Internal Medicine Practice Questions — USMLE Step 2 CK — Page 72

Match each clinical presentation with the most appropriate first-line targeted or empiric antimicrobial therapy.

Click a left item, then click its matching right item

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Answer

The camper with wrist/ankle rash requires oral doxycycline (RMSF); the IV drug user with right-sided endocarditis requires intravenous vancomycin (MRSA); the college student with purpuric meningitis requires intravenous ceftriaxone (Meningococcus); and the farmer with broad-based budding yeast requires oral itraconazole (Blastomycosis).

Each pathogen or clinical syndrome has a highly specific first-line antimicrobial agent guided by local epidemiology, resistance patterns, and pharmacokinetics (such as CNS penetration for meningitis or intracellular activity for rickettsial disease).

Step-by-Step Solution

1

Analyze the tick-borne disease vignette.

Identify Rocky Mountain Spotted Fever based on the North Carolina location and centripetal petechial rash starting on extremities.

Recognizing the classic triad of fever, headache, and distal rash points directly to Rickettsia rickettsii, which must be treated with doxycycline.

2

Analyze the infective endocarditis vignette.

Identify right-sided (tricuspid) endocarditis complicated by septic pulmonary emboli in an intravenous drug user.

Staphylococcus aureus is the most common pathogen in this demographic, necessitating robust empiric MRSA coverage with vancomycin.

3

Analyze the central nervous system infection vignette.

Identify meningococcal meningitis based on the demographic (dormitory resident) and characteristic purpuric rash.

Neisseria meningitidis is a leading cause of bacterial meningitis in this age group and requires a third-generation cephalosporin like ceftriaxone for optimal CNS penetration and coverage.

4

Analyze the systemic fungal infection vignette.

Identify Blastomyces dermatitidis based on geography (Ohio), verrucous skin lesions, and broad-based budding yeast morphology.

Matching the morphologic description to the pathogen determines the choice of an azole antifungal, specifically itraconazole, for non-life-threatening systemic disease.

Key Concept

Selection of optimal empiric or targeted antimicrobial therapy based on clinical presentation, epidemiologic risk factors, and microbiological clues.

Question 1422Question →

A $32$ -year-old man comes to the clinic to establish care after recently testing positive for human immunodeficiency virus (HIV). He is currently asymptomatic and has no history of opportunistic infections. Vital signs are within normal limits. Physical examination reveals no lymphadenopathy, oral thrush, or skin lesions. Laboratory evaluation shows a CD4 T-lymphocyte count of $38/\mu\text{L}$ and an HIV RNA viral load of $280,000$ copies/mL. Serologic testing is positive for *Toxoplasma gondii* IgG antibodies. An interferon-gamma release assay is negative. An antiretroviral therapy (ART) regimen consisting of bictegravir, emtricitabine, and tenofovir alafenamide is initiated today. In addition to ART, which of the following is the most appropriate prophylactic antimicrobial regimen for this patient?

Trimethoprim-sulfamethoxazole and azithromycin

Azithromycin only

Trimethoprim-sulfamethoxazole only

Trimethoprim-sulfamethoxazole and fluconazole

No prophylactic antimicrobials are indicated

Show answer & explanation

Answer: Trimethoprim-sulfamethoxazole only

Answer

Trimethoprim-sulfamethoxazole only

The correct answer provides targeted prophylaxis for the exact pathogens this patient is at risk for without inappropriately prescribing unneeded antimicrobials. A CD4 count

< 200/\mu\text{L}

necessitates prophylaxis against *Pneumocystis jirovecii* pneumonia, and a count

< 100/\mu\text{L}

combined with positive IgG antibodies requires prophylaxis against *Toxoplasma gondii*. Trimethoprim-sulfamethoxazole provides highly effective coverage for both. Although the CD4 count is

< 50/\mu\text{L}

, primary prophylaxis for *Mycobacterium avium* complex (MAC) is no longer recommended for patients who are immediately starting antiretroviral therapy.

Step-by-Step Solution

1

Analyze the patient's CD4 count and serologic status.

The CD4 count is

38/\mu\text{L}

(which is

< 200/\mu\text{L}

and

< 100/\mu\text{L}

) and Toxoplasma IgG is positive.

To identify which opportunistic pathogens the patient is currently at high risk for acquiring.

2

Identify the required primary prophylaxis regimens.

Prophylaxis is urgently required for Pneumocystis jirovecii (CD4

< 200/\mu\text{L}

) and Toxoplasma gondii (CD4

< 100/\mu\text{L}

with positive IgG). Trimethoprim-sulfamethoxazole effectively covers both.

To select the appropriate evidence-based antimicrobial agent.

3

Determine if Mycobacterium avium complex (MAC) prophylaxis is needed.

MAC prophylaxis (such as azithromycin) is not indicated because the patient is initiating fully suppressive antiretroviral therapy (ART) today.

Contemporary guidelines have removed the recommendation for MAC prophylaxis in patients starting ART, even when the CD4 count is

< 50/\mu\text{L}

.

Key Concept

In patients with HIV, primary prophylaxis for Mycobacterium avium complex (MAC) is no longer recommended if antiretroviral therapy is initiated immediately, but prophylaxis for Pneumocystis jirovecii and Toxoplasma gondii is still required based on CD4 thresholds.

Question 1423Question →

A 50-year-old male presents to the outpatient clinic reporting progressive weakness and a metallic taste in his mouth over the last several weeks. He has a 15-year history of poorly controlled hypertension. His blood pressure is $165/95 \text{ mm Hg}$ , pulse is $84/\text{min}$ , and respiratory rate is $22/\text{min}$ . Physical examination reveals trace bilateral lower extremity edema and a pale complexion. Laboratory studies are obtained and reveal the following:

Serum chemistry:
$Na^+$ : $140 \text{ mEq/L}$
$K^+$ : $5.2 \text{ mEq/L}$
$Cl^-$ : $102 \text{ mEq/L}$
$HCO_3^-$ : $12 \text{ mEq/L}$
Blood urea nitrogen: $85 \text{ mg/dL}$
Serum creatinine: $5.5 \text{ mg/dL}$

Arterial blood gas (room air):
pH: $7.25$
$pCO_2$ : $26 \text{ mm Hg}$
$pO_2$ : $95 \text{ mm Hg}$

Based on these findings, which of the following best describes this patient's current acid-base status?

High anion gap metabolic acidosis with appropriate respiratory compensation

High anion gap metabolic acidosis with superimposed respiratory acidosis

High anion gap metabolic acidosis with superimposed respiratory alkalosis

Normal anion gap metabolic acidosis with appropriate respiratory compensation

Primary respiratory alkalosis with appropriate metabolic compensation

Show answer & explanation

Answer: High anion gap metabolic acidosis with appropriate respiratory compensation

Answer

High anion gap metabolic acidosis with appropriate respiratory compensation

This patient has a high anion gap metabolic acidosis secondary to advanced chronic kidney disease (uremia). The diagnosis requires a systematic approach to the arterial blood gas and serum chemistry. The patient is acidemic (

pH = 7.25

). The primary driver of the acidemia is the low bicarbonate (

12 \text{ mEq/L}

), confirming a metabolic acidosis. Next, the anion gap is calculated as

Na^+ - (Cl^- + HCO_3^-) = 140 - (102 + 12) = 26 \text{ mEq/L}

. Because this is significantly higher than the normal range (

8-12 \text{ mEq/L}

), it is a high anion gap metabolic acidosis. Finally, Winter's formula (

1.5 \times HCO_3^- + 8 \pm 2

) is used to assess for a mixed disorder. The expected

pCO_2

is

(1.5 \times 12) + 8 = 26 \pm 2 \text{ mm Hg}

(range

24-28 \text{ mm Hg}

). Since the patient's measured

pCO_2

(

26 \text{ mm Hg}

) matches the expected value perfectly, this is a simple, fully compensated high anion gap metabolic acidosis.

Step-by-Step Solution

1

Determine the primary acid-base disturbance by evaluating the pH, pCO2, and bicarbonate.

The pH is

7.25

(acidemia),

pCO_2

is

26 \text{ mm Hg}

(low), and

HCO_3^-

is

12 \text{ mEq/L}

(low).

An acidic pH paired with a low bicarbonate identifies the primary process as a metabolic acidosis.

2

Calculate the serum anion gap using the formula:

AG = Na^+ - (Cl^- + HCO_3^-)

.

AG = 140 - (102 + 12) = 26 \text{ mEq/L}

.

Differentiating between a normal anion gap (

8-12 \text{ mEq/L}

) and a high anion gap guides the differential diagnosis. An AG of

26 \text{ mEq/L}

confirms a high anion gap metabolic acidosis, likely secondary to uremia given the elevated BUN and creatinine.

3

Apply Winter's formula to determine the expected respiratory compensation:

Expected\ pCO_2 = (1.5 \times HCO_3^-) + 8 \pm 2

.

Expected\ pCO_2 = (1.5 \times 12) + 8 \pm 2 = 18 + 8 \pm 2 = 26 \pm 2 \text{ mm Hg}

(range

24-28 \text{ mm Hg}

).

Calculating expected

pCO_2

is necessary to identify if a secondary, superimposed respiratory disorder is present.

4

Compare the measured

pCO_2

with the calculated expected

pCO_2

range.

The measured

pCO_2

is

26 \text{ mm Hg}

, which is exactly equal to the calculated expected value.

Because the measured value falls perfectly within the expected range, there is appropriate respiratory compensation without a superimposed respiratory disorder.

Key Concept

Evaluation of metabolic acidosis requires a step-wise approach: first calculating the anion gap, followed by calculating the expected respiratory compensation using Winter's formula (

Expected\ pCO_2 = 1.5 \times HCO_3^- + 8 \pm 2

).

Estimated Time:1m 0s

Question 1424Question →

An executive health screening is performed for a 45-year-old man who reports a 6-month history of significant fatigue, reduced libido, and a constant feeling of coldness. Physical examination shows a heart rate of $56/min$ , normal blood pressure, and delayed relaxation of the deep tendon reflexes. Laboratory evaluation reveals:

Thyroid-stimulating hormone (TSH): $1.1 \mu U/mL$ (Normal: $0.4 - 4.0 \mu U/mL$ )
Free thyroxine (T4): $0.4 ng/dL$ (Normal: $0.9 - 1.7 ng/dL$ )

Which of the following additional findings is most likely to be present in this patient?

Elevated serum anti-thyroid peroxidase antibody titers

Enlarged, firm, and rubbery thyroid gland on palpation

Elevated serum luteinizing hormone concentration

Decreased serum adrenocorticotropic hormone concentration

Elevated serum thyroid-stimulating immunoglobulin levels

Show answer & explanation

Answer: Decreased serum adrenocorticotropic hormone concentration

Answer

Decreased serum adrenocorticotropic hormone concentration

The patient's laboratory results (low free T4 with an inappropriately normal TSH) are diagnostic of central hypothyroidism, which is caused by a failure of the pituitary gland or hypothalamus to produce sufficient TSH. This is frequently due to a mass lesion such as a pituitary adenoma. When the anterior pituitary gland is compromised, other hormones are also frequently deficient (panhypopituitarism). Therefore, a decreased serum adrenocorticotropic hormone (ACTH) concentration, as well as decreased gonadotropins (LH, FSH) causing his reduced libido, would most likely be present.

Step-by-Step Solution

1

Interpret the thyroid function tests.

The patient has a low free T4 level, indicating hypothyroidism, but the TSH level is within the normal reference range.

To establish the primary hormonal abnormality.

2

Determine the etiology of the hypothyroidism based on the TSH response.

A low free T4 with an inappropriately normal (or low) TSH points to central (secondary) hypothyroidism, typically due to pituitary or hypothalamic dysfunction.

Primary hypothyroidism would present with an elevated TSH due to a lack of negative feedback on the intact pituitary gland.

3

Identify associated findings of pituitary dysfunction.

Patients with central hypothyroidism often have panhypopituitarism, which involves deficiencies in other anterior pituitary hormones, including adrenocorticotropic hormone (ACTH) and gonadotropins.

To predict what other clinical or laboratory abnormalities the patient might have.

Key Concept

Diagnosis of central hypothyroidism and recognition of associated panhypopituitarism

Estimated Time:1m 0s

Question 1425Question →

A 58-year-old woman is brought to the emergency department due to a 1-day history of fever, chills, and progressive shortness of breath. She completed her second cycle of systemic chemotherapy (docetaxel and cyclophosphamide) for node-positive breast cancer 8 days ago. Medical history is significant for ischemic cardiomyopathy (left ventricular ejection fraction 40%) and moderate chronic obstructive pulmonary disease. Her temperature is 38.9°C (102.0°F), blood pressure is 84/54 mm Hg, pulse is 118/min, and respirations are 24/min. Pulse oximetry shows 91% on room air. The patient appears lethargic. Jugular venous pressure is 6 cm H2O. Lung auscultation reveals crackles in the right lower lung base. Heart sounds are rapid but regular, with no S3 gallop. The extremities are warm to the touch. Laboratory results are as follows:

Hemoglobin: 9.8 g/dL
Leukocyte count: $600/\mu L$
Absolute neutrophil count: $120/\mu L$
Platelet count: $110,000/\mu L$
Creatinine: 1.4 mg/dL
Thyroid-stimulating hormone (TSH): $0.4\ \mu U/mL$
Free T4: $0.9\ ng/dL$

Which of the following is the most appropriate next step in the management of this patient?

Obtain blood cultures and administer intravenous cefepime

Administer intravenous furosemide and noninvasive positive pressure ventilation

Administer oral azithromycin and discharge with close outpatient follow-up

Transport the patient immediately for a CT pulmonary angiography

Administer intravenous levothyroxine and hydrocortisone

Show answer & explanation

Answer: Obtain blood cultures and administer intravenous cefepime

Answer

Obtain blood cultures and administer intravenous cefepime

The correct action is to obtain blood cultures and administer intravenous cefepime. This patient has febrile neutropenia (defined as a temperature > 38.3°C and an absolute neutrophil count < 500/μL), which is a life-threatening oncologic emergency. Her hypotension (84/54 mm Hg) and warm extremities strongly suggest distributive shock secondary to sepsis, likely from a pulmonary source given the right lower lobe crackles. In high-risk patients (e.g., those with hemodynamic instability or profound neutropenia), blood cultures must be drawn and empiric intravenous broad-spectrum antibiotics with anti-pseudomonal activity (such as cefepime, meropenem, or piperacillin-tazobactam) must be initiated immediately to prevent rapid clinical deterioration and death.

Step-by-Step Solution

1

Calculate Absolute Neutrophil Count (ANC) and evaluate vital signs.

ANC is 120/μL (< 500/μL) and patient is hypotensive with fever.

Identifies the clinical syndrome as high-risk febrile neutropenia with septic shock.

2

Differentiate the etiology of shock based on physical exam findings.

Warm extremities, normal JVP, and lack of an S3 gallop indicate distributive (septic) shock rather than cardiogenic shock.

Prevents inappropriate administration of diuretics which would worsen hypotension.

3

Determine the required initial therapeutic intervention.

Immediate blood cultures followed by an anti-pseudomonal beta-lactam (cefepime).

Febrile neutropenia is an oncologic emergency requiring emergent empiric broad-spectrum antibiotic therapy.

Key Concept

High-risk febrile neutropenia presenting with septic shock requires immediate empiric broad-spectrum intravenous antibiotics with anti-pseudomonal coverage.

Question 1426Question →

For each clinical presentation described below, select the most appropriate initial antimicrobial agent according to current guidelines.

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Answer

The presentations correspond to Lyme disease (Doxycycline), Herpes zoster (Valacyclovir), Group A Streptococcal pharyngitis (Penicillin V), and Gonococcal urethritis (Ceftriaxone).

Each match correctly pairs a classic infectious disease syndrome with its universally accepted standard-of-care antimicrobial therapy.

Step-by-Step Solution

1

Identify the primary diagnosis for each specific clinical presentation.

The diagnoses are early localized Lyme disease, herpes zoster, streptococcal pharyngitis, and gonorrhea.

Accurate clinical and laboratory diagnosis is required to select the appropriate pathogen-directed therapy.

2

Determine the guideline-recommended first-line antimicrobial for each established diagnosis.

Lyme disease requires doxycycline; herpes zoster requires valacyclovir; streptococcal pharyngitis requires penicillin V; gonorrhea requires ceftriaxone.

First-line agents maximize clinical efficacy while minimizing antimicrobial resistance and side effects.

Key Concept

First-line antimicrobial therapy for common outpatient infectious diseases

Question 1427Question →

A 42-year-old woman is diagnosed with severe, seropositive rheumatoid arthritis characterized by symmetric polyarthritis involving the metacarpophalangeal joints, morning stiffness lasting 2 hours, and bone erosions on radiography. She is preparing to begin long-term pharmacotherapy. Arrange the following clinical steps in the correct chronological sequence according to current consensus guidelines for the escalating management of rheumatoid arthritis.

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Answer

The correct chronological sequence is: initiate methotrexate, evaluate the clinical response at 3 months, perform an interferon-gamma release assay, prescribe a TNF inhibitor, and finally switch to an alternative mechanism biologic if the TNF inhibitor fails.

Rheumatoid arthritis management follows a strict algorithmic escalation. Methotrexate is the universal first step. Because csDMARDs require time to work, a 3-month evaluation is necessary before deciding on failure. If the disease remains active, biologic escalation is warranted. However, the initiation of any biologic (especially TNF inhibitors) requires immediate prior screening for latent tuberculosis and hepatitis B/C to prevent fatal reactivation. Once cleared, the TNF inhibitor is added. Finally, if the patient fails the TNF inhibitor trial, standard practice is to switch to a biologic with a different mechanism of action rather than cycling through another TNF inhibitor.

Step-by-Step Solution

1

Identify the standard first-line pharmacotherapy for a new diagnosis of severe rheumatoid arthritis.

The first step is initiating methotrexate alongside folic acid supplementation.

Methotrexate is the most effective initial csDMARD, serves as the anchor drug for rheumatoid arthritis, and reduces the risk of anti-drug antibodies if biologics are used later.

2

Determine the appropriate timeframe for evaluating the initial therapy.

The second step is evaluating the patient at a 3-month follow-up.

Conventional DMARDs take several months to reach full efficacy; premature escalation before an adequate trial should be avoided.

3

Recognize the required safety prerequisites before escalating to biologic therapy.

The third step is performing an interferon-gamma release assay (IGRA).

Biologics strongly increase the risk of tuberculosis reactivation, making infectious screening a mandatory chronological gatekeeper before their initiation.

4

Select the appropriate next line of therapy following csDMARD failure.

The fourth step is prescribing a TNF inhibitor as an add-on therapy.

Adding a biologic DMARD to background methotrexate is the standard of care for methotrexate non-responders.

5

Determine the management strategy if the initial biologic fails.

The final step is switching to an alternative mechanism biologic.

Patients who do not respond to a TNF inhibitor are typically transitioned to a biologic with a different mechanism of action, such as an IL-6 inhibitor or CD20 monoclonal antibody.

Key Concept

The stepwise escalation of pharmacotherapy in rheumatoid arthritis emphasizes initial csDMARD use, mandatory infectious screening immediately prior to biologic therapy, and class-switching upon primary biologic failure.

Estimated Time:1m 30s

Question 1428Question →

A $34$ -year-old woman is evaluated in the emergency department for a $2$ -day history of heavy gingival bleeding, recurrent epistaxis, and a large bruise on her thigh after minor trauma. Her temperature is $37.9^\circ\text{C}$ ( $100.2^\circ\text{F}$ ), pulse is $112/\text{min}$ , and blood pressure is $105/65 \text{ mm Hg}$ . Physical examination reveals pallor, diffuse petechiae over the chest and extremities, and continuous oozing of blood from the intravenous line insertion site. Laboratory studies show:

Test	Value	Normal Range
Hemoglobin	$7.8 \text{ g/dL}$	$12.0-15.5 \text{ g/dL}$
Platelet count	$18,000/\text{mm}^3$	$150,000-400,000/\text{mm}^3$
Leukocyte count	$32,000/\text{mm}^3$	$4,500-11,000/\text{mm}^3$
Prothrombin time	$21 \text{ sec}$	$11-15 \text{ sec}$
aPTT	$45 \text{ sec}$	$25-40 \text{ sec}$
Fibrinogen	$80 \text{ mg/dL}$	$200-400 \text{ mg/dL}$

A peripheral blood smear demonstrates numerous atypical mononuclear cells with folded nuclei, heavily granulated cytoplasm, and bundles of rod-shaped cytoplasmic inclusions.

Arrange the following management steps in the most appropriate chronological sequence for this patient.

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Answer

The correct sequence is: Administer all-trans retinoic acid (ATRA) -> Perform bone marrow aspiration and biopsy -> Obtain molecular confirmation of the PML-RARA fusion -> Initiate definitive induction therapy with arsenic trioxide.

The presentation of pancytopenia, severe coagulopathy (prolonged PT/aPTT, low fibrinogen), and a peripheral smear showing atypical cells with prominent bundles of Auer rods (faggot cells) is the classic manifestation of Acute Promyelocytic Leukemia (APL) complicated by disseminated intravascular coagulation (DIC). Because this coagulopathy can rapidly lead to fatal hemorrhage, the absolute first step in management is the immediate administration of all-trans retinoic acid (ATRA). This decision must be based purely on clinical and morphologic suspicion. ATRA forces the differentiation of leukemic promyelocytes into mature neutrophils, rapidly improving the coagulopathy. Once ATRA is administered and the patient's bleeding diathesis is acutely managed (often with cryoprecipitate, fresh frozen plasma, and platelets), a bone marrow aspiration and biopsy should be performed to secure the diagnostic material. The samples obtained are then sent for cytogenetic or molecular testing to confirm the presence of the

\text{t}(15;17)

translocation, which creates the PML-RARA fusion protein. Finally, once the diagnosis is definitively confirmed, combination induction therapy (often incorporating arsenic trioxide and/or an anthracycline alongside ATRA) is initiated to achieve complete remission.

Step-by-Step Solution

1

Analyze the clinical presentation and laboratory findings.

The patient has pancytopenia, clinical signs of disseminated intravascular coagulation (DIC), and atypical cells with bundles of Auer rods (faggot cells).

These findings are highly specific for Acute Promyelocytic Leukemia (APL), a medical emergency driven by the PML-RARA fusion protein.

2

Determine the most urgent, life-saving intervention.

Administration of all-trans retinoic acid (ATRA) is the immediate priority.

APL causes severe DIC leading to a high rate of early hemorrhagic death. ATRA induces differentiation of leukemic promyelocytes, rapidly resolving the coagulopathy, and must not be delayed.

3

Sequence the diagnostic and definitive treatment steps following initial stabilization.

Bone marrow biopsy is followed by molecular testing, which is then followed by targeted combination therapy.

Tissue acquisition must precede molecular confirmation. Once the specific genetic lesion is confirmed, final chemotherapeutic adjustments (such as adding arsenic trioxide) are made.

Key Concept

In patients with suspected Acute Promyelocytic Leukemia (APL) presenting with severe coagulopathy, all-trans retinoic acid (ATRA) must be administered immediately based on clinical suspicion, prior to bone marrow biopsy and molecular confirmation, to prevent fatal hemorrhage.

Estimated Time:1m 30s

Question 1429Question →

Match each clinical presentation with the most likely corresponding serum and urine laboratory findings.

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Answer

The correct matches correlate specific clinical syndromes with their pathognomonic acid-base and electrolyte derangements: Sjögren syndrome with Type 1 RTA, diabetic nephropathy with Type 4 RTA, vomiting with volume-responsive metabolic alkalosis, small cell lung cancer with SIADH, and lithium use with nephrogenic diabetes insipidus.

Each clinical vignette provides classic epidemiological and historical clues that point to a specific pathophysiology, which then dictates the expected serum and urine biochemical findings.

Step-by-Step Solution

1

Analyze the clinical vignette for the 32-year-old woman with Sjögren syndrome and kidney stones.

Diagnose Type 1 (distal) Renal Tubular Acidosis.

Sjögren syndrome is a classic autoimmune cause of distal RTA, which leads to calcium phosphate stones due to abnormally alkaline urine and bone buffering of the acidosis.

2

Analyze the diabetic patient's presentation with reduced GFR.

Diagnose Type 4 Renal Tubular Acidosis.

Diabetic nephropathy damages the juxtaglomerular apparatus, reducing renin and aldosterone, leading to hyperkalemia and a mild metabolic acidosis with appropriately acidic urine.

3

Analyze the patient with intractable emesis.

Diagnose volume-responsive metabolic alkalosis.

Gastric acid loss generates alkalosis, and volume depletion maintains it, with the kidney avidly reabsorbing chloride to restore volume (urine Cl < 20 mEq/L).

4

Analyze the smoker with a central lung mass.

Diagnose SIADH.

Ectopic ADH secretion from small cell lung cancer causes water retention, euvolemic hyponatremia, and natriuresis (urine Na > 40 mEq/L).

5

Analyze the bipolar patient on lithium presenting with polyuria.

Diagnose nephrogenic diabetes insipidus.

Lithium impairs ADH action in the collecting duct, leading to large volumes of dilute urine and hypernatremia if water access is insufficient.

Key Concept

Accurate diagnosis of acid-base and electrolyte disorders requires integrating the patient's clinical history (e.g., autoimmune disease, diabetes, fluid losses, malignancies, medications) with expected serum and urine biochemical patterns.

Estimated Time:3m 0s

Question 1430Question →

Match each patient's clinical presentation with the primary pathophysiologic mechanism or underlying diagnosis responsible for their electrolyte and acid-base disturbances.

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Answer

The correct matches link each distinct clinical presentation to its core pathophysiologic defect. Type 1 RTA matches to impaired distal hydrogen secretion; Type 2 RTA to impaired proximal bicarbonate reabsorption; Type 4 RTA to hypoaldosteronism; Gitelman syndrome to a distal tubule NCCT defect; and surreptitious vomiting to volume depletion with secondary hyperaldosteronism.

Each vignette represents a pathognomonic presentation for a specific nephrology disorder. Matching requires identifying the disease from the clinical clues (e.g., Sjogren for Type 1 RTA, Myeloma for Type 2 RTA, Diabetes for Type 4 RTA, hypocalciuria for Gitelman, and low urine chloride for vomiting) and linking it to its known pathophysiologic mechanism at the level of the nephron.

Step-by-Step Solution

1

Evaluate the acid-base and potassium status for each clinical vignette.

Patients 1, 2, and 3 have a normal anion gap metabolic acidosis (NAGMA). Patients 4 and 5 have metabolic alkalosis with hypokalemia.

Categorizing into acidosis versus alkalosis immediately narrows the differential diagnosis to Renal Tubular Acidosis (RTA) syndromes versus volume depletion/tubulopathies.

2

Differentiate the NAGMA patients (1, 2, and 3) by their serum potassium levels and urine pH.

Patient 3 has hyperkalemia, which is diagnostic of Type 4 RTA. Patients 1 and 2 have hypokalemia. Patient 1 has a urine pH > 5.5 (diagnostic of Type 1 RTA), while Patient 2 has a urine pH < 5.5 (diagnostic of Type 2 RTA).

Potassium is the key differentiator for Type 4 RTA. Urine pH distinguishes Type 1 (distal failure to acidify) from Type 2 (intact distal acidification once threshold is reached).

3

Differentiate the hypokalemic metabolic alkalosis patients (4 and 5) by their urine chloride levels and physical exam findings.

Patient 5 has a low urine chloride and physical signs of bulimia (vomiting). Patient 4 has hypocalciuria and normal blood pressure without vomiting signs, pointing to Gitelman syndrome.

Urine chloride distinguishes volume-depleted states such as vomiting (< 20 mEq/L) from renal potassium wasting syndromes like Gitelman or Bartter syndrome (> 20 mEq/L).

Key Concept

Differentiation of complex acid-base and electrolyte disorders requires integrating serum potassium, urine pH, urine chloride, and specific clinical features to identify the precise tubular or systemic defect.

Estimated Time:2m 0s

Question 1431Question →

Match each clinical presentation and coagulation profile with the most likely underlying hematologic diagnosis.

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Answer

Presentation 1 matches von Willebrand disease, 2 matches Hemophilia A, 3 matches DIC, 4 matches Vitamin K antagonist effect, and 5 matches Antiphospholipid syndrome.

Correctly identifying hematologic disorders requires integrating clinical signs (mucosal vs. joint bleeding, thrombosis vs. hemorrhage) with specific laboratory patterns. von Willebrand disease alters bleeding time and mucosal hemostasis. Hemophilia A causes isolated intrinsic pathway defects (prolonged aPTT) with deep joint bleeding. DIC globally consumes both platelets and factors. Vitamin K antagonists primarily affect the extrinsic pathway (isolated prolonged PT initially). Antiphospholipid syndrome presents with paradoxical thrombosis and an artifactual, non-correcting prolonged aPTT.

Step-by-Step Solution

1

Analyze presentation 1 focusing on mucosal bleeding and prolonged bleeding time.

Identify von Willebrand disease.

Prolonged bleeding time with normal platelets indicates a platelet function defect, typical of vWD which also sometimes prolongs aPTT.

2

Analyze presentation 2 focusing on joint bleeding and prolonged aPTT that corrects.

Identify Hemophilia A.

Correction on a mixing study confirms a factor deficiency (Factor VIII or IX) rather than an inhibitor. Hemarthrosis is classic for hemophilia.

3

Analyze presentation 3 focusing on sepsis and consumptive coagulopathy.

Identify Disseminated intravascular coagulation (DIC).

Simultaneous depletion of platelets and coagulation factors (prolonging both PT and aPTT) with elevated D-dimer is the hallmark of DIC.

4

Analyze presentation 4 focusing on isolated prolonged PT in an anticoagulated patient.

Identify Vitamin K antagonist effect.

Warfarin inhibits vitamin K-dependent factors. Factor VII has the shortest half-life, so PT prolongs before aPTT.

5

Analyze presentation 5 focusing on thrombosis, recurrent miscarriages, and non-correcting aPTT.

Identify Antiphospholipid syndrome.

A prolonged aPTT that fails to correct with normal plasma indicates the presence of an inhibitor (lupus anticoagulant), which is paradoxically prothrombotic.

Key Concept

Differentiation of bleeding and thrombotic disorders using clinical presentation, platelet count, PT, aPTT, and mixing studies.

Question 1432Question →

An 18-year-old male with homozygous sickle cell disease is brought to the emergency department due to a two-day history of progressively worsening chest pain, productive cough, and subjective fevers. Initial vital signs show a temperature of 38.8°C (101.8°F), blood pressure of 118/76 mm Hg, heart rate of 112/min, and respiratory rate of 26/min. Pulse oximetry reveals an oxygen saturation of 87% on room air. Physical examination is notable for scleral icterus and decreased breath sounds with crackles over the right lower lung fields. Laboratory evaluation demonstrates a hemoglobin of 7.2 g/dL, leukocyte count of 16,500/mm³, and reticulocyte count of 12%. A chest radiograph reveals a new consolidation in the right lower lobe.

What is the most appropriate chronological sequence for the management of this patient's condition?

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Answer

The correct chronological sequence is to first administer supplemental oxygen and analgesia, followed by empiric intravenous antibiotics, then perform an exchange red blood cell transfusion if clinical deterioration occurs, and finally prescribe daily oral hydroxyurea for long-term prevention after recovery.

The management of acute chest syndrome (ACS) follows a stepwise approach based on acuity. The absolute first priority is stabilization with supplemental oxygen to reverse hypoxia-induced sickling, accompanied by rapid pain control. Once the patient is stabilized, empiric antibiotics (e.g., ceftriaxone and azithromycin) are given because underlying pulmonary infections are the most common trigger for ACS and cannot be reliably distinguished from infarction. If the patient's respiratory status continues to decline or if they present with severe disease (e.g., needing mechanical ventilation), red blood cell exchange transfusion is indicated to rapidly replace HbS with normal hemoglobin. Finally, after the patient has recovered from the acute episode, long-term preventive therapy with hydroxyurea is initiated in the outpatient setting to increase fetal hemoglobin and reduce the frequency of future crises.

Step-by-Step Solution

1

Analyze the clinical presentation.

The patient has sickle cell disease and presents with fever, chest pain, hypoxia, and a new pulmonary infiltrate, which is diagnostic for acute chest syndrome (ACS).

Establishing the diagnosis of ACS determines the specific treatment pathway.

2

Determine the immediate resuscitative priorities.

Hypoxia and pain promote further red blood cell sickling. Providing supplemental oxygen and parenteral analgesics is the first necessary intervention.

Reversing the acute triggers of sickling prevents the microvascular occlusion from worsening.

3

Identify the underlying trigger and initial medical therapy.

Infection is a leading cause of ACS. Empiric antibiotics covering typical and atypical organisms must be started promptly after initial stabilization.

Pneumonia often triggers or is indistinguishable from ACS, making early antimicrobial therapy the standard of care.

4

Determine the intervention for potential clinical deterioration.

If respiratory status worsens despite initial measures, an exchange transfusion is necessary to acutely lower the hemoglobin S concentration.

Rapid removal of sickled cells restores adequate microvascular perfusion and oxygenation in refractory or severe cases.

5

Establish a long-term preventive plan.

Hydroxyurea therapy is planned for the outpatient setting once the patient recovers from the acute crisis.

Hydroxyurea increases fetal hemoglobin (HbF) and is indicated to prevent future episodes, but it has no role in acute management.

Key Concept

The management of acute chest syndrome in sickle cell disease begins with immediate supportive care (oxygen, pain control, fluids), followed by empiric antibiotics for potential infectious triggers, exchange transfusion for severe or refractory cases, and finally, long-term prevention with hydroxyurea.

Estimated Time:1m 30s

Question 1433Question →

An otherwise healthy 42-year-old male is evaluated in the ambulatory care center due to a painful swelling on his right thigh. The lesion has been progressively enlarging over the past three days. He takes no medications and has no significant past medical history. Vital signs demonstrate a temperature of 37.1°C (98.8°F), blood pressure of 122/78 mm Hg, and a heart rate of 74/min. Physical examination of the right anterior thigh reveals a 3-cm, highly tender, fluctuant, erythematous nodule with a central purulent punctum. There is no significant surrounding induration, and no regional lymphadenopathy is appreciated. Which of the following is the most appropriate next step in management?

Incision and drainage only

Incision and drainage followed by oral clindamycin

Incision and drainage followed by intravenous vancomycin

Oral dicloxacillin monotherapy

Topical mupirocin application

Show answer & explanation

Answer: Incision and drainage only

Answer

Incision and drainage only

The correct approach is incision and drainage only. The patient presents with a simple, uncomplicated cutaneous abscess, characterized by a fluctuant, tender nodule with a purulent center. In an otherwise healthy, immunocompetent patient with a single small abscess (typically <5 cm), no systemic signs of infection (such as fever or tachycardia), and minimal surrounding cellulitis, the definitive treatment is mechanical source control. Incision and drainage alone provides excellent cure rates. Systemic antibiotics are not indicated in this scenario.

Step-by-Step Solution

1

Evaluate the clinical presentation to determine the type and severity of the infection.

The patient has a localized, 3-cm fluctuant mass with a purulent punctum and normal vital signs, indicating a simple, uncomplicated cutaneous abscess.

Categorizing the infection is necessary to determine if both source control and systemic antibiotics are required.

2

Apply current treatment guidelines for an uncomplicated cutaneous abscess.

The standard of care for a single, small abscess in an immunocompetent patient without systemic symptoms is mechanical drainage.

Source control is the most critical intervention for purulent collections.

3

Determine if adjunctive antibiotics are indicated.

Adjunctive antibiotics are unnecessary as the patient lacks high-risk features (e.g., severe extensive surrounding cellulitis, systemic inflammatory response syndrome, immunocompromise).

Prescribing antibiotics when not indicated violates principles of antimicrobial stewardship.

Key Concept

Management of uncomplicated cutaneous abscesses

Question 1434Question →

An 18-year-old female gymnast is brought to the university health clinic by her roommate. She has been vomiting persistently for the past four days. The roommate mentions she has observed similar episodes in the past, though not this severe. Physical examination shows dry mucous membranes, poor skin turgor, and a pulse of 112/min.

Laboratory studies show the following:
- $Na^+$ : 139 mEq/L
- $K^+$ : 2.9 mEq/L
- $Cl^-$ : 94 mEq/L
- $HCO_3^-$ : 36 mEq/L

Arterial blood gas analysis on room air reveals:
- pH: 7.52
- $pCO_2$ : 48 mm Hg
- $pO_2$ : 94 mm Hg

Based on these findings, which of the following best characterizes this patient's acid-base status?

Primary metabolic alkalosis with appropriate respiratory compensation

Primary metabolic alkalosis with a superimposed primary respiratory acidosis

Primary metabolic alkalosis with a superimposed primary respiratory alkalosis

Primary respiratory acidosis with compensatory metabolic alkalosis

Primary respiratory alkalosis with compensatory metabolic acidosis

Show answer & explanation

Answer: Primary metabolic alkalosis with appropriate respiratory compensation

Answer

Primary metabolic alkalosis with appropriate respiratory compensation

This patient has a pH of 7.52, indicating an alkalemia. Her significantly elevated

HCO_3^-

of 36 mEq/L establishes that the primary disorder is a metabolic alkalosis, which is classically seen with severe vomiting (due to loss of gastric hydrochloric acid and volume contraction). To determine if a mixed disorder is present, the expected respiratory compensation must be calculated. The lungs compensate for metabolic alkalosis via hypoventilation, which increases the

pCO_2

. The formula for expected compensation is: Expected

pCO_2 = 40 + [0.7 \times (measured\ HCO_3^- - 24)] \pm 2

. For this patient, the expected

pCO_2 = 40 + [0.7 \times (36 - 24)] = 40 + 8.4 = 48.4 \pm 2

mm Hg (range 46.4 to 50.4 mm Hg). The patient's actual measured

pCO_2

of 48 mm Hg falls perfectly within this range, indicating an appropriate physiological respiratory compensation with no superimposed secondary acid-base disorder.

Step-by-Step Solution

1

Evaluate the pH to determine the overall acid-base direction.

The pH is 7.52, indicating an alkalemia (pH > 7.45).

The primary disorder must align with the direction of the pH deviation.

2

Examine the

pCO_2

and

HCO_3^-

to identify the primary etiology.

The

HCO_3^-

is significantly elevated at 36 mEq/L, which drives the alkalemia.

Elevated bicarbonate in the setting of alkalemia defines a primary metabolic alkalosis. This is consistent with the patient's history of vomiting, which causes loss of gastric acid (

H^+

) and volume contraction.

3

Calculate the expected respiratory compensation.

Expected

pCO_2 = 40 + [0.7 \times (36 - 24)] = 40 + [0.7 \times 12] = 40 + 8.4 = 48.4

mm Hg. The normal tolerance range is typically

\pm 2

mm Hg (46.4 - 50.4 mm Hg).

The lungs compensate for metabolic alkalosis by hypoventilating to retain

CO_2

. The formula

0.7 \times \Delta HCO_3^-

determines if the respiratory response is adequate.

4

Compare the measured

pCO_2

to the expected range.

The patient's actual

pCO_2

is 48 mm Hg, which is within the expected range.

Because the actual

pCO_2

matches the expected compensation, there is no superimposed secondary acid-base disorder.

Key Concept

Metabolic alkalosis respiratory compensation calculation

Question 1435Question →

A 19-year-old man with type 1 diabetes mellitus is brought to the emergency department due to lethargy, deep and rapid breathing, and a fruity breath odor. Laboratory results show a blood glucose of $580 \text{ mg/dL}$ , arterial pH of $7.12$ , serum bicarbonate of $10 \text{ mEq/L}$ , and a serum potassium of $5.6 \text{ mEq/L}$ . He is diagnosed with severe diabetic ketoacidosis (DKA).

Arrange the following management steps in the optimal chronological sequence for this patient.

Drag items to arrange them in the correct order

Show answer & explanation

Answer

The optimal sequence for managing diabetic ketoacidosis is: initial fluid resuscitation with

0.9\%

normal saline, followed by an intravenous insulin infusion, addition of potassium when levels drop into the normal range, addition of dextrose when glucose reaches

200 \text{ mg/dL}

, and finally transitioning to subcutaneous insulin when the anion gap closes.

Management of DKA requires a strict protocol to safely resolve the metabolic derangements. Initial fluid resuscitation with

0.9\%

normal saline restores intravascular volume. Once potassium is confirmed

>3.3 \text{ mEq/L}

, an intravenous regular insulin infusion is started to halt ketogenesis. As insulin therapy shifts potassium intracellularly, potassium must be added to maintenance fluids when serum levels drop

<5.2 \text{ mEq/L}

. Because blood glucose drops faster than ketones are cleared,

5\%

dextrose is added when glucose reaches

200 \text{ mg/dL}

to prevent hypoglycemia while maintaining the insulin drip. Finally, transition to subcutaneous insulin occurs once the anion gap closes and the patient can tolerate oral intake.

Step-by-Step Solution

1

Administer a rapid intravenous bolus of

0.9\%

normal saline

Restores intravascular volume and tissue perfusion

Severe osmotic diuresis leads to profound volume depletion. Reversing this shock state is the absolute top priority.

2

Initiate a continuous intravenous regular insulin infusion

Halts lipolysis and ketogenesis

Insulin drives glucose into cells and stops ketone production. It can be safely started because the initial potassium is well above the

3.3 \text{ mEq/L}

threshold.

3

Add potassium chloride to the intravenous fluids once serum potassium falls below

5.2 \text{ mEq/L}

Prevents severe hypokalemia

Despite total body potassium depletion, initial serum potassium is often high or normal due to acidemia. As insulin therapy drives potassium into cells, levels drop rapidly, requiring proactive supplementation.

4

Add

5\%

dextrose to the intravenous fluids once serum glucose reaches

200 \text{ mg/dL}

Prevents hypoglycemia while allowing insulin to continue

Blood glucose levels typically normalize faster than the ketoacidosis resolves. Dextrose must be given so the insulin drip can safely continue to close the anion gap.

5

Transition to a subcutaneous basal-bolus insulin regimen

Establishes long-term glycemic control

This transition is safe only when the acute crisis has resolved (evidenced by a closed anion gap) and the patient is able to eat.

Key Concept

Diabetic Ketoacidosis (DKA) Stepwise Management

Estimated Time:2m 0s

Question 1436Question →

A $62$ -year-old man with poorly controlled type 2 diabetes mellitus is admitted to the hospital with a non-healing ulcer on the plantar aspect of his right foot. The ulcer is surrounded by $4$ cm of erythema and warmth. During physical examination, a sterile metal probe easily reaches the underlying bone. His temperature is $38.2^\circ\text{C}$ ( $100.8^\circ\text{F}$ ), blood pressure is $130/80$ mm Hg, and pulse is $96$ /min. Laboratory studies show a leukocyte count of $14,500/\text{mm}^3$ . He is started on empiric intravenous vancomycin and piperacillin-tazobactam. A bone biopsy is performed on the second day of admission. By day $5$ , his fever has resolved, and the erythema has significantly decreased. The bone biopsy cultures grow only Staphylococcus aureus, which is sensitive to oxacillin, cefazolin, and clindamycin, but resistant to penicillin. No Gram-negative bacilli or anaerobes are isolated. Which of the following is the most appropriate next step in pharmacotherapy?

Discontinue the current regimen and begin intravenous cefazolin

Continue the current regimen of intravenous vancomycin and piperacillin-tazobactam

Discontinue intravenous vancomycin and continue intravenous piperacillin-tazobactam

Discontinue intravenous piperacillin-tazobactam and continue intravenous vancomycin

Discontinue the current regimen and begin oral ciprofloxacin and clindamycin

Show answer & explanation

Answer: Discontinue the current regimen and begin intravenous cefazolin

Answer

Discontinue the current broad-spectrum regimen and begin intravenous cefazolin to specifically target Methicillin-Susceptible Staphylococcus aureus (MSSA).

The correct answer is to discontinue the broad-spectrum regimen and begin intravenous cefazolin. This patient presented with a diabetic foot infection complicated by osteomyelitis, which appropriately prompted empiric therapy with vancomycin and piperacillin-tazobactam. The gold standard for diagnosing the causative organism in osteomyelitis is a bone biopsy. The culture unequivocally identified Methicillin-Susceptible Staphylococcus aureus (MSSA) as the sole pathogen, with no Gram-negative or anaerobic organisms isolated. According to the core principles of antimicrobial stewardship, therapy must be de-escalated to the most narrow-spectrum, effective agent once culture and susceptibility data are available. Intravenous cefazolin (or an anti-staphylococcal penicillin such as nafcillin) is the treatment of choice for MSSA osteomyelitis because it is highly efficacious, narrow-spectrum, and avoids the selective pressure for multi-drug resistant organisms.

Step-by-Step Solution

1

Identify the primary diagnosis and clinical scenario.

The patient has a diabetic foot ulcer with underlying osteomyelitis (indicated by a positive probe-to-bone test), initially appropriately treated with empiric broad-spectrum antibiotics.

To establish the baseline clinical state and the original indication for broad-spectrum therapy.

2

Interpret the definitive diagnostic data.

Bone biopsy culture at day 5 shows exclusively Staphylococcus aureus that is sensitive to oxacillin, confirming it is Methicillin-Susceptible S. aureus (MSSA).

Bone biopsy is the gold standard for defining the microbiology of osteomyelitis, superseding the initial assumption of a polymicrobial infection.

3

Apply principles of antimicrobial stewardship.

The empiric broad-spectrum coverage (vancomycin and piperacillin-tazobactam) must be de-escalated to target only MSSA.

To prevent antibiotic resistance, reduce toxicity, and provide the most efficacious targeted therapy for the specific pathogen isolated.

4

Select the optimal definitive pharmacotherapy.

Intravenous cefazolin is chosen.

Cefazolin is a first-generation cephalosporin and the drug of choice for severe MSSA infections, providing narrow-spectrum, highly bactericidal activity.

Key Concept

Antimicrobial stewardship dictates the de-escalation of empiric broad-spectrum antibiotics to targeted, narrow-spectrum therapy based on definitive culture results; intravenous cefazolin (or an anti-staphylococcal penicillin) is the treatment of choice for MSSA osteomyelitis.

Question 1437Question →

A female university student in her early $20$ s is evaluated in the rheumatology clinic for a $6$ -week history of profound fatigue and stiffness in her proximal interphalangeal joints. She notes that the skin across her cheeks becomes persistently red and painful after brief sun exposure. Over the past $14$ days, she has developed noticeable bilateral ankle swelling. Her blood pressure is $145/92$ mmHg. Laboratory evaluation shows a serum creatinine of $1.4$ mg/dL, and urinalysis demonstrates $3+$ proteinuria with red blood cell casts. Arrange the following clinical interventions in the standard chronological sequence for the definitive diagnostic workup and targeted management of this patient's underlying condition.

Drag items to arrange them in the correct order

Show answer & explanation

Answer

The correct chronological sequence is: 1) ANA screening, 2) Confirmatory anti-dsDNA/complement testing, 3) Percutaneous renal biopsy, 4) Targeted induction immunosuppressive therapy.

The evaluation of suspected Systemic Lupus Erythematosus (SLE) follows a strict sequence beginning with highly sensitive screening (ANA). If this is positive, highly specific markers (anti-dsDNA, anti-Smith) are evaluated to confirm the diagnosis. Because this patient exhibits clear signs of renal involvement (edema, proteinuria, RBC casts, elevated creatinine), a renal biopsy is the absolute critical next step to classify the lupus nephritis. Only after the histologic class is definitively established can the appropriate, targeted induction immunosuppressive therapy be safely initiated.

Step-by-Step Solution

1

Analyze the patient's clinical presentation.

The combination of inflammatory arthritis, photosensitive malar rash, and new-onset nephropathy (hypertension, edema, proteinuria, RBC casts) is highly suspicious for Systemic Lupus Erythematosus (SLE) with lupus nephritis.

Recognizing the syndrome dictates the necessary systemic workup.

2

Determine the optimal first diagnostic test.

Antinuclear antibody (ANA) assay is ordered first.

ANA is the most sensitive screening test for SLE and is universally the first step in the serologic evaluation of suspected connective tissue diseases.

3

Determine the subsequent confirmatory test.

Anti-dsDNA, anti-Smith, and complement levels (C3, C4) are measured.

Because ANA is sensitive but not specific, these highly specific markers confirm the diagnosis of SLE and establish baseline disease activity.

4

Address the end-organ involvement.

A percutaneous renal biopsy is performed.

Clinical and laboratory evidence of nephritis requires histologic classification (Classes I-VI) because treatment pathways diverge significantly based on the tissue pathology.

5

Determine the final management step.

Targeted induction immunosuppression is initiated.

Aggressive regimens (e.g., cyclophosphamide, mycophenolate) carry significant toxicity and are specifically indicated for proliferative forms of lupus nephritis (Class III and IV) as proven by biopsy.

Key Concept

Sequential evaluation and management of suspected Systemic Lupus Erythematosus and lupus nephritis

Estimated Time:1m 0s

Question 1438Question →

Match the following classic urinalysis sediment findings with the most appropriate renal pathology or clinical syndrome.

Click a left item, then click its matching right item

Show answer & explanation

Answer

Muddy brown granular casts match with acute tubular necrosis; RBC casts match with nephritic syndrome; WBC casts match with acute interstitial nephritis or pyelonephritis; fatty casts match with nephrotic syndrome; and broad waxy casts match with chronic kidney disease.

Each type of urinary cast provides specific clues about the anatomical site and mechanism of renal injury. Muddy brown casts reflect tubular cell death (ATN). RBC casts reflect glomerular bleeding (nephritic syndrome). WBC casts reflect interstitial inflammation (AIN or pyelonephritis). Fatty casts reflect lipiduria due to hyperlipidemia from severe proteinuria (nephrotic syndrome). Broad waxy casts reflect stasis in enlarged tubules of failing kidneys (CKD).

Step-by-Step Solution

1

Analyze the urinalysis finding of muddy brown granular casts.

Matches with acute tubular necrosis (ATN).

These casts represent necrotic tubular epithelial cells that have sloughed off into the tubular lumen due to toxic or ischemic injury.

2

Analyze the finding of red blood cell (RBC) casts.

Matches with nephritic syndrome.

RBC casts form when red blood cells pass through an inflamed and damaged glomerular basement membrane into the tubules.

3

Analyze the finding of white blood cell (WBC) casts.

Matches with acute interstitial nephritis or pyelonephritis.

WBC casts indicate inflammation in the tubulointerstitium (infection or allergic reaction) rather than the glomerulus.

4

Analyze the finding of fatty casts with a 'Maltese cross' appearance.

Matches with nephrotic syndrome.

Nephrotic syndrome is characterized by heavy proteinuria, leading to compensatory hyperlipidemia and subsequent lipiduria.

5

Analyze the finding of broad waxy casts.

Matches with chronic kidney disease.

Broad waxy casts form in dilated, hypertrophic tubules that have reduced flow in the setting of advanced and chronic renal disease.

Key Concept

Urinalysis cast patterns and associated renal pathologies

Question 1439Question →

A 45-year-old man is evaluated for treatment-resistant hypertension. His blood pressure remains consistently greater than 150/90 mm Hg despite documented compliance with a three-drug antihypertensive regimen that includes a thiazide diuretic. Recent laboratory testing revealed unprovoked hypokalemia with a serum potassium level of 2.9 mEq/L. The physician strongly suspects primary hyperaldosteronism and plans a complete diagnostic workup to determine if the patient is a candidate for surgical cure. Arrange the following diagnostic and management steps in the most appropriate chronological sequence for the evaluation of this patient.

Drag items to arrange them in the correct order

Show answer & explanation

Answer

The correct chronological sequence is to first screen with the aldosterone-to-renin ratio, confirm the diagnosis with a saline infusion test, localize the anatomy with an adrenal CT scan, and finally perform adrenal venous sampling to establish functional lateralization prior to surgery.

The evaluation of primary hyperaldosteronism follows a highly structured algorithm. The initial mandatory step is screening with the plasma aldosterone concentration to plasma renin activity ratio. If this ratio is elevated, the diagnosis must be biochemically confirmed with a suppression test, such as an intravenous saline infusion, which will fail to suppress aldosterone levels in patients with autonomous production. Once biochemically confirmed, the workup transitions to localization, beginning with a high-resolution adrenal CT scan. Because non-functioning adrenal incidentalomas are highly prevalent, particularly in middle-aged and older adults, an anatomic CT scan alone cannot reliably determine the source of aldosterone hypersecretion. Therefore, adrenal venous sampling is typically required in surgical candidates to functionally confirm unilateral disease (e.g., an aldosterone-producing adenoma) versus bilateral adrenal hyperplasia.

Step-by-Step Solution

1

Screening

Measure the ratio of plasma aldosterone concentration to plasma renin activity.

Screening is the universally required first step in the workup for suspected endocrine hypersecretion syndromes to determine if invasive or time-consuming testing is warranted.

2

Confirmation

Perform an intravenous saline infusion test.

Because screening tests have high sensitivity but lower specificity, a confirmatory test (such as saline infusion or oral sodium loading) is necessary to prove that the hormone secretion is autonomous and fails to suppress.

3

Anatomic Localization

Obtain a high-resolution CT scan of the adrenal glands.

Anatomy must be visualized first to rule out large suspected carcinomas and to assess for the presence of unilateral or bilateral adrenal nodules.

4

Functional Lateralization

Conduct adrenal venous sampling.

Anatomic imaging alone cannot reliably distinguish a functioning nodule from an incidental non-functioning nodule. Adrenal venous sampling confirms which adrenal gland is actively hypersecreting the hormone before a surgical adrenalectomy is performed.

Key Concept

The diagnostic algorithm for primary hyperaldosteronism follows a strict sequence: initial biochemical screening, confirmatory suppression testing, anatomic localization via CT scan, and functional lateralization via adrenal venous sampling.

Question 1440Question →

A 26-year-old male athlete undergoes an independent medical evaluation required for a specialized life insurance policy. He reports feeling exceptionally well and currently runs approximately $30\text{ miles}$ per week. His family history is notable for a younger brother diagnosed with attention-deficit/hyperactivity disorder, but there is no known history of autoimmune or endocrine diseases.

Vital signs include a heart rate of $64\text{/min}$ and a blood pressure of $118/74\text{ mm Hg}$ . Physical examination reveals a normal-sized, non-tender thyroid gland without palpable nodules. There is no evidence of proptosis, lid lag, hyperreflexia, or resting tremor.

Laboratory studies demonstrate:

Parameter	Patient Value	Reference Range
Thyroid-stimulating hormone (TSH)	$8.4 \mu\text{U/mL}$	$0.4-4.2 \mu\text{U/mL}$
Free thyroxine (T4)	$3.1\text{ ng/dL}$	$0.8-2.7\text{ ng/dL}$
Free triiodothyronine (T3)	$6.8\text{ pg/mL}$	$2.3-4.2\text{ pg/mL}$

An MRI of the brain with gadolinium contrast demonstrates a normal pituitary gland without sellar or suprasellar masses.

Which of the following is the most likely underlying mechanism for this patient's laboratory abnormalities?

Mutation in the gene encoding the thyroid hormone receptor

Monoclonal proliferation of anterior pituitary thyrotrope cells

Production of autoantibodies directed against thyroid peroxidase

Immunoglobulin-mediated activation of the thyrotropin receptor

Surreptitious ingestion of synthetic exogenous levothyroxine

Show answer & explanation

Answer: Mutation in the gene encoding the thyroid hormone receptor

Answer

The correct answer is a mutation in the gene encoding the thyroid hormone receptor, causing Resistance to Thyroid Hormone (RTH).

The correct answer identifies a mutation in the thyroid hormone receptor (specifically the beta isoform). This causes Resistance to Thyroid Hormone (Refetoff syndrome). The peripheral tissues and pituitary gland are resistant to T3/T4, preventing normal negative feedback. Consequently, the pituitary secretes more TSH, which drives the thyroid to produce high levels of T4 and T3. The patient remains clinically euthyroid (asymptomatic, normal heart rate) because the abnormally high hormone levels are just enough to overcome the receptor resistance.

Step-by-Step Solution

1

Analyze the laboratory pattern.

The patient has elevated Free T4 and Free T3 paired with an elevated TSH.

This pattern indicates a failure of negative feedback, narrowing the differential to central hyperthyroidism (TSHoma) or Resistance to Thyroid Hormone (RTH).

2

Evaluate the clinical presentation.

The patient has a normal heart rate (64/min) and lacks any symptoms of thyrotoxicosis.

TSHomas typically produce symptomatic hyperthyroidism, whereas patients with RTH are usually clinically euthyroid because the elevated hormone levels compensate for the receptor defect.

3

Correlate with imaging findings.

The brain MRI is completely normal.

A normal MRI effectively rules out a TSH-secreting pituitary macroadenoma, confirming the diagnosis of Resistance to Thyroid Hormone.

Key Concept

Resistance to Thyroid Hormone (RTH)

Estimated Time:1m 30s

Internal Medicine

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