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PHAMACOLOGY - Cardiology > Treatment of Angina > Flashcards

Treatment of Angina Flashcards

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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

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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?

Study These Flashcards
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?

Study These Flashcards
A

LIVER metabolism is significant

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

25
What CCB side effects are most common in the Dihydropyridines? • Name them
``` ***diffs tied to MOA between CCB types*** • Excessive Vasodilation • GI irritation = nausea • Peripheral Edema • Coronary Steal ``` Dihydropyridines: Amoldipine, Nefidipine, Nicadipine, Isradipine, Felodipine
26
What CCB side effects are most common in Non-Dihydropyridines? • Name them
Verapamil and Diltiazem: • Bradycardia, Asystole, AV BLOCK • Congestive Heart Failure • Constipation (Verapamil)
27
What is the MAJOR PROBLEM with using Verapamil and Diltiazem with a Beta-Blocker?
• AV BLOCK - pt. would drop dead
28
What are some drugs that may reduce the efficacy of Verapamil? • why?
Rifampin and phenobarbital *These drugs are CYP3A4 inducers and may cause Reduced plasma levels of Verapamil
29
What Adverse side effect is common to both the dihydropyridines and non-dihyropyridines?
PERIPHERAL EDEMA
30
T or F: it is safe to use dihydropyridines with Beta Blockers.
True, not a risk of AV block here
31
Which CCB causes constipation and pretty much any other side effect associated with Beta Blockers?
• Verapamil
32
What are the 3 different types of Angina?
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
What two major factors contribute to angina? | • what affects these factors?
Demand: • HR, Contractility, Afterload (wall tension) ``` O2 Supply: • Coronary Vascular Resistance • Perfusion Pressure • Collateral Blood Flow • Heart Rate and Mechanics ```
34
What is the difference between Prinzmetal's angina and unstable and exertional angina? • Angiograms? • Prognosis?
Prinzmetal • Caused by Vasospasm - not an increase in myocardial O2 demand • Angiograms are normal • Px is Excellent
35
What are the 3 general approaches to treating Angina?
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
How does altering chronotropy or ionotropy benefit the heart?
• 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
What is the Primary Drug of Choice in the Treatment of most Angina?
* 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
Where are the predominant effects of each class of CCBs?
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
Which of the classes of CCBs MUST ALWAYS be given with a Beta blocker? • which is the 1st line therapy when switching to CCBs?
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
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?
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
T or F: in general Nitrates are the preferred way to treat angina.
True, use Nitrates before switching to Calcium Channel blockers
42
What are some situations in which you might use a CCB over a Nitrate in Angina?
**If possible switch to a dihyrdopyridine** * To Reduce AFTERLOAD in cases of - VALVULAR insufficiency * Reduces Aortic or Mitral Valvular insufficiency
43
Besides Asthma and COPD, what are some cases in which it Non-Dirhydropyridine Drugs should be used to treat angina? • name them
Verapamil and Diltizem * Labile (Variable glucose levels) Insulin Dependent Diabetes * Severe Peripheral Vascular Disease with Rest Pain Depression
44
What type of angina is most effectively treated by a calcium channel blocker? • what is not effectively treated?
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
WHAT IS YOUR 1ST CHOICE OF THERAPY IN ANGINA?
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
What positive effects do Beta blockers have for people with angina? • what important things can they not do for these people?
• 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
What drugs are Beta blockers use with in order to make up for their short comings in angina treatment?
• 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
T or F: Beta blockers and nitrates are ideal in treatment in all types of angina?
FALSE, beta blockers DO NOT prevent vasospasm associated with Prinzmetal;s angina (no vasospastic protection)
49
T or F: Beta Blockers are good for patients who have angina and have had a previous MI.
True, beta blockers REDUCE V-FIB and mortality associated with MIs
50
Ranolazine • MOA • Why does it suck?
* 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
Ranolzaine • Adverse Reactions • Contraindications
• 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
What is the role of the 3 general treatments for angina in actually preventing angina in people with Coronary Heart disease?
* Beta-Blockers - decrease episodes * Nitrates - no effect * CCB's - variable
53
Someone is treated with a beta blocker and nitrate to prevent unstable angina. What else should they be started on?
* 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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