TEST Normal Limits DIAGNOSTICS

CBC RBC DECREASED RBC causes: anemia (microcytic hypochromic, normocytic, normochromic
0.40-0.50 Male anemia)
0.35-0.45 Female INCREASED RBC causes: polycythemia vera, secondary polycythemia, vigorous exercise,
high altitude
CBC Hemtocrit DECREASED:
Adult (male): 42-53 Anemias, recovery after blood loss, hemodilution (pregnancy, edematous states,
% recumbency)
(female): 37-47 INCREASED: polycythemia, erythrocytosis of dehydration, hemoconcentration (in shock
assoc trauma, surgery, burns), high altitude
%
CBC Hb 135-175 g/L male At birth high due to the fact that low oxygen in-utero
120-160 g/L Female Adult value at age 15
ASSESS ANEMIA/Polycythemia and their therapeutic responses
Decreased Hbg: ANEMIA (all types), blood loss/fluid reconstitution, edematous states,
pregnancy,
Increased Hbg: polycythemia vera, secondary polycythemia, vigorous exercise and high
altitude, (hemoconcentration)untreated shock assoc. with fluid loss, dehydration
(hemoconcentration)
CBC MCV Adult: 80-97 fL INCREASED MCV causes:
Volume • Megaloblastic anemia (b12 and/or folate deficiency),
• Spurious macrocytic anemia (aplasia, myelofibrosis, hyperglycemia, cold
agglutinins)
• Reticulocytosis
• Liver disease
• Drugs
• AIDS
DECREASED MCV causes:
• Iron deficiency anemia*
• Defects in porphyrin synthesis (hereditary sideroblastic anemia, acquired
sideroblastic anemia, pyridoxine responsive anemia, lead poisoning)
• Hemolytic anemia (thalassemia minor*)
• Marked RBC fragmentation
• Hereditary spherocytosis
• postsplenectomy
CBC MCH Adult: 27.5-33.0 pg Parallel MCV
Mean cell
Hb
CBC MCHC Adult: 305-360 g/L DECREASED:
Mean cell • iron def anemia
Hb • Defects in porphyrin synthesis (hereditary sideroblastic anemia, acquired
concentrati sideroblastic anemia, pyridoxine responsive anemia, lead poisoning)
on • Hemolytic anemia (Thalassemia minor*)
INCREASED: hereditary spherocytosis
WBC Neutrophil ADULT: 50-70 % INCREASED:
s • newborn, pregnancy, delivery, emotional disturbances, n/V, strenuous physical
2.0 – 7.5 xE9/L activity, UV light, cold sever stress, heat
• Bacterial infections, (some viral), mycotic, spirochetal rickettsial and parasitic
infections,
• acuter RA, Rhematic Fever, vasculitis, myositis, hypersensitivity reactions,
• uremia, diabetic acidosis, eclampsia, throid storm
• hemorrhage, hemolytic anemia, leukemias, myeloproliferatrive disorders
• burns, MI, Gangrene, malignant Neoplasia
• drugs: heparin, digitalis, Epi, lithium, histamines, corticosteroids
• allergies
DECREASED:
• bacterial: typhoid fever, paratyphoid, brucellosis, septicemia
• viral: hepatitis, MONO, measles, rubella, influenza, chicken pox, Colorado tick fever
• protoza (MALARIA)
• aplastic anemia, vit b12-folate def, agranulocytosis, SOL in bone marrow
• Bone marrow depressants (radiation, cytotoxic drugs, benzes), reactions to drugs
• Collagen vascular diseases: LUPUS, RA, MONO, Hypersplenism (lv disease, storage
diseases)
WBC Lymphocyt ADULT: 50-70 % INCREASED:
es • Viral: mono, hepatitis, CMV, Herpes zoster, herpes simiplex,m mumps, chicken pox,
1.0-3.5 xE9/L viral pneumonia, measles
• Bacteril: pertussis, brucellosis, typhoid & paratyphoid, TB, syphilis
• Ulcerative colitis, serum sickness, idiopathic thrombocytopenic pupura
• Hypoadreanlism, hyperthyroid
• LEUKEMIA (ACCUTE & CHRONIC); aplastic anemia, agraulocytosis, MULTIPLE
MYELOMA,
DECREASED:
• Cushing’s
• Corticosteroid therapy
• AIDS, immunosuppresive therapy
 • Military TB, Hodgkin’s disease, Lupus, terminal carinoma, renal failure
WBC Mono ADULT: 1-6 % INCREASED:
cytes • Bacterial & viral & parasitic (malaria) & other infections
0.0-1.0 xE9/L • Preleukemic
• Leukemia: CML, AML
• Lymphomas: Hodgkins disease NHL
• Polycythemia vera
• Perarteritis nodosa, lupus, RA, ulcerative colitis, cirrhosis, malignancies
WBC Eosino Adult: 1-5 % INCREASED:
phils Eosinophils 0.0- • PARASITIC infections
0.5 xE9/L • Allergic diseases: asthma, seasonal rhinitis
• Skin: atopic dermatitis, eczema,
• Pulmonary: hypersensitivity pneumonitis
• Malignancies: ovarian, villous of UB, LU, mets from vulvar/penile, adenocarcinoma
of colon
• IgA deficiency
• DRUGS: gold, iodides, ampicillin, phenytoin
• Fungal infections
• IBS
WBC Basophils ALL: 0-1% INCREASED:
Basophils 0.0- • Chronic hypersensitivity to food/drugs
0.2 xE9/L • Polycythemia vera, basophilic leukemia, chronic granulocytic leukemia
• MAST CELL DISEASE: urticaria pigmentosa
• Chronic hemolytic anemia, ulcerative colitis, myxedema
Glucose Adults: 3.6-6.0 mmol/L Below Normal – hypoglycemia (has to be less than 50mg/dL to be to get diagnosis) causes:
• POSTPRANDIAL: alimentary hyperinsulinism (gastrectomy, gastrojejunostomy,
pyloroplasty, Vagotomy), Hereditary fructose intolerance, galactosemiam, leucine
sensitivity, idiopathic
• Falciparum Malaria, Reye’s syn, LV disease (advanced), Malnutrition, Renal
Glycosuria, Islet Beat cell tumor (insulinoma), malignancy, Hypoglycin ingestion,
neonatal hypoglycemia, Dormandy’s syn, endocrine hypofunhctions (Addison’s),
enzyme deficiencies,
• Factitious: insulin, oral hypoglycemic agents, high dose salicylates, glycogenic
enzyme deficiencies, autoimmune insulin syn,
• Artifactual: polycythemia vera, bacterial, failure to separate clot
Above Normal – hyperglycemia causes:
 • DM (with signs of polydipsia/polyuria/weight lose/ketonuria),
• acute pancreatitis,
• Endocrine hyperfunctions (cushing’s, pheochromocytoma, acromegaly,
hypothalamic lesions, carcinoid synd, thyrotoxicosis, glycagonoma,
somatostatinoma),
• Hemochromatosis,
• DRUGS: steroids, epinephrine/norepinephrine, Benzothiadiazine diuretics, phenytoin
STRESS: shock, trauma, CVA, MI and burns
HbA1C 0.040-0.060 mmol/L (4%-6%) Measure of chronic blood sugar
**** I think in class he quotes 7 % as acceptable for a diabetic under good control
s-TSH PRIMARY HYPOTHYROID: decrease total T4 & Free T4, increase s-TSH
0.35-5.00 miu/L SECONDARY HYPOTHYROID: decrease Total T4 & Free T4, decrease s-TSH
T3 ADULT: 3.5-6.5 pmol/L HYPERTHYROID: increase Total T4, increase Free T4, decrease s-TSH
THYROTOXICOSIS: normal Total T4 & Free T4, decrease s-TSH, increase T3
T4 Adults: 9-23 pmol/L Causes of HYPERTHYROID: throidittis, graves disease with acute iodide loading,
thyrotoxicosis, antithyroid drugs
Thyroxine Causes of THYROTOXICOSIS: diffuse goiter (grave’s disease), toxic multinodular goiter,
(plummer syndrome) Toxic adenoma.
Causes of HYPOTHYROID: Hashimoto’s, throid cancer, etc
AST Adult: 10-40 U/L • AST is measured in evaluation of conditions causing tissue damage, m/c Myocardial
Infarction and LV dz
aspartate • AST is primarily used to detect and monitor LV parenchymal dz
amino • AST is more sensitive, but less specific than ALT in detecting LV dz
transferase • Widespread tissue distribution
• Elevated in a wide variety of conditions:
• Lv dzs: hepatitis, cholestasis – intrahepatic and extrahepatic, alcoholism, drug
toxicity (e.g. acetaminophen)
• Heart: acute MI (98% of px – rise and fall a few hours after CPK levels rise and fall),
acute myocarditis (any cause)
• Skeletal muscle (SKM): skm dz, trauma
• RBCs: haemolytic anemia (severe), megaloblastic anemia
• Other: malignancy, infectious mononucleosis, CHF, acute renal infarction, acute
pulmonary infarction, acute pancreatitis, tissue necrosis, third degree burns,
seizures, eclampsia, heparin therapy, other drugs (oral contraceptives,
acetaminophen, aspirin, isoniazid, codeine, cortisone)
Highly Elevated levels:
 • Very high values, over 500, may be found in LV dz, large necrotic tumours,
CHF and shock
• Greatly increase in acute LV damage e.g. viral hepatitis, toxic damage
Moderately Elevated levels:
• Cirrhosis, metastatic cancer, obstructive jaundice and infectious mono
Decreased AST:
• pyridoxine (B6) deficiency
• chronic dialysis
ALT Adult: 5-42 U/L • Evaluates LV dz
(Alanine • Distribution limited to LV and KI thus changes are much more specific to LV damage
aminotrans than AST
ferase • Elevation of AST AND ALT is highly suggestive of LV dz
• If values are greater than 10x normal, sever hepatocellular damage is
suspected
• Elevation of ALT occurs in:
• LV disease
• CHF
• Infectious mono
• Acute MI
• Acute renal infarction
• SKM disease
• Acute pancreatitis
• Heparin therapy
Serum Adult: 135-148 mmol/L Hyponatremia (results from water retention or salt loss or both → cell swelling and
Sodium intracellular hypotonicity)
Clinical sx depend on level of serum sodium and how rapidly the decrease occurs; sx are
Potentially Life primarily neurological
Causes:
Threatening values:
< 120mmol/L or > • Isotonic Hyponatremia (plasma osmolality 280-295) – hyperproteinemia;
155mmol/L hyperlipidemia
• Hypertonic Hyponatremia (plasma osmolality >295) –
hyperglycemia;mannitol;glycerol
• Hypotonic Hyponatremia (plasma osmolality <280) – m/c form; dx made on
basis of plasma and urine Na as follows:
 Plasma Volume Urine Na Diagnosis
Hypovolemic > 30mmol/L Renal losses
• diuretic therapy
• osmotic diuresis
• salt-wasting nephropathy
• adrenal insufficiency
• proximal renal tubular
acidosis
• metabolic alkalosis
• pseudo-hypoaldosteronism
• cerebral salt-wasting
<30mmol/L Extrarenal losses
• GIT
• Sweat
• Third space (Burns, ascites,
effusions)
Euvolemic (normal >20mmol/L • Excess ADH (SIADH –
volume) syndrome of inappropriate
ADH secretion, Drugs, Pain)
• Water intoxication (IV
therapy, psychogenic water
drinking, tap water enema)
• Glucocorticoid defc
• hypothyroidism
Hypervolemic <10mmol/L Edematous
• CHF
• Cirrhosis
• Nephrotic syndrome
>30mmol/L Renal failure (acute or chronic) Hypernatremia
(→elevated serum osmolality → intracellular dehydration → cell shrinkage)
Clinical sx include:
• Pathologically = marked brain cell shrinkage → mechanical trauma intracranially
• Extensive vascular damage
• Venous and capillary congestion
• Subarachnoid and intracerebral hemorrhages w/ cortical venous thrombosis and areas
of venous infarction
• Neuro sx occur in 50% of pxs
 Treatment:
• Over zealous tx may lead to seizures ( which can be difficult to tx)
Causes:
Sodium excess
• Excess sodium bicarbonate
• Hypertonic IV fluids
• Sodium chloride tablets
• Ingestion of sea water (480mmol/L)
• Improperly mixed formula
• Aldosteronism (primary or secondary)
• Cushing’s syndrome
Water Deficient
• Central diabetes insipidus (i.e. hypopituitarism)
• Nephrogenic diabetes insipidus
• Diabetes mellitus
• Excessive sweating
• Inadequate water intake
• Lack of thirst (adipsia)
• Increased insensible water loss (i.e. normal losses in day from minor sweating,
breathing, etc. are increased)
Water deficit in Excess of Sodium Deficit (i.e. lost more water than than Na, despite having
lost Na too)
• Diarrhea (common in pediatric cases w/ enteric dz)
• Osmotic diuretics
• Diabetes mellitus
• Obstructive Uropathy
• Renal dysplasia
Serum Adult: 3.5-5.3mmol/L The concentration of intracellular K is 130mmol/L; the serum concentration of K is 3.5 to
Potassium 5.0mmol/L – thus only 2 to 3%of K is extracellular and thus SERUM K REFLECTS K
STORES
Potentially Life Hypokalemia
Causes: 3 mechanisms of loss
threatening values: 1. urinary loss
<2.5mmol/L • Diuretics (thiazides, loop diuretics)
>6.5mmol/L • Mg depletion
• Antibiotics (Carbenicillin, Amphotericin B)
• Increased mineralcorticoid (Florinef; carbenoxolone – mineralcorticoid-like activity
 on distal tubule; licorice, chewing tobacco)
• Renal tubular acidosis (type I – distal or type II – proximal)
• Bartter’s syndrome (rare genetic dz characterized by hypokalemia, alkalosis and
normal to low blood pressure)
• Hyperaldosteronism
• Cushing’s syndrome or disease
• CAH (11 or 17 hydroxylase defc)
• High renin states
2. GIT loss
• Vomiting
• Nasogastric suction
• Pyloric obstruction
• Diarrhea
• Malabsorption
• Villous adenoma
• Enama and laxative abuse
• Biliary drainage
• Enteric fistula
3. mvmt of K from extracellular to intracellular fluid
• Alkalosis
• Na-K-ATPase stimulation (insulin – promotes entry of K into cells; beta 2 agonists;
catecholamines)
• Familial hypokalemic periodic paralysis
• Barium intoxication
• Hypothermia
• Frozen deglycerolyzed RBC transfusion
• Acute myeloid leukemia

Other: decrease K intake; sweating

Hyperkalemia
Causes:
1. Redistribution
• Metabolic or respiratory acidosis
• Drugs: insulin; beta adrenergic blockade; argining infusion; succinylcholine;digitalis
toxicity
• Hyperkalemic periodic paralysis
2. Renal failure – m/c cause

Anion gap Upper limit of normal:
15mmol/L
Borderline: 12-20mmol/L
Lower limit of normal:
<5mmol/L
Anion gap = (Na) – [(Cl) +
CO2 content]
Normal found by substituting
the normal values for Na, Cl
and CO2
Normal anion gap = (140) –
(103 + 25) = 12mmol/L
• Acute or chronic w/ oliguria
3. Aldosterone antagonists
• Spironolactone;triamterene;amiloride
4. Adrenogenital syndrome
• 21 hydroxylase defc
5. Adrenal insufficiency
• Px on long term corticosteroids w/ sudden discontinuance
6. Hypoaldosteronism
• Addison’s dz
7. Potassium load
• Massive muscle necrosis
• IV therapy (i.e. w/ K supplements or to pxs w/ renal dz)
• Blood transfusion of old blood leads to hemolysis
8. Significant thrombocytosis or leukocytosis
9. Artefactual increase
• Hemolyzed serum
• Repeated fist clenching during venipuncture
• Delayed separation of serum from cells
Increased Anion Gap
Causes:
• Renal failure (phosphate and sulphate accumulation)
• Ketoacidosis (diabetic, alcoholic, or starvation)
• Lactic acidosis
• Toxic agents (salicylates poisoning; ethylene glycol [oxalic acid]; methyl alcohol [formic
acid]; paraldehyde [acetic acid] – rare; propyl alcohol
Mnemonic: A MUDPIE – A= aspirin, M = methyl alcohol, U = uremia, D = diabetic
ketoacidosis, P = paraldehyde, I = idiopathic lactic acidosis, E = ethylene glycol
Note: only 4 clinical conditions are associated w/ high anion gap metabolic acidosis
1. renal failure
2. ketoacidosis
3. lactic acidosis
4. drugs/toxins
Thus, in the absence of renal failure or drugs/toxins, and increase in anion gap is assumed
to be ketoacidosis or lactic acidosis
Other less common causes of increases:
• increase in uncalculated cations such as hypercalcemia, hypermagnesemia,
hyperkalemia, lithium intoxication, and polymyxin B (antibiotic used for resistant gram –
 ve bacteria) administration

Low Anion Gap

Causes: m/c
• Multiple myeloma
• Hypnatremia
• Hypoabluminemia
• Bromide ingestion
Serum Cl Child and Adult Increased Serum Chloride
95-110 mmol/L Causes:
1. Hyperchloremic Metabolic Acidosis (chloride increases as bicarbonate decreases to
maintain electrical neutrality)
2. Respiratory Alkalosis (hydrogen ions from intracellular sources enter the extracellular
fluid and bicarb moves into the RBCs in exchange for Cl, thus minimizing extracellular
alkalosis)
3. Renal Dz
• Pyelonephritis
• Polycystic renal dz
• Obstructive uropathy
• Renal tubular acidosis
4. Severe dehydration e.g. diabetes mellitus
5. Diabetes Insipidus
6. IV saline
Decrease Serum Chloride
Causes:
1. Renal Loss
• Loop diuretics
• Salt-losing nephropathies
• Bartter’s syndrome
2. GI loss
• Nasogastric suction
• Gastric outlet obstruction (e.g. pyloric stenosis)
• Zollinger-Ellison syndrome (pancreatic or duodenal tumour causing excess gastrin
secretion leading to peptic ulcers)
• Congenital Chloride-losing enteropathy
• Secretory diarrhea
3. Other
• Metabolic alkalosis (bicarb is increase thus Cl decreases to maintain
 electroneutrality)
• Respiratory acidosis (chronic) (Cl excretion is must accompany renal compensation
for respiratory acidosis)
• CHF
• Overhydration
• SIADH
• Overtreatment w/ hypotonic solutions
• Dietary defc
• Burns
• Addison’s dz
• Perspiration (Cystic Fibrosis)
Carbon 24-30mmol/L CO2 is the serum content of bicarbonate and carbonic acid
Dioxide CO2 = HCO3 +H2CO3
Content = HCO3 + (PCO2 x 0.03)
• The bicarb concentration is about 20 times that of carbonic acid, thus the CO2 content
approximates the value of bicarb
Decreased CO2 Content
• Metabolic acidosis
Mildly Decreased CO2 Content
• Chronic respiratory alkalosis w/ compensation
Increased CO2 Content
• Metabolic alkalosis
Mildly Increased CO2 Content
• Chronic respiratory acidosis w/ compensation
Ferritin 10-291ug/L < 40 ug/L is probably iron deficient

Cholesterol Total: up to 6.19 mmol/Lm targets based on 10 yr CVDz assessment, Can J Card.2006;22(11):913-927.; ON Assoc Med
HDL > 1.3 mmol/L Lab 2004

LDL < 3.2 mmol/L

Trig < 2.11

mmol/L
Urine ** ALSO see lecture notes posted on ESNIPS Sp Gr 1.005-1.030
Analysis pH 5.0-8.0
(dipstick, Leukocytes neg; Nitrites neg; Protein neg; Glucose neg; Ketones
UA) neg; Urobilinogen neg; Bilirubin neg; Blood neg; Color pale
yellow; Clarity clear
NORMALS
Diabetes Diagnosis:
1) unequivocal elevation of plasma glucose together with classical signs OR
2) elevation of fasting plasma glucose on more than one occasion OR
3) Elevated plasma glucose after glucose challenge on more than one occasion

IN ADULTS
1) classical symptoms plus RANDOM glucose > 200 mg/dL
2) AM fasting glucose > 140 mg/dL on two occasions OR
3) Oral glucose challenge (75 g) where glucose values >200mg/dL at 2 hours and some time between 0 & 2 hours on more than
one occasion

IN PREGNANCY:
Oral glucose challenge:
fasting > 105 mg/dL, 1
hour > 190 mg/dL,
2 hours > 165mg/dL,
3 hours > 145 mg/dL ** having two or more of the values elevated