All cardio Flashcards
1
Q
What are toxicities associated w/ statins?
A
- birth defects (use BABAs during pregnancy) 2. hepatotoxicity 3. myopathy (rhabdomyolysis) 4. drug-drug interactions (esp w/ amlodipine)
2
Q
Name the statins and their MoA
A
atorvastatin, rosuvastatin, simvustatin, pravastain, lovastain inhibit HMG CoA reductase (rate-limiting step of cholesterol synthesis, increase uptake of LDL)
3
Q
Name the classes that increase refractory period (including those that increase APD and those that do not)
A
APD increased: IA (because of K+), III
No change in APD: IB, IC, adenosine
4
Q
Bivalirudin
A
Direct-acting thrombin inhibitor (IV)
5
Q
Name the thiazides, MoA and side effects
A
Hydrochlorothiazide and chlorthalidone inhibits Na/Cl symporter hypokalemia, alkalosis
6
Q
what makes vasculature different than other structures in the body? What receptors does it have? What dominates?
A
No parasympathetic receptors; mediated by a1 and B2 a1 dominates so constriction typically wins
7
Q
What is the MoA of BABAs?
A
increase elimination of bile acids, drawing more out of the liver (only way to excrete cholesterol) also increases LDL receptors to pull more LDL out of bloodstream
8
Q
Name the K+ sparing drugs, MoA, and side effects
A
2 MoA: 1. aldosterone receptor antagonists: spironolactone, eplerenone (both = steroid hormones) 2. Enac blockers: triamterene;
spironolactone similar to estradiol so leads to gynecomastia
9
Q
Rank the relative strength of Na channel blockers
A
IC (flecainide and propafenone) = strongest
IA (procainamide) = middle
IB (lidocaine) = weakest
10
Q
FXa drugs (direct and indirect)
A
Direct apixaban (oral) rivaroxaban (oral) endoxaban (oral) No parenteral drugs Indirect: Fondaparinux (SubQ) Enoxaparin (SubQ)
11
Q
What is a1’s primary role? Where are these located/how do the receptors work?
A
SM contraction (sympathetic) eye and bladder contraction - in conjunction w/ B2
Also very important for vascular constriction and dilation (a1 dominates so constriction typically wins dominates)
12
Q
name an a2 agonist and describe how it works + a cardio application
A
clonidine - a2 agonist so it inhibits NE from presynaptic neuron and counterintuitively blocks sympathetic signals - use for HTN
13
Q
what is the role of a2?
A
inhibits NE from presynaptic neuron and postsynaptically induces smooth muscle contraction like a1 COUNTERINTUITIVELY: blocks sympathetic signals
14
Q
How do COX 1/2 inhibitors work and what’s an important anti-platelet?
A
Aspirin Targets thromboxane, decreases platelet aggregation and activation Use for unstable angina, stroke, and MI
15
Q
What does a direct versus indirect thrombin inhibitor mean?
A
Indirect-acting drugs use antithrombin to impact thrombin (or inhibit Vit K reductase in case of warfarin) **includes indirect anti-Xa drugs like Fondaparinux and Enoxaparin Direct-acting drugs directly bind to thrombin (Factor II)
16
Q
Abciximab
A
GpIIb/IIIa inhibitor These are the receptors for fibrin, which prevents fibrinogen bridges from forming (prevents platelet plug)
17
Q
Propafenone
A
IC Na+ blocker (strong)
Don’t use in pts w/ structural abnormalities
Increases threshold potential (decreases automaticity), increases RP (no increase in APD), and decreases conduction velocity
18
Q
Which drugs should you avoid using w/ patients who have structural abnormalities?
A
Class IC drugs because they bind tightly to Na+ and are proarrhythmic
19
Q
Parenteral direct-acting anti-thrombotic drugs
A
Argatroban and bivalirudin
20
Q
Losartan
A
ARB
21
Q
Name the drugs that decrease conduction velocity
A
IA, IC, Class II, Class IV, adenosine
22
Q
What are the fibric acid derivatives (FADs)? What are they mainly used for?
A
Gemfibrozil and fenofibrate Lowering TAGs
23
Q
What are the GpIIb/IIIa inhibitors?
A
Abciximab, eptifibatide, tirofiban
24
Q
Name Class III side effects
A
All K+ blockers besides for Amiodarone: prolong QT and association w/ Torsades (including Procainamide)
Amiodarone - prolongs QT but no Torsades (has multiple mechanisms); hypo/hyperthyroidism or blue skin/tongue tint
25
B1-selective only drugs
metropolol and atenolol (also called selective B blockers) - both used for HTN, metoprolol used for HF
26
What drugs can you use in the case of HIT?
Direct-acting thrombin inhibitors
27
What's the MoA of FADs?
1. directly stimulate LDL receptor (draw out of circulation) 2. stimulate lipoprotein lipase (decreases TAGs in circulation) 3. promotes breakdown of FFAs
28
B blockers used for HTN + selectivity
atenolol (B1), metoprolol (B1), carvedilol (a1, B1-3)
29
Name the classes that decrease automaticity for antiarrhythmics
All classes
30
name an a1 antagonist and describe how it works
prazosin counters SM contraction by blocking a1 and leads to vasodilation, thus decreasing BP
31
Side effects of warfarin
birth defects, increased bleeding risk when combined w/ other medications (e.g. FADs, NSAIDs, amiodarone), variation in Vit K in diet can be a challenge
32
what receptors are used by GI and what are their effects?
M3 and B2; M3 = contraction, B2 = relaxation for GI
33
amlodipine
DHP CCBx
34
Valsartan
ARB
35
Name the 3 broad mechanisms/goals of antiarrhythmics
1. decrease automaticity
2. increase refractory period (can increase APD or have no impact on APD)
3. can slow conduction velocity
36
Parenteral indirect-acting anti-thrombotic drugs
FII+FXa Unfractionated heparin FXa Fondaparinux Enoxaparin
37
What is B1's primary role?
stimulates SA/AV nodes
38
What is the main difference between epi and NE sensitivity's to receptors?
NE has low affinity for B2 (this was emphasized in the ANS and cardio lecture)
39
Lisinopril
ACEi
40
Name the class II anti-arrhythmic drugs and describe their mechanism
B-blockers (B1 antagonists)
Block epi and NE, decrease sympathetic reseponse, DECREASE PHASE 4 SLOPE
Atenolol, metoprolol, carvediol, propanolol
41
Anti-thrombin (FII) drugs, direct and indirect
Direct: Argatroban (IV) Bivalirudin (IV) Dabigtran (oral) Indirect: U. heparin (IV) Warfarin
42
a 1, 2, B 1, 2 - selective agonist
epinephrine (broncodilation, SM relaxation, among other impacts)
43
Lidocaine
Weak Na+ block with unclear mechanism (beyond increasing threshold potential)
Decreases automaticity, increases RP w/ no increase in APD
44
epinephrine
a1/2, B 1/2 - selective agonist
45
diazoxide
hyperpolarizes smooth muscle cells and inhibits contraction parenteral; used for hypertensive emergencies
46
Chlorathalidone
thiazide diuretic inhibits Na/Cl symporter hypokalemia, alkalosis
47
Solatol
Class III K+ blocker
Increases APD
Prolongs QT and is associated w/ Torsades
48
propanolol
B1/2/3 - selective antagonist (B blocker), decreases cardiac output
Anti-arrhythmic (decreases Phase 4 slope)
49
What drugs would you use to treat angina and HTN at same time?
B blockers or CCBx
50
B1 antagonists
metoprolol, atenolol, carvedilol, propandolol (B blockers)
Primarily works by decreasing the slope of Phase 4 depolarization and decreasing HR
51
how is a2 different from other receptors?
effects of a2 work on presynaptic neuron (inhibits the release of NE from presynaptic neuron, but postsynaptically, a2 induces smooth muscle contraction like a1)
52
Name the 2 types of Ca channel blockers and the drugs that fall into both
Both reduce strength of contraction non-DHPs (also anti rhythmics) verapamil, diltiazem DHPs amlodipine, nifedipine, nimodipine
53
What is a cholesterol absorption stimulator? How does it work?
Alirocumab stimulates LDL receptor to increase the amount of LDL absorbed into the liver; does the by blocking PCSK9 PCSK9 promotes the breakdown of the LDL receptor, so alirocumab stabilizes against degradation
54
Side effects of a1 antagonists
orthostatic hypotension (prazosin)
55
What is B2's primary role?
SM relaxation (sympathetic) for GI, lungs, salivary glands, etc.
In eye and bladder, used in conjunction w/ a1
56
Flecainide
IC Na+ blocker (strong)
Don't use in pts w/ structural abnormalities
Increases threshold potential (decreases automaticity), increases RP (no increase in APD), and decreases conduction velocity
57
Rivaroxaban
Direct-acting Xa-inhibitor (oral)
58
Procainamide
Class IA, Na+ K+ blocker
Associated w/ Torsades
Reduces automaticity (Increases threshold potential), increases refractory period, and decreases conduction velocity
Moderate Na+ block
59
What role do M3 and B2 play in the uterus?
M3 - contractions, B2, relaxation (L+D plus menstrual applications)
60
Fenofibrate MoA + side effects
FAD 1. directly stimulate LDL receptor (draw out of circulation) 2. stimulate lipoprotein lipase (decreases TAGs in circulation) 3. promotes breakdown of FFAs Watch for drug-drug interactions (statins, warfarin, etc.)
61
What mechanisms should you try to use for structural defects/reeentry
Increase the refractory period, decrease conduction velocity
62
Ivabradine (didn't really discuss this in class but it's on the drug chart)
If (HCN) channel inhibitor
63
3 types of diuretics for HTN
1. loop diruetics 2. thiazides 3. K-sparing
64
non-selective parasympathetic antagonist used to increase cardiac output or to dilate eyes
Atropine
65
atenolol
B1 antagonist, B blocker (decreases cardiac output)
Anti-arrhythmic (decreases Phase 4 slope)
Also used for HTN
66
Diltiazem
Class IV Ca++ channel blocker (non-DHP)
Slows nodal depolarization (decreases automaticity), decreases conduction velocity
Also used for HTN
67
Verapamil
Class IV Ca++ channel blocker (non-DHP)
Slows nodal depolarization (decreases automaticity), decreases conduction velocity
Also used for HTN
68
Describe how adenosine works
Increases max diastolic potential (cell is more negative between action potentials)
Opens K+ channels, slows CA influx, is a nodal agent
69
Alirocumab MoA
cholesterol absorption stimulator; stimulates LDL receptor to increase the amount of LDL absorbed into the liver; does this by blocking PCSK9; PCSK9 promotes the breakdown of the LDL receptor, so alirocumab stabilizes against degradation
70
What receptors are used by salivary glands and what are their effects? \*\*what do you need to remember about the sympathetic receptor in this case?
for salivation - M3 = watery, B2 = thick (sympathetic) \*\*note B2's primary role is SM relaxation, not induction of secretion
71
Enoxaparin
Indirect-acting Xa-inhibitor (SubQ)
72
dobutamine
B1 agonist, increases cardiac output
Use in cases of cardiogenic shock (acute HF) to increase CO (also use milrinone, mentioned in HF lecture - phosphodiesterase 3 antagonist)
Routine use of ionotropes does not improve mortality (may shorten life)
73
metropolol
B1 antagonist, B blocker (decreases cardiac output)
Anti-arrhythmic (decreases Phase 4 slope)
Also used for HTN and HF
74
Amiodarone
Class III K+ blocker
Increases APD
Prolongs QT but not associated w/ Torsades
Hyper/hypothyroidism, blue skin/tongue tint
75
nifedipine
DHP CCBx
76
Eplerenone
K-sparing diuretic, aldosterone receptor antagonist
77
carvedilol
a1, B1/2/3 (nonselective) antagonist (B blocker), decreases cardiac output
Anti-arrhythmic (decreases Phase 4 slope)
Also used for HTN and HF
78
Isoproterenol
B1 and B2 agonist synthetic drug similar to dobutamine (discussed in ANS and cardio lecture)
79
Oral indirect-acting anti-thrombotic drugs
Warfarin (vitamin K reductase inhibitor)
80
what role do the following play in urinary control? a1, M3, and B2
M3 - parasympathetic control (contraction - detrusor) B2 - sympathetic control (relaxation - detrusor) a1 - sympathetic control (contraction - internal urethral sphincter) somatic control - external urethral sphincter (nicotinic receptor)
81
Colestipol + side effects
BABA - increase elimination of bile acids, drawing more out of the liver (only way to excrete cholesterol) also increases LDL receptors to pull more LDL out of bloodstream Use during pregnancy, severe GI tox
82
Name the Class I anti-arrhythmic drugs + subclasses, and describe their mechanism
Na+ channel blockers - increase threshold potential and make it harder to depolarize
Slow resetting of NA+ channels
IA - Procainamide
IB lidocaine
IC flecainide, propafenone
83
What are M3's primary roles?
SM contraction, secretion (parasympathetic)
84
What are the categories of anti-platelet drugs?
COX 1/2 inhibitors, P2Y12 inhibitors, GpIIb/IIIa inhibitors
85
ACE inhibitor MoA, drugs + side effects
captopril and lisinopril prevent conversion of angiotensin I to II by inhibiting ACE angiodema and cough (due to build-up of bradykinin), hyperkalemia, be careful w/ first trimester of pregnancy
86
When should you be careful with ACE inhibitors?
During pregnancy - teratogenic during 1st trimester (messes up fetus's blood supply)
87
B1 agonist, name and function
dobutamine, increases cardiac output
88
What's a comorbidity you should consider for ACE inhibitors + ARBs?
Is protective against diabetic nephropathy compared to other drugs
89
When should you take BABAs?
1 hour before other drugs or 3 hours after (can interfere w/ absorption)
90
Spironolactone
K-sparing diuretic, aldosterone receptor antagonist gynecomastia
Used for HF
91
clonidine
a2 agonist, used for HTN
92
name an a2 agonist and describe MoA/use
clonidine, HTN, acts presynaptically in anti-sympathetic ways
93
What type of muscle does not fire action potentials?
Vascular smooth muscle (under involuntary control - hormones, ANS neurotransmitters like adrenergic receptors, local stimuli)
94
Argatroban
Direct-acting thrombin inhibitor (IV)
95
prazosin
a1 antagonist - counters SM contraction and leads to vasodilation, decreasing BP; used for HTN
can cause orthostatic hypotension
96
Triamterene
K-sparing diuretic, Enac blocker
97
What other effects do statins have?
Cardioprotective effects such as: 1. increases in NO 2. stabilizing plaques and decrease risk of thrombosis 3. decrease inflammation 4. decrease platelet activation and VTE risk
98
Eptifibatide
GpIIb/IIIa inhibitor These are the receptors for fibrin, which prevents fibrinogen bridges from forming (prevents platelet plug)
99
Dronedaron
Class III K+ blocker
Increases APD
Prolongs QT and is associated w/ Torsades
100
Side effects of B1 and B2 antag
B - need to be careful w/ diabetes b/c messes up insulin B2 - watch for asthma/COPD due to bronchioconstriction
101
Niacin MoA + side effects
reduces secretion of VLDL and reduces the amount of lipid in circulation flushing, pruritus, insulin resistance (not used very often)
102
What is a cholesterol absorption inhibitor? How does it work?
Ezetimibe 1. blocks absorption from GI tract (blocks NPCI receptor) 2. also stimulates LDL receptor to absorb more from bloodstream
103
Dabigitran
Direct-acting thrombin inhibitor (oral)
104
Prasugrel
P2Y12 inhibitor (targets ADP receptor)
105
describe mediators of urinary control
parasympathetic control - detrusor muscle (M3), contracts to put pressure on bladder during times of rest; sympathetic control - detrusor muscle (B2) - relaxes during times of stress (decreasing urge to urinate) sympathetic control - urethra (a1) - contracts during times of stress (also so you don't pee yourself) but is inhibited when at rest; external sphincter - somatic control
106
What are the Vitamin K-dependent factors?
2, 7, 9, 10 protein C and S
107
Name the vasodilator MoAs (column 2 on drug chart) and name side effects
1. cGMP levels - relaxation 2. K+ openers - hyper polarize cells and inhibit contraction 3. Ca channel blockers Gingival enlargement (not sure if for all?)
108
Atropine
non-selective parasympathetic antagonist (indirect) used to increase cardiac output (tx bradycarida) or to dilate eyes
Decreases Phase 4 slope by blocking ACh receptors (increases threshold)
109
nimodipine
DHP CCBx
110
P2Y12 inhibitors - describe MoA and name drugs
targets ADP receptor and prevents platelets from using energy Clopidogrel, prasugrel, ticagrel
111
Dofelitide
Class III K+ blocker
Increases APD
Prolongs QT and is associated w/ Torsades
112
Apixaban
Direct-acting Xa-inhibitor (oral)
113
What are side effects of FADs?
Myopathy (especially when used in combo w/ statins... FADs decrease statin absorption in liver which increases serum levels of statins and contribute to myopathy) Also increases bleeding risk from warfarin (does same thing as it does w/ statins and increases amount in bloodstream)
114
name an a1 agonist and describe how it works
phenylephrine; increases BP by increasing vascular constriction Activates voltage-gated Ca++ channels, increases SR release (increases contraction)
115
What should you combine ezetimibe w/ and why?
Statins so that HMG CoA reductase doesn't increase synthesis of cholesterol
116
Describe the differences between direct and indirect acting parasympathetic drugs; give an example of an indirect drug
Direct - target the receptor (mAchR) - Ach mimics indirect - target acetylcholinesterase (AchE) in the synapse, AchE inhibitors atropine = indirect
117
Ezetimibe MoA
1. blocks absorption from GI tract (blocks NPCI receptor) 2. also stimulates LDL receptor to absorb more from bloodstream
118
Clopidogrel
P2Y12 inhibitor (targets ADP receptor)
119
Which statins are highly effective?
Atorvastatin and rosouvastatin
120
describe how phenylephrine works
a1 agonist; increases BP by increasing vascular constriction
121
Endoxaban
Direct-acting Xa-inhibitor (oral)
122
Tirofiban
GpIIb/IIIa inhibitor These are the receptors for fibrin, which prevents fibrinogen bridges from forming (prevents platelet plug)
123
What are statins best used for? What can you combine them with?
Lowering LDL and TAGs Many other anti-lipid drugs, esp ezetimibe
124
Which statins interact poorly w/ amlodipine?
atorvastatin, simvustatin, lovastatin
125
hydralazine
changes cGMP levels and induces vascular relaxation
Used for HF
126
How should you try to modify abnormal impulse formation
decrease automaticity (can target nodal rate or myocytes with premature beats)
127
Captopril
ACEi
128
Name the Class IV drugs and describe their mechanism
Diltiazem and verapamil (non-DHPs)
Slow AV/SA depolarization (similar to class I except nodally focused)
129
Tacagrelor
P2Y12 inhibitor (targets ADP receptor)
130
Name the loop diuretics, MoA, and side effects
furosemide inhibits Na/K/Cl symporter; hypokalemia, alkalosis; \*\*preferred during pregnancy compared to other diuretics
131
What is M2's role?
parasympathetic control; slows SA/AV node
132
Which HTN drugs lead to hyperkalemia and hypokalemia?
Hyper: ACE inhibitors and ARBs Hypo: loop diuretics and thiazides
133
ARB MoA, drugs + side effects
losartan, valsartan blocks receptor of angio II (prevents aldosterone/RAAS system effects) risk of hyperkalemia and arrhythmia, be careful w/ first trimester
134
Name the Class III antiarrhythmics and describe their mechanism
K+ blockers
Increase AP duration (increase refractory period and slow repol)
Amiodarone, dronedaron, dofelitide, solatol
135
What are the BABAs? When should you use them? Toxicities?
Colestipol Use during pregnancy Can cause severe GI tox
136
Hydochlorothiazide
thiazide diuretic inhibits Na/Cl symporter hypokalemia, alkalosis
137
Gemfibrozil MoA + side effects
FAD 1. directly stimulate LDL receptor (draw out of circulation) 2. stimulate lipoprotein lipase (decreases TAGs in circulation) 3. promotes breakdown of FFAs Watch for drug-drug interactions (statins, warfarin, etc.)
138
How do GpIIb/IIIa inhibitors work and when are they used?
These are the receptors for fibrin, which prevents fibrinogen bridges from forming (prevents platelet plug) angioplasty and stent placement
139
Adenosine
Antiarrhythmic
Makes cell more depolarized at baseline (increases max diastolic potential)
Slows Ca++ influx, opens K+ channels
Works through all 3 paths
140
Oral direct-acting anti-thrombotic drugs
FII Dabigitran FXa Apixiban Rivaroxaban Endoxaban
141
Furosemide
Loop diuretic inhibits Na/K/Cl symporter hypokalemia, alkalosis \*\*preferred during pregnancy compared to other diuretics
142
Fondaparinux
Indirect-acting Xa-inhibitor (SubQ)
143
When are statins usually taken?
Often at night (not all)
144
carvedilol selectivity
a1, B1, 2, 3
145
What drugs do you use for HF? Contraindications?
Entresto; ACEi or ARB (contra to ACEi: angiodema, advanced renal disease), B blockers (metoprolol or carvdedilol; contra = bronchospasm or acute HF or bradycardia), aldosterone antagnoists (spirolactone and eplerenone - contra= hyperkalemia or advanced renal disease); use other diruetics for symptom control w/ wet HF
146
Good review of uses of specific B blockers for reference
147
Digitalis/digoxin
Inhibits Na+ export via Na/K+ ATPase, promoting Ca++ retention and increased inotropy (contractility)
Narrow therapeutic window before toxicity (including arrhythmias, confusion, seizures, visual disturbances, N/V, etc)
148
What are considerations related to diurertics in HF that you should keep in mind?
May be toxic to kidneys, have no mortality benefit; helpful to reduce the amount of fluid in a "wet" patient to get them out of pulmonary edema zone
Use loop diurertics (e.g. furosemide) for HF (aldosterone antag aka K-sparing diuretics often used as first-line treatment due to mortality benefit)
Thiazides rarely used in HF
149
Isosorbibe mononitrate + hydralazine (BiDil)
Drug controversially used only for African American/Black patients in HF... interesting tie-ins w/ social medicine as pointed out by Dr. Saunders early in the semster
See actual BiDil ad w/ Snoop Dogg (and this article for more info: https://www.healthaffairs.org/doi/abs/10.1377/hlthaff.W5.455?journalCode=hlthaff)
150
Summarize HF drugs that improve mortality and those that improve symptoms
