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PHRM 845: Therapeutics III > Ischemia > Flashcards

Ischemia Flashcards

1
Q

Describe the flow of blood within the heart?

A
  • Deoxygenated blood come into the RIGHT ATRIUM via the superior and inferior vena cava.
  • It then travels to the RIGHT VENTRICLE where it is pumps out into the lungs via the pulmonary arteries.
  • Oxygenated blood is returned to the LEFT ATRIUM from the lungs from the pulmonary veins.
  • It then travels to the LEFT VENTRICLE where it is pumps out to the body via the atora.
  • Repeat
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2
Q

What are the Hemodynamic Parameters?

A
  • Preload, Afterload, Heart Rate, Contractility
  • ALL affect cardiac output
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3
Q

What do the Hemodynamic Parameters measure?

A

Oxygen supply and demand to the myocardium

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4
Q

What is the main cause of Myocardial Ischemia?

A

An imbalance between Supply and Demand
- Increased oxygen consumption [caused by increased HR, Contractility, Afterload, Preload] will INCREASE demand.
- Decreased Coronary Blood Flow [caused by vasospasm, fixed stenosis, thrombus] will DECREASE supply.

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5
Q

What is Preload?

A

The amount of blood that is entering the ventricles [how much the ventricles are streched] - End Diastolic Volume

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6
Q

Cause and effects on Preload?

A

Dilation of the Veins will DECREASE preload.
- Decrease in preload will DECREASE O2 consumption [the heart isn’t stretching as much]
- Decrease in preload will INCREASE perfusion [myocytes are receiving more O2]

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7
Q

What is Afterload?

A

The resistance that the ventricles must overcome to circulate the blood [to help shoot blood out into the body]

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8
Q

Cause and effect on Afterload?

A

Dilation of the Arteries will DECREASE aferload.
- Decrease in afterload will DECREASE O2 consumption [blood is able to leave the heart easier, lowering the myocyte work load, increasing perfusion]

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9
Q

What is myocardial prefusion?

A

It is the ability of the myocytes to receive oxygen, it also shows how well blood flows through the heart.

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10
Q

Explain the process of the formation of atherosclerotic plaques?

A

-Monocytes move into the cell where they become macrophages.
- The macrophages take up the LDL, becoming a fatty streak
- Eventually the plaque will rupture forming a thrombus

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11
Q

What are the types of Angina?

A

Variant Angina [Printzmetal’s], Stable Angina [Fixed stenosis], Unstable Angina [thrombus]

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12
Q

Describe what happens within Variant Angina [Printzmetal’s]?

A

Also known as Vasospasm Angina, the arteries will spasm eventually becoming stuck closed
- SUPPLY ischemia [because of DECREASED blood flow in]
-Occurs often at rest or night

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13
Q

Describe what happens within Stable Angina [Fixed Stenosis]?

A

An atherosclerotic plaque is formed in the arteries where they become partially blocked
- DEMAND ischemia [because the supply is DECREASED so the demand is much higher]

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14
Q

Describe what happens within Unstable Angina [Thrombus]?

A

The atherosclerotic plaque ruptures resulting in platelet aggregation and the formation of the Thrombus, blocking the arteries
- SUPPLY ischemia [because of the DECREASE in blood flow]

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15
Q

What is a STEMI?

A

STEMI: ST Elevated Myocardial Infarction
- COMPLETE Blockage on the vessel due to plaque rupture and thrombus formation
- The ST wave is elevated [major sign]

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16
Q

What is an NSTEMI?

A

NSTEMI: Non-ST Elevated Myocardial Infarction
- PARTIAL Blockage on the vessel due to plaque rupture and thrombus formation
- The ST wave is NOT elevated [major sign]

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17
Q

How to treat angina?

A

INCREASE oxygen delivery:
- Vasodilators or Antithrombics [increase the supply]
DECREASE oxygen demand:
- Vasodilators and Cardiac Depressants [decrease HR, Contractility, Pressure]

18
Q

What is the mechanism of action for the formation of NO?

A
  • L-Arginine is converted into L-Citruline where NO is released from the Endothelium into the vascular smooth muscle
  • It then reacts with GUANYLATE CYCLASE where it formed cGMP, and cGMP dephosphorylates MLC causing RELAXATION.
19
Q

What is the activity of the Organic Nitrates?

A
  • Mainly cause the dilation of the Veins [decreasing PRELOAD]
  • Can dilate the Coronary Arteries [decreasing AFERLOAD]
20
Q

With medications are the Organic Nitrates?

A

Glyceryl Trinitrate, Isosorbide Mononitrate, Isosorbide Dinitrate

21
Q

Describe the mechanism fo Nitrate Tolerance?

A

Caused by frequent or high doses of GTN
- They slowly inactivate ALDH2 in mitochondria [so GTN can’t be made into NO] resulting in no vasodilation

22
Q

What are the classes of Calcium Channel Blockers?

A

Dihydropyridines [“-pines”], Benzthiazepines [Diltiazem], Phenylalkylamines [Verapamil]
- DHP = “-pines”
- NON DHP = Verapamil and Diltiazem

23
Q

What is the mechanism of action for the CCBs?

A

They block the extracellular Ca2+ from entering into the cell
- Decreasing the formation of the Ca + Calmodulin complex = decreasing the constriction caused by MLCK [dilation of the arteries]

24
Q

What is the activity of the CCBs?

A

Mainly the dilation of the arteries
- NO dilation of the Veins [Veins do not use extracellular Ca2+]

25
Q

Explain how DHP differs from NON DHP?

A
  • DHP [Amlodipine] will bind between the proteins on the out side of the Calcium Channel, blocking it
  • NON DHP [Verapamil] will just bind directly into the channel, blocking it that way
26
Q

What is the mechanism of action for Beta-Blockers?

A

They block the Beta receptors within the myocardium from getting stimulated by Noepi and Epi [adrenaline].
- Decreased Noepi/Epi will decrease the activation of Adenylyl Cyclase, resulting in a decreased cAMP, causing VASODILATION
- Epi will increase the HR and Contraction

27
Q

What is the activity of Beta-Blockers?

A

Help reduce oxygen usage and depress the heart
- Main treatment in Stable Angina

28
Q

Which Beta-Blockers are Cardioselective and which aren’t?

A

B1: Metoprolol, Atenolol, Bisoprolol, Nebivolol
[Heart Selective]
B2: Propranolol, Nadolol, Labetolol, Sotaolol,
[Lung Selective]
Mixed: Carvedilol, Labetolol
[B1, B2, A Selective]

29
Q

What patients shouldn’t get a Beta-Blocker?

A

Patients that have Asthma, already have a LOW heart rate, Heart Failure [because of negative intropic activity]

30
Q

What is reflex tachycardia?

A
  • When the blood pressure is decreased, the heart will beat faster in an attempt the increase it.
  • The vagus nerve and the carotid nerve both help with this within the arteries.
31
Q

What are some medical ways that we can combat Reflex Tachycardia?

A
  • If the blood pressure is to high, we can give a Nitrate to lower that; but HR will INCREASE [can give Beta-Blocker to help lower that heart rate]
  • If CCBs increase preload too much, then we can use Nitrates to lower it
32
Q

What is a Hyperpolarization-activated Cyclic Nucleotide [HCN]?

A
  • Work within the SA node in the heart, causing th hyperpolarization of the cells by the influx of Na+
  • cAMP will activate these channels
33
Q

What is the action of Ivabradine?

A
  • Will block the HCN block completely, not allowing Na+ to enter, stopping the Hyperpolarization [slowing heart rate]
34
Q

What is the way that we treat Unstable Angina?

A
  • Want to block the formation of Thrombus
  • Aspirin, P2Y12, Heparin
35
Q

What are the MHG-CoA Reductase Inhibitors?

A

“-Statins”

36
Q

What is the mechanism of action for the Statins?

A
  • They block the conversion of HMG-CoA into Mevalonate, which will decrease the formation of cholesterol, causing the decrease in plaque formation
37
Q

What is the purpose of Aspirin in Unstable Angina?

A
  • Its a COX-1 Platelet inhibitor; Blocks the TXA2 synthesis, stopping the recruitment and formation fo platelets
38
Q

What is the mechanism of action for P2Y12 Inhibitors?

A
  • They inhibit the P2Y12 ADP receptor, preventing platelet activation
39
Q

What are the P2Y12 Inhibitors?

A

Clopidogrel, Ticagrelor, Cangrelor

40
Q

What is the mechanism of action for the GP IIb/IIIa inhibitors?

A
  • They inhibit the GP IIb/IIIa receptor, preventing the platelet aggregation

PHRM 845: Therapeutics III (25 decks)

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