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PHAMACOLOGY - Cardiology > Treatment of Angina > Flashcards

Treatment of Angina Flashcards

1
Q

Nitroglycerine

• MOA

A
  • Nitroglycerine (glycerine with three nitrates) is ingested then denitrated to release NO that goes to activate Guanylate Cyclase
  • Guanylate Cyclase generates cGMP that goes on to activate PKG that mediates smooth muscle relaxation
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2
Q

What are the 2 main effects of nitroglycerine?

A

VENOdilation = reduction in PRELOAD
• Decreased Pressure during diastole increasing subendocardial bloodflow

ARTERIAL dilation = Reductino in AFTERLOAD

CORONARY vasodilation
• SELECTIVE vasodilation of epicardial and collateral coronary vessels
• REVERSES/PREVENTS coronary VASOSPASM

**ONLY DRUG that produces venodilation and reduction in preload*

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3
Q 
What other effects does nitroglycerine have on hemodynamics (besides reduced preload and venodilation)? 
• BP
• HR
• Vascular Resistance 
• Cardiac Output
A

BP: unchanged or SLIGHT reflexive increase

HR: unchanges or SLIGHT reflexive increase

Vascular Resistance - DECREASE PULMONARY vascular resistance

Cardiac Output: slight reduction

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4
Q

What are some different methods of administration for nitroglycerine?

A
  • Oral
  • Transdermal (patch)
  • Mucosal
  • Intravenous
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5
Q

What are the main adverse side effects associated with nitrates?

A

HYPOTENSION: Results from higher doses of nitrates that cause ARTERIAL vasodilation
• Reflex tachycardia or WORSENING Angina
• Dizziness, Orthostatic HypoTN, SYNCOPE

HEADACHE: Vasodilation of meningeal vasomotor arteries

RASH: caused by LONG acting nitrates (cutaneous patches)

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6
Q

What drugs are contraindicated with nitrates?

A

BONER PILLS - both cause act on the cGMP pathway, may result in MYOCARDIAL ISCHEMIA

Sildenifil = Viagra

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7
Q

What is the problem with dosing the nitrates?

A

TOLERANCE - Dosing has to be sporadic to keep your body from adjusting to the continuous exposure

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8
Q

What are the mechanisms of Nitrate Tolerance?

A

CYSTEINE STORES DEPLETED
• cysteine is vital for the conversion of nitrates to nitric oxide

VOLUME EXPANSION
• just increase the amount of fluid in the vasculature

NEUROHUMORAL ACTIVATION
• would lead to volume expansion via RAAS

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9
Q

Should you terminate Nitrate treatment immediately if a patient gets hypotensive on IV nitrates?

A

NO - this can cause abrupt vasospasm

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10
Q

What are the 2 groups of CCBs (calcium channel blockers)?

A
  • Dihydropyridine

* Non-dihyropyridine

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11
Q

What drugs are classified as Dihydropyridine CCBs?

A 
"dipines"
• Amlodipine 
• Nefidipine 
• Nicardipine 
• Felodipine 
• Isradipine
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12
Q

What two drugs are the Non-dihyropyridines?

A
  • Verapamil (group: phenylalkyamines)

* Diltiazem (group: benzothiazapines)

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13
Q

What 3 conditions are often treated by use of CCB’s?

A
  1. ANGINA
  2. HYPERTENSION
  3. SUPRAVENTRICULAR arrhythmias (atrial flutter, Atrial Fibrillation, Paroxysmal SVT)
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14
Q

Why does increased Ca2+ cause contraction in:
• Cardiac Myocytes
• Smooth Muscle

A

Cardiac:
• Ca2+ binds to TROPONIN C and reduces inhibition of ACTIN-MYOSIN cross-bridges

Smooth:
• CALMODULIN activates MLCK which PHOSPHORYLATES MYOSIN and triggers contraction

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15
Q

How does calcium inside the cell increase 10x in a period of only a few msec?

A
  • Release from the ER/SR

* Capacitive Ca2+ entry

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16
Q

Why don’t CCB’s cause effects on all systems in the body that highly dependent on Ca2+ like neurons?

A
  • They only act on Voltage Dependent Large Conductance (L-TYPE CALCIUM CHANNELS)
  • Cardiovascular system = really the only place these are found

other calcium channel types remain unaffected)

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17
Q

Differentiate the dependence the different parts of the heart on L-type Calcium Channels.

A

Atria and Ventricles
• Ca2+ used to activate contractile machinery

SA and AV nodes:
• L-type channels are activated after the initial voltage increase induced by T-type channels

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18
Q

How do the CCBs modulate the actions of calcium channels?

A

ALL:
• Reduce the magnitude of the Ca2+ current

Verapamil and Diltiazem (non-dihydropyridines)
• Slow the recovery of the channel

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19
Q

What is the effects of CCBs on Cardiac and Venous/Arterial Smooth Muscle?

A

Cardiac Muscle:
• Reduces FREQUENCY and FORCE of contraction - Reduced CO

Arterial:
• Relaxation of arterial smooth muscle

Veins = NO EFFECT

Lack of effect on veins means that AFTERLOAD is reduces but preload is not

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20
Q

Differentiate the effects of Dihyropyridines and Non-dihydropyridines on Smooth muscle and Cardiac tissue.

A

Dihyropyridines:
• ONLY VASODILATE but they work on BOTH CORONARY AND Peripheral Arteries

Non-dihydropyridines:
• EQUIPOTENT on Cardiac Tissue and Vasculature

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21
Q

How does the mechanism of action explain the differences in effect of the Dihydropyridines and Non-dihydropyridines?

A

Dihydropyridines:
• ONLY Bind at a PARTICULAR VOLTAGE so Target SMOOTH muscle - which stays at a pretty CONSTANT VOLTAGE

Non-Dihyropyridines:
• BIND INSIDE the Ca2+ channels so they need channels that are constantly OPENING AND CLOSING TO GET INSIDE AND PERFORM ACTION

Cardiac Muscle is best at doing the opening and closing thing

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22
Q

Calcium Channel Blockers:
• Bioavailability
• Elimination
• Halflife

A

Bioavailability:
• Rapid GI absorption and EXTENSIVE 1st PASS metabolism reduces bioavailability

Elimination:
• Drug Terminated via Hepatic Metabolism

Halflife:
• SHORT for most of these EXCEPT for - Isradipide and Felodipine

23
Q

What is the Bolus effect of CCBs?

• how has it been prevented?

A

Bolus Effect:

• Rapid absorption leads to REFLEX TACHYCARDIA, Headache, CORONARY STEAL

24
Q

What precautions should you take with CCBs in a patient who has liver cirrhosis?
• which drugs would grapefruit juice be bad for?

A

LIVER metabolism is significant

non-dihydropyridines are acted on by CYP3A4
• Verapamil > Diltiazem

25
Q

What CCB side effects are most common in the Dihydropyridines?
• Name them

A 
***diffs tied to MOA between CCB types***
• Excessive Vasodilation
• GI irritation = nausea
• Peripheral Edema 
• Coronary Steal

Dihydropyridines: Amoldipine, Nefidipine, Nicadipine, Isradipine, Felodipine

26
Q

What CCB side effects are most common in Non-Dihydropyridines?
• Name them

A

Verapamil and Diltiazem:
• Bradycardia, Asystole, AV BLOCK
• Congestive Heart Failure
• Constipation (Verapamil)

27
Q

What is the MAJOR PROBLEM with using Verapamil and Diltiazem with a Beta-Blocker?

A

• AV BLOCK - pt. would drop dead

28
Q

What are some drugs that may reduce the efficacy of Verapamil?
• why?

A

Rifampin and phenobarbital

*These drugs are CYP3A4 inducers and may cause Reduced plasma levels of Verapamil

29
Q

What Adverse side effect is common to both the dihydropyridines and non-dihyropyridines?

A

PERIPHERAL EDEMA

30
Q

T or F: it is safe to use dihydropyridines with Beta Blockers.

A

True, not a risk of AV block here

31
Q

Which CCB causes constipation and pretty much any other side effect associated with Beta Blockers?

A

• Verapamil

32
Q

What are the 3 different types of Angina?

A

Unstable Angina
• Caused by atherosclerosis and thrombosis blocks blood supply

Prinzmetal’s
• Vasospasm blocks blood flow

Exertional (stable) Angina
• caused by atherosclerosis only symptomatic when heart’s oxygen demands are increased

33
Q

What two major factors contribute to angina?

• what affects these factors?

A

Demand:
• HR, Contractility, Afterload (wall tension)

O2 Supply: 
• Coronary Vascular Resistance
• Perfusion Pressure
• Collateral Blood Flow
• Heart Rate and Mechanics
34
Q

What is the difference between Prinzmetal’s angina and unstable and exertional angina?
• Angiograms?
• Prognosis?

A

Prinzmetal
• Caused by Vasospasm - not an increase in myocardial O2 demand
• Angiograms are normal
• Px is Excellent

35
Q

What are the 3 general approaches to treating Angina?

A
  1. Increased Coronary Blood Flow
  2. Reduce Myocardial O2 consumption by:
    • NEGATIVE CHRONOTROPIC EFFECT
    • NEGATIVE IONOTROPHIC EFFECT
    • Reduction in PRELOAD or AFTERLOAD
  3. Prevention of Platelet Deposition/aggregation
36
Q

How does altering chronotropy or ionotropy benefit the heart?

A

• Heart is Perfused during Diastole when Subendocardium is Relaxed and Vessels are not smushed

CHRONOTROPY - increases TIME spend in Diastole so the subendocardial vessels fill more

IONOTROPY - decreases FORCE so that so much blood is not forced out of the tissue with each stroke

37
Q

What is the Primary Drug of Choice in the Treatment of most Angina?

A
  • Beta Blockers are considered 1st drug of choice in angina
  • CCBs reserved for those who cant tolerate Beta Blocker or for people whose angina is UNCONTROLLED by Beta-Blocker + Nitrate
38
Q

Where are the predominant effects of each class of CCBs?

A

Non-Dihydropyridine:
• act DIRECTLY on the Heart to decrease work by SLOWING AV conduction (via Ca2+ inhibit)
• PREVENTS Reflex Vasospasm (some action on smooth mm.)

Dihydropyridine:
• VASCULAR effects predominate increasing CORONARY perfusion and DECREASING AFTERLOAD
• REFLEX Cardiac stimulation

39
Q

Which of the classes of CCBs MUST ALWAYS be given with a Beta blocker?
• which is the 1st line therapy when switching to CCBs?

A

Dihydropyridines - MUST be given with a Beta blocker to prevent reflex tachycardia that results from extensive vasodilation

Dihydropyridines are the PREFERRED method of CCB treatment for Angina - except in cases of Asthma or COPD

40
Q

While Dihydropyridines are the preferred method of CCB treatment for Angina, Verapamil, and Diltiazem are given to patients with COPD or Asthma, why is this?

A

Dihydropyridines MUST be given with a Beta blocker, but beta blockers can’t be given with Asthma or COPD b/c of bronchoconstriction

• Verapamil and Diltiazem act mostly on myocytes but ALSO prevent the reflex function of vessels

41
Q

T or F: in general Nitrates are the preferred way to treat angina.

A

True, use Nitrates before switching to Calcium Channel blockers

42
Q

What are some situations in which you might use a CCB over a Nitrate in Angina?

A

If possible switch to a dihyrdopyridine

  • To Reduce AFTERLOAD in cases of - VALVULAR insufficiency
  • Reduces Aortic or Mitral Valvular insufficiency
43
Q

Besides Asthma and COPD, what are some cases in which it Non-Dirhydropyridine Drugs should be used to treat angina?
• name them

A

Verapamil and Diltizem

  • Labile (Variable glucose levels) Insulin Dependent Diabetes
  • Severe Peripheral Vascular Disease with Rest Pain Depression
44
Q

What type of angina is most effectively treated by a calcium channel blocker?
• what is not effectively treated?

A

Good At Treating:
• Exertional and Vasospastic Angina

NOT effective at treating:
Coronary Heart Disease (causing Angina)
• does NOT reduce reinfarction of CHD death
• causes impaired LV function causing INCREASED morbidity and mortality

Beta blockers are much more effective at helping patients with Coronary Artery Disease –> so dihydropyridines would probably be your best option

45
Q

WHAT IS YOUR 1ST CHOICE OF THERAPY IN ANGINA?

A

Beta Blockers, only use CCBs for people who can’t take beta blockers (asthma, COPD) and in people whose angina isn’t under control with Beta-Blocker + Nitrate

46
Q

What positive effects do Beta blockers have for people with angina?
• what important things can they not do for these people?

A

• Reduction in HR
• Reduction in Ionotropy
• Reduction in Afterload
—> these all increase perfusion in diastole/time spent in diastole

they CANNOT:
• Prevent Coronary Vasospasm

47
Q

What drugs are Beta blockers use with in order to make up for their short comings in angina treatment?

A

• Often given with NITRATE or CCBs (dihydropyridines) to add protection against CORONARY vasospasm

Nitrates: DILATE Coronaries, reduce LVEDP, and LV volume

Dihydropyridines: prevent VASOSPASM and reduce vascular resistance

48
Q

T or F: Beta blockers and nitrates are ideal in treatment in all types of angina?

A

FALSE, beta blockers DO NOT prevent vasospasm associated with Prinzmetal;s angina (no vasospastic protection)

49
Q

T or F: Beta Blockers are good for patients who have angina and have had a previous MI.

A

True, beta blockers REDUCE V-FIB and mortality associated with MIs

50
Q

Ranolazine
• MOA
• Why does it suck?

A
  • Partial Fatty acid oxidase inhibitor, increases Glucose Oxidation and efficiency of O2 use in Heart
  • Late Sodium Current Inhibitor
  • No effect on HR or BP (no hemodynamic effects)

This drug is expensive and doesn’t relieve attacks of angina and also may interact with Digoxin

51
Q

Ranolzaine
• Adverse Reactions
• Contraindications

A

• dizziness, headache, constipation, inc. in serum creatinine and BUN (not major), syncope

contraindications
• don’t give with CYP3A4 inhibitors
• Don’t give to ppl. with long QT or using class Ia or III antiarrhythmics
• Fucks up Digoxin Dosing

52
Q

What is the role of the 3 general treatments for angina in actually preventing angina in people with Coronary Heart disease?

A
  • Beta-Blockers - decrease episodes
  • Nitrates - no effect
  • CCB’s - variable
53
Q

Someone is treated with a beta blocker and nitrate to prevent unstable angina. What else should they be started on?

A
  • ASPRIN - anyone whose had a cardiac event, MI etc. should take it
  • warfarin works too but its more expensive and dosing is a pain in the ass

PHAMACOLOGY - Cardiology (11 decks)

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