Cardio and Blood vessels Flashcards

1
Q

Treatment for temporal giant cell arteritis and takayasu arteritis

A

Corticosteroids

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

Treatment of polyarteristis nodosa

A

corticosteroids

cyclophosphatimide

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

What is the treatment for a kid with kawasaki disease

A

ASA

IVIG

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

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

Wegener’s granulomatosis treatment

A

Cyclophospahmide (MAINLY)

corticosteroids

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

CHF treatment

A

ACEI

also beta blocker, spironolactone, ARB

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

treatment for a PDA and MOA

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Treatment for Transposition of great vessels

A

PGE to maintain a patent ductus arteriosus until surg

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

Treatment for torsades pointes

A

Magnesium sulfate

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

Treatment for essential HTN

A

Diuretics
ACEI
ARBs
calcium channel blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

First line treatment for essential HTN

A

diuretics

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

CHF treatment

A

Diuretics
ACEI
ARBs
Beta blocker*

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

First line treatment

A

diuretics

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

What kind of CHf are beta blocker contraindicated

A

decompensated

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

What must be used in DM pt with HTN

A

ACEI

ARBS

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

List the DHP calcium channel blockers

A

Nifedipine

amlodopine

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

List the nonDHP calcium channel blockers

A

Verapamil

diltiazem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Calcium channel blockers clinical uses

A
Angina
Prinzmetal's angina
arrythmias
HTN
Raynaud's  phenomena
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Which of the calcium channel blocker is not used for arrythmias

A

nifedipine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Calcium channel blocker MOA

A

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

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

Describe the order of how CCblockers on the vascular smooth muscle

A

Amlodipine=nifedipine>diltiazem.varapamil

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

describe the order of how CCblocker on the heart

A

Verapamil>diltiazem>amlodipine=nifedipine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

CCblockers toxicity

A

cardiac depression
peripheral edema
flushing
dizziness

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

CCblockers toxicity specific for verapamil

A

constipation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
CCblockers toxicity specific for NonDHP
AV block
26
Hydralazine use
Severe HTN CHF first line for preg HTN with methyldopa
27
hydralazine MOA
increase cGMP --SM relaxation--VD arteriole and reduce afterload
28
hydralazine toxicity
``` fluid retension nausea HA angina Lupus like syndrome compensatory tachycardia ```
29
Hydralazine is contraindicated in
Angina/CAD
30
What drug is given with hydralazine to prevent reflex tachycardia
B-blocker
31
List the diuretics
``` furosemide Thiazide spironolactone eplerenone triamterene Amiloride ```
32
List the ARBs
s
33
List the ACEI
Captopril, Enalapril,lisinopril
34
Malignant HTN treatment
``` nitroprusside nicardipine clevidipine labetalol fenoldopam ```
35
Nitroprusside MOA
Short acting direct release of NO to increase cGMP
36
Nitroprusside toxicity
Cyanide toxicity
37
FenoldopamMOA
a dopamine D1 receptor agonist that causes vasodilation of coronary, peripheral, renal, and splanchnic --decreasing BP and increasing natriuresis
38
Nitroglycerin and isosorbide dinitrate MOA
Relases NO--increase cGMP--SM relaxation--VENOdilation--decreased preload
39
Nitroglycerina and isosorbide dinitrate clinical use
Angina | pulmonary edema
40
Nitrates/isosorbide dinitrate toxicity
``` Reflex tachy HypoTN flushing HA Monday disease ```
41
Statins MOA
inhibit conversion of HMG-CoA to mevalonate
42
Statins effects
decrease LDLcholesterol decreases TGs increase HDL
43
Statin side effects
hepatotoxic | rhabdomyolysis
44
Niacin MOA
inhibits lipolysis | reduces hepatic VLDL secretion into circulation
45
Niacin effect
increase HDL | decrease TGs and LDL
46
Niacin toxicities
Red flushed face--give ASA hyperglycemia--acanthosis nigircan hyperuricemia-- makes gout bad
47
List the bile acid resins
Cholestyramine colestipol colesvelam
48
Bile acid resin MOA and effect
prevent intestinal RAb of bile acids so that liver must use chol to make more reduce LDL
49
Bile acid resins toxicity
GI discomfort reduce absorption of fat soluble ADEK Chol Gall stones
50
Ezetimbe is a
cholesterol absorption blocker at small intestine brush border
51
Ezetimbe effects and toxicity
reduce LDL Rare LFTs diarrhea
52
Fibrates( the "fibrozil and the fibrates") MOA
upregulate lipoprotein lipase activity ---increase TG clearance
53
Fibrates toxicity
Myositis hepatotoxicity chol gallstones`
54
Digoxin MOA
glycoside that directly inhibits Na/K ATPase leading to indirect inhibition of the Na/Ca exchanger----increase intracellular Ca---increase contractility
55
Digoxin also stimulate
vagus nerve---decrease HR
56
Digoxin use
CHF to increase contractility | AFib to reduce conduction thru AV node and depress SA node
57
Factor predisposing to digoxin toxicity
Renal failure hypokalemia quinidine
58
digoxin toxicity
N/V/D blurry yellow vision Hyperkalemia
59
Digoxin EKG
``` Prolong PR lower QT ST scooping T-wave inversion arrythmias AV block ```
60
Class I antiarrhythmics MOa
Na+ channel blocker decreasing phase 0 depolorization and increasing the threshold for firing
61
Class I antiarrhythmics are state dependent. what does this mean?
They selectively depress tissue that is frequently depolorized
62
What increases the toxicities of all the class I antiarrythmics
hyperkalemia
63
List the class IA antiarrhythmics
Quinidine Procainamide disopyramide
64
Class IA anitarryhthmic specific MOA
increase AP duration increase effectice refractory period increase QT interval
65
quinidine toxicity
headache | tinnitus
66
Procainamide toxicity
reversible SLE-like sxs
67
Class IA collective toxicity
thrombocytopenia | QTprolongation--- torsadesde pointes
68
disopyramide toxicity
heart failure
69
List the class IB antiarryhthmics
Lidocaine TOcainide Mexiletine phenytoin
70
Class IB preferentially affect
ichemic or depolarized purkinje and ventricular tissue by decreasing AP duration
71
Which antiarrythmics are good Post MI and digitalis induced arrythmias
Class IB lidocaine Tocainide Mexiletine
72
Class IB antiarrythmics toxicity
Act as local anesthetics CNS stimulation or depression Cardiac depression
73
List the class IC antiarrythmic drugs
Flecaine | propafenone
74
Class IC antiarrythmic drugs are contraindicated in
structural heart disease and post MI
75
The class IC antiarrythmic drugs are only really used for
as a last resort for refractory tachyarrythmias
76
Class IC antiarrythmics toxicity
pro-arrythmia esp post-MI | significantly prolongs refractory AV node
77
List the class II antiarrythmics
``` B-blockers: metoprolol propanalol esmolol atenolol timolol ```
78
MOA of the class II antiarrythmics
decrease cAMP and ca2+ levels that lead to decrease SA and AV nodal activity decrease phase 4
79
Class II antiarrythmics clinical uses
Vtachy SVT slowing ventricular rate during A-fiband flutter
80
Class II antiarrythmics toxicity
Impotence exacerbation of asthma cardiac:bradycardia, Av block, CHF CNS: sedation sleep alterations, may mask hypoglycemia
81
Toxicity unique to metoprolol
dyslipidemia
82
toxicity unique to propranolol
exacerbate vasospasm in Prinzmetal's angina
83
List the class III antiarrythmics
``` K+channel blocker Amiodarone Ibutilide Dofetilide Sotalol ```
84
Class III antiarrythmics MOA
increase AP duration increase ERP? increase QT interval
85
Check these for amiodarone
PFTs LFTS TFTs
86
Amiodarone toxicity
``` pulmonary fibrosis hepatotoxicity hypothyroidism or hyperthyroidism corneal deposits skin deposits--blue gray neurologic effects constipation cardiovascular: brady, heart block, CHF ```
87
Which antiarrythmic has all class I,II, III, and Iv effects and why
Amiodarone | alters the lipid membrane
88
Sotalol toxicity
torsades de pointes | excessive beta block
89
Ibutilide toxicity
torsades
90
List the class IV antiarrythmics
Ca+channel blocker: verapamil diltiazem
91
Class IV antiarrythmics MOa
decrease conduction velocity increase ESR increase PR interval
92
Class IV antiarrythmics clinical use
prevention of nodal arrythmias ex SVT
93
Class IV antiarrythmics toxicity
constipation flushing edema CV effect: CHf, AV block,sinus node depression
94
Adenosine MOA
increase K+ extrusion out of the cell causing hyperpol | decreases influx of ca
95
What is the drug of choice for dx and abolishing SVT
adenosine
96
These two thing block adenosine's effect
theophyline | caffeine
97
Adenosine toxicity
flushing hypotension chest pain
98
Mg2+ uses
torsades depointes | digoxin toxicity