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NU 560 Pharmacotherapeutics > Unit 3 > Flashcards

Unit 3 Flashcards

1
Q

Do ACEs and ARBs affect arterial vasculature, venous vasculature, or both?

A

Both

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2
Q

Do CCBs affect arterial vasculature, venous vasculature, or both?

A

Arterial

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3
Q

Do diuretics affect arterial vasculature, venous vasculature, or both?

A

venous
long term use can affect arterial

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4
Q

Do BBs affect arterial vasculature, venous vasculature, or both?

A

both

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5
Q

Do alpha agonists/blockers affect arterial vasculature, venous vasculature, or both?

A

both

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6
Q

Do nitrates affect arterial vasculature, venous vasculature, or both?

A

Both

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7
Q

Goal SBP and DBP for Age>60

A

<150
<90

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8
Q

Goal SBP and DBP for Age<60

A

<140
<90

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9
Q

Goal SBP and DBP for DM and CKD

A

<140
<90

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10
Q

Goal SBP and DBP for CKD only

A

<130
<80

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11
Q

ALL patients with DM and/or CKD with albuminuria >300 should receive what

A

ACE or ARB

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12
Q

How to treat HTN in non-black with no cormorbidities or just DM

A

thiazide
ACE/ARB
CCB

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13
Q

How to treat HTN in a black patient with no comorbidities or just DM

A

thiazide
CCB

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14
Q

statins MOA

A

inhibit HMG CoA reductase which inhibits LDL production in the liver

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15
Q

2 examples of high dose statins

A

atorvastatin 80mg
rosuvastatin 40mg

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16
Q

when to prescribe a high dose statin

A

> 75 with ASCVD
LDL>190
DM 40-75 no ASCVD and LDL 70-189 and estimated risk >7.5% for serious CV event in 10 years

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17
Q

monitoring for statins

A

baseline lipid panel and LFTs
recheck in 3 mo
if at goal, monitor lipids q3-12 months

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18
Q

education for statins

A

avoid grapefruit juice
Many med interactions due to CYP3A involvement

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19
Q

SE of statins (4)

A

myalgia– rhabdo/renal failure
headache
fatigue
GI distress
elevated LFTs

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20
Q

how to manage SE of statins

A

d/c statin, if symptoms resolve, r/s at lower dose, if tolerated, dose can be gradually increased. If unable to achieve recommended dose, consider non-statins

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21
Q

6 medications for angina

A

ACEs/ARBs
Spironolactone
Nitrates
BB
CCB
AP- aspirin

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22
Q

2 short acting medications for angina

A

nitro SL
isordil SL

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23
Q

2 long acting medications for angina

A

nitro topical/transdermal patch
isosorbide IR/ER

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24
Q

MOA BB

A

block beta 1 and/or beta 2 receptors centrally and peripherally, leading to decreased cardiac output and sympathetic outflow

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25
Q

BB contraindications (6)

A

bradycardia
2nd and 3rd degree HB
decompensated heart failure
severe bronchospastic disease
caution in asthma and COPD

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26
Q

SE of BB (8)

A

fatigue
drowsiness
bronchospasm
N/V
bradycardia
AV conduction abnormalities
CHF
mask hypoglycemia

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27
Q

MOA CCB

A

inhibit the movement of calcium ions across a cell membrane leading to cardiac muscle relaxation and vasodilation. Non-dihydropyridines decrease HR and slow cardiac conduction at the AV node. Dihydropyridines are potent vasodilators.
Dihydropyridines- nifedipine, amlodipine
Non dihydropyridine- verapamil, diltiazem

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28
Q

CCB non-dihydropyridines contraindications (2)

A

heart block and sick sinus syndrome (avoid in LV failure)

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29
Q

nifedipine contraindications (2)

A

essential HTN or HTN emergency (inconsistent fluctuations in BP and reflex tachycardia)

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30
Q

SE non-dihydropyridines (3)

A

GI upset
peripheral edema
hypotension

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31
Q

SE dihydropyridine (4)

A

headache
flushing
palpitations
peripheral edema

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32
Q

MOA ACEIs

A

prevent the conversion of angiotensin I to angiotensin II. Inhibit the degradation of bradykinin and increase the synthesis of vasodilating prostaglandins

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33
Q

ACEI contraindications (3)

A

b/l renal artery stenosis (acute renal failure)
pregnancy (avoid in women childbearing age)
hx of angioedema

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34
Q

SE ACEIs (6)

A

cough
rashes
dizziness
hyperkalemia
angioedema
laryngeal edema

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35
Q

MOA ARBs

A

block the binding of angiotensin II to the angiotensin II receptor which blocks the vasoconstriction and aldosterone-secreting effects

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36
Q

ARB contraindications (3)

A

b/l renal artery stenosis
pregnancy
caution in renal/hepatic impairment

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37
Q

SE ARBs (8)

A

dizziness
URI
viral infection
fatigue
diarrhea
sinusitis
pharyngitis
rhinitis

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38
Q

Loop diuretics MOA

A

inhibit the reabsorption of sodium and chloride in the proximal and distal tubules and the loop of Henle

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39
Q

Loop diuretics contraindications (5)

A

anuria
hepatic coma
severe electrolyte depletion
hypersensitivity to sulfas
ethacrynic acid contraindicated in infants

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40
Q

Loop diuretics SE (6)

A

hypokalemia
hypomagnesemia
hypercalcemia
hyperuricemia
hyperglycemia and hyperlipidemia in high doses

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41
Q

Thiazide diuretics MOA

A

inhibits Na, K, and Cl reabsorption in the distal tubule

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42
Q

Thiazide diuretics contraindications (2)

A

anuria
hypersensitivity to sulfas

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43
Q

Thiazide diuretics SE (6)

A

hypokalemia
hypomagnesemia
hypercalcemia
hyperuricemia
hyperglycemia
hyperlipidemia

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44
Q

potassium sparing diuretics MOA

A

interfere with sodium reabsorption at the distal tubule, decreasing potassium secretion

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45
Q

aldosterone receptor antagonists MOA

A

inhibit the effect of aldosterone by competitively binding to aldosterone receptors in the cortical collecting duct. Leads to decreased reabsorption of sodium and water and decrease potassium secretion

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46
Q

Potassium-Sparing Diuretics/Aldosterone Receptor Antagonists contraindications (4)

A

hyperkalemia, Addison disease, anuria, patients taking eplerenone

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47
Q

Potassium-Sparing Diuretics/Aldosterone Receptor Antagonists SE (4)

A

gynecomastia, hirsutism, menstrual irregularities, gout symptoms

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48
Q

Central Alpha-2 Receptor Agonists MOA

A

inhibit action of adrenaline on smooth muscle in blood vessel walls, dilating both arterioles and veins and cause relaxation of smooth muscle
Clonidine

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49
Q

Central Alpha-2 Receptor Agonists contraindications

A

use with tadalafil, sildenafil, and vardenafil (increased risk of symptomatic hypotension)

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50
Q

Central Alpha-2 Receptor Agonists SE (5)

A

first-dose phenomenon:
dizziness
faintness
palpitations
syncope
ortho hypotension

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51
Q

class 1 antiarrhythmics

A

sodium channel blockers:
procainamide
lidocaine
quinidine

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52
Q

what leads to quinidine toxicity

A

substrate of CYP3A4 (interacts with ketoconazole, erythromycin, amio, verapamil, diltiazem, rifampin, phenobarbital, phenytoin)

inhibitor of CYP2D6 (interacts with BB)

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53
Q

what leads to procainamide toxicity

A

renal impairment leads to accumulating levels

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54
Q

what leads to lidocaine toxicity

A

reduced hepatic blood flow d/t HFrEF delays metabolism

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55
Q

Class II antiarrhythmics

A

beta blockers

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56
Q

Class III antiarrhythmics

A

potassium channel blockers:
amiodarone
dronedarone
sotalol
dofetilide

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57
Q

what leads to amio and dronedarone toxicity

A

substrate of CYP3A4
inhibitor of CYO3A4, 2C9, 2D6

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58
Q

what not to give with amio and drondarone (9)

A

azoles
cyclosporine
clarithromycin
ritonavir
rifampin
phenobarbital
phenytoin
carbamazepine
St. John’s Wort

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59
Q

what leads to sotalol toxicity

A

poor renal function

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60
Q

what drugs lead to dofetilide toxicity (7)

A

cimetidine
dolutegravir
ketoconazole
HCTZ
megestrol
prochlorperazine bactrim
verapamil

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61
Q

what leads to dofetilide toxicity

A

poor renal function

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62
Q

class IV antiarrhythmics

A

CCB

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63
Q

what leads to diltiazem and verapamil toxicity

A

substrate and inhibitor of CYP3A4 do use cautiously with other meds that are metabolized by that isozyme

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63
Q

what leads to digoxin toxicity

A

poor renal function
electrolyte disturbance predispose the myocardium to the toxic effects of dig

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64
Q

3 drug interactions of dig

A

amio
dronedarone
verapamil

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65
Q

MOA of digoxin

A

predominant antiarrhythmic effect on the AV node of conduction system.

affects the ANS by stimulating the parasympathetic division increasing vagal tone which slows conduction through AV node

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66
Q

indication of digoxin

A

slow electrical impulse conduction through the AV node, slowing ventricular rate in AF and AFL

great for HFrEF with concomitant AF/AFL d/t to its positive inotropic effect

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67
Q

onset and peak of digoxin

A

6-8 hours

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68
Q

MOA amio

A

reduces automaticity and conduction velocity and prolongs refractoriness

blocks the rapid and slow components of the delayed rectifier potassium current

blocks sodium channels

non-selective beta blocking activity

weak CCB properties

minimal to no negative inotropic effects- safe for HFrEF

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69
Q

amio indications

A

management of acute VT/VF and AF

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70
Q

amio pharacodynamics (4)

A

poor oral bioavailability
large vol of distribution
long half life
loading dose needed

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71
Q

amio SE (10)

A

pulmonary toxicity
corneal microdeposits
thyroid abnormalities
N/V
hepatotoxicity
prolonged QT
photosensitivity
blue/gray skin
heart block
tremors

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72
Q

How do ACE/ARBs help with heart failure

A

reduce afterload
prevent cardiac remodeling

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73
Q

How do BB help with heart failure

A

reduce mortality, decrease O2 demand and workload

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74
Q

How do diuretics help with heart failure

A

reduce preload

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75
Q

how do nitrates help with heart failure

A

relax vasculature (coronary and systemic) to impact O2 supply and demand

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76
Q

Textbook treatment order for heart failure

A
  1. ACE (ARB if not tolerated) and BB
  2. Diuretic
  3. Digoxin
  4. ARB, aldosterone agonist, hydral/isosorbide
77
Q

How to treat AF/AFL with normal LV function

A

IV diltiazem, IV verapamil, IV BB
dig too slow onset

78
Q

How to treat AF/AFL with reduced LV function

A

IV BB or IV digoxin

79
Q

indication of EPO

A

treats anemia in ESRD who can’t produce enough EPO due to renal damage
if hgb <10 to avoid transfusion

80
Q

How is EPO given

A

SQ 3x/week

81
Q

Education for patients on EPO

A

take multivitamin d/t renal restrictive diet and iron supplement

82
Q

contraindications of EPO

A

uncontrolled HTN or sensitivity to mammalian products/albumin

83
Q

SE of EPO (6)

A

HTN
HA
seizure
nausea
edema
fatigue

84
Q

monitoring for patients on EPO (10)

A

H&H
ferritin
transferrin
B12
folate
BP
clotting times
plts
BUN and Cr

85
Q

4 indications for AP therapy

A

ischemic stroke prevention and treatment
add on to AC for mechanical valve
post-ACS to prevent CV death, MI, stroke
prevent thrombosis s/p PCI

86
Q

indications of ASA

A

post ACS
prevent thrombosis
add-on AC

87
Q

ASA platelet dysfunction

A

lasts for 7-10 days after day of d/c
d/t lifespan of the platelets exposed to ASA
irreversible

88
Q

onset of ASA

A

5 minutes

89
Q

onset of plavix

A

2 hours

90
Q

how long to d/c plavix before surgery

A

5-7 days

91
Q

SE of ASA (3)

A

GI upset
bleeding
potentiate PUD

92
Q

SE of plavix (3)

A

diarrhea
bruising
bleeding

93
Q

3 contraindications for AP

A

active GI bleed
ICH
PUD

94
Q

how to manage a patient with initiation of warfarin

A

start with warfarin + injectable AC
d/c LMWH when INR therapeutic
don’t bridge with direct thrombin inhibitor (dabigatran)

95
Q

Contraindications for ACs (10)

A

active bleed
recen ICH
intracranial mass (at high risk bleeding)
end stage liver disease
severe thrombocytopenia
recent trauma
immediate post-op ocular or CNS surgery
spinal catheters
aneurysms

96
Q

7 labs to consider before initiating ACs

A

PT
INR
aPTT
UA
CBC
LFT
pregnancy test

97
Q

3 considerations for LMWH or DOAC

A

body wt
Cr
CrCl

98
Q

3 ACs/APs to prevent VTE

A

Lovenox
warfarin
DOACs

99
Q

3 ACs/APs to prevent stroke in AF

A

DOACs
ESRD: xarelto or eliquis

100
Q

AC/AP for prosthetic valve

A

warfarin (and sometimes ASA)

101
Q

2 ACs/APs for TAVR

A

ASA+plavix for 3-6 months then ASA for life

102
Q

3 ACs/APs for ischemic stroke

A

ASA
ASA/dipyridamole
plavix

103
Q

4 ACs/APs for MI s/p PCI

A

ASA
plavix
prasugrel
ticagrelor

104
Q

recombinant EPO indication

A

treatment of anemia in chronic renal failure, zidovudine admin (HIV med) and chemo admin
(Darbepoetin - long acting version) not indicated for zidovudine

105
Q

is warfarin safe in pregnancy

A

no

106
Q

is heparin safe in pregnancy

A

yes

107
Q

is ASA/plavix safe in pregnancy

A

only if there is a dire need

108
Q

indication for DOACs

A

fast onset
VTE treatment and AF

109
Q

MOA of recombinant EPO

A

stimulates production of RBCs in erythroid tissues in bone marrow

110
Q

why is iron supplementation for anemia important

A

iron is needed for the creation of heme groups needed for hgb and myoglobin

111
Q

where is excess iron stored

A

liver
spleen
bone marrow

112
Q

when are DOACs inappropriate to prescribe

A

MI
ischemic stroke
prosthetic heart valves

112
Q

education regarding taking iron supplements

A

empty stomach or with OJ because an acidic environment is needed for absorption

113
Q

DOAC monitoring

A

renal and hepatic function
prodrug and excreted by kidney
may need to renally dose

114
Q

reversal for warfarin

A

vit K
FFP

115
Q

reversal for dabigatran and pradaxa

A

idarucizumab

116
Q

Xa inhibitors (-aban) reversal agent

A

andexanet

117
Q

7 medications that worsen HF

A

flecainide
disopyramide
sotalol
dronedarone
a-blockers (-zosins)
CCBs
moxonidine

118
Q

mechanisms of antibiotic resistance (6)

A

-bacterial enzyme production
-alteration of bacterial cell membranes (inhibiting abx from entering the cell)
-activation of efflux pumps expels abx out of the intracellular space back across the cell membrane
-alteration of abx target site of action, mutations alter the ribosomal binding site
-alteration of target enzymes
-overproduction of target enzymes leading to resistance

119
Q

3 ways abx work

A

interference with cell wall synthesis
interference with nucleic acid synthesis
interference with protein synthesis

120
Q

PCN MOA

A

inhibition of cell wall synthesis, binds to PCN-binding proteins

121
Q

Cephalosporins MOA

A

inhibition of cell wall synthesis, binds to PCN-binding proteins

122
Q

Monobactams MOA

A

inhibition of cell wall synthesis, binds to PCN-binding proteins

123
Q

Carbapenems MOA

A

inhibition of cell wall synthesis, binds to PCN-binding proteins

124
Q

Beta-Lactam/Beta-Lactamase inhibitors MOA

A

inhibition of cell wall synthesis, binds to PCN-binding proteins

125
Q

Fluroquinolones MOA

A

Inhibits DNA gyrase and topoisomerase IV enzymes which are needed to coil the bacteria DNA

126
Q

Macrolides MOA

A

inhibits bacterial protein synthesis by binding to the 50S ribosomal subunit

126
Q

Amioglycosides and tetracyclines MOA

A

inhibit bacterial protein synthesis by binding to the smaller 30S ribosomal subunit

127
Q

Sulfa MOA

A

inhibit the incorporation of para-amiobenzoic acid, the basic building block bacteria use to synthesize dihydrofolic acid which is required for bacterial cell growth

127
Q

glycopeptide MOA

A

cell wall active agent

127
Q

clindamycin MOA

A

binds to 50S subunit of bacterial ribosome and inhibits protein synthesis

128
Q

flagyl MOA

A

interacts with bacterial DNA causing strand breakage and results in protein synthesis inhibition

129
Q

Glycopeptide SE (2)

A

Red-man syndrome
nephrotoxicity

130
Q

red man syndrome

A

histamine mediated phenomenon affiliated with infusion rate
pruritus
flushing of head, neck, face
hypotension

131
Q

fluoroquinolones bioavailability

A

highly bioavailable

132
Q

fluoroquinolones distribution

A

most tissues and body fluids except CNS

133
Q

fluoroquinolones half life

A

4-12 hours

134
Q

fluoroquinolones excretion

A

renal

135
Q

what type of organism does PCN treat

A

gram positive

136
Q

what type of organism do cephalosporins treat

A

gram positive ad negative

137
Q

what type of organism does clinda treat

A

gram positive and MRSA

138
Q

what type of organism does vanco treat

A

MRSA and gram positive

139
Q

what type of organism do carbapenems treat

A

gram positive and negative

140
Q

what type of organism do tetracyclines treat

A

gram positive and some gram negatives

141
Q

what type of organism do fluoroquinolones treat

A

gram negative and some gram positive

142
Q

what type of organism do aminoglycosides treat

A

gram negative

143
Q

what type of organism do macrolides treat

A

gram positive and some negatives

144
Q

cephalosporins absorption

A

well absorbed in GI tract

145
Q

cephalosporins distribution

A

penetrates well into tissues and body fluids with high concentrations in urinary tract. 3rd and 4th gen penerate CSF

146
Q

cephalosporin excretion

A

kidney except ceftriaxone which is excreted by the liver

147
Q

beta lactams distribution

A

most body tissues except CSF

148
Q

beta lactams excretion

A

glomerular filtration so check renal function

149
Q

how to treat MRSA (2)

A

vancomycin
bactrim

150
Q

most common SE of antibiotic treatment

A

c diff

151
Q

treatment of c diff

A

PO vanco

152
Q

most common SE of PCN

A

hypersensitivity

153
Q

most common SE of beta-lactam and BLI

A

GI effects
hypersensitivity

154
Q

most common SE of cephalosporins and monobactams

A

safe class with favorable toxicity profile

155
Q

most common SE of carbapenems

A

neurotoxicity (seizure)

156
Q

most common SE of quinolones

A

hepatotoxicity
QTC prolongation
GI upset

157
Q

most common SE of macrolides

A

GI upset

158
Q

most common SE of aminoglycosides

A

nephrotoxicity
ototoxicity

159
Q

most common SE of tetracycline

A

GI side effects
hepatotoxicity

160
Q

most common SE of sulfas

A

rash
fever
GI effects
SJS

161
Q

most common SE(4) glycopeptides

A

fever, chills, phlebitis, red man syndrome

162
Q

most common SE of clinda

A

c diff

163
Q

azithromycin half life

A

50-60 hours

164
Q

sulfa half life

A

hours to days

165
Q

tetracyclines half life

A

short acting- 8
long acting- 16-18

166
Q

vanco half life

A

5-11 hours

167
Q

HIV lab values post exposure

A

CD4+ will rapidly decline 2-3 weeks post exposure and HIV RNA with increase greatly

168
Q

Diagnosis of HIV labs

A

presence of HIV RNA or p24 antigen
negative or indeterminate HIV antibody test
CD4 and plasma HIV RNA viral load

169
Q

normal CD4+ T-cell count

A

500-1600

170
Q

what does a CD+ T-cell count of less than 200 indicate

A

AIDS malignancies

171
Q

undetectable viral load number

A

<20-75 copies/ml

172
Q

Reverse transcriptase inhibitors MOA

A

work in target cells to interfere with the transcription of RNA or DNA

173
Q

proteases inhibiors MOA

A

activity late in the reproduction phase of the HIV virus inhibiting the ability of the polyprotein chains to break apart and create new chains of the virus

174
Q

what is the outcome of protease inhibitor

A

decrease the production of viral RNA

175
Q

fusion inhibitor MOA

A

Prevents fusion of the virus to the cell membrane of the CD4 host cell

176
Q

integrase inhibitor MOA

A

prevents integration of viral DNA into the host cell’s genome

177
Q

CCR5 antagonist MOA

A

Blocks the CCR5 receptor on the CD4 cell membrane. Not all viruses use this receptor for cell entry

178
Q

5 goals of HIV treatment

A

maximal suppression of viral load to undetectable levels
restoration and preservation of immune system function
enhance QOL and duration of life
reduce M&M from HIV-related complications
prevent HIV transmission

179
Q

who is eligible for ART therapy

A

all patients regardless of CD4+ count should be offered treatment as soon as possible with ART

180
Q

10 labs before initiating ART

A

H&P
CBC
BMP
LFTs
fasting lipid profile and glucose
urinalysis
CD4+
T-cell count
viral load

181
Q

recommended starting ART

A

2 reverse transcriptase inhibitors and a third drug (either protease or integrase inhibitor)

182
Q

how often or check CD4+ count after ART initiation and why

A

3-6 months to assess response for first 2 years of treatment and to determine the necessity of opportunistic infection prophylaxis

183
Q

how often or check CD4+ count when consistently above the threshold for risk of opportunistic infection

A

300-500
yearly

184
Q

how often or check CD4+ count when consistently above 500 after 2 years of ART

A

optional

185
Q

how often to check viral load after therapy initiated or changed

A

immediately before treatment
2-8 weeks later
q4-8 weeks until less than 200
q3-4 months (6 months if immunologically stable and fully suppressed viral load for at least 2 years)

186
Q

education for HIV

A

Adherence is the most crucial factor to success-stopping a medication can increase resistance
create a med plan
discuss how to take meds properly
lifesyle changes
SE to monitor for
develop a support system

NU 560 Pharmacotherapeutics (5 decks)

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