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Golden Numbers, Scoring and Grading Systems

Characterise symptoms => ask around cause => ask around effects => ask around predisposition and past history => check off red flags => check of pitfalls and masquerades.

Go to Resources
Haem/Onc Heart Lungs Kidneys: Kidney Health Australia Neurol Gastro/Surg Endo Urol Infectious: ASHM website (National STI Management Guidelines, Sexual Health Society of Victoria). ASHM = Australasian Society for HIV Medicine, Viral Hepatitis and STIs. Hepatitis Australia Information Line, Hepatitis Resource Centre website Immun/Allergy:, Aus Prescriber Anaphylaxis Wall Chart Paeds: Royal Children's Hospital Clinical Guidelines ( Health for Kids Guideline Development Group. Women's Men's Mental Health: GP Psych Support Rheum Ortho/Sports: Hands @ Australian hand therapy association. Derm ENT/Maxfax Opthalm Burns: Alfred Hospital and Royal Children's Hospital Melbourne have guidelines ( DKA: Asutralian Paediatric Endocrine Group A guidelines.

Killer disease rankings:

1. Ischaemic heart disease (the second most common cause of death among 35yos!). 2. Stroke, 7% men 11% women, 1 every 10 minutes (all cancers combined trumps stroke as 2nd highest cause) 3. Alzheimer's dementia 4. Trachea, bronchus and lung cancer

Cancer morbidity/mortality
Commonest 2003 (Combined): NMSC, Bowel, Breast, Prostate, Melanoma, Lung. Commonest 2003 (Men): NMSC, Prostate, Bowel, Lung, Melanoma. Commonest 2003 (Women): NMSC, Breast, Bowel, Melanoma, Lung. Biggest killer 2003 (Combined): Lung, Bowel, Prostate, Breast, Pancreas (a 2011 HTT article puts pancreatic cancer 4th). Biggest killer 2003 (Men): Lung, Prostate, Bowel, Unknown Primary, Pancreas. Biggest killer 2003 (Women): Lung, Breast, Bowel, Unknown Primary, Pancreas. Gastric cancer: Second highest cancer killer worldwide, though incidence falling. Cancer with most rapidly increasing incidence worldwide? Oesophageal cancer (among overweight, middle aged men with GORD). Highest incidence in Japan (also China).

Chemo side effects: Neutropaenia, NVD, skin changes, peripheral neuropathy, tiredness, hair loss, mouth ulcers.

Known Familial Cancer Syndromes

Peutz-Jehgers syndrome (STK11/LKB1 mutation) Familial breast cancer (BRCA and BRCA2 mutations) Familial atypical mole melanoma syndrome (with p16 mutation) Hereditary pancreatitis (PRSS1 mutation).

Prognosis including 5-Year Cancer Survival Rates

Overall 5-year survival all cancers? 58%. TCC bladder: Superficial (75%) >80%, Invasive 50-60%. RCC: T1 90-100%, T2-3 60%, mets 0-20%. Prostate cancer 10yr survival with active surveillance? 95%. Chance of RCC <3cm metastasising: 0.2%. 5yr survival for first stroke? <50%. 10yr survival for first stroke? 20%. How much higher is mortality among PD patients overall? 2-5%. What is the reduction in life expectancy as a result of MS? 5-10 years. Proportion of MS patients with significant disability at 5yrs? 5%. Proportion of MS patients disability free at 20yrs without therapy? 10-20% (80% of RRMS eventually transition to secondary progressive, lose ability to walk independently and many dement). Over what period do most MS pts become disabled? 2-4 decades. What percentage of PD patients have dyskinaesias + fluctuations in response to levodopa at 6 years? 75%. What is the acute vestibular syndrome substantial-complete recovery rate with high dose corticosteroids (methylpred) at 12mo? 76%. What is the prognosis of motor neurone disease? Progressive disability and death within 2-3 years. What is the prognosis of Ramsay Hunt? Little data, but generally poorer than Bell's palsy with age and diabetes poor prognostic indicators (tight glycaemic control recommended). What is the age-adjusted mortality risk for Alzheimer's? 4-fold. What is the age-adjusted mortality risk for FTD? 6 to 8-fold. What proportion of NAFLD patients die of cirrhosis? Simple steatosis rarely progresses. Non-alcoholic steatohepatitis tends to progress over time, but tends to be less histologically severe and progresses more slowly than alcoholic steatohepatitis. It may stay stable for a number of years. 9% with steatohepatitis progress to cirrhosis and 30% of these die within 10 years (ie 2.9% of people with non-alcoholic steatohepatitis die of it). What is the rate of HCC in cryptogenic cirrhosis? 7%. What proportion of diabetics have NAFLD? 49-75% (and diabetes is a poor prognostic indicator for all negative end-points in NAFLD including the most common cause of death, cardiovascular death). Untreated HCV: At 20yrs (47% moderate liver damage, 7% cirrhosis, 1% liver failure or cancer); at 40yrs (45% moderate liver damage, 20% cirrhosis, 5% liver failure or cancer). Prognosis of children infected with HBV? 1/4 die of cirrhosis or liver cancer. Gastro-oesophageal cancers? <30% at 5yrs overall (but very much depends on type and stage). Colorectal cancer diagnoses that eventually die of the disease? Just under half. 5 year survival according to ACPS stage: A 90%, B 70%, C 50%, D <10%.

Pancreatic cancer? 5% 5-year survival, 90% dead within a year. Gastric cancer 5-year survival? 25%. What is the 5-year survival of T1 and T2 laryngeal cancer with laser surgery + radiotherapy => 85%.

Grading and Classification Systems

TNM grading system: TX (primary tumour can not be assessed), T0 (no evidence of primary tumour), Tis (carcinoma in situ), T1 (invasion of lamina propria ie mucosa/submucosa), T2 (invasion of muscularis propria), T3 (invasion of adventitia/serosa or surrounding fat), T4 (invasion of surrounding organs/structures or peritoneum). NX (regional nodes can not be assessed), N0 (no regional node metastasis), N1 (1-2 node regional metastasis for OG cancer, 3-4 nodes for colorectal cancer), N2 (3-6 node regional metastasis for OG cancer, >4 nodes for CRC), N3 (>7 node regional metastasis). MX (not able to assess distant mets), N) (no distant mets), N1 (distant mets). Renal cysts: Bosniak categories 1-4 (1 is simple cyst, 2 probably benign cyst, 3 probably malignant, 4 definitely malignant based on septation/calcification, wall thickness, density) Renal cell carcinoma (usually clear cell carcinoma): Fuhrman grading system based on nuclear characteristics of RCC. Bladder cancer (urothelial cell carcinoma): Muscle invasive (cystectomy + urinary diversion + lymphadenectomy + adjuvant chemo if node positive +/- neoadjuvant chemo to shrink tumour before surgery) vs non-muscle invasive (transurethral resection of all visible tumours and adjuvant intravesical BCG for high grade tumours). TNM classification used. Prostate cancer: Gleason scoring system based on 5 histological patterns of cancer (helpfully numbered 1 to 5) => pathologist identifies two most prevalent patterns and adds their numbers together => in practice, combinations of patterns 1 and 2 rarely reported => Gleason 6 (3+3) has a fairly good prognosis, 7 is intermediate (3+4 is better than 4+3, as 3 predominates), and Gleason 8-10 tumours have poor prognoses. Prolapse: Grade 1 (into vagina), 2 (to introitus), 3 (outside vagina), 4 (completely outside vagina). Erectile Dysfunction: Sexual Health Inventory for Men (Mnemonic: See HIM). Prostatism/LUTS: International Prostate Symptom Score Sheet: <7 mild (manage with watchful waiting), >8 mod-severe (urodynamics then decide). Risk of BPH progression: IPSS >8, age >70, PSA >1.4, Qmax <12, residual >100mL. What is the bacteriuria cutoff for diagnosis of UTI on MSU? 10^5 colony forming units per mL. MS severity? Kurtzke Extended Disability Status Scale (EDSS): 0-1 no deficit, 6-7 wheel chair, 8-9 bedbound. Stroke severity at presentation? National Institute of Health Stroke Scale (NIHSS) .. useful pre-hospital and in ED. Indication for admission follow the NINDS (National Institute of Neurological Disorders and Stroke) score .. and NINDS is also where the 3h rule for rtPA use comes from. What are the differentials of stroke in GPland? Migraine, hypoglycaemia, seizures. TIA score ? need for urgent specialist assessment. ABCD2 score (age>60 = 1, BP>140/90 = 1, clinical/unilat-weak=2.aphasia-only=1, duration>60min = 2, less = 1, diabetes = 1), >4 need assessment in <24h, >7 is highest risk. Low risk => review in <2wks. What proportion of TIA clinic attendees don't have TIAs? 1/3. CHADS2-VASC for anticoagulation in AF: 0 = aspirin or nothing; 1 = aspirin or warfarin; >1 warfarin. Check HAS-BLED score for bleeding risk. C: CHF, HTN, A>75yo=2pts, DM, Stroke (or TIA), Vasc Dx, A>65yo=1pt, Sex=F. Warfarin is generally underutilised in AF. Classification of strokes (TACI/LACI/PACI/POCI): Oxfordshire Community Stroke Project subgroups .. based on clinical presentation and useful for

prognosis, as opposed to TOAST classification which is based on investigation findings and potentially more useful in guiding treatment. Severity of Sporadic Idiopathic Parkinson's Disease: Hoehn and Yahr stage 0: no signs of disease; stage 1: unilateral disease, no impairment of balance; stage II: bilateral disease, no impairment of balance; stage III: balance impairment, mild to moderate disease; physically independent; stage IV: severe disability but still able to walk or stand unassisted; stage V: wheelchair-bound or bedridden unless assisted. Modified H&Y Scale has additional 1.5 and 2.5 scores. Global severity assessment encompassing impairment and clinical findings. Severity of Parkinson's Disease: Unified Parkinson's Disease Rating Scale (score >30 severe), designed to monitor impairment. Depression Scales: Beck Depression Inventory, Geriatric Depression Scale. ADL scale for use in dementia? Dementia outcome measurement suite. Cognitive function: MMSE, GPCog, RUDAS for migrants, KICA for ATSIs. C-spine injury imaging criteria: Follow either NEXUS (sens: 99.6%, spec: 12.9%) or Canadian C-Spine (sens: 100%, spec 42.5%). Controversial which is better. NEXUS criteria (1 out of: midline tenderness, altered LOC, focal deficit, probable intoxication, distracting injury => image). If imaging indicated, immobilise neck immediately. Traumatic Brain Injury: International Classification of Diseases (ICD) injury severity score. When to do CT for head injury in kids: British CHALICE guidelines (Children's Head Injury Algorithm for Prediction of Important Clinical Events): Witnessed LOC >5mins, amnesia >5mins, abnormal drowsiness, 3+ episodes vomiting, clinical suspicion of nonaccidental injury, post-traumatic seizure in non-epileptic, ED GCS <14 for child <15 in infant, suspect open/depressed skull fracture or tense fontanelle, evidence of BOS#, focal neurological deficit, lesion >5cm in infants, high impact trauma. Not validated but useful. Stool type: Bristol stool chart. Chronic HCV fibrosis: Metavir scoring system: 1 (mild) to 4 (severe) based on findings of enlargement of portal system, septae, cirrhosis. Oesophageal cancers: Siewert classification: Type I (above GOJ) and Type II (through GOJ) => oesophagectomy; Type III (below GOJ) => total gastrectomy. TNM classification used to grade them. Barrett's oesophagus: No dysplasia (87%), low grade dysplasia (11%), high grade dysplasia (1.2%). NHMRC and Australian Cancer Network screening guidelines CRC risk categories? 1. Cat 1: No family history. FOBTs q2yrs (biannually) from 50yo stopping at 75yo with consecutive negative tests. 2. Cat 2: 1 first degree family member with CRC at >55yo. FOBT biannually and consider sigmoidoscopy every 5 years. 3. Cat 3: 1 first degree relative with CRC at <55yo or 2+ first or second degree relatives on same side of family with CRC at >55yo? Colonoscopy every 5yrs from 50yo or 10yrs younger than first case, FOBTs annually in intervening years. 4. Cat 4: 3+ relatives on same side of family with CRC or any of the following: 2+ relatives with multiple cancers in same person, CRC with multiple adenomas, CRC at <50yo, family member with known relevant gene mutation=> genetic screening, bowel cancer specialist, annual scopes from 12-15yo in FAP (then drop back to q3yrs at 3035yo), scopes q1-2yrs from 25yo or 5yrs younger than first diagnosed relative in HNPCC, consider FOBTs in off years. CAPP2 trial supports aspirin for pts with HNPCC genes. FOBTs: faecal immunochemical test better than guaiac test. 5. What frequency of colonoscopy screening in pts with HNPCC family history? Yearly (accelerated progression of disease). Hereditary Non-Polyposis Colorectal Cancer: When to refer for genetic testing: (1) Bethesda guidelines; (2) Amsterdam criteria (when genetically proven diagnosis not possible).

1. Bethesda: CRC<50yo, more than one tumour (in time or space), tumour with MSI-H histology and <60yo, HNPCC tumour in <50yo relative, 2+ relatives with HNPCC. 2. Amsterdam: >3 cases in family, (>2 first degree relatives, two successive generations affected, >1 case at <50yo, FAP excluded). Colorectal cancer: Australian Clinico-Pathological Staging System (ACPS .. a modification of Dukes classification) => A (tumour confined to bowel wall: T1/T2 N0, 90% five year survival), B (tumour invasion through bowel wall: T3/T4 N0, 70% five year survival), C (N1 M0 any stage of tumour invasion, 50% five year survival), D (M1, <10% five year survival). Haemorrhoids symptom grades based on history not examination: Grade 1 (internal, never prolapse, only symptom bleeding), Grade 2 (prolapse on straining with spontaneous reduction, symptom regular bleeding), Grade 3 (prolapse on straining and need to be replaced manually but then stay there), Grade 4 (permanently prolapsed or if replaced reprolapse on walking or mild exercise, symptoms can include itching, throbbing, paradoxically less bleeding). Pancreatitis: Ranson's criteria => uses various haematological and biochemical parameters as well as vitals and age at admission and at 48h to predict outcomes. Burn size? Patient's palm+fingers surface area = 1%. Rule of 9s for adults, Lund and Browder chart for kids. Depth of burn = cap refill and pain (superficial dermis = painful, pink with brisk cap refill .. progressively less painful until full thickness, painless, paler wound). Superficial or epidermal burn = first degree (red, pain, no blisters); partial thickness or dermal burn = second degree (red, pain, blisters, less pain/colour as as burn goes deeper); full thickness = third degree (white, dry, painless). Dermal burns: Superficial => red, blanches with brisk CRT, painful. Deep => mottled, sluggish CRT, less painful. Sports head injuries: SCAT2: Sport Concussion Assessment Tool 2. Chandler's stages of orbital cellulitis: (1) Preseptal: eyelid swelling, no proptosis , opthalmoplegia or loss of vision; (2) Orbital cellulitis: inflammation of orbital fat; (3) subperiosteal abscess; (4) orbital abscess; (5) cavernous sinus thrombosis.

Diagnostic Criteria
MS: 2010 McDonald criteria => 2 attacks and 2 objective clinical lesions separated in time and space, no further investigations required for dx. Less than this, need MRI to confirm. In reality, MRI is always sought. Evoked potentials also useful. CSF in unclear cases to distinguish from tumours (oligoclonal bands not specific to MS though), infection, inflammatory disease. Aquaporin 4 antibodies help distinguish MS from Devic's. PD: UK Parkinson's Disease Society Brain Bank criteria: Bradykinaesia + 1 other feature (rigidity, resting tremor, postural instability) and other causes ruled out. But always refer to neurologist for diagnosis. Migraine and migrainous vertigo: International Headache Society criteria for migraine and Migraines are >5x headaches lasting 4h-3d and >2 of 1. unilateral, 2. throbbing, 3. moderate-severe, 4. aggravated by routine activities causing avoidance behaviour, 5. nausea/vomiting or photo/phonophobia, 6. secondary cause ruled out by investigations or not likely on history (5-60min aura). Neurhauser criteria for migrainous vertigo (one criteria & exclusion of other diagnoses). Post-concussive syndrome: Head injury with LOC preceding symptoms by maximum of 4 weeks + >3 out of headache/dizziness/lethargy/noise-intol; irritability/lability/depression/anxiety; subjective cognitive/memory/concentration problems but no neuropsychiatric findings; insomnia; reduced alcohol intake; preoccupation with fear of brain damage and taking on sick/hypochondriachal role.

Irritable bowel syndrome: Rome III criteria, but no symptom/test pathognomonic: >6mo, >3d per months for last 3mo. Recurrent abdominal pain or discomfort with 2+ of the following: Improvement with defaecation, change in frequency of bowel motions, chnge in form of stool (Bristol stool chart).

Fractures and Injuries

Thumb injuries: 1. Bennett fracture: Thumb jammed end on fracturing base of 1st carpometacarpal and displacing digit proximally. Intra-articular fracture dislocation of 1st carpometacarpal (medial fragment attached to volar ligament and rest of metacarpal displaced proximally by pull of adductor pollicis longus and adductor pollicis => inherently unstable, needs referral to hand surgeon). 2. Skier's thumb (acute) aka gamekeeper's thumb (chronic)? Thumb MCP sprain of ulnar collateral (often forced abduction/hyperextension in ball sports) => pinch grasp painful and weakened => complete tear needs surgery. Stener lesion if ruptured ligament sits outside adductor aponeurosis => painful lump best observed from dorsal view. Metacarpal fractures: Transverse fractures => reduce and immobilise in thumb spica cast. Finger extensor tendon rupture 1. Mallet finger (extensor tendon rupture at DIP): Forced flexion injury of DIP, rupture of extensor tendon or avulsion # => can present normally and develop flexion deformity => isolate DIP in resisted ROM => requires surgery (treatable up to 3mo) and strict use of splint. 2. Boutonierre deformity (extensor tendon rupture at PIP): PIP hyperflexion injuries/dislocations presenting already reduced and unremarkable => occult extensor digitorum rupture => boutonierre deformity over time if not referred for repair. Finger flexor tendon rupture and volar plate fracture: 1. Flexor tendon rupture: Grabbing, missed tackle incident, forced extension => finger in relative extension compared to others =>urgent xrays for associated avulsion # and immediate referral as irreparable after 7-10d. 2. Volar plate (finger) fracture (EASILY MISSED): Finger jammed by ball => forced hyperextension of PIP => avulsion fracture of volar (palmar) plate => permanent loss of function if not identified and managed with special exercises and splint.

Drug Doses
Paracetamol: 15mg/kg QID Ibuprofen: 10mg/kg TDS Amoxicillin: 40-50mg/kg/d in 3 divided doses

Golden Numbers
What is the prevalence of TB globally? 1/3. Endocrinology What target serum Vitamin D should be aimed for in replacement therapy: 50nmol/L. At what TSH should thyroxine treatment be offered regardless of T4/T3: 10 (normal is <2.5). What is a normal thyroxine replacement requirement 1.6mcg/kg (start with 50mcg in the elderly or in pts with high TSH but normal T4, 25mcg in frail elderly). What is the target TSH in replacement therapy? 0.5 - 5 traditionally, new evidence suggests 0.3 - 3 better. What is the recommended daily calcium intake? 1200mg.

What HbA1c is required to diagnose diabetes? 6.5%, 48mmol/mol. What target HbA1c should be aimed for with treatment? 7%, 53mmol/mol. How much daily insulin does a type 2 diabetic typically require? Normal insulin requirement: 0.5-2IU/kg/d. How much daily insulin does a type 1 diabetic typically require? 0.5-1IU/kg/d. How to start insulin? If pt on maximal oral therapy, with symptomatic hyperglycaemia (BSL >15, HBA1C >9), start insulin at once. Starting doses: Basal insulin start with 10 (aiming for FBG 6, some say 5.5). Rapid-acting insulin start with 4 (aiming for postprandial BSL 15 at 2h: don't aim too low ie <8 as rapid-acting insulin isn't that rapid and delayed hypos common). Pt directed increases of 1 unit a day of basal insulin (of 5U every 2-3d), or go by the following: if fasting BSL <4.4/hypo cut by 2u ... is 4.5-7.0 don't change ... if 7.110.0 increase by 2u ... >10.0 increase by 4u. For morning dose, go on previous predinner BSL, for evening dose go on FBG. What to do about insulin dose if planning to eat a big meal? Add 2-4U insulin, monitor BSL and make a note for next time. What to do about insulin dose if exercising+++? Cut insulin by 25-50%, monitor BSL and make a note for next time. Urology How to manage kidney stone according to size? <5mm will probably pass, those <1cm & asymptomatic can be watched (xray at 6mo then annually, or US/CT if stone lucent), those >1cm (or <1cm but sympt) need treatment with SWL day surg, those >1.5cm need treatment with percutaneous nephrolithotomy, difficult involving narrow calyces may require open nephro/pyelolithotomy. Will the ureteric stone pass? >7mm unlikely to pass, 4-6mm 50% pass, <2mm 95% pass. If no infection, give it 4wks to pass (drinking water won't help as body sends water to other kidney). Proportion of people over 50yo with renal cysts? 50%. Proportion of RCCs diagnosed incidentally? 50% (classic triad of loin pain, palpable mass and haematuria now rare). Renal mass size indicating better prognosis? <4cm (Up to 1/3 are benign and if malignant, many are slow growing and have excellent post-nephrectomy prognosis). Proportion of RCC pts with mets at time of diagnosis? 1/3 Definition of urinary frequency? >8 voids in 24h. Definition of polyuria? >40mL/kg/d. Definition of nocturnal polyuria? >20-30% daily urine passed at night. % of men with bladder outlet obstruction who also have detrusor instability? 40-50%. Frequency of UTIs needed to justify prophylactic antibiotics: >3-4. Chronic postvoid residual associated with UTIs? >30mL. Large postvoid residual? >200mL = probable detrusor dysfunction = poor response to treatment likely. What is considered to be a low bladder capacity in urodynamic filling tests? 400mL. What is considered to be a normal detrusor pressure rise during urodynamic filling tests? 10cm H2O. What pressure rise during filling tests indicates detrusor instability? 15cm H2O. What proportion of men develop prostate cancer in their lifetime? 1 in 9 (80% of 80yos). What is the male patient's lifetime risk of dying of prostate cancer? 3%. What is the lowest TNM grade of prostate cancer can be palpated on DRE? T2 (still confined to prostate .. vs T3 which has breached the capsule or involves seminal vesicles). DRE is used as a means of clinical staging. What proportion of suspicious nodules detected on DRE turn out to be malignant? 1/3.

At what age is it reasonable to start screening for prostate cancer? 55yo (PSA and DRE) or at 40yo if any family history (can do a one-off at 40 to help stratify future risk. What prostate cancer detection rate does the recommended biopsy cut-off of 2.5ng/mL provide? 36%. What PSA velocity is an indication for biopsy? 0.35ng/mL/yr (other indications: PSA above age specific reference range, abnormal DRE). 0.03ng/mL/yr is average in a pt without prostate cancer. Velocity >0.35ng/mL/yr => 5 fold risk of prostate cancer death. Old threshold of clinical significance 0.75ng/mL/yr too high. What are the significant PSA doubling time (PSADT) values for inferring whether a cancer is localised or metastatic? <9mo likely metastatic, >1yr likely localised to prostate. What are the useful free-to-total PSA ratios helpful in discerning prostate cancer from other pathology (Catalona trial)? FTTR >25% reassuring (90-98% detection rate and if cancer present, probably not clinically significant); FTTR <10% suspicious for cancer (cancer releases more bound PSA, BPH releases more free PSA). What PSA level in men with prostate cancer indicates searching for mets? >20ng/mL. After surgery, what PSA level indicates biochemical recurrence and the need for salvage radiotherapy? 0.2ng/mL. When should PSA be undetectable after prostatectomy? <12wks (if not, cancer persisting). After radiotherapy for prostate cancer, what PSA indicates biochemical recurrence? 2.0ng/mL above the nadir (Phoenix definition). When is the PSA nadir after prostatic radiotherapy? c18mo. What proportion of patients undergoing TRUS prostate biopsy suffer sepsis as a complication? Up to 3% (sometimes with a 2-3 day delay). How often should PSA be repeated after radical prostatectomy? At 6-12 weeks, then every 6mo for 5yrs (every 3-4 months if Gleason >8), then annually. How much increased risk does one first degree family member with prostate cancer confer on a man? 2.5 fold. What is the reported NNT for prevention of prostate cancer deaths by screening? About 1400 (less than that of breast screening at about 1500). How many prostate cancers need to be treated (this includes by active surveillance as well as surgery or radiotherapy) to save 1 life? 48. What is the incidence of urinary incontinence 12 months after radical prostatectomy? <10%. What proportion of previously potent men experience erectile dysfunction after radical prostatectomy compared to external beam radiotherapy or brachytherapy? >50% for ERBT and prostatectomy, 40% for brachytherapy (EBRT impotence tends to have delayed onset, while that of surgery tends to be at its worst immediately after and gradually improve). What proportion of men having brachytherapy get acute urinary retention? 10% (urethral strictures also in 10%). What is does active surveillance of prostate cancer involve? DRE and PSA q3mo for 2yrs then q6mo. Biopsy at 6mo and 18mo then q5yrs. What proportion of men experience erectile dysfunction? 40% of adult men to some degree, 1/4 in 50-60yo age group rising to almost 3/4 of 70yos (c10% of non-diabetics and c30% of diabetics develop complete erectile dysfunction). What spinal nerve levels control micturition and erections in men? S2-4 (pudendal nerve). What percentage of healthy men with erectile dysfunction have penile arterial disease visible on Doppler? 90%. Below what serum testosterone level will supplementation have a benefit in terms of improved erections? <7nmol/L (however there is no agreement on a definite level at which replacement should be considered and testosterone has more effect on libido than erections). When and what treatment should be offered for erectile dysfunction after radical prostatectomy? PDE5 inhibitor trial at 6wks (efficacy depends on whether nerve sparing

surgery possible), then prescribe PGE1 injections or vacuum device with periodic (q3mo) testing of PDE5 inhibitors for nerve recovery. What proportion of men with Peyronie's disease spontaneously recover? Rule of thirds. Over period of 2 years, 1/3 recover, 1/3 stay the same and 1/3 deteriorate. How much earlier does ED occur in diabetics? 10-15 years. What is a normal urinary flow (Qmax)? >20-30mL/sec in women, >15mL/sec in men. What erectile dysfunction figure has traditionally been quoted for patients post-TURP? 58%. How many men experience retrograde ejaculation post-TURP? 70%. How many men suffer post-TURP urethral strictures? 3-5%. What percentage of men still have LUTS after surgical procedure for BPH? 40%. Neurology Mean age and gender of MS patients? 3s & 4s: 30-40yo, 3/4 female. What proportion of MS cases are primary progressive? 15-20%. How effective are B-interferons and glatiramer in MS? Prevent progression from CIS to definite MS, reduce relapse by 30% and also number of active lesions on MRI. What effect do B-interferons and glatiramer acetate have in MS? 30% reduction in relapse and 50% reduction in relapse on MRI. How long does a TIA last? 1-24h with no imaging changes (>60mins scores higher on ABCDE2 for increased risk of CVA, so >1h bad). What is the risk of a TIA patient having a stroke within a week? 5-7%. What percentage of stroke patients restroke within a year? 8-12%. What proportion of strokes are ischaemic? 85% (5% SAH, 10% Primary Intracerebral Haemorrhage). What is the definition of crescendo TIA? 2 in a week (disregard ABCD2 and refer). What is the sensitivity of CT for subarachnoid haemorrhage at 1wk? 50% (the later the presentation the worse the sensitivity .. opposite for infarcts). When do ischaemic brain infarcts become apparent? 48-72h. What is the limit for thrombolysis post-CVA? 3h (evidence suggests useful even beyond this period to 4.5h but not beyond this .. advanced imaging can detect penumbra). What proportion of stroke patients currently receive rtPA? 10% .. delayed presentation and lack of local facilities or expertise limits use. Early assessment by stroke team = good outcome (phone advice by stroke team better than nothing). What is the "NNT" of rtPA? 10 (extra 1 in 10 leaves hospital independent, at cost of 7 haemorrhages, 4 fatal). What is the "NNT" for aspirin? 100 (but recommended to exclude haemorrhage before giving or continuing antiplatelet). What is the "NNT" for stroke unit? 25. Is immediate anticoagulation beneficial in CVA? No. Aspirin vs lifestyle in secondary ischaemic stroke prevention? Lifestyle 3x as effective over long term (esp maintaining normal BP). Aspirin dosage in secondary iscaemic stroke prevention? 160-300mg/d. What about pts with PICH haemorrhagic strokes on blood thinners? Stop, reverse if possible, in general don't restart. What level of stenosis for carotid endarterectomy? 70% and symptomatic (other factors include age, gender, if stenosis smooth or ulcerated and if CVA/TIA/eye-event). The earlier the better and CAE generally better than stenting. What chance of stroke with carotid endarterectomy? 20-30% in 3/12 (CEA marginally favoured over stenting in terms of risk reduction at this time). CVA badness: >60yo, >60mins, sugar, shitty BP 140/90, signs on one side.

What proportion of TIA presentations have ischaemic strokes? 50%. At what stage would you try to lower BP in acute stroke? About 230/140 in ischaemic stroke or 180/110 for haemorrhagic stroke. Don't try to lower BP (esp in pt with potentially compromised swallow) outside hospital. Drugs approved to lower BP in stroke pts are labetolol, hydralazine, clonidine. What are the 7d and 1mo mortality rates for stroke? 10 and 20%. What proportion of low risk strokes (PACI, POCI, LACI) are independent at 1yr? 50%. What is the bleeding complication rate for thrombolysis in stroke? 7 in 100. What reduction in future vascular events does smoking cessation bring? Halves it. What is the secondary risk reduction achieved in lowering BP by 12/5mmHg? 43% at 4yrs. What benefit does a 1mmol/L reduction in LDL give? 1/4 less vascular events in 5 years. What is the annual risk of major bleeds using aspirin and clopidogrel together? 1%. What is the incidence of PD in patients >60yo? 1% (falls with increasing age). What is the prevalence of PD? 4.5-21 per 100,000. What proportion of PD diagnoses are disproven on autopsy? 25%. What proportion of typical PD patients have a family history compatible with austosomal dominant or recessive inheritance? 10-15%. What proportion of IPD patients never have a tremor? 25%. How frequently is single Epley manouevre successful in BPPV? 85%. How long does recovery from acute vestibular neuronitis take? 3-5 days for acute phase of contiuous vertigo and vomiting, but up to a year to learn to compensate for loss of balance. What proportion of AVS patients never regain vestibular function? 30-70%. What proportion of AVS patients respond well to high dose steroids? 76%. What age group get BPPV? >50yo. How long should benzos be used in acute vertigo? 24-48h How long does BPPV take to resolve? 6-8 weeks untreated. 24-48h treated. What proportion of vertigo has inner ear as its source? 85%. What proportion of alert, neurologically intact minor trauma pts with normal CT but persistent midline C-spine tenderness have C-spine, disc, ligamentous injury identified on MRI? 21% (cervical spondylosis strongly associated with injury severity). How much longer do MND patients survive on Riluzole? 3-6mo. How much survival benefit does non-invasive ventilation have for MND patients? 12mo. When does MND strike? 40-60yo. What proportion of MND patients suffer cognitive impairment? 60% (so possible link to other neurodegenerative disease especially frontotemporal dementia). What is the average time from onset of symptoms to diagnosis in MND? 14mo (the earlier the better so biopsychosociospiritual needs of patients can be met and affairs put in order). What proportion of MND patients are living at home 4 weeks before death? 70%. How frequently does Bell's palsy recur? 12% of cases. Age of onset of various dementias? FTD 40-60yo (similar to MND), PD >55yo increasing with age then decreasing among elderly, PSP >60yo, Alzheimer's/vascular/alcoholism incidence increases with age. What proportion of early-onset dementia is FTD? 10-12% (after Alzheimer's and vascular, alcohol is fourth). Where do the dementias rank in later life? Alzheimer's, vascular, mixed, dementia with Lewy bodies, FTD, PD. What proportion of Alzheimer's pts respond to cholinesterase inhibitors? 20-30%. How many TBI patients will recover from depressive sequelae spontaneously? 50% (sertraline proven effective treatment .. also try music therapy, exercise, counselling). How soon after mild TBI do cognitive deficits resolve? 1-3 months (in mod-severe cases,

can continue improving for 2 years). How many post-TBIs have personality changes 12mo out? >50% (irritability, impatience, depression, dixfficulty socialising, apathy). How many post-TBI patients have irritability and depressive temperament at 5yrs? >60% and >40% respectively (can be chronic problems). What proportion of TBI patients are legally intoxicated on presentation? 42%. What is legal intoxication? >100mg/dL blood alcohol. What is the sensitivity and specificity of CAGE questionnaire following TBI? 86% and 91%. What proportion of post-TBI patients develop epilepsy? 10%. How often do chronic daily headaches occur? >15d/mo. How long do prolonged headaches last? >4h. What are the different types of brief (<4h) episodic (<15d/mo) primary headaches? Cluster headaches, trigeminal autonomic cephalalgia, idiopathic primary stabbing headache (vs prolonged headaches like migraine and tension headache, while episodic primary triggered headaches have varying duration). What are the most frequent brief (<4h) primary headaches? Chronic cluster headache, chronic paroxysmal hemicrania, short-lasting unilateral neuralgiform headache attacks wth conjunctival injection and tearing (SUNCT syndrome) (vs chronic migraine, chronic tension headache, hemicrania continua which last >4h). What are the 1st, 2nd, 3rd commonest forms of headache? Tension headache, systemic infection, migraine. What to do if suspecting SAH at >7d? CTA (within 7d = CT and if normal LP). How long off work for BPPV? 1 week to return to normal activities. Gastroenterology: What percentage of people >60yo develop diverticulae? 60% (mostly sigmoid due to pressure forcing mucosal lining through weak points in muscularis). What percentage of people >60yo get symptomatic diverticulitis? 10-20% (15% of this number get complications). What is the gender breakdown of IBS? Twice as many women as men. Where does IBS rate as cause of absenteeism? Second highest cause after colds. Increased incidence of Coeliac antibodies and biopsy changes in people with IBS symptoms? 3 fold and 4 fold. Prevalence of microscopic colitis in IBS-D patients? 2.3%. What caecal diameter on xray is a concern in terms if perforation risk? 10cm. What is the estimated prevalence of NAFLD? 20-30% (with 3-5% having the more advanced form non-alcoholic steatohepatitis). Histological definition of NAFLD? Hepatic steatosis of >5%. What proportion of the obese are estimated to have hepatic steatosis and non-alcoholic steatohepatitis? 75% and 20%. What is the current (2012-3) rate of childhood obesity in the USA? 30%. What is the association of PCOS with NAFLD? Strong association (PCOS is a marker for NAFLD as 40-50% of PCOS-sufferers have NAFLD). What proportion of cryptogenic liver disease patients are obese or diabetic? 50-75% (NAFLD common in diabetics, not diabetes common in NAFLD). What proportion of NAFLD patients have metabolic syndrome? 30%. What weight reduction can significantly reduce hepatic steatosis? Modest loss of 5-10%. What proportion of people aiming to lose weight manage to maintain 10% wt loss to 1yr? <20% (and most of them regain most if it over the following 3-5yrs). What additional risk of NAFLD does high waist to hip ratio cause in normal weight middle

aged men? Doubles it. How many Australian have been exposed to Hep C (2013 article, 2010 figure)? c304,000 (267,000 living with chronic Hep C). What age group has the most Hep C sufferers? 20-39yo (65%). What proportion of new HCV patients are IV drug users? 90% What proportion of Hep C sufferers in Australia have moderate to severe disease? 48,000. What proportion of acute Hep C infections are symptomatic? 10% (rarely causes acute liver failure). Whta is the rate of sampling error on liver biopsies for HCV? 20%. What are the most prevalent HCV genotypes in Australia? GT 1a and 1b at 55% (then HCV 3). What percentage of Hep C patients clear the virus and over what period? 15-40% over 2-6 months (Check says 25%). What proportion of Hep C patients go on to suffer chronic infection and complications? 85% develop chronic infection. 20% of these progress to advanced liver disease with cirrhosis +/HCC over 20-30 years. What is the likelihood of dying of HCC (a common complication of chronic Hep C) within a year of diagnosis? 33%. What proportion of Hep C liver transplant patients have cirrhosis in the transplanted liver at 5 years? 30%. What is the risk of heterosexual Hep C transmission? <5%. What is the risk of vertical Hep C transmission? Up to 5% (15% if HIV positive). What is the overall potential cure rate of HCV? 70%. Which Hep C genotypes respond well or poorly to antivirals? Poorly => GTs 1 or 4 (40-50% sustained viral response, or with new triple therapy in the immuno-naive up to 70%); Well => GTs 2 and 3 (70-80% SVR). SVR is absence of virus at 6mo, which equates to 99% chance of remaining negative on long term follow up. What is central obesity? Waist >94cm in men, >80cm in women. What is an elevated fasting BSL? >5.6mmol/L. What is raised BP in context of screening for metabolic syndroms in young person? >130/85. What is the cut-off for elevated triglycerides? 1.7mmol/L. Biochemical definition of cholestasis? ALP >200U/L (>2x ULN, or ALP:ALT 3:1). Causes include biliary obstruction, preg, erythromycin/oestrogen, infiltration eg malignancy). Common picture is ALP >2x ULN + GGT >5x ULN + ALT <5x ULN ... ALT rise doesn't occur in pregnancy. Biochemical definition of hepatocellular damage? ALT >200U/L (>5x ULN or ALT:ALP 3:1). Causes include Hep ABC, EBV, CMV, alcohol, fatty liver, paracetamol, metal overload, hypoxia, autoimmune disorders). Common picture is ALT >5x ULN + elevated GGT and ALP <2x ULN. AST/ALT ratio suggestive of alcohol as cause of deranged LFTs? >2.. AST/ALT ratio consistent with cirrhosis? >1 (HTT 2010 says ALT:AST <0.8). In regard to ribavirin teratogenicity, how long after finishing Hep C treatment should a patient wait before conception? 6mo. Serological criteria for HBV referral for consideration of treatment? HBV DNA >2000IU/mL and ALT >1-2x normal (HTT 2010 says >10,000IU/mL). What proportion of patients clear HBV infections from serum and from liver? 95% in 2-6mo from serum, HBV never cleared from liver so in older age or immunosuppression the disease can flare up again. How often to surveill for HCC? If no FHx and no cirrhosis, AFP and ultrasound every 6mo.

What HBV DNA level in a pregnant woman is the threshold for antivirals to prevent vertical transmission at birth? >107IU/mL. Treatment is in addition to standard HBV vaccine and HBIg given at birth. In what proportion of dysphagia (difficulty swallowing) cases can cause be identified on history alone? 85%. What is the perforation risk for a routine diagnostic upper endoscopy? 1: 10,000 (1-2% if dilatation required). What group is affected by eosinophilic oesophagitis? Caucasian men aged in their 20s and 30s. How effective is the six-food elimination diet in eosinophilic oesophagitis? Reduction of symptoms in 90% of patients. What proportion of the general population have Schatzki's rings? 7%, most asymptomatic. What is the risk and suggested surveillance of Barrett's oesophagus? 0.5%/yr risk of oesophageal adenocarcinoma. Surveillance endoscopies with biopsy every 2-3 years. How long does the effect of botox injections last (eg in achalasia)? 3-6mo. What initial response rate does balloon dilatation have in achalasia? 90%. How about surgical myotomy for achalasia? 95% (better longevity of relief with 85% still symptom free at 5yrs). What proportion of the Australian population have IBS? 10%. What is the gender breakdown in IBS? Women outnumber men 2:1. What percentage of IBS patients improve or lose their symptoms over time? >50%. What proportion of IBS patients respond to a low FODMAP diet? 75%. What age group is most affected by oesophageal cancer? 50-60yo overweight, white men with GORD. Effect of caustic injury, achalasia on oesophageal SCC risk? 1000-fold and 100-fold risk. Effect of GORD, obesity and combination (obesity + weekly reflux for 10yrs) on AC of the oesophagus/GOJ? 4-fold, 3-to-6-fold, and 16.5-fold (synergistic effect). Effect of smoking on oesophageal/GOJ AC? 2-to-3-fold increase. What effect does Barrett's oesophagus have on oesophageal AC risk? 125-fold increase, though most Barrett's pts die of other causes. Mortality of OG surgery? <3%. Rate of recurrent laryngeal nerve palsy after oesophagectomy? 5% (esp after neck incision). What is the lifetime incidence of colorectal cancer? 1 in 21 (Australia has one of the highest rates in the world). What proportion of CRCs occur in pts with defined genetic causes? 2-3%. What proportion of bowel cancer patients have hereditary polyposis as a cause? <1%. What proportion of bowel cancer patients have HNPCC (previously Lynch Syndrome)? 23% (risk to HNPCC gene carriers might be up to 90%). At what age should bowel cancer generallly begin? 50yo. What is the false negative rate of FOBT? 30%. Need to ensure patients don't take false reassurance from negative result ... "if you have any symptoms we need to investigate further". What is the latent time from polyp to bowel cancer? 5-10 years. What is current CRC screening practice in Australia? Recently initiated national screening program involves FOBT kits being sent to people at 50, 55 and 65yo (despite evidence and NHMRC guidelines). What proportion of patients have mets at time of diagnosis with CRC? >25%. How often is permanent end colostomy required in rectal cancer? 10%. What reduction in local recurrence of rectal cancer does radiotherapy give when added to surgery? Halves it.

What is the 5yr survival benefit of adjuvant chemo in ACPS stage C CRC? 20%. What is the 5yr survival rate after resection of mets in CRC? Some series suggest 50% (up from 25%) for liver or lung mets. But remember resection is only attempted in the few patients with isolated mets. Disseminated mets are incurable. What is the prevalence of Coeliac's disease in Australia? 1:100 (but population screening not recommended as not cost effective and tests imperfect). What effect does positive first degree family history have on risk of Coeliac's? Increases it 10-fold. What proportion of Coeliac's sufferers complain of fatigue? 80%. What proportion of newly diagnosed Coeliac's patients have a low BMD? 1/3. What proportion of Coeliac's patients experience ataxia, peripheral neuropathy? 6-10%. What proportion of Coeliac's patients have IgA deficiency? 2-5% (causing tTG and DGP to be falsely negative). Below what age is serological testing for Coeliac's considered unreliable? 4yo. Do genetic testing on blood or a buccal scrape if concerned. Gluten challenge in patients who have put themselves on a gluten-free diet: how much gluten and for how long before testing? Equivalent of 4 slices of bread a day for 6 weeks. What are the Coeliac's genes and what proportion of pts with Coeliac's have them? HLADQ8 and HLA-DQ2, 99.6% (1/3 of the population has these so not useful in screening, but useful in pts refusing gluten challenge). How many duodenal biopsies should be taken when testing for Coeliac's? 4 (changes can be patchy). What is the earliest a repeat small bowel biopsy should be done in coeliac's after instituting a gluten-free diet? 18mo. How soon should symptoms of Coeliac's resolve on a strict gluten-free diet? 3-6mo. What proportion of newly diagnosed Coeliac's patients in Australia are malnourished and what proportion overweight? 4% and 34% respectively. Most pts gain 6% body weight in the first year on a gluten-free diet. What proportion of Coeliac's patients are also lactose intolerant? 10-20%. What percentage of health adults and healthy neonates carry C difficile in their stools? 2% and 70% respectively. What proportion of US and UK inpatients carry C difficile in their stools? 20%. What is the rate of C difficile carriage in some nursing homes? 50%. What proportion of patients with C difficile colitis have had antibiotics in the preceding 3 months? <50%. When is C difficile colitis considered hospital-acquired? If it occurs at >48 after admission and <12wks post discharge (a significant proportion of patients with hospital-acquired C difficile colitis are discharged before symptoms begin). What proportion of C difficile colitis patients relapse after treatment? 35%. What is the age cut off for treating non-sinister PR bleeding as simple haemorrhoids without referring for colonoscopy? 40yo. How long does healing take after haemorrhoidectomy? 8-10 weeks of excruciating pain. How long does Rectogesic (topical GTN) take to allow anal fissure healing? 6-8 weeks. How long does botox take to heal anal fissures? Most healed when effect wears off at 3/12. What proportion of pancreatitis cases are caused by gallstones or alcohol? 80% in western countries (gallstones most common cause of acute cases then alcohol; alcohol causes 60% of chronic cases). What proportion of acute pancreatitis cases are caused by malignancy? <5%. What degree of elevation in lipase/amylase supports diagnosis of pancreatitis? >3 times normal.

What CRP level is used to define severe acute pancreatitis? >150 (but only peaks at 48h). What is the ideal timing of cholecystectomy in gallstone pancreatitis? Same admission, or if not possible then within 4wks of discharge. How frequent are peripancreatic fluid collections in acute pancreatitis? 25% of cases. How long should peripancreatic collections be managed conservatively for? >12wks. What is steatorrhoea in terms of excess fat excretion? >15g/d. What proportion of pancreatic cancer patients present at an advanced and non-surgically resectable stage of disease? >80%. What proportion of resectable pancreatic tumours are of the pancreatic head? 60-70%. What proportion of pancreatic tumours are of exocrine origin? >90%. What increased risk of pancreatic cancer does smoking confer? Odds ratio 1.77 (normalises after 15yrs of abstinence). What proportion of pancreatic cancer is thought to be familial? 10%. What is the 30-day mortality after Whipple's procedure (pancreatoduodenectomy) in high volume centres? <4%. How frequently is neoadjuvant downstaging of pancreatic cancer successful? <5%. What is standard post-operative follow up after cancer resection? Clinic visits q3mo to 2yrs, then q6mo to 5yrs (then annually in some types of cancer). What proportion of patients suitable for pancreatic surgery (pancreatic cancer stage 1) are not having it according to a recent US data review? Half. What is the complication rate of pancreatic biopsy (FNA)? 0.5 - 3%. What proportion of chronic pancreatitis cases are hereditary? 1%. What increased risk of pancreatic cancer do pts with hereditary chronic pancreatitis have? 50-fold. Risk conferred by having one or two parents with Crohn's? 5% and 35%. Risk conferred by having one or two parents with ulcerative colitis? 1.5%. What is the lifetime incidence of extraintestinal manifestations in pts with IBD? Up to 1:3. What proportion of patients experience AEs on thiopurine drugs? 15% (10% need to stop as a result)? What percentage of patients taking thiopurines develop pancreatitis? 1-3%. What proportion of UC patients require colectomy for refractory disease? 30%. What is the effect of IBD on pregnancy? Rule of thirds: 1/3 better, 1/3 same, 1/3 worse. What is the potential effect of mesalazine on bowel cancer risk in IBD? 50% reduction. What proportion of GP presentations are related to GORD? 10%. What is the increased risk of PUD conferred by helicobacter? !:4 - 1:10 (and increased cancer risk). What are typical findings on upper endoscopy for dyspepsia without alarm symptoms? 77% normal, 15.5% reflux oesophagitis, 5% ulcer. What proportion of oesophageal cancer cases have dyspepsia? 40%. What proportion of oesophageal AC is due to sedentariness and obesity? 37%. What proportion of duodenal and non-NSAID gastric ulcers are associated with helicobacter infection? 90%. Risk of dyspepsia in NSAID use (including aspirin)? 10-20% of patients taking NSAIDs have dyspepsia and 5-15% have to stop as a result (only 1.5-2% have complications in form of PUD). Under what age is gastric cancer rare? 50yo. What proportion of peptic ulcers are healed by PPIs at 2wks and 1mo? 60% and 94%. Relative efficacy of medical treatments for GORD? Increased dose PPI (100% effective), single dose PPI (80%), H2 antagonists or cisapride (50%), antacids (20%), lifestyle (20%). How long to delay endoscopy after stopping acid suppression? 4 weeks => higher diagnostic

yield. What is biochemical definition of hepatitis? ALT >5x ULN. How frequently should cirrhotics be surveilled for HCC? AFP and US q6mo. What proportion of kids get appendicitis and when? 1%, 10-12yo. What percentage of kids get UTIs? 8% of girls, 2% of boys. Typical age when testicular torsion occurs? 10-12yo. Typical age when inguinal hernia occurs in kids? Usually <1yo but can be any age. Emergency Paeds parameter calculations 1. Weight (Age + 4) x 2 2. ETT diameter Age/4 + 4 3. Defibrillation: 4j/kg (mono or biphasic) 4. Fluid requirements: Resuscitation 20mL/kg; Daily maintenance 100mL/kg for first 10kg, 50mL/kg for second 10kg, 20mL/kg for the rest; Hourly maintenance 4, 2, 1. 5. Adrenaline 0.1ml/kg 1:10,000 6. Pulse 160 - (age x 5) 7. SBP 80 + (age x 2) 8. ETT length Age/2 + 12 LMA sizes: 4 for adults, 2 for kids. ETT sizes: 6 for kids, 7 for women, 8 for men (have smaller sizes and half sizes available). Dobutamine dose in septic/cardiogenic shock: 2.5-10mcg/kg/min. Sedation: Midazolam 0.1mg/kg and fentanyl 1mg/kg. Defibrillation dose in arrest: 200j biphasic (1-4j/kg in kids) or 360j monophasic. When to stop resuscitation: Documented asystole >10mins, pupils fixed/dilated >10mins, no ROSC >15mins (exceptions: temp <33deg, kids, drug overdose). How often to use adrenaline in arrest: after 2nd shock then every 2nd loop (1mg of 1:10,000 or 0.1mg/kg of 1:10,000 for kids). What is the ratio of compressions to ventilations? 30:2 in adults (many question the need for ventilation at all), 15:2 in kids. ROSC rates after resuscitation for witnessed out of hospital arrests? 25%. ROSC rates after resuscitation for witnessed out of hospital arrests if rhythm VF/PVT? 45%. Discharge from hospital rate after out-of-hospital cardiac arrest? 7.6%. How long can an IO needle be left in situ? 24h before risk of osteomyelitis. Temporising measure rather than long-term alternative to central line => try to get central venous access within the first 24h. How long to try with IV before reaching for IO in arrest? 90-120 seconds (< 2 minutes). Proportion of deaths in Australia accounted for by suicide? 1.6%. What proportion of deaths for men 20-39yo are accounted for by suicide? 20% (men 4 times as likely as women to die by suicide). Prevalence of suicidal ideation? 2.3%. What proportion of suicides initially present with self harm? 50%. What proportion of suicides see their GP in the month beforehand? 45%. Proportion of serious violence including homicide attributable to psychosis? <10%. What proportion of scaphoid #s have normal initial xray? 1/3. Healing times for burns? First degres <7d, superficial dermal 7-14d with discolouration, deep dermal 21d with hypertrophic scarring, full thickness doesn't heal on its own. Time from exposure to arrest in anaphylaxis? Foods 30mins, venoms 15mins, iatrogenic 5mins. Adrenaline dose and route in anaphylaxis? 0.01mg/kg of 1:1000 to max 0.5mg in lateral thigh. If no response to 3 repeated IMIs, IV infusion.

What proportion of anaphylactic reactions are biphasic. 2-20%. Recommended duration of post-acute observation to exclude biphasic course? 4-6h in ED., overnight if reaction severe. What SaO2 is acceptable in paeds patient? >94% (<90% on 100% oxygen => need assisted ventilation). When to re-xray hand fractures? 1 week (and 2 weeks for MCPs). How to examine PIP collateral ligaments? MCPs at 90deg, PIPs at 30deg, lateral stress. Duration of immobilisation in hand fractures? 1-4 weeks (mostly 3 weeks) except mallet fracture which is 6-8 weeks. Proportion of angio-oedema cases attributed to ACEIs? 30%. GCS at what time indicative of severity of sports related concussion? 6h (most sports head injuries are assessed as mild at this time). Rate of concussions in AFL and rugby? 5 injuries per team season. How long does recovery from concussion usually take? 10-14d in >90% of cases. Proportion of sports head injuries who get "post-concussion syndrome" (ie symptoms lasting >3mo)? <1%. Increase in relative risk of depression in later life after concussion? 2-3 times. Accounting for pseudohyponatraemia in DKA? Add 2mmol sodium for every 5.5mmol glucose over 5.5mmol (hypernatraemia present at >150mmol/L). In what age group is DKA more prevalent at diagnosis? <5yo. Onset of action of nebulised adrenaline? 10-30mins. What proportion of parents report personality changes in their kids after mild head injury? Nearly 1/3. Over what period do most symptoms of post-concussive syndrome resolve? Within 3 months. Proportion of salivary pleomorphic adenomas that become malignant? 10% at 10-15yrs. Proportion of head and neck cancers occuring in oral cavity and amenable to examination without specialised equipment? 50%. What sized LN is considered suspicious? >10mm (>20mm is malignant until proven otherwise). If metastatic neck nodes identified, what proportion of primaries will be head and neck tumours? 75%. Risk of needle track seeding on FNA? 1:1000. Laryngitis when to worry? >3wks (another source says duration of hoarseness suggestive of structural lesion in smoker? >10d). Proportion of world affected by allergic rhinosinusitis? 10-25%. Percentage of pts diagnosed by physicians as having chronic rhinosinusitis? 2-4%. Proportion of asthmatics with chronic sinus symptoms? >80%. What age group is affected by chronic rhinosinusitis? Increases in incidence till 60yo then falls off. What is "chronic" in chronic sinusitis? >12wks. How common are nasal polyps? 4% of population. What proportion of asthmatics have nasal polyps? Up to 15%. Proportion of AOE caused by fungal infection (esp aspergillus)? 10%. What proportion of AOM resolves on its own? 80%. Complication rate of AOM? 1%. Incidence of blindness in orbital cellulitis? 10%. Proportion of nosebleeds that originate from Little's area? 90%. Recurrence rates of quinsy? 10-20%. Proportion of Australians and older Australians with hearing loss? 27% and 87%.

Proportion of patients with reduced disability and improved QOL with hearing aids? 70% and just over half. Under what age is it safe to assume all teeth are deciduous? <6yo. What extra-oral dry time confers poorer reimplantation prognosis in avulsed tooth? >60min. Duration of splinting of avulsed tooth? 14d. Proportion of ISSHL patients reporting balance problems, vertigo? 50%. When to worry about a mouth ulcer? >3wks (esp if solitary and palpable). What frequency tuning fork used for Weber's test? 512Hz, middle C. When to check hearing in AOM? 10d. Which CN affected first in Ramsay Hunt syndrome? 7. In what age groups is sore throat rare? <4yo and >45yo (common from 4-8yo and in teens). What age group tends to get bacterial throat infections? 3-13yo. In what age group is quinsy common? 20-50yo. When to consider prophyactic antibiotics for tonsillitis? 5 episodes a year. Duration of antibiotics in AOM? 5d. Duration of antibiotics in GABHS tonsillitis? 10d.

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Urology Need to review: renal masses. Storage symptoms: UTI, bladder stones, bladder cancer, overactive bladder, interstitial cystitis. Voiding symptoms: BPE, bladder neck stenosis, urethral stricture, poor detrusor contractility. Overactive bladder syndrome describes symptom cluster of urinary urgency (+/urge incontinence) and usually frequency and nocturia. Detrusor overactivity is a urodynamic observation of contraction during filling (neurogenic or idiopathic). Prostate doesn't need to be enlarged to obstruct urethra (inner transitional zone can grow). Most prostate cancers are posterior, where TRUS biopsy samples taken from. BPH and catheters: Avoid indwelling catheters if possible. Permanent suprapubic catheterisation or intermittent self catheterisation more appropriate. Alpha-antagonists for BPE and PBS: Prazosin on PBS but more side effects, tamsulosin is not on PBS. Treatment of BPE? 1st medical rx with alpha-antagonists (prazosin on PBS, tamsulosin not on PBS) or steroidal anti-androgens (finasteride/dutasteride .. block conversion of testosterone to DHEAS) => then for smaller prostates, repeated ablative surgery is an option (transurethral needle ablation TUNA, transurethral microwave therapy TUMT) => then for large prostates, definitive cavitating surgery (green light laser prostatectomy if available, or holmium laser enucleation or TURP). Surgical treatment for BPH? Cavitating vs ablative. Medical treatment of overactive bladder syndrome (detrusor instability, urge incontinence .. inc in setting of BPH)? Watchful waiting (address exacerbating factors like fluid intake, coffee, alcohol, spicy foods, constipation mx, diuretics only in the morning etc .. plus continence/urology therapist: voiding diary, gradual extension of intervoid times, freeze and squeeze method), then antimuscarinics (oxybutynin/Ditropan on PBS, solifenacin/Vesicare not on PBS), alpha antagonists if BPH implicated. Phytotherapy like saw palmetto probably no better than placebo for LUTS/BPH. Meds for voiding/obstructive symptoms like hesitancy and weak stream? Alpha antagonists (prazosin/Minipres etc) block alpha1a receptors relaxing bladder neck

smooth muscle; 5a-reductase inhibitors (finasteride/Proscar etc) block conversion of testosterone to DHEAS and reduce prostate size. Combination (Duodart) for resistant cases. Meds for storage symptoms like urgency, frequency, nocturia? Antimuscarinic therapy (oxybutynin/Ditropan etc) block M acetylcholine receptors and reduce dysfunctional detrusor contraction. Urinary retention rarely occurs when using antimuscarinics for LUTS in patients with BPE. Patients with macroscopic haematuria or persistent microhaematuria and urothelial carcinoma risk factors score urology referral regardless of cytology. Continence therapy: Supervised pelvic floor exercises for stress incontinence; bladder diary, timed voids (gradually lengthening time) or freeze and squeeze for urge incontinence. LUTS urology referral criteria? Haematuria, recurrent infections, bladder stones, renal impairment. Sterile pyuria, asymptomatic bacteriuria? Investigate for TB, bladder stones, foreign bodies, cancer, diverticulae, chronic retention, upper urinary tract abnormalities. If leukocyte esterase alone is positive on UA are bacteria present? 50% of the time bacteria present (If nitrites alone are positive, there is a UTI). If leuks+ nits-, decision to treat based on symptoms. When should you check for clearance of urinary bacteria after treating? In pregnant women. What are risk factors for uroepithelial cancer? Smoking, cyclophosphamide, radiation, chemicals (benzene, anilene dyes). Urine cytology? 3 specimens on 3 different days. UTI treatment in women? Trimethoprim 300mg/nocte for 3d or cephalexin 500mg BD for 5 days (go to 10d if immunocompromised, pregnant as complete eradication desirable). How to reduce risk of UTIs? Hydration (2L water a day to avoid stasis), good hygeine, postcoital voiding, front to back wiping, cotton underwear, avoid diaphragm use, cranberry juice may help. Treatment options for recurrent UTIs? Trial of self start therapy (pt has emergency supply of antibiotics and MSU request/pot at home, and takes MSU then starts therapy if symptomatic) or postcoital prophylaxis depending on pattern. Then longterm prophylaxis (eg daily low dose cephalexin or trimethoprim for 3/12) plus ultrasound. The urology referral, further investigation for urinary tract abnormalities if problem persists. Pelvic floor exercises: Handout available on Melbourne Women's and Children's Hospital.

Neurology Check C-spine first before doing any head manouevres when examining patient with vertigo. Cause of MS: genetic (T cell receptor variability) & environmental (6x higher incidence in Tassie than north Qld ? vitamin D link (supplementation used though not proven), late exposure to EBV and high titres associated, weak link with smoking). Immunological but process still unclear. What areas does MS affect? Eloquent areas like optic nerve, corpus callosum, cerebellum/pons, periventricular white matter, spinal cord (plaques often occur in "non-eloquent" areas too, but these are asymptomatic). Thought of as white matter disease but actually also causes demyelination in grey areas too causing cognitive

impairment. Fluffy white matter lesions also very very common in brains of normals (one spot per decade is a rule of thumb) so referring for just-in-case patients is fraught .. causes including migraine, scuba diving, trauma, small vessel disease. What pattern does MS follow? Young patient, symptoms building slowly over days then gradually resolving over weeks. MRI used to monitor silent progression. What are the phases? Primary autoimmune assault on CNS amenable to immunotherapy and late, less treatable degenerative phase. What is the basis of treatment for MS and what are its risks? Immunosuppression, reactivation of herpes infections, JC virus, infection-related malignancies (cervical, stomach cancer and lymphoma). RRMS first line treatment? Self injected B-interferon 1a (Avonex, Rebif) or 1b (Betaferon) which inhibit gamma-interferon, reduce cytokine release and augment suppressor T cell function .. common AE of flulike effects (exprected due to role of interferon in infections => often suppressed by pretreating with NSAIDs), seizures, headache or depression; glatiramer acetate (Copaxone) which may block presentation of myelin antibodies to T lymphocytes. Supplement vitamin D even though evidence not yet in .. no harm. RRMS second line treatment? Natalizumab (Tysabri) which acts as regional immunosuppressant by inhibiting leukocyte migration to CNS (more effective but 1:1000 get reactivation of JC virus causing progressive multifocal leukoencephalopathy aka PML). Also fingolimod, oral medication with promise blocking exit of lymphocytes from lymph nodes. Both more effective than first line agents in reducing disease activity. What salvage options are available for aggressive or difficult-to-treat MS? Chemo immunosuppressive agents mitoxantrone (risks => late course acute myeloid leukaemia, CCF) or cyclophosphamide. Low to zero tolerance for disease activity. If disease activity, neurologists will escalate treatment but in reality toxic third line drugs rarely used these days. What should be done to reduce risks of salvage treatments? The risks in using potent immunosuppressants for MS can be reduced by ensuring immunisation is up to date, screening for latent TB, surveillance for skin and cervical cancer, and avoidance of osteoporosis What drug best in pregnant women? Glatiramer (B1). What is the treatment for acute relapses of RRMS? Methylprednisolone IV for 3/7 (can cause avascular necrosis of hip and predictable steroid effects). Disease modifying treatments only approved by PBS for RRMS. How long do we treat before calling response to DMTs suboptimal? 6mo. Treatment of spasticity in MS? Physio and baclofen combination, botox if bedbound. Treatment of pain (inc trigeminal neuralgia) and spasm in MS? Carbamazepine (Eccentric AEs like drowsiness and ataxia), with capsaicin, gabapentin/pregabalin, tricyclics as back up. Treatment of fatigue in MS? Conservative measures, then expensive modafanil, then sometimes amantadine. Treatment of tremor in MS? Clonazepam, propranolol. Treatment of bladder symptoms in MS? Anticholinergics (oxybutinin), alpha blockers (tamsulosin), desmopressin, intermittent self catheterisation, intravesical nerve blocks, botox. What are side effects of first line drugs? Side effects of beta interferons include flulike symptoms, injections-site reactions, a mild neutropenia or elevated LFTs What stage does cognitive impairment occur in MS? All stages (but especially secondary progressive), often affects employability.

What are good prognostic factors in MS? Young, female, normal initial MRI, optic neuritis or isolated sensory symptoms as CIS, full recovery from first attack, initial relapsing/remitting course, long interval to second attack, no disability at 5yrs. Spinal lesions => poor prognosis. MS mimics: Autoimmune like neuromyelitis optica (Devic's disease => involves optic nerve and long tracts) or acute disseminated encephalomyelitis (monophasic, more explosive than MS, usually in kids), vasculitis/APS, tumour, connective tissue (SLE/Sjogren's), sarcoidosis, neuro-Behcet's, infection (HIV, syphilis, schistosomiasis). What factors are involved in young (<40yo) stroke? Thrombophilia or valvular heart disease. Less obvious risk factors for stroke (after HTN, smoking, age etc)? FHx, other vascular disease, thrombophilia, vasculitis, extracranial arterial dissection. Cerebral Infarcts: TACI (total anterior: large infarct with triad of hemiparesis, higher defects and hemianopia, 20% early mortality and high morbidity), LACI (lacunar: small, deep white matter infarct with pure sensory, motor, ataxic, dysarthria/clumsiness, amnestic, low incidence of embolic diathesis), PACI (partial anterior: less severe with 1 or 2 TACI symptoms), POCI (posterior: large variety of brainstem and cerebellar type strokes, never due to carotid pathology) ? TA: higher cerebral dysfunction (dysphasia, dyscalculia etc), homonymous visual field defect, ipsilateral sensory/motor defect. LA: pure motor or sensory. PA: 2/3 from TACI, higher cerebral dysfunction, more limited sensory or motor deficit (eg one limb), PO: ipsi CN palsy and contra sensorimotor deficit, bilateral sensorimotor deficit, conjugate gaze disorder, cerebellar dysfunction but no ataxic hemiparesis, isolated homonymous visual field defect. What are the criteria for diagnosing ischaemic CVA? Symptoms and no findings on CT (risk factors supportive). CT signs of ischaemic stroke? Local cortical/gyral swelling and sulcal effacement (narrowing) secondary to cytotoxic oedema. Also hyperdense middle cerebral artery sign (backed up blood in occluded artery). What is plain brain CT good for? Mass lesions (cancer/abscess), acute haemorrhage. Does CTB involve clinically significant cerebral radiation exposure? No, even with enhanced CT techniques using higher doses of radiation. When is brain imaging warranted? Vascular territory uncertain, pathology uncertain, need to exclude haemorrhage (anticoagulants or long duration of symptoms). Specialist review recommended before imaging. Trend is towards CT angio. Early carotid doppler important as endarterectomy +/- stenting has strong role in prevention of early stroke recurrence. Less thought of tests in CVA? TTE if any evidence of cardiac pathology/thrombus/shunts. What is the role of aspirin in secondary prevention of stroke? 160-300mg beneficial with a large NNT but low rate of AEs. Clopidogrel more effective but only in PVD patients. Several guidelines recommend dipyrimadole+aspirin combo as first line but AEs a problem (headaches, flushing, GI effects) .. clopidogrel only in those that don't tolerate. CAPRIE => clopidog better than asp; MATCH => lower ischaemic stroke, higher bleeding rate, balance in favour of combination. CHARISMA => adding clopidogrel no added benefit. Lifestyle vs aspirin? Lifestyle (BP, lipids, smoking, BSL .. especially the first 3) 3x more effective than aspirin long term. BP is king, treat to vague target of <140/90 (gradually to avoid AEs).

PPIs (except pantoprazole) inhibit effect of clopidogrel. Benefit of carotid endarterectomy (CEA) or stenting highest early on after first stroke/TIA. CEA better short term, but by intermediate term thay even out. What ischaemic CVAs does CT miss? Small, acute, posterior fossa. Benefits of thrombolysis in ischaemic stroke? Recovery time and functional outcomes (1 in 10 extra patients walks out of hospital). Benefits of stroke unit in all stroke patients? 1 in 25 extra patients walk out of hospital. Benefits of aspirin in ischaemic stroke? 1 in 100 extra patients walks out of hospital. Benefits of anticoagulation in ischaemic stroke? None. Advise pts call 000 if any focal neurological symptoms rather than calling GP => improved thrombolysis rates and improved outcomes. What is the stroke authority in Australia called? National Stroke Foundation. What are the guidelines for stroke rehab? Stroke Foundation Guidelines (National Stroke Foundation Clinical Guidelines for Stroke Rehabilitation and Recovery). What is the driving exclusion period for stroke? 1 month. Is anticoagulation safe and effective in the elderly (>75yo)? Yes, BAFTA trial. In what circumstance is anticoagulation better than antiplatelet in stroke? Not in SR or left atrial thrombus present, ESPRIT trial. What are two indicated medical treatments in secondary prevention of ischaemic strokes (and the studies behind them)? Highest tolerated dose of statin (40 simva, 80 atorva => SPARCL and Heart Protection trials), statins effective in secondary prevention independent of lipid lowering effect; lower BP with ACEI and diuretic once acute phase of initial stroke resolves even if normotensive (PROGRESS trial). What are some straightforward carotid territory stroke symptoms? Amaurosis fugax or aphasia. Which strokes have the highest mortality? TACI and PICH (primary intracerebral haemorrhage). Is a marginal/improving stroke patient safe to be at home? 50mL swallow test, if voice gurgly or if any cough IV hydration needed so send to ED. What if TIA symptoms occur in appropriately anticoagulated patient? Question diagnosis: ? seizures, hypoglycaemia, ominous causes of ischaemia like malignancy or bacterial endocarditis. Is it OK to have an elderly pt on anticoagulation and antiplatelet? Generally risk>benefit. What are contraindications to MRI? Pacemakers and defibrillators. What effect does smoking have on incidence of PD? Reduces it. What is the most common cause of PD? Sporadic Idiopathic Parkinson's Disease (IPD). What is the most common cause of autosomal dominant PD identified so far? PARK 8 (10-20% of dominantly inherited cases and also 1-2% of IPD cases). What is gene is associated with autosomal recessive inheritance and early onset PD, especially if sibling affected? PARK 2 (Parkin). ... article doesn't mention if this is the most common. Is onset generally earlier in genetically inherited PD? Yes. Why does drooling occur in PD? Problems swallowing, not excessive salivation. What proportion of IPD patients have both action and resting tremor? Half. Is cog-wheeling unique to PD? No, any pt with tremor may have it. What is retropulsion? The "pull test" (pulling sharply on pt's shoulders from behind) makes them take more than one step back.

At what stage of PD does hypomimia (reduced facial expression) occur? Early, along with disturbance of posture. What symptoms/signs go against a diagnosis of IPD? Symmetrical motor manifestations, early and severe autonomic dysfunction, early dementia, early and frequent falls, poor response to levodopa, lack of tremor (though 25% of IPD patients never have tremor), rapid progression to Hoehn and Yahr stage III (within a year). What symptoms support diagnosis of IPD? Early loss of smell, asymmetrical/intermittent motor signs including tremor which can be resting+action or resting only, bradykinaesia, seborrheic dermatitis, late appearance of dementia and autonomic instability. What do early, frequent falls suggest? A form of PD other than IPD (progressive supranuclear palsy or multiple system atrophy). What is the typical PD tremor? 4-5Hz resting tremor (distal>proximal, upper>lower limb, often asymmetric in early disease, can be intermittent, can occur in chin/lips/tongue). 25% never have tremor and 10% have resting and action tremor. When to refer to neurologist in PD? (1) Diagnosis, (2) Initiation of pharmacotherapy, (3) Advanced disease. Do cognitive changes in PD always = dementia? No. Is there any treatment that slows progression in PD? No. Should meds be started in PD if there is no functional impairment? No. What non-pharmacological treatments are proven in PD? Exercise programs = improved motor function; speech therapy = stronger voice; silk sheets = improved rolling in bed; reduced protein in diet for pts taking levodopa (protein may impair absorption). Which is more likely to cause dyskinaesias, levodopa (dopamine precursor that can cros BBB) or dopamine agonists (ropinirole, pramipexole)? Levodopa. What drug gives mild symptomatic improvement in early PD? Selegiline (MAO-B antagonist). What are the alternatives to treat non-tremor predominant PD? Levodopa (+benserazide/carbidopa), selegiline (mild, early disease), amantadine, dopamine agonists (ropinirole, pramipexole). What is entacapone? Carboxymethytransferase (COMT) inhibitor (protects L-Dopa from gut breakdown). Added, along with DAs, in advancing disease. What are two alternatives for tremor-predominant disease? Amantadine (antiviral and anti-Parkinsonian .. antiPD action poorly understood, weak NMDA agonist and anticholinergic) anticholinergics (benztropine, biperiden, procyclidine, orphenedrine, diphenhydramine, trihexylphenidyl etc). What agent should be used for nausea in PD? Domperidone, doesn't cross BBB (not metoclopramide or prochlorperazine which do cross BBB, worsening of PD symptoms). What antipsychotics are first choice for treatment of psychosis in PD? Atypicals (quetiapine first line, clozapine sometimes), definitely not typical/traditional. What to do in PD with falls? Review meds and refer to specialist. When is surgery beneficial in PD? Levodopa resistant PD with severe dyskinaesias and motor fluctuations (no effect on cognition or disease progression, and only partial effect on postural instability, falls, dysarthria, on-period freezing). Treatment for orthostatic hypotension? Increase salt/water intake, domperidone, pyridostigmine, fludrocortisone, octreotide. What is the definition of vertigo? Sense of motion (sudden rotational vertical or horizontal motion) when there is none => always organic involving vestibular

apparatus or central connections. Dizziness is a more general term for disequilibrium encompassing true vertigo and pseudovertigo (1. lightheadedness, 2. pre/syncope, 3. disequilibrium). Why is true vertigo? Asymmetrical firing of vestibular neurons => neurons in vestibular nucleus on one side of brain stem fire less frequently than those on the other side. Dizziness history? Rotation vs blackout sensation vs unsteady on feet, pattern and previous bouts, exacerbants like posture or movement, nausea/vomiting/tinnitus/deafness/palpitations/CP, visual disturbance, recent illnesses, medications (antiHTN, diuretics, antidepressants, tranquilisers, aspirin/salicylates, quinine). Dizziness examination? Cardiovascular inc postural BP and thorough neurological, otoscopic, C-spine. What are the commonest causes of true vertigo? BPPV, vestibular neuronitis and acute viral labyrinthitis (viral labyrinthitis is basically the same as vestibular neuronitis, except that the whole of the inner ear is involved causing deafness and tinnitus to arise simultaneously with severe vertigo). What are the probability causes of untrue vertigo? Dizziness caused by anxiety, postural hypotension (inc innocent senile orthostatic hypotension, med or hydration relation or due to autonomic failure), vasovagal, motion sickness, post head injury. Don't forget ear wax => commoner cause of true vertigo in elderly than recognised. Treatment of senile orthostatic hypotension: Get up slowly, exercise legs before doing so, wear firm, elastic stockings. Serious causes of dizziness not to be missed? Cancer (acoustic neuroma, posterior fossa tumour, brain abscess; cardiovascular (arrhythmia, AMI, AS); cerebrovascular (vertebrobasilar insufficiency, brainstem infarct eg PICA thrombosis; MS). Pitfalls of vertigo? Ear wax, otosclerosis, arrhythmia, hyperventilation, AOD, cough or micturition syncope, vestibular migraine, PD, Meniere's, postural orthostatic tachycardia syndrome. Seven masquerades all possible. Pt may be trying to tell you depressed or anxious. Difference between viral labyrinthitis and acute vestibular neuronitis syndrome? Labyrinthitis involves whole inner ear causing vertigo, deafness, tinnitus. What causes BPPV? Overactivity of one vestibular nucleus. How long is true vertigo? It is never long-lasting as the brain adapts. Questions to ask in vertigo? Is it true vertigo (world spinning vs faintness vs feeling of imbalance vs anxiety etc). Is it recurrent? ... Recurrent = mostly harmless. Single attack = investigate for brainstem or cerebellar cause vs vestibular neuronitis syndrome (aka labrynthitis). Is it triggered? Spontaneous = Meniere's, labrynthitis aka vestibular neuronitis syndrome; triggered = BPPV, alcohol-induced, vestibular migraine, loud-noise-or-straining-triggered (perilymph fistula or superior semicircular canal dehiscence caused by trauma: eg water-skiing or barotrauma while scuba diving => electrocohleography and temporal bone imaging can help => treatment surgical), situational/anxiety-provoked (eg fear of heights or crowded places, mal debarquement => can last years, associated with anxiety, responds to CBT and SSRIs). Single episodes of vertigo: Acute labrynthitis (vestibular neuronitis syndrome) vs cerebellar infarct/haemorrhage. Labrynthitis => controversy over whether viral or ischaemic as nerve and artery traverse same course. Examination in vertigo? Whisper test, characterise nystagmus as peripheral or central (clues to central cause: direction change, ie left beating on left-gaze and right-beating on right gaze; not the same in both eyes; purely vertical), head

impulse test to identify peripheral cause (testing for defect in vestibulo-ocular reflex by getting pt to focus on your nose while you rapidly rotate their head 20deg to one side, with positive test showing abnormality on that side ... fast movement but small angle to prevent vertebral artery injury); Dix Hallpike to identify BPPV (below). Check for Parkinsonism, visual problems, spinal pathology like cervical sponsylosis (distal sensation, reflexes), peripheral neuropathy. Gentamicin/Aminiglycosides can damage vestibular system causing vertigo but no hearing loss => pt typically notices oscillopsia when they get home (jiggling bad home-movie effect on movement due to loss of VOR) => do head impulse, get them to read Snellen chart while you jiggle their head slightly causing a 1-2 point reduction in vision, or do Romberg with them standing on a pillow => image them (MRI brain and spine) then mx with vestibular rehab. Significance of head impulse? Peripheral not central cause of vertigo. What is Alexander's law? Nystagmus more prominent when looking towards side of quick phase (indicates peripheral, inner ear cause). What are the characteristics of peripheral nystagmus? Unidirectional regardless of direction of gaze (note: reversibility is a feature of BPPV on doing Dix Hallpike), same in both eyes, not pure vertical, accentuated by looking to side of quick phase. Meniere's: Overdiagnosed => episodic unprovoked attacks of usually-unilateral vertigo lasting >20mins to 4-8h with vomiting+++, spontaneous horizontal nystagmus, tinnitus (roaring/buzzing/tinny-sounds), aural fullness like experienced travelling on a plane preceding attack (noticed in retrospect), fluctuating low freq sensorineural hearing deficit (unable to use phone on affected side) that initially recovers between attacks but later deteriorates, disequilibration/nausea lasting for days in between, late in course can have brief and unprovoked "drop attacks" or otolithic crises where they suddenly fall. Cause of Meniere's? Presumed to be increased endolymphatic fluid pressure in canals. Examination? Weber for sensorineural deafness, nystagmus, caloric test (instil warm and cold water into external aufitory canal). Examination largely normal between attacks as hearing often recovers. Can be low level loss. Investigation? Audiometry (SN deafness of 30-40dB, loudness recruitment), electrocochleography. Treatment for acute vertigo in Meniere's? Reassurance not malignant. Start with IV benzodiazepines, then oral diazepam 5mg q8-12h, prochlorperazine IMI or suppositories (not recommended by some authorities) or ondansetron wafers (jury split on betahistine/Serc and generally not used in Australia). Meniere's diagnosis? Audiogram showing fluctuating low-freq sensorineural hearing loss; electrocochleogram measuring electrical signal from cochlea in response to externally applied sounds. Meniere's treatment? Check 2011 supports classic management recommendation was NEAT approach: Nutrition (optimal low fat diet), Exercise, Avoid CATSSS (coffee, alcohol, tobacco, sugar, salt and social drugs), Tranquility (relaxation, meditation, recreation, CBT, sedative). No evidence for avoiding alcohol/coffee. Tobacco should be avoided for other reasons. Low salt diet still stands (nothing with >120mg/100g serve), refer to dietician. Also direct to Meniere's Australia, consider thiazide. Monitor electrolytes. No evidence for avoidance of alcohol/coffee. Avoid tobacco for other reasons. Resistant cases? Transtympanic genta => partial chemical labrynthectomy with permanent loss of some vestibular function in treated ear. Acute Vestibular Syndrome (AVS) is a syndrome of acute vestibular failure => presumptive cause vestibular neuronitis (aka acute labrynthitis) => controversy

whether viral or ischaemic (recent evidence suggests reavtivated HSV1 in vestibular ganglion) => acute/unprovoked/persistent (3-5d, much longer than attacks of Meniere's) vertigo in youngish patient often after "flu" with mixed horizontal-torsional nystagmus with rapid phase away from affected ear and when looking away from affected ear (Alexander's law), nausea and vomiting, no hearing loss or tinnitus, no other neurological signs, ends with brain stem adaptation but with residual ataxia due to unilateral vestibular hypofunction => caloric stimulation confirms vestibular pathology => serious pathology to exclude is suppuration of middle ear, mastoiditis (fever; tenderness, swelling and redness of mastoid process) => treat oral pred 100mg/d reducing over 3 weeks (Check says 9d), fluids and aggressive physio rehab exercises despite resistance due to symptoms. One cause of Meniere's is thought to be viral labyrinthitis. Treatment of Acute Vestibular Syndrome (presumptive cause HSV in labrynth)? Acutely: lie still in bed on ear of affected side, keep gaze in position that eases symptoms, antiemetics and fluid resusc if necessary. Vestibular suppression with IM then PO diazepam in first 24-48h but sparingly thereafter (Check suggests stat IM followed by PO prochlorperazine as vestibular suppressant, but this is actually only good for nausea and has more rebound). Diazepam reduces brainstem response to vestibular stimuli. Consider steroids (similar to Bell's palsy treatment). Antivirals controversial - evidence does not support routine use. Later: Vestibular adaptation exercises or even formal vestibular physio. Vestibular neuronitis triad: Acute vertigo, nausea, vomiting. Acute labyrinthitis triad: Acute vertigo, nausea, vomiting, hearing loss +/- tinnitus. What if recurs after several weeks? Postvestibular neuronitis BPPV (Rx: Epley or Sermont manouevres), decompensation (cause unclear => formal investigations, physio), migraine, Meniere's, vascular vertigo, recurrent vestibulopathy. Benign Paroxysmal Positional Vertigo: clustered attacks of triggered vertigo/nystagmus 1-60secs provoked by head movement lasting days, nausea but rarely vomiting, not disabling, caused by calcium crystals shaking loose from utricle and saccule and entering semicircular canals where they become gravity detectors. Spontaneous resolution in 6-8 weeks or 24-48h with treatment (most idiopathic but st associated with head trauma especially, but also vestibular neuronitis, labrynthitis, vertebrobasilar ischaemia, bed rest, middle ear surgery). Dix-Hallpike manouevre to test for BPPV (done 3 times, with head left, centre and right) = sitting to lying with head 45deg rotated, 45deg below horizontal and bad ear down => rotational nystagmus with latency, fatiguability, reversibility. Put pillow/s behind shoulders as alternative to using end of bed. Rotational nystagmus => posterior semicircular canal => treat with Epley manouevres; horizontal-only or bilateral positive tests => lateral canals => 360deg Epley and have vomit bucket ready or referral to specialist vertigo clinic. What controversial condition touted by Check 2011 can also present similarly? Cervicogenic vertigo. Some think aetiology of BPPV is cervicogenic rather than because of otoliths but this is very controversial and unproven. Contraindications to Dix-Hallpike or Sermont-Epley manouevres? Neck pain, stiffness, injury, spondylosis, severe vertigo/nystagmus. Have vomit bowl at the ready. Treatment for BPPV? Epley manouevre in office (supplemented by Brandt-Daroff at home), reassurance, return to normal activities at 1wk .. if >2yrs of refractory symptoms and known site of lesion (ie virtually never so rarely used) surgery can be used to sever the nerve to the semicircular canal. Epley manouevre to treat posterior BPPV? Done by doctor as an office procedure. One minute spent in each head position and 10mins with head neutral at the end.

Do Hallpike manouevre with bad ear down then still lying rotate head 90 degrees the other way then roll onto the side pt is now facing then sit up side-on. NHMRC level 1 evidence for posterior BPPV. Not responding? Suspect central cause or ant/horiz canal involvement and refer for formal vestibular function testing. Do at-home Brandt-Daroff exercises work for vertigo? No, they are old, useless and even the inventors have abandoned them. Check still bats for them so for exam purposes probably recommend supplementing Epley with Brandt and Daroff: pt sits on edge of bed with head at 45 degrees left then quickly lies sideways with head off end of bed, stays there 30secs or till vertigo/nystagmus stops, then sits back up with head in same position then holds for 30secs, then turns head to right and repeats. Done 3 times a day. Spontaneous horizontal nystagmus before Hallpike manouevre? Peripheral cause other than BPPV. No latency (10-20sec), reversal or fatiguability (at 30-40secs) after Hallpike manouevre? Not BPPV (Hallpike only positive in posterior semicircular canal BPPV, the most common type, not anterior or horizontal semicircular canal BPPV). Remember mild cases of BPPV might have vertigo but not nystagmus on DixHallpike, and in these circumstances Epley manouevre won't help => advise to come back if getting worse. What if no clear cut diagnosis of treatment-responsive BPPV? (1) MRI Circle of Willis and internal auditory canals if available; if not then high quality CT with fine cuts through posterior fossa; (2) high quality audiogram and vestibular function testing at ENT dept. Red flags for central cause of vertigo: Unaccustomed headache, unable to stand/walk, spontaneous direction changing nystagmus, spontaneous vertical nystagmus, normal head impulse, additional focal neurological signs. Positive Romberg's? Peripheral disorder (sensory or vestibular input) eg tabes dorsalis, B12. Unstable prior to Romberg's and no change with manouevre? Cerebellar or other central lesion. Central Positional Vertigo (CPV) causes? MS, cerebellar idisease, brainstem ischaemia, migraine. Less severe symptoms than BPPV but nystagmus persists with stationary head. Spontaneous vertical (up or down beating) or direction changing nystagmus with no latency, reversibility or fatiguability? Central cause. Sudden onset episodic vertigo in elderly patient, lasting 10-15mins at a time with veering, slurred speech, numbness in legs, numbness and weakness in legs, no symptoms in between => veterbrobasilar insufficiency or TIAs in vertebrobasilar artery territory. Rarely occurs with vertigo alone, usually a whole cluster of symptoms are this area is densely packed with vital structures. Examination for vertebrobasilar insufficiency? Cardiovascular, especially vessels of neck and arms. Complete neurological examination including CNs. Management of suspected vertebrobasilar insufficiency? ABCD2 score => specialist referral, preferably stroke unit. Investigations would include FBC, UEC, BSL, lipids, ECG, CT or MRI, angiography. What would the probability diagnosis be for a young pt with episodic vertigo, occasional vomiting, lasting for minutes to days, sometimes but not always followed by headache, +/- recognisable triggers (ask about these)? Migrainous vertigo aka vestibular migraine. Migraine: Severe headache, often hormonal, hemicranial, throbbing, and sometimes associated with visual auras, nausea, photophobia and phono- phobia.

Vertigo due to vestibular migraine => (1) Must have history of migraine headaches and possibly also family history of migraines. (2) Often very sensitive to motion (unable to read in a car). (3) Features may include waking with severe vertigo/ataxia after well the night before, getting up to vomit, then lying propped up and extremely still (partner moving about room causes symptoms), day 1 worst, lasts 1-3d, hangover effect. Triptans useless for vertigo. For frequent attacks, encourage NEAT lifestyle, try amitriptyline or topiramate as prophylaxis (also on the list but with less evidence are propranolol, pizotifen, verapamil). Probability diagnosis for young man with dizzy spells when standing from sitting or moving around, associated with veering, using minocycline for acne? Minocyclineinduced vestibular neuronitis. Other drugs that can cause vestibulopathy? Salicylates, strep/genta/tetracyclines, phenytoin, antidepressants/hypertensives/histamines, quinidine, tranquilisers (phenothiazines, benzos), diuretics at high doses, GTN, alcohol, cocaine. Treatment for drug-induced vestibulopathy? Withdraw medication and treat expectantly (antiemetics for nausea if needed). Symptoms and signs of hyperventilation? SOB, palpitations, sweating, dry mouth, aerophagy, agitation, fatigue, malaise, extremity/perioral parasthaesias, carpopedal spasm. What causes symptoms in hyperventilation? CO2 loss => metab alkalosis => free plasma H+ depleted and borrowed from protein-H+ plasma complexes => Ca++ takes place of H+ bound to protein => hypocalcaemia. Diagnosis of hyperventilation? Get pt to breathe heavily for 2 minutes to reproduce symptoms. Treatment of hyperventilation? Assess for anxiety, depression. Reassurance no physical cause. Treat by consciously slowing breathing rate or breathing into paper (not plastic) bag or hands. Minor tranquilisers as last resort with referral if appropriate. Syncope and presyncope in young patients? Reflex syncope (micturition, fright, standing etc) vs POTS (postural orthostatic tachycardia syndrome +> "orthostatic intolerance" with tachycardia and reduced ventricular filling, can be disabling with myriad symptoms including chest pain and fatigue, refer to syncope unit). Should all pts with single, severe attack of vertigo be imaged for cerebellar infarct or haemorrhage? Yes, preferably MRI in first 2-3d but if not then CT. Importance is that some need surgical decompression of posterior fossa to relieve brainstem compression or hydrocephalus and once identified investigation for thromboembolic source or vertebrobasilar pathology needed. Normal pressure hydrocephalus triad? Ataxia, dementia, incontinence. Curable with VP shunt. Does acoustic neuroma cause vertigo? No. It is a benign, slow-growing Schwannoma allowing plenty of time for neuroadaptation. It causes unilateral tinnitus, unilateral hearing loss and sometimes imbalance (unsteady gait). What nerves does acoustic neuroma affect? CN VIII but also V and VII. What are the key tests for diagnosis of acoustic neuroma? Audiology (SN loss with auditory brain stem response showing absence of waveforms and latency of 5th wave; MRI). Treatment neurosurgical. How often is isolated vertigo due to vertebral artery compression? The case would be widely published if it happened. Most people have a reserve in the form of 2 vertebral arteries and being such a vital CNS region there would be other devastating effects if it was the cause. Is recurrent isolated dizziness often due to TIA/CVA? No. If it's recurrent, it's not

TIA/CVA. What are some dangerous treatment options for vertigo? Chiropractic neck manipulation (risks vertebral artery dissection/stroke .. also useless as dizziness doesn't come from neck), prochlorperazine (only useful for nausea and risks Parkinsonian effects). Can uncomplicated otitis media cause vertigo? No. Inner ear viral infections may, but unless sequalae of severe suppurative labrynthitis occurs the middle ear is completely separate from the inner ear and a middle ear infection will not cause vertigo. Can a loop of artery in the internal auditory canal cause vertigo? No, often appears on MRI reports but is no longer considered a relevant finding. Vertigo triggered by loud noise? Occurs in pts with structurally abnormal inner ear (perilymph fistula 2 to trauma/barotrauma) Is dementia genetic? Most cases are sporadic, but if strong family history especially early onset counsel and consider referral for genetic testing. What are the causes of vertigo? Peripheral (labyrinth&CN8: acute vestibular syndrome, Meniere's, BPPV, drugs, trauma, acoustic neuroma), Central (brainstem ischaemia/tumour, vertebrobasilar insufficiency, cerebellar degeneration, MS, migraine). Why is explicit diagnosis of dementia important? It attracts extra funding via the Aged Care Funding Instrument. What can a pt do to reduce risk of dementia and improve cognitive function? Address cardiovascular risk (reduce BP, lipids, BSL, weight, alcohol intake, smoking), exercise regularly, engage socially and do cognitive training (eg crosswords, Sudoku). What is a reasonable approach to dementia diagnosis? DDDDDD (Dementia instrument, delirium, drugs, depression instrument, daily activities, driving) Case finding on clinical suspicion (problem is that tools are not sensitive or specific enough for general population screening) by (1) Clinical history (collaborative assessment of cognition, behaviour, psychological state), (2) Physical examination (for causes of delirium: UTI, CCF, visual/hearing impairment), (3) ADL assessment (including safety: driving/falls ... and nutrition: Dementia outcome measurement suite), (4) medication review (home medications review, deprescribe as many meds possible esp anticholinergics/sedatives), (5) depression instrument (Geriatric Depression Scale), (6) cognitive function instrument (MMSE, GPCog, RUDAS for migrants, KICA for ATSIs). Routine investigations to order in dementia? FBC, (UEC not mentioned), LFT, ESR, calcium, TSH, B12 and folate, non-contrast CT brain. Recommended: CXR, fasting lipids, ECG, MSU. Consider: Fasting BSL, fasting homocysteine, HIV serology. Special investigations: EEG, MRI, PET, apolipoprotein E (E4 status increases risk of dementia), neuropsychological assessment. Treatment of dementia? Try to identify type of dementia, address lifestyle and meds, treat other reversible causes (hypoxia due to CCF or lung disease etc), refer to Alzeimer's Australia (and Commonwealth Respite and Carelink, and Dementia Hotline, and Dementia Behaviour Management Advisory Service), address legal issues (will, power of attorney, guardianship, advanced care directives), and if still in decline despite more conservative measures consider anti-dementia meds in consultation with specialist (cholinesterase inhibitors for mild-mod Alzheimer dementia: donepezil, rivastigmine, galantamine; NMDA inhibitor memantine for moderately severe disease ... PBS authority rules complex so check carefully and no clear stopping rules. Recheck cognitive function at 6mo). As disease progresses, ACAT may be mobilised.

When to refer dementia patients? Unsure of diagnosis, patient young/atypical, symptoms/signs atypical, psychosis or behavioural disturbance, multiple/complex comorbidities, considering anti-dementia meds. Histological findings of pts with frontotemporal dementia? "tau" and "ubiquitin" inclusions (the former related to MAPT gene and the latter to the progranulin gene both on Ch17). What are the types of dementia? Alzheimer's, frontotemporal, vascular, progressive supranuclear palsy, Parkinson's disease, alcohol (inc binge drinking). What are the pathological features of different kinds of dementia? Alzheimer's = tau (amyloid plaques and tangles); FTD = tau and ubiquitin inclusions; vascular = white matter ischaemia and stroke; PSP = tau pathologies; PD = Lewy bodies. What forms of dementia have early STM loss as a feature? Alzheimer's, vascular. Which forms of dementia have early frontal lobe symptoms/signs? Frontotemporal and progressive supranuclear palsy. What forms of dementia feature movement symptoms? Progressive supranuclear palsy, Parkinson's disease, very late in Alzheimer's. What types of dementia feature dysphasia? Occurs in semantic FTD, increases with age in Alzheimer's, varies in vascular. What are the types of FTD? Behavioural variant (lost inhibition, emotion/empathy, reactivity, insight, planning with intact memory .. may have changed eating habits, eg preferring sweet foods), semantic (Pick's disease: increasing difficulty with naming, word meaning, comprehension; paraphrasias ie substituting similar words like "aunt" for "sister"; fluent but non-sensical speech; difficulty recognising unfamiliar objects or faces, memory becomes a problem later), progressive nonfluent aphasia (slow, laboured speech with phonemic errors but naming and comprehension less affected; abstract thinking, math, memory and behaviour affected later). Can overlap with MND, PSP, corticobasilar degeneration. Is neuroimaging (MRI, CT, SPECT) diagnostic in FTD? Helpful yes, diagnostic no. FTD can occur without imaging signs and other dementias can show selective atrophy or hypoperfusion of frontotemporal areas too. Diagnosis clinical on basis of neuropsychiatric testing. Which forms of dementia respond to cholinesterase inhibitors? Alzheimer's (2030%), vascular, some with PD. Not useful in FTD. What treatment is there for FTD? No disease modifying agents. Symptomatic only. Aggression => distraction or letting pt play it out; trial SSRI or low-dose atypical antipsychotic, support carer and refer as necessary (psychogeries often required). Wandering => paint doors same colour as walls and put "no exit" signs up, childproof fences can help, put clocks/calendars/signs up to orientate pt, reduce noise levels, put name/address/RTS tag on patient in case lost. Sexual disinhibition => distraction, clothing modification to inhibit undressing, if refractory try SSRI or atypical antipsychotic. Apathy => encourage group activities at local day activity centre. Hygiene => compromise with shower/bath on alternate days and sponge down on other days. Repetitive behaviour => SSRIs approved but studies show useless, try redirection or engaging in other activities. What does the prefrontal cortex do? Motivation (damage = apathy), social norms, emotion, attention, organisation/choice/planning, recollection, programming of motor actions (implementation and monitoring, when to stop or continue). What C-spine trauma imaging to order? International guidelines suggest CT, but ATLS is sticking to plain film first dogma with targeted axial CT to areas of suspected injury or if entire C-spine not visualised on plain film in the face of evidence that this is suboptimal. Go with radiologist-reported CT unless unavailable

(in which case do 5-view plain film series of all 7 vertebrae and have reported by radiologist). Abnormal neurological or imaging findings warrant referral to acute trauma unit for further assessment. Significance of wear and tear changes in C-spine trauma imaging? Wear and tear of intervertebral joints and discs (aka spondylosis) is a red flag predictor of occult injury. What collar should be used before C-spine imaging? Any well-fitting semi-rigid collar OK (Laerdal Stifneck OK for a few hours; 2-piece Philadelphia collar a more comfortable longer term option). If none available, rigid surface, neutral supine position, sandbags, rolled towels and tape OK. What to do with late presentations of neck pain after trauma? Treat as for acute injury as soft tissue healing unpredictable in adults meaning gradual instability and deformity can occur leading to delayed catastrophic defects. Pain lateral to the midline less likely to indicate significant disc or ligamentous injury. Treatment of delayed or persistent neck pain with imaging negative for injury (or significant spondylosis)? Avoid soft collar +> causes wasting and dependence. Antiinflammatories, adequate follow up, early mobilisation, physio. What are some complications of traumatic brain injury? Depression (27%), anxiety (20%), schizophrenia (2x as common), cognitive impairment (2/3), seizures (10%), somatic complaints (headache, dizziness, pain, insomnia to >50%), postconcussion syndrome (15%, criteria above). What are classic features of TBI-related depression? Hopelessness, worthlessness, anhedonia. What works for depression in TBI? Sertraline, maybe music therapy, exercise, counselling. What treatment works for anxiety/PTSD post-TBI? Small amount of evidence for CBT in mild cases, neurorehabilitation in moderate cases. What about schizophrenia post-TBI? Standard treatment. What about cognitive impairment (trouble with letter writing, memory, paperwork)? Memory aids, reminders, cognitive rehabilitation (dopamine agonists and mindfulness meditation don't work). What are the differentials for a 58yo smoker with history of infected prosthetic hip joint suffering lower limb neurology and back pain, imaging showing degeneration, circumferential epidural enhancement, discitis and pathological fracture with cord compression? Osteomyelitis, malignancy. What is the presentation of spinal osteomyelitis? Indolent back pain +/- fever but rarely early neurological deficits (L>T>C spine). Organism usually S aureus. What are the complications of spinal osteomyelitis? Crush fracture => neurological impairment; abscess formation. What are the risk factors for spinal osteomyelitis? >Middle aged men, >1 comorbidity (DM, alcohol+++, renal disease, IVDU, malignancy, immunosuppression), surgery in past <6mo especially involving prostheses/grafts or indwelling devices. Spread most often haematogenous (abundant, slow flowing blood supply) , but can also be direct innoculation or contiguous spread. What is the best test for suspected spinal osteomyelitis? MRI most sensitive (xray and CT miss cases, especially early in course). Gallium bone scans also sens/spec. What is motor neurone disease (most common form = amyotrophic lateral sclerosis)? Progressive neurodegenerative disease characterised by motor systems failure resulting in death of nerves responsible for all voluntary movements => limb paralysis, weakness of muscles of speech and swallowing, ultimately respiratory failure.

What causes MND? Unknown. 5-10% familial. Toxins/chemicals/metals, trauma suggested as possible agents. What does diagnosis of motor neurone disease rely on? Clinical criteria, specifically the presence of upper (eg. spasticity, hyper-reflexia) and lower (eg. muscle wasting, fasciculations and weakness) motor neurone features all in same part of body eg arm or leg. No pathognomonic test .. still a diagnosis of exclusion. Pt's can present with difficulty writing, turning key, opening bottles, leg heaviness, tripping, foot drop, problems climbing stairs etc and evidence of wasting.Bulbar onset MND presents with slurred speech and tongue fasciculations. What are the most useful ancillary tests to support diagnosis of MND? Neurophysiological studies (NCS and electromyography) => support diagnosis, identify subclinical disease and extent of neuron loss and exclude mimics. Transcranial magnetic stimulation can may be useful to identify upper motor neuron dysfunction. MRI useful to exclude MS. What treatments should be offered? Referral to specialist MND clinics (contact MND Australia for info) to enable multidisciplinary approach, referral to support networks like MND Australia, EPC/GPMP, Riluzole (neuroprotective anti-glutamate drug) slows progression by 3-6mo (more recent analyses suggest benefit may be greater in concert with other measures .. monthly FBC, LFT initially), non-invasive ventilation relieves symptoms related to respiratory failure and prolongs survival by up to 12mo, percutaneous endoscopic gastrostomy (PEG) feeding tubes for pts with bulbar MND to prevent aspiration, assist pt to get affairs in order. Neurologist with special interest may be good option in rural areas with no MND clinic, and in some areas GP may need to act as case manager. Does stem cell treatment have a role? Still unproven, no positive results yet and "stem cell centres" in the Ukraine and China thus far lack published data or follow up. What benefit does a specialist-coordinated multidisciplinary team approach have in MND? QOL and survival benefit. Establish end of life directives early on. What are some palliative treatments in MND? Lorazepam for SOBOE, diazepam/morphine for breathlessness at rest or choking, morphine for pain, midazolam for agitation/distress, for excessive saliva or chesty secretions use glycopyrolate or hyoscine sulfate or amitriptyline, for thick saliva use NS or acetylcysteine nebs, use coloxyl and senna or movicol for constipation, magnesium/carbamazepine for muscle cramps, baclofen/clonazepam for muscle spasm/spasticity, carbamazepine or gabapentin for fasciculations, SSRI/SNRI/TCA for depression/lability, claustrophobia). What is Ramsay Hunt syndrome? Reactivation of zoster in geniculate ganglion of CN7 => otalgia, unilateral CN7 palsy, vesicles on TM (+/- external ear, dermatomal), vertigo, tinnitus, +/- deafness. Histopathology shows inflammation and neuritis of the facial nerve. Herpes zoster may also affect other cranial nerves, especially V, VI, VIII, IX and X. What would signify brainstem involvement In Ramsay Hunt? Ataxia. What is the treatment for Ramsay Hunt? Hospital, IV antivirals (aciclovir) more effective if started in <72h, followed by oral antivirals. Steroids controversial. Benzos (diazepam 5mg q4-6h) for vertigo. Long-acting opioids (oxycontin) may be needed for pain. What is Bell's palsy? Commonest cause of acute unilateral facial nerve paralysis (can also involve other CNs). Recurs in 12%, more commonly in pts with DM, immune compromise, family history. Be sure to exclude nasties before making initial diagnosis.

What type of salivary tumour can transform from benign to malignant possibly causing facial palsy? Pleomorphic adenoma (of salivary gland) transforming to adenocarcinoma. What other rare cause of LMN facial nerve palsy should be considered? Malignant otitis externa spreading to involve skull base (pseudomonas osteomyelitis of temporal bone in elderly, diabetic or immunosuppressed patients). Three-pronged reatment of Ramsay Hunt? (1) Facial nerve recovery (within 72h, start antivirals to inhibit viral replication and steroids for pain/residualweakness/synkinesis, despite Cochrane finding lack of RCTs to prove efficacy), (2) Postherpetic neuralgia management (age-related, use gabapentin weaning at 6mo), (3) Eye care (examine for complete closure, lubricating drops in day and taping at night, consider ophthalm referral for temporary tarsorraphy). Additional analgaesia may be needed initially. Is revaccination of oldies warranted to prevent shingles? Yes. Shingles Prevention Study showed 50% lower incidence among pts >60yo vaccinated with high titre live attenuated zoster vaccine and lower rate of postherpetic neuralgia in those that did get shingles. Approved for pts >50yo, but not on PBS. What are NCS used for? Test how nerves in arms/legs working, one damaged or more general impairment? Used to investigate weakness or parasthaesias (CTS, diabetic peripheral neuropathy). Pacemaker compatability with NCS should be checked with cardiologist. Pt only feels tapping sensation. Headache classification? Primary/secondary, brief/prolonged, frequent/episodic. What are the exceptions to the "brain tumours don't present as headaches" rule? Pituitary tumours, cancer elsewhere (mets). What is the cause of migraine? No vasospasm but wave of neural inhibition. Migraine treatment? Treat symptoms, prevent recurrence, treat cause ... treat symptoms with aspirin 900mg (or NSAID eg diclofenac instead if <16yo) taken with ice water at onset + metoclopramide to overcome gastric stasis. Move to triptan if headache not budging at 2h (cause non-cardiac chest tightness). Rescue with ergot/triptan IMIs or suppositories, with opioids+antiemetics as last resort .. for frequent flyers use headache diary, prevention with psychology/exercise/physio/acupuncture and meds starting with B-blockers (propranolol) then amitriptyline then valproate. What about opioids in migraine? Avoid except in for rescue situations. What is a complication of heroic migraine preventer methylsergide? Retroperitoneal fibrosis. What causes transformed migraines? Prolonged use of anti-migraine medications or analgaesics (withdrawal from codeine, triptans etc). What should be done in medication overuse headaches? Abrupt withdrawal is indicated (even of opioids as weaning doesn't work), inpatient treatment best but can do as outpatient with 1-2 weeks off work if patient insists ... treatment includes IV dihydroergotamine or lignocaine, then stick to NSAIDS with others esp opioids only >monthly, triptans 1-2x a week. Ergots can become abused and even NSAIDS. Tension headache treatment? Treat cause, symptoms, recurrence ... treat symptoms with aspirin/NSAIDS in acute cases // prevent recurrence with amitriptyline and avoid NSAIDS in chronic cases // supplement both with exercise, physio (massage, mobilisation, manipulation, posture correction), relaxation therapy (yoga, meditation), CBT. No evidence for SSRIs/TCAs. Cluster headache treatment? Triptan 1st line. 100% O2 helps some. Methylsergide and lithium as back up. Prevention with uptitrating verapamil (while monitoring ECG) or prednisolone 75mg/d.

Sex headache? Most likely benign sex headache but need to exclude SAH urgently. If proven benign, propranolol for 3-4 weeks is reasonable (2nd line verapamil). Hemicrania continua treatment? Indomethacin. Does CT exclude SAH? No, need LP, so don't do outpatient CTs looking for SAH, send straight to ED as the pt will need to go there anyway whatever the CT shows. Treatment of exertional/sex headache? Propranolol, verapamil. What are the serious acute and subacute headache causes? SAH, meningitis, encephalitis, acute obstructive encephalitis, TA. What is one possible complication of neck manipulation? Vertebral artery dissection. What is the symptoms most clearly associated with temporal arteritis? Jaw claudication (scalp tenderness frequent, headache variable). Is giant cell arteritis the only headache that responds to steroids? No, so not a good diagnostic tool (sinusitis, spondylosis, cluster, migraine can respond). Trigeminal neuralgia cause? Commonest is innocent irritating loop of artery entering pons (vs red flaggers like compressive lesion or demyelination). Pain focussed on one division of trigeminal nerve and severity fluctuates from episode to episode. Treat with carbamazepine, which sometimes fails due to inadequate dosing. Cluster headache triad: Eye pain, lacrimation, responds to O2/triptan.

Gastroenterology: Dysphagia classification? Oropharyngeal (trouble initiating with choking/coughing and nasal regurgitation) vs oesophageal (food sticking in chest), motility problem (early cough, liquids and solids) vs mechanical obstruction (late cough, solids only). What does coughing, choking or difficulty initiating suggest in dysphagia? Oropharyngeal level problem: dysmotility common (CVA, PD etc), obstructive cause rare (neoplastic/inflammatory mass, cricopharyngeal bar => Zenker's diverticulum). What does food hold-up in the lower retrosternal area indicate? Oesophageal (Motility common: Barrett's, achalasia, diffuse oesophageal spasm, eosinophilic oesophagitis // vs Mechanical rare: int/external mass compression, Schatzi's etc). What does dysphagia for solids only suggest? Mechanical obstruction (stricture, cancer) rather than motility problem (achalasia, oesophageal spasm, weak peristalsis). What important questions should be asked in cases of dysphagia? Localisation (cervical vs restrosternal), solids only or both solids and liquids (mech vs dysmot), duration and rate of progression (neoplasm), persistence of symptoms when not swallowing (globus), presence of reflux (GORD), cancer risk factors (smoking, alcohol), history of atopy (eosinophilic oesophagitis), medical history (ENT surgery, RTx, connective tissue diseases, cardiovascular and neurological disease, medications that might exacerbate (anticholinergics, bisphosphonates). What connective tissue disease is associated with reflux? Scleroderma. What medications can cause dysphagia? Medications that cause xerostomia (including anticholinergics like solifenacin/Vesicare for overactive bladder) or ulceration/stricture (bisphosphonates, potassium supplements). Examination in dysphagia? Swallow (50mL water); nutritional status and wt; obvious signs of neurological disease (speech); mouth (for thrush, acid erosion from reflux, oropharyngeal lesion); skin and joints (scleroderma), inspect neck/chest (surgical scars or radiotherapy tattoos), palpate neck (LNs, thyroid nodule, any other mass); brief cardiovascular examination for stroke risk (AF, murmurs, carotid bruit). What if pt presents with typical GORD symptoms (heartburn, regurgitation)? 4 week trial of PPI reasonable.

Steps in investigation? Oesophageal symptoms => trial of PPI if uncomplicated GORD and no red flags => barium swallow, then if abnormal endoscopy, then if normal manometry. Oropharyngeal symptoms => barium swallow then if abnormal referral. Advantages of investigating with barium swallow? Available, non-invasive, cost effective, good for detecting Zenker's diverticulum, cricopharyngeal bar, strictures, webs, rings, mass lesions. It is possible to assess dysphagia with liquids and solids, but testing for solids (eg with bread dipped in barium) is operator dependent and needs to be specifically requested. Disadvantages of barium swallow? Less sensitive in dysmotility conditions (like achalasia). Who should have upper endoscopy? All patient with significant oesophageal dysphagia to rule out obstructive lesion and malignancy (useless for abnormalities near upper oesophageal sphincter and in pharynx like Zenker's diverticulum). What is the gold standard test for diagnosing oesophageal motor disorders once mechanical obstruction excluded by endoscopy? Oesophageal manometry. What is eosinophilic oesophagitis? Allergic-immune condition with increased eosinophilic infiltration of oesophageal mucosa leading to stiffening and fibrosis, and impairment of peristalsis => multiple concentric mucosal rings, linear furrowings, microabscesses. How does eosinophilic oesophagitis present? Male Caucasians 20-39yo with acute food bolus obstruction or chronic, non-progressive dysphagia (also chest pain and reflux). How is eosinophilic oesophagitis diagnosed? Scope and mucosal biopsy (the only way to diagnose). What is treatment of eosinophilic oesophagitis? PPIs, a course of swallowed fluticasone, and in kids a six food elimination diet (cow's milk protein, wheat, soy, eggs, seafood and peanuts). What is Schatzki's ring compared to oesophageal web? Mucosal ring at GOJ caused by reflux (as compared to exactly the same thing at other levels in oesophagus). Known as "steakhouse syndrome" because symptoms experienced when swallowing large boluses. Dx prone-oblique views during barium swallow => Rx for all webs including Schatzi's dilatation during endoscopy + adjuvant PPI. What are three causes of mucosal strictures? Iron deficiency (Plummer-Vincent syndrome), bullous dermatological disorders, and pill-induced ulceration with subsequent stricture formation (oral bisphosphonates) => bougie dilatation +/- stent if difficult + PPI for reflux (steroid injection sometimes used if rapidly recurrent). What are the biggest risk factors for oesophageal SCC? Smoking and alcohol consumption. What causes oesophageal adenocarinoma? Reflux => Barrett's oesophagus => oesophageal adenocarcinoma. Highest risk group for Barrett's and oesophageal AC? Male smokers with long-term GORD symptoms. Commonest oesophageal malignancy? Adenocarcinoma has overtaken SCC. Best diagnostic test for oesophageal malignancies? Upper endoscopy + biopsy. Treatment of oesophageal malignancies? Surgery + chemoradiotherapy. Stenting sometimes used as bridging or palliative modality. How is achalasia best characterised? Immune mediated motor neurodegeneration => impaired relaxation of the lower oesophageal sphincter and defective/absent peristalsis => belching, regurgitation, chest pain, heart burn, wt loss => better with repeated swallows => bird's beak appearance on barium swallow and dilated

oesophagus with residues on scope. Monometric findings in achalasia (memorise in case of picture question)? No lower oesophageal sphincter relaxation indicated by no change in pressure in lower high pressure zone and no peristaltic contraction. Achalasia treatment? Balloon dilatation, botox injections (generally not recommended due to lower success rates and only 3-6mo effect), surgical myotomy (favoured by younger patients). Which is more common, achalasia or diffuse oesophageal spasm? Achalasia. Diffuse oesophageal spasm rare, high amplitude simultaneous contractions (only 5% show typical corkscrew appearance on barium swallow) => usually benign course, improving with time, trial of CCBs or nitrate donors (sildenafil, isosorbide) but response often poor, botox better, myotomy as last resort. What is weak peristalsis? Non-specific manometric diagnosis characterised by low amplitude contractions unable to contract strongly enough to clear bolus. What is dyspepsia? Upper abdominal or retrosternal pain, discomfort, heartburn, nausea, vomiting. Causes of dyspepsia? Reflux oesophagitis commonest in western countries. PUD, functional dyspepsia, OG cancer (rare cause). Few cases due to helicobacter in absence of ulcer (helicobacter now much more a problem in elderly due to poorer hygiene during their childhood. Rare causes of dyspepsia? Diabetes, hypercalcaemia. Dyspepsia risk factors? NSAIDs, smoking (dose dependent), alcohol, SE status, obesity, other meds (COX2 inhibitors, pred, antibiotics, SSRIs). Causes of PUD? Helicobacter then NSAIDs. Also smoking. How does GORD happen? Acid reflux across lax lower oesophageal sphincter. Are COX2 inhibitors (celecoxib, meloxicam) less likely to cause dyspepsia? No, but less likely to cause PUD. Causes of GORD? Smoking (dose dependent), fats, caffeine, alcohol, CCBs (reduce sphincter tone), theophylline. Never helicobacter. Does helicobacter cause GORD? No, in fact it may be protective by raising gastric pH. Helicobacter only causes dyspepsia via ulceration. Will treating helicobacter resolve dyspepsia? No, in absence of ulcer. History suggestive of PUD? Family history of PUD, smoking, periodicity of symptoms, pain on empty stomach, NSAIDs, SSRIs, COX2 inhibitors (associated but less strongly so). Useful history in GORD? Most commonly heartburn (retrosternal pain), reflux and history of possible precipitants (inc NSAIDs, caffeine, chocolate, alcohol, fatty/spicy foods). Seek red flags and ask about cough, wheeze, hoarseness, sore throat, water/acid brash, dysphagia, odynophagia. Diagnosis of GORD? Rapid symptomatic improvement with acid suppression and prompt relapse on cessation (represent for investigation if not improving at 2-4 weeks). Prompt relapse on cessation of PPI virtually diagnostic. How common is helicobacter infection? Becoming rarer among kids/teens. More common in the elderly (infected during childhood). Best tests? Serology cheap, available and accurate for detection. Urea breath test best non-invasive option to confirm eradication as serology may remain positive for 12mo. Neither give information on presence/absence of complications. Dyspepsia treatment approaches? H pylori neg => probably no ulcer => trial of PPI then refer if refractory. H pylori positive => ulcer possible => options are (1) refer for scope or (2) treat, suppress with PPI and refer if symptoms persist (probably the better option on balance).

Does referral for endoscopy for dyspepsia detect treatable upper GI cancers? No. Treatment and resistance? Amoxi and clarithro and either omeprazole or esomeprazole for a wk. Resistance to clarithro and metronidazole confirmed in Australia. Confirm eradication in pts with complicated PUD or comorbidities. Choice of analgaesic in high GI risk? Low CV risk => COX2 inhibitor. High CV risk => avoid NSAIDs, but if absolutely necessary naproxen + PPI (CV risk wins). Choice of NSAID in low GI risk? Low CV risk => traditional NSAID. High CV risk and on aspirin => naproxen + PPI. Contribution of biliary or sphicter of Oddi dysfunction in dyspepsia? Unknown but probably small. When is upper endoscopy indicated? Red flags or GORD unresponsive at 2-4 weeks (cease PPI first). Red flags of dysphagia? Anaemia, melaena or bloody stools, dysphagia, jaundice, early satiety, wt loss, symptoms refractory to acid suppression. Does gastric cancer usually cause dyspepsia? Rarely. Is oesophageal cancer a common cause of dyspepsia? No, it is a rare cause but if present causes dyspepsia in 40% of cases. Are most NSAID-associated gastric erosions and ulcers painful? No, most present with GI haemorrhage. Risks of GORD? Barrett's oesophagus and oesophageal adenocarcinoma. What effect does combination of clopidogrel and aspirin have on GI bleeding risk in patients with coronary stents? Synergistically increases it. Most effective medical treatments for GORD? Increased dose PPI (100% effective), single dose PPI (80%), H2 antagonists or cisapride (50%), antacids (20%), lifestyle (20%). How long should patients stay on a PPI? If severe oesophagitis seen on scope, risk of stricture/bleeding necessitate maintenance on PPI. Initial 1-2 week trial or ondemand acid suppression or antacid treatment may be as effective as regular acid suppression for some. Classification of gastro-oesophageal cancers: SCC of oesophagus, AC of distal oesophagus and GOJ, AC of remainder of stomach. Risk factors for oesophageal SCC? Smoking, alcohol, vitamin AC deficiency, caustic ingestions, achalasia. Risk falls after quitting smoking/alcohol. Risk factors for oesophageal/GOJ AC? GORD/Barrett's, obesity, smoking, red meat, alcohol. Risk factors for gastric AC? Smoking, low SE status, poor diet (low protein, high carb), salted/pickled foods, vitamin ACE deficiencies, helicobacter pylori infection (other associations: pernicious anaemia, gastric intestinal metaplasia and previous gastric surgery). Diagnosis of OG (oesophageal and gastric) cancers? Screening in low risk populations like Australia not recommended, but case finding may be worthwhile in high-risk and dyspeptic patients. Screening endoscopy recommended in longstanding GORD (esp obese male pts). At what stage do patients typically first experience symptoms in OG cancer? Late. Does upper endoscopy improve survival in gastric cancer? No. What symptoms are the most reliable predictors of OG cancer? Dysphagia, A>55yo. Upper GIT red flags: A>55yo, dysphagia, diagnosis unclear, refractory symtoms, anaemia, anorexia, vomiting, abdominal mass, wt loss, GI bleeding. Refer if one or more present. What is Barrett's oesophagus? Metaplastic condfition where squamous oesophageal epithelium is replaced by columnar epithelium (seen macroscopically

and on biopsy). What treatments reduce progression of Barrett's oesophagus? PPIs may do so but unproven (NSAIDs may also reduce risk, combined PPI+NSAID trial underway in UK). GORD surgery provides symptomatic relief and reduces rate of progression to cancer more effectively than PPIs. Endoscopic mucosal resection has replaced oesophagectomy to excise tissue affected by high grade dysplasia or non-invasive cancer (long term endoscopic surveillance required). Ablation (Argon ablation and more expensive radiofrequency ablation aka HALO) techniques show promise. What degree of dysplasia do most pts with Barrett's oesophagus have? None. What risks does PPI use carry? Osteoporotic hip fracture due to reduced calcium absorption in low acid environment (insufficient evidence for prophylactic bisphosphonates). Calcum and vitamin D supplementation should be considered if on long-term acid suppression, may increase risk of colonisation with C difficile esp in elderly (controversial), reduced clopidogrel absorption. Headache, diarrhoea, hypomagnesaemia, rarely irreversible interstitial nephritis, CAP and enteric infections. How is OG cancer diagnosed? CT or barium swallow suggestive but endoscopy and (at least 7) biopsies needed for diagnosis. Staging: CT chest/abdo/pelvis for mets or locoregional spread; endoscopic ultrasound for loco-regional spread only when it will affect treatment (eg surgery called off if invasion of aorta present); in oesophageal/GOJ cancer, CT-PET superior to CT-ultrasound combined (radiolabelled glucose uptake increased in malignant tissue due to higher metabolic rate ... used in GOJ cancer only); laporoscopy to detect occult peritoneal/liver spread in GOJ/stomach cancer (allows peritoneal washings for cytology, which if positive may preclude curative surgery). How is fitness for surgery assessed? QOL, exercise tolerance, thorough cardiopulmonary assessment (TTE, EST, cardiopulmonary stress test), review by experienced anaesthetist. What is the usefulness of narrow band imaging and chromo-endoscopy? Used during endoscopy to improve visualisation and localisation of structures or tissue types and hence improve diagnostic yield of endoscopy. Not diagnostic in or of themselves. Does higher OG cancer risk carry forward to first and second generation migrants from Japan and China? Yes. How is T1a (confined to mucosa) gastric/oesophageal disease treated? Day stay endoscopic mucosal resection (EMR) as risk of LN involvement <3%. Risk of LN involvement 14-20% in T1b so EMR not considered in these cases. What is the default treatment for OG cancer? Gold standard is surgery. How is SCC of the upper third of the oesophagus managed? Radical chemoradiotherapy alone as primary treatment. How about mid and distal oesophageal SCC? Multimodal treatment (surgery +/chemotherapy or chemoradiotherapy) vs chemoradiotherapy alone as primary treatment. Treatment of choice is neoadjuvant therapy (no consensus if radiotherapy should be added) then oesophagectomy if pt fit enough. What is the traditional, open method of oesophagectomy? Ivor-Lewis oesophagectomy. What is the standard procedure for proximal gastric cancer? Total gastrectomy with Roux-en-Y reconstruction. How about distal gastric cancer? Subtotal gastrectomy. What are the symptoms of post-gastrectomy dumping syndrome? Postprandial reflux , pain, bloating, diarrhoea.

What are the possible causes of diarrhoea after total gastrectomy? Poor mixing of pancreatic enzymes with food in reconstructed foregut (supplement pancreatic enzymes) or bacterial overgrowth in reconstructed small bowel (carbon-14 deoxycholate breath test). Can refer for colonoscopy to r/o colonic pathology. What are symptoms of bile reflux after total gastrectomy? Heartburn, upper abdo pain and bilious vomiting => prokinetics and cytoprotectives. How are post-oesophgectomy GORD and dumping syndromes managed? Refer to dietician especially for dumping syndrome. PPI for GORD (or cytoprotective sucrulfate after gastrectomy) and prokinetic for dumping. Vitamin deficiencies after OG surgery? Vitamin B12, lipid soluble vitamins, iron. What are the sequelae of recurrent laryhngeal nerve palsy after oesophagectomy? Hoarseness and aspiration risk. What to do in recurrence of symptoms after treatment or when suspecting recurrence? CEA, CA 19-9, CT, endoscopy and occasionally PET. Treatment of recurrent laryngeal nerve palsy? Teflon injection as filler to hold paralysed vocal cord in medial position. Differentials of postprandial RUQ pain radiating to back, nausea, pale stools, dark urine, jaundice and mild RUQ tenderness? Biliary colic (postprandial pain and nausea suggestive), acute cholecystitis, choledocholithiasis (obstructive symptoms suggestive), Mirizzi syndrome (external compression of common bile duct by impacted stone in neck of gallbladder or cystic duct, less common), acute cholangitis (more likely if fever present), gallstone pancreatitis, hepatitis. Biliary colic triad? Severe pain, vomiting, pain radiation. Acute cholangitis triad (Charcot's triad)? RUQ pain, fever, jaundice. Biliary conditions needing urgent hospitalisation, IV ABx and surgery? Acute cholangitis, cholecystitis, gallstone pancreatitis (more fulminant course with perforation/sepsis risk). Biliary colic, symptomatic choledocholithiasis or comorbidities/DM/immunosupp => also score a hospital stay. Biliary investigations? FBC (? WCC), LFT (medical vs surgical jaundice), lipase, UEC (in case contrast studies needed), upper abdo US (sensitive and specific for cholelithiasis and good for assessing whole biliary tree, identifying medical vs surgical jaundice). MR cholangiopancreatography may be used by surgeons to distinguish choledocholithiasis from Mirizzi syndrome and avert ERCP. Hepatocyte dysfunction vs cholestasis? AST + ALT up in the former. Bilirubin, ALP and GGT up in the latter. But picture can be mixed. Gallstone disease treatment? Asymptomatic stones => don't usually need treatment. Conservative mx of symptomatic disease => high rates of recurrence. Lap chole is standard treatment and virtually as safe acutely as electively in hands of specialist laporoscopic surgeons. Treatments for symptomatic choledocholithiasis? ERCP (with sphincterotomy, stone extraction) then lap chole, vs lap chole with intraoperative cholangiogram +/- bile duct exploration (open bile duct exploration and chole less common). Treatment/referral for uncomplicated biliary colic? Refer early as biliary colic is a warning sign and delayed diagnosis/treatment results in complications (cholecystectomy at <24h from onset of biliary colic reduces complications and conversion to open cholecystectomy). What is NAFLD? Hepatic manifestation of metabolic syndrome linked to insulin resistance ranging in severity from simple hepatic steatosis through to non-alcoholic steatohepatitis, cirrhosis, liver failure and liver cancer. Diagnosis problematic as no non-invasive, sensitive test to distinguish benign hepatic steatosis from more serious NASH and inherent difficulties in monitoring response to treatment by

biopsy makes management data flawed and inconsistent => so no consensus on management. What is the leading reason for liver transplantation and is this expected to change in the future? Now => Hep C. NAFLD expected to be the leading reason for liver transplantation in future. What is the link between insulin resistance and NAFLD? Insulin resistance underpins pathogenesis and progression of NAFLD. What causes NAFLD? Increased visceral adipose tissue => increased circulating hormones +/- mitochondrial dysfunction => insulin resistance (reduced production of insulin sensitiser adiponectin in obesity amplifies insulin resistance) => increased release of fatty acids from visceral fat (also dietary and genetically increase lipogenesis) => preferential uptake of FFAs from portal circulation by liver => increased formation of triglycerides, reduced release of stored triglycerides from hepatocytes due to reduced apolipoprotein synthesis and microsomal transfer protein gene polymorphisms => increased reactive oxygen species via mitochondrial and peroxisomal FFA oxidation process (also M1 macrophages in adipose tissue activated, releasing TNFa and IL6) => increased hepatocyte apoptosis with rate of injury/apoptosis driving progression to fibrosis (exact mechanism of progression unknown). What contribution to hepatic stellate cells make in chronic liver damage? Produce excess extracellular matrix leading to fibrosis. Is central adiposity predictive of NAFLD? Yes (as well as high waist-hip ratio, diabetes, hypertension, high triglycerides, PCOS). What are some secondary causes of NAFLD? Hep C (esp genotype 3 .. mediates insulin resistance and causes fatty liver in 50% of pts), OSA-related hypoxia, glucocorticoids, amiodarone, tamoxifen, HAART, jejunoileal bypass, prolonged TPN. Can alcohol-induced and non-alcoholic steatosis be distinguished on histopathology? No, distinction can only be made on history and this is difficult as well as alcohol use often under-reported. What about patients with hepatic steatosis or steatohepatitis who drink at "safe levels"? There is no such thing as some pts more sensitive to toxic effects of alcohol than others and in any case history often unreliable. What are components of metabolic syndrome? Insulin resistance, abdominal obesity, hypertriglyceridaemia, low HDL, HTN. Do children with parents or siblings who have NAFLD exhibit higher risk for NAFLD? Yes. How does the liver store fat? As triglycerides. What form of fat releases more fatty acids, subcutaneous or visceral? Visceral (so visceral fat more closely associated with insulin resistance and NAFLD). Is adipose tissue an inert depot of stored energy? No, it is a dynamic organ capable of secreting hormones and cytokines perpetuating changes in favour of insulin resistance. Is insulin-sensitiser adiponectin release reduced in obesity? Yes. How do NAFLD patients present? Asymptomatic unless advanced liver disease present, when jaundice/ascites/encephalopathy etc present. Signs of advanced liver disease? Jaundice, ascites, oedema, encephalopathy, GI bleeding, fatigue, muscle wasting. What are poor prognostic indicators in NAFLD? Diabetes, cirrhosis, age, other causes of liver disease (alcohol, Hep C, haemochromatosis). When to go looking for or suspect NAFLD? All metabolic syndrome patients. Are LFTs sensitive/specific for NAFLD severity or progression to steatohepatitis?

No, not sensitive or specific. Normal LFTs can persist despite histological progression to NASH or early cirrhosis. Abnormal LFTs (frequently AST and ALT 25x upper limit of normal with deranged bilirubin/albumin late in course) are a signal for investigation, but little more. What test is essential to detect euglycaemic insulin resistance? 2-hour glucose tolerance test with paired hourly glucose and insulin levels. What are the histological changes associated with NASH? Steatosis with mixed lobular inflammation and ballooning of hepatocytes. Why is liver biopsy not routine in NAFLD despite being diagnostic gold standard? Invasive with risk of complications, cost, sampling variability due to patchy steatosis. What is the de facto imaging investigation of choice in NAFLD? Ultrasound, accessible, cheap, no radiation (but not sensitive if steatosis <25-30% of liver, doesn't accurately predict histopathology, operator dependent). What is treatment for NAFLD? No proven medical treatment, primary prevention of obesity is the holy grail. Remove cause (5-10% wt loss through low GI diet and moderate-vigorous exercise, bariatric surgery for the morbidly obese only). Metformin may improve aminotransferase levels and some histological data but not convincing enough to recommend routine use. Glitazones may improve NAFLD but at expense of wt gain and possible CCF complications, so not taken up widely. Orlistat showed histological improvements, but related to wt loss not direct effect. No evidence for alternatives like antioxidants, N-acetylcysteine, zinc, folate etc. Why is it difficult to lose weight once you put it on? New, higher homeostatic set point and not possible to lower set point again through subsequent weight loss. How do low fat/energy diets compare to ad libitum low GI diets in overweight/obese patients? Meta-analysis => low GI diets => lower weight, lower fat, better lipid profile. What are the benefits of moderate to vigorous exercise? Decreases body weight, total fat, insulin resistance. Improves glucose tolerance, lipid profile, hypertension. Vigorous better. What is the most commonly notified disease in Australia? Hep C. Can you be reinfected with Hep C if you have had it and cleared it? Yes. Does liver transplantation effectively eliminate the Hep C virus? No, infection of the graft occurs in 100% of cases. How is Hep C transmitted? Blood borne only (not in other bodily fluids) mainly through injecting drug use (90%) or unsafe medical/surgical procedures, occasionally tattooing or acupuncture. There is a risk of sexual transmission for MSMs with HIV esp through anal sex (risk of heterosexual transmission low at <5%). Mums shouldn't be discouraged from breastfeeding unless nipples cracked/bleeding. No need for elective Caesarian (perinatal transmission 2-5%). What kind of virus is Hep C? RNA flavivirus. What tests to order in HCV diagnostic panel? antiHCV antibodies and LFTs (HCV RNA if antibodies). What is the window period for HCV? Advise to retest at 3mo (often along with HIV). What is the serological picture for a person who has cleared HCV? anti-HCV antibodies positive, HCV RNA negative. What follow-up tests to order in HCV+ patient? Check genotype and HCV quantitative PCR aka "viral load" (determines length of treatment and potential response to it). Assess for cirrhosis as this will affect treatment choices: LFTs, UEC (cirrhosis affects sodium, renal failure a contraindication to ribavirin), FBC (platelets, macrocytosis as indication of alcohol use, interferon causes cytopaenias),

INR/PT(synthetic function), ultrasound, and AFP if cirrhosis identified. Check TSH as interferon treatment can cause hyper/hypothyroidism. Check for other poor prognostic indicators like diabetes and metabolic syndrome: BSL (interferon can worsen control), lipids. Check for HAV immune status and HBV immune/infectious status (Hep A IgG, antiHBs/antiHBc/HBsAg) ... vaccinate if necessary. Check for other conditions that could give the liver a double whammy: HIV, iron studies, serum copper, caeruloplasmin, autoimmune screen, alpha1 antitrypsin level. How does the Hep C virus cause necroinflammation, fibrosis and cirrhosis? Indirectly via inflammatory response due to its presence in hepatocytes. Poor prognostic indicators? MOLDiE: Male, old or obese, long duration, diabetes or metabolic syndrome, ethanol abuse. Why has development of a vaccine been difficult? Hep C is highly heterogenous with multiple quasispecies even within same individual. Six main genotypes with different distribution and varying response to antivirals: genotype 1a and 1b most common worldwide, with these two and genotype 3a the most common in Australia. What is the most important predictor of likely response to antiviral treatment? Virus genotype (GTs 1 least responsive then GT 4. GTs 2 and 3 respond better). However, this does not influence disease progression or prognosis. How is Hep C diagnosis made? Combination of serum anti-HCV antibodies and confirmatory HCV RNA. Is liver biopsy a prerequisite for starting treatment for chronic HCV? No, it is the gold standard for determining severity of fibrosis and useful in terms of prognostic information, but not necessary to initiate treatment. What non-invasive tests is available to assess liver fibrosis in HCV and HBV? Transient elastography (FibroScan), determines velocity of elastic shear-waves through liver. Serum biomarkers (low platelets and reversed AST:ALT ratio .. ALT higher in chronic HCV, but in cirrhosis this is reversed. Validated serological markers of fibrosis Hepascore (using validated serological markers of fibrosis) mainly used in SA and WA. What is the goal of HCV treatment? Viral eradication (sustained virological response or SVR => HCV RNA absent at 6mo). Does SVR result in regression of fibrosis? Yes, even in advanced stages. Who should be considered for HCV antiviral treatment? All Metavir F3 and F4 patients. Treatment naive patients with compensated chronic liver disease who desire treatment and have no contraindications regardless of whether or not ALT normal. Who should wait? Weigh risks vs benefits in pts with mild disease despite longstanding infection or elderly patients. If fibrosis absent or mild, might be worth waiting 4-5 years for improved treatments. How common and severe are side effects of interferon treatment in chronic HCV? Common and often severe: flulike symptoms, anorexia/diarrhoea and wt loss, insomnia and anxiety/depression), low libido, rashes or worsened psoriasis, hair loss, cytopaenias, hyper/hypothyroidism, worsened glycaemic control. Rarely: interstitial lung disease, cardiomyopathy, retinopathy. What about ribavirin side effects? Rash/pruritis, URT congestion, haemolytic anaemia, teratogenicity What is the significance of RVR (rapid viral response) during antiviral treatment for HCV? Patients who experience RVR (HCV RNA not detectable at 4 weeks) have >90% chance of virus eradication regardless of treatment regimen as long as they complete it. What are boceprevir and telaprevir and what are their advantages and

disadvantages? Direct acting antivirals that competitively inhibit protease complex involved in HCV replication. Combined with PEG-IFN and ribavirin they yield much higher rates of virological cure and treatment duration is often shorter if fibrosis not advanced (only available for use in HCV GT 1). Adverse effects associated with standard PEG-IFN plus ribavirin treatment are no more frequent when protease inhibitor added. However, dosing schedules are demanding and complex though, and resistance is a major issue so can not be used as monotherapy (without interferon) or dose modified. Major cause of protease inhibitor resistance is interferon resistance (often due to previous treatments). Severe anaemia requiring transfusion or EPO can occur, often requiring modified ribavirin dose. What is PEG-IFN: Pegylated interferon. What is the duration of triple therapy? 24 to 48 weeks depending on drug and response. Side effects of protease inhibitors? Anaemia+++ (esp boceprevir). Boceprevir causes dysgeusia (bad taste) => reduced appetite => wt loss. Telaprevir causes rash in 1/3 to 1/2 of patients, sometimes severe (SJS/TEN) and in 1/4 of patients perianal itching/burning. Perianal symptoms usually resolve when treatment stopped. What are contraindications to new triple therapy? Same as old therapeutic regimen: organ failure (decompensated cirrhosis, severe cardiac disease, other organ transplant, ribavirin contraindicated in renal failure), special groups (pregnant or breastfeeding, kids), active autoimmune disease, unstable mental illness, uncontrolled DM. Can new triple therapy be used in paediatric patients? No, data relating to response rates and safety in children are lacking. Who to screen for HCV? Haemophilia, Haemodialysis, drug Habit, Homosexuals with HIV, Home country, Hospital workers, inHerited, jailHouse. IVDUs (present or past), transfusions/transplants before 1990, associated conditions like haemophilia/HIV or dialysis and deranged LFTs, incarceration, unsafely performed tattoos or piercings, emergency medical workers or those with hx needlestick, MSM with HIV, kids of HCV positive mothers, migrants from HCV prevalent countries like Egypt (poor infection control in past parenteral schisto treatment). What general advice to give to pt with HCV? Sterile needle practices, drug substitution (methadone etc), condoms for people with multiple partners or MSM HIV+s, don't share potentially contaminated implements (inc toothbrushes/razors), vaccinate for HAV and HBV, healthy lifestyle/wt, advise on efficacy of treatment, psych support. What about pt with risk factors who tests negative? Vaccinate against HAV (and HBV if risk factors or close contacts with disease), address the risk factors (IVDU cessation, sterile needles, not sharing razors etc, safe sex if MSM/HIV and for other infections, healthy lifestyle messages including alcohol moderation), regular review. Can pts who have cleared HCV donate blood? No, but they can be organ donors due to chort supply and low risk of transmission. What investigations to order for ab obese, binge drinking, sporadic IV drug user who feels well and has no findings on physical examination? FBC, UEC, LFT (? fatty liver), Hep B/C and HIV (IV drug use .. order HBsAg, antiHBs, antiHBc, antiHCV1, HIV serology), fasting lipids (alcohol => hypertriglyceridaemia), fasting BSL (metabolic syndrome in obese patient), Hep A serology to assess immunity and possible need for vaccination. What are antiHBc and antiHBs? Hepatitis B core antibody, hepatitis B surface antibody.

Consenting pts for Hep B, Hep C and HIV testing? Risk assessment, what positive/negative results mean, discussion of reason for test, meaning of positive or negative result, window period, ways to reduce the risk of transmission, discussion about confidentiality, availability of treatment, assessment of social supports, arrange follow-up to discuss results. Sexual health screening if indicated. Consenting may take more than one consult in pts LOTE/ATSI patients and may need interpreter. What if antiHCV antibodies positive and HCV RNA negative? Repeat RNA test in 6mo to confirm. Support/information for HCV patients and pregnant/planning women with HCV? Hepatitis Australia Information Line, Hepatitis Resource Centre website, Pregnancy, birth and beyond resource for women with hepatitis C. Lethargy screen? FBC, iron studies, UECs, LFTs, fasting BSL, TSH, CRP (+/ESR). Blood test results suggestive of cirrhosis? Anaemia, thrombocytopaenia, transaminitis with AST/ALT ratio >1, low albumin. Further investigations in pt suspected to have cirrhosis? HAV IgG (? need for vaccination), HBsAg/antiHBs/antiHBc/antiHCV (HBV and HCV are potential causes), INR (? synthetic function of liver), fasting iron studies (? haemochromatosis), upper abdominal ultrasound. Follow up once cirrhosis confirmed? Check AFP for HCC, HCV genotype and viral load if relevant, refer to gastroenterologist for scope ? varices. Lifelong follow up monitoring for liver function and HCC (ultrasound and AFP every 6mo), lifestyle intervention inc minimising alcohol and avoiding hepatotoxins, managing weight (HCV and cirrhosis associated with insulin resistance). Signs of cirrhosis? Hard liver edge, splenomegaly (portal hypertension), muscle wasting, subclinical hepatic encephalopathy. Signs of decompensated cirrhosis? Jaundice, ascites/oedema, coagulopathy, variceal bleeding, hepatorenal syndrome, encephalopathy, muscle wasting and weakness => refer to specialist centre for liver transplant assessment. Blood test for acute vs resolved/immunised HAV? HAV IgM and IgG. Step 1 of HBV serology: screening for infection? HBsAg, antiHBs and antiHBc, then other tests depending on results. Step 1 of interpreting HBV serology? HBsAg, antiHBs, antiHBc, ALT. If surface antigen positive => active infection => go to step 2. Vaccination: antiHBs (surface antibody) only positive. Infection cleared from serum: antiHBs and antiHBc (surface and core antibodies) positive but HBsAg (surface antigen) negative. Acute infection: all positive, including antiHBc IgM. Chronic infection: antiHBc and HBsAg positive, antiHBs and others neg. Infectious? High titre (HBV DNA level) Step 2 of HBV serology (note all phases below can be seen in acute or chronic HBV)? What phase is the infection in? Do physical examination, HBeAg, antiHBe, HBV DNA level, LFT/FBC/INR/AFP, liver ultrasound. Discuss transmission prevention (HBV and other BBVs, screen household). Immune tolerance: HBeAg+ and HBV DNA titre high (acute infection), antiHBe(no immune response yet), normal LFTs. Immune clearance: HBeAg+, antiHBe+ and HBV DNA titre falling (immune system response), abnormal LFTs. At risk of progression so refer for consideration of antivirals and consider screening for HCC q6mo (AFP and ultrasound).

Immune control: antiHBe+, HBeAg- and HBV DNA titre low (disease controlled by immune system), normal LFTs. Immune escape: antiHBe+ and HBeAg- but HBV DNA rising and abnormal LFTs (immune system has lost control of virus). At risk of progression so refer for consideration of antivirals and consider screening for HCC q6mo (AFP and ultrasound). 10-20% will go on to immune escape. Monitoring patients in immune tolerance phase chronic HBV? LFTs, HBV DNA every 6mo (? only funded every 12mo) What HBsAg positive groups should definitely be surveilled for HCC? Asian men >40yo, Asian women >50yo, Africans >20yo, cirrhotics, FHx HCC. Geographical regions associated with high rates of HBV? China (>50% of HCC worldwide) and other parts of Asia. Also ATSIs. What is the difference between HCC in HBV and HCV? In HBV, cancer can occur in absence of cirrhosis. How common are HAV outbreaks in Australia? Rare but occasionally occur when water contaminated with sewage. What is different about viral hepatitis infections in kids? It is milder, serum clearance may not occur. What is the difference clinically between viral hepatitis and drug/alcohol induced hepatitis? Systemic symptoms seen in viral hepatitis but not in drug-induced hepatitis. Tests to order in suspected acute hepatitis? LFT, FBC, INR, UEC all appropriate (Medicare won't fund a full hepatitis viral screen, so in acute illness order HBsAg, HAV IgM and antiHCV). What additional tests to order in HBsAg+ pts (new diagnosis of acute or chronic Hep B infections)? HBeAg, antiHBe, HBV DNA viral load (? stage of infection). HAV, HCV, HDV, HIV serology. FBC, LFT, INR/APTT, AFP, liver ultrasound including portal venous doppler. Treatment of acute HBV? Advise treatment not required as immune system will clear infection from serum in 2-3mo with liver settling back to normal function (but that infection will remain dormant in liver), encourage contact tracing (to check for infection and immune status), always go over risk of transmission to others and of picking up other BBVs (prophylaxis). Address D&A issues if relevant. What if HBV is cleared from serum but LFTs don't normalise? Check for HCV (remember window period). How is HBV transmitted? Primarily an STI in Australia. In high prevalence countries, transmission usually vertical, so check mum and siblings of cases. Horizontal (from peer) transmission can occur, esp in kids. What is a healthy carrier of HBV? There is no such thing. This term (referring to a HBsAg/antiHBe positive, LFT normal state) predates understanding of natural history of HBV. All HBV+ patients should be surveilled for progression of disease to a more advanced phase. Can pts with chronic HBV infection have progressive liver disease despite normal examination and normal ALT? Yes. What other possibilities need to be considered in a pt with chronic HBV and new finding of deranged LFTs? Alcoholic steatohepatitis, NAFLD, medication, biliary disease, HCC, liver mets, combination of the above. Management of ATSI patient in immune escape phase of HBV? Refer for consideration of HBV treatment, multidisciplinary approach involving aboriginal health worker, manage other comorbid conditions especially alcohol (abstinence preferable with pharmacotherapeutic support if necessary) and metabolic syndrome

with GPMP/TCA and mobilising support of aboriginal health service (remoteness shouldn't be a barrier with telehealth and shared care protocols). Surveill for HCC q6mo from 50yo if no FHx, cirrhosis. Check family members for infection, vaccination status and vaccinate if necessary. What antivirals are used to treat HBV and what effect do they have? Lifelong entecavir or tenofovir, reduce risk of disease progression, HCC and transmission (compliance likely to be an important issue). Issues in pregnant migrant from rural Asia? Interpreter, cultural safety, general health (risk of BBVs), health during this pregnancy, vaccination history (rubella, pertussis, influenza, varicella), family history (DM, multiple births, chromosomal abnormalities genetic conditions, social supports. Advise re medication effects, importance of healthy diet/exercise, prevention of listeriosis and toxoplasmosis, supplementation with folate/iodine (consideration of vitamin D, calcium, iron if deficient). Investigations including first trimester screening for Downs. Discussion of models of antenatal care. Antenatal screening tests? FBC, blood group and antibodies, HBsAg, HIV, rubella IgG and syphilis serology, vitamin D, MSU (reasonable in pt from high HBV prevalence country to also do HBsAg, antiHBs, antiHBc, LFTs). What happens to HBV infection during pregnancy? Usually less liver inflammation due to immunosuppressed state, but in some the disease can flare up and in rare cases this can be life threatening. What treatment to offer pregnant woman with active HBV infection in immune tolerant phase? Refer to specialist antenatal clinic with link to specialist HBV treatment service (they will monitor HBV DNA titre 3 monthly during pregnancy ? need for third trimester treatment to prevent vertical transmission along with standard HBV vaccination at <24h ... if mum HBeAg+, HBIg given to bub at different NA should be monitored for 6 months after birth for flare up. Check contacts. What is the AHSM portal? Australian Society for HIV Medicine portal, gives information not only on HIV testing but also HBV and HCV testing. Does mode of delivery affect vertical transmission in HBV? No. Significance of different LFT pictures? 1. Hepatocellular picture: ALT = most sensitive and specific test for hepatocyte injury and >5x ULN (>200) indicates hepatitis. Common picture is ALT >5x ULN + elevated GGT and ALP <2x ULN. Common causes Hep ABCE, EBV/CMV, drugs. Other causes: autoimmune. 2. Cholestatic picture: ALP >2x ULN + GGT >5x ULN + ALT <5x ULN is a cholestatic picture. Cholestasis not surgical, but also medical: drug induced injury, infiltration (cancer/sarcoid), PBC/PSC. ALT rises because bile accumulation hepatotoxic (doesn't occur in cholestasis of pregnancy). 3. Mildly elevated bilirubin: Non specific. Important uses are to accurately identify impaired liver function in presence of known cirrhosis and useful prognostic indicator in cholestatic cirrhosis (PSC). 4. Low albumin: Poor nutrition, enhanced breakdown (malignant cachexia, HIV), haemodilution (2nd trim pregnancy, blood taken from IV drip arm), protein loss (nephrosis, protein losing enteropathy), cirrhosis (even borderline values significant). 5. Elevated AST: Alcoholic liver disease, cirrhosis, Wilson's disease, some drug reactions. ALT:AST <0.8) specific but not sensitive for cirrhosis and alcoholic liver disease (other sources cite ALT:AST <1:2 as specific for alcoholic liver disease). 6. Elevated GGT: First one to rise (in any process: cholestasis, hepatitis, infiltrative, cirrhosis) as located on hepatocyte surface. Most common cause of GGT rise +

small rise in ALT = NAFLD (clinical correlation and check bsl/lipids). ALP+GGT up means ALP of liver origin not bone. Sensitive but not specific marker of infiltration (cancer, sarcoid) as well as alcohol, drugs (eg anticonvulsants). Can be useful in monitoring alcohol abstinence. Sometimes never explained and in some situations can be ignored. What are the surrogate "liver function" tests? Platelet count (hypersplenism + reduced hepatic protein thrombopoeitin production) and PT/INR (reduced synthetic function). Platelet levels fall in parallel to degree of fibrosis. Does low levels of clotting factors 2, 7, 9 and 10 respond well to vitamin K? No, because vitamin K deficiency is not the problem but synthetic function. What is serum AFP? An oncofetal protein that rises in pregnancy, cirrhosis and HCC. How frequently should pts with cirrhosis be surveilled for HCC? US and AFP q6mo (supervised program to ensure they aren't lost to follow up). What causes GGT to rise? Hepatocellular injury, increased synthesis/release stimulated by enzyme inducing agents (alcohol and wide range of other drugs), bile acid levels rise (acting as detergent, releasing it from cell membrane). When can I ignore an isolated elevated GGT and stop retesting? Asymptomatic, not alcohol dependent, healthy diet/exercise, normal waist circumference, 2+ normal scans. Drugs that need regular monitoring of LFTs? Isoniazid (TB antibiotic), methotrexate, synthetic retinoids, ketoconazole, terbinafine, some anticancer drugs, prolonged minocycline. Not statin, don't even check before starting, effect on LFTs mild and transient and in fact deranged LFTs is almost an indication to take a statin. What other drugs may cause drug-induced hepatitis? Antidiabetics, antihypertensives, paracetamol, herbal/OTCs, recreational drugs (ecstasy) What is more important in diagnosing early hepatotoxic drug reactions, symptoms or LFT changes? Symptoms. Symptoms of hepatotoxic drug reaction? Malaise, nausea, dyspepsia, facial discomfort, fever. What autoantibodies are associated with autoimmune hepatitis? ANA, smooth muscle and liver/kidney microsomal antibodies. How are severe cases of autoimmune hepatitis treated? Prednisone and azathioprine. Is cholestasis always related to surgical biliary obstruction? No. Can be medical => drugs, hepatitis, autoimmune, liver malignancy. Does cholestasis always cause jaundice and bilirubinuria? No, as there are degrees of obstruction. Why does anaemia occur in liver disease? Portal hypertensive gastropathy => chronic blood loss (occasionally more substantial bleeding from same lesions, PUD or varices). How are gallstones thought to cause pancreatitis? Smaller stones more problematic => obstruct pancreatic duct => pancreatic enzymes activated => auto-digestion of pancreas. What meds can cause pancreatitis? Diuretics (thiazide/loop), steroids, antibiotics (metronidazole/tetracycline), azathioprine, valproate. Other causes: ERCP, hypercalcaemia, hyperlipidaemia (lipoproteins), trauma, autoimmune (Ig4-related), viral (mumps, cocksackie B, viral hepatitis), ostructing tumour. Who typically presents with alcohol-induced acute pancreatitis? Young men consuming >80g alcohol a day (not predictable or dose dependent, so genetic

factors probably involved). Can be hereditary => 50-fold increase in pancreatic cancer risk. Presentation of acute pancreatitis? Sometimes profound shock and haemodynamic instability. Usually severe epigastric pain radiating to back, anorexia, nausea and vomiting, sometimes rigors => check for Grey Turner and Cullen signs. Are amylase/lipase always diagnostic of acute pancreatitis? No. Levels 3x normal strongly suggestive but not diagnostic. How to diagnose acute pancreatitis and simultaneously rule out other causes of abdominal pain? CT with contrast, pancreatic protocol at >48h after onset of symptoms due to lag in imaging findings (also order ultrasound within 24h to examine biliary tree ... often difficult due to pain/gas ... repeat on resolution). Blood test helpful to monitor clinical course of acute pancreatitis? CRP. Initial management priorities? Identify and reverse organ failure (es renal and respiratory). Are peripancreatic fluid collections and pseudocysts usually managed surgically? No, most resolve spontaneously. Watch and wait for >12wks. How does chronic pancreatitis present? Epigastric pain (radiating to back, episodic or constant, associated with nausea/vomiting, can decrease over time as pancreas "burns out") or loss of exocrine/endocrine function (steatorrhoea and effects of reduced insulin/glucagon ... occurs late in course which is when some present). Signs of chronic pancreatitis? Wt loss, malnutrition ... sometimes abdominal mass, jaundice, gastric outlet obstruction, splenomegaly, signs of chronic liver disease (can get left sided portal hypertension with ascites and gastric varices). Diagnosis of chronic pancreatitis? No single lab test. Amylase/lipase can be normal. Contrast-enhanced CT with pancreatic protocol highly sensitive/specific. Endoscopic ultrasound sensitive/specific looking at parenchyma and ductal system and allows FNA if needed, MRCP has replaced ERCP in diagnosis, calcifications on plain film diagnostic if present. Pancreatic exocrine function tests including 3-day faecal fat as well as faecal elastase-1 and serum trypsinogen sometimes needed (sensitive/specific in advanced disease). Management of pain in chronic pancreatitis? NSAIDs and opioids, coeliac plexus block or thorascopic splanchnectomy considered if oral analgaesia failsm surgery sometimes needed, enzyme replacement controversial. Management of malnutrition? Enzyme replacement (Creon) with every meal, and if refractory then trial of PPI (stomach acid thought to degrade ingested enzymes). Management of diabetes? Oral hypoglycaemics don't work. Insulin needed and diabetes often brittle. What imaging to order for suspected biliary obstruction or fatty liver? US. What imaging to order for suspected liver cancer? CT. Are morphological changes of pancreatic parenchyma in chronic pancreatitis reversible? No. Risk factors for pancreatic cancer? Smoking (OR 1.77), high BMI, chemicals in dyes (beta-naphthylamine, benzidine), chronic pancreatitis. Longstanding diabetes not associated but new-onset diabetes is .. consider case finding in new diabetics with unusual symptoms. Presenting symptoms of pancreatic cancer? Wt loss, jaundice, abdominal/back pain, dyspepsia, nausea, depression (high index of suspicion in non-specific and persistent abdominal symptoms and in new-onset T2DM at early age or with unusual features like wt loss and abdominal symptoms). What are problems with CA 19.9 as a screening tool? High false positive rate as present in healthy individuals so need to correlate with radiological findings, some

people genetically unable to produce it, can be elevated in other conditions (pancreatitis, obstructive jaundice due to choledocholithiasis and cirrhosis). Diagnosis of pancreatic cancer? Contrast CT with pancreatic protocol => multidisciplinary meeting => endoscopic ultrasound and FNA +/- MRI/laporotomy => staging and management as appropriate. When to treat an unidentified pancreatic mass seen on imaging as malignant? Always - cancer until proven otherwise => FNA biopsy (and CA 19-9 may be useful in this scenario). Why is endoscopic ultrasound-guided FNA biopsy used in pancreatic masses? The risk of needle track seeding. What is treatment of choice for pancreatic cancer? Pancreatoduodenectomy (Whipple procedure, perioperative mortality <4% ... only <20% of patients have resectable tumours at diagnosis but of these half may not be getting it) and adjuvant chemotherapy (gemcitabine). All patients should be offered adjuvant chemo. What treatment can be used in pancreatic cancer patients who are not surgical candidates and have obstructive jaundice, pruritis? ERCP => biliary stent. What could present as subacute to chronic RIF pain and mass? Inflammatory mass (Chrohn's ileal stricture, unusual), infectious mass (appendicitis with phlegmon, more likely acute than chronic), gynae (ovarian cyst/malignancy/PID), rare (lymphoma, benign renal tumour). What effect does smoking have in IBD? Protective worsens outcome in Crohn's, improves it in UC. What are some features of IBS: Fluctuating symptoms absent between exacerbations (constant symptoms not in keeping with IBS), nausea but not vomiting, no palpable mass ... IBD commonly misdiagnosed as IBS esp early on. Bloody diarrhoea frequently absent in early IBD. History to elicit in the IBD vs IBS history? The above and also SOCRATES of pain, nature of diarrhoea (past and present), appetite, wt loss, fever, perianal disease (fissures, abscesses, past and present) and oral disease, menstrual history, DUB, LUTS, previous investigations/scopes (terminal ileal Crohn's lesions may be missed on scopes not going the distance). Is PR bleeding always present in IBD? No. Non invasive tests to assist in IBD vs IBS diagnosis? FBC, ESR, CRP, iron studies (faecal calprotectin and lactoferrin are sensitive new markers of inflammation used in detecting intestinal inflammation). Scans available in GPland to investigate IBS vs IBD? CT and small bowel barium studies (judicious use of CT scans especialy in young patients due to concerns about radiation). What scans are available in GPland to assess IBS vs IBD? CT or small bowel barium studies (be judicious about use of CT). When is capsule endoscopy PBS funded? Recurrent/persistent/active bleeding, anaemia, upper endoscopy and colonoscopy inconclusive. What is the long term management of Crohn's? Multidisciplinary IBD clinic referral (if available). Immunomodulatory therapy with steroids and thiopurines (azathioprine) which aim to avoid the need for surgery. Mild colitis can be treated with mesalazine aka mesalamine (similar action to sulfasalazine but without sulfa allergy problem). Should also address risk of osteoporosis as a result of malabsorption and steroids. Immunisations to prevent infections associated with immunosuppression. Long term screening for colon cancer. Psychological support. What to make of late middle aged patient with LIF pain worse on movement or coughing, low grade temp, looser motions but no blood/mucous, normal

examination and obs? Uncomplicated diverticulitis. Other possible diagnoses? IBD and bowel cancer. Management of uncomplicated (no perforation, abscess, fistula, obstruction) diverticulitis? Inpatient management if diabetic, immunosuppressed, elderly, comorbidities. Otherwise, outpatient management with liquid diet (once episode settles change to high fibre diet) and broad spectrum antibiotics covering aerobes and anaerobes (Augmentin Duo Forte or cipro and metronidazole if allergic to penicillin). Review at 48-72h and expect improvement at that time. Paracetamol for pain, avoid codeine due to constipation. TIming of colonoscopy in relation to diverticulitis? 4-6 weeks after acute episode settles, not during acute phase as there is an increased risk of perforation (could do sigmoidoscopy for distal IBD/cancer but this adds little to acute management. Also, diverticulitis doesn't confer higher risk of bowel cancer but if >50, abdo pain and altered bowel habit it is reasonable to screen with scope). Is it common to have recurrent diverticulitis or to need surgery? Few patients get further episodes and most of those that do still don't require surgery. Only need surgery if peritonitis, uncontrolled sepsis, obstruction, fistula (surgery based on number of episodes + complications + risk). Dietary changes to prevent further episodes? High fibre may prevent further diverticulae but no evidence it will prevent further bouts of diverticulitis (nuts and seeds unproven to help). Differential and investigation of dysuria, pneumaturia and faecaluria? Colovesical fistula (causes: often diverticulitis, need to rule out Crohn disease, carcinoma), CT with oral contrast. Treatment of colovesical fistula? Resection of involved loop of bowel, primary reanastomosis, bladder repair all at same time. What are the core symptoms of IBS? Abdominal pain or discomfort, altered bowel habits and abdominal bloating with or without distension (many others can be present including symptoms outside GI system). Symptoms simultaneous and recurrent/chronic. If isolated symptoms, diagnosis is functional XYZ (diarrhoea, bloating, constipation). Differentials? IBS, fructose intolerance, Coeliac's, IBD (less likely than IBS), giardiasis, colorectal cancer. Pathogenesis of IBS? What physiologic processes underlie gut dysfunction in IBS? Enteric nervous system disturbance including visceral hypersensitivity (VH), aberrant gut motility responses and aberrant somatic muscle reflexes. Luminal distension => bloating, dysmotility, reduced passage of gas through small bowel, or creating osmotic load and increasing transit. Short-chain carbohydrates called FODMAPs (esp fructose and lactose) implicated in some patients. Cause of ENS dysfunction in IBS? Genetic vs environmental contribution still unclear. Low grade inflammation often present and can be triggered by severe gastroenteritis (post-infectious IBS) or by foods. Microbiota density and functional properties contribute to symptoms more than composition of microbes. Is IBS caused by somatisation, depression/anxiety? No. Types? IBS-D (IBS diarrhoea predominant), IBS-M (mixed), IBS-C (constipation). Conditions associated with IBS? GORD, functional dyspepsia, non-cardiac chest pain, chronic fatigue syndrome, fibromyalgia, migraines, TMJ dysfunction, dyspareunia, interstitial cystitis. Making diagnosis? Not a diagnosis of exclusion => screen all pts for Coeliac's (tTA and total IgA: serology 3x more likely to be positive, and biopsy-proven Coeliac's 4x more likely in pts with IBS-like symptoms), FBC (? anaemia) and CRP (? systemic

inflammation) => if red flags (mild tenderness is not a red flag) refer for further investigation and specialist opinion. TSH, stool MCS/OCP, iron studies are low yield in average risk patients but often ordered anyway. Further investigations in suspected IBS? Convincing chronic diarrhoea scores faecal MCS/OCP and maybe therapeutic trial of metro/tinidazole for giardia; cyclical pelvic pain in women scores a bimanual examination and pelvic ultrasound (ovarian cancer rare but important); breath hydrogen for fruc/lactose intolerance not diagnostic but can help determine therapeutic approaches (or refer to dietician for trial of low-FODMAP diet). No evidence for testing intestinal permeability, food specific IgG, salivary IgA, faecal microbial or fatty acid content. When to arrange colonoscopy in patients with IBS symptoms? Low yield in patients <50yo with no alarm symptoms. Order in pts with acute/severe/progressive symptoms, patients >50yo, or IBS-D patients with red flags (inc ileoscopy for IBD and random colonic biopsies with microscopic colitis). Bowel symptoms red flags: A>50yo, progressive/severe, major change, nocturnal/waking symptoms (diarrhoea interrupting sleep or severe nocturnal pain), persistent daily diarrhoea, rectal bleeding (not just blood on paper), anaemia, unintentional wt loss, recurrent vomiting, strong FHx IBD/Coeliac's or GI/ovarian cancer, fever, abnormal examination(not mild tenderness). Management of IBS? Meds not first line. Harness the placebo effect, give dietary and lifestyle advice, refer to dietician if necessary and reserve medications as stopgaps or adjunct treatments. Targets for treatment: (1) Global symptoms; (2) Individual symptoms; (3) Complications (procedures & polypharmacy) Treatment for global symptoms? Reassurance (sometimes the only treatment required .. harness the placebo), food diary, trial of low FODMAP diet or other dietary exclusions, probiotics, altered fibre intake (modest effect: can help in IBS-C if clearly deficient; try reducing in IBS-D), non-absorbable antibiotic rifaximin has prolonged/mild benefit in some (off label and caution re microbial resistance), antidepressants, CBT/hypnotherapy. Treatment for diarrhoea: Opioid antagonists (loperamide, diphenoxylate ... codeine not recommended), bile salt binders (cholestyramine), anticholinergics (hyoscine, TCAs ..slow transit time), probiotics, antibiotics (above). Treatment for constipation: Laxatives (iso-osmotic/Movicol, osmotic/Lactulose .. stimulants not recommended), fibre supplements (if deficient, modest benefit), prokinetic (Prucolapride, SSRIs), probiotics. Treatment for pain/bloating: Antispasmodics (mebeverine/Colofax, peppermint oil, hyoscine), antidepressants, probiotics, antibiotics (above), analgaesics not recommended. Treatment for complications: Liberal reassurance => explanation re "visceral hypersensitivity" or "brain-gut disorder". Multidisciplinary approach for patients who don't accept this. What are FODMAPS: Poorly digested short chain carbs (like fructose and lactose) that create osmotic load and ferment in the gut. Hydrogen breath test or refer to dietician for trial of low FODMAP diet. FODMAP containing foods: Wheat, various fruit and veg (apples, pears, stonefruits, honey), onions, dairy (milk, yoghurt, ice cream), legumes. What is the role of probiotics and prebiotics? Probiotics effectivetargeted treatment improving all core symptoms but only transient in gut so need to be taken long term, few side effects. Prebiotics (inulin) supposed to increase effect of probiotics and increase good gut bacteria have no evidence and may actually increase symptoms. What about diets low in naturally occurring chemicals (low in salicylates, amines,

glutamates): good scientific basis but little hard evidence. Refer to dietician. Can gluten cause functional gut symptoms in pts without Coeliac's? Yes, emerging new evidence for "gluten intolerance" but gluten-free is a fallback position at present. Do all patients score dietician referral? No, symptoms must be serious enough to warrant effort and patient must be willing and able to put changes in place. What about CAMs (complementary & alternative meds)? Anecdotal evidence only. What is the aim of psychotherapy in IBS? Address interaction between pt's biology, behaviour, cognitive processes, early life factors and sociocultural environment. What is the evidence for and role of psychological therapies? Mixed results hampered by their relegation to use as third line treatments in difficult patients. Not first line but definitely underused and should not be reserved for pts with comorbid psychiatric disorders. CBT and hypnotherapy are best validated and may have effect on gut even in absence of any effect on underlying psychological disorder. When to refer to gastroenterologist? Only if red flags, abnormal results indicating need for scope or further investigation/advice needed to rule out other pathology (or if patient doesn't accept diagnosis). Is there any difference in mortality between IBS sufferers and the general population? No. Future investigations and treatments in IBS? Tests of neutrophil-derived inflammatory proteins in stool may guide treatment (calprotectin), drugs likely to target ENS/CNS responses and gut inflammation (mesalazine), low gluten/chemical/protein diets may be used, psychological treatments may aim to alter gut physiology not psychological dysfunction. What do colicky abdominal pain, distension and absolute constipation (no stool or flatus) suggest? Large bowel obstruction. Differentials of large bowel obstruction? Colorectal cancer, diverticulitis, sigmoid diverticulitis, IBD, pseudo-obstruction. Management of large bowel obstruction? Urgent ED referral to confirm diagnosis and manage (if still passing flatus, urgent outpatient appointment OK). What complication could follow if problem untreated? Closed loop obstruction (competent ileocaecal valve closing one end, downstream obstruction eg tumour at the other, caecum most distensible so RIF pain occurs despite obstruction elsewhere) => perforation, peritonitis. Investigations for large bowel obstruction? Plain films erect and supine and CT with rectal contrast (distended bowel, inability of contrast to pass obstruction). What is the age distribution of colorectal AC? Increasing frequency from 30yo, no sex predilection. Risk factors for CRC? Diet: High fat, high animal protein, high energy, low fibre diet associated with increased incidence (protective benefits of calcium, vitamin D, folate, selenium, antioxidants remains to be proven). Alcohol: Beer and spirit consumption probably increases risk more effect than wine. Smoking: on balance probably does contribute. Coeliac's disease. Does aspirin halve incidence of colorectal cancer? Unproven and can't be recommended due to potential AEs. Benefit seen in studies may be due to increased bleeding at an earlier stage in disease process. If exercise protective againts CRC? Colon cancer yes, rectal cancer no. Reasons unclear (increased transit, immunehormonal effects?). Why screen for CRC? It has a clear premalignant phase where disease preventable or modifiable. Where to check for quantified risk of bowel cancer? NHMRC and Australian Cancer

Network screening guidelines. What cancers are pts with HNPCC gene mutations at higher risk for? GIT (AC oesophagus/stomach, pancreatic cancer, CRC), gynae (uterine, ovarian), renal. What are HNPCC genes? DNA mismatch repair genes hMLH1, hMMSH2, hMSH6, hPMS2. Who should be referred for genetic testing/counselling for HNPCC? 1st deg relatives of pts with gene (usually identified from biopsy sample) => otherwise Bethesda criteria => Amsterdam criteria if no genetic testing possible. Should FOBT be done in pt who reports PR bleeding? No, but yes to DRE. How does FOBT screening compare to screening for other cancers in terms of cost and efficacy? Slightly more expensive than mammographic screening, much more effective than Pap smear screening, and prostate screening completely unproven. What patients is FOBT screening appropriate for? Asymptomatic, average risk patient or asymptomatic patients with relative risk <2. Bowel cancer screening in coeliac pts? Colonoscopy reasonable not mandatory. What about flexi sigmo/colonoscopy screening? Unproven or infeasible. What about virtual colonoscopy with CT, or CEA? Resolution not good enough yet for CT screening and no evidence. CEA only elevated in advanced or metastatic disease, never in polyposis (the screening target). Also, can be elevated in other conditions. What are symptoms of bowel polyps? Usually none. What are CRC symptoms? Rectal bleeding (esp independent of defaecation), persistent altered bowel habit (frequency, consistency, calibre), abdominal pain. Rectal cancer can cause straining and sense of incomplete evacuation. Can present as iron def anaemia. Can experienced clinicians tell benign from malignant bleeding clinically? No. When to refer a pt with rectal bleeding for colonoscopy? >40yo + SSx, elderly, FHx, red flags. Is there any alternative to colonoscopy as an investigation for rectal bleeding? Other tests substandard (but helical CT, aka virtual colonoscopy, or barium aenema + flexi-sig can be used if pt can not tolerate colonoscopy or colonoscopy can not be technically completed). Good polyps vs bad polyps? Hyperplastic polyps don't increase lifetime CRC risk. Adenomas increase risk even after removed => repeat scope at 4-6yrs (or sooner if high risk features eg >1cm diam). Surveillance after excision of high-risk (multiple, high-grade, villous, >1cm) adenomas => rpt colonoscopy in 1-3 years. Why is preoperative staging important in rectal tumours? Pelvis is confined space so any spread outside wall of bowel lumen complicates excision => accurate staging (MRI or endorectal UC, not CT) helps in making decisions re preop downstaging treatments, eg radiotherapy. What is the use of digitalised combination of PET & CT? Improved identification of previously occult metastatic disease. Is metastatic bowel cancer always incurable? No, sometimes both mets and primary resectable and with addition of chemo/radiotherapy may be for cure. Treatment of obstructing sigmoid tumour? Emergent Hartmann procedure (primary colo-colic reanastomosis problematic as proximal colon ischaemic due to distension) => stapling off of rectal stump, end colostomy => reanastomosing at a later date. Treatment of obstructing right sided tumour? Tumour resection with primary ileocolic reanastomosis.

What is the operation of choice for rectal cancer? ARSE: Anterior resection with primary reanastomosis if there is any rectum left below tumour. If anus and sphincter have to be removed an abdomino-perineal resection and permanent end colostomy is done (10% of cases). Does open bowel surgery have better outcomes than laporoscopic surgery? No, laporoscopic surgery at least equivalent. What chemo is used in CRC and in which ACPS stage of cancer? 5-flouroracil or capecitabine based, benefits stage C pts only (LN positive, no mets). Also bevacizumab/Avastin, an anti-VEGF monoclonal antibody, can be used to retard angiogenesis and so tumour growth. Side effects of 5FU/capecitabine treatments? Diarrhoea, mucositis, peripheral neuropathy, photosensitive rash. What is the role of radiotherapy in CRC? Only used in rectal tumours as toxic to small bowel. Neoadjuvant vs adjuvant is controversial, but neoadjuvant probably better (halves risk of local recurrence which is a particular risk in rectal cancer). Which have a worse prognosis in CRC, mets presenting synchronously with primary tumour or developing later? Synchronous presentation worse. When is colonic stenting an appropriate choice? Colonic obstruction, advanced metastatic disease and short life expectancy. What follow up is recommended after surgery for CRC? 3 monthly clinic visits (GP or specialist) for 2 years, then 6 monthly visits up to 5 years. What is checked at bowel cancer follow up appointments? Physical examination and CEA at each visit. What 5yr survival benefit does intensive follow up of CRC yield? 5%. Where to refer patients for information on Coeliac's and the gluten-free diet? Coeliac Australia website, mobile phone app ... pts can join if they have a doctor's letter confirming they have Coeliac's. Refer to dietician with experience in Coeliac's. What other autoimmune disorders are people with Coeliac's prone to? T1DM, autoimmune thyroiditis, autoimmune hepatitis, Addison's disease, vitiligo. What is gluten? Protein with gliadin+glutelin found in wheat, barley, rye and oats. How does Coeliac's present? IBS-like symptoms, fatigue, iron-deficiency anaemia (due to malabsorption not bleeding), folate deficiency, osteoporosis, infertility and recurrent miscarriage in untreated women, mood disorders, neurological symptoms (cerebellar ataxia, peripheral neuropathy), dermatitis herpetiformis, abnormal LFTs. Not rectal bleeding. Can Coeliac's cause cancer? Yes (small bowel lymphoma, colorectal cancer, oesophageal cancer and adenocarcinoma of jejunum). Risk returns to normal after 5 years on gluten-free diet. Conditions associated with coeliac or with coeliac as possible cause? Cancer, refractoriness, lactose intolerance, IBS, Crohn's. Is fatigue in Coeliac's dependent on iron deficiency anaemia? No. What blood test results should prompt serological testing for Coeliac's? Fe-def anaemia or deranged LFTs (anaemia can be mixed macro/microcytic due to malabsorption of both iron and folate). What causes osteopaenia and osteoporosis in Coeliac's? Chronic inflammation and malabsorption of calcium and vitamin D. Does Coeliac's cause elevated CRP? Not usually (a distinction that can be helpful when considering Coeliac's vs IBD). What age group and gender does osteoporosis affect in Coeliac's? Young patients, no gender predilection. Which coeliac patients should have DEXA scans? All newly diagnosed patients

regardless of symptoms (Medicare subsidised). What is dermatitis herpetiformis? Itchy, purplish, flexural rash. Does depression and anxiety resolve on gluten-free diet in patients with coeliac? Can do, independent of effects in terms of anaemia/fatigue. What blood tests are recommended for investigation of coeliac? Tissue transglutaminase (tTG) antibodies, deamidated gliadin peptide (DGP) antibodies (not anti-gliadin antibodies or anti-endomysial antibodies) and total IgA. Under what circumstances is coeliac testing less reliable? In smokers, kids <4yo, IgA deficiency, patients eating a gluten free diet (pts have to be consuming gluten for serology or biopsy to be accurate). What effect can IgA deficiency have on coeliac testing results? IgA based serology including tTG and DGP can be falsely negative (levels fall on a gluten-free diet). Is HLA-DQ8 or DQ2 testing more useful when positive or negative? Negative. Gold standard diagnostic test for coeliac? Small bowel biopsy (4 samples). What are histopathological findings? Patchy partial, subtotal or total villous atrophy with hyperplastic crypts. Close link between symptoms, serology and tissue damage? Little connection (and after 12mo on gluten-free diet serology and histology can still be discordant). What tests should be ordered once diagnosis made? FIZ BOD: Folate, Iron, Zinc, B12, Osteoporosis and D (DEXA and vitamin D). Why do coeliac patients need pneumococcal vaccination? Hyposplenism which occurs for unknown reasons and puts them at risk of bacterial infections. Repeat small bowel biopsy at 1yr to confirm healing? No, healing takes years. Coeliac-safe foods? CRiSP-QT: Corn, Rice, Soy, Potato, Quinoa, Tapioca. Is avoidance of obvious gluten-containing foods like wheat-based cereals, bread and pasta enough to improve symptoms and are "diet-holidays" OK? No and no. What are some less obvious items containing gluten? OTC/prescribed meds, nutritional supplements. What should patients expect to happen on a gluten-free diet? Resolution of symptoms over 3-6mo and wt increase of c6%. Classic presentation of C difficile colitis? Patient presenting with persistent watery diarrhoea up to 10-15x a day during or after a course of antibiotics. When to test for C difficile? Pt with significant diarrhoea and taking antibiotic at or within 12wks of presentation; diarrhoea >14d. What is the gastrocolic reflex? The urge to defaecate after meals. What are the likely reasons for the increased incidence of C difficile colitis? Increased carriage rates, strains with increased virulence, widespread and inappropriate antibiotic use, ageing population. How is C difficile spread? Faecal oral route. What makes C difficile so readily transmissible? Hardy spores resistant to alcoholbased disinfectants (stress handwashing with soap and water). What are risk factors for C difficile colitis? Antibiotics, A>65yo (for hospital-acquired C difficile diarrhoea only), immunosuppression (hospital chemo patients especially vulnerable), IBD (high index of suspicion; test stools if not responding to usual therapy), gastric acid suppression (maybe, FDA has put warning on box). Why are nursing home residents more vulnerable to C difficile? High carrier rate, frequent antibiotic use and difficulties in toileting elderly, infirm patients. Are patients carrying C difficile at the time of admission more or less likely to get diarrhoea while admitted? Less. How does C difficile rank alongside other causes of bacterial diarrhoea? 1st in the US, increasing in Australia.

Age of pts with community-acquired vs hospital-acquired C diff diarrhoea? Pts with community-acquired disease younger. Should all nursing home residents be screened/treated to eradicate C diff? No. What antibiotics are particularly strongly associated with C difficile diarrhoea? Broad spectrum penicillins (amoxi/ampicillin), broad spectrum cephalosporins, fluouroquinolones (also clindamycin .. any antibiotic can be a cause, even metronidazole and vancomycin which are used to treat C difficile). Worldwide use of what class of antibiotics may be associated with rise of the most significant hypervirulent C difficile strain NAP1/BI/027 (has been identified in Australia)? Fluouroquinolones. Are PPIs a definite risk factor for acquiring C difficile? Controversial. How is C difficile diagnosed? (1) Stool glutamate dehydrogenase (produced by all strains of C difficile) then C diff toxin if positive, (2) Stool C difficile PCR (the gene test) is sensitive and specific. Note: C difficile toxin testing on its own has false negatives because it requires a certain threshold of toxin to be present; culture is slow and difficult; colonoscopy/biopsy not mandatory, but can be helpful if diagnosis unclear (eg pts with IBD) => yellow pseudomembrane that can be washed off. What is first line treatment for C difficile colitis? Oral metronidazole 400mg TDS (IV metronidazole if unable to tolerate oral meds) with oral vancomycin as back up. Why has it been difficult to prove efficacy of probiotics? So many different strains of probiotic bacteria available, which may have a variable effect on the colonic flora of different individuals. How are recurrences treated? First recurrence => retry first line agent (metronidazole) although less likely to be successful; then try tapered doses of PO vancomycin or "pulse" therapy. What are some promising new treatments for recurrent cases? Faecal microbiota transplant from gut of healthy individuals, novel antibiotics (rifaximin, nitazoxanide .. fidaxomicin most promising as specifically targets C diff without altering colonic flora), immunotherapy with monoclonal antibodies to neutralise toxin, probiotics. PR bleeding red flags: Blood altered (dark/melaena), bleeding independent of defaecation, blood in/on stool, change in bowel habit, wt loss, anorexia, abdominal pain or distension. Risk factors for haemorrhoids? Women => childbirth. All => forced/hard stool, diet. How do haemorrhoids occur? No valves in anal veins => straining at stool increases pressure dramatically in veins of anal cushions (part of anal valve mechanism) => arterioles compensate by increasing pressure/flow making problem worse => once stretched, cushions don't go back to normal size => endothelium stretched thinner and bleeds => large haemorrhoids prolapse. Symptoms of haemorrhoids? PR bleeding (bright red, on paper, only on defaecation), itching, throbbing, discomfort not pain, prolapsed anal cushions. How useful is examination in diagnosing haemorrhoids? Not very, examination often normal, good history much more important. Seeking innocent cause of PR bleeding on history? Straining (going at home in morning even when not feeling like it should be discouraged as causes piles/fissures), deferring defaecation. When to refer likely haemorrhoidal bleeding for colonoscopy? >40, FHx, red flags. Drugs used in haemorrhoids? Combined antibiotic (framycetin), astringent analgaesic (cinchocaine), antiinflammatory and antipruritic (hydrocortisone).. Conservative treatment of haemorrhoids? No straining, increase fluids/fibre (vegies, wheat bran, psyllium husk), OTCs with astringent/cinchocaine (vasoconstriction and local analgaesia), steroid/hydrocortisone (anti-inflammatory/oedema, antipruritic),

antibiotic/framycetin (for superinfection that can worsen symptoms) ... Scheriproct, Proctosedyl, Anusol. Does size determine treatment of haemorrhoids? No, symptomatic grade. What causes itching and throbbing in haemorrhoids? Usually prolapse. Management of recurrent symptoms? Don't sit on haemorrhoids! In recurrences, suspect other or more sinister cause and refer for specialist opinion? haemorrhoids vs fissure, fistula, SCC of anus. What is the goal of haemorrhoid surgery? Shrink the piles to stop the prolapse (not excision). Surgical methods used? Grade 1-2: injections (recurrences frequent); Grade 2-3: rubber banding (recurrences frequent); Grade 3-4: haemorrhoidectomy (vs rectal haemorrhoidopexy vs HAL-RAR). How does sclerotherapy work? Phenol or almond oil => irritation, thrombosis and sclerosis of haemorrhoidal vessels. What are side effects of rubber banding procedure? Significant pain and bleeding. How long does healing take after haemorrhoidectomy? 8-10 weeks (and excruciatingly painful). What about new alternatives to haemorrhoidectomy? Stapled haemorrhoidopexy (less painful but has rare/serious complications like rectovaginal fistula and pelvic sepsis requiring colostomy); or US-guided haemorrhoidal artery ligation and rectoanal repair HAL-RAR (7-10d discomfort only). How are thrombosed haemorrhoids managed? ANAL conservative management: Analgaesia (strong), Nitrates (GTN/Rectogesic), Antibiotics (metronidazole), Lactulose. Refer if BNO. How easy are anal fissures to spot? Very hard except with proctoscope. Diagnose on history of painful defaecation and bright red blood on toilet paper only (pain on sitting is a red flag for cancer => refer). What stops anal fissures from healing? Pain related sphincter spasm and resulting ischaemia. Do most topical haemorrhoid creams work for anal fissure? No, topical GTN (Rectogesic) is only treatment => relieves sphincter spasm, allowing healing. How effective is anal sphincter botox for anal fissure? As successful and sphincterotomy and without the risk of passive faecal incontinence long term. What if botox (especially repeated botox) fails to relieve symptoms of anal fissure? Consider evacuatory disorder or pelvic organ prolapse. Are antibiotics to be used for pilonidal/perianal abscesses (pain+++, fluctuant mass) or anal sepsis? No, treatment is surgical excision. What is the aim of pilonidal abscess surgery? Tension-free, primarily closed wound which avoids midline scar and flattens natal cleft (simple excisions +/- primary closure do the opposite and recurrence rates are high) => refer, difficult to do well. What age groups are most affected by IBD? Teens and young adults with second peak in middle age. What are typical symptoms of IBD? Pain and diarrhoea with blood and mucous, and often constitutional symptoms (fatigue, fever, wt loss). What part of bowel does UC affect? Large bowel only, mucosa and submucosa only. Symptoms not always proportional to degree of disease. How do extraintestinal manifestations relate in time and severity? May precede and may be severe. What is the pattern of IBD arthritis? Peripheral arthritis usually asymmetrical, large joint (rarely symmetrical small joint occurs), and axial (enthesitis) includes sacroileitis and ankylosing spondylitis.

Why does anaemia occur in IBD? Blood loss, malabsorption, iron deficiency, anaemia of chronic disease. What other gastrointestinal disease can be associated with Crohn's? Coeliac's. What effect does smoking have in IBD? Worsens Crohn's (quitting can induce remission while continuing to smoke increases relapses and reduces likellhood of remission), improves UC (some patients choose to continue smoking rather than having chronic colitis). Do kids of IBD patients have a higher risk of disease? Yes, small increase, younger onset (<5% for 1 parent with IBD). What use is stool analysis in diarrhoea? Can help distinguish IBS, infection or IBD. What if it is unclear if a patient has Crohn's or UC? Order pANCA (elevated in UC), and anti-Saccharomyces cerevisiae antibodies, ASCA (elevated in Crohn's). Not sensitive or specific enough for use in the general population (can be elevated in healthy patients). What are limitations of steroids in IBD? Aside from the obvious like risk of opportunistic infection and osteoporosis, steroids do not maintain remission in CD or UC and don't heal mucosa in active CD. What are steroids used for in IBD? High dose steroids used for rapid control of acute, severe symptoms. What IBD drug can cause reversible male infertility? Sulfasalazine/Salazopyrin (if planning to start family, switch to mesalazine). Note PBS requires this be tried first before other 5ASA mesalazine preparations. What are the other side effects of this drug? Headache, nausea, rash (sulfa allergy), teratogenicity (spina bifida). Rarer, more serious effects include bone marrow suppression and hepatotoxicity (hepatotoxicity and bone marrow failure surveillance: do baseline FBC, LFT and recheck weekly for the first month ... regularly therafter). Benefits of thiopurines (azathioprine, 6-mercaptopurine)? Heal mucosa in CD, induce remission and reduce chance of relapse. What are the important side effects of thiopurines (azathioprine, 6-mercaptopurine)? Flulike symptoms, nausea, drug-induced hepatitis, bone marrow suppression, alopecia, increased BCC/SCC (not melanoma), very occasionally pancreatitis. Purine affecting drugs? Azathioprine, allopurinol. What other drug greatly increases toxicity of thiopurines? Allopurinol. What are some of the risks of antiTNFa treatment? Profound immunosuppression with reactivation of TB, Hep B or C, exacerbation of HPV, increased non-Hodgkins lymphoma risk. What is the hierarchy of drugs in UC? Steroids still have limited use for acute phase. First line is 5ASAs ... either sulfasalazine PO or mesalazine topically (then mesalazine orally) for UC. Then for either UC or CD: thiopurines (azathioprine or 6MP), then methotrexate. What is the hierarchy of drugs in CD? 5ASAs not useful. Steroids still have very limited use for acute phase (they don't cause mucosal healing). then most need long-term thiopurine (azathioprine or 6MP), then methotrexate, then antiTNFa monoclonal antibodies for severe and unresponsive or fistulising CD (IV infliximab/Remicade, or SC adalimumab/Humira ... patient preference) can be prescribed by gastroenterologist. What causes osteoporosis in IBD? Primarily chronic inflammation, combined with malnutrition, malabsorption and steroid treatment. Important for GP to identify and address reduced bone density, inadequate calcium intake and vitamin D deficiency. Is elective appendicectomy effective in IBD? No, results of studies disappointing.

Is surgery curative in CD? No. What is an unpalatable dietary CD treatment that is effective but mainly restricted to use in kids? Elemental diet (no normal food .. all necessary calories consumed in liquid diet with amino acids). Do spicy foods, excessive alcohol, high fat or other foods that cause GI upset actually worsen inflammation in IBD? No, but they can aggravate symptoms and should be avoided. What diseases need to be screened for prior to starting antiTNFa drugs? Latent TB, Hep B and C, cervical cancer (Pap). How is latent TB screened for? CXR and quantiferon gold. Live vaccines to avoid in all immunosuppressed patients? BCG, MMR, varicella, yellow fever, typhoid live vaccine, adenovirus, cholera live vaccine, oral polio (no longer used). If required, should be given prior to starting treatment. Biggest practical issues are varicella vaccination in non-exposed patients and yellow fever vaccination in patients wanting to travel to areas where it is endemic. Should make sure pts for immunosuppression are Hep A and B vaccinated and up to date with all other scheduled vaccinations. Who is considered immunosuppressed? Course of steroids, biologic agent or immunomodulator in last 3/12. Infants of mums on immunosuppressive therapy during pregnancy should not have live vaccinations in first 6-12mo of life. How useful is IM iron in iron deficiency anaemia? Poorly absorbed and shouldn't be used. Use oral iron + vitamin C, then IV iron infusion if this is insufficient (iron polymaltose 1000-1500mg ... safe and effective). Should women continue treatment during pregnancy? Generally yes. Why avoid corticosteroids in first trimester of pregnancy? Slightly increased risk of cleft lip/palate. What is the risk of sulfasalazine in pregnancy? Folate deficiency => spina bifida (double the dose of supplementation). Is azathioprine teratogenic? No evidence malformations increased but trend to advise avoidance during breastfeeding due to traces in breast milk and unknown safety though many have breastfed without adverse effects. What about antiTNFa drugs in pregnancy? No evidence of malformations, but best avoided from wk 22 as effect on fetal immunity unclear (if used during pregnancy, no live vaccines in 1st year of life). Is methotrexate safe in pregnancy? Causes malformations (men and women planning to conceive should avoid for 6mo beforehand) What effect does breastfeeding have on risk of IBD in infants? Reduces it. What to tell pts about increased bowel cancer risk in IBD? Risk mainly in pts with long-term uncontrolled disease. No worse than having bowel cancer in family in terms of increased risk. What are the benefits and risks of colonoscopy? Benefits: allows direct inspection of mucosa and biopsy. Risks include perforation, bleeding after polypectomy, vasovagal episodes due to bowel prep. Not a harmless procedure. What is the hygiene hypothesis? It is possible that exposure to large number of gastrointestinal infections during childhood reduces risk of IBD. Are most perianal fissures, fistulas and abscesses caused by Crohn's? No, but it should be considered as it causes disease from mouth to anus and transmural inflammation. What investigations may be used to investigate suspected small bowel disease? CT enterography, small bowel MRI, small bowel capsule endoscopy. Features suggestive of surgical cause in paediatric abdominal pain? Asymmetrical

pain, sudden onset, signs of peritonism, bilious vomiting. Clinical picture of "mesenteric adenitis" (parents struggle with other name: "nonspecific abdominal pain"): 2-3d periumbilical pain, relatively constant but some exacerbations, radiating to RIF, st nausea, rarely vomiting, recent viral illness, modhigh temp (38-39deg), mod tachycardia, mild cervical lymphadenopathy, generalised abdominal tenderness, ketonuria only, mildly elevated WCC with lymphocytosis, imaging unhelpful, recurrent => Rx: acknowledge pain, explain, give fluids, antipyretics/analgaesics (admit for obs if symptoms severe or unsure). What does acute appendicitis look like in kids? Often classic presentation => periumbilical pain migrating to RIF, usually 1-2x vomits then refuse to eat, diarrhoea, urinary symptoms, low grade temp (in pre-school kids just looks like acute gastro and only becomes apparent after perforation => phlegmon ... CRP >50 useful in this setting). Leukocytes on UA and normal WCC at 3-4d point away from it, though leuks can be found due to transmural bladder inflammation if in contact with appendix. Re-examination by same clinician after a period can be useful if symptoms/signs not severe. What is first choice imaging in appendicitis in kids (often after period of observation)? US (esp in older girls as allows for assessment of adnexae .. graded pressure over McBurney's point may be used as a technique in specialist centres where diagnosis remains unclear). CT in very select group only. When to order a stool culture in paediatric gastroenteritis? If symptoms severe enough to warrant surgical review. Should children with proven UTI be radiologically investigated for VUR or other urological abnormality? Debatable. What is one not infrequent "red herring" paediatric abdominal pain presentation? Pneumonia. Common presentation of intussusception? Episodic colicky abdominal pain, vomiting after recent viral illness. Red currant jelly stool rare. Cause of intussusception? In rare case (older kids) polyp, Meckel's diverticulum, lymphoma acts as pathological lead point. HSP predisposed. Investigation of intussusception? Ultrasound highly sensitive and specific. Golden rules of the scrotum? Always carefully examine the scrotum/testes of any boy with abdominal pain (torsion and hydrocoele can present in this way), acute hydrocoele (caused by mesenteric adenitis => increased fluid accumulation in previously occult hydrocoele) does not cause testicular tenderness, suspected torsion scores urgent surgical referral. Presentation of testicular torsion? 12-15yo with sudden, usually nocturnal testicular pain, sweating and pallor => don't scan, refer! How does malrotation with small bowel volvulus present? Usually first few weeks of life but can present late, even in adulthood. Bilious vomiting is hallmark. Upper GI contrast is diagnostic gold standard. Urgent resuscitation and surgical correction to avoid loss of small bowel and reliance on TPN. Inguinal hernia age of presentation in kids? Can occur at any age but most commonly <1yo. Differentials in recurrent paediatric abdominal pain should include? CF, coeliac disease, biliary dyskinaesia, short segment Hirschprung disease, pelvi-ureteric junction obstruciton.

Emergency BLS Algorithm: DRSABCDE: Danger: PPE

Response: AVPU/GCS (A = GCS 15; V = GCS 9 - 14; P = 4- 8; U <3), use mobile phone app for GCS. Send for help (inc thinking about hospital transfer) and SHAVED (sugar, hypovolaemia, anaphylaxis, VF/VT, epilepsy, drug overdose). Airway and C-spine: Look/listen/feel; collar and sandbags; suction; positioning, Guedels/nasopharyngeal; ETT size (Age/4) + 4; LMA (4 for females, 5 for males, 6 for big males). Breathing: Look/listen/feel (trachea, percussion, auscultation), sats probe, RR, O2, mask & bag-valve-mask, ventilator and capnography. Circulation: Monitor/defibrillation; BP cuff (BP and HR); CRT; IV lines and fluids: bloods (inc glucose); adrenaline/inotropes; wt (age + 4) x2. Disability and defibrillation: Glucose, neurological failure (PEARL), rhythm check. Exposure: Uncover, check everywhere; take temp. Severe asthma vs severe croup: Asthma give IV salbutamol then IV adrenaline. Croup give nebulised adrenaline + oral steroids then inhaled salbutamol. The 4 Hs: Hypoxia, hypovolaemia, hypothermia, hypo/hyperkalaemia. The 4 Ts: Thrombus, Tension PTx, Tamponade, Toxins. What to make of wide-complex tachycardia: VT till proven otherwise. Do chronic and paroxysmal AF differ in morbidity? No. AF causes: Cardiovascular (LVF, valvular, sick sinus, myocarditis, HTN); Pulmonary (PE, parenchymal disease, OSA); Endocrine (hyperthyroidism), Toxic (alcohol, cocaine, caffeine), General (acute illness, surgical abdomen, surgery, vagal, vomiting, exercise). What are current key messages in resuscitation? Importance of compressions, simplification of drug regimens, importance of post-resuscitation care. When to start compressions? Unresponsive and not breathing normally (this includes agonal breathing). When to shock in VF or pulseless VT? As soon as defibrillator attached and rhythm checked, then go into first cycle. When to stop/start compressions in relation to defibrillation? Only once defibrillator charged and operator says stand clear, then recommence after shock without checking rhythm (only doable with manual defibrillators as semi-automatic ones need static period to assess rhythm and charge). What are the 4 drugs used in cardiorespiratory arrest? Electricity, O2, adrenaline (1mg every 2nd cycle with 100mL NS push behind it ... every 4 and a bit minutes) and amiodarone (300mg IV after third defibrillation). Is atropine used in asystole? Not in arrested patient, but still used in bradycardia. ROSC achieved, then what (post-resuscitation care)? Treat the cause (4Hs and 4Ts), attend to detail (correct electrolytes, BSL), cooling for 24h with cold saline or cooling devices. How to check C-spine? If pt upright, stand behind them and palpate with both thumbs in deep circular motions on each spinous process from nuchal ridge to at least T1, them over facet joints on either side. If supine, loosen collar and reach behind with one hand and palpate with fingers, spinous processes and facet joints. What abnormalities are sought palpating C-spine? tenderness, gaps/steps, oedema, haematoma, muscle spasm. How to achieve adequate flow through IO cannula? Use a pressure bag or put a BP cuff around normal bag. Can you recannulate the same bone with another IO needle after 24h? No, extravasation will occur.

Factors associated with risk to self? >7/10 high risk 1. Sex (male), 2. Age (older) 3. Depression (guilt, hopelessness) 4. Previous attempts (family hx) 5. Ethanol abuse (or other drugs) 6. Rational thinking loss (impulsivity, problem solving deficit) 7. Social supports lacking (or recent social stressors) 8. Organised plan 9. No spouse 10. Sickness Important aspects of suicidal ideation to explore? (1) Lethality of considered method and potential for serious injury; (2) Intent/planning and desire to live vs desire to die (precipitating events); (3) Impulsivity, loss of insight/judgement (morbid jealousy, delusions of persecution). Which is more closely associated with mental illness, suicide or homicide/violence? Suicide. Factors associated with risk to others? Static (previous violence best predictor, 10x more frequent in males, late teens to early twenties, personality disorder esp antisocial, impulsivity, previous substance abuse) vs dynamic (substance use, negative affect of anger/humiliation/irritation, social factors/conflict, acute positive symptoms of psychosis esp hallucinations or thought insertion). What does evidence suggest is best practice re suicide, violence risk assessment? Unclear, very little evidence, all methods have poor sensitivity/specificity. How to ask about suicide? Note plans/preparation are a red flag of immediate risk. 1. How does the future seem to you? 2. Do you ever feel like giving up? 3. Does it ever get so bad you want to die? 4. How severe/frequent are the thoughts? 5. Have you made any plans? 6. Have you ever come close to doing something? 7. What stops you? Best treatment for suicide risk? Treat underlying disorder, empathic and nonjudgemental listening. When to manage pt with suicidal ideation in the community? Ideas fleeting, resisted and lacking intent. Referral to outpatient psychiatric, addictions or psychotherapy service creates a safety net and instils some hope. When to refer potential suicide for inpatient care? MI PAIN: Mental Illness or disorder, organised Plan, Alcohol or drugs, Impulsivity, No supports or protective factors. Should "no self harm" contracts be used? No, no evidence for them. Safety plan including follow up, online resources and help lines for out-of-hours emergencies can be used (GP Psych support website). Can you break confidentiality if pt threatens to commit violence against a third party? Yes, overriding "pulic interest", preferably done via police. Fracture rules? Where one bone is broken go looking for another fracture or dislocation. Frequently missed fracture sites? Scaphoid (radial side), triquetrum (second row ulnar side), proximal forearm. What is the most common FOOSH fracture in adults? Radial head (jammed against capitellum, often occult on xray).

What is the most common fracture in kids? Supracondylar #, extension injury. Xray signs include disrupted cortex, fat pads, line from anterior cortex not bisecting capitellum as it should. Check neurovascular status. What is the main complication of supracondylar fractures? Volkmann contracture due to forearm compartment syndrome and muscle/nerve necrosis. Management of radial head fracture? Pain control, short period of immobilisation in backslab and sling, early restoration of function. What is a Monteggia fracture? # proximal ulna with dislocation of radial head (at proximal end of radius) => check neurovascularly intact. Extremity x-ray checklist: Right patient, >2 well-exposed orthogonal views (right angles), fat pads (esp around joints), cortices, margins of image (? second, occult fracture). Standard suspected scaphoid fracture management? Abduction cast (thumb spica) for 10 days then folow up xray, but advanced imaging esp CT increasingly used to avoid unnecessary treatment. What is the position of the thumb in a spica cast? Aligned with forearm and index finger (like holding a can of soft drink). What is the main risk with scaphoid fractures? Non-union and avascular necrosis. What does anterior sail sign and posterior fat pad of distal humerus mean? Fracture with effusion till proven otherwise (supracondylar in kids, radial head in adults). What is the weakest point around joints in kids vs adults? Growth plate in kids and tendons, ligaments in adults. What is the most common type of Salter Harris fracture? Type 2 through growth plate and metaphysis but sparing epiphysis. Identifying (anterior) dislocation of shoulder on xray? Widened gap between humeral head and glenoid on AP, plus humeral head not lying over Y-intersection of coracoid, acromion and scapular body on lateral view. Treatment of calcific tendinosis of supraspinatus tendon? Trial of steroid injection, rarely surgical removal. Approach to interpreting C-spine films? Quality: (Are 7 vertebrae visible on lateral film, are 2 views included, is exposure adequate?); Lost alignment (LAT: anterior vertebral bodies, posterior vertebral bodies, spinolaminar line / AP: spinous processes); Precervical soft tissue widening (normal = <7mm at C2 and <20mm at C7); C1 and C2 (Check base of peg on peg view; check lateral masses of C1 exactly aligned with C2 and distance between peg and masses equal). What if xray and CT normal but midline tenderness present? MRI for disc or ligamentous injury. Causes of pulmonary infiltrates on xray? Fluid, pus, cells (neoplasm), blood. What do fluffy infiltrates suggest? Alveolar origin. Approach to chest xray interpretation? Quality (name, rotation, side marker), diaphragm (elevated, flattened, tented, displaced air), heart (size, silhouette), hila (position, clarity, size), costophrenic angles, lungs (infiltrates, air bronchograms, masses, vascularity), bones. Key question in lower abdominal pain to rule out obstruction? Flatus? Signs of small bowel obstruction on plain film? Valvulae conniventes visible (cross entire lumen in contrast to haustra of large bowel), >3-4 air fluid levels visible and loops of bowel >3cm. Check for air under diaphragm. Most common causes of SBO? Adhesions, hernias, tumour, Crohn's strictures. Common causes of dilated large bowel? Pseudo-obstruction (gas visible in rectum), sigmoid volvulus, obstructing carcinoma. Check for air under diaphragm. Size of caecum indicating high risk of perforation as a result of complete large

bowel obstruction (>10cm .. also dilated small bowel loops). What does initial minor burn management involve? First aid (including analgaesia and RICE factors which may affect healing .. no ice!), assessment of area/depth of burn, dressing +/- debridement of blisters, review. 1. First aid: Cool the burn, warm the patient (avoid hypothermia in kids). Cold running water for >20mins effective within first 60min (analgaesic, promotes healing). Hydrogel products (Burnshield/Burnaid) good temporary dressings and second best to cold water for cooling. Elevation reduces oedema/pain. Analgaesia => cold water, occlusive dressing, oral analgaesia. 2. Assess: Palm, rule of 9s, Lund and Browder, then assess depth (pain, colour). 3. Dressings: Absorptive early on when exudate present (paraffin gauze, gauze, Meolin) then nonadherent (Opsite) or moist hydrocolloids (Duoderm, Comfeel). 4. Review within 48h. What does blistering suggest? Partial thickness wound. To pop or not to pop blisters? No consensus, but blisters <6mm less likely to pop on their own and less likely to cover deep wounds so leave alone as they provide moist healing environment. Might be better to debride large blisters on presentation to allow wound assessment. If already ruptured, debriding all necrotic tissue and foreign matter best to prevent infection although controversy exists on value of blister roof as dressing. Do topical/oral antibiotics speed recovery in burns? No evidence unless clearly contaminated (eg immersion in dirty water). What about the role of silver-containing (antimicrobial) dressings? Unproven and silver sulfadiazine may delay partial thickness burn healing. Can use antimicrobials later if signs of critical colonisation ("covert infection") to avoid antibiotics. Burns unit referral criteria: Inhalation burn injury, electrical burn injury, chemical burn injury, >10% TBSA or full thickness >5% TBSA, special areas, special groups (kids <12mo or ? abuse, pregnant, elderly, infirm), burns plus (burns + trauma). Wound bed preparation: TIMES 1. T: Tissue nonviable or deficit: Surgical, sharp debridement to remove necrotic/infected tissue in acute/chronic wounds, plus dressings to promote autolytic and nontoxic chemical debridement ... increased interest in sterile "greenbottle fly" larvae. 2. I: Infection or Inflammation: Tumor, calor, dolor, rubor normal, copious purulent and malodorous exudate with grey or dark red and friable/bleeding granulation tissue and rolled edges not. Commensals like staph aureus and corynebacterium promote healing but critical colonisation point reached where cytokines and MMPs cause static healing. RX: Prudent antiseptic dressings to avoid using systemic antibiotics. 3. M: Moisture balance must be maintained: Desiccation inhibits epithelialisation, chronic wound fluid MMPs degrade proteins (fibronectin and vitronectin) and interfere with growth factors. 4. E: Edges advancing or undermined: Dessication of wound bed, hypergranulation and debris inhibit epithelialisation. Hypergranulation, rolled/undermined edges can occur from bacterial imbalance. Biopsy if suspecting malignancy. 5. S: Surrounding skin: Assess for stasis, sensation (peripheral neuropathy), fragility of skin, staining (haemosiderosis, or violaceous colour of pyoderma gangrenosum or vasculitis), striae, sinister characteristics of malignancy. Dressings to maintain moisture balance: Hydrocolloids/gels to Kaltostat to Allevyn to Mesorb to Vacutex to ostomy bags. Dry wound: Hydrogels/hydrocolloids (Duoderm, Comfeel), interactive wet

dressings (TenderWet). Minimal exudate: Hydrogels/hydrocolloids (DuoDerm, Comfeel), non-adherent semi-permeable films (OpSite), calcium alginate (Kaltostat). Moderate exudate: Calcium alginate (Kaltostat), hydrofibre (silver-impregnated Aquacel), foam dressings (Allevyn), Heavy exudate: Extra absorbent dry dressings (Mesorb, Exudry), capillary wicking agents (Vacutex), wound/ostomy bags. Debriding dressings: Autolytic debridement: Hydrogels/colloids including amorphous hydrogels (SoloSite) and hydrogel gel-sheets or impregnanted gauze (Curagel). Chemical debridement: Iodine dressings (Iodosorb), wound honey (MediHoney), hypertonic dressings (Curasalt, Mesalt). Antimicrobial dressings: Iodine dressings (Iodosorb) or tulle gras (Inadine), chlorhexidine tulle gras (Bactigras), wound honey (MediHoney), silver impregnated dressings (Aquacel). Diagnosing anaphylaxis? Any life threatening hypotension without clear alternate cause is anaphylaxis till proven otherwise. Anaphylaxis vs syncope? Syncope recovers when lying flat. Blood test for anaphylaxis? Mast cell tryptase level may be useful if diagnosis uncertain but low sensitivity so need serial measurements at presentation, 1h and in convalescence to give 75% sensitivity (less useful in food allergies) ... especially useful if course protracted or biphasic. Do swelling, respiratory distress and hypotension all need to be present to diagnose anaphylaxis? No, one is enough, high index of suspicion, and hypotension may be absolute or relative (>30% drop from baseline). What to make of pt with anaphylaxis on exercise after eating a specific food? Summation anaphylaxis (eg food-dependent exercise induced anaphylaxis). Treatment of anaphylaxis? O2, avoid upright position, BP cuff tourniquets on arms (SBP by palpating for pulse and get IV access), IM adrenaline 0.01mg/kg of 1:1000 to 0.5mg, fluid bolus (start at 20mL/kg and go up to 50mL/kg in first 20mins), obs every 5mins, next think of metaraminol, prepare for CPR. Bronchodilators and IV steroids can sometimes help with bronchospasm. IV antihistamine should never be first line management. Inserting an IV line in anaphylaxis? Inflate BP cuff on arm to just below systolic. Adrenaline dose and route? 0.01mg/kg of 1:1000 to max 0.5mg in lateral thigh up to three doses then go to IV adrenaline infusion. What if IM adrenaline doesn't work (3 times) => poor absorption => IV infusion => if this fails, selective vasoconstrictor like metaraminol or vasopressin. What if hypertension, nausea, vomiting, shaking, arrhythmia develops => adrenaline toxicity => no further boluses. Post-acute treatment for anaphylaxis? Anaphylaxis management plan, medi-alert epi pen (adrenaline autoinjector) if risk of accidental exposure. Thorough and regularly repeated education needed. Insect sting reactions may respond to desensitisation. Can also try if medication allergy and few alternative agents. Investigation of allergen by immunologist as complex. When to prescribe adrenaline autoinjector? Anaphylaxis and risk of subsequent exposure (all food and insect allergies etc, not medication allergies). What investigations/treatments have no scientific basis? Cytotoxic or Vega testing, hair analysis, kinesiology. What about the "just need a new Epi-Pen script" presentation? Trigger for long consult to check allergen identified, avoidance strategies clear, Medi-Alert bracelet

worn, action plan in place and know how to use autoinjector, comorbidities that reduce reserve capacity well managed. Paeds primary survey? Start with first glance "Paeds Assessment Triangle or PAT": (1) Appearance (TICLS: tone, interactivity, consolability, look/gaze, speech/cry), (2) WOB (posture, movements, visual signs, audible signs), (3) Circulation (colour, MM, CRT) => then primary survey ABCDE. For disability: tone/gaze/cry. Secondary survey: SAMPLE history (signs/symptoms, allergies, meds, past history, last meal/liquid, events). What do the European Resuscitation Council list as vascular access site of choice? Intraosseous, esp if child having CPR (medial, proximal tibia 1-2cm below tuberosity). Give up on IV after 90-120secs of trying. Recommended office emergency drugs: Salbutamol*, O2*, Ceftriaxone*, Adrenaline (1:1000* and 1:10,000), anticonvulsant agent (eg midazolam), corticosteroids, atropine, naloxone, normal saline (* essential). Essentials = SOCA. Diagnosis of meningococcal septicaemia? High index of suspicion in kids with nonspecific symptoms of fever, lethargy, myalgia, vomiting, headache. If non-blanching rash => hospital and administer IV antibiotics before transfer. Kernig's sign? Flex hip to 90deg with knee extended => pain. Brudzinski's sign? Flex neck => flexion of hips/knees. Treatment for meningococcal sepsis? (1) IV Ceftriaxone/Cefotaxime most preferred, PenG (benzylpenicillin) recommended, if unavailable then Ampicillin, and if penicillin & cephalosporin hypersensitivity then cloramphenicol. Most meningococcal isolates are penicillin sensitive, but some other bugs (S pneum, H infl) can present similarly so ceftriaxone first choice. What is croup: Parainfluenza, influenza or other viral infection related laryngotracheobronchitis => NPA not required. Croup triad: URTI before stridor, respiratory distress, barking cough. Treatment of croup: (1) Oral steroids for almost all (1mg/kg oral pred enough unless too sick to swallow - often BD for 4 doses). (2) Inhaled adrenaline (4mL 1:1000 with high flow O2 (though SaO2 usually OK), lasts 2h so monitor till after this period) for severe cases. Only side effects mild: pallor and tachycardia. Hospital admission if not responding or severe symptoms/signs (AMRs+++, unable to feed). (3) Salbutamol for associated bronchoconstriction but upper airway obstruction should be treated with adrenaline first. (4) Paracetamol or ibuprofen for discomfort. No antibiotics. Onset of action of nebulised adrenaline? 10-30mins. Is SaO2 useful in croup? No, upper airway problem so low SaO2 is a late sign. Is stridor a feature of asthma? No, stridor comes from teh upper airway. What is mild traumatic brain injury (aka concussion)? Shear, acceleration, deceleration forces cause functional disturbance via altered patterns of neuron activation (poorly understood pathophysiology). No structural injury or changes on imaging. Most specific symptoms? LOC, confusion, attention deficit ("not themselves"), amnesia, balance disturbance ... may not always be present and sometimes delayed onset. Suspect after any collision or direct trauma to head. Who to observe at home and who to observe at practice/ED? HOME: No LOC, no altered mental state, <1x vomiting. HOSPITAL: LOC (any LOC probable concussion / >5mins LOC possible structural lesion), headache, seizure, lump, vomiting 2 or more times => only release if alert, interactive, drinking OK. How long should minor head injury patients be monitored? No evidence. Should parents wake kids with minor head injuries through night to check? No.

Red flags for structural head injury (when parents should represent and you should worry/refer)? Mechanism of injury, progression ... worsening headache not responding to paracetamol, persistent vomiting, LOC >1min or later deterioration in conscious state (GCS <12), amnesia, objective neurological deficit or ataxia, blood/discharge from ears/nose, haemophilia or anticoagulants, delayed onset of fitting/spasms especially in kids. Pts should get better over 10-14d not the other way around. Also consider ? non-accidental injury in kids as a referral criteria. Imaging what and when? Never xray skull. CHALICE guidelines to determine need for head CT (above). How much ionising radiation in CT head compared to CXR? 115 CXRs = 1x CTB. Lower threshold for scanning if <2yo plus SSx, suspect non-accidental injury, haemophilia, anticoagulants, LOC >5mins. Grade and prognosis of concussion? SCAT2 helpful guide, but no instrument accepted. Prognostic modifiers: Symptoms (esp duration >10d), signs (>1min LOC, amnesia), sequelae (seizures >1min), temporal (in relation to previous injuries: "second impact syndrome"), threshold (repeated concussions, progressively less force required), age (<18yo), co/premorbidities (migraine, depression or other MH/sleep disorder), medication (psychoactive, anticoagulants), behaviour (dangerous style of play), sport (high risk sport). What is "second impact syndrome"? Aka "acute, progressive, diffuse cerebral oedema". Consensus is that return to play and reinjury before recovery can cause "second impact syndrome" (potentially fatal and delayed recovery), esp in younger athletes. "Graduated return to play protocol"? No return to play until full recovery: graduated return to play guided by symptoms, signs and using neuropsychiatric testing: (1) Complete rest, once asymptomatic go to 2; (2) Light aerobic exercise, no resistance work; (3) Sport-specific exercise (running in football) and progressive addition of resistance work; (4) Non-contact training drills; (5) Full contact training drills after medical clearance; (6) Game play. What does rest mean after concussion? No physical activity, stress (altitude/flying), cognitive load (study, video games, computer), alcohol/drugs, driving. Moat commonly reported symptoms after mild head injury? Headache and personality changes => neuropsychological assessment if persistent. What proportion of parents report personality changes in their kids after mild head injury? Nearly 1/3. Over what period do most symptoms of post-concussive syndrome resolve? Within 3 months. Is it common for people to get cognitive decline or depression later in life as a result of concussion? Relative risk of depression 2-3, cumulative cognitive deficit risk unclear but probably rare. C-Spine clearance? DAINTY (distracting injury, alcohol or drugs, injury mechanism, neurological deficits, tenderness in midline, YES => get pt to raise arms to touch your hand (any numbness/tingling), remove collar and get pt to turn head 45deg left and 45deg right, then all the way left and right. If no pain, remove collar. Bite management? Liberal lavage, antibiotics, tetanus toxoid (consider Hep B status if human bite), If associated fracture refer for washout. Secondary, loose closure at 3d if still clean. Regular review. Hand laceration management? Examine movement/sensation/circulation (ROM, light touch and pain, CRT, pulses) before using local. Excessive pain with active/resisted movements ? tendon injury. Copious lavage, loose suturing to allow drainage delayed closure OK in wounds presenting after 6h. Tetanus toxoid and

comsider antibiotics. When to refer hand injuries? Compound fracture, fractures with rotation deformity (examine fingers end-on and with DIP/PIP joint flexion) deeper structures on view, tendon or nerve injury, circulatory compromise. Low threshold for xray as many fractures (esp avulsion) occult. Hand immobilisation? Minimise as hand susceptible to permanent loss of ROM (mostly about 3 weeks except mallet fracture which is 6-8) => early exercises and dynamic splints. "Safe position" is >70deg MCP flexion, minimal PIP flexion, 30deg wrist dorsiflexion. Common causes of sore throat? Viral pharyngitis, strep tonsillitis, chronic sinusitis with postnasal drip. Serious sore throat diagnoses? Epiglottitis, cardiac pain, oesophageal perforation (Booerhave syndrome), retropharyngeal abscess/perforation. Other causes of epiglottitis? Staph aureus in adults, chemical burns (cement dust), tehrmal burns (if thinking of epiglottitis clarify H influenzae vaccination status). How does Booerhave syndrome happen and what are complications? Usually forceful vomiting => rupture of distal oesophagus at weakest point => retrosternal, pleuritic pain, SOB, dysphagia, odynophagia. Occasionally after blunt trauma and very rarely by cold carbonated drinks consumed quickly => oesophageal spasm and gas expansion increasing pressure and causing rupture. Complications: pneumonia, mediastinitis, empyema, sepsis, MOF. Treatment: transfer urgently for specialist surgery & antibiotics, fluids. Causes of angio-oedema? Inherited or acquired C1 inhibitor deficiency, medications (ACEIs most frequently), environmental exposures (eg bee stings). Why is ACEI-induced angio-oedema different? Bradykinin and substance P mediated not mast cell degranulation and histamine mediated. Non pitting oedema of head, neck, mouth without urticaria (occasionally isolated angio-oedema of instestine so consider as unusual cause of abdominal pain. Thought to often have average onset at 12-14mo of treatment (can occur early). Risk lower in diabetics, higher in females and smokers and possibly people on aspirin/NSAIDs or immunosuppresssants. Avoid gliptins + ACEIs! Treatment often steroids and antihistamines but unproven in this setting. Indicators of need to secure airway in angio-oedema? Marked base of tongue and floor of mouth oedema. Differentials of pelvic pain in pregnancy? Common in early pregnancy. Miscarriage, ectopic, heterotopic, ovarian torsion, ruptured ovarian cyst or corpus luteum, PID, red degeneration of fibroid, GI or urinary tract pathology. Heterotopic pregnancy (simultaneous intra and extrauterine pregnancies) risk factors? Assisted reproductive technologies (1:100 ... rare in natural conception). previous ectopic, smoking, endometriosis, PID, previous tubal surgery. Usually missed and diagnosed on rupture, but diagnosis possible by TVUS. Management of heterotopic pregnancy? Usually surgical (laparoscopy or laparotomy) but medical treatment sometimes tried (TVUS-guided injection of hyperosmolar glucose or KCL into gestational sac). Anticholinergic syndrome red flags? Dizziness, blurred vision, dry mouth, dilated pupils. Can be caused by improperly prepared lupini beans. Management of anticholinergic syndrome? Supportive with benzodiazepines for agitation/psychosis and physostigmine for central ACS. Risk factors for DKA? Puberty, female, higher mean HbA1c, higher reported insulin doses, lower SE status, mental health problems. What is DKA? No insulin => osmotoc diuresis (dehydration, K and PO4 depletion)

and peripheral/hepatic lipolysis (ketoacidosis) => hyperkalaemic dehydration (low total body K and PO4). DKA triggers? UTI, AMI, pneumonia. T1DM/DKA clues: Polyuria, polydipsia, return of nocturnal enuresis early ... then wt loss, chest or abdominal pain, altered breathing, ketosis, confusion, shock. DKA investigations? BSL, ABG (cap/venous in kids), UEC, urinalysis (ketones, glucose) and UMCS, ECG, CXR. Obs in DKA? Q30min BP, HR, UO / Q1h capillary BSL / Q2h UEC (potassium). What does high serum BSL and urine ketones+++ imply? High risk of DKA (as opposed to starvation state which would present with low serum BSL). DKA management: DRSABCDE and call for specialist advice. 1. Fluid:: Calculate deficit + 24h maintenance fluids (deficit usually 40-80mL/kg). Give 1/3 volume in 5-6h (normal saline). Keep NBM. Don't go past 1.5-2x daily requirements. Once BSL <15 switch to 5%D and N/2 at 50-100mL/h. 2. Potassium: Cardiac monitor. Replace K once/if <6mmol (5mmol/kg/d at 40mmol per litre of fluid) and check at least Q2h. 3. Sodium (correct by adding 2mmol for every 5.5mmol glucose over 5.5mmol/L).: If >150mmol/L use N/2 to rehydrate and slow the process to 48-72h. 4. IV Insulin (Novorapid, Humalog, Actrapid): Bolus 0.15iu/kg (100iu/1000mL and flush 100mL through line first to saturate binding to giving set), then 0.05 to 0.15iu/kg/h (0.05 preschoolers, 0.1 for school kids, 0.15 for adults). Ideally initiated in PICU or diabetes ward, but depending on setting SC doses may be recommended to stabilise pt until IV can be started. Usual NS fluid bolus in DKA in shocked/dry kids? Bolus 10-20mL/kg over 1-2h. DKA Complications? Severe infection, arterial thrombosis, shock, lactic acidosis, cerebral oedema. Signs of cerebral oedema? HTN, bradycardia, low SaO2, headache, confusion. Risk factors for and treatment of cerebral oedema in DKA? Risks => low arterial CO2, high arterial nitrogen, sodibic treatment, smaller increase in sodium during treatment. Treatment => fluid restrict, 0.45% NS, mannitol. Paediatric vital signs: 1. RR: <1yo 30-40 / 2-5yo 25-30 / 5-12yo 20-25 / >12yo 15-20 (Min drops by 5s. Max drops by 10, 5, 5). 2. HR: <1yo 110-160 / 2-5yo 95-140 / 5-12yo 80-120 / >12yo 60-100 (Max drops by 20s. Min drops by 15, 15, 20). 3. SBP: <1yo 70-90 / 2-5yo 80-100 / 5-12yo 90-110 / >12yo 100-120 (Min and max both rise by 10s). 4. Reduced UO: Infant <2mL/kg/h / child <1mL/kg/h / adult 0.5-1mL/kg/h. Meningitis treatment? Ceftriaxone (Benzylpenicillin OK esp if closer to civilisation but doesn't cover other possible pathogens). Dexamethasone and aciclovir.

Ear Nose and Throat, Head and Neck, Dental AOM causative organisms? S. pneum, H infl, M catarr. What are the different types of otitis media? 1. Acute otitis media: Inflammation & likely pus collection in middle ear. 2. Unresponsive otitis media: Clinical symptoms, signs after >48h of treatment. 3. Chronic suppurative otitis media: Persistent inflammation with perforation and draining exudate >6 weeks. 4. Recurrent acute otitis media: >3 episodes in 6mo, >4 episodes in 12mo. 5. Otitis media with effusion (serous otitis media): Residual collection without

symptoms, signs or inflammation lasting 6-16 weeks. Half of kids will have effusion at 1 month post AOM, 10% will have one at 3 months. 6. Myringitis: Inflammation of TM +/- otitis externa. Diagnosis of otitis media? Clinical => ear pain, temps, anorexia/vomiting. Bulging, inflamed/injected, dull, non-mobile TM (Be aware, this can also occur in viral URTI .. and pt will not respond to antibiotics). Culture of discharge does not aid diagnosis. Diagnostic accuracy of GPs diagnosing effusion? <50% (ENT surgeons only 75%). Risk factors for otitis media? Static: 6-11mo, not first child, ATSI, cleft lip/palate, immunodeficient. Modifiable: Daycare, tobacco smoke, bottle feeding, horizontal feeding, dummies (inadvertent sharing), not vaccinated for 13vPCV. How to explain otitis media? Very common for bugs get in behind babies/kids eardrums because eustachian tubes from back of throat are shorter and more horizontal than in adults. Also softer and more easily blocked, so fluid doesn't drain away as easily. Problem can be infection and pus in the middle ear, leftover fluid from an old infection, or infection of the eardrum itself (sometimes with an infection of the outer ear too). This causes pain, temperature, loss of appetite, vomiting and sometimes hearing problems. Antibiotics are not always needed because they are not that good at curing these infections and don't get rid of the fluid build-up (the body clears most of them on its own). Best first-option treatment is rest, pain relief, wait and see. Sometimes the eardrum bursts, which releases the fluid and relieves the symptoms. The eardrum heals on its own and there are rarely any long-term problems if this happens. Complications like infection of the mastoid bone behind the ear and meningitis are rare. If the problem happens repeatedly or there is fluid behind the eardrum still there after 3 months and hearing is affected it may be worthwhile seeing ENT specialist for possible grommets (which create a hole in the eardrum to drain fluid to the outer ear), but this involves an operation and has risks. So it is a last resort. Give fact sheet to parents/carers (at end of NSW Health reading). Otitis media historical features important in deciding management? Consider cause => recurrent infections at different sites ? immunodeficiency; swimming may be good for CSOM in remote aboriginal communities but >60cm underwater forces bugs into middle ear (think about taking a break). Consider prognosis => first year of regular contact with other kids => less likely to have ongoing infections. Consider effects => concerns about hearing? TM appearance in AOM? Most specific features are bulging, loss of light reflex and loss of normal contour. Early: Cloudy, bulging, vascularised => Mid: red, bulging as disease progresses => Late: dull and retracted/neutral if effusion present. Immobile. TM appearance in AOM vs OME? AOM bulging, OME neutral or retracted. Management of otitis media? Distinguish AOM from myringitis and OME! Check hearing. Be sparing with antibiotics (Definitely not in first 24h, only benefit is modest reduction in symptoms after 3-7d). 1. Initial treatment of AOM? Rest in warm room with adequate humidity..(1) If >2yo and not very ill, give high dose paracetamol (15mg/kg q6h) or ibuprofen (10mg/kg q8h) for pain/temps and topical benzocaine if no perf. Give script for amoxi 5/7 course to fill if not better at 48h. Notify teachers, keep ear dry. (2) If higher risk (<2yo, preverbal, severe pain or illness, perf, ATSI, cochlear implant), antibiotics straight away. Reassess in 48-72h (24h if <2yo). 2. Which antibiotics? In kids: 5d amoxicillin 1st line (40-50mg/kg/d in 3 divided doses), cephalosporin/cefaclor 2nd line. In adults: 5d amoxicillin or augmentin duo forte (doxy and macrolides also work). 3. Treatment at review? If looks to be resolving with or without perf, keep ears dry, see again in 3 months (hearing test at 10d). If not responding (persisting

pain/discharge), affecting school work, or red flags present (reduced LOC, facial paralysis) => consider differentials/complications, seek advice and consider augmentin duo (to cover resistant strep). Also saline spray to clear mucous, steroid spray to reduce adenoids (won't open eustachian tubes), keep ear dry. Decongestants only if nasal congestion present. 4. If suppurative: Tissue spears (+ povidone iodine 5% instilled with 20mL syringe and plastic tubing first if chronic). Cipro/Ciloxan drops OK in perfs (not Ciproxin). 5. When to check hearing? At 10d. 6. When to refer? Referral for myringotomy and tympanostomy if effusion + retraction at >3 months + hearing loss on audiometry. Also if 3x AOM in 6 months or 4x AOM in 12 months, retracted TM. Complications of AOM? Mastoiditis, cholesteatoma (temporal bone cyst), meningitis, brain abscess, facial paralysis. <1% incidence. Spotting mastoiditis? Unremitting pain esp at night, fever, bulging/red TM and swollen/tender mastoid process => CT not MRI. Cleaning ears? Suction if available. If not, then tissue spears. Indications for ear ventilation tubes? Chronic OM with effusion >4/12 with significant hearing deficit or vision problems, language delay, learning difficulties, TM damage with retraction pockets (to prevent damage to ossicles). Use of prophylactic antibiotics? Some efficacy but only if unable to tolerate GA or infection with tubes in (risk of resistance). When to do adenoidectomy? 2nd set of grommets or significant nasal obstruction (doesn't prevent recurrent AOM). Otitis externa organisms? Staph aureus, pseudomonas aeruginosa. Function of cerumen? Lysozymes, immunoglobulins, acidic pH (4-5) => protective barrier and part of immune system. Wheat bran wax in Asians, darker/thicker balls of wax in Caucasians/Africans. Removal of wax? Cotton wool brooch curettage or suction under direct vision +/cerumenolytic (docusate sodium aka Waxsol best). Not syringing, especially if tight canal, outer ear infection or eczema, TM not visible, complete occlusion deep in canal. Ear candles not recommended 2 to paraffin impaction risk. Alternatively, warm olive oil. Removal of foreign bodies? Lateral ear canal => easily removed. Deep ear canal => good illumination, blunt microforcepts, brace using side of pt's head, refer kids to specialist. Insects => flush with sterile water +/- kill with olive oil. Can insects cause perfs? Yes, ticks are a particular problem. Activities predisposing to exostoses? Swimming/surfing (cold water) => periosteal reaction and bone deposition gradually occluding canal, causing conductive hearing loss, wax plugging, infection => surgical removal in rare problematic cases. What are osteomata? Benign, often pedunculated tumours arising from anteriorsuperior side of bony-cartilage junction. Rarely a problem. OE vs OM? OE = summer, swimming, pain on manipulation of tragus/pinna, fullness/deafness, pseudomonas/staph on swab, TM normal or mildly inflamed, can be hard to visualise, mobile; OM = winter, URTI, less painful except right before perf, TM red/opaque and immobile, bubbles may be seen on popping ears. What predisposes to AOE? Too much or too little cerumen (eg from swimming), trauma, dermatitis. Examination in AOE? Pinna, tragus, mastoid, canal (? foreign object), TM. Cranial nerve examination mandatory (In malignant AOE CN 7 hit first, then 9,10,11, 12 and if petrous bones involved, 5 and 6 affected).

Prevention of otitis externa? Avoid water/humidity (shampoo then hair dryer, acetic acid and alcohol drops, ear plugs), avoid trauma (cotton buds, paper clips), avoid syringing if tight/twisted canals, treat dermatitis or systemic illness (diabetes, HIV etc), avoid neomycin drops (atopic reaction), treat discharging OM. Acute otitis externa (external canal cellulitis) treatment? Education, regular aural toilet, ear drops 7-10d, analgaesia. No evidence for antiseptic vs antimicrobial, quinolone vs aminoglycoside, antimicrobial vs antimicrobial+steroid, but topical better than systemic. Kenacomb Otic has antifungal and antimicrobial but not effective against pseudomonas, ototoxic. Sofradex similar to Kenacomb, cheaper, no antifungal action. Ciproxin HC effective against pseudomonas, staph aureus, ototoxic. Ciloxan not ototoxic. Fungal otitis externa treatment? Usually caused by prolonged antibacterial drop use. Aural toilet and Locacorten-Vioform (flumethasone-cliquinol) ... sometimes acidifying solutions all that is required, other options are clotrimazole drops, or fill the ear with canesten. Kenacomb Otic treats both fungal and bacterial (not P aerug). Viral otitis externa treatment? Vesicles on TM => mastoid/scalp pain, loss of taste ant 2/3 of tongue, lost lacrimation, tinnitus/vertigo, LMN facial palsy => herpes zoster oticus aka Ramsay Hunt syndrome => antivirals, steroids, eye protection or patching => recovery not as good as for Bell's palsy. Serious mimics of otitis externa? Cholesteatoma, malignant otitis externa. When to use oral antibiotics? Complicated AOE, diabetic/immunosuppressed. How to use ear drops? Lie on side with affected ear upwards, manipulate tragus in circular motion, stay there for a few minutes. Getting the drops through tight canal? Ear wick, change every 48h. Analgaesia? Paracetamol, NSAIDs, benzocaine/Auralgin drops if no perf, topical steroids in antibiotic drops, codeine/oxycodone for stronger pain. What does malignant otitis externa (skullbase osteomyelitis) look like? Pathognomonic signs is granulation tissue on floor of cartilaginous canal near junction with bony canal => elderly, diabetic or immunocompromised with unremitting pain, discharge, malaise/fever, not responding to treatment => CN palsies with CN 7 hit first => aggressive, prolonged systemic and topical antibiotics needed (hyperbaric oxygen effective in specialist centres) => technetium scans positive months after successful treatment. How does age-related hearing loss happen? Mostly sensorineural. Peipheral: Accumulated genetic damage, diminishing neural/supportive cochlear cells (cumulative effects of noise, ototoxins, vascular pathology, middle ear infections). Central: primary changes => reduced brain cells involved in processing and lipofuscin accumulation; secondary => effects of vacular disease and respiratory failure on hearing centre of brain => both cause difficulty localising or judging gaps in sound. Auditory deprivation causes neuroplastic changes in brain. What is sensorineural hearing loss? Loss 2 to damage along pathway from cochlea to cochlear nerve to higher auditory centres. Cochlear vs retrocochlear defects? Cochlear => speech understanding scores in line with pt's hearing thresholds (hear and understand speech but over narrower decibel range). Retrocochlear => poor speech understanding scores compared to "hearable" decibel range (hear but can't make out speech even within narrowed decibel range). Depression rates in elderly patients with hearing deficits? Almost twice as high. Is it safe to assume a patient who can hear easily during one-on-one conversation has no functional hearing problem? No, ask about hearing in real-world situations.

Do's and don't of speaking to someone with hearing impairment? DO get attention by touch, wait till they can see you, position self close, enunciate and speak at normal rate, reduce background noise, clue to changes in topic, rephrase. DON'T speak from another room or while walking away, speak directly to ear, shout, cover mouth, repeat statements. What are hearing-assistive devices? Devices that transmit sound from a source (eg TV audio) directly to individual via wired or wireless technology. with output via earphones or existing hearing aid. What are alerting devices? Devices designed to convert auditory alerts (doorbell, smoke alarm to visual or tactile stimuli). In-the-ear (ITE) vs behind-the-ear (BTE) devices? BTE larger so bigger battery pack, greater gain/amplification, easier/larger controls. ITE don't protrude but lack advantages of BTE & fitting crucial as inadvertent ventilation causes feedback++. Problems with hearing aids? Pts not satisfied with quality of government-subsidised aids; difficulty with ear moulds (due to altered wax production/migration, skin and hair in elderly patients); moulds get blocked with wax; pts more prone to AOE; pts with single-sided deafness difficult to fit with traditional air-conducton aids as they struggle with distorted sound compared to normal ear. Options if not suitable for BTE or ITE devices (due to microtia, aural atresia, discharging ears, derm problems)? Baha bone-anchored implant (titanium coupling implanted in bone with ear or body worn microphone, stimulus bilateral so localisation not perfect), middle ear implants (amplify sounds through ossicular chain, no occlusion of canal, reduced distortion at higher gain in higher frequencies, stimulus unilateral improving localisation), cochlear implants (most implantees adults, transmastoid approach, new partial deafness implantation tech preserves residual natural cochlear function, can stimulate specific frequency spectrum, hybrid air-conduction hearing aid and cochlear implant devices available). Hearing loss red flags? Asymmetrical (cerebellopontine angle tumour eg vestibular schwannoma), cranial nerve defects (destructive inflammatory or neoplastic process in temporal bone), ear canal or middle ear mass (SCC or adenoid cystic carcinoma), deep ear pain (inflammatory or neoplastic process in temporal bone), discharging ear ("). How often to recheck hearing in pts with hearing aids? Yearly. Blocked nose differentials? URTIs, ARS/CRS, septal deviation, turbinate hypertrophy, polyps and neoplasms, adenoid hypertrophy, rhinitis medicamentosa, nasal valve dysfunction, FB. Acute rhinosinusitis (<12wks): Usually viral, but if >10d suspect bacterial. Infection of nasal passages and sinuses (unified airway). Rhinorrhoea (st purulent), obstruction, pressure/fullness, malaise, fever, cough, reduced smell. Bacterial causes same as AOM + staph aureus => rx is amoxicillin or macrolide if hypersensitivity. Can be hard to distinguish from viral URTI, so overdiagnosed. Allergic rhinitis/rhinosinusitis (ARS) vs chronic rhinosinusitis (CRS)? 1. ARS => IgE mediated after allergy exposure (often seasonal cycles, family history) => vascular congestion and mucous hypersecretion => itch, sneeze, watery rhinorrhoea, itchy/watery eyes. 2. CRS (>12wks) => final common pathway of numerous processes, involves mucosal oedema from persistent inflammation => mainly obstruction and thick discharge (also: facial pressure, headache, halitosis, lost sense of smell). Incomplete resolution with exacerbations. Can ARS and CRS happen together? Yes, ARS is one cause. ARS history/investigation? Ask about exposure to pets, dust, cleaning products;

asthma history; meds including NSAIDs, BBs, ACEIs, OCPs, nasal decongestants which can cause congestion. Look for polyps, deviation, allergic crease. Order RAST or send for skin prick testing with specialist (higher anaphylaxis risk), immunological assessment if suspecting immunodeficiency, pre-post spirom. ARS treatment? Education, avoidance (little evidence it works: reduce soft furnishings, vacuum regularly with high efficiency particulate aka HEPA air filter, use protective bedding, low temp and humidity environments better) => pharmacotherapy (intermittent => oral antihistamines give excellent control; <3d bursts of oxymetazoline/a-agonist // persistent => oral antihistamine, intranasal steroids minimal systemic absorption but can sting/dry). Ocular antihistamines (antistine privine). Other treatments for ARS? Intranasal anticholinergics (not first line but good for rhinorrhoea, vasomotor rhinitis in elderly), cromones (difficult dosing/compliance), leukotriene antagonists (on par with H1-antagonists but not as good as steroids). Resistant ARS? ENT referral for inferior turbinoplasty as adjunct, short course oral steroids, immunology referral for immunotherapy (long therapeutic times and potential anaphylaxis or failure). Some causes of CRS? Structural (Polyps, tumours, deviated septum, trauma), systemic/medical (CF, HIV, GORD, autoimmune diseases), allergic rhinosinusitis, infections (viral colds, bacterial, fungal .. or allergic reactions to fungal infections), irritants (smoking only proven to affect mucosa in vitro). Examination in CRS? Otoscope or headlight => mucopus, deviation, polyps, turbinate hypertrophy. Also swelling/erythema of cheeks/forehead/orbit, eye movements, meningism. Investigations to confirm CRS? Assessed on mucosal thickness on CT or nasoendoscopy. CT: sinus opacification, air-fluid level, mucosal thickness. CRS management? Nasal saline irrigation, intranasal corticosteroids (recognising neither of these get to sinuses), directed antibiotic therapy .=> continue steroids for 3 months then try stopping. Resistant cases of CRS? Culture-directed antibiotics after 2 failed courses (macrolides appealing due to antibacterial plus anti-inflammatory effect, 3mo course). Treat concomitant allergic rhinosinusitis. With polyps or persistence >1/12, short course of oral steroids, then ENT referral for consideration of surgery (number of exacerbations needed for surgery not clear, asthmatics' pulmonary function can be improved with polyp surgery). Desensitisation injection therapy if allergy identified. Causes of intranasal swelling? Septal deviation, hypertrophic turbinate, inflammatory polyp. 1. Benign inflammatory polyp = probability diagnosis (if no septal deflection). Uniform, slightly translucent, lateral wall beneath middle turbinate, can occlude entire passage or present at nares. 2. Hypertrophic turbinate: Can look like a polyp, more opaque, also lateral wall, sensitive to touch, reduced by decongestant spray. 3. Also consider: Antrochoanal polyp, inverted papilloma, or other sinonasal inflammatory or neoplastic aetiologies. What are polyps? Subgroup within CRS (all polyps have CRS, not all CRS have polyps), chronic focal inflammatory change causing ballooning of inflamed mucosa. Chronic vs intermittent rhinosinusitis? <>12wks. Persistent vs episodic allergic rhinosinusitis? <>4d/wk for <>4wks. How does QOL effect of chronic rhinosinusitis compare to COPD, back pain? Similar.

What classifies allergic rhinits as mild, moderate, severe? Sleep, ADLs. Where do nasal polyps arise? Lateral nasal wall and middle meatus. Does CRS generally cause pain? No, chronic mucosal inflammation is a rare generator of significant pain. Is loss of smell as significant predictor of CRS? Yes (less consistent, but if present it is the strongest indicator). Does allergic rhinitis predispose to chronic rhinosinusitis? No evidence for this, but they can coexist. Are nasal passages and sinuses separate units? No, unified airway. Secondary sinonasal conditions? CF, immunodeficiency, mucociliary problems, fungal disease, systemic vasculitis and granulomatous diseases, cocaine abuse, neoplasm => referral mandatory. What does unilateral, purulent discharge suggest? Dental infection or FB. What does unilateral, clear discharge suggest? CSF leak. What does cacosmia suggest (confirm objective halitosis directly or with family)? Look for dental infection or FB. Does anterior rhinoscopy help diagnose CRS? No, little role. How is culture collected in CRS? Direct endoscopic collection from middle meatus (must be of directly visualised mucopus as random swab usually contaminated with mixed flora). Cardinal endoscopic features of CRS? Mucosal oedema, polyps, discharge, crusting. Imaging of sinuses? No to plain films, yes to CT. Do CT scan findings correlate well with symptoms? No. Do chemical and physical methods of limiting allergen exposure work in mitesensitive perennial allergic rhinosinusitis? No. What does fungal ball, mycetoma look like? CT shows "double density" within involved sinus => surgery to remove (antifungals not indicated). Delay till nasal steroids kick in? 2 weeks. How to apply nasal steroids? Head forward, opposite hand to opposite nose => directs spray to middle meatus. What can be tried as additives to nasal douches? Xylitol, mupirocin. Sinus red flags? Unilateral obstruction/discharge, blood in saliva/snot (? neoplasia), cacosmia (foul smell when none exists), constitutional symptoms (neoplasm or inflammatory disorder), symptoms suggesting CF/Katagener's in paeds population (cough, SOB, recurrent RTIs), symptoms suggesting expansion into orbit (periorbital oedema, epiphora, diplopia, reduced vision, ophthalmoplegia), neurological symptoms (severe frontal headache, meningism, focal neurol deficits). Samter triad? Polyposis + asthma + aspirin sensitivity. Notoriously difficult to manage, refractory to medical and surgical therapy, may require frequent courses of oral steroids and nasal polypectomies. Multidisciplinary approach (chest, ENT, endo, immuno). Most common complication of acute rhinosinusitis? Periorbital (preseptal) cellulitis. Orbital cellulitis = postseptal cellulitis. Periorbital cellulitis = preseptal cellulitis. Preseptal (periorbital) vs postseptal (orbital) cellulitis: Orbital cellulitis is posterior to connective tissue barrier called orbital septum, confined space causes pressure on structures including optic nerve => proptosis, ophthalmoplegia, blindness in 10%. Spread is usually from ethmoid sinuses through bone or via thromobophlebitis. Chandler's stages of orbital cellulitis: (1) Preseptal: eyelid swelling, no proptosis , opthalmoplegia or loss of vision; (2) Orbital cellulitis: inflammation of orbital fat; (3)

subperiosteal abscess; (4) orbital abscess; (5) cavernous sinus thrombosis. Periorbital cellulitis treatment => oral antibiotics and specialist review. Orbital cellulitis treatment => IV antibiotics and if that fails, surgical drainage. Factors predisposing to epistaxis? Most idiopathic. Local (cold/dry air + digital trauma, inflammation, anatomical abnormalities, tumours, AV malformations), systemic disease (coagulation abnormalities like von Willebrand disease, vascular diseases, cardiac/pulmonary disease, HTN controversial), drugs (blood thinners inc ginseng and gingko, intranasal steroids, cocaine). Epistaxis history? Characterise symptoms: laterality, duration/quantity, from nose or down throat, previous episodes / Seek cause: Recent URTI, blockage, discharge, crust, digital trauma, meds, alcohol/drugs, past ARS or systemic disease, other sites of bleeding/bruising. Epistaxis examination? Haemodynamic status, source of bleed (hard, use PPE, good lighting and suction) checking nostrils/septum/pharynx, other signs directed by history. Treatment of epistaxis? Head tilted forward, press soft part of nose towards face for 10mins while mouth breathing (90% of bleeds from Kieselbach's plexus in Little's area in anterior cartilagenous septum which branches off from int/ext carotids, bleeding here responds to pressure), ice to forehead and nape of neck => decongestant and anaesthetic (lignocaine and phenylephrine spray) to allow examination => try cautery with silver nitrate sticks which cause chemical burn, being careful not to perforate septum => failing this, pack (posteriorly not superiorly) with nasal tampons like Surgicel, Kaltostat or balloon catheters like RapidRhino and leave for 1-4d (consider antibiotics to prevent toxic shock syndrome) => failing this ED. When to send to ED? Shock, bleeding despite pinching/packing, blood down back of throat, recurrent anterior bleed not responding to cautery, comorbidities, coagulation defects, suspect mass or AV malformation, postsurgery => arterial ligation may be needed. Posterior bleeding source? Suspect sphenopalatine arterial branches => unclear trigger, endoscopy to identify. Risks of posterior bleeding? Airway compromise, aspiration, uncontrollable haemorrhage. Recurrent, profuse epistaxis? Suspect hereditary haemorrhagic telangiectasia (Osler disease), lack of smooth muscle and elastic tissue in vessel walls. Adolescent male, recurrent epistaxis? Suspect juvenile angiofibroma. Recurrent with persistent obstruction? Suspect neoplasm. Approach to sore throat? Is the airway safe? Can diptheria/epiglottitis/cancer be excluded? Does the pt need surgical drainage, antibiotics, both? Consider severe tonsillitis with membrane as EBM. Be aware of complications like abscess, febrile convulsions. Sore throat causes by age? Rare in kids <4 or adults >45yo. Common in 4-8yo, teens. Mostly viral pharyngitis, but significant minority strep pyog tonsillitis or EBV (antibiotics cause adverse reaction). Hard to pick cause clinically: red throat no exudate may be bacterial or viral as may swollen tonsils with follicular exudate. 1. KIDS: Rare <4yo and can present atypically (pharyngitis/tonsillitis presenting with vomiting, abdo pain and fever not sore throat). Infection usually viral, bacterial becomes more common from 3-13yo. Other possibilities: (primary HSV) gingivostomatitis, epiglottitis, croup (laryngotracheobronchitis), laryngitis, oral thrush (more bad taste than sore throat), aphthous ulcers, FBs, postnasal drip (eg allergic rhinitis), irritation (smoke or dry air).

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2. ADULTS: Very sore throat, heavy exudate, toxic appearance => think primary HSV as well as strep throat. 3. OLDIES: Take seriously .. may be viral infection, but must exclude pharyngeal cancer (triad: painful swallowing, referred ear pain, hoarseness). Also think zoster (lesions usually in oral cavity and on face), candidiasis (metallic taste => excude DM). Serious causes of sore throat? Haemophilus influenzae epiglottitis (2-4yo, rapid onset febrile illness, no cough, unable to swallow), strep pharyngitis and its complications, diptheria, HIV/AIDS, DM/thrush, throat cancer, blood dyscrasias (acute leukaemia, neutropaenia, aplastic anaemia, agranulocytosis), supraglottic foreign body (not visible on examination). Pitfalls of sore throat? Dagnosing angiose EBV as GABHS (both cause exudative tonsillitis) => giving penicillin => severe rash. Also adenovirus, primary HIV, trauma (FB, burns, irritants), vocal abuse, mouth breathing due to nasal obstruction, tonsilloliths (hallitosis, vague sore throat, recurrent tonsillitis), NSAIDS, thyroiditis. Red flags of sore throat: Persistent fever, failed ABx, medication-induced agranulocytosis, drooling, sharp pain when swallowing, swelling+++, candidiasis. Sore throat history? Sore throat vs deep pain in throat vs neck pain, point to source of pain, associated symptoms (metallic taste, fever, nasal stuffiness/discharge), ear or other pain. Also smoking, other irritants, asthma/steroids, immunisations (diptheria). Sore throat history and investigation? general (toxicity, pallor of leukaemia, nasal stuffiness of EBV, hallitosis of strep throat), neck (tenderness, lymph nodes), ears, sinuses, oral cavity (ulcers, abnormal masses or swelling, redness, exudate). Consider swab, FBC/smear, BSL, Monospot (blood), ASOT. 1. Viral pharyngitis: mild redness, prominent lymphoid patches on oropharynx. 2. Candidiasis: small patches of exudate on palate or other structures. 3. EBM: large whitish-yellow membrane on both tonsils +/- petechiae, swollen uvula => FBC (atypical lymphocytes) + Monospot bloods (IgMs better in early illness). 4. GABHS: generalised redness/swelling of tonsils and pharynx with pockets of pus => swabs controversial (do it if worried about diptheria, TB or institutional outbreaks). Sore throat treatment: 1. Supportive: rest, soothing fluids and icy poles, analgaesia (aspirin for adults, paracetamol or ibuprofen for kids), aspirin gargles, don't overuse topical lozenges or sprays (sensitising), <3d of decongestants for runny nose. When to refer sore throat? Epiglottitis in kids, inaccessible FB, peritonsillar/retropharyngeal abscess, recurrent tonsillitis and adenoid hypertrophy, suspicion of HIV/diptheria, no response to treatment, generalised/undiagnosed disorders. Specific causes to watch out for? 1. Streptococcal (GABHS) tonsillopharyngitis: Pharynx, tonsils, both. Uncommon <3yo and >40yo. Four features: systemically unwell (T >38, toxic), tender anterior cervical LNs, tonsillar swelling with white-spot exudate, no cough (+/- dysphagia, throat pain st worse on talking, hallitosis). Examination: Inflamed/swollen pharynx, swollen tonsils with pockets of yellow pus, very enlarged/tender tonsillar LNs. Investigations: Throat swab 90% sensitive, whether/who to swab controversial partly because asymptomatic carriage common ... Murtagh's suggests only swab if suspecting diptheria or in boarding schools etc. Precise diagnosis = positive culture + 4x rise in ASOT. In pharyngitis, pt infectious for 1 week after acute phase (reduced to 24h if



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treated). Exclude from school till 24h after treatment started. Toothbrushes carry GABHS - don't share. When to use antibiotics: Contentious, can shorten duration of disease but resistance is a problem (analgaesia and throat gargles often all that is needed). Use clinical judgment => more likely to treat if existing RHD, scarlet fever, quinsy or peritonsillar cellulitis, pts in special communities (ATSIs). If using antibiotics, stick to 10d course of Pen V (roxithromycin if allergic, benzathine penicillin if non-compliant, avoid amoxicillin => risk of EBV rash). Antibiotics protect from rheumatic fever but not post-strep glomerulonephritis. When to use prophylactic antibiotics: if >5 episodes a year and affecting life. Quinsy (peritonsillar abscess): Peak incidence 20-50yo. Previously thought to be due to spread of GABHS tonsillitis, but now thought to be primary infection of Weber's (salivary) gland. Can be anaerobe, haemophilus or staph aureus. Symptoms: lateralised throat pain, increasing difficulty swallowing, referred ear pain, trismus. Signs: mass with medially displaced uvula, hot-potato voice. Treatment: needle aspiration or incision/drainage if pointing (not "hot tonsillectomy" as was done in the past). Oral pen V likely to fail .. use IM procaine penicillin or clindamycin. If not yet pointing, diagnosis is peritonsillar cellulitis, a transitional stage, treated with antibiotics and supportive care. Ongoing symptoms and smoking history, need to exclude cancer. EBV (Infectious monoucleosis): History: Suspect in 15-30yo with prodromal fever, sore throat, lymphadenopathy 1-4 weeks (peaks at 7d) +/- malaise, anorexia, myalgia, skin rash. Examination: nasal voice, often petechiae on palate, enlarged tonsils +/- white exudate, peri-orbital oedema, (posterior cervical) lymphadenopathy, splenomegaly (50%), jaundice +/- hepatomegaly (510%), rash (primary or secondary to amoxi/ampicillin). EBV testing: Controversial, but one possible strategy = FBC for atypical lymphocytes, absolute lymphocytosis + Monospot blood test first ... then IgM tests later if still uncertain (more specific). Heterophile antibody tests are blood tests that work via RBC agglutination; they include Monospot (horse RBC agglutination) and Paul-Bunnell test (sheep RBC agglutination). They are cheap and fast but false negatives occur in early illness (esp week 1). IgM and IgG to viral capsid antigen (EBVCA), IgM to early antigen, and antibody to nuclear antigen (EBNA) are more sensitive/specific and most expensive. EBV PCR more sensitive/specific than heterophile tests (only vaildated in kids) but also expensive. Pt can remain infectious for up to a year. Exclusion from school not necessary (per NHMRC guidelines). Viral pharyngtis: Commonest cause of sore throat. Prodromal coryza, hoarseness, cough, conjunctivitis, nasal stuffiness. Few signs, mild redness, no exudate, sometimes lymphoid patches, no large/tender tonsillar lymph nodes. Diptheria: Corynebacterium diptheriae, onset insidious and affected by previous immunisation, antibiotics (fatal form almost always in non-immunised pts). History: Insidious, mild-mod fever, mild sore throat/dysphagia. Examination: pallor, ill-looking, large tonsils, pharynx inflamed and oedematous, spreading pseudomembrane (usually grey-green), large LNs, bull neck. Investigation: throat swab. Treatment: antitoxin, penicillin or erythromycin, isolation. Candida pharyngitis: HIV, DM, corticosteroids (inc inhalers), broad spectrum antibiotics, dentures, debility => bad (metallic) taste and sometimes pain/dysphagia => widespread milky white plaque that can be scraped off to show bleeding/ulcerated surface => find underlying cause, nystatin suspension rinse/swallow (or amphotericin lozenges). Acute epiglottitis: Life threatening in kids, often missed in adults because

airway not obstructed => sore throat, dysphagia, drooling, tender neck (+ airway compromise in kids) => don't examine throat with tongue depressor (risk of losing airway) => hospital + IV cefotaxime. 8. Laryngeal cancer => 1st tests to order CT neck, chest with contrast, FNA of mass; consider flexible fibre-optic laryngoscopy, biopsy, whole body PET/CT. Oropharyngeal cancer => biopsy, PET-CT head/neck. 9. Others: Herpangina (rare and self limiting; Cocksackie virus; small vesicles on soft palate, uvula, anterior fauces that rupture and form small ulcers), HSV pharyngitis (primary infection similar to GABHS pharyngitis but ulcers go beyond tonsils). Are throat swabs helpful in distinguishing bacterial from viral tonsillitis? No. Advice to patient with mononucleosis? Long duration of symptoms, avoidance of contact sports for 6 weeks, monitoring of LFTs. What is stertor? Noisy breathing due to oropharyngeal obstruction (distinct from stridor). What to make of symptoms c/w tonsillitis but normal looking tonsils? Pathology further down aerodigestive tract. Function of larynx? Protect airway from foreign substances and phonation. Smoking and hoarseness? Smoking history + hoarseness >10d => laryngeal lesion till proven otherwise => ENT, Maxfax referral. Dysphonia history? URTI, smoking (ever), recent voice abuse, trauma/surgery, vomiting or reflux, coughing or throat clearing, associated dysphagia or neck lumps, referred ear pain, metabolic disease, FHx aerodigestive cancer. Dysphonia examination? Nose, nasal airway, oral cavity, tongue, pharynx, neck (diffuse LA + no preceding URTI => ? lymphoma // unilateral mid-neck LA => ? upper airway malignancy // thyroid enlargement with retrosternal extension can be cause). "Eeee test" aka maximum phonation time - normal is >10s at normal volume/pitch. "Sliding eeee test" - inability to perform smoothly suggests hyperfunctional voice disorders or organic laryngeal pathology. "Crescendo eeee test" - loud to soft and soft to loud. What does reduced maximum phonation time mean? Lung disorder, vocal fold paralysis, psychogenic cause. Gold standard for laryngeal assessment? Flexible fibreoptic rhinolaryngoscopy (during speaking, singing, swallowing etc). Recent development in dynamic assessment? Videokymography. Commonest causes of chronic laryngitis? Smoking, alcohol, laryngopharyngeal reflux, voice misuse. Are GORD and laryngopharyngeal reflux part of the same spectrum? No. What conditions are commonly confused with voice dysfunction? Hyper and hyponasality. What causes diplophonia and breathiness? Nodules (take months-years of vocal abuse to form). Which are commoner, vocal cord nodules or cysts? Nodules (cysts are often misdiagnosed as nodules). Which needs surgery, which voice therapy? Nodules => voice therapy; Cysts => surgery. Causes of hoarseness? Acute vs chronic, inflammatory (viral laryngitis) vs structural (nodules). 1. Voice abuse: ACUTE: Muscle tension dysphonia (occupational or situational, loud/prolonged use of voice, excessive tension, poor breathing technique, puts pt at risk of structural lesions, diagnosed on hx and laryngoscopy to exclude






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other causes => voice therapy); Haemorrhages (acute onset after barracking, shouting, singing, vomiting, weightlifting, URTI, NSAIDs, anticoagulants etc, subepithelial bleeding and swelling => conservative mx unless doesn't resolve then needs surgery to suction out blood). CHRONIC: Nodules (common, bilateral, at point of max vibration on free edge of cords, problems at higher pitches => voice therapy first + fluids, PPIs, lifestyle, occasional aspirin gargles, no point in surgery as will recur); Cysts (rarer, unilateral, deeper in cord => don't respond to voice therapy, need surgery). Smoking: Polyps (uni/bilateral on free edge of cord, dampened vibration in affected cord and different frequency, problems at lower pitches with gravelly voice called "fry" => voice therapy has no role in primary treatment, once present for >6wks needs surgery); Diffuse polypoidal degeneration aka Reinke oedema (also seen in hypothyroidism, build up of gelatinous material in Reinke space of floppy cords as mechanism to protect from irritants => quit smoking for 3 months, then surgery to one side at a time to slice open vocal folds and squeeze/suction this material out); Laryngeal SCC (peristent hoarseness in smoker +/- dysphagia, odynophagia, neck lump, referred ear pain is cancer till proven otherwise => refer for scope under LA => laser surgery or radiotherapy). Laryngopharyngeal reflux: Distinct from GORD. Not diagnosed or excluded by gastroenterologist on upper endoscopy. Investigated by laryngoscopy, flexible transnasal oesophagoscopy (under LA in seated position). Also postnasal drip. Infection/Inflammation: Viral laryngitis is the commonest cause of hoarseness, rarely bacterial, physical findings don't match symptoms (slight swelling but no movement disorder), no specific treatment and topical/oral steroids controversial; Papillomas/HPV (more aggressive in kids, hoarseness/stridor and SOB, repeated operations, intralesional cidofovir injections, laser vaporisation in adults, one type associated with development of aerodigestive tract cancer). Vocal ulcer granulomas: Can form after trauma during intubation followed by repeated throat clearing by pt, ulceration and reparative granuloma formation, hoarseness and sharp localised pain => diagnosis and cessation of throat clearing, if not it can reach a size that endangers airway and needs excision. Iatrogenic/Injury: Oedema/granuloma, arytenoid dislocation, recurrent laryngeal nerve injury. Soft tissue: Commonly due to ETT/LMA => oedema => usually resolves over <6wks. Sometimes from vocal cord granuloma or arytenoid dislocation resulting in immobile vocal fold => ENT referral for laryngoscopy. For granuloma: vocal therapy + acid suppression + surgery. Neurological: Recurrent laryngeal nerve trauma in surgery (cervical laminectomy via the anterior approach, thyroid surgery, carotid endarterectomy, cardiac surgery, surgery for oesophageal cancer). Can recover => cord often augmented with autologous fat or synthetic filler. Also speech therapy. Also postviral mononeuritis of recurrent laryngeal nerve, infiltration by tumour (eg at apex of lung). Ageing: Presbylaryngitis, age related atrophy of intrinsic laryngeal muscles, bowing of cords, loss of pitch and projection, often earlier in women (many secondary factors also present) => voice therapy first, then if severe fillers can be injected to augment vocal folds. Metabolic: Hypo/hyperthyroidism, amyloidosis, rheumatoid arthritis. Sulcus vocalis: Furrow along free edge causing it to be bowed, glottis doesn't close completely, breathy hoarseness => surgery. Mixed causes: Chronic laryngitis, Can be due to voice abuse, tobacco

smoking, alcohol, laryngopharyngeal reflux, voice rough and forced with lower pitch than normal, fold smooth and glistening, free edge rough and swollen => address cause. What does voice therapy involve? DO: rest voice (1-5d, not longer as muscles can atrophy), hydration (6-8 glasses/d), air humidification (no eucalyptus etc as drying). DON'T: prolonged loud speaking/shouting/singing or loud whispering, repetitive throat clearing, irritants (smoke), dehydration (caffeine, antihistamines, anticholinergics). Timing of various causes of dysphonia? Constant = structural and traumatic; intermittent = muscle tension, GORD, postnasal drip. Commonest cause of dysphonia? Viral laryngitis, to 3wks (if longer refer). Diagnosis of muscle tension dysphonia? Typical history + laryngoscopy to exclude other path and demonstrate muscle tension. Mx is voice therapy. Differentials of throat tightness? Angina/AMI, allergy, globus pharyngeus. Medications for dysphonia? Antibiotics useless, steroids only for autoimmune causes. What does acute onset of unilateral salivary gland pain, swelling and fever suggest? Bacterial sialadenitis. What does intermittent unilateral salivary gland swelling and pain suggest? Chronic sialadenitis with calculi. What does bilateral salivary gland symptoms suggest? Viral infection or systemic cause. What does painless, slow growing, unilateral salivary gland mass suggest? Neoplasm. Where does the parotid gland open? Near the second upper molar (Stensen's duct). Where does Wharton's (submandibular) gland open? Anterior floor of mouth. Which gland produces serous and which mucoid saliva? Parotid = serous; Wharton's = mucoid. What viruses can cause sialadenitis? Mumps (commonest), coxsackie, EBV, CMV, HIV, influenza => treatment supportive (warm compresses, analgaesia, oral hygiene, fluids). Which gland is typically affected by bacterial sialadenitis? Parotid (unilateral). Who gets bacterial sialadenitis (usually by retrograde infection)? Debilitated patients, diabetics, Sjogren's, ductal obstruction with salivary stones, poor oral hygiene, periodontal/dental disease. What bacteria is usually involved in bacterial sialadenitis? Staph aureus. What antibiotics should be used? Diclox/fluclox or first generation cephalosporin. How does a salivary stone present? Recurrent postprandial pain and swelling, palpable stone. Which stones are radio-opaque on plain film? Submandibular (80% radio-opaque), not parotid. Is ultrasound useful? Yes, gives information about gland, ductal dilatation, and can identify stones as small as 1mm. Which stones should not be massaged out? Submandibular, as you can force them proximally and make excision more difficult. Initial management of sialolithiasis? Massage out, sialologues (gum, lemon drops), anti-inflammatories. Only use antibiotics if clear signs of infection. Salivary and oral effects of Sjogren's? Xerostomia, painless enlargement of salivary glands, sialadenitis, sialolithiasis, oral candidiasis. Treatment of xerostomia? DON'T use drying meds, foods, mouthwashes (alcohol and alcohol-containing mouthwashes, coffee, carbonated drinks), salty/spicy foods

which can cause pain in dry mouth. DO increase intake of water or other sugarless beverages, use sialologues (sugar free gum/drops), saliva substitutes (aquae, saliva orthana), moist/soft foods at room temp or moisten foods with broth/gravy/sauce, rinse before and after meals with water, dilute alcohol-free lemon+glycerin/sodium-flouride/chlorhex mouthwash, use humidifier especially at night, glycerin/paraffin oil to lips. Sometimes pilocarpine (use limited by side effects and can't be used in asthma/CCF). What proportion of salivary gland tumours occur in the parotid? 75%. What proportion of parotid vs submandibular tumours are benign? 75% vs 50%. Is nerve palsy a common sign in salivary gland malignancy? No. What to make of an isolated, painless swelling of a salivary gland? Malignancy till proven otherwise. Salivary lump history? History of mass, associated pain, weakness of facial muscles or tongue (malignancy), history of skin malignancies of face/scalp, prior radiation exposure. Salivary lump examination? Bimanual palpation, check oral cavity, cervical LNs. How does a benign salivary lump look and feel? Slow growing, firm, mobile, wellcircumscribed and not fixed, no nodes. How does a malignant lump look and feel? Rapidly growing, fixed to surrounding structures, nodes present. Where are benign lumps often found? Inferior pole of parotid below angle of jaw. What are the commonest benign salivary gland masses? Pleomorphic adenoma (usually lower pole of parotid, slow growing, non-tender, no palsy), Warthin's tumour (parotid only). Commonest cause of "salivary gland cancer"? Skin cancer mets (outside gland). What is the commonest actual salivary gland tumour? Mucoepidermoid (rare). Where does Warthin's tumour occur? Lower pole of parotid gland, upper neck below angle of jaw. What to do with a slow-growing, unilateral salivary gland lump? Order FNA, refer. Treatment of pleomorphic adenoma vs Warthin's tumour? Superficial parotidectomy (not enucleation), preserving facial nerve is priority so complete excision sometimes impossible, can rarely recur. For Warthin's tumour enucleation is sufficient but in reality formal dissection done to identify facial nerve. What causes Warthin's tumour? Smoking. What salivary tumours are more likely to metastasise to cervical LNs? Submandibular. What is the aim of adjuvant radiotherapy in salivary gland malignancies? To reduce local recurrence (use is controversial). Do post-surgical salivary fistulae need repair? Usually not, heal spontaneously. What is Frey's syndrome? Sweating over salivary gland during eating (autonomic fibres reattach to sweat glands instead of salivary glands after surgery => treatment surgical). What does a reactive node present like? Rapid onset, painful, antecedent infection. What does a malignant neck lump present like? Gradual onset (>6wks), painless, risk factors (mainly smoking with drinking as a cofactor .. also asbestos, nickel and wood dust, GORD). What does a metastatic node look/feel like? Multiple, rock hard, non-tender, fixed. What is the main factor in head and neck cancer? Smoking (alcohol is a potentiating cofactor). Red flags of primary head and neck malignancy? Hoarseness (larynx), dysphagia or odynophagia (cancer of pharynx or oesophagus), SOB (trachea/lungs), wt loss

(distant visceral malignancy). When to investigate a neck lump further? Smoker >40yo, drinker, >6 weeks, salivary gland or thyroid lump, red flags. When not to worry about nodes? Small, reactive nodes in kids. Multiple, <1cm, mobile, painless nodes normal in kids <15yo. Watch for 1-2 weeks, consider broad spectrum antibiotics. What to make of >6wks LN enlargement in children? Cat scratch fever, sarcoidosis, TB, and the longer they are there the greater the suspicion of lymphoma. What landmarks are palpable in the neck? Hyoid bone, thyroid cartilage (Top down order: hyoid bone, thyroid cartilage with Adam's apple, cricoid cartilage, trachea), transverse process of 1st cervical vertebra (just below mastoid). Borders of anterior triangle: Mandible, sternomastoid, clavicle (further subdivided into superior and inferior carotid, submandibular and suprahyoid). Borders of posterior triangle: Mastoid, base of skull (occiput), sternomastoid, clavicle (further subdivided into subclavian and occipital triangles). How to find the thyroid isthmus? 2-3 tracheal rings below the cricoid cartilage. How does a normal thyroid gland feel? Barely palpable. What to do if you see a lesion on throat examination? Palpate it if possible, as well as surrounding area and anterior floor of mouth. What and where are the most common congenital neck lumps? Thyroglossal cyst (remanant of descent of thyroid), 75% midline, the rest para-midline, discrete firm lumps that rise with swallowing or protrusion of tongue. What is a branchial cyst and what does it look like? Peristence of second branchial cleft, cystic, anterior to sternomastoid below mandible, present as infected mass that responds to antibiotics => surgical excision. What is a ranula? Cystic swelling in floor of mouth caused by saliva escaping from sublingual salivary glands, can become "plunging ranula" going through floor of mouth to neck => surgery if symptomatic. What are cystic hygromas? Congenital, intermittent, brilliantly transilluminating, lymphoid base-of-tongue lesions seen in infants. Causes of inflammatory lymphadenitis? VIral (influenza, parainfluenza, EBV, CMV, HSV, HIV), bacterial (bartonella henselai aka "cat scratch fever", actinomyces), fungal (coccidiomycosis), parasitic (toxoplasmosis). Most common benign soft tissue tumour of neck? Lipoma. What to make of thyroid lumps? Benign and malignant processes can coexist, so refer all thyroid lumps for investigation. What does a papillary thyroid tumour look like? (1) Isolated, non-tender thyroid mass or (2) Single, non-tender enlarged LN in lateral neck or below thyroid in midline (Delphian node). LN levels and their likely primary cancer sources: 1. Level 1 (submental): Submandibular gland, oral/tongue SCC. 2. Level 2 (upper jugular .. just under angle of jaw): Cutaneous, tonsil, oropharyngeal. 3. Level 3 (middle jugular .. mid neck under angle of jaw): Larynx, pharynx, thyroid, most relevant in smokers with suspected throat cancer. 4. Level 4 (lower jugular .. lower neck under angle of jaw): Hypopharynx, thyroid, cutaneous, mets from cancers outside head and neck, rarely larynx. 5. Level 5 (posterior triangle): Any cancer of upper aerodigestive tract or scalp/nape cancers, nasopharyngeal. 6. Level 6 (anterior compartment): Midline almost always thyroid, rarely laryngeal. Best imaging for neck mass? Constrast CT.

Best test for tissue diagnosis of neck lump? FNA (1:1000 risk of needle track seeding). What if lymphoma suspected? FNA with flow cytometry. When to worry about oral lesion (patch or ulcer)? Persists >3wks after cause gone. What do malignant oral lesions look like? 1. Erythroplakia or leukoplakia => malignant or premalignant. Usually a speckled red and white (can be all red or all white), nodular, patch/ulcer on (1) ventral/lateral tongue; (2) floor of mouth; (3) buccal mucosa. // SCC accounts for 90% of oral malignancies (Risks: tobacco, cannabis, alcohol, sunlight, immunosuppression/HIV, lymphoma, meds). Lip => good prognosis. Intraoral => morbidity/mortality+++. Treat: surgery +/- radiotherapy +/- chemo. 2. Others: Mucoepidermoid carcinoma (commonest salivary gland tumour => painless, hard, nodular, slow-growing tumour), lymphoma, Kaposi's sarcoma, malignant melanoma. What do benign oral masses look like? 1. Epulis: Gum swelling coming from periodontal membrane between two teeth (site of caries or irritation from partial denture). Treat: excision + curettage of origin + extraction of involved teeth. 2. Other: Pyogenic granuloma (minor trauma => pyogenic gum-lip granuloma => excision); retention/mucous cysts (trauma to salivary glands => cysts of various size and number, st on tonsils => incision or marsupialisation for larger ones); ranula (large, unilateral, transparent-blue cyst with surface vessels on floor of mouth, sometimes bursts and returns => marsupialisation); fibrous/fibroepithelial hyperplasia (poorly fitting dentures => chronic inflammation => hyperplasia on floor of mouth); haemangioma (blanching purple, sessile/nodular swelling esp on vermillion border, floor of mouth or tongue => treatment cosmetic) ... pleomorphic adenoma, squamous papillomas, polyps, exostoses from mandible/maxilla or hard palate, blood blisters (from dentures), torus palatinus. Benign causes of red patches? Reduced epithelial layer => cheek biting, candidiasis, geographic tongue, haem disorders, dermatoses. Benign causes of white patches? Thickened epithelial layer => trauma (aspirin, tea tree oil burn), infection (candidiasis - plaque rubs off), dermatoses. What does oral candidiasis look like? "More a bad taste than a pain". Tender white/yellow curdlike plaques, easily rubbed off to show red mucosa, metallic taste, dysphagia, hallitosis, sensitivity to acidic substances (toothpaste). Think: immunodeficiency/HIV, meds, (Abx, steroids, cytotoxics), nutritional/anaemia (iron, folate, B6), DM. Diagnosis: clinical (wet prep + potassium hydrochloride => spores, mycelia). Treat: underlying cause, multivitamin, nystatin rinse/swallow (or myconazole gel, amphotericin or nystatin lozenges), decontaminate dentures with chlorhex or dilute White King scrub. If immunosuppressed or unresponsive, oral fluconazole. What do oral dermatoses look like? Potentially premalignant lichen planus, SLE (uncommonly pemphigus vulgaris, mucous membrane pemphigoid) => biopsy/histo. LP: >45yo, asymptomatic or painful white-lace on mucosa/tongue +/- erosions. SLE: oral lesions can be first sign, usually lateral hard palate, similar to LP. Treat: mouthwash (chlorhex or tetracycline/nyastatin or lignocaine) and corticosteroids (topical, injection, oral), refer. Causes of bacterial biofilm known as dental plaque? Hyposalivation and poor oral hygiene => inflamed periodontal tissues. Brush twice a day with soft-bristled toothbrush and flouride paste, floss and use mouthwash. Avoid dry mouth. Dental referral.

Causes of xerostomia? Mouth breathing, salivary gland dysfunction (Sjogren's, stones), meds (antihistamines, decongestants, analgaesics, antidepressants, diuretics, antihypertensives, smoking cessation meds), depression, dehydration (inc diabetes, diarrhoea, renal failure), anaemias. Symptoms: burning, hallitosis pain, bad/reduced taste, difficulty with speech/chewing/swallowing => increased caries and thrush. Xerostomia treatments? Change predisposing meds, avoid drying mouthwashes, increase intake of sugarless beverages, frequent sips of water, rinse before and after meals with water, sialologues (sugar free gum/drops), saliva substitutes (aquae, saliva orthana), lemon+glycerin or sodium flouride mouthwash, glycerin/paraffin oil to lips, diluted alcohol free mouthwash (chlorhex), moist/soft foods at room temp or moisten foods with broth/gravy/sauce, avoid alcohol, coffee and carbonated drinks, use humidifier especially at night. Sometimes pilocarpine (use limited by side effects and can't be used in asthma/CCF). Avoid salty/spicy foods which can cause pain in dry mouth. Effects of smoking on oral cavity? Risks => periodontal disease and cancer. Heat, dryness, immune suppression => increased calculus (tartar), bone loss and pocket depth. Same degree of plaque. Same or less gingival inflammation. Differentials of bony ulcer in mouth (osteochemonecrosis)? Bisphosphonates (BRONJ: Bisphosphonate-Related OsteoNecrosis of the Jaw), trauma (poorly fitting dentures), cancer, infection. Diagnostic criteria for BRONJ? Current/previous bisphosphonates, exposed and necrotic maxillofacial bone >8wks, no radiotherapy. Who is at higher risk of BRONJ? Highest in pts on high dose IV bisphosphonates for malignancy. Very rare in pts just taking for osteoporosis but risk increased with dental extractions. Other cofactors are: poorly controlled DM, concurrent corticosteroids, chemo or immunosuppressive drugs like methotrexate, age, alcohol abuse, smoking. How does BRONJ occur? Stress fractures from mastication => impaired repair due to bisphosphonate action with reduced blood supply and tumoricidal effects. Prevention of BRONJ? Dental assessment/treatment before starting bisphosphonates, avoid dental surgery while taking, dental review q3-6mo while taking, good oral hygiene, well fitting dentures, use soft denture liners, educate on warning signs (jaw pain+++, numbness, denture sore spots, oral odour, infection). Management of osteochemonecrosis? OPG +/- panoramic and periapical films (but changes often not present till late) and prompt maxfax referral. They will likely do incisional biopsy for diagnosis, then curettage of necrotic bone with soft tissue closure, antibiotics (amoxi or clinda) and antiseptic mouth washes BD with monitoring q 2-3 weeks till healed. Adjust dentures, fit soft lining. Should long-term bisphosphonates be ceased before dental procedures? Not usually recommended as they persist in bone, but antiangiogenesis effects may be refuced if they are stopped aiding mucosal healing. Oral problems caused by GORD? Dental erosion, temperature sensitivity, mucosal ulceration, loss of taste, halitosis. Treatment of GORD in relation to dental disease? PPI half to one hour before meal closest to time of day when symptoms worst, review in 8 weeks, refer to dentist. Lifestyle changes in GORD? Smaller meals, avoid lying down within 3h of eating, fluids between meals not with them, reduce alcohol intake, reduce caffeine intake as well as chocolate, fatty/spicy foods, citrus and tomato-based products, raise head of bed by 15-20cm with timber blocks. Prevention of dental erosion in GORD? Adhere to GORD treatment, antiacid at first

sign of reflux, hold milk in mouth after reflux noticed, rinse with flouride toothpaste and water if reflux noticed, chew sugar free gum (saliva is buffer), good oral hygiene, bicarb containing toothpaste (buffer), apply alkaline toothpaste or gel with finger before sleeping, frequent applications of low concentration flouride, rinse frequently with neutral pH mouthwash, avoid brushing immediately after reflux and avoid abrasive toothpastes. What can a dentist do about damage caused by GORD? From banding composites on damaged areas to full mouth reconstruction. Symptoms and signs of bruxism? Muscle spasms of head/neck/ear, pain on chewing/waking. Tender masseter/temporalis and TMJ. What causes bruxism? Stress, malocclusion, habit. What damage does bruxism cause? Accelerated tooth wear (canines and central/lateral incisors affected first and worst becoming flatter), cracks and pits form plaque traps, bone loss and widening of periodontal ligament space. Treatment? Education can help treat daytime bruxism, manage stress/anxiety (psychological support, communication strategies, biofeedback, sleep therapy), dental referral fto fit protective nighttime mouthguard or even occlusal adjustment procedures. If antidepressant is cause, consider changing. Muscle relaxants unproven but may help short term, specific masticatory muscle or TMJ exercises can help with pain. Symptoms and signs of odontogenic infections? Toothache, periodontal swelling, malaise, fever. Red, tender gum mass, percussive dental tenderness. Serious sequelae of dental infections? Parapharyngeal or mediastinal spread via deep fascial planes threatening airway or causing septic shock. Symptoms that would suggest serious pathology? Dysphagia, difficulty breathing or opening mouth. Bugs involved? Mixed with anaerobes (Porphyromonas etc) and some facultative anaerobe streps. Management of periodontal infections? Surgical drainage of pus is mainstay, antibiotics as adjunct only, plus analgaesia, fludis. When to use antibiotics in periodontal infections? Cellulitis, susceptible, sick, stridor, stuck in the sticks. Cellulitis (not simple oedema or abscess, which can be treated by drainage alone), susceptible (immunosuppression/comorbidities), sick (systemic spread), stridor (compromised airway), stuck (cause can't be removed immediately). What antibiotics to use and for how long? 5d course of Pen V, amoxicillin, or clindamycin if allergic. If not responding or deep infection, add metronidazole. If deep, rapidly spreading or high risk patient (diabetic etc) => admission for cultures, debridement, 3wks of IV antibiotics. Why might someone with dementia have poor dentition? Behavioural factors (resisting oral healthcare, not getting usual flouride exposure), oral hygiene factors (unable to self care and resist care from others), dietary factors (sugary foods, meds given in jam/puree, coffee, alcohol), dysphagia (requires soft foods, frequent small meals, food in mouth for longer => in dysphagia, intensive oral care w dentists, speechies, GPs needed to maintain dental health), reduced saliva, polypharmacy (anticholinergics, diuretics etc). Use of sedatives in dental treatment of dementing patients? Shortest acting option (oxazepam, temazepam), start at low dose and consider increasing over subsequent visits, monitor during and after for falls/aspiration risk (no eating until meds wear off, safe mobilistion needs to be assessed with onset and offset). Should avulsed primary teeth be replaced? No. How to handle avulsed teeth? Hold by the crown, avoid rubbing root or rinsing in

water unless obvious surface contamination. What is the safest place to store a tooth? The socket if possible, even if not fully repositioned. Mould aluminium foil over teeth to hold in place. Next best is milk. Important history in avulsed tooth presentation? LOC or other concerning nondental injuries (ED transfer), history matches injury (non-accidental injury), tetanus vax status, extra-oral dry time ><60mins (if >60min out of mouth and not in storage media reimplantation less successful due to necrotic periodontal ligament, and reimplantation method different). Why is it important that all teeth and fragments are accounted for? Fragments embedded in lip, swallowed or inhaled (may need xrays to find them). Definitive management of avulsed tooth? See dentist at tertiary or dental hospital. Bracket and wire splint across adjacent teeth for 14d, antibiotics and soft diet. First step in assessing sudden unilateral tinnitus, blocked sensation, hearing loss? Weber test (512Hz, middle C, tuning fork or get patient to hum) => midline (N), louder in bad ear (conductive), louder in good ear (sensorineural). Differentials in sudden conductive hearing loss (otalgia suggestive)? Wax vs AOE vs AOM (fluid indicates blocked eustachian tube => topical or oral decongestants). Differentials in sudden sensorineural hearing loss (painless suggestive)? Probably idiopathic sudden sensorineural hearing loss (ISSHL) => emergent ENT referral => consensus in favour of steroids (pred), antivirals advocated but no evidence, 1/3 improve spontaneously. Differentials: acoustic neuroma (st sudden), herpes zoster oticus (Ramsay Hunt => look for vesicles => antivirals and steroids). Cause of ISSHL? Debated. Maybe viral, maybe microvascular event involving vestibular circulation. Differentials of acute facial nerve palsy? Bell's palsy (commonest, idiopathic), Ramsay Hunt (look for vesicles, otalgia => antivirals, steroids, eye protection, management of postherpetic neuralgia), pleomorphic adenoma of parotid, malignant otitis externa. What proportion of ISSHL patients report disturbed balance? 50%. Causes of halitosis? Oral (most common) vs ENT/resp and other causes ... mainly bacterial putrefaction of food debris + gum inflammation (alcohol, smoking, dry mouth aggravate problem). Treatment of halitosis? Treat underlying conditions (dental, neoplastic, pulmonary TB, hairy tongue, rhinosinusitis). Review meds responsible for xerostomia (isosorbide dinitrate, various antidepressants). Avoid smoking, alcohol, onion, garlic, peppers, curry, hot salami, cheese. Maintain hydration. Brush teeth/tongue. Use mouthwash. Floss and use sugarless gum. Refer to dentist. Red flags of sore mouth? Signs of dehydration (kids: herpetic gingivostomatitis); soft palate petechiae (gingivostomatitis or tonsillopharyngitis); oral ulcers LONE, LONG, PLUS (>3 weeks or plus skin or bowel disorders); oral candidiasis; glossodynia (depression). Intraoral bony exostoses usually normal variation (sometimes syndrome like Gardner's). Also trismus, dysphagia, breathing difficulty. Differentials of mouth ulcers? Apthous, traumatic, lichenoid (drug), herpetic. Apthous ulcers: Most common. Cause unproven, ? HSV6, nutritional, autoimmune. 3-5mm diameter, round/oval, red margin, sloughy base on lining epithelium. Ask: ? skin/bowel problems, medication, stress. For symptoms: Topical lignocaine jelly/ointment with cotton bud then 2 mins later SM33 paint (gel for kids) .. or EMLA with cotton bud for 5 mins. For healing: RCTs support tetracycline/nyastatin mouthwash, topical/lozenge/spray steroids if not HSV (triamcinolone or others), topical chloramphenicol, sucrulfate+water mouthwash, diclofenac+hyaluronan. Major ulcers: locally injected or oral steroids. Also:

squeezed teabag, tea tree oil, acupuncture. Traumatic ulcers: Sports, biting, hot or hard food, over brushing, dentures, sharp teeth, braces, aspirin burns, iatrogenic causes (dental trauma/neglect is common cause of mouth/tongue pain). Treat: remove cause, warm saline +/topical anaesthetic mouthwashes (eg benzocaine/Cepacaine, benzydamine/Difflam). Lichenoid shallow ulcers due to meds like gold, NSAIDs, carbimazole, antihypertensives and cytotoxics. Herpetic ulcers: Secondary HSV can present in many ways (eg maxillary trigeminal => unilateral buccal mucosa). Facial ulceration or soft palate petechiae ? EBV. Topical analgaesic (Difflam) + valciclovir if <48h. If severe, IV valganciclovir and hydration. Also, angular cheilitis (red/sore/macerated corners of mouth => Fe/B-malnutrition, thrush, poor-fitting dentures, dermatitis => treat cause). Investigation of oral ulcers? Consider FBC, swabs, autoantibodies, syphilis serol, BSL, B12/folate, biopsy. What are the probability, serious and pitfall diagnoses of gum symptoms? 1. Probably: trauma (brushing, dentures), infection (hygiene/gingivitis), drugs (warfarin). 2. Serious causes: oral cancer (eg epulis), blood dyscrasia (AML), acute HSV. 3. Pitfalls: Trench mouth (anaerobes => necrotising ulcerative gingivitis aka "Vincent infection" - in ill young adults under stress => procaine penicillin), autoimmune (SLE, lichen planus), hereditary haemorrhagic telangiectasia, malabsorption, scurvy, vWD. What is gingivitis and how is it treated/prevented? Painless red/swollen gums near teeth, easy bleeding, hallitosis, plaque with calculus (tartar). Leads to periodontitis = recession, alveolar bone loss or periodontal pocketing, loosening. Treat: 10d of chlorhex mouthwash BD, amoxicillin for abscess (+ metronidazole if severe). Prevent: abrasive flouride toothpaste and small medium-soft brush, aim at gingival margin with small horizontal motion, floss, regular dental review. What causes tongue symptoms? Trauma, apthous ulcers, geographic tongue, HSV in kids, fissured tongue, atrophic glossitis. Serious: cancer/HIV. Pitfalls: anaemia/malnutrition, glossopharyngeal neuralgia, lichen planus, median rhomboid glossitis, Crohn's disease, Behcet syndrome, Coeliac disease. Don't forget depression, glossodynia. 1. Painful tongue: Characterise symptoms/associations (worse with spicy food => migratory glossitis or median rhomboid glossitis). Common causes similar to sore mouth/throat => think of trauma (sharp tooth or dentures or meds), infecion (primary HSV or hand foot and mouth in miserable kids), xerostomia in elderly (meds, mouth breathing, Sjogren's), background illness (diabetes or immunosuppression), strawberry tongue (scarlet fever vs Kawasaki disease), macroglossia (acromegaly, myxoedema, amyloidosis) ... glossodynia (painful tip of tongue) consider depression => think of checking FBC, B12/folate/iron, lesion swab or biopsy. 2. Geographic tongue (aka erythema migrans aka migratory glossitis): Benign, self-limiting hypersensitivity reaction with changing (within weeks) areas of desquamation on top/sides of tongue with red patches and white-grey edges like a relief map. Can be aggravated by stress, tobacco, alcohol, cannabis, spicy foods => reassure, if painful gargle benzocaine/Cepacaine, if persistent low-dose inhaled glucocorticoid. Check for Coeliac disease. 3. Black/hairy tongue: ABx/steroids/tranqs or debility => long papillae due to overgrowth or less wear => bad taste/breath => treat with 8 segments sliced

pineapple sucked on back of tongue for 40 seconds then chewed/swallowed for 10d).