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_MS2 Cardio > 8/24- Pharmacotherapy of Angina > Flashcards

8/24- Pharmacotherapy of Angina Flashcards

1
Q

What drugs are commonly used to treat angina?

A
  • Organic Nitrates
  • Beta-blockers
  • CCBs
  • Potassium (K) channel openers

(Never Buy Kathryn Cookies)

  • Endothelin receptor blockers
  • Na channel blockers
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2
Q

How do organic nitrates help angina? Examples?

A

Dilate veins, coronary arteries and other blood vessels

  • isosorbide mononitrate
  • isosorbide dinitrate
  • nitroglycerin
  • Sodium nitroprusside
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3
Q

How do beta blockers help angina? Examples?

A

Decrease oxygen demand

—olols

  • Atenolol
  • Bisoprolol
  • Metoprolol
  • Propranolol
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4
Q

How do CCBs help angina? Examples?

A

Decrease heart rate and contractility

  • Verapamil and Diltiazem

Dihydropyridines dilate blood vessels (****dipine)

  • Amlodipine (long-acting is useful)
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5
Q

How do K channel openers help angina? Examples?

A

—-dil and Hydralazine

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6
Q

What is angina?

A

Pain caused by ischemia of nerves innervating the organ

  • Sx due to imbalance between organ’s oxygen supply and demand toward normal
  • Pain resolved by restoration of organ oxygen supply and demand toward normal
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7
Q

T/F: angina occurs only in the heart?

A

False- can occur in many organs

(heart, abdominal organs, extremities/skeletal muscle)

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8
Q

What is angina in the extremities (skeletal muscle) called?

A

Intermittent claudication

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9
Q

T/F: angina never occurs in the brain

A

True- nerves in the brain are not innervated by pain receptors (but BVs in the brain are)

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10
Q

What is angina pectoris?

A

Characteristic sudden, severe, pressing chest pain radiating to the neck, jaw, back and arms (referred pain)

  • Due to insufficient coronary blood flow (causing ischemia)
  • Imbalance typically during exertion, stress, spasm of vascular sm, obstruction of BVs (plaque)
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11
Q

Is angina accompanied by cell death?

A

No- not yet

  • Pain is just a cry for help; if untreated, -> MI
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12
Q

What spinal levels does cardiac angina/referred pain involve?

A

T1-T4 (left arm and shoulder more common)

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13
Q

What are the 3 types of angina?

A
  • Stable
  • Unstable
  • Prinzmetal
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14
Q

Describe stable angina.

Treatment? Response to NG?

A
  • Most common type
  • Caused by reduction in perfusion due to coronary atherosclerosis
  • Heart becomes vulnerable whenever there is increased demand due to physical activity, emotional stress, etc
  • Typically up to about 70% artery occlusion

Treat with:

  • Nitroglycerin (vasodilator)- promptly relieves pain
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15
Q

Describe unstable angina. What is used to treat it?

Response to NG? Treatment?

A
  • Between stable angina and MI
  • Occurs more frequently (and increasingly so) than stable angina
  • Precipitated with progressively less effort
  • Often unrelated to exercise and occurs at rest
  • 70-99% artery occlusion
  • Symptoms NOT relieved by rest or nitroglycerin

Treatment:

- Aspirin

- Clopidogrel (Plavix)- preferred

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16
Q

Describe Prinzmetal angina. Response to NG?

A

Aka variant angina

  • Uncommon pattern of episodic angina that occurs at rest and is due to coronary artery spasm
  • Responds to NG and CCBs
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17
Q

What factors increase oxygen supply?

Increase oxygen demand?

A

Supply:

  • Coronary blood flow
  • Transmural blood flow
  • Coronary collateral blood flow
  • Diastolic perfusion time
  • Pressure gradient (DBP - LVEDP)

Demand:

  • Ventricular wall tension (preload + afterload)
  • Heart rate
  • Cardiac contractility
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18
Q

Which of the following 2nd messengers in the smooth muscle promote dilation of BVs?

A. Ca

B. Diacylglycerol

C. cAMP

D. cGMP

E. cAMP and cGMP

F. IP3

A

Which of the following 2nd messengers in the smooth muscle promote dilation of BVs?

A. Ca

B. Diacylglycerol

C. cAMP

D. cGMP

E. cAMP and cGMP

F. IP3

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19
Q

Therapy: ways to increase oxygen supply?

Decrease oxygen demand?

A

Increase supply:

  • Dilated coronary arteries
  • Increased diastolic time (decreased HR)

Decreased demand:

  • Decrease in preload or afterload
  • Decrease HR
  • Decrease contractility
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20
Q

What causes contraction of the smooth muscle around BVs (molecularly)? Source?

A

Ca-mediated; two sources:

  • outside cells
  • inside cells (SR)

The higher the cytoplasmic Ca levels, the more contraction

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21
Q

What is the effect of cAMP (PKA) in the smooth muscle?

A

Relaxation

  • recall: albuterol
22
Q

What promotes relaxation of the smooth muscle? Contraction?

A

Relaxation:

  • cGMP
  • cAMP
  • (Ca channel blockers, –dipine)

Contraction:

  • Increased Ca
23
Q

Mechanism of action for CCBs?

A

(–dipines)

  • Block L-type Ca channels that allow Ca into sm cell (of vascular smooth muscle)
  • Decreased cellular Ca -> decreased contraction
  • Results in decreased MVO2
24
Q

How is smooth muscle contraction regulated by endothelial cells?

A

ACh or bradykinin act on endothelial cells to increase eNOS levels (inducible nitric oxide synthase)

  • Results in increase in NO and relaxation of vascular smooth muscle (thus increased blood flow)
  • NO also keeps platelets inactive
25
Q

What are some pharmacological approaches to dilate blood vessels (relax vascular smooth muscle)?

A
  • AT1 antagonists
  • ACE inhibitors
  • Ca chanel blockers
  • K channel openers
  • alpha 1 antagonists
  • ET A/B antagonists
  • PDE5 inhibitors
  • Nitrates
26
Q

What are nitrates used to treat?

A

- Stable angina pectoris

- Unstable angina pectoris (along with aspirin and Clopidogrel)

- Acute MI (controversial; isosorbide dinitrate recommended)

- Hypertension

- Acute and chronic heart failure

- Pulmonary HTN

27
Q

What is the mechanism of action of nitrates?

A

All nitrates act by increasing NO

  • Spontaneous degradation
  • Conversion by enzymes (in plasma, endothelial cell, and sm cells)
  • NO, cGMP, PKG increased
  • Myosin phosphatase increase
  • Myosin-phosphate decreases
  • NO-bound K channels open and membrane hyperpolarizes
  • SM/BVs dilation increases
28
Q

What are the sites of action of organic nitrates?

How do they work in each place to help angina?

A

- Heart: coronary arteries: increase O2 supply by dilating large epicardial arteries

- Arteries: decrease afterload and MVO2

- Veins: drastically decrease preload and decrease MVO2

29
Q

What are the 3 commonly used nitrates?

A
  • Nitroglycerin
  • Isosorbide dinitrate
  • Nitroprusside
30
Q

Compare characteristics of the common nitrates

A

Nitroglycerin: half life 5-40 min

Isosorbide dinitrate: half life 1-4 hrs

  • SH groups required for NO formation
  • Acetylcysteine will prolong duration

Nitroprusside: half life 1-2 min (short!)

  • Spontaneously decomposes
  • Close monitoring required b/c of cyanide poisoning
  • Metabolized by liver and excreted by kidneys
  • Less specific; works in all tissues

ALL:

  • Low bioavailability
  • Metabolized in gut and liver
31
Q

What is the mechanism of nitrate tolerance?

When does it occur?

How can you prevent it?

A

Mechanism:

  • Impaired NG bioconversion by mitochondria
  • Reduced bioactivity of NO
  • Activation of vasoconstrictor renin-angiotensin-aldosterone system and sympathetic nervous system in response to vasodilation (reversible by ACEIs)

Develops after 12-24 hrs of continuous exposure to exogenous nitrates (but not to sodium nitroprusside)

Prevention:

  • Intermittent therapy with a 7-12 hr nitrate-free period daily
32
Q

Contraindication for nitroglycerine?

A

Anemia (severe)

  • Nitrates may make worse by hemodilution

Hypotension

People taking Sildenafil (Viagra)

  • Cannot degrade cGMP so giving nitrates will decrease BP too much and cause tachycardia with increased MVO2

Acute MI

  • Still used by many Increased intracranial pressure
  • Will dilate cerebral arteries -> even more ICP

Pericardial tamponade

  • Due to excess fluid in pericardial sac

Restrictive CM (due to rigid ventricle)

  • Pts with diastolic dysfunction depend on preload to keep up cardiac output
33
Q

Adverse reactions to NG?

A

CNS:

  • Headache (severe and throbbing duet o BV dilation)
  • Flushing

Hematological

  • Hemodiultion; methemoglobinemia (with ferric iron; ferrus is normal)
  • Prolonged bleeding time (NO inhibits platelet aggregation)
  • Thrombocytopenia
  • Cyanide poisoning (with nitroprusside)

Cardiovascular:

  • Reflex tachycardia
  • Paradoxical angina
  • Bradycardia
  • Hypotension (edema)
  • Paradoxical HTN
  • Arrhythmias
34
Q

What are some drug-drug interactions to be aware of with NG?

A
  • Acetylcysteine: hypotension
  • Altepase (tPA): increased altepase clearance
  • Aspirin- increased NG concentrations
  • DihydroErgotamine (DE)- increased DE plasma concentrations (DE dilates BVs)
35
Q

What suffix do beta blockers use?

A

–olol

36
Q

What are the effects of beta blockers?

A
  • Decrease sympathetic stimulation
  • Decrease HR
  • Decrease oxygen demand
  • Increase refractory period
  • Increase diastolic perfusion time
  • Decrease conduction velocity
  • Decrease contractility
  • Decrease oxygen demand (beta blockers with ISA like Pindolol are contraindicated)
37
Q

Adverse effects of beta blockers?

A

- Bronchoconstriction: B2 blockade of airway may precipitate/worsen asthma

Metoprolol and Atenolol are cardioselective;

Propanolol is b1 = b2… But all beta blockers are nonselective at higher concentrations)

- Bradycardia: B1 blockade (pts with conduction problems should avoid)

- Hypotension

- Sudden withdrawal syndrome after chronic use (angina, MI)

38
Q

Effects of CCBs?

A
  • Decreased HR (SA node, AV node)
  • Decreased conduction velocity
  • More dilated BVs
  • Decreased afterload
  • Decreased MVO2
39
Q

What are the three classes of CCB drugs? Specificity?

A

Amlodipine and DihydroPyridINE

  • Specific to BVs

Diltiazem

  • BVs- heart

Verapamil

  • Cardiac specific
40
Q

What is the mechanism of K channel openers?

A

Open ATP-mediated K channels to hyperpolarize cells and clsoe Ca channels in arterioles

41
Q

Uses of K channel openers? Side effects?

A

Used in severe or refractory HTN

  • NOT first choice
  • NOT for angina pain

Side effects:

  • Flushing
  • Headache
  • Hypotension
  • Reflex tachycardia
  • Angina pain
  • Hirsutism (promotes hair growth)–Rogaine (Minoxidil) used to treat male baldness
42
Q

What suffix is used for K channel openers?

A

—dil

43
Q

What is hydralazine? Uses? Side effects?

A

Direct arterial vasodilator

  • Mechanism unknown
  • NOT a first line drug (leads to reflex tachycardia)
  • Drug induced lupus is a frequent side effect
44
Q

What is endothelin? Mechanism of action?

Example? Uses?

A
  • Peptide released by endothelial cells
  • Contracts sm cells
  • Can also relax sm indirectly via NO
  • Ex) Bosentan- used to treat severe pulmonary HTN
45
Q

What is Ranolazine? Mechanism of action? Uses? Side effects?

A

- Na channel blocker: inhibits late phase of Na current, resulting in less cytoplasmic Ca and reduced MVO2

  • 2nd line drug with many warnings

Side effects:

  • QT prolongation
  • Many drug interactions
46
Q

Why use sodium nitroprusside with cyanide toxicity?

A

Most powerful among the three nitrates

  • Dilates arteries more; decreased afterload
  • Coronary blood flow increases
47
Q

T/F: diuretics can be used to treat angina?

A

Truish- 2nd line and experimental

48
Q

I-Clicker:

A 56-year old patient complains of chest pain following any sustained exercise. He is diagnosed with atherosclerotic angina. He is prescribed sublingual nitroglycerin for treatment of acute chest pain.

Which of the following adverse effects is more likely to be experienced by this patient?

A. Hypertension

B. Throbbing headache

C. Bradycardia

D. Sexual dysfunction

E. Anemia

A

Which of the following adverse effects is more likely to be experienced by this patient?

A. Hypertension

B. Throbbing headache

C. Bradycardia

D. Sexual dysfunction

E. Anemia

49
Q

A 56-year old patient complains of chest pain following any sustained exercise. He is diagnosed with atherosclerotic angina. He is prescribed sublingual nitroglycerin and a beta blocker for treatment of acute chest pain. The beta blocker has the added benefit of preventing which of the following side effects of sublingual nitroglycerin?

A. Dizziness

B. Methemoglobinemia

C. Throbbing headache

D. Reflex tachycardia

E. Edema

A

The beta blocker has the added benefit of preventing which of the following side effects of sublingual nitroglycerin?

A. Dizziness

B. Methemoglobinemia

C. Throbbing headache

D. Reflex tachycardia

E. Edema

  • Dilate veins so BP decreases
50
Q

A 68-year-old man has been successfully treated for exercise-induced angina with short-acing nitrates for several years. He recently has been complaining about being awakened at night with chest pain.

Which of the following drugs would be useful in preventing this patient’s noctural angina?

A. Hydralazine

B. Nitroglycerin (sublingual)

C. Isosorbide dinitrate (sublingual)

D. Verapamil

E. Nitroglycerin (transdermal)

A

Which of the following drugs would be useful in preventing this patient’s noctural angina?

A. Hydralazine

B. Nitroglycerin (sublingual)

C. Isosorbide dinitrate (sublingual)

D. Verapamil

E. Nitroglycerin (transdermal)

  • Want a nitrate that will last a long time
  • Transdermal lasts 8-14 hrs (can work overnight)

_MS2 Cardio (35 decks)

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