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Pharmacology > Cardio and Blood vessels > Flashcards

Cardio and Blood vessels Flashcards

1
Q

Treatment for temporal giant cell arteritis and takayasu arteritis

A

Corticosteroids

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2
Q

Treatment of polyarteristis nodosa

A

corticosteroids

cyclophosphatimide

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3
Q

What is the treatment for a kid with kawasaki disease

A

ASA

IVIG

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4
Q

What is the only instance where you would give a kid ASA?

What is the MOA

A

Kawasaki disease

It blocks release of thromboxane from cyccloxygenase thereby inhibiting PLTs aggregation and thrombus formation

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5
Q

Wegener’s granulomatosis treatment

A

Cyclophospahmide (MAINLY)

corticosteroids

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6
Q

CHF treatment

A

ACEI

also beta blocker, spironolactone, ARB

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7
Q

treatment for a PDA and MOA

A

Indomethacin—-inhibits PGE which is what keeps the PDA open

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8
Q

Treatment for Transposition of great vessels

A

PGE to maintain a patent ductus arteriosus until surg

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9
Q

Treatment for torsades pointes

A

Magnesium sulfate

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10
Q

Treatment for essential HTN

A

Diuretics
ACEI
ARBs
calcium channel blockers

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11
Q

First line treatment for essential HTN

A

diuretics

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12
Q

CHF treatment

A

Diuretics
ACEI
ARBs
Beta blocker*

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13
Q

First line treatment

A

diuretics

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14
Q

What kind of CHf are beta blocker contraindicated

A

decompensated

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15
Q

What must be used in DM pt with HTN

A

ACEI

ARBS

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16
Q

List the DHP calcium channel blockers

A

Nifedipine

amlodopine

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17
Q

List the nonDHP calcium channel blockers

A

Verapamil

diltiazem

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18
Q

Calcium channel blockers clinical uses

A 
Angina
Prinzmetal's angina
arrythmias
HTN
Raynaud's  phenomena
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19
Q

Which of the calcium channel blocker is not used for arrythmias

A

nifedipine

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20
Q

Calcium channel blocker MOA

A

block voltage gated calcium channels of only cardiac and smooth muscle to decrease contractility

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21
Q

Describe the order of how CCblockers on the vascular smooth muscle

A

Amlodipine=nifedipine>diltiazem.varapamil

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22
Q

describe the order of how CCblocker on the heart

A

Verapamil>diltiazem>amlodipine=nifedipine

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23
Q

CCblockers toxicity

A

cardiac depression
peripheral edema
flushing
dizziness

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24
Q

CCblockers toxicity specific for verapamil

A

constipation

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25
Q

CCblockers toxicity specific for NonDHP

A

AV block

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26
Q

Hydralazine use

A

Severe HTN
CHF
first line for preg HTN
with methyldopa

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27
Q

hydralazine MOA

A

increase cGMP –SM relaxation–VD arteriole and reduce afterload

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28
Q

hydralazine toxicity

A 
fluid retension
nausea
HA
angina
Lupus like syndrome
compensatory tachycardia
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29
Q

Hydralazine is contraindicated in

A

Angina/CAD

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30
Q

What drug is given with hydralazine to prevent reflex tachycardia

A

B-blocker

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31
Q

List the diuretics

A 
furosemide
Thiazide
spironolactone
eplerenone
triamterene
Amiloride
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32
Q

List the ARBs

A

s

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33
Q

List the ACEI

A

Captopril, Enalapril,lisinopril

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34
Q

Malignant HTN treatment

A 
nitroprusside
nicardipine
clevidipine
labetalol
fenoldopam
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35
Q

Nitroprusside MOA

A

Short acting direct release of NO to increase cGMP

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36
Q

Nitroprusside toxicity

A

Cyanide toxicity

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37
Q

FenoldopamMOA

A

a dopamine D1 receptor agonist that causes vasodilation of coronary, peripheral, renal, and splanchnic –decreasing BP and increasing natriuresis

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38
Q

Nitroglycerin and isosorbide dinitrate MOA

A

Relases NO–increase cGMP–SM relaxation–VENOdilation–decreased preload

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39
Q

Nitroglycerina and isosorbide dinitrate clinical use

A

Angina

pulmonary edema

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40
Q

Nitrates/isosorbide dinitrate toxicity

A 
Reflex tachy
HypoTN
flushing
HA
Monday disease
41
Q

Statins MOA

A

inhibit conversion of HMG-CoA to mevalonate

42
Q

Statins effects

A

decrease LDLcholesterol
decreases TGs
increase HDL

43
Q

Statin side effects

A

hepatotoxic

rhabdomyolysis

44
Q

Niacin MOA

A

inhibits lipolysis

reduces hepatic VLDL secretion into circulation

45
Q

Niacin effect

A

increase HDL

decrease TGs and LDL

46
Q

Niacin toxicities

A

Red flushed face–give ASA
hyperglycemia–acanthosis nigircan
hyperuricemia– makes gout bad

47
Q

List the bile acid resins

A

Cholestyramine
colestipol
colesvelam

48
Q

Bile acid resin MOA and effect

A

prevent intestinal RAb of bile acids so that liver must use chol to make more
reduce LDL

49
Q

Bile acid resins toxicity

A

GI discomfort
reduce absorption of fat soluble ADEK
Chol Gall stones

50
Q

Ezetimbe is a

A

cholesterol absorption blocker at small intestine brush border

51
Q

Ezetimbe effects and toxicity

A

reduce LDL
Rare LFTs
diarrhea

52
Q

Fibrates( the “fibrozil and the fibrates”) MOA

A

upregulate lipoprotein lipase activity —increase TG clearance

53
Q

Fibrates toxicity

A

Myositis
hepatotoxicity
chol gallstones`

54
Q

Digoxin MOA

A

glycoside that directly inhibits Na/K ATPase leading to indirect inhibition of the Na/Ca exchanger—-increase intracellular Ca—increase contractility

55
Q

Digoxin also stimulate

A

vagus nerve—decrease HR

56
Q

Digoxin use

A

CHF to increase contractility

AFib to reduce conduction thru AV node and depress SA node

57
Q

Factor predisposing to digoxin toxicity

A

Renal failure
hypokalemia
quinidine

58
Q

digoxin toxicity

A

N/V/D
blurry yellow vision
Hyperkalemia

59
Q

Digoxin EKG

A 
Prolong PR
lower QT
ST scooping
T-wave inversion
arrythmias
AV block
60
Q

Class I antiarrhythmics MOa

A

Na+ channel blocker decreasing phase 0 depolorization and increasing the threshold for firing

61
Q

Class I antiarrhythmics are state dependent. what does this mean?

A

They selectively depress tissue that is frequently depolorized

62
Q

What increases the toxicities of all the class I antiarrythmics

A

hyperkalemia

63
Q

List the class IA antiarrhythmics

A

Quinidine
Procainamide
disopyramide

64
Q

Class IA anitarryhthmic specific MOA

A

increase AP duration
increase effectice refractory period
increase QT interval

65
Q

quinidine toxicity

A

headache

tinnitus

66
Q

Procainamide toxicity

A

reversible SLE-like sxs

67
Q

Class IA collective toxicity

A

thrombocytopenia

QTprolongation— torsadesde pointes

68
Q

disopyramide toxicity

A

heart failure

69
Q

List the class IB antiarryhthmics

A

Lidocaine
TOcainide
Mexiletine
phenytoin

70
Q

Class IB preferentially affect

A

ichemic or depolarized purkinje and ventricular tissue by decreasing AP duration

71
Q

Which antiarrythmics are good Post MI and digitalis induced arrythmias

A

Class IB
lidocaine
Tocainide
Mexiletine

72
Q

Class IB antiarrythmics toxicity

A

Act as local anesthetics
CNS stimulation or depression
Cardiac depression

73
Q

List the class IC antiarrythmic drugs

A

Flecaine

propafenone

74
Q

Class IC antiarrythmic drugs are contraindicated in

A

structural heart disease and post MI

75
Q

The class IC antiarrythmic drugs are only really used for

A

as a last resort for refractory tachyarrythmias

76
Q

Class IC antiarrythmics toxicity

A

pro-arrythmia esp post-MI

significantly prolongs refractory AV node

77
Q

List the class II antiarrythmics

A 
B-blockers:
metoprolol
propanalol
esmolol
atenolol
timolol
78
Q

MOA of the class II antiarrythmics

A

decrease cAMP and ca2+ levels that lead to decrease SA and AV nodal activity
decrease phase 4

79
Q

Class II antiarrythmics clinical uses

A

Vtachy
SVT
slowing ventricular rate during A-fiband flutter

80
Q

Class II antiarrythmics toxicity

A

Impotence
exacerbation of asthma
cardiac:bradycardia, Av block, CHF
CNS: sedation sleep alterations, may mask hypoglycemia

81
Q

Toxicity unique to metoprolol

A

dyslipidemia

82
Q

toxicity unique to propranolol

A

exacerbate vasospasm in Prinzmetal’s angina

83
Q

List the class III antiarrythmics

A 
K+channel blocker
Amiodarone
Ibutilide
Dofetilide
Sotalol
84
Q

Class III antiarrythmics MOA

A

increase AP duration
increase ERP?
increase QT interval

85
Q

Check these for amiodarone

A

PFTs
LFTS
TFTs

86
Q

Amiodarone toxicity

A 
pulmonary fibrosis
hepatotoxicity
hypothyroidism or hyperthyroidism
corneal deposits
skin deposits--blue gray
neurologic effects
constipation
cardiovascular: brady, heart block, CHF
87
Q

Which antiarrythmic has all class I,II, III, and Iv effects and why

A

Amiodarone

alters the lipid membrane

88
Q

Sotalol toxicity

A

torsades de pointes

excessive beta block

89
Q

Ibutilide toxicity

A

torsades

90
Q

List the class IV antiarrythmics

A

Ca+channel blocker:
verapamil
diltiazem

91
Q

Class IV antiarrythmics MOa

A

decrease conduction velocity
increase ESR
increase PR interval

92
Q

Class IV antiarrythmics clinical use

A

prevention of nodal arrythmias ex SVT

93
Q

Class IV antiarrythmics toxicity

A

constipation
flushing
edema
CV effect: CHf, AV block,sinus node depression

94
Q

Adenosine MOA

A

increase K+ extrusion out of the cell causing hyperpol

decreases influx of ca

95
Q

What is the drug of choice for dx and abolishing SVT

A

adenosine

96
Q

These two thing block adenosine’s effect

A

theophyline

caffeine

97
Q

Adenosine toxicity

A

flushing
hypotension
chest pain

98
Q

Mg2+ uses

A

torsades depointes

digoxin toxicity

Pharmacology (13 decks)

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