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Pharmacology > Nurs 605 Module 8 > Flashcards

Nurs 605 Module 8 Flashcards

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
Q

What allergy would a patient have if advised to avoid thiazides?

A

sulfa allergy

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26
Q

What are the uses of thiazides?

A

HTN

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27
Q

What is the first line drug in HTN?

A

usually thiazide or thiazide like medication

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28
Q

What are adverse effects of thiazides?

A 
metabolic effects
hyponatremia
hyperglycemia
hypouricemia
hypokalemia
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29
Q

Discuss combination therapy in HTN

A

combination therapy is needed in approximately 50% of the population with HTN

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30
Q

What are some combinations of antihypertensives that should be avoided and why?

A

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
Q

In Canada, what is the recommended age and SBP when you would offer HTN tx?

A

> 160 SBP

>60 years of age with HTN

32
Q

What does the evidence say about decreasing a SBP from 160 to 150? (ARRs)

A

all cause mortality 1.2%

CV related mortality 4.3%

33
Q

What does the evidence say about treating adults >80 with HTN?

A

similar to >60 age trends

CV related mortality similar, but because of age, can’t reduce all cause mortality

34
Q

At what SBP are we putting patients at risk for adverse events of hypotension? What is the evidence surrounding this?

A

decreasing to < 140 SBP increases risk of adverse events such as syncope and hypotension
evidence weak

35
Q

What does the evidence say about decreasing to <135 SBP?

A

low quality evidence
increased risk of adverse events
small overall ARR of 1.6% (small increase but adverse events)

36
Q

What is the evidence surrouding a decreased BP of <120 vs. 140 SBP? Where did this evidence come from?

A

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
Q

At what diastolic BP do we put patients at risk?

A

anything lower than DBP <60

38
Q

What does the evidence suggest about bloodpressure guidelines in HTN patients with DM?

A

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
Q

What are some common thaizide medications for HTN?What is the evidence surroudnig superiority of these meicdations/

A

HCTZ and chlorthalidone
both are equal in terms of reducing BP
chlorthalidone has longer half life but reduction of BP is similar

40
Q

After taking an initial dose of ramipril, what is the % of BP lowering effect?

A

60-70% after the first dose of ramipril

41
Q

Is there a difference between ramipril and perindopril?

A

pharmacodynamics yes
clinicallly, no
both work similarly

42
Q

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?

A

no, considered contraindicated if hx of angioedema

continuation of acei may escalate angioedema leading to life threatening outcomes

43
Q

cough is an adverse effect of ACEi. when would cough start after initiation of therapy and how long after discontinuation will cough cease?

A

usually occurs within 2 weeks of initiation

days or months for resolution

44
Q

ARBs are less studied than ACEinihibitors; so less evidence about CV related morbidity and mortality
same as ACE1-60-70% reduction at starting dose

A

just FYI

45
Q

Discuss peripheral edema in CCB

A

increases with continued dose
longer duration of drug will increase peripheral edema
peripheral edema is dose related

46
Q

What are some drug interactions and their potential adverse effects with CCB?

A

erythromycin, clarithromycin - increased risk of AKI in older adults
statins-reduce dose of CCB

47
Q

Compare beta blockers with ARBs, ACEi, CCB and thiazides; what is the outcome of BBs?

A

BBs do not reduce CV related outcomes. have higher rates of adverse events due to adverse effects

48
Q

A 65 year old man presents with an ongoing BP of 150/80 what would be your next steps?

A

continue assessment, offer treatment, thiazide diueretic first

49
Q

What are the risk of aiming for a BP <130SBP?

A

increased CV risks and adverse effects

smaller ARR in CV events (1-2% )

50
Q

What is the difference between primary and secondary prevention of cardiovascular disease?

A

primary- no prev. hx or CVD

secondary- hx of MI or unstable angina

51
Q

What are the hard and soft endpoints/goals for those on statin therapy?

A

hard: decreased all cause mortality, decreased major cornoary events
soft: no hispitalizations, revascularize

52
Q

Discuss statin clinical trials (who was in it, what was excluded)

A

male, middle age, caucasian particpants
less represented women, ethnic groups
excluded: non compliant, non adherent, intolrated statins or unresponsive to statins

53
Q

discuss the overall evidence of statins in the use of primary prevention. in the female population? in older populations?

A

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
Q

describe the overall evidence of statins in the use of secondary prevention.

A

**secondary prevention- someone who has a history of unstable angina or MI
MCE ARR 3.8%
ACM ARR 1.8%

55
Q

Statins should be offered to patients who have a recent MI, regardlless of their LDL leve

A

FYI

56
Q

Would you start someone who is a diabetic on statins? if yes, why, if no, why?

A

probably not if they do not have a secondary coronary disease or cardiovascular disease
risk scores to assess whether they need a statin

57
Q

Why would you not start a patient on a statin based on their LDL-C levels?

A

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
Q

What is the evidence surrounding choosing a statin>

A

not one is better than the otehr

look at tolerabilty, patient cost, drug interactions

59
Q

What antibiotic increases statin doses and should be avoided?

A

macrolides

60
Q

Which statin has the least amount of drug interactions?

A

pravastatin

61
Q

Which are high potency statins? low potency?

A

high potency- atorvastatin, rosuvastatin
low potency- everything else
neither is superior to another

62
Q

What are the dosing strategies of statins? and which are supported by evidence?

A

fixed dose
treat to target
LDL targets
evidece based: fixed dose; no evidece to treat to target or LDL-C

63
Q

What are some common drug interactions with statins? And how would we minimize these interactions?

A

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
Q

What are the adverse effects of statins?

A

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
Q

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

A

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
Q

What is the mechanism of action of statins?

A

inhibits the HmG-CoG

interrupts cholesterol pathway=cannot build up fatty levels of cholesterol in the body

67
Q

What do statins do to lipids and lipoprotein levels

A

decreases LDL

decreaed tryglycerides, increases HDL

68
Q

What is the mechanism of action of ezetrimibe?

A

stops absorption of cholesterol in the GI tract

69
Q

What is the mechansim of action of resins?

A

binds to bile acids and prevents reabsorption of bile acids (which is needed for the cholesterol pathway)

70
Q

What is angina pectoris?

A

aka stable angina
when the heart doesn’t receive enough oxygen
ususally caused by CAD
manifests as tightness, squeezing to the chest

71
Q

What are some pharmacological treatments for angina pectoris?

A

nitrates- venodilator -encourages O2 perfusion to the heart
beta blockers- decreases heart rate, contractility and BP
CCB-controls HR, contractility
Antiplatelets-stablizes plaque

72
Q

Describe the monitoring for side effects of amiodarone.

A

monitor liver enzymes at baseline and q 6 months–can cause elevated AST, ALT

Thyroid function tests-can cause hypothyroidism, hyperthyroidism

73
Q

Describe the management of a patient with atrial fibrillation who is controlled by rate and anticoagulation alone.

A

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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