Clinical Chemistry Final Exam Study Guide PDF

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Summary

Professor Stephanie Rink
Comprehensive objectives for the final exam for Fall of 2018
Red highlights indicate reference ranges that will not be provided on the exam
Blue highlights indicate equations to memorize...

Description

Diseases and Disorders Renal Disease

Pathophysiology

Acute Glomerulonephritis

Immunologic process – inflammation and damage Poststreptococcal Non-Poststreptococcal

Chronic Glomerulonephritis

Lengthy glomerular inflammation may lead to glomerular scarring and eventual loss of functioning nephrons

Nephrotic Syndrome

Increased permeability to glomerular basement membrane

Lower UTI (Cystitis)

Bladder infection

Upper UTI (Acute Pyelonephritis)

Kidney Infection

Chronic Renal Failure

Progressive loss of renal function, leading to end stage renal disease

Physical/Chemical Eval Protein – mild; can reach nephrotic levels Blood – positive (degree variable) Protein – heavy Blood – positive (usually small) Specific Gravity – low, isosthenuric Protein – severe Blood – positive (usually small) Decreased transferrin Hypoalbuminemia Mild proteinuria Mild hematuria Positive Nitrite Positive Leukocyte Esterase Alkaline pH Same as for lower urinary tract infection, with the only difference being presence/absence of casts Glycosuria Proteinuria Hematuria Isosthenuria ↑ Ischemia-Modified Albumin Decreased GFR (20:1 (elevated creatinine)

Reference Range or Formula 6-20 mg/dL 0.9-1.3 mg/dL

Post-renal hyperuremia (obstruction)

Normal ratio, both BUN & Creatinine elevated Renal hyperuremia (glomerular damage)

Elevated in: Severe liver disease Ammonia

Reye’s Syndrome, Cirrhosis, Viral Hepatitis

Impaired renal function Blood urea increased, converts to ammonia in intestines

Hyperuricemia Uric Acid

Gout, renal failure, renal calculi, excess ethanol

Hypouricemia Severe liver disease, defective tubular reabsorption

Creatinine Clearance (CC) Glomerular Filtration Rate (GFR)

Assesses GFR More sensitive than CC Decreased in glomerular disease

CC(mL/min) = (UV)/P

Spectrophotometer Formula/Beer’s Law

Cu = (Au/As)*Cs

Carbohydrate Disease

Diabetes Mellitus

Testing FPG = ≥ 126mg/dL Casual Plasma Glucose = ≥ 200mg/dL (plus diabetes sx) OGTT = ≥ 200mg/dL HbA1C = ≥ 6.5%

Normal Reference Ranges

2/4 must be met on 2 different days

Prediabetes

Gestational Diabetes

FPG = ≥ 100 < 126mg/dL (impaired fasting glucose) OGTT = ≥ 140 < 200mg/dL (impaired glucose tolerance) OGTT Fasting = ≥ 95mg/dL 1hr = ≥ 180mg/dL 2hr = ≥ 155mg/dL 3hr = ≥ 140mg/dL

Fasting plasma glucose: 70-100mg/dL OGTT: AST AST/ALT ratio ALT AST/ALT ratio >2 Increased ALP AST/ALT ratio >2.0 Mildly increased ALP Markedly increased GGT Markedly increased total bilirubin Hyperammonemia (increased NH3) Markedly increased ALP Increased AST, ALT, total bilirubin BUN/Creatinine Ratio >20:1 (elevated creatinine)

Cardiac Disease

Analytes Myoglobin

CK-MB Acute Myocardial Infarction Troponin greatest specificity for acute MI

CRP Ischemia-Modified Albumin

Testing Rises: 1-3 hrs Peaks: 12 hrs Falls: 1 day Rises: 4-8 hrs Peaks: 24 hrs Falls: 2-3 days Rises: 3-6 hrs Peaks: 10-24 hrs Falls: 5-14 days Rises: 6-12hrs Not exclusive to AMI Early marker produced by any ischemic event (CA, renal disease, liver disease)

Myeloperoxidase (MPO) Lp-PLA2 Lipo(a)

Cardiovascular Risk

hs-CRP

Congestive Heart Failure

BNP marker for heart failure

Elevations: atheromatous plaque instability Elevations: increased risk of cardiovascular event Inflammation >30 mg/dL = 2-fold risk of atherosclerosis Hereditary 3.0 mg/L = HIGH RISK >10.0 mg/L = acute inflammatory condition 500 pg/mL = congestive heart failure

Anions, Cations, & Acid-Base Balance Disease Respiratory Acidosis

Defect Accumulation of pCO₂ Hypoventilation

Lab Values pH: decreased pCO₂: increased

Deficit of pCO₂ Respiratory Alkalosis

Metabolic Acidosis

Metabolic Alkalosis Reference Ranges 7.35 - 7.45 32-48 mmHg 23-29 mmHg

Measurement

Hyperventilation, early salicylate poisoning, excessive mechanical ventilation

Deficit of HCO₃Renal failure – reduced excretion of acids Ketoacidosis (Diabetes)

Accumulation of HCO₃Ingestion of excess alkali (antacids), hypokalemia, hyperaldosteronism

pH pCO₂ HCO₃-

Formula

Decrease

overhydration SIADH

Osmolality

2(Na) + (Glucose/20) + (BUN/3)

Osmolal Gap

Measured Osmolality - Calculated Osmolality

Anion Gap

(Na) - (Cl) - (HCO₃-)

Cations

Sodium 135-145 mmol/L

HCO₃-: normal (uncompensated), increased (compensated) pH: increased pCO₂: decreased HCO₃-: normal (uncompensated), decreased (compensated) pH: decreased pCO₂: normal (uncompensated), decreased (compensated) HCO₃-: decreased pH: increased pCO₂: normal (uncompensated), increased (compensated) HCO₃-: increased

Increase

Dehydration Cushing’s Syndrome Hyperaldosteronism

Increase dehydration hyperglycemia uremia ethanol Lactic acidosis Ketones Ethanol/Methanol

↑ unmeasured cations

↓ unmeasured cations

↓ unmeasured anions

↑ unmeasured anions

Decrease Overhydration Pseudohyponatremia Renal Failure Addison’s Disease Hypoaldosteronism Inversely related

Potassium 3.5-5.0 mmol/L

Calcium 8.6-10.2 mmol/L

Intravascular hemolysis Acidosis Renal Failure Addison’s Disease Hypoaldosteronism Primary Hyperparathyroidism

Insulin use Alkalosis Cushing’s Syndrome Hyperaldosteronism Primary Hypoparathyroidism Pseudohypoparathyroidism

Inversely related

(Ionized Calcium

PTH & Vit. D = ↑ Ca Calcitonin = ↓ Ca

- active form)

Magnesium

Poor diet/starvation/alcoholism Prolonged IV therapy Hyperparathyroidism Hyperaldosteronism Hyperthyroidism Hypercalcemia

Hypothyroidism Hypoaldosteronism ( Hypopituitarism (↓ GH) Antacids, Laxatives, Enemas PTH = ↑ Mg

Aldosterone, Thyroxine, GH = ↓ Mg

Anions

Increase

Phosphorous Chloride 98-107 mmol/L

Bicarbonate 23-29 mmHg

Decrease INVERSELY RELATED TO Ca

PTH = ↓ HPO4

Metabolic Acidosis

Metabolic Alkalosis

changes in Cl parallel changes in Na

Metabolic Alkalosis

Metabolic Acidosis

Inversely related

Toxicology Alcohol Ethanol Isopropanol Methanol Ethylene Glycol

Increased Osmolal Gap + + + +

Metabolic Increased Acidosis Anion Gap + + + +

Serum Acetone + -

Other testing Trinder’s Reagent Glutathione

Ca Oxalate Crystals +

Other significant findings Hyperuricemia (↑ uric acid)

Purpose/Indication Salicylate poisoning produces purple color

↓ = Acetaminophen overdose carboxyhemoglobinemia (CO₂ poisoning)

Co-Oximetry

cherry-red skin appearance

methemoglobinemia cyanosis, chocolate-brown blood

Retention Factor (Rf)

Distance moved by Component/Total Distance moved by Solvent

Class

Drug

Metabolite

Cardiac

Procainamide

N-Acetylprocainamide (NAPA)

Tricyclic Antidepressant

Amitriptyline

Nortriptyline

Imipramine

Desipramine

Cocaine

Benzoylecgonine

Endocrine – Pituitary Primary: problem with the thyroid gland Secondary: problem with the pituitary gland

Disease Primary Hyperthyroidism – Grave’s Disease Secondary Hyperthyroidism Primary Hypothyroidism – Hashimoto’s Disease Secondary Hypothyroidism Endocrine – Adrenal

T3 ↑ ↑ ↓ ↓

T4 ↑ ↑ ↓ ↓

TSH ↓ ↑ ↑ ↓

Primary: problem with the adrenal gland Secondary: problem with the pituitary gland

Cushing’s Disease Cortisol ACTH High Dose Dexamethasone Suppression CRH Stimulation ↑ ↓ ↑ Primary Hyperadrenalcorticalism No change ↑ ↑ ↑↑ Secondary Hyperadrenalcorticalism Successful Suppression ↑ ↑ ↑ ACTH-Secreting Tumor No change Addison’s Disease Cortisol ACTH ACTH Stimulation ↓ ↑ Minimal to NO ↑ cortisol Primary Hypoadrenalcorticalism ↓ ↓ Gradual ↑ in cortisol Secondary Hypoadrenalcorticalism Aldosteronism Aldosterone levels Plasmin Renin activity Primary Hyperaldosteronism – Conn’s Syndrome ↑ ↓ Adrenal adenoma or adrenal hyperplasia

Secondary Hyperaldosteronism

↑

↑

Decreased blood flow to kidney

Hyporeninemic Hypoaldosteronism

Furosemide will ↑ aldosterone

Kidney disease: diabetes, interstitial nephritis, multiple myeloma

Hyperreninemic Hypoaldosteronism

No effect with furosemide

Aldosterone production inhibited

 Catecholamines Adrenal Tumors Associated with ↑ Pheochromocytoma Neuroblastoma

Compounds Elevated Catecholamines – epinephrine, norepinephrine, dopamine Vanillylmandelic Acid, Metanephrines Catecholamines – epinephrine, norepinephrine, dopamine Vanillylmandelic Acid, Metanephrines Homovanillic Acid

Endocrine – Gonadal Disease Hypergonadotropic Hypogonadism Hypogonadotropic Hypogonadism

LH ↑ ↓

FSH ↑ ↓

Testosterone ↓ ↓

Lab Math/Quality Assurance Coefficient of variation (CV) % = SD(100)/Mean Sensitivity = True Pos/(True Pos + False Neg) Positive Predictive Value = True Pos/(True Pos + False Pos) Specificity = True Neg/(True Neg + False Pos) Negative Predictive Value = True Neg/(True Neg + False Neg) SDI = (Your lab’s result – Group mean)/Group SD % w/v concentration MW not a factor ex. 2% solution = (2g/100mL)*(g OR mL) = g OR mL % w/w concentration solute/total ex. Prepare 400g of a 20% Ehrlich’s reagent in HCl solution. 400g * 0.2 = 80g Ehrlich’s 400g - 80g = 320g HCl % v/v concentration solute/total ex. Concentration of a solution prepared by adding 75mL ethanol to 175mL water. 75mL/(75+175)mL = 0.3 = 30% V1C1 = V2C2 w1/v1 = w2/v2 Molarity = (g/L)/GMW GMW = aw/ve Normality = M * VE Convert between molarity and normality M = N/VE Convert between mEq/L and mg/dL mEq = (mg/dL)/GMW mg/dL = (mEq/L * GMW)/10 GMW = aw/ve Dilutions...