Free FPGEE sample questions

Use the standard identification steps. Gram-positive cocci in clusters are staphylococci (streptococci grow in chains or pairs). The catalase test separates staphylococci (positive) from streptococci and enterococci (negative). The coagulase test then separates Staphylococcus aureus (positive) from coagulase-negative staphylococci such as S. epidermidis and S. saprophyticus.

S. aureus causes skin and soft tissue infections, bacteremia, endocarditis, osteomyelitis and toxin-mediated disease. Knowing whether it is MSSA or MRSA decides therapy: an anti-staphylococcal beta-lactam (cefazolin, nafcillin, oxacillin) for MSSA, and vancomycin, daptomycin or linezolid for MRSA.

IgG is the only antibody class actively transported across the placenta. Transport uses the neonatal Fc receptor (FcRn) on placental syncytiotrophoblast cells, and it increases sharply in the third trimester. Maternal IgG protects the newborn for roughly the first 6 months of life.

This explains several practice points: Tdap and RSV vaccines given during pregnancy protect the newborn through maternal IgG; preterm infants have less maternal antibody; and maternal IgG autoantibodies (Graves TSH-receptor antibodies, anti-Rh antibodies) can cross and affect the fetus.

A loading dose fills the volume of distribution to the target concentration at once: Loading dose = (Vd × Cp target) ÷ F (F = 1 for IV).

Step 1, total Vd: 0.7 L/kg × 70 kg = 49 L. Step 2, loading dose: 49 L × 15 mg/L = 735 mg.

The loading dose depends on Vd, not clearance; the maintenance dose depends on clearance (maintenance rate = CL × Cpss ÷ F). If an oral form with F = 0.5 were used, the loading dose would double to 1470 mg.

Use the Henderson–Hasselbalch equation for a weak acid: pH = pKa + log([ionized A⁻] / [un-ionized HA]). So log(ionized/un-ionized) = pH − pKa = 1.4 − 4.4 = −3, and the ratio = 10⁻³, i.e., 1 : 1000.

Rule of thumb: an acid in an acidic environment stays mostly un-ionized ("like in like"), and the un-ionized form is lipid-soluble and crosses membranes. A base in an acidic environment is mostly ionized. Each pH unit away from the pKa changes the ratio tenfold. Note that even for weak acids, most absorption happens in the small intestine because of its huge surface area.

Build the 2 × 2 table: TP = 90, FN = 10 (disease present); TN = 80, FP = 20 (disease absent).

Specificity = TN ÷ (TN + FP) = 80 ÷ 100 = 80%. It is the share of healthy people correctly identified as negative.

The other values from the same table: sensitivity = TP ÷ (TP + FN) = 90%; positive predictive value = TP ÷ (TP + FP) = 90 ÷ 110 = 81.8%; negative predictive value = TN ÷ (TN + FN) = 80 ÷ 90 = 88.9%; accuracy = (TP + TN) ÷ total = 170 ÷ 200 = 85%. Memory aid: SpPIn (a highly Specific test, when Positive, rules In) and SnNOut (a highly Sensitive test, when Negative, rules Out).

Absolute risk reduction (ARR) = control event rate − treatment event rate = 20% − 15% = 5% = 0.05. Number needed to treat (NNT) = 1 ÷ ARR = 1 ÷ 0.05 = 20.

So 20 patients must be treated for the study period to prevent one stroke. Round NNT up to the next whole number. For comparison, the relative risk reduction (RRR) = ARR ÷ control rate = 5 ÷ 20 = 25%, and the relative risk = 15 ÷ 20 = 0.75. RRR can make a small benefit look large, which is why NNT is useful for clinical decisions.

Prasugrel has a boxed warning: it is contraindicated in patients with a history of stroke or TIA because of a higher risk of intracranial bleeding, and it is generally not recommended in patients 75 years or older (except high-risk situations such as diabetes or prior MI). Body weight below 60 kg also raises bleeding risk (the maintenance dose is reduced to 5 mg in that case). This patient has all three risk factors.

Ticagrelor (with aspirin no higher than 100 mg daily) or clopidogrel are the options. Dual antiplatelet therapy (DAPT) after ACS is usually continued for 12 months, with shorter courses considered for high bleeding risk. Ticagrelor side effects include dyspnea and bradyarrhythmias; clopidogrel effectiveness is reduced in CYP2C19 poor metabolizers.

For heart failure, the target serum digoxin level is about 0.5–0.9 ng/mL; higher levels add toxicity without benefit. Her level of 2.4 ng/mL is high, and her symptoms are classic toxicity: GI (nausea, anorexia), neurologic (confusion, fatigue) and visual (yellow-green tint, halos). Arrhythmias are the dangerous effects: frequent PVCs, bigeminy, AV block, and paroxysmal atrial tachycardia with block.

Digoxin is renally cleared, so older adults with low CrCl and low body weight need lower doses (often 0.125 mg daily or less). Hypokalemia, hypomagnesemia and hypercalcemia increase toxicity, because potassium competes with digoxin at the Na/K-ATPase. Interacting drugs that raise digoxin levels: amiodarone, verapamil, dronedarone, clarithromycin. Life-threatening toxicity is treated with digoxin immune fab (DigiFab).