Unit 3 Flashcards
1
Q
Do ACEs and ARBs affect arterial vasculature, venous vasculature, or both?
A
Both
2
Q
Do CCBs affect arterial vasculature, venous vasculature, or both?
A
Arterial
3
Q
Do diuretics affect arterial vasculature, venous vasculature, or both?
A
venous
long term use can affect arterial
4
Q
Do BBs affect arterial vasculature, venous vasculature, or both?
A
both
5
Q
Do alpha agonists/blockers affect arterial vasculature, venous vasculature, or both?
A
both
6
Q
Do nitrates affect arterial vasculature, venous vasculature, or both?
A
Both
7
Q
Goal SBP and DBP for Age>60
A
<150
<90
8
Q
Goal SBP and DBP for Age<60
A
<140
<90
9
Q
Goal SBP and DBP for DM and CKD
A
<140
<90
10
Q
Goal SBP and DBP for CKD only
A
<130
<80
11
Q
ALL patients with DM and/or CKD with albuminuria >300 should receive what
A
ACE or ARB
12
Q
How to treat HTN in non-black with no cormorbidities or just DM
A
thiazide
ACE/ARB
CCB
13
Q
How to treat HTN in a black patient with no comorbidities or just DM
A
thiazide
CCB
14
Q
statins MOA
A
inhibit HMG CoA reductase which inhibits LDL production in the liver
15
Q
2 examples of high dose statins
A
atorvastatin 80mg
rosuvastatin 40mg
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
17
Q
monitoring for statins
A
baseline lipid panel and LFTs
recheck in 3 mo
if at goal, monitor lipids q3-12 months
18
Q
education for statins
A
avoid grapefruit juice
Many med interactions due to CYP3A involvement
19
Q
SE of statins (4)
A
myalgia– rhabdo/renal failure
headache
fatigue
GI distress
elevated LFTs
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
21
Q
6 medications for angina
A
ACEs/ARBs
Spironolactone
Nitrates
BB
CCB
AP- aspirin
22
Q
2 short acting medications for angina
A
nitro SL
isordil SL
23
Q
2 long acting medications for angina
A
nitro topical/transdermal patch
isosorbide IR/ER
24
Q
MOA BB
A
block beta 1 and/or beta 2 receptors centrally and peripherally, leading to decreased cardiac output and sympathetic outflow
25
BB contraindications (6)
bradycardia
2nd and 3rd degree HB
decompensated heart failure
severe bronchospastic disease
caution in asthma and COPD
26
SE of BB (8)
fatigue
drowsiness
bronchospasm
N/V
bradycardia
AV conduction abnormalities
CHF
mask hypoglycemia
27
MOA CCB
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
28
CCB non-dihydropyridines contraindications (2)
heart block and sick sinus syndrome (avoid in LV failure)
29
nifedipine contraindications (2)
essential HTN or HTN emergency (inconsistent fluctuations in BP and reflex tachycardia)
30
SE non-dihydropyridines (3)
GI upset
peripheral edema
hypotension
31
SE dihydropyridine (4)
headache
flushing
palpitations
peripheral edema
32
MOA ACEIs
prevent the conversion of angiotensin I to angiotensin II. Inhibit the degradation of bradykinin and increase the synthesis of vasodilating prostaglandins
33
ACEI contraindications (3)
b/l renal artery stenosis (acute renal failure)
pregnancy (avoid in women childbearing age)
hx of angioedema
34
SE ACEIs (6)
cough
rashes
dizziness
hyperkalemia
angioedema
laryngeal edema
35
MOA ARBs
block the binding of angiotensin II to the angiotensin II receptor which blocks the vasoconstriction and aldosterone-secreting effects
36
ARB contraindications (3)
b/l renal artery stenosis
pregnancy
caution in renal/hepatic impairment
37
SE ARBs (8)
dizziness
URI
viral infection
fatigue
diarrhea
sinusitis
pharyngitis
rhinitis
38
Loop diuretics MOA
inhibit the reabsorption of sodium and chloride in the proximal and distal tubules and the loop of Henle
39
Loop diuretics contraindications (5)
anuria
hepatic coma
severe electrolyte depletion
hypersensitivity to sulfas
ethacrynic acid contraindicated in infants
40
Loop diuretics SE (6)
hypokalemia
hypomagnesemia
hypercalcemia
hyperuricemia
hyperglycemia and hyperlipidemia in high doses
41
Thiazide diuretics MOA
inhibits Na, K, and Cl reabsorption in the distal tubule
42
Thiazide diuretics contraindications (2)
anuria
hypersensitivity to sulfas
43
Thiazide diuretics SE (6)
hypokalemia
hypomagnesemia
hypercalcemia
hyperuricemia
hyperglycemia
hyperlipidemia
44
potassium sparing diuretics MOA
interfere with sodium reabsorption at the distal tubule, decreasing potassium secretion
45
aldosterone receptor antagonists MOA
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
46
Potassium-Sparing Diuretics/Aldosterone Receptor Antagonists contraindications (4)
hyperkalemia, Addison disease, anuria, patients taking eplerenone
47
Potassium-Sparing Diuretics/Aldosterone Receptor Antagonists SE (4)
gynecomastia, hirsutism, menstrual irregularities, gout symptoms
48
Central Alpha-2 Receptor Agonists MOA
inhibit action of adrenaline on smooth muscle in blood vessel walls, dilating both arterioles and veins and cause relaxation of smooth muscle
Clonidine
49
Central Alpha-2 Receptor Agonists contraindications
use with tadalafil, sildenafil, and vardenafil (increased risk of symptomatic hypotension)
50
Central Alpha-2 Receptor Agonists SE (5)
first-dose phenomenon:
dizziness
faintness
palpitations
syncope
ortho hypotension
51
class 1 antiarrhythmics
sodium channel blockers:
procainamide
lidocaine
quinidine
52
what leads to quinidine toxicity
substrate of CYP3A4 (interacts with ketoconazole, erythromycin, amio, verapamil, diltiazem, rifampin, phenobarbital, phenytoin)
inhibitor of CYP2D6 (interacts with BB)
53
what leads to procainamide toxicity
renal impairment leads to accumulating levels
54
what leads to lidocaine toxicity
reduced hepatic blood flow d/t HFrEF delays metabolism
55
Class II antiarrhythmics
beta blockers
56
Class III antiarrhythmics
potassium channel blockers:
amiodarone
dronedarone
sotalol
dofetilide
57
what leads to amio and dronedarone toxicity
substrate of CYP3A4
inhibitor of CYO3A4, 2C9, 2D6
58
what not to give with amio and drondarone (9)
azoles
cyclosporine
clarithromycin
ritonavir
rifampin
phenobarbital
phenytoin
carbamazepine
St. John's Wort
59
what leads to sotalol toxicity
poor renal function
60
what drugs lead to dofetilide toxicity (7)
cimetidine
dolutegravir
ketoconazole
HCTZ
megestrol
prochlorperazine bactrim
verapamil
61
what leads to dofetilide toxicity
poor renal function
62
class IV antiarrhythmics
CCB
63
what leads to diltiazem and verapamil toxicity
substrate and inhibitor of CYP3A4 do use cautiously with other meds that are metabolized by that isozyme
63
what leads to digoxin toxicity
poor renal function
electrolyte disturbance predispose the myocardium to the toxic effects of dig
64
3 drug interactions of dig
amio
dronedarone
verapamil
65
MOA of digoxin
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
66
indication of digoxin
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
67
onset and peak of digoxin
6-8 hours
68
MOA amio
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
69
amio indications
management of acute VT/VF and AF
70
amio pharacodynamics (4)
poor oral bioavailability
large vol of distribution
long half life
loading dose needed
71
amio SE (10)
pulmonary toxicity
corneal microdeposits
thyroid abnormalities
N/V
hepatotoxicity
prolonged QT
photosensitivity
blue/gray skin
heart block
tremors
72
How do ACE/ARBs help with heart failure
reduce afterload
prevent cardiac remodeling
73
How do BB help with heart failure
reduce mortality, decrease O2 demand and workload
74
How do diuretics help with heart failure
reduce preload
75
how do nitrates help with heart failure
relax vasculature (coronary and systemic) to impact O2 supply and demand
76
Textbook treatment order for heart failure
1. ACE (ARB if not tolerated) and BB
2. Diuretic
3. Digoxin
4. ARB, aldosterone agonist, hydral/isosorbide
77
How to treat AF/AFL with normal LV function
IV diltiazem, IV verapamil, IV BB
dig too slow onset
78
How to treat AF/AFL with reduced LV function
IV BB or IV digoxin
79
indication of EPO
treats anemia in ESRD who can't produce enough EPO due to renal damage
if hgb <10 to avoid transfusion
80
How is EPO given
SQ 3x/week
81
Education for patients on EPO
take multivitamin d/t renal restrictive diet and iron supplement
82
contraindications of EPO
uncontrolled HTN or sensitivity to mammalian products/albumin
83
SE of EPO (6)
HTN
HA
seizure
nausea
edema
fatigue
84
monitoring for patients on EPO (10)
H&H
ferritin
transferrin
B12
folate
BP
clotting times
plts
BUN and Cr
85
4 indications for AP therapy
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
indications of ASA
post ACS
prevent thrombosis
add-on AC
87
ASA platelet dysfunction
lasts for 7-10 days after day of d/c
d/t lifespan of the platelets exposed to ASA
irreversible
88
onset of ASA
5 minutes
89
onset of plavix
2 hours
90
how long to d/c plavix before surgery
5-7 days
91
SE of ASA (3)
GI upset
bleeding
potentiate PUD
92
SE of plavix (3)
diarrhea
bruising
bleeding
93
3 contraindications for AP
active GI bleed
ICH
PUD
94
how to manage a patient with initiation of warfarin
start with warfarin + injectable AC
d/c LMWH when INR therapeutic
don't bridge with direct thrombin inhibitor (dabigatran)
95
Contraindications for ACs (10)
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
7 labs to consider before initiating ACs
PT
INR
aPTT
UA
CBC
LFT
pregnancy test
97
3 considerations for LMWH or DOAC
body wt
Cr
CrCl
98
3 ACs/APs to prevent VTE
Lovenox
warfarin
DOACs
99
3 ACs/APs to prevent stroke in AF
DOACs
ESRD: xarelto or eliquis
100
AC/AP for prosthetic valve
warfarin (and sometimes ASA)
101
2 ACs/APs for TAVR
ASA+plavix for 3-6 months then ASA for life
102
3 ACs/APs for ischemic stroke
ASA
ASA/dipyridamole
plavix
103
4 ACs/APs for MI s/p PCI
ASA
plavix
prasugrel
ticagrelor
104
recombinant EPO indication
treatment of anemia in chronic renal failure, zidovudine admin (HIV med) and chemo admin
(Darbepoetin - long acting version) not indicated for zidovudine
105
is warfarin safe in pregnancy
no
106
is heparin safe in pregnancy
yes
107
is ASA/plavix safe in pregnancy
only if there is a dire need
108
indication for DOACs
fast onset
VTE treatment and AF
109
MOA of recombinant EPO
stimulates production of RBCs in erythroid tissues in bone marrow
110
why is iron supplementation for anemia important
iron is needed for the creation of heme groups needed for hgb and myoglobin
111
where is excess iron stored
liver
spleen
bone marrow
112
when are DOACs inappropriate to prescribe
MI
ischemic stroke
prosthetic heart valves
112
education regarding taking iron supplements
empty stomach or with OJ because an acidic environment is needed for absorption
113
DOAC monitoring
renal and hepatic function
prodrug and excreted by kidney
may need to renally dose
114
reversal for warfarin
vit K
FFP
115
reversal for dabigatran and pradaxa
idarucizumab
116
Xa inhibitors (-aban) reversal agent
andexanet
117
7 medications that worsen HF
flecainide
disopyramide
sotalol
dronedarone
a-blockers (-zosins)
CCBs
moxonidine
118
mechanisms of antibiotic resistance (6)
-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
3 ways abx work
interference with cell wall synthesis
interference with nucleic acid synthesis
interference with protein synthesis
120
PCN MOA
inhibition of cell wall synthesis, binds to PCN-binding proteins
121
Cephalosporins MOA
inhibition of cell wall synthesis, binds to PCN-binding proteins
122
Monobactams MOA
inhibition of cell wall synthesis, binds to PCN-binding proteins
123
Carbapenems MOA
inhibition of cell wall synthesis, binds to PCN-binding proteins
124
Beta-Lactam/Beta-Lactamase inhibitors MOA
inhibition of cell wall synthesis, binds to PCN-binding proteins
125
Fluroquinolones MOA
Inhibits DNA gyrase and topoisomerase IV enzymes which are needed to coil the bacteria DNA
126
Macrolides MOA
inhibits bacterial protein synthesis by binding to the 50S ribosomal subunit
126
Amioglycosides and tetracyclines MOA
inhibit bacterial protein synthesis by binding to the smaller 30S ribosomal subunit
127
Sulfa MOA
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
glycopeptide MOA
cell wall active agent
127
clindamycin MOA
binds to 50S subunit of bacterial ribosome and inhibits protein synthesis
128
flagyl MOA
interacts with bacterial DNA causing strand breakage and results in protein synthesis inhibition
129
Glycopeptide SE (2)
Red-man syndrome
nephrotoxicity
130
red man syndrome
histamine mediated phenomenon affiliated with infusion rate
pruritus
flushing of head, neck, face
hypotension
131
fluoroquinolones bioavailability
highly bioavailable
132
fluoroquinolones distribution
most tissues and body fluids except CNS
133
fluoroquinolones half life
4-12 hours
134
fluoroquinolones excretion
renal
135
what type of organism does PCN treat
gram positive
136
what type of organism do cephalosporins treat
gram positive ad negative
137
what type of organism does clinda treat
gram positive and MRSA
138
what type of organism does vanco treat
MRSA and gram positive
139
what type of organism do carbapenems treat
gram positive and negative
140
what type of organism do tetracyclines treat
gram positive and some gram negatives
141
what type of organism do fluoroquinolones treat
gram negative and some gram positive
142
what type of organism do aminoglycosides treat
gram negative
143
what type of organism do macrolides treat
gram positive and some negatives
144
cephalosporins absorption
well absorbed in GI tract
145
cephalosporins distribution
penetrates well into tissues and body fluids with high concentrations in urinary tract. 3rd and 4th gen penerate CSF
146
cephalosporin excretion
kidney except ceftriaxone which is excreted by the liver
147
beta lactams distribution
most body tissues except CSF
148
beta lactams excretion
glomerular filtration so check renal function
149
how to treat MRSA (2)
vancomycin
bactrim
150
most common SE of antibiotic treatment
c diff
151
treatment of c diff
PO vanco
152
most common SE of PCN
hypersensitivity
153
most common SE of beta-lactam and BLI
GI effects
hypersensitivity
154
most common SE of cephalosporins and monobactams
safe class with favorable toxicity profile
155
most common SE of carbapenems
neurotoxicity (seizure)
156
most common SE of quinolones
hepatotoxicity
QTC prolongation
GI upset
157
most common SE of macrolides
GI upset
158
most common SE of aminoglycosides
nephrotoxicity
ototoxicity
159
most common SE of tetracycline
GI side effects
hepatotoxicity
160
most common SE of sulfas
rash
fever
GI effects
SJS
161
most common SE(4) glycopeptides
fever, chills, phlebitis, red man syndrome
162
most common SE of clinda
c diff
163
azithromycin half life
50-60 hours
164
sulfa half life
hours to days
165
tetracyclines half life
short acting- 8
long acting- 16-18
166
vanco half life
5-11 hours
167
HIV lab values post exposure
CD4+ will rapidly decline 2-3 weeks post exposure and HIV RNA with increase greatly
168
Diagnosis of HIV labs
presence of HIV RNA or p24 antigen
negative or indeterminate HIV antibody test
CD4 and plasma HIV RNA viral load
169
normal CD4+ T-cell count
500-1600
170
what does a CD+ T-cell count of less than 200 indicate
AIDS malignancies
171
undetectable viral load number
<20-75 copies/ml
172
Reverse transcriptase inhibitors MOA
work in target cells to interfere with the transcription of RNA or DNA
173
proteases inhibiors MOA
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
what is the outcome of protease inhibitor
decrease the production of viral RNA
175
fusion inhibitor MOA
Prevents fusion of the virus to the cell membrane of the CD4 host cell
176
integrase inhibitor MOA
prevents integration of viral DNA into the host cell’s genome
177
CCR5 antagonist MOA
Blocks the CCR5 receptor on the CD4 cell membrane. Not all viruses use this receptor for cell entry
178
5 goals of HIV treatment
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
who is eligible for ART therapy
all patients regardless of CD4+ count should be offered treatment as soon as possible with ART
180
10 labs before initiating ART
H&P
CBC
BMP
LFTs
fasting lipid profile and glucose
urinalysis
CD4+
T-cell count
viral load
181
recommended starting ART
2 reverse transcriptase inhibitors and a third drug (either protease or integrase inhibitor)
182
how often or check CD4+ count after ART initiation and why
3-6 months to assess response for first 2 years of treatment and to determine the necessity of opportunistic infection prophylaxis
183
how often or check CD4+ count when consistently above the threshold for risk of opportunistic infection
300-500
yearly
184
how often or check CD4+ count when consistently above 500 after 2 years of ART
optional
185
how often to check viral load after therapy initiated or changed
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
education for HIV
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
