CV- UWORLD Flashcards
101- Q 18. Varicose vein
- key words for defining it?
- major complication
- TORTIOUS, DILATED vein
- skin ulceration due to poor blood circulation
- It is possible that it can lead to stasis and SUPERFICIAl thrombosis. Systemic thromboembolic event (ex: PE) is not common.
101- Q 18. What is pathophysiology of intermittent claudication?
peripheral ARTERY thromboembolic event
*usually do NOT involved veins
101- Q 24. Explain what happens to peripheral resistance of arteries.
Arterial resistance increases due to compensatory action by RAAS
HF -> decreased CO -> decreased renal perfusion
-> more renin -> increased vasoconstriction and sodium retention -> exacerbation of CHF
- think CHF as DOWNWARD SPIRALING process: it gets exacerbated over time
101- Q 24. What happens to lung compliance in CHF?
CHF -> pulmonary edema -> alveolar gets sticky -> decreased lung compliance
101- Q 33. How previous MI affect possibility for rupture during new MI?
Previous MI forms fibrotic scar tissue, making it LESS LIKELY to rupture during new MI
101- Q 34. Describe histologic finding in cardiac myxoma
scattered cells within mucopolysaccharide stroma
- buzzword: MUCOPOLYSACCHARIDE STROMA
101- Q 36. Which condition is most commonly associated with nonbacterial thrombotic endocarditis?
advanced malignancy
102- Q 4. Pathophysiology of development of pulmonary HTN due to pulmonary congestion in left sided HF
pulmonary congestion
- > damage to endothelium
1. decreased NO/ increased ENDOTHELIN due to endothelial dysfunction -> vasoconstriction
- over time, pulmonary endothelium remodeling
- > intimal thickening
-> pulmonary HTN
102- Q 7. common cardinal vein gives rise to what structure?
SVC
102- Q 15. pathogenesis of Janeway lesions in bacterial endocarditis
septic emboli
: emboli infected with bacteria on valve
-> dislodged from valve and deposit in peripheral skin region -> Janeway lesion
- NOT immune complex mediated damage
102- Q 18. Anatomy: penetration at each region leads to damage to what structure?
- left sternal border 2nd intercostal
- left sternal border 4th intercostal
- 5th intercostal along midclavicular line
- pulmonary trunk
- right ventricle (most anterior)
- I picked pulmonary trunk, but this will be noted at 2nd intercostal. It’s pretty high up
- left lung
102- Q 26. Why non-dihydropine CCB (verapamil) doesn’t work on skeletal muscle?
skeletal muscle cells do have L-type Ca2+ channel (target of verapamil). It also has dihydropine Ca2+ channel that is mechanically linked to RyR receptor, which release Ca2+ from SR.
skeletal muscle contraction is NOT MOSTLY DEPENDENT in extracellular Ca2+, rather it is intracellular Ca2+ released from SR.
Thus. blocking L-type Ca2+ is not enough to prevent skeletal muscle contraction
103- Q 11. Nitroprusside
- MOA
- effect on preload? afterload?
- side effect
- short acting balanced dilation of BOTH artery and vein via direct release of NO
- decrease BOTH preload and afterload
- major side effect is cyanide toxicity (it releases cyanide)
103- Q 13. Eccentric hypertrophy vs. concentric hypertrophy: compare etiologies
Eccentric: volume driven
- AR, MR
- dilated cardiomyopathy
- MI (MI -> not pumping blood well, residual blood remaining -> eccentric dilation)
Concentric: pressure driven (thick muscle layer)
- aortic stenosis
- chronic HTN
103- Q 16. Three side effects of hydralazine
- hypotension (headache)
- fluid retention
: decreased BP -> RAAS - SLE like symptom (anti-histone antibody)
- reflex tarchycardia
103- Q 16. Does reflex tachycardia by hydralazine cause transient hypertension?
NO. Although it causes reflex tachy, vasodilation outweighs reflex tachy effect.
Sudden withdrawal of hydralazine may cause transient hypertension tho
103- Q 26. Describe which TWO structures are involved in outflow obstruction in HCM
- thickened septum
- mitral valve leaflet
Thickened septum + ANTERIOR motion of MITRAL VALVE LEAFLET together obstructs outflow
103- Q 28. Which enzyme within atherosclerotic plaque is responsible for MI?
metalloproteinase
It is RUPTURE of plaque that leads to COMPLETE OCCLUSION, which leads to MI
103-Q 34. What is physical exam findings of dry beriberi by thiamine deficiency?
high output cardiac failure
: collapsing carotid pulse, displaced apical impulse
103- Q 39. Mitral valve regurgitation
- preload
- afterload
- left ventricular ejection fraction
- preload: increased, blood flew back up to atrium will fill more blood during next round of diastole
- afterload: REDUCED
- this is little tricky to understand, but decreased outflow (due to loss of some blood flowing back to atrium), there is less resistance in outflow
- EF: increased. with more preload/ less afterload, more EF
104- Q 9. Which three drugs may cause coronary artery steal syndrome? why?
adenosine, dipyradamole, regadenoson
these drugs are coronary artery selective vasodilators. Dilation of other vessels (pericardial or systemic) will shunt blood away from coronary artery, which will not cause coronary artery syndrome
104- Q 12. Which tissues extract oxygen most from artery?
myocardium. They work fucking harder than other organs or tissues.
Thus, coronary sinus has the lowest oxygen content compared to any veins
Compare how splitting and S4 sound differently
I wrote it down in FA p.271
104- Q 28. How exactly does vegetation happen in bacterial endocarditis?
STERILE vegetation forms first as FIBRIN deposits on PREVIOUSLY DAMAGED VALVE (for s.aureus, it can directly happen on new valve)
- > bacteria sit on FIBRIN DEPOSIT
- > septic emboli-> which can be further dislodged into peripheral skins -> Janeway lesions
104- Q34. What is the most common cause of claudication?
atherosclerosis
105- Q 32. Milrinone (this drug is not in 2016 FA, but in 2017 FA)
- MOA
- indication
- side effects (2)
- PDE-3 inhibitor (like theophyline)
- > increase cAMP
1. increase intracellular Ca2+ - > increase ionotropy/ chronotropy (in cardiomyocyte)
- inhibit MLCK -> vasodilation (vascular smooth muscle)
- acute decompensated HF
- side effects: hypotension, arrythmia
105- Q34. What is risk in catheterization of femoral vein above inguinal ligament (compared to below inguinal ligament)
above inguinal ligament catheterization increases risk for retroperitoneal hemorrhage
106- Q 7. What is paradoxical embolism? what heart condition is associated with it?
History of DVT, and stroke after it without having pulmonary symptoms (like PE)
ASD (widened S2 splitting on auscultation)
106- Q 25. What is the most common cause of mitral stenosis?
rheumatic fever
ACUTE rheumatic fever starts with mitral REGURGITATION
At late stage (CHRONIC rheumatic fever), fibrous thickening and fusion of valve leaflets lead to mitral STENOSIS
- bacterial endocarditis does NOT cause mitral stenosis, rather it is most common cause of MVP
106- Q 38. What is the most common underlying valvular pathology for development of subacute bacterial endocarditis
MVP is the most common underlying valvular pathology
- subacute bacterial endocarditis is developed from PREVIOUSLY DAMAGED valve.
- rheumatic fever also predisposes the subacute bacterial endocarditis, but not common due to recognition and well established treatment for group A strep
107- Q 1. Apart from crescendo-decrescendo cystolic ejection murmur, what is additional feature of aortic stenosis murmur?
- Loudest at base of heart (top part, bottom is apex)
- murmur radiates to carotid (neck)
107- Q 7. Exercise and Heart work. What should I think?
early exercise: both SV and HR increase
late exercise: only HR increase
*** It is HR that limits cardiac output!! Duration of DIASTOLE is the majority of HR. Thus it is DIASTOLIC TIME that limits cardiac output.
107- Q 8. which TWO ion channels are responsible for decreased intracellular Ca2+ during muscle relaxation phase? Location of each channel?
- NCX (Na+/Ca2+ exchanger) in T tubule
- SERCA (Ca2+-ATPase) in SR
107- Q 12. Niacin causes flushing by what molecule?
prostaglandin
107- Q 16. What forms fibrous caps in artherosclerosis?
Extracellular matrix proteins (collagen, elastin) synthesized by VASCULAR SMOOTH MUSCLE
107- Q 28. Fenoldopam
- MOA
- indication
- side effects
- dopamine D1 agonist
- > increase renal vasodilation -> increase natriuresis
- can also dilate other vessels (coronary, peripheral, splanchnic)
- fenolDOPAM= DOPAMine
- indicated for hypertensive crisis
- hypotension, reflex tachy
107- Q 32. Stroke history, renal embolism, clear lungs. What heart condition should I think?
atrial fibrilation
-> stasis -> thrombosis -> SYSTEMIC EMBOLISM
vs. DVT: PULMONARY EMBOLISM
107- Q 34. Describe location of AV node
Interatrial septum near opening of coronary sinus
107- Q 40. Where is coronary sinus located?
lying on atrioventricular grove on posterior of heart
107- Q 40. where do three leads of pace maker goes?
RA, RV, LV (via coronary sinus)
109- Q5. What property of atherosclerotic plaque explains absence of myocardial necrosis?
slow growth
- slow growth of atherosclerotic plaque allows time to develop collateral arteries
109 -Q9. Listening heart murmur at the end of expiration would result in what? by what mechanism?
It will intensify (accentuate) sound
- end of expiration results in decreasing lung volume and bridging the heart closer to chest wall
108- Q 3. Two cardiac conditions in Marfan syndrome
- MVP
- dissecting aortic aneurysm
: defective fibrilin -> loss of sheets around elastin
-> CYSTIC MEDIAL NECROSIS of aorta
108- Q 4. What is isolated systolic hypertension? what is most common cause of it?
increased systolic BP, but NORMAL diastolic BP
associated with AORTIC STIFFENING due to aging
- this makes sense: stiff aorta will increase more tension in systole as heart is pumping against stiff aorta, while diastolic pressure will not be that much affected because during diastole, blood is not really pushing against stiff aorta
108- Q8. Loss of contraction happens how long after onset of ischemia?
within 1 min.
It is super quick.
108- Q 19. Which part of aorta is most susceptible to get ruptured by trauma?
aortic isthmus
- this region, right next to L. subclavian artery, is relatively immobile as it is tethered by ligamentum arteriosum
