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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
If we are blocking ACE then we are preventing Angiotensin 1 converting to angiotensin 2 which causes what
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)
26
Captropril Assessment
Obtain BP Measure Potassium levels Obtain CBC with differential (related to possible Neutropenia side effect of ACE inhibitors)
27
Ace inhibitors and relationship with Bradykinin?
ACE inhibitors block the breakdown of bradykinin, causing protein level of bradykinin to rise, vessels widen and we see Vasodilation Cough Angioedema (rarely)
28
3 Hard no's of ACE inhibitors?
Pregnancy Hisotry of angioedema Renal artery stenosis
29
MAR considerations for ACE inhibitors (Captopril)
``` Antihypertensives Anything potassium related Diuretics NSAIDS (relation to double whammy effect on kidneys) Lithium ```
30
Ongoing Eval and interventions for both ACE and ARBS
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)
31
Reason why prescribing both ARBS and ACE inhibitors
Hypertension Post MI Heart failure Can slow nephropathy
32
Dosing of Ace inhibitors?
Low and slow and by mouth (PO)
33
What is Losartan
Angiotensin 2 Receptor Blocker (ARBS)
34
ACE inhibitors dosing
Nearly all are oral and given with food
35
You need to give ARBS with food?
No with or without food. Oral drug
36
Adverse reaction of Losartan
Common: hypotension | Serious/rare: Angioedema and fetal injury
37
Same 3 hard nos of ARBS
Pregnancy, history of angioedema, renal artery stenosis
38
Assessment when giving ARBS (Losartan)
Blood pressure
39
Look at MAR what to note in ARBS (losartan)
Antihypertensive drugs and Diuretics | BOTH INCREASE POSSIBLY OF HYPOTENSIVE CRISIS
40
Verapamil and Diltiazem are what
Calcium channel blockers (Very similar to Beta blockers)
41
Calcium channel blockers (Verapamil and Diltiazem) both used for what
Essential hypertension Cardiac dysrhthmias Angina pectoris
42
What do the orphans do
Dilate peripheral arterioles lowering afterload Dilation of coronaries increases perfusion Decrease in HR, AV conduction, force of contraction
43
Do not take the orphans with
Beta blockers or Grapefruit juice
44
Will you have reflex tachycardia with calcium channel blockers
No because of the effect they have on the heart in addition- unlike prazosin
45
Common side affect of Verapamil and Diltiazem
Constipation (V) | Dizziness, facial flushing, edema (D and V)
46
Hard nos of Calcium channel blockers (Exact same as Beta blockers)
2 or 3rd degree AV block and Sinus bradycardia
47
Before giving CCB Orphans
Obtain HR and BP, (standing and supine) chest pain history, ECH, renal and liver function
48
CCB administration
PO Sustained release or Immediate release
49
Ongoing Eval and interventions of CCB orphans
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
Dihydropyridines Use
Also a calcium channel blocker | Angina pectoris and essential HTN
51
MOA of Dihydropyridines (Nifedipine)
Dilation of peripheral arterioles lower afterload
52
Could you have reflex tachycardia with Dihydropyridines
Yes
53
Dosing of dihydropyridines
Using Sr limits adverse effects(Effects begin in 20 peak at 6 hours) Immediate release- Begin immediately peak in 30 minutes
54
Do not take Dihydropyridines with
Digoxin
55
Same nursing assessment for Dihydropyridines as Orphans
Obtain HR and BP (standing and supine) chest pain history, renal and liver function
56
Ongoing evals for Dihydropyridines
Monitor for increased peripheral edema, discuss falls, immediate release can cause reflex tachycardia ad a beta blocker may be prescribed to aid
57
Adverse effects of dihydropyridines (same as orphans)
Dizziness, facial flushing, HA, edema
58
dihydropyridines hard no
2nd or 3rd degree AV block
59
Hydralazine
Select dilation of arterioles, lowering afterload
60
Nitroprusside difference from Nitroglycerin
Nitroprusside dilates both arterioles and veins
61
Nitroglycerin Use
Reduction and frequency/intensity of angina attacks
62
Nitroglycerin MOA on stable angine
Acts on vascular smooth muscle to cause dilation of coronary veins by converting to nitric oxide, lowering preload, thus reducing O2 demand
63
Nitroglycerin MOA on Variant Angina
Relaxes coronary vasopspasm which increases O2 supply
64
Nitroglycerin Absorption and Metabolism
Highly lipid soluble and rapid inactivation
65
How do we give Nitroglycerin
Topical or Buccal
66
Obtain What prior to giving nitrogylcerin and ask what
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
Administration rules of Nitroglycerin
Buccal: Max 3 dose, 5 minute intervals, if outpatient call 911 after the first dose Minimum of 8 hour drug free window
68
Ongoing evals and interventions with nitrogylcerin
Assess for s/s of relief discuss fall precautions Educate client on storage light (dark container) temp (sensitive to heat) age (expiration)
69
Class 1 other antidysrhythmic drugs
Class - Lidocaine (Blocks cardiac NA channels) Class 2- Beta blockers Class 3- Block K Channels (amiodarone) Class 4- Calcium channel blockers
70
HMG-CoA reductase inhibitors (Statins) Use and MOA | Liver says- you cholesterol goons need to get in here stat"
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
Pharmacokinetics of Statins
Heavy first pass effect, metabolized by CYP3A4
72
Are there any adverse effects of Statins
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
Atorvastatin (Lipitor) Assess what prior to admin
LFTS
74
3 hard nos to Atorvastatin (Lipitor)
Viral or Alcoholic hepatitis, pregnancy, grapefruit juice
75
Administration of Atorvastatin
PO without regard to meals | Preferably in the evening (When body is processing lipids)
76
Ongoing eval and interventions of Lipitor
Educate client to notify of any muscle pain or tenderness occur and also assess for any signs and symptoms of relief
77
Colesevelam (Welchol) Use and MOA
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
Pharmacokinetics of Bile Acid Sequestrants
Biologically Inert | Don't actually absorb into bloodstream, all work done in GI)
79
Adverse Effect on Welchol
Constipation
80
Drug interactions with Colesevelam
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
Assessment Bile Acid Sequestrants
Measure lab values of baseline cholesterol, LDL, HDL, and TGs
82
Administration of Bile Acid Sequestrants
PO without regard to meals | If receiving powder or granules, mix with water or juice to limit esophageal irritation
83
Ongoing eval and interventions of bile acid sequestrants
S/S relief increase dietary fiber and fluids so no constipation note timing of drugs that interfere
84
Ezetimibe Use and MOA & adverse
Use: Adjunct to diet modification to reduce LDL and cholesterol MOA: Act on small intestine to inhibit dietary cholesterol absorption Possible gallstones
85
Drug Interactions
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
Fibrates (Gemfibrozil) Use and MOA
Use: For lowering TG levels and raises HDL MOA: not fully understood
87
Fibrate adverse reactions
Gallstones, myopathy, hepatotoxic
88
Anticoagulants primarily treat what
Used primarily to prevent thrombosis in veins and the atria of the heart
89
Heparin MOA
Helps antithrombin inactivate clotting factors: Primarily thrombin and factor Xa (10)
90
Can you take Heparin when pregnant
Yes, the drug wont cross the placenta
91
Purpose of taking Heparin
MI, PE, Massive DVT, line patency, DVT prophylaxis
92
Pharmacokinetics of heparin and labs we check
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
IV administration 2 things- check with patient then check with labs
Weight based bolus | aPTT or Anti-Xa measured once every 6 hours

Pharmacology (6 decks)

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