Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

A

methyldopa
nifedipine
labetalol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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

A

ACEi
ARBs
direct renin inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A 
(-osin)
prazosin
tamsulosin
terazosin
doxazosin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

MOA of prazosin

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

difference of tamsulosin, terazosin, doxazosin from prazosin

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

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

A

benign prostatic hypertrophy (BPH)

help kidney stones pass

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

which is the most selective beta1 blocker?

A

bisoprolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

characteristic of esmolol

A

short half life as a beta1 blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is contraindicated for propranolol?

A

peripheral vascular disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is the drug of choice for gestational HTN?

A

alpha-methyldopa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

list the alpha2 agonists

A

clonidine

alpha-methyldopa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

MOA of clonidine

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

is clonidine used as first line or adjuvant therapy?

A

adjuvant therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

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

A

alpha-methldopa

hydralazine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what happens with an abrupt withdrawal of alpha2 agonists?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

list the prostanoids (4)

A 
(-prost)
epoprostenol
treprostenil
iloprost
selexipag
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

pharmacokinetics of epoprostenol

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

pharmacokinetics of treprostenil

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
pharmacokinetics of iloprost
INHALATION 6-9 times/day
26
disadvantage of selexipag
expensive af
27
drugs used to treat PAH
prostanoids endothelin antagonists PDE-5 inhibitors guanylate cyclase sensitizers
28
MOA of prostaonids
mimics action of endogenous prostacyclin - vascular dilation - inhibits platelet aggregation - decreases pulmonary vascular resistance tx PAH
29
list the endothelin antagonists (3)
bosentan amrbisentan macitentan
30
which drug(s) nonspecifically blocks ETa and ETb endothelin receptors?
bosentan | macitentan
31
which drug(s) specifically only blocks ETa endothelin receptors?
ambrisentan
32
adverse effects of bosentan
hepatotoxicity | teratogenesis
33
drug interactions of bosentan and macitentan
accelerates metabolism of via CYP450 - warfarin - oral contraceptives (use 2 forms of BC!)
34
adverse effects of ambrisentan
teratogenesis
35
advantage of ambrisentan over bosentan?
does NOT accelerate metabolism of warfarin or OCPs (but still use 2 forms of BC)
36
adverse effects of epoprostenol and treprostenil
sepsis due to chronic catheter | life-threatening problems if pump becomes clogged
37
adverse effects of iloprost
fainting due to hypOtension
38
MOA of PDE-5 inhibitors for treatment of ED and HTN
selective blocks PDE-5 enzymes --> decrease degradation of cGMP --> incr cGMP --> longer erections (tx of ED) and vasodilation (tx of HTN)
39
dangerous drug interactions and effects of PDE-5 inhibitors
``` with alpha blockers (for HTN) --> severe hypOtension with nitrates (for angina) --> severe hypOtension ```
40
rare adverse effects of PDE-5 inhibitors
visual disturbance | priapism
41
MOA of guanylate cyclase sensitizer
1. sensitives soluble guanylate cyclase (sGC) to endogenous NO 2. directly stimulates sGC independent of NO - -> incr cGMP --> vasodilation tx PAH
42
list the guanylate cyclase sensitizer (1)
riociguat
43
if CCB vapopressor test is (+) which drugs should be used to treat pulmonary HTN?
nifedipine, diltiazem, amlodipine
44
when do you use combination therapy to treat PAH?
when the disease and sx become progressively worse
45
list the ACE inhibitors (4)
``` (-pril) captopril enalapril benazepril lisinopril ```
46
list the angiotensin receptor blockers/ARBs (3)
(-sartan) losartan valsartan candesartan
47
list the renin inhibitors (1)
aliskiren
48
list the calcium channel blockers used for treating HTN (4) -- 2 groups
dihydropyridines: (-dipine) nifedipine amlodipine non-dihydropyridines: verapamil diltiazem
49
list the direct vasodilators (3)
hydralazine nitroprusside minoxidil
50
list the HMG-CoA Reductase Inhibitors
``` (STATINS) atorvastatin fluvastatin lovastatin pitavastatin pravastatin rosuvastatin simvastatin ```
51
list the statins in order of potency for reducing LDL levels
atorvastatin rotuvastatin simvastatin lovastatin pitavastatin pravastatin fluvastatin
52
how do HMG-CoA reductase inhibitors (statins) treat lipid disorders?
inhibit HMG-CoA reductase in order to lower LDL levels (greatest decrease in LDL levels compared to all other lipid disorder drugs)
53
how are beta blockers useful in the treatment of angina pectoris? (MOA)
work to decrease the O2 demand of the myocardium seen in classic angina/angina pectoris - improve myocardial perfusion - decrease contractility - decrease BP - decrease afterload
54
list the beta blockers used for chronic ischemic heart disease (4)
propanolol nadolol metoprolol atenolol
55
contraindications of beta blockers for IHD
``` ASTHMA peripheral vascular disease T1DM bradyarrhythmias AV conduction dysfunction ```
56
adverse effects of beta blockers for IHD
``` reduced CO bronchoconstriction impaired liver glucose mobilization incr VLDL, decr HDL sedation, depression sympathetic hyper responsiveness upon abrupt withdrawal ```
57
list the PDE-5 inhibitors that can be used specifically for ED (4)
tadalafil sildenafil (viagra) vardenafil avanafil
58
absolute contraindication for PDE-5 inhibitors
people on organic nitrates | causes incr NO --> incr cAMP bc no PDE-5 to degrade --> excessive hypotension
59
list the anti fungal drugs/drug classes (4)
amphotericin B flucytosine azoles echinocandins
60
list the echinocandins (3)
(-fungin) caspofungin micafungin anidulafungin
61
list the azoles (7)
imidazole ketoconazole ``` triazole itraconazole fluconazole voriconazole posaconazole ```
62
MOA of amphotericin B
forms a complex with ergosterol and disrupts the fungal plasma membrane --> leakage of intracellular ions and macromolecules --> cell death
63
MOA of flucytosine
taken up into fungal cell membrane by cytosine permease converted to 5-FU --> FdUMP and FUTP --> inhibit DNA and RNA synthesis, respectively
64
how do amphotericine B and flucytosine work together in combination therapy?
synergistically enhances the penetration of flucytosine through amphotericin-damaged fungal cell membranes
65
which anti fungal agent has the broadest spectrum of action?
amphotericin B
66
what situation could lead to resistance to ampotericin B?
impaired ergosterol binding from either - decreased membrane concentration of ergosterol - modified ergosterol that has less affinity for amphotericin B
67
what situation could lead to resistance to flucytosine?
altered metabolism of flucytosine, which can develop rapidly in monotherapy
68
what are the immediate adverse effects that can present with amphotericin B?
immediate reactions related to IV infusion: ms spasms, F/C, hypotension, headache
69
what are the long term adverse effects that can present over time with amphotericin B?
renal damage: decreased renal perfusion, renal tubular injury and dysfunction anemia seizures
70
what are the adverse effects of flucytosine?
bone marrow toxicity with anemia, leukopenia, and thrombocytopenia derangement of liver enzymes (less frequently)
71
MOA of azoles
reduction of ergosterol synthesis by inhibition of fungal CYP450 enzymes
72
which azoles are used for treatment of aspergillus spp. infections? (3)
itraconazole posaconazole voriconazole
73
what is the azole of choice to treat invasive aspergillosis?
vorizonazole
74
what is the azole of choice to treat mucocutaneous candidiasis?
fluconazole
75
what is the azole of choice to treat and used as secondary prophylaxis of cryptococcal meningitis?
fluconazole
76
which azole is the only one with significant activity against mucormycosis?
posaconazole
77
which azole has the widest therapeutic index? what does this allow for?
fluconazole | allows for more aggressive dosing
78
what situation could lead to resistance to azoles?
up regulation of fungal CYP450 causes standard azole dosages to be less efficacious
79
what azole has less selectivity? what does this mean for it's effects?
ketoconazole | has a greater propensity for adverse effects
80
adverse effects of azoles (if any)
in general are RELATIVELY NONTOXIC minor upset GI sx can cause abnormalities in liver enzymes
81
which azoles have the potential adverse reaction of inhibiting mammalian CYP3A4?
voriconazole | posaconazole
82
what are some of the specific toxicities that could be seen with vorizonazole?
VISUAL DISTURBANCES rash elevated hepatic enzymes
83
MOA of echinocandins
inhibition of glucan synthase --> inhibit synthesis of Beta (1-3)-glucan at the fungal cell wall --> disrupted fungal cell wall --> cell death
84
what situation could lead to resistance to echinocandins?
point mutations in glucan synthase -- do not give to pts if they have this!
85
adverse effects of echinocandins (if any)
well tolerated minor GI side effects flushing
86
list the SABAs (5)
``` albuterol terbutaline metaproterenol pirbuterol levalbuterol ```
87
list the LABAs (5)
``` formoterol salmeterol indacaterol vilanterol olodaterol ```
88
list the anticholinergic bronchodilators (4)
atropine ipratropium tiotropium (LAMA) aclidinum (LAMA)
89
list the methylxanthine bronchodilators (3)
theophylline theobromine caffeine
90
list the inhaled corticosteroids/ICS (7)
``` beclomethasone budesonide ciclesonide flunisolide fluticasone mometasone triamcinolone ```
91
list the leukotriene receptor antagonists/lipoxygenase inhibitors (3)
zafirlukast montelukast zileuton
92
MOA of B2 agonists bronchodilators (SABAs and LABAs)
induce adenylyl cyclase --> incr intracellular cAMP --> bronchodilation
93
how is terbutaline administered?
only beta2 agonist available for subQ injection
94
which SABA is given for a more immediate and sustained delivery?
terbutaline
95
which B2 agonists are used only in pts 12+ yo?
terbutaline (SABA) | pirbuterol (SABA)
96
which B2 agonist is used only in pts 4+ yo?
levalbuterol (SABA)
97
in general, when are SABAs used?
during acute bronchospasmic attacks
98
in general, when are LABAs used?
maintenance/long-term management of COPD or asthma
99
what must LABAs be concomitantly used with?
long-term asthma control medication such as ICS
100
LABAs increase the risk of...
asthma-related deaths | asthma-related hospitalizations
101
which B2 agonist is used for exercise induced bronchospasm (EIB) in pts 4+ yo?
salmeterol (LABA)
102
MOA of anticholinergic bronchodilators
blocks ACh from binding to receptors --> inhibit PNS effects
103
what agents are most widely used in asthma/COPD?
anti-muscarinic agents (anticholinergics like atropine) | methylxanthines
104
what is an advantage of ipratropium over atropine?
it is a potent atropine analog that is poorly absorbed after aerosol administration and therefore is relatively free of systemic atropine-like effects
105
are anticholinergics/antimuscarinics used more for acute treatment or long-term maintenance?
long-term/maintenance tx for bronchospasm for COPD mostly
106
what is an important caution for dosing of atropine? (certain diseases to look out for and why)
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
MOA of methylxanthine bronchodilators
inhibit phosphodiesterase (PDE) --> incr cAMP --> bronchodilator
108
methylxanthines should be used with extreme caution in patients with...
active PUD seizure disorders cardiac arrhythmias
109
first line therapy for patients with persistent asthma? | what is added if low doses do not control sx?
ICS | add LABA as next step
110
which ICS (2) have the potential to cause candida infections?
ciclesonide | fluticasone
111
which ICS (2) have a risk of causing adrenal insufficiency + death in asthmatic patents?
beclomethasone | triamcinolone
112
which ICS (2) are contraindicated in patients with severe hypersensitivity to milk proteins?
budesonide | mometasone
113
in general, when are ICS agents used?
in maintenance treatment or as prophylaxis for asthma
114
which ICS (1) is only used in patients 12+ yo?
ciclesonide
115
which ICS (2) are used in patients 4+ yo? which (1) for patients 5+ yo? which (1) for patients 6+ yo?
4+ fluticasone mometasone 5+ beclomethasone 6+ budesonide
116
which ICS (1) requires a couple months to recover HPA function after withdrawal from systemic corticosteroids?
beclomethasone
117
common combinations of ICS + LABAs (3)
fluticasone + salmetrol mometasone + formoterol budesonide + formoterol
118
steps (4) for treatment of mild persistent to severe persistent asthmatics
1. ICS low dose 2. ICS low dose + LABA 3. ICS high dose + LABA 4. ICS high dose + LABA + OCS
119
MOA of zafirlukast vs. montelukast vs. zileuton
zafirlukast: selectively (-) LTD4 and LTE4 montelukast: selectively (-) LTE4 and CysLTI zileuton: inhibits 5-lipoxygenase --> (-) LTB4, C4, D4, E4 formation
120
major adverse effect of zafirlukast
hepatotoxicity (life threatening hepatic failure)
121
major contraindication of zileuton
active liver disease or persistent hepatic function enzyme elevations >3x ULN
122
which leukotriene receptor antagonists / lipoxygenase inhibitors is used to treat allergies and prevent asthma attacks?
montelukast
123
which leukotriene receptor antagonists / lipoxygenase inhibitors are used as prophylaxis and in the chronic tx of asthma? age restrictions of each?
zafirlukast (5+ yo) | zileuton (12+ yo)
124
list the oral corticosteroids/OCS (1)
prednisone
125
list the monoclonal Abs (1)
omalizumab
126
major adverse effect of omalizumab and what setting it must be administered in
can lead to anaphylaxis -- must only be given in the hospital to manage potential anaphylaxis
127
which cholinergic drugs can be used to treat sx associated with airway restriction? what receptors do they activate or inhibit? what is the outcome?
antimuscarinics/parasympatholytics = ipratropium and tiotropium which antagonize/inhibit M3 receptors (smooth muscle and glands) --> bronchodilation (tx asthma, COPD)
128
genetic variations (2) that affect the pharmacokinetic and pharmacodynamic responses of warfarin (Coumadin)...
polymorphisms in biotransforming ENZYMES polymorphisms in DRUG TARGETS
129
list the adrenergic receptors and their coinciding G-proteins
``` 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
list the G-proteins and their single transduction pathways
``` Gq = incr IP3-DAG Gi = decr cAMP Gs = incr cAMP ```
131
general target tissue and action of: alpha1 adrenergic receptors
vascular smooth ms (BV), pupillary dilator muscles, prostrate CONTRACTION - vasoconstriction (reflex bradycardia) - incr BP - incr MAP - dilate pupils
132
general target tissue and action of: alpha2 adrenergic receptors
CNS, platelets, nerve terminals decr sympathetic tone inhibit NT release some vasoconstriction
133
general target tissue and action of: beta1 adrenergic receptors
heart and JG cells CONTRACTION - incr myocardial contractility - incr HR - incr SA and AV node activity - incr renin release
134
general target tissue and action of: beta2 adrenergic receptors
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
general target tissue and action of: D1 adrenergic receptors
smooth muscle DILATION of renal blood vessels
136
general target tissue and action of: D2 adrenergic receptors
nerve endings modulate transmitter (NT) release
137
list the endogenous catecholamines (3)
epinephrine norepinephrine dopamine
138
``` list the general effects of epinephrine on: - cardiac fxn - vascular tone - respiratory system - skeletal ms - blood glucose levels (think of the receptors it targets) ```
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
list the general effects of norepinephrine on: - cardiac fxn - vascular tone (think of the receptors it targets)
cardiac stimulation, but decr HR vasoconstriction incr peripheral vascular resistance (PVR) and BP
140
what are the predominant adrenergic receptors for epinephrine?
a1 = a2; B1 = B2
141
what are the predominant adrenergic receptors for norepinephrine?
a1 = a2; B1 >> B2
142
what are the predominant adrenergic receptors for dopamine?
D1 = D2 >> B1 >> a1
143
general effects of dopamine (think of the receptors it targets)
D1 stimulation = vasodilation D2 stimulation = suppressed NE release high doses B1 = cardiac effects higher doses a1 = vasoconstriction
144
list the beta adrenergic agonists (3) and their target receptors
isoproterenol: NON-SELECTIVE, B1 = B2 dobutamine: selective B1 albuterol: selective B2
145
adverse effects of beta blockers
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
what situations/sx (3) require a switch from non-selective to selective beta blockers?
switch to B1 selective if... - respiratory sx of bronchospasm and incr airway resistance - exacerbation of peripheral vascular disease (excess vasodilation) - hypoglycemic episodes
147
pharmacodynamic effects of isoproterenol (non-selective beta agonist)
B1: (+) inotropic and chronotropic action, incr CO B2: vasodilator, decr arterial pressure, bronchodilation
148
pharmacodynamic effects of dobutamine (selective B1 agonist, some a1 activity)
potent inotropic action, less prominent chronotropic action
149
pharmacodynamic effects of albuterol (selective B2 agonist)
bronchodilation | relaxation of uterus
150
list the non-selective beta blockers (3)
propanolol pindolol nadalol
151
list the B1 selective blockers (5)
``` ABEAMS atenolol betaxolol esmolol acebutolol metoprolol ```
152
list the alpha agonist drugs (2) and their target receptors
``` phenylephrine = a1 clonidine = a2 ```
153
list the non-selective alpha antagonists (2)
phentolamine (reversible) | phenoxybenzamine (irreversible)
154
list the a1 selective antagonists (3)
-OSIN prazosin tamsuolsin doxazosin
155
list the mixed alpha and beta blockers (2)
(non-selective B and a1 blockers) labetolol carvedilol
156
MOA of ACE inhibitors
inhibition of ACE --> prevention of conversion of angiotensin I to angiotensin II (potent vasoconstrictor) --> incr renin activity and decr aldosterone secretion --> lowered BP
157
adverse effects of ACEi
cough (tickle) | angioedema (can be deadly if tongue swells)
158
MOA of ARBs
competitive non peptide angiotensin II receptor blocker --> blocks the vasoconstriction and aldosterone-secreting effects of angiotensin II
159
advantage of ARBs over ACEi
ARBs induce a more complete inhibition of the RAAS than ACEi
160
important note about candesartan's binding:
relatively irreversible binding
161
which ARB goes through extensive first-pass metabolism via CYP2C9 and CYP3A4 to active metabolite E-3174? what is special about E-3174?
losartan E-3174 is 10x more potent than losartan
162
in which situation are adverse effects of ARBs more likely seen?
diabetic nephropathy
163
MOA of aliskiren
direct renin inhibitor --> blockade of conversion of Ang I to Ang II --> decr BP
164
what is the prototypical dihydropyridine CCB?
nifedipine
165
MOA and effects of calcium channel blockers
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
which CCB has the most potent negative inotropic effect?
verapamil (cardio-specific!)
167
drug used as the first line tx for HTN for nonblack populations without CKD but with DM:
nifedipine
168
instead of ACEi or ARBS, thedrug used as the first line tx for HTN for black populations without CKD but with DM:
nifedipine
169
off label indications of nifedipine:
hypertensive emergency in pregnancy pulmonary HTN preterm labor
170
when administered via IV, what do verapamil and diltiazem treat? (1)
supraventricular tachyarrhytmias (SVT) ... essentially rate control
171
when administered PO, what does verapamil treat? (3)
primary HTN (first line) angina pectoris SVT
172
when administered PO, what does diltiazem treat? (3)
``` primary HTN (first line) classic stable and vasospastic angina pectoris ```
173
which direct vasodilator(s) directly vasodilate the arterioles (with little effect on veins) of smooth muscles?
hydralazine | minoxidil
174
which direct vasodilator(s) directly vasodilate the arterioles AND veins of smooth muscles?
nitroprusside
175
which direct vasodilator can be used in hypertensive emergencies in pregnancy (pre-eclampsia)?
hydralazine
176
which direct vasodilator can be used in a hypertensive crisis?
nitroprusside
177
adverse effects of minoxidil in CV and in endocrine/metabolic effects
CV: pericardial effusion w/ tamponade endo/metab: sodium and water retention
178
adverse effect of nitroprusside
thiocyanate toxicity --> tinnitus, metabolic acidosis, muscle twitching, mitosis, hyperoxemia
179
list the thiazide diuretics (3)
hydrochlorathiazide metolazone chlorthalidone
180
list the loop diuretics (4)
``` -SEMIDE furosemide torsemide bumetanide ethacrynic acid ```
181
list the K+ sparing diuretics (4)
Na-channel blockers - amiloride - triamterene aldosterone antagonist - spironolactone - eplerenone
182
list the aquaretics (2)
-VAPTAN conivaptan tolvaptan
183
which diuretics treat HTN and edema?
thiazide loop K+ sparing
184
which diuretics treat euvolemic and hypervolemic hyponatremia?
aquaretics
185
MOA and site of action of loop diuretics
Na-K-Cl cotransporter blockers at the thick ascending loop of Henle
186
MOA and site of action of thiazide diuretics
Na-Cl contransporter blocker at the distal convolute tubule
187
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)?
loop diuretic
188
advantage of loop diuretics over thiazides in treatment of HTN
loops still work in patients with LOW RBF and GFR (good for patients who are unresponsive to other diuretics)
189
main clinical application of thiazide diuretics (hydrochlorothiazide)
management of mild-to-moderate HTN... either alone or in combo with other agents
190
MOA and site of action of K+ sparing diuretics
either block epithelial Na+ channels/ENaC (triamterene, amiloride) or antagonize aldosterone (spironolactone, eplerenone) at the cortical collecting duct
191
main clinical application of K+ sparing diuretics
counteracts K+ loss induced by other diuretics when treating HTN or HF (adjunct use)
192
MOA and site of action of aquaretics
blocks ADH receptor in the collecting duct --> excrete free water (pee a lot)
193
what is an off-label use of HCTZ?
calcium nephrolithaisis
194
what are the class 1 antiarrhythmic drugs?
sodium channel blockers
195
list the class 1A antiarrhythmic drugs (3)
quinidine procainamide disopyramide
196
list the class 1B antiarrhythmic drugs (2)
lidocaine | mexiletine
197
list the class 1C antiarrhythmic drugs (2)
flecainide | propafenone
198
MOA of class 1A antiarrhythmics
blocks Na+ (OPEN) and K+ channels | decrease slope of phase 0
199
effects of class 1A antiarrhythmics on AP and ECG
prolong AP duration by reducing repolarizing influx prolong QRS (ventricular depolarization) and QT intervals
200
MOA of class 1B antiarrhythmics
block Na+ channels (only bind INACTIVATED channels) | do NOT block K+ channels
201
effects of class 1B antiarrhythmics on AP and ECG
SHORTEN AP duration do NOT prolong QT duration, prolong QRS interval (ventricular depolarization) when tissue is damaged
202
MOA of class 1C antiarrhythmics
block Na+ channels (only bind ACTIVATED/OPEN channels) -- slow impulse conduction
203
effects of class 1C antiarrhythmics on AP and ECG
do NOT prolong AP duration do NOT prolong QT duration, prolong QRS interval (ventricular depolarization)
204
class 1 antiarrythmics drugs are state-dependent. In which state do they bind their respective channels?
1A and 1C bind activated/open Na channels | 1B binds inactivated Na channels
205
rank the class 1 antiarrhythmics from highest to lowest affinity to Na+ channels
``` strongest binding affinity 1C 1A 1B lowest binding affinity ```
206
which antiarrhythmic class 1 drug is effective in SUSTAINED ventricular tachycardias and arrhythmias associated with MI?
procainamide (class 1A)
207
which is the least toxic drug of the class 1 antiarrythmics?
lidocaine (class 1B)
208
cardiac adverse effects of the class 1A antiarrythmics (3)
QT prolongation induction of torsade de pointes arrhythmias & syncope excessive inhibition of conduction
209
extra cardiac adverse effects of quinidine
GI side effects: diarrhea, N/V | thrombocytopenia
210
extra cardiac adverse effects of procainamide
Lupe erythematous (SLE) syndrome with arthritis, pleuritis, pulmonary disease, hepatitis, and fever
211
extra cardiac adverse effects of disopyramide
atropine-like symptoms - urinary retention - dry mouth - blurred vision - constipation - exacerbation of glaucoma
212
which class 1 antiarrythmic drug could be used to terminate ventricular tachycardia in the setting of an ACUTE MI?
lidocaine
213
neurologic adverse effects of lidocaine
``` paresthesia tremor slurred speech convulsions nystagmus muscle twitching confusion loss of coordination ```
214
which class 1 antiarrythmic is used to treat ventricular arrhythmias and relieve chronic pain due to diabetic neuropathy and nerve injury?
mexiletine
215
which class 1 antiarrythmic is used to treat supraventricular arrhythmias in patients with structural dz and has some weak beta-blocking activity?
propafenone
216
cardiac adverse effect of class 1C antiarrythmics
exacerbate ventricular arrhythmias
217
extra cardiac adverse effects of propafenone
metallic taste | constipation
218
class 1 antiarrhythmics and their effects on K+ channels
``` 1A = block K+ channels 1B = do NOT block K+ channels 1C = block some K+ channels ```
219
pharmacokinetics of dissociation from Na channels for class 1 antiarrythmics
``` 1A = slow impulse conduction 1B = dissociate with fast kinetics (less severe side effects!) 1C = dissociate with slow kinetics ```
220
MOA and effects of amiodarone on the heart
block K+ channels --> causes bradycardia and slows AV conduction causes peripheral vasodilation
221
effects of amiodarone on AP and ECG
prolong AP duration prolong QT interval
222
what does amiodarone usually treat?
recurrent VTach | AFIB
223
adverse effects of amiodarone
``` AV block bradycardia hypo or hyperTHYROIDISM fatal pulmonary fibrosis hepatitis photodermatitis ```
224
what metabolizes amiodarone? drugs that inhibit this metabolizer have what effect on amiodarone?
metabolized by CYP3A4 amiodarone's half-life is affected by drugs that inhibit (cimetidine) or induce (rifampin) CYP3A4
225
what is the elimination time of amiodarone like?
very long elimination half-life (weeks - months) | effects are maintained 1-3 months after discontinuation
226
what effect does amiodarone have on other CYP enzymes? what does this mean?
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions