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PHARMACOLOGY > 19-Drugs for Angina, MI and CVA > Flashcards

19-Drugs for Angina, MI and CVA Flashcards

1
Q

When arterial blood supply is narrowed due to atherosclerosis, what 3 events could occur? (related to cardiovascular and cerebrovascular function…)

A
  1. Angina pectoris
  2. Acute myocardial infarction
  3. Cerebrovascular accident (TIA, stroke)
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2
Q

What part (region) of the heart do the coronary arteries supply?

A

The myocardium!

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3
Q

What is the relationship between hypertension and atherosclerosis? (general answer)

A
  • High blood pressure puts excess force on the vasculature (coronary arteries) causing injury.
  • Injury causes inflammation and inflammation is directly related to the immune system
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4
Q

Described the process of atherosclerosis (COMPLEX answer)

A
  • HTN causes endothelial injury (coronary arteries) and inflammation stimulates
  • Inflammation causes the tight junctions between the endothelial cells to widen which allows LDL to enter the tunica intima
    (**High cholesterol levels often due to poor diet; there is an association between HTN and high cholesterol)
  • Inflammation activates the immune system and immune cells (monocytes, T-lymphocytes) migrate to the “site of injury”
  • Monocytes differentiate into macrophages once inside the intima
  • Macrophages engulf oxidized LDL to “neutralize” it but lysosomes can’t break down LDL
  • Macrophages will continue to eat up LDL and will become larger and larger. Macrophage is now called a “foam cell”
  • Foam cells become so big that they rupture (spit out oxidized LDL, enzymes, cellular components) causing more damage and inflammation
  • This causes a vicious cycle of inflammation –> immune cell recruitment –> foam cell –> rupture –> damage –> inflammation
  • When the immune system can’t fight the “infection”, the body “walls” off the fatty plaque
  • T-lymphocytes secrete cytokines inducing smooth muscle migration around the fatty plaque. This narrows the artery lumen impairing blood vessel elasticity and causes it to narrow

= ATHEROSCLEROSIS

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5
Q

What are the impacts of atherosclerosis:

a. narrowed arteries
b. reduces blood flow to organs/tissues
c. increased total peripheral resistance (causing HTN)
d. reduced vascular elasticity
e. reduced response to sympathetic stimuli
f. all of the above

A

f - all of the above!!

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6
Q

T or F: We can rely on the body’s immune system response to fighting infection to control the atherosclerosis.

A

FALSE! The immune system – in the case of atherosclerosis – makes the problem WORSE (vicious cycle). We often need to incorporate a change in lifestyle and pharmacological approach

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7
Q

Define angina pectoris (general pathology of angina)

A
  • acute chest pain arising from inadequate oxygen supply to the myocardium –> results in transient ischemia
    (supply does not meet the demand)
  • the inadequate oxygen supply typical results from atherosclerosis because it decreases blood flow which decreases oxygen delivery
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8
Q

Why does the inadequate oxygen to the myocardium cause pain?

A
  • there is not enough oxygen to maintain aerobic metabolism so the body switches to anaerobic metabolism for energy. This results in an accumulation of lactic acid which irritates the myocardial nerve fibers transmitting a pain message to the cardiac nerves
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9
Q

What are some common signs/symptoms of angina?

A
  • panic, pallor, dyspnea, diaphoresis, tachycardia, elevated blood pressure
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10
Q

T or F: For angina pectoris, if the demand on the heart is decreased (ex: client rests from exercise), the pain will slowly subside.

What about for myocardial infarction?

A

TRUE! Typically when the provoking factor is eliminated (exercise, stress, strong emotion, etc.), the patient’s pain will subside.

This is NOT TRUE for myocardial infarction. Myocardial infarction results from a fully occluded vessel and the pain associated with this will not be alleviated until the client seeks out medical intervention.

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11
Q

T or F: The ischemia associated with angina pectoris is permanent.

A

FALSE! The ischemia associated with angina pectoris is transient (or reversible).

On the other hand, the ischemia associated with MI is permanent.

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12
Q

What happens with the coronary artery is completely occluded?

A

Myocardial Infarction

  • complete ischemia
  • myocytes being to die in about 20 minutes unless blood supply is restored
  • necrotized tissues release enzyme markers of tissue injury (toponin) which can be used to confirm MI vs. unstable angina
  • often results in permanent damage
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13
Q

How long does an angina attack typically last? How about MI?

A
  • angina attack lasts for about 10-15 minutes

- pain associated with MI lasts for at least 30min (often lasts until medical intervention is achieved)

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14
Q

What is stable angina?

A
  • predictable frequency, duration and intensity, no associated myocardial damage, relief with rest
  • probably won’t progress to MI
  • lifestyle change and meds can often be suffice to manage condition
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15
Q

What is unstable angina?

A
  • variable intensity, occurs during periods of rest, increased frequency, no associated myocardial damage
  • increased risk of MI
  • medical emergency
  • atherosclerotic plaque is disrupted, exposing the injured endothelium to platelet and coagulation. This results in transient ischemia as the affected vessel narrows further
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16
Q

What are some non-pharmacological management options for angina pectoris?

A
  • limit alcohol consumption
  • eliminate foods high in cholesterol, saturated fats and sodium
  • control hyperlipidemia
  • control HTN
  • regular exercise + maintenance of optimal weight
  • control blood glucose levels
  • abstain from using tobacco products
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17
Q

What are the two main therapeutic goals for treating angina pectoris? (general answer)

A
  • reduce the intensity and frequency of attacks

- reduce myocardial oxygen demand or improve oxygen supply to the myocardium

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18
Q

What are the four main ways in improve oxygen demand to the myocardium?

A
  • slow heart rate
  • reduce force of cardiac contraction
  • dilate veins (reduce volume of blood sent to heart [preload])
  • dilate arterioles (reduces TPR [afterload])
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19
Q

What are the 3 main drugs classes used to treat angina pectoris?

A
  1. Nitrates
  2. Beta-blockers
  3. Calcium channel blockers
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20
Q

How does nitroglycerin help terminate an angina attack?

A
  • It facilitates the formation of nitric acid, a potent vasodilator for vascular smooth muscle
  • it relaxes coronary arteries and venous smooth muscle allowing oxygenated blood to move to the myocardium, reducing the pain
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21
Q

Which vessels are mostly affected by nitroglycerin – coronary arteries or coronary veins? Why?

A
  • coronary arteries are less affected by nitroglycerin compared to coronary veins because atherosclerosis primarily occurs in the coronary arteries causing them to be less elastic and not able to dilate as well
  • only the healthy (uneffected) coronary arteries dilate with nitric oxide
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22
Q

How does the dilation of venous smooth muscle help relieve angina pectoris?

A
  • decreases amount of blood returning to the heart (preload)

- decreases cardiac output, workload, and oxygen demand

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23
Q

How does the minor dilation of arterial smooth muscle help relieve angina pectoris?

A
  • increase blood flow to myocardium

- improves oxygen supply to myocardium

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24
Q

Briefly describe the administration protocol for short-acting nitrate – nitroglycerin

A
  • sublingual route (tablet or spray), IV or topical, extended release forms
  • first line therapy for treating angina attack
  • take nitro upon attack and wait 5 min. If no improvement, take another dose and wait 5 min. Patient can take max 3 doses in 15 minutes –> risk of hypotension
  • if symptoms persist after 3 doses within a 15 minute span, seek medical attention
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25
Q

Briefly describe the administration protocol for long-acting nitrate – isosorbide dinitrate

A
  • decreases intensity and frequency of angina attacks
  • oral & transdermal
  • common for pts to develop tolerance to the medication so it is important that the patch is removed for 12-16hrs/day or withhold at nighttime oral dose
  • can not discontinue abruptly –> risk MI
  • no longer first line therapy for angina prophylaxis because is does not reduce morality in clients with CAD
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26
Q

What are some possible side effects of nitrates?

A

All adverse effects are related to vasodilation and decrease in blood flow (most blood supply in the periphery):
- throbbing headache, dizziness, weakness, hypotension, reflex tachycardia

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27
Q

What are the two main drug-drug interactions with nitrates?

A
  • erectile dysfunction drugs can cause life-threatening hypotension (phosphodiesterase-5 inhibitors)
  • alcohol (vasodilator)
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28
Q

Why would a beta antagonist be prescribed for angina pectoris? What is it mode of action?

A
  • first line therapy for prevention of chronic stable angina
  • blocks the sympathetic innervation to the heart reducing cardiac workload, slowing heart rate and reducing contractility. Together, these changes decrease oxygen demand
  • beta blockers help to decrease the frequency and intensity of angina attacks with no risk of tolerance
  • beta blockers are ideal for clients with HTN & CAD
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29
Q

What populations (3 in particular) should be cautioned about using beta blockers?

A
  • use with caution in those with asthma and COPD (block sympathetic input to the lungs)
  • exacerbated depression (adrenergic tone has an effect on mood)
  • hypoglycemia risk for diabetics (inhibited SNS masks hypoglycemia symptoms)
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30
Q

What are some adverse effects of beta adrenergic antagonists?

A

fatigue, weakness, bradycardia, hypotension, sleep disturbances

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31
Q

Why is a rapid withdrawal from beta blockers discouraged? (in terms of treating angina pectoris)

A
  • rapid withdrawal worsens angina symptoms.

- it is recommended that the dose be reduced over 1-2 weeks

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32
Q

What is the main reason why calcium channel blockers would be prescribed?

A

used for the prevention of chronic stable angina in clients who cannot tolerate beta-blockers

33
Q

How do calcium channel blockers help treat angina? (What is the mode of action?)

A
  • block calcium ion channels so that calcium is not available for contraction
  • this inhibition results in relaxed arteriolar smooth muscle which lowers BP and decreases afterload, and it decreases HR which reduces the workload
  • this allows the supply of oxygen to meet the demand of the myocardium
34
Q

What is a selective CCB?

A

inhibits Ca+ in smooth muscle of vasculature and causes vasodilation

35
Q

What is a non-selective CCB?

A
  • inhibit Ca+ in vasculature and the heart muscle –> reduced HR
  • these are the class of CCB to treat angina
  • second line of therapy for angina pectoris
36
Q

What are some adverse effects of CCB?

A
  • all side effects are related to reduced cardiac output and smooth muscle dilation
  • dizziness, light-headedness, fatigue, bradycardia, flushing, nausea
  • HYPOTENSION and reflex tachycardia
37
Q

Why do patient’s taking CCBs need to avoid grapefruit juice?

A

CCBs are metabolized by CYP 450 and grapefruit juice inhibits CYP 450 resulting in a toxic amount of the CCBs in the body

38
Q

What is the biomarker used to determine whether someone has unstable angina or is having an MI?

A

Necrotized tissues release enzyme markers of tissue injury (troponin) which can be used to confirm MI vs. unstable angina

39
Q

How does coronary artery disease progress to MI?

A
  • plaque ruptures and hemorrhages and exposed plaque activates the coagulation cascade
  • platelets are recruited to develop clots which end up occluding the coronary artery leading to myocardial ischemia and necrosis
  • pieces of unstable plaque break away and block small vessels that supply parts of the myocardium or to other organs including the kidneys, eyes and brain
40
Q

What are the goals of therapy for MI?

A
  • reduce myocardial oxygen demand
  • restore blood supply to the damaged myocardium (through surgery or thrombolytic drugs)
  • control dysrhythmias
  • reduce post-MI mortality
  • control pain with analgesics
41
Q

What drugs are typically prescribed to reduce post-MI mortality?

A
  • antiplatelets, anti-coagulants, statins
42
Q

What are the 6 steps of the pharmacological management of an MI? What class of medications would be used to achieve each step?

A
  1. Restore blood supply to the damaged myocardium
    - thrombolytics within 12 hrs of onset; ideally 30 min
  2. Reduce myocardial oxygen demand
    - nitrates, beta blockers, ACE inhibitors
  3. Control or prevent MI-associated dysrhythmias
    - beta blockers (slow impulse conduction suppressing dyshythmias)
  4. Reduce post-MI mortality
    - ASA, beta-blocker, ACE inhibitors, statins
  5. Manage sever pain and anxiety with analgesics
    - opiates (morphine)
  6. Prevent enlargement of the thrombus
    - anticoagulant, antiplatelet
43
Q

Which type of stroke is more common – thrombotic or hemorrhagic?

A

THROMBOTIC!

  • 80% thrombotic (something occluding the vessel)
  • 20% hemorrhagic (vessels have ruptured)
44
Q

What are some of the warning signs of stroke?

A
  • signs and symptoms dependent on the brain areas affected

- some universal symptoms include paralysis on one side, vision problems, dizziness, speech problems, headache

45
Q

What are some preventive treatments for thrombotic CVAs? (pharmacological and non-pharmacological)

A
  • lifestyle management (exercise, diet, stress, etc.)
  • antihypertensive drugs
  • antiplatelet therapy
  • anticoagulant therapy
46
Q

What is the first line therapy for thrombotic strokes? What MUST be done before this therapy is used?

A
  • a thrombolytic agent should be administered within 3 hours of the brain attack
  • thrombolytics can help restore function in the affected brain areas
  • as CT scan MUST be done before thrombolytics are administered. If the pt is suffering from an hemorrhagic stroke, the thrombolytic agent will make the stroke worse and the pt could die
47
Q

Which organ recovers better from ischemia – the brain or the heart?

A
  • the heart
  • MI have as a 12hr window and CVA has a 3hr window
  • CVAs often results in some form of permanent damage whereas someone can have an MI and recover back to full health
48
Q

T/F: HTN sets stage for atherosclerosis

A

true

49
Q

What is within macrophages that do not allow for LDL to be neutralized?

A

lysosomes

50
Q

Where does pain begin and radiate with angina?

A

Left shoulder and left arm

  • go into jaw
  • thoracic back
  • stomach (females)
51
Q

What is the chest pain like for Angina pectoris?

A
  • steady, intense pain

- rushing/constricting

52
Q

What can help reduce anginal symptoms?

A

sitting down and relaxing heart rate

53
Q

What is onset of angina pectoris associated with?

A
  • physical exertion or emotional excitement

- increase oxygen demand

54
Q

How long do angina pectoris symptoms normally last for?

A

10-15 after rest

55
Q

What can be prescribed to help terminate attack sooner?

A

nitroglycerin

56
Q

When does unstable angina occur?

A

during rest; having heart beat can be too much

57
Q

T/F: Unstable angina can be associated with MI and is a medical emergency?

A

True

58
Q

T/F: stable angina needs to be treated like a medical emergency?

A

FALSE; can be monitored and maintained with medication, not going to suffer from MI most likely

59
Q

T/F: unstable angina needs to be treated like a medical emergency

A

TRUE

60
Q

What is the first line therapy for terminating an angina attack? and why?

A

ntirates

- act as a vasodilator for vascular smooth muscle

61
Q

Function of nitrates

A
  • relax coronary arteries
  • dilate of venous smooth muscle
  • dilation of arterial smooth muscle
62
Q

How are nitroglycerin nitrates administered? Short or Long Acting?

A
  • short acting

- sublingual route with spray or tablet

63
Q

Function of nitroglycerin

A
  • terminate an angina attack or prior to physical activity
64
Q

Protocol for nitroglycerin

A
  • rest, take drug and wait 5 min

- if no improvement take another dose

65
Q

What is the maximum amount of doses for nitroglycerin in a 15 min time period?

A
  • 3 doses; if symptoms still occur seek help
66
Q

How are isosorbide dinitrate nitrates administered and are they long or short acting?

A
  • long acting

- oral and transdermal routes

67
Q

How long should a nitrate patch be removed for?

A

12-16 hours a day

68
Q

Do you need to gradually come of a nitrate long acting medication or can you do it instantly?

A
  • need to have a slow withdrawal to prevent risk of MI
69
Q

In what forms are short acting nitroglycerin available in?

A
  • PO
  • IV
  • topical
  • extended release forms
70
Q

Whom should take caution when taking nitrates?

A
  • those with hypotension, hypervolemia and pre existing conditions limiting cardiac output
71
Q

Which is the first drug of choice for chronic stable angina?

A

beta adrenergic antagonists

72
Q

Function of beta adrenergic antagonists

A
  • reduce cardiac workload
  • slows heart rate
  • reduces contractility
  • decreases oxygen demand
73
Q

Who are beta adrenergic antagonists ideal for?

A
  • clients with hypertension and CAD

- reduces risk of MI and frequency and intensity of angina episodes

74
Q

When taking a beta adrenergic antagonist who should use with caution?

A
  • asthma
  • copd
  • depression
  • diabetes
75
Q

Does rapid withdrawal worsens or help angina?

A
  • worsen; reduce dose over 1-2 weeks
76
Q

Are beta blockers and calcium channel blockers used to treat or prevent chronic stable angina?

A

prevent

77
Q

When are calcium channel blockers used to treat angina?

A

used when clients cannot tolerate beta blockers

78
Q

How do you determine the type of stroke?

A

need CT

  • same risk factors of hypertension and CAD
  • signs and symptoms dependent on brain areas affected

PHARMACOLOGY (27 decks)

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