CVS pathology Flashcards by Lauren Lamb

A 69 yo woman presents with crushing substernal chest pain and nausea. Lab studies show elevated serum levels of cardiac proteins (CK-MB: 8.5 ng/mL; troponin-l: 3.2 ng/mL). a diagnosis of MI is confirmed by ECG. Despite treatment, the patient becomes hypotensive and resuscitation attemps are unsuccessful. A cross section of the patient’s Rt. coronary a. at autopsy is shown in the image. which of the following pathologic changes are evident in this autopsy specimen?

A. arteritis and atherosclerosis

B. atherosclerosis and thrombosis

C. microanurysm and canalization

D. thromboid and calcification

E. vasodilation and arteritis

B. atherosclerosis and thrombosis. the arrow is pointing to the thrombus that is occupying the lumen of the vessel.

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A 70 yo woman complains of throbbing unilateral headache and vision problems. She reports weight loss and mandibular pain while eating. the pt. also has a history (Hx) of recurrent bouts of fever accompanied by malaise and muscle aches. Physical examination reveals nodular enlargement of the temporal artery with pain on palpation. A biopsy is obtained (shown in the image) what is the appropriate diagnosis?

A. Giant cell arteritis

B. hypersensitivity angitis

C. kawasaki disease

D. polyarteritis nodosa

E. Wegner granulomatosis

A. Giant cell arteritis.

It presents as:

Headache (sup. Temporal a.)
Vision problems (ophthalmic a.)
Jaw claudication
Polymyalgia rheumatica
Elevated ESR
Normal CK
Inflammation but NO destruction
Segmented lesions

Negative biopsy doesn’t exclude disease- may just be section without disease

see it in Adults > 50

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Corticosteroids (ex. Prednisone)
Give tx (corticosteroids) ASAP to avoid blindness in pt

MOA: Decreases inflammation
Toxicity:

Cushing like symptoms

Moon face
Red/purple striae

Immunosuppression
Ulcers
Pancreatitis
Cataracts
Osteoporosis
Obesity
Diabetes
Changes in mood

Euphoria
Psychosis

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A 20 yo woman complains of double vision, fainting spells, tingling of the fingers of her left hand, and numbness of the fingers of her right hand. physical examination reveals absence of pulse in her right arm. laboratory tests show elevated erythrocyte sedimentation rate (ESR) and thrombocytosis. an arteriogram (shown) demonstrates narrowing and occlusion of branching arteries, including the rt. subclavian a. the pt subsequently develops heart failure and dies of massive pulmonary edema. at autopsy, the aorta has a thickened wall and shows vasculitis and fragmentation of elastic fibers. which of the following is the most likely dx?

A. buerger disease

B. Churg Strauss disease

C. Kawasaki disease

D. Giant cell granulomatous arteritis

E. Takayasu arteritis

E. Takayasu arteritis.

it affects young woman
AKA pulseless disease
Adults <50 yrs old
it’s granulomatous large vessel vasculitis involving aortic arch vessels (Brachiocephalic trunk, Left common carotid a., and Left subclavian a.)

Absent upper extremity pulse (pulseless disease)
Discrepancy in BP betw. The arms (> 10 mm Hg)
Visual defects
Night sweats
Arthritis
Myalgias
Skin nodules
Stroke

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Tx: corticosteroids

MOA: Decreases inflammation
Toxicity:

Cushing like symptoms

Moon face
Red/purple striae

Immunosuppression
Ulcers
Pancreatitis
Cataracts
Osteoporosis
Obesity
Diabetes
Changes in mood

Euphoria

psychosis

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Systemic HTN is defined as pressure:

pressure ≥ 140/90 mm Hg

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What is true of the etiology of primary HTN?

the etiology is unknown in 95% of cases

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What are the risk factors for primary HTN?

Age

Race (AA are at incr. risk, asians are at decr. risk)

Obesity

stress

lack of physical activity

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what is a common cause of secondary HTN?

renal artery stenosis

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what is etiology of renal a. stenosis (renovascular HTN) in elderly males?

atherosclerosis

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what is the etiology of renal a. stenosis (renovascular HTN) in young women?

Fibromuscular dysplasia. Fibromuscular dysplasia is a developmental defect of the blood vessel wall, resulting in irregular thickening of large and medium sized arteries, especially the renal a.

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what is fibromuscular dysplasia?

it’s a developmental defect of the blood vessel wall, resulting in irregular thickening of large and medium sized arteries, especially the renal a. it mainly affects young females.

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what is the pathophysiology of renovascular HTN?

stenosis decreases blood flow to the glomerulus
juxtaglomerular apparatus (JGA) responds by secreting renin, which converts angiotensinogen to angiotensin I
Angiotensin I is converted to angiotensin II (ATII) by angiotensin converting enzyme (ACE).
ATII raises blood pressure (BP)
incr. in BP leads to HTN w/ incr. plasma renin and unilateral atrophy due to decr. blood flow of the affected kidney [this is not seen in primary HTN].

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What are the ways that angiotensin II (ATII) incr. BP?

contracting arteriolar smooth muscle, incr. TPR
promoting adrenal release of aldosterone, which incr. resorption of sodium in the distal convoluted tubule (expanding plasma volume)

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What are the two classifications of HTN?

Benign and malignant

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what is benign HTN?

It’s a mild or moderate elevation in blood pressure.

most cases of HTN are benign

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what are characteristics of benign HTN?

It’s clinically silent

vessel changes occur gradually in response to a persistent stable elevated blood pressure (BP).

see tissue ischemia and brain vessel fragility

vessels and organs are damaged slowly over time

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what is malignant HTN?

it’s severe elevation in blood pressure > 200/120 mm Hg

it comprises <5% of HTN cases

what is the etiology of malignant HTN?

it may arise from preexisting benign HTN

it may arise de novo

it can be a complication of essential HTN

it can be a complication of secondary HTN

what are characteristics of malignant HTN?

it has an accelerated clinical course

see sudden, marked incr. in diastolic BP

it presents with acute, destructive changes and proliferative responses in the small vessel walls (intimal only)

these acute destructive changes result in cessation of blood flow to the small vessels which results in multiple foci of tissue necrosis

see acute organ damage due to ischemic coagulative necrosis

What is most common cause of endocarditis?

Streptococcus viridans (S. viridans) infection

what is most common cause of endocarditis in IV drug abusers?

S. aureus infection

Presentation: chest pain that arises w/ exertion or emotional stress. the chest pain lasts <20 minutes and radiates to the left arm or jaw, diaphoresis, and shortness of breath. see ST depression on ECG (shown). ST depression is due to subendocardial infarction. it represents reversible injury to myocytes, NO necrosis.

Etiology: atherosclerosis of coronary arteries w/ >70% stenosis. the stenosis results in decreased blood flow which results in inability to meet the metabolic demands of the myocardium during exertion.

Tx: rest or nitroglycerin

what is the condition?

Stable angina

Stable angina presents as retrosternal chest pain that arises w/ exertion or emotional stress. the chest pain lasts <20 minutes and radiates to the left arm or jaw, diaphoresis, and shortness of breath. see ST depression on ECG (shown). ST depression is due to subendocardial infarction. it represents reversible injury to myocytes, NO necrosis.

stable angina is due to atherosclerosis of coronary arteries w/ >70% stenosis. the stenosis results in decreased blood flow which results in inability to meet the metabolic demands of the myocardium during exertion.

the treatment for stable angina is rest or nitroglycerin

Presentation: it’s chest pain that occurs at rest. it represents reversible injury to myocytes, no necrosis. ECG shows ST depression (shown) due to subendocardial infarction (ischemia). There is high risk of progression to MI.

Etiology: rupture of an atherosclerotic plaque w/ thrombosis and incomplete (>90%) occlusion of a coronary artery. if chest pain occurs at rest then the coronary arteries are >90% stenotic.

Tx: nitroglycerin, aspirin, ß-blockers, statins, heparin, or glycoprotein IIb/IIIa inhibitors.

what is the disorder:

unstable angina

unstable angina is chest pain that occurs at rest. it represents reversible injury to myocytes, no necrosis. ECG shows ST depression (shown) due to subendocardial infarction (ischemia). There is high risk of progression to MI.

unstable angina is due to rupture of an atherosclerotic plaque w/ thrombosis and incomplete (>90%) occlusion of a coronary artery. if chest pain occurs at rest then the coronary arteries are >90% stenotic.

the treatment for unstable angina is nitroglycerin, aspirin, ß-blockers, statins, heparin, or glycoprotein IIb/IIIa inhibitors.

it's episodic chest pain unrelated to exertion/ at rest it's due to coronary a. vasospasm it represents reversible injury to myocytes (no necrosis) EKG shows ST elevation (pictured) due to transmural ischemia (MI) tx: Ca²⁺channel blockers (verapamil, diltiazem, nifedipine, amlodipine) and nitrates (nitroglycerin, isosorbide dinitrate) what is the disorder

Prinzmetal (AKA variant) angina Prinzmetal angina is episodic chest pain unrelated to exertion/ at rest it's due to coronary a. vasospasm it represents reversible injury to myocytes (no necrosis) EKG shows ST elevation (pictured) due to transmural ischemia (MI) tx: Ca2+ channel blockers (verapamil, diltiazem, nifedipine, amlodipine) and nitrates (nitroglycerin, isosorbide dinitrate)

Which congenital heart conditions present with early cyanosis (neonatal cyanosis) due to Right to Left shunt (pictured)?

the 5 T's Truncus arteriosis Tricuspid atresia Tetralogy of fallot Transposition of the great vessels Total anomalous pulmonary these cardiac malformations result in shunting of deoxygenated blood from the pulmonary circulation (rt heart) into oxygenated blood in the systemic circulation (left heart). the addition of deoxygenated blood to oxygenated blood decreases the partial pressure of O₂ in the systemic blood and causes early cyanosis.

what conditions cause late cyanosis due to left to right shunts (pictured)?

VAPid diseases VSD ASD PDA

what disorder is associated w/ truncus arteriosus and tetralogy of fallot?

22q11 deletions

what disorder is associated w/ VSD and ASD?

Down's syndrome (trisomy 21)

A karyotype of a 17 year old girl is pictured. what cardiac defect may she have?

coarctation of the aorta

A 32 year old prima 1 gravida 0 is 7 months along. she has DM2. what cardiac defect may her child have?

transposition of the greater vessels

It's characterized by a single large vessel arising from both ventricles. etiology: the truncus failed to divide it presents w/ early cyanosis deoxygenated blood from the rt ventricle mixes w/ oxygenated blood from the left ventricle before pulmonary and aortic circulations separate. what is the disorder?

truncus arteriosus

it's characterized by pulmonary artery arising from the left ventricle and aorta arising from the right ventricle creating 2 independent circuits. it's associated w/ maternal diabetes it presents w/ early cyanosis b/c the pulmonary and systemic circuits don't mix, they are 2 independent circuits. the heart looks like an egg (pictured) and the aorta is ant. to the pulmonary trunk/artery. this condition is incompatible w/ life unless there is a PDA which allows mixing of blood. PGE can be given at birth to maintain a PDA until a definitive surgical repair is performed. this condition results in RVH and atrophy of the left ventricle. what is the disorder?

Transposition of the great vessels transposition of the great vessels is associated w/ maternal diabetes transposition of the great vessels presents w/ early cyanosis b/c the pulmonary and systemic circuits don't mix, they are 2 independent circuits. the heart looks like an egg and the aorta is ant. to the pulmonary trunk. this condition is incompatible w/ life unless there is a PDA or VSD which allows mixing of blood (pictured). PGE can be given at birth to maintain a PDA until a definitive surgical repair is performed. this condition results in RVH and atrophy of the left ventricle.

it's characterized by stenosis of the rt ventricular outflow tract, RVH, VSD, and an aorta that overrides the VSD there is a rt to left shunt w/ early cyanosis in this condition the degree of stenosis determines the extent of shunting and cyanosis pts learn to squat in response to a cyanotic spell. squatting incr. arterial resistance decreasing shunting and allowing more blood to reach the lungs. will see boot shaped heart on X-ray (pictured) and hyaline aorta. it is associated with 22Q11 deletions (DiGeorge syndrome) what is the disorder?

Tetralogy of fallot tetralogy of fallot is characterized by stenosis of the rt ventricular outflow tract, RVH, VSD, and an aorta that overrides the VSD there is a rt to left shunt w/ early cyanosis in tetralogy of fallot the degree of stenosis determines the extent of shunting and cyanosis tetralogy of fallot pts learn to squat in response to a cyanotic spell. squatting incr. arterial resistance decreasing shunting and allowing more blood to reach the lungs. will see boot shaped heart on X-ray and hyaline aorta. it is associated with 22Q11 deletions (DiGeorge syndrome)

it occurs when the tricuspid valve orifice fails to develop, so there is a membrane between the rt atrium and rt ventricle. the rt ventricle is hypoplastic. it's often associated w/ ASD resulting in a right to left shunt. it presents w/ early cyanosis what is the disorder?

tricuspid atresia tricuspid atresia occurs when the tricuspid valve orifice fails to develop, so there is a membrane between the rt atrium and rt ventricle. the rt ventricle is hypoplastic. tricuspid atresia is often associated w/ ASD resulting in a right to left shunt. tricuspid atresia presents w/ early cyanosis

In this condtion, oxygen-rich blood returns from the lungs to the right atrium or to a vein flowing into the right atrium, instead of the left side of heart. In other words, blood simply circles to and from the lungs and never gets out to the body. For the infant to live, an atrial septal defect (ASD), PDA, or patent foramen ovale (passage between the left and right atria) must exist to allow oxygenated blood to flow to the left side of the heart and the rest of the body. it presents with early cyanosis. what is the condition?

Total anomalous pulmonary venous return (TAPVR) In TAPVR oxygen-rich blood returns from the lungs to the right atrium or to a vein flowing into the right atrium, instead of the left side of heart. In other words, blood simply circles to and from the lungs and never gets out to the body. For the infant to live, an atrial septal defect (ASD), PDA, or patent foramen ovale (passage between the left and right atria) must exist to allow oxygenated blood to flow to the left side of the heart and the rest of the body. TAPVR presents with early cyanosis.

it's a defect in the septum that divides the right and left ventricles it's the most common congenital heart defect it's associated w/ fetal alcohol syndrome (FAS) and trisomy 21 (Down's) it results in left to right shunt. the size of the defect determines the extent of shunting and age at presentation. small defects are often asymptomatic large defects can lead to eisenmenger syndrome, reversal of shunt (L to R goes to R to L), late cyanosis, RVH, polycythemia, and clubbing tx: surgical closure for larger defects. small defects may close spontaneously there are 2 types: membranous and muscular what is the disorder?

ventricular septal defect (VSD) VSD is a defect in the septum that divides the right and left ventricles VSD is the most common congenital heart defect VSD is associated w/ fetal alcohol syndrome (FAS) and trisomy 21 (Down's) VSD results in left to right shunt. the size of the defect determines the extent of shunting and age at presentation. small defects are often asymptomatic large defects can lead to eisenmenger syndrome, reversal of shunt (L to R goes to R to L), late cyanosis, RVH, polycythemia, and clubbing tx: surgical closure for larger defects. small defects may close spontaneously there are 2 types: membranous and muscular

in this type of VSD the hole is higher up near the valves

membranous VSD

in this type of VSD the hole is below the valves near the trabeculated/muscular area

muscular VSD

It's a defect in the septum that divides the right and left atria it results in L to R shunt and split S2 on auscultation b/c the incr. in blood in right heart delays closure of pulmonary valve a complication of this disorder is paradoxical emboli, a kind of stroke or other form of arterial thrombosis caused by embolism of a thrombus (blood clot) of venous origin through a lateral opening in the heart, such as a patent foramen ovale. it has 2 types, ostium secundum (most common in general population) and ostium primum (most common in trisomy 21 pts) what is the disorder?

atrial septal defect (ASD) ASD is a defect in the septum that divides the right and left atria ASD results in L to R shunt and split S2 on auscultation b/c the incr. in blood in right heart delays closure of pulmonary valve a complication of ASD is paradoxical emboli, a kind of stroke or other form of arterial thrombosis caused by embolism of a thrombus (blood clot) of venous origin through a lateral opening in the heart, such as a patent foramen ovale. it has 2 types, ostium secundum (most common in general population) and ostium primum (most common in trisomy 21 pts)

this type of ASD is the most common type in the general population 90% of ASD cases are this type

Ostium secundum

A 2 yeard old child w/ Down's (trisomy 21) has an ASD what type of ASD is he most likely to have?

ostium primum

it's a failure of the ductus arteriosus to close it's associated w/ congenital rubella it results in L to R shunt betw. the aorta and the pulmonary artery during development, the ductus arteriosus normally shunts blood from the pulmonary artery to the aorta, bypassing the lungs it's asymptomatic at birth with holosystolic "machine-like" murmur. it may lead to eisenmenger syndrome, resulting in lower extremity (LE) cyanosis Tx: indomethicin which decreases PGE, resulting in closure of the ductus arteriosus what is the disorder?

patent ductus arteriosus (PDA) PDA is a failure of the ductus arteriosus to close PDA is associated w/ congenital rubella PDA results in L to R shunt betw. the aorta and the pulmonary artery during development, the ductus arteriosus normally shunts blood from the pulmonary artery to the aorta, bypassing the lungs PDA is asymptomatic at birth with holosystolic "machine-like" murmur. a PDA may lead to eisenmenger syndrome, resulting in lower extremity (LE) cyanosis Tx: indomethicin which decreases PGE, resulting in closure of the PDA

it's the narrowing of the aorta. it's classically divided into infantile and adult forms. infantile form is associated w/ a PDA. it lies distal to the aortic arch, but proximal to the PDA. the infantile form presents as lower extremity cyanosis in infants, often at birth the infantile form is associated w/ Turner syndrome the adult form is not associated w/ a PDA. it lies distal to the aortic arch. the adult form presents as HTN in the upper extremities and hypotension w/ a weak pulses in the lower extremities (LE); classically discovered in adulthood. collateral circulation develops across the intercostal arteries; engorged arteries cause notching of ribs on x-ray (pictured). it's associated w/ bicuspid aortic valve. what is the disorder?

coarctation of the aorta coarctation of the aorta is the narrowing of the aorta. it's classically divided into infantile and adult forms. infantile form is associated w/ a PDA. it lies distal to the aortic arch, but proximal to the PDA. the infantile form presents as lower extremity cyanosis in infants, often at birth the infantile form is associated w/ Turner syndrome the adult form is not associated w/ a PDA. it lies distal to the aortic arch. the adult form presents as HTN in the upper extremities and hypotension w/ a weak pulses in the lower extremities (LE); classically discovered in adulthood. collateral circulation develops across the intercostal arteries; engorged arteries cause notching of ribs on x-ray (pictured). it's associated w/ bicuspid aortic valve.