Mbbs Year 2 Cvs Block (Random Lectures)

Front 1

structure of valvular cusps: differences of AV valve and SL valve (2). Name dense and loose c.t.

Back 1

AV: inner dense c.t.; SL: outer dense c.t.; dense c.t. = valve fibrosa; loose c.t. = valve spongiosa

Front 2

common reason of development of valvular disease

Back 2

mechanical injury (leads to fibrosis on preserved architecture), inflammation (fibrosis and visualization), degenerative (deposit of chol and Ca)

Front 3

pathophysiology: describe how mitral valve stenosis and aortic valve stenosis lead to heart failure

Back 3

https://www.dropbox.com/sh/7pmuqwim8sq7n6e/E8tPkiOnMR/cvs_flashcard1.png

Front 4

Calcific aortic stenosis: symptoms and signs for CAS (11pts)

Back 4

asymptomatic, angina, visual disturbance, congestive heart failure, synope during exertion, fatigue, palpitation, apex beat change, dyspnea, systolic ejction murmur, small amplitude pulse, systolic thrill,

Front 5

Mitral annular calcification (MAC):

Back 5

source of thrombi & emboli leading to stroke, infective endocarditis

Front 6

Mitral valve proplapse: etiology (2) and predisposition (1)

Back 6

Mitral valve: myxomatous (mucus in c.t.) in the mitral valve, anomaly of c.t., predisposition: Marfan's Syndrome

Front 7

Mitral valve proplapse: Features of histology (2)

Back 7

ballooning, thickened rubbery valve, mucoid material deposit on the valve

Front 8

signs and complications of mitral valve prolapse (9)

Back 8

usually asymptomatic, angina, palpitation, migraine headache, CHF, stroke, IE, anxiety

Front 9

Aschoff bodies appears in acute state of Rheumatic fever. what is Aschoff bodies?

Back 9

foci of fibrinoid degeneration surrounded by lymphocytes

Front 10

Pancarditis which three?

Back 10

pericarditis, myocarditis, verrucae vegetations

Front 11

in infective endocarditis, ___________ vegetation is formed? what is it?

Back 11

friable vegetations: destruction of underlying cardiac tissue.

Front 12

complications of infective endocarditis

Back 12

sepsis, sepsis emboli, abscess formation, death, destruction of the valve result in sudden hemodynamic disturbance

Front 13

Libman Sacks endocarditis: predisposition

Back 13

Systemic Lupus Erythematosis (SLE): autoimmune disease in which the body's immune system mistakenly attacks healthy tissue.

Front 14

complications of hypertension at four sites:

Back 14

heart: LVH, vessels: atherosclerosis, hypertrophy, fibrinoid necrosis, aneurysm formation, atherosclerosis, brain: haemorrhage, infarction and stroke, kidney: nephrosclerosis

Front 15

hypertension: MULTIfactorial (3)

Back 15

imbalance between renin activity & salt conc., Overactive sympathetic system (hyperkinetic), peripheral resistance

Front 16

Secondary Hypertension causes (4)

Back 16

endocrine diseases, kidney disease (renal artery stenosis), pheochromocytoma, adrenal adenomas

Front 17

Loop diuretics: site (1) and mechanism (3)

Back 17

Loop of Henle, inhibit Na-K-2Cl co-transporter, reabsorption of Ca and Mg, K+ and H+ excretion

Front 18

Loop diuretics adverse effects (4)

Back 18

electrolyte disturbances, hypokalemia, alkalosis, hypovolemia, hypersensitivity, skin rash

Front 19

thiazide diuretics: site (1) and mechanisms (3)

Back 19

act on early stage of distal convoluted tubules, inhibit Na-Cl cotransporter, stimulate Na/Ca exchanger, K+ and H+ excretion

Front 20

Potassium-sparing diuretics: site (1) and mechanisms (3) (spironolactone and apiloride)

Back 20

site: collecting tubule, spironolactone inhibits the effect of aldosterone (which decrease K+ and H+ excretion), apiloride blocks epithelial Na channel

Front 21

statin: mechanism (2)

Back 21

inhibitor of HMG CoA reductase ie. decrease syn. of chol. in liver; increase synthesis of LDL Receptors

Front 22

Bile acid binding resins mechanism (4)

Back 22

reabsorption of chol decrease, increase syn,; increase syn,. of LDL receptor; increase hepatic TG synthesis

Front 23

digoxin mechanism 3pt

Back 23

Inhibit Na/K ATPase; Sensitize baroreflex; increase vagal effect

Front 24

β-stimulants (dopamine) mechanism 3pt

Back 24

Activate β-receptors, increase syn. cAMP, increase Ca channel opening

Front 25

Nitrates (nitroglycerin) mechanisms (2)

Back 25

venodilation to lower venous return, relax smooth muscle to restore flow; final: decrease cardiac work

Front 26

ivabradine mechanism mechanism (2)

Back 26

decrease funny current, decrease SA node packmaker rate, decrease HR

Front 27

β-blockers (propanolol) mechanism (2)

Back 27

Block β receptor in heart => low HR, contractility, BP, ...

Front 28

Ca channels blockers which two drugs?

Back 28

dihydropyidine, verapamil

Front 29

dihydropyidine mechanism (2)

Back 29

Vascular effects (dihydropyidine) low Ca entry => relax coronary, spasm => store flow; Relax vessel => low BP, Cardiac work

Front 30

verapamil mechanism (1)

Back 30

Cardiac effects (verapamil) low Ca entry =>low contraction, Cardiac work

Front 31

describe the renin-agiotensin-aldosterone system and its final effects (4+3)

Back 31

http://www.ganfyd.org/images/1/1f/Neurohormonal.JPG