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Pharm > CV > Flashcards

CV Flashcards

1
Q

Beta one receptors effect ____ while beta two receptors effect _____

A

Heart; Lungs

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2
Q

What are the beta adrenergic antagonists MOA

A

Inhibit symp. stimulation - lowering BP/HR (1) and blocking bronchodilation (2)

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3
Q

If patient taken off beta blocker too quickly, what condition can happen?

A

Rebound cardiac excitation

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4
Q

Beta blockers are used cautiously in which types of patient population? (Three discussed) Why?

A

Diabetics because beta two receptors normally inc. glucose levels in blood; therefore blocking causes hypoglycemia
Pt with history of severe allergic reactions b/c epinephrine (treatment) won’t be effective
Pt with COPD (including asthma) b/c beta 2 receptors normally cause bronchodilation if stimulated

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5
Q

Beta blockers are subdivided into 3 groups. Give the distinctions of each generation in regards to the receptor it affects.

A

1st - affect beta 1 and 2
2nd - cardioselective (beta 1)
3rd - has vasodilating actions (beta 1,2,alpha 1)

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6
Q

If patient HR is under ____ or BP systolic under _____ hold beta blocker

A

60; 90

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7
Q

Common 1st generation beta blocker

A

Propanolol

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8
Q

Common 2nd generation beta blocker

A

Metoprolol

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9
Q

3 beta blockers approved for heart failure

A

Bisoprolol
Carvedilol
Metoprolol

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10
Q

Common 3rd generation beta blocker

A

Labetolol - used in HTN crisis

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11
Q

Centrally acting alpha2 agonists MOA

A

Action: stimulate the alpha2 receptors in the CNS, which decreases sympathetic outflow of the neurotransmitter norepinephrine (NE).

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12
Q

Two common centrally acting alpha 2 agonists

A

Clonidine

Methyldpoa

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13
Q

Adrenergic Neuron-Blocking agents MOA

A

Action: inhibit the uptake of NE into storage vesicles resulting in depletion of catecholamines & serotonin from central & peripheral axon terminals.

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14
Q

First line drug class for treating HTN

A

Diuretics

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15
Q

Name the 4 subclasses of diuretics and where does each work in kidney

A

Loop - work in loop of henle
thiazide - early distal convoluted tubule
potassium sparing - late distal convoluted tubule & collecting duct
osmotic - proximal convoluted tubule

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16
Q

Loop diuretics MOA

A

Action/uses: inhibit sodium & water reabsorption in loop of henle - promotes excretion of water, sodium and potassium

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17
Q

Common loop diuretic drug

A

Furosemide (Lasix)

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18
Q

Which electrolytes to monitor when on diuretic

A

Mg, K, Na, Cl

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19
Q

How to administer potassium

A

NEVER give IV push, only IVPG (no more than 10mEq/hr) and IV fluids ( no more than 40mEq/liter) or PO

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20
Q

How to recognize thiazide drug class (suffix) and MOA

A

-thiazide

promote excretion of sodium, chloride, potassium, and water by decreasing their reabsorption in the distal tubule

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21
Q

Potassium sparing MOA

A

promote excretion of sodium & water by inhibiting sodium-potassium exchange in the distal tubule

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22
Q

Two subcategories to potassium sparing drug class and common drugs to each

A

Aldosterone antagonists- Spironolactone
- inhibit action of aldosterone
Non-aldosterone antagonists (works faster and more direct) - Amiloride HCL and triamterene
- fluid which has built up in the tissues of the lungs or body is drawn back into the bloodstream to replace the fluid passed out by the kidneys. This eases symptoms such as edema (pulmonary and extremity)

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23
Q

Osmotic diuretic MOA and drug name

A

MOA: most of the drug stays in the nephron creating an osmotic force. It inhibits passive reabsorption of water.
Mannitol

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24
Q

Uses of mannitol and unique a/e

A

Prophylaxis of renal failure
Reduction of increased intracranial pressure (Inc. ICP)
Reduction of intraocular pressure
A/E: edema! watch pt with CHF or pulmonary edema closely

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25
Q

Name the 4 category drugs that work on RAAS

A

ACE inhibitors
ARBs
Direct Renin inhibitors
Aldosterone Antagonists

26
Q

ACE inhibitor (suffix) and MOA

A

-pril
Action: interrupt the RAAS in 1 of 3 ways:
- Inhibit conversion of angiotensin I to angiotensin II
- Decrease aldosterone secretion
- Compete w/ angiotensin II to block its effect

27
Q

ACE inhibitor results in a dec in ______ hormone and increase in ______ hormone.

A 
Dec. angiotensin II:
 - Vasodilation
 - Dec. blood volume
 - Dec. cardiac & vascular remodeling 
 - Potassium retention
Inc. Bradykinin(by inhibiting its degradation)
 - Vasodilation
 - Cough
 - Angioedema (rare)
28
Q

A/E of -pril

A

cough
first dose hypotension
hyperkalemia
angioedema

29
Q

If first dose hypotension occurs while on ace inhibitors, three steps to take

A

Diuretics temporarily discontinued
BP monitored for several hours after taking
Supine position 2-4 hours esp. if feel lightheaded

30
Q

Angiotenson II receptor blockers (ARBs) MOA

A

Action: blocks access of angiotensin II to its receptors in blood vessels and all other tissues.

31
Q

What is alternative to ACE inhibitors (-pril) that does not inhibit bradykinin (no cough) nor raise potassium in blood?

32
Q

How to know ARBs (suffix)

33
Q

Direct renin inhibitor MOA

A

binds tightly w/ renin & inhibits the cleavage of angiotensinogen into angiotensin I. Works earlier than other drugs in this category

34
Q

Only drug in direct renin inhibitor category?

35
Q

MOA of calcium channel blockers

A

Decrease myocardial contractility by preventing the influx of calcium ions into the cells
Decreased oxygen demand
Dilate coronary & peripheral arteries

36
Q

Suffix of calcium channel blockers

37
Q

Unique a/e to nifedipine

A

gingival hyperplasia

reflex tachycardia

38
Q

Three categories to calcium channel blockers (Very Nice Drugs)

A

Verpamil
Nifedipine
Diltiazem

39
Q

Out of three subcategories of calcium channel blockers, which two can treat dysrhythmias such as A-flutter, SVT, and A-fib?

A

Verpamil and Diltiazem

40
Q

Hydralazine MOA, Use, and unique a/e

A

Action: causes selective dilation of arterioles by action on vascular smooth muscle
Used in HTN crises and chronic heart failure (short term fix reducing afterload)
A/E reflex tachycardia

41
Q

Sodium Nitroprusside MOA, Use, and unique a/e

A

Venous and arteriole dilation
Used in HTN emergency
a/e thiocyanate toxicity (observe for loc changes and delirium), cyanide poisoning

42
Q

Anti hypertensives approved in pregnancy

A

Methylodopa, Labetalol, Hydralazine, long acting Nifedipine

43
Q

Treatment for angina

A

nitroglycerine
If not successful – add beta blocker
If not successful – add or substitute w/ CCB

44
Q

Labs for bleeding and clotting time

A

PT - Prothrombin Time (11-13sec)
INR - International Normalized Ratio (.8-1.1sec)
APTT - Activated Partial Thromboplastin Time (normal=40 seconds

45
Q

2 classes of antithrombotic drugs

A
  • antiplatelet drugs: (arterial) antiplatelet agents prevent platelets from clumping and also prevent clots from forming and growing
  • anticoagulant drugs: (venous) anticoagulants slow down clotting, thereby reducing fibrin formation and preventing clots from forming and growing
46
Q

Heparin MOA

A

Anti coag that prevents the continuation of the clotting cascade via binding with Anti-thrombin III making the enzyme 2000s more potent

47
Q

Main Heparin A/E

A

Heparin-induced thrombocytopenia (HIT): is an antibody-mediated reaction characterized by a profound decrease in platelets

48
Q

Antidote for heparin

A

Protamine Sulfate

49
Q

Common Low Molecular Weight Heparin

A

Lovenox; a fragment of standardized heparin - advantage b/c of less a/e

50
Q

Warfarin MOA

A

Anti-coag; Interferes with hepatic synthesis of vitamin K-dependent clotting factors (II, VII, IX, and X).

51
Q

Warfarin Antidote

52
Q

Aspirin MOA

A

Anti-platelet; suppresses platelet aggregation by irreversible inhibition of cyclooxygenase which is an enzyme needed by platelets to synthesize thromboxane A2

53
Q

Anti-platelet MOA and drugs in class (other than ASA)

A

block P2Y12 ADP receptors on the platelet surface and thereby prevent ADP-stimulated aggregation
Clopidogrel (Plavix)
Prasugrel (Effient)
(-gril) and Ticagrelor

54
Q

Thrombolytic Agents MOA and drugs suffix

A

dissolve the clot by converting plasminogen to plasmin, which lyses the thrombi & fibrinogen.
- plase

55
Q

Anti-Dysrhythmic Meds

A

1) Quinidine, Phenytoin, Lidocaine
2) Propanolol
3) Amiodorone
4) Verpamil and Diltiazem
Others: Digoxin, Adenosine, Magnesium Sulfate

56
Q

HMG-CoA reductase inhibitors MOA and suffix

A

MOA: decrease the rate of cholesterol production by inhibiting HMG-CoA reductase. The liver requires HMG-CoA reductase to produce cholesterol.
(-statin) - category X

57
Q

Medication Protocol for MI

A 
MONA / MONA B
Morphine 
Oxygen 
Nitroglycerin
Aspirin
(Beta Blocker)
58
Q

Digoxin Teaching

A

Monitor apical pulse for 1 full min before administering. Withhold dose and notify health care professional if pulse rate is <60 bpm in an adult, <70 bpm in a child, or <90 bpm in an infant.

59
Q

Digoxin A/E

A

Anorexia (early sign)
Nausea, vomiting
Visual disturbances

60
Q

-statin a/e

A

Myopathy: soreness, weakness, increase in CPK levels

hepatotoxic

Pharm (5 decks)

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