Uworld Pathophysio Cardio Flashcards

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1
Q

—– shock can present with either hyper- or hypothermia. The initial disturbance is peripheral vasodilation leading to decreased systemic vascular resistance, decreased central venous pressure, and decreased pulmonary capillary wedge pressure. A compensatory increase in sympathetic drive causes an increase in cardiac output; the resulting high flow rates lead to incomplete oxygen extraction in the tissues, resulting in high mixed venous oxygen saturation.

A

Septic

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2
Q

This presentation of hypotension, tachycardia, jugular venous distension with clear lungs, and pulsus paradoxus (manifesting as loss of palpable pulse during inspiration) is consistent with —–. This is most likely due to the patient’s recent viral illness causing viral pericarditis with significant pericardial fluid accumulation

A

cardiac tamponade

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3
Q

Severe —- typically presents with right-sided heart failure. Patients can have distended jugular veins, pulsatile and tender hepatomegaly, abdominal distension with ascites, and lower extremity edema. The lungs are clear on auscultation in the absence of concomitant left-sided heart disease. Cardiac examination typically reveals a holosystolic murmur best heard at the left lower sternal border; the murmur intensifies with maneuvers that increase right ventricular preload (eg, deep inspiration, leg raise).

A

tricuspid regurge

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4
Q

Permanent pacemaker placement can cause —- because the right ventricular lead passes through the tricuspid valve orifice and can disrupt valve closure.

A

TR

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5
Q

Calcification and thickening of the pericardium are common features of constrictive —- on CT. Clinical findings include slowly progressive dyspnea, peripheral edema, and ascites.

A

pericarditis

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6
Q

The ventricular myocardium secretes —– in response to the ventricular stretch and strain that typically occurs with volume overload. BNP, along with atrial natriuretic peptide secreted by the atrial myocardium, stimulates vasodilation and salt and water excretion to help relieve volume overload.

A

brain natriuretic peptide (BNP)

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7
Q

Eccentric ventricular hypertrophy results in a dilated cavity with relatively thin ventricular walls due to the addition of myocardial contractile fibers in series in response to chronic volume overload. Chronic aortic regurgitation can result from —– dilation and is a common cause of eccentric hypertrophy.

A

aortic root

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8
Q

Renal infarction presents with flank pain, hematuria, elevated lactate dehydrogenase, and a wedge-shaped kidney lesion on CT scan. The most common cause of renal infarction is systemic —–, often due to thrombus formation during atrial fibrillation. The brain and kidneys are more likely than other organs to suffer embolic infarctions because they are perfused at a higher rate.

A

thromboembolism

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9
Q

This young patient’s repeated episodes of palpitations are suggestive of paroxysmal supraventricular tachycardia, and the physician suspects Wolff-Parkinson-White (WPW) syndrome. WPW syndrome is caused by an accessory conduction pathway (bundle of Kent) that allows electrical conduction impulses to bypass the —- node and cause preexcitation of the ventricles. This preexcitation leads to characteristic findings on baseline ECG, including a shortened PR interval (often <0.12 seconds), early upslope of the QRS complex (delta wave), and a widened QRS complex.

A

atrioventricular

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10
Q

Early disseminated Lyme disease can have cardiac involvement (Lyme carditis) that most commonly manifests with varying degrees of —- block. Patients may be asymptomatic, but those with complete AV conduction block are likely to have dyspnea, lightheadedness, or syncope

A

atrioventricular (AV) conduction

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11
Q

patient with recurrent episodes of syncope while shaving most likely has carotid sinus hypersensitivity (CSH). When carotid sinus baroreceptors detect increased blood pressure, the brainstem responds by increasing parasympathetic tone (slows the heart rate) and reducing sympathetic tone (induces vasodilation). In some individuals, especially elderly men, the carotid sinus baroreceptors become overly sensitive to tactile stimulation, triggering an exaggerated vasovagal response with marked peripheral vasodilation (ie, decreased ——).

A

systemic vascular resistance

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12
Q

decreased pulmonary capillary wedge pressure (PCWP) and increased right atrial pressure (RAP), indicate impaired blood flow from the —– to the left side of the heart (right-sided heart failure). Common causes of right-sided heart failure include obstruction of pulmonary circulation (eg, pulmonary arterial hypertension, pulmonary embolism) and right ventricular infarction (likely in this patient due to multiple cardiovascular risk factors)

A

right ventricle

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13
Q

—– disease) is a segmental, inflammatory vasculitis that affects the small- and medium-sized arteries and veins of the distal extremities with inflammatory, intraluminal thrombi and sparing of the vessel wall. It is usually seen in young, heavy smokers, and can present with digital ischemia and ulceration, extremity claudication, Raynaud phenomenon, and superficial thrombophlebitis.

A

Thromboangiitis obliterans (Buerger

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14
Q

This patient has chronic constitutional and pulmonary symptoms associated with patchy lung infiltrates/cavitation and laboratory findings of glomerulonephritis (hematuria, increased creatinine). These findings are suggestive of granulomatosis with polyangiitis (GPA), a small vessel vasculitis associated with antineutrophilic cytoplasmic antibodies (ANCA). Patients with GPA generally present with weeks or months of constitutional symptoms (eg, arthralgias, fatigue, low-grade fever, weight loss) and manifestations in the following areas:

Upper airway: otitis media, nasal crusting/ulcers, rhinorrhea

Lower airway: hoarseness, cough, stridor, hemoptysis, pulmonary infiltrates

Kidney: rapidly progressive glomerulonephritis

Laboratory evaluation frequently shows anemia of chronic disease due to elevated levels of inflammatory cytokines and renal insufficiency due to glomerulonephritis (eg, microscopic hematuria, red cell casts, negative nitrate/bacteriuria).

histopathology will show a necrotizing arteritis with granulomatous inflammation (eg, epithelioid histiocytes, multinucleated giant cells) and a mixture of surrounding inflammatory cells. Veins and capillaries are also frequently affected.

A
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15
Q

Signs of —- include jugular venous distension, muffled heart sounds, and hypotension (Beck triad), as well as reduced point of maximal impulse, cool extremities, and clear lungs.

A

tamponade

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16
Q

A ruptured posteromedial papillary muscle causes acute mitral —–, which can abruptly lead to cardiogenic shock. Patients are expected to have shortness of breath and lung crackles due to acute pulmonary edema.

A

regurgitation

17
Q

Fatty streaks are the earliest lesions of atherosclerosis and can be seen as early as the second decade of life. They appear as a collection of lipid-laden —– (foam cells) in the intima that can eventually progress to atherosclerotic plaques.

A

macrophages

18
Q

Concentric hypertrophy is characterized by uniform thickening of the ventricular wall and narrowing of the ventricular cavity due to increased —-load (eg, chronic hypertension, aortic stenosis).

Eccentric hypertrophy is characterized by reduced ventricular wall thickness with an associated increase in chamber size due to volume overload.

A

after

19
Q

—— is associated with a decrease in LV chamber size, predominantly through shortening of the apex-to-base dimension accompanied by a leftward bowing of the lower interventricular (sigmoid) septum.

A

Aging

20
Q

—— 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 equal 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 significant RVOT obstruction shunt more deoxygenated blood across the VSD to the aorta and are more cyanotic.

A

Tetralogy of Fallot (TOF)

21
Q

The most common histologic findings in —–related aortic root disease include fragmentation and loss of the elastic lamellae with fibrosis and cystic medial degeneration (replacement of collagen, elastin, and smooth muscle by a basophilic mucoid extracellular matrix with irregular fiber cross-linkages and cystic collections of mucopolysaccharide). Cystic medial degeneration also occurs with normal aging, but is accelerated in —- syndrome.

A

Marfan

22
Q
A
23
Q

The mitral valve is the valve most frequently affected by —. Mitral valve prolapse (MVP) is the most common underlying valvular disease predisposing to the development of — in developed countries, particularly when it is associated with coexistent mitral regurgitation. Microscopic deposits of platelets and fibrin occur spontaneously in individuals with valvular disease secondary to endocardial injury from turbulent blood flow. These deposits then become colonized by microorganisms (eg, viridans streptococci) during episodes of bacteremia (eg, following dental extraction).

A

IE

24
Q

Peripheral edema results from the accumulation of fluid in the interstitial spaces. Factors that promote edema include elevated capillary hydrostatic pressure, decreased plasma oncotic pressure, sodium and water retention, and impaired lymphatic drainage.

In chronic heart failure, increased —- initially offsets factors favoring edema, whereas acute changes (eg, venous thrombosis, heart failure decompensation) are more likely to produce edema.

A

lymphatic drainage

25
Q

Hypertrophic cardiomyopathy is a common cause of sudden cardiac death (SCD) in young adults. Histologic features include cardiomyocyte hypertrophy and myofiber disarray with increased interstitial fibrosis. The structural disarray creates a substrate for —– that can lead to SCD.

A

ventricular arrhythmia (eg, ventricular tachycardia, ventricular fibrillation) that can lead to SCD.

26
Q

Myocardial hibernation refers to a state of chronic myocardial ischemia in which both myocardial metabolism and function are reduced to match a concomitant reduction in coronary blood flow (due to moderate/severe flow-limiting stenosis). This new equilibrium prevents myocardial necrosis. Chronically hibernating myocardium demonstrates decreased expression and disorganization of contractile and cytoskeletal proteins, altered adrenergic control, and reduced calcium responsiveness. These changes lead to decreased contractility and left ventricular (LV) — dysfunction. However, coronary revascularization and subsequent restoration of blood flow to hibernating myocardium improves contractility and LV function

A

systolic

27
Q

Hypertension is the single most important risk factor for the development of intimal tears leading to —–. Hypertension, smoking, diabetes mellitus, and hypercholesterolemia are all major risk factors for atherosclerosis, which predisposes more to aortic aneurysm formation.

A

aortic dissection

28
Q

Atrial septal defects cause wide, fixed splitting of the second heart sound due to right-sided volume overload from left-to-right shunting. Uncorrected defects can lead to irreversible medial hypertrophy of the pulmonary arteries with pulmonary hypertension and reversal to right-to-left shunting (ie, —– syndrome).

A

Eisenmenger

29
Q

The major defects in tetralogy of Fallot are right ventricular outflow tract (RVOT) obstruction and a ventricular septal defect (VSD). In many patients, activities (eg, feeding, crying) can precipitate cyanotic episodes (tet episodes) by causing a dynamic increase in RVOT obstruction. During these episodes right ventricular pressure is increased and pulmonary arterial and left atrial pressures are ——– as blood is shunted away from the pulmonary circulation (ie, right-to-left shunting through the VSD).

A

decreased

30
Q

In unilateral renal artery stenosis, the narrowed renal artery causes hypoperfusion of the affected kidney with subsequent ischemic damage (eg, tubular atrophy, interstitial ischemia, glomerular crowding). In contrast, the contralateral kidney is exposed to high blood pressure and typically shows changes of hypertensive nephrosclerosis (eg, arteriolar wall thickening due to hyaline or hyperplastic arteriolosclerosis).

A

boop

31
Q
A