Internal Medicine Alıştırma Soruları — USMLE Step 2 CK — Sayfa 117

Soru 2321Soru →

A $75$ -year-old retired teacher arrives at the outpatient clinic reporting a one-week history of worsening shortness of breath. He states that he has been waking up gasping for air in the middle of the night and now must sleep propped up on three pillows. He has a $40$ -pack-year smoking history and suffered an anterior myocardial infarction $4$ years ago. Vital signs show a blood pressure of $150/90$ mmHg, heart rate of $105$ /min, respiratory rate of $24$ /min, and oxygen saturation of $91\%$ on ambient air. Pulmonary auscultation reveals dependent, coarse crackles in both lower lung fields with absent wheezing and a normal expiratory phase. Cardiovascular examination is notable for an S3 gallop and jugular venous distention to $12$ cm $H_2O$ . Which of the following is the most appropriate initial pharmacological intervention?

Intravenous furosemide

Inhaled albuterol and ipratropium

Oral prednisone

Intravenous piperacillin-tazobactam

Oral azithromycin

Cevabı ve açıklamayı göster

Cevap: Intravenous furosemide

Cevap

Intravenous furosemide

The correct intervention is intravenous furosemide. This patient presents with classic signs and symptoms of acute decompensated heart failure (ADHF), including orthopnea, paroxysmal nocturnal dyspnea, an S3 gallop, elevated jugular venous pressure, and bibasilar crackles. Given his history of a myocardial infarction, he likely has ischemic cardiomyopathy. The cornerstone of initial therapy for patients presenting with ADHF and volume overload is intravenous loop diuretics, which rapidly decrease preload and relieve pulmonary congestion.

Adım Adım Çözüm

1

Identify the primary clinical syndrome from the patient's signs and symptoms.

The patient exhibits orthopnea, paroxysmal nocturnal dyspnea, an S3 gallop, elevated jugular venous pressure, and bibasilar crackles, which point to acute decompensated heart failure (ADHF).

Recognizing the constellation of signs associated with volume overload and left ventricular failure is necessary to guide therapy.

2

Differentiate the presentation from other potential respiratory causes, specifically COPD.

Although the patient has a significant smoking history, the absence of wheezing, a normal expiratory phase, and the presence of prominent cardiac signs (S3, elevated JVP) make a COPD exacerbation highly unlikely.

Differentiating between ADHF and COPD is critical because their treatments (diuresis vs. bronchodilators/steroids) are vastly different.

3

Select the appropriate initial pharmacological intervention for the diagnosed condition.

Intravenous loop diuretics (like furosemide) should be administered.

Loop diuretics rapidly reduce volume overload, thereby decreasing ventricular preload and relieving pulmonary congestion.

Anahtar Kavram

Differentiating acute decompensated heart failure from a COPD exacerbation based on clinical signs, and initiating prompt diuresis.

Tahmini Süre:1m 0s

Soru 2322Soru →

A 68-year-old man is evaluated in the hospital prior to planned discharge. He was admitted 5 days ago for an acute exacerbation of heart failure. His medical history is notable for ischemic cardiomyopathy with a left ventricular ejection fraction of 30%, type 2 diabetes mellitus, and mild chronic obstructive pulmonary disease (COPD).

During this hospitalization, he has received aggressive diuresis with intravenous furosemide, achieving a net negative fluid balance of $6.5 \text{ L}$ . He currently feels well and denies shortness of breath.

Vital signs are temperature $37.0^\circ\text{C} (98.6^\circ\text{F})$ , blood pressure $118/74 \text{ mm Hg}$ , pulse $78/\text{min}$ , and respiratory rate $14/\text{min}$ . Oxygen saturation is 96% on room air.

Physical examination reveals absent jugular venous distension and no lower extremity edema. Auscultation of the lungs reveals decreased breath sounds at the right lung base.

A chest radiograph demonstrates a small-to-moderate right-sided pleural effusion, which is unchanged from admission. Because the effusion has not resolved with diuresis, a diagnostic thoracentesis is performed to rule out other etiologies.

Laboratory Test	Serum	Pleural Fluid
Total protein	$7.0 \text{ g/dL}$	$3.9 \text{ g/dL}$
Albumin	$3.6 \text{ g/dL}$	$1.9 \text{ g/dL}$
Lactate dehydrogenase (LDH)	$190 \text{ U/L}$	$125 \text{ U/L}$

Pleural fluid analysis also shows a leukocyte count of $150/\text{mm}^3$ (predominantly mononuclear) and a glucose level of $98 \text{ mg/dL}$ .

Arterial blood gas analysis on room air:

Parameter	Value
pH	$7.45$
$PaCO_2$	$46 \text{ mm Hg}$
$PaO_2$	$72 \text{ mm Hg}$
$HCO_3^-$	$31 \text{ mEq/L}$

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

Observation and transition to oral diuretics

Escalate to broad-spectrum intravenous antibiotics

Administer systemic corticosteroids and scheduled bronchodilators

Place a tube thoracostomy for pleural fluid drainage

Administer intravenous acetazolamide

Cevabı ve açıklamayı göster

Cevap: Observation and transition to oral diuretics

Cevap

Observation and transition to oral diuretics

The most appropriate next step is observation and transition to oral diuretics. This patient has a pleural effusion that initially appears exudative by Light's criteria (pleural-to-serum protein ratio of

0.55 > 0.5

; pleural-to-serum LDH ratio of

0.65 > 0.6

). However, he has been aggressively diuresed for heart failure (net negative

6.5 \text{ L}

). Diuresis removes water from the pleural space faster than proteins and LDH, concentrating the fluid and converting a transudate into a 'pseudo-exudate'. When clinical suspicion for a transudate remains high despite Light's criteria suggesting an exudate, the serum-to-pleural fluid albumin gradient (similar to the SAAG for ascites) should be calculated. A gradient

> 1.2 \text{ g/dL}

confirms a transudate. This patient's gradient is

1.7 \text{ g/dL}

(

3.6 - 1.9

), confirming the effusion is a transudate secondary to his known heart failure. Because he is now clinically euvolemic (no JVD, no edema, normal vitals) and the etiology is benign, no further acute intervention is needed; he can be safely observed and transitioned to oral maintenance diuretics.

Adım Adım Çözüm

1

Evaluate the pleural fluid using Light's criteria.

The fluid meets criteria for an exudate (pleural-to-serum protein ratio is 0.55 [> 0.5] and LDH ratio is 0.65 [> 0.6]).

Initial classification of pleural fluid is required to formulate a differential diagnosis.

2

Calculate the serum-to-pleural fluid albumin gradient.

The gradient is 1.7 g/dL (3.6 g/dL - 1.9 g/dL), which is > 1.2 g/dL, indicating a transudate.

In patients receiving diuretics, transudates can become concentrated as water is removed from the pleural space, falsely appearing as exudates by Light's criteria (a 'pseudo-exudate'). The albumin gradient corrects for this.

3

Interpret the acid-base status.

pH 7.45, elevated HCO3, and elevated PaCO2 indicate a fully compensated contraction alkalosis secondary to aggressive diuresis.

Ensures no superimposed acute respiratory failure from the patient's underlying COPD is present.

4

Determine the appropriate management.

Observation and transition to oral diuretics.

The patient is clinically euvolemic (absent JVD, no edema, negative 6.5 L fluid balance), and the effusion is a resolving transudate from heart failure, requiring no further invasive or acute medical intervention.

Anahtar Kavram

Patients undergoing active diuresis for heart failure can develop 'pseudo-exudates' where pleural fluid meets Light's criteria for an exudate but is actually a concentrated transudate; this is confirmed by a serum-to-pleural fluid albumin gradient > 1.2 g/dL.

Soru 2323Soru →

During morning rounds in the intensive care unit, a physician evaluates a patient who was admitted $24$ hours ago for severe right lower lobe pneumonia complicated by septic shock. The patient is a $72$ -year-old retired mechanic with a past medical history of ischemic cardiomyopathy (ejection fraction $35\%$ ) and type 2 diabetes mellitus. He is currently receiving targeted intravenous antibiotics based on rapid polymerase chain reaction testing, intravenous lactated Ringer's solution, and a continuous norepinephrine infusion.

Over the last hour, the patient has become increasingly agitated and diaphoretic. His temperature is $38.8^\circ$ C ( $101.8^\circ$ F), blood pressure is $86/52$ mm Hg, pulse is $118$ /min, and respiratory rate is $32$ /min. Physical examination demonstrates prominent use of the sternocleidomastoid and scalene muscles. Lung auscultation reveals coarse crackles at the right lung base.

Serum chemistry panel:

Parameter	Result	Reference Range
Sodium	$138$ mEq/L	$136-145$ mEq/L
Potassium	$4.8$ mEq/L	$3.5-5.0$ mEq/L
Chloride	$100$ mEq/L	$95-105$ mEq/L
Bicarbonate	$10$ mEq/L	$22-28$ mEq/L

Arterial blood gas (on

4

L/min nasal cannula):

Parameter	Result	Reference Range
pH	$7.07$	$7.35-7.45$
PaCO $_2$	$36$ mm Hg	$35-45$ mm Hg
PaO $_2$	$62$ mm Hg	$75-105$ mm Hg

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

Intravenous bolus of furosemide

Intravenous infusion of sodium bicarbonate

Endotracheal intubation and mechanical ventilation

Addition of intravenous micafungin to the antimicrobial regimen

Transport for a computed tomography angiography of the chest

Cevabı ve açıklamayı göster

Cevap: Endotracheal intubation and mechanical ventilation

Cevap

Endotracheal intubation and mechanical ventilation

The correct option is endotracheal intubation and mechanical ventilation. This patient is in septic shock with a high anion gap metabolic acidosis (Anion Gap =

138 - (100 + 10) = 28

). Appropriate respiratory compensation for this degree of metabolic acidosis is calculated using Winter's formula: Expected PaCO

_2

=

(1.5 \times \text{HCO}_3^-) + 8 \pm 2

. For this patient, Expected PaCO

_2

=

(1.5 \times 10) + 8 = 23 \pm 2

mm Hg. The patient's actual PaCO

_2

is

36

mm Hg. Although

36

mm Hg falls within the standard reference range, it is significantly higher than the expected

23

mm Hg. This indicates a superimposed primary respiratory acidosis. Clinically, the patient is breathing at

32

/min and using accessory muscles. The combination of increased work of breathing and an inappropriately elevated PaCO

_2

signifies diaphragmatic fatigue and impending respiratory arrest. The most appropriate next step to secure the airway and support ventilation is endotracheal intubation.

Adım Adım Çözüm

1

Calculate the anion gap to identify the primary metabolic disturbance.

Anion Gap =

138 - (100 + 10) = 28

mEq/L.

An elevated anion gap (

> 12

) confirms a primary high anion gap metabolic acidosis, expected in septic shock (lactic acidosis).

2

Calculate the expected PaCO2 using Winter's formula to assess respiratory compensation.

Expected PaCO

_2

=

(1.5 \times 10) + 8 \pm 2 = 23 \pm 2

mm Hg.

This determines what the lungs should be doing to compensate for the severe metabolic acidosis.

3

Compare the actual PaCO2 to the calculated expected PaCO2.

The actual PaCO

_2

(

36

mm Hg) is significantly higher than the expected PaCO

_2

(

23

mm Hg).

A PaCO2 higher than expected indicates a concomitant primary respiratory acidosis, meaning the patient is failing to ventilate adequately.

4

Synthesize the laboratory findings with the clinical presentation to determine the immediate intervention.

The patient requires endotracheal intubation.

Tachypnea with accessory muscle use, coupled with an inability to mount an appropriate respiratory compensation, indicates severe diaphragmatic fatigue and impending respiratory arrest.

Anahtar Kavram

Patients with severe metabolic acidosis must hyperventilate to compensate. A 'normal' PaCO2 in the setting of severe metabolic acidosis indicates respiratory muscle fatigue and impending respiratory failure, requiring immediate mechanical ventilation.

Soru 2324Soru →

Match each classic electrocardiographic (ECG) description to its corresponding cardiac condition.

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Cevap

Mobitz type I block presents with progressive PR lengthening and a dropped QRS; atrial flutter shows sawtooth waves; Wolff-Parkinson-White syndrome features a delta wave and short PR interval; acute pericarditis is marked by diffuse ST elevations and PR depressions.

Each listed ECG finding is a pathognomonic hallmark of its respective condition. Mobitz type I involves progressive AV node fatigue (Wenckebach). Atrial flutter generates macroreentrant circuits leading to sawtooth waves. WPW syndrome creates early ventricular depolarization via an accessory pathway, visible as a delta wave. Acute pericarditis causes diffuse subepicardial inflammation, reflecting as widespread ST elevations and PR depressions.

Adım Adım Çözüm

1

Analyze each electrocardiographic description provided in the left column.

Identified four distinct textbook patterns: Wenckebach periodicity, sawtooth baseline, pre-excitation features, and diffuse inflammatory changes.

Recognizing classic ECG patterns is foundational to linking them to their corresponding physiological or pathological causes.

2

Correlate the identified ECG patterns with the specific clinical diagnoses provided in the right column.

Matched the patterns to Mobitz type I block, atrial flutter, WPW syndrome, and acute pericarditis respectively.

This establishes the definitive diagnostic link required to complete the matching task.

Anahtar Kavram

Classic Electrocardiographic (ECG) Patterns in Cardiovascular Disease

Tahmini Süre:1m 0s

Soru 2325Soru →

A nephrologist is evaluating laboratory data and urinalysis findings from several patients. Match each clinical laboratory presentation with its most likely underlying etiology.

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Cevap

The presentations map to Prerenal azotemia (concentrated urine, low FENa), Acute tubular necrosis (muddy brown casts, high FENa), Type 1 RTA (high urine pH, kidney stones), Type 4 RTA (hyperkalemia, diabetes), and Acute glomerulonephritis (RBC casts), respectively.

Each laboratory and clinical profile correctly corresponds to a specific nephrologic disorder based on pathophysiologic mechanisms of sodium handling, concentrating ability, acid-base balance, and glomerular integrity.

Adım Adım Çözüm

1

Analyze the urinalysis and electrolyte parameters for the first two items to differentiate forms of acute kidney injury.

Low FENa and high osmolality indicate intact tubular function responding to hypoperfusion (prerenal). High FENa, low osmolality, and muddy brown casts indicate intrinsic tubular damage (acute tubular necrosis).

Differentiating prerenal from intrinsic renal failure relies on markers of tubular concentrating ability and sodium handling.

2

Evaluate the acid-base and electrolyte profiles for the next two items to distinguish forms of renal tubular acidosis (RTA).

A positive urine anion gap with high urine pH and stones points to Type 1 RTA. Hyperkalemia in a diabetic patient points to Type 4 RTA.

RTAs share non-anion gap metabolic acidosis but are differentiated by serum potassium, urine pH, and specific clinical associations.

3

Assess the urinary sediment in the final item.

RBC casts and dysmorphic RBCs indicate glomerular origin of hematuria.

RBC casts are pathognomonic for glomerulonephritis.

Anahtar Kavram

Interpretation of urinalysis, electrolyte panels, and acid-base status to diagnose renal etiologies.

Soru 2326Soru →

An evaluation for secondary amenorrhea and spontaneous bilateral galactorrhea is initiated for a 29-year-old female. She reports her last menstrual period occurred 8 months ago, prior to which her cycles were regular every 28 days. Over the past several months, the patient has also noted worsening constipation, generalized sluggishness, and increased sensitivity to cold environments. She takes no daily medications, and a urine pregnancy test is negative. Vital signs show a temperature of 36.2 °C (97.1 °F), blood pressure of 114/72 mm Hg, and a pulse of 54/min. Physical examination demonstrates delayed relaxation of the Achilles tendon reflexes.

Laboratory studies reveal:
Thyroid-stimulating hormone (TSH): $58.0 \ \mu\text{U/mL}$ (Normal: $0.4-4.0 \ \mu\text{U/mL}$ )
Free thyroxine (T4): $0.4 \ \text{ng/dL}$ (Normal: $0.9-2.4 \ \text{ng/dL}$ )
Prolactin: $82 \ \text{ng/mL}$ (Normal: $< 25 \ \text{ng/mL}$ )

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

Administer oral levothyroxine

Obtain a magnetic resonance image of the brain

Initiate therapy with cabergoline

Measure serum insulin-like growth factor 1

Perform a visual field examination

Cevabı ve açıklamayı göster

Cevap: Administer oral levothyroxine

Cevap

Administer oral levothyroxine

The correct answer addresses the root cause of the patient's symptoms. The patient has primary hypothyroidism, evidenced by her fatigue, cold intolerance, bradycardia, delayed deep tendon reflexes, elevated TSH, and low free T4. In primary hypothyroidism, the lack of circulating thyroid hormone removes negative feedback on the hypothalamus, resulting in increased production of thyrotropin-releasing hormone (TRH). TRH stimulates the anterior pituitary to release not only TSH but also prolactin. The resulting hyperprolactinemia suppresses gonadotropin-releasing hormone (GnRH) pulsatility, leading to secondary amenorrhea and galactorrhea. The most appropriate next step is to treat the primary hypothyroidism with levothyroxine. Normalizing thyroid hormone levels will restore negative feedback, lower TRH, normalize prolactin levels, and resolve the amenorrhea and galactorrhea.

Adım Adım Çözüm

1

Interpret the clinical presentation and laboratory results.

The patient has signs of hypothyroidism (bradycardia, delayed reflexes, cold intolerance) confirmed by high TSH and low free T4, alongside moderate hyperprolactinemia.

Establishing the primary physiological derangement is required before deciding on further diagnostic or therapeutic interventions.

2

Connect the primary hypothyroidism to the hyperprolactinemia.

Primary hypothyroidism causes a loss of negative feedback, leading to increased hypothalamic secretion of thyrotropin-releasing hormone (TRH).

TRH stimulates lactotrophs in the anterior pituitary to secrete prolactin, in addition to stimulating thyrotrophs to secrete TSH.

3

Determine the effect of hyperprolactinemia on the menstrual cycle.

Elevated prolactin inhibits the pulsatile release of gonadotropin-releasing hormone (GnRH), leading to secondary amenorrhea and galactorrhea.

This explains the patient's absence of menses and breast discharge.

4

Select the most appropriate next step in management.

Administer oral levothyroxine to treat the primary hypothyroidism.

Treating the root cause will normalize TRH levels, which in turn will normalize TSH and prolactin levels, resolving all symptoms without the need for pituitary imaging or dopamine agonists.

Anahtar Kavram

Hyperprolactinemia secondary to primary hypothyroidism

Tahmini Süre:1m 15s

Soru 2327Soru →

A 38-year-old woman presents to the emergency department with a 1-week history of worsening fatigue, spontaneous gum bleeding, and easy bruising. Her temperature is 37.8°C (100°F), blood pressure is 110/70 mm Hg, and pulse is 105/min. Physical examination is notable for diffuse petechiae across her chest and extremities, as well as oozing from her intravenous catheter site.

Laboratory studies show:

Parameter	Result
Leukocyte count	$28,000/\mu L$
Hemoglobin	$8.2 \text{ g/dL}$
Platelet count	$18,000/\mu L$
Prothrombin time (PT)	$22 \text{ sec}$
Activated PTT	$48 \text{ sec}$
Fibrinogen	$90 \text{ mg/dL}$

A peripheral blood smear demonstrates numerous atypical promyelocytes with multiple needle-like cytoplasmic inclusions.

Arrange the following steps in the most appropriate chronological sequence for the management of this patient's condition.

Öğeleri doğru sıraya koymak için sürükleyin

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Cevap

The correct sequence of management is: Administration of ATRA, followed by bone marrow aspiration and biopsy, then confirmation of the PML-RARA fusion gene, and finally the initiation of comprehensive induction therapy.

Acute promyelocytic leukemia (APL) is a medical emergency that classically presents with pancytopenia and severe disseminated intravascular coagulation (DIC). The pathognomonic finding is a peripheral smear with atypical promyelocytes containing numerous Auer rods (needle-like inclusions). Because the risk of catastrophic bleeding is extremely high, the standard of care dictates that all-trans retinoic acid (ATRA) must be administered immediately based on clinical and morphological suspicion alone. ATRA induces the differentiation of the leukemic promyelocytes, rapidly reversing the coagulopathy. Once the patient is stabilized and ATRA is initiated, a bone marrow aspiration and biopsy should be performed to secure the diagnosis. From this marrow sample, cytogenetic or molecular studies (such as FISH or RT-PCR) are run to definitively confirm the presence of the t(15;17) translocation and the resulting PML-RARA fusion gene. Only after this definitive confirmation is the comprehensive induction regimen (such as the addition of arsenic trioxide) fully committed to for curative intent.

Adım Adım Çözüm

1

Identify the clinical presentation as acute promyelocytic leukemia (APL) complicated by disseminated intravascular coagulation (DIC).

The patient has pancytopenia, coagulopathy (prolonged PT/aPTT, low fibrinogen), and a smear showing atypical promyelocytes with Auer rods (needle-like inclusions).

Recognizing this classic presentation is essential because APL is a hematologic emergency requiring immediate specific intervention.

2

Determine the most critical immediate intervention.

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

ATRA forces the malignant promyelocytes to differentiate, which rapidly improves the life-threatening coagulopathy. It must be given upon suspicion without waiting for genetic confirmation.

3

Determine the diagnostic sequence following stabilization.

A bone marrow aspiration and biopsy is performed next.

Tissue is required to formally diagnose the leukemia and perform specific cytogenetic and molecular tests.

4

Identify the confirmatory test and subsequent long-term management.

The PML-RARA fusion gene is confirmed, leading to comprehensive induction therapy.

Definitive targeted treatment (e.g., adding arsenic trioxide) requires confirmation of the t(15;17) translocation, establishing the final step in this initial sequence.

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 alone, prior to waiting for definitive bone marrow biopsy and cytogenetic confirmation.

Alternatif Yöntem

While managing the specific leukemia, concurrent supportive care with cryoprecipitate (to keep fibrinogen > 150 mg/dL) and platelets (to keep > 30,000-50,000/µL) should occur simultaneously with ATRA administration.

Tahmini Süre:1m 30s

Soru 2328Soru →

Correlate the following clinical scenarios involving suspected central nervous system infections with the most appropriate empiric or targeted pharmacotherapy.

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Cevap

1: Empiric bacterial meningitis >50 years is treated with ceftriaxone, vancomycin, and ampicillin. 2: Cryptococcal meningitis is treated with liposomal amphotericin B and flucytosine. 3: Neurologic Lyme disease is treated with intravenous ceftriaxone. 4: HSV encephalitis is treated with intravenous acyclovir. 5: Post-neurosurgical meningitis is treated with vancomycin and cefepime.

Each clinical scenario uniquely points to a distinct central nervous system infection etiology requiring a specific therapeutic approach based on current Infectious Diseases Society of America (IDSA) guidelines.

Adım Adım Çözüm

1

Analyze each patient's demographic profile, exposure history, and immune status.

Identified a healthy older adult, a severely immunocompromised HIV patient, an outdoor worker with a previous erythema migrans rash, an adult with rapidly progressive encephalopathy, and a post-neurosurgical patient.

Host factors and epidemiologic exposures dictate the most likely etiology of central nervous system infections.

2

Evaluate the localized signs and cerebrospinal fluid (CSF) findings.

Correlated neutrophilic pleocytosis with bacterial meningitis, mononuclear pleocytosis with elevated pressure to fungal/cryptococcal infection, hemorrhagic CSF with temporal lobe edema to HSV, and lymphocytic pleocytosis with facial palsy to neurologic Lyme.

CSF profiles (neutrophilic vs. lymphocytic/mononuclear) and imaging findings help differentiate bacterial, viral, fungal, and spirochetal causes.

3

Select the guideline-recommended antimicrobial regimen for each specific diagnosis.

Matched age-based bacterial coverage, targeted fungal induction therapy, anti-spirochetal cephalosporin therapy, antiviral therapy, and anti-pseudomonal/MRSA coverage accordingly.

Delivering precise empiric or targeted therapy prevents significant morbidity and mortality associated with central nervous system infections.

Anahtar Kavram

Selection of empiric and targeted antimicrobial regimens for central nervous system infections must be strictly tailored to patient age, immune status, unique exposures, and specific cerebrospinal fluid profiles.

Soru 2329Soru →

A 34-year-old woman is evaluated in the emergency department for sudden-onset, severe, and cramping mid-abdominal pain that began 8 hours ago. The pain is continuous but worsens in waves. She has had three episodes of vomiting, which recently became bilious. Her past medical history is significant for a laparoscopic Roux-en-Y gastric bypass performed 2 years ago for class III obesity, resulting in a 45-kg (99-lb) weight loss. Her temperature is 37.8°C (100.0°F), pulse is 115/min, blood pressure is 108/68 mm Hg, and respirations are 18/min. Physical examination reveals an anxious patient in obvious distress. The abdomen is mildly distended with focal tenderness in the mid-abdomen, but there is no rebound tenderness or rigidity. Bowel sounds are high-pitched.

Laboratory results:
Leukocyte count: 14,500/mm³
Hemoglobin: 13.2 g/dL
Serum sodium: 138 mEq/L
Serum potassium: 3.6 mEq/L
Blood urea nitrogen: 24 mg/dL
Serum creatinine: 1.1 mg/dL
Serum lactate: 3.2 mmol/L (Normal: 0.5 - 2.2 mmol/L)

A computed tomography (CT) scan of the abdomen and pelvis with intravenous contrast reveals dilated loops of small bowel with a transition point. The mesenteric vessels appear rotated around a central axis, and there is mild adjacent mesenteric edema. There is no free intraperitoneal air.

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

Urgent operative exploration

Gastrointestinal decompression with a double-lumen tube and bowel rest

Initiation of empiric broad-spectrum antimicrobial therapy

Diagnostic esophagogastroduodenoscopy

Administration of an oral water-soluble contrast agent

Cevabı ve açıklamayı göster

Cevap: Urgent operative exploration

Cevap

Urgent operative exploration

The correct answer is urgent operative exploration. This patient presents with acute small bowel obstruction (SBO) symptoms, leukocytosis, and an elevated serum lactate level. She has a history of a Roux-en-Y gastric bypass (RYGB), which places her at high risk for an internal hernia (e.g., through Petersen's space or the mesojejunal defect). The CT finding of mesenteric vessels rotated around a central axis (the 'mesenteric swirl' sign) is highly specific for a volvulus or internal hernia. These conditions create a closed-loop obstruction, where a bowel segment is occluded at two adjacent points. This rapidly compromises vascular supply, leading to ischemia, necrosis, and perforation if not immediately addressed. The presence of tachycardia, leukocytosis, and an elevated lactate (indicating anaerobic metabolism from hypoperfusion) strongly suggests early bowel ischemia. Therefore, urgent surgical intervention is required to reduce the hernia, assess bowel viability, and repair the mesenteric defects.

Adım Adım Çözüm

1

Analyze the patient's history and acute presentation.

The patient has acute small bowel obstruction (SBO) symptoms (colicky pain, bilious vomiting, dilated loops with a transition point) and a history of a Roux-en-Y gastric bypass (RYGB).

Identifying prior abdominal surgeries helps determine the specific etiology of the SBO.

2

Interpret the specific imaging and laboratory findings.

CT shows a 'mesenteric swirl' sign, diagnostic of an internal hernia. Laboratories show leukocytosis and an elevated lactate level.

The swirl sign indicates a closed-loop obstruction, while elevated lactate and WBCs suggest impending bowel ischemia.

3

Determine the appropriate management strategy based on the obstruction type.

The patient requires urgent operative exploration.

Unlike simple adhesive SBOs which may be managed conservatively, closed-loop obstructions with signs of ischemia mandate immediate surgical intervention to prevent bowel necrosis and perforation.

Anahtar Kavram

Patients with a history of Roux-en-Y gastric bypass who present with signs of a small bowel obstruction and a 'mesenteric swirl' on CT likely have an internal hernia. This creates a closed-loop obstruction with a high risk of rapid bowel ischemia, necessitating urgent operative exploration rather than conservative management.

Soru 2330Soru →

A $61$ -year-old man with decompensated cirrhosis secondary to metabolic dysfunction-associated steatohepatitis (MASH) is evaluated in the progressive care unit for acute kidney injury. He was admitted four days prior for tense ascites, at which time he underwent an uncomplicated $6$ -liter therapeutic paracentesis. Currently, he reports feeling fatigued but denies abdominal pain, fever, or shortness of breath. His daily urine output has declined to $350$ mL over the past $24$ hours. Spironolactone and furosemide were discontinued two days ago when an initial rise in creatinine was noted.

A urine culture collected on admission grew $>100,000$ CFU/mL of *Escherichia coli* pan-susceptible to all tested agents, and he has been receiving targeted oral amoxicillin.

Vital signs are temperature $37.1^\circ$ C ( $98.8^\circ$ F), blood pressure $96/58$ mmHg, and pulse $86$ /min. Physical examination reveals scleral icterus, a protuberant abdomen with a positive fluid wave, and bilateral pitting edema up to the mid-calves.

Laboratory findings:
Hemoglobin: $10.2$ g/dL
Leukocyte count: $6,800/\mu$ L
Serum sodium: $131$ mEq/L
Blood urea nitrogen: $68$ mg/dL
Serum creatinine: $2.8$ mg/dL (baseline at admission: $1.1$ mg/dL)
Urine sodium: $8$ mEq/L
Urinalysis: occasional hyaline casts, no red blood cells, negative for protein

A repeat diagnostic paracentesis performed this morning yields fluid with a total leukocyte count of $120/\mu$ L and $15\%$ neutrophils. An ultrasound of the kidneys shows normal cortical echogenicity without hydronephrosis. Over the preceding $24$ hours, the patient received a continuous infusion of intravenous isotonic crystalloid totaling $2.5$ liters, but his repeat serum creatinine today remains unchanged at $2.8$ mg/dL.

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

Intravenous administration of albumin

Initiation of midodrine and octreotide therapy

Escalation of antimicrobial therapy to intravenous piperacillin-tazobactam

Consultation for urgent hemodialysis

Evaluation for transjugular intrahepatic portosystemic shunt

Cevabı ve açıklamayı göster

Cevap: Intravenous administration of albumin

Cevap

The correct answer is the intravenous administration of albumin.

The correct answer is the intravenous administration of albumin. Hepatorenal syndrome (HRS-AKI) is a unique form of functional renal failure in patients with advanced cirrhosis, characterized by severe renal vasoconstriction. However, because these patients have profound splanchnic vasodilation and reduced effective circulating volume, pre-renal azotemia from volume depletion is the most common cause of acute kidney injury. In cirrhosis, crystalloid solutions rapidly shift into the extravascular space (third-spacing) due to portal hypertension and hypoalbuminemia, making them highly ineffective at expanding the effective arterial volume. Therefore, before diagnosing HRS and initiating vasoconstrictor therapy, current AASLD guidelines mandate a volume expansion challenge specifically with intravenous albumin (typically 1 g/kg/day for 2 consecutive days). The lack of response to 2.5 liters of isotonic crystalloids does not fulfill this diagnostic requirement.

Adım Adım Çözüm

1

Identify the etiology pattern of acute kidney injury in this patient.

The patient has pre-renal physiology (indicated by a low urine sodium of 8 mEq/L and occasional hyaline casts) with no response to 2.5 liters of intravenous crystalloids.

Differentiating true volume depletion from hepatorenal syndrome (HRS-AKI) is the critical diagnostic branch point.

2

Determine if the diagnostic criteria for Hepatorenal Syndrome have been met.

The criteria have not been met. Diagnosis requires the absence of renal improvement after at least 48 hours of diuretic withdrawal and plasma volume expansion specifically with intravenous albumin.

Crystalloids freely diffuse out of the intravascular space in cirrhosis due to profound portal hypertension and hypoalbuminemia, making them inadequate for expanding effective arterial volume.

3

Select the next best step in management based on guidelines.

The patient must receive an intravenous albumin challenge (1 g/kg/day).

To adequately treat potential uncorrected pre-renal azotemia and complete the diagnostic workup for HRS-AKI.

Anahtar Kavram

Diagnosis of Hepatorenal Syndrome (HRS-AKI) requires failure of renal function to improve after a therapeutic volume expansion challenge with intravenous albumin; crystalloid fluids are inadequate for this purpose.

Tahmini Süre:1m 30s

Soru 2331Soru →

A 32-year-old man presents to the emergency department with a 4-week history of productive cough, occasional hemoptysis, low-grade fevers, and night sweats. He has experienced a 5-kg (11-lb) unintentional weight loss during this time. The patient immigrated to the United States from a region highly endemic for tuberculosis two months ago. His temperature is 37.8°C (100.0°F), blood pressure is 120/78 mm Hg, pulse is 88/min, and respiratory rate is 16/min. Physical examination reveals bronchial breath sounds and crackles in the right upper lung field. The clinical presentation is highly suspicious for active pulmonary tuberculosis. Arrange the following management steps in the most appropriate chronological order.

Öğeleri doğru sıraya koymak için sürükleyin

Cevabı ve açıklamayı göster

Cevap

The correct sequence of steps is: 1) Place the patient in an airborne infection isolation room with negative pressure, 2) Obtain a posterior-anterior and lateral chest radiograph, 3) Obtain sputum specimens for acid-fast bacilli smear and culture, and 4) Initiate empiric four-drug therapy with rifampin, isoniazid, pyrazinamide, and ethambutol.

The proper sequence for managing a patient with high clinical suspicion for active pulmonary tuberculosis begins with protecting public health. Immediate airborne infection isolation is the absolute first priority. Once the patient is isolated, the diagnostic workup begins with a chest radiograph to identify characteristic pulmonary lesions. This is followed by the collection of sputum specimens for definitive microbiologic diagnosis. Finally, empiric anti-mycobacterial therapy is initiated only after all diagnostic cultures have been collected, ensuring the medications do not interfere with culture yield.

Adım Adım Çözüm

1

Assess the risk of airborne transmission.

The patient's symptoms (chronic cough, hemoptysis, weight loss) and epidemiologic history strongly suggest active tuberculosis.

Identifying the high risk of a highly contagious airborne disease dictates the immediate need for strict infection control.

2

Implement immediate infection control measures.

The patient is placed in an airborne infection isolation room.

To prevent the aerosolized spread of Mycobacterium tuberculosis to healthcare personnel and other patients in the emergency department.

3

Perform initial diagnostic imaging.

A chest radiograph is obtained (often via portable machine).

To rapidly evaluate for structural lung abnormalities indicative of tuberculosis, such as apical consolidations or cavitations.

4

Secure definitive microbiologic diagnostic samples.

Sputum specimens are collected for AFB smear, culture, and nucleic acid amplification testing.

To confirm the diagnosis microbiologically and obtain crucial drug susceptibility testing prior to introducing medications.

5

Initiate empiric targeted pharmacotherapy.

A four-drug regimen (RIPE) is started.

To begin treating the active infection safely after all necessary diagnostic samples have been securely obtained.

Anahtar Kavram

Management Sequence for Suspected Active Pulmonary Tuberculosis

Tahmini Süre:1m 30s

Soru 2332Soru →

A clinician is evaluating four non-diabetic adult patients who presented with recurrent episodes of neuroglycopenia. A 72-hour fasting test was performed for each patient. Match each patient's laboratory profile obtained during the symptomatic hypoglycemic episode (glucose $<55\text{ mg/dL}$ ) to the most likely underlying etiology.

Soldaki öğeye tıklayın, sonra eşleşen sağdaki öğeye tıklayın

Cevabı ve açıklamayı göster

Cevap

Profile 1 matches Insulinoma; Profile 2 matches Exogenous insulin; Profile 3 matches Secretagogue ingestion; Profile 4 matches Non-islet cell tumor hypoglycemia.

Each patient's hypoglycemia etiology is systematically determined by evaluating the presence of endogenous insulin production (C-peptide), precursor processing (proinsulin), and exogenous secretagogues.

Adım Adım Çözüm

1

Evaluate serum insulin levels during the hypoglycemic episode.

Profiles 1, 2, and 3 show high insulin (insulin-mediated). Profile 4 shows low insulin (non-insulin-mediated).

This differentiates hyperinsulinemic states from causes like severe liver failure, adrenal insufficiency, or NICTH where insulin is appropriately suppressed.

2

Analyze C-peptide levels in the hyperinsulinemic profiles.

Profile 1 and 3 have high C-peptide. Profile 2 has low C-peptide.

C-peptide is co-secreted with endogenous insulin. High insulin with low C-peptide proves the insulin came from an exogenous source.

3

Check the secretagogue screen and proinsulin levels for profiles with high C-peptide.

Profile 1 has a negative screen and high proinsulin. Profile 3 has a positive screen.

This step distinguishes between autonomous tumoral secretion of insulin (insulinoma) and pharmacologically stimulated endogenous secretion (sulfonylureas/meglitinides).

Anahtar Kavram

Diagnostic evaluation of fasting hypoglycemia using the insulin, C-peptide, and oral hypoglycemic agent screen axis.

Soru 2333Soru →

A 68-year-old man is brought to the emergency department for worsening shortness of breath, increased sputum production, and confusion over the past 24 hours. He has very severe chronic obstructive pulmonary disease (COPD) and uses home oxygen therapy. The patient's wife reports that for the past 3 days, he has also had multiple episodes of large-volume, watery diarrhea.

Vital signs are temperature 37.6°C (99.7°F), blood pressure 110/70 mm Hg, pulse 115/min, and respirations 26/min. Physical examination shows a barrel chest, diffuse bilateral wheezing, and a prolonged expiratory phase. The mucous membranes are dry.

Laboratory results from today are as follows:

Serum chemistries:

Test	Result
Sodium	135 mEq/L
Potassium	3.5 mEq/L
Chloride	102 mEq/L
Bicarbonate	23 mEq/L
Blood urea nitrogen	28 mg/dL
Creatinine	1.2 mg/dL

Arterial blood gas:

Test	Result
pH	7.17
PaCO2	66 mm Hg
PaO2	50 mm Hg
HCO3-	23 mEq/L

A review of the patient's electronic medical record reveals an arterial blood gas obtained during a routine clinic visit 2 months ago when he was feeling well:

Baseline Arterial blood gas:

Test	Result
pH	7.36
PaCO2	56 mm Hg
PaO2	62 mm Hg
HCO3-	31 mEq/L

Which of the following combinations of acid-base disorders best describes this patient's current condition?

Acute-on-chronic respiratory acidosis and normal anion gap metabolic acidosis

Acute-on-chronic respiratory acidosis and high anion gap metabolic acidosis

Acute respiratory acidosis and normal anion gap metabolic acidosis

Chronic respiratory acidosis and normal anion gap metabolic acidosis

Uncompensated acute respiratory acidosis

Cevabı ve açıklamayı göster

Cevap: Acute-on-chronic respiratory acidosis and normal anion gap metabolic acidosis

Cevap

Acute-on-chronic respiratory acidosis and normal anion gap metabolic acidosis

The correct answer is acute-on-chronic respiratory acidosis and normal anion gap metabolic acidosis. The patient's baseline ABG shows a compensated chronic respiratory acidosis (PaCO2

56 \text{ mm Hg}

, HCO3-

31 \text{ mEq/L}

). Today, his PaCO2 has acutely increased to

66 \text{ mm Hg}

(an acute increase of

10 \text{ mm Hg}

). For an acute rise in PaCO2, the HCO3- should increase by

1 \text{ mEq/L}

per

10 \text{ mm Hg}

rise in PaCO2. Therefore, his expected HCO3- is

32 \text{ mEq/L}

(

31 + 1

). His actual HCO3- is

23 \text{ mEq/L}

, which is significantly lower than expected, indicating a concurrent metabolic acidosis. The anion gap is calculated as

135 - (102 + 23) = 10 \text{ mEq/L}

, which is normal. This normal anion gap metabolic acidosis is clinically supported by his 3-day history of severe diarrhea, which causes profound gastrointestinal bicarbonate loss.

Adım Adım Çözüm

1

Analyze the baseline arterial blood gas.

The baseline ABG shows a PaCO2 of 56 mm Hg and HCO3- of 31 mEq/L, consistent with a compensated chronic respiratory acidosis.

Establishing the patient's baseline is necessary to correctly interpret the current acute changes in patients with severe COPD.

2

Evaluate the current PaCO2 and calculate the expected compensation.

The PaCO2 has acutely increased by 10 mm Hg (from 56 to 66 mm Hg). The expected acute increase in HCO3- is 1 mEq/L, making the new expected HCO3- 32 mEq/L (31 + 1).

In acute respiratory acidosis, the HCO3- increases by 1 mEq/L for every 10 mm Hg increase in PaCO2.

3

Compare actual HCO3- to expected HCO3-.

The actual HCO3- is 23 mEq/L, which is significantly lower than the expected 32 mEq/L. This indicates a superimposed metabolic acidosis.

A lower-than-expected bicarbonate level in the setting of respiratory acidosis confirms a concurrent metabolic acidosis.

4

Calculate the anion gap.

Anion Gap = Na+ - (Cl- + HCO3-) = 135 - (102 + 23) = 10 mEq/L. This is within the normal range.

The anion gap differentiates between a normal anion gap and a high anion gap metabolic acidosis. The normal gap points to GI bicarbonate loss from diarrhea.

Anahtar Kavram

Patients with chronic respiratory acidosis who develop an acute exacerbation require step-wise acid-base analysis utilizing their baseline ABG values to accurately calculate expected compensation and identify superimposed metabolic disorders.

Tahmini Süre:2m 0s

Soru 2334Soru →

Match each patient's acquired acid-base and electrolyte derangement profile with the pharmacological agent most likely responsible for these findings.

Soldaki öğeye tıklayın, sonra eşleşen sağdaki öğeye tıklayın

Cevabı ve açıklamayı göster

Cevap

The correct answer links the hypocalciuric alkalosis to thiazide diuretics, the hyperchloremic acidosis with alkaline urine to carbonic anhydrase inhibitors, the hypercalciuric alkalosis to loop diuretics, and the hyperkalemic acidosis to aldosterone antagonists.

Each pharmacological agent acts on a specific segment of the nephron, creating a unique signature of electrolyte and acid-base changes based on the localized transport mechanisms disrupted.

Adım Adım Çözüm

1

Analyze the primary acid-base disturbance described in each presentation.

Two profiles exhibit metabolic alkalosis (patients 1 and 3), and two exhibit a normal anion gap metabolic acidosis (patients 2 and 4).

Categorizing the primary acid-base derangement immediately narrows down the physiological mechanism of action.

2

Differentiate the causes of metabolic alkalosis based on the urinary calcium handling.

Patient 1 presents with hypocalciuria (characteristic of thiazides), while Patient 3 presents with hypercalciuria (characteristic of loop diuretics).

Thiazides and loop diuretics both cause hypokalemic contraction alkalosis, but they have profoundly opposite effects on renal calcium handling.

3

Differentiate the causes of metabolic acidosis based on potassium levels and urine pH.

Patient 2 shows an alkaline urine pH due to bicarbonate wasting, identifying a carbonic anhydrase inhibitor. Patient 4 shows hyperkalemia, identifying an aldosterone antagonist.

Acetazolamide causes a proximal RTA-like picture with hypokalemia, whereas spironolactone causes a Type 4 RTA-like picture defined by hyperkalemia.

Anahtar Kavram

Diuretic-induced acid-base and electrolyte derangements can be precisely distinguished by their unique downstream effects on serum potassium, acid-base balance, and urinary calcium handling.

Tahmini Süre:1m 30s

Soru 2335Soru →

An occupational health physician refers a 41-year-old male to an internist after discovering a resting heart rate of $112\text{/min}$ during an annual workplace screening. The patient reports experiencing intermittent palpitations, profound heat intolerance, and a 5-kg (11-lb) weight loss over the past three months despite a significantly increased appetite. He has no significant past medical history and takes no medications. His blood pressure is $150/85\text{ mmHg}$ . Physical examination demonstrates warm and moist skin, a fine resting tremor in both hands, and a diffusely enlarged, non-tender thyroid gland. No proptosis or periorbital edema is observed.

Laboratory studies yield the following results:

Laboratory Test	Result	Reference Range
Thyroid-stimulating hormone (TSH)	$6.8\text{ }\mu\text{U/mL}$	$0.4 - 4.0\text{ }\mu\text{U/mL}$
Free thyroxine (T4)	$3.2\text{ ng/dL}$	$0.9 - 1.7\text{ ng/dL}$
Free triiodothyronine (T3)	$7.1\text{ pg/mL}$	$2.0 - 4.4\text{ pg/mL}$

Which of the following is the most appropriate next step in diagnosing the underlying cause of this patient's condition?

Magnetic resonance imaging of the brain

Radioactive iodine uptake scan

Measurement of thyroid-stimulating immunoglobulins

Measurement of serum thyroglobulin levels

Ultrasonography of the thyroid gland

Cevabı ve açıklamayı göster

Cevap: Magnetic resonance imaging of the brain

Cevap

Magnetic resonance imaging of the brain

This patient presents with classic clinical features of thyrotoxicosis, confirmed by elevated serum free T4 and free T3 levels. In primary hyperthyroidism (such as Graves disease or toxic nodular goiter), the elevated circulating thyroid hormones exert negative feedback on the pituitary gland, leading to a profoundly suppressed TSH level. However, this patient's TSH is inappropriately elevated. The combination of high thyroid hormone levels and an elevated or normal TSH indicates a central (secondary) cause of hyperthyroidism, which is most commonly due to a TSH-secreting pituitary adenoma. The most appropriate next diagnostic step is a magnetic resonance imaging (MRI) scan of the brain to visualize the expected pituitary macroadenoma.

Adım Adım Çözüm

1

Analyze the patient's symptoms and vital signs.

The patient exhibits classic signs of thyrotoxicosis, including resting tachycardia, heat intolerance, weight loss, and a fine tremor.

To establish the primary clinical syndrome before interpreting laboratory values.

2

Evaluate the provided laboratory values.

Free T4 and Free T3 are elevated, confirming thyrotoxicosis. However, the TSH is also inappropriately elevated rather than suppressed.

To determine whether the hyperthyroidism is primary (thyroid origin) or secondary (central origin).

3

Interpret the combination of elevated thyroid hormones and elevated TSH.

This pattern indicates secondary (central) hyperthyroidism, as a normal pituitary gland would completely suppress TSH production in the presence of high circulating T4 and T3.

To identify the pathophysiologic mechanism of the disease.

4

Determine the next best step in diagnostic management based on the central etiology.

Imaging of the brain is indicated to visualize a suspected TSH-secreting pituitary adenoma.

Definitive diagnosis and subsequent surgical planning for a pituitary tumor require direct visualization via MRI.

Anahtar Kavram

Secondary (central) hyperthyroidism is characterized by elevated circulating thyroid hormones (Free T4 and T3) alongside an inappropriately normal or elevated TSH. The most appropriate next step in evaluation is a pituitary MRI to identify a TSH-secreting pituitary adenoma.

Soru 2336Soru →

A 22-year-old man with a history of type 1 diabetes mellitus is brought to the emergency department due to progressive lethargy, nausea, vomiting, and diffuse abdominal pain over the past 24 hours. He reports having a severe sore throat and fever for the last three days. His temperature is 37.5°C (99.5°F), blood pressure is 92/58 mm Hg, pulse is 128/min, and respirations are 28/min and deep. Physical examination reveals dry mucous membranes, delayed capillary refill, and a fruity breath odor. Laboratory evaluation reveals:

Laboratory Test	Result
Serum glucose	580 mg/dL
Serum sodium	132 mEq/L
Serum potassium	3.1 mEq/L
Serum chloride	98 mEq/L
Serum bicarbonate	10 mEq/L
Blood urea nitrogen	35 mg/dL
Serum creatinine	1.6 mg/dL
Arterial pH	7.15
Urinalysis	Large ketones, large glucose

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

Öğeleri doğru sıraya koymak için sürükleyin

Cevabı ve açıklamayı göster

Cevap

The correct sequence is: Intravenous 0.9% sodium chloride bolus → Intravenous potassium chloride → Continuous intravenous regular insulin infusion → Add 5% dextrose to intravenous fluids → Subcutaneous long-acting insulin.

The correct sequence prioritizes immediate life-saving interventions while preventing iatrogenic complications. Intravenous fluids (0.9% NaCl) are universally the first step in DKA to restore volume and renal perfusion. Next, because the patient's potassium is critically low (< 3.3 mEq/L), potassium chloride must be given before insulin to prevent life-threatening hypokalemia. Once potassium is confirmed to be ≥ 3.3 mEq/L, an intravenous insulin infusion is started to halt ketogenesis. As glucose levels fall below 250 mg/dL, dextrose is added to the fluids to prevent hypoglycemia while allowing continued insulin administration to close the anion gap. Finally, once the anion gap resolves and the patient can eat, they are transitioned to subcutaneous insulin.

Adım Adım Çözüm

1

Assess volume status and initiate fluid resuscitation.

Intravenous 0.9% normal saline is given immediately.

The patient is hypotensive, tachycardic, and severely dehydrated due to osmotic diuresis; volume expansion is always the first priority.

2

Evaluate initial serum potassium level before administering insulin.

Intravenous potassium chloride is administered next.

The patient's potassium is 3.1 mEq/L (below the critical 3.3 mEq/L threshold). Insulin causes an intracellular shift of potassium, so giving insulin now would cause life-threatening hypokalemia.

3

Initiate insulin therapy once potassium is safe.

Continuous intravenous regular insulin infusion is started.

Insulin is required to stop ketogenesis and close the anion gap. It is safe to start only after potassium is ≥ 3.3 mEq/L.

4

Monitor glucose and adjust intravenous fluids.

Dextrose 5% is added to the intravenous fluids.

When serum glucose reaches 200-250 mg/dL, dextrose must be added to prevent hypoglycemia while the insulin infusion continues to clear ketones.

5

Transition to maintenance diabetes therapy.

Subcutaneous long-acting insulin is administered.

This is done when the anion gap is closed (usually ≤ 12 mEq/L) and the patient can eat, allowing for the eventual discontinuation of the IV insulin drip (1-2 hours later).

Anahtar Kavram

In the management of diabetic ketoacidosis, if the initial serum potassium is < 3.3 mEq/L, potassium repletion must precede insulin therapy to prevent severe, potentially fatal insulin-induced hypokalemia.

Soru 2337Soru →

Emergency medical services bring a 72-year-old woman to the hospital after her daughter found her profoundly lethargic at home. According to the daughter, the patient has had severe, watery, non-bloody diarrhea for the past five days. Her past medical history is significant for severe chronic obstructive pulmonary disease requiring home oxygen therapy, hypertension, and osteoarthritis. Upon arrival, the patient is difficult to arouse.

Temperature is $37.2^\circ\text{C}$ ( $99.0^\circ\text{F}$ ), blood pressure is $88/54$ mmHg, pulse is $114$ /min, and respiratory rate is $26$ /min. Physical examination reveals dry mucous membranes, delayed capillary refill, and decreased breath sounds bilaterally with a prolonged expiratory phase.

Arterial blood gas (room air) and serum chemistries are obtained:

Laboratory Parameter	Result
Arterial pH	$7.21$
$\text{PaCO}_2$	$42$ mmHg
$\text{PaO}_2$	$56$ mmHg
Sodium	$139$ mEq/L
Potassium	$3.1$ mEq/L
Chloride	$114$ mEq/L
Bicarbonate	$15$ mEq/L
Blood urea nitrogen (BUN)	$48$ mg/dL
Creatinine	$2.1$ mg/dL

Which of the following best describes this patient's underlying acid-base disturbance?

Mixed non-anion gap metabolic acidosis and respiratory acidosis

Mixed high anion gap metabolic acidosis and respiratory acidosis

Non-anion gap metabolic acidosis with appropriate respiratory compensation

High anion gap metabolic acidosis with appropriate respiratory compensation

Mixed non-anion gap metabolic acidosis and respiratory alkalosis

Cevabı ve açıklamayı göster

Cevap: Mixed non-anion gap metabolic acidosis and respiratory acidosis

Cevap

Mixed non-anion gap metabolic acidosis and respiratory acidosis

The correct answer is a mixed non-anion gap metabolic acidosis and respiratory acidosis. The first step in evaluating this patient's acid-base status is identifying the primary disorder: the

pH

is

7.21

(acidemia) and the serum bicarbonate is

15

mEq/L (decreased), signifying a primary metabolic acidosis. Next, the anion gap must be calculated:

\text{Na}^+ - (\text{Cl}^- + \text{HCO}_3^-) = 139 - (114 + 15) = 10

mEq/L. Because this falls within the normal physiologic range (

8-12

mEq/L), the patient has a normal anion gap (hyperchloremic) metabolic acidosis, which directly corresponds to her history of profound watery diarrhea causing massive gastrointestinal bicarbonate loss. The final step is assessing the adequacy of respiratory compensation using Winter's formula: Expected

\text{PaCO}_2 = (1.5 \times 15) + 8 \pm 2 = 30.5 \pm 2

mmHg. For appropriate respiratory compensation, her

\text{PaCO}_2

should fall between

28.5

and

32.5

mmHg. However, her measured

\text{PaCO}_2

is

42

mmHg. Because her measured

\text{PaCO}_2

is substantially higher than expected, she is retaining

\text{CO}_2

, representing a superimposed, concurrent primary respiratory acidosis. This occurs because her severe underlying chronic obstructive pulmonary disease and lethargy prevent her from achieving the necessary compensatory hyperventilation.

Adım Adım Çözüm

1

Analyze the primary acid-base disorder by looking at pH and bicarbonate.

The arterial pH is

7.21

(acidemia) and serum bicarbonate (

\text{HCO}_3^-

) is

15

mEq/L (low). This indicates a primary metabolic acidosis.

Establishing the direction of the primary disorder dictates which compensatory formula must be applied.

2

Calculate the anion gap (AG) to determine the etiology of the metabolic acidosis.

AG = \text{Na}^+ - (\text{Cl}^- + \text{HCO}_3^-) = 139 - (114 + 15) = 139 - 129 = 10

mEq/L.

A normal AG (

8-12

mEq/L) confirms a non-anion gap metabolic acidosis, which in this patient is due to profound gastrointestinal bicarbonate loss from diarrhea.

3

Determine expected respiratory compensation using Winter's formula.

Expected

\text{PaCO}_2 = (1.5 \times \text{HCO}_3^-) + 8 \pm 2

. Here,

(1.5 \times 15) + 8 = 22.5 + 8 = 30.5 \pm 2

(range

28.5

to

32.5

mmHg).

Winter's formula determines the physiologic

\text{CO}_2

elimination expected in response to a specific degree of metabolic acidosis.

4

Compare the measured

\text{PaCO}_2

to the expected

\text{PaCO}_2

.

The measured

\text{PaCO}_2

is

42

mmHg, which is significantly higher than the maximum expected value of

32.5

mmHg.

An inappropriately elevated

\text{PaCO}_2

indicates a concurrent primary respiratory acidosis, secondary to hypoventilation from her underlying chronic obstructive pulmonary disease and severe fatigue.

Anahtar Kavram

Identifying mixed acid-base disorders using the anion gap and Winter's formula

Soru 2338Soru →

Match each Hepatitis B virus (HBV) serologic profile to its most accurate clinical interpretation.

Soldaki öğeye tıklayın, sonra eşleşen sağdaki öğeye tıklayın

Cevabı ve açıklamayı göster

Cevap

Profile 1 matches Acute Hepatitis B; Profile 2 matches Resolved past infection; Profile 3 matches Vaccine-induced immunity; Profile 4 matches Chronic Hepatitis B.

Hepatitis B serology requires sequential interpretation. HBsAg determines active versus absent infection. Core antibodies (Anti-HBc IgM vs IgG) distinguish acute from chronic/past exposure. Surface antibodies (Anti-HBs) determine immunity. HBeAg correlates with infectivity.

Adım Adım Çözüm

1

Evaluate the presence of HBsAg.

Profiles 1 and 4 have positive HBsAg, indicating active infection (acute or chronic). Profiles 2 and 3 have negative HBsAg, indicating absence of active infection.

HBsAg is the primary marker of active HBV infection.

2

Differentiate the active infections (Profiles 1 and 4) using Anti-HBc.

Profile 1 has Anti-HBc IgM (acute). Profile 4 has Anti-HBc IgG (chronic).

IgM antibodies against the core antigen indicate recent, acute exposure, whereas IgG indicates past or ongoing chronic exposure.

3

Differentiate the non-active/immune profiles (Profiles 2 and 3) using Anti-HBc.

Profile 2 has Anti-HBc IgG, meaning the patient was exposed to the actual virus (resolved natural infection). Profile 3 is negative for all core antibodies.

The HBV vaccine only contains surface antigen. Therefore, vaccinated individuals will only develop Anti-HBs, never Anti-HBc.

Anahtar Kavram

Interpretation of Hepatitis B Serologic Panels

Soru 2339Soru →

Match each diagnostic laboratory profile with the most likely etiology of thyrotoxicosis.

Soldaki öğeye tıklayın, sonra eşleşen sağdaki öğeye tıklayın

Cevabı ve açıklamayı göster

Cevap

Exogenous levothyroxine intake matches the profile of low RAIU and undetectable thyroglobulin. Subacute granulomatous thyroiditis matches low RAIU and elevated thyroglobulin. Graves disease matches diffusely increased RAIU. A TSH-secreting pituitary adenoma matches central hyperthyroidism with an increased alpha-subunit.

The diagnosis of thyrotoxicosis relies on a structured laboratory algorithm. Primary hyperthyroidism presents with a suppressed TSH and elevated Free T4. Within this category, high radioactive iodine uptake (RAIU) indicates new hormone synthesis (e.g., Graves disease with a diffuse pattern). Low RAIU indicates release of preformed hormone or an exogenous source. These are distinguished by serum thyroglobulin, which is released from damaged follicles in destructive thyroiditis (elevated) but suppressed in exogenous hormone ingestion (undetectable). Conversely, central hyperthyroidism presents with a normal or elevated TSH despite high Free T4; TSH-secreting adenomas typically also hypersecrete the alpha-subunit.

Adım Adım Çözüm

1

Evaluate the TSH and Free T4 relationship to determine the origin.

Low TSH with high Free T4 indicates primary hyperthyroidism. Normal or high TSH with high Free T4 indicates central hyperthyroidism (TSH-secreting adenoma).

This establishes whether the source of thyrotoxicosis is driven by the pituitary or is independent of it.

2

Assess the radioactive iodine uptake (RAIU) in patients with primary hyperthyroidism.

High RAIU suggests active de novo hormone synthesis (e.g., Graves disease). Low RAIU suggests release of preformed hormone or exogenous intake.

RAIU distinguishes hyperactive glandular synthesis from thyroid destruction or factitious thyrotoxicosis.

3

Use serum thyroglobulin to differentiate the specific causes of low RAIU thyrotoxicosis.

Elevated thyroglobulin indicates thyroid follicular destruction (subacute thyroiditis). Undetectable thyroglobulin indicates an exogenous hormone source (exogenous levothyroxine intake).

Thyroglobulin is released during follicular damage but is suppressed when taking exogenous pure levothyroxine.

Anahtar Kavram

Diagnostic evaluation of thyrotoxicosis using thyroid function tests, radioactive iodine uptake, and serum markers.

Soru 2340Soru →

A 29-year-old man is evaluated in the hospital for ongoing fever. He was admitted 4 days ago with high fevers, chills, and pleuritic chest pain. His medical history is significant for opioid use disorder with active intravenous heroin use. On admission, his temperature was 39.2°C (102.6°F). Physical examination revealed a new holosystolic murmur at the lower left sternal border. Computed tomography of the chest showed multiple peripheral cavitary lesions. Two sets of blood cultures were drawn, and he was started on empiric intravenous vancomycin and ceftriaxone. A transthoracic echocardiogram demonstrated a 1.5-cm mobile vegetation on the anterior leaflet of the tricuspid valve. Today, the patient's temperature is 38.4°C (101.1°F). The admission blood cultures are now growing methicillin-susceptible *Staphylococcus aureus* (MSSA). Which of the following is the most appropriate next step in pharmacotherapy?

Discontinue current antibiotics and start intravenous cefazolin

Continue intravenous vancomycin and discontinue intravenous ceftriaxone

Continue intravenous vancomycin, discontinue intravenous ceftriaxone, and add intravenous gentamicin

Discontinue current antibiotics and start oral linezolid

Discontinue current antibiotics and start intravenous daptomycin

Cevabı ve açıklamayı göster

Cevap: Discontinue current antibiotics and start intravenous cefazolin

Cevap

Discontinue current antibiotics and start intravenous cefazolin

The correct answer requires recognizing that for severe, invasive infections caused by methicillin-susceptible Staphylococcus aureus (MSSA), antistaphylococcal beta-lactams (such as cefazolin, nafcillin, or oxacillin) are the superior treatment choice. Although vancomycin is an appropriate initial empiric choice to cover potential MRSA, it has slower bactericidal activity against MSSA compared to beta-lactams. Continuing vancomycin once MSSA is confirmed is associated with prolonged bacteremia, higher rates of treatment failure, and increased mortality. Therefore, the most appropriate next step in antibiotic stewardship and patient management is to discontinue both the vancomycin and the ceftriaxone (which was covering gram-negatives) and initiate targeted therapy with intravenous cefazolin.

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1

Identify the primary diagnosis based on the clinical presentation

The patient has native valve right-sided infective endocarditis complicated by septic pulmonary emboli.

The combination of intravenous drug use, a new tricuspid regurgitation murmur, cavitary lung lesions, a large tricuspid vegetation, and positive blood cultures confirms the diagnosis.

2

Evaluate the current empiric antibiotic regimen against the culture results

The patient is receiving empiric vancomycin and ceftriaxone, but the pathogen is identified as methicillin-susceptible Staphylococcus aureus (MSSA).

Broad-spectrum empiric therapy must be narrowed and optimized once the exact pathogen and its susceptibilities are identified.

3

Determine the optimal targeted pharmacotherapy for the identified pathogen

Therapy should be de-escalated to an intravenous antistaphylococcal beta-lactam, such as cefazolin, nafcillin, or oxacillin.

Beta-lactams provide superior bactericidal activity, faster clearance of bacteremia, and significantly improved survival rates compared to vancomycin for MSSA endovascular infections.

Anahtar Kavram

De-escalation of empiric therapy to an antistaphylococcal beta-lactam (e.g., cefazolin, nafcillin) is the standard of care for methicillin-susceptible Staphylococcus aureus (MSSA) endocarditis, as beta-lactams are clinically superior to vancomycin for MSSA.

Internal Medicine

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