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Chemistry
| Question | Answer |
|---|---|
| Glucose | • Fasting reference range for serum or plasma : 70-99mg/dL • Arterial and capillary values: 2-3 mg/dL higher • Normal CSF values are two-thirds (approximately 60-65%) of plasma levels |
| Hormonal activity affecting serum glucose levels | • Insulin • Glucagon • ACTH • Growth Hormone • Cortisol • Human Placental Lactogen • Epinephrine • T3 and T4 |
| Insulin effects of glucose | • Source: Beta cells of islets of Langerhans of pancreas • Action: ⬇ serum glucose, stimulates glucose uptake by cells |
| Glucagon effects of glucose | • Source: Alpha cells of pancreas • Action: ⬆ glucose, stimulates glycogenolysis (breakdown of glycogen glucose) |
| ACTH effects of glucose | • Source: anterior pituitary • Action: ⬆ glucose, insulin antagonist (interferes or inhibits) |
| Growth Hormone effects of glucose | • Source: anterior pituitary • Action: ⬆ glucose, insulin antagonist, acromegaly=hyperglycemia |
| Cortisol effects of glucose | • Source: adrenal cortex • Action: ⬆ glucose, stimulates gluconeogenesis (glucose from non-carbohydrate sources) |
| Human Placental Lactogen effects of glucose | • Source: placenta • Action: ⬆ glucose, insulin antagonist |
| Epinephrine effects of glucose | • Source: adrenal medulla • Action: ⬆ glucose, stimulates glycogenolysis, pheochromocytoma-lumor of adrenal medulla --> hyperglycemia |
| T3 and T4 effects of glucose | • Source: thyroid gland • Action: ⬆ glucose, stimulates glycogenolysis |
| GAG CHET to remember what cause in increase of glucose | • Glucagon • ACTH • Growth Hormone • Cortisol • Human Placental Lactogen • Epinephrine • T3 and T4 |
| Symptoms of decrease or no insulin production | • Tired • Polyuria • Increase thirst and hunger • Weight loss • Poor wound healing |
| Lab test for diabetes | • Increase glucose in blood and urine • May have increased cholesterol • Diabetic acidosis: decreased Na, increased K, decreased Cl, +Ketones in blood and urine |
| Fasting blood sugar range | • Normal: 70-99 mg/dL • Diabetes >126 mg/dL |
| Post prandial sugar (PPS) 2hrs after meal range | • Normal < 126 mg/dL • Diabetes >200 mg/dL |
| Post-loading glucose range | • Similar to PPS <126 mg/dL • Glucose load is standardized • Diabetics ≥ 200mg/dL |
| Glucose tolerance test (GTT) standard dose 75g | • Diagnostics of diabetes mellitus > 150 mg/dL after 2 hours, > 200 mg/dL after 2 hours • Perform if FBS and PPS are normal |
| Intravenous glucose tolerance test (V-GTT) | • Poor absorption (flat curve with oral GTT) OR patient who cannot tolerate a large glucose load (vomiting) |
| O’Sullivan test (for gestational diabetes) | • Standard dose 50g • Probable gestational diabetes > 150mg/dL at 1 hour • Follow up with oral GTT |
| Glycosylated Hemoglobin (A1C, Hgb A1C) | Test used to monitor glucose • Assessment of long term control • Average glucose level over 60 days (2-3 months) |
| Microalbumin | Test used to monitor glucose • Detects small amounts of protein in urine of diabetic patients to assess renal damage |
| C Peptide of insulin (reflects pancreatic insulin secreting) | Test used to monitor glucose • Normal 1:1 (insulin: C-peptide) • Diabetes > 1:1 • C-peptide ⬇ after insulin injection |
| Human plasma lipids are | Cholesterol, triglycerides, phospholipids, and non-esterified fatty acids |
| Lipids combine with proteins in the liver to form | Lipoproteins |
| Lipoproteins are | • Low density lipoproteins (LDL) • High density lipoproteins (HDL) • Very low density lipoproteins (VLDL) |
| Low density lipoproteins (LDL) | Bad, brings cholesterol to the cells <100mg/dL |
| High density lipoproteins (HDL) | Good, Helpful it takes cholesterol from the cells >60mg/dL |
| Very low density lipoproteins (VLDL) | Bad 2-30mg/dL |
| Fast lipid test is how many hours | 12hrs |
| General info about protein | •Most are made and broken down in the liver, Carbon, hydrogen, oxygen, and nitrogen are the primary constituents of protein molecules • Basic unit- amino acids linked together • Breakdown in the body produces urea and ammonia |
| Electrophoresis | Direction of migration of proteins in an electrical field is determined by the surface charge of the protein |
| Electrophoresis: Protein at a higher pH than its isoelectric point is blank and migrates towards the blank | • Negatively charged • Anode (positive charge) |
| Electrophoresis: blank has the largest number of free negative charges and migrates most rapidly traveling the greatest distance from the application point | Albumin (smallest M.W.) |
| Urine and serum protein electrophoresis is exactly the same except urine must be what before application | Concentrated |
| Electroendosmosis causes what to migrate toward the cathode even though they are slightly negatively charged (due to...) | • Gamma globulins • (due to the electrical charge on the support medium) |
| Electrophoresis; what is the pH need to be in order for the 6 major bands to migrate | pH 8.6 |
| Electrophoresis: what are the 6 major bands | • Pre-albumin • Albumin • Alpha-1 • Alpha-2 • Beta • Gamma |
| Electrophoresis support media include | • Agarose gel • Starch gel • Cellulose acetate |
| Electrophoresis stains include | • Amido Black • Ponceau S • Coomassie Brilliant Blue |
| Electrophoresis specimen collection and handling | • Plasma samples (mistaken as serum) result in fibrinogen peak migrating between gamma and beta fractions • Recollect sample and repeat to verify that peaks are not fibrinogen |
| Remember Protein Electrophoresis: Abbie Albumin is attracted to Andy Anod because of his Positive attitude | |
| Clinical significance Albumin | • Largest plasma protein fraction • Regulator of osmotic pressure • Transport protein b/c of ease of binding with blood components • Causes ⬇ values:⬇ synthesis (liver impartment), malabsorption/malnutrition, nephrotic syndrome (renal loss), burns |
| Clinical significance Alpha-1-globulins: Alpha1-antitrypsin (AAT | • ⬆ in acute phase and pregnancy • ⬇ associated with emphysema in neonates |
| Clinical significance Alpha-1-globulins: Alpha-1-fetoprotein (AFP) | • ⬆ values • ⬆ in amniotic fluid and serum in neural tube defects (spina bifida) • Liver cancer marker • ⬇ associated with Down’s syndrome |
| Clinical significance Alpha-2-globulins: Haptoglobin | • Binds free hemoglobin • ⬆ in acute phase and nephrotic syndrome • ⬇ in hemolysis and liver diseases |
| Clinical significance Alpha-2-globulins: Ceruloplasmin | • Transport copper • ⬆ in acute phase and pregnancy • ⬇ in Wilson’s disease |
| Clinical significance o Beta globulin | • Carrier proteins for iron (transferrin) and lipids (lipoproteins) • ⬆ in: elevated beta lipoprotein (LDL) Iron deficiency anemia |
| Clinical significance o Gamma globulin | • ⬆ in: Chronic inflammation Cirrhosis or viral hepatitis Collagen diseases Paraproteins (monoclonal bands, gammopathies) • ⬇ in congenital or acquired immunodeficiency |
| General info about enzymes | • Organic catalysts responsible for most reactions in the body |
| Enzymes in lab measurements are affected by | • Concentration of reactants • pH (optimum pH varies with each enzyme) • Temperature (optimum usually 37°C) • Ionic strength • Presence of activators or inhibitors |
| Total CK (Creatine Kinase) | • ⬆ in muscle, cardiac, or brain damage • Higher reference range in males due to greater muscle mass and physical activity • Normal 22-192U/L (units/Liter) |
| CK has 2 subunits | • M and B • BB is most negatively charged; therefore migrates furthest toward anode • Cardiac muscle = CK-MM and CK-MB • Skeletal muscle = CK-MM • Brain, GI, prostate, uterus = CK-BB |
| Troponin | • troponin is a contractile protein that is cardiac-specific • It consists of 3 subunits • Normal 0-0.4 ng/mL |
| Troponin subunits | • TnC • TnI TnI assays are available and produce similar diagnostic results as TnT • TnT Currently used in some laboratories for detection of AMI ⬆ increases the serum 4 hours after MI and peaks at 2-5 days |
| LD (Lactate Dehydrogenase) increased in | • MI- “flipped” isoenzyme pattern (LD1>LD2) • Liver disease • Muscle trauma • Renal infarct • Hemolytic diseases • Pernicious anemia |
| LD (Lactate Dehydrogenase) source of error | • Hemolyzed specimens- “flipped” isoenzyme pattern • Prolonged contact of serum to cells |
| LD (Lactate Dehydrogenase) Isoenzymes -2 chains (M and H) | • LDL1 = HHHH = Heart, RBCs, kidney- fastest fraction (anode) • LD2 = MHHH = heart • LD3 = MMHH = lung • LD4 = MMMH = many tissues • LD5 = MMMM = skeletal muscle and liver- slightly toward cathode |
| AST (Aspartate Transaminase) | • Found in cardiac muscle, liver, RBCs, and other tissue • ⬆ in MI, liver disease, muscle trauma, renal infarct, hemolysis • Normal 5-40U/L |
| ALT (Alanine Transaminase) | • ⬆ in in liver damage • 7-56U/L |
| GGT (Gamma-Glutamyl Transferase) | • ⬆ in liver disease (highest in biliary obstruction and cirrhosis) • Pre-employment drug screens (⬆ in alcoholics) • Spectrophotometric method- gamma-glutamyl-p-nitroanilide + glyclglycine GGT nitroaniline |
| ALP (Alkaline Phosphatase) | • Found in bone, intestinal mucosa, renal tubule cells, biliary tree (liver), leukocytes, placenta • Disorders of liver (obstructive jaundice due to gallstones or malignancy) • Growth in children- rapid skeletal growth • 3 trimester of pregnancy |
| Amylase | • Produced in salivary & pancreatic glands • Highest elevations seen in pancreatitis and obstruction to pancreatic ducts (malignancy) • Lower elevations seen in obstruction of salivary glands (mumps) • Urine remains ⬆ longer than serum in pancreatitis |
| Lipase | • ⬆ in pancreatitis • Remains elevated longer than amylase • More specific for acute pancreatitis |
| ACP (Acid Phosphatase) | • Highest elevations seen in metastasizing carcinoma of the prostate • ⬆ in bone disease or cancers that metastasize to breast cancer • Tartrate-resistant portion elevated in hairy cell leukemia • In seminal fluid useful for rape cases |
| Cholinesterase | • Erythrocyte acetylcholinesterase and plasma pseudocholinesterase • Destroys acetylcholine after nerve impulse transmission • ⬇ in serious neuromuscular effects; decrease is clinically significant • ⬇ results investigate of organophosphate poisoning |
| Cardiac Markers to Evaluate Possible Acute Myocardial Infarction | • CK-MB followed by CK-MM 1 to raise within 24hrs normal in 2-3days • AST raise 24-48hrs normal 4-6days • LD raise in 48-72days • Myoglobin: (muscle)⬆ in muscle damage in AMI. Raise within 30mins |
| Remember MI enzymes: MiCal | Mical had an MI. His CK rise first, followed by AST and lastly LD |
| What Liver markers are elevated | • AST: highest in hepatitis • ALT: highest in hepatitis, liver specific • LD: in many tissues other than liver • ALP: biliary obstruction; slightly elevated in hepatitis • 5'NT: biliary obstruction • GGT: liver specific; highest in alcoholism |
| Remember Elevated Liver enzymes: ABC | • Alcoholism • Biliary obstruction • Cirrhosis |
| Remember Hepatis VS Obstruction | • HeATitis herb: ⬆ AST, ALT, GGT, Bilirubin • Plugged up Paul: ⬆ ALP, 5'NT=5 fingers, GGT, Bilirubin |
| What Muscle Disorders elevate what enzymes | • CK • AST • Aldolase |
| What enzymes are elevated in Acute Pancreatitis | • ⬆ in amylase (serum and urine); remains elevated longer in urine • ⬆ in lipase- more specific than amylase |
| Electrolytes | • Sodium (NA+) • Potassium (K+) • Chloride (Cl¯) |
| Sodium (NA+) | • Major cation of extracellular fluid • 85% is reabsorbed in the kidney tubules • Reference range = 135-145mM/L • Hyponatremia Cushing’s syndrome Dehydration Hyperaldosteronism (causes ⬇ renal reabsorption) |
| Potassium (K+) | • Major cation of intracellular fluid • Range = 3.5-5.5mM/L • 23X higher in cells than in plasma • Separate serum from cells quickly to prevent K+ from shifting to serum • False ⬆ in K+ Hemolysis EDTA contamination Prolonged tourniquet |
| Hypokalemia and hyperkalemia may cause | Heart arrhythmias and/or neuromuscular symptoms inkling weakness and paralysis |
| What can cause o Hyperkalemia | • Diabetic acidosis (metabolic) • Intravascular hemolysis • Severe burns • Renal failure |
| What can cause o Hypokalemia | • Insulin injections • Alkalosis • GI losses • Hyperaldosteronism (⬇ renal reabsorption) |
| Ion-Selective electrode (ISE) Analysis for | NA+ and K+ • Na+ electrode- glass electrode selective for Na+ • Liquid ion-exchange membrane electrode, incorporating the antibiotic valinomycin in used to measure K+ |
| Chloride (Cl¯) | • Major anion of extracellular fluid • Maintains hydration, osmotic pressure and the normal anion-cation balance • Reference rand = 98-106mM/L • Chloride generally follows Na+ so ⬆ and ⬇ in same conditions |
| What causes Hypochloremia | • Diabetic acidosis (excessive acid production) • Renal failure (diminished acid secretion) • Prolonged vomiting (loss of gastric HCL) |
| What causes Hyperchloremia | • Excess loss of HCO3 GI Loss Renal tubular acidosis Mineral corticoid deficiency |
| Sweat chloride | • ⬆ in cystic fibrosis • Sweat is collected by iontophoresis using drug, pilocarpine, to induce sweating • >60mM/L - cystic fibrosis |
| Chloride shift | • Buffering system of the blood (far acid-base balance) • HCO¯3 ion is pulled out of the erythrocyte and Cl¯ moves into the erythrocyte resulting in ⬇ serum Cl¯ |
| CO2 (Total Carbon Dioxide) | • CO2 + HCO¯3 + H2Co3 = total CO2 • Reflects bicarbonate (HCO¯3 ) |
| Anion GAP | • Calculation that reflects differences between unmeasured cations and anions • Major unmeasured cations • Major unmeasured anions • (Na+) + (K+) - Cl¯) + (HCO¯3) OR *** (Na+)- (Cl¯) + (HCO¯3) *** • Reference range = 8-18mM/L |
| What causes ⬆ anion gap | • ⬆ in concentration of unmeasured anions Ethanol ketones • ⬇ in unmeasured cations Low serum Mg++ Low serum Ca++ |
| What causes ⬇ anion gap | • ⬇ in unmeasured anions- albumin loss • ⬆ in unmeasured cations High serum Mg++ High serum Ca++ Lithium therapy |
| Osmolality | • Measures of the total concentration (number) of dissolved particles in a solution (molecular weight, size, density, or type of particle does not matter) • Can be measured directly |
| Calculated Osmolality | = 2Na + Glucose/18 + BUN/2.8 |
| Increased osmo = | Increased thirst |
| Can compare calculated osmolality to the measured osmolality; a measured osmolality that is >10 higher than the calculated osmolality indicates | Presence of exogenous unmeasured anion (methanol, ethanol, ketone bodies, etc.) |
| Remember conditions causing increased in unmeasured anions (ethanol, ketones. etc.): SLUMPED | • Salicylate intoxication • Lactic acidosis • Unmeasured ions • Methanol • Polyethylene glycol • Ethanol • Diabetic ketoacidosis |
| Magnesium (MG++) | Ca++ channel blocking agent (affects heart) |
| What causes increased Magnesium (MG++) | Renal failure |
| What causes decreased Magnesium (MG++) | • Cardiac disorders • Diabetes mellitus • Diuretics, alcohol and other drugs |
| Calcium (Ca++) | • Combines with phosphate in the bone • Controlled by 3 hormones: PTH (parathyroid) ⬆ ionized Ca++ Calcitonin inhibits bone reabsorption (⬇ Ca++) Vitamin D causes ⬆ absorption in the intestines (⬆ Ca++) |
| What causes Hypercalcemia- muscle weakness, disorientation | • Hyperparathyroidism • Cancer with bone metastasis • Multiple myeloma • Renal failure |
| What causes Hypocalcemia- tetany (in cases of tetany suspect Ca FIRST then Mg or K) | • Hypoparathyroidism • ⬇ serum albumin • ⬇ vitamin D (malabsorption, inadequate diet)- impaired bone release, impaired renal reabsorption |
| What can cause false decreases in Calcium (Ca++) | Using EDTA tubes, EDTA chelates Ca++ |
| Phosphorous | • Majority of phosphate in body expressed as phosphorous; lab measures inorganic phosphorous (PO4) only • Inverse relationship with Ca++ (when Ca++ is ⬆, PO4 is ⬇ and vice versa) |
| What causes increase Phosphorous | • Hypoparathyroidism • Chronic renal failure • Excess vitamin D |
| What causes decrease Phosphorous | • Hyperparathyroidism • Impaired renal absorption |
| Iron | • Over 65% of total body iron is in hemoglobin- O2 transport • Transported by transferrin, haptoglobin, and hemopexin • Stored as ferritin and hemosiderin |
| TIBC (total iron-binding capacity) | • Measures transferrin levels • Excess ferric salts are added to serum to saturate binding sites on transferrin • Unbound iron is precipitated with magnesium carbonate • After centrifugation, the supernatant is analyzed for iron |
| Normal serum iron range | 500-1600ug/l |
| Normal transferrin saturatoion | 20-55% |
| Normal TIBC | 2500-4000ug/l |
| Normal serum ferritin | 15-200ug/l |
| Lab assessment of Iron: storage iron depletion (no anemia) | • Serum iron: normal • Transferrin saturation: normal • TIBC: normal • Serum ferritin: ⬇ |
| Lab assessment of iron: Iron deficiency anemia | • Serum iron: ⬇ • Transferrin saturation: ⬇ • TIBC: ⬆ • Serum ferritin: ⬇ |
| Lab assessment of iron: Anemia of chronic disease (inflammation) | • Serum iron: ⬇ • Transferrin saturation: ⬇ • TIBC: ⬇ • Serum ferritin : ⬆ |
| Lab assessment of iron: Thalassemia | • Serum iron: ⬆ • Transferrin saturation: ⬆ • TIBC: ⬇ • Serum ferritin: ⬆ |
| Lab assessment of iron: Hemochromatosis | • Serum iron: ⬆ • Transferrin saturation: ⬆ • TIBC: ⬇ • Serum ferritin: ⬆ |
| Lab assessment of iron: Sideroblastic anemia | • Serum iron: ⬆ • Transferrin saturation: ⬆ • TIBC: normal • Serum ferritin: ⬆ |
| Acid-Base Balance equation | pH= pKa + log (HCO3-)/(H2CO3) |
| Sample collection and handling for Acid-Base Balance testing | • Anticoagulant- sodium heparinate (heparin) • Must use anaerobic collection for blood pH and blood gas studies |
| Effects of blood gas if blood is exposed to air | • CO2 and PCO2 ⬇ • pH ⬆ • PO2 ⬆ |
| Effects of blood gas if testing is prolonged (>20mins) | • Blood should be placed on ice to prevent glycolysis which leads to: CO2 and PCO2 ⬆ pH ⬆ PO2 ⬇ |
| Effects of blood gas if there are bubbles in the syring | • pH ⬆ • PCO2 ⬇ • PO2 ⬇ |
| Effects of blood gas testing is longer than 30min not on ice | • pH ⬇ • PCO2 ⬆ • PO2 ⬇ |
| Remember factors affecting blood gases | • pH flies through the air but fails after sitting (air ⬆pH, prolonged sitting ⬇pH) • Paco (PCO2) fails from the air but rises after sitting (air ⬇PCO2, prolonged sitting ⬆PCO2) • O2: exposure to air causes ⬆PO2, prolonged sitting causes loss air ⬇PO2 |
| pH for blood gases | • Negative log of H+ • 7.35-7.45 |
| PCO2 for blood gases | • Partial pressure or tension of CO2 in blood • 35-45mm Hg |
| HCO3 for blood gases | • Bicarbonate-calculated • 22-26m/v/L |
| PO2 for blood gases | • Oxygen tension- partial pressure of oxygen • 85-105mm Hg |
| Remember blood gas normal | • PO2 I like my oxygen at 100 but will do 90 • PCO2 is half of PO2 =45 • HCO3 is half of PCO2 =around 23 • pH is 1/3 of HCO3 = around 7.4 |
| Metabolic Acidosis | • Primary bicarbonate deficit: Diabetic ketoacidosis (⬆ acid production) Renal disease (⬇ H+ excretion) Prolonged diarrhea (excessive HCO¯3 loss) Late salicylate poisoning |
| Compensatory mechanisms for Metabolic Acidosis | • Primarily respiratory- hyperventilation ⬇ PCO2 • Some renal (if kidney function is normal) - ⬆ excretion of H+ and reabsorption of HCO¯3 |
| Lab findings in Metabolic Acidosis | • ⬇ pH, HCO¯3, CO2, and PCO2 • Acid urine |
| Metabolic Alkalosis | • Primary HCO¯3 excess • Seen in: NaHCO¯3 infusion Citrate (anticoagulant in blood transfusions) Antacids (contain HCO¯3) Vomiting (HCL loss, prolonged vomiting leads to alkalosis due to GI loss of HCO¯3) K+ depletion Diuretic therapy |
| Compensatory mechanisms for Metabolic Alkalosis | • Primarily respiratory- hypoventilation- ⬆ retention of CO2 • Some renal- ⬇ excretion of H+ and ⬆ reabsorption of HCO¯3 |
| Lab findings in Metabolic Alkalosis | ⬆ pH, HCO¯3, CO2, and PCO2 |
| Respiratory Acidosis | • Primary CO2 excess • Seen in: Emphysema Pneumonia Rebreathing of air (paper bag) |
| Compensatory mechanisms for Respiratory Acidosis | • Mainly renal- ⬆ H+ excretion and HCO¯3 reabsorption • Some respiratory (if defect is not in the respiratory center) |
| Lab finings in Respiratory Acidosis | • ⬇ pH • ⬆ HCO¯3, CO2, and PCO2 |
| Respiratory Alkalosis | • Primary CO2 deficit • Seen in: Hyperventilation (blowing off too much CO2) Early salicylate poisoning |
| Compensatory mechanisms for Respiratory Alkalosis | Mainly renal- ⬇ H+ excretion |
| Lab finings in Respiratory Alkalosis | • ⬆ pH and HCO¯3 • ⬇ PCO2 and CO2 |
| Compensatory mechanisms that is renal | • Respiratory Acidosis ⬆ HCO3 • Respiratory Alkalosis ⬇ HCO3 |
| Compensatory mechanisms that is lung | • Metabolic Alkalosis ⬇ pCO2 • Metabolic Alkalosis ⬆ pCO2 |
| Remember compensatory mechanisms respiratory | Compensation occurs in respiratory when Carbo (Bicarb-HCO3) gets made at pH for playing with Paco (PCO2) so Carbo hops on Pacos side of the seesaw = pH goes up while PCO2 and HCO3 go down. pH comes down and PCo2 and HCO3 go up. |
| Remember compensatory mechanisms metabolic | Compensation occurs in metabolic when Paco (PCO2) decided to crash the swinging 2some and hops on with pH and Carbo (Bicarb-HCO3) = now all go up and all go down |
| Evaluation Acid-Base Disorders | •Look at the pH to determine acidosis or alkalosis • Look at the PCO2 and HCO¯3 to see where they fall in relation to their ‘normal’ PCO2 seesawing with pH? (Respiratory) HCO¯3 swinging with pH? (Metabolic) • If the pH is normal, full compensation |
| Evaluation Acid-Base Disorders: partial compensation has occurred if | If the main compensatory mechanism has kicked in but the pH is still out of normal range |
| Evaluation Acid-Base Disorders: if a primary dysfunction is respiratory function results in change in PCO2 (seesaw) the main compensation factor will be | HCO¯3 (Metabolic) |
| Evaluation Acid-Base Disorders: if a primary dysfunction in metabolic function results in a change in HCO¯3 (swing) the main compensating factor will be | PCO2 (Respiratory) |
| Remember Acid-Base status: ROME, Respiratory, Opposite, | • pH and Paco (PCO2) hop on the seesaw up and down. When they are on opposite directions from normal the status is respiratory. (respiratory=opposite) • pH >7.45 = alkalosis • pH <7.35 = acidosis |
| Remember Acid-Base status: ROME, Metabolic, Equal | • pH runs off and joins Carbo (Bicarb-HCO3) on the swing. Both go up and down together the status is metabolic. (metabolic=equal) • pH >7.45 = alkalosis • pH <7.35 = acidosis |
| Hemoglobin Derivatives | • Hemoglobin breakdown products include porphyrins, bilirubin, and urobilinogen • Hemoglobin of aged or damaged RBCs converted to bilirubin |
| Protoporphyrin =Fe++ ----> | Heme |
| Heme + globin ----> | Hemoglobin |
| Lab analysis of Porphyrins and related compounds | • Urine with large amounts of porphyrins show a red or port wine color • All porphyrins have a characteristic pink fluorescence (can be quantitated using a UV spectrophotometer) • Uroporphyrins can be extracted into n-butanol |
| Lab analysis of Bilirubin: Diazotization methods | • Evelyn and Malloy (classic method) Bilirubin + diazatized sulfanilic acid-->azobilirubin (purple) Total bilirubin reacts with diazo reagent in methyl alcohol read in 30min Conjugated bilirubin (direct) reacts with diazo reagent in H2O read in 1min |
| Lab analysis of Bilirubin: Diazotization methods: direct and indirect | • Direct = conjugated = water soluble • Indirect = unconjugated = insoluble in water |
| Specimen collection and handling of Bilirubin | • Bilirubin is light sensitive therefore sample should be stored in the dark/amber color tube • Lipemia- falsely ⬆ results • Hemolysis- falsely ⬇ results |
| Bilirubin and Disease states general info | • When unconjugated bilirubin is ⬆ there will be a ⬆ in urine urobilinogen (due to U amount reabsorbed from intestine and filtered by kidney) • When conjugated bilirubin (water soluble) is ⬆it will appear in urine |
| Bilirubin and Disease conditions Pre-hepatic jaundice | • (i.e. hemolytic anemia) ⬆RBC destruction-->⬆unconjugated bilirubin Liver function normal; conjugation occurs at normal rate--> normal conjugated bilirubin and no bilirubin in urine ⬆unconjugated bilirubin-->⬆urine urobilinogen |
| Bilirubin and Disease conditions Hepatic jaundice | • (i.e. viral hepatitis, cirrhosis) ⬆ unconjugated bilirubin, ⬆ conjugated bilirubin and ⬆urobilinogen due to liver dysfunction ⬆ conjugated bilirubin-->⬆ urine bilirubin ⬆ urine urobilinogen |
| Bilirubin and Disease conditions Post-hepatic (obstructive) jaundice | • Conjugated and unconjugated bilirubin cannot be metabolized properly; “backup” into plasma • ⬇ urobilinogen (due to backup) prevents conjugated bilirubin from entering intestine to be broken down into urobilinogen • Stool may become clay colored |
| Plasma/serum and Urine Bilirubin and Disease states: Pre-hepatic jaundice (hemolytic anemia) | Plasma/serum • Unconjugated: ⬆ •Conjugated: normal Urine • Bilirubin: 0 • Urobilinogen: ⬆ |
| Plasma/serum and Urine Bilirubin and Disease states: Hepatic (cirrhosis, viral hepatitis) | Plasma/serum • Unconjugated: ⬆ •Conjugated: ⬆ Urine • Bilirubin: 0 or ⬆ • Urobilinogen: ⬆ |
| Plasma/serum and Urine Bilirubin and Disease states: Post-hepatic (chronic jaundice) | Plasma/serum • Unconjugated: normal •Conjugated: ⬆ Urine • Bilirubin: ⬆ • Urobilinogen:⬇ |
| Remember HDN....bilirubin cannot be conjugated in neonates | • Serum indirect (unconjugated) bilirubin ⬆, conjugated bilirubin is normal • Unconjugated (H2O insoluble) can't be execrated in urine, no urinary bilirubin • Unconjugated bilirubin can't be broken down by intestinal bacteria so no urine urobilinogen |
| Toxicology and Therapeutic Drug Monitoring: Immunochemical methods | • Immunochemical methods Enzyme-multiplied immunologic technique (EMIT) detects drugs of abuse Fluorescence polarization immunoassay (FPIA) monitors therapeutic drug levels |
| Toxicology and Therapeutic Drug Monitoring: Chromatographic Techniques | • Chromatographic Techniques Thin-Layer Chromatography (TLC) High-Performance Liquid Chromatography (HPLC) Gas Chromatography-Mass Spectrophotometry (GC-MS ‘Gold standard’ technique for confirmation of screening methods |
| Therapeutic Drug Monitoring: Specimen collection | • Wait 4 steady-state reached • 5.5 half-lives to reach steady state & 5.5 half-lives to clear drug • Trough specimen (lowest concentration) drawn immediately b4 next dose • Peaks are usually drawn 1-2 hours after an oral dose and vary for IV/IM |
| Goal of Therapeutic Drug Monitoring | To achieve the therapeutic range, avoiding concentrations that are sub-therapeutic or toxic |
| Therapeutic Drug Monitoring general info | • Each drug has its own rate of absorption, peak time, amount of binding to proteins, metabolism, and rate of excretion • Most common methods are immunoassays (RIA, EIA, and FPIA) • HPLC and GC |
| What type of method is best for Therapeutic Drug Monitoring | • High-Performance Liquid Chromatography (HPLC) and Gas Chromatography (GC) More sensitive and can measure parent drug and metabolites Disadvantages- expense, time, and the expertise required |
| Aminoglycosides (Antibiotics) generic name | • Gentamicin Amikacin Vancomycin • Tobramycin- less toxic to kidney than gentamicin |
| Aminoglycosides (Antibiotics) | • Inhibits bacterial protein synthesis; treat severe infections by gram-neg bacteria • Monitor toxic range to prevent damage to hearing (ototoxic) and kidneys (nephrotoxic) • RIA and EIA |
| Chloramphenicol | Toxic levels can result in aplastic anemia |
| Anti-arrhythmic and other Cardio-active Drugs | • Digoxin- RIA is preferred method • Disopyramide- GC, HPLC, ELISA • Procainamide- immunoassays (NAPA metabolite) • Quinidine- fluorescence, HPLC • Lidocaine- immunoassay, GLC, HPLC |
| Anti-convulsion’s generic names | • Carbamazepine • Ethosuximide • Phenobarbital • Phenytoin (Dilantin-brand) • Primidone (metabolite phenobarb) • Valproic acid |
| Anti-convulsion’s | • Alter transmission of nerve impulses to prevent epileptic seizures • Immunoassays, GC, HPLC (Gas Chromatography and High-Performance Liquid Chromatography) |
| Psychotropic (Antidepressants): Tricyclics | • Amitriptyline/Nortriptyline • Imipramine/Desipramine • GC method preferred because multiple drugs may be given and active metabolites are often present |
| Psychotropic (Antidepressants): Lithium | • Used to treat manic-depression • Flame emission photometry, ISEs |
| Bronchodilator | • Theophylline • Narrow therapeutic window & short half-life • Metabolized by liver Liver impairment can ⬆ levels Signs of toxic nausea, headache, irritability, insomnia Severe toxic arrhythmias, seizures, death • Caffeine metabolite in baby |
| Bronchodilator: High-Performance Liquid Chromatography (HPLC) measures | Theophylline and metabolites (caffeine and dyphylline) |
| Acute Poisoning: Substances | • Cyanide • Carbon monoxide • Alcohol- ethanol most common, enzymatic- alcohol dehydrogenase • Arsenic • Heavy metals • Iron • Salicylates- metabolic acidosis- respiratory alkalosis • Organophosphates • Acetaminophen |
| Acute Poisoning: Organophosphates | • CNS symptoms- diagnosis depends on history of exposure (pesticides), symptoms, and lab measurements of erythrocyte acetylcholinesterase and plasma pseudocholinesterase • Both are ⬇ in poisoning • Plasma portion is more sensitive but less specific |
| Acute Poisoning: Acetaminophen | Liver damage from accumulation of toxic metabolite 48 hours after ingestion; antidote helpful if given in first 24 hours |
| Non-Protein Nitrogens (NPN) general info | • All NPNs (urea, creatinine, uric acid, ammonia)⬆ in plasma in renal impairment; referred to as azotemia • Suspected renal impairment, best lab test is glomerular filtration rate (GFR) • Creatine clearance evaluates GFR (more sensitive than BUN/Creat) |
| Creatine clearance = | Urine creat/plasma creat X volume 24hr urine/1440 (min/24hr) • Expressed in mls/min |
| Creatine clearance correct for body surface = | creat clear X 1.73/area(nomogram) |
| Creatinine | • From creatine from muscle • Can also be measured to evaluate renal function; NOT as sensitive as GFR • Classic method is the Jaffe reaction |
| Blood Urea Nitrogen (BUN) | • ⬆ in impaired renal function • Rises more rapidly than serum creatinine • Methods: Colorimetric method & Enzymatic method • BUN/creatinine ratio is normally about 10:1-20:1 |
| Blood Urea Nitrogen (BUN) methods: Colorimetric method | Uurea reacts with diacetyl monoxime to form a colored complex |
| Blood Urea Nitrogen (BUN) methods: Enzymatic method | Uurease hydrolyzed urea into ammonia which can be measured spectrophotometically or with ISSE Inhibited by anticoagulant, sodium fluoride Must NOT use anticoagulant for ANY enzyme analysis |
| Uric Acid | • End product of purine metabolism • ⬆ in gout, renal failure, and leukemia |
| Uric Acid method: Colorimetric method | • Urine acid reduces phophotungstic acid to tungsten blue which is measured spectrophotometically • Interferents include lipids and several drugs |
| Uric Acid method: Enzymatic assays are based on | The uricase reaction in which allantoin and H2O2 are produced and H2O2 is coupled to give a color product |
| Ammonia | • Derived from the action of bacteria on the contents of the colon • Metabolized by the liver normally • ⬆ plasma ammonia is toxic to the CNS |
| Hyperammonemia | • Advanced liver disease (most common) Reye’s syndrome Cirrhosis Viral hepatitis • Impaired renal function Blood urea is ⬆ (⬆ excretion into intestine, where it is converted to ammonia) |
| Ammonia specimen collecting and handling | • Sample must be placed on ice, centrifuged, and analyzed immediately (nitrogenous constituents will metabolize to ammonia causing false ⬆) • Poor venipuncture technique (probing) Incompletely filling tube |
| Endocrinology: Thyroid Hormones general info | • Stimulate many cell metabolic processes • Necessary for normal growth and development • TRH (thyrotropin releasing hormone) |
| TRH (thyrotropin releasing hormone) | • Stimulates the pituitary to release TSH • TSH stimulates the thyroid gland to produce both thyroxine (T4) and triiodothyronine (T3) |
| In the tissue T4 is converted to | T3 (the physiologically active product) |
| T4 concentration is much blank than T3 | Higher |
| T4 is bound to | Thyroxine-binding prealbumin (TBPA) and albumin |
| Only the blank fractions are metabolically active; the rest is for storage | Free • T4 99.97% is bound and 0.3% free • T3 99.5% bound and 0.5% free |
| Hyperthyroidism (⬆ T3 and T4) | • Symptoms include weight loss, heat intolerance, hair loss, nervousness, tachycardia, and tremor. • Most common cases is Grave’s disease • Pregnancy |
| Grave’s disease | • Autoimmune disorder • Antibodies to thyroid-stimulating hormone (TSH) receptors • Causes thyroid hyperactivity and suppression of TSH • Lab findings: Normal or ⬆ T3 and ⬆ T4 ⬇ TSH and anti-microsomal antibodies |
| Hypothyroidism | • Symptoms include fatigue, weight gain, decreased mental and physical output, cold intolerance • Cretinism- congenital • Myxedema- severe thyroid deficiency in adults • Hashimotos Thyroiditis |
| Hashimotos Thyroiditis | • Thyroid autoantibodies (antithyroglobulin and antimicrosomal antibodies) • Lab findings: ⬇ T3 and T4 ⬆ TSH |
| Test for Thyroid function | • Total thyroxine (T4) • Free T4 • Direct T3- RIA or EIA • T3 uptake |
| Remember Thyroid sisters go getter Gertrude Graves and morbid Matilda Myxedema | • Gertrude Graves everything is racing (⬆ T3 and T4 except ⬇TSH) • Matilda Myxedema everything is low (⬇ T3 and T4 except ⬆ TSH) |
| Androgens | • Male sex hormones, secondary sexual characteristics • Secreted by the testes, adrenals, and ovaries • ⬆ testosterone- precocious puberty in boys, testicular tumors, masculinization in females • ⬇ in hypogonadism |
| Estrogens | • Female sex hormones • Secreted by ovaries Estradiol- secondary sexual characteristics Estrone- metabolite of estradiol Estriol |
| Estriol | • ⬆ during fetal development in pregnancy • Steady increase should occur in the 3rd trimester • Monitors the integrity of the feto-placental unit • Decline or sudden change indicates a complication of the pregnancy |
| Increased estrogen | Precocious puberty in girls, feminization in males, pregnancy, oral contraceptives, polycystic ovary disease |
| Aldosterone | • Mineralocorticoid • Produced in adrenal cortex • Maintains blood pressure, promotes sodium reabsorption and potassium secretion |
| Hyperaldosteronism- Conn’s Disease | • ⬆ Na • ⬇ K • Hypertension |
| Hypoaldosteronism | • ⬇ Na and Cl • ⬇ cortisol • ⬇ hemoglobin • ⬇ urinary steroids • ⬇ ACTH in damage to hypothalamus or pituitary; ⬆ ACTH in adrenal damage |
| Cortisol | • Glucocorticoid • Produced in adrenal cortex • Functions Causes ⬆ glucose through gluconeogenesis and decreased carbohydrate use Inhibits protein synthesis Immunosuppressive and anti-inflammatory • Diurnal variation (highest in morning) |
| Increased Cortisol without diurnal variation | Cushing’s syndrome • Diabetes mellitus, ⬇ plasma protein and hypertenstion • Truncal obesity, facial hair, ‘buffalo hump’, osteoporosis, scant menses |
| Decreased Cortisol | Addison’s disease • ⬇ Na and Cl • ⬇ cortisol • ⬇ hemoglobin • ⬇ urinary steroids • ⬇ ACTH in damage to hypothalamus or pituitary; ⬆ ACTH in adrenal damage |
| Test for Adrenal Cortex Function | • Cortisol • Dexamethasone • Aldosterone • Renin • ACTH |
| Test for Adrenal Cortex Function: Dexamethasone | • Suppresses cortisol in normal individuals • No suppression in Cushing’s • ⬆ in depression |
| Test for Adrenal Cortex Function: Aldosterone | • RIA • ⬆ in upright position |
| Test for Adrenal Cortex Function: Renin | • Estimated by angiotensin I generation • Very unstable (sample must be frozen immediately) • ⬆ in upright position • ⬇ in Conn’s |
| Test for Adrenal Cortex Function: ACTH | • RIA • Distinguishes between primary and secondary hyperaldosteronism |
| Remember the Steroid brothers Cushy Carl and Anemic Addison | • Cushy's problem is everything, ⬆ cortisol, glucose, Na, urinary steroids, ALD (aldosterone) • Addison's problem is everything is down, ⬇ cortisol, Na and Cl, Hgb, ALD, urinary steroids |
| Catecholamines | • Produced in adrenal medulla (chromaffin cells) Epinephrine, norepinephrine, and dopamine Homovanillic acid (HVA) is a metabolite of dopamine Metabolites of epinephrine include metanephrines and vanillylmandelic acid (VMA) |
| Test for catecholamines | • Metanephrines in urine, best screen for pheochromocytoma • VMA- screen for pheochromocytoma • HVA- screen for neuroblastoma • Catecholamines |
| Gastrointestinal hormones | • Gastrin- ⬆ in Zollinger-Ellison syndrome • Serotonin |
| Serotonin | • Vasoconstrictor in platelets, brain, other tissues • ⬆ production in tumors of chromaffin cells of GI tract • Measure breakdown 5-hydroxy-indole-acetic acid (5-HIAA), in urine • 5-HIAA falsely ⬆from drugs or food-bananas, pineapples, & chocolate |
| Oral glucose tolerance test results: • Fasting =75mg/dL • 30mins =82mg/dL • 1hr =85mg/dL • 90mins =80mg/dL • 2hrs =78mg/dL The results correlate with: • normal curve • diabetes • hypoglycemia • poor gastric absorption | Poor gastric absorption |
| What test would you ordered to monitor a diabetic patient's long term control • C-peptide of insulin • Glycosylated hemoglobin • Fasting plasma glucose • Postprandial plasma glucose | Glycosylated hemoglobin is the specific hemoglobin fractions to which glucose molecules become irreversibly attached. Average glucose level during the last 3 months |
| Lipid results • Cholesterol =175mg/dL (ref 140-200) • Triglycerides =205mg/dL (ref 40-155) • Serum turbid with cream layer on top These results most likely reflect: • Non-fasting • Normal • Nephrotic syndrome • Diabetes mellitus | Non-fasting specimens result in increased trigs and chylomicrons but do not affect cholesterol results. |
| What is the protein fraction that migrates most rapidly towards the anode is: • Albumin • Alpha-1 • Beta • Gamma | Albumin migrates the fastest because of its small size and negative charge |
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