Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardio Exam 2 > lecture 6 > Flashcards

lecture 6 Flashcards

1
Q

myocardial ischemia (IHD)

A

imbalance between myocardial O2 supply and demand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

IHD contributing factors

A
  1. increased sympathetic outflow-> incr HR, ventricular wall tension & ventricular contractility-> incr myocardial demand
  2. decreased coronary blood flow due to coronary vasospasm &/or coronary atherosclerosis (CAD)-> decreased myocardial O2 supply
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

coronary artery disease

A

a condition in which coronary arteries are narrowed by the formation of atherosclerotic plaques

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

main symproms of myocardial ischemia

A
  1. angina

2. decreased exercise tolerance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

myocardial ischemia generally preceds

A

MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

2 distinct characteristics of MI

A
  1. sudden interruption of blood supply to the myocardium by rupture of a plaque resulting in thrombosis
  2. myocardial function is compromised & tissue can become necrotic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

IHD short term goal of therapy

A

prevent/reduce symptoms of angina that limits exercise capability & quality of life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

IHD long term goals of therapy

A

prevent events of myocardial ischemia (MI, arrhythmias, HF) & reduce mortality (extend life)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

IHD treatment

A
  • risk factor modification

- nonpharm therapy: revascularization, coronary artery bypass grafting, percutaneous transluminal coronary angioplasty

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

pharmacological agents used

A
  • nitrates
  • beta blcokers
  • CCB
  • anticoagulants
  • antiplatelet agents
  • thrombolytic agents
  • statins
  • ACEI
  • pure antianginal drugs
  • morphine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

pharmacological treatments improved the balance between O2 supply & demand by:

A
  • dilating the coronary vasculature (increase O2 supply)

- reducing cardiac workload (decrease demand)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

organic nitrates MOA

A
  • prodrugs
  • upon metabolism release NO
  • NO is also biosynthesized in different tissues by NOS
  • Potent vasodilator
  • NO stimulates guanylyl cyclase-> incr cGMP-> dec intracellular Ca & MLC dephosphorylation-> SM relaxation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

hemodynamic effects of low dose nitrates

A
  • preferentially dilate veins compared to arterioles-> decreased venous return & preload & decreased left & right ventricular chamber size
  • (slight decr. in BP)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

hemodynamic effects of high dose nitrates

A
  • cause further venous pooling & decrease arteriol resistance
  • activation of compensatory sympathetic reflexes (tachycardia)
  • cronary blood flow may increase transiently, but it will decrease again if cardiac output & BP are decreased significantly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

total & regional coronary blood flow (low to moderate doses of nitrates)

A
  1. vasodilate & restore the flow in epicardial vessels
  2. do not impair autoregulation in smaller vessels
  3. decrease intracavitary systolic & diastolic pressures-> incr blood flow to the subendocardium
  4. dilate cardiac veins (may improve cardiac microcirculation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

nitrate effects on myocardial O2 requirements

A
  • incr ventous capacitance-> decr venous return-> decr preload-> reduced O2 demand & incr blood flow to subendocardium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

antianginal effects of nitrates

A
  1. reduction of venous return & myocardial O2 demand- primary effect*
  2. dilation of epicardial coronary arteries-> improved blood flow & O2 supply
  3. NO in plts-> antiplt effect (modest, but important)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

tolerance to nitrates

A

repeated/continuous use of (high) doses of nitrates may lead to marked attenuation of their pharmacological effects (tachyphylaxis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

nitrate side effects

A
  1. HA
  2. transient dizziness & weakness
  3. postural/orthostatic hypotension
  4. drug rash
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

caution using nitrates with

A

PDE5 inhibitors-> severe hypotension!

PDE5I inhibit the conversion of cGMP to GMP-> incr cGMP-> vasodilation

21
Q

PDE5 inhibitors

A

sildenafil (viagra)
tadalafil (cialis)
vardenafi (levitra)

22
Q

nitrate drugs

A 
nitroglycerin
isosorbide dinitrate
isosorbide mononitrate
nitroglycerin IV
nitroglycerin patch
23
Q

nitrates

A
  • all have a large first pass effects
  • all but isosorbine mono have short T1/2 & high clearance rates
  • large interindiviual variations in plasma conc.
24
Q

nitroglycerin concentrations are effected by

A
  • route of admin
  • IV: highest
  • oral: lowerst
25
Q

sublingual NTG

A

usually taken during anginal attack or in anticipation of exercise or stress-induced attack

26
Q

IV NTG

A

mainly in clinic for acute coronary syndrome

27
Q

chewable, oral & transdermain Nitrates

A

long-term prophylaxis of angina

28
Q

what type of beta receptors are in the heart?

A

beta 1

29
Q

what are the effects of beta 1 stimulation

A
  • tachycardia, contraction force increase, impulses travel in heart faster too, O2 demand is increased
  • chrono (inc HR)
  • dromo (AV node conduction)
  • iono (incr contraction force)
30
Q

with beta-blocker use, are we targeting O2 supply or demand

A

O2 demand

31
Q

Beta 1 blockers are effective in the treatment of

A
  • exertional angina: reduce severity & frequency of attacks, cardioprotective effects
  • UA & MI: reduce recurrent episodes & improve mortality
32
Q

Beta blockers can result in

A
  • profound decreases in LV function

- caution in pts with limited cardiac reserve (critically depend on adrenergic stimulation)

33
Q

DHP CCB act on

A

arteries/arteriole

  • decr. peripheral resistance
  • coronary vasodilation
  • improved contractility & ventricular function
  • improved coronary blood flow
  • HR & CO may increase
34
Q

NonDHP CCBs act on

A

the heart

35
Q

what CCBs would you use in someone suffering from IHD?

A

NonDHPs

- DHPs can still be useful

36
Q

CCB MOA

A

block L type Ca channels-> decr influx of Ca-> relaxation

37
Q

nicardipine (DHP) may have selectivity for

A

coronary vessels

38
Q

parenteral anticoagulants

A
  • UFH & LMWH facilitate binding of thrombin to antithrombin-> several coagulation factors, incl fibrinogen are NOT acivated
39
Q

oral anticoagulants

A
  • warfarin/ vit K antagoinst inhibit vit K epoxide reductase-> vit K is NOT reduced (recovered) to activate coagulation factors (7,9,10,2)
40
Q

anticoagulants

A
  • prevent progression of thrombosis & systemic embolization
  • reduce recurrent episodes of UA & MI
  • usually are used in combo with other drugs to achieve better therapeutic outcome
41
Q

factors that cause activation & aggregation of plts

A

TX-A2, thrombin, ADP, collagen, etc

- can serve as targets to inhibit plt activation

42
Q

aggregated plts

A

form the initial hemostatic plug at sites of vascular injury & are key played in thrombus formation

43
Q

antiplt agents

A

aspirin

44
Q

aspirin

A
  • NSAID that inactivates COX1 & inhibits TX-A2 formation from arachidontic acid in plts
  • 50-320mg/day: complete & permanent inactivation of COX1 w/out clinically sig effect on COX2
45
Q

COX1 ->

A
  • PGs & TX-A2

- plt aggregation & vasoconstriction

46
Q

COX2->

A
  • PGs & prostacyclins

- vasorelaxation & antiplt effect

47
Q

aggrenox

A

aspirin/ ER dipyridamole

48
Q

common side effect of aggrenox

A

HA- usually disappears upon continuation of therapy

49
Q

dipyridamole MOA

A
  • inhibits adenosine uptake in plts-> inc adenosine on surface-> A2 stimulation-> incr cAMP in plts-> decr plt activation
  • inhibits PDE-> inc cGMP-> SM relaxation & decr plt activation

Cardio Exam 2 (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions