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Pharmacology > Cardiac- Exam 1 > Flashcards

Cardiac- Exam 1 Flashcards

1
Q

Prazosin (Minipress) Act on what receptors

A

A1 Receptors in veins and arteries.

Reduces preload and afterload

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2
Q

Prazosin Prescribed for

A

Essential Hypertension (Problem is with blood vessels)

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3
Q

Common Adverse effects of Prazosin

A

Reflex tachycardia- no influence over heart so it can respond in panic if baroreceptors are not being stretched
Nasal congestion- Dilation of blood vessels in nasal mucosa produced leaky capillaries and cause congestion

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4
Q

Prazosin is antagonist or agonist?

A

Alpha-andrenergic antagonist (Blocking mechanism)

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5
Q

Serious side effect of Prazosin

A

Orthostatic hypertension (dilation of veins) lots of vascular volume chilling in your venous vasculature

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6
Q

Pre administration of Prazosin

A

Obtain HR and BP for a baseline

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7
Q

Thinks to look for in a MAR with someone being prescribed Prazosin

A

Diuretics (low blood volume) and anti-hypertensives. Anything that will double up on lowing hypertension- double whammy

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8
Q

Evaluations and Interventions of Prazosin

A

Assess for efficacy and discuss fall precautions

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9
Q

Types of beta blockers

A

First Generation and second generation

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10
Q

First generation beta blockers do what

A

Non-selective. Block beta 1 and beta 2

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11
Q

What is propanolol

A

First gen beta blocker

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12
Q

What is metoprolol

A

Second gen beta blocker

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13
Q

What does second gen beta blockers like metoprolol do

A

Cardio selective. Only block beta 1 receptors in heart

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14
Q

Beta Blockers treat what 3 things

A

Hypertension
Angina pectoris
Cardiac dysrhythmias

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15
Q

Where are sites of action of beta 2 blockers

A

Receptors on arterioles located in heart, lungs, and skeletal muscles

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16
Q

Common adverse reaction of both metoprolol and propanolol

A

Bradycardia

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17
Q

Serious/rare side effects of both Propanolol and metoprolol

A

AV block and Rebound cardiac excitation- dont stop them suddenly

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18
Q

Serious rare effects of just Propanolol

A

Bronchoconstriction- related to beta receptors in lungs
inhibition of glycogenolysis
Depression (P) is lipid soluble so can cross BBB

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19
Q

Hard no for prescribing either beta blocker

A

Sinus bradycardia and 2 or 3 AV block

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20
Q

Assessment of Beta blockers

A

Obtain HR and BP
chest pain history
ECG - know what baseline rhythm looks like

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21
Q

Be aware of what then administering either beta blocker

A

First dose effect- possibly give at night to avoid adverse postural hypotension

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22
Q

Ongoing eval and intervention of Beta blockers

A

Assess for signs/symptoms of overshooting the mark
Adverse for adverse effects in Beta 2, in other sites of action other than heart
discuss fall precautions

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23
Q

What is Catopril

A

ACE inhibitor

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24
Q

Catopril is prescribed to treat what

A

Hypertension, post MI, HF to reduce workload of heart, and can also slow nephropathy

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25
Q

If we are blocking ACE then we are preventing Angiotensin 1 converting to angiotensin 2 which causes what

A

Kidney: Wont cause kidneys to hold onto sodium and fluid
Adrenal glands: Wont secrete aldosterone which causes sodium and fluid retention in kidneys but also peeing out potassium. So you will retain all your potassium
Heart: Wont stimulate muscle hypertrophy and fibrosis in the heart
Blood vessels: Wont cause vasoconstriction, so you will vasodillate
Brain: Will not stimulate sympathetic outflow in the brain (NO fight or flight response)

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26
Q

Captropril Assessment

A

Obtain BP
Measure Potassium levels
Obtain CBC with differential (related to possible Neutropenia side effect of ACE inhibitors)

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27
Q

Ace inhibitors and relationship with Bradykinin?

A

ACE inhibitors block the breakdown of bradykinin, causing protein level of bradykinin to rise, vessels widen and we see
Vasodilation
Cough
Angioedema (rarely)

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28
Q

3 Hard no’s of ACE inhibitors?

A

Pregnancy
Hisotry of angioedema
Renal artery stenosis

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29
Q

MAR considerations for ACE inhibitors (Captopril)

A 
Antihypertensives
Anything potassium related
Diuretics
NSAIDS (relation to double whammy effect on kidneys)
Lithium
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30
Q

Ongoing Eval and interventions for both ACE and ARBS

A

Discuss Fall precautions
Monitor BP closely for first 2 hours (First dose effects)
Obtain WBC count and diff every 2 weeks for first 3 months (Just with ACE inhibitors)

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31
Q

Reason why prescribing both ARBS and ACE inhibitors

A

Hypertension
Post MI
Heart failure
Can slow nephropathy

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32
Q

Dosing of Ace inhibitors?

A

Low and slow and by mouth (PO)

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33
Q

What is Losartan

A

Angiotensin 2 Receptor Blocker (ARBS)

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34
Q

ACE inhibitors dosing

A

Nearly all are oral and given with food

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35
Q

You need to give ARBS with food?

A

No with or without food. Oral drug

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36
Q

Adverse reaction of Losartan

A

Common: hypotension

Serious/rare: Angioedema and fetal injury

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37
Q

Same 3 hard nos of ARBS

A

Pregnancy, history of angioedema, renal artery stenosis

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38
Q

Assessment when giving ARBS (Losartan)

A

Blood pressure

39
Q

Look at MAR what to note in ARBS (losartan)

A

Antihypertensive drugs and Diuretics

BOTH INCREASE POSSIBLY OF HYPOTENSIVE CRISIS

40
Q

Verapamil and Diltiazem are what

A

Calcium channel blockers (Very similar to Beta blockers)

41
Q

Calcium channel blockers (Verapamil and Diltiazem) both used for what

A

Essential hypertension
Cardiac dysrhthmias
Angina pectoris

42
Q

What do the orphans do

A

Dilate peripheral arterioles lowering afterload
Dilation of coronaries increases perfusion
Decrease in HR, AV conduction, force of contraction

43
Q

Do not take the orphans with

A

Beta blockers or Grapefruit juice

44
Q

Will you have reflex tachycardia with calcium channel blockers

A

No because of the effect they have on the heart in addition- unlike prazosin

45
Q

Common side affect of Verapamil and Diltiazem

A

Constipation (V)

Dizziness, facial flushing, edema (D and V)

46
Q

Hard nos of Calcium channel blockers (Exact same as Beta blockers)

A

2 or 3rd degree AV block and Sinus bradycardia

47
Q

Before giving CCB Orphans

A

Obtain HR and BP, (standing and supine) chest pain history, ECH, renal and liver function

48
Q

CCB administration

A

PO Sustained release or Immediate release

49
Q

Ongoing Eval and interventions of CCB orphans

A

Assess for S/S of overshooting the beta 1 blockage effects- bradycardia, AV node blockade, severe hypotension
Increase dietary fiber and fluids as appropriate to limit constipation (V)
Monitor for increased peripheral edema
Discuss fall precautions

50
Q

Dihydropyridines Use

A

Also a calcium channel blocker

Angina pectoris and essential HTN

51
Q

MOA of Dihydropyridines (Nifedipine)

A

Dilation of peripheral arterioles lower afterload

52
Q

Could you have reflex tachycardia with Dihydropyridines

A

Yes

53
Q

Dosing of dihydropyridines

A

Using Sr limits adverse effects(Effects begin in 20 peak at 6 hours)
Immediate release- Begin immediately peak in 30 minutes

54
Q

Do not take Dihydropyridines with

A

Digoxin

55
Q

Same nursing assessment for Dihydropyridines as Orphans

A

Obtain HR and BP (standing and supine) chest pain history, renal and liver function

56
Q

Ongoing evals for Dihydropyridines

A

Monitor for increased peripheral edema, discuss falls, immediate release can cause reflex tachycardia ad a beta blocker may be prescribed to aid

57
Q

Adverse effects of dihydropyridines (same as orphans)

A

Dizziness, facial flushing, HA, edema

58
Q

dihydropyridines hard no

A

2nd or 3rd degree AV block

59
Q

Hydralazine

A

Select dilation of arterioles, lowering afterload

60
Q

Nitroprusside difference from Nitroglycerin

A

Nitroprusside dilates both arterioles and veins

61
Q

Nitroglycerin Use

A

Reduction and frequency/intensity of angina attacks

62
Q

Nitroglycerin MOA on stable angine

A

Acts on vascular smooth muscle to cause dilation of coronary veins by converting to nitric oxide, lowering preload, thus reducing O2 demand

63
Q

Nitroglycerin MOA on Variant Angina

A

Relaxes coronary vasopspasm which increases O2 supply

64
Q

Nitroglycerin Absorption and Metabolism

A

Highly lipid soluble and rapid inactivation

65
Q

How do we give Nitroglycerin

A

Topical or Buccal

66
Q

Obtain What prior to giving nitrogylcerin and ask what

A

Blood pressure, make sure they haven’t take viagra (sildenafil- hard no), assess for any other anti hypertensives (double whammy) and PMH of any alcohol use

67
Q

Administration rules of Nitroglycerin

A

Buccal: Max 3 dose, 5 minute intervals, if outpatient call 911 after the first dose
Minimum of 8 hour drug free window

68
Q

Ongoing evals and interventions with nitrogylcerin

A

Assess for s/s of relief
discuss fall precautions
Educate client on storage light (dark container) temp (sensitive to heat) age (expiration)

69
Q

Class 1 other antidysrhythmic drugs

A

Class - Lidocaine (Blocks cardiac NA channels)
Class 2- Beta blockers
Class 3- Block K Channels (amiodarone)
Class 4- Calcium channel blockers

70
Q

HMG-CoA reductase inhibitors (Statins) Use and MOA

Liver says- you cholesterol goons need to get in here stat”

A

Use: Most effective drug for lowering LDL and total cholesterol, can raise HDL and lower TG- primary prevention method
MOA: Increase the # of LDL receptors on hepatic cells- pull bad cholesterol out of circulation for processing

71
Q

Pharmacokinetics of Statins

A

Heavy first pass effect, metabolized by CYP3A4

72
Q

Are there any adverse effects of Statins

A

Typically well tolerate and side effects are not common but the serious ones are

  1. Myopathy (muscle weakness) & Rhabdomyolysis
  2. Hepatotoxicity
  3. New onset diabetes, memory loss, cataracts
73
Q

Atorvastatin (Lipitor) Assess what prior to admin

A

LFTS

74
Q

3 hard nos to Atorvastatin (Lipitor)

A

Viral or Alcoholic hepatitis, pregnancy, grapefruit juice

75
Q

Administration of Atorvastatin

A

PO without regard to meals

Preferably in the evening (When body is processing lipids)

76
Q

Ongoing eval and interventions of Lipitor

A

Educate client to notify of any muscle pain or tenderness occur and also assess for any signs and symptoms of relief

77
Q

Colesevelam (Welchol) Use and MOA

A

Bile Acid sequestrant
Use: Reduce LDL cholesterol levels, typically used as adjunct to statins
MOA: Does what Statins do in addition to
Hide Bile acids- binds to bile acids in the GI tract and promotes excretion vs absorption
- Need cholesterol to make bile so you are just hitting with a double whammy

78
Q

Pharmacokinetics of Bile Acid Sequestrants

A

Biologically Inert

Don’t actually absorb into bloodstream, all work done in GI)

79
Q

Adverse Effect on Welchol

A

Constipation

80
Q

Drug interactions with Colesevelam

A

Certain drugs can form insoluble complexes and mess with fat breakdown absorption so take these meds 1 hour prior to bile acid sequestrants or 4 hours after (Thiazide diuretics, digoxin, warfarin, some antibiotics)

81
Q

Assessment Bile Acid Sequestrants

A

Measure lab values of baseline cholesterol, LDL, HDL, and TGs

82
Q

Administration of Bile Acid Sequestrants

A

PO without regard to meals

If receiving powder or granules, mix with water or juice to limit esophageal irritation

83
Q

Ongoing eval and interventions of bile acid sequestrants

A

S/S relief
increase dietary fiber and fluids so no constipation
note timing of drugs that interfere

84
Q

Ezetimibe Use and MOA & adverse

A

Use: Adjunct to diet modification to reduce LDL and cholesterol
MOA: Act on small intestine to inhibit dietary cholesterol absorption
Possible gallstones

85
Q

Drug Interactions

A

Statin and ezetimibe- may increase myopathy (S an E my-opathy)
Fibrates and Ezetimibes- dont mix well
Bile acid Sequestriants and Ezitmibe- space timing of administration

86
Q

Fibrates (Gemfibrozil) Use and MOA

A

Use: For lowering TG levels and raises HDL
MOA: not fully understood

87
Q

Fibrate adverse reactions

A

Gallstones, myopathy, hepatotoxic

88
Q

Anticoagulants primarily treat what

A

Used primarily to prevent thrombosis in veins and the atria of the heart

89
Q

Heparin MOA

A

Helps antithrombin inactivate clotting factors: Primarily thrombin and factor Xa (10)

90
Q

Can you take Heparin when pregnant

A

Yes, the drug wont cross the placenta

91
Q

Purpose of taking Heparin

A

MI, PE, Massive DVT, line patency, DVT prophylaxis

92
Q

Pharmacokinetics of heparin and labs we check

A

D: Binds nonspecifically to plasma proteins and endothelial cells
M: Short half life (administer often)
Labs:
Activated partial thromboplastin time (aPTT)
Anti-Factor Xa Heparin Assay (anti-Xa)

93
Q

IV administration 2 things- check with patient then check with labs

A

Weight based bolus

aPTT or Anti-Xa measured once every 6 hours

Pharmacology (6 decks)

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