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Pharm II > Antihypertensives/vasodilators > Flashcards

Antihypertensives/vasodilators Flashcards

1
Q

Hypertensive urgency

A

Severe asymptomatic hypertension >180/>120

Without acute end organ injury

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2
Q

Hypertensive Emergency

A

Severe hypertension >180/>120

With acute end organ injury

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3
Q

Vasodilators

A

Drugs that dilate vasculature

Subdivided: arterial vs venous

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4
Q

Differentiate between antihypertensives and vasodilators

A

All systemic vasodilators are antihypertensives

BUT

All antihypertensives are NOT vasodilators

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5
Q

Preop chronic hypertension control

A

Hypertension associated with increased perioperative adverse events

If inadequately controlled- greater intraop swings in BP may be cause of these adverse events

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6
Q

Organ perfusion in hypertension

A

Auto regulation is right shifted

=organ hypoperfusion at higher BPs

the heart is also working harder-consuming more O2= increase in LV dysfunction and MIs

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7
Q

Intraop complications of hypertension

A

Bleeding- in specific operations

Trauma to vessel anastomoses

Extension of aortic dissections

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8
Q

Calcium Channel blockers MOA

A

Disrupt movement of Ca through calcium channels in vascular AND CARDIAC tissues

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9
Q

Classes of CCBs and preferred muscle/tissue

A

Dihydropyridines- amlodipine. Smooth muscle» cardiac

Phenylalkylamines- verapamil. Cardiac>smooth muscle

Benzothiazepines- diltiazam Smooth muscle> cardiac

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10
Q

Physiology of CCBs

A

Decrease afterload (via SVR)- can be used to treat arterial vasospasm

Negative inotropic/chronotropic/dromotropic agents

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11
Q

Clinical utility of CCBs

A

Ischemic heart disease

Acute hypertensive events

Aortic dissection

Cerebral and coronary vasospasm (nimodipine)

Antiarrhythmics- depress electrical impulses in SA and AV nodes- useful in atrial tachycardias

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12
Q

CCB adverse effects

A

Prolong Neuromuscular blockade

Dihydropyridines- reflex tachycardia

Non-dihydropyridines heart block when combined with Beta blockers

Flushing/ankle edema?

Decreased hepatic clearance related to decreased CO

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13
Q

Note on B1 selectivity

A

All “selective” beta blockers show B2 blockade at high doses

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14
Q

Chronic beta blocker therapy in the perioperative setting

A

Should be continued!

Withdrawal is associated with increased morbidity and mortality

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15
Q

Why are Beta blockers helpful in ischemic heart disease?

A

They decrease myocardial oxygen supply

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16
Q

Explain antihypertensives effect of beta blockers

A

Decrease CO -negative inotropy

Decrease renin release

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17
Q

Beta blockers in setting of tachyarrhythmias

A

Some have a membrane stabilizing effect

Inhibit action potential propagation across myocardial membrane

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18
Q

BB in CHF

A

HFREF EF<40%
Improves survival

Beneficial effect on LV remodeling- improves performance

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19
Q

Beta blocker elimination

A

Primarily hepatic

Esmolol- red cell cholinesterases

20
Q

Beta blocker contraindications

A

2nd and 3rd degree block in absence of pacemaker….

Class IV CHF?

21
Q

Adverse effects BB

A

Exacerbates bronchospastic lung disease (nonselective)
Exacerbates LHF and PVD

Masks hypoglycemia symptoms associated with insulin OD

22
Q

ACE/ARB in perioperative period

A

Controversial but the only class that can be held 24 hr prior to surgery

-potentially holding lowers risk of death and postoperative vascular events

23
Q

What do you give in setting of induction hypotension in an ACE/ARB patient that has continued the medication?

A

Vasopressin

24
Q

ACE MOA

A

Block conversion of angiotensin I to angiotensin II

25
Q

ARAs MOA

A

Angiotensin receptor ANTAGONIST

Antagonize effect of angiotensin II at AT1 receptors- no impact on ACE

26
Q

Physiologic effects of ACE/ARAs

A

Mitigate effect of angiotensin II on VSM

Increase parasympathetic tone

Decrease impact of aldosterone on distal convoluted tubule= Na/water loss

Inhibit ACE mediated breakdown of kinins =enhanced vasodilation (ACE only)

27
Q

ACE/ARA clinical use

A

Hypertension

Diabetic neuropathy- slows progression of CKD

Chronic CHF- afterload reduction and regression of ventricular remodeling

28
Q

ACE elimination

A

Renal

29
Q

Adverse effects ACE/ARAs

A

Hypotension- inducing vasoplegia

Hyperkalemia!!!

Cough- ACE specific

Anemia

Angioedema ACE>ARA

30
Q

Classes of diuretics

A

Thiazides (chlorthalidone, metolazone)

Loop diuretics (furosemide, bumetanide)

Potassium-sparing diuretics (spironolactone, amiloride)

31
Q

Loop diuretics clinical utility

A

Volume overload

Weak antihypertensive effect

32
Q

Uses for spironolactone

A

Hypertension associated with hyperaldosteronism

And chronic CHF

33
Q

Electrolyte abnormality in thiazide diuretics

A

Hyponatermia

34
Q

When do you see HYPER kalemia in diuretics use

A

K-sparing diuretics especially in combination with ACE inhibitors

35
Q

MOA alpha-1 adrenergic blockers

A

Inhibition of norepinephrine mediated vaso constriction

36
Q

Name some alpha blockers

A

ZOSIN

Doxazosin
Terazosin
Prazosin

37
Q

Difference between phentolamine and phenoxybenzamine

A

Phentolamine- binds competitively-short acting

Phenoxybenzamine- binds irreversibly, long acting

38
Q

GPCRs for A1 and A2

A

A1- Gq

A2- Gi

39
Q

WTF is Fenoldopam

A

Dopamine Agonist

DA-1 receptor

Arteriolar vasodilation with decreased afterload

Increased renal perfusion

Coronary vasodilation

Does not cross BBB

40
Q

Fenoldopam kinetics/dynamics

A

Onset- 5 minutes
Duration 30-60

Hepatic metabolism

41
Q

Adverse effects Fenoldopam

A

Hypotension….
Increased intraocular pressure
Reflex tachycardia
Hypokalemia
Cutaneous flushing

42
Q

Action of direct vasodilators

A

NO on vessel wall

43
Q

Nbitroprusside

A

Tachyphylaxis with prolonged infusion

Photosensitive

Arterial and venous vasodilation

44
Q

Nitroprusside Degradation

A

Reacts with Hb to form Cyanide and NO

45
Q

3 pathways to cyanide poisoning in nitroprusside and max dose

A
  1. Cyanomethemoglobin- disrupts carrying capacity oh O2
  2. Thiocyanate- consumes thiosulfate B12

3-cytochrome oxidase- disruption of aerobic respiration

<2mcg/kg/min

46
Q

Nitroglycerin

A

Tachyphylaxis

Primarily Venous- preload reduction

Reflex tachycardia

Coronary vasodilation- does NOT cause steal

Can relieve opioid induced biliary spasm

Hepatic metabolism

47
Q

Hydralazine

A

Arterial vasodilation

Hypertension in pregnancy
CHF with reduced EF

Variable IV onset

Hepatic via acetylation- some patients see reduced acetylation which can lead to lupus like symptoms

Pharm II (8 decks)

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