L49-therapeutic Control Of Ischemia Flashcards

1
Q

Agents that improve ischemic symptoms

A
Inc coronary flow
Inc O2 supply 
Vasodilators:
▪️Organic nitrates 
▪️Calcium channel blockers
▪️Potassium channel openers
Dec cardiac work
Dec O2 demand 
-ve inotropes
▪️beta blockers
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2
Q

What do organic nitrates act on

A

Venular

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3
Q

Types of organic nitrates

A

Rapid acting: nitroglycerine

Short acting: isosorbide mono and dinirate

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4
Q

Mechanism of nitrates

A

Act on GSH-transferase
Release on nirite ion in endothelial cell
Act as NO donner mimicking action of endogenous NO

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5
Q

Functions of nitrates

A

Vasodilation

Cytoprotection of endothelium

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6
Q

Side effects of nitrates

A

Tachycardia
Flush and headache
Syncope

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7
Q

How can there be an inc myocardial oxygen supply

A

Dilatation of collaterals which redistributes flow

Dilatation of large and resistant vessels which dec the BP and dec afterload

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8
Q

What are the dihydropamines and what are they selective to

A

Nifedipine and amlodipine

Act on VSMCs

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9
Q

What acts on cardiomyoctes

A

Verampril

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10
Q

What has an intermediate action on both cardiomyocytes and VSMCs

A

Diltaizem

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11
Q

Mechanism of Ca channel blockers

A

Bind to: L type and T type
In VSMCs they dec entry of extracellular Ca and cause vasorelaxation dec bp and afterload
In cardiomyocytes they dec entry of Ca and dec CICR from SR dec contraction and dec hr having a -ve dromotropic effect

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12
Q

Why should we never use short acting nifepidine

A

Sudden dec in bp and reflex tachycardia which causes myocardial hypo perfusion and can lead to death
Use instead long acting amlodipine

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13
Q

What do K channel openers do

A

Vasodilator action
Opening of Atp sensitive k channels causing hyper polarization and inhibits L type ca channel which dec VSMCs contraction in arteriolar
Used as second line therapy

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14
Q

What do beta blockers do

A

-ve inotropic and chronotropic
Dec CO and afterload
Dec RAAS which dec cardiac work and O2 demand
Leads to bradycardia
Which prolongs diastole and inc coronary filling as well as perfusion time which inc myocardial O2 supply

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15
Q

B1 selective drugs

A

Nebivolol
Atenolol
Bisoprolol
Metoprolol

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16
Q

What can nitrates be combined with

A

Non dihydroprine group or with beta blockers to limit decrease blood pressure and reflex tachycardia

17
Q

What can calcium channel blockers be used with

A

Dihydropyridines since they don’t dec contractility and given if also HF
Non-dihydropyridines since they dont cause vasodilation but dec contractility so give for angina if HF is not severe and no bradycardia can be give if hypotension exist

18
Q

What can beta blockers be used with

A

Nitrates since they abolish its induced reflex tachycardia

With dihydropydrine calcium channel blockers but not verampril nor diltiazem for fear of conduction defect

19
Q

What is the mechanism of Pfox inhibitors

A

The shift cardio myocytes metabolism to the utilization of carbohydrates which lower the O2 demand rather than free fatty acids to spare O2 to the ischemic myocardium
They prevent beta oxidation via inhibiting enzyme responsible for transfer of free fatty acids across the mitochondrion membranes

20
Q

Agents used to prevent develop of thrombos

A

Aspirin or clopidogrel

21
Q

To hold progression of atherosclerosis

A

Statins

22
Q

To limit cardiac demand and dysrhythmias

A

Beta blockers

23
Q

To dump in the RASS damaging effects specially in presence of hypertension

A

Ace inhibitors

24
Q

What is given before and during transfer in treatment of acute myocardial infarction

A

GTN and sublingual up to three doses at five minute intervals
Analgesic such as morphine for pain
Chewable aspirin plus loading dose clopidogrel
If needed CPR or 02 or Ivy fluids

25
Q

What is given in the ER than ICU or CCU units

A

To relieve symptoms : IV GTN infusion plus analgesic IV
To open occluded vessel:
pry PCI
fibrinolytics 

26
Q

The drugs given to improve survival

A

Early beta blockers
Early statins
Ace inhibitors