Module 6 cardiac Flashcards
(132 cards)
1
Q
What are the risk factors for CV disease?
A
gender, age cigarette smoking, DM, HTN, dyslipidemia
2
Q
Which lipoproteins are associated with hyperlipidemia?
A
Decreased amount of High-density lipoproteins (HDL-C)
3
Q
At which point in the cholesterol synthesis pathway do the statins intervene?
A
HMG CoA- inhibits this step to decrease the amount of endogenous cholesterol in our body
4
Q
What does the LDL-C do? And what are the important aspects to remember?
A
“Bad” cholesterol
60% of total cholesterol in body
transports cholesterol to peripheral cells
excess initiates atherosclerosis
predictor for CV disease
Primary target of cholesterol lowering therapy
5
Q
What is HDL-C and what does it do?
A
“Good” cholesterol
20-30% of cholesterol in body
transports cholesterol from peripheral tissues and vessels to liver and kidneys for removal
6
Q
What is VLDL-C and what is its purpose?
A
Made up of triglycerides
produced by liver
precursor to LDL
7
Q
There are primary and secondary causes of hyperlipidemia. What are the primary causes?
A
genetics
8
Q
There are primary and secondary causes of hyperlipidemia. What are the secondary causes?
A
Diet (high fat)
Underlying disease (DM, Liver disease, CRF, alcoholism)
Medications (estrogens, protease inhibitors, steroids, thiazides, beta blockers)
9
Q
What effect does estrogen have on cholesterol?
A
decreases LDL
increases HDL
but increases triglycerides
10
Q
What determines the patient’s LDL goal?
A
Coronary hear disease risk assessment
Risk factor status
11
Q
What are the determinants of the CHD risk assessment?
A
MI Myocardial ischemia angina coronary angioplasty coronary artery surgery DM Peripheral arterial disease AAA Carotid artery disease
12
Q
What are the risk factors to count after the CHD risk assessment is complete?
A
Cigarette smoking
Hypertension (140/90)
Low HDL (45, women =/> 55)
13
Q
After completing the Framingham scoring, your patient has a 10year risk of >20%, what is their LDL-C goal?
A
<100mg/dl
14
Q
After completing the Framingham scoring, your patient has a 10year risk of </= 20%, what is their LDL-C goal?
A
<130 mg/dl
15
Q
For those patients with 0-1 risk factor and no need for further risk factor assessment, what would their LDL-C goal be?
A
<160 mg/dl
16
Q
What are the items to score in the Framingham risk assessment?
A
Age Total cholesterol Smoking status HDL level Systolic blood pressure
17
Q
What is the normal/accepted HDL range?
A
40-60 mg/dl
18
Q
What is the accepted/normal level for total cholesterol?
A
<200 mg/dl
19
Q
What does a lipoprotein analysis include?
A
total cholesterol
LDL-C
HDL-C
triglycerides
20
Q
What is the accepted/normal for triglycerides?
A
<150 mg/dl
21
Q
What is considered the “cornerstone” in LDL-lowering therapy?
A
Lifestyle changes
22
Q
What are the 4 lifestyle modifications encouraged in lowering LDL levels?
A
Reduce intake of cholesterol
soluble fiber intake of 10-25g/d
Weight reduction
Increased physical activity
23
Q
Describe the progression of drug therapy in primary prevention of hyperlipidemia.
A
- Initiate statin or bile acid sequestrant or nicotinic acid
- In 6 weeks, if goal not acheived, intensify same medications
- In 6 weeks, if goal acheived, treat other lipid risk factors. If goal not acheived, refer to specialist.
- Monitor Q4-6 months
24
Q
What is the main concern in increasing the lipid lowering medications?
A
rhabdomyolosis
25
What are the four drug classifications used in treatment of dyslipidemia?
HMG CoA Reductase Inhibitors (Statins)
Bile acid sequestrants
nicotinic acid (Niacin)
Fibric acids
26
What are the contraindications in using HMG CoA Reductase inhibitors?
Liver disease (absolutely do not use)
CYP450meds
Antifungals
macrolides
27
Name the HMG CoA Reductase inhibitors.
```
lovastatin (Mevacor)
pravastatin (Pravachol)
simvastatin (Zocor)
fluvastatin (Lescol)
atorvastatin (Lipitor)
rosuvastatin (Crestor) newest
```
28
When do the HMG CoA Reductase inhibitors work best?
when taken before bed
29
What are the major side effects of HMG CoA reductase inhibitors?
Myopathy
| increased liver enzymes
30
Are bile acid sequestrants systemic acting?
No
31
What effect do bile acid sequestrants have on triglycerides?
increases triglyceride levels
32
What are the side effects of bile acid sequestrants?
GI distress/constipation
| decreased absorption of other drugs (HCTZ, warfarin, digoxin, thyroid meds, BBs, statins)
33
When is the use of bile acid sequestrants contraindicated?
TG level of more than 400
| dysbetalipoproteinemia (increases TG = acute pancreatitis)
34
What are the common bile acid sequestrants used?
cholestyramine (Questran)
colestipol (Colestid)
colesevelam (Welchol)
35
Which medication is used to raise the HDL level once the LDL goal has been reached?
Nicotinic acid
36
What does nicotinic acid do?
decreases the production of VLDL which eventually becomes LDL and raises HDL
37
What are the side effects of nicotinic acid?
flushing, hyperglycemia, hyperuricemia, upper GI distress, hepatotoxicity
38
When is nicotinic acid contraindicated?
liver disease
severe gout
peptic ulcer
39
What is an important aspect in patient education regarding nictonic acid?
Side effects lessen over time
40
What is the major drug interaction in using fibric acids?
Warfarin - more warfarin is available in blood, increasing anticoagulant effect
41
What do fibric acids do?
decreases hepatic TG production and VLDL synthesis
42
Name the 2 fibric acids used.
gemfibrozil (Lopid)
| fenofibrate (Tricor)
43
What does ezetimibe (Zetia) do?
inhibits the absorption of cholesterol by the small intestine
44
What drug interactions are of concern in using ezetimibe (Zetia)?
fibric acids and cyclosporines block the absorption of Zetia
45
What is the purpose of taking fish oil (omega-3 fatty acids)?
decreases TG/VLDL
46
What are the main risks associated with a triglyceride level > 500?
pancreatitis, increased risk for atherosclerosis
47
What is the treatment for hypertriglyceridemia?
```
dietary fat restriction
ETOH restriction
weight reduction
treat coexisting conditions
medications: fibric acids, niacin, fish oil, statins
```
48
What are the four types of medications used in treating Coronary Artery Disease?
Nitrates
Beta Blockers
Calcium Channel Blockers
49
What do nitrates do?
Reduce cardiac preload
| Dilate coronary arteries
50
What are the 3 nitrates commonly prescribed?
Nitroglycerin
isosorbide dinitrate
isosorbide mononitrate
51
What is the timeframe that a patient being treated with nitrates should be nitrate FREE?
8-12 hours
52
What is the first line nitroglycerin agent?
Sublingual nitroglycerin
53
What do beta blockers do?
Decrease heart rate
reduce blood pressure
decrease contractility
54
What is the treatment plan for CAD?
1. Initiate aspirin
2. Sublingual NTG
3. NTG vs. CCB vs BB
4. Maximize single agent
5. combination treatment
55
90% of patients with HTN havethis type of HTN.
Essential
56
According to JNC 8, how is a non-black patient treated with blood pressure >140/90?
Thiazide type diuretic and ACEI, ARB, or CCB
57
According to JNC 8, how is a black patient treated with blood pressure >140/90?
Thiazide type diuretic or CCB
58
Which drugs affect heart rate and contractility?
BBs
CCBs
Centrally acting adrenergics
59
What effects does the parasympathetic system have on the cardiac system?
Stimulates smooth muscle, cardiac muscle and decreases heart rate
60
What effects does the sympathetic system have on the cardiac system?
Stimulates the heart rate, vasoconstricts vessels in skin and visceral and vasodilates vessels in skeletal muscle
61
What is the mechanism of action for adrenergic drugs?
decreased BP, HR, venous return, CO, and cardiac workload
62
What are the centrally acting alpha2-receptor agonists?
clonidine (Catapres)
| methyldopa (Aldomet)
63
What are the 5 types of adrenergic drugs?
Centrally and peripherally acting adrenergic neuron blockers
Centrally acting alpha2-receptor blockers
peripherally acting alpha1-receptor blockers
Peripherally acting beta-receptor (beta blockers)
both cardioselective (beta1) and nonselective(beta1 and beta2)
Pheripherally acting dual alpha1 and beta-receptor blockers
64
What type of drugs are the -zosin's?
Adrenergic: peripheral alpha1-vlockers
65
Describe the mechanism of action in peripheral alpha1-blockers.
Decreased BP, peripheral resistance
Promotes vasodilation
No change in CO
66
What are the beta blockers mechanism of action?
reduces BP by reducing HR
reduces renin secretion
decreases myocardial contractility
results in decreased HR, BP, CO, SVR, and cardiac workload
67
What is the mechanism of action in dual action alpha1 adn beta-receptor blockers?
Decreased HR
vasodilation
results in decreased BP, HR, SVR, and improves CO
also useful in CHF
68
What is clonidine and when is it useful?
central acting alpha2-receptro agonist
| among other things, useful in management of withdrawal symptoms of opioid or nicotine dependent persons
69
What are the most common side effects of adrenergic drugs?
Dry mouth
Drowsiness, sedation
constipation
70
Which drugs end in -olol or -lol?
Beta blockers
71
Which drugs end in -pril?
ACE inhibitors
72
What are ACE inhibitors used for?
used for first line therapy in CHF and HTN
73
What are ACE inhibitors sometimes combined with?
CCBs or thiazide diuretics
74
Once ACE converts angiotensin I to angiotensin II, what does angiotensin II do?
Potent vasoconstrictor that causes aldosterone secretion from the adrenal glands
75
What are the effects of ACE inhibitors?
decreased afterload
systemic vasodilation
decreases Na and H2O reabsorption
decreases BP
76
Name the most common ACEIs
captopril (Capoten)
enalapril (Vasoec)
lisinoptil (Prinivil and Zestril)
quinapril (Accupril)
77
Which ACEI is used in diabetic patients, and why?
captopril (Capoten)
| It is renal protective
78
Which ACEIs are newer with long half-lives and require once a day dosing?
lisinopril (Prinivil and Zestril)
| quinapril (Accupril)
79
Which ACEI may be used in patients with liver dysfunction?
captopril (Capoten)
| lisinopril (Prinivil and Zestril)
80
What are the adverse effects of ACEIs?
```
Fatigue
Dizziness
HA
Mood changes
Impaired taste
Possible hyperkalemia
Dry, nonproductive cough
Angioedema (rare but potentially fatal)
First dose hypotension
```
81
What is the suffix associated with ARBs?
-sartan
82
What is special about ARBs in reference to its side effects, as compared with ACEIs?
No dry cough
| Less likely to cause hyperkalemia
83
Name the most common ARBs.
losartan (Cozaar, Hyzaar)
valsartan (Diovan)
sprosartan (Teveten)
irbesartan (Avapro)
84
What is the mechanism of action in calcium channel blockers (CCBs)?
causes smooth muscle relaxation by blocking the binding of calcium to its receptors, preventing muscle contraction
85
What are the effects of CCBs?
decreased peripheral smooth muscle tone
decreased systemic vascular resistance
decreased BP
decreased HR
86
What are the suffixes associated with CCBs?
- zem
- mil
- dipine
87
Name the most common CCBs.
benzothiazepines: diltiazem (Cardizem)
phenylalkamines: verapamil (Calan)
dihydropyridines: amlodipine (Norvasc)
nifedipine (Procardia)
88
What are the indications for use of CCBs?
```
angina
HTN
dysrhythmias
migraines
Raynauds disease
```
89
What are the adverse effects of CCBs?
```
hypotension
papitations
tachycardia
worsening of CHF
constipation, nausea
rash
flushing
peripheral edema
dermatitis
```
90
What are the effects of diuretics?
```
decreased preload
decreased CO
decreased total peripheral resistance
which results in
decreased workload on the heart and BP
```
91
What are the most common vasodilators?
diazoxide (Hyperstat)
hydralazine HCl (Apresoline)
minoxidil (loniten)
sodium nitroprusside (Nipride, Nitropress)
92
What are the 3 types of diuretics?
thiazide
loop
potassium-sparing
93
What are the most common thiazide and thiazide-like drugs used?
```
thiazides:
HCTZ
all end in -zide
thiazide-like:
metolazone (Zarozolyn)
```
94
What is the mechanism of action in thiazide/thiazide-like drugs?
action primarily in the distal convouted tubule
inhibits tubular reabsorption of Na, Cl, K ions
results in systemic vascular resistance
95
What is the minimum creatinine clearance for use of thiazides?
30-50 ml/min
| metolazone: 10 ml/min
96
What are the adverse effects of thiazide diuretics?
```
dizziness
HA
blurred vision
paresthesias
decreased libido
anorexia
n/v/d
impotence
urticaria
photosensitivity
hypokalemia
hyperglycemia
```
97
Name the common loop diuretics.
bumetanide (Bumex)
furosemide (Lasix)
torsemide (Demedex)
98
How do loop diuretics work?
act directly on the ascending limb of the loop of Henle to inhibit Cl and Na resorption
Increases renal prostaglandins, resulting in the dialtion of blood vessels and reduced peripheral vascular resistance
99
Loop diuretics adverse effects are similar to thiazides except for what?
No decreased libido, no impotence/photosensitvity
| risk for hematologic concerns
100
Name the potassium sparing diuretics.
also known as aldosterone inhibiting diuretics:
amiloride (Midamor)
spironolactone (Aldactone)
triamterene (Dyrenium)
101
When are potassium supplements not recommended when using diuretics?
when potassium levels exceed 3 mEq/L
102
Name some foods high in potassium.
```
bananas
oranges
dates
apricots
raisins
broccoli
green beans
potatoes
meats
fish
legumes
```
103
What drug toxicity is of concern with diuretic drug therapy?
digitalis
104
Which type of heart failure is most common?
Systolic
105
What are the common causes of chronic heart failure (CHF)?
```
HTN
CAD
idiopathic
valvular disease
viral
genetic abnormalities
drug induced: anticancer, ETOH, cocaine, immunomodulating drugs
```
106
What are the first line agents used for CHF?
ACEIs
107
What do positive inotropic drugs do?
increase the force of myocardial contraction
108
What do negative chronotropic drugs do?
decrease HR
109
What do negative dromotropic drugs do?
slows cardiac conduction through the tissue
110
What are the common drug classes used in treatment of CHF?
```
ACEIs
Angiotensin II receptor blockers (ARBs)
Beta blockers
Aldosterone blocking agents
cardiac glycosides
```
111
What is the therapeutic level for digoxin?
0.5 - 2 ng/ml
112
Name the therapy used in digoxin toxicity.
Digoxin immune Fab (Digibind)
113
Name the conditions that predispose a patient to digoxin toxicity.
hypokalemia, hypomagnesemia, hypercalcemia
cardiac pacer
hepatic dysfunction
dysrhythmias
hypothyroid, respiratory, or renal disease
advanced age
114
When would you hold digoxin?
apical pulse less than 60 or greater than 120
| s/s toxicity
115
What foods should be avoided while taking digoxin and why?
High fiber
| fiber binds with digitalis
116
What are the contraindications for the use of warfarin?
```
pregnancy
psychosis/senility
alcoholism
hepatic disease
high bleeding risk
```
117
What is the length of treatment for warfarin for the use of cardioversion?
3 weeks prior to cardioversion
118
What is the initial dosing for warfarin?
5mg every day for 2-3 days
119
What is the target INR in warfarin therapy for most patients? for those with a mechanical heart valve?
2-3
| 2.5-3.5
120
What is the antidote for warfarin in the case of toxicity?
Vitamin K
121
What is the general rule for monitoring INR in warfarin therapy?
Monitor INR twice weekly, till patients have 2 consecutive INRs in range, then may monitor every 4 weeks as stable. Remember that an INR today is the dose change 3-5 days ago.
122
The average change in INR due to amiodarone when taken with warfarin is what?
increase of 44%
123
How much would you need to decrease the warfarin dose if a patient would need to take amiodarone?
50% reduction
124
Name the medications that interact with warfarin (increases INR).
```
antiobiotics
amiodarone
zafirlukast
sulfa/trimeth
flagyl
HMG CoA Reductase inhibitors
fibric acid derivatives
```
125
What effect does chronic alcoholism have on warfarin therapy?
decreases INR
126
What are the effects of vitamin K, herbals, and ASA on warfarin therapy.
vitamin K: decreases INR
herbals: increase INR
ASA: increases INR
127
Weekly dose changes should be approximately how much in warfarin therapy?
5-20% of total weekly dose
128
JNC-7 recommends which diagnostic tests before initiating treatment form HTN?
```
12 lead EKG
urinalysis with albumin
blood glucose and hematocrit
serum potassium
creatinine and GFR
serium calcium
lipid profile
```
129
When treating HTN pharmacologically, what is the drug of choice for patients with DM, CHF, and MI?
ACEIs
130
Which HTN medication may make cognitive dysfunction and dementia worse?
central alpha2 agonists
131
What is preeclampsia?
HTN and proteinuria after 20 weeks
132
HTN is higher in which ethnic/racial group?
African Americans
