CVS pathology Flashcards
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.
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
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 treatment?
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
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
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. what is the treatment for this disease?
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
Systemic HTN is defined as pressure:
pressure ≥ 140/90 mm Hg
What is true of the etiology of primary HTN?
the etiology is unknown in 95% of cases
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
what is a common cause of secondary HTN?
renal artery stenosis
what is etiology of renal a. stenosis (renovascular HTN) in elderly males?
atherosclerosis
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.
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.
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].
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)
What are the two classifications of HTN?
Benign and malignant
what is benign HTN?
It’s a mild or moderate elevation in blood pressure.
most cases of HTN are benign
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
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.
