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Pathopharmacology Intro > Module 2 > Flashcards

Module 2 Flashcards

1
Q

Cholesterol is an important building block in what 4 things?

A

Estrogen/testosterone, Vitamin D, Cortisol, Bile Acid.

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2
Q

What percentage of cholesterol is exogenous and what percentage is endogeneous?

A

Exogenous = 25%, Endogenous = 75%.

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3
Q

Where is endogenous cholesterol made?

A

In the liver.

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4
Q

What is hypercholesterolemia? What are other names for it?

A

Too much cholesterol. Otherwise known as hyperlipidemia or dyslipidemia.

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5
Q

When should cholesterol screening start?

A

At age 20.

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6
Q

Why do we normally check cholesterol after fasting?

A

Because meals can alter the level of cholesterol short term.

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7
Q

What is total cholesterol score used for?

A

Used to assess risk for heart disease and atherosclerosis.

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8
Q

What is the “equation” to find the total cholesterol score?

A

HDL + LDL + triglyceride/5 = total cholesterol.

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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.

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10
Q

What is the ideal HDL level for women and men?

A

Women: > 45 mg/dL
Men: >55 mg/dL.

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11
Q

What is the ideal LDL level?

A

< 100 mg/dL.

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12
Q

What is the range for triglycerides?

A

40-150.

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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.

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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).

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15
Q

What is arteriosclerosis?

A

Thickening/hardening of arterial wall.

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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.

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17
Q

What are the steps in atherosclerotic plaque formation?

A
  1. Endothelial damage
  2. Lipid molecules are able to attach to the innermost layer of the vein/artery
  3. Migration of leukocytes / smooth muscle cells into the vessel wall
  4. Foam cell formation (macrophages engulfing lipids)
  5. Degradation of cellular matrix
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18
Q

Plaque with large lipid cores are more prone to what?

A

Rupture.

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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.

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20
Q

What is C-Reactive protein (CRP)? What does it typically indicate?

A

Marker of inflammation. Typically indicates increased risk of disease state.

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21
Q

Almost all instances of atherosclerosis can lead to what?

A

Coronary artery disease and insufficient delivery of oxygen to heart.

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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.

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23
Q

What are HMG-CoA reductase inhibitors?

A

Statins.

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24
Q

What do statins do?

A

Inhibits HMG-CoA reductase which inhibits the formation of cholesterol.

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25
Q

What things are included in clinical ASCVD?

A

Acute coronary syndrome, history of MI, stable / unstable angina, coronary revascularization, stroke / TIA, PAD.

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26
Q

Is HMG-CoA reductase a permanent fix?

A

No, this is something the person will have to continue to take in order to continue the benefits.

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27
Q

What are the specific effects of statins?

A

Decrease LDL by 21-63%, increase HDL by 5-22%, decrease 6-43%.

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28
Q

What are 3 adverse reactions to statins?

A

Myopathy, rhabdomyolysis, and hepatotoxicity.

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29
Q

What is myopathy?

A

Muscle weakness.

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30
Q

What is rhabdomylosis?

A

Breakdown of muscle fibers that release a damaging protein into the blood that can lead to acute kidney failure.

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31
Q

What is hepatotoxicity?

A

Damage to the liver from medication.

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32
Q

Atorvastatin (Lipitor) is a:

A

Statin / HMG-CoA reductase inhibitor.

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33
Q

Simvastatin (Zocor) is a:

A

Statin / HMG-CoA reductase inhibitor.

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34
Q

Rosuvastatin (Crestor) is a:

A

Statin / HMG-CoA reductase inhibitor.

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35
Q

How long does it take to see effects of statins?

A

About 2 weeks.

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36
Q

What statins usually need to be taken at night?

A

Simvastatin and rosuvastatin.

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37
Q

Statins may cause what type of discomfort? What helps relieve it?

A

GI discomfort, taking it with food may help.

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38
Q

What type of drugs should someone taking statins avoid?

A

Drugs that increase myopathy and/or rhabdo and also alcohol.

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39
Q

Ezetimibe (Zetia) is a:

A

Cholesterol absorption inhibitor.

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40
Q

What do cholesterol absorption inhibitors do?

A

Blocks cholesterol absorption in the jejunum.

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41
Q

Are cholesterol absorption inhibitors 1st or 2nd line therapies?

A

2nd line.

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42
Q

What medication is usually taken in combination with cholesterol absorption inhibitors? Why?

A

Statins - it has a 15-20% greater decrease in LDL than alone.

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43
Q

What 4 things are monitored / checked before initiating cholesterol medication therapies?

A
  1. Fasting lipid panel
  2. ALT levels (this is from the liver)
  3. Creatine kinase (indicates muscle breakdown)
  4. Identify secondary causes
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44
Q

How does the RAAS pathway flow?

A

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

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45
Q

What does aldosterone do?

A

Causes the kidneys to retain more sodium (which causes increased fluid retention) and increases BP.

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46
Q

Angiotensin II is a potent __________.

A

Vasoconstrictor.

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47
Q

Does stress influence the RAAS?

A

Yes, chronic stress stimulates renin and starts the RAAS.

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48
Q

What division of the nervous system is the primary driver of the BP regulation process?

A

Sympathetic nervous system.

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49
Q

What do arterial baroreceptors do?

A

Sense BP changes and can impact vasodilation / vasoconstriction accordingly. Can also impact HR to change BP.

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50
Q

How does vascular autoregulation help blood pressure?

A

It alters the resistance in arterioles to change BP.

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51
Q

What is considered normal blood pressure?

A

Less than 120
AND
Less than 80

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52
Q

What is considered elevated blood pressure?

A

120-129
AND
Less than 80

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53
Q

What is considered hypertension stage 1?

A

130-139
OR
80-89

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54
Q

What is considered hypertension stage 2?

A

140+
OR
90+

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55
Q

What is considered a hypertensive crisis?

A

180+
AND OR
120+

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56
Q

Primary hypertension is the same thing as:

A

Essential hypertension.

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57
Q

What type of hypertension is caused by unknown reasons?

A

Primary / essential hypertension.

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58
Q

What are three interactions that may play a part in essential hypertension?

A

SNS, RAAS, and natriuretic peptides.

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59
Q

What are natriuretic peptides?

A

Chemicals/hormones that help control water and sodium retention.

60
Q

What are the risk factors for primary hypertension? (there are 11)

A

Smoking
Excessive sodium intake
Hyperlipidemia
Genetics
Obesity
Age
Sedentary lifestyle
Stress
African American
High alcohol consumption
Insulin resistance

61
Q

What is secondary hypertension?

A

Hypertension with a known cause that is related to an underlying disease or disorder.

62
Q

What is the best way to treat secondary hypertension?

A

To treat the underlying cause.

63
Q

What are some end-organ damage that can be seen with unmanaged hypertension?

A

Chest pain (heart damage)
Headache (brain damage)
Visual changes (eye damage)
Weakness/pain in extremities

64
Q

What are the cardiac implications of long term uncontrolled BP?

A

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
Q

What are the renal implications of long term uncontrolled hypertension?

A

Increased SNS and RAAS -> decreased blood flow / increased inflammation -> leads to decreased function and permeant damage.

66
Q

What are the brain implications of long term uncontrolled hypertension?

A

Higher risk for stroke, aneurysm, or hemorrhaging.

67
Q

What are the eye implications of long term uncontrolled hypertension?

A

Increased retinal pressure -> retinopathy and blindness

68
Q

What are the lower extremity implications of long term uncontrolled hypertension?

A

Gangrene

69
Q

What are the two types of hypertensive crises?

A

Hypertensive urgency and hypertensive emergency.

70
Q

Does hypertensive urgency or hypertensive emergency lead to end-organ damage?

A

Hypertensive emergency.

71
Q

How do you treat hypertensive urgency?

A

With oral agents to gradually lower BP.

72
Q

How do you treat hypertensive emergencies?

A

With IV medications to aggressively lower BP within minutes - hours.

73
Q

What are some potential causes of hypertensive urgency?

A

Anxiety, pain, abrupt withdrawal from BP meds.

74
Q

What are some symptoms of hypertensive emergencies?

A

Headache, blurry vision.

75
Q

What are the three types of diuretics?

A

Potassium sparing, thiazide, and loop.

76
Q

In general, how do diuretics lower blood pressre?

A

Increase urinary output (decrease circulating volume)
Decreases arterial resistance
Decreases cardiac output by blocking sodium / chloride reabsorption

77
Q

What type of antihypertensive medication is usually first line?

A

Diuretics.

78
Q

What type of diuretic is 1st line management of mild hypertension?

A

Thiazide

79
Q

Hydrochlorothiazide (Hydrodiuril) is a:

A

Thiazide diuretic

80
Q

What is the mechanism of action of thiazide diuretics?

A

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
Q

What are the side effects of thiazide diuretics? (5)

A

Electrolyte and metabolic disturbances
Orthostatic hypotension
Worsen renal insufficiency
Hyperuricemia
Elevated levels of glucose, cholesterol, and triglycerides

82
Q

What specific electrolyte disturbance can happen with thiazide diuretics?

A

Hypokalemia.

83
Q

Furosemide (Lasix) is a:

A

Loop diuretic

84
Q

What is the mechanism of action of loop diuretics?

A

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
Q

Which diuretic has the most profound diuresis?

A

Loop diuretics

86
Q

What are potential routes for loop diuretics?

A

IV or PO

87
Q

What are potential side effects of loop diuretics? (4)

A

Hypokalemia
Dehydration
Hypotension
Ototoxicity

88
Q

What is the normal potassium range?

A

3.5-5.0

89
Q

Spironolactone (Aldactone) is a:

A

Potassium-sparing (aldosterone ANTAGONIST)

90
Q

What is the mechanism of action of potassium-sparing diuretics?

A

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
Q

Why would someone take a potassium sparing diuretic in addition to another antihypertensive medication?

A

Lowers the chance of hypokalemia.

92
Q

What are the side effects of potassium sparing diuretics? (2)

A

Hyperkalemia
Endocrine effects (deepened voice, impotence, irregular menstrual cycles, gynecomastia)

93
Q

What are the 3 types of sympatholytic antihypertensives?

A

Alpha-adrenergic blockers
Centrally acting alpha-2 agonists
Beta adrenergic blockers

94
Q

Metoprolol, propranolol, and carvedilol are all:

A

Beta adrenergic blockers (aka Beta blockers)

95
Q

Which beta blocker is selective?

A

Metoprolol

96
Q

Which beta blocker is non-selectice?

A

Propranolol

97
Q

Which beta blocker is receptive to only alpha and beta receptors?

A

Carvedilol

98
Q

Where are beta 1 receptors located?

A

In the heart

99
Q

Where are beta 2 receptors located?

A

In the lungs

100
Q

Blocking beta 1 receptors has what effects?

A

Decreased contractility, decreases HR (those two things together are going to decrease cardiac output), and decrease renin secretion.

101
Q

Blocking beta 2 receptors has what effects?

A

Increases airway resistance and increases vascular resistance.

102
Q

What is the mechanism of action of beta adrenergic blockers?

A

Increase nitric oxide -> vasodilation

Blocks stimulation of beta-1 receptors -> decrease HR and contractility

103
Q

What are 4 side effects of beta-blockers?

A

Fatigue/lethargy
Bradycardia
Hypotension
Can mask hypoglycemia in diabetic patients (would have tachycardia)

104
Q

What are the nursing considerations of beta adrenergic blockers?

A

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
Q

Why is rebound HTN a problem?

A

Can put a patient in critical risk for cardiovascular events, stroke, and death.

106
Q

When should a beta adrenergic blocker be held?

A

HR less than 60, and systolic BP less than 100

107
Q

Clonidine (Catapress) is an:

A

Alpha-2 adrenergic agonist.

108
Q

Would someone with newly diagnosed hypertension be prescribed clonidine first? why?

A

No, because of the high side effect profile.

109
Q

What is the primary indication for clonidine?

A

Primary hypertension.

110
Q

What routes are clonidine usually given?

A

PO or transdermal.

111
Q

Where can transdermal clonidine be applied?

A

Upper chest, upper outer arm, lower abdomen, and hip

112
Q

What is the key nursing action for alpha-2 adrenergic agonists?

A

Do not stop abruptly due to the potential for rebound HTN.

113
Q

What are some side effects of alpha-2 adrenergic agonists? (3)

A

Drowsiness, potential for rebound HTN, may worsen pre-existing liver disease

114
Q

Doxazosin (Cardura) is a:

A

Selective alpha-1 blocker

115
Q

What is the mechanism of action of selective alpha-1 blockers?

A

Directly blocks sympathetic nervous system and decreases peripheral vascular resistance

116
Q

Are alpha-1 blockers used first line?

A

No

117
Q

What are the side effects of selective-1 blockers? (2)

A

Hypotension, dizziness

118
Q

What are the 3 types of RAAS blockers?

A

ACE inhibitors, ARBs, Renin inhibitors

119
Q

Captopril (capoten) and lisinopril (zestril) are both:

A

ACE (angiotensin converting enzyme) inhibitors

120
Q

Are ACE inhibitors first line therapies? Why?

A

Yes, they are safe and efficacious.

121
Q

What is the mechanism of action of ACE inhibitors?

A

Block angiotensin converting enzyme -> inhibits production of angiotensin II (stops powerful vasoconstriction) and inhibits aldosterone secretion (less water retention)

122
Q

Which of the hypertensive medication classes has some renal protective effects?

A

ACE inhibitors

123
Q

What are some side effects of ACE inhibitors? (5)

A

First dose hypotension
Dry, persistent nonproductive cough
Dizziness
Rash
Angioedema

124
Q

What is first dose hypotension? What drug class is it associated with?

A

A drop in BP in the first 6-8 hours. Associated with ACE inhibitors.

125
Q

What is angioedema? What population is mostly affected?

A

Swelling under the skin that can affect the larynx. More common in African Americans.

126
Q

Are ACE inhibitors safe for pregnant women? Why?

A

No, it is teratogenic.

127
Q

Losartan (cozaar) is an:

A

Angiotensin receptor blocker (ARB)

128
Q

What is the mechanism of action for angiotensin receptor blockers?

A

Blocks the action of angiotensin II after it is formed -> causes vasodilation, increases sodium and water excretion

129
Q

What are the indications for angiotensin receptor blockers?

A

Hypertension, heart failure, and stroke progression

130
Q

What are the side effects for angiotensin receptor blockers (ARBs)

A

Potential for angioedema

131
Q

Can pregnant patients be prescribed angiotensin receptor blockers?

A

No.

132
Q

Aliskiren (tekurna) is a:

A

Renin inhibitor

133
Q

What is the mechanism of action of renin inhibitors?

A

Direct inhibition of renin -> induces vasodilation, decreased blood volume, decreases SNS, and inhibits cardiac and vascular hypertrophy.

134
Q

What are some side effects of renin inhibitors (2)

A

GI discomfort, potential for hyperkalemia (especially in diabetic patients).

135
Q

Can a patient take a renin inhibitor if they are pregnant?

A

No

136
Q

How long does it take for renin inhibitors to take full effect?

A

Several weeks

137
Q

Nifedipine (procardia) and nicardipine (cardene) are bothh:

A

Calcium channel blockers

138
Q

What is the mechanism of action for calcium channel blockers?

A

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
Q

What are some side effects of calcium channel blockers? (6)

A

Orthostatic hypotension, bradycardia, may precipitate AV block, headache, GI discomfort, peripheral edema

140
Q

What are the two primary indications for calcium channel blockers?

A

Hypertension and chest pain

141
Q

Can calcium channel blockers be given IV?

A

Yes

142
Q

If a patient is taking calcium channel blockers for hypertension and begins having peripheral edema, what should they be prescribed?

A

Diuretic

143
Q

What populations of people are calcium channel blockers best for?

A

African Americans and elderly.

144
Q

Hydralazine (apresoline) is a:

A

Vasodilators

145
Q

What is the mechanism of action of vasodilators?

A

Work directly on arterial and venous smooth muscles and cause relaxation -> decreases systemic and peripheral vascular resistance

146
Q

What is the indication for vasodilators?

A

Hypertension

Pathopharmacology Intro (6 decks)

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