Internal Medicine Alıştırma Soruları — USMLE Step 2 CK — Sayfa 104

Soru 2061Soru →

A 31-year-old female patient presents to the primary care clinic for evaluation of profound exhaustion, persistent constipation, and chronic cold intolerance that has worsened over the past 5 months. She also reports amenorrhea since the delivery of her child 10 months ago. Her obstetric history is significant for a complicated vaginal delivery involving a severe postpartum hemorrhage, which necessitated massive transfusion protocols and intensive care unit admission. Following discharge, she noticed an inability to lactate. Current vital signs show a temperature of 36.4°C (97.5°F), blood pressure of 105/70 mmHg, pulse of 58/min, and respiratory rate of 14/min. Physical examination is notable for coarse, dry skin, delayed relaxation phase of the deep tendon reflexes, and a marked absence of axillary and pubic hair.

Laboratory evaluation reveals the following:

Test	Result	Reference Range
Thyroid-stimulating hormone (TSH)	1.4 µU/mL	0.5 - 5.0 µU/mL
Free thyroxine (T4)	0.5 ng/dL	0.9 - 2.4 ng/dL

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

Initiate levothyroxine therapy

Measure serum thyroid peroxidase antibodies

Measure morning serum cortisol

Order an ultrasound of the thyroid gland

Reassure the patient and repeat thyroid function tests in 6 weeks

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Cevap: Measure morning serum cortisol

Cevap

Measure morning serum cortisol

The patient's presentation of fatigue, cold intolerance, constipation, amenorrhea, and failure to lactate following a severe postpartum hemorrhage is classic for Sheehan syndrome (postpartum ischemic necrosis of the pituitary gland). Her laboratory results show a low free T4 with an inappropriately normal TSH, confirming central hypothyroidism. In patients with suspected hypopituitarism, it is critical to evaluate for central adrenal insufficiency (secondary adrenal insufficiency) before initiating thyroid hormone replacement. Thyroid hormone increases the metabolic clearance of cortisol. If levothyroxine is given to a patient with undiagnosed adrenal insufficiency, it can rapidly deplete the remaining cortisol and precipitate a life-threatening adrenal crisis. Therefore, the most appropriate next step is to measure a morning serum cortisol level to assess adrenal function.

Adım Adım Çözüm

1

Analyze the patient's history and physical examination findings.

The patient has symptoms of hypothyroidism (fatigue, cold intolerance, delayed reflexes), hypogonadism (amenorrhea, loss of pubic hair), and prolactin deficiency (inability to lactate) following a massive postpartum hemorrhage.

This constellation of symptoms points toward ischemic necrosis of the pituitary gland, known as Sheehan syndrome.

2

Interpret the thyroid function tests.

The free T4 is low, confirming hypothyroidism, but the TSH is inappropriately normal (instead of being elevated).

A lack of TSH elevation in the setting of low T4 confirms a central (secondary) cause of hypothyroidism rather than primary thyroid failure.

3

Determine the safest next step in management.

Because panhypopituitarism involves multiple hormone deficiencies, adrenal function must be evaluated by measuring morning serum cortisol before any thyroid hormone replacement is given.

Administering levothyroxine increases the basal metabolic rate and the clearance of cortisol. In a patient with concurrent central adrenal insufficiency, this can quickly deplete remaining cortisol stores and precipitate a fatal adrenal crisis.

Anahtar Kavram

In patients with central hypothyroidism (e.g., from Sheehan syndrome), adrenal function must be evaluated with a morning serum cortisol level before initiating levothyroxine to prevent precipitating a life-threatening adrenal crisis.

Soru 2062Soru →

A 55-year-old man with a 15-year history of poorly controlled type 2 diabetes mellitus presents to the clinic with a deep, non-healing ulcer on the plantar surface of his right foot. Examination reveals a 2-cm wide ulcer with surrounding erythema, edema, and purulent exudate. The patient is afebrile, but underlying osteomyelitis is highly suspected. Arrange the following steps in the correct sequential order for the diagnostic evaluation of this patient, starting with the most appropriate initial step and concluding with the definitive diagnostic procedure.

Öğeleri doğru sıraya koymak için sürükleyin

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Cevap

The correct diagnostic sequence begins with a bedside clinical evaluation (probe-to-bone test), followed by baseline initial imaging (plain radiography). If initial imaging is inconclusive, advanced imaging (MRI) is performed, culminating in the definitive diagnostic test (bone biopsy).

The established diagnostic algorithm for suspected osteomyelitis progresses systematically from the least invasive and most accessible clinical tests to more sensitive imaging, and finally to definitive invasive procedures. Clinical examination via probing is the immediate first step. Plain radiographs act as the standard initial imaging to assess gross bony abnormalities and alternative diagnoses. Because early osteomyelitis may not be visible on X-ray for up to 14 days, an MRI is subsequent to evaluate marrow edema. Ultimately, a bone biopsy provides the definitive microbiological diagnosis necessary for tailoring long-term antibiotic therapy.

Adım Adım Çözüm

1

Perform a probe-to-bone test.

Assesses the depth of the ulcer and likelihood of bone involvement.

It is the most accessible, rapid, and least invasive initial clinical assessment for suspected osteomyelitis.

2

Order plain radiographs of the foot.

Rules out fractures, soft tissue gas, and evaluates for late-stage periosteal elevation or cortical erosion.

Standard initial imaging modality that must precede advanced imaging to serve as a baseline.

3

Order magnetic resonance imaging (MRI).

Detects early signs of osteomyelitis such as bone marrow edema.

Required when plain radiographs are non-diagnostic but clinical suspicion remains high, owing to its superior sensitivity.

4

Perform a bone biopsy.

Provides histological confirmation and accurate microbiological cultures.

Serves as the definitive gold standard for diagnosis and ensures appropriate pathogen-directed antibiotic therapy.

Anahtar Kavram

Diagnostic sequencing for diabetic foot osteomyelitis

Tahmini Süre:1m 0s

Soru 2063Soru →

A 54-year-old man presents to the emergency department with a 2-hour history of vomiting bright red blood and passing dark, tarry stools. His blood pressure is 90/60 mmHg, and his pulse is 118/min. Arrange the following management steps in the most appropriate chronological sequence for this patient.

Öğeleri doğru sıraya koymak için sürükleyin

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Cevap

The correct sequence is: Fluid resuscitation, followed by IV proton pump inhibitor, then esophagogastroduodenoscopy, and finally Helicobacter pylori testing and treatment.

The management of acute upper gastrointestinal bleeding follows a strict physiological priority list. Establishing circulation with intravenous fluids directly addresses the immediate life threat of hypovolemic shock. Once the patient is stabilized, an intravenous proton pump inhibitor is given to create a favorable gastric pH for clot formation. Esophagogastroduodenoscopy is then safely performed for definitive hemostasis. Finally, addressing the root cause (such as an H. pylori infection) is done in the post-acute phase to prevent future recurrence.

Adım Adım Çözüm

1

Assess hemodynamic status and begin fluid resuscitation.

The patient's hypotension and tachycardia indicate hemorrhagic shock, requiring immediate large-bore IV access and crystalloid fluids.

Circulation must be secured before any specific diagnostic or therapeutic maneuvers can be safely attempted.

2

Initiate pharmacologic acid suppression therapy.

Administration of an IV proton pump inhibitor increases gastric pH.

A higher gastric pH promotes hemostasis and clot stability over the bleeding site in the upper gastrointestinal tract.

3

Perform endoscopic diagnosis and treatment.

Esophagogastroduodenoscopy (EGD) is conducted to locate and treat the exact source of bleeding.

EGD allows for direct visualization and targeted therapeutic interventions, but is only safe once the patient is hemodynamically stable.

4

Implement secondary prevention measures.

Test for H. pylori and initiate appropriate eradication therapy if the result is positive.

Treating the underlying cause prevents future episodes of peptic ulcer bleeding and is part of the post-acute care plan.

Anahtar Kavram

In acute upper gastrointestinal bleeding, hemodynamic stabilization with intravenous fluids is the absolute first priority, followed by pharmacologic acid suppression, urgent endoscopic intervention, and finally long-term preventative care.

Soru 2064Soru →

A 64-year-old man is brought to the emergency department by his family due to a 2-day history of increasing confusion, low-grade fever, and abdominal discomfort. The patient has a history of decompensated cirrhosis secondary to metabolic dysfunction-associated steatotic liver disease (MASLD). He takes furosemide, spironolactone, and lactulose, but his family reports he has been less compliant with his medications over the past week. His temperature is $38.0^\circ\text{C}$ ( $100.4^\circ\text{F}$ ), blood pressure is $105/65\text{ mmHg}$ , and heart rate is $98/\text{min}$ . Physical examination reveals scleral icterus and a distended abdomen with shifting dullness. There is diffuse, mild abdominal tenderness without rebound or guarding. Asterixis is present.

Laboratory results are as follows:

Laboratory Parameter	Result
Hemoglobin	$10.5\text{ g/dL}$
Leukocyte count	$11,500/\text{mm}^3$
Platelet count	$82,000/\text{mm}^3$
Total bilirubin	$3.8\text{ mg/dL}$
Blood urea nitrogen	$36\text{ mg/dL}$
Serum creatinine	$1.6\text{ mg/dL}$

A diagnostic paracentesis is performed, yielding cloudy yellow fluid. Ascitic fluid analysis reveals:

Ascitic Fluid Analysis	Result
Total leukocyte count	$1,000/\text{mm}^3$
Neutrophils	$85\%$
Total protein	$1.1\text{ g/dL}$

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

Intravenous ceftriaxone and albumin

Intravenous ceftriaxone alone

Intravenous ceftriaxone and metronidazole

Intravenous piperacillin-tazobactam and vancomycin

Oral ciprofloxacin and intravenous albumin

Cevabı ve açıklamayı göster

Cevap: Intravenous ceftriaxone and albumin

Cevap

The most appropriate next step is to initiate intravenous ceftriaxone and albumin.

The correct answer is to administer both intravenous ceftriaxone and albumin. This patient's presentation of fever, confusion, and abdominal tenderness in the setting of cirrhosis strongly suggests spontaneous bacterial peritonitis (SBP). The diagnosis is confirmed by an ascitic fluid absolute neutrophil count of

850/\text{mm}^3

(diagnostic threshold is

\geq 250/\text{mm}^3

). Empiric treatment requires a third-generation cephalosporin (e.g., ceftriaxone) to cover enteric gram-negative organisms. Furthermore, SBP frequently triggers severe renal vasoconstriction, leading to hepatorenal syndrome (HRS). To prevent HRS, intravenous albumin is indicated in patients who meet high-risk criteria: a serum creatinine

> 1.0\text{ mg/dL}

, blood urea nitrogen (BUN)

> 30\text{ mg/dL}

, or total bilirubin

> 4.0\text{ mg/dL}

. Because this patient has a creatinine of

1.6\text{ mg/dL}

and a BUN of

36\text{ mg/dL}

, concurrent albumin administration is essential to reduce mortality.

Adım Adım Çözüm

1

Calculate the absolute neutrophil count in the ascitic fluid to confirm the diagnosis.

The absolute neutrophil count is

1,000 \times 0.85 = 850/\text{mm}^3

.

An ascitic fluid neutrophil count

\geq 250/\text{mm}^3

is diagnostic for spontaneous bacterial peritonitis (SBP).

2

Determine the optimal empiric antibiotic regimen for community-acquired SBP.

Intravenous third-generation cephalosporins (e.g., ceftriaxone or cefotaxime) are the treatment of choice.

They provide excellent coverage against the most common pathogens responsible for SBP, which are enteric gram-negative organisms (such as Escherichia coli and Klebsiella pneumoniae).

3

Evaluate the patient's renal function to determine if adjunctive therapy is indicated.

The patient has a blood urea nitrogen (BUN) of

36\text{ mg/dL}

and a serum creatinine of

1.6\text{ mg/dL}

.

Patients with SBP are at high risk for developing acute kidney injury (hepatorenal syndrome). Intravenous albumin is indicated if the patient has a BUN

> 30\text{ mg/dL}

, a serum creatinine

> 1.0\text{ mg/dL}

, or a total bilirubin

> 4.0\text{ mg/dL}

.

Anahtar Kavram

Diagnosis of spontaneous bacterial peritonitis requires an ascitic fluid absolute neutrophil count

\geq 250/\text{mm}^3

; treatment involves a third-generation cephalosporin and intravenous albumin for patients with elevated creatinine, BUN, or bilirubin.

Soru 2065Soru →

A $32$ -year-old woman is evaluated in the outpatient clinic for progressive exertional dyspnea and fatigue over the past $8$ months. She has no prior medical conditions and does not use tobacco. Vital signs are within normal limits, though pulse oximetry shows $94\%$ on ambient air. Physical examination is notable for a prominent right ventricular heave, a loud pulmonic component of the second heart sound ( $P_2$ ), and trace lower extremity pitting edema. The lungs are clear to auscultation. A chest radiograph reveals enlarged central pulmonary arteries with rapid tapering of the peripheral vessels. Electrocardiography shows right axis deviation.

Arrange the following diagnostic and therapeutic steps in the most appropriate sequential order for evaluating and managing this patient's suspected condition, from first to last.

Öğeleri doğru sıraya koymak için sürükleyin

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Cevap

The correct sequence is: Transthoracic echocardiography, followed by a V/Q scan, then right heart catheterization, followed by vasoreactivity testing with inhaled nitric oxide, and finally the initiation of targeted pulmonary vasodilator therapy.

The standard diagnostic algorithm for suspected pulmonary hypertension begins with a transthoracic echocardiogram to estimate pulmonary pressures and evaluate for left-sided heart failure. If echocardiography suggests pulmonary hypertension, the next essential step is a V/Q scan to evaluate for chronic thromboembolic pulmonary hypertension (CTEPH), as CTEPH is potentially curable with surgical pulmonary thromboendarterectomy. Once CTEPH and other secondary causes (like interstitial lung disease) are ruled out, a right heart catheterization is required to definitively confirm pulmonary arterial hypertension. During the catheterization, vasoreactivity testing (e.g., with inhaled nitric oxide) must be performed. Finally, the specific results of the invasive hemodynamic and vasoreactivity testing guide the initiation of targeted medical therapy.

Adım Adım Çözüm

1

Identify the primary clinical syndrome.

The patient presents with classic signs of isolated right heart strain and pulmonary hypertension (dyspnea, clear lungs, right ventricular heave, loud P2).

Recognizing pulmonary hypertension is required to enter the correct diagnostic algorithm.

2

Determine the initial non-invasive screening test.

Transthoracic echocardiography is ordered first.

Echocardiography estimates pulmonary artery systolic pressure and evaluates for left heart disease, which is the most common overall cause of pulmonary hypertension.

3

Select the appropriate imaging to rule out thromboembolic disease.

A ventilation/perfusion (V/Q) scan is performed next.

A V/Q scan is more sensitive than CT pulmonary angiography for chronic thromboembolic pulmonary hypertension (CTEPH) and must be done prior to invasive hemodynamics.

4

Confirm the diagnosis invasively.

Right heart catheterization is performed.

Direct measurement of mean pulmonary arterial pressure (mPAP) and pulmonary capillary wedge pressure (PCWP) is required to formally diagnose Group 1 Pulmonary Arterial Hypertension (PAH).

5

Test for vasoreactivity and initiate appropriate treatment.

Inhaled nitric oxide is administered during catheterization, followed by starting appropriate vasodilator therapy.

Vasoreactivity testing determines if the patient will respond to calcium channel blockers; otherwise, specific advanced PAH therapies are selected based on the definitive hemodynamic profile.

Anahtar Kavram

The precise sequential diagnostic algorithm for evaluating suspected pulmonary hypertension.

Soru 2066Soru →

A 52-year-old woman is evaluated in the emergency department for severe, watery diarrhea over the past five days. She reports feeling profoundly weak. She has no significant past medical history. Her blood pressure is 105/65 mm Hg, pulse is 112/min, and respiratory rate is 22/min. Physical examination shows dry mucous membranes and delayed capillary refill.

Laboratory results:
- Serum sodium: 138 mEq/L
- Serum potassium: 3.2 mEq/L
- Serum chloride: 114 mEq/L
- Serum bicarbonate: 12 mEq/L
- Arterial blood gas (room air): pH 7.24, PaCO2 24 mm Hg, PaO2 96 mm Hg

Using Winter's formula, calculate the patient's expected PaCO2. (Provide the exact median numerical value in mm Hg, excluding the ±2 range)

Cevabı ve açıklamayı göster

Cevap: 26

Cevap

26

In the setting of a primary metabolic acidosis (as seen in this patient with severe diarrhea and a low serum bicarbonate), the lungs compensate by increasing ventilation to blow off

CO_2

. Winter's formula,

Expected PaCO2 = (1.5 \times HCO_3^-) + 8 \pm 2

, is used to determine if the respiratory compensation is appropriate. By plugging in the patient's bicarbonate of 12 mEq/L, the calculation is

(1.5 \times 12) + 8 = 26

. The median expected PaCO2 is 26 mm Hg. Since the patient's measured PaCO2 is 24 mm Hg (which falls within the

26 \pm 2

range of 24-28 mm Hg), she has an appropriately compensated simple metabolic acidosis.

Adım Adım Çözüm

1

Recall Winter's formula for respiratory compensation.

Expected PaCO2 = (1.5 \times HCO_3^-) + 8

This formula predicts the appropriate compensatory decrease in PaCO2 for a given drop in bicarbonate during simple metabolic acidosis.

2

Identify the serum bicarbonate value from the laboratory panel.

HCO_3^-

= 12 mEq/L

The bicarbonate concentration is the primary variable driving the expected respiratory compensation.

3

Substitute the bicarbonate value into Winter's formula.

Expected PaCO2 = (1.5 \times 12) + 8

Setting up the equation allows for the direct calculation of the target PaCO2.

4

Complete the arithmetic calculation.

18 + 8 = 26

Yields the exact median expected PaCO2 in mm Hg, before applying the

\pm 2

range.

Anahtar Kavram

Calculation of expected respiratory compensation (Winter's formula) in metabolic acidosis

Soru 2067Soru →

A 38-year-old man presents to the emergency department with a 3-day history of bleeding gums, frequent epistaxis, and a diffuse rash. He has no significant past medical history. His temperature is $37.6^\circ\text{C}$ ( $99.7^\circ\text{F}$ ), blood pressure is $112/70$ mm Hg, and pulse is $105$ /min. Physical examination reveals widespread petechiae and ecchymoses over his trunk and extremities, as well as active mucosal bleeding in the oral cavity. Laboratory studies show:

Laboratory Test	Result
Hemoglobin	$7.8$ g/dL
Leukocyte count	$32,000/\mu\text{L}$
Platelet count	$18,000/\mu\text{L}$
Prothrombin time (PT)	$22$ seconds
Activated partial thromboplastin time (aPTT)	$48$ seconds
Fibrinogen	$85$ mg/dL (Normal: $150-400$ mg/dL)

A peripheral blood smear demonstrates numerous atypical promyelocytes containing multiple needle-like cytoplasmic inclusions (Auer rods).

Based on the suspected diagnosis, arrange the following management and diagnostic steps in the most appropriate chronological order.

Öğeleri doğru sıraya koymak için sürükleyin

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Cevap

The correct chronological sequence for managing suspected acute promyelocytic leukemia is: 1) Initiate therapy with all-trans retinoic acid (ATRA), 2) Perform a bone marrow aspiration and biopsy, 3) Confirm the diagnosis via fluorescence in situ hybridization (FISH) for t(15;17), and 4) Administer post-remission consolidation therapy.

The correct management sequence for acute promyelocytic leukemia prioritizes immediate life-saving therapy over definitive diagnostic confirmation. ATRA is initiated first based on peripheral blood smear findings to reverse DIC. A bone marrow biopsy is then performed to formally diagnose the leukemia and obtain a sample for FISH. FISH is subsequently performed on this sample to identify the t(15;17) translocation. Finally, consolidation therapy is administered weeks later, once the patient has achieved complete remission.

Adım Adım Çözüm

1

Recognize the clinical presentation and laboratory findings suggestive of Acute Promyelocytic Leukemia (APL).

The patient has pancytopenia, coagulopathy consistent with disseminated intravascular coagulation (DIC), and a peripheral smear showing promyelocytes with Auer rods.

Identifying APL is crucial because it is a hematologic emergency that dictates immediate, specific intervention to prevent fatal hemorrhage.

2

Determine the most critical initial intervention before pursuing definitive diagnostic testing.

Initiate all-trans retinoic acid (ATRA) therapy.

ATRA induces differentiation of the leukemic cells and rapidly resolves the DIC, significantly reducing early mortality. It must not be delayed for bone marrow biopsy or molecular confirmation.

3

Establish the sequence for definitive diagnostic confirmation.

Perform a bone marrow aspiration and biopsy, followed by molecular testing (FISH) for the t(15;17) translocation.

A bone marrow sample is required to confirm the diagnosis morphologically and provide the specimen for FISH, which definitively identifies the PML-RARA fusion gene.

4

Identify the long-term management step after initial stabilization and remission induction.

Administer post-remission consolidation therapy.

Consolidation therapy is given after the patient achieves remission to eradicate minimal residual disease and prevent relapse.

Anahtar Kavram

In patients with suspected acute promyelocytic leukemia (APL), all-trans retinoic acid (ATRA) must be administered immediately based on clinical and morphological suspicion to treat life-threatening coagulopathy, prior to definitive confirmation with bone marrow biopsy and genetic testing.

Soru 2068Soru →

Currently admitted to the intensive care unit, a $76$ -year-old man with ischemic cardiomyopathy (left ventricular ejection fraction $20\%$ ) is being managed for a severe heart failure exacerbation. He has been receiving continuous intravenous furosemide for the past four days. Over the last $48$ hours, his net fluid balance is negative $6$ liters. Today, he develops an insidious onset of severe, diffuse abdominal pain. He is grimacing in bed and requesting intravenous analgesia.

Vital signs include a temperature of $37.1^\circ\text{C}$ , heart rate of $112$ /min (irregularly irregular), blood pressure of $85/55$ mmHg, and respiratory rate of $22$ /min. Physical examination reveals a flat, soft abdomen that is surprisingly non-tender to deep palpation. There is no guarding, rigidity, or rebound tenderness. Bowel sounds are diminished.

Laboratory studies are significant for:
Leukocyte count: $16,500/\text{mm}^3$
Blood urea nitrogen: $55 \text{ mg/dL}$
Creatinine: $2.1 \text{ mg/dL}$ (baseline $1.0 \text{ mg/dL}$ )
Lactate: $4.8 \text{ mmol/L}$ (Normal: $0.5-2.2 \text{ mmol/L}$ )

CT angiography of the abdomen and pelvis demonstrates diffuse, smooth narrowing of the superior mesenteric artery and its primary branches with an alternating pattern of spasm and dilation. No distinct endoluminal filling defects or abrupt vascular cutoffs are visualized. The bowel wall appears mildly thickened, but no pneumatosis intestinalis or free intraperitoneal air is present.

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

Continuous intravenous heparin infusion

Immediate exploratory laparotomy

Intra-arterial infusion of papaverine

Intravenous administration of piperacillin-tazobactam and clinical observation

Intravenous administration of norepinephrine

Cevabı ve açıklamayı göster

Cevap: Intra-arterial infusion of papaverine

Cevap

Intra-arterial infusion of papaverine

This patient's presentation is highly characteristic of non-occlusive mesenteric ischemia (NOMI). NOMI typically occurs in elderly patients with underlying cardiovascular disease (e.g., severe heart failure) who suffer a systemic low-flow state. In this scenario, massive diuresis resulted in intravascular volume depletion and hypotension. In response to reduced cardiac output, the body selectively vasoconstricts the splanchnic circulation to maintain blood flow to the brain and heart. This profound vasospasm causes severe abdominal pain out of proportion to the physical exam and drives up serum lactate.

The diagnosis is confirmed via CT angiography showing diffuse mesenteric narrowing and an alternating pattern of spasm and dilation (often described as a "string of sausages" appearance) without any actual clot or mechanical obstruction. Because there is no mechanical occlusion, surgical embolectomy and systemic anticoagulation are ineffective. The appropriate management involves hemodynamic resuscitation, discontinuation of vasoconstrictive or volume-depleting agents (stopping the furosemide), and direct intra-arterial infusion of a vasodilator (such as papaverine) into the superior mesenteric artery to physically break the splanchnic spasm.

Adım Adım Çözüm

1

Analyze the patient's risk factors and clinical presentation.

The patient has severe heart failure and experienced massive diuresis, leading to hypotension, elevated creatinine (pre-renal acute kidney injury), and severe abdominal pain out of proportion to the physical exam.

Pain out of proportion to exam combined with elevated lactate in a hypotensive state points heavily toward acute mesenteric ischemia.

2

Interpret the diagnostic imaging findings in the context of the presentation.

CT angiography shows diffuse arterial narrowing and spasm without any discrete thrombus or embolus.

These specific imaging findings, combined with a low-flow state (hypovolemia from diuresis and poor cardiac output), distinguish non-occlusive mesenteric ischemia (NOMI) from occlusive thromboembolic ischemia.

3

Determine the definitive treatment for this specific pathology.

The primary treatment is resolving the vasospasm by stopping the inciting factors (furosemide) and administering catheter-directed intra-arterial vasodilators, such as papaverine.

Since there is no physical clot to retrieve or bypass, systemic anticoagulants or immediate surgery will not fix the underlying perfusion deficit.

Anahtar Kavram

Non-occlusive mesenteric ischemia (NOMI)

Tahmini Süre:1m 45s

Soru 2069Soru →

Match each of the following clinical presentations with the most likely diagnosis.

Soldaki öğeye tıklayın, sonra eşleşen sağdaki öğeye tıklayın

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Cevap

1 matches with Whipple disease; 2 matches with Celiac disease; 3 matches with Carcinoid syndrome; 4 matches with VIPoma.

Each clinical presentation aligns precisely with a distinct gastroenterologic syndrome characterized by its pathognomonic features: PAS-positive macrophages for Whipple disease, dermatitis herpetiformis for celiac disease, right-sided heart disease with flushing for carcinoid syndrome, and the WDHA triad for VIPoma.

Adım Adım Çözüm

1

Analyze the first vignette focusing on the PAS-positive macrophages and systemic manifestations.

Identified as Whipple disease due to the classic combination of malabsorption, arthralgias, neurologic symptoms, and histologic findings.

PAS-positive macrophages are pathognomonic for Tropheryma whipplei infection in the context of these clinical symptoms.

2

Evaluate the second vignette highlighting the dermatologic and hematologic findings.

Identified as Celiac disease.

The combination of malabsorption, iron deficiency anemia, and dermatitis herpetiformis is classically seen in celiac disease due to gluten sensitivity.

3

Examine the third vignette focusing on episodic flushing and cardiac involvement.

Identified as Carcinoid syndrome.

Serotonin secretion from a carcinoid tumor leads to flushing, diarrhea, and right-sided valvular heart lesions (tricuspid regurgitation).

4

Assess the fourth vignette noting the biochemical triad.

Identified as VIPoma.

The presentation of watery diarrhea, severe hypokalemia, and achlorhydria constitutes the WDHA syndrome caused by a VIP-secreting tumor.

Anahtar Kavram

Differential diagnosis of chronic diarrhea syndromes based on characteristic systemic, dermatologic, and biochemical manifestations.

Soru 2070Soru →

Match each clinical presentation with its underlying pathophysiologic mechanism or characteristic pathologic finding.

Soldaki öğeye tıklayın, sonra eşleşen sağdaki öğeye tıklayın

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Cevap

The correct pairings match each patient's clinical presentation to the underlying disease pathophysiology: the man with inflammatory back pain has Ankylosing Spondylitis (driven by enthesitis), the woman with recurrent ulcers has Behçet syndrome (a systemic vasculitis with pathergy), the woman with muscle weakness and rash has Dermatomyositis (complement-mediated microangiopathy), and the woman with widespread pain without inflammation has Fibromyalgia (central sensitization).

Each vignette represents a classic presentation of a distinct rheumatologic disorder, perfectly aligning with one distinct pathophysiologic mechanism provided in the options. Diagnosing the condition based on the constellation of symptoms allows for direct correlation to its pathologic basis.

Adım Adım Çözüm

1

Analyze each clinical vignette to establish the most likely diagnosis.

Patient 1 has ankylosing spondylitis; Patient 2 has Behçet syndrome; Patient 3 has dermatomyositis; Patient 4 has fibromyalgia.

Identifying the specific rheumatologic condition is the necessary first step before determining its underlying mechanism.

2

Evaluate the pathophysiologic descriptions and link them to the identified diagnoses.

Ankylosing spondylitis pairs with enthesitis; Behçet syndrome pairs with vasculitis/pathergy; dermatomyositis pairs with complement-mediated microangiopathy; fibromyalgia pairs with central pain sensitization.

Matching the disease to its core pathologic mechanism confirms understanding of disease etiology as tested on the exam.

Anahtar Kavram

Pathophysiologic mechanisms of common rheumatologic and autoimmune conditions.

Soru 2071Soru →

A $48$ -year-old man is evaluated in the hospital on day $5$ of an admission for severe acute pancreatitis. He originally presented with severe, radiating epigastric pain, nausea, and a serum lipase level of $3,200\text{ U/L}$ . The patient has a $10$ -year history of heavy alcohol consumption. He has been strictly nil per os (NPO) and is receiving intravenous crystalloid fluids and opioid analgesics. Today, his temperature is $38.4^\circ\text{C}$ ( $101.1^\circ\text{F}$ ), blood pressure is $118/74\text{ mmHg}$ , pulse is $108/\text{min}$ , and respirations are $18/\text{min}$ . Physical examination reveals persistent epigastric tenderness to deep palpation without rebound tenderness or guarding. Bowel sounds are hypoactive. Laboratory studies show:

Leukocyte count: $16,500/\text{mm}^3$
Total calcium: $7.8\text{ mg/dL}$
Albumin: $2.0\text{ g/dL}$
Liver function tests: Within normal limits

A repeat computed tomography (CT) scan of the abdomen with intravenous contrast demonstrates an area of non-enhancement involving approximately $40\%$ of the pancreatic body and tail, consistent with pancreatic necrosis. There is no visible gas within the peripancreatic fluid collection. Which of the following is the most appropriate next step in management?

Continue supportive care and initiate enteral nutrition

Initiate intravenous imipenem-cilastatin

Administer intravenous calcium gluconate

Perform CT-guided fine-needle aspiration of the pancreas

Schedule endoscopic retrograde cholangiopancreatography

Cevabı ve açıklamayı göster

Cevap: Continue supportive care and initiate enteral nutrition

Cevap

Continue supportive care and initiate enteral nutrition

The correct management is to continue supportive care and initiate enteral nutrition. This patient is exhibiting signs of Systemic Inflammatory Response Syndrome (SIRS), which frequently occurs during the first week of severe acute pancreatitis. SIRS manifests with fever, tachycardia, and leukocytosis, mimicking infection. However, the CT scan confirms sterile pancreatic necrosis by the absence of gas within the fluid collection. Evidence-based guidelines strongly advise against the prophylactic use of broad-spectrum antibiotics (such as carbapenems) for sterile necrosis, as they do not decrease the incidence of infected necrosis or mortality. Instead, early enteral nutrition (via nasogastric or nasojejunal tube) should be initiated. Enteral feeding maintains the intestinal mucosal barrier, thereby preventing bacterial translocation from the gut and actively reducing the risk of subsequent necrosis infection.

Adım Adım Çözüm

1

Interpret the clinical presentation and timing.

The patient is on day

5

of severe acute pancreatitis and has developed a fever and leukocytosis.

To distinguish between early Systemic Inflammatory Response Syndrome (SIRS), which is expected, and late infected necrosis.

2

Analyze the imaging and laboratory findings.

The CT scan confirms sterile necrosis (no gas present). The total calcium is

7.8\text{ mg/dL}

, but correcting for an albumin of

2.0\text{ g/dL}

yields a normal corrected calcium of

9.4\text{ mg/dL}

.

To rule out infected necrosis and true hypocalcemia, both of which would require specific interventions.

3

Select the appropriate management strategy based on findings.

Supportive care combined with the initiation of enteral nutrition is chosen.

Enteral feeding is preferred over parenteral nutrition to maintain the gut mucosal barrier, and prophylactic antibiotics are contraindicated for sterile necrosis.

Anahtar Kavram

Management of sterile pancreatic necrosis and expected SIRS in severe acute pancreatitis.

Soru 2072Soru →

A $78$ -year-old man is brought to the clinic by his son for a routine follow-up. The patient has a history of advanced Parkinson disease and neurogenic bladder, which is managed with a chronic indwelling urethral catheter. The son reports that over the past week, the urine in the collection bag has become notably turbid and foul-smelling. The patient is otherwise acting at his baseline; he has had no fevers, chills, abdominal pain, or changes in oral intake. Vital signs are temperature $37.0^\circ\text{C}$ ( $98.6^\circ\text{F}$ ), blood pressure $132/82\text{ mm Hg}$ , pulse $74\text{/min}$ , and respirations $14\text{/min}$ . Physical examination demonstrates a soft, non-tender abdomen and no costovertebral angle tenderness. There is no leakage or erythema around the urethral meatus.

A urinalysis is obtained directly from the catheter port:

Test	Result
Color	Turbid
Specific gravity	$1.015$
Leukocyte esterase	Positive
Nitrites	Positive
WBC	$50\text{/hpf}$
Bacteria	Many

A urine culture grows $>100,000\text{ CFU/mL}$ of *Klebsiella pneumoniae*. Which of the following is the most appropriate next step in management?

Reassurance and continued observation

Exchange the indwelling catheter and observe

Initiate oral ciprofloxacin

Initiate oral nitrofurantoin

Bladder irrigation with sterile saline

Cevabı ve açıklamayı göster

Cevap: Reassurance and continued observation

Cevap

Reassurance and continued observation

The correct management is reassurance and continued observation. This patient has asymptomatic bacteriuria (ASB) in the setting of a chronic indwelling urinary catheter. Virtually all patients with chronic indwelling catheters will develop bacteriuria within

2

to

4

weeks. The presence of cloudy, foul-smelling urine, pyuria (positive leukocyte esterase and elevated WBC count), and positive nitrites on urinalysis are expected findings of chronic colonization. They do not distinguish ASB from catheter-associated urinary tract infection (CAUTI). A diagnosis of CAUTI requires the presence of systemic signs of infection (e.g., fever, altered mental status, hemodynamic instability) or localized urinary symptoms (e.g., flank pain, pelvic discomfort) with no other identifiable source. In the absence of these symptoms, treatment with antibiotics is contraindicated, as it does not prevent future symptomatic infections and strongly promotes antimicrobial resistance.

Adım Adım Çözüm

1

Evaluate the patient's clinical symptoms in the context of a chronic indwelling catheter.

The patient has turbid, foul-smelling urine but no systemic signs of infection (normal temperature and hemodynamics) or localized symptoms.

Determining the presence of true symptoms is required to distinguish clinical infection from expected bacterial colonization.

2

Interpret the urinalysis and urine culture results.

The urinalysis demonstrates pyuria and the culture is positive for a high bacterial load of Klebsiella pneumoniae.

While these findings indicate the presence of bacteria and inflammation, they are nearly universal in patients with chronic catheters and do not confirm an active infection.

3

Determine the appropriate management plan based on the diagnosis of asymptomatic bacteriuria (ASB).

The diagnosis is ASB, which requires reassurance and observation without antimicrobial therapy or catheter exchange.

Antibiotic treatment of ASB does not improve outcomes, fails to prevent future infections, and actively contributes to antimicrobial resistance.

Anahtar Kavram

Cloudy, foul-smelling urine and pyuria are expected findings in patients with chronic indwelling urinary catheters and do not constitute indications for antibiotic therapy in the absence of systemic or localized signs of infection.

Soru 2073Soru →

Following a one-week vacation in a tropical resort, a 32-year-old female presents to the outpatient clinic reporting 48 hours of frequent, watery bowel movements. She describes having three to four loose stools per day accompanied by mild abdominal cramping. She denies seeing blood or mucus in the stool and has not experienced fever, chills, nausea, or vomiting. Her medical history is unremarkable, and she takes no daily medications. Vital signs show a temperature of 37.1°C (98.8°F), blood pressure of 118/76 mmHg, and heart rate of 78/min. On physical examination, the abdomen is soft and non-tender with active bowel sounds. The patient requests an antibiotic prescription to ensure she can return to work tomorrow. Which of the following is the most appropriate management plan for this patient?

Symptomatic management with fluid replacement

Empiric therapy with oral ciprofloxacin

Empiric therapy with oral azithromycin

Empiric therapy with oral metronidazole

Empiric therapy with oral vancomycin

Cevabı ve açıklamayı göster

Cevap: Symptomatic management with fluid replacement

Cevap

Symptomatic management with fluid replacement

The patient presents with classic symptoms of mild traveler's diarrhea, characterized by a few loose stools per day and mild cramping, but lacking systemic toxicity or dysentery (bloody stools). The vast majority of these cases are caused by viral pathogens or self-limiting bacterial infections such as enterotoxigenic Escherichia coli (ETEC). The standard of care for mild traveler's diarrhea is supportive, focusing on oral fluid and electrolyte replacement. Antimicrobial therapy is not indicated due to the self-limiting nature of the illness and the principles of antibiotic stewardship.

Adım Adım Çözüm

1

Analyze the clinical presentation.

The patient has mild, watery diarrhea with no warning signs (no high fever, no gross blood, no severe abdominal pain) following recent travel.

Categorizing the severity of traveler's diarrhea dictates the necessity of antimicrobial therapy.

2

Determine the appropriate intervention.

Supportive care with oral rehydration is selected.

Current guidelines recommend against the routine use of antibiotics for mild traveler's diarrhea to prevent antibiotic resistance and adverse effects.

Anahtar Kavram

Management of mild traveler's diarrhea emphasizes supportive care over antimicrobial therapy.

Soru 2074Soru →

A 52-year-old woman with a history of type 1 diabetes mellitus is brought to the emergency department after $3$ days of intractable vomiting and generalized abdominal pain. She ran out of her prescribed insulin $4$ days ago. On physical examination, she appears lethargic with dry mucous membranes and decreased skin turgor. Temperature is $37.2^\circ$ C ( $99.0^\circ$ F), blood pressure is $95/60$ mm Hg, pulse is $118$ /min, and respirations are $26$ /min and deep.

Laboratory studies reveal:

Test	Result	Reference Range
Serum sodium	$140$ mEq/L	$136-145$ mEq/L
Serum potassium	$4.8$ mEq/L	$3.5-5.0$ mEq/L
Serum chloride	$92$ mEq/L	$98-106$ mEq/L
Serum bicarbonate	$14$ mEq/L	$22-28$ mEq/L
Blood urea nitrogen	$42$ mg/dL	$7-18$ mg/dL
Serum creatinine	$1.6$ mg/dL	$0.6-1.2$ mg/dL
Blood glucose	$480$ mg/dL	$70-110$ mg/dL

Assume a normal anion gap of $12$ mEq/L and a normal serum bicarbonate of $24$ mEq/L.

What is the patient's calculated delta ratio (also known as the $\Delta$ AG / $\Delta$ HCO $_3^-$ ratio)?

Cevabı ve açıklamayı göster

Cevap: 2.2

Cevap

The calculated delta ratio is 2.2.

The patient's clinical presentation of diabetic ketoacidosis combined with intractable vomiting strongly suggests a mixed acid-base disorder. Diabetic ketoacidosis causes a high anion gap metabolic acidosis (HAGMA), while vomiting induces a metabolic alkalosis due to the loss of gastric hydrochloric acid. To confirm this mathematically, the delta ratio is calculated. The patient's measured anion gap is

140 - (92 + 14) = 34

mEq/L. The change in anion gap (

\Delta\text{AG}

) is

34 - 12 = 22

mEq/L. The change in bicarbonate (

\Delta\text{HCO}_3^-

) is

24 - 14 = 10

mEq/L. Dividing the

\Delta\text{AG}

by the

\Delta\text{HCO}_3^-

yields a ratio of

2.2

. In a pure HAGMA, the drop in bicarbonate should be roughly equivalent to the rise in the anion gap (ratio between

1.0

and

2.0

). A delta ratio

> 2.0

indicates that the bicarbonate level has not fallen as much as expected, which confirms the presence of a concurrent metabolic alkalosis.

Adım Adım Çözüm

1

Calculate the patient's anion gap (AG).

\text{AG} = 140 - (92 + 14) = 34

mEq/L

Establishing the initial anion gap is necessary to identify the presence of a high anion gap metabolic acidosis and to compute the delta anion gap.

2

Calculate the change in anion gap (

\Delta\text{AG}

).

\Delta\text{AG} = 34 - 12 = 22

mEq/L

The numerator of the delta ratio represents how much the anion gap has increased above the normal baseline.

3

Calculate the change in bicarbonate (

\Delta\text{HCO}_3^-

).

\Delta\text{HCO}_3^- = 24 - 14 = 10

mEq/L

The denominator of the delta ratio represents how much the bicarbonate has decreased below the normal baseline due to buffering the excess acid.

4

Divide

\Delta\text{AG}

by

\Delta\text{HCO}_3^-

.

\text{Delta Ratio} = \frac{22}{10} = 2.2

The resulting ratio categorizes the nature of the acid-base disorder, determining if a concomitant metabolic alkalosis or normal anion gap metabolic acidosis is present.

Anahtar Kavram

In a high anion gap metabolic acidosis, calculating the delta ratio (

\Delta

AG /

\Delta

HCO

_3^-

) helps uncover hidden, concurrent mixed acid-base disorders such as a superimposed metabolic alkalosis.

Alternatif Yöntem

Instead of using the delta ratio, clinicians frequently calculate the 'corrected bicarbonate' (or expected bicarbonate) by adding the

\Delta\text{AG}

to the patient's measured bicarbonate:

14 + 22 = 36

mEq/L. Because this value is significantly higher than the normal

24

mEq/L, it leads to the exact same clinical conclusion of a superimposed metabolic alkalosis.

Tahmini Süre:2m 0s

Soru 2075Soru →

Evaluate the following four clinical scenarios describing patients with symptomatic thyrotoxicosis. Match each clinical vignette to the specific histopathologic or molecular etiology driving the patient's condition.

Soldaki öğeye tıklayın, sonra eşleşen sağdaki öğeye tıklayın

Cevabı ve açıklamayı göster

Cevap

The correct pairings identify Graves disease (autoantibodies activating receptors), subacute thyroiditis (granulomatous destruction), toxic multinodular goiter (autonomous focal production), and postpartum thyroiditis (lymphocytic infiltration).

Graves disease is driven by TSH receptor-stimulating autoantibodies, leading to diffuse iodine uptake. Subacute thyroiditis involves viral-induced granulomatous destruction, causing a painful goiter and low uptake due to follicular rupture. Toxic multinodular goiter involves autonomous nodules, showing patchy uptake on imaging. Postpartum thyroiditis is a painless lymphocytic inflammation occurring within a year of delivery, also causing low uptake due to the release of preformed hormone.

Adım Adım Çözüm

1

Analyze the radioactive iodine uptake (RAIU) and physical exam findings for each clinical scenario.

Scenarios 1 and 3 demonstrate increased uptake, indicating true hyperthyroidism (increased de novo hormone synthesis). Scenarios 2 and 4 demonstrate decreased uptake, indicating a destructive thyroiditis (release of preformed hormone).

RAIU separates thyrotoxicosis into states of overproduction versus states of glandular destruction or exogenous intake.

2

Differentiate the hyperthyroid states (Scenarios 1 and 3).

Scenario 1 describes diffuse uptake with unique extrathyroidal manifestations (exophthalmos), pointing to Graves disease (autoantibody-mediated). Scenario 3 describes patchy uptake with a lumpy gland in an older adult, pointing to toxic multinodular goiter (autonomous focal nodules).

The pattern of uptake (diffuse vs. patchy) correlates directly with the underlying diffuse molecular trigger versus focal somatic mutations.

3

Differentiate the destructive thyroiditis states (Scenarios 2 and 4).

Scenario 2 features a painful neck, high ESR, and viral prodrome, indicating subacute granulomatous thyroiditis. Scenario 4 features a painless neck in a postpartum patient, indicating postpartum lymphocytic thyroiditis.

Pain and systemic inflammation distinguish granulomatous destruction from painless autoimmune lymphocytic destruction.

Anahtar Kavram

Differential diagnosis of thyrotoxicosis utilizing clinical presentation, physical examination, and radioactive iodine uptake patterns to identify underlying pathophysiologic mechanisms.

Soru 2076Soru →

A patient is hospitalized for the management of an acute, swollen, and exquisitely tender left knee. Diagnostic arthrocentesis performed at admission yielded opaque, purulent synovial fluid, prompting the immediate initiation of empiric antimicrobial therapy with intravenous vancomycin and intravenous ceftriaxone. Over the past 48 hours, the patient has demonstrated marked clinical improvement, with complete resolution of fever and a significant decrease in joint effusion. The microbiology laboratory subsequently contacts the team to report that the admission synovial fluid culture is growing *Streptococcus pyogenes* (Group A Streptococcus). The isolate demonstrates standard susceptibility patterns to all tested beta-lactams, macrolides, and fluoroquinolones. In accordance with the principles of antimicrobial stewardship, which of the following is the most appropriate next step in the pharmacologic management of this patient?

Transition to intravenous penicillin G

Maintain the current regimen of intravenous vancomycin and ceftriaxone

Discontinue ceftriaxone and maintain intravenous vancomycin

Transition to intravenous piperacillin-tazobactam

Transition to oral trimethoprim-sulfamethoxazole

Cevabı ve açıklamayı göster

Cevap: Transition to intravenous penicillin G

Cevap

The most appropriate next step is to transition to intravenous penicillin G.

The correct answer is to transition the patient to intravenous penicillin G. The cornerstone of antimicrobial stewardship in the inpatient setting is 'de-escalation.' When a patient presents with a severe, potentially limb- or life-threatening infection (such as septic arthritis), it is appropriate to start broad-spectrum empiric therapy (e.g., vancomycin for MRSA and ceftriaxone for Gram-negative organisms). However, once blood or synovial fluid cultures identify the causative pathogen and its susceptibility profile, the antibiotic regimen MUST be narrowed to the most targeted, effective agent. *Streptococcus pyogenes* (Group A Streptococcus) is exquisitely susceptible to penicillin. Transitioning to penicillin G provides optimal bactericidal activity while minimizing collateral damage to the patient's microbiome and preventing the development of resistant organisms.

Adım Adım Çözüm

1

Identify the pathogen and its typical susceptibility profile.

The pathogen is Streptococcus pyogenes (Group A Streptococcus), which is universally susceptible to penicillin.

Accurate pathogen identification allows for targeted antimicrobial therapy.

2

Evaluate the current empiric antibiotic regimen against the identified pathogen.

The patient is on vancomycin (covers MRSA and other Gram-positives) and ceftriaxone (covers many Gram-negatives and some Gram-positives). This is excessively broad for a confirmed Group A Strep infection.

Empiric regimens are designed to cover all likely pathogens before cultures finalize, but must be narrowed once data is available.

3

Apply principles of antimicrobial stewardship to select the optimal definitive therapy.

Therapy should be de-escalated to the narrowest spectrum agent that is highly effective against the pathogen. Intravenous penicillin G (or ampicillin/cefazolin) is the drug of choice.

Targeted therapy minimizes toxicity, reduces the risk of Clostridioides difficile infection, and prevents the emergence of multi-drug resistant organisms.

Anahtar Kavram

Antimicrobial de-escalation (Stewardship)

Soru 2077Soru →

A 72-year-old man is evaluated for severe shortness of breath on postoperative day 3 following a right hemicolectomy for colon cancer. Yesterday, his hemoglobin was 6.5 g/dL, and he was prescribed 2 units of packed red blood cells. The infusion of the second unit was completed 30 minutes ago. He has a history of essential hypertension, diet-controlled type 2 diabetes mellitus, and osteoarthritis. His temperature is 37.1°C (98.8°F), blood pressure is 168/94 mm Hg, pulse is 112/min, and respirations are 24/min. Pulse oximetry shows 88% on room air. Physical examination reveals distended jugular veins evaluated at 9 cm above the sternal angle. Cardiac auscultation shows a regular tachycardia with a prominent S3 gallop. Lung auscultation reveals bilateral crackles at the lung bases. Trace bilateral pedal edema is present. What is the most appropriate next step in management?

Intravenous furosemide

Inhaled albuterol and ipratropium

Intravenous broad-spectrum antibiotics

Removal of central venous catheter and blood cultures

Rapid infusion of 0.9% normal saline

Cevabı ve açıklamayı göster

Cevap: Intravenous furosemide

Cevap

Intravenous furosemide

The correct intervention is the administration of a loop diuretic. This patient is presenting with Transfusion-Associated Circulatory Overload (TACO), characterized by respiratory distress, hypertension, tachycardia, and signs of cardiogenic pulmonary edema (JVD, S3 gallop, basilar crackles) occurring within 6 hours of a blood transfusion. Patients at extremes of age or with underlying cardiac/renal dysfunction are at highest risk. Management involves immediate cessation of the transfusion, respiratory support (supplemental oxygen or positive pressure ventilation), and diuresis (e.g., intravenous furosemide).

Adım Adım Çözüm

1

Analyze the patient's vital signs and timing of symptom onset.

The patient developed acute dyspnea, hypoxia (88%), and hypertension (168/94 mm Hg) within 30 minutes of receiving a second unit of packed red blood cells.

Establishing the temporal relationship to the transfusion helps narrow the differential to acute transfusion reactions.

2

Evaluate the physical examination findings.

The patient has jugular venous distention, an S3 gallop, and bilateral basilar crackles.

These findings are pathognomonic for left-sided heart failure and systemic volume overload.

3

Synthesize data to determine the specific transfusion reaction and select the appropriate intervention.

The combination of respiratory distress, hypertension, and cardiogenic pulmonary edema following a transfusion indicates Transfusion-Associated Circulatory Overload (TACO). The correct management is diuresis.

TACO is caused by fluid volume excess overwhelming the cardiovascular system, requiring loop diuretics like furosemide alongside supplemental oxygen.

Anahtar Kavram

Transfusion-Associated Circulatory Overload (TACO) management

Tahmini Süre:1m 30s

Soru 2078Soru →

A 68-year-old man with a history of severe chronic obstructive pulmonary disease and hypertension is brought to the emergency department by his daughter due to worsening confusion and decreased urine output over the past 48 hours. He recently had a gastrointestinal illness with severe nausea and poor oral intake, leading to profound dehydration. His current medications include lisinopril and tiotropium. Temperature is 37.1°C (98.8°F), blood pressure is 88/52 mm Hg, pulse is 112/min, and respirations are 26/min. Physical examination shows dry mucous membranes, diminished breath sounds bilaterally with a prolonged expiratory phase, and delayed capillary refill.

Laboratory studies reveal the following:
Sodium: $136\text{ mEq/L}$
Potassium: $5.1\text{ mEq/L}$
Chloride: $95\text{ mEq/L}$
Bicarbonate: $12\text{ mEq/L}$
Blood urea nitrogen: $72\text{ mg/dL}$
Creatinine: $4.1\text{ mg/dL}$ (baseline $1.1\text{ mg/dL}$ )

Arterial blood gas (on room air):
pH: $7.18$
pCO2: $34\text{ mm Hg}$
pO2: $62\text{ mm Hg}$

Which of the following best characterizes this patient's acid-base status?

High anion gap metabolic acidosis and concurrent respiratory acidosis

High anion gap metabolic acidosis with appropriate respiratory compensation

High anion gap metabolic acidosis and concurrent respiratory alkalosis

Normal anion gap metabolic acidosis and concurrent respiratory acidosis

Primary respiratory acidosis with appropriate metabolic compensation

Cevabı ve açıklamayı göster

Cevap: High anion gap metabolic acidosis and concurrent respiratory acidosis

Cevap

High anion gap metabolic acidosis and concurrent respiratory acidosis

The correct diagnosis is a high anion gap metabolic acidosis with a concurrent respiratory acidosis. The patient's primary disorder is a metabolic acidosis (pH

7.18

,

HCO_3^-

12\text{ mEq/L}

). The anion gap is elevated at

29\text{ mEq/L}

(

136 - [95 + 12]

), confirming a high anion gap metabolic acidosis (likely uremic/lactic secondary to severe hypoperfusion and AKI). To assess the respiratory response, Winter's formula must be applied:

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

. The patient's measured

pCO_2

is

34\text{ mm Hg}

. Because

34\text{ mm Hg}

is significantly greater than the expected maximum of

28\text{ mm Hg}

, he has a superimposed respiratory acidosis. His history of severe COPD limits his ability to mount an appropriate hyperventilatory response.

Adım Adım Çözüm

1

Analyze the basic pH and primary disturbance.

The pH is

7.18

(acidemia) and the

HCO_3^-

is markedly low at

12\text{ mEq/L}

, indicating a primary metabolic acidosis.

Establishing the primary acid-base disorder is the necessary first step before assessing for mixed disorders.

2

Calculate the Anion Gap (AG).

AG = Na^+ - (Cl^- + HCO_3^-) = 136 - (95 + 12) = 136 - 107 = 29\text{ mEq/L}

.

An elevated AG (normal

8-12\text{ mEq/L}

) confirms a high anion gap metabolic acidosis (HAGMA), in this case likely due to severe acute kidney injury (uremia) from hypoperfusion.

3

Calculate the expected respiratory compensation using Winter's formula.

Expected\ pCO_2 = (1.5 \times HCO_3^-) + 8 \pm 2 = (1.5 \times 12) + 8 \pm 2 = 18 + 8 \pm 2 = 26 \pm 2\text{ mm Hg}

(Range:

24-28\text{ mm Hg}

).

This formula determines if the patient's respiratory system is adequately blowing off

CO_2

in response to the metabolic acidemia.

4

Compare expected

pCO_2

to measured

pCO_2

.

The measured

pCO_2

is

34\text{ mm Hg}

, which is greater than the expected range of

24-28\text{ mm Hg}

.

Because the actual

pCO_2

is higher than expected, the patient has a superimposed (concurrent) respiratory acidosis, likely because his severe COPD prevents adequate compensatory hyperventilation.

Anahtar Kavram

Diagnosis of mixed acid-base disorders requires calculating the anion gap and using Winter's formula to determine if respiratory compensation is appropriate.

Tahmini Süre:1m 30s

Soru 2079Soru →

Review the following clinical scenarios involving patients with diverticular disease. Correlate each specific presentation with its most appropriate next step in management based on current clinical guidelines.

Soldaki öğeye tıklayın, sonra eşleşen sağdaki öğeye tıklayın

Cevabı ve açıklamayı göster

Cevap

Match mild uncomplicated diverticulitis to conservative management without antibiotics; abscess >4cm to percutaneous drainage; purulent/feculent peritonitis to emergent laparotomy; and frequent recurrent episodes to elective resection.

The correct pairings align with current clinical guidelines for diverticular disease, which stratify treatment by disease severity (uncomplicated vs. complicated) and the presence of hemodynamic instability or peritonitis.

Adım Adım Çözüm

1

Analyze the first scenario (mild uncomplicated diverticulitis).

Identify a lack of systemic toxicity or surgical complications.

Determines that conservative therapy without antibiotics is the standard of care to prevent antimicrobial resistance.

2

Analyze the second scenario (5-cm pericolic fluid collection).

Identify complicated diverticulitis with a large abscess.

Abscesses >3-4 cm generally require percutaneous drainage in addition to therapeutic antibiotics.

3

Analyze the third scenario (diffuse rigidity, hypotension, free air).

Identify generalized peritonitis (Hinchey III/IV).

Life-threatening peritonitis requires immediate surgical exploration, typically with a Hartmann procedure, as medical management will fail.

4

Analyze the fourth scenario (recurrent uncomplicated episodes).

Identify a severe quality-of-life impact from chronic recurrences.

Patients with multiple symptomatic recurrences are ideal candidates for elective sigmoid resection to prevent future episodes.

Anahtar Kavram

Management of Diverticular Disease

Soru 2080Soru →

Match each clinical presentation of glomerular disease with its most characteristic renal biopsy or immunofluorescence finding.

Soldaki öğeye tıklayın, sonra eşleşen sağdaki öğeye tıklayın

Cevabı ve açıklamayı göster

Cevap

IgA nephropathy matches with mesangial IgA deposition; PSGN matches with subepithelial humps; Goodpasture syndrome matches with linear IgG deposition; Membranous nephropathy matches with subepithelial 'spike and dome' deposits.

Each clinical scenario distinctly describes a specific glomerular disease that corresponds precisely to a unique pathological finding: IgA nephropathy correlates with mesangial deposits, PSGN with subepithelial humps, Goodpasture syndrome with linear IgG deposition, and membranous nephropathy with a spike and dome pattern.

Adım Adım Çözüm

1

Analyze the first clinical vignette regarding the timing of hematuria relative to the upper respiratory infection.

The concurrent nature of the hematuria and infection identifies IgA nephropathy.

Synpharyngitic hematuria differentiates IgA nephropathy from post-infectious etiologies, and is confirmed by mesangial IgA deposition on biopsy.

2

Evaluate the second presentation involving a pediatric patient with delayed-onset hematuria and edema following a skin infection.

The distinct latency period of two weeks points to poststreptococcal glomerulonephritis (PSGN).

PSGN requires time for immune complex formation and deposition, classically forming subepithelial humps visible on electron microscopy.

3

Assess the third patient presenting with rapidly progressive pulmonary-renal syndrome.

Hemoptysis combined with acute kidney injury strongly suggests Goodpasture syndrome.

Anti-glomerular basement membrane (anti-GBM) antibodies attack both alveolar and glomerular basement membranes, yielding a linear IgG immunofluorescence pattern.

4

Examine the adult patient with nephrotic range proteinuria and an underlying malignancy.

The clinical picture correlates with membranous nephropathy.

Solid organ tumors are classic secondary causes of membranous nephropathy, which reveals subepithelial deposits generating a 'spike and dome' appearance on silver staining.

Anahtar Kavram

Identifying primary and secondary glomerular diseases based on their classic clinical presentations and pathognomonic histopathological findings.

Tahmini Süre:1m 30s

Internal Medicine

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Alternatif Yöntem

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