ENDOCRINE SYSTEM2011 COVERAGE

ANATOMY AND PHYSIOLOGY PITUITARY DISORDERS ADH DISORDERS ADRENAL GLANDS DISORDERS THYROID GLAND DISORDERS PARATHYROID GLANDS DISORDERS DIABETES MELLITUS PITUITARY DISORDERS

1. HYPERPITUITARISM 2. HYPOPITUITARISM ADH DISORDERS

1. SYNDROME OF INAPPROPRIATE ADH 2. DIABETES INSIPIDUS ADRENAL GLANDS DISORDERS

1. CONNS DISEASE 2. CUSHINGS DISEASE 3. ADDISONS DISEASE 4. PHEOCHROMOCYTOMA THYROID GLAND DISORDERS

1. GOITER 2. HYPERTHYROIDISM 3. HYPOTHYROIDISM PARATHYROID GLANDS DISORDERS 1. HYPERPARATHYROIDISM 2. HYPOPARATHYROIDISM DIABETES MELLITUS

1. TYPE I 2. TYPE II 3. GESTATIONAL DM WHAT IS ENDOCRINE SYSTEM? IT IS A SYSTEM COMPOSED OF DIFFERENT ENDOCRINE ORGANS. RELEASES HORMONES INTO THE BLOOD STREAM. ITS A DUCTLESS SYSTEM HORMONES ARE CHEMICAL SUBSTANCES PRODUCED OR RELEASED BY AN ENDOCRINE ORGANS, ALSO KNOWN AS THE MESSENGER. ANATOMY AND PHYSIOLOGY HYPOTHALAMUS-PITUITARY AXIS HYPOTHALAMUS PITUITARY GLAND ANTERIOR PG OR ADENOHYPOPHYSIS TSH THYROID GLAND THYROID HORMONES ACTH ADRENAL CORTEX CORTISOL (AGA) GH BONES AND MUSCLES, GLUCAGON MSH SKIN - MELANIN FSH OVARY- ESTROGEN SPERM PRODUCTION LH GRAAFIAN FOLLICLE PROGESTERONE SPERM MATURATION PROLACTIN - BREAST MILK PRODUCTION POSTERIOR PG OR NEUROHYPOPHYSIS ADH KIDNEYS (DCT) WATER REABSORPTION OXYTOCIN BREAST AND UTERUS - CONTRACTION HOW DOES IT WORK?

H POSITIVE FEEDBACK ESTROGEN

PROGESTERONE INHIBITORY FEEDBACK PROLACTIN OXYTOCIN NEGATIVE FEEDBACK MSH ADH GH ACTH TSH HYPOTHALAMUS - SPIN SENSOR OF HORMONAL FLUCTUATION POSITIVE FEEDBACK INHIBITORY FEEDBACK NEGATIVE FEEDBACK PITUITARY DISORDERS HYPOPITUITARISM HYPERPITUITARISM HYPOPITUITARISM CAUSE SIMMONDS, SHEEHANS CHROMOPHOBIC PITUITARY TUMOR

DX USE THE S/SX MRI

S/SX OXY & PROLACTIN (GALACTORRHEA) FSH & LH (AMENORRHEA)

MSH (ALBINISM) ACTH (ADDISONS) GH (DWARFISM) ADH (DI) TSH (HYPOTHYROIDISM) MX BROMOCRIPTINE TO LOWER PROLACTIN SANDOSTATIN TO REDUCE THE TUMOR SURGERY: TRANS SPHENOIDAL HYPOPHYSECTOMY HORMONE REPLACEMENT THERAPY SOMATOTROPIN TO REPLACE GH LEVOTHYROXINE TO REPLACE TH HYDROCORTISONE TO REPLCE CORTISOL VASOPRESSIN TO REPLACE ADH

HYPERPITUITARISM CAUSE BASOPHILIC PIT. TUMOR ACIDOPHILIC PIT. TUMOR

DX USE THE S/SX MRI

S/SX FSH & LH (AMENORHEA) OXY & PROLACTIN (GALACTORRHEA) MSH (SKIN PIGMENTATION) ACTH (CUSHINGS) GH (GIGANTISM OR ACROMEGALY) ADH (SIADH)

TSH (HYPERTHYROIDISM) MX BROMOCRIPTINE TO LOWER PROLACTIN AND GH SANDOSTATIN TO REDUCE THE TUMOR SURGERY: TRANSSPHENOIDAL HYPOPHYSECTOMY ACROMEGALY

ARTHRITIS CARPAL TUNNEL SYNDROME OSTEOPOROSIS KYPHOSIS HYPERTENSION ARTERIOSCLEROSIS HEART ENLARGEMENT HEART FAILURE AN ENLARGED JAW THICKENED TONGUE ENLARGED AND WEAKENED HANDS COARSENED FACIAL FEATURES OILY OR LEATHERY SKIN PROMINENT SUPRAORBITAL RIDGE PITUITARY DISORDERS HYPOPITUITARISM S/SX OXY & PROLACTIN (GALACTORRHEA) FSH & LH (AMENORRHEA) MSH (ALBINISM) ACTH (ADDISONS) GH (DWARFISM)

 ADH (DI) TSH (HYPOTHYROIDISM) HYPERPITUITARISM S/SX ) FSH & LH (AMENORHEA) OXY & PROLACTIN (GALACTORRHEA) MSH (SKIN PIGMENTATION) ACTH (CUSHINGS) OR ACROMEGALY) GH (GIGANTISM ADH (SIADH) TSH (HYPERTHYROIDISM STEREOTAXIC HYPOPHYSECTOMY STEREOTAXIS IS A THREE-DIMENSIONAL AIMING TECHNIQUE USING X RAYS OR SCANS FOR GUIDANCE. INSTRUMENTS CAN BE PLACED IN THE BRAIN WITH PINPOINT ACCURACY THROUGH TINY HOLES IN THE SKULL. STEREOTAXIS IS ALSO USED TO DIRECT RADIATION WITH SIMILAR PRECISION USING A GAMMA KNIFE TRANSSPHENOIDAL HYPOPHYSECTOMY

HYPOPHYSECTOMY IS A PROCEDURE TO ACCESS AND REMOVE THE PITUITARY GLAND (A). TO ACCESS IT, AN INCISION IS MADE BENEATH THE PATIENT'S UPPER LIP TO ENTER THE NASAL CAVITY (B). A SPECULUM IS INSERTED, AND SPECIAL FORCEPS ARE USED TO REMOVE THE PITUITARY TUMOR (C). TRANSSPHENOIDAL HYPOPHYSECTOMY PREOP DRUG: BROMOCRIPTINE (PARLODEL) TO LOWER GH AND PROLACTIN OCTREOTIDE (SANDOSTATIN) TO REDUCE TUMOR POSTOP CARE HEAD ELEVATION FOR 2 WEEKS NASAL PACKING, MOUTH CARE INCREASE ICP PRECAUTIONS OBSERVE FOR CSF LEAKAGE (HALO SIGN)

 WATCHOUT DIABETES INSIPIDUS-POLYURIA DI SIADH DIABETES INSIPIDUS CAUSE: SURGERY, TRAUMA, TUMOR ADH S/SX FVD, HYPERNATREMIA POLYURIA URINE OUTPUT, URINE SG BV, FVD, HCT AND PLASMA OSMOLALITY SODIUM (BLOOD) THIRST REHAB: LIFELONG SUPPLEMENT OF HORMONES, MAC ADH ABNORMALITY

MANAGEMENT LIFE TIME PITRESSIN OR VASOPRESSIN FLUID RESUSCITATION

SYNDROME OF INAPPROPRIATE ANTI DIURETIC HORMONE CAUSE: TUMOR, DRUGS ADH S/SX FVE, HYPONATREMIA OLIGURIA URINE OUTPUT, URINE SG BV, FVE, HCT AND PLASMA OSMOLALITY SODIUM (BLOOD)

MANAGEMENT TRANSSPHENOIDAL HYPOPHYSECTOMY RESTRICT FLUIDS

 DI

COMPARISON

CAUSE: SURGERY, TRAUMA, TUMOR ADH-POLYURIA S/SX FVD, HYPERNATREMIA POLYURIA URINE OUTPUT, URINE SG BV, FVD, THIRST , HCT AND PLASMA OSMOLALITY SODIUM (BLOOD) MANAGEMENT LIFE TIME PITRESSIN OR VASOPRESSIN FLUID RESUSCITATION

SIADH CAUSE: TUMOR, DRUGS ADH-OLIGURIA S/SX FVE, HYPONATREMIA OLIGURIA URINE OUTPUT, URINE SG BV, FVE, HCT AND PLASMA OSMOLALITY SODIUM (BLOOD)

MANAGEMENT TRANSSPHENOIDAL HYPOPHYSECTOMY RESTRICT FLUIDS

ADRENAL GLANDS ABNORMALITY CONNS DISEASE CUSHINGS PRIMARY (DISEASE) SECONDARY (SYNDROME)

ADDISONS DISEASE PRIMARY SECONDARY

PHEOCHROMOCYTOMA CONNS DISEASE CAUSE: PRIMARY (ADENOMA) HYPERSECRETIONS OF ALDOSTERONE ONLY

DX: SERUM ELECTROLYTES (NA, K) URINE ( ALDOSTERONE) IMAGING (MRI)

CONNS DISEASE S/SX AND INTERVENTION: HYPERNATREMIA: NEUROLOGIC (SEIZURE) INTERVENTION: RESTRICT NA, NEUROLOGIC ASSESSMENT, SEIZURE PRECAUTIONS FVE: HPN, EDEMA, CHF INTERVENTION: I&O, RESTRICT WATER, KVO, DIURETICS (K SPARER) HYPOKALEMIA: INVERTED T WAVE, ARRHYTHMIAS, CARDIAC ARREST, CONSTIPATION, MUSCLE WEAKNESS INTERVENTION: GIVE ORAL SUPPLEMENT, KALIUM DURULE (TABLET), IV KCL (INCORPORATED TO 1 L OF PNSS), CARDIAC MONITOR,

CONNS DISEASE SURGERY: BILATERAL ADRENALECTOMY (SCOPIC) POSTOP: WATCHOUT ADDISONS DISEASE S/SX REHAB: LIFETIME STEROIDS, MEDIC ALERT CARD (MAC), WATCHOUT ADDISONS AND CUSHINGS

CUSHINGS DISEASE CAUSE PRIMARY: TUMOR AT THE ADRENAL CORTEX

SECONDARY : TUMOR AT THE PITUITARY GLAND

DX: DX: 24 HOUR URINE CORTISOL, PLASMA CORTISOL, DEXAMETHASONE SUPPRESSION ( ACTH: 2 C.D.) S/SX CORTISOL - CATABOLISM ALDOSTERONE NA, H20, K GLUCOCORTICOID - HYPERGLYCEMIA ANDROGEN FEMALES ARE AFFECTED

MX PRIMARY: ADRENALECTOMY SECONDARY: HYPOPHYSECTOMY

ADDISONS DISEASE CAUSE PRIMARY: ADRENAL CORTEX ATROPHY SECONDARY: PIT. GLAND ATROPHY

DX: 24 HOUR URINE CORTISOL, PLASMA CORTISOL, ACTH STIMULATION TEST ( CORTISOL 1 A.D.) S/SX CORTISOL - WEAKNESS ALDOSTERONE - NA, H20,K GLUCOCORTICOID - HYPOGLYCEMIA ANDROGEN MALES ARE AFFECTED

MX SYPMTOMATIC LIFETIME STEROIDS ADDISONIAN CRISIS

COMPARISON CUSHINGS DISEASE CAUSE

PRIMARY: TUMOR AT THE ADRENAL CORTEX SECONDARY : TUMOR AT THE PITUITARY GLAND

DX: 24 HOUR URINE CORTISOL, PLASMA CORTISOL, DEXAMETHASONE SUPPRESSION ( ACTH: 2 C.D.) S/SX CORTISOL ALDOSTERONE GLUCOCORTICOID ANDROGEN

MX PRIMARY: ADRENALECTOMY SECONDARY: HYPOPHYSECTOMY

ADDISONS DISEASE CAUSE PRIMARY: ADRENAL CORTEX ATROPHY SECONDARY: PIT. GLAND ATROPHY

DX: 24 HOUR URINE CORTISOL, PLASMA CORTISOL, ACTH STIMULATION TEST ( CORTISOL 1 A.D.)

S/SX CORTISOL ALDOSTERONE GLUCOCORTICOID ANDROGEN

MX SYPMTOMATIC LIFETIME STEROIDS

CUSHINGS DISEASE CAUSE DX S/SX CX MX MEDICAL MANAGEMENT: 1. MITOTANE ADRENAL CYTOTOXIC 2, METYRAPONE REDUCE HYPERADRENALISM CAUSED BY ECTOPIC ACTH 3. AMINOGLUTETHIMIDE (CYTADREN) ADRENAL STEROID INHIBITOR, ANTINEOPLASTIC

INSTRUCTION IN USING STEROIDS TAKEN IN THE MORNING INCREASED THE DOSE DURING HIGH LEVEL OF STRESS HIGHLY INDIVIDUALIZE (DOSING) WATCHOUT FOR SIDE EFFECTS: CUSHINGOID (TRUNKAL OBESITY, MOON FACIE, BUFFALO HUMP) HIRSUTISM OR VIRILISM PANCYTOPENIA, GLAUCOMA, CORNEAL ULCERATION NOTE: S/SX OF CUSHINGS DISEASE STEROIDS SIDE EFFECTS

HYPERTENSION, THROMBOEMBOLISM WEIGHT GAIN, MOON FACE, TRUNKAL OBESITY, BUFFALO HUMP PRONE TO INFECTION GI BLEEDING GLAUCOMA, CORNEAL ULCERATION MUSCLE WASTING, POOR WOUND HEALING OSTEOPOROSIS HYPERGLYCEMIA

ACNE VIRILIZATION (MUSCULINE EFFECT IN WOMEN) ADDISONS DISEASE PHEOCHROMOCYTOMA CAUSE: TUMOR IN THE ADRENAL MEDULLA DX:

EPI AND NOR-E (BLOOD), CATECHOLAMINES - FROM E AND NOR-E (BLOOD), VANILLYL MANDELIC ACID VMA (URINE-24H COLLECTION) REFLECTION OF CATECHOLAMINES METANEPHRINE (24 H URINE) REFLECTION OF EPINEPHRINE PHEOCHROMOCYTOMA S/SX: RELATED TO HIGH LEVEL OF EPINEPHRINE AND NOREPINEPHRINE HYPERTENSION, TACHYCARDIA, ARRHYTHMIAS (SYMPATHETIC RELATED ALSO), BLOOD SUGAR AND GLYCOSURIA

INTERVENTION: ER CASE DRUG OF CHOICE (REGETINE), SURGERY: BILATERAL ADRENALECTOMY

THYROID GLAND DISORDERS

1. GOITER 2. HYPERTHYROIDISM 3. HYPOTHYROIDISM GOITER CAUSE: IODINE DEFICIENT (40 FG/DAY OF IODINE) HYPOTHYROIDISM (COMPENSATORY ENLARGEMENT) HYPERTHYROIDISM (HYPERTROPHY)

DX: HISTORY AND PE (I,P,A) BLOOD EXAM (T3 AND T4) IMAGING (THYROID SCAN) FNAB (FINE NEEDLE ASPIRATION BIOPSY)

S/SX: ENLARGEMENT (VISIBLE) MAY LEAD TO TRACHEAL OBSTRUCTION MAYBE HYPERTHYROID OR HYPOTHYROID S/SX

INTERVENTION: PREVENTION (EAT SEA FOODS, AVOID GOITROGENIC FOODS) THYROIDECTOMY GOITER

HYPERTHYROIDISM CAUSE: AUTOIMMUNE DISEASE (GRAVES DISEASE) DX: RADIOACTIVE IODINE UPTAKE (UPTAKE) THYROID SCAN (HOT SPOT, T.N.G.) PBI, T3, T4

S/SX: BMR, THYROID STORM MX: SYMPTOMATIC ANTI-THYROID DRUGS RADIOACTIVE IODINE (HIGH) SURGICAL THYROIDECTOMY

HYPOTHYROIDISM CAUSE: AUTOIMMUNE DISEASE (HASHIMOTOS THYROIDITIS) DX:

RADIOACTIVE IODINE UPTAKE (UPTAKE) THYROID SCAN (COLD SPOT, N.T.N.G.) PBI, T3, T4

S/SX: BMR, MYXEDEMA COMA MX: SYMPTOMATIC LIFE TIME SUPPLEMENT OF SYNTHETIC T3 AND T4

HYPERTHYROIDISM CAUSE: AUTOIMMUNE DISEASE (GRAVES DISEASE) DX: RADIOACTIVE IODINE UPTAKE (UPTAKE) THYROID SCAN (HOT SPOT, T.N.G.) PBI, T3, T4

S/SX: BMR, THYROID STORM MX: SYMPTOMATIC ANTI-THYROID DRUGS RADIOACTIVE IODINE (HIGH) SURGICAL THYROIDECTOMY

HYPOTHYROIDISM CAUSE: AUTOIMMUNE DISEASE (HASHIMOTOS THYROIDITIS) DX: RADIOACTIVE IODINE UPTAKE (UPTAKE) THYROID SCAN (COLD SPOT, N.T.N.G.) PBI, T3, T4

S/SX: BMR, MYXEDEMA COMA MX: SYMPTOMATIC

LIFE TIME SUPPLEMENT OF SYNTHETIC T3 AND T4

HYPERTHYROID & HYPOTHYROID MANIFESTATIONS HYPERTHYROIDISM ANTI-THYROID DRUGS THIONAMIDES (PROPYLTHIOURACIL) METHIMAZOLE (TAPAZOLE), CARBIMAZOLE AXN: DEC SYNTHESIS OF LIFETIME MEDS, 3X/DAY SIDE EFFECT: AGRANULOCYTOSIS (REPORT SORE THROAT) LIVER DISEASE (JAUNDICE, ABDL PAIN) THYROID HORMONES, MAY TAKE SEVERAL WEEKS TO TAKE EFFECT

RADIOACTIVE IODINE 123-I OR 131-I AXN: DESTROY THYROID TISSUE DISADVANTAGE: DESTRUCTION OF THE THYROID GLAND CAN NOT BE CONTROLLED AND IT MIGHT LEAD TO SEVERITY OF THE ENTIRE GLAND AVOID CONTACT WITH FECES AND URINE (FLUSH TOILET 2-3X) RADIOACTIVE IODINE PAINLESS PROCEDURE, 1 OR MORE CAPSULES TAKEN PO (LEAD CONTAINER) LIQUID FORM IS ALSO AVAILABLE RADIATION EMITTED IS ABLE TO REDUCE THE SIZE OF THE THYROID WASTES ARE EXCRETED VIA FECES, URINE, SWEAT, BREAST MILK AND SALIVA (RADIATION HAZARD) SAFETY PRIVATE ROOM (2-5 DAYS ISOLATION) SURGICAL THYROIDECTOMY SSKI SATURATED SOLUTION OF POTASSIUM IODIDE (LUGOLS) IS GIVEN PREOP TO DECREASE THYROID VASCULARITY GIVEN WITH JUICE TO DISGUISE TASTE, GIVEN WITH STRAW TO PREVENT STAINING OF TEETH SE: SIALORRHEA IODISM OR IODINE TOXICITY (SWELLING OF BUCCAL MUCOSA, SALIVATION, CORYZA, SKIN ERUPTION)

POSTOP: THYROIDECTOMY AIRWAY PATENCY MONITOR BLEEDING WATCHOUT THYROID CRISIS CHECK FOR TETANY (PARATHYROID GLAND IS SEVERED) HOARSENESS OF VOICE-LARYNGEAL NERVE DAMAGE POSITION: SUPINE OR SEMI FOWLERS, NO HYPERFLEXION AND HYPEREXTENSION OF THE NECK, HEAD MIDLINE, NO PILLOW!!!

HYPOTHYROIDISM SYNTHETIC THYROID HORMONES

LIFETIME MEDS, 3X/DAY T4 SYNTHROID, LEVOTHYROID T3 CYTOMEL T3 & T4 PROLOID T3 GIVEN NGT, FASTER THAN T4 T4 GIVEN PARENTERALLY SIDE EFFECT: ADRENAL INSUFFICIENCY NOTE: 3-12 WEEKS OF MEDICATIONS BEFORE SIGNS AND SYMPTOMS DISAPPEAR HYPERCALCEMIA CAUSE: HYPERPARATHYHROIDISM S/SX: DEEP BONE PAIN LITHIASIS FORMATION HYPOPHOSPHATEMIA (LOW ENERGY STORE) SHORTENED QT INTERVAL MNGMT: PARATHYROIDECTOMY, HYDRATION, PREVENT FRACTURE REDUCE CA INTAKE, DIALYSIS HYPOCALCEMIA CAUSE: HYPOPARATHYHROIDISM S/SX: TETANY: TINGLING, TROUSSEAU, CHVOSTEK AND LARYNGEAL SPASM

HYPERPHOSPHATEMIA (WIDE CALCIFICATION) LENGTHENED QT INTERVAL (TORSADES DE POINTES) MNGMT: ORAL, TABLET AND IV )CALCIUM GLUCONATE) RESPIRATORY SUPPORT FOR LARYNGEAL SPASM COMPARATIVELY HYPERCALCEMIA CAUSE: HYPERPARATHYHROIDISM S/SX: DEEP BONE PAIN LITHIASIS FORMATION HYPOPHOSPHATEMIA (LOW ENERGY STORE) SHORTENED QT INTERVAL MNGMT: PARATHYROIDECTOMY, HYDRATION, PREVENT FRACTURE REDUCE CA INTAKE, DIALYSIS HYPOCALCEMIA CAUSE: HYPOPARATHYHROIDISM S/SX: TETANY: TINGLING, TROUSSEAU, CHVOSTEK AND LARYNGEAL SPASM HYPERPHOSPHATEMIA (WIDE CALCIFICATION) LENGTHENED QT INTERVAL (TORSADES DE POINTES) MNGMT: ORAL, TABLET AND IV )CALCIUM GLUCONATE) RESPIRATORY SUPPORT FOR LARYNGEAL SPASM HYPOCALCEMIA

PARATHYROID GLANDS DISORDERS 1. HYPERPARATHYROIDISM 2. HYPOPARATHYROIDISM DIABETES MELLITUS

1. TYPE I 2. TYPE II 3. GESTATIONAL DM PHYSIOLOGY ALPHA CELL GLUCAGON (GLYCOGENOLYSIS)

BLOOD SUGAR

BETA CELL INSULIN (GLYCOGENESIS) BLOOD SUGAR

DELTA CELL SOMATOSTATIN INHIBITORY TO GH AND TSH

PHYSIOLOGY OF GLUCAGON PHYSIOLOGY OF INSULIN TERMINOLOGIES GLYCOGENESIS: GLUCOSE TO GLYCOGEN (INSULIN) GLYCOGENOLYSIS: GLYCOGEN TO GLUCOSE (GLUCAGON) GLUCONEOGENESIS: GENERATION OF GLUCOSE FROM NON-CHO ( FATS AND PROTEIN) LIPOGENESIS: GLUCOSE TO FATTY ACIDS LIPOGENOLYSIS: BREAKDOWN OF FATS (GOOD-EXERCISE) KETOGENESIS: BREAKDOWN OF FATS (BAD-DM) FORMATION OF KETONE BODIES-DKA

DM COVERAGE

1. CAUSE 2. DX 3. S/SX 4. CX 5. MX COMPARISON

NIDDM-TYPE II ADULT ONSET (40Y/O) DECREASED INSULIN TO NORMAL GENETIC, HEREDITARY

INSULIN RESISTANT (CELL) (SUGAR) OBESITY

IDDM-TYPE I JUVENILE ONSET ZERO INSULIN (SUGAR) GENETIC, HEREDITARY AUTOIMMUNE (COXSACKIE VIRUS) VIRAL

WHAT WILL HAPPEN IF YOU HAVE GLUCOSE INTOLERANCE? PATHOPHYSIOLOGY OF DIABETES MELLITUS (TYPE I AND II) HYPERGLYCEMIA S/SX: 4 PS POLYURIA POLYDIPSIA POLYPHAGIA PARESTHESIA POOR WOUND HEALING RECURRENT INFECTIONS HYPOGLYCEMIA S/SX: ADRENERGIC - HR, RR, BP, SWEATING, TREMORS, PALPITATIONS, NERVOUSNESS AND PALLOR NEUROLOGIC HEADACHE, LIGHT HEADEDNESS, SLURRED SPEECH, AND LOC IF CONSCIOUS GIVE 10-15 GM OF SIMPLE SUGAR, 5-6 PCS. OF CANDIES, 3 GLUCOSE TABLET OR 4 OZ OF JUICE IF UNCONSCIOUS GIVE 1 MG OF GLUCAGON SQ OR IM, 50% OF DEXTROSE SOLUTION IV BOLUS

NURSING DIAGNOSIS DECREASED TISSUE PERFUSION (BRAIN, HEART, KIDNEYS) SECONDARY TO HYPEROSMOLALITY ALTERATION IN ELIMINATION INCREASED URINARY OUTPUT SECONDARY TO HYPEROSMOLALITY RISK FOR FLUID VOLUME DEFICIT SECONDARY TO INCREASED URINARY OUTPUT AND HYPEROSMOLALITY ALTERATION IN ADL SECONDARY TO POLYURIA RISK FOR SKIN BREAKDOWN SECONDARY TO PARESTHESIA AND NEUROPATHY NURSING DIAGNOSIS RISK FOR CARDIOVASCULAR DISEASES SECONDARY TO HYPERLIPIDEMIA ALTERATION IN METABOLISM (FATS AND PROTEIN CATABOLISM) SECONDARY TO CELLULAR HYPOGLYCEMIA FLUIDS, ELECTROLYTES AND ACID BASE IMBALANCES SECONDARY BODY COMPENSATION (FVD, ACIDOSIS) {K, PO4, MG} ALTERATION IN BREATHING PATTERN SECONDARY TO DKA (KUSSMAULS) SENSORY PERCEPTION DEFICIT SECONDARY TO CATARACT, GLAUCOMA, RETINOPATHY, AND NEUROPATHY NURSING DIAGNOSIS DISTURBANCE IN BODY IMAGE SECONDARY TO CACHEXIA KNOWLEDGE DEFICIT SECONDARY TO ILLNESS PROGRESSION (LIFELONG DISEASE AND NO CURE) ANXIETY RELATED TO PROGNOSIS OF THE DISEASE SEXUAL ACTIVITY DISTURBANCE RELATED TO NEUROPATHY, HYPERLIPIDEMIA (ERECTILE DYSFUNCTION) NURSING DIAGNOSIS ALTERED NUTRITION BALANCE SECONDARY TO DIETARY CHANGES (AVOID SIMPLE SUGAR AND FATS) NONCOMPLIANCE SECONDARY LIFESTYLE CHANGES, DISEASE PROGRESSION, DIETARY REGIMEN ETC CAREGIVER STRAIN HOW TO DETECT GLUCOSE INTOLERANCE? RANDOM BLOOD SUGAR (NO NPO) BLOOD IS WITHDRAWN ANYTIME 200 MG/DL 2X

3 PS S/SX POLYURIA POLYDIPSIA

POLYPHAGIA HOW TO DETECT GLUCOSE INTOLERANCE? 2-HOUR POSTPRANDIAL TEST (AFTER MEAL) NPO 8-12 HOURS BLOOD EXTRACTION (BASELINE AND FBS) 75 GM OF SUGAR (ORAL) BLOOD EXTRACTION AFTER 2 HOURS 200 MG/DL (+)

HOW TO DETECT GLUCOSE INTOLERANCE? OGTT ORAL GLUCOSE TOLERANCE TEST NPO 8-12 HOURS BLOOD EXTRACTION (BASELINE AND FBS) 75 GM OF SUGAR (ORAL) BLOOD EXTRACTION EVERY HOUR (1ST, 2ND, 3RD, 4TH) 200 MG/DL (+)

HOW TO DETECT GLUCOSE INTOLERANCE? FASTING BLOOD SUGAR NPO 8-12 HOURS 110 MG/DL NPO 8H (+)

HOW TO DETECT GLUCOSE INTOLERANCE AND COMPLIANCE? GLYCOSYLATED HEMOGLOBIN A1C (HBA1C) NO SPECIAL PREP GLUCOSE MOLECULES REACT WITH HEMOGLOBIN (GLYCATED HB-120 DAYS) 6.5% INDICATES POOR CONTROL OF BLOOD GLUCOSE LEVELS HAVE BEEN ASSOCIATED WITH CARDIOVASCULAR DISEASE, NEPHROPATHY AND

RETINOPATHY.

DIAGNOSTIC EVALUATION

1. RANDOM BLOOD SUGAR (NO NPO) 2. 2H POSTPRANDIAL TEST (NPO) 3. OGTT (NPO) 4. FASTING BLOOD SUGAR (NPO) 5. GLYCOSYLATED HBA1C (NO NPO) INTERVENTIONS

NIDDM TYPE II MANAGEMENT: DIET EXERCISE WEIGHT REDUCTION ORAL HYPOGLYCEMIC AGENT (OHA) BIDS (INSULIN AND OHA) INSULIN HHNKS OR HONKS IDDM TYPE I MANAGEMENT: DIET EXERCISE MAINTAIN WEIGHT NO OHA INSULIN DKA DEHYDRATION IV FLUIDS (ISOTONIC, PNSS) HYPERGLYCEMIA INSULIN IV DRIP (REGULAR INSULIN ONLY) NO KETOACIDOSIS

DEHYDRATION IV REPLACEMENT HYPERGLYCEMIA INSULIN IV DRIP (REGULAR INSULIN ONLY) KETOACIDOSIS TREAT WITH INSULIN IF SEVERE GIVE NAHCO3 (CSF ACIDOSIS, HYPOKALEMIA)

DIET (AVOID SIMPLE SUGAR, EXCHANGE LIST) 50%, 30%, 20% (CHO, FATS, CHON) NON DIABETIC 50%,20%,30% (CHO, FATS, CHON) DIABETIC 4/9/4 KCAL/GM (CHO, FATS, CHON) 2,800 KCAL/DAY RDA

SIMPLE SUGAR OR MONOSACCHARIDES CAKES, COOKIES, CANDIES AND ICE CREAM USUALLY CONTAIN WHITE TABLE SUGAR MILK (GALACTOSE)-DAIRY PRODUCTS HONEY FRUITS MOLASSESARNIBAL PUTANGBENGE!!! SIMPLE VS COMPLEX CARB SIMPLE CARBOHYDRATES OR SIMPLE SUGARS THESE CARBS ARE BROKEN DOWN AND DIGESTED VERY QUICKLY, BUT MOST SIMPLE CARBS CONTAIN REFINED SUGARS AND VERY FEW ESSENTIAL VITAMINS AND MINERALS. EXAMPLES INCLUDE TABLE SUGAR, FRUIT JUICE, MILK, YOGURT, HONEY, MOLASSES, MAPLE SYRUP AND BROWN SUGAR. COMPLEX CARBOHYDRATES THE COMPLEX CARBS TAKE LONGER TO DIGEST AND ARE PACKED WITH FIBER, VITAMINS AND MINERALS. EXAMPLES INCLUDE VEGETABLES, WHOLE GRAIN BREADS, OATMEAL, LEGUMES, BROWN RICE AND WHEAT PASTA. DRUGS THAT CAN CONTROL BLOOD SUGAR. ORAL HYPOGLYCEMIC AGENT (OHA) INSULIN ORAL HYPOGLYCEMIC AGENTS

1. SULFONYLUREAS - STIMULATES INSULIN SECRETIONS AND INCREASES TISSUE SENSITIVITY TO INSULIN

2. BIGUANIDES DECREASES INTESTINAL UPTAKE AND HEPATIC PRODUCTION OF GLUCOSE AND INCREASES TISSUE SENSITIVITY 3. ALPHA GLUCOSIDASE INHIBITOR SLOWS CARBOHYDRATE ABSORPTION 4. THIAZOLIDINEDIONES INSULIN SENSITIZER, INCREASES TISSUE SENSITIVITY TO INSULIN ORAL HYPOGLYCEMIC AGENTS

1. SULFONYLUREAS,GLIPIZIDE, EUGLUCON SE: HYPERSENSITIVITY, HEADACHE, GI UPSET 2. BIGUANIDES, GLUCOPHAGE, METFORMIN SE: LACTIC ACIDOSIS, GI UPSET, METALLIC TASTE, TAKE B12 AND FOLIC ACID 3. ALPHA GLUCOSIDASE INHIBITOR, GLUCOBAY SE: FLATULENCE, GI UPSET 4. THIAZOLIDINEDIONES, AVANDIA SE: LIVER DISEASE TYPES OF INSULIN

1. IMMEDIATE ACTING HUMALOG (LISPRO)

2. SHORT ACTING REGULAR SEMILENTE HUMULIN R NOVOLIN R

3. INTERMEDIATE ACTING LENTE NPH OR NEUTRAL PROTAMINE HAGEDORN HUMULIN N NOVOLIN N

4. LONG ACTING ULTRA LENTE FACTS ABOUT INSULIN

SOURCE OF INSULIN

X BOVINE X PORCINE HUMOLOGUE-BEST HUMOLOGUE INSULIN FACTS ABOUT INSULIN FACTS ABOUT INSULIN INSULIN IN USE, ROOM TEMP., 36-46F, 1 MONTH, NO FRIDGE STOCK OF INSULIN BOTTLES MUST BE REFRIGERATED WHEN NOT IN USE FACTS ABOUT INSULIN ALWAYS CHECK BLOOD SUGAR BEFORE INSULIN ADMINISTRATION BGM 80-110 MG/DL < 80 HYPO > 110 HYPER > 250 HHNKS > 300 DKA FACTS ABOUT INSULIN GIVEN BEFORE MEAL FACTS ABOUT INSULIN ROTATE THE SITE EVERY 2 WEEKS SITE ABDOMEN (BEST SITE), UPPER ARMS, UPPER BUTTOCKS

AN INCH SPACING EVERY SHOT FACTS ABOUT INSULIN ROUTE SQ

PINCH OR 45 FOR THIN PATIENT 90 FOR REGULAR CLIENT FACTS ABOUT INSULIN MIXED INSULIN 70/30 REGULAR (CLEAR) FIRST TO BE DRAWN FOLLOWED BY NPH (CLOUDY) FACTS ABOUT INSULIN TUBERCULIN SYRINGE 1ML INSULIN SYRINGE 100 UNITS FACTS ABOUT INSULIN INSULIN SLIDING SCALE USE REGULAR INSULIN ONLY PRIME TUBING FIRST (100 U INSULIN) INCORPORATED TO PNSS CHECK HYPOK DRILL: ADMISTER 300 UNITS OF REGULAR INSULIN IN 500 ML OF PNSS. DELIVER 28 UNITS/HOUR. HOW MANY DROPS/MINUTE? DF 60. HOW MANY HOURS TO CONSUME? FORMULA: ML/HOUR 300 U INSULIN:500ML PNSS :: 28 U INSULIN/H : X ML/H (300X )= (500X28) 300X = 14,000 X = 14,000/300 X = 46.66ML/H OR 46.66 GTTS/MIN

DURATION IN HOUR TVI/ML PER HOUR

500/46.66 10.7 HOURS

FACTS ABOUT INSULIN INSULIN PUMP EXTERNAL BATTERY OPERATED NEEDLE IS INSERTED SQ THAT DELIVERS REGULAR INSULIN, 1 UNIT/HOUR (DAYTIME) FAST ACTING (LISPRO) FREQUENT BLOOD GLUCOSE MONITORING IS ADVISED $ 5K US FACTS ABOUT INSULIN LIPODYSTROPHY IS A COMPLICATION IF THE SITE OF INJECTION IS NOT ROTATED PROPERLY, IT CAN ALSO ALTER THE RATE OF INSULIN ABSORPTION. GOOD SITE MUST BE SUPPLE SKIN. FACTS ABOUT INSULIN HYPERINSULINISM TREMORS, HUNGER AND DIAPHORESIS WILL MANIFEST DAWN PHENOMENON COMMON IN TYPE I, HYPERGLYCEMIA IN THE MORNING SOMOGYI PHENOMENON REBOUND HYPERGLYCEMIA AFTER INSULIN ADMINISTRATION (GRADUAL REDUCTION OF INSULIN IS THE KEY TO MANAGE IT AND GIVE A SNACK )

THANK YOU

FUNDA LECTURE CENTRAL VENOUS CATHETERS SWAN GANZ OR PULMONARY CATHETERS IV KCL THORACENTESIS PERICARDIOCENTESIS

PARACENTESIS URINARY CATHETERS REMINDERS DIABETIC KIT FOOT CARE S/SX OF CX: (VISUAL, URINE, LOC, BP, DYSPNEA ETC.) MAC BGM REGULAR CHECK UP LAB EXAMS DIET (AVOID SIMPLE SUGAR, EXCHANGE LIST) 50/30/20 (CHO, FATS, CHON) NON DIABETIC 50/20/30 (CHO, FATS, CHON) DIABETIC 4/9/4 KCAL/GM (CHO, FATS, CHON) 2,800 KCAL/DAY RDA

THANK YOU HYPOTHALAMUS-PITUITARY AXIS PITUITARY DISORDERS

1. PITUITARY TUMOR 2. HYPERPITUITARISM 3. HYPOPITUITARISM 4. DIABETES INSIPIDUS (DI) 5. SYNDROME OF INAPPROPRIATE ADH (SIADH) PITUITARY TUMOR CAUSE: BASOPHILIC CUSHINGS SYNDROME EOSINOPHILIC OR ACIDOPHILIC GIGANTISM OR ACROMEGALY CHROMOPHOBIC HYPOPITUITARISM

DX: SCAN AND S/SX S/SX: INCREASED ICP, HEADACHE, PAPILLEDEMA (VISUAL DISTURBANCE), OTHER S/SX IS DEPENDENT ON THE TYPE OF TUMOR CX: HORMONE IMBALANCES MX: HYPOPHYSECTOMY BROMOCRIPTINE (PARLODEL) TO LOWER GH AND PROLACTIN OCTREOTIDE (SANDOSTATIN) TO REDUCE TUMOR

COMPARISON HYPERPITUITARISM CAUSE: BASOPHILIC CUSHINGS SYNDROME EOSINOPHILIC OR ACIDOPHILIC GIGANTISM OR ACROMEGALY

DX: SCAN AND S/SX S/SX: FSH, LH, OXY, PRO (FLOP) TSH, ADH, GH, MSH ACTH (TAGMA) CX: RELATED TO HORMONE IMBA. MX: HYPOPHYSECTOMY HYPOPITUITARISM CAUSE CHROMOPHOBIC HYPOPITUITARISM SHEEHANS SYNDROME SIMMONDS DISEASE

DX: SCAN AND S/SX S/SX: FSH, LH, OXY, PRO (FLOP) TSH, ADH, GH, MSH ACTH (TAGMA) CX: RELATED TO HORMONE IMBA. MX: HYPOPHYSECTOMY AND SUPPLEMENT OF HORMONES HYPERPITUITARISM CAUSE

DX S/SX CX MX HYPOPITUITARISM NURSING PROBLEMS DECREASED TISSUE PERFUSION (BRAIN, HEART, KIDNEYS) SECONDARY TO HYPEROSMOLALITY ALTERATION IN ELIMINATION INCREASED URINARY OUTPUT SECONDARY TO HYPEROSMOLALITY RISK FOR FLUID VOLUME DEFICIT SECONDARY TO INCREASED URINARY OUTPUT AND HYPEROSMOLALITY ALTERATION IN ADL SECONDARY TO POLYURIA AND PARESTHESIA RISK FOR SKIN BREAKDOWN SECONDARY TO PARESTHESIA AND NEUROPATHY NURSING PROBLEMS RISK FOR CARDIOVASCULAR DISEASES SECONDARY TO HYPERLIPIDEMIA ALTERATION IN METABOLISM (FATS AND PROTEIN CATABOLISM) SECONDARY TO CELLULAR HYPOGLYCEMIA FLUIDS, ELECTROLYTES AND ACID BASE IMBALANCES SECONDARY BODY COMPENSATION ALTERATION IN BREATHING PATTERN SECONDARY TO DKA SENSORY PERCEPTION DEFICIT SECONDARY TO CATARACT, RETINOPATHY, NEUROPATHY NURSING PROBLEMS DISTURBANCE IN BODY IMAGE SECONDARY TO CACHEXIA KNOWLEDGE DEFICIT SECONDARY TO ILLNESS PROGRESSION ANXIETY RELATED TO PROGNOSIS OF THE DISEASE SEXUAL ACTIVITY DISTURBANCE RELATED TO NEUROPATHY, HYPERLIPIDEMIA (ERECTILE DYSFUNCTION) NURSING PROBLEMS ALTERED NUTRITION BALANCE SECONDARY TO DIETARY CHANGES NONCOMPLIANCE SECONDARY LIFESTYLE CHANGES, DISEASE PROGRESSION, DIETARY REGIMEN ETC CAREGIVER STRAIN