Module 2 Flashcards
1
Q
Cholesterol is an important building block in what 4 things?
A
Estrogen/testosterone, Vitamin D, Cortisol, Bile Acid.
2
Q
What percentage of cholesterol is exogenous and what percentage is endogeneous?
A
Exogenous = 25%, Endogenous = 75%.
3
Q
Where is endogenous cholesterol made?
A
In the liver.
4
Q
What is hypercholesterolemia? What are other names for it?
A
Too much cholesterol. Otherwise known as hyperlipidemia or dyslipidemia.
5
Q
When should cholesterol screening start?
A
At age 20.
6
Q
Why do we normally check cholesterol after fasting?
A
Because meals can alter the level of cholesterol short term.
7
Q
What is total cholesterol score used for?
A
Used to assess risk for heart disease and atherosclerosis.
8
Q
What is the “equation” to find the total cholesterol score?
A
HDL + LDL + triglyceride/5 = total cholesterol.
9
Q
What is the ideal range of cholesterol, what is considered borderline high, and what is considered high?
A
Ideal: 100-200 mg/dL
Borderline: 200-239 mg/dL
High: 240+ mg/dL.
10
Q
What is the ideal HDL level for women and men?
A
Women: > 45 mg/dL
Men: >55 mg/dL.
11
Q
What is the ideal LDL level?
A
< 100 mg/dL.
12
Q
What is the range for triglycerides?
A
40-150.
13
Q
What is wrong in people with familial hypercholesterolemia?
A
Defect in LDL receptors in the liver -> do not respond to HMG-CoA reductase inhibitors -> liver cannot remove LDL from the blood -> elevated LDL cholesterol levels.
14
Q
What are some risk factors for high cholesterol?
A
Age, family history, smoking, HTN, DM, physical inactivity, poor diet (high in saturated fat).
15
Q
What is arteriosclerosis?
A
Thickening/hardening of arterial wall.
16
Q
What 4 things can lead to atherosclerotic plaque formation?
A
Injury to the endothelium, cigarette smoking (which damages the endothelium), chronic hypertension, and hyperglycemia.
17
Q
What are the steps in atherosclerotic plaque formation?
A
- Endothelial damage
- Lipid molecules are able to attach to the innermost layer of the vein/artery
- Migration of leukocytes / smooth muscle cells into the vessel wall
- Foam cell formation (macrophages engulfing lipids)
- Degradation of cellular matrix
18
Q
Plaque with large lipid cores are more prone to what?
A
Rupture.
19
Q
Why is a plaque with a large lipid core rupturing a problem?
A
Can block artery which would stop blood flow and oxygenation somewhere.
20
Q
What is C-Reactive protein (CRP)? What does it typically indicate?
A
Marker of inflammation. Typically indicates increased risk of disease state.
21
Q
Almost all instances of atherosclerosis can lead to what?
A
Coronary artery disease and insufficient delivery of oxygen to heart.
22
Q
How can someone lower the cholesterol in their blood?
A
Decrease LDL and increase HDL, increase exercise and improve diet (low saturated fats), medications, weight control, stop smoking.
23
Q
What are HMG-CoA reductase inhibitors?
A
Statins.
24
Q
What do statins do?
A
Inhibits HMG-CoA reductase which inhibits the formation of cholesterol.
25
What things are included in clinical ASCVD?
Acute coronary syndrome, history of MI, stable / unstable angina, coronary revascularization, stroke / TIA, PAD.
26
Is HMG-CoA reductase a permanent fix?
No, this is something the person will have to continue to take in order to continue the benefits.
27
What are the specific effects of statins?
Decrease LDL by 21-63%, increase HDL by 5-22%, decrease 6-43%.
28
What are 3 adverse reactions to statins?
Myopathy, rhabdomyolysis, and hepatotoxicity.
29
What is myopathy?
Muscle weakness.
30
What is rhabdomylosis?
Breakdown of muscle fibers that release a damaging protein into the blood that can lead to acute kidney failure.
31
What is hepatotoxicity?
Damage to the liver from medication.
32
Atorvastatin (Lipitor) is a:
Statin / HMG-CoA reductase inhibitor.
33
Simvastatin (Zocor) is a:
Statin / HMG-CoA reductase inhibitor.
34
Rosuvastatin (Crestor) is a:
Statin / HMG-CoA reductase inhibitor.
35
How long does it take to see effects of statins?
About 2 weeks.
36
What statins usually need to be taken at night?
Simvastatin and rosuvastatin.
37
Statins may cause what type of discomfort? What helps relieve it?
GI discomfort, taking it with food may help.
38
What type of drugs should someone taking statins avoid?
Drugs that increase myopathy and/or rhabdo and also alcohol.
39
Ezetimibe (Zetia) is a:
Cholesterol absorption inhibitor.
40
What do cholesterol absorption inhibitors do?
Blocks cholesterol absorption in the jejunum.
41
Are cholesterol absorption inhibitors 1st or 2nd line therapies?
2nd line.
42
What medication is usually taken in combination with cholesterol absorption inhibitors? Why?
Statins - it has a 15-20% greater decrease in LDL than alone.
43
What 4 things are monitored / checked before initiating cholesterol medication therapies?
1. Fasting lipid panel
2. ALT levels (this is from the liver)
3. Creatine kinase (indicates muscle breakdown)
4. Identify secondary causes
44
How does the RAAS pathway flow?
Starts with low fluid volume (or when there is a decreased renal perfusion) stimulating kidneys to release renin -> causes the liver to convert angiotensinogen to angiotensin I -> travels to lungs -> angiotensin I is converted to angiotensin II by angiotensin converting enzyme -> angiotensin II acts on adrenal glands to release aldosterone -> nephron ability to retain fluid increases
45
What does aldosterone do?
Causes the kidneys to retain more sodium (which causes increased fluid retention) and increases BP.
46
Angiotensin II is a potent __________.
Vasoconstrictor.
47
Does stress influence the RAAS?
Yes, chronic stress stimulates renin and starts the RAAS.
48
What division of the nervous system is the primary driver of the BP regulation process?
Sympathetic nervous system.
49
What do arterial baroreceptors do?
Sense BP changes and can impact vasodilation / vasoconstriction accordingly. Can also impact HR to change BP.
50
How does vascular autoregulation help blood pressure?
It alters the resistance in arterioles to change BP.
51
What is considered normal blood pressure?
Less than 120
AND
Less than 80
52
What is considered elevated blood pressure?
120-129
AND
Less than 80
53
What is considered hypertension stage 1?
130-139
OR
80-89
54
What is considered hypertension stage 2?
140+
OR
90+
55
What is considered a hypertensive crisis?
180+
AND OR
120+
56
Primary hypertension is the same thing as:
Essential hypertension.
57
What type of hypertension is caused by unknown reasons?
Primary / essential hypertension.
58
What are three interactions that may play a part in essential hypertension?
SNS, RAAS, and natriuretic peptides.
59
What are natriuretic peptides?
Chemicals/hormones that help control water and sodium retention.
60
What are the risk factors for primary hypertension? (there are 11)
Smoking
Excessive sodium intake
Hyperlipidemia
Genetics
Obesity
Age
Sedentary lifestyle
Stress
African American
High alcohol consumption
Insulin resistance
61
What is secondary hypertension?
Hypertension with a known cause that is related to an underlying disease or disorder.
62
What is the best way to treat secondary hypertension?
To treat the underlying cause.
63
What are some end-organ damage that can be seen with unmanaged hypertension?
Chest pain (heart damage)
Headache (brain damage)
Visual changes (eye damage)
Weakness/pain in extremities
64
What are the cardiac implications of long term uncontrolled BP?
Hypertrophy of the left ventricle due to the need to overcome pressure to pump blood out to the body -> increased work -> higher risk of heart failure or heart attack
Accelerated progression of atherosclerosis
Increased risk of aortic aneurysm due to weakened vessel walls.
65
What are the renal implications of long term uncontrolled hypertension?
Increased SNS and RAAS -> decreased blood flow / increased inflammation -> leads to decreased function and permeant damage.
66
What are the brain implications of long term uncontrolled hypertension?
Higher risk for stroke, aneurysm, or hemorrhaging.
67
What are the eye implications of long term uncontrolled hypertension?
Increased retinal pressure -> retinopathy and blindness
68
What are the lower extremity implications of long term uncontrolled hypertension?
Gangrene
69
What are the two types of hypertensive crises?
Hypertensive urgency and hypertensive emergency.
70
Does hypertensive urgency or hypertensive emergency lead to end-organ damage?
Hypertensive emergency.
71
How do you treat hypertensive urgency?
With oral agents to gradually lower BP.
72
How do you treat hypertensive emergencies?
With IV medications to aggressively lower BP within minutes - hours.
73
What are some potential causes of hypertensive urgency?
Anxiety, pain, abrupt withdrawal from BP meds.
74
What are some symptoms of hypertensive emergencies?
Headache, blurry vision.
75
What are the three types of diuretics?
Potassium sparing, thiazide, and loop.
76
In general, how do diuretics lower blood pressre?
Increase urinary output (decrease circulating volume)
Decreases arterial resistance
Decreases cardiac output by blocking sodium / chloride reabsorption
77
What type of antihypertensive medication is usually first line?
Diuretics.
78
What type of diuretic is 1st line management of mild hypertension?
Thiazide
79
Hydrochlorothiazide (Hydrodiuril) is a:
Thiazide diuretic
80
What is the mechanism of action of thiazide diuretics?
Works on distal convoluted tubule to inhibit the reabsorption of sodium, potassium, and chloride -> fluid loss through urine -> decrease cardiac output
Relaxes arterioles -> decreases peripheral vascular resistance
81
What are the side effects of thiazide diuretics? (5)
Electrolyte and metabolic disturbances
Orthostatic hypotension
Worsen renal insufficiency
Hyperuricemia
Elevated levels of glucose, cholesterol, and triglycerides
82
What specific electrolyte disturbance can happen with thiazide diuretics?
Hypokalemia.
83
Furosemide (Lasix) is a:
Loop diuretic
84
What is the mechanism of action of loop diuretics?
Inhibits the kidneys ability to reabsorb sodium in the loop of Henle -> more sodium in the urine (more fluid) -> less fluid in the blood vessels -> decreases cardiac output
85
Which diuretic has the most profound diuresis?
Loop diuretics
86
What are potential routes for loop diuretics?
IV or PO
87
What are potential side effects of loop diuretics? (4)
Hypokalemia
Dehydration
Hypotension
Ototoxicity
88
What is the normal potassium range?
3.5-5.0
89
Spironolactone (Aldactone) is a:
Potassium-sparing (aldosterone ANTAGONIST)
90
What is the mechanism of action of potassium-sparing diuretics?
Block the action of aldosterone (which causes retaining of salt and fluid) -> holding some amount of potassium while you are releasing sodium and water.
91
Why would someone take a potassium sparing diuretic in addition to another antihypertensive medication?
Lowers the chance of hypokalemia.
92
What are the side effects of potassium sparing diuretics? (2)
Hyperkalemia
Endocrine effects (deepened voice, impotence, irregular menstrual cycles, gynecomastia)
93
What are the 3 types of sympatholytic antihypertensives?
Alpha-adrenergic blockers
Centrally acting alpha-2 agonists
Beta adrenergic blockers
94
Metoprolol, propranolol, and carvedilol are all:
Beta adrenergic blockers (aka Beta blockers)
95
Which beta blocker is selective?
Metoprolol
96
Which beta blocker is non-selectice?
Propranolol
97
Which beta blocker is receptive to only alpha and beta receptors?
Carvedilol
98
Where are beta 1 receptors located?
In the heart
99
Where are beta 2 receptors located?
In the lungs
100
Blocking beta 1 receptors has what effects?
Decreased contractility, decreases HR (those two things together are going to decrease cardiac output), and decrease renin secretion.
101
Blocking beta 2 receptors has what effects?
Increases airway resistance and increases vascular resistance.
102
What is the mechanism of action of beta adrenergic blockers?
Increase nitric oxide -> vasodilation
Blocks stimulation of beta-1 receptors -> decrease HR and contractility
103
What are 4 side effects of beta-blockers?
Fatigue/lethargy
Bradycardia
Hypotension
Can mask hypoglycemia in diabetic patients (would have tachycardia)
104
What are the nursing considerations of beta adrenergic blockers?
Need to be weaned off of the medication due to rebound HTN
If non-selective beta blocker - patients with asthma or breathing conditions should not use due to the blocking beta 2 receptors
105
Why is rebound HTN a problem?
Can put a patient in critical risk for cardiovascular events, stroke, and death.
106
When should a beta adrenergic blocker be held?
HR less than 60, and systolic BP less than 100
107
Clonidine (Catapress) is an:
Alpha-2 adrenergic agonist.
108
Would someone with newly diagnosed hypertension be prescribed clonidine first? why?
No, because of the high side effect profile.
109
What is the primary indication for clonidine?
Primary hypertension.
110
What routes are clonidine usually given?
PO or transdermal.
111
Where can transdermal clonidine be applied?
Upper chest, upper outer arm, lower abdomen, and hip
112
What is the key nursing action for alpha-2 adrenergic agonists?
Do not stop abruptly due to the potential for rebound HTN.
113
What are some side effects of alpha-2 adrenergic agonists? (3)
Drowsiness, potential for rebound HTN, may worsen pre-existing liver disease
114
Doxazosin (Cardura) is a:
Selective alpha-1 blocker
115
What is the mechanism of action of selective alpha-1 blockers?
Directly blocks sympathetic nervous system and decreases peripheral vascular resistance
116
Are alpha-1 blockers used first line?
No
117
What are the side effects of selective-1 blockers? (2)
Hypotension, dizziness
118
What are the 3 types of RAAS blockers?
ACE inhibitors, ARBs, Renin inhibitors
119
Captopril (capoten) and lisinopril (zestril) are both:
ACE (angiotensin converting enzyme) inhibitors
120
Are ACE inhibitors first line therapies? Why?
Yes, they are safe and efficacious.
121
What is the mechanism of action of ACE inhibitors?
Block angiotensin converting enzyme -> inhibits production of angiotensin II (stops powerful vasoconstriction) and inhibits aldosterone secretion (less water retention)
122
Which of the hypertensive medication classes has some renal protective effects?
ACE inhibitors
123
What are some side effects of ACE inhibitors? (5)
First dose hypotension
Dry, persistent nonproductive cough
Dizziness
Rash
Angioedema
124
What is first dose hypotension? What drug class is it associated with?
A drop in BP in the first 6-8 hours. Associated with ACE inhibitors.
125
What is angioedema? What population is mostly affected?
Swelling under the skin that can affect the larynx. More common in African Americans.
126
Are ACE inhibitors safe for pregnant women? Why?
No, it is teratogenic.
127
Losartan (cozaar) is an:
Angiotensin receptor blocker (ARB)
128
What is the mechanism of action for angiotensin receptor blockers?
Blocks the action of angiotensin II after it is formed -> causes vasodilation, increases sodium and water excretion
129
What are the indications for angiotensin receptor blockers?
Hypertension, heart failure, and stroke progression
130
What are the side effects for angiotensin receptor blockers (ARBs)
Potential for angioedema
131
Can pregnant patients be prescribed angiotensin receptor blockers?
No.
132
Aliskiren (tekurna) is a:
Renin inhibitor
133
What is the mechanism of action of renin inhibitors?
Direct inhibition of renin -> induces vasodilation, decreased blood volume, decreases SNS, and inhibits cardiac and vascular hypertrophy.
134
What are some side effects of renin inhibitors (2)
GI discomfort, potential for hyperkalemia (especially in diabetic patients).
135
Can a patient take a renin inhibitor if they are pregnant?
No
136
How long does it take for renin inhibitors to take full effect?
Several weeks
137
Nifedipine (procardia) and nicardipine (cardene) are bothh:
Calcium channel blockers
138
What is the mechanism of action for calcium channel blockers?
Blocks calcium access to cells -> decrease contractility and conductivity of heart and decreases demand for oxygen
Causes vasodilation of the smooth muscles of peripheral arteries
139
What are some side effects of calcium channel blockers? (6)
Orthostatic hypotension, bradycardia, may precipitate AV block, headache, GI discomfort, peripheral edema
140
What are the two primary indications for calcium channel blockers?
Hypertension and chest pain
141
Can calcium channel blockers be given IV?
Yes
142
If a patient is taking calcium channel blockers for hypertension and begins having peripheral edema, what should they be prescribed?
Diuretic
143
What populations of people are calcium channel blockers best for?
African Americans and elderly.
144
Hydralazine (apresoline) is a:
Vasodilators
145
What is the mechanism of action of vasodilators?
Work directly on arterial and venous smooth muscles and cause relaxation -> decreases systemic and peripheral vascular resistance
146
What is the indication for vasodilators?
Hypertension
