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PATHO/PHARM I > Week 7: > Flashcards

Week 7: Flashcards

1
Q

Arteriosclerosis

A

Arteriosclerosis is a condition characterized by thickening and hardening of the vessel wall.

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2
Q

What is a form of arteriosclerosis?

A

Atherosclerosis

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3
Q

Atherosclerosis

A

Atherosclerosis is a form of arteriosclerosis that is caused by the accumulation of lipid-laden macrophages within the arterial wall,

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4
Q

What does Atherosclerosis lead to the formation of?

A

Plaque

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5
Q

What does Atherosclerosis being with?

A

Atherosclerosis begins with injury to the endothelial cells that line artery walls.

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6
Q

Causes of endothelial injury:

A

Possible causes of endothelial injury include the common risk factors for atherosclerosis, such as
smoking, hypertension, diabetes,
increased levels of low-density lipoprotein (LDL),
decreased levels of high-density lipoprotein (HDL),
and autoimmunity.

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7
Q

Fatty streak

A

accumulation of foam cells

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8
Q

Fibrous plaque

A

Smooth muscle cells in the region of endothelial injury proliferate, produce collagen, and migrate over the fatty streak, forming a fibrous plaque

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9
Q

complicated plaques

A

Plaques that have ruptured.

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10
Q

How many types of lipoproteins are there:

A

There are six major classes of plasma lipoproteins.

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11
Q

Three major lipoproteins important in coronary atherosclerosis?

A
  1. Very low density lipoproteins (VLDLs)
  2. Low density lipoproteins (LDLs)
  3. High density lipoproteins (HDLs)
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12
Q

Major core lipid of VLDLs

A

Triglycerides

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13
Q

Major core lipid of LDLs

A

Cholesterol

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14
Q

Of all the lipoproteins, which is the greatest contributor to coronary atherosclerosis?

A

Of all lipoproteins, LDLs make the greatest contribution to coronary atherosclerosis.

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15
Q

What does LDLs do?

A

Delivery of cholesterol to nonhepatic tissues

Designed to drop cholesterol where its needed and where its not.

LDLs, whose function is the delivery of cholesterol to peripheral tissues,

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16
Q

High Density lipoproteins major core lipid:

A

Cholesterol

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17
Q

What does HDLs do?

A

Pick up cholesterols or fats and brings them back to the liver for further processing.

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18
Q

Purpose of HDLs

A

HDLs promote cholesterol removal.

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19
Q

Desirable Total Cholesterol

A

Less than 200mg/dL

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20
Q

Optimal LDL cholesterol

A

less than 100mg/dl

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21
Q

High HDL Cholesterol optimal

A

60mg/dl or higher

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22
Q

Three things supposed to be done first before pharmacological intervention of _____:

A
  1. Smoking cessation
  2. Diet
  3. Exercise
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23
Q

How does diet help with lowering cholesterol?

A

The central feature of the diet is reduced intake of cholesterol and saturated fats:

Intake of trans fats—should be minimized.

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24
Q

What type of cholesterol does diet lower?

A

LDLs

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25
Q

How does exercise impact cholesterol levels?

A

It raises HDLs

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26
Q

How does smoking cessation effect cholesterol levels?

A

Raises HDLs

Lowers LDLs

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27
Q

When should you use Drug therapy to treat Cholesterol?

A

When life changes (diet, exercise, smoking cessation) do not work

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28
Q

What is the most effective drug for lowering LDLs

A

HMG-CoA Reductase Inhibitors (Statins)

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29
Q

Drug families used to lower LDLs

A
  1. HMG-CoA Reductase Inhibitors (Statins)
  2. Bile acid sequestrants
  3. Nicotinic acid (Niacin)
  4. Fibrates
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30
Q

What is a beneficial side effect of drugs used to lower LDLs?

A

Virtually all of the drugs that we use to lower LDL cholesterol have the added benefit of increasing HDL cholesterol, at least to some degree. This rise of HDL, therefore, can be considered a beneficial “side effect.”

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31
Q

Nonlipid beneficial cardiovascular actions of Statins:

A
  1. Promote plaque stability
  2. Reduce the risk for cardiovascular (CV) events
  3. Increased bone formation
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32
Q

What is the mechanism of action for Statins?

A

Inhibits the HMG-CoA Reductase enzyme which makes cholesterol?

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33
Q

Why is it better to take statins at night?

A

Because most of your cholesterol is made at night.

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34
Q

Common Adverse Effects of Statins?

A

Headache
Rash
GI disturbances

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35
Q

Rare Adverse Effects of Statins?

A

Myopathy
Rhabdomyolysis
Hepatotoxicity

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36
Q

Bile acid sequestrant side effects:

A

Constipation

Some effect vitamin absorption

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37
Q

Nicotinic- what does it do?

A

Lowers triglycerides

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38
Q

Adverse Effect of Nicotinic acid is:
What is done to treat this effect?

A

Skin (flushing, itching)
Take an antihistamine to counteract this effect

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39
Q

Fibrates- why are they generally not used for cholesterol?

A

They have a significant amount of hepatotoxicity

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40
Q

What do Fibrates do to treat cholesterol?

A

Reduce levels of TGs

Does not reduce LDLs

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41
Q

Other products used to Alter Plasma Lipid Levels

A

Lovazo
Fish Oil
Plant stanol and sterol esters
Estrogen
Cholestin

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42
Q

Coronary Artery Disease (CAD)

A

Any vascular disorder that narrows or occludes the coronary arteries leading to myocardial ischemia.

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43
Q

Most common cause of CAD

A

Atherosclerosis

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44
Q

Modifiable Risk Factors to CAD:

A

Dyslipidemia
Hypertension
Cigarette smoking
Diabetes and insulin resistance
Obesity/sedentary lifestyle
Atherogenic diet

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45
Q

Nonmodifiable Risk Factors to CAD:

A

Increased age
Family history
Male gender

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46
Q

How does coronary artery disease affect perfusion

A

It decreases perfusion, which causes ischemia or ultimately necrosis.

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47
Q

Angina

A

Chest pain

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48
Q

When is anginal pain precipitated?

A

Anginal pain is precipitated when the oxygen supply to the heart is insufficient to meet oxygen demand.

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49
Q

Drug therapy of angina has two goals:

A
  1. Prevention of MI and death
  2. Prevention of myocardial ischemia and anginal pain
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50
Q

What is cardiac associated angina?

A

Is ischemia of the myocardium- lack of oxygen

It is local temporary deprivation of the coronary blood supply

51
Q

Three types of angina:

A
  1. Stable (exertional) angina
  2. Prinzmetal (variant) angina
  3. Unstable angina
  4. Silent ischemia
52
Q

Stable (exertional) angina causes:

A

Emotional excitement

Large meals-blood goes to gut

Cold exposure-vasoconstriction

53
Q

Stable angina- how long does it last

A

Lasts less than 5 minutes

54
Q

Stable angina- what is the physiological cause

A

Lack of blood flow

55
Q

Why is stable angina predictable?

A

Because it occurs with exertion

56
Q

Prinzmetal (variant) angina

A

occurs because of vasoconstriction because of vasospasm

57
Q

How long does variant angina last

A

less than 5 minutes

*rest doesn’t stop it

58
Q

How to treat variant angina:

A

Variant angina is treated by increasing cardiac oxygen supply.

59
Q

Silent ischemia

A

Lack of blood flow; we don’t know about it because there is no chest pain

60
Q

Unstable angina

A

The opposite of stable angina

61
Q

Antianginal drugs

A

(i.e., drugs that prevent myocardial ischemia and anginal pain)

62
Q

Three families of anti anginal agents:

A
  1. organic nitrates (e.g., nitroglycerin),
  2. beta blockers (e.g., metoprolol), and
  3. calcium channel blockers (CCB; e.g., verapamil).
63
Q

What is a fourth agent usually combined with first line agents for angina?

A

Ranolazine

64
Q

Cardiac oxygen demand is determined by:

A
  1. Heart rate
  2. Contractility
  3. Preload
  4. Afterload
65
Q

Drugs that reduce HR, Contractility, Preload and Afterload decrease what?

A

Drugs that reduce these factors reduce oxygen demand.

66
Q

Oxygen supply is determined by what>

A

myocardial blood flow

67
Q

When does myocardial perfusion take place:

A

myocardial perfusion takes place only during diastole (i.e., when the heart relaxes).

68
Q

Why does myocardial perfusion not take place during systole?

A

Perfusion does not take place during systole because the vessels that supply the myocardium are squeezed shut when the myocardium contracts.

69
Q

Angina pectoris has three forms.

A

(1) chronic stable angina (exertional angina),

(2) variant angina (Prinzmetal’s or vasospastic angina), and

(3) unstable angina.

70
Q

WHat is the underlying cause of exertional angina?

A

CAD

71
Q

CAD is characterized by:

A

(CAD), a condition characterized by deposition of fatty plaque in the arterial wall.

72
Q

In people with CAD, what happens?

A

in people with CAD, arterioles in the affected region are already fully dilated during rest. Thus, when exertion occurs, there is no way to increase blood flow to compensate for the increase in oxygen demand. The resultant imbalance between oxygen supply and oxygen demand causes anginal pain.

73
Q

In a healthy heart, how is oxygen demand dealt with?

A

In the healthy heart, as cardiac oxygen demand rises, coronary arterioles dilate, causing blood flow to increase. The increase keeps oxygen supply in balance with oxygen demand

74
Q

What is the goal of antianginal therapy?

A

The goal of antianginal therapy is to reduce the intensity and frequency of anginal attacks.

75
Q

Two remedies to handle anginal pain:

A
  1. Increase O2 supply
  2. Decrease O2 demand
76
Q

Why is it impossible to remedy stable angina by increasing O2 supply?

A

Because the underlying cause of stable angina is occlusion of the coronary arteries, there is little we can do to increase cardiac oxygen supply.

77
Q

How do the four antianginal drugs (organic nitrates, beta blockers, and CCBs and ranolazine) relieve the pain of the stable angina?

A

All four groups relieve the pain of stable angina primarily by decreasing cardiac oxygen demand

78
Q

Why are organic nitrates used for stable angina?

A

Decrease oxygen demand by dilating veins, which decreases preload

79
Q

Why are organic nitrates used for variant angina?

A

Increase oxygen supply by relaxing coronary vasospasm

80
Q

Why are Beta Blockers used for Stable angina?

A

Decrease oxygen demand by decreasing heart rate and contractility

81
Q

Why are Beta Blockers used for variant angina?

A

They are NOT used

82
Q

Why are CCBs used for Stable angina?

A

Decrease oxygen demand by dilating arterioles, which decreases afterload (all calcium blockers), and by decreasing heart rate and contractility (verapamil and diltiazem)

83
Q

Why are CCBs used for variant angina?

A

Increase oxygen supply by relaxing coronary vasospasm

84
Q

Why are Ranolazine used for stable angina?

A

Appears to decrease oxygen demand, possibly by helping the myocardium generate energy more efficiently

85
Q

Why are Ranolazine used for variant angina?

A

NOT used

86
Q

What are the most frequently used antianginal drugs?

A

organic nitrates

87
Q

How do organic nitrates relieve angina?

A

By causing vasodilation

88
Q

What is the prototype organic nitrate?

A

Nitroglycerin

89
Q

What does nitroglycerin work directly on?

A

Nitroglycerin acts directly on vascular smooth muscle (VSM) to promote vasodilation.

90
Q

What type of vessels do nitroglycerin usually work on at therapeutic doses?

A

At usual therapeutic doses, the drug acts primarily on veins.

Dilation of arterioles is only modest.

91
Q

Principal adverse effects of Nitroglycerin?

A

Principal adverse effects—headache, hypotension, and tachycardia—occur secondary to vasodilation.

92
Q

How does Nitroglycerin lowers Bp?

A

Nitroglycerin lowers blood pressure—primarily by decreasing venous return and partly by dilating arterioles.

93
Q

How does Nitroglycerin cause reflex tachycardia?

A

By lowering blood pressure, the drug can activate the baroreceptor reflex, causing sympathetic stimulation of the heart.

The resultant increase in both heart rate and contractile force increases cardiac oxygen demand, which negates the benefits of therapy.

94
Q

When Nitroglycerin is administered sublingually, how is it absorbed?

A

When administered sublingually (beneath the tongue), nitroglycerin is absorbed directly through the oral mucosa into the bloodstream.

95
Q

What happens to sublingual nitroglycerin (hint- having to do with liver)

A

sublingual nitroglycerin bypasses the liver and thereby temporarily avoids inactivation.

Because the liver is bypassed, sublingual doses can be low (between 0.3 and 0.6mg). These doses are about 10 times lower than those required when nitroglycerin is dosed orally.

96
Q

How do beta blockers reduce anginal pain?

A

Beta blockers reduce anginal pain primarily by decreasing cardiac oxygen demand, principally through blockade of beta1 receptors in the heart, which decreases heart rate and contractility.

97
Q

Prototype CCB

A

Verapamil

98
Q

What is Myocardial infarction (MI) known as?

A

Heart attack

99
Q

What is Myocardial infarction (MI) defined as?

A

MI is defined as necrosis of the myocardium (heart muscle) resulting from local ischemia (deficient blood flow)

100
Q

What is the underlying cause of MI?

A

The underlying cause is partial or complete blockage of a coronary artery.

101
Q

In simple terms, what is STEMI?

A

Complete interruption of regional myocardial blood flow

102
Q

ST elevation MI (STEMI)- why is it called this?

A

This class of MI is called ST-elevation MI (STEMI), because it causes elevation of the ST segment on the electrocardiogram (ECG).

103
Q

Risk factors of STEMI?

A

Risk factors for STEMI include advanced age, family history of MI, sedentary lifestyle, high serum cholesterol, hypertension, smoking, and diabetes.

104
Q

When does acute MI occur?

A

Acute MI occurs when blood flow to a region of the myocardium is stopped because of platelet plugging and thrombus formation in a coronary artery almost always at the site of a fissured or ruptured atherosclerotic plaque.

105
Q

Acute STEMI is diagnosed by the presence of?

A

Acute STEMI is diagnosed by the presence of:

chest pain,
characteristic ECG changes, and elevated serum levels of myocardial cellular components (troponin, creatine kinase).

106
Q

When do myocardial cells release intracellular proteins?

A

When myocardial cells undergo necrosis, they release intracellular proteins (e.g., cardiac troponins, creatine kinase).

107
Q

What are the best serum markers for STEMI?

A

Today cardiac-derived troponins, cardiac troponin I and cardiac troponin T, are considered the best serum markers for STEMI.

108
Q

Before relying on cardiac derived troponin, what biomarker did physicians rely on?

A

Before cardiac troponins became the preferred biomarkers for STEMI, clinicians relied on measurement of the MB isoenzyme of creatine kinase (CK-MB).

109
Q

What is the goal of management of STEMI

A

The goal is to bring cardiac oxygen supply back into balance with oxygen demand.

110
Q

Management of STEMI includes?

A

Reperfusion therapy

111
Q

Reperfusion therapy

A

which restores blood flow to the myocardium, and by reducing myocardial oxygen demand.

112
Q

What is the routine drug therapy for when STEMI is suspected?

A

Oxygen

Aspirin

NSAIDs

Morphine

Beta Blockers

Nitroglycerin

113
Q

What does supplemental O2 do when given for suspected STEMI?

A

Supplemental oxygen, administered by nasal cannula, can increase arterial oxygen saturation and can thereby increase oxygen delivery to the ischemic myocardium.

114
Q

What does Aspirin do when given for suspected STEMI?

A

Aspirin suppresses platelet aggregation, producing an immediate antithrombotic effect.

115
Q

What does NSAIDs do when given for suspected STEMI?

A

According to the 2013 guideline, routine use of nonsteroidal antiinflammatory drugs (NSAIDs) other than aspirin should be discontinued.

116
Q

What does morphine do when given for suspected STEMI?

A

In addition to relieving pain, morphine can improve hemodynamics.

By promoting venodilation, the drug reduces cardiac preload.

117
Q

What does beta blockers do when given for suspected STEMI?

A

When given to patients undergoing acute STEMI, beta blockers (e.g., atenolol, metoprolol) reduce cardiac pain, infarct size, and short-term mortality.

Recurrent ischemia and reinfarction are also decreased.

118
Q

In patients with STEMI, nitroglycerin has several beneficial effects:

A

In patients with STEMI, nitroglycerin has several beneficial effects: It can (1) reduce preload and thereby reduce oxygen demand; (2) increase collateral blood flow in the ischemic region of the heart; (3) control hypertension caused by STEMI-associated anxiety; and (4) limit infarct size and improve LV function.

119
Q

How do we accomplish reperfusion?

A
  1. fibrinolytic drugs (also known as thrombolytic drugs) or with
  2. percutaneous coronary intervention (PCI), usually balloon angioplasty coupled with the placement of a stent.
120
Q

Fibrinolytic drugs

A

Fibrinolytic drugs dissolve clots by converting plasminogen into plasmin, a proteolytic enzyme that digests the fibrin meshwork that holds clots together.

121
Q

Three fibronylitic drugs available for MI treatment?

A

alteplase (tPA), reteplase, and tenecteplase.

122
Q

When is the best time to start fibrinolytics?

A

Current guidelines suggest a target of 30minutes or less for the time between entering the emergency department and starting fibrinolysis.

123
Q

All patients undergoing fibrinolytic therapy should receive what?

A

All patients undergoing fibrinolytic therapy should receive an anticoagulant (IV heparin, bivalirudin, enoxaparin, fondaparinux) plus antiplatelet drugs (aspirin plus clopidogrel but not a GP IIb/IIIa inhibitor, such as abciximab)

124
Q

All post MI patients should take four drugs?

A

All post-MI patients should take four drugs: (1) a beta blocker;
(2) an ACE inhibitor or an ARB; either
(3a) an antiplatelet drug (aspirin, clopidogrel, ticagrelor, or prasugrel) or
(3b) an anticoagulant (warfarin); and (
4) a statin. All four should be taken indefinitely.

PATHO/PHARM I (28 decks)

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