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CARDIOVASCULAR QBANK (UWORLD) EXAM| 252
QUESTIONS WITH ANSWERS|2025-2026|A+ GRADED
Pathology -Age: 64 years man -Difficult walking for 6 months; experiencing muscle cramps in his right thigh after walking a block on level ground -The cramps subside quickly with rest. He has also had decreased sexual performance. -Medical history: hypercholesteremia and MI; smokes (daily) -Afebrile, normal BP and pulse; cardiac auscultation (normal S1 and S and equal vesicular breath sounds over bilateral lungs) -Abdomen soft (without masses), no peripheral edema, nor muscle tenderness, nor muscle weakness; cause of patient's symptoms? a)Granulomatous inflammation of the arterial media b)Homogenous acellular thickening of the arteriolar wall c)Lipid-filled arterial intimal plaques d)Medial band-like arterial calcification e)Onion-like concentric thickening of the arteriolar walls Answer: Choice C (Lipid-filled arterial intimal plaques)
-Patient’s muscle pain (occurs with exercise and remits with rest)= intermittent claudication; smoking is an important risk factor -Claudication is usually due to atherosclerosis of the large arteries, specifically resulting from fixed stenoses caused by lipid-filled intimal plaques that bulge into arterial lumen (atheromas). These stenoses prevent a sufficient increase in blood flow to muscles during exercise, leading to ischemic muscle pain. The pain is rapidly relieved by rest, as residual blood flow is adequate to meet the metabolic demands of resting, but not exercising muscle -Thigh claudication is suggestive of occlusive disease of the ipsilateral external iliac artery or its more distal branches (i.e., common femoral, superficial femoral, profunda femoris arteries). Accompanying impotence and/or gluteal claudication suggests more proximal aortoiliac occlusion (so called Leriche syndrome), which, in addition to affecting the external iliac artery, also diminishes blood flow to the internal pudendal and gluteal branches of the internal iliac artery Choice A= Granulomatous inflammation of the arterial media occurs in temporal (giant cell) arteritis, the most common form of systemic vasculitis in adults. The condition typically affects patients age >50 years and causes headache, facial pain, jaw claudication and visual loss
Hyperplastic arteriolosclerosis (pic in answer) Monckeberg arteriolosclerosis -Age: 19 years man -Transitioning care from his pediatrician; recently changed his glasses for myopia, he otherwise has no symptoms; no medications; vitals are normal -Physical exam: tall with long upper extremities and fingers. Face appears narrow with down-slanted palpebral fissures, flattened malar bones, and a small jaw -Lungs are clear on auscultation. Late-systolic murmur is present at cardiac apex. Abdomen is soft and nontender with no organomegaly. Cause of patient's murmur? a)Aortic root dilation b)Aortic valve cusp fusion c)Endocardial fibrous deposition d)Myxomatous mitral degeneration e)Papillary muscle dysfunction
Answer: Choice D (Myxomatous mitral degeneration) -The patient has clinical features of Marfan syndrome, an autosomal dominant disorder caused by mutations in the FBN gene encoding fibrillin-1, a main component of extracellular matrix microfibrils. Fibrilling-1 provides support to elastic fibers and helps maintain connective tissue integrity. It also regulates extracellular matrix remodeling by binding to and sequestering transforming growth factor-beta (TGF-beta) -In Marfan syndrome, defective fibrillin-1 is unable to bind TGF- beta. The resulting overexpression of free, active TGF-beta leads to increased production of matrix metalloproteinases, which cleave elastic fibers and other components of the extracellular matrix, reducing tissue integrity. Within the mitral valve, this process results in fragmentation of elastic fibers and decreased collagen density and pooling of glycosaminoglycans (myxomatous mitral degeneration) -The elongated, floppy mitral valve leaflets prolapse into the atrium which causes a midsystolic click on auscultation and allows for mitral valve regurgitation. This regurgitation flow is characterized by a mid-to-late systolic apical murmur, as seen in this patient; severe regurgitation may produce a holosystolic murmur
Turner syndrome -Age: 42 years woman -Comes to ED for evaluation of chest pain. She was moving furniture in her summer house 2 days ago when she experienced sharp pain in the left side of the sternum that quickly subsided. Since then, the patient has had episodic pain with deep inspiration or trunk movement. She has no fever or cough. -History: hypertension; father died of MI at age 67. Not smoker. High BP (same BP in right and left arm), pulse and RR (normal) -Localized tenderness to palpation at the left sternal border. Lungs are clear to auscultation, and cardiac exam (normal hear sounds without gallops or murmurs). Abdomen is soft and nontender. No peripheral edema. Cause? a)Acute pericarditis b)Aortic dissection c)Costochondritis d)Esophageal spasm e)Gastroesophageal reflux disease f)Panic disorder g)Pneumonia
h)Pulmonary arterial hypertension i)Pulmonary embolism j)Unstable angina Answer: Choice C (Costochondritis) -This patient’s chest pain is most likely due to Costosternal syndrome (also known as costochondritis or anterior chest wall syndrome) involving regional chest wall. It usually occurs after repetitive activity and involves the upper costal cartilage at the costochondral or Costosternal junctions. The pain is typically reproduced with palpation and worsened with movement or changes in position (e.g., horizontal arm flexion). Patients typically do not have palpable warmth, swelling or erythema Choices A, G and I= Conditions causing inflammation of the pleura or pericardium can cause sharp pain worsened with inspiration. Pericarditis often follows an upper respiratory viral syndrome. The pain of pericarditis is typically worse when lying flat and relieved by leaning forward. Examination may show a pericardial friction rub. Pulmonary embolism can cause pleural inflammation with chest pain. However, such cases are typically due to large emboli and are associated with significant hypoxia and shortness of breath. Pneumonia usually presents with fever, cough, and shortness of breath. None of these conditions would be associated with focal tenderness of the chest wall
-Age: 68 years man -Brought to ED with chest pain. For the last year, the patient has had exertional chest pain that has progressively worsened. He was shoveling snow this morning when the pain become unbearable. He has smoked a pack of cigarettes daily for 40 years -High BP; normal pulse; exam: mild diaphoresis -Lungs: clear to auscultation. ECG= ST and T wave changes suggestive of ischemia. Cardiac enzymes are elevated. Emergent coronary angiography is performed, which demonstrates significant atherosclerotic involvement of the left anterior descending and circumflex arteries. Development of these vascular lesions most likely involved growth factors released from which of the following sources? a)B lymphocytes b)Eosinophils c)Erythrocytes d)Mast cells e)Neutrophils f)Platelets Answer: Choice F (Platelets) The development of atherosclerotic plaque, or atheroma, involves a multistep process:
-Initially, factors including hyperlipidemia, hypertension, hyperglycemia, and smoking triggers endothelial injury and/or dysfunction. This leads to increased vascular permeability, enhanced leukocyte adhesion, and a higher propensity for thrombosis. -Lipoproteins (i.e., LDL and oxidized LDL) enter the arterial wall intima and begin to accumulate. Monocytes adhere to the endothelial wall and enter into the intima as well; these cells transform into macrophages and engulf lipid particles to become foam cells. Platelets adhere to the abnormal endothelium and become activated -Growth factors, namely platelet-derived growth factors (PDGF), are released from platelets, activated macrophages, and endothelial cells. This triggers smooth muscle (SMC) recruitment from the media and proliferation in the intima Over time, progressive SMC proliferation and accumulation of necrotic debris (due to macrophage/foam cell and SMC death) lead to growth of the atheroma. SMCs encourage plaque stability by synthesizing collagen, whereas activated inflammatory cells break down collagen and contribute to plaque instability. HDL likely extracts lipids from the intima back into the bloodstream and helps slow atheroma development Choice A= B lymphocytes are not known to play a significant role in atheroma development. However, T lymphocytes in the arterial intima
-An echocardiogram shows defects in the lower part of the interatrial septum and the interventricular septum. This patient's condition is most likely associated with? a)22q11.2 deletion b)Autosomal trisomy c)Fibrillin mutation d)Frataxin mutation e)Hamartin gene mutation f)Sex chromosome monosomy Answer: Choice B (Autosomal trisomy) -This patient’s echocardiogram suggests a complete atrioventricular (AV) canal defect, the most common type of cardiac defect in patients with Down syndrome, an autosomal trisomy. Failure of endocardial cushion fusion results in ostium primum atrial septal defect, a ventricular septal defect and a single AV valve. Significant left-to-right shunting and AV valve regurgitation lead to excessive pulmonary blood flow and symptoms of heart failure (e.g., tachypnea, poor feeding). Auscultator findings of AV valve regurgitation (holosystolic, best heard at apex) and increased pulmonary venous return (mid-diastolic rumble) are characteristic. Choice A= DiGeorge syndrome (22q11.2 deletion) is characterized by thymic aplasia (T cell deficiency) and hypoparathyroidism
(hypocalcemia). It is associated with tetralogy of Fallot, truncus arteriosus, and transposition of the great vessels Choice C= Marfan syndrome (fibrillin-1 mutation) is associated with cystic medial necrosis of the aorta, which may result in dissecting aortic aneurysms and aortic valve regurgitation. Mitral valve prolapse is also common, but septal defects are not Choice D= Mutations in frataxin, a mitochondrial protein important in iron homeostasis and respiratory function, cause Friedreich ataxia. It is characterized by spinocerebellar degeneration and is associated with hypertrophic cardiomyopathy, but not septal defects Choice E= Mutations in tuberin and hamartin are seen in tuberous sclerosis. These patients may develop cardiac rhabdomyomas in ventricular walls and AV valves, cutaneous angiofibromas (adenoma sebaceum), central nervous system hamartomas, and renal cysts. However, septal defects are not characteristic Choice F= A missing sex chromosome (monosomy) is seen in Turner syndrome (45, XO), which is associated with bicuspid aortic valve (most common cardiac lesion) and coarctation of the aorta
-Brought to ED due to an episode of syncope. The patient was recently discharged back to a nursing home after being hospitalized for a urinary tract infection. -History: coronary artery disease and takes aspirin, clopidogrel, and atorvastatin -Medical conditions: type 2 diabetes, hypertension; doesn't use tobacco -Low BP (68/32) and pulse (118). Invasive hemodynamic monitoring reveals an elevated right atrial pressure of 17mmHg and a pulmonary capillary wedge pressure of 7mmHg (normal 8-10mmHg); most likely cause? a)Anaphylactic shock b)Gastrointestinal bleeding c)Right ventricular infarction d)Septic shock e)Severe aortic stenosis Answer: Choice C (Right ventricular infarction) -This patient is in shock (e.g., severe hypotension, end organ dysfunction (syncope)) due to an unknown cause. Hemodynamic monitoring (e.g., pulmonary artery catheterization) shows decreased pulmonary capillary wedge pressure (PCWP) and increased right atrial pressure (RAP), which indicated impaired blood flow from the right ventricle to the left side of the heart (right-sided heart failure). Common causes of right-sided HF= obstruction of pulmonary
circulation (e.g., pulmonary hypertension, pulmonary embolism) and right ventricular infarction (likely in this patient due to multiple cardiovascular risk factors) -In right ventricular infarction, the right ventricle is unable to effectively pump blood forward into the pulmonary arteries, causing increased pressure in the right atrium (i.e., elevated central venous pressure). The decreased RV outflow also lowers PCWP (an indicator of left-sided preload), which subsequently reduces cardiac output and causes hypotension. A reflexive increase in heart rate is mostly intact in this patient, though it is often impaired in RV infarction due to frequent ischemic involvement of the conduction system Choices A and D= Anaphylactic and septic shock are associated with peripheral vasodilation and massive fluid shift to the extravascular space. The depleted intravascular volume lowers the mean circulatory filling pressure, reducing both RAP and PCWP, while hypotension caused by widespread peripheral vasodilation leads to a compensatory increase in cardiac output Choice B= GI bleeding can cause hypovolemic shock with decreased RAP, PCWP, and cardiac output. Decreased cardiac output triggers an increase in sympathetic tone with peripheral vasoconstriction (increased systemic vascular resistance) to help maintain perfusion pressure
e)Splenic flexure Answer: Choice E (Splenic flexure) -This patient’s bilateral hippocampal necrosis is characteristic of the effect of global cerebral ischemia due to systemic hypotension. The hippocampus is particularly vulnerable during shock because of the high metabolic demand of its CA1 pyramidal neurons. Watershed areas located between the distal terminal branches of 2 different vascular territories (border zones) are also susceptible to ischemia because they have a low baseline perfusion pressure and poorly tolerate sustained decreases in systemic BP Important watershed areas in the body include: -Gastrointestinal
- Splenic flexure: the border zone supplied by branches of the superior and inferior mesenteric arteries -Brain: the borders of the areas supplied by the anterior cerebral artery, middle cerebral artery and posterior cerebral artery
-Age: 24 years man -Evaluated for episode of syncope. He was out jogging when he felt lightheaded and passed out, but he didn't sustain any head injury -The patient has had 2 similar episodes of lightheadedness while jogging over the last year, but this was the first time he passed out. He considers himself in good health and has no other medical problems -The patient does not smoke or do drugs. His father suddenly at age
- On physical exam, he has a harsh systolic murmur. Transthoracic echocardiography shows asymmetric interventricular septal hypertrophy. The patient's symptoms are most likely explained by left ventricular outflow obstruction created by which of the following structures? a)Aortic valve cusp and interventricular septum b)Aortic valve cusp and papillary muscle c)Aortic valve cusps d)Ascending aorta and interventricular septum e)Mitral valve leaflet and interventricular septum Answer: Choice E (Mitral valve leaflet and interventricular septum) -This patient’s presentation suggests hypertrophic cardiomyopathy (HCM), an autosomal dominant disorder resulting from mutations in cardiac sarcomere proteins. HCM is characterized by asymmetric ventricular septal hypertrophy and variable, dynamic left ventricular outflow (LVOT) obstruction. Systolic anterior motion of the mitral valve
