Internal Medicine

3151 soru

Tüm türler3,151 Çoktan seçmeli1,611 Çoklu seçim73 Sayısal81 Eşleştirme714 Sıralama672

A 71-year-old woman is brought to the emergency department from a skilled nursing facility due to progressively worsening altered mental status over the past 24 hours. Her medical history includes chronic obstructive pulmonary disease, type 2 diabetes mellitus, and hypertension. Vital signs are temperature $38.9^\circ\text{C}$ ( $102.0^\circ\text{F}$ ), blood pressure 82/50 mmHg, pulse 118/min, and respirations 26/min. Oxygen saturation is 94% on room air. Physical examination reveals dry mucous membranes and suprapubic tenderness. The lungs are clear to auscultation bilaterally. Cardiac examination shows tachycardia with a regular rhythm and no murmurs.

Laboratory and diagnostic results are as follows:

Test	Result	Reference Range
Sodium	$138\text{ mEq/L}$	136-145 $\text{mEq/L}$
Potassium	$4.8\text{ mEq/L}$	3.5-5.0 $\text{mEq/L}$
Chloride	$102\text{ mEq/L}$	95-105 $\text{mEq/L}$
Bicarbonate	$12\text{ mEq/L}$	22-28 $\text{mEq/L}$
Blood urea nitrogen (BUN)	$45\text{ mg/dL}$	7-18 $\text{mg/dL}$
Creatinine	$2.1\text{ mg/dL}$	0.6-1.2 $\text{mg/dL}$
Serum lactate	$5.2\text{ mmol/L}$	0.5-1.0 $\text{mmol/L}$
Thyroid-stimulating hormone (TSH)	$0.2\text{ \mu U/mL}$	0.4-4.0 $\text{\mu U/mL}$
Free thyroxine (T4)	$0.7\text{ ng/dL}$	0.9-1.7 $\text{ng/dL}$

Arterial blood gas (room air):

Parameter	Result
pH	$7.28$
PaCO2	$26\text{ mmHg}$
PaO2	$88\text{ mmHg}$

Urinalysis shows 3+ leukocyte esterase, positive nitrites, and >50 leukocytes/hpf. A central venous catheter is placed, and aggressive intravenous fluid resuscitation is initiated. Blood and urine cultures are pending.

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

Administer intravenous ceftriaxone

Administer intravenous levothyroxine

Administer intravenous sodium bicarbonate

Administer intravenous furosemide

Perform endotracheal intubation

Cevabı ve açıklamayı göster

Cevap: Administer intravenous ceftriaxone

Cevap

The correct action is to administer intravenous ceftriaxone, as the patient is in septic shock and requires immediate empiric antibiotic therapy while fluid resuscitation continues.

The correct answer emphasizes treating the fundamental cause of the patient's critical condition. She is in septic shock secondary to a urinary tract infection, evidenced by fever, hypotension, lactic acidosis, and a markedly abnormal urinalysis. The immediate priorities in septic shock are restoring perfusion (intravenous fluids) and eliminating the source of infection (empiric broad-spectrum antibiotics, such as ceftriaxone, targeting gram-negative enteric organisms). All of her other derangements (acidosis, altered thyroid labs) are secondary to this primary process.

Adım Adım Çözüm

Diagnose the primary clinical syndrome based on vital signs and localizing laboratory data.

The patient has fever, hypotension, tachycardia, and a urinalysis positive for leukocyte esterase and nitrites, confirming a diagnosis of septic shock secondary to urosepsis.

Identifying the primary cause of instability dictates the most urgent life-saving interventions: fluids and empiric antibiotics.

Analyze the acid-base status using the arterial blood gas and basic metabolic panel.

The anion gap is

138 - (102 + 12) = 24

, indicating a high anion gap metabolic acidosis (due to a lactate of

5.2\text{ mmol/L}

). Using Winter's formula (

1.5 \times 12 + 8 \pm 2

), the expected PaCO2 is

24-28\text{ mmHg}

. The measured PaCO2 is

26\text{ mmHg}

, meaning the respiratory compensation is perfect.

Calculating expected compensation is crucial to determine if a secondary respiratory disorder exists that might require mechanical ventilation or other airway interventions.

Interpret the abnormal thyroid function tests in the context of the current clinical picture.

The low TSH and low free T4 represent euthyroid sick syndrome (non-thyroidal illness syndrome), a physiologic down-regulation of the hypothalamic-pituitary-thyroid axis during severe acute illness.

Preventing inappropriate treatment for laboratory abnormalities that are secondary to the primary critical illness avoids iatrogenic harm.

Anahtar Kavram

In patients presenting with septic shock and multiorgan derangements, management must prioritize reversing the underlying infection and hypoperfusion (fluids and antibiotics) while recognizing appropriate physiologic adaptations like respiratory compensation for metabolic acidosis and euthyroid sick syndrome.

Tahmini Süre:1m 30s

Soru 502Soru →

A 32-year-old G1P0 woman at 30 weeks gestation comes to the emergency department due to progressively worsening shortness of breath and orthopnea over the past two weeks. She says she has to prop herself up on three pillows at night to breathe comfortably. Medical history is significant for Hodgkin lymphoma diagnosed 5 years ago, which was successfully treated with six cycles of a chemotherapy regimen containing doxorubicin. She also has a history of mild asthma for which she uses an albuterol inhaler as needed. Her temperature is 37.0°C (98.6°F), blood pressure is 112/70 mm Hg, pulse is 108/min, and respirations are 24/min. Pulse oximetry is 94% on room air. Physical examination shows prominent jugular venous distention. Cardiac auscultation reveals a regular rate and rhythm with an apical S3 gallop. Lung auscultation reveals fine bibasilar crackles without wheezing. There is 2+ bilateral pitting edema in the lower extremities. Laboratory studies show:

Parameter	Result
Hemoglobin	11.2 g/dL
Leukocyte count	9,200/mm³
Thyroid-stimulating hormone (TSH)	2.1 µU/mL (normal: 0.4–4.0 µU/mL)
Arterial blood gas (room air):
pH	7.48
pCO₂	28 mm Hg
HCO₃⁻	20 mEq/L

Which of the following is the most likely underlying mechanism for this patient's current presentation?

Oxidative damage to cardiomyocytes leading to left ventricular dilation

Physiologic volume expansion and diaphragmatic elevation typical of late gestation

Airway smooth muscle constriction and bronchial mucosal inflammation

Autoimmune destruction of thyroid gland follicles leading to hormone deficiency

Primary metabolic acidosis with appropriate respiratory compensation

Cevabı ve açıklamayı göster

Cevap: Oxidative damage to cardiomyocytes leading to left ventricular dilation

Cevap

The correct answer is oxidative damage to cardiomyocytes leading to left ventricular dilation.

The correct answer identifies the pathophysiology of anthracycline-induced cardiotoxicity. The patient is presenting with classic signs of acute decompensated heart failure, including orthopnea, an S3 gallop, elevated jugular venous pressure, and pulmonary crackles. Her history of receiving doxorubicin (an anthracycline) puts her at high risk for dose-dependent cardiotoxicity. Anthracyclines generate reactive oxygen species that cause oxidative damage to cardiomyocytes, leading to myocyte necrosis and replacement fibrosis, which manifests as a dilated cardiomyopathy. The profound physiological volume expansion and increased cardiac output required during pregnancy act as significant stressors that frequently unmask previously asymptomatic, compensated ventricular dysfunction in cancer survivors.

Adım Adım Çözüm

Analyze the patient's acute clinical presentation and physical exam findings.

The presence of orthopnea, jugular venous distention, an S3 gallop, bibasilar crackles, and peripheral edema strongly indicates acute decompensated heart failure (fluid overload).

Identifying the active clinical syndrome is the necessary first step to determine the underlying etiology.

Connect the heart failure diagnosis to the patient's past medical history.

The patient received doxorubicin for Hodgkin lymphoma 5 years ago. Doxorubicin is a known anthracycline.

Anthracyclines are notorious for causing irreversible, dose-dependent cardiotoxicity presenting as dilated cardiomyopathy.

Explain the trigger for her acute decompensation at this specific time.

The normal physiologic plasma volume expansion that peaks in the late second and early third trimester of pregnancy has increased her cardiac preload.

Increased cardiac demand during pregnancy frequently acts as a stressor that unmasks underlying, previously asymptomatic anthracycline-induced ventricular dysfunction.

Anahtar Kavram

Anthracycline-induced cardiotoxicity (dilated cardiomyopathy) unmasked by the physiological volume expansion of pregnancy.

Soru 503Soru →

A $68$ -year-old woman comes to the emergency department reporting severe difficulty breathing and wheezing for the past two days. She has a history of type 2 diabetes, hypertension, and severe chronic obstructive pulmonary disease (COPD). She reports a recent upper respiratory tract infection. Her home medications include metformin, lisinopril, and a tiotropium inhaler. She has been using her rescue albuterol inhaler multiple times today with minimal relief.

She reports an increase in breathlessness, but states her sputum remains clear and sparse. She denies chest pain, orthopnea, paroxysmal nocturnal dyspnea, or swelling in her legs. Temperature is $37.2^\circ\text{C}$ ( $99.0^\circ\text{F}$ ), pulse is $118\text{/min}$ , blood pressure is $138/86\text{ mmHg}$ , and respiratory rate is $28\text{/min}$ . Pulse oximetry shows $88\%$ on room air.

Physical examination reveals an anxious woman using accessory muscles of respiration. Lung auscultation demonstrates diffuse, bilateral expiratory wheezing with a prolonged expiratory phase. Jugular venous pressure is estimated at $6\text{ cm H}_2\text{O}$ . Trace bilateral pedal edema is noted, which the patient states is chronic.

Laboratory studies:

Test	Result	Reference Range
Leukocyte count	$9,200\text{/mm}^3$	$4,000-11,000\text{/mm}^3$
B-type natriuretic peptide (BNP)	$65\text{ pg/mL}$	$< 100\text{ pg/mL}$
Procalcitonin	$0.03\text{ ng/mL}$	$< 0.1\text{ ng/mL}$

Arterial blood gas (room air):

Parameter	Result	Reference Range
pH	$7.32$	$7.35-7.45$
PaCO $_2$	$56\text{ mmHg}$	$35-45\text{ mmHg}$
PaO $_2$	$58\text{ mmHg}$	$75-105\text{ mmHg}$
HCO $_3^-$	$28\text{ mEq/L}$	$22-28\text{ mEq/L}$

A rapid multiplex respiratory polymerase chain reaction (PCR) panel is positive for rhinovirus. Chest radiograph shows lung hyperinflation with flattened hemidiaphragms. There is no focal consolidation, pleural effusion, or cardiomegaly.

Which of the following interventions are indicated for the initial management of this patient? (Select 2)

Geçerli olan tümünü seçin

Administer nebulized short-acting bronchodilator therapy

Administer systemic glucocorticoid therapy

Initiate diuresis with a loop diuretic

Start empiric therapy with cefepime and vancomycin

Use Winter's formula to evaluate expected respiratory compensation

Cevabı ve açıklamayı göster

Cevap: Administer nebulized short-acting bronchodilator therapy; Administer systemic glucocorticoid therapy

Cevap

The correct initial management steps are administering nebulized short-acting bronchodilator therapy and administering systemic glucocorticoid therapy.

The correct interventions are administering nebulized short-acting bronchodilator therapy and systemic glucocorticoid therapy. This patient is experiencing a severe acute COPD exacerbation, indicated by her accessory muscle use, tachypnea, acute-on-chronic respiratory acidosis, and failure of outpatient therapy. The standard of care in the emergency department includes immediate nebulized short-acting beta-agonists (often combined with muscarinic antagonists like ipratropium) to reverse bronchoconstriction, alongside early administration of systemic glucocorticoids (oral or intravenous) to treat underlying inflammation and expedite recovery.

Adım Adım Çözüm

Analyze the clinical presentation and physical exam.

The patient has an acute exacerbation of COPD, characterized by increased dyspnea, diffuse wheezing, accessory muscle use, and hyperinflation on the chest radiograph.

To establish the primary diagnosis and rule out alternative causes of dyspnea such as acute decompensated heart failure or pneumonia.

Interpret the laboratory and arterial blood gas (ABG) data.

Normal BNP and procalcitonin rule out heart failure and bacterial pneumonia, respectively. The ABG demonstrates an acute-on-chronic respiratory acidosis (pH 7.32, PaCO2 56 mmHg, HCO3 28 mEq/L) consistent with severe airway obstruction.

To appropriately stage the severity of the exacerbation and verify that the primary derangement is respiratory.

Determine the appropriate evidence-based bundle of interventions.

Standard protocol for a severe COPD exacerbation requires immediate inhaled short-acting bronchodilators, systemic glucocorticoids, and supplemental oxygen. Antibiotics are withheld because she lacks purulent sputum and has a confirmed rhinovirus infection.

Bronchodilators relieve acute bronchospasm, glucocorticoids reduce underlying airway inflammation, and targeted therapy prevents unnecessary antibiotic exposure.

Anahtar Kavram

The initial pharmacological management of moderate-to-severe acute COPD exacerbations includes inhaled short-acting bronchodilators and early administration of systemic glucocorticoids. Antibiotics are reserved for patients with purulent sputum or those requiring mechanical ventilation.

Tahmini Süre:1m 30s

Soru 504Soru →

A 55-year-old man comes to the clinic due to a 4-week history of progressive abdominal swelling, early satiety, and lower extremity edema. He has a 15-year history of heavy alcohol consumption but stopped drinking one month ago. His temperature is 37.0°C (98.6°F), blood pressure is 112/68 mm Hg, and pulse is 88/min. Physical examination reveals scleral icterus, multiple spider angiomas on the upper chest, and shifting dullness on abdominal percussion. Trace pitting edema is present bilaterally in the lower extremities. A diagnostic paracentesis is performed.

Test	Result
Serum albumin	3.4 g/dL
Ascitic fluid albumin	0.8 g/dL
Ascitic fluid total protein	1.5 g/dL
Ascitic fluid leukocyte count	200/mm³ (10% neutrophils)

What is the primary pathophysiologic mechanism responsible for this patient's abdominal fluid accumulation?

Elevated right atrial and post-hepatic venous pressure

Increased intrahepatic vascular resistance

Heavy proteinuria leading to decreased plasma oncotic pressure

Direct peritoneal inflammation due to an infectious pathogen

Transmural bowel ischemia secondary to mechanical obstruction

Cevabı ve açıklamayı göster

Cevap: Increased intrahepatic vascular resistance

Cevap

Increased intrahepatic vascular resistance is the correct mechanism, as evidenced by a SAAG >= 1.1 g/dL and ascitic total protein < 2.5 g/dL, which strongly points to cirrhosis.

The correct mechanism is increased intrahepatic vascular resistance, which is the hallmark of cirrhosis. This patient's clinical signs (spider angiomas, icterus, alcohol history) strongly suggest cirrhosis. Diagnostically, the Serum-Ascites Albumin Gradient (SAAG) is calculated by subtracting ascitic albumin from serum albumin (

3.4 - 0.8 = 2.6

g/dL). A SAAG

\geq 1.1

g/dL indicates portal hypertension. To differentiate the cause of portal hypertension, ascitic total protein is evaluated: levels

< 2.5

g/dL point to intrahepatic (cirrhotic) causes, while levels

\geq 2.5

g/dL point to post-hepatic causes like right heart failure. This patient's low protein confirms cirrhosis.

Adım Adım Çözüm

Calculate the Serum-Ascites Albumin Gradient (SAAG).

SAAG = 3.4 \text{ g/dL} - 0.8 \text{ g/dL} = 2.6 \text{ g/dL}

SAAG is the most accurate initial test to differentiate ascites caused by portal hypertension from other causes.

Interpret the SAAG value.

A SAAG of

2.6

g/dL is

\geq 1.1

g/dL, confirming the presence of portal hypertension.

Portal hypertension drives fluid into the peritoneal cavity via increased hydrostatic pressure, leaving larger albumin molecules in the serum.

Evaluate the ascitic fluid total protein.

The total protein is

1.5

g/dL, which is

< 2.5

g/dL.

In the setting of portal hypertension, a low ascitic protein (< 2.5 g/dL) indicates an intrahepatic source (cirrhosis), whereas a high protein (>= 2.5 g/dL) indicates a post-hepatic source (right heart failure).

Anahtar Kavram

Cirrhotic ascites is characterized by a Serum-Ascites Albumin Gradient (SAAG) >= 1.1 g/dL and an ascitic fluid total protein < 2.5 g/dL, resulting from increased intrahepatic vascular resistance.

Tahmini Süre:1m 15s

Soru 505Soru →

An 80-year-old male resident of an assisted living facility is brought to the urgent care clinic complaining of excruciating right knee pain that started abruptly 24 hours ago. His medical history is significant for generalized osteoarthritis and well-controlled heart failure. His current temperature is $37.8^\circ C$ ( $100.0^\circ F$ ), blood pressure is $135/82$ mmHg, and heart rate is $88$ /min. Examination of the right knee demonstrates prominent swelling, marked warmth, and erythema, with passive range of motion severely limited by pain. Synovial fluid aspirated from the joint reveals a leukocyte count of $32,000/\mu L$ (88% segmented neutrophils). Polarized light microscopy identifies numerous rhomboid-shaped crystals exhibiting weak positive birefringence. Gram stain is negative for bacteria. Plain films of the affected joint exhibit linear calcification of the meniscal cartilage. Which of the following is the most appropriate next step in management?

Intra-articular injection of a glucocorticoid

Initiation of intravenous vancomycin and ceftriaxone

Administration of intravenous furosemide

Measurement of serum thyroid-stimulating hormone levels

Urgent orthopedic consultation for arthroscopic joint lavage

Cevabı ve açıklamayı göster

Cevap: Intra-articular injection of a glucocorticoid

Cevap

Intra-articular injection of a glucocorticoid

The patient's presentation is classic for an acute flare of calcium pyrophosphate deposition (CPPD) disease, or pseudogout. The pathognomonic findings are rhomboid-shaped, weakly positively birefringent crystals on synovial fluid analysis and chondrocalcinosis on plain radiography. For a patient with a monoarticular flare—especially an elderly patient with significant comorbidities like heart failure, where NSAIDs are relatively contraindicated—intra-articular glucocorticoids are the safest and most effective targeted first-line therapy.

Adım Adım Çözüm

Analyze the synovial fluid analysis and microscopy findings.

The fluid shows

32,000/\mu L

leukocytes (inflammatory but non-purulent) and rhomboid-shaped, weakly positively birefringent crystals.

Identifying the specific crystal type is required to differentiate between gout (needle-shaped, negatively birefringent) and pseudogout (rhomboid-shaped, positively birefringent).

Identify the primary diagnosis based on combined clinical and laboratory clues.

The diagnosis is an acute flare of Calcium Pyrophosphate Deposition (CPPD) disease, commonly known as pseudogout, supported by the imaging finding of chondrocalcinosis.

Accurate diagnosis dictates specific pharmacotherapy and rules out life-threatening conditions like septic arthritis.

Determine the optimal acute management for this specific patient.

Intra-articular glucocorticoids are selected over systemic NSAIDs or colchicine.

The patient is elderly with heart failure. NSAIDs can exacerbate heart failure and cause renal impairment. Localized therapy with an intra-articular injection safely and rapidly treats a monoarticular flare.

Anahtar Kavram

Diagnosis and acute management of calcium pyrophosphate deposition (CPPD) disease (pseudogout).

Tahmini Süre:1m 0s

Soru 506Soru →

Match each patient's clinical presentation with the underlying pathophysiology that best explains their bleeding disorder.

Soldaki öğeye tıklayın, sonra eşleşen sağdaki öğeye tıklayın

Cevabı ve açıklamayı göster

Cevap

Match the clinical vignettes to their corresponding pathophysiological mechanisms: Placental abruption to consumptive coagulopathy (DIC); Isolated petechiae in a healthy woman to IgG autoantibodies (ITP); Heavy menses and epistaxis to multimeric glycoprotein deficiency (vWD); Hemarthrosis with X-linked history to intrinsic tenase complex factor deficiency (Hemophilia); ESRD bleeding to uremic toxin-induced platelet dysfunction.

Each patient presentation contains classic hallmark signs for a specific bleeding disorder. Placental abruption is a classic trigger for DIC (consumptive coagulopathy). Isolated mucocutaneous bleeding in a young woman points to ITP (autoantibody-mediated). Mucosal bleeding with an autosomal dominant inheritance pattern indicates vWD (vWF deficiency). Hemarthrosis with an X-linked inheritance pattern strongly suggests Hemophilia (Factor VIII/IX deficiency). Finally, bleeding in a dialysis patient is typical for uremic platelet dysfunction (toxin-mediated).

Adım Adım Çözüm

Analyze the clinical presentation of the pregnant patient with placental abruption and bleeding from IV sites.

Identified as Disseminated Intravascular Coagulation (DIC).

Placental abruption is a major trigger for DIC due to massive release of tissue factor, leading to widespread consumption of coagulation factors.

Evaluate the 35-year-old woman with isolated petechiae and mucosal bleeding.

Identified as Immune Thrombocytopenic Purpura (ITP).

ITP presents with isolated thrombocytopenia (causing mucocutaneous bleeding) in an otherwise healthy individual, driven by anti-GPIIb/IIIa IgG autoantibodies.

Assess the 17-year-old girl with mucosal bleeding (heavy menses, epistaxis) and a dominant family history.

Identified as von Willebrand Disease (vWD).

vWD is the most common inherited bleeding disorder, presenting with mucosal bleeding due to a defect in vWF, which bridges platelets to the endothelium and stabilizes Factor VIII.

Review the presentation of the 5-year-old boy with hemarthrosis and an affected maternal uncle.

Identified as Hemophilia A or B.

Deep tissue bleeding (hemarthrosis) and an X-linked recessive inheritance pattern are classic for hemophilia, which involves intrinsic pathway factor deficiencies.

Examine the bleeding presentation in the 45-year-old man with end-stage renal disease.

Identified as Uremic Platelet Dysfunction.

Uremia leads to the buildup of toxins that impair platelet function, causing abnormal bleeding despite normal platelet numbers.

Anahtar Kavram

Pathophysiology and clinical presentation of bleeding disorders

Soru 507Soru →

A $34$ -year-old woman comes to the clinic for evaluation of a $4$ -week history of palpitations, anxiety, sweating, and a $3$ -kg ( $6.6$ -lb) weight loss. She works as a medical assistant and reports high stress levels. She has no neck pain, dysphagia, or recent viral illnesses. Her temperature is $37.1^\circ\text{C}$ ( $98.8^\circ\text{F}$ ), blood pressure is $135/85\text{ mm Hg}$ , and pulse is $112\text{/min}$ . Physical examination reveals warm, moist skin and a fine resting tremor. The eyes appear normal without proptosis. The thyroid gland is normal in size, non-palpable, and non-tender.

Laboratory studies show:
Thyroid-stimulating hormone (TSH): $<0.01\text{ }\mu\text{U/mL}$
Free thyroxine (T4): $2.9\text{ ng/dL}$ (Normal: $0.9-1.7\text{ ng/dL}$ )

A radioactive iodine uptake (RAIU) scan reveals $1\%$ uptake at $24$ hours (Normal: $15\%-30\%$ ).

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

Measurement of serum thyroglobulin

Measurement of thyroid-stimulating immunoglobulins

Initiation of methimazole therapy

Ultrasound of the thyroid gland

Measurement of 24-hour urinary iodine excretion

Cevabı ve açıklamayı göster

Cevap: Measurement of serum thyroglobulin

Cevap

Measurement of serum thyroglobulin

The correct answer is measurement of serum thyroglobulin. This patient has thyrotoxicosis characterized by a suppressed TSH, elevated free T4, and a low radioactive iodine uptake (RAIU). A low RAIU indicates decreased de novo synthesis of thyroid hormone. The differential diagnosis includes destructive thyroiditis (e.g., painless/silent thyroiditis, subacute thyroiditis), iodine-induced thyrotoxicosis, or exogenous thyroid hormone intake. Serum thyroglobulin is a precursor protein synthesized by normal thyroid follicular cells and co-secreted with endogenous thyroid hormone. In destructive thyroiditis, preformed thyroglobulin is released from damaged follicles, resulting in elevated serum levels. Conversely, exogenous thyroid hormone administration suppresses TSH, which in turn suppresses endogenous thyroglobulin production, leading to low serum thyroglobulin levels. Because this patient works in the medical field (increasing access to medications) and lacks symptoms of viral subacute thyroiditis (like neck pain), distinguishing between painless thyroiditis and factitious thyrotoxicosis is critical. Measuring thyroglobulin is the definitive next step to make this distinction.

Adım Adım Çözüm

Identify the primary clinical syndrome.

The patient has clinical signs of thyrotoxicosis confirmed by a suppressed TSH and an elevated free T4.

Establishing the biochemical presence of primary thyrotoxicosis is the required first step before determining the underlying etiology.

Interpret the radioactive iodine uptake (RAIU) scan.

The RAIU is severely suppressed at 1%, which is well below the normal range.

A low RAIU indicates that the thyroid gland is not actively synthesizing new hormone, ruling out causes like Graves disease or toxic nodular goiter.

Formulate a differential diagnosis for low-uptake thyrotoxicosis.

The differential is narrowed to destructive thyroiditis (e.g., painless or subacute thyroiditis), iodine-induced thyrotoxicosis, or exogenous thyroid hormone intake (factitious thyrotoxicosis).

These conditions cause thyrotoxicosis through the release of preformed hormone or external ingestion, thereby suppressing TSH and halting de novo synthesis.

Select the most definitive test to differentiate between endogenous destruction and exogenous ingestion.

Measurement of serum thyroglobulin.

Thyroglobulin is co-secreted with endogenous thyroid hormone. It is elevated in destructive thyroiditis but suppressed in exogenous hormone use.

Anahtar Kavram

Differentiating causes of thyrotoxicosis with low radioactive iodine uptake (RAIU) using serum thyroglobulin levels.

Soru 508Soru →

An oncologist evaluates a $45$ -year-old hospitalized male patient for persistent fever and new respiratory symptoms. The patient is currently on day $15$ of induction chemotherapy for acute lymphoblastic leukemia. His hospital course has been complicated by profound neutropenia. Three days prior, after recording a temperature of $39.2^\circ\text{C}$ ( $102.6^\circ\text{F}$ ), he was started on empiric intravenous piperacillin-tazobactam. Despite this intervention, his fevers have remained unremitting. This morning, he developed right-sided pleuritic chest pain and experienced an episode of hemoptysis. Current vital signs include a temperature of $38.9^\circ\text{C}$ ( $102.0^\circ\text{F}$ ), blood pressure of $112/72 \text{ mm Hg}$ , pulse of $110/\text{min}$ , and respiratory rate of $20/\text{min}$ . Pulse oximetry shows $94\%$ on room air. Pulmonary auscultation reveals focal crackles and decreased breath sounds in the right upper lung zone. Laboratory analysis demonstrates a leukocyte count of $200/\text{mm}^3$ with an absolute neutrophil count of $40/\text{mm}^3$ . A high-resolution non-contrast computed tomography scan of the chest reveals a $2.5\text{-cm}$ right upper lobe dense macroscopic nodule surrounded by a peripheral zone of ground-glass attenuation. Which of the following is the most appropriate next step in the pharmacologic management of this patient?

Initiate intravenous vancomycin

Initiate intravenous meropenem

Initiate intravenous furosemide

Initiate intravenous voriconazole

Initiate intravenous fluconazole

Cevabı ve açıklamayı göster

Cevap: Initiate intravenous voriconazole

Cevap

The correct answer is to initiate intravenous voriconazole, as the clinical picture and radiographic findings strongly point to invasive pulmonary aspergillosis.

The correct answer is to initiate intravenous voriconazole. This patient has profound, prolonged neutropenia and presents with unremitting fever despite empiric broad-spectrum antibacterial therapy, pleuritic chest pain, and hemoptysis. His chest computed tomography scan reveals a macroscopic nodule surrounded by a zone of ground-glass attenuation, commonly known as the 'halo sign'. This constellation of clinical and radiographic findings is highly characteristic of invasive pulmonary aspergillosis. The halo sign pathologically represents an area of pulmonary hemorrhage surrounding an angioinvasive fungal infarction. Intravenous voriconazole is the first-line treatment of choice for invasive aspergillosis, offering improved survival and reduced toxicity compared to older therapies.

Adım Adım Çözüm

Identify the primary clinical syndrome and immunocompromised state.

The patient has persistent febrile neutropenia despite broad-spectrum antibacterial therapy, now complicated by pleuritic chest pain and hemoptysis.

Establishing the failure of initial antibacterial therapy in a profoundly neutropenic patient shifts the diagnostic focus toward opportunistic fungal infections.

Interpret the radiographic findings on the chest computed tomography scan.

The scan reveals a dense nodule surrounded by a ground-glass opacity, known classically as the 'halo sign'.

The halo sign is highly specific in severely immunocompromised patients for angioinvasive organisms (most commonly Aspergillus species), with the ground-glass area representing local hemorrhage.

Determine the optimal pharmacologic intervention for the suspected pathogen.

Intravenous voriconazole is the most appropriate addition to the patient's regimen.

Voriconazole is the established first-line drug of choice for invasive pulmonary aspergillosis, yielding better outcomes and lower toxicity than older alternatives like amphotericin B.

Anahtar Kavram

Invasive pulmonary aspergillosis typically presents in patients with prolonged, profound neutropenia as persistent fever, pleuritic chest pain, and hemoptysis; chest imaging classically demonstrates a nodule surrounded by a ground-glass 'halo sign', and the first-line treatment is voriconazole.

Soru 509Soru →

A 65-year-old man is evaluated on postoperative day 3 for acute-onset right knee pain and swelling. The patient underwent an uncomplicated laparoscopic cholecystectomy for acute calculous cholecystitis. His medical history is significant for hypertension, type 2 diabetes mellitus, and chronic kidney disease. His home medications include amlodipine, insulin glargine, and atorvastatin. His temperature is 38.2°C (100.8°F), blood pressure is 145/85 mm Hg, pulse is 95/min, and respiratory rate is 16/min.

Physical examination shows a swollen, erythematous, and exquisitely tender right knee with a large effusion. Range of motion is severely limited due to pain. The surgical incisions are clean, dry, and intact.

Laboratory studies show:

Test	Result
Leukocyte count	12,500/mm³
Serum creatinine	2.6 mg/dL (baseline 2.4 mg/dL)

Arthrocentesis of the right knee is performed. Synovial fluid analysis shows a leukocyte count of 45,000/mm³ with 85% neutrophils. Polarized light microscopy reveals negatively birefringent, needle-shaped crystals. Gram stain of the synovial fluid shows no organisms.

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

Intravenous vancomycin and ceftriaxone

Blood and urine cultures with chest radiography

Intra-articular triamcinolone injection

Oral naproxen

Measurement of serum uric acid level

Cevabı ve açıklamayı göster

Cevap: Intra-articular triamcinolone injection

Cevap

Intra-articular triamcinolone injection

The correct answer is intra-articular triamcinolone injection. The patient is experiencing an acute gout flare, evidenced by severe monoarticular inflammation and the presence of negatively birefringent, needle-shaped crystals in the synovial fluid. Postoperative status is a classic trigger for gout due to fluid shifts and systemic stress. First-line treatments for acute gout include nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, and corticosteroids. However, this patient's severe chronic kidney disease (creatinine 2.6 mg/dL) represents an absolute contraindication to NSAID therapy. Colchicine must also be heavily dose-adjusted or avoided in advanced renal failure. While oral systemic corticosteroids are an option, they may significantly disrupt glycemic control in a patient with type 2 diabetes. Therefore, an intra-articular corticosteroid injection is the most appropriate and targeted next step, maximizing local anti-inflammatory efficacy while minimizing systemic adverse effects.

Adım Adım Çözüm

Diagnose the underlying condition.

Acute gout flare.

The patient has acute monoarthritis with negatively birefringent, needle-shaped crystals on synovial fluid analysis, which is diagnostic for gout. The flare was likely precipitated by surgical stress and fluid shifts.

Identify relevant patient comorbidities.

Severe chronic kidney disease and type 2 diabetes mellitus.

The laboratory panel shows a markedly elevated serum creatinine, indicating significant baseline renal impairment.

Select the safest first-line therapy.

Intra-articular corticosteroid injection.

NSAIDs are contraindicated due to the chronic kidney disease. Systemic corticosteroids could exacerbate his diabetes. For a single affected joint, an intra-articular injection provides rapid relief with minimal systemic side effects.

Anahtar Kavram

Management of acute gout flares must be tailored to patient comorbidities. NSAIDs and colchicine are often contraindicated in severe chronic kidney disease, making intra-articular corticosteroids the preferred treatment for monoarticular involvement.

Tahmini Süre:1m 15s

Soru 510Soru →

Match each patient's clinical scenario with the most appropriate next step in management.

Soldaki öğeye tıklayın, sonra eşleşen sağdaki öğeye tıklayın

Cevabı ve açıklamayı göster

Cevap

The correct matching aligns the COPD exacerbation with systemic steroids and antibiotics, the diuretic-induced metabolic alkalosis with isotonic saline and potassium, the asymptomatic bacteriuria with catheter removal (no antibiotics), and the severe subclinical hypothyroidism with levothyroxine replacement.

Each clinical vignette maps directly to a definitive first-line intervention in general internal medicine. The COPD exacerbation meets criteria for triple therapy (steroids, bronchodilators, antibiotics). The volume-contracted metabolic alkalosis resolves with isotonic saline and potassium. The asymptomatic bacteriuria requires strict antibiotic avoidance and catheter discontinuation. The subclinical hypothyroidism with TSH >10 mIU/L requires thyroid hormone supplementation.

Adım Adım Çözüm

Analyze each clinical presentation to determine the primary underlying diagnosis and its severity.

Diagnoses identified: Acute COPD exacerbation, contraction alkalosis with hypokalemia, asymptomatic bacteriuria, and severe subclinical hypothyroidism.

Accurate diagnosis is required before selecting the most appropriate evidence-based intervention.

Apply current clinical guidelines and management algorithms for each identified condition.

Matched each condition to its definitive pharmacological or stewardship-based intervention.

General internal medicine requires synthesizing presentations across multiple organ systems and applying distinct therapeutic guidelines simultaneously.

Anahtar Kavram

Application of targeted, evidence-based management pathways across varied internal medicine presentations, emphasizing antibiotic stewardship and proper endocrine laboratory interpretation.

Soru 511Soru →

A 58-year-old man with a 15-year history of type 2 diabetes mellitus and peripheral neuropathy presents to the outpatient clinic with a 3-week history of a nonhealing ulcer on the plantar surface of his left hallux. He reports no fever, chills, or systemic symptoms. Vital signs are within normal limits. Physical examination reveals a 2-cm, deep ulceration with a hyperkeratotic border and mild surrounding erythema. There is no fluctuance or gross purulence. The physician suspects underlying osteomyelitis. Arrange the following steps in the most appropriate sequential order for the optimal diagnostic workup and management of this patient's condition.

Öğeleri doğru sıraya koymak için sürükleyin

Cevabı ve açıklamayı göster

Cevap

The correct sequence begins with bedside clinical evaluation (probing the ulcer), followed by initial imaging (plain radiographs), advanced imaging if needed (MRI), definitive microbiological diagnosis (bone biopsy), and finally, targeted treatment (pathogen-directed antibiotics).

In a hemodynamically stable patient presenting with a diabetic foot ulcer and suspected osteomyelitis, the standard of care follows a logical progression from least invasive to most definitive. Probing the ulcer to bone is a clinical exam maneuver with high predictive value. Plain radiographs are the appropriate initial imaging step. Since plain films can be falsely negative early in the disease process, MRI is the subsequent step to confirm the diagnosis and anatomical extent. Once osteomyelitis is confirmed radiographically, a bone biopsy is necessary to identify the specific pathogens, as superficial swab cultures are unreliable. Finally, because the patient is clinically stable without signs of sepsis, antimicrobial therapy is safely withheld until after the biopsy is obtained, allowing for targeted rather than empiric broad-spectrum treatment.

Adım Adım Çözüm

Probe the ulcer base with a sterile, blunt metal instrument.

Assesses whether bone is palpable.

This is a direct extension of the physical examination. Palpating bone has a high positive predictive value for underlying osteomyelitis and is the definitive first bedside step.

Obtain plain radiographs of the left foot.

Screens for gross bony abnormalities or soft tissue gas.

Plain radiography is universally the first-line imaging test to rule out other etiologies (like fractures or foreign bodies) and assess for advanced osteomyelitis (e.g., periosteal elevation, cortical disruption).

Obtain a magnetic resonance imaging (MRI) scan of the left foot.

Provides high-resolution soft tissue and bone marrow assessment.

Because plain films often remain normal for up to two weeks following the onset of bone infection, MRI is required to detect early bone marrow edema characteristic of osteomyelitis.

Perform a percutaneous or surgical bone biopsy for microbiological culture.

Identifies the causative organism(s) and their susceptibility profile.

Diabetic foot infections are frequently polymicrobial, and surface swab cultures do not correlate well with deep bone pathogens. A definitive bone biopsy is the gold standard for diagnosis and must precede antibiotics in stable patients.

Initiate pathogen-directed systemic antimicrobial therapy.

Treats the confirmed infection with a narrow, targeted regimen.

In hemodynamically stable patients without systemic symptoms or severe limb-threatening infection, antibiotics should be withheld until bone cultures are obtained to ensure targeted, effective therapy.

Anahtar Kavram

The diagnostic and management sequence for suspected diabetic foot osteomyelitis in a clinically stable patient prioritizes definitive microbiological diagnosis via bone biopsy prior to the initiation of antimicrobial therapy.

Soru 512Soru →

Emergency medical personnel transport a $61$ -year-old male to the hospital shortly after he experienced the sudden onset of severe, crushing retrosternal chest pain. The pain began while he was resting and is accompanied by profound diaphoresis. His medical history includes type 2 diabetes mellitus, hyperlipidemia, and a $35$ pack-year smoking history. Upon arrival, he appears pale and lethargic. Vital signs demonstrate a blood pressure of $84/52$ mmHg and a heart rate of $56$ /min. Physical examination reveals prominent distention of the jugular veins when the patient is positioned at a $45^\circ$ angle. Auscultation of the chest demonstrates completely clear lung fields bilaterally. Cardiac auscultation reveals bradycardia but no murmurs, rubs, or gallops. An electrocardiogram is rapidly obtained and shows $3$ -mm ST-segment elevations in leads II, III, and aVF, along with reciprocal ST-segment depressions in leads I and aVL. Which of the following is the most appropriate initial intervention to address this patient's hemodynamic state?

Rapid infusion of isotonic saline

Intravenous injection of furosemide

Sublingual application of nitroglycerin

Bolus dose of intravenous metoprolol

Prompt endotracheal intubation

Cevabı ve açıklamayı göster

Cevap: Rapid infusion of isotonic saline

Cevap

Rapid infusion of isotonic saline.

The patient's clinical presentation of profound hypotension, jugular venous distention, and completely clear lung fields, combined with an inferior ST-elevation myocardial infarction (STEMI in leads II, III, and aVF), is the classic triad of an acute right ventricular infarction. Because the ischemic right ventricle loses its ability to pump effectively, it becomes highly dependent on elevated venous return (preload) to force blood through the pulmonary circulation and maintain adequate left ventricular filling. The correct initial management for the resulting cardiogenic shock is volume expansion with a rapid infusion of isotonic fluids (e.g., normal saline). This maximizes right ventricular preload and subsequently improves overall cardiac output.

Adım Adım Çözüm

Analyze the electrocardiogram findings.

ST-segment elevations in the inferior leads (II, III, and aVF) confirm the diagnosis of an acute inferior ST-elevation myocardial infarction (STEMI).

Identifying the location of the infarction is critical for predicting potential mechanical or hemodynamic complications.

Interpret the physical examination findings in the context of the infarction.

The classic triad of hypotension, elevated jugular venous pressure (JVP), and clear lung fields points strongly to concurrent right ventricular infarction.

Up to half of inferior STEMIs involve the right ventricle. The right ventricle fails to pump blood forward, causing blood to back up (JVP) while the left ventricle remains under-filled (causing clear lungs and hypotension).

Determine the optimal hemodynamic intervention.

The impaired right ventricle becomes highly dependent on venous return (preload) to push blood into the pulmonary circulation. Intravenous fluids are required to increase this preload.

Interventions that decrease preload (like nitrates or diuretics) will precipitate profound cardiovascular collapse in this setting.

Anahtar Kavram

Right ventricular infarction classically presents with hypotension, elevated jugular venous pressure, and clear lungs; it requires maintenance of right ventricular preload with intravenous fluid boluses and absolute avoidance of preload-reducing agents such as nitrates and diuretics.

Tahmini Süre:1m 0s

Soru 513Soru →

A 42-year-old woman comes to the clinic reporting significant weight gain, worsening fatigue, and the development of dark hair on her face and chest over the past 8 months. Her medical history is unremarkable, and she takes no medications. On physical examination, her blood pressure is 160/100 mm Hg. She has a rounded face with plethora, truncal obesity with prominent supraclavicular fat pads, and several wide, purplish striae on her abdomen. Proximal muscle weakness is noted when she attempts to stand from a seated position. The physician suspects endogenous hypercortisolism. Assuming each step's result dictates the need for the subsequent one in a classic ACTH-dependent pathway, arrange the following diagnostic steps in the most appropriate chronological order.

Öğeleri doğru sıraya koymak için sürükleyin

Cevabı ve açıklamayı göster

Cevap

The correct sequence for evaluating Cushing syndrome is to first confirm hypercortisolism, then determine ACTH dependence, followed by imaging of the suspected source, and finally invasive venous sampling if imaging is inconclusive.

The evaluation of Cushing syndrome must follow a strict stepwise algorithm to avoid incorrect diagnoses. The first requirement is to establish the presence of hypercortisolism using tests like 24-hour urinary free cortisol, late-night salivary cortisol, or a low-dose dexamethasone suppression test. Once confirmed, plasma ACTH is measured to distinguish between ACTH-independent causes (e.g., adrenal adenoma, where ACTH is suppressed) and ACTH-dependent causes (e.g., pituitary adenoma or ectopic ACTH syndrome, where ACTH is normal or elevated). If the condition is ACTH-dependent, a pituitary MRI is performed since Cushing disease is the most common cause. If the MRI does not reveal a definitive adenoma (typically defined as >=6 mm), inferior petrosal sinus sampling (IPSS) is required. IPSS measures ACTH in the venous drainage of the pituitary and compares it to peripheral blood; a central-to-peripheral ACTH gradient confirms a pituitary source, whereas the absence of a gradient suggests an ectopic source.

Adım Adım Çözüm

Confirm hypercortisolism with a 24-hour urinary free cortisol test.

Establishes the diagnosis of Cushing syndrome.

It is necessary to definitively prove the patient has pathological excess cortisol before attempting to determine the underlying source.

Measure the early morning plasma ACTH level.

Categorizes the Cushing syndrome as ACTH-dependent or ACTH-independent.

This fundamentally branches the diagnostic algorithm. Low ACTH points to an adrenal source, while normal/high ACTH points to a pituitary or ectopic source.

Perform a pituitary MRI.

Visualizes the pituitary gland to identify a potential adenoma.

Since pituitary adenomas (Cushing disease) are the most common cause of ACTH-dependent Cushing syndrome, imaging this gland is the next logical non-invasive step.

Perform inferior petrosal sinus sampling (IPSS).

Differentiates between pituitary and ectopic ACTH secretion by measuring ACTH gradients.

Required when ACTH is elevated but the pituitary MRI does not show a definitive adenoma (typically >6 mm), preventing unnecessary pituitary surgery in patients who might actually have an ectopic neuroendocrine tumor.

Anahtar Kavram

The diagnostic algorithm for Cushing syndrome involves a stepwise approach: first establishing hypercortisolism, next determining ACTH dependence, and finally localizing the source of hormone overproduction.

Tahmini Süre:1m 30s

Soru 514Soru →

A 19-year-old man comes to the university health clinic due to a painful swelling in his right axilla that has been worsening over the past 4 days. He is a collegiate wrestler and reports that several of his teammates have recently been treated for similar skin lesions. He has no significant past medical history and takes no medications. Vital signs are temperature 37.0°C (98.6°F), blood pressure 118/76 mm Hg, pulse 74/min, and respirations 14/min. Physical examination shows a 3.5-cm, exquisitely tender, erythematous, and fluctuant nodule in the right axilla. There is no surrounding induration or erythema extending beyond the nodule, and no regional lymphadenopathy is appreciated. Which of the following is the most appropriate next step in management?

Incision and drainage of the lesion

Incision and drainage followed by oral trimethoprim-sulfamethoxazole

Oral cephalexin therapy

Intravenous vancomycin therapy

Swab of the overlying skin for bacterial culture

Cevabı ve açıklamayı göster

Cevap: Incision and drainage of the lesion

Cevap

Incision and drainage of the lesion

The patient presents with a mild, purulent skin and soft tissue infection (cutaneous abscess). In healthy, immunocompetent patients who do not exhibit signs of systemic inflammatory response (such as fever, tachycardia, or tachypnea) and who lack extensive surrounding cellulitis, the definitive treatment is incision and drainage alone. Systemic antibiotics are not routinely indicated for simple abscesses following adequate source control, as they do not significantly improve cure rates and contribute to unnecessary antibiotic exposure.

Adım Adım Çözüm

Evaluate the clinical presentation and physical examination findings.

The patient has a 3.5-cm, exquisitely tender, erythematous, fluctuant nodule without systemic signs (such as fever or tachycardia) or extensive surrounding cellulitis.

Determining the severity of a skin and soft tissue infection (SSTI) dictates the need for surgical versus medical intervention.

Classify the infection according to clinical guidelines.

This is classified as a mild, purulent skin and soft tissue infection (simple abscess).

Guidelines stratify purulent SSTIs into mild (no systemic signs), moderate (systemic signs present), and severe (failed previous treatment, deep infection, or immunocompromise).

Determine the most appropriate next step in management based on the classification.

The primary and definitive treatment for a mild, uncomplicated abscess is incision and drainage alone.

Source control is curative for simple abscesses. Adding systemic antibiotics does not significantly improve outcomes in healthy individuals and violates antimicrobial stewardship.

Anahtar Kavram

The standard of care for a mild, uncomplicated cutaneous abscess in an immunocompetent patient without systemic signs of illness is incision and drainage alone; adjunctive systemic antibiotics are not indicated.

Soru 515Soru →

A 42-year-old woman is evaluated in the emergency department for severe, colicky left flank pain radiating to the groin and gross hematuria. For the past year, she has experienced progressive generalized muscle weakness, persistent dry eyes, and a dry mouth. Blood pressure is 120/76 mm Hg, and pulse is 88/min. Laboratory studies show:

Laboratory Test	Result
Serum sodium	$139$ mEq/L
Serum potassium	$2.8$ mEq/L
Serum chloride	$115$ mEq/L
Serum bicarbonate	$14$ mEq/L
Serum creatinine	$1.1$ mg/dL
Arterial pH	$7.27$
Arterial $PaCO_2$	$29$ mm Hg
Arterial $PaO_2$	$98$ mm Hg

Urinalysis	Result
pH	$6.8$
Blood	Large
Protein	Trace

A non-contrast CT of the abdomen and pelvis reveals a 5-mm calculus in the left ureter and bilateral medullary nephrocalcinosis. Which of the following is the most likely primary pathophysiologic mechanism responsible for this patient's laboratory and imaging findings?

Impaired apical hydrogen ion secretion in the distal tubule

Defective sodium-bicarbonate cotransport in the proximal tubule

Decreased epithelial sodium channel activity in the cortical collecting duct

Increased gastrointestinal loss of bicarbonate-rich fluids

Accumulation of unmeasured organic anions due to decreased glomerular filtration

Cevabı ve açıklamayı göster

Cevap: Impaired apical hydrogen ion secretion in the distal tubule

Cevap

The primary pathophysiologic mechanism is impaired apical hydrogen ion secretion in the distal tubule (Type 1 Renal Tubular Acidosis).

The correct option identifies the defect seen in Type 1 (distal) RTA: an inability of the

\alpha

-intercalated cells in the distal tubule to secrete hydrogen ions. This defect leads to a normal anion gap metabolic acidosis, profound hypokalemia (as the kidney wastes potassium in an attempt to retain sodium without exchanging hydrogen), and a persistently alkaline urine (pH > 5.5). The combination of alkaline urine and hypocitraturia creates an environment highly susceptible to calcium phosphate precipitation, leading to bilateral medullary nephrocalcinosis and urolithiasis. Furthermore, Type 1 RTA is classically associated with autoimmune diseases, specifically Sjögren syndrome and rheumatoid arthritis, perfectly matching the patient's sicca symptoms and joint history.

Adım Adım Çözüm

Calculate the serum anion gap to classify the metabolic acidosis.

AG = Na^+ - (Cl^- + HCO_3^-) = 139 - (115 + 14) = 10

mEq/L.

An anion gap between 8 and 12 mEq/L indicates a normal anion gap metabolic acidosis (NAGMA), ruling out etiologies like lactic acidosis, ketoacidosis, and uremia.

Evaluate the respiratory compensation using Winter's formula.

Expected

PaCO_2 = (1.5 \times 14) + 8 \pm 2 = 29 \pm 2

mm Hg. The measured

PaCO_2

29

mm Hg.

Confirming appropriate respiratory compensation ensures there is no mixed acid-base disorder (e.g., concurrent respiratory alkalosis or acidosis) complicating the clinical picture.

Analyze the serum potassium and urine pH in the context of a NAGMA.

The patient has severe hypokalemia (

2.8

mEq/L) and an inappropriately alkaline urine (pH

6.8

In the setting of NAGMA, a high urine pH (

> 5.5

) and hypokalemia specifically point toward a distal renal tubular defect (Type 1 RTA), as the kidney fails to excrete

H^+

Integrate the clinical and imaging findings to confirm the etiology.

The patient has signs of Sjögren syndrome (dry eyes/mouth, muscle weakness from hypokalemia) and nephrocalcinosis with kidney stones.

Type 1 RTA is highly associated with autoimmune diseases like Sjögren syndrome and uniquely causes nephrocalcinosis/calcium phosphate stones due to alkaline urine and low urinary citrate.

Anahtar Kavram

Type 1 (distal) renal tubular acidosis presents with a normal anion gap metabolic acidosis, hypokalemia, urine pH > 5.5, and nephrocalcinosis, often in the setting of autoimmune disorders like Sjögren syndrome.

Soru 516Soru →

A $72$ -year-old man is evaluated in the intensive care unit due to abnormal laboratory results. He was admitted $8$ days ago for severe sepsis secondary to complicated pyelonephritis, which required intravenous antibiotics and vasopressor support. He has steadily improved; vasopressors were discontinued $3$ days ago, and he is currently breathing comfortably on room air. He has a medical history of type $2$ diabetes mellitus and benign prostatic hyperplasia. His temperature is $36.9^\circ\text{C}$ ( $98.4^\circ\text{F}$ ), blood pressure is $130/80\text{ mm Hg}$ , and pulse is $78\text{/min}$ . Physical examination shows a tired-appearing man. His neck is supple with no thyromegaly or palpable nodules. Laboratory studies show:

Laboratory Test	Result	Reference Range
Thyroid-stimulating hormone (TSH)	$0.15\ \mu\text{U/mL}$	$0.4-4.0\ \mu\text{U/mL}$
Free thyroxine (T4)	$0.7\ \text{ng/dL}$	$0.9-1.7\ \text{ng/dL}$
Total triiodothyronine (T3)	$40\ \text{ng/dL}$	$80-200\ \text{ng/dL}$
Morning serum cortisol	$22\ \mu\text{g/dL}$	$5-25\ \mu\text{g/dL}$

Which of the following is the most appropriate next step in the management of this patient's thyroid findings?

Magnetic resonance imaging of the pituitary gland

Administration of oral liothyronine

Reassurance and reevaluation of thyroid function after clinical recovery

Administration of intravenous levothyroxine

Initiation of methimazole therapy

Cevabı ve açıklamayı göster

Cevap: Reassurance and reevaluation of thyroid function after clinical recovery

Cevap

Reassurance and reevaluation of thyroid function after clinical recovery

The correct approach is reassurance and reevaluation of thyroid function after clinical recovery. This patient's laboratory findings (low TSH, low free T4, and profoundly low total T3) in the context of recent severe sepsis are classic for nonthyroidal illness syndrome, also known as euthyroid sick syndrome. During severe illness, caloric deprivation, or major surgery, there is decreased peripheral conversion of T4 to active T3, leading to low T3 levels (early phase). As the illness persists and becomes more severe, TSH and T4 levels also drop. This is considered a physiologic adaptation to reduce metabolic demand during stress rather than true thyroid gland dysfunction. Treatment with thyroid hormone replacement does not improve clinical outcomes and is not indicated. Thyroid function tests should be repeated 4 to 6 weeks after recovery from the acute illness if clinical suspicion remains.

Adım Adım Çözüm

Analyze the thyroid function tests.

The patient has low TSH, low free T4, and markedly low total T3.

Identifying the specific pattern of thyroid hormone derangement is the first step in diagnosis.

Correlate the laboratory findings with the clinical context.

The abnormal labs occurred in the setting of severe sepsis, a critical illness, without signs of preexisting thyroid or pituitary disease.

Context differentiates true endocrine pathology from physiologic adaptations to stress.

Determine the diagnosis and next best step in management.

The diagnosis is nonthyroidal illness syndrome (euthyroid sick syndrome), for which the standard of care is observation and retesting after recovery.

Treatment with exogenous thyroid hormone is not beneficial and may be harmful in this condition.

Anahtar Kavram

Nonthyroidal illness syndrome (euthyroid sick syndrome) presents with low T3, low or normal T4, and low or normal TSH in critically ill patients, requiring only observation.

Soru 517Soru →

A 58-year-old woman comes to the clinic reporting a 6-week history of a progressively enlarging mass on the right side of her face. She also reports soaking night sweats and a 4-kg (8.8-lb) unintentional weight loss over the past 2 months. She has a 12-year history of primary Sjögren syndrome, which is managed with artificial tears and pilocarpine. Physical examination reveals a 4-cm, firm, non-tender, immobile mass in the right parotid region. Right-sided cervical lymphadenopathy is also present. Her past parotid enlargements associated with her autoimmune disease were bilateral, soft, and fluctuated in size. Laboratory studies show an elevated lactate dehydrogenase (LDH) level. Which of the following is the most likely etiology of this patient's new symptoms?

B-cell non-Hodgkin lymphoma

Pleomorphic adenoma

Suppurative parotitis

Sialolithiasis

Exacerbation of Sjögren syndrome

Cevabı ve açıklamayı göster

Cevap: B-cell non-Hodgkin lymphoma

Cevap

B-cell non-Hodgkin lymphoma

The correct answer is B-cell non-Hodgkin lymphoma. Patients with primary Sjögren syndrome have a substantially increased risk (estimated at 15 to 44 times that of the general population) of developing B-cell non-Hodgkin lymphoma, most commonly mucosa-associated lymphoid tissue (MALT) lymphoma or diffuse large B-cell lymphoma. The classic presentation of this malignant transformation is a new, progressively enlarging, unilateral, firm, and non-tender mass in a major salivary gland (often the parotid), accompanied by regional lymphadenopathy and systemic B-symptoms such as night sweats and unintentional weight loss. An elevated LDH level further supports a highly proliferative malignant process. While benign, bilateral, soft parotid enlargement is a common baseline feature of Sjögren syndrome, a unilateral, firm, fixed mass represents a critical red flag for lymphoma.

Adım Adım Çözüm

Analyze the patient's baseline medical history.

The patient has a 12-year history of primary Sjögren syndrome.

Establishing the chronic underlying disease helps identify associated long-term complications and distinguishes them from new, unrelated conditions.

Identify the key clinical features of the current presentation.

The patient has a new-onset, firm, immobile, unilateral parotid mass accompanied by cervical lymphadenopathy, systemic B-symptoms (night sweats, weight loss), and elevated LDH.

Differentiating these progressive, alarming features from her baseline chronic, bilateral, soft parotid swelling is critical.

Correlate the new clinical findings with the underlying disease risk profile.

Sjögren syndrome is strongly associated with an increased risk of developing B-cell non-Hodgkin lymphoma, which perfectly matches the presentation of a malignant salivary mass and systemic symptoms.

Recognizing this specific epidemiological association leads directly to the correct malignant etiology.

Anahtar Kavram

Patients with primary Sjögren syndrome have a markedly increased risk (up to 44-fold) of developing B-cell non-Hodgkin lymphoma. A new, progressively enlarging, unilateral, firm parotid mass accompanied by B-symptoms should immediately raise suspicion for malignant transformation.

Soru 518Soru →

Match each clinical vignette to the autoantibody profile most specific for the suspected underlying rheumatologic or autoimmune condition.

Soldaki öğeye tıklayın, sonra eşleşen sağdaki öğeye tıklayın

Cevabı ve açıklamayı göster

Cevap

The clinical vignettes describe Mixed Connective Tissue Disease (Anti-U1 RNP), Antisynthetase syndrome (Anti-Jo-1), Sjögren syndrome (Anti-Ro/La), Diffuse cutaneous systemic sclerosis (Anti-Scl-70), and Antiphospholipid syndrome (Anticardiolipin/Anti-beta-2-glycoprotein I).

Each vignette represents a classic USMLE presentation of a distinct rheumatologic disorder with a highly specific serologic marker. Mixed Connective Tissue Disease requires anti-U1 RNP. Antisynthetase syndrome features myositis, interstitial lung disease, and 'mechanic's hands' corresponding to anti-Jo-1. Sjögren syndrome's sicca symptoms map to anti-Ro/SSA and anti-La/SSB. Diffuse systemic sclerosis with pulmonary involvement maps to anti-Scl-70. Antiphospholipid syndrome's recurrent fetal loss and thrombosis correlate with anticardiolipin and anti-beta-2-glycoprotein I antibodies.

Adım Adım Çözüm

Analyze the first vignette to identify the combination of Raynaud phenomenon, puffy hands, and overlapping features of multiple connective tissue diseases.

Diagnose Mixed Connective Tissue Disease (MCTD), which is defined by the presence of anti-U1 RNP antibodies.

MCTD requires anti-U1 RNP for definitive classification alongside its characteristic overlapping clinical presentation.

Evaluate the second vignette featuring interstitial lung disease, myositis, and hyperkeratotic skin on the lateral fingers.

Identify 'mechanic's hands' and diagnose Antisynthetase syndrome, highly associated with Anti-Jo-1 antibodies.

Anti-Jo-1 is an antibody directed against histidyl-tRNA synthetase and is a hallmark of this specific inflammatory myopathy phenotype.

Review the third vignette describing severe dry eyes, dry mouth, and parotid gland enlargement.

Diagnose Sjögren syndrome, heavily correlated with Anti-Ro/SSA and Anti-La/SSB antibodies.

These antibodies target ribonucleoprotein complexes and are classic serologic markers for Sjögren syndrome.

Assess the fourth vignette demonstrating diffuse skin thickening extending to the trunk, along with bibasilar reticular opacities.

Diagnose diffuse cutaneous systemic sclerosis (SSc), linked to Anti-Scl-70 antibodies.

Anti-Scl-70 is specific to the diffuse subtype of SSc and is predictive of a higher likelihood of interstitial lung disease.

Examine the fifth vignette detailing unprovoked thrombosis and recurrent second-trimester pregnancy loss.

Diagnose Antiphospholipid syndrome, tested via Anticardiolipin and anti-beta-2-glycoprotein I antibodies.

These are part of the core diagnostic laboratory criteria for Antiphospholipid syndrome alongside lupus anticoagulant.

Anahtar Kavram

Correlation of specific serologic autoantibody profiles with their distinct rheumatologic clinical syndromes.

Soru 519Soru →

A $72$ -year-old man is evaluated in a skilled nursing facility due to a $4$ -day history of frequent, watery, foul-smelling stools and diffuse lower abdominal cramping. Two weeks ago, he completed a $7$ -day course of oral amoxicillin-clavulanate for a chronic obstructive pulmonary disease exacerbation. His temperature is $37.8^{\circ}\text{C}$ ( $100.0^{\circ}\text{F}$ ), blood pressure is $128/78\text{ mm Hg}$ , and pulse is $92/\text{min}$ . Physical examination reveals mild, diffuse abdominal tenderness without guarding or rebound. Laboratory testing shows a leukocyte count of $14,000/\text{mm}^3$ and a serum creatinine of $1.1\text{ mg/dL}$ . A stool enzyme immunoassay is positive for both glutamate dehydrogenase antigen and *Clostridioides difficile* toxins A and B. Which of the following is the most appropriate targeted pharmacotherapy for this patient's current condition?

Oral fidaxomicin

Intravenous vancomycin

Oral metronidazole

Intravenous metronidazole

Fecal microbiota transplantation

Cevabı ve açıklamayı göster

Cevap: Oral fidaxomicin

Cevap

Oral fidaxomicin

The patient has an initial episode of non-severe *Clostridioides difficile* infection (CDI), characterized by characteristic diarrhea following recent antibiotic exposure, a leukocyte count

< 15,000/\text{mm}^3

, and a serum creatinine

< 1.5\text{ mg/dL}

. According to current guidelines, the preferred first-line treatment for an initial episode of CDI is oral fidaxomicin. Oral vancomycin is an acceptable alternative. Fidaxomicin is specifically favored because of its narrow spectrum of activity (preserving normal gut flora) and its association with significantly lower rates of CDI recurrence.

Adım Adım Çözüm

Analyze the clinical presentation and recent history.

The patient has new-onset watery diarrhea and abdominal cramping following a recent course of amoxicillin-clavulanate.

Identifying the clinical syndrome and risk factors points toward antibiotic-associated diarrhea.

Interpret the diagnostic test results.

Stool immunoassay is positive for GDH antigen and C. difficile toxins A and B, confirming the diagnosis.

Positive GDH confirms the presence of the organism, while positive toxins confirm the toxigenic strain causing active infection.

Assess disease severity.

The patient has a leukocyte count of 14,000/mm^3 (which is less than 15,000/mm^3) and a normal serum creatinine, with no signs of shock or megacolon.

Severity classification determines the appropriate route and choice of antimicrobial therapy.

Select the guideline-recommended first-line therapy.

Oral fidaxomicin or oral vancomycin is indicated for an initial episode of non-severe C. difficile infection.

Current IDSA/SHEA guidelines prioritize oral fidaxomicin due to its narrow spectrum and lower recurrence rates.

Anahtar Kavram

The first-line pharmacotherapy for an initial episode of non-fulminant Clostridioides difficile infection is oral fidaxomicin or oral vancomycin.

Soru 520Soru →

A 28-year-old man with a 5-year history of ulcerative colitis is admitted to the hospital with a severe disease flare, characterized by up to $12$ bloody bowel movements daily and severe abdominal cramping. He was started on high-dose intravenous methylprednisolone $3$ days ago. Today, he appears profoundly lethargic and confused. Vital signs show a temperature of $39.4^\circ\text{C}$ ( $102.9^\circ\text{F}$ ), blood pressure of $88/50\text{ mm Hg}$ , and pulse of $132/\text{min}$ . Physical examination reveals a markedly distended, tympanitic abdomen with diffuse rigidity, involuntary guarding, and absent bowel sounds. Laboratory studies show a leukocyte count of $24,000/\text{mm}^3$ and serum lactate of $5.1\text{ mmol/L}$ . An upright chest radiograph reveals free air under the right hemidiaphragm. The patient's legally appointed healthcare proxy (his brother) is en route to the hospital and is currently unreachable by phone. His girlfriend, who is at the bedside, requests that the medical team wait for the brother before proceeding with any major interventions. What is the most appropriate next step in the management of this patient?

Escalate medical therapy by adding broad-spectrum intravenous antibiotics

Delay surgical intervention until the legally appointed proxy provides consent

Proceed immediately with an exploratory laparotomy

Transport the patient for a computed tomography scan of the abdomen and pelvis

Administer an intravenous sodium bicarbonate infusion to normalize the pH

Cevabı ve açıklamayı göster

Cevap: Proceed immediately with an exploratory laparotomy

Cevap

Proceed immediately with an exploratory laparotomy

This patient has a history of severe ulcerative colitis and now presents with altered mental status, hemodynamic instability, diffuse peritonitis, and free air under the diaphragm on a chest radiograph. This presentation is highly consistent with a perforated toxic megacolon. A perforated viscus with signs of peritonitis and septic shock is an absolute surgical emergency requiring immediate exploratory laparotomy. Although the patient lacks decision-making capacity and his designated healthcare proxy is unreachable, the ethical and legal principle of implied consent permits physicians to provide immediate, life-saving treatment without waiting for formal authorization. Delaying care for consent or further imaging would likely be fatal.

Adım Adım Çözüm

Analyze the clinical presentation and diagnostic findings.

The patient has severe ulcerative colitis complicated by a perforated toxic megacolon (indicated by pneumoperitoneum, diffuse rigidity, and septic shock).

Identifying the complication is critical for determining the urgency of the intervention.

Determine the definitive medical or surgical requirement.

A perforated viscus with hemodynamic instability mandates emergent surgical source control (exploratory laparotomy).

Medical management alone is uniformly fatal once gross perforation and peritonitis have occurred.

Apply medical ethics principles regarding consent in emergencies.

Proceed with surgery under implied consent.

The patient lacks decision-making capacity (lethargic/confused), the condition is immediately life-threatening, and the legal proxy is temporarily unreachable.

Anahtar Kavram

Emergent surgical management of a perforated toxic megacolon and the application of implied consent in life-threatening emergencies.

ÖncekiSayfa 26 / 158Sonraki

Internal Medicine

Cevap

Adım Adım Çözüm

Anahtar Kavram

Sık Yapılan Hatalar

Cevap

Adım Adım Çözüm

Anahtar Kavram

Sık Yapılan Hatalar

Cevap

Adım Adım Çözüm

Anahtar Kavram

Sık Yapılan Hatalar

Cevap

Adım Adım Çözüm

Anahtar Kavram

Sık Yapılan Hatalar

Cevap

Adım Adım Çözüm

Anahtar Kavram

Sık Yapılan Hatalar

Cevap

Adım Adım Çözüm

Anahtar Kavram

Sık Yapılan Hatalar

Cevap

Adım Adım Çözüm

Anahtar Kavram

Sık Yapılan Hatalar

Cevap

Adım Adım Çözüm

Anahtar Kavram

Sık Yapılan Hatalar

Cevap

Adım Adım Çözüm

Anahtar Kavram

Sık Yapılan Hatalar

Cevap

Adım Adım Çözüm

Anahtar Kavram

Sık Yapılan Hatalar

Cevap

Adım Adım Çözüm

Anahtar Kavram

Sık Yapılan Hatalar

Cevap

Adım Adım Çözüm

Anahtar Kavram

Sık Yapılan Hatalar

Cevap

Adım Adım Çözüm

Anahtar Kavram

Sık Yapılan Hatalar

Cevap

Adım Adım Çözüm

Anahtar Kavram

Sık Yapılan Hatalar

Cevap

Adım Adım Çözüm

Anahtar Kavram

Sık Yapılan Hatalar

Cevap

Adım Adım Çözüm

Anahtar Kavram

Sık Yapılan Hatalar

Cevap

Adım Adım Çözüm

Anahtar Kavram

Sık Yapılan Hatalar

Cevap

Adım Adım Çözüm

Anahtar Kavram

Sık Yapılan Hatalar

Cevap

Adım Adım Çözüm

Anahtar Kavram

Sık Yapılan Hatalar

Cevap

Adım Adım Çözüm

Anahtar Kavram