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CPR Remediation > Pharmacology > Flashcards

Pharmacology Flashcards

Follows LOs for - drugs for lipid disorders - drugs used in chronic IHD - drugs for asthma and COPD - pulmonary HTN - drugs for HTN - ED pharmacology - anti-fungal pharmacology - cholinergics - adrenergics - biotransformation - anti-arrhythmic drugs other decks - "CPR II" class: "(2) Intro to Pharmacology (Iszard)" deck - "CPR II" class: "(9.1) Intro to Cholinergic drugs (Kruse)" deck - "CPR II" class: "(9.2) CIS I Cholinergic drugs (Kruse)" deck

1
Q

list the current first line drugs for treating HTN

A

thiazide diuretics (chlorthalidone, HCTZ)
ACEi (captopril, enalapril, benazepril, lisinopril)
ARBs (losartan, valsartan, candesartan)
CCB dihydropyridines (amlodipine, nifedipine)
CCB non-dihydropyridines (verapamil, diltiazam)

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2
Q

anti-hypertensive drugs that are safe to use in pregnancy (3)

A

methyldopa
nifedipine
labetalol

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3
Q

anti-hypertensive drugs that should NEVER be used during pregnancy (3)

A

ACEi
ARBs
direct renin inhibitors

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4
Q

list the alpha antagonist drugs used to treat HTN (4)

A 
(-osin)
prazosin
tamsulosin
terazosin
doxazosin
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5
Q

MOA of prazosin

A

competitive antagonist of alpha1-AR –> vasodilation –> decreased peripheral resistance and BP

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6
Q

difference of tamsulosin, terazosin, doxazosin from prazosin

A

each selectively antagonist alpha 1a, 1b, and 1c specifically

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7
Q

other clinical applications of tamsulosin, terazosin, doxazosin (other than tx of HTN)

A

benign prostatic hypertrophy (BPH)

help kidney stones pass

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8
Q

characteristic adverse effects of alpha antagonists (-osins)

A

orthostatic hypotension, syncope, palpitations, edema

retrograde ejaculation, priapism, urinary frequency

dizziness, drowsiness, decreased energy, weakness

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9
Q

which is the most selective beta1 blocker?

A

bisoprolol

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10
Q

characteristic of esmolol

A

short half life as a beta1 blocker

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11
Q

adverse effects of propranolol

A

bronchospasm, dyspnea

cold extremities

disrupted sleep

bradycardia, AV block, CHF, cardiogenic shock, hypotension, syncope

hyperglycemia, hyperkalemia, hyperlipidemia, hypoglycemia

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12
Q

what is contraindicated for propranolol?

A

peripheral vascular disease

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13
Q

what beta blocker is lipid soluble? what effects does that have?

A

metoprolol is lipid soluble –> more likely to produce adverse CNS effects (lethargy, confusion, nightmares)

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14
Q

what is the drug of choice for gestational HTN?

A

alpha-methyldopa

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15
Q

list the alpha2 agonists

A

clonidine

alpha-methyldopa

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16
Q

MOA of clonidine

A

crosses the BBB –> acts on CNS –> shuts down sympathetic flow (alpha 2 effects)

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17
Q

is clonidine used as first line or adjuvant therapy?

A

adjuvant therapy

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18
Q

adverse effects of clonidine

A

REBOUND HTN IF DOSE MISSED
bradycardia or tachycardia, AV block, arrhythmia, syncope, etc.

drowsiness, fatigue, dizziness

xerostomia, upper abd pain

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19
Q

what two drugs have the adverse effect of drug-induced SLE-like syndrome?

A

alpha-methldopa

hydralazine

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20
Q

what happens with an abrupt withdrawal of beta blockers?

A

excessive cardiac stimulation in response to normal SNS tone (receptors become unmasked) –> tachycardia, HTN, MI, angina, arrhythmia (REBOUND HTN)

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21
Q

what happens with an abrupt withdrawal of alpha2 agonists?

A

excessive SNS tone (breaks have been released) –> REBOUND HTN

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22
Q

list the prostanoids (4)

A 
(-prost)
epoprostenol
treprostenil
iloprost
selexipag
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23
Q

pharmacokinetics of epoprostenol

A

very short half life (6 min!)
continuous IV
drugs must be kept cold

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24
Q

pharmacokinetics of treprostenil

A

longer half-life (4 hrs)
subQ infusion but very painful
does NOT need to be refrigerated

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25
Q

pharmacokinetics of iloprost

A

INHALATION 6-9 times/day

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26
Q

disadvantage of selexipag

A

expensive af

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27
Q

drugs used to treat PAH

A

prostanoids
endothelin antagonists
PDE-5 inhibitors
guanylate cyclase sensitizers

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28
Q

MOA of prostaonids

A

mimics action of endogenous prostacyclin

  • vascular dilation
  • inhibits platelet aggregation
  • decreases pulmonary vascular resistance

tx PAH

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29
Q

list the endothelin antagonists (3)

A

bosentan
amrbisentan
macitentan

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30
Q

which drug(s) nonspecifically blocks ETa and ETb endothelin receptors?

A

bosentan

macitentan

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31
Q

which drug(s) specifically only blocks ETa endothelin receptors?

A

ambrisentan

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32
Q

adverse effects of bosentan

A

hepatotoxicity

teratogenesis

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33
Q

drug interactions of bosentan and macitentan

A

accelerates metabolism of via CYP450

  • warfarin
  • oral contraceptives (use 2 forms of BC!)
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34
Q

adverse effects of ambrisentan

A

teratogenesis

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35
Q

advantage of ambrisentan over bosentan?

A

does NOT accelerate metabolism of warfarin or OCPs (but still use 2 forms of BC)

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36
Q

adverse effects of epoprostenol and treprostenil

A

sepsis due to chronic catheter

life-threatening problems if pump becomes clogged

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37
Q

adverse effects of iloprost

A

fainting due to hypOtension

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38
Q

MOA of PDE-5 inhibitors for treatment of ED and HTN

A

selective blocks PDE-5 enzymes –> decrease degradation of cGMP –> incr cGMP –> longer erections (tx of ED) and vasodilation (tx of HTN)

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39
Q

dangerous drug interactions and effects of PDE-5 inhibitors

A 
with alpha blockers (for HTN) --> severe hypOtension
with nitrates (for angina) --> severe hypOtension
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40
Q

rare adverse effects of PDE-5 inhibitors

A

visual disturbance

priapism

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41
Q

MOA of guanylate cyclase sensitizer

A
  1. sensitives soluble guanylate cyclase (sGC) to endogenous NO
  2. directly stimulates sGC independent of NO
    - -> incr cGMP –> vasodilation

tx PAH

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42
Q

list the guanylate cyclase sensitizer (1)

A

riociguat

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43
Q

if CCB vapopressor test is (+) which drugs should be used to treat pulmonary HTN?

A

nifedipine, diltiazem, amlodipine

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44
Q

when do you use combination therapy to treat PAH?

A

when the disease and sx become progressively worse

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45
Q

list the ACE inhibitors (4)

A 
(-pril)
captopril
enalapril
benazepril
lisinopril
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46
Q

list the angiotensin receptor blockers/ARBs (3)

A

(-sartan)
losartan
valsartan
candesartan

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47
Q

list the renin inhibitors (1)

A

aliskiren

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48
Q

list the calcium channel blockers used for treating HTN (4) – 2 groups

A

dihydropyridines:
(-dipine)
nifedipine
amlodipine

non-dihydropyridines:
verapamil
diltiazem

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49
Q

list the direct vasodilators (3)

A

hydralazine
nitroprusside
minoxidil

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50
Q

list the HMG-CoA Reductase Inhibitors

A 
(STATINS)
atorvastatin
fluvastatin
lovastatin
pitavastatin
pravastatin
rosuvastatin
simvastatin
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51
Q

list the statins in order of potency for reducing LDL levels

A

atorvastatin
rotuvastatin

simvastatin

lovastatin
pitavastatin
pravastatin

fluvastatin

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52
Q

how do HMG-CoA reductase inhibitors (statins) treat lipid disorders?

A

inhibit HMG-CoA reductase in order to lower LDL levels (greatest decrease in LDL levels compared to all other lipid disorder drugs)

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53
Q

how are beta blockers useful in the treatment of angina pectoris? (MOA)

A

work to decrease the O2 demand of the myocardium seen in classic angina/angina pectoris

  • improve myocardial perfusion
  • decrease contractility
  • decrease BP
  • decrease afterload
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54
Q

list the beta blockers used for chronic ischemic heart disease (4)

A

propanolol
nadolol
metoprolol
atenolol

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55
Q

contraindications of beta blockers for IHD

A 
ASTHMA
peripheral vascular disease
T1DM
bradyarrhythmias
AV conduction dysfunction
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56
Q

adverse effects of beta blockers for IHD

A 
reduced CO
bronchoconstriction
impaired liver glucose mobilization
incr VLDL, decr HDL
sedation, depression
sympathetic hyper responsiveness upon abrupt withdrawal
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57
Q

list the PDE-5 inhibitors that can be used specifically for ED (4)

A

tadalafil
sildenafil (viagra)
vardenafil
avanafil

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58
Q

absolute contraindication for PDE-5 inhibitors

A

people on organic nitrates

causes incr NO –> incr cAMP bc no PDE-5 to degrade –> excessive hypotension

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59
Q

list the anti fungal drugs/drug classes (4)

A

amphotericin B
flucytosine
azoles
echinocandins

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60
Q

list the echinocandins (3)

A

(-fungin)
caspofungin
micafungin
anidulafungin

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61
Q

list the azoles (7)

A

imidazole
ketoconazole

triazole
itraconazole
fluconazole
voriconazole
posaconazole
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62
Q

MOA of amphotericin B

A

forms a complex with ergosterol and disrupts the fungal plasma membrane –> leakage of intracellular ions and macromolecules –> cell death

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63
Q

MOA of flucytosine

A

taken up into fungal cell membrane by cytosine permease

converted to 5-FU –> FdUMP and FUTP –> inhibit DNA and RNA synthesis, respectively

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64
Q

how do amphotericine B and flucytosine work together in combination therapy?

A

synergistically enhances the penetration of flucytosine through amphotericin-damaged fungal cell membranes

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65
Q

which anti fungal agent has the broadest spectrum of action?

A

amphotericin B

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66
Q

what situation could lead to resistance to ampotericin B?

A

impaired ergosterol binding from either

  • decreased membrane concentration of ergosterol
  • modified ergosterol that has less affinity for amphotericin B
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67
Q

what situation could lead to resistance to flucytosine?

A

altered metabolism of flucytosine, which can develop rapidly in monotherapy

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68
Q

what are the immediate adverse effects that can present with amphotericin B?

A

immediate reactions related to IV infusion: ms spasms, F/C, hypotension, headache

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69
Q

what are the long term adverse effects that can present over time with amphotericin B?

A

renal damage: decreased renal perfusion, renal tubular injury and dysfunction

anemia

seizures

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70
Q

what are the adverse effects of flucytosine?

A

bone marrow toxicity with anemia, leukopenia, and thrombocytopenia

derangement of liver enzymes (less frequently)

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71
Q

MOA of azoles

A

reduction of ergosterol synthesis by inhibition of fungal CYP450 enzymes

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72
Q

which azoles are used for treatment of aspergillus spp. infections? (3)

A

itraconazole
posaconazole
voriconazole

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73
Q

what is the azole of choice to treat invasive aspergillosis?

A

vorizonazole

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74
Q

what is the azole of choice to treat mucocutaneous candidiasis?

A

fluconazole

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75
Q

what is the azole of choice to treat and used as secondary prophylaxis of cryptococcal meningitis?

A

fluconazole

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76
Q

which azole is the only one with significant activity against mucormycosis?

A

posaconazole

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77
Q

which azole has the widest therapeutic index? what does this allow for?

A

fluconazole

allows for more aggressive dosing

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78
Q

what situation could lead to resistance to azoles?

A

up regulation of fungal CYP450 causes standard azole dosages to be less efficacious

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79
Q

what azole has less selectivity? what does this mean for it’s effects?

A

ketoconazole

has a greater propensity for adverse effects

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80
Q

adverse effects of azoles (if any)

A

in general are RELATIVELY NONTOXIC

minor upset GI sx
can cause abnormalities in liver enzymes

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81
Q

which azoles have the potential adverse reaction of inhibiting mammalian CYP3A4?

A

voriconazole

posaconazole

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82
Q

what are some of the specific toxicities that could be seen with vorizonazole?

A

VISUAL DISTURBANCES
rash
elevated hepatic enzymes

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83
Q

MOA of echinocandins

A

inhibition of glucan synthase –> inhibit synthesis of Beta (1-3)-glucan at the fungal cell wall –> disrupted fungal cell wall –> cell death

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84
Q

what situation could lead to resistance to echinocandins?

A

point mutations in glucan synthase – do not give to pts if they have this!

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85
Q

adverse effects of echinocandins (if any)

A

well tolerated

minor GI side effects
flushing

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86
Q

list the SABAs (5)

A 
albuterol
terbutaline
metaproterenol
pirbuterol
levalbuterol
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87
Q

list the LABAs (5)

A 
formoterol
salmeterol
indacaterol
vilanterol
olodaterol
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88
Q

list the anticholinergic bronchodilators (4)

A

atropine
ipratropium
tiotropium (LAMA)
aclidinum (LAMA)

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89
Q

list the methylxanthine bronchodilators (3)

A

theophylline
theobromine
caffeine

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90
Q

list the inhaled corticosteroids/ICS (7)

A 
beclomethasone
budesonide
ciclesonide
flunisolide
fluticasone
mometasone
triamcinolone
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91
Q

list the leukotriene receptor antagonists/lipoxygenase inhibitors (3)

A

zafirlukast
montelukast
zileuton

92
Q

MOA of B2 agonists bronchodilators (SABAs and LABAs)

A

induce adenylyl cyclase –> incr intracellular cAMP –> bronchodilation

93
Q

how is terbutaline administered?

A

only beta2 agonist available for subQ injection

94
Q

which SABA is given for a more immediate and sustained delivery?

A

terbutaline

95
Q

which B2 agonists are used only in pts 12+ yo?

A

terbutaline (SABA)

pirbuterol (SABA)

96
Q

which B2 agonist is used only in pts 4+ yo?

A

levalbuterol (SABA)

97
Q

in general, when are SABAs used?

A

during acute bronchospasmic attacks

98
Q

in general, when are LABAs used?

A

maintenance/long-term management of COPD or asthma

99
Q

what must LABAs be concomitantly used with?

A

long-term asthma control medication such as ICS

100
Q

LABAs increase the risk of…

A

asthma-related deaths

asthma-related hospitalizations

101
Q

which B2 agonist is used for exercise induced bronchospasm (EIB) in pts 4+ yo?

A

salmeterol (LABA)

102
Q

MOA of anticholinergic bronchodilators

A

blocks ACh from binding to receptors –> inhibit PNS effects

103
Q

what agents are most widely used in asthma/COPD?

A

anti-muscarinic agents (anticholinergics like atropine)

methylxanthines

104
Q

what is an advantage of ipratropium over atropine?

A

it is a potent atropine analog that is poorly absorbed after aerosol administration and therefore is relatively free of systemic atropine-like effects

105
Q

are anticholinergics/antimuscarinics used more for acute treatment or long-term maintenance?

A

long-term/maintenance tx for bronchospasm for COPD mostly

106
Q

what is an important caution for dosing of atropine? (certain diseases to look out for and why)

A

dose should be restricted to 2-3 mg when recurrent use of atropine is essential in pts with CAD to avoid atropine-induced tachycardia

107
Q

MOA of methylxanthine bronchodilators

A

inhibit phosphodiesterase (PDE) –> incr cAMP –> bronchodilator

108
Q

methylxanthines should be used with extreme caution in patients with…

A

active PUD
seizure disorders
cardiac arrhythmias

109
Q

first line therapy for patients with persistent asthma?

what is added if low doses do not control sx?

A

ICS

add LABA as next step

110
Q

which ICS (2) have the potential to cause candida infections?

A

ciclesonide

fluticasone

111
Q

which ICS (2) have a risk of causing adrenal insufficiency + death in asthmatic patents?

A

beclomethasone

triamcinolone

112
Q

which ICS (2) are contraindicated in patients with severe hypersensitivity to milk proteins?

A

budesonide

mometasone

113
Q

in general, when are ICS agents used?

A

in maintenance treatment or as prophylaxis for asthma

114
Q

which ICS (1) is only used in patients 12+ yo?

A

ciclesonide

115
Q

which ICS (2) are used in patients 4+ yo? which (1) for patients 5+ yo? which (1) for patients 6+ yo?

A

4+
fluticasone
mometasone

5+
beclomethasone

6+
budesonide

116
Q

which ICS (1) requires a couple months to recover HPA function after withdrawal from systemic corticosteroids?

A

beclomethasone

117
Q

common combinations of ICS + LABAs (3)

A

fluticasone + salmetrol
mometasone + formoterol
budesonide + formoterol

118
Q

steps (4) for treatment of mild persistent to severe persistent asthmatics

A
  1. ICS low dose
  2. ICS low dose + LABA
  3. ICS high dose + LABA
  4. ICS high dose + LABA + OCS
119
Q

MOA of zafirlukast vs. montelukast vs. zileuton

A

zafirlukast: selectively (-) LTD4 and LTE4
montelukast: selectively (-) LTE4 and CysLTI
zileuton: inhibits 5-lipoxygenase –> (-) LTB4, C4, D4, E4 formation

120
Q

major adverse effect of zafirlukast

A

hepatotoxicity (life threatening hepatic failure)

121
Q

major contraindication of zileuton

A

active liver disease or persistent hepatic function enzyme elevations >3x ULN

122
Q

which leukotriene receptor antagonists / lipoxygenase inhibitors is used to treat allergies and prevent asthma attacks?

A

montelukast

123
Q

which leukotriene receptor antagonists / lipoxygenase inhibitors are used as prophylaxis and in the chronic tx of asthma? age restrictions of each?

A

zafirlukast (5+ yo)

zileuton (12+ yo)

124
Q

list the oral corticosteroids/OCS (1)

A

prednisone

125
Q

list the monoclonal Abs (1)

A

omalizumab

126
Q

major adverse effect of omalizumab and what setting it must be administered in

A

can lead to anaphylaxis – must only be given in the hospital to manage potential anaphylaxis

127
Q

which cholinergic drugs can be used to treat sx associated with airway restriction? what receptors do they activate or inhibit? what is the outcome?

A

antimuscarinics/parasympatholytics = ipratropium and tiotropium which antagonize/inhibit M3 receptors (smooth muscle and glands) –> bronchodilation (tx asthma, COPD)

128
Q

genetic variations (2) that affect the pharmacokinetic and pharmacodynamic responses of warfarin (Coumadin)…

A

polymorphisms in biotransforming ENZYMES

polymorphisms in DRUG TARGETS

129
Q

list the adrenergic receptors and their coinciding G-proteins

A 
alpha 1 (a1 A, B, D) = Gq
alpha 2 (a2 A, B, C) = Gi
beta1 = Gs
beta2 = Gs
dopamine 1 = Gs
dopamine 2-4 = Gi
dopamine 5 = Gs
130
Q

list the G-proteins and their single transduction pathways

A 
Gq = incr IP3-DAG 
Gi = decr cAMP
Gs = incr cAMP
131
Q

general target tissue and action of: alpha1 adrenergic receptors

A

vascular smooth ms (BV), pupillary dilator muscles, prostrate

CONTRACTION

  • vasoconstriction (reflex bradycardia)
  • incr BP
  • incr MAP
  • dilate pupils
132
Q

general target tissue and action of: alpha2 adrenergic receptors

A

CNS, platelets, nerve terminals

decr sympathetic tone
inhibit NT release
some vasoconstriction

133
Q

general target tissue and action of: beta1 adrenergic receptors

A

heart and JG cells

CONTRACTION

  • incr myocardial contractility
  • incr HR
  • incr SA and AV node activity
  • incr renin release
134
Q

general target tissue and action of: beta2 adrenergic receptors

A

respiratory sm ms, uterine sm ms, vascular sm ms, skeletal muscle

DILATION

  • vasodilation (reflex tachycardia)
  • bronchodilation
  • sm ms relaxation
  • promote K+ uptake
  • (+) glycogenolysis, gluconeogenesis (hyperglycemia)
135
Q

general target tissue and action of: D1 adrenergic receptors

A

smooth muscle

DILATION of renal blood vessels

136
Q

general target tissue and action of: D2 adrenergic receptors

A

nerve endings

modulate transmitter (NT) release

137
Q

list the endogenous catecholamines (3)

A

epinephrine
norepinephrine
dopamine

138
Q 
list the general effects of epinephrine on:
- cardiac fxn
- vascular tone
- respiratory system 
- skeletal ms
- blood glucose levels 
(think of the receptors it targets)
A

cardiac fxn = B1: incr contractility, HR, AV conduction velocity

vascular tone = B2 and a1: vasodilation, incr systolic BP

respiratory system = B2 and a1: bronchodilation, decr bronchial secretions

skeletal ms = B2: ms tremor, promote K+ uptake

blood glucose = B2: promote liver glycogenolysis and gluconeogenesis (hyperglycemia)

139
Q

list the general effects of norepinephrine on:
- cardiac fxn
- vascular tone
(think of the receptors it targets)

A

cardiac stimulation, but decr HR
vasoconstriction
incr peripheral vascular resistance (PVR) and BP

140
Q

what are the predominant adrenergic receptors for epinephrine?

A

a1 = a2; B1 = B2

141
Q

what are the predominant adrenergic receptors for norepinephrine?

A

a1 = a2; B1&raquo_space; B2

142
Q

what are the predominant adrenergic receptors for dopamine?

A

D1 = D2&raquo_space; B1&raquo_space; a1

143
Q

general effects of dopamine (think of the receptors it targets)

A

D1 stimulation = vasodilation
D2 stimulation = suppressed NE release
high doses B1 = cardiac effects
higher doses a1 = vasoconstriction

144
Q

list the beta adrenergic agonists (3) and their target receptors

A

isoproterenol: NON-SELECTIVE, B1 = B2
dobutamine: selective B1
albuterol: selective B2

145
Q

adverse effects of beta blockers

A

sedation, sleep disturbances, depression

incr airway resistance (bronchoconstriction)

depression of HR, contractility, excitability; exacerbate PVR

incr VLDL, decr HDL

hypoglycemic episodes

abrupt discontinuation leading to compensatory responses

  • enhance cardiac stimulation
  • arrhythmias
146
Q

what situations/sx (3) require a switch from non-selective to selective beta blockers?

A

switch to B1 selective if…

  • respiratory sx of bronchospasm and incr airway resistance
  • exacerbation of peripheral vascular disease (excess vasodilation)
  • hypoglycemic episodes
147
Q

pharmacodynamic effects of isoproterenol (non-selective beta agonist)

A

B1: (+) inotropic and chronotropic action, incr CO
B2: vasodilator, decr arterial pressure, bronchodilation

148
Q

pharmacodynamic effects of dobutamine (selective B1 agonist, some a1 activity)

A

potent inotropic action, less prominent chronotropic action

149
Q

pharmacodynamic effects of albuterol (selective B2 agonist)

A

bronchodilation

relaxation of uterus

150
Q

list the non-selective beta blockers (3)

A

propanolol
pindolol
nadalol

151
Q

list the B1 selective blockers (5)

A 
ABEAMS
atenolol
betaxolol
esmolol
acebutolol
metoprolol
152
Q

list the alpha agonist drugs (2) and their target receptors

A 
phenylephrine = a1
clonidine = a2
153
Q

list the non-selective alpha antagonists (2)

A

phentolamine (reversible)

phenoxybenzamine (irreversible)

154
Q

list the a1 selective antagonists (3)

A

-OSIN
prazosin
tamsuolsin
doxazosin

155
Q

list the mixed alpha and beta blockers (2)

A

(non-selective B and a1 blockers)
labetolol
carvedilol

156
Q

MOA of ACE inhibitors

A

inhibition of ACE –> prevention of conversion of angiotensin I to angiotensin II (potent vasoconstrictor) –> incr renin activity and decr aldosterone secretion –> lowered BP

157
Q

adverse effects of ACEi

A

cough (tickle)

angioedema (can be deadly if tongue swells)

158
Q

MOA of ARBs

A

competitive non peptide angiotensin II receptor blocker –> blocks the vasoconstriction and aldosterone-secreting effects of angiotensin II

159
Q

advantage of ARBs over ACEi

A

ARBs induce a more complete inhibition of the RAAS than ACEi

160
Q

important note about candesartan’s binding:

A

relatively irreversible binding

161
Q

which ARB goes through extensive first-pass metabolism via CYP2C9 and CYP3A4 to active metabolite E-3174? what is special about E-3174?

A

losartan

E-3174 is 10x more potent than losartan

162
Q

in which situation are adverse effects of ARBs more likely seen?

A

diabetic nephropathy

163
Q

MOA of aliskiren

A

direct renin inhibitor –> blockade of conversion of Ang I to Ang II –> decr BP

164
Q

what is the prototypical dihydropyridine CCB?

A

nifedipine

165
Q

MOA and effects of calcium channel blockers

A

inhibit Ca2+ from entering the “slow channels” or select voltage-sensitive areas of vascular smooth muscle and myocardium during depolarization –> coronary vasodilation + myocardial O2 delivery + negative inotrope (decr contractility)

166
Q

which CCB has the most potent negative inotropic effect?

A

verapamil (cardio-specific!)

167
Q

drug used as the first line tx for HTN for nonblack populations without CKD but with DM:

A

nifedipine

168
Q

instead of ACEi or ARBS, thedrug used as the first line tx for HTN for black populations without CKD but with DM:

A

nifedipine

169
Q

off label indications of nifedipine:

A

hypertensive emergency in pregnancy
pulmonary HTN
preterm labor

170
Q

when administered via IV, what do verapamil and diltiazem treat? (1)

A

supraventricular tachyarrhytmias (SVT)

… essentially rate control

171
Q

when administered PO, what does verapamil treat? (3)

A

primary HTN (first line)
angina pectoris
SVT

172
Q

when administered PO, what does diltiazem treat? (3)

A 
primary HTN (first line)
classic stable and vasospastic angina pectoris
173
Q

which direct vasodilator(s) directly vasodilate the arterioles (with little effect on veins) of smooth muscles?

A

hydralazine

minoxidil

174
Q

which direct vasodilator(s) directly vasodilate the arterioles AND veins of smooth muscles?

A

nitroprusside

175
Q

which direct vasodilator can be used in hypertensive emergencies in pregnancy (pre-eclampsia)?

A

hydralazine

176
Q

which direct vasodilator can be used in a hypertensive crisis?

A

nitroprusside

177
Q

adverse effects of minoxidil in CV and in endocrine/metabolic effects

A

CV: pericardial effusion w/ tamponade

endo/metab: sodium and water retention

178
Q

adverse effect of nitroprusside

A

thiocyanate toxicity –> tinnitus, metabolic acidosis, muscle twitching, mitosis, hyperoxemia

179
Q

list the thiazide diuretics (3)

A

hydrochlorathiazide
metolazone
chlorthalidone

180
Q

list the loop diuretics (4)

A 
-SEMIDE
furosemide
torsemide
bumetanide
ethacrynic acid
181
Q

list the K+ sparing diuretics (4)

A

Na-channel blockers

  • amiloride
  • triamterene

aldosterone antagonist

  • spironolactone
  • eplerenone
182
Q

list the aquaretics (2)

A

-VAPTAN
conivaptan
tolvaptan

183
Q

which diuretics treat HTN and edema?

A

thiazide
loop
K+ sparing

184
Q

which diuretics treat euvolemic and hypervolemic hyponatremia?

A

aquaretics

185
Q

MOA and site of action of loop diuretics

A

Na-K-Cl cotransporter blockers at the thick ascending loop of Henle

186
Q

MOA and site of action of thiazide diuretics

A

Na-Cl contransporter blocker at the distal convolute tubule

187
Q

which diuretic would be used if there was a need for massive and rapid fluid removal (i.e. acute pulmonary edema, hepatic edema, cardiac edema, renal edema)?

A

loop diuretic

188
Q

advantage of loop diuretics over thiazides in treatment of HTN

A

loops still work in patients with LOW RBF and GFR (good for patients who are unresponsive to other diuretics)

189
Q

main clinical application of thiazide diuretics (hydrochlorothiazide)

A

management of mild-to-moderate HTN… either alone or in combo with other agents

190
Q

MOA and site of action of K+ sparing diuretics

A

either block epithelial Na+ channels/ENaC (triamterene, amiloride) or antagonize aldosterone (spironolactone, eplerenone) at the cortical collecting duct

191
Q

main clinical application of K+ sparing diuretics

A

counteracts K+ loss induced by other diuretics when treating HTN or HF (adjunct use)

192
Q

MOA and site of action of aquaretics

A

blocks ADH receptor in the collecting duct –> excrete free water (pee a lot)

193
Q

what is an off-label use of HCTZ?

A

calcium nephrolithaisis

194
Q

what are the class 1 antiarrhythmic drugs?

A

sodium channel blockers

195
Q

list the class 1A antiarrhythmic drugs (3)

A

quinidine
procainamide
disopyramide

196
Q

list the class 1B antiarrhythmic drugs (2)

A

lidocaine

mexiletine

197
Q

list the class 1C antiarrhythmic drugs (2)

A

flecainide

propafenone

198
Q

MOA of class 1A antiarrhythmics

A

blocks Na+ (OPEN) and K+ channels

decrease slope of phase 0

199
Q

effects of class 1A antiarrhythmics on AP and ECG

A

prolong AP duration by reducing repolarizing influx

prolong QRS (ventricular depolarization) and QT intervals

200
Q

MOA of class 1B antiarrhythmics

A

block Na+ channels (only bind INACTIVATED channels)

do NOT block K+ channels

201
Q

effects of class 1B antiarrhythmics on AP and ECG

A

SHORTEN AP duration

do NOT prolong QT duration, prolong QRS interval (ventricular depolarization) when tissue is damaged

202
Q

MOA of class 1C antiarrhythmics

A

block Na+ channels (only bind ACTIVATED/OPEN channels) – slow impulse conduction

203
Q

effects of class 1C antiarrhythmics on AP and ECG

A

do NOT prolong AP duration

do NOT prolong QT duration, prolong QRS interval (ventricular depolarization)

204
Q

class 1 antiarrythmics drugs are state-dependent. In which state do they bind their respective channels?

A

1A and 1C bind activated/open Na channels

1B binds inactivated Na channels

205
Q

rank the class 1 antiarrhythmics from highest to lowest affinity to Na+ channels

A 
strongest binding affinity
1C
1A
1B
lowest binding affinity
206
Q

which antiarrhythmic class 1 drug is effective in SUSTAINED ventricular tachycardias and arrhythmias associated with MI?

A

procainamide (class 1A)

207
Q

which is the least toxic drug of the class 1 antiarrythmics?

A

lidocaine (class 1B)

208
Q

cardiac adverse effects of the class 1A antiarrythmics (3)

A

QT prolongation
induction of torsade de pointes arrhythmias & syncope
excessive inhibition of conduction

209
Q

extra cardiac adverse effects of quinidine

A

GI side effects: diarrhea, N/V

thrombocytopenia

210
Q

extra cardiac adverse effects of procainamide

A

Lupe erythematous (SLE) syndrome with arthritis, pleuritis, pulmonary disease, hepatitis, and fever

211
Q

extra cardiac adverse effects of disopyramide

A

atropine-like symptoms

  • urinary retention
  • dry mouth
  • blurred vision
  • constipation
  • exacerbation of glaucoma
212
Q

which class 1 antiarrythmic drug could be used to terminate ventricular tachycardia in the setting of an ACUTE MI?

A

lidocaine

213
Q

neurologic adverse effects of lidocaine

A 
paresthesia
tremor
slurred speech
convulsions 
nystagmus
muscle twitching
confusion
loss of coordination
214
Q

which class 1 antiarrythmic is used to treat ventricular arrhythmias and relieve chronic pain due to diabetic neuropathy and nerve injury?

A

mexiletine

215
Q

which class 1 antiarrythmic is used to treat supraventricular arrhythmias in patients with structural dz and has some weak beta-blocking activity?

A

propafenone

216
Q

cardiac adverse effect of class 1C antiarrythmics

A

exacerbate ventricular arrhythmias

217
Q

extra cardiac adverse effects of propafenone

A

metallic taste

constipation

218
Q

class 1 antiarrhythmics and their effects on K+ channels

A 
1A = block K+ channels
1B = do NOT block K+ channels
1C = block some K+ channels
219
Q

pharmacokinetics of dissociation from Na channels for class 1 antiarrythmics

A 
1A = slow impulse conduction
1B = dissociate with fast kinetics (less severe side effects!)
1C = dissociate with slow kinetics
220
Q

MOA and effects of amiodarone on the heart

A

block K+ channels –>

causes bradycardia and slows AV conduction

causes peripheral vasodilation

221
Q

effects of amiodarone on AP and ECG

A

prolong AP duration

prolong QT interval

222
Q

what does amiodarone usually treat?

A

recurrent VTach

AFIB

223
Q

adverse effects of amiodarone

A 
AV block
bradycardia
hypo or hyperTHYROIDISM
fatal pulmonary fibrosis
hepatitis 
photodermatitis
224
Q

what metabolizes amiodarone? drugs that inhibit this metabolizer have what effect on amiodarone?

A

metabolized by CYP3A4

amiodarone’s half-life is affected by drugs that inhibit (cimetidine) or induce (rifampin) CYP3A4

225
Q

what is the elimination time of amiodarone like?

A

very long elimination half-life (weeks - months)

effects are maintained 1-3 months after discontinuation

226
Q

what effect does amiodarone have on other CYP enzymes? what does this mean?

A

inhibits many CYP enzymes – this may affect the metabolism of many other drugs

*all meds should be carefully reviewed in pts on amiodarone

CPR Remediation (2 decks)

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