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Pharmacology > Final Exam > Flashcards

Final Exam Flashcards

1
Q

Major pathophysiological characteristics of asthma

A

airway narrowing & inflammation mostly in medium-sized bronchi
airway hyperresponsiveness
Th2 cell response

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2
Q

Th2 high inflammation asthma

A

early onset allergic asthma, adult-onset eosinophilic nonallergic asthma, & exercised-induced
respond well to inhaled corticosteroids (ICS), monoclonal antibodies to IgE, and Th2-targeted therapeutics

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3
Q

adult-onset eosinophilic nonallergic asthma

A

chronic sinusitis, nasal polyps, exacerbated by aspirin
high eosinophils in sputum & blood
tx= ICD & IL-5 monoclonal antibodies

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4
Q

nonallergic, Th2 low asthma

A

severe adult onset
high neutrophils in sputum
triggered by= URI, pollution, smoke. Obesity worsens
*Poor response to ICS

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5
Q

preferred method of measuring expiratory flow to dx asthma > 5 y/o

A

spirometry (* may be normal if asx)
peak expiratory flow can be used if needed

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6
Q

3 things to measure asthma control

A

freq/severity of sx
use of SABA
impact on life (restricting activity? impacting sleep?)

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7
Q

non-pharm interventions for asthma sx control

A

no smoking
physical activity; warm up & take SABA 5-20 min before
occupational exposure
stop NSAIDs if worsen sx
beta blocker to cardioselective
allergens
weight loss, avoid sulfites (beer, wine, shrimp, dried fruit)
vaccinations (flu, covid)
emotions
weather
outdoor pollen/allergens ***all patients w/ asthma tested for allergens

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8
Q

long term/maintenance med classes for asthma

A

inhaled corticosteroids (ICS)
inhaled long-acting beta agonists (LABA)
oral leukotriene receptor antagonists (LTRA)
inhaled long acting muscarinic antagonists (LAMA)
biologic agents

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9
Q

quick relief meds for asthma

A

short acting beta agonist (SABA)
ICS-formoterol (steroid + LABA)
short acting muscarinic antagonist (SAMA)
short bursts of systemic corticosteroids

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10
Q

theophylline’s place in asthma/COPD therapy & why fallen out of favor?

A

higher risk of SE and not recommended; weak efficacy.
nausea and other gastrointestinal disturbances, cardiac arrhythmias, and CNS excitation, leading to a narrow therapeutic window.

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11
Q

who qualifies for ICS tx in asthma

A

all people w/ persistent asthma at least 2 days each month

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12
Q

ICS dosing considerations

A

flat dose-response curve
smoking decreases response
2 weeks of therapy needed to see significant clinical effects

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13
Q

ICS adverse effects & interactions

A

oral candidiasis
cough
dysphonia
pneumonia in high dose
long term- decreased BMD, adrenal suppression
genetic variant causes wide range of response to ICS

interaction= cushings & adrenal insufficiency when potent inhibitors of CYP3A4 (ritonavir, itraconazole, ketoconazole) with high dose ICS so avoid

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14
Q

last line for asthma tx

A

systemic corticosteroids when all other add on tx options have been expended
assess barriers to asthma control before adding

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15
Q

when are LABAs (long acting inhaled beta 2 agonists) used for asthma & ex

A

acts as bronchodilator
add-on maintenance not controlled on ICS alone
as effective as doubling ICS dose or adding LTRA
**black box= NEVER used alone w/o ICS bc risk exacerbations/death

ex- salmeterol, formoterol, vilanterol

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16
Q

LAMAs (long acting muscarinic antagonists)
mech. of action, indication, SE, ex (w/ onset/duration)

A

mechanism of action: inhibit acetylcholine effect on muscarinic receptors in airways and protect against cholinergic mediated bronchoconstriction

indication: uncontrolled asthma, already taking ICS or ICS & LABA

SE=(think anticholinergic) urinary retention, dry mouth, HA, URI

ex: tiotropium bromide; onset 30 min x24 hr; umeclidinium

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17
Q

LTRA (leukotriene receptor antagonists)
mech. of action, indication, SE & interactions

A

mech. of action= anti-inflammatory that either inhibit 5-lipoxygenase or antagonize leukotriene D4 effects. Oral med so convenient but significantly less effective than ICS

indication= steroid sparing; *beneficial for asthma + allergic rhinitis, aspirin sensitivity, exercise-induced bronchospasm

SE = **black box warning serious mental health SE for montelukast; neuropysch SE (sleep disorder, aggression, suicide)
hepatotoxicity (zileuton & zafirlukast)
CYP 2C9 metabolism= drug interactions

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18
Q

biologic agents for asthma indication & action

A

poor sx control despite all recommendations
target Th2 inflammation to reduce steroid use, fewer exacerbations, improved lung function

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19
Q

anti-IgE monoclonal antibody for asthma
action, indication, SE, ex

A

omalizumab

action= inhibits binding of IgE to receptors on mast cells & basophils that decreases inflammation & allergic response

indication= mod-severe asthma, not controlled on ICS, positive skin test or reactivity to aeroallergens & high IgE

SE= injection site reaction, anaphylaxis rare but possible so *monitor x2 hours x3 months then reduce to 30 min. *rx epinephrine

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20
Q

IL-5 & IL-5R antagonist monoclonal antibody
indication, action, SE, ex

A

indication= severe exacerbations, high eosinophils
action= prevention of eosinophils
ex= mepolizumab, reslizumab, benralizumab
SE= nasopharyngitis, HA, hypersensitivity, worse asthma, URI. Long term effects unknown

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21
Q

IL-4 receptor alpha antagonist monoclonal antibody
indication, action, SE, ex

A

dupilumab
high IgE and eosinophil count
inhibit IL-4 and IL-13 signaling in Th2 inflammation
SE= injection site pain, transient blood eosinophilia

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22
Q

macrolides & asthma
indication, action, ex

A

azithromycin 500mg 3x/week decreases asthma sx
uncontrolled medium-high dose ICS/LABA
benefits from anti-inflammatory NOT antimicrobial properties
tx x6 months

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23
Q

SABAs for asthma
indication, action, use, SE, ex

A

action= reverse acute airway obstruction d/t bronchoconstriction & block early-phase response to antigen in asthma exacerbation. Increase mucociliary clearance and stabilize mast cell membranes. PRN only, not scheduled
onset < 5 min, lasts 4-6 hours

indication= asthma exacerbation; use with ICS

use= 4-10 puffs Q20 min up to 1 hour in severe acute exacerbation. Shouldn’t have repeated use over 1-2 days

SE= use without ICS increases risk of death, reduced lung function, urgent healthcare!
tachycardia, tremor, hypokalemia

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24
Q

ICS (budesonide)-formoterol

A

low dose ICS-formoterol as maintenance and reliever therapy (MART) is recommended for all adolescents and adults (80/4.5 mcg); maxium dose of formoterol 72 mcg

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25
Q

I.C.E

A

ICE= inhaler technique, compliance, environment
evaluate at every step of asthma control

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26
Q

when can asthma severity be determined

A

severity can only be determined once asthma is controlled and the individual is utilizing their lowest effective dose

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27
Q

short-acting muscarinic antagonists (SAMA)
onset/duration, indication

A

ipratropium bromide (MDI or neb)
onset 15 min, lasts 4-8 hrs
add to SABA in mod-severe exacerbation in ED only

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28
Q

tx if acute asthma doesn’t respond to SABA

A

systemic corticosteroids
oral route > IV in acute asthma
5-7 days, no taper needed

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29
Q

tx chronic asthma, sx < 2/month

A

PRN low dose budesonide/formoterol or low dose ICS when SABA taken

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30
Q

tx asthma sx > or = 2 sx/month

A

low dose ICD w/ SABA PRN or PRN low dose ICS/formoterol

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31
Q

asthma sx most days or waking up d/t asthma at least 1x/week tx

A

low dose ICD/formoterol as controller & reliever or low dose ICD/LABA with PRN SABA or medium dose ICS with SABA

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32
Q

tx daily sx, waking up w/ sx 1x/week or more or FEV1 < 65%

A

high dose ICD w/ PRN SABA +- oral steroid burst or medium dose ICS/formoterol daily and PRN +- oral steroid burst

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33
Q

well-controlled, partly controlled and uncontrolled asthma

A

Sx in 1 month: daytime asthma sx > 2x/week, nighttime waking d/t asthma, reliever needed > 2x/week, activity limitation d/t asthma

well controlled= yes to NONE of the sx listed

partly controlled= yes to 1-2 of sx

uncontrolled= yes to 3-4 of sx

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34
Q

risk factors asthma exacerbations

A

uncontrolled sx
freq. use SABA
inadequate ICS
low FEV1 (esp. if < 60% predicted)
major psych/socioeconomic problems
exposures to smoke, allergens
comorbid: obesity, rhinosinusitis, food allergy
sputum/blood eosinophilia, elevated FeNO
pregnancy
hx intubation or tx ICU for asthma
1+ severe exacerbations in past 12 months

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35
Q

intermittent asthma characteristics and tx

A

infrequent trigger exposure (ex. exercise induced); still have chronic inflammation

preferred tx: ICS/formoterol PRN or PRN SABA w/ low dose ICS. Can use SABA alone but increased risk of severe exacerbations

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36
Q

tx for moderate persistent asthma

A

single maintenance and reliever therapy (SMART) of ICS/formoterol (both control & reliever)

addition of LAMA, biologic agents, and/or oral steroids may be considered if unable to control on SMART alone

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37
Q

what is step up asthma therapy mean

A

control-based tx, meds adjusted in continuous cycle w/ assessment, tx, review
f/u 1-3 months after change to regimen
always assess adherence and technique

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38
Q

when to step down asthma therapy

A

monitor Q3-12 months, step down once control maintained x3 months
gradual decrease; if too quick can increase risk of serious exacerbation even if sx are still controlled

*taper down ICS dose by 25%-50% at 3 month intervals
complete d/c of ICS not recommended

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39
Q

for asthma exacerbations, what to do if adherence to ICS is a problem

A

increase ICS dose during acute exacerbations

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40
Q

what to do if worsening asthma sx persist x48 hr

A

add oral steroid

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41
Q

parts of asthma self management action plan

A

corticosteroid rx for exacerbation PRN
PEF (daily in am or when sx worsen) for mod/severe persistent asthma w/ poor perception or unexplained response

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42
Q

PEF asthma plan

A

personal best PEF over 2-3 week period when receiving optimal tx
subsequent are compared to personal best
80-100% of personal best means therapy acceptable
50-79% of personal best means impending exacerbation
< 50% of personal best means medical alert, use PRN immediately, steroids, go to ER

PEF alone not used to determine severity of airflow limitation bc poor technique or inflammation of small airways in severe exacerbation that PEF can’t detect

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43
Q

Dx of COPD

A

Spirometry is required to make a clinical diagnosis of COPD. The presence of a post-
bronchodilator FEV1/FVC < 0.70 confirms the presence of persistent airflow limitation
and of COPD

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44
Q

genetic factor in COPD

A

rare hereditary deficiency of alpha 1 antitrypsin (AAT) can cause premature/accelerate emphysema

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45
Q

COPD patho

A

repeated exposure to noxious particles/gas= chronic inflammation= patho change central/peripheral airways, lung parenchyma, pulmonary vasculature= obstruction. Imbalance proteases & antiproteases in lungs and oxidative stress

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46
Q

do all smokers develop COPD

A

no but all have inflammation

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47
Q

difference between asthma & COPD inflammation

A

asthma= inflammation from eosinophils and mast cells
COPD= inflammation from neutrophils, macrophages, CD8+ T lymphocytes. Some w/ COPD have eosinophils & respond better to bronchodilators & corticosteroids, may indicate co asthma

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48
Q

GOLD category of severity COPD based on FEV1

A

GOLD 1 mild= 80% predicted or greater
GOLD 2 moderate- 50% to 79% predicted
GOLD 3 severe= 30% to 49% predicted
GOLD 4 very severe= less than 30% predicted

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49
Q

what to use for COPD sx assessment

A

CAT
score of 10 or more need inhaled long acing bronchodilators

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50
Q

COPD treatment domain grades

A

A= low risk, less sx, GOLD 1-2, <= 1 exacerbation/year, mMRC 0-1, CAT < 10

B= low risk, more sx, GOLD 1-2, <= 1 exacerbation/year, mMRC >= 2, CAT >= 10

C= high risk, less sx, GOLD 3-4, >= 2 exacerbations/year, mMRC 0-1, CAT < 10

D= high risk, more sx, GOLD 3-4, >= 2 exacerbations/year, mMRC >= 2, CAT >= 10

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51
Q

what’s the only intervention proven to slow decline of FEV1 & slow COPD progression

A

smoking cessation
no meds shown to modify progressive decline in lung function or prolong survival

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52
Q

considered 1st line tx COPD (though GOLD doesn’t distinguish)

A

LAMA (long acting anticholingergics)

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53
Q

recommended labs COPD

A

CBC (elevated hct > 55% d/t polycythemia)
AAT level
ABGs if pulse ox < 92%

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54
Q

how to address smoking cessation in COPD

A

encourage every visit; “5 As” :

Ask: identify/document tobacco use status
Advise: strongly urge to quit
Assess: Is user willing to attempt to quit?
Assist: use counceling/pharm to help pt willing to quit
Arrange: scheduled f/u preferably within first week of quit date

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55
Q

pulmonary rehab

A

within 2 weeks of hospitalization
2x/week x6-8 weeks
max tolerated load or interval & strength training, education, self management interventions aimed at behavior change

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56
Q

when O2 in COPD

A

stable COPD with PsO2 <= 55 mm Hg, or O2 sat <= 88%, or evidence pulmonary HTN/edema d/t HF/polycythemia

ABGs after 60-90 days

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57
Q

Mainstay tx for symptomatic COPD

A

bronchodilators PRN or scheduled
increase FEV1, reduce sx, reduce freq/severity exacerbations/hospital, improve exercise tol., pulmonary rehab efficacy, and health status

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58
Q

adverse effects SABA & LABA

A

dose related
palpitations, tachycardia, cough, hypokalemia, sleep disturbance, tremor

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59
Q

ex antimuscarinics

A

ipratropium, tiotropium, aclidinium, glycopyrrolate
promote bronchodilation, decrease mucus
not one better than other

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60
Q

LABA or LAMA mod-very severe COPD

A

LAMA more effective at reducing exacerbations/hospital, fewer adverse effects

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61
Q

methylxanthine/theophylline & COPD

A

limited use d/t narrow therapeutic index, drug interact, questionable efficacy, adverse effects
reserved for those who cant use inhaled meds or still sx after appropriate bronchodilators

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62
Q

methylxanthine/theophylline interractions/adverse effects

A

interacts (through CYP450) with age, tobacco smoke (induce metabolism & increase clearance), and marijuana

SE: HA, heartburn, insomnia, tachycardia, palpitations, tremor
Dose-related= n/v, seizures, arryhthmias

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63
Q

tx COPD group a

A

few sx, low exacerbation risk

bronchodilator (SABA)

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64
Q

tx COPD group b

A

more sx, low exacerbation risk

LABA or LAMA

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65
Q

tx COPD group c

A

few sx, high exacerbation risk

LAMA

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66
Q

tx COPD group D

A

more sx, high exacerbation risk

LAMA or LAMA + LABA or ICS + LABA

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67
Q

when to use ICS in COPD

A

mod-very severe COPD w/ increased exacerbation risk, not controlled by first line (LAMA)
prevents exacerbations when high serum eosinophils

*monotherapy not recommended. Combine with LABA

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68
Q

phosphodiesterase-4 (PDE-4) inhibitor in COPD

A

Roflumilast (oral)
reduce inflammation
severe-very severe COPD associated w/ bronchitis & h/o exacerbations
little effect on sx/quality of life
SE: diarrhea, nausea, weight loss, HA, insomnia, low appetite, abdominal pain, neuropsych effects

*avoid in underweight & depression

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69
Q

med with pneumonia risk COPD

A

ICS

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70
Q

combination therapy COPD

A

when not responding to monotherapy
LAMA/LABA preferred
triple LAMA/LABA/ICS reduce mortality in severe-very severe

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71
Q

vaccines for COPD

A

annual flu
PPSV23 regardless of age
PCV13 > 65 and/or comorbidities/immunocompromised/smoker

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72
Q

tx for all AAT deficient COPD pt

A

alpha 1 augmentation therapy

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73
Q

other pharm meds for COPD

A

N-acetylcysteine= mucolytic

*prophylaxis w/ macrolides (azithromycin); greatest benefits in smokers

anti-interleukin-5 monoclonal antibodies (mepolizumab) with triple therapy

vitamin D if low levels

beta blockers for cardioprotection

chinese medicines when added to standard regimen

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74
Q

meds for COPD exacerbation

A

*SABA with or w/o ipratropium is standard
d/c LAMA if using ipratropium d/t anticholinergic effects

systemic corticosteroids esp w/ high serum eosinophils

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75
Q

ABX in COPD exacerbation

A

use when increased sputum purulence & volume or increased dyspnea or all, or patients who need mechanical vent.

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76
Q

“other” tx COPD exacerbation

A

thromboprophylaxis
fluids
higher risk of repeat exacerbation or cardio event after exacerbation

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77
Q

what’s allergic rhinitis (AR) and other term used to describe d/t common concurrent sx

A

allergen-induced IgE mediated inflammatory condition of the lining of the nose and upper respiratory tract

aka allergic rhinoconjunctivitis d/t ocular sx

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78
Q

4 approaches to tx for AR (allergic rhinitis)

A

avoidance of allergen triggers
patient/caregiver education
pharmacotherapy
immunotherapy

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79
Q

goals of tx of AR (since NO “cure”)

A

min. freq/severity of sx
prevent comorbid disorders (ex asthma)
improve QOL
improve work/school performance/attendance
min. adverse effects of tx

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80
Q

non-pharm. tx AR

A

*avoid triggers
nasal saline

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81
Q

first line and second line tx AR

A

1: intranasal corticosteroids for mod-severe persistent and oral antihistamines for mild intermittent

2 (sometime first in certain pt): oral decongestants, intranasal mast cell stabilizer (cromolyn), intranasal antimuscarinic (ipratropium) and intranasal saline irrigation

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82
Q

why intranasal steroid for AR tx

A

anti-inflammatory most effective to treat nasal congestion (inflammation in late phase AR)

recommended as MONOTHERAPY vs combo w/ antihist. initially

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83
Q

INCS examples, onset, duration, administration

A

not one better than the other
fluticasone, budesonide, ciclesonide, mometasone, triamcinolone
onset 3-4 hr but up to 12 hr so use regularly. Max fax can be delayed 14 days
if severe nasal congestion IN may not be effective d/t limited exposure to nasal mucosa

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84
Q

INCS admin technique and SE

A

head down, spray lateral away from septum to prevent septum irritation & med down esophagus
SE: dryness irritation, burning, mild epistaxis, RARE nasal septum perforation
systemic SE concern: adrenal suppression, osteoporosis, ocular effects

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85
Q

INCS admin technique and SE

A

head down, spray lateral away from septum to prevent septum irritation & med down esophagus
SE: dryness irritation, burning, mild epistaxis, RARE nasal septum perforation
systemic SE concern: adrenal suppression, osteoporosis, ocular effects

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86
Q

antihistamines for AR

A

histamine 1 (H1) receptors; inverse agonists
little effect on nasal congestion
onset 1-2 hours for oral 15 min nasal
first & second generation oral
IN are second generation, need rx, anti-inflammatory effects: azelastine and olopatadine, SE bitter taste.

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87
Q

first vs second generation antihistamines

A

1st generation= 6 chemical classes from diphenhydramine > chlorpheniramine. do not routinely use d/t CNS & antimuscarinic SE (caution in elderly & w/ other meds with SE)

2nd generation= cetirizine, loratadine, acrivastine; less antimuscarinic SE. Not 1 superior to another
*need adjustment w/ renal impairment
* effective alone for mild or intermittent AR; preferred d/t fewer SE

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88
Q

what if on antihistamine for AR but persistent nasal congestion

A

add decongestant
maybe use oral w/ IN
or mod-sever seasonal AR use both INCS and IN antihistamine

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89
Q

oral decongestants
onset SE & contraindications

A

onset: oral 30 min, IN 5-10 min

SE: CNS or cardiovascular d/t SNS stimulation so HTN, insomnia, nervousness, irritability, anxiety, tremor, HA, hallucinations, decreased appetite
IN SE: persistent rebound congestion rhinitis medicamentosa **only use x3 days*

contraindicated (oral):
cardiac hx > use IN decongestant instead
BPH & other bladder outlet conditions can have increased urinary retention
DM
hypothyroidism
glaucoma esp closed angle

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90
Q

mast cell stabilizer for AR

A

cromolyn (OTC IN product)
less effective than INCAS, oral and IN antihistamines
helps early & late effects of AR
onset 4-7 days but not maximal until 2 weeks; can be PRN if episodic

well tolerated; burning sneezing bad taste nosebleed
FOUR times daily
**best in pediatric & pregnant with mild or intermittent sx

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91
Q

leukotriene receptor antagonist for AR

A

montelukast
For AR reserved for pt who can’t tolerate/don’t respond to first line tx
recommended over antihistamines in perennial AR
better for nasal congestion and rhinorrhea
SE: neuropsych, HA, GI, rash

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92
Q

antimuscarinic agent for AR

A

ipratropium IN spray
reserved for those whose rhinorrhea not controlled by other therapy

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93
Q

tx of AR in children

A

USE: second gen. antihistamine and/or INCS, montelukast chewable option, IN ipratropium in unresponsive > 5, *cromolyn mild or intermittent d/t excellent safety

avoid combo meds > unintentional OD
no first generation antihistamines

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94
Q

tx AR in pregnancy

A

USE: nasal saline, physical exercise, external nasal strip, 2nd gen. antihistamines generally safe, cromolyn safe but less efficacious

AVOID: oral decongestants, not a lot of data on fetal risk w/ INCS

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95
Q

BP value to start pharmacologic tx to lower BP if h/o CAD, DM or CKD, PCE score for CVD risk >= 10%, or greater than 65

A

SBP >= 130-140, DBP >= 80-90
for above 65 y/o SBP >= 130 warrants tx

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96
Q

when to start pharm. tx to lower BP in person w/o comorbid. or age >= 65

A

SBP >= 140 or DBP >= 90

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97
Q

how long to wait between each antihypertensive drug change

A

2 weeks for full effect

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98
Q

what class of med can be used at any stage of HTN if indicated

A

beta blocker

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99
Q

when to start TWO antihypertensive drugs for HTN

A

dual therapy for stage 2 HTN > 160/100

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100
Q

two med classes known to be more effective as initial antiHTN therapy in older people and blacks

A

thiazide and CCB

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101
Q

what population to try to avoid diuretic for HTN & what to use instead

A

younger patients to avoid long term exposure to metabolic side effects of diuretics
use CCB instead
also consider metabolic effects of beta blockers

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102
Q

what to avoid for HTN tx in advance CKD

A

potassium sparing diuretics (ex spironolactone); refer to specialist if > 3 drugs required at max dose

103
Q

step care approach to initiation/titration of antihypertensive meds (1-4)

A

Step 1:
ACE or ARB
or
CCB or
thiazide diuretic

Step 2:
ACE or ARB plus
CCB or thiazide

Step 3:
ACE or ARB plus
CCB plus
thiazide

Step 4:
ACE or ARB plus
CCB plus
thiazide plus
spironolactone

104
Q

antihypertensives to avoid in pregnancy and child bearing age

A

ACE inhibitors and ARBs or d/c as soon as pregnancy dx

105
Q

diuretic for significant kidney dysfunction

A

loop diuretic instead of thiazide

106
Q

4 classes of antihypertensives (ABCD) and two categories

A

ACE/ARB, beta blockers, CCB, diuretics

category 1 (AB)= block RAAS
category 2 (CD)= other pathways

combo between two categories more potent than combo from within one category

107
Q

normal, elevated, stage 1, stage 2 hypetension

A

normal < 120 AND < 80
elevated 120-129 AND < 80
stage 1= 130-139 OR 80-89
stage 2= >= 140 OR >= 90

108
Q

tx elevated BP (120-129/<80)

A

nonpharm therapy
reassess 3-6 months

109
Q

tx stage 1 HTN (130-139/80-89) if ASCVD risk < 10% or greater than 10%

A

less than 10% nonpharm therapy reassess 3-6 months

> = 10% risk nonpharm. AND antihypertensive med, reassess in 1 month, if goal not met assess adherence then consider intensification

110
Q

resistant HTN

A

failure to achieve BP goals despite adherence to optimal doses of THREE meds of diff. classes (one usually diuretic) OR need 4+ meds
screen for secondary causes

111
Q

non pharm tx HTN

A

rarely sufficient to reach goal BP
lower dietary Na (2.4g) increase K intake
low fat diet (esp. saturated), high fruits/veggies
weight reduction
physical activity
mod ETOH consumption
smoking cessation

112
Q

who gets greater benefit from Na restriction

A

low PRA (salt sensitive), DM, metabolic syndrome, CKD, older, black

113
Q

first line diuretics baseline initial therapy for HTN

A

thiazide esp. chlorthalidone (more potent that HCTZ)

114
Q

metabolic SE thiazides

A

hyperlipidemia, hyperglycemia, low K, low Mg, hyperuricemia, hypercalcemia

if CrCl < 30 loop diuretic indicated

115
Q

loop diuretic admin for HTN

A

BID except torsemide which is QD d/t long half life

116
Q

SE loop diuretics

A

excessive diuresis > low Na and hypotension
low K, low Mg, low Ca

117
Q

ex K sparing diuretics and SE

A

triamteren and amiloride
SE: high K especially w/ renal impairment, NSAIDs, K supplements, or ACE/ARBs which spare K

118
Q

aldosterone antagonists for HTN- properties, ex, SE

A

spironolactone, eplerenone
K sparing effects; helpful in resistant HTN

SE: hyperkalemia esp in renal impairment or ACE/ARB, NSAIDs, salt substitutes (contain K)
gynecomastia

119
Q

beta blockers for HTN indication, contraindication

A

NOT first line tx for HTN; lack positive outcomes in elderly. CYP2D6 metabolism

good for comorbidities: CAD, HFrEF, recent MI

contraindicated= asthma or COPD and PVD if non selective
usually avoid in DM, block ssx hypoglycemia
avoid w/ diuretics usually

120
Q

non selective, selective, vasodilatory beta blockers

A

non selective= propranolol, timolol, nadolol
selective= metoprolol, atenolol, bisoprolol
vasodilatory= labetolol, carvedilol

121
Q

CCB for HTN
indication, first line (dihydropyridine vs nondihydropyridine), ex, SE

A

effective esp. in elderly & blacks
coronary vasodilatory properties so also good for angina

first line= dihydropyridine CCB nifedipine and amlodipine BUT associated w/ edema; okay to give if dx HF but not routinely recommended

nondihydropyridine= verapamil, diltiazem negative inotropic effects block cardiac conduction good for a-fib + HTN. AVOID in LVEF

122
Q

anihypertensive for HTN + angina or dysrhythmia like a fib

A

CCB

123
Q

first line for HTN w/ DM, HF, MI, CKD, stroke

A

ACEi

124
Q

ACEi indication for HTN, SE,

A

inhibition of angiotensin II synthesis = reduces artery tone and changes intraglomerular pressure (lowers GFR; d/c or reduce if GFR > 30% lower)
more effective for HTN when given diuretic
don’t combine with ARB for HTN

first line for HTN w/ DM, HF, MI, CKD, stroke
SE: high K, persistent dry cough, less common= kidney injury, angioedema esp in black/caribbean origin

125
Q

Angiotensin receptor blockers (ARBs) for HTN

A

more effective for HTN when given diuretic
don’t combine with ACEi for HTN
SE angioedema

126
Q

renin inhibitor for HTN

A

aliskiren

127
Q

alpha 1 blocker for HTN

A

doxazosin, terazosin, prazosin
NOT used as monotherapy!
add-on (4th/5th line)
**Usually combine with thiazide to min. edema from fluid/Na retention

indicated for elderly men w/ prostatism

SE: dizzy, palps, syncope r/t orthostatic hypotension, priapism, vivid dreams, depression, asthenia

doxazosin= increased cardiovascular and cerebrovascular events

128
Q

central alpha 2 agonists indication, mech. of action, SE

A

clonidine, methyldopa, guanfacine, guanabenz
limited use d/t SE but good for pregnancy or add-on in resistance

mech. of action: reduce sympathetic outflow increase parasympathetic

SE: orthostasis, sedation, dry mouth, vision disturbances, rebound HTN w/ abrupt d/c of clonidine

129
Q

direct vasodilators for HTN

A

hydralazine and minoxidil
resistant HTN; relax smooth muscle
***admin w/ betta blockers and diuretics d/t tachycardia and fluid retention
SE: pericardial effusion, T wave change, hypertrichosis

130
Q

HTN and angina tx

A

beta blockers or long acting CCB

131
Q

HTN post MI tx

A

esp. with reduced LVEF
beta blockers and ACEi/ARB

aldosterone antagonists if reduced LVEF and DM or HF sx

132
Q

HTN tx with HF

A

BP target < 130/80
beta blockers, ACEi/ARBs, aldosterone antagonists aka mineralocorticoid receptor antagonists
diuretics only if evidence of fluid volume overload for sx relief

*****Blacks= combo isosorbide dinitrate and hydralazine

133
Q

HTN tx with DM but no CKD

A

depends if black or not

black= thiazide or CCB or both; consider ACEi/ARB if albuminuria cr

non-black= ACEi/ARB, thiazide, CCB

134
Q

HTN tx if CKD

A

ACEi/ARB to slow progression of renal disease
ACEi w/ thiazide if ho stroke/TIA

135
Q

HTN tx with a fib

A

ARB or nondihydropyridine CCB= verapamil, diltiazem negative inotropic effects block cardiac conduction good for a-fib + HTN

136
Q

HTN tx considerations if age > 65

A

lower starting doses d/t SE esp. postural hypotension
avoid rapid volume depletion and titration

137
Q

population with diminished response to ACEi/ARB

A

blacks (better w/ diuretics and CCB)
Asians should use RAASi and CCB with/without diuretic

138
Q

antihypertensive med for pregnancy

A

preferred= methyldopa, nifedipine, labetalol
fetal risk can’t be r/o

139
Q

right side vs left side HF sx

A

right= systemic congestion
left= pulmonary sx

140
Q

what controls HR

A

ANS > sympathetic stimulation of beta adrenergic receptors= increased HR so increased CO

141
Q

preload

A

measure of ventricular filling pressure at end of diastole r/t volume of blood in LV before systole
determined by venous return, ventricular relaxation, atrial contraction

142
Q

heart contractility

A

inotropic state of heart; intrinsic property of cardiac muscle incorporating fiber shortening and tension development
influenced by adrenergic nerve activity & circulating catecholamines epi/norepi

143
Q

compensatory mechanisms that worsen HF

A
  1. preload & frank-starling mechanism
    - decreased CO > RAAS > increase fluid/Na to increase CO but heart can’t contract fully and increased preload worsens CO
  2. tachycardia and increased afterload
    - low CO > increased HR from SNS norepi on beta adrenergic receptors > increased CO acutely then increased cardiac O2 demand> ischemia, proarrythmia, further impair
  3. cardiac remodeling and ventricular hypertrophy
    - regulated by angiotensin II and aldosterone; change in size/shape of heart to maintain CO
    - hypertrophy = growth of myocytes. Reduce cardiac stress acutely but then leads to myocyte death d/t increased O2 demand. Contributes to diastolic dysfunction
144
Q

RAAS and SNS in HF

A

vasoconstriction to redistribute blood but increases afterload (resistance to ventricular ejection) so maladaptive = further decrease in CO, cont. stim of compensatory response, cycle of neurohormonal activation

145
Q

neurohormonal activation to compensate for decreased CO in HF

A

RAAS, SNS, endothelin, vasopressin, natriuretic peptides, nitric oxide

146
Q

angiotensin II

A

vasoconstriction to increase vascular resistance and BP

147
Q

aldosterone

A

released from adrenal glands;
sodium and water retention, electrolyte abnormalities (low K & Mg)= increased arrhythmias
causes SNS stimulation

148
Q

norepinephrine

A

SNS activation; adaptive role in HF by increasing HR and contractility and mediate vasoconstriction
cardiotoxic & risk for arrythmia & ischemia
contribute to hypertrophy/remodeling
elevated in proportion of HF severity

149
Q

endothelin

A

vasocontrictor
meds failed to improve outcomes in HFrEF

150
Q

arginine vasopressin

A

vasoconstriction & trophic effects on heart, free water retention
hyponatremia
meds failed to improve HFrEF prognosis

151
Q

Natriuretic peptides ANP & BNP

A

regulate Na/water balance
released when cardiac chamber wall stretched
BNP biomarker for HF

152
Q

bradykinin

A

linked to RAAS through ACE
vasodilatory peptide, elevated in HF

153
Q

nitric oxide

A

vasodilatory hormone from endothelium, high in HF

154
Q

antihypertensives that can precipitate or exacerbate HF

A

antiarrythmics (disopyramide, dronedarone, etc)
beta blockers
CCB

155
Q

HF classifications per NYHA and ACC/AHA
functional class (numbers) can reverse, staging (letters) does not reverse

A

N/a // A = risk w/o structural heart disease or sx

I // B,C = structural heart disease w/o limitation of activity or sx HF. Ordinary physical activity doesn’t cause sx

II // C = structural heart disease, slight limitation in activity or sx HF. Ordinary activity= fatigue, palps, dyspnea, angina

III // C = structural heart disease w/ marked limitation in activity. Comfortable at rest, less than ordinary activity = sx

IV // C,D = structural heart disease that results in inability to carry on activity w/o discomfort, sx at rest. D is end-stage HF

156
Q

goals of tx of HF overall & per stage

A

no cure; prevent/reduce sx, hospitalizations, slow progression, improve QOL, prolong survival

157
Q

goals of tx of HF overall & per stage

A

no cure; prevent/reduce sx, hospitalizations, slow progression, improve QOL, prolong survival

A= risk factor control to reduce onset
B= pharm. to reduce further damage/slow progression
C= additional therapies for sx and decrease morbidity/mortality
D= shifts toward palliative care and QOL issues

158
Q

most common etiology of HF

A

ischemic heart disease

159
Q

pharm. therapy by HF stage

A

A= reduce risk, antihypertensives, lipid lowering, ACEi/ARB
B= ACEi/ARB, beta blockers
C= diuretics and ACEi/ARB, ARNI (Sacubitril/valsartan ), beta blockers, aldosterone receptor antagonist. Blacks may not respond to ACEi/ARB, use hydralazine & isosorbide dinitrate. Can add digoxin & ivabradine for sx
D= mechanical support, transplant, continuous IV vasoactive therapies

160
Q

diuretics in HF

A

used for relief of acute sx of congestion and maintenance of euvolemia. Morbidity not mortality. Lowest effective dose. Dose based on sx/fluid
all pt with sx volume overload
can be PRN if mild congestion but scheduled if persistent

thiazide and loop

thiazides weaker so NOT monotherapy usually for mild congestion; not used with impaired renal function

**Loop mostly used in HF; retain function in impaired renal function. Each is equally effective. Torsemide if don’t respond to furosemide

161
Q

maximal response to diuretics in HF

A

reduced; ceiling dose where there’s limited added benefit
d/t diuretic resistance bc of compensatory increase in Na absorption
aside from increasing dose, increase frequency to 2-3x/day or combine loop with thiazide (metolazone most often)

162
Q

Diuretic SE/concerns w/ HF

A

hypokalemia > arrhythmia & death
hypomagnesemia
renal insufficiency d/t overdiuresis
reduction in renal flow amplified if take ACEi/ARB too

163
Q

neurohormonal agents for HF

A

ACEi, ARBs, beta blockers, aldosterone receptor antagonists

164
Q

what should all patients at risk for HF regardless of sx receive

A

ACEi

165
Q

ACEi for HF (mech. of action, contraindications, SE)

A

no one better than another
slows progression
RAAS, slow breakdown bradykinin= vasodilation

absolute contraindications: h/o angioedema, bilateral renal artery stenosis, preganancy
relative: unilateral renal artery stenosis, renal insufficiency, hypotension, hyperkalemia, cough
can either help or worsen renal function depending; if increases Cr/BUN, hold or decrease diuretic

risk of hypotension esp w/ initiation and dose increase; hold diuretic

166
Q

thiazide or loop diuretic for HF

A

Loop
rarely will increasing the dose of a thiazide diuretic be sufficient to treat
symptoms of volume overload in HF.

No edema= no diuretic

167
Q

how are meds dosed for HF

A

target doses (those that were proven to minimize mortality in clinical trials)
if cannot tolerate, then highest tolerated dose

*targeting high ACEi dose should not prevent starting beta blocker or aldosterone receptor antagonist on the grounds of limited BP
*ACEi have target dose, but benefit even at lower doses for ALL heart failure pts.

168
Q

how are meds for HF titrated

A

up over several weeks based on tolerability

169
Q

ARBs for HF

A

second-line despite equivalent benefit to ACEi d/t ACEi having more clinical trial experience
no cough bc doesn’t induce bradykinin like ACEi

can be considered if angioedema w/ ACEi but carefully d/t potential cross-sensitivity

monitor renal function, BP, K

170
Q

what tx if HF patient intolerant or contraindicated to ARBs or ACEi

A

hydralazine and isosorbide dinitrate

171
Q

sacubitril/valsartan in HF

A

angiotensin receptor/neprilysin inhibitor (ARNI)
sacubitril needs to be combined with ARB so there’s not elevated angiotensin II

***warranted in pt with symptomatic HFrEF who are tolerating ACEi or ARB. That should be replaced with sacubitril/valsartan

more risk of hypotension; contraindicated for use with ACEi d/t angioedema risk. *36 hr washout period needed when switching

172
Q

hydralazine and isosorbide dinitrate in HF

A

isosorbide dinitrate is a nitrate
cause vasodilation to reduce preload

hydralazine reduces afterload through smooth muscle relaxation

nitric oxide beneficial in HF; blacks respond well likely d/t imbalance nitric oxide production

consider as add on for black patient already on ACEi or ARB

low doses, titrate to target based on tolerability

SE: HA, hypotension, tachycardia, dose-dependent risk for lupus with hydralazine

173
Q

beta adrenergic antagonists for HF

A

aka beta blockers
block SNS effect at beta adrenergic receptors which outweighs acute neg. inotropic effects if used judiciously

***initiate in all HF patients class I-IV or stage B-D if stable
mortality reduction for metoprolol succ. (selective) and carvedilol (non selective)

*Low dose, Slow titration over weeks to months when stable and euvolemic
volume overload at time of beta blocker initiation increases risk of worse sx

may cause short term worsening HF sx

carvedilol lowers BP more and greater risk of dizziness/hypotension

174
Q

what if patient started on beta blocker gets mild congestion

A

increase diuretic
if severe, reduction of dose considered

175
Q

ACEi and beta blocker for HF dosing

A

low doses of both= greater benefit that high dose of only one drug class

176
Q

mineralcorticoid receptor antagonists (MRAs) for HF

A

spironolactone and eplerenone
inhibit aldosterone that produce weak diuretic effects while sparing K

eplerenone doesn’t have endocrine adverse effects

use bc suppress aldosterone not for diuretic;

*recommended in symptomatic pt LVEF <= 35% or post MI w/ LVEF <= 40% w/ sx or DM

SE= hyperkalemia, gynecomastia, menstrual irregularities

177
Q

digoxin for HF

A

positive inotropic effects; increase intracellular Na thus increased Ca during systole
reduces hospitalization but not survival
numerous adverse effects and toxicity is concern
concentration should be below 1

*indicated to decrease hospitalizations in pt remain sx despite tx

may help to slow rate with a fib and HF but beta blocker more effective

serum drug monitoring with changes in renal function, suspected toxicity, addition/subtraction interacting drug

178
Q

digoxin toxicity

A

nonspecific- fatigue weakness
CNS: delirium, confusion, psychosis
GI: n/v anorexia
visual disturbances
arrhythmias
electrolyte disturbances: hypokalemia, hypomagnesemia, hypercalcemia

179
Q

Ivabradine for HF

A

HFrEF with elevated resting HR > 70, LVEF <= 35%, class II and III, NSR, max tolerated doses or contraindication to beta blocker
lowers HR w/o effecting BP or contractility

180
Q

CCB for HF

A

nondihydropyridine (diltiazem & verapamil) worsen HF

dihydropyridine (amlodipine and felodipine) are ok for HFrEF but not routinely recommended
use for angina or uncontrolled HTN

181
Q

anticoagulants for HF

A

aspirin can increase hospitalization d/t interaction with RAAS inhibitors; only use with ischemic etiology

warfarin preferred and non vitamin K anticoag. if compelling indication like a fib
based on individual factors

182
Q

pathological cause ischemic heart disease (IHD) & sx

A

stenosis in coronary arteries = ischemia/decreased O2 blood to heart muscle
vasospasms worsen (Prinzmetal angina= spasms w/o significant plaque; uncommon)

sx: angina, non ST elevation MI, ST elevation MI
since r/t increased O2 demand not acute change in supply, typically angina d/t stress or exercise

183
Q

risk factors IHD

A

modifiable: HTN, DM, dyslipidemia, cigarettes, EOTH, obesity BMI > 30, low fruit/veggies

nonmod: men >= 45, women >= 55, men & postmenopausal women, family hx

184
Q

HF + IHD + HTN tx

A

Patients with conditions such as IHD often have multiple comorbidities. Evaluation and treatment of these patients require comprehensive management. BBs have demonstrated benefits and should be part of all patients’ therapy with stable HF. The caveat was that only metoprolol succinate, carvedilol, and bisoprolol are approved for use in HF. Therapy of IHD recommends BB as first line therapy (barring contraindications). Contemporary clinical outcomes have demonstrated superiority with carvedilol, but in general the only BB that should not be used are those with ISA. Considering both conditions then, it would be prudent to choose
a BB beneficial for both conditions (metoprolol succinate, carvedilol and bisoprolol).

beta blocker can’t be initiated if acute HF, needs to be stabilized first; low dose, slow titration d/t risk of initial worsening HF sx

185
Q

what to do for IHD if patient on beta blocker, still sx, resting HR 55-60

A

Beta blockers are considered first line therapy and should be dosed to a
resting HR of 55-60 BPM. If the patient is still symptomatic at that HR, then doses
cannot be increased, but rather an additional agent (usually a DHP CCB) is added.

186
Q

goals of tx of IHD

A

prevent ACS & death
alleviate angina sx
prevent recurrent angina
prevent progression of disease
reduce complications
avoid/min tx SE

187
Q

first-line tx for primary/secondary prevention in IHD

A

lifestyle mod
statins (regardless of lipids) or HMG-CoA reductase inhibitors
ACEi or ARB
antiplatelet therapy (aspirin)
beta blocker especially in HFrEF or h/o MI

188
Q

why ACEi for IHD

A

vasculoprotective effects (anti-inflammatory, anitplatelet, improved endothelial function, arterial compliance/tone)

189
Q

when to initiate aspirin and P2Y12 (clopidogrel; dual antiplatelet therapy) in IHD

A

recent ACS, stent placement

190
Q

tx for prinzmetal or variant angina

A

if high BP= CCB
if low BP= long acting nitrate

191
Q

alternative to beta blocker in IHD

A

if high BP= CCB
if low BP or low HR= long acting nitrate

192
Q

dosing of meds in IHD

A

start low, care uptitration PRN to control sx or cardiovascular risk factors

193
Q

who gets high vs mod intensity statin therapy & add on for IHD

A

high intensity= pretty much everyone; esp. very high risk ADCVD d/t h/o ASCVD event or multiple high risk conditions
mod to high in pt. >= 75 y/o

ezetimibe if ASCVD on max statin LDL > 70

194
Q

who with IHD should receive antihypertensive therapy & first line

A

BP >= 130/80

ACEi, ARBs, beta blockers w/o ISA

195
Q

If IHD & BP still high despite first line tx & has angina, what do you add

A

dihydropyridine CCB (nifedipine and amlodipine)

196
Q

dihydropyridine CCB

A

nifedipine and amlodipine)

197
Q

nondihydropyridine CCB

A

diltiazem and verapamil

198
Q

If IHD & BP still high despite first line tx & DOES NOT have angina, what do you add

A

dihydropyridine CCB, thiazide, and/or mineralcorticoid receptor antagonists (MRA)

*think about steps to HTN tx

199
Q

meds recommended for DM with IHD

A

**#1 (regardless of A1C) GLP-1 receptor agonists liraglutide, semaglutide, dulaglutide
or
SGLT2i empagliflozin, canagliflozin

200
Q

aspirin in IHD

A

all pt with IHD esp. if h/o MI w/o contraindications
75mg-162mg
if contraindicated/not tolerated, use alternative like clopidogrel

201
Q

what can alter effectiveness of P2Y12 clopidogrel

A

pt on meds that lower CYP2C19 activity like PPI

202
Q

what ACEi for IHD

A

ramipril or perindopril

203
Q

first line tx of acute sx angina

A

short acting nitrates
but not initial monotherapy

204
Q

nitrates for angina in IHD
mech of action, onset/duration/administration, contraindication, SE

A

venodilation to reduce preload which reduces O2 demand and relief of sx
higher doses reduce afterload and BP
relieve vasospasms
can be given 2-5 min before activity to prevent angina

onset 1-3 min. Repeat Q5 min x3 or until sx resolve. Last x30 min. Isosorbide dinitrate lasts 2 hrs.

SE: standing= lightheaded, dizzy, hypotension

**contraindication= use of phosphodiesterase type 5 inhibitor (sildenafil, vardenafil, tadalafil) bc risk of significant hypotension and reduced cardiac perfusion. Don’t take within 24-48 hours!!

205
Q

nitrate pt education on admin

A

seated position
911 if sx don’t improve/worsen x5 min after first dose
keep in original glass container, tighten
repeated use not harmful

206
Q

what drugs prevent ischemic sx in IHD

A

beta blockers, CCB, nitrates, ranolazine
*no evidence that these improve survival

207
Q

what med for initial therapy to prevent angina in IHD

A

beta blockers in absence of contraindications esp. h/o MI or HFrEF

208
Q

beta blockers for IHD dosing considerations & contraindications

A

low initial dose, titration based off sx/response
dose to resting HR 55-60
max HR w/ exercise 100 or less or 20 beats above resting

contraindications: HR < 50, AV conduction defects, caution w/ meds that suppress AV conduction (digoxin, verapamil, diltiazem)

relative contraindications: asthma, COPD, severe depression

**Caution w/ DM, may mask tachycardia/tremor w/ hypoglycemia. Also alter glucose metabolism if insulin dependent

209
Q

CCB in IHD

A

recommended in IHD when beta blockers contraindicated or not tolerated. Can be used in combo if beta blockers alone unsuccessful
*more effective in unpredictable angina r/t spasms!

inhibits Ca into smooth muscle > less contraction > vasodilation and reduced afterload (reduce cardiac O2 demand)

***nondihydropyridines verapamil & diltiazem have neg chronotropic effects so better for angina!!! reminder dihydropyridines better for HF

better to avoid short acting!

contraindication to verapamil & diltiazem= bradycardia and conduction disease; also not good in HF

210
Q

combo beta blocker and CCB in IHD

A

long acting dihydropyridine CCB recommended d/t risk bradycardia and AV block

211
Q

what population to avoid CCB

A

HFrEF; can exacerbate d/t neg inotropic effects
amlodipine and felodipine exceptions

212
Q

long acting nitrates for IHD

A

limited d/t tolerance with continuous use; loss of antianginal effects within 24 hr
best way to avoid= 8-12 hr intervals w/o nitrate use (when sleeping)

SE: hypotension, dizzy, flushing, HA
tx with APAP, resolves with cont. use

213
Q

why is monotherapy with nitrates for prevention of ischemia in IHD avoided and what is needed?
when can it be used as monotherapy?

A

increase sympathetic response/HR > increase O2 demand secondary to nitrate venodilation

**add to baseline therapy with beta blocker or CCB or combo of both

can be used if baseline low BP or sx hypotension with low dose BB/CCB

214
Q

ranolazine for IHD

A

anti-ischemic agent, unknown action
reduced angina, increases exercise capacity but doesn’t reduce incidence of Major adverse cardiovascular events (MACE)

*min. effect on BP/HR so option if low at baseline
*expensive!!! so reserved for those who don’t respond to first line

SE: prolonged QT, dizziness, constipation, HA, nausea

contraindications: hepatic disease, digoxin, cyclosporin, should lower statin/metformin, CYP3A4 meds: ketoconazole, clarithromycin, phenytoin, carbamazepine

215
Q

pharm with no benefit or cause harm in IHD

A

hormone replacement, folic acid, antioxidants, st. johns wort
COX-2i & NSAIDs increase risk MI and stroke

216
Q

4 statin benefit groups for dyslipidemia? Who falls into groups and recommendation for each?

A
  1. established ASCVD risk (secondary prevention)
    -high intensity statin, no PCE risk estimator needed
  2. primary prevention w/ high LDL 190+
    -high intensity statin, no PCE risk estimator needed
  3. primary prevention w/ DM, age 40-75 regardless of LDL
    -moderate intensity statin
  4. primary prevention w/o DM, age 40-75, 10 year ASCVD risk 7.5% +, LDL 70-189
    - check CAC score; usually high intensity
217
Q

desirable cholesterol, LDL, HDL, triglycerides

A

Cholesterol < 200
non HDL < 130
LDL < 100 (aim for < 70 in high risk)
HDL > 60 (low would be < 40 in men < 50 women)
TG < 150

218
Q

nonpharmacologic tx dyslipidemia

A

plant stanols/sterols & fiber
weight loss
exercise >= 150 min/week mod intensity, 75 min vigorous
dietary cholesterol < 200
reduced trams and saturated fats

219
Q

PCE risk groups for ASCVD

A

low risk < 5%
borderline 5-7.4%
intermediate 7.5-19.9%
high > 20%

220
Q

high, moderate, low intensity statin doses and expected decrease in LDL

A

high (>= 50%)
atorvastatin 40mg target 80mg
rosuvastatin 20mg target 40 mg

moderate (30-49%)
atorvastatin 10mg target 20mg
rosuvastatin 5mg target 10mg
simvastatin 20-40mg
pravastatin 40mg target 80mg
lovastatin 40mg target 80mg
fluvastatin 80mg
pitavastatin 1-4mg

low (< 30%)
simvastatin 10mg
pravastatin 10-20mg
lovastatin 20mg
fluvastatin 20-40mg

221
Q

When to add ezetimibe or PCSK9i to statin

A

50% reduction goal in ASCVD not met or LDL remains > 70

222
Q

risk of having and tx high triglycerides

A

TG >500 risk of pancreatitis esp. if > 1000. Tg primary target for intervention
reduce fats/carbs, no ETOH, weight, exercise
goal reduce < 150

> 1000 niacin, fibrates, OM3FA
500-999 triglyceride lowering agent or statin
AVOID bile sequestrants if TG 300+
200-499 *statins first line

223
Q

statins (HMG-CoA reductase inhibitors) for dyslipidemia

A

preferred med
reduce ASCVD risk and mortality
usually taken in PM when produce most cholesterol (atorvastatin, rosuvastatin anytime)
well-tolerated
CYP450 metabolism (except pravastatin and pitavastatin)
takes 4-6 weeks for max effect

224
Q

adverse effects statins & who’s at higher risk

A

elevated LFT, statin-associated muscle sx (SAMS): rhabdo., myopathy, myalgia

obtain baseline LFTs and CK

higher risk for SAMS: small body, DM, CKD, periop., multi meds like fibrates, cyclosporine, azoles, macrolifes, verapamil, amiodarone, grapefruit juice, ETOH abuse

r/o secondary causes: vit D deficiency, hypothyroidism, muscle disorders

other SE: high A1c, may cause DM, memory loss, confusion. Cardiac benefit usually outweighs risk

225
Q

how to handle SAMS

A

screen Q6-12 weeks after start/change med and each visit

CK level if sx (muscle pain, weak, tender, brown urine)
if CK < 3x upper limit of normal, cont. statin & monitor
CK > 3x normal but < 10x cont. if mild sx, repeat CK x1 week
CK increasing, statin d/c, CK reassessed when sx resolve
CK > 10x normal, stop statin, fluids
CK > 40x normal= rhabdo so ER, risk ARF

226
Q

cholesterol absorption inhibitors for dyslipidemia

A

ezetimibe
reduces LDL by 18%, TG 7-9%, mod increase HDL
usually used as add on to statin when reductions not achieved or intol. of statins
2 weeks for max effect
contraindicated in liver disease or unexplained elevated LFT

227
Q

bile acid sequestrants/resins for dyslipidemia

A

cholestyramine, colestipol, colesevelam (“coles-“)
lower LDL only and may even increase triglycerides
usually adjunct to statins if ezetimibe and PCSK9i not option or can’t tolerate statin

they aren’t absorbed so GI effects- flatulence, bloating, constipation
*can inhibit absorption of other drugs (digoxin, warfarin, thyroxine, thiazides, beta blockers, fat soluble vitamins, folic acid) take 1 hr before or 4 hr after

228
Q

ATP citrate lyase inhibitors for dyslipidemia

A

bempedoic acid
reduces LDL 15-25% and up to 38% when with ezetimibe

indicated for use WITH ezetimibe for familial HeFH or need additional LDL lowering agent after max statin
SE: increase uric acid

229
Q

niacin for dyslipidemia

A

aka B3
limited d/t SE: flushing, hepatotoxicity, pruritus
aspirin or NSAID 30 prior or w/ food, avoid hot liquid & EOTH, slow titration, can reduce flushing & pruritus
suppls. labeled “no flush” pointless/ineffective for lowering LDL

230
Q

fibrates for dyslipidemia

A

gemfibrozil
decrease triglycerides 20-60%, increase HDL 9-30%. *most effective at lowering TG
primarily used for high TG/low HDL

SE: dyspepsia, abd. pain, diarrhea, flatulence, rash, muscle pain, fatigue, cholecystitis, elevated LFTs. DO NOT increase glucose or uric acid like niacin, risk of bleeding with warfarin
with statin or renal insufficiency SAMS can occur

CK & LFTs before therapy & if sx. Increased INR if take warfarin

contraindicated: avoid if renal dysfunction eGFR < 30, gallbladder disease, liver dysfunction

231
Q

OM3FA for dyslipidemia

A

lower triglycerides 45%
DHA in it can increase LDL but EPA lowers

232
Q

microsomal triglyceride transport inhibitors for dyslipidemia

A

lomitapide
when with max lipid med, lowers LDL 40%
SE: GI, elevated LFT
risk of hepatotoxicity so need REMS program
pregnancy category X

233
Q

antisense oligonucleotide inhibitor of Apo B-100 sythesis for dyslipidemia

A

mipomersen
1x/week SQ injection
when with max lipid med, lowers LDL 25%
risk of hepatotoxicity so need REMS program
pregnancy risk B

234
Q

PCSK9 inhibitors for dyslipidemia

A

alirocumab and evolocumab
SQ human monoclonal antibodies
reduce LDL 48-71% with statins

**add to max tolerated satin in very high risk ASCVD; add ezetimibe first d/t cost

235
Q

metabolic syndrome

A

elevated waist circumference (truncal obesity)
elevated TG >150
low HDL < 40 men < 50 women
high BP > 130/85
high fasting glucose >= 100

236
Q

Heparin mech. of action, clotting factor inhibition, how is therapy monitored/adjusted? Labs?

A

UFH > LMWH in renal pt CrCl < 30

UFH:
rapid anticoag. in acute VTE
augments natural anticoagulant AT (antithrombin)
dose correlated with pt weight
*achieve therapeutic aPTT within 24h; other labs: whole blood clotting time, ACT, antifactor Xa, plasma heparin concentration. h/h, BP, platelets.
close monitoring, periodic adjustment
antidote= protamine sulfate

LMWH (dalteparin & enoxaparin/Lovenox):
improved properties; more predictable anticoag.
mediated through pentasaccharide sequence that binds to AT
not as much monitoring/dose changes
CBC; sometimes antifactor Xa activity measurement needed if underweight, obese, or renal impair.
can admin at home/outpatient uncomplicated VTE
***pregnancy; don’t cross placenta; NEED to monitor Xa activity Q4-6 weeks

237
Q

Heparin vs LMWHs and fondaparinux

A
238
Q

Mech. of action warfarin, clotting factor inhibition, how it initiated/monitored/adjusted? Labs?

A

use decreased in favor to DOACs
inhibits production of vitamin K-dependent coag. factors (prothrombin & others) and anticoag. proteins.

*no effect on circulating coag. factors & antithrombotic activity delayed 5-7 days!!!

**Need overlap w/ heparin, LMWH, or fondaparinux bc paradoxical hypercoag. state first few days!

metabolism in liver CYP & varies greatly between pts. Genotype info recommended.

dose depends on response through freq. labs; adjustments based on weekly dose

adjusted for INR 2-3; INR Q2-3 days x1 week then weekly then Q2 weeks, Q4-6 weeks
consider pt related influences on dose too

SE: bleeding, necrosis, purple toe syndrome, teratogenic

239
Q

Why is warfarin initiation overlapped with either heparin or LMWHs when initiated?

A

warfarin doesn’t achieve antithrombotic effect for several days
paradoxical hypercoag. state first few days!

overlap x5 days until INR 2+ for 24-48 hrs

240
Q

How to manage elevated INR w/ warfarin

A

vitamin K
if life-threatening bleeding fresh-frozen plasma

241
Q

Significant interactions w/ warfarin (rx & OTC)

A

pharmacokinetic
change in hepatic metabolism or binding to plasma protein

pharmacodynamic
enhance/diminish effect of warfarin but don’t alter INR

increase effect:
APAP
amiodarone
ETOH
ABX
fluoxetine, sertraline, fluvoxamine
flu vaccine
omeprazole
testosterone
cranberry
garlic
ginger
celery
onion
parsley
tumeric

lower effect:
sucralfate
ETOH
phenytoin, phenobarbital, carbamazepine
st john’s wort
green tea
ginseng
coQ10

bleeding risk:
ASA, NSAID
clopidogrel
LMWH, heparin

242
Q

When are antiplatelets like aspirin indicated? Alternative if sensitive to ASA?

A

IHD

243
Q

oral direct thrombin inhibitors and oral direct Xa inhibitors (DOACs) indication/MOA/monitoring

A

Xa inhibitors (rivaroxaban, apixaban) for hip/knee replacement, superior to LMWH. No lab monitoring or dosing adjustments, oral admin.

oral direct thrombin inhibitors (DTI) dabigatran for hip replacement only. Can’t be used CrCl < 30 or with P-gp

244
Q

oral direct thrombin inhibitors (DTI) and oral direct Xa inhibitors (NOACs) compared to warfarin

A
245
Q

who should receive VTE prophylaxis

A

patients with mod-high risk VTE unless contraindicated

246
Q

drug with most protection against VTE in medical pt and major ortho surgery pt

A

low molecular weight heparins (LMWHs) when compared to unfractionated heparin (UH) and warfarin

247
Q

approved meds to prevent VTE in hospitalized general med/surg pt

A

UFH 5000 unit SQ Q8-12h
enoxaparin 40mg SQ daily
dalteparin 2500-5000 units SQ daily
fondaparinux 2.5mg SQ daily
also betrixaban

248
Q

prevent of VTE following MAJOR ortho surgery

A

UFH, **LMWH, **fondaparinux, adjusted dose warfarin, asa, direct oral anticoags (apixaban, dabigatran, edoxaban, rivaroxaban)

249
Q

how long VTE prophylaxis for total knee, hip or hip fx repair?

A

Minimum 10-14 days but extend to 35 d/t VTE risk up to 1 month

250
Q

factor Xa inhibitors for VTE (parenteral & oral aka DOAC)

A

parenteral: fondaparinux
indirect inhibitor of factor Xa, anticoag activity by accelerating AT
SQ daily; anticoag x2-4 days after d/c
No routine monitoring/dose adjust
few drug interactions; don’t affect platelets
Help w/ tx and alternative if pt has HIT bc not affecting by heparin antibodies

oral aka direct oral anticoagulants (DOACs) : apixaban, rivaroxaban, edoxaban, betrixaban
VTE/PE tx
monotherapy, NO NEED for parenteral overlap
warfarin better as preventing death d/t VTE, these lower bleeding risk
no routine monitoring/dose adjust; aPTT, INR, PT have no place in therapy
take w/ food, avoid with renal impairment

251
Q

Direct thrombin inhibitors (DTIs) for VTE (parenteral & oral)

A

Bind to thrombin and prevent interactions w/ their substrates

parenteral: *drug of choice VTE + HIT
*argatroban, bivalirudin, desirudin, lepirudin
do not require AT unlike heparins; predictable

oral: dabigatron
**need overlap treatment w/ UFH & LMWH 5-10 days first
no monitoring/dose adjust needed
aPTT to monitor but not widely used

252
Q

**preferred tx for acute VTE tx and if CrCl < 30

A

LMWH or fondaparinux preferred over UFH unless CrCl < 30 then UFH preferred

253
Q

**preferred tx for long term/extended VTE tx phase

A

DOACs (rivaroxaban, apixaban)

254
Q

preferred tx for acute, long term, extended phase treatment for cancer related thrombosis

A

LMWH; ex: Enoxaparin (Lovenox)

Pharmacology (12 decks)

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