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CV Module Pharm > Intro to CV Pharm > Flashcards

Intro to CV Pharm Flashcards

1
Q

What are the two branches of ANS? What do they play an important role in?

A

ANS is comprised of two balancing systems, the SNS and the PSNS branches, which play a very important role in regulating the heart and the tone of the vascular system.

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2
Q

In the control of cardiac and vascular function, drug therapy involves blockade of ANS at what five locations?

A
  1. The Heart (beta receptors)
  2. vasculature
  3. Vasomotor center in the brain
  4. Sympathetic nerve terminals
  5. Autonomic ganglia
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3
Q

What ANS drugs act directly on the heart? What is their effect?

A

Beta-blockers→slow HR and contractility (and impact renin release from JGA in kidney)

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4
Q

What ANS drugs act directly on the vasculature? What is their effect?

A

Alpha blockers→reduce smooth muscle tone

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5
Q

What ANS drugs act on the vasomotor center in the brain? Effect?

A

Miscellaneous drugs→reduce centrally the level of SNS activity (and renin release, by consequence)

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6
Q

What ANS drugs act on sympathetic nerve terminals? Effect?

A

Transmitter-depleting agents (Reserpine)→ to reduce the result of sympathetic nerve activation

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7
Q

What is the effect of ANS drugs acting on autonomic ganglia?

A

reduced activity in both the SNS and PSNS branches, the overall effect being related to the respective prevailing tone.

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8
Q

What is the common name ending of α1 antagonists? Mechanism of action? Side effects?

A

the “AZOSINS”; they block α1-R’s on arterioles and venules;

Side effects: orthostatic hypotension and syncope, especially on 1st dose.

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9
Q

What are two examples of α2 agonists? Mech of action? Side effects?What is unique about Methyldopa?

A

Clonidine and Methlydopa; they decrease sympathetic outflow (decrease CO and BP) by stimulating presynaptic α2-R’s in the CNS which then inhibit release of nt.
Side effects: Rebound HTN (compensatory mechanisms become predominant), dry mouth, sedation, bradyarrhythmias
Methyldopa is a prodrug converted to the active form α-methyl-NE, and it’s coombs test positive.

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10
Q

What is the common name ending of β-blockers? Mechanism of action? Side effects?

A

The “OLOLs” (or if it has an additional action just “LOL”). They block postsynaptic β-R’s.
Side effects: CV disturbances, impotence, SLEEP DISTURBANCES/Sedation (lipophilic ones that can cross BBB), Asthma

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11
Q

Why are β-blockers contraindicated in asthmatics?

A

β2-R’s are important in the lungs for relaxation of bronchial smooth muscle. So, nonspecific β-blockers will inhibit this and cause bronchoconstriction, which is bad for asthmatics. β1-specific blockers are less likely to cause this, but are still rarely given to asthmatics.

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12
Q

What is the postganglionic sympathetic terminal blocker? Its mechanism of action? Why is it rarely used?

A

Reserpine; It destroys adrenergic synaptic vesicles, thereby depleting NE and decreasing its release.
Reserpine is rarely used b/c it has a number of side effects: depression, sedation, dry mouth, edema, bradycardia, NIGHT TERRORS (it can access the CNS)

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13
Q

What are the ganglionic blockers? Mech of action? Why are they rarely used?

A
  1. Hexamethonium 2. Trimethaphan
    They are ganglionic nicotinic receptor antagonists that inhibit postsganglionic neurons.
    They are rarely used b/c they have a lack of specificity and inhibit both sympathetic and PS tone→global ANS blockage
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14
Q

What are four type of drugs that act on vascular smooth muscle cells?

A
  1. CCBs
  2. Drugs acting thru NO (nitroso-vasodilators)
  3. Drugs opening K+ Channels
  4. D1 agonists
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15
Q

What are the two major types of CCBs? Their mechanisms of action?

A
  1. The PINES→ block L-type Ca2+ channels in vascular smooth muscle (selective)
  2. (non-PINES) Diltiazem and Verapamil→block L-type CC’s in CARDIAC and vascular smooth muscle cells (they slow conduction thru the AV node)
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16
Q

What are the side effects of CCB’s?

A

CONSTIPATION and GI disturbances→ b/c Ca2+ is involved in contraction of smooth muscle in GI system. If you take that away, you get stasis in the GI system
BRADYCARDIA (slowing of HR) and AV block→b/c non-PINES have direct effects on heart.
Edema, headache, dizziness

DOUBLE CHECK ALL THE SIDE EFFECTS IN THIS NOTECARD SET WITH THE PPT

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17
Q

Which CCB causes tachycardia?

A

Nifedipine

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18
Q

What are two nitroso-vasodilator drugs (act thru NO)? What is their mechanism of action?

A
  1. Hydralazine 2. Nitroprusside

They release NO, which stimulates guanylate cyclase to increase cGMP levels→VSM relaxation

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19
Q

What are the side effects of Hydralazine?

When is nitroprusside used, and what are its side effects?

A

Hydralazine→Reversible LUPUS-like syndrome, edema, arteriolar dilation
Nitroprusside→a) it’s used for hypertensive emergencies and to treat cyanide poisoning b) side effects: arteriolar and venous dilation

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20
Q

What are K+channel-opening drugs? Their mechanism of action?

A
  1. Minoxidil 2. Diazoxide

They open K+ channels→ hyperpolarization of vascular smooth muscle (VSM)

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21
Q

What are the indications and side effects of minoxidil and diazoxide?

A

Minoxidil: used for severe HTN; side effects include HIRSUTISM, pericardial effusion, edeme
Diazoxide: for HT emergencies and tx hypoglycemia (cause hyperglycemia

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22
Q

What is a D1 agonist drug? Its mechanism of action? When is it used?

A

Fenoldapam; vasodilates renal vessels and is used for HT emergencies

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23
Q

How does diazoxide cause hyperglycemia in addition to relaxation of VSM?

A

It opens K+ channels→hyperpolarization of VSM cell→inhibition of opening of voltage-gated Ca2+ channels→DECREASED Ca2+ ENTRY, which is required for insulin secretion→reduced insulin secretion→HYPERGLYCEMIA.

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24
Q
  1. What is the result of Fenoldopam (D1 agonist binding its receptor) on VSM cells?
  2. What is the effect of it binding its receptor in sympathetic ganglia?
A
  1. It binds to D1 receptors on VSM cells causing direct vasodilation of RENAL and mesenteric vascular beds. Thus, it helps maintain renal perfusion.
  2. The D1-R in symp ganglia is located on the presyn membrane (heterorec). So, activation of this receptor has an inhibitory effect of transmission thru the ganglia, but ????there’s still an effect on the postsyn membrane of the adrenergic synapse
25
Q

What is meant by the dose-dependent specificity of dopamine and its agonists like Fenoldopam?

A

At increased concentrations, it becomes less specific for D-R’s and begins to act on other sympathetic receptors such as alpha and beta receptors.

26
Q

Are ACEi’s or ARBs more effective/complete in inhibiting the actions of ANGII? Why?

A

ARBs tend to have better and more complete inhibitory actions. ACEi’s are not absolute, as patients have other enzymes that can produce a small amount of ANGII. However, ARBs block the end point of ANGII signaling.

27
Q

What is a fairly common adverse affect of ACEi’s that does not occur with ARBs?

A

A very dry and irritating cough. This is b/c ACEi’s increase bradykinin levels, and this causes the cough.

28
Q

What are two contraindications ACEi’s and ARBs?

A
  1. Renal Artery Stenosis or other situations where the pt has pre-existing renal disease, where the pt is relying on the RAAS for renal perfusion, so blocking it has negative consequences.
  2. Pregnancy
  3. Conditions increasing the risk of hyperkalemia
29
Q

What are the side effects of ACEi’s? ARBs?

A

ACEi’s: COUGH, hyperkalemia, angioedema, renal damage in pre-existing renal disease
ARBs: same as ACEi’s, but NOT COUGH

30
Q

What is the side effect of aliskerin (renin inhibitor)?

A

Hyperkalemia

31
Q

What are thiazides useful for?

A

Rx of mild HTN

32
Q

What are side effects of thiazides?

A

Decreased K, Mg, Na

Increased Ca2+, uric acid, glucose, LDL-C, triglycerides

33
Q

What are loops useful for?

A

Moderate to severe HTN

34
Q

What are the side effects of loops?

A

Decreased K, Mg, Na, Ca2+

Increased Uric acid, glucose, LDL-C, triglycerides

35
Q

What are the side effects of spironolactone (aldosterone antagonist)?

A

Hyperkalemia, metabolic acidosis, GYNECOMASTIA

36
Q

What is an advantage of aldosterone antagonists?

A

they are SAFE for use during PREGNANCY

37
Q

Pregnancy: what drugs are indicated? What drugs are contraindicated?

A

Indicated: α-methyl-dopa and hydralazine
Contraindicated: ACEi’s and ARBs

38
Q

Diabetes: what drugs are indicated? What drugs are contraindicated?

A

Indicated: ACEi’s, ARBs (also diuretics)
Contraindicated: high dose BBs

39
Q

Heart Failure: what drugs are indicated? What drugs are contraindicated?

A

Indicated: ACEi’s
Contraindicated: BBs (high doses), Verapamil/Diltiazem

40
Q

COPD/Astham: what drugs are indicated? What drugs are contraindicated?

A

Indicated: CCBs
Contraindicated: BB (esp nonselective); also ACEi’s are not recommended bc they cause the dry cough which can initiate an asthma attack

41
Q

What are the initial agents indicated in the Rx of HTN in pt’s with CKD?

A

ACEi’s, ARB’s (increase RBF)

42
Q

What drug is used in the treatment of HTN with BPH?

A

α-blockers

43
Q

What drugs are contraindicated in pt’s with severe depression? (3)

A
  1. BBs
  2. Reserpine
  3. α-methyl-dopa
    These three can get into the CNS
44
Q

What drugs are the initial agents used in the Rx of CV problems post-MI? (3)

A
  1. BBs
  2. Spironolactone
  3. Cardiac CCBs
    (ACEi’s are also acceptable)
45
Q

Which drugs are the initial agents for prophylaxis of recurrent stroke in the Rx of HTN? (2)

A
  1. Diuretics

2. ACEi’s

46
Q

What three classes of drugs are used in the Rx of angina?

A
  1. Nitrates
  2. CCBs
  3. BBs
47
Q

What are the clinical uses of nitrates? (2)

A
  1. Acute angina (nitroglycerin)

2. Pulmonary edema

48
Q

What are the side effects of nitrates? (4)

A
  1. Reflex tach
  2. Orthostatic hypotension
  3. Headache
  4. Tachyphylaxis
49
Q

What are the clinical uses of CCBs? (3)

A
  1. Angina
  2. HTN
  3. SVT (except Nifedipine)
50
Q

What are the side effects of CCBs? (3)

A
  1. Cardiac depression
  2. Peripheral edema
  3. Constipation
51
Q

What are the clinical uses of BBs? (3)

A
  1. Angina
  2. HTN
  3. Arrhythmia
52
Q

What are the side effects of BBs? (3)

A
  1. Impotence
  2. Depression
  3. Bradycardia
53
Q

Which drug is a cardiac glycoside? What is its mechanism of action?

A

Digoxin; it’s a Na/K-ATPase INHIBITOR

54
Q

What is the result of Digoxin acting on the Na/K-ATPase?

A

Inhibition of Na/K-ATPase→increased intracellular [Na+]→Activation of Na-Ca2+ Exhanger→increased intracellular [Ca2+]→increase in CO (increased inotropy) and vasoconstriction (increased VSM tone) due to smooth muscle contraction

55
Q

Why is vasoncontriction not an adverse of Digoxin Rx?

A

The increase in CO caused by digoxin leads to decreased SNS activity, which leads to reduction in vascular tone, which compensates for the vasoconstriction.

56
Q

What is a disadvantage of Rx with Digoxin?

A

It has a very NARROW therapeutic index/window.

57
Q

What is the classic adverse effect of Digoxin?

A

Visual disturbances→pt sees HALOS around light sources

58
Q

What is the antidote to decrease Digoxin levels when its toxicities become significant? How does it work?

A

Digibind: it binds up free digoxin and allows it to be excreted

CV Module Pharm (13 decks)

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