Chemistry Flashcards
(526 cards)
1
Q
AST is mainly found in what tissues?
A
Cardiac muscle.
Liver.
Skeletal muscle.
2
Q
A threefold elevation in AST can mean what?
A
Liver disease.
Rhabdomyolysis.
3
Q
At what time of day are AST and ALT highest?
A
In the afternoon.
4
Q
Tissues that contain LD1 and LD2.
A
Heart.
Red blood cells.
Kidneys.
5
Q
Tissues that contain LD4 and LD5.
A
Liver.
Skeletal muscle.
6
Q
Tissues that contain LD3.
A
Lungs.
Spleen.
Lymphocytes.
Pancreas.
7
Q
How to establish the hepatobiliary origin of alkaline phosphatase.
A
Measure 5’ nucleotidase or GGT.
8
Q
Which isoenzyme of alkaline phosphatase is most susceptible to heat and urea?
A
The isoenzyme of bone.
9
Q
Which isoenzymes of alkaline phosphatase are most susceptible to L-phenylalanine?
A
The isoenzymes of placenta and intestine.
10
Q
Physiological causes of elevated alkaline phosphatase (3).
A
Pregnancy.
Bone growth.
Postprandial state in group O or group B Lewis-positive secretors.
11
Q
Medications that can raise the alkaline phosphatase.
A
Oral contraceptives.
NSAIDS.
12
Q
Main source of 5’ nucleotidase.
A
Biliary epithelium.
13
Q
Main sources of ammonia.
A
Skeletal muscle and gut.
14
Q
Hyperammonemia: Causes in adults (3).
A
Liver failure.
Bypass of portal circulation.
Protein overload in the gut.
15
Q
Hyperammonemia: Pediatric cause.
A
Inborn error of metabolism.
16
Q
Hyperammonemia: Surgical cause.
A
Ureterosigmoidostomy.
17
Q
Hyperammonemia: Microbiological cause.
A
Infection with urea-splitting organisms.
18
Q
Hyperammonemia: Pharmacological causes.
A
Valproic acid.
TPN.
19
Q
Origin of urobilinogen.
A
Bacterial metabolism of conjugated bilirubin in the gut.
20
Q
What is δ-bilirubin?
A
Bilirubin that is covalently bound to albumin as a result of prolonged hyperbilirubinemia.
Very slowly cleared from the blood.
21
Q
How is conjugated bilirubin measured?
A
Directly, i.e. without the use of an accelerator.
22
Q
How is unconjugated bilirubin measured?
A
Use of an accelerator (alcohol) permits all bilirubin to be measured.
Total bilirubin − conjugated bilirubin = unconjugated bilirubin.
23
Q
Conditions that increase the delivery of unconjugated bilirubin to the liver.
A
Right heart failure.
Cirrhosis.
24
Q
Gilbert’s syndrome:
A. Definition.
B. Drugs that cause a similar condition.
A
A. Unconjugated hyperbilirubinemia due to mildly impaired conjugation; uptake of unconjugated bilirubin by the hepatocyte may also be impaired.
B. Rifampin, probenecid.
25
Crigler-Najjar syndrome:
A. Definition.
B. Cause of secondary disease.
A. Unconjugated hyperbilirubinemia due to impaired conjugation within the hepatocytes.
B. Hypothyroidism.
26
Dubin-Johnson syndrome:
A. Definition.
B. Pharmacological causes.
A. Conjugated hyperbilirubinemia due to impaired secretion into the canaliculus.
B. Estrogen, cyclosporine.
27
Cholestasis leads to what type of hyperbilirubinemia?
Conjugated.
28
Cholestatic vs. hepatocellular jaundice: Which one causes ___?
A. a greater elevation of alkaline phosphatase
B. a greater elevation of AST and ALT
C. elevated cholesterol
D. pruritus
A,C,D: Cholestatic.
B: Hepatocellular.
29
Relation of elevated PT to liver disease.
Indicates severe impairment of hepatocellular synthetic function.
30
Effect on immunoglobulins of
A. Autoimmune hepatitis.
B. Primary biliary cirrhosis.
A. Elevated IgG.
B. Elevated IgM.
31
Effect of liver disease on the ratio of serum albumin to serum immunoglobulins.
Decreased due to decreased albumin and increased immunoglobulins.
32
Physiologic neonatal jaundice:
A. Time of onset.
B. Velocity of rise in total bilirubin.
C. Time of peak of total bilirubin.
D. Usual maximum of total bilirubin.
A. About 2-3 days after delivery.
B. No more than 5 mg/dL/day.
C. Usually by day 4 or 5 after delivery.
D. No more than 20 mg/dL.
33
Pathological neonatal jaundice:
A. Time of onset.
B. Velocity of rise of total bilirubin.
C. Time of peak of total bilirubin.
D. Value of conjugated bilirubin.
A. Sometimes within the first 24 hours after delivery.
B. More than 5 mg/dL/day.
C. May continue to rise for more than a week.
D. >2 mg/dL.
34
Pathologic jaundice: Leading causes.
Sepsis.
Hemolytic disease of the newborn.
35
In uncomplicated pancreatitis, when does serum amylase rise and return to normal?
Rise: 2-24 hours.
Return to normal: 2-3 days.
36
Possible meaning of a prolonged rise in serum amylase with pancreatitis.
A complication such as a pseudocyst.
37
Relation of high serum amylase to pancreatitis.
Does not correlate with severity of pancreatitis but is more specific for pancreatitis.
38
Serum lipase:
A. How long it stays elevated in pancreatitis.
B. Advantages over serum amylase.
A. Up to 14 days.
B. More specific for pancreatitis; not affected by renal clearance.
39
Normal serum amylase in pancreatitis:
A. How often?
B. Associated types of pancreatitis.
A. In about 10% of cases.
B. Alcoholic; chronic relapsing.
40
Nonpancreatic causes of elevated serum amylase (9).
DKA.
Acute cholecystitis.
Peptic ulcer disease.
Bowel obstruction.
Bowel ischemia.
Ectopic pregancy.
Salpingitis.
Renal insufficiency.
Macroamylasemia.
41
Ranson's criteria upon admission:
Age: >55 years.
WBC >16,000.
AST >250.
LDH >350.
Glucose >200.
42
Ranson's criteria: After admission.
48 hours after admission:
```
Increase in BUN >5 mg/dL.
Calcium less than 8 mg/dL.
PaO₂ less than 60 mmHg.
Base deficit greater than 4 mEq/L.
Fluid sequestration >6 L.
Decrease in hematocrit >10%.
```
43
72-hour quantitation of fecal fat:
A. Procedure.
B. Interpretation.
A. High-fat diet is given for 3 days before collection and during the 3 days of the collection.
B. Fecal fat >20 g/day suggests exocrine pancreatic dysfunction.
44
Fluid chemistry: Pancreatic pseudocyst.
Elevated amylase and CA 19-9.
Normal CEA.
45
Fluid chemistry: Serous cystadenoma.
Deceased amylase, CA 19-9, CEA.
46
Fluid chemistry: Mucinous cystic neoplasm.
Elevated CEA, CA 19-9.
Normal amylase.
47
Fluid chemistry: Intraductal papillary neoplasm.
Elevated amylase, CEA.
Normal or elevated CA 19-9.
48
Fluid chemistry: Solid-cystic tumor.
Decreased amylase, CA 19-9, CEA.
49
Isoenzymes of creatine kinase.
CK-BB: Brain; fastest migration.
CK-MB: Mostly cardiac muscle; intermediate migration.
CK-MM: Mostly skeletal muscle; slowest.
50
Relative index:
A. Definition.
B. Interpretation.
A. Ratio of CK-MB to total CK.
B. A value >5% implies cardiac origin.
51
Macro-CK (type 1): Clinical association; migration.
Found in healthy elderly women.
Faster than CK-MM but slower than CK-MB.
52
Macro-CK, type 2:
A. Synonym.
B. Migration.
C. Clinical association.
A. Mitochondrial CK.
B. Slower than MM.
C. May be seen in advanced malignancy.
53
Troponin: Reference value.
Everything up to the 99th percentile.
54
Troponin: Non-ischemic cardiac causes of elevation (3).
Pericarditis.
Myocarditis.
Heart failure.
55
Troponin: Non-cardiac causes of elevation (5).
Pulmonary embolism.
Intracranial insults.
Shock.
Sepsis.
Renal insufficiency.
56
Troponin: Causes of analytical false positives.
Heterophile antibodies.
Fibrin.
57
Diagnosis of myocardial infarction: Abnormal initial troponin value.
Requires at least 20% elevation in cardiac TnI at 3 or 6 hours, plus supporting clinical evidence.
58
Diagnosis of myocardial infarction: Normal initial troponin value.
Requires at least a 50% increase in cardiac TnI at 3 or 6 hours, plus supporting clinical evidence.
59
Indication that elevated troponin may be of non-cardiac origin.
Chronic elevation.
60
Half-lives of BNP and NT-pro-BNP.
BNP: 20 minutes.
NT-Pro-BNP: 1-2 hours.
61
Albumin: Half-life.
17 days.
62
Prealbumin: Half-life.
48 hours.
63
Prealbumin: Functions.
Transport of the complex of vitamin A and retinoic-acid-binding protein.
Transport of thyroxine.
64
Prealbumin: Appearance of band on electrophoresis.
Serum: Inconspicuous.
CNS: Prominent.
65
How acute inflammation affects the serum proteins.
Albumin, prealbumin, and transferrin are decreased.
γ-globulins may be normal or decreased.
Everything else is increased.
66
How chronic inflammation affects the serum proteins.
Decreased: Albumin, prealbumin.
Increased: Everything else.
67
α₁ band of SPEP: Main component.
α₁-Antitrypsin.
68
α₂ band of SPEP: Main components.
α₂-Macroglobulin.
Haptoglobin.
Ceruloplasmin.
69
β₁ band of SPEP: Main component.
Transferrin.
70
β₂ band of SPEP: Main components.
IgA, C3.
71
γ band of SPEP: Main components.
Immunoglobulins, CRP.
72
Proteins found at the interfaces between bands on SPEP.
Albumin-α₁: HDL.
α₁-α₂: GC globulin, α₁-antichymotrypsin, α₁-acid glycoprotein.
α₂-β₂: Hemoglobin if there is hemolysis.
β₁-β₂: LDL.
β₂-γ: Fibrinogen if there is incomplete clotting.
73
Significance of α₂-macroglobulin (2).
Elevated in renal disease and liver disease.
Retained in the nephrotic syndrome.
74
Transferrin: Appearance on CSF electrophoresis.
Double peak due to partial asialation (to form the tau protein).
75
CRP: Analytic sensitivity of highly sensitive assays.
Detect as little as 0.5 mg/L.
76
CRP: Stratification of values.
3-10 mg/dL: Associated with low-level chronic inflammation and poor outcomes from cardiovascular events.
Greater than 10 mg/dL: Associated with inflammation and collagen-vascular diseases.
Less than 3 mg/dL: Normal.
77
SPEP: Nephrotic syndrome.
Fading of all bands except that of α₂-macroglobulin.
78
SPEP pattern: Acute inflammation.
Increased α₁ and α₂ bands.
Normal or decreased γ-globulins.
Everything else is decreased.
79
SPEP pattern: Cirrhosis.
Decreased albumin.
β-γ bridging.
Blunting of α₁ and α₂ bands.
80
Biclonal gammopathy:
A. Incidence.
B. Most common with which immunoglobulin?
A. 3-4% of M proteins.
B. IgA (because of monomers and dimers).
81
Pseudo-M spike: Causes (7).
```
Hemoglobin.
Fibrin.
Excess transferrin.
Excess CRP.
Excess of tumor markers, esp. CA 19-9.
Certain antibiotics.
Radiocontrast agents.
```
82
SPEP: Typical location of
A. IgG.
B. IgA.
C. IgM.
A. γ region.
B. β₂ region.
C. β-γ interface.
83
UPEP pattern: Glomerular proteinuria.
Bands at albumin and α₁ regions.
84
UPEP pattern: Tubular proteinuria.
Loss of small proteins that are normally filtered by the tubules, e.g. β₂-microglobulin, α₁-microglobulin, and light-chain immunoglobulins.
85
Causes of overflow proteinuria.
Hemoglobinuria.
Myoglobinuria.
Bence Jones proteins.
86
Type I cryoglobulins:
A. Definition.
B. Clinical associations.
A. Monoclonal immunoglobulins.
B. Multiple myeloma, Waldenström's macroglobulinemia.
87
Type II cryoglobulins:
A. Definition.
B. Clinical association.
A. Monoclonal IgM + polyclonal IgG.
B. Rheumatoid arthritis: The monoclonal IgM often has specificity for the Fc portion of IgG.
88
Type III cryoglobulins:
A. Definition.
B. Clinical association.
A. Polyclonal IgG and polyclonal IgM.
B. Rheumatoid arthritis.
89
Which cryoglobulins are considered mixed?
Types II and III.
90
Mixed cryoglobulinemias: Clinical associations (5).
Hepatitis C.
Chronic liver disease.
Chronic infections.
Lymphoproliferative disorders.
Autoimmune diseases.
91
Mixed cryoglobulinemias: Manifestations of the systemic immune-complex disease (7).
```
Palpable purpura (LCV).
Arthralgias.
Hepatosplenomegaly.
Lymphadenopathy.
Anemia.
Sensorineural deficits.
Glomerulonephritis.
```
92
Mixed cryoglobulinemias:
A. Most common type of renal disease.
B. How this disease appears on EM.
A. Membranoproliferative glomerulonephritis, type II.
B. Subendothelial electron-dense deposits in a fingerprint-like pattern.
93
SPEP: Usual pH.
8.6.
94
Immunofixation electophoresis: Steps.
1. Patient's sample is placed in 6 wells.
2. Electric current is applied.
3. Antisera for IgG, IgA, IgM, and κ and λ light chains are added.
95
Steps of immunophenotyping (immunofixation).
1. Patient's sample is added.
2. Microspheres with bound antibodies to IgG, IgA, IgM, and κ and λ light chain are added.
3. Electric current is applied.
4. Where the abnormal spike disappeared, one can see which bead took it away.
96
Cause of spurious hyponatremia.
Drawing the sample proximal to an intravenous or central line.
97
Pseudohyponatremia:
A. Type of analyzer affected.
B. Causes.
A. Any that uses the indirect method, in which the sample must be diluted first.
B. Hyperproteinemia, hypertriglyceridemia, hypercholesterolemia.
98
Pseudohyponatremia: Effect on osmolality and osmolality gap.
Osmolality is normal, but there is an increased osmolality gap.
99
Hypertonic hyponatremia: Causes.
Hyperglycemia.
Mannitol.
100
Hyponatremia due to hyperglycemia: Correction factor.
ΔNa = [1.6 × (serum glucose - 100)] / 100.
101
In the setting of true hypo-osmotic hyponatremia, what suggests that renal disease may be the cause?
Urine Na >30 mEq/L.
102
Hypovolemic hypo-osmotic hyponatremia: Causes (8).
Urine Na below 30: Vomiting, diarrhea, third-spacing.
Urine Na above 30: Diuretics, renal insufficiency, adrenal insufficiency, renal tubular acidosis, cerebral salt-wasting syndrome.
103
Euvolemic hypo-osmotic hyponatremia: Causes (5).
Urine Na below 30: Psychogenic polydipsia.
Urine Na above 30: SIADH, hypothyroidism, adrenal insufficiency, drugs (desmopressin, SSRIs, TCAs, MDMA, chlorpropamide).
104
Hypervolemic hypo-osmotic hyponatremia: Causes (4).
Cirrhosis.
Nephrosis.
CHF.
Renal failure.
105
Hypernatremia: Basic etiologies.
Inability to drink water.
Iatrogenic.
Diabetes insipidus.
106
Central diabetes insipidus: Causes.
Mass or trauma affecting the neurohypophysis and/or the hypothalamus.
107
Nephrogenic diabetes insipidus: Causes (6).
```
Renal medullary disease.
Hypercalcemia.
Hypokalemia.
Renal tubular acidosis.
Fanconi's syndrome.
```
Drugs: Demeclocycline, lithium, gentamicin, amphotericin B.
108
Hypokalemia is associated with which types of renal tubular acidosis?
Types 1 and 2.
109
Hypokalemia: Five eponymous diseases that can cause it.
Bartter's syndrome.
Gitelman's syndrome.
Liddle's syndrome.
Cushing's syndrome.
Conn's syndrome.
110
Hypokalemia can result from what other electrolyte abnormality?
Hypomagnesemia.
111
Hypokalemia: How to recognize a possible renal cause.
Urine K >30 mEq/day.
112
Hypokalemia: Nonrenal causes (3).
GI losses: Vomiting, diarrhea, villous adenoma, nasogastric suction.
Metabolic alkalosis.
Correction of diabetic ketoacidosis.
113
Hyperkalemia: Artifactual causes in vitro.
Leukocytosis.
Clotting.
Hemolysis.
114
Hyperkalemia: Artifactual causes during phlebotomy.
Blood draw proximal to infusion of potassium.
Excessive fist clenching.
Prolonged use of tourniquet.
Use of small-bore needle.
Traumatic blood draw.
115
True hyperkalemia: Causes (6).
Acidosis.
Addison's disease.
Iatrogenic.
Potassium-sparing diuretics.
Renal failure.
Rhabdomyolysis.
116
Relation between hyperkalemia and acidosis.
Acidosis is nearly always associated with hyperkalemia.
Exception: Renal tubular acidosis, types 1 and 2.
117
How much of calcium is bound to albumin?
About 50%.
118
How does pH affect the amount of free calcium?
Acidosis increases it.
Alkalosis decreases it.
119
Hypercalcemia: Finding on EKG.
High-peaked T waves.
120
Hypercalcemia: Neurological manifestations.
Lethargy.
Slowed mentation.
Depression.
Hyporeflexia.
121
Hypercalcemia: Possible gastroenterological complications.
Peptic-ulcer disease.
Pancreatitis.
122
Primary hyperparathyroidism: Laboratory findings (4).
Hypercalcemia.
Hypophosphatemia.
Increased ratio of chloride to phosphate.
Increased urinary cAMP.
123
Humoral hypercalcemia of malignancy: Causes (6).
```
SCC.
HCC.
RCC.
T-ALL.
Breast carcinoma.
Hypercalemic variant of small-cell carcinoma of the ovary.
```
124
Familial hypocalciuric hypercalcemia: Gene and its location.
CASR (calcium-sensing receptor) on 3q21.1.
125
Type of diuretic associated with hypercalcemia.
Thiazide.
126
Endocrinological causes of hypercalcemia (3).
Addison's disease.
Acromegaly.
Hyperthyroidism.
127
Forms of parathyroid hormone: Biological activities and half-lives.
Intact and N-terminal: Active; 5 minutes.
C-terminal and mid-portion: Inactive; longer half-life.
128
Hypocalcemia: Findings on EKG.
Low-voltage T waves.
Prolonged QT interval.
Dysrhythmias.
129
Leading cause of primary hypoparathyroidism.
Iatrogenic.
130
Relationship between hypomagnesemia and PTH secretion.
Transient or mild hypomagnesemia may stimulate secretion.
Prolonged or severe hypomagnesemia may suppress it.
131
Hypocalcemia: Genetic cause.
DiGeorge's syndrome.
132
Classes of diuretics that may cause hypocalcemia.
Loop diuretics.
Osmotic diuretics.
133
How renal failure can lead to hypocalcemia.
The excess serum phosphate chelates the calcium.
134
Acidemia vs. acidosis.
Acidemia: Acidic pH of the blood.
Acidosis: A condition that will lead to acidemia unless there is compensation.
135
Henderson-Hasselbalch equation.
pH = pKa + log([base]/[acid]).
7.4 = 6.1 + log[(24)/(0.03 × 40)].
136
Clue that a given acid-base disorder may be metabolic (or respiratory).
Metabolic: pH and bicarbonate move in the same direction.
Respiratory: pH and bicarbonate move in opposite directions.
137
Anion gap: Formula.
AG = [Na] − [Cl] − [bicarbonate].
138
Why is the anion gap normal in some forms of metabolic acidosis?
Because the chloride is elevated.
139
Causes of a decreased anion gap.
Hypoalbuminemia.
Paraproteinemia.
140
Osmolal gap: Formula and normal value.
OG = Measured osmolality − (2[Na] − [glucose]/18 − [BUN]/2.8).
Normal value: <10.
141
Causes of metabolic acidosis with an increased anion gap.
```
Methanol.
Uremia.
Diabetic ketoacidosis.
Paraldehyde.
Alcoholic ketoacidosis.
Lactic acidosis.
Ethylene glycol.
Salicylates.
```
142
Causes of metabolic acidosis with a normal anion gap.
```
Diarrhea.
Renal tubular acidosis.
Ureterosigmoidostomy.
NH₄Cl.
Carbonic anhydrase inhibitors.
```
TPN.
Recovery from diabetic ketoacidosis.
143
Causes of an increased osmolal gap with metabolic acidosis.
Ethylene glycol, propylene glycol.
Methanol.
Paraldehyde.
Ethanol (sometimes).
144
Causes of increased osmolal gap without metabolic acidosis.
```
Isopropanol.
Mannitol.
Acetone.
Glycerol.
Ethanol (sometimes).
Sorbitol.
```
145
How to tell whether metabolic alkalosis will respond to chloride.
Urine Cl less than 10 mEq/L: Responsive.
Urine Cl greater than 10 mEq/L: Resistant.
146
Causes of chloride-responsive metabolic alkalosis.
```
Diuretics.
Vomiting.
Villous adenoma.
Nasogastric suction.
Carbenicillin.
Contraction alkalosis.
```
147
Causes of chloride-resistant metabolic alkalosis.
```
Bartter's syndrome.
Milk-alkali syndrome.
Cushing's syndrome.
Hyperaldosteronism.
Exogenous corticosteroids.
Licorice.
```
148
Relationship between BUN and GFR.
The BUN underestimates the GFR, especially at higher concentrations of BUN.
149
Azotemia vs. uremia.
Azotemia: Elevated BUN.
Uremia: Azotemia with toxic effects.
150
Relationship between creatinine and GFR.
The creatinine overestimates the GFR, especially at higher concentrations of creatinine.
151
Creatinine clearance: Formula, typical reference range (including units).
CrCl = (urine creatinine ÷ plasma creatinine) × (urine volume ÷ time).
80-120 mL/minute.
152
At what point does the relationship between creatinine and GFR become linear?
When GFR is about half normal.
153
Nonglomerular influences on creatinine.
Muscle mass.
Muscle activity.
Muscle injury.
Protein intake.
Age, race, gender.
154
Ratio of BUN to creatinine: Normal.
About 10 to 1.
155
Ratio of BUN to creatinine: Causes of high value.
Prerenal azotemia.
Early postrenal azotemia.
156
Ratio of BUN to creatinine: Types of renal failure with a normal value.
Intrarenal azotemia.
Late postrenal azotemia.
157
Cystostatin C: Utility.
Estimates the GFR.
Strongly predicts cardiovascular mortality in patients with chronic renal disease.
158
Proteinuria:
A. Normal value.
B. Definition of "significant proteinuria".
A. 150 mg/day.
B. >300 mg/day.
159
Value of a random urine sample in screening for proteinuria.
A random urine protein and a concurrent urine creatinine are as good as a 24-hour urine protein in screening for proteinuria.
160
Proteinuria:
A. Sensitivity of the urine dipstick.
B. Sensitivity of the microalbuminuria screen.
A. 30 mg/dL.
B. 0.3 mg/dL.
161
Significant microalbuminuria:
A. Type of specimen.
B. Measured analytes and their units.
A. Random urine.
B. Albumin and creatinine in mg/g.
162
β₂-microglobulin and lysozyme.
A. Handling by the nephron.
B. Clinical utility.
A. Freely filtered by the glomerulus and completely reabsorbed by the tubules.
B. Their presence in the urine suggests renal tubular dysfunction.
163
Who should be testing annually for chronic kidney disease (according to the National Kidney Foundation)?
Those with diabetes, hypertension, or a family history of renal disease.
164
Chronic kidney disease: Recommended screening tests.
Microalbuminuria screen.
Estimated GFR.
165
Chronic kidney disease: Definition.
Estimated GFR <60
- or -
Microalbuminuria for 3 consecutive months.
166
Chronic kidney disease: Stages.
Stage 1: GFR >90 but with microalbuminuria.
Stage 2: GFR between 60 and 89.
Stage 3: GFR between 30 and 59.
Stage 4: GFR between 15 and 29.
Stage 5 (renal failure): GFR below 15, or dialysis dependent
167
Acute renal failure: Three basic types.
Prerenal, intrarenal, postrenal.
168
Intrarenal acute renal failure: Leading causes.
Acute glomerulonephritis.
Acute tubular necrosis.
169
Acute tubular necrosis: Leading causes.
Ischemia, toxins.
170
Urinary sediment: Glomerulonephritis.
Dysmorphic red cells, red-cell casts.
171
Urinary sediment: Acute tubular necrosis.
Tubular casts.
172
Urinary sediment: Pyelonephritis.
White-cell casts.
173
Urinary sediment: Allergic interstitial nephritis.
Eosinophils.
174
Drugs that cause acute tubular necrosis.
Contrast agents, aminoglycosides, amphotericin B.
175
Drugs that cause acute glomerular injury.
Cyclosporine, penicillamine.
176
Drugs that cause acute tubulointerstitial nephritis.
NSAIDs.
177
Fraction excretion of sodium: Formula.
FENa = (urine Na × plasma Cr) / (urine Cr × plasma Na).
178
Prerenal vs. intrarenal acute renal failure:
A. Ratio of BUN to creatinine.
B. Fractional excretion of sodium.
C. Fractional excretion of urea.
A. Prerenal: >10 to 1; intrarenal: about 10 to 1.
B. Prerenal: Less than 1%.
C. Prerenal: Less than 35%.
179
Hepatorenal syndrome: Frequent cause.
Profound fluids shifts resulting from treatment of ascites.
180
Bilirubin: Maximal absorbance by scanning spectrophotometry.
450 nm.
181
Oxyhemoglobin: Maximal absorbance.
About 410 nm.
182
Amniotic-fluid bilirubin: Range at which absorbances are measured.
340 to 560 nm.
183
What is the ΔOD450?
The difference between the measured absorbance at 450 nm and the theoretical absorbance based on the assumption that amniotic fluid contains no pigment.
184
What is a Liley chart used for?
To estimate the severity of fetal hemolysis. The ΔOD450 is plotted against the gestational age.
185
hCG: Molecular structure.
α subunit: Shared with FSH, LH, and TSH.
β subunit: Unique.
186
hCG: Leading cause of false positives.
Heterophile antibodies.
187
hCG: Conditions associated with pituitary production.
Pituitary tumor.
Postmenopausal state.
188
hCG: When it becomes detectable in a normal gestation.
At about 6-8 days after conception.
189
hCG: Phase and frequency of doubling.
About every 48 hours during the first trimester.
190
hCG: Peak during normal gestation.
About 100,000 mIU/mL near the end of the first trimester, followed by a slight decline and a plateau early in the 2nd trimester.
191
hCG: Causes of high value in an intrauterine pregnancy (4).
Multiple gestation.
Polyhydramnios.
Eclampsia.
Hemolytic disease of the fetus.
192
hCG: Clue to an ectopic pregnancy.
Failure to rise at least 66% within 48 hours.
However, this can be seen in up to 20% of normal pregnancies, and up to 20% of ectopic pregnancies show a normal rise in hCG.
193
hCG: Level after removal of
A. Ectopic pregnancy.
B. Uncomplicated molar pregnancy.
A. Can remain elevated for several weeks.
B. Can remain elevated for up to 10 weeks.
194
hCG: Schedule of monitoring after removal of uncomplicated molar pregnancy.
hCG is measured weekly until undetectable for 3 weeks, and then monthly for 1 year.
195
"Quad" screen:
A. Components.
B. When performed.
C. Sensitivity for detection of Down's syndrome.
A. hCG, AFP, unconjugated estradiol, dimeric inhibin A.
B. At 18 weeks of gestation.
C. 78%.
196
"First trimester" test:
A. Components.
B. When performed.
C. Sensitivity for Down's syndrome.
A. hCG, pregnancy-associated plasma protein A, thickness of nuchal fold as estimated by ultrasonography.
B. At 10-13 weeks.
C. 83%.
197
Integrated screens:
A. Components of the "serum integrated screen".
B. Components of the "full integrated screen".
C. Sensitivity of the latter for Down's syndrome.
A. hCG, AFP, uE, DIA, PAPP-A.
B. All of the above plus nuchal-fold thickness.
C. 88%.
198
How are serum gestational markers expressed for purposes of calculation?
As multiples of the mean (MoM).
199
What makes the cutoff between "positive" and "negative" in prenatal screening for Down's syndrome?
The theoretical risk for Down's syndrome in a child born to a healthy 35-year-old mother, i.e. 1 in 270.
200
Serum markers: Down's syndrome.
Elevated hCG, DIA.
Decreased AFP, uE.
201
Serum markers: Edwards' syndrome.
hCG, AFP, and uE are all decreased.
202
Serum markers: Neural-tube defect.
Elevated AFP.
Normal hCG.
Decreased uE.
203
Use of test for fetal fibronectin.
Absence of FF has a strong NPV, but its presence does not have a high PPV for imminent preterm birth.
204
Use of transvaginal ultrasound to predict imminent preterm birth.
High NPV but not a high PPV.
205
Fetal-lung maturity.
A. Accelerating factor.
B. Impeding factor.
A. Stressful pregnancy, i.e. corticosteroids.
B. Maternal diabetes mellitus.
206
Fetal-lung maturity: When testing becomes relevant.
At 32-38 weeks of gestation.
207
Fetal-lung maturity: Best specimen for testing.
Uncontaminated amniotic fluid.
208
Fetal-lung maturity: When a confirmatory test is indicated.
When the screening test yields a result below the cutoff for maturity.
209
Normal ratio of lecithin to sphingomyelin.
At least 2.5 to 1.
210
Ratio of lecithin to sphingomyelin: Confounding factors and their effects.
Meconium falsely decreases the ratio.
Blood normalizes it to 1.5.
211
Fetal-lung maturity: Preferred method of testing in diabetic mothers.
Phospatidylglycerol concentration.
212
Phospatidylglycerol concentration:
A. Advantage of this method.
B. Disadvantage.
A. Not affected by blood or meconium.
B. Cannot be used until 35-36 weeks of gestation.
213
Lamellar-body count:
A. Value that indicates fetal-lung maturity.
B. Limitations.
A. At least 50,000/mL.
B. Blood and meconium.
214
Fluorescence-polarization method: What is measured?
The ratio of surfactant to albumin, in mg/g.
215
Fluorescence-polarization method: Cutoffs for maturity and immaturity.
Maturity: Above 55 mg/g.
Immaturity: Below 40 mg/g.
216
How do the following analytes change during pregnancy?
A. Albumin.
B. Calcium.
C. Creatinine.
A. Decreases.
B. Decreases, but ionized calcium remains the same.
C. Decreases.
217
How do the following analytes change during pregnancy?
A. Fibrinogen.
B. BUN.
C. Urine protein.
A. Increases.
B. Decreases by about half.
C. Roughly doubles.
218
How do hematocrit and hemoglobin change during pregnancy?
Hematocrit: -4 to -7%.
Hemoglobin: -1.5 to -2 mg/dL.
219
What happens to responsiveness to insulin during pregnancy?
Human placental lactogen, secreted early in the third trimester, imparts relative insulin resistance.
220
How does the half-life of a drug affect the timing of doses?
A dose is given at the completion of each half-life.
221
By what kinetics are most drugs eliminated in the body?
By first-order (exponential) kinetics.
Elimination of ethanol follows zero-order kinetics.
222
Steady state:
A. Definition.
B. When it typically occurs.
A. The state in which the amount of drug entering the body equals the amount of drug leaving it.
B. After 4-5 half-lives.
223
How does the chemical composition of a drug influence its volume of distribution?
Lipophilic drugs have a large volume of distribution.
Hydrophilic drugs have a smaller volume of distribution.
224
Volume of distribution: Units and formula.
Volume of distribution =
Dose (mg) / concentration in plasma (mg/L) / body weight (kg).
225
What value of ___ would suggest alteration of urine to be tested for drugs of abuse?
A. creatinine
B. nitrite
A. Less than 20 mg/dL.
B. Greater than 500 mg/dL.
226
Window of detection: Cannabinoids.
Single use: 3 days.
Chronic use: Up to 30 days.
227
Window of detection: Benzodiazepines.
2-10 days, depending on the drug.
228
Window of detection: Amphetamines.
2-3 days.
229
Window of detection: Barbiturates.
3-15 days, depending on the drug.
230
Window of detection: Opiates.
2-3 days.
231
Window of detection: Ethanol.
One day.
232
Window of detection: Cocaine.
2-3 days.
233
Ethanol: Metabolism.
Converted by alcohol dehydrogenase to acetaldehyde, which is then converted by aldehyde dehydrogenase to acetic acid.
234
Ethanol: Ratio of concentration in breath to concentration in whole blood.
1 to 2100.
235
Ethanol: Correlation of concentration in the blood to clinical manifestations.
```
>0.05%: Sobriety.
0.05-0.1%: Euphoria.
0.1-0.2%: Excitement.
0.2-0.3%: Confusion.
0.3-0.4%: Stupor.
>0.4%: Coma and death.
```
236
Ethanol: Use of GGT to monitor consumption.
A normal GGT suggests abstinence for at least 4 weeks.
237
Ethanol: Use of carbohydrate-deficient transferrin to monitor consumption.
At least as sensitive and probably more specific than GGT.
238
Class of drugs associated with hyperthermia, dry skin, flushing, mental-status changes.
Anticholinergics.
239
Class of drugs associated with hypertension, mydriasis, tachycardia, anxiety.
Adrenergics.
240
Class of drugs associated with increased secretions, vomiting, gastrointestinal cramps, miosis.
Cholinergics / organophosphates.
241
Oxygen-saturation gap: Definition, normal value.
The difference between the oxygen saturation measured by co-oximetry and that measured by pulse oximetry.
Normally <5%.
242
Causes of abnormally high venous oxygen content.
Carbon monoxide.
Cyanide.
Hydrogen sulfide.
Azides.
243
Causes of increased oxygen-saturation gap.
Carbon monoxide.
Cyanide.
Hydrogen sulfide.
Methemoglobin.
244
How can one determine whether ethanol is responsible for an increased osmolal gap?
Modified calculated osmolality =
2*[Na] + [glucose]/18 + [BUN]/2.8 + [ethanol]/4.6.
245
Metabolites of each of the following alcohols:
A. Methanol.
B. Ethylene glycol.
C. Isopropanol.
A. Formaldehyde, formic acid.
B. Glycolic acid, oxalic acid.
C. Acetone.
246
Lead: Tissues in which it gets distributed.
Erythrocytes, bones, kidneys.
247
Lead toxicity: Mechanisms.
Binding to sulfhydryl groups.
Direct toxicity to mitochondria.
248
Lead toxicity: Affected enzymes of heme synthesis.
δ-ALA dehydratase.
Ferrochelatase.
249
Lead toxicity: Metabolites of heme synthesis that accumulate.
Zinc protoporphyrin.
Free erythrocyte protoporphyrin.
250
Lead toxicity: Other affected enzymes of erythrocytes.
5' nucleotidase.
ATPase of sodium channel.
251
Lead toxicity: Relationship to iron deficiency.
Both conditions increase the ZPP and the FEP.
Iron deficiency exacerbates lead toxicity.
252
Lead toxicity: Classical neurological sign.
Bilateral wrist drop.
253
Lead toxicity: Renal effects.
Glycosuria.
Aminoaciduria.
Phosphaturia.
254
Lead toxicity: Gastrointestinal effect.
Abdominal pain.
255
Lead toxicity: Diagnostic concentration.
At least 10 μg/dL in venous blood (by atomic-absorption spectrophotometry).
256
Carbon monoxide: Normal source; normal value of carboxyhemoglobin.
From the breakdown of heme.
<1%.
257
Carbon monoxide toxicity: Mechanisms.
Binding to hemoglobin.
Inhibition of cellular oxidative pathways.
258
Carbon monoxide toxicity: Nonspecific tests.
Anion gap.
Lactate level.
Cyanide level.
Cardiac enzymes.
259
Carbon monoxide toxicity: Specific test.
Co-oximetry.
260
Carbon monoxide toxicity: Correlation of level of carboxyhemoglobin to clinical manifestations.
>2%: Normal smoker.
2-6%: Normal nonsmoker.
10-20%: Dyspnea on exertion.
20-50%: Headache, lethargy, syncope.
>50%: Coma and death.
261
Acetaminophen toxicity: Phases.
1. Mild nausea and abdominal pain that abate within hours.
2. Progressive liver injury beginning after 24 hours.
3. Fulminant hepatic failure.
4. Recovery, transplant, or death.
262
When can one use the Rumack-Matthew nomogram?
No sooner than 4 hours after ingestion of acetaminophen.
263
Acetaminophen: Potentially toxic dose in healthy individuals.
150 mg/kg.
264
Acetaminophen: Nontoxic metabolism.
Conjugation with sulfate or glucuronide.
265
Acetaminophen: Toxic metabolite and its effect.
N-Acetyl-p-benzoquinoneimine.
Causes necrosis in zone 3 (centrilobular).
266
Cyanide toxicity: Mechanism.
Inhibits cytochrome a3, thus uncoupling the electron-transport chain.
267
Cyanide toxicity: Laboratory findings.
Anion gap with lactic acidosis.
Hyperglycemia.
Increased venous oxygen content.
268
Cyanide toxicity: Treatment.
Sodium nitrite and amyl nitrite convert hemoglobin to methemoglobin, which binds cyanide.
Sodium thiosulfate converts cyanide to nontoxic thiocyanate.
269
Salicylate toxicity: Associated acid-base abnormalities.
Respiratory alkalosis due to direct stimulation of medulla.
Metabolic acidosis, at first compensatory and then due to inhibition of oxidative pathways.
Respiratory acidosis due to CNS depression.
270
Arsenic toxicity: Distribution of arsenic in body fluids and tissues.
Skin, hair, nails, urine.
271
Arsenic toxicity: Mechanism.
Inhibits oxidative production of ATP.
272
Acute arsenic toxicity: Affected body systems.
Gastrointestinal tract: Nausea, vomiting, abdominal pain, bloody diarrhea.
Hematopoietic system: Basophilic stippling, cytopenias.
273
Chronic arsenic toxicity: Affected tissues.
```
Nerves (peripheral neuropathy).
Kidneys (nephropathy).
Skin (hyperpigmentation, hyperkeratosis).
Nails (transverse lines).
Marrow (myelodysplasia).
```
274
Arsenic toxicity: Best and worst tests.
Best: 24-hour urinary arsenic excretion.
Worst: Blood arsenic concentration.
275
Tricyclic antidepressants: Toxic effects.
Anticholinergic effects.
Prolongation of the QRS complex.
Ventricular dysrhythmias.
276
Organophosphate / carbamate toxicity: Laboratory tests.
Each of the following should be decreased:
Red-cell cholinesterase (more specific).
Plasma pseudocholinesterase (more sensitive).
277
Acute mercury intoxication: Clinical manifestations.
Respiratory distress.
Renal failure.
278
Chronic mercury intoxication: Clinical syndromes.
Acrodynia: Autonomic dysfunction, painful desquamating rash of palms and soles.
Erethism: Personality changes, irritability, loss of fine-motor coordination.
279
Mercury toxicity: Laboratory tests.
Elemental mercury: 24-hour urinary mercury excretion.
Organic mercury: Analysis of whole blood or hair.
280
Digoxin: Half-life.
36 hours.
281
Digoxin: When to take the sample for measurement of the drug level.
8-12 hours after the last dose.
282
Digoxin: Factors that can increase toxicity.
```
Hypercalcemia.
Hypomagnesemia.
Hypokalemia.
Hypoxia.
Hypothyroidism.
Quinidine.
Calcium-channel blockers.
```
283
Conditions that predispose to the production of digoxin-like immunoreactive substances (4).
Pregnancy.
Neonatal state.
Liver failure.
Renal failure.
284
Procainamide: Metabolite.
N-acetylprocainamide: Synthesized in the liver but cleared by the kidneys; has pharmacological activity of its own.
285
Aminoglycosides: Monitoring.
Peak: Efficacy.
Trough: Toxicity.
286
Lithium: Therapeutic range.
0.4 to 1.2 mmol/L.
287
Lithium: Range of possible toxicity.
>1.5 mmol/L.
288
Lithium: Schedule of routine monitoring.
Every 1-3 months, 12 hours after the last dose.
289
Lithium: Half-life.
8-40 hours.
290
Lithium: Monitoring after initiation of therapy or a change in dose.
After about 5 half-lives or about 2-8 days.
291
Lipoproteins: Lipids.
Chylomicrons, VLDL: Triglycerides.
IDL, LDL, HDL: Cholesterol.
292
Lipoproteins: Associated apolipoproteins.
```
Chylomicrons: B48, A-1, C-II, E.
VLDL: B100, C, E.
IDL: B100, E.
LDL: B100.
HDL: A-1, C, E.
```
293
Chylomicrons: Fate in the bloodstream.
Lipoprotein lipase removes the monoglycerides and the free fatty acids.
The remnants are taken up by the liver or the LDL receptor.
294
VLDL: Origin.
Hepatic metabolism and repackaging of triglycerides and cholesterol.
295
VLDL: Fate.
Lipoprotein lipase metabolizes it to IDL or eventually to LDL.
296
LDL: Purpose and fate.
Main carrier of cholesterol to cells.
Taken up by means of its apo-B100 and the LDL receptor.
297
HDL: Origin.
Synthesized in the liver.
298
Measured lipoproteins.
Total cholesterol, HDL, triglycerides.
299
Calculated estimate of VLDL:
A. Formula.
B. Invalidating factors.
A. VLDL ≈ Triglycerides ÷ 5.
B. Chylomicrons are present, TG >400 mg/dL, or there is type 3 dyslipidemia.
300
Method of direct measurement of lipoproteins.
Ultracentrifugation.
301
Effect of excess of lipoproteins on refrigerated plasma.
Chylomicrons: Cream layer.
VLDL: Turbidity or opacity.
Others: No visible change.
302
Lipid excess associated with eruptive xanthomas.
Triglycerides.
303
Lipoprotein excess associated with periorbital xanthelasma.
LDL.
304
Dyslipidemias associated with increased triglycerides and normal cholesterol.
Type I: Chylomicrons.
Type IV: VLDL.
Type V: Chylomicrons and VLDL.
305
Dyslipidemias associated with increased LDL and normal triglycerides.
Type IIa.
306
Dyslipidemias associated with increase in both triglycerides and LDL.
Type IIb: VLDL and LDL.
Type III: IDL and remnant lipoproteins.
307
Dyslipidemias associated with tendinous xanthomas.
Types IIa, IIb, and III.
308
Familial hypercholesterolemia:
A. Underlying defect.
B. Inheritance.
C. Lethal state.
A. Lack of LDL receptors.
B. Autosomal dominant.
C. Homozygosity.
309
Familial hypercholesterolemia:
A. Apolipoproteins normally taken up by the receptor.
B. Resulting lipoprotein excesses in disease.
A. Apo-B100, apo-E.
B. VLDL, IDL, LDL.
310
Hyper-apo-B-lipoproteinemia:
A. Associated dyslipidemia.
B. Excess lipoprotein.
C. Mechanism of disease.
A. Type IIa.
B. LDL.
C. The mutant apo-B100 does not bind normally to the LDL receptor.
311
IDL: Origin and fate.
Arises from the action of endothelial lipoprotein lipase on VLDL.
IDL gets taken up by the LDL receptor or converted by hepatic lipoprotein lipase to LDL.
312
Lp(a).
LDL with an added apolipoprotein A.
Increase in Lp(a) is associated with atherosclerosis.
313
Familial LPL deficiency: Associated type of dyslipidemia.
Type I.
314
Apolipoprotein C-II deficiency:
A. Associated type of dyslipidemia.
B. Mechanism of disease.
A. Type I.
B. Apolipoprotein C-II is needed for lipoprotein lipase to be able to act on chylomicrons.
315
Familial hypertriglyceridemia: Associated type of dyslipidemia.
Type IV.
316
Familial dysbetalipoproteinemia: Associated type of dyslipidemia.
Type III.
317
Familial combined hyperlipidemia:
A. Associated types of dyslipidemia.
B. Inheritance.
C. Underlying defect.
A. Types IIa, IIb, and IV.
B. Autosomal dominant.
C. Overproduction of apolipoprotein B100.
318
Hypercholesterolemia: Major primary cause.
Familial hypercholesterolemia.
319
Hypercholesterolemia: Secondary causes (7).
```
Diabetes.
Hypothyroidism.
Cholestasis.
Cyclosporine.
Loop diuretics.
Thiazide diuretics.
Nephrotic syndrome.
```
320
Hypertriglyceridemia: Primary causes.
LPL deficiency.
Apo-C-II deficiency.
Familial hypertriglyceridemia.
Familial combined hyperlipidemia.
321
Hypertriglyceridemia: Secondary causes (10).
```
Diabetes.
Pregnancy.
Obesity.
Renal insufficiency.
Hepatitis.
Nephrotic syndrome.
β-blockers.
Isotretinoin.
Corticosteroids.
Ethanol.
```
322
Mixed hypertriglyceridemia and hypercholesterolemia: Primary causes.
Familial combined hyperlipidemia.
Dysbetalipoproteinemia.
323
Tangier disease: Laboratory abnormalities.
Low total cholesterol.
Absence of HDL and apolipoprotein A-1.
324
Tangier disease: Clinical manifestations.
Deposition of cholesterol esters in tonsils, spleen, lymph nodes, corneas, and blood vessels.
325
Low HDL: Secondary causes.
Obesity.
Inactivity.
Smoking.
Anabolic steroids.
326
Risk factors for coronary heart disease.
Smoking.
Hypertension.
Low HDL.
Family history of early CHD.
Age.
327
Total cholesterol: Stratification (in mg/dL).
Desirable: <200.
Borderline: 200-239.
High: 240 or higher.
328
LDL cholesterol: Stratification (in mg/dL).
Optimal: Less than 100.
Near-optimal: 100-129.
Borderline: 130-159.
High: 160-189.
Very high: 190 or higher.
329
LDL target: Patient with 0 or 1 major risk factors.
<160 mg/dL.
330
LDL target: Patient with 2 or more major risk factors.
<130 mg/dL.
331
Coronary-heart-disease equivalents.
Diabetes.
Non-cardiac atherosclerosis.
Framingham risk for MI of 20% within 10 years.
332
Normal ratio of C peptide to insulin.
5-15 to 1.
333
Glycolysis in an unseparated tube of blood:
A. Rate.
B. Prevention.
A. About 5-10 mg/dL/hour.
B. NaF; takes 1-2 hours to act.
334
Correlation of glucose level in whole blood with that in plasma.
Whole-blood glucose tends to run about 10-15% lower.
335
How to use the HbA1c to estimate the average blood glucose.
Average glucose = (28.7 × HbA1c) − 46.7.
336
Hypoglycemia: Classification based on symptoms.
Fasting (neuroglycopenic): Gradual onset; altered mental status.
Reactive: Faster onset, more profound hypoglycemia; adrenergic symptoms.
337
Fasting hypoglycemia: Causes (other than fasting).
```
Insulinoma.
Nesidioblastosis.
Sarcomas, large.
Errors of metabolism.
Liver disease, end-stage.
```
338
Reactive hypoglycemia: Causes.
Dumping syndrome.
Early diabetes mellitus, type 2.
Fructose intolerance, hereditary.
Galactosemia.
339
Diabetes mellitus, type I: Targets of autoantibodies.
Insulin.
Islet cells.
Glutamic acid decarboxylase.
Insulinoma antigens IA2 and ICA512.
340
Diabetes mellitus, type I: Associated HLA loci.
DR3, DR4.
341
Diagnosis of nongestational diabetes mellitus: Methods (4).
HbA1c >= 6.5.
Fasting plasma glucose >=126 mg/dL.
Random plasma glucose >=200 mg/dL, plus supporting clinical evidence.
Plasma glucose >=200 mg/dL at 2 hr in a 75-g OGTT.
342
When are pregnant women tested for ___?
A. diabetes mellitus, type 2
B. gestational diabetes
A. At the first prenatal visit.
B. At 24-28 weeks of gestation.
343
75-gram OGTT: Values at which gestational diabetes is diagnosed.
Fasting: >= 92 mg/dL.
At 1 hr: >= 180 mg/dL.
At 2 hr: >= 153 mg/dL.
344
Monitoring of HbA1c: Frequency and goal.
At least twice a year; <7%.
345
Additional tests used in the monitoring of diabetes.
Annual tests:
- Estimated GFR based on creatinine.
- Microalbuminuria screen.
- Lipid panel.
346
Serum potassium in diabetic ketoacidosis.
Initially high due to metabolic acidosis, but drops due to transcellular shifts.
Total-body potassium is severely depleted.
347
Major serum ketones and their detection.
Acetone, acetoacetic acid, β-hydroxybutyrate.
The last is not detected by the nitroprusside method.
348
How hyperglycemic hyperosmotic non-ketotic coma (HHNC) differs from DKA.
HHNC:
```
Associated with diabetes mellitus, type 2.
Glucose often >1000.
Osmolality often >330.
Normal ketones.
Normal bicarbonate.
```
In HHNC and DKA, total K+ is severely depleted.
349
Tumor markers: Sources of error in their measurement.
Hook's effect can cause a falsely low values.
Heterophile antibodies can cause falsely low or falsely high values.
350
PSA: Percentage of men with an elevated value who have prostate cancer.
30-40%.
351
Guaiac test: How it works.
Hemoglobin has intrinsic peroxidase activity and can oxidize guaiac in the presence of hydrogen peroxide.
352
Guaiac test: Sources of error.
False positives: NSAIDs, exogenous heme, exogenous peroxidase.
False negative: Excessive intake of vitamin C.
353
CEA: Uses in colon cancer.
Preoperative prediction of outcome.
Postoperative monitoring.
354
CEA: Correlation of value with stage of colon cancer.
CEA is elevated in
25% of patients with disease confined to the colon,
50% of patients with nodal metastasis,
75% of patients with distant metastasis.
355
Non-colonic cancers in which CEA can be elevated.
```
Pancreatic.
Medullary thyroid.
Cervical.
Lung.
Urothelial.
Breast.
Stomach.
```
356
Benign causes of elevated CEA (7).
Peptic-ulcer disease.
Inflammatory bowel disease.
Pancreatitis.
Biliary obstruction.
Cirrhosis.
Smoking.
Hypothyroidism.
357
Thyroglobulin: Source of error.
Antithyroglobulin antibodies.
358
CA 125: Malignant causes of elevation.
Carcinomas of
- Ovary (nonmucinous).
- Fallopian tube.
- Endometrium.
- Pancreas.
- Breast.
- Colon.
359
CA 125: Benign causes of elevation.
```
Pregnancy.
Pelvic inflammatory disease.
Benign ovarian cyst.
Leiomyoma.
Endometriosis.
Ascites.
```
360
MUC1 protein: Epitopes of interest as tumor markers.
CA 27.29.
CA 15-3.
361
MUC1 protein: Relation of epitopes to stage of cancer.
Both epitopes are elevated in 60-70% of women with breast cancer of advanced stage.
362
CA 19-9: Relationship to cancer.
Elevated in 80% of patients with pancreatic adenocarcinoma at presentation.
363
CA 19-9: Source of error.
Absence of Lewis antigens.
364
α-fetoprotein: Benign causes of elevation.
Pregnancy.
Cirrhosis.
Hepatitis.
365
β₂-microglobulin: General cause of elevation.
Cell death.
366
β₂-microglobulin: Use as a tumor marker.
Independent prognostic factor in multiple myeloma.
367
Serotonin: Chemical name, major metabolite.
5-hydroxytryptamine.
5-hydroxyindoleacetic acid.
368
Products of foregut carcinoids.
5-hydroxytryptophan.
Histamine.
Catecholamines.
369
Products of midgut carcinoids.
Usually serotonin only.
370
Products of hindgut carcinoids.
Usually none.
371
Metabolism of catecholamines.
Epinephrine -> metanephrine -> vanillylmandelic acid.
Norepinephrine -> normetanephrine -> vanillylmandelic acid.
372
Metabolism of DOPA and dopamine.
Both are metabolized to homovanillic acid.
373
Neuroblastoma: Relatively specific tumor markers.
Vanillylmandelic acid and homovanillic acid.
374
Neuroblastoma: Nonspecific tumor markers.
Neuron-specific enolase.
Ferritin.
LDH.
375
NMP 22 test: Analyte; use.
The nuclear mitotic apparatus (NuMA) released by the dying cells of urothelial carcinoma.
376
BTA (bladder tumor antigen) test: Analytes.
Complement factor H.
Complement factor H−related protein.
377
Cause of hyperthyroidism other than elevated T4.
Elevated T3.
378
Proteins that bind thyroxine.
Thyroxine-binding globulin.
Prealbumin.
379
Causes of increase in thyroxine-binding globulin.
Estrogens.
Pregnancy.
Oral contraceptives.
Active hepatitis.
Hypothyroidism.
380
Causes of decreased thyroxine-binding globulin.
Hypoproteinemia.
Androgens.
Cortisol.
381
Correlation of T3 resin uptake with thyroid function.
High uptake: Hyperthyroidism.
Low uptake: Hypothyroidism.
382
Reverse T3: Definition; clinical significance.
Alternate metabolite of T4.
Elevated in the euthyroid sick syndrome.
383
Use of TRH in the work-up of hypothyroidism.
Increased secretion of TSH: Thyroidal problem.
Weak or no response: Pituitary problem.
384
Situations in which measuring the TSH alone may miss hypothyroidism.
Neonatal state.
Pituitary dysfunction.
Hypothalamic dysfunction.
385
What should be done when a low TSH is accompanied by a normal free T4?
Measure the free T3 to exclude T3 toxicosis.
386
Graves' disease: Autoantibodies.
Thyroid-stimulating antibodies.
Anti-thyroid peroxidase (antimicrosomal).
Anti-thyroglobulin.
387
Drugs that can cause hypothyroidism.
Iodine.
Lithium.
Interleukin-2.
IFN-α.
388
Hashimoto's thyroiditis: Antibodies.
Anti-thyroid peroxidase.
Anti-thyroglobulin.
389
Neonatal hypothyroidism: Leading cause.
Thyroidal dysgenesis.
390
Neonatal hypothyroidism: Other causes (5).
Dyshormonogenetic goiter.
Refetoff's syndrome.
Hypopituitarism.
Maternal autoantibodies.
Maternal drugs.
391
Euthyroid sick syndrome: Results of tests of thyroid function.
Elevated reverse T3.
Decreased T3.
Normal T4 and TSH.
392
Amiodarone: Effects on the thyroid function.
Often causes hyperthyroidism in iodine-poor areas and hypothyroidism in iodine-rich areas.
393
Lithium: Effect on thyroid function.
Prevents release of thyroxine.
394
Serum cortisol: Diurnal variation and relevance to testing.
Serum cortisol is highest around 8 a.m. and lowest around midnight.
A low morning cortisol suggests adrenal insufficiency. A high midnight cortisol suggests Cushing's syndrome.
395
Urine free cortisol: Advantage, disadvantage.
Not affected by diurnal variation.
Requires collection of urine for 24 hours.
396
Dexamethasone: Normal effect.
Suppresses secretion of cortisol and ACTH.
397
Low-dose dexamethasone suppression test: Purpose.
To determine whether a patient has Cushing's syndrome (hypercortisolism).
398
Low-dose dexamethasone suppression test: Types.
Standard: Two days.
Rapid: Overnight.
399
Low-dose dexamethasone suppression test: Causes of failure of suppression.
Hypercortisolism.
Severe stress.
Depression.
Alcoholism.
400
High-dose dexamethasone suppression test: Purpose.
To determine whether a patient has Cushing's disease (ACTH-producing pituitary adenoma).
401
High-dose dexamethasone suppression test: Interpretation.
Suppression: Pituitary adenoma.
No suppression: Measure plasma ACTH.
- High: Ectopic ACTH.
- Low: Primary hypercortisolism.
402
CRH stimulation test: Interpretation.
Exaggerated secretion of ACTH: Pituitary adenoma.
No response: Ectopic ACTH or primary hypercortisolism.
403
Cushing's syndrome: Recommended screening tests.
Low-dexamethasone suppression test.
24-hour urinary cortisol, or one-time serum or salivary cortisol collected at midnight.
404
ACTH-dependent Cushing's syndrome: Additional confirmatory test.
Sampling of bilateral inferior petrosal sinuses.
405
Hypercortisolism: Leading cause.
Exogenous corticosteroids.
406
Hormones secreted by the basophilic cells of the anterior pituitary.
FSH, LH, ACTH, TSH.
407
Adrenal insufficiency: Screening tests.
Cosyntropin stimulation test.
Morning cortisol.
408
Adrenal insufficiency: Additional test and its interpretation.
Plasma ACTH . . .
- High: Primary adrenal insufficiency.
- Low or normal: Pituitary disease or cessation of exogenous corticosteroids.
409
Adrenal insufficiency: Leading cause.
Autoimmune disease.
410
Adrenal insufficiency: Congenital causes.
Congenital adrenal hyperplasia.
Adrenoleukodystrophy.
411
Adrenal insufficiency: Pharmacological causes.
Ketoconazole.
Etomidate.
Mitotane.
412
Addisonian crisis: Acid-base disorder.
Metabolic acidosis.
413
Secondary adrenal insufficiency: Clinical differences from primary adrenal insufficiency.
Secondary adrenal sufficiency:
- Not as severe.
- Preserved mineralocorticoid function.
- No hyperpigmentation.
414
Hyperaldosteronism: Primary causes.
Adrenal hyperplasia.
Adrenal adenoma.
415
Hyperaldosteronism: Secondary causes.
Renal-artery stenosis.
Renin-secreting tumor.
416
Hyperaldosteronism: Acid-base and electrolyte abnormality.
Metabolic alkalosis.
Hypokalemia.
417
Hyperaldosteronism: Screening and confirmatory tests.
Screening: Ratio of plasma aldosterone concentration to plasma renin activity.
Confirmatory: 24-hour urinary aldosterone.
418
Congenital adrenal hyperplasia: Most common types.
21-hydroxylase deficiency.
11-hydroxylase deficiency.
419
21-hydroxylase: Location of gene.
6p21.3.
420
21-hydroxylase deficiency: Clinical manifestations.
Adrenal hyperplasia.
Virilization.
Salt-wasting in about one third of patients.
421
21-hydroxylase deficiency: Laboratory findings.
Increased ACTH.
Decreased cortisol and aldosterone.
Increased 17-ketosteroids and 17-α-hydroxyprogesterone.
422
11-hydroxylase deficiency: Laboratory findings.
Increased ACTH.
Decreased cortisol.
Increased 17-ketosteroids, deoxycorticosterone, and 11-deoxycortisol.
423
The stalk effect.
Disruption of the pituitary stalk leads to a decrease in all hormones except prolactin, whose secretion is normally inhibited by dopamine secreted by the hypothalamus.
424
Growth hormone: Stimulants of secretion.
Exercise.
Fasting.
Sleep.
Insulin.
Arginine.
425
Growth hormone: Tests for hypersecretion.
Markedly high random level of GH.
IGF-1: If low or normal, then there is no excess of GH.
Failure of glucose infusion to suppress GH.
426
Use of FSH level to diagnose early menopause.
A persistently high FSH suggests ovarian failure.
427
Hyperprolactinemia: Clinical manifestations in each sex.
Women: Galactorrhea, amenorrhea.
Men: Gynecomastia, testicular atrophy, impotence.
428
Hyperprolactinemia: Pharmacological cause.
Phenothiazines.
429
Nephrogenic diabetes insipidus: Physiologic cause.
Normal aging.
430
Diabetes insipidus: Diagnosis.
Overnight water-deprivation test.
If urine osmolality increases progressively, then DI is excluded.
Otherwise, urine osmolality will increase in response to exogenous ADH in central DI but not in nephrogenic DI.
431
What happens to postmortem glucose (2), and why?
Blood: Increases due to glycogenolysis.
Vitreous fluid: Decreases due to glycolysis.
432
What abnormality of glucose concentration can be diagnosed postmortem?
Diabetic ketaacidosis -- in vitreous fluid.
433
What happens to BUN and creatinine after death?
They remain stable.
434
What happens to sodium and chloride after death (2)?
Blood: They decrease immediately after death.
Vitreous fluid: They remain stable.
435
What happens to potassium after death (2)?
Blood, CSF: It increases abruptly.
Vitreous fluid: It increases linearly.
436
Postmortem chemical pattern of dehydration.
Increase in Na, Cl, BUN, creatinine.
Relatively normal K.
437
Postmortem chemical pattern of uremia.
Elevated BUN, creatinine.
Relatively normal Na, Cl, K.
438
Postmortem chemical pattern of decomposition.
Increased K.
Decreased Na, Cl.
Relatively normal BUN, creatinine.
439
Value of measuring postmortem tryptase.
A low or normal value makes anaphylaxis unlikely, but a high value does not prove it.
440
"Renal threshold" for glucose.
180 mg/dL.
441
Cause of glycosuria other than hyperglycemia.
Tubular dysfunction.
442
Sugars detected by the urine dipstick.
Mainly glucose; sensitivity for the other reducing substances is relatively low.
443
A test for sugars in the urine other than the dipstick.
Benedict's copper sulfate method detects glucose, fructose, galactose, lactose, maltose, and pentoses but not sucrose.
444
Types of proteinuria that are not associated with disease.
Positional.
Intermittent.
Exercise-induced.
445
Detection of ketones in the urine.
The dipstick detects acetoacetate better than acetone and does not detect β-hydroxybutyrate at all.
446
How to recognize hemoglobinuria.
Dipstick is positive for blood.
Haptoglobin is low.
Microscopy reveals hemosiderin-laden macrophages.
447
How to recognize myoglobinuria.
Dipstick is positive for blood.
Creatine kinase is elevated.
No evidence of hemoglobinuria.
448
Causes of increased urinary urobilinogen.
Liver disease.
Hemolysis.
449
Causes of false-positive leukocyte esterase.
Eosinophils.
Trichomonads.
450
Tests on the urine dipstick that may be inhibited by ascorbic acid.
Blood.
Bilirubin.
Glucose.
Leukocyte esterase.
Nitrite.
451
Urine pH:
A. In most cases of acidosis.
B. In renal tubular acidosis.
A. Around 6.
B. >=6.5.
452
Crystal morphology: Calcium oxalate.
"Envelopes".
453
Crystal morphology: Uric acid.
Squares, diamonds, rods.
454
Crystal morphology: Triple phosphate.
"Coffin lids".
455
Crystal morphology: Ammonium biurate.
"Thorn apples".
456
Crystal morphology: Cystine.
Hexagons.
457
Crystal morphology: Tyrosine.
"Sheaves of wheat".
458
Crystal morphology: Cholesterol.
"Broken window panes".
459
Crystal morphology: Sulfa.
"Fans".
460
Crystal morphology: Bilirubin.
Yellow-brown needles.
461
Top five urinary stones in order of decreasing frequency.
Calcium oxalate.
Calcium phosphate.
Triple phosphate.
Uric acid.
Cystine.
462
Factor predisposing to the formation of all types of urinary stones.
Low urinary volume.
463
Oxalate stones: Additional predisposing factors (3).
Hypercalciuria.
Oxaluria.
Low urinary citrate.
464
Oxalate stones: Disease associations.
Crohn's disease.
Resection or bypass of small bowel.
465
Calcium phosphate stones: Predisposing factors (2).
Hypercalciuria.
Alkaline urinary pH.
466
Triple-phosphate stones: Predisposing factor.
Infections by urea-splitting organisms.
467
Urate stones: Predisposing factors.
Hyperuricosuria.
Acidic urinary pH.
468
Cystine stones: Associated disease.
Cystinuria, an autosomal-recessive disorder of renal handling of cysteine, ornithine, lysine, and arginine.
469
Red blood cells: Glomerular-type bleeding (3).
Dysmorphic red cells.
Red-cell casts.
Erythrophagocytosis.
470
Red blood cells: Nonglomerular-type bleeding.
Normal morphology.
471
Hyaline casts: Clinical associations.
Renal disease.
Dehydration.
Heat injury.
Vigorous exercise.
472
Red-cell casts: Clinical association.
Glomerulonephritis.
473
White-cell casts: Clinical association.
Tubulointerstitial nephritis, esp. pyelonephritis.
474
Tubular casts: Clinical association.
Acute tubular necrosis.
475
Granular casts: Clinical associations.
Renal disease.
Dehydration.
Heat injury.
Vigorous exercise.
476
Waxy casts: Clinical associations.
Severe renal disease.
477
Broad casts: Clinical association.
End-stage renal disease.
478
Fatty casts:
A. Clinical association.
B. Unique morphology.
A. Nephrotic syndrome.
B. "Maltese cross" pattern with polarized light.
479
Amorphous crystals: Clinical association.
Usually insignificant.
480
Oxalate crystals: Toxicological association.
Ethylene glycol.
481
Biurate crystals:
A. Predisposing factor.
B. Clinical association.
A. Alkaline urinary pH.
B. Usually insignificant.
482
Tyrosine crystals: Clinical associations (3).
Tyrosinosis.
Liver disease.
Hyperbilirubinemia.
483
Pink xanthochromia: Interpretation.
Free hemoglobin in the CSF, as in subarachnoid hemorrhage.
484
Yellow xanthochromia: Interpretation.
Old (12 hours to 2 weeks) hemorrhage.
485
Artifactual xanthochromia: Causes (6).
Melanin.
Increased CSF protein (>150 mg/dL).
Severe hyperbilirubinemia.
Carotenoids.
Rifampin.
Delay of examination >1 hour.
486
Possible signs of a truly bloody tap.
Persistence of blood in all tubes.
Xanthochromia.
Hemosiderin-laden macrophages, erythrophagocytosis.
487
CSF protein: Normal value.
15-45 mg/dL.
488
CSF albumin: Normal ratio to serum albumin.
1 to 230.
489
How to detect a CSF leak from the nose or ear.
CSF has
- Less glucose.
- A double transferrin peak and a prominent prealbumin peak.
- Asialated transferrin.
490
CSF glucose relative to serum glucose:
A. Normal.
B. In bacterial meningitis.
A. About 60%.
B. <30%.
491
CSF IgG index:
A. Purpose.
B. Formula.
A. To assess for intrathecal production of immunoglobulin while controlling for a leak in the blood-brain barrier.
B. CSF IgG ÷ serum IgG / CSF albumin ÷ serum albumin.
492
Oligoclonal bands: Sensitivity and specificity for multiple sclerosis.
Sensitivity: 50-75%.
Specificity: 95-97%.
493
CSF: Normal cell count in adults and neonates.
Adults: 0-5/mL.
Neonates: 0-20/mL.
494
CSF: Normal lymphocyte percentage in adults and in neonates.
Adults: 30-90%.
Neonates: 10-40%.
495
CSF: Normal monocytes percentage in adults and in neonates.
Adults: 10-50%.
Neonates: 50-90%.
496
Bacterial meningitis: Typical CSF cell count.
1000 to 10,000/mL.
497
Bacterial meningitis: Typical concentration of protein in the CSF.
>100 mg/dL.
498
Bacterial meningitis: Dominant leukocytes.
Neutrophils; lymphocytes may predominate in partially treated infections.
499
Viral meningitis: Dominant leukocytes.
Neutrophils early, lymphocytes later.
500
Viral meningitis: Typical glucose concentration in CSF.
Normal; may be decreased in herpes encephalitis.
501
Light's criteria.
Any of the following will make it an exudate:
Effusion protein >= 0.5 that of serum.
Effusion LDH >= 0.6 that of serum.
Effusion LDH >= ⅔ of the upper limit of normal for the serum.
502
Transudates: Causes (3).
Cirrhosis.
Nephrosis.
CHF.
503
Chylous vs. pseudochylous effusions: Origin.
Chylous: Obstruction or disruption of the thoracic duct.
Pseudochylous: Lipids from dead cells.
504
Chylous vs. pseudochylous effusions: Chemical differences.
Chylous: Triglycerides often >110 mg/dL; chylomicrons on electrophoresis.
Pseudochylous: Triglycerides <50 mg/dL; no chylomicrons.
505
Congestive heart failure:
A. Frequent location of effusion.
B. Possible effect of treatment.
A. Right hemithorax.
B. Conversion of transudate to exudate.
506
Empyema: Criteria.
Neutrophils often >100,000/mL.
pH <7.2.
Bacteria on Gram stain.
507
Tuberculous pleural effusion: Laboratory findings.
Predominantly lymphocytic.
Few mesothelial cells.
Elevated adenosine deaminase.
508
Effusion associated with pulmonary embolism: Laboratory findings.
Usually bloody.
May show hyperplasia and/or atypia of mesothelial cells.
509
Pleural effusion associated with collagen-vascular disease: Chemical findings.
Often
LDH >700.
pH less than 7.2.
Glucose less than 30.
510
Pleural effusion associated with collagen-vascular disease: Cytological findings.
Much fibrin.
Few mesothelial cells.
Occasional histiocytes.
511
Neutrophilic pleural effusion: Causes.
Pulmonary embolism (early).
Empyema.
512
Lymphocytic pleural effusion: Causes.
Lymphoma.
Lymphatic obstruction.
Tuberculosis.
513
Eosinophilic pleural effusion: Causes.
Previous instrumentation.
Introduction of air into the pleural space.
514
Lack of mesothelial cells in a pleural effusion: Causes.
Rheumatoid pleural effusion.
Tuberculosis.
Pleurodesis.
515
Serum-ascites albumin gradient: Interpretation.
A value of greater than 1.1 g/dL suggests portal hypertension.
516
Peritoneal fluid: Significance of neutrophils.
A count of more than 250/mm³ suggests infection.
517
Peritoneal fluid: Significance of Gram stain.
A negative stain does not exclude spontaneous bacterial peritonitis.
Florid positivity suggests secondary bacterial peritonitis.
518
Synovial fluid: Effect of inflammation.
Reduces viscosity.
519
Normal synovial fluid: WBC count, neutrophils (%), difference in glucose from serum.
0-150.
<25%.
0-10.
520
Noninflammatory effusion: WBC count, neutrophils (%), difference in glucose from serum.
0-3000.
<25%.
0-10.
521
Inflammatory effusion: WBC count, neutrophils (%), difference in glucose from serum.
3000-75,000.
30-75%.
0-40.
522
Septic, gouty, or RA effusion: WBC count, neutrophils (%), difference in glucose from serum.
>100,000.
>90%.
0-100.
523
Septic arthritis: Significance of Gram stain.
Positive in only about half of cases.
524
Monosodium urate crystals: Length and birefringence.
2-20 μm, negatively birefringent needles.
525
Calcium pyrophosphate crystals: Length, birefringence.
2-20 μm, weakly positively birefringent "rhomboids, rods, or rectangles".
526
ALT is mainly found in what tissues?
Liver.
Kidney.
