Exam 1 Flashcards
(203 cards)
1
Q
unfractionated heparin route
A
IV/SC
2
Q
LMWH prototype
A
enoxaparin (Lovenox)
3
Q
LMWH route
A
SC
4
Q
vitamin K antagonist prototype
A
Warfarin (coumadin)
5
Q
Fondaparinux route
A
IV/SC
6
Q
contraindications to unfractionated heparin
A
active bleeding, history of heparin-induced thrombocytopenia
7
Q
contraindications to LMWH
A
active bleeding, hx of heparin-induced thrombocytopenia, CrCl<30
8
Q
contraindications to fondaparinux
A
active bleeding, CrCl<30
9
Q
contraindications to warfarin
A
active bleeding, pregnancy (ok in breastfeeding)
10
Q
reversal for forms of heparin
A
protamine
11
Q
reversal for fondaparinux
A
none
12
Q
reversal for warfarin
A
vitamin K, 4-factor prothrombin complex concentrate
13
Q
advantages to unfractionated heparin
A
preferred in renal impairment or dialysis, has reversal agent, short half-life
14
Q
disadvantages to unfractionated heparin
A
less predictable kinetics require close monitoring. Reduced efficacy and safety compaired to LMWH. SC route is hard for patients
15
Q
advantages to LMWH
A
preferred over UFH due to improved efficacy and safety. More predictable kinetics mean less monitoring. Longer half-life allows for more infrequent dosing
16
Q
disadvantages of LMWH
A
renal impairment may preclude use, only partial reveriability
17
Q
advantages of fondaparinux
A
predictable kinetics, long half-life, may be easier to use in morbid obesity
18
Q
disadvantages of fondaparinux
A
Renal impairment may preclude use, no reversal agent
19
Q
disadvantages of warfarin
A
Drug-diet interactions, drug-drug interactions, drug-disease state
20
Q
conditions affecting warfarin dosing
A
Age>75, liver disease, low albumin, decompensated CHF, drug interactions, thyroid storm
21
Q
warfarin initial dose
A
2.5-3.0 mg/day
22
Q
DOACs factor 10a inhibitors prototypes
A
apixaban (Eliquis), rivoroxaban (Xarelto)
23
Q
DOACs factor IIa inhibitors prototypes
A
dabigatran
24
Q
DOACs route
A
PO
25
contraindications to DOACs
active bleeding, pregnancy, severe renal impairment, bariatric surgery, known GI absorption problems
26
DOACs (factor Xa) reversal
adexanet alpha (Andexxa)
27
DOACs (factor 2a) reversal
Praxbind (idarucizumab)
28
stopping apixiban
stopping abruptly can increase risk of stroke (short half/life)
29
stroke prevention in non-valvular afib
DOACs/warfarin
30
stroke prevention in valvular afib
warfarin
31
guidelines for anticoagulation with cardioversion
Pt should be anticoagulated for 3 weeks prior to cardioversion if Afib has been present for >48 hours
32
Where are DVT Pt's treated
majority outpatient
33
treatment for DVT
DOACs or Warfarin
34
conventional DVT treatment
warfarin/LMWH bridge for first 5 days, until INR is >2 for >24 hours
35
Single drug DOAC DVT treatment
rivaroxaban or apixaban starting at a higher dose and then switching to a lower dose
36
DOAC DVT treatment with bridge
LMWH for first 5 days then switch to dabigatran/edoxaban
37
duration of anticoagulant treatment after DVT
minimum 3 months
38
First line antihypertensive classes
ACEI, ARB, thiazides, CCB (dihydropyridines)
39
ACEI mechanism
blocks ACE to inhibit formation of angiotensin II, leading to vasodilation
40
ACEI side effects
hypotension, dizziness, hyperkalemia, angioedema teratogen
41
ACEI is especially first line for what conditions
HTN with DM or CDK
42
ACEI monitoring
Potassium, creatinine, BP
43
ARB mechanism
block angiotensin 2 receptors on blood vessels, reducing systemic vascular resistance
44
ARB side effects
hypotension, dizziness, headache, hyperkalemia, angioedema
45
ARB monitoring
Potassium, creatinine, BP
46
Thiazide advantages
effective at BP control with less diuresis than other types of diuretics
47
which thiazide is preferred
chlorthalidone
48
mechanism of thiazides
inhibit Na/Cl transporter in distal tubule, increasing Na and Cl excretion
49
side effects of thiazides
Hyperglycemia, hyperlipidemia, uremia, hypercalcemia, hypokalemia, metabolic alkalosis, hypotension, sun sensitivity, hyponatremia/magnesemia/phosphatemia. Arrhythmias, SJS
50
thiazides cautions
caution with history of gout, less effective in Pts with CrCl<30
51
CCB dihydropyridines prototype
amlodipine
52
CCB mechanism
Bind to L-type calcium channels on vascular smooth muscle, cardiac myocytes, and cardiac nodal tissue to block entry of calcium into the cells. More selective for vascular cells with minimal direct cardiac effects
53
CCB side effects
hypotension, dizziness, peripheral edema
54
CCB monitoring
BP
55
thiazides monitoring
Blood pressure
Urine output
Electrolytes (potassium, sodium, magnesium, calcium): within 1 week of initiation; frequently during first few months; at least yearly thereafter
Uric acid: within 2-6 weeks of initiation; “routinely” thereafter
SCr/BUN: baseline; then 1-2 times per year
Glucose: baseline and at least once per year
56
CCBs, non-dihydropyridines prototype
diltiazem, verapamil
57
CCBs, non-dihydropyridines mechanism
same as dihydropyridines except these are selective for cardiac myocytes with less effects on systemic vasodilation
58
When would a beta blocker be part of a first-line HTN treatmetn
in cases of stable ischemic heart disease or heart failure
59
which BBs to use for heart failure with reduced ejection fraction
metoprolol succinate, carvedilol, bisoprolol
60
beta blockers mechanism
Bind to beta-adrenergic receptors and inhibit the effects of catecholamines (norepinephrine and epinephrine) at these receptors
61
side effects of CCBs non-dihydropyridine
hypotension, dizziness, constipation, bradycardia
62
monitoring CCBs non-dihydropyridine
BP, HR
63
side effects of BBs
Bronchospasm, bradycardia, hypotension (~1%), dizziness, fatigue, depression
64
cautions of BBs
do not initiate if in decompensated HF, may mask symptoms of hypoglycemia, caution in asthma/COPD, contraindicated in severe bradycardia
65
Loop diuretics mechanism
Inhibit sodium-potassium-chloride cotransporter in the thick ascending limb
66
loop diuretics side effects
hypomagnesemia; hypokalemia; hyperuricemia; hypotension; metabolic alkalosis, ototoxicity, SJS
67
loop diuretics caution
not generally used for HTN
68
loop diuretics monitoring
BP, urine output, electrolytes within 1 week of intitiation, uric acid, creatinine, BUN glucose, blood dyscrasias
69
Potassium-sparing diuretics prototype
triamterene
70
Potassium-sparing diuretics mechanism
Directly inhibit sodium channels in distal renal tubule. Have small effects alone for HTN, so they're used in hypokalemia in pt's with HTN.
71
Potassium-sparing diuretics side effects
hyperkalemia, hyperuricemia, hypotension, anemia, thrombocytopenia
72
Potassium-sparing diuretics monitoring
BP, urine output, electrolytes (esp K) within 1 week, uric acid, Cr/BUN, glucose, blood dyscrasias
73
Potassium-sparing diuretics cautions
not for use in anuric, hyperkalemic patients, those who take potassium, or those with significant renal disease
74
aldosterone antagonist diuretics mechanism
Block the action of aldosterone at distal segment of the distal tubule; compete for the aldosterone-dependent sodium-potassium exchange site in distal tubule cells increased secretion of water and sodium
75
aldosterone antagonist diuretics uses
primary hyperaldosteronism and resistant hypertension, add-on for HF
76
aldosterone antagonist side effects
hyperkalemia; GI upset; gynecomastia (spironolactone); hyperglycemia; hyponatremia, hypomagnesemia
Severe side effects: Cardiac arrhythmias/cardiac death (due to hyperkalemia), Stevens-Johnson syndrome, Agranulocytosis
77
aldosterone antagonist cautions
same as for K-sparing diuretics
78
which drug class is last-line for HTN
alpha-2 agonists
79
alpha-2 agonist examples
clonidine, methyldopa
80
alpha 2 agonist mechanism
Alpha-2 receptor agonists act as vasodilators; act in the central nervous system to reduce sympathetic outflow from the CNS decreased peripheral resistance, renal vascular resistance, heart rate and blood pressure
81
alpha 2 agonist side effects
dry mouth; dizziness; sedation/fatigue; hypotension
| Severe side effects: heart block; rebound hypertension (with abrupt discontinuation –clonidine
82
vasodilators example
hydralazine
83
vasodilators mechanism
Highly specific action on arterial vessels reduces vascular resistance and arterial pressure (possibly due to opening of K+ channels, inhibition of Ca release, or formation of NO)
84
vasodilators side effects
hypotension; edema; palpitations; reflex tachycardia; headaches; flushing
Severe side effects: lupus-like syndrome (~10%)
85
vasodilators dosage note
2-3 times daily
86
aldosterone antagonist monitoring
BP, urine output, electrolytes (esp. K) within 1 week, Cr/BUN
87
indications for antihypertensives
BP>130/80 with 10-year ASCVD risk>10% OR BP>140/90
88
target BP for most patients
130/80
89
nitroglycerin action
venodilation reduces preload. Epicardial vessels are dilated. Alleviate coronary spasm
90
nitroglycerin cautions
contraindicated with recent cialis or viagra use
91
IV/SL nitro indications
acute relief of angina
92
PO/transdermal nitro indications
chronic prophylaxis of angina
93
PO forms of nitro
start with isosorbide
94
transdermal forms of nitro
nitro patch/ointment
95
how to use nitro for angia prophylaxis
must have 12 hour nitrate free interval to avoid tolerance
96
nitro side effects
HA, syncope, hypotension, dizzines, reflex tachycardia
97
onset of IV nitro
1-2 minutes
98
how to take SL nitro
one tablet every 5 minutes, up to 3 doses (onset 1-3 minutes)
99
how to use nitro patch
12 hours on, 12 hours off
100
how to use nitro ointment
place every 6-8 hours during the day
101
how to take PO nitro
TID or BID depending on type
102
most popular form of chronic angina management
isosorbide mononitrate extended release (QD)
103
fibrinolytic contraindications
active bleeding, intracranial hemorrhage, bleeding issues, suspected aortic dissection, severe HTN
104
examples of fibrinolytics
tPA (alteplase), tenecteplase
105
fibrinolytics mechanism
activate plasminogen
106
clopidogrel indications and class
P2Y12 receptor inhibitor, ACS/MI/stroke/PAD
107
which anti-platelet is used for ACS with PCI only
prasurgrel
108
which antiplatelet is considered the best but is most expensive
tricagrelor
109
last-line antianginal drug in patients with refractory angina
ranolazine
110
CCB post-MI benefits
reduce afterload and cardiac workload, dilate coronary arteries, reduce HR/contractility, relieve chest pain
111
ACE/ARB post-MI benefits
Limit post‐infarction left ventricular dilatation and hypertrophy (remodeling) and
preserve ventricular pump function
• Decrease progression to CHF, reinfarction, and mortality
• Patients with left ventricular ejection fraction (LVEF) < 40% derive the most benefit
112
BB post-MI benefits
• Lower heart rate and cardiac contractility,
ultimately leading to a reduction in cardiac
workload
• Limit myocardial damage and mortality
113
what anticoagulant to use during MI
heparin product
114
clopidogrel dosage
300-600 loading, 75 mg daily
115
Prasugrel dosage
60 mg loading dose, then 5-10 mg once daily
116
ticagrelor dosage
180 mg loading, then 60-90 mg twice daily
117
unfractionated heparin mechanism
binds to antithrombin III to inhibit activity of activated coagulation factors
118
heparin products origin
porcine intestinal tissue
119
unfractionated heparin half life
1-1.5 hours
120
unfractionated heparin pharmacokinetics
nonlinear
121
unfractionated heparin dosing
largely weight-based
122
unfractionated heparin monitoring
chromogenic anti-Xa level, aPTT, CBC
123
major complication of HIT
thrombosis
124
LMWH mechanism
binds to antithrombin III, inhibits activity of coag factors Xa>IIa
125
LMWH pharmacokinetics
linear
126
LMWH onset/half-life
about 4 hours for both
127
LMWH excretion
renal (must account for kidney function)
128
LMWH side effect that's different from heparin
burning on injection
129
fondaparinux mechanism
binds factor Xa
130
fondaparinux origin
synthetic
131
LMWH/fondaparinux monitoring
anti-Xa level, renal function, CBC
132
which parenteral anticoagulant to use for CKD patients
unfractionated heparin
133
warfarin route
PO only
134
warfarin metabolism
hepatic
135
warfarin half-life
very long
136
when to use lower initial dose of warfarin
age over 75, liver disease, low albumin, decomp CHF, drug interactions etc
137
what to do if miss dose of warfarin
still take if within 8 hours of usual time
138
baseline INR
0.8-1.2
139
when to check INR for warfarin
baseline, within 3-5 days of initiation, then every 1-8 weeks
140
what baseline labs to get before warfarin
albumin, LFTs, INR, CBC
141
warfarin adverse effects
bleeding/bruising, warfarin necrosis, hair loss/thinning, purple toe syndrome
142
2 classes of DOACs
factor Xa inhibitors (apixaban, rivaroxaban), factor IIa inhibitors (dabigatran)
143
DOACs exretion
renal (to varying degrees)
144
DOACs half life
much shorter than warfarin
145
DOACs pharmacokinetics
linear
146
which DOAC must be taken with food
rivaroxaban
147
which DOAC must be kept in original packaging
dabigatran
148
DOACs drug-drug interactions
minimal, based on CYP3A4 and P-gp systems
149
DOACs missed dose
take as soon as you remember
150
p-gp inducer effect on DOACs
makes them get metabolized faster = higher risk of clot
151
p-gp inhibitor effect on DOACs
makes them get metabolized slower - more risk of bleeding
152
do you check INR for DOAC
no
153
anticoagulant to use in pregnancy
lovenox
154
DOAC follow up
1-3 months initially, 6-12 months thereafter
155
non-valvular AF
absence of moderate-severe mitral stenosis or mechanical valve
156
risk stratification for stroke in A-fib scale
CHAD2DS2-VASc
157
when to offer anticoagulation per CHADS-VASc
score of 1 (male) or 2 (female)
158
NSAIDs with anticoagulant
avoid
159
SA/AV nodal tissue is primarily dependent on what electrolyte
calcium
160
ventricular myocytes are primarily dependent on what electrolyte
sodium
161
ventricular myocyte action potential phase 0
rapid influx of sodium (channels open)
162
ventricular myocyte action potential phase 1
Sodium channels close, K+ leaks out
163
ventricular myocyte action potential phase 2
Calcium channels open, calcium comes in while K leaves
164
ventricular myocyte action potential phase 3
Ca channels close, K leaves
165
ventricular myocyte action potential phase 4
resting potential
166
what causes abnormal automaticity
cell membrane is abnormally permeable to sodium in phase 4, ectopic foci compete with SA node
167
most common mechanism for arrhythmias
reentry
168
what is re-entry
indefinite propagation of an impulse originating from the SA node with activation of previously refractory tissue
169
3 requirements for re-entry
2 pathways for impulse conduction, an area of unidirectional block in 1 pathway, triggering stimulus (usually a premature beat)
170
goal of antiarrhythmic drugs
restore and maintain sinus rhythm without causing a rhythm disturbance
171
class 1 antidysrhythmic aka
sodium channel blocker
172
class 4 antidysrhythmic aka
calcium channel blocker
173
class 3 antidysrhythmic aka
potassium channel blocker
174
class 2 antidysrhythmic aka
beta blocker
175
class 1 affects which phase
0
176
class 4 affects which phase
2
177
class 3 affects which phase
3
178
class 2 affects which phase
4
179
class 1A
moderate Na channel blockers, procainamide
180
class 1B
weak Na channel blockers, Lidocaine
181
class 1C
strong Na channel blockers, flecainide
182
class 3 prototype
amiodarone
183
class 5 antiarrthyhmics
AN nodal blockers
184
class 5 examples
adenosine, digoxin
185
which class 1 exhibit use-dependence in diseased myocardium
1b
186
main uses of 1a/1b
acute ventricular dysrhythmias
187
main uses of 1c
cardioversion/sinus rhythm maintenance in a fib
188
major contraindication of 1c
structural heart disease
189
which antiarrhythmics are used for "pill in the pocket" for palpitations
1c (recurrent a fib), must take with BB/CCB to slow AV conduction
190
most commonly used antiarrhythmic class
3
191
major caution of class 3
QT prolongation
192
what is the "son of amiodarone"
dronedarone
193
which class 3 requires inpatient monitoring on initiation
sotalol, dofetilide
194
fatal complication of amiodarone
pulmonary fibrosis
195
monitoring for amiodarone
TSH, liver function, PFT
196
blue man syndrome
amiodarone-induced photosensitivity
197
amiodarone drug-drug interactions
warfarin, digoxin, beta blockers, CCBs, simvastatin (increases effects of these), grapefruit juice (increases affect of amiodarone)
198
half-life of amiodarone
1-2 months
199
side effects of sotalol
bradycardia, dizziness, fatigue
200
what antiarrhythmic classes cause long QT
1a, 3
201
what electrolyte derangements can cause long QT/torsades
hypokalemia, hypomagnesemia
202
flecainide side effects
CNS disturbances
203
lidocaine side effects
confusion, dizziness, seizures
