Nurs 605 Module 8 Flashcards
What does ACE inhibitor stand for?
Angiotensin converting enzyme inhibitr
Describe the mechanism of action for ACE inhibitors
inhibits conversion of angiotensin 1 to angiotensin 2
What are some adverse effects of ACE inhibitors and why do they occur?
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
What are the uses of ACE inhibitors?
hypertension
congestive heart failure
diabetic nephropathy
What are the benefits of using ACE inhibitors
decreased BP
relatively low cost
decreased morbidity and mortality
What does ARB stand for?
angiotensin receptor blocker
Describe the mechanism of action for ARBS
similar to ACE inhibitors
works to block the angiotensin II receptor
decreases vasopressin and aldosterone = lowered BP
When would you choose to use an ARB?
when ACE inhibitors are not tolerated
What are the risks of combining both ARBs and ACEIs?
can potentially place the patient in hypotension, synconpe
decreased renin levels
don’t combine them-risk outweighs the benefit
What are some adverse events associated with ARBs?
hyperkalemia
What are contraindications for use of ARBs?
not to be used in pregnancy
Which ethnic group is at greater risk of angioedema when using ACE inhibitors?
african american descent (5% increased risk of angioedema with ACEI)
When would you choose to use a beta blocker?
not used as first line treatment due for various side effects
can be used in heart failure patients
What is the mechanism of action of beta blockers?
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
What are the adverse effects of beta blockers?
edema-due to increased sodium and water retention
arrythmias- due to decreased contractility
decreased HR- due to decreased epinephrine
bronchospasms/dyspnea- due to bronchoconstriction
What are the contraindications of beta blockers
not to be used in those with asthma as drug can further cause bronchoconstriction
not to be used in those with heart blocks
What are the indications of use for beta blockers?
HTN (not first line)
heart failure
angina pectoris
Patients cannot abruptly stop beta blockers; what is the reason for this?
can lead to rebound tachycardia and arrythmias
should be tapered
Describe the mechanism of action of calcium channel blockers (CCB)
CCBs work on the calcium channels of the AV node to decrease AV conduction
disrupts movement of calcium through the calcium channels
Two sub classes of CCB; what are they and common drugs in that class
non dihydropyridine- diltiazem and veramipril
dihydropyridine- amlopidine, felodipine
What are adverse effects of CCB?
gingival hyperplasia
bradycardia, hypotension
constipation
peripheral edema
What are the contraindications of CCB?
heart failure
What are the uses of CCB?
HTN
angina pectoris
arrythmias
Describe the mechanism of action of thiazide diuretics
inihibits the reabsorption of sodium and calcium in the distal tubule
What allergy would a patient have if advised to avoid thiazides?
sulfa allergy
What are the uses of thiazides?
HTN
What is the first line drug in HTN?
usually thiazide or thiazide like medication
What are adverse effects of thiazides?
metabolic effects hyponatremia hyperglycemia hypouricemia hypokalemia
Discuss combination therapy in HTN
combination therapy is needed in approximately 50% of the population with HTN
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
In Canada, what is the recommended age and SBP when you would offer HTN tx?
> 160 SBP
>60 years of age with HTN
What does the evidence say about decreasing a SBP from 160 to 150? (ARRs)
all cause mortality 1.2%
CV related mortality 4.3%
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
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
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)
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
At what diastolic BP do we put patients at risk?
anything lower than DBP <60
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
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
After taking an initial dose of ramipril, what is the % of BP lowering effect?
60-70% after the first dose of ramipril
Is there a difference between ramipril and perindopril?
pharmacodynamics yes
clinicallly, no
both work similarly
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
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
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
Discuss peripheral edema in CCB
increases with continued dose
longer duration of drug will increase peripheral edema
peripheral edema is dose related
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
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
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
What are the risk of aiming for a BP <130SBP?
increased CV risks and adverse effects
smaller ARR in CV events (1-2% )
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
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
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
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
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%
Statins should be offered to patients who have a recent MI, regardlless of their LDL leve
FYI
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
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
What is the evidence surrounding choosing a statin>
not one is better than the otehr
look at tolerabilty, patient cost, drug interactions
What antibiotic increases statin doses and should be avoided?
macrolides
Which statin has the least amount of drug interactions?
pravastatin
Which are high potency statins? low potency?
high potency- atorvastatin, rosuvastatin
low potency- everything else
neither is superior to another
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
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)
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
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
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
What do statins do to lipids and lipoprotein levels
decreases LDL
decreaed tryglycerides, increases HDL
What is the mechanism of action of ezetrimibe?
stops absorption of cholesterol in the GI tract
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)
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
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
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
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)
