uWORLD Cardio Pathophysiology QuestionBank, 100% proven pass rate.

uWORLD Cardio Pathophysiology QuestionBank, 100% proven pass rate. Document Content and Description Below uWORLD Cardio Pathophysiology QuestionBank, 100% proven pass rate. uWORLD: A 67 yo man comes to the ED due to progressive SOB and chest tightness. he has no lightheadedness or syncope. The patie nt takes lisinopril for HTN and metformin for Type 2 DM. He has smoked a pack of cigarettes daily of the last 40 years. The blood pressure cuff is inflated to 140 mmHg and the pressure is released very slowly. At 120 mmHg, intermittent Korotkoff sounds are head only during expiration. At 100mmHg, Korotkoff sounds are heard throughout the respiratory cycle The physical examination finding can be seen in the following? - ☑☑Pericardial disease > Pulsus paradoxus is defined by a decrease in systolic blood pressure of > 10 mmHg with *inspiration*. It is most commonly seen in patients with cardiac tamponade but can also occur in severe asthma, chronic obstructive pulmonary disease, and constrictive pericarditis > Inspiration causes an increase in systemic venous return, resulting in increased right heart volumes. Under normal conditions, this results in expansion of the right ventricle into the pericardial space with little impact on the left side of the heart. However, in conditions that impair expansion into the pericardial space )eg, acute cardiac tamponade), the increased right ventricular volume occurring with inspiration leads to *bowing of the inter ventricular septum* toward the left ventricle. This leads to a decrease in left ventricular (LV) end-diastolic volume and stroke volume, with a resultant decrease in systolic pressure during inspiration. A patient has pulses paradoxus. The patient is tachypeneic and unable to speak in full sentences. Examination revels prolonged expiration and prominent bilateral wheezing. Heart sounds are nonroman. Chest imaging shows a normal-sized heart and hyper inflated lungs with a flattened diaphragm. Beside ECG revels no intrapericardial fluid accumulation or pericardial thickening. Which of the following physiologic changes is most likely to provide immediate relief in this patient? - ☑☑cAMP accumulation in smooth muscle cells > Asthma and chronic obstructive pulmonary disease (COPD) exacerbation are the most frequent causes of pulses paradoxus in the absence of significant pericardial disease. Beta-adrengeric agonists control acute asthma and COPD exacerbations by causing bronchial smooth muscle relaxation via increase intracellular cAMP. uWORLD: A 35 yo man is evaluated for progressive fatigue and SOB. Recently, he has noticed bilateral leg swelling and abdominal distention despite overall weight loss. He does not use tobacco, alcohol, or illicit drugs. Despite treatment, the patient dies several weeks later. Autospy revels significant endocardial thickening with dense fibrous deposits around the tricuspid and pulmonary valves as well as moderate pulmonary valve stenos. The left-sided cardiac chambers and valves are normal. Measuring the levels of which substances would have helped in diagnosing this patient? - ☑☑Urinary 5-hydroxyindolearcretic acid > Carcinoid syndrome typically presents with episodic flushing, secretary diarrhea and wheezing. It can lead to pathognomonic plaque-like deposits of fibrous tissue on the right-sided endocardium, causing tricuspid regurgitation and right-sided heart filature. Elevated 24 hour urnary 5-hydroxyindoleacetic acid can confirm the diagnosis. > The autospy findings - endocardial thickening and fibrosis of tricuspid and pulmonary valves - are chracerstic of *carcinoid heart disease.*. Carcinoids are well-differentiated neuroendocrine turbos found most commonly in the distill small intestine and proximal colon, with a strong propensity for metastasis to the liver. These tumors secrete seers products (including histamine, serotonin, and vasoactive intestinal peptide) that are metabolized in the liver. In patients with liver metastasis, these hormones are relased directly into the systemic circulation, leading to carcinoid syndrome. > Carcinoid heart diseases is caused by excessive secretion of *serotonin*, which stimulates fibroblast growth and fibrognesis. Pathognomic plaque-like *deposits of fibrous tissue* occur most commonly on the *endocardium*, leading to *tricuspid regurgitation*, pulmonic valvulpathy, and right-sided heart failure )eg ascites, peripheral edema). Endocardial fibrosis and thickening are generally limited to the right heart as vasoactive products and inactivated distally by pulmonary vascular endothelial monoamine oxidase. FYI - Measuring of plasma cortisol: Used for diagnosing adrenal insufficiency and Crushing syndrome - Measuring of homocysteine: elevation may contribute to arterial and venous thrombosis and to the development of atherosclerosis. - Measuring of plasma phenylalanine: May be elevated in patients with phenylalanine hydroxylase deficiency, resulting in central nervous system damage/intellectual disability : - Measuring of porphobilinogen: May be elevated in the porphyria, which are caused by deficiencies of the heme synthesis enzymes. The porphyries may produce cutaneous lesions, skin photosensitivity, or attacks of abdominal pain and neurological disturbances (acute intermittent porphyria) - Measuring of vanillymandelic acid: by product of norepinephrine and epinephrine, and can be used to detect *neuroblastoma* and other tumors of neural crest origin uWorld: A 62 yo woman comes to the hospital with intermittent but progressive substernal chest pain over the last 36 hours. Medical history includes HTN and hyperlipidemia, but the patient has been poorly compliant with her medication regimen and outpatient follow-up. She previously smoked a pack daily for 30 years but quit last year. Her blood pressure is 130/75 mmHg and pulse is 73/min. ECG on admission shows normal sinus rhythm with a 2-mm ST segment elevation in leads V2-V5. The patient is treated with medical management. However, on the fifth day of hospitalization she dies suddenly, despite adequate resuscitation. Which is the most likely cause of death in the patient? - ☑☑Profound hypotension > Rupture of the left ventricular free wall is a catastrophic mechanical complication of anterior wall myocardial infarction (MI) that usually occurs within the first 5-14 days after MI. Rupture leads to hemoperricardium and cardiac tamponade, causing profound hypertension and shock with rapid progression to pulseless electrical activity and death. > This patient most likely died from profound hypotension due to *ruptured left ventricular free wall*. Her initial presentation of substernal chest discomfort and ST segment elevation in anterior precordial leads in consistent with acute *anterior wall myocardial infarction (MI)*. Free wall rupture is a catastrophic mechanical complication that usually occurs within the first 5-14 days after a large anterior transmural MI (from left anterior descending occlusion). During this timeframe, the infarcted myocardium is substantially weakened by coagulative necrosis, neutrophilic and macrophage infiltration, and enzymatic lysis of myocardial connective tissue. Abrupt rupture of the left ventricle leads to *hemopericardium* and *cardiac tamponade*. Patients have sudden onset of chest pain and *profound hypotension and shock*, with rapid progression to pulseless electrical activity and death. FYI: > Carotid artery occlusion = can lead to ischemic symptoms (hemiparesis, vision changes) but does not typically cause sudden death. > Hypertensive emergency can lead to aortic dissection = that typically presents with tearing chest or back pain. Hypertension and shock can occur with retrograde extension of the dissection into he pericardial cavity or contrary arteries, with resultant hemoperricardium or MI, respectively. However, this patient's presentation of intimal normal blood pressure and ST segment elevation is more suggestive of acute MI with subsequent cardiac rupture. uWORLD: A 18 yo women is referred to cardiologist after a heart murmur is discovered during routine checkup. The patient is healthy and has no symptoms. Past medical history is unremarkable. She runs daily and wants to start actively training for a half marathon. She is concerned that the murmur is a sign of heart disease and would prevent her from pursuing her athletic activities. She has no family history of sudden cardiac death. Auscultation reveals a midsystolic click that is followed by a short late-systolic mummer at the cardiac apex. The mummer disappears with equating. This patient's condition is most likely related to an abnormality involving which of the following tissues? - ☑☑connective tissue > Cardiac auscultation in patients with mitral valve prolapse (MVP) typically reveals a non ejection (eg. mid systolic) click and mid- to late systolic mummer of mitral regurgitation. MVP is most often caused by defects in mitral valve connective tissue proteins that predispose to myxomatous degeneration of the mitral leaflets and chord tendineae. > The presence of a midstylic click following to a mid- to late systolic mummer at cardiac apex that disappears with squatting is most consistent with *mitral valve prolapse* (MVP) with mitral regurgitation (MR). The click results from sudden tensing of the charade tendineae as they are pulled taut by the ballooning valve leaflets. The mummer is due to malalignment of the valve margins during systole. *Manevuvers* that change left ventricular (LV) volume and cavity size can change the timing and intensity of the murmur. *Squatting* from a standing position *increases venous return* and *LV volume*, helping to bring the valve leaflets into a more normal anatomic arrangement. This, in turn, decrease the degree of MVP, causing a delay in the onset of click during systole, and systolic mummer typically becomes shorter or disappears. FYI > Hypertrophic cardiomyopathy (HCM) also presents with a systolic mummer at the cardiac apex that decreases in intestnity with squatting (due to increased left ventricle volume and decreased outflow tract obstruction). However, a mid systolic click, which is classic for MVP, is not heard with HCM. uWORLD: A 66 yo man with DM is brought to the host pail due to sudden-onset chest pain and nausea. BP is 70/60 mmHg and pulse is 60/min. Lungs are clear on auscultation. ECG shows ST-segment elevation in leads II, III, and aVG. Chest x-ray is unremarkable. The patient is diagnosed with an inferior wall myocardial infarction. Emergency cardiac cauterization revel complete occlusion of the proximal right coronary artery. He is persistently hypotensive in the cardiac cauterization laboratory. Which of the following hemodynamic findings is most likely to be obsessed (cardiac output, Pulmonary capillary wedge pressure, Central venous pressure; Will it increase/decrease?)? - ☑☑Increase CO Decrease Pulmonary Capillary Wedge pressure Increase Central Venous Pressure This patient is in cariogenic shock after suffering a left ventricular (LV) inferior wall MI. The inferior wall of the LV is supplied by the posterior descending artery, which arises off the dominant right canary artery. Because the right coronary artery also gives off marginal branches that supply most of the right ventricle (RV), inferior wall MI is often associated with r*right ventricular infarction(. > Infarction of the RV results in decreased RV stroke volume, which in turn leads to *diminished* LV filling and *cardiac output* in spite of preserved LV systolic function (Frank-Starling mechanism). TV dilation and elevated diastolic pressures also cause a shift of the interventrciular septum toward the LV cavity, further impairing LV filling and cardiac output, contributing to systemic hypotension and shock. Because left-sided filling pressures are reduced, *pulmonary capillary wedge pressure* also *decrease* as it estimates left atrial pressure. In addition, patients have *elevated central venous pressure* due to RV dysfunction and impaired forward flow. uWORLD: A 45 yo woman who recently immigrated to the US is hospitalized with exertion dyspnea and fatigue. She has no significant past medical history and takes no medication. The patient's BP is 110/80 mmHg and heart rate is 90/min and regular. After cardiopulmonary examination, the physician suspects mitral stenos. Which of the following is the most useful measure for assessing the degree of stenosis? - ☑☑A2-to-opening snap time interval > On auscultation, the best indicator of mitral stenosis (MS) severity is the length of time between S2 (specifically the A2 component, caused by aortic valve closure) and the opening snap (OS). The OS occurs due to abrupt tensing of the valve leaflets as the mitral valve reaches its maximum diameter during forceful opening. > Left-sided S3 and/or S4 gallops are generally absent in MS, since left ventricular filling is normal or decreased. Ex. A 4 month old baby is brought to the cardiology clinic by his parents for continued followed-up of tetralogy of Fallot. The diagnosis was made during routine antenatal sonography, and the pregnancy and delivery were otherwise uncomplicated. The infant has been seen frequently in the clinic and has not had any cyanosis, respiratory distress, and difficulty feeding. The parents become concerned when their son's surgical plan is discussed because he does not have the clinical signs that other children with metrology of Fallot demonstrate. Which is the major determinant of symptoms severity in this condition? - ☑☑Right ventricular Outflow Tract Obstruction > *Tetraology of Fallot* is characterized by ventricular septal defect (VSD), overriding aorta, right ventricular outflow tract (RVOT) obstruction and right ventricular hypertrophy. The VSD generally is large, which allows for haul pressure in the right and left ventricles. Therefore, it is the amount of *RVOT obstruction* that determines how much deoxygenated blood is delivered to the systemic circulation. > Infants with no or minimal RVOT obstruction, such as this patient, deliver more deoxygenated blood to the lungs and appear cyanotic. The degree of RVOT obstruction is *dynamic* and can increase suddenly, leading to profound cyanosis ("tet spells". These can be caused by dehydration or hyperventilation but are usually idiopathic. uWORLD: A 62 yo man comes o the office for follow-up of hypertension. He was diagnosed with HTN 10 years ago and has been treated with a number of different medications. However, the patient has had to discontinue several medications due to side effects such as dizziness, palpitations, and headaches. Currently he takes ramipril and chlothalidone and is tolerating them well. BP is 160/92 mmHg and was 158/89 mmHg at his most recent prior visit. ECG shows sinus bradycardia (55/min) with PR interval prolongation (280 sec). Which of the following medications would be most effective for lowering this patient's blood pressure without worsening his ECG abnormalities? - ☑☑Nifedipine > DO NOT GIVE Non-hydropyrmidine Ca2+ channel blockers (Verapamil, Diltilzaem) OR beta-blockers because they depress the AV node further worsening the bradycardia. > Calcium channel blockers inhibit the L-type channel on vascular smooth muscle and cardiac cells. Dihydropyridines (eg nifedipine, amlodipine) primary affect peripheral arteries and cause vasodilation. Nondihydropyridines (eg. verapamil, diltiazem) affect the myocardium and can cause bradycardia and slowed atrioventricular conduction. uWORLD: A 45 yo man comes to the ED because of severe chest pain, diaphoresis, and palpitations. The patient dies two hours after the onset of his symptoms. Autospy reveals 100% occlusion of the left anterior descending artery. At the time of the patient's death, light microscopy of the affected myocardium would most likely demonstrate which of the following? - ☑☑Normal myocardium Timeline > 0-4 hours - minimal change > 4-12 hrs- early coagulation necrosis, edema, hemorrhage, wavy fibers, > 12-24 hrs - coagulation necrosis and marginal contraction band necrosis > 1 to 5 days - coagulation necrosis and neutrophilic infiltrate > 5 to 10 days - macrophage phagocytosis of dead cells > 10 to 14 days - granulation tissue and neovascularization > 2 weeks to 2 months - collagen deposition/scar formation uWORLD: A 60 yo man comes to the ED with acute substernal chest pain, nausea, and diaphoresis. The patient has a history of liver cirrhosis, hypertension, and hyperlipidemia. He quit smoking 3 months ago but previously smoked a pack of cigarettes daily for 25 years. ECG shows ST elevations in leads II, III, and aVF. He is diagnosed with a MI and, after careful discussion of risks and benefits, repercussion therapy is not performed due to underlying cirrhosis and history of vatical bleeding. The patient is eventually discarded from the hospital with conservative management. Twelve day after his MI, he dies suddenly. Light microscopy would most likely show what changes to the myocardium of the inferior wall? - ☑☑Granulation tissue with neovascularization > Sudden cardiac death *12 days* after MI is most likely due to *ventrciular arrhythmias* originating from the infarcted myocardium. The microscopic diagnosis of MI depends on the presence of necrotic myocardium, with areas of acute inflammation and necrosis separated from viable myocardium. After the initial event, several characteristic microscopic changes occur in the infarcted zone in a specifyic temporal sequence with some overlap in different stages. > *During the second week* after MI, the damage tissue is replaced by *granulation tissue* and *neovascularization* is found in the infarct zone. uWORLD: A 72 yo man with long-standing dyspnea was seen int eh clinic after experiencing an episode of syncope. Physical examination showed weak and slowly rising arterial pulses. Cardiac auscultation showed a harsh mid systolic mummer best heard at the second right intercostal space with decreased intensity of the second heart sound. ECG and echocardiogram confirmed the diagnosis of severe aortic stenosis. Two months later, the patient comes to the ED with palpitations and increased SOB. His blood pressure is 90/60 mmHg and his heart rate is 130/min with an irregularly irregular rhythm. ECG shows new-onset arterial fibrillation without significant ST-segment or T-wave changes. Chest x-rays show bilateral pulmonary edema. Which of the following hemodynamic changes is most likely associated with this patient's current presentation? - ☑☑Sudden decrease in left ventricular preload > Patients with severe AS already have reduced cardiac output due to significant valvular obstruction, which can be exacerbated by the sudden *loss of normal atrial contraction* that contributes to ventricular filling. Atrial contraction is especially important for these patients as many have concentric left ventricular (LV) hypertrophy and therefore reduced LV compliance. As a result, they become dependent on atrial contraction to maintain adequate LV filling. > In patients with chronic aortic stenosis, and concentric left ventricular hypertrophy, atrial contraction contributes significantly to left ventricular filling. Loss of atrial contraction due to atrial fibrillation can reduce left ventricular preload and cardiac output sufficiently to cause systematic hypertension. Decreased forward filling of the left ventricle can also result in backup of blood in the left atrium and pulmonary veins, leading to acute pulmonary edema. uWORLD: An 82 yo man comes to the office due to progressive dyspnea and fatigue over the last ear, which now limits his daily activities. He also noticed bilateral swelling of his feet. The patient has HTN, which is controlled with amlodipine. His BP is 122/72 mmHg and pulse is 55/min. Physical examination reveals elevated jugular venous pressure with rapid 'y' descent and a prominent S4. Abdominal examination shows moderate ascites. The patient has 3+ bilateral lower extremity pitting edema. Echocardiogram reveals left atrial enlargement with marked left ventricular hypertrophy and normal left ventricular ejection fraction. Complete good count, basic metabolic panel, and serum, and urine protein electrophoresis are within normal limits. What is the most likely diagnosis of this patient? - ☑☑Senile amyloidosis > This patient's clinical presentations (eg. progressive exertion dyspnea, edema, ascites, elevated jugular venous pressure and rapid 'y' descent, prominent S4) and echocardiogram findings (eg. left atrial enlargement, left ventricular hypertrophy, normal ejection fraction) are consistent with *diastolic heart failure* due to restrictive cardiomyopathy. > *Restrictive cardiomyopathy* can be idiopathic or caused by infiltrative disease (eg, amyloidosis, sarcoidosis, hemochromatosis), radiation fibrosis, or endomycardial fibrosis. Although most cases are associated with normal ventricular wall thickness. Infiltrative conditions such as cardiac amylosisis may lead to significant *ventricular hypertrophy*. Infiltrative diseases can also cause conduction system abnormalities (eg, bradycardia) that may ultimately require pacemaker implantation* The fourth heart sound (S4) is a low frequency sound heard at the end of diastole just before S1. It is due to decreased left ventricular compliance and is often associated with _____________________ and ____________________. - ☑☑Restrictive cardiomyopathy; left ventricular hypertrophy uWORLD: A 54 yo Caucasian male comes to the ED with retrosternal chest pain of 30 min duration. The patient also complains of sweating and mild dyspnea. A single table of nitro is delivered sublingually, and the patient's pain decreases significantly. The patient has experienced several similar episodes of pain over the last 12 hours, all of which resolved spontaneously. Which of the following ultrastructural changes would most likely indicate irreversible myocardial cell injury in this patient? - ☑☑Mitochondrial vacuolization > Mitochondrial vacuolization is typically a sign of irreversible cell injury, signifying that the involved mitochondria are permanently unable to generate ATP. Reversible injury: > Myofibril relaxation > Disaggregation of polysomes denotes the dissociation of rRNA from mRNA in reversible ischemic/hypoxic injury. > Disaggregation of granular and fibrillar elements of the nucleus is associated with reversible cell injury > Triglyceride droplet accumulation is characteristic of reversible cell injury, especially in hepatocytes, and also in striated muscle cells and renal cells. > Glycogen loss is another early and reversible cellular response to injury uWORLD: A 45 yo man comes to the clinic due to recurrent palpitations accompanied by chest discomfort and SOB. A year ago, he was diagnosed with paroxysmal atrial fibrillation treated with rate control using a beta blocker. Past medical history is also significant for HTN and obesity. ECG shows left atrial enlargement, normal left ventricular ejection fraction, and no significant valvular disease. 24-hour Holter monitoring reveals bursts of atrial fibrillation associated with the patient's symptoms. He is initiated on dofetilide to maintain normal sinus rhythm. This medication exerts its main effect on which portion of the action potential curve? - ☑☑Phase 3 (last repolarization) > Class III antiarrhymic drugs amiodarone, stall, dofetilide) predominately block potassium channels and inhibit the outward potassium current during the phase, leading to prolongation of repolarization, action potentials duration, and the QT interval on ECG. > uWORLD: A 42 yo male is brought to the ED complaining of severe headaches and oliguria. His blood pressure is 240/150 mmHg and his heart rate is 90/min. On ophthalmologic exam, there is papilledema bilaterally. Which of the following is the most likely pathological process associated with his patient's condition? - ☑☑Onion-like concentric thickening of arteriolar walls > This patient presents in hypertensive crisis, a condition defined as a persistent diastolic pressure exceeding 130 mmHg that is often associated with acute vascular damage. Hyper plastic arteriolosclerosis, which can result from diastolic pressures >120-130 mmHg, presents as onion-like > Hyp