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Pharm > Quiz 3 > Flashcards

Quiz 3 Flashcards

1
Q

Cytochrome P-450 Nomenclature

A
  • CYP2D6
    • CYP=cytochrome P-450
    • 2=family (40% homology)
    • D=sub-family (55% homology)
    • 6=individual form
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2
Q

CYP2D6

A
  • met 25% clinical drugs
  • genetic polymorphism
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3
Q

Genetic Polymorphism

A
  • how quickly drugs met determined by amt of enz
    • poor
    • intermediate
    • efficient
    • ultrarapid
      • 5-10% whites
      • 0-2% blacks
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4
Q

Slow v. Fast Metabolizers

A
  • based on amt of 2D6 d/t gen polymorphism
  • primarily 2D6, others to lesser
  • Fast met never reach MEC
  • Slow met tox build-up
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5
Q

Newborn Metabolism

A
  • not metabolically competent
  • extra-utero liver dev
  • Gray Baby Syndrome: chloramphenicol tox d/t poor glucuronidation
    • virtually no phase-2 enz
    • build up to tox levels
  • Fetal met poor overall - only CYP3A sub-fam
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6
Q

Elderly Metabolism

A
  • dim met and excretion
  • dim enz induction
  • multiple drugs (avg 10 inpatient)
  • dose using escalation strategy
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7
Q

LFT’s

A
  • AST/ALT from hep cell destruction
    • tell about destruction - NOT fx
    • adv cirrhotic liver dz - normal LFT’s because not much left to destroy
  • Albumin - dec -> dec in fx
  • Conj bili - inc unconj bili -> dec in fx
  • Clotting factors - normal = good fx
  • No clinical test to determine how liver met drugs
    • =>dosing escalation strategy
      • look for effects v tox of drugs
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8
Q

Disease State and Met

A
  • Recognize risk for poor met and dose less agressively, escalate
    • hepatitis, CA’s, etc
  • Fx dec w/ acute or chronic liver dz
  • Drug cleared by liver -> overdose danger
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9
Q

Gender diff in met

A
  • significance not well understood, gen dose same m/f
  • ex:
    • contraceptives - diff prob hormonally based
      • menses can effect Pkin
    • N-Demethylation of erythromycin f>m
    • Propanolol oxidation m>f
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10
Q

Preg met

A
  • smoking inc CYP1A sub-fam in placenta
  • poss profound induction
    • may need inc anticonvulsants (dec after delivery)
      • can be monitored with blood levels

*** Sz drugs/smoking/preg ***

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11
Q

Enzyme Induction

A
  • some prec drugs inc amt of enz that met other obj drugs
  • carbamazepine/tegretol enhances own met, inc in enz that met itself
    • dosage change alters liver capacity to met
  • larger doses of prec means larger changes in liver met/induction
    • higher doses more clin sig
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12
Q

Slow Onset/Slow Offset

A
  • onset: 5 days
  • max effect: 2 wks
  • offset: 3+ wks
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13
Q

Important Enz Inducers

A

Think sz drugs..

  • barbs
  • phenytoin
  • primidone
  • carbamazepine
  • rifampin (TB, potent)
  • ritonavir (AIDS, potent, tons of interactions)
  • smoking (1A family)
  • EtOH (chronic)
  • charbroiled meat (theophyline)

Look up pt other drugs!!

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14
Q

Enz Inhibition

A
  • most common reported drug/drug interaction
  • decrease activity of cytochrome P450 enz
  • inc plasma conc and pharm resp of obj drug
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15
Q

Pro-Drugs and induction/inhibition

A
  • reverse effects
  • ex: inh normally slows met of drug, raising levels
    • inh of pro-drug slows activation lowering level of active drug
  • ex: induction normally speeds met of drug, lowering levels
    • induction of pro-drug speeds activation speeding the increase of active drug production - poss tox
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16
Q

Fast Onset/Fast Offset

A
  • enz inh onset begins as prec reaches critical conc
    • max intensity within 24h
    • offset usually within 24h of d/c prec
  • need to recognize quickly for quick reversal
    • potentially more dangerous than slow - must recognize quickly
    • can be reversed quickly
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17
Q

Pharmacokinetic

A
  • change in plasma conc
  • as with ind and inh
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18
Q

Pharmacodynamic Interactions

A
  • no change in plasma conc, but change in the conc/effect relationship
  • 2 drugs, diff effect than either alone
    • ant - one inc hr, one decr
    • syn/additive therapeutic effects = desired
    • syn/additive adverse sfx - avoid
  • advantage when using drugs with different sfx
    • inc desired effect w/o increasing sfx
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19
Q

Additive CNS Depressant Effects

A

Usually not single drug at high amt, but additive effects

  • EtOH
  • analgesics
  • antihistamines
  • barbs
  • benzos
  • BB’s - esp propanolol, cross BBB
  • anticonvulsants
  • sedatives
  • phenothiazides
  • TCA’s
  • Anesthetics
  • m. relaxants
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20
Q

Additive Anticholinergic Effects

A
  • Drying effects, const, urinary ret, sedation
  • Drugs:
    • antipsychotics - haldoperidol
    • antidepressants - amitriptyline
    • antiparkinson - benztropine
    • anticholinergic - scopolamine
    • antispasmotic - dicyclomine
    • antihistamine - diphenhydramine
    • anxiolytics - benzo’s
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21
Q

ACh antagonist example

A
  • pt w/ Alz dim gets donepezil, cholinesterase inh, inc ACh
  • develops urinary incontinence, gets tolterodine, anticholinergic, blocks ACh
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22
Q

Ginkgo biloba

A
  • antiplatlet effects
  • inc bleeding w/ ASA, warfarin, ticlopidine, clopidogrel, dipyridamole
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23
Q

Ginseng

A
  • inc INR
  • warfarin
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24
Q

Kava

A
  • additive CNS depression
  • benzos, barbs, antipsychotics, EtOH
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25
Q

Garlic

A
  • antiplatlet
  • ASA, warfarin, ticlopidne, clopidogrel, dipyridamole
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26
Q

Ginger

A
  • potent thromboxane synthetase inh
  • warfarin
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27
Q

St. John’s Wort

A
  • MAOi
    • phenelzine - MAOi
    • pseudoephedrine/ephedra potentiated by MAOi
  • SSRI activity - seratonin overload
    • fluoxetine, paroxetine
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28
Q

Cardiac Output

A
  • HR x SV
  • SV
    • preload (forced in)
    • afterload (resistance)
    • contractility (inotropes)
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29
Q

Frank-Starling

A
  • inc preload stretches cardiac m, inc contractility
    • primary compensatory mec to inc CO
  • SV/preload (LVEDV/P)
    • normal fx in steep range where inc LVEDV/P has big inc in SV
    • LV dysfx curve is flatter, so LVEDV/P inc shows little inc in SV
      • eventually attempted preload inc backs up system to fluid volume overload = sx
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30
Q

Correlation of Sx/Hemodynamics in HF

A
  • Most/classic assumption: sx imply HD changes, improved sx imply HD improvement
  • Some: inc EF, sx remain OR dec EF, no sx
  • Cannot assume like -> 2 separate goals in tx
    • improve sx
    • improve HD
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31
Q

Causes of Death in HF

A
  • dec perfusion of vital organs
  • arrhythmias
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32
Q

Mech of CHF progression

A
  • cardiac remodeling = change in geometry of left ventricle
    • chamber dilation - more blood in, more CO, good thing
    • hypertrophy - more muscle inc strength, good thing
      • too much m dec compliance
    • spherical shape - inc contractile strength, good
      • over time inc mech strains, leaky valves
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33
Q

Causes of Cardiac Remodeling

A
  • Neurohormonal systems - these can be targeted with drugs
    • Ang II
    • NEPI
    • ALD
    • Natruiuretic peptides
    • Arginine Vasopressin
    • Endothelin
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34
Q

How to improve performance

A
  • short term sx benefit, no HD effects - in ICU, acutely ill
    • positive inotropes
    • dec impedence
      • relax peripheral vessels, vasodilators
  • slow remodeling process, dec risk of major cardiac event
    • ACEi, BB, experimental agents
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35
Q

NYHA Functional Classification

A
  • functional status at a point in time, sx control, not criteria for tx
    • sx = fatigue, dyspnea, palpatations, fluid overload/edema
  • Class I - no sx w/ normal activity
  • Class II - sx w/ normal activity
  • Class III - sx w/ less than normal activity, ok at rest
  • Class IV - sx at rest, inc discomfort w/ inc activity

Can move up and down classes, class II with illness -> class IV, back to class II when recover from illness

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36
Q

Criteria for evaluation of HF pts

A
  • functional status
  • fluid status
  • EF
  • other
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37
Q

Functional status criteria

A
  • NYHA Classification
  • Exercise testing during graded exercise
  • QOL instruments
  • Peak O2 consumption during graded exercise
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38
Q

Fluid status criteria

A

majority of sx associated with fluid overload

  • body wt
  • JVD
  • pulm/hep congestion/edema
  • peripheral edema (legs, abd, presacral)
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39
Q

EF criteria

A
  • single most important measurement - gold standars w/o cath
    • distinguish systolic HF from other processes
  • Quantitative measurement
    • Left vent EF
    • LV dimensions, geometry, thickness, regional motion, spherical changes
  • repeat w/ important changes in clinical status
40
Q

Other criteria

A
  • invasive HD testing
    • R heart cath
  • electrophysiologic testing - EP testing - give drug to cause arrhythmia and see which agent will treat this pt arrhythmia
  • neurohormonal eval - BNP ->fluid overload, preload
    • do not predict extent of damage
41
Q

Classification of HF

A
  • Tx guidelines focus here, where NYHA is sx control
  • AHA and ACC (college of cardiologists)
  • Stages A-D
42
Q

Stage A

A
  • at risk w/o structural changes or sx of HF
    • HTN #1 risk factor is long term HTN
    • Atherosclerosis
    • DM
    • Obesity
    • Met syndrome
    • Cardiotoxic drug use (adriomycin chemotherapy)
    • Family hx cardiomyopathy
43
Q

Stage B

A
  • Structural heart dz w/o sx HF (compensatory mechanisms)
    • previous MI
    • LV remodeling/hypertrophy or dec EF
    • asymptomatic valvular dz (mitral regurg or aortic stenosis)
44
Q

Stage C

A
  • struct dz w/ current or hx sx (SOB, edema, dyspnea, paroxysmal nocturnal dyspnea)
45
Q

Stage D

A
  • refractory HF requiring specialized intervetions
  • marked sx at rest despite max medical therapy
    • recurrently hospitalized/cannot be safely d/c’d w/o spec interventions
46
Q

HF Prevention

A
  • Prevent initial injury
    • treat hyperlip, sys/dia HTN, stop smoking
  • Prevent further injury
    • thrombolytic/angioplasty in AMI
    • ACEi or BB
    • ACEi and BB
  • Prevention of post-injury deterioration
    • ACEi
47
Q

Some therapeutic strategies

A
  • remove underlying cause - repair congenital defects, valvular lesions, treat HTN and endocarditis
  • remove precipitating cause - infections arrhythmias, drugs
  • control of HF state - dec workload, inc pump performance, control excess salt/water
  • avoid CCB’s (neg inotropes), NSAIDS, some antiarrhythmic agents
48
Q

Agents with no current role in HF

A
  • coenzyme Q10
  • carnitine
  • inosine
  • vitamins
  • growth hormone
49
Q

Rationale for diuretics

A
  • SV/preload curve is flat in range of sx
  • dec preload below sx range w/o sig dec in SV
  • similar preload dec in non-HF would drastically dec SV
  • MOA
    • block reabs Na from tubule system back into blood, therefore water
      • trap Na in tubule system and pee out with water
50
Q

Salt Restriction

A
  • max level of salt reduction that is tolerable to pt is goal
  • effects of diuretics can be overcome w/ high salt diet
  • no salt added in cooking or at table
51
Q

Thiazides

A
  • work at distal tubule
    • 5-8% of Na reabsorption here, so weak
  • not really used in HF
  • not effective w/ CrCl<30, as in HF w/ renal insufficiency
  • don’t work chronically as diuretics (2 wks), abs Na earlier than distal tubule
  • # 1 antihypertensive, not by dec volume though, mech unk
  • 25-50mg q day, start w/ 10mg in elderly
52
Q

Loop Diuretics

A
  • Block Na reabs in asc LOH
  • 20-25% dec reabs
  • work in mod-severe HF
  • work in RF (inc dose req)
  • high ceiling diuretics
    • HCTZ diminished returns
    • Loops diuresis inc w/ dose, up to causing renal failure
      • lasix 99% usage
      • 20-40 mg q 6-8h until diuresis ensues
      • give effective dose 1-2 qd to maintain edema control
53
Q

Diuretic ADR - Hypo K

A
  • hypokalemia - more V loss, more K loss
    • HF prone to hypoK d/t hyperALD
      • dec renal perf P results in kidney RAAS activation
      • hyperALD=hypoK, now adding drug that dec K
    • arrhythmias - d/t hi or lo K, #1 cause of death in HF
      • monitor K all the time
    • ass w/ lo Mg also - Mg involved in reabs of K
  • dig - can cause arrhythmias w/ lo K, so caution
    • dz state (HF->ALD->hypoK->arrhythmias)
    • diuretic (dec K)
    • adding dig inc arrhythmias w/ lo K = perfect storm for Ventricular Arrhythmias
54
Q

Hypo K tx/prevention

A
  • ACEi/ARB dec ALD and its K wasting effects
  • Spironolactone = ALD ant
  • K supplements or K sparing diuretics
    • caution w/ACEi (hyper K)
    • caution w/impaired renal fx
    • K dose 40-100mEq/day tx, 20 prevent
55
Q

Diuretic ADR - prerenal azotemia/hypotension

A
  • diuretic goal is to remove 1 kg/day
  • overaggressive diuresis depletes intravascular V, proximal tube reabs water and urea
  • prerenal azotemia is max goal for diuresis
  • BUN:Cr>10-20:1 -> dec dose
  • ARF is next step
  • normal mech is Alb to draw fluid from tiss d/t onc/osm P
56
Q

Diuretic Resistance

A
  • HF is most common setting for diuretic resistance
  1. slow abs in gut = dec Cmax - IV or inc PO dose
  2. inc tubular Na reabs - block reabs at 2 points, dramatic inc
    1. thiazide + furosemide (HCTZ potent in this combo)
    2. metolazone 5-10mg + furosemide
  3. Avoid NSAIDs - afferent dilation d/t prostaglandins, effect of NSAID is to dec filtrate to glom/tubules
    • can cause ARF in HF
57
Q

Diuretic money slide

A
  • inc urinary Na excretion, dec sx fluid retention
    • dec JVP, pulm congestion, ascites, peripheral edema, wt
  • improve cardiac fx by dec preload, which was too high for heart to handle effectively
  • inc exercise tolerance
  • effects not sustained in monotherapy, also need to treat remodeling aspect of dz
  • cannot sub ACEi for diuretic, will work initially because blocks ALD which is causing fluid retention
  • dose: too lo dim resp to ACEi, too hi hypotension and renal insufficiency w/ACEi
58
Q

When to use diuretics

A
  • pt w/ sx of volume overload
59
Q

Diuretics as monotherapy in HF

A
  • don’t do it.
  • even if sx improved/controlled
  • dec volume -> neurohormonal/RAAS activation
    • drives remodeling and dz progression long term
    • inc electrolyte depletion

—> malpractice

  • ACEi or BB w/ diuretic needed to offset remodeling changes
60
Q

Diuretic Initiation and Maintenance

A
  • low initial dose - 20-40mg qd furosemide
  • titrate to inc UO/dec wt 0.5-1 kg/day
  • loops preferred, esp in renal impairment and high fluid retention
  • goals of therapy:
    • reduce sx
    • eliminate physical signs of fluid retention
      • restore JVP toward normal
      • eliminate edema
61
Q

Angiotensin II effects

A
  1. Potent vasoconstrictor - inc afterload
  2. Causes norepi release - causes arrhythmias
  3. Causes ALD release - fluid retention
62
Q

ACE

A
  1. ang I -> ang II
  2. breaks down bradykinins
    • ACEi -> build up of bradykinins -> cough
      • use ARB to avoid cough
63
Q

ACEi’s

A
  • -prils
  • effects
    • dec sx - dyspnea
    • prolong exercise tol
    • dec hospitalization, ER
    • work in mild, mod, severe HF - inc LV EF
    • can be used in combo w/ other drugs - +/- digoxin, w/ diuretic to dec dose, ok w/BB’s
    • dec morb/mort - death, dz progression
64
Q

Who should be on an ACEi?

A
  • HF d/t LV systolic dysfx - unless unable to tolerate
  • any systolic dysfx
  • mild, mod, sev HF
  • LV EF <35-40%
  • w/ diuretic in fluid retention
  • ok w/ dig or BB
65
Q

ACEi cautions

A
  • Use w/ caution
    • SBP<80
    • Cr>3
    • bil renal art stenosis
    • K>5.5
  • Not used
    • previous life-threatening rxn like angioedema
    • pregnancy = teratogen
66
Q

ACEi initiation in HF

A
  • Assess fluid status, if depleted hold diuretic 24-48h
  • Dosing (start safe/low w/ captopril short acting, switch to = dose long acting once dosage established)
    • risk of hypotension 6.25mg captopril and monitor for 2h
      • (severe LV dysfx, SBP<100, Na<135)
    • >75yo 12.5mg captopril qd and titrate as tol
    • hypertensive 25mg captopril TID
    • others 12.5mg TID
  • 48h phone call - dizzy/weak?
  • 1 wk f/u visit - modify if +Cr 0.5, K>5.5, sx hypotension
  • 2-3wk titration to 150mg capt, 20mg enal/lisin qd =effective tx dose
67
Q

ACEi risk of hypotension

A
  • hypotension
    • most common ADR in HF, usually asymptomatic
    • concern w/dec renal fx, blurred vision, syncope - often w/init
    • more common w/ very active RAAS, hypoNa, recent rapid diuresis
    • w/ inc risk, hold diuretic 1-2 days
    • guideline states “all attempts should be made to continue ACEi” - Need RAAS blockade with ACEi or ARB
68
Q

ACEi risk of dec renal fx

A
  • in dec renal perfusion, GFR dep on ang-mediated efferent arteriole vasoconstriction
  • high risk in NYHA class IV, hypoNa, w/NSAIDs
  • mgt:
    • dec diuretic, try again
    • mild-mod azotemia may need to be accepted in order to continue ACEi in HF (not just HTN)
69
Q

ACEi risk of K retention

A
  • may cause cardiac conduction disturbances
  • highest risk w/
    • dec renal fx
    • K supplements
    • DM (dec renal fx)
70
Q

ACEi risk of cough

A
  • non-productive
  • disappears 1-2wks after d/c
  • recurs w/ rechallenge
    • switch to ARB
71
Q

ARB’s

A
  • -sartan
  • sfx, risks, hypotension, renal dysfx, hypoK… same as ACEi
  • no cough
  • possibly less risk of angioedema, but let someone else take that risk, may be malpractice
72
Q

BB’s

A
  • used to be contraindicated in HF, now drug of choice
    • neg chronotropes, poss neg inotropes, but…
  • block sympathetic NS effects…
    • vasoconstriction
    • cardiac hypertrophy
    • provoke arrhythmias
    • promote hypoK
  • protective benefit greater than neg risk of BB
    • so come with restrictions
  • sx benefit and dec m/m
73
Q

When to use BB’s

A
  • stable NYHA class II/III
    • class IV severly decomp, negs outweigh benefits
  • LV EF<34-40%
  • added to ACEi and diuretic
  • DM particularitly experience dec m/m, despite poss masking of hypoglycemia
74
Q

When not to use BB’s

A
  • bronchospastic dz - asthma, COPD w/bronchoconstrictive component
  • symptomatic brady
  • advanced HB - II/III
  • acutely decomp HF
    • req intense diuresis
    • req hospitalization
75
Q

Heart Block

A
  • 1st long PR
  • 2nd occasional dropped QRS
  • winkyback longer and longer PR interval til the drop
  • 3rd complete A/V separation
76
Q

BB init/maint

A
  • not class effect, only use…
  • start low w/
    • 3.125 carvedilol (also alpha1 ant)
    • 1.25 bisoprolol
    • 12.5 metoprolol SR
  • 2x dose q 2-4wks to highest tolerable dose
    • hypotension, brady, fluid retention, worsening HF
    • more improvement w/ higher doses
  • may need to back of ACEi to inc BB, then bring ACEi back
    • ACEi at tx dose, BB at highest tolerable
  • don’t mess with diuretic - d/t poss fluid ret, worsening HF
77
Q

BB risks

A
  • hypotension
    • carv d/t a1 block/vasodilation
      • more common w/ first or inc dose (react not overreact)
      • tolerance w/ continued use
    • dec ACEi temporarily
    • avoid fluid ret by maintaining diuretic dose
  • Fluid ret + worsening HF d/t neg effect on efficiency (neg chron/ino)
    • pulm/peripheral congestion
    • daily wt + adjust diuretic
    • optimize fluid status before starting BB
  • Brady/HB - usually asymptomatic, dose dependent, dec dose hr<50, 2/3 deg HB
78
Q

CCB’s

A
  • lack of evidence supporting efficacy
  • safety concerns esp verapamil - avoid in HF
  • known neg inotropes
  • no substantial benefits in HF
79
Q

Dig benefits

A
  • dec sx and improve clinical status
    • QOL
    • fx capacity, no effect on remodeling
    • exercise tolerance
  • no dec m/m, risk of death or hospitalization
80
Q

When to use dig

A
  • not replace other drugs, maximize then add to them for sx relief
  • early or late in therapy
  • preferred in Afib - dig dec ventricular response, Afib worsening HF, get rid of Afib, get rid of symptomatic HF
  • not in class I, ie not if no sx
81
Q

Dig init/maint

A
  • >70y, impaired renal fx, or really small
    • 0.125mg
  • otherwise 0.25mg
  • no data on optimal dose or serum conc
    • don’t get aggressive - may cause arrhythmias
  • serum level - only test if concerned about tox
82
Q

Dig risks

A
  • arrhythmias
  • GI sx
  • Neurologic complaints (halo?)
83
Q

Factors predisposing dig toxicity

A
  • hypoK
    • augmented cardiac effects
    • get arrhythmias in therapeutic range
    • intracellular K more important than serum K
  • hypoMg
  • met alk
  • hyperCa
  • underlying heart dz
  • hypoThy - altered dist, abs, renal excretion, R sensitivity
84
Q

Hydralazine-Nitrate Combo

A
  • option when ACEi intol
  • little evidence of either alone
  • many w/HF cannot tolerate sfx of doses used in clinical trials
  • hyd=art dil, nit=ven dil -> dec pre and afterload
    • orthostasis major concern
  • particular benefit shown to African-American pts
85
Q

Bidil

A
  • isosorbide dinitrate 20mg/hydralazine 37.5mg
    • $2 combo branded tab
    • $0.29 generic tabs
  • indication: tx HF as adjunct to std tx in self-identified black pts
    • improve survival
    • prolong time to hosp for HF
    • improve pt reported fx status
86
Q

Bidil trial

A
  • African-American Heart Failure Trial (A-HeFT)
    • double blind, placebo controlled
    • 1,050 self-id black pts w/ NYHA class II-IV HF
    • all continued std tx
    • trial halted d/t sig higher mortality in placebo group (10.2% v 6.2%)
    • 21% of pts d/c Bidil d/t adverse effects (placebo = 12%)
  • Concerns
    • proved Bidil add-on therapy works in blacks, which was already known, not that it doesn’t work in whites
    • “self-reported” blacks
    • AE’s - HA/severe HA, orthostatic dizziness
87
Q

ALD ant

A
  • spironolactone - NOT “K sparing diuretic” (only Amiloride and Triamterene), dif MoA
    • only works w/ high ALD levels (HF and chronic liver dz)
  • In class IV HF - was avoided as just one more drug to effect K
    • low dose (<25mg)
    • dec death/hosp
    • early term of study d/t unethical to withhold from control group
    • worse HF, higher ALD - the better it works
  • lactone ring - hormonal effects - gynecomastia, menstral irreg, ED, libido, hirsutism — Eplerenone doen’t have these sfx but cost more and only 10% see these sfx, would be overcharging 90%, sfx temporary
88
Q

Entresto

A
  • combo ARB and Neprilysin Inh = ARNI
    • valsartan + sacubitril
    • HFrEF
    • dec CV deaths, hosp, all cause mortality compared to enalapril (ACEi only)
    • deg amyloid peptides in brain - dimentia concern but outweighed by severe HF
89
Q

NP

A
  • Atrial and Brain = ANP and BNP
  • produced in response to inc LV filling in fluid overload
  • causes natriuresis + diuresis -> dec art P -> imp HD (wedge P)
    • not just a marker, works to alter overload state
90
Q

Nesiritide

A
  • synth BNP
  • +inotrope, great in HF w/ severe HD changes
    • dec dyspnea and wedge P (good)
  • $$, IV only, hypotension (bad)
  • no dec in m/m in HF, chronically
  • approved and used in acute decomp HF
91
Q

Omapatrilat

A
  • neprilysin inh and ACEi
    • inc NP by inh degradation
  • dec BP and inc HD (good)
  • inc freq/sev angioedema (bad)
  • no sig ben over enalapril, d/c’d dev
92
Q

Stage A guideline recommendations

A
  • Stage A = risk… dec risk
    • control HTN, lipids, DM
    • stop smoking, EtOH, illicit drug use
    • echo w/fam hx cardiomyopathy or using cardiotoxic meds
    • use ACEi if you can find a good reason
      • atherosclerosis, DM, HTN
93
Q

Stage B guideline recommendations

A
  • stage B =struct dz w/o sx… stage A recs plus…
  • BB+ACEi/ARB/ARNI if hx MI, regardless of EF
  • ACEi if dec EF and no sx HF, even if no MI
  • ARB if hx MI, w/o HF, if ACEi intol and low EF
  • ARNI in class II or III HFrEF, even if tolerating ACEi/ARB
  • Dig not used w/ low EF, NSR and no sx HF
  • Diuretics not used w/o sx HF
94
Q

Stage C guideline recommendations

A
  • stage C=struct dz+hx/current sx… stage A+B plus…
  • diuretics+salt restriction if evidence of fluid ret
  • ACEi if sx HF and dec LVEF unless contraindicated, else ARB
  • BB’s for stable pt w/ sx HF dec LVEF unless contraindicated
  • avoid NSAIDs, antiarrhythmics and CCB’s
  • ALD ant reasonable in mod sev to sev sx HF if renal fx and K monitored - Cr<2.5m/<2f, K<5
  • hydralazine/nitrate reasonable if sx still w/ ACEi and BB, or if ACEi/ARB intol
  • ARB addition may be considered if sx w/ conventional tx
  • ACEi, ARB and ALD ant not recommended together (hyperK risk)
95
Q

CrCl formula

A

CrCl in ml/min…

(140-age)IBW

CrCl = ——————- x (*.85 for females)

(Cr)(72)

  • IBW
    • male 50kg + (2.3 x inches over 5ft)
    • female 45kg + (2.3 x inches over 5ft)

Pharm (7 decks)

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