Brainscape's Knowledge GenomeTM

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


See full index

Pharm II > CV > Flashcards

CV Flashcards

1
Q

Stage 1 HTN

A

130/80 to 139/89

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

Stage 2 HTN

A

> or = 140/90

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

Most common form of HTN with no clear pathophysiology

A

Essential (primary) HTN

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

The presence of __________ properties results in less bradycardia & negative inotropic effects compared with “pure” beta blockers. (Carvedilol, labetalol) However these properties may result in __________

A

Alpha blocking; orhtostatic hypotension

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

Prazosin, terazosin, & doxazosin are oral selective _________ resulting in vasodilating effects on ______ vaculature

A

Postsynaptic a1 antagonists; BOTH arterial and venous

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

Why are a1 antagonists unlikely to elicit reflex increses in CO and renin release?

A

They do not block a2 receptors which leaves intact the normal inhibitory effect on NorEpi release from nerve endings

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

______ & _______ are non-selective a blockers used almost exclusively in the management of pheochromocytoma

A

Phenoxybenzamine; phentolamine

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

Used to relieve vasospasm of Raynaud’s phenomenon and preop in preparation of pts with pheochromocytoma

A

Prazosin

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

Nearly completely metabolized with < 60% bioavailability after oral admin which suggest first-pass hepatic metabolism. This makes this drug suitible for pts with renal failure

A

Prazosin

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

If a pt taking prazosin exhibits hypotension during epidural anesthesia preventing compensatory vasoconstriction, what would be the best choice to increase SVR?

A

Epinephrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How does clonidine work in neuraxial placement?

A

Inhibits substance P release and nociceptive neuron firing produced by noxious stimulation

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

When does clonidine peak? Half time? Duration?

A

Peak plasma: 60 -90 min;
H/t: 9-12 hrs (50% m liver, 50% unchanged in urine);
D of hypotensive effect: 8 hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Clonidine’s effect on postsynaptic a2 receptors in CNS affects anesthesia how?

A

A 50% decrease in anesthetic requirements for inhaled anesthetics and injected drugs in pts pretreated with clonidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What causes rebound htn with abrupt discontinuation of clonidine?

A

> 100% increase in circulating concentrations of catecholamines and intense peripheral vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

ACE inhibitors are most effective in treating which type of HTN?

A

Systemic HTN secondary to increased renin production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

First line therapy for systemic htn, CHF, and MR. also more effective/safer in diabetics.

A

ACE inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

ACE inhibitors decrease ______ & ______ which leads to?

A

Angiotensin II & plasma aldosterone;

Reduced vasoconstricion and reduction of Na and water retention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

ACE inhibitors block the breakdown of ________, an endogenous vasodilator substance which contributes to the antihypertenzive effects of these drugs

A

Bradykinin

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

If respiratory distress develops d/t ACE/ARB inhibitors, what should be given?

A

Epi 0.3 - 0.5 ml of a 1:1,000 dilution SQ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

_________ is possible with ACE/ARBs d/t decreased production of aldosterone

A

Hyperkalemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Can ACE inhibitors be used in renal pts?

A

Caution with preexisitng renal dysfunciton, C/I in renal artery stenosis (⬇️ glomerular filtration rate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Exaggerated hypotension attributed to continued ACE inhibitor therapy has been responsive to?

A

Crystalloids and/or admin of catecholamine or vasopressin (works on NO) infuison

23
Q

CCB inhibit Ca influx through voltage-sensitive ______ Ca channels in vascular smooth muscle. Do they work on arteries, veins, or both?

A

L-type; arterial specific

24
Q

_____ & ______ are less potent vasodilators & have (-) inotropic & chronotropic activity limiting their use in pts with cardiac dz.

More used for antiarrhythmic action

A

Verapamil & diltiazem

25
Q

The _________ CCB are potent vasodilators and are relatively safe to use in pts with heart failure & cardiac conduction defects, EXCEPT large doses of short-acting ________. Why?

A

Dihydropyridines;
Nifedipine;
It may acutely lower the BP and cause myocardial ischemia

26
Q

Inhibition of PDE prevents the breakdown of?

A

cAMP & cGMP

27
Q

What is the effect of PDE inhibition?

A

Vascular smooth muscle relaxation & for PDE3 inhibitors positive inotropy from intracellular Ca mobilization

28
Q

NO is administered by inhalation to produce?

A

Relaxation of the pulmonary arterial vasculature

29
Q

Does inhaled NO affect systemic circulation? Why?

A

Pulmonary circulation not systemic d/t its extremely rapid uptake by hemoglobin (half life < 5 sec)

30
Q

How does NO improve oxygenation?

A

By dilating vessels in alveoli where it is locally delivered, it improves oxygenation by improving ventilation-perfusion matching

31
Q

What can happen if NO is given in the presence of left heart dysfuntion?

A

The increased pulmonary blood flow can precipitate acute left heart failure and pulmonary edema

32
Q

SNP is a direct-acting nonselective peripheral vasodialtor that causes relaxation where?

A

Arterial and venous vascular smooth muscle only

33
Q

Onset & duration of SNP

A

O: almost immediate
D: transiet requiring continuous IV administration

34
Q

MOA of SNP

A

SNP interacts with oxyhemoglobin, dissociating immediately & forming methemoglobin while releasing cyanide and NO. NO activates guanylate cyclase increasing cGMP. cGMP inhibits Ca entry into vascular smooth muscle & increases Ca uptake by smooth ER to produce vasodilation. (Prodrug)

35
Q

The SNP infusion rates greater than ________ per minute IV result in dose-dependent accumulation of cyanide and the risk of CN toxicity myst be considered

A

2mcg/kg

36
Q

Thiocyanate is ____ less toxic than cyanide

A

100-fold

37
Q

________ can produce pulmonary vasodilation equivalent to the degree of systemic arterial vasodilation

A

Nitroglycerin

38
Q

MOA of hydralazine

A

Direct systemic arterial vasodilator which both hyperpolarizes smooth muscle cells and activates guanylate cyclase to produce vasorelaxation

39
Q

Why is hydralazine not recommended for pts with myocardial ischemia or CAD?

A

The arterial vasodilation produces a reflex SNS stimulation with resulitng increases in HR and contractility

40
Q

A dopamine type 1 receptor agonist that causes systemic arterial dilaiton through increasing cAMP

A

Fenoldopam

41
Q

The _______ state occurs during the upstroke of the AP and the _______ state occurs during the plateau phase of repolarization

A

Active; inactivated

42
Q

Drug-induced torsades de pointes is often a/w?

A

Bradycardia bc QTc interval is longer at slower HR

43
Q

________ is thought to reflect a reentrant tachycardia and easily degenerates to v fib

A

Wide complex ventricular rhythm

44
Q

Slows phase 0 depolarization in ventricular muscle fibers

A

IA (Na channel blocker)

45
Q

Shortens Phase 3 repolarization in ventricular muscle fibers

A

IB (Na channel blockers)

46
Q

Markedly slows Phase 0 depolarization in ventricular muscle fibers

A

IC (Na channel blockers)

47
Q

Inhibits Phase 4 depolarization in SA and AV nodes

A

II (B blockers)

48
Q

Prolongs Phase 3 repolarization in ventricular muscle fibers

A

III (K channel blocker)

49
Q

Inhibits action potential in SA and AV nodes

A

IV (CCB)

50
Q

Which drugs increase the duration of action potential?

A 
Class IA, class III.
Class II & IV increase PR interval
51
Q

MOA of adenosine in heart

A

Binds to A1 receptor (Gi protein) > opens K channesl > hyperpolarization.
Also ⬇️ cAMP in cardiac cells > ⬇️Ca entry > slow HR & conduction

52
Q

MOA of adenosine in vascular smooth muscle

A

Binds with A2 receptor (Gs protein) causing ⬆️ cAMP > vasodilaiton

53
Q

______ antagonize adenosine; _______ potentiates it

A

Xanthines (caffeine); dipyridamole (adenosine uptake inhibitor)

Pharm II (8 decks)

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