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Pharmacology > Nurs 605 Module 8 > Flashcards

Nurs 605 Module 8 Flashcards

(73 cards)

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1
Q

What does ACE inhibitor stand for?

A

Angiotensin converting enzyme inhibitr

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2
Q

Describe the mechanism of action for ACE inhibitors

A

inhibits conversion of angiotensin 1 to angiotensin 2

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3
Q

What are some adverse effects of ACE inhibitors and why do they occur?

A

decreased GFR- inhibition of conversion inhibits the contriction of the efferent arteriole in the GFR = too relaxed
increased bradykinin production leads to cough
angioedema -facial flushing and swelling, can occur days to weeks post initiation of therapy

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4
Q

What are the uses of ACE inhibitors?

A

hypertension
congestive heart failure
diabetic nephropathy

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5
Q

What are the benefits of using ACE inhibitors

A

decreased BP
relatively low cost
decreased morbidity and mortality

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6
Q

What does ARB stand for?

A

angiotensin receptor blocker

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7
Q

Describe the mechanism of action for ARBS

A

similar to ACE inhibitors
works to block the angiotensin II receptor
decreases vasopressin and aldosterone = lowered BP

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8
Q

When would you choose to use an ARB?

A

when ACE inhibitors are not tolerated

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9
Q

What are the risks of combining both ARBs and ACEIs?

A

can potentially place the patient in hypotension, synconpe
decreased renin levels
don’t combine them-risk outweighs the benefit

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10
Q

What are some adverse events associated with ARBs?

A

hyperkalemia

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11
Q

What are contraindications for use of ARBs?

A

not to be used in pregnancy

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12
Q

Which ethnic group is at greater risk of angioedema when using ACE inhibitors?

A

african american descent (5% increased risk of angioedema with ACEI)

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13
Q

When would you choose to use a beta blocker?

A

not used as first line treatment due for various side effects
can be used in heart failure patients

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14
Q

What is the mechanism of action of beta blockers?

A

several mechanism of actions- primarily works to block beta 1 and beta 2 receptors
blocks receptor in the AV node, SA node= decreased HR and contractility
decreased peripheral vascular resistance= blocks vaso constriction, increases vasodilation = slows HR
blocks renin production in the kidneys-affects angiontensin II and aldosterone to lower BP

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15
Q

What are the adverse effects of beta blockers?

A

edema-due to increased sodium and water retention
arrythmias- due to decreased contractility
decreased HR- due to decreased epinephrine
bronchospasms/dyspnea- due to bronchoconstriction

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16
Q

What are the contraindications of beta blockers

A

not to be used in those with asthma as drug can further cause bronchoconstriction
not to be used in those with heart blocks

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17
Q

What are the indications of use for beta blockers?

A

HTN (not first line)
heart failure
angina pectoris

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18
Q

Patients cannot abruptly stop beta blockers; what is the reason for this?

A

can lead to rebound tachycardia and arrythmias

should be tapered

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19
Q

Describe the mechanism of action of calcium channel blockers (CCB)

A

CCBs work on the calcium channels of the AV node to decrease AV conduction
disrupts movement of calcium through the calcium channels

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20
Q

Two sub classes of CCB; what are they and common drugs in that class

A

non dihydropyridine- diltiazem and veramipril

dihydropyridine- amlopidine, felodipine

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21
Q

What are adverse effects of CCB?

A

gingival hyperplasia
bradycardia, hypotension
constipation
peripheral edema

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22
Q

What are the contraindications of CCB?

A

heart failure

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23
Q

What are the uses of CCB?

A

HTN
angina pectoris
arrythmias

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24
Q

Describe the mechanism of action of thiazide diuretics

A

inihibits the reabsorption of sodium and calcium in the distal tubule

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25
What allergy would a patient have if advised to avoid thiazides?
sulfa allergy
26
What are the uses of thiazides?
HTN
27
What is the first line drug in HTN?
usually thiazide or thiazide like medication
28
What are adverse effects of thiazides?
``` metabolic effects hyponatremia hyperglycemia hypouricemia hypokalemia ```
29
Discuss combination therapy in HTN
combination therapy is needed in approximately 50% of the population with HTN
30
What are some combinations of antihypertensives that should be avoided and why?
most combimations are safe avoid ARB + ACEi= does not show increased improvement in HTN but increased risk of adverse effects such as dizziness, syncope, hypotension avoid ARB/ACE + BB = increaased adverse effects; can be used if there is an indication to do so such as post MI or heart failure
31
In Canada, what is the recommended age and SBP when you would offer HTN tx?
>160 SBP | >60 years of age with HTN
32
What does the evidence say about decreasing a SBP from 160 to 150? (ARRs)
all cause mortality 1.2% | CV related mortality 4.3%
33
What does the evidence say about treating adults >80 with HTN?
similar to >60 age trends | CV related mortality similar, but because of age, can't reduce all cause mortality
34
At what SBP are we putting patients at risk for adverse events of hypotension? What is the evidence surrounding this?
decreasing to < 140 SBP increases risk of adverse events such as syncope and hypotension evidence weak
35
What does the evidence say about decreasing to <135 SBP?
low quality evidence increased risk of adverse events small overall ARR of 1.6% (small increase but adverse events)
36
What is the evidence surrouding a decreased BP of <120 vs. 140 SBP? Where did this evidence come from?
evidence comes from SPRINT trial overall, harms are greater than outcome leads to greater risk of adverse events and increased poypharmacy ARR 1.6% but ARI 2.2% (harms outweigh the benefit
37
At what diastolic BP do we put patients at risk?
anything lower than DBP <60
38
What does the evidence suggest about bloodpressure guidelines in HTN patients with DM?
unlikely that results with differ in DM patients with HTN if BP is lowered simiarly, increased risk of adverse events standard BP guidelines should apply to these patients <140-160/90-100
39
What are some common thaizide medications for HTN?What is the evidence surroudnig superiority of these meicdations/
HCTZ and chlorthalidone both are equal in terms of reducing BP chlorthalidone has longer half life but reduction of BP is similar
40
After taking an initial dose of ramipril, what is the % of BP lowering effect?
60-70% after the first dose of ramipril
41
Is there a difference between ramipril and perindopril?
pharmacodynamics yes clinicallly, no both work similarly
42
If a patient has historically had angioedema- is it still appropriate to prescribe ACEi or ARBs? What occurs if ACEi is continued in a person with angioedema?
no, considered contraindicated if hx of angioedema continuation of acei may escalate angioedema leading to life threatening outcomes
43
cough is an adverse effect of ACEi. when would cough start after initiation of therapy and how long after discontinuation will cough cease?
usually occurs within 2 weeks of initiation | days or months for resolution
44
ARBs are less studied than ACEinihibitors; so less evidence about CV related morbidity and mortality same as ACE1-60-70% reduction at starting dose
just FYI
45
Discuss peripheral edema in CCB
increases with continued dose longer duration of drug will increase peripheral edema peripheral edema is dose related
46
What are some drug interactions and their potential adverse effects with CCB?
erythromycin, clarithromycin - increased risk of AKI in older adults statins-reduce dose of CCB
47
Compare beta blockers with ARBs, ACEi, CCB and thiazides; what is the outcome of BBs?
BBs do not reduce CV related outcomes. have higher rates of adverse events due to adverse effects
48
A 65 year old man presents with an ongoing BP of 150/80 what would be your next steps?
continue assessment, offer treatment, thiazide diueretic first
49
What are the risk of aiming for a BP <130SBP?
increased CV risks and adverse effects | smaller ARR in CV events (1-2% )
50
What is the difference between primary and secondary prevention of cardiovascular disease?
primary- no prev. hx or CVD | secondary- hx of MI or unstable angina
51
What are the hard and soft endpoints/goals for those on statin therapy?
hard: decreased all cause mortality, decreased major cornoary events soft: no hispitalizations, revascularize
52
Discuss statin clinical trials (who was in it, what was excluded)
male, middle age, caucasian particpants less represented women, ethnic groups excluded: non compliant, non adherent, intolrated statins or unresponsive to statins
53
discuss the overall evidence of statins in the use of primary prevention. in the female population? in older populations?
**primary prevention-someone who has not had a hx of MI** ARR 1.2% coronary events reduction (very small, 66 people over 5 years) all cause mortality? likely <0.5%, not demonstrated women: no reduction in MCE or ACM older adult: insufficient evidence
54
describe the overall evidence of statins in the use of secondary prevention.
**secondary prevention- someone who has a history of unstable angina or MI MCE ARR 3.8% ACM ARR 1.8%
55
Statins should be offered to patients who have a recent MI, regardlless of their LDL leve
FYI
56
Would you start someone who is a diabetic on statins? if yes, why, if no, why?
probably not if they do not have a secondary coronary disease or cardiovascular disease risk scores to assess whether they need a statin
57
Why would you not start a patient on a statin based on their LDL-C levels?
surrogate marker, meaning may not be clinically relevant no supporting evidence and no refuting evidence re: starting statin therapy to treat target levels remember**primary prevention ARR is low when using statin as a prohphylaxis
58
What is the evidence surrounding choosing a statin>
not one is better than the otehr | look at tolerabilty, patient cost, drug interactions
59
What antibiotic increases statin doses and should be avoided?
macrolides
60
Which statin has the least amount of drug interactions?
pravastatin
61
Which are high potency statins? low potency?
high potency- atorvastatin, rosuvastatin low potency- everything else neither is superior to another
62
What are the dosing strategies of statins? and which are supported by evidence?
fixed dose treat to target LDL targets evidece based: fixed dose; no evidece to treat to target or LDL-C
63
What are some common drug interactions with statins? And how would we minimize these interactions?
antifungals macrolides warfarin CCBs minimize interactions by: avoiding interacting drugs, stopping statin if on macrolide short term, monitoring for adverse effects, reduce statin dosage if needed (amiodarone)
64
What are the adverse effects of statins?
usually occur at high doses of statins- rhabdomyolisis and myopathies simvastastin 80mg specifically incresaed myopathies and rhabdo - if no problesm x 12 months, can continue dose, but if new on statin, don't start on high dose diabetees? evidece unclear, ARI 0.4% neuropathy elevated liver enzymes
65
Discuss aspergillosis, abspetos, ammonia, managanese and avian protein inhalation toxicity What areas of work are these pathogens most likley to be found and what are the acute and chronic concerns
asbestos- mining, farming=fibrosis, lung cancer aspergillosis-farmers lung- farmers, moldy hay=bronchoconstriction, cough, chest tightness ammonia-construction and metal work=pulmonary edema avian protein- bird handlers and exposure to droppings=bronchoconstriction, cough, chest tightness
66
What is the mechanism of action of statins?
inhibits the HmG-CoG | interrupts cholesterol pathway=cannot build up fatty levels of cholesterol in the body
67
What do statins do to lipids and lipoprotein levels
decreases LDL | decreaed tryglycerides, increases HDL
68
What is the mechanism of action of ezetrimibe?
stops absorption of cholesterol in the GI tract
69
What is the mechansim of action of resins?
binds to bile acids and prevents reabsorption of bile acids (which is needed for the cholesterol pathway)
70
What is angina pectoris?
aka stable angina when the heart doesn't receive enough oxygen ususally caused by CAD manifests as tightness, squeezing to the chest
71
What are some pharmacological treatments for angina pectoris?
nitrates- venodilator -encourages O2 perfusion to the heart beta blockers- decreases heart rate, contractility and BP CCB-controls HR, contractility Antiplatelets-stablizes plaque
72
Describe the monitoring for side effects of amiodarone.
monitor liver enzymes at baseline and q 6 months--can cause elevated AST, ALT Thyroid function tests-can cause hypothyroidism, hyperthyroidism
73
Describe the management of a patient with atrial fibrillation who is controlled by rate and anticoagulation alone.
rate control- beta blockers, or CCB (monitor HR, hypotension, gingival hyperplasia) anticoagulation- warfarin, ASA, or NOACs (monitor INR)

Pharmacology (13 decks)

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