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PHAR 121 > Arterial Thrombosis > Flashcards

Arterial Thrombosis Flashcards

1
Q

What can arterial thrombosis cause?

A

Ischemic necrosis of tissue supplied by the artery

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2
Q

What is the first phase of arterial thrombosis development?

A

LDL enters the sub-endothelial space

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3
Q

What is artherosclerosis?

A
  • A disease of the arteries
  • Often asymptomatic
  • Artherosclerotic plaque pushing aginst arterial wall
  • LDL is the main player
  • Ischemia or infarction can occur if they rupture
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4
Q

What happens when the arthersclerotic plaque ruptures?

A

Platlets –> Circulating cells that aggregate on damaged blood vessel walls
- If the platlet response is big enough, can block the artery completly

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5
Q

What happens if platlets block an artery to the heart?

A
  • Oxygen cannot perfuse out of arteries
  • Cardiac cells still being told to contract –> creating a demand for oxygen and energy supply is gone
    Cardiac cells suffocate
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6
Q

Define Ischemia

A
  • inadequate blood flow to a tissue
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7
Q

What occurs if ischemia is complete? What areas of the body does this occur?

A
  • Myocardial Infarction –> Coronary artery –> coronary artery disease
  • Stroke –> cerebrovascular event –> cerebra arteries –> cerebrovascular disease
  • Arteries of the limbs –> Peripheral arterial disease
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8
Q

Platlets

A
  • Fragments of larger, multinucleated cells (megakaryocytes)
  • No nucleus
    Contain granules in cytoplasm
    Contain COX-1 enzyme
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9
Q

What is the role of platlets?

A

Adhere to damaged wall
Aggregate to form a platlet plug
Activate coagulation cascade and other platlets

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10
Q

How do platlets adhere to injured areas?

A
  • Glycoprotein Ib receptors
  • Expressed on platlet surface
  • Affinity for subendothelial substrates (Collagen and Von Willebrand Factor)
  • cause platlets to adhere to injured area
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11
Q

How are platelets activated?

A

1) Exposure to subendothelial surfaces (adherence/ GP Ib binding)
2) Exposure to activators such as:

Thromboxane
ADP
Thrombin
Serotonin
Platlet Activating factor (PAF)

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12
Q

How does activation of platlets promote aggregation?

A
  • Emergence of GP IIb/IIIA receptor
  • receptor that promotes platlet agggregation
    FIBRINOGEN CONNECTS THE GP IIB/IIIA RECEPTORS OF TWO PLATLETS TOGETHER
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13
Q

What is fibrinogen?

A
  • the precursor of fibrin - final product of coagulation cascade
  • links platlets to ensure aggregation
  • localizes substrate for clot formation at site of damage
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14
Q

Once platlets are activated they release?

A
  • Release stored granules of:

Adenosine Diphosphate (ADP)
Thromboxane A2

  • Results in the activation of resting platlets and initiates the coagulation cascade
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15
Q

What is prostacyclin (PGI2)?

A
  • produced by endothelial cells
  • Promotes vasodilation and decrease platlet aggregation
  • Synthesized from arachadonic acid
  • Same precursor as thromboxane A2
  • Produced by the enzyme familiy –> CYCLOOXYGENASE-2
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16
Q

Cyclooxygenase types:

A
  • COX-1 –> Converets arachdonic acid to thromboxane A2
  • COX-2 –> Converts aracdonic acid to prostacyclin (PGI2)
17
Q

Thromboxane A2 is a….

A

Platlet Activator

18
Q

Prostacylin is a…

A

platlet inhibitor

19
Q

ASA inhibits….

A
  • COX 1 AND COX 2
  • 50-100 x more potent for COX-1
20
Q

What amount of ASA will inhibit only COX-1?

A
  • 81 mg
21
Q

How does ASA work?

A
  • Irreversible inhibitor of COX (mainly COX-1) –> Prevents formation of thromboxane A2
  • Platelets cannot regenerate COX as no nucleus
  • Allows for OD dosing despite short half life
22
Q

Why is ASA used over NSAIDS?

A
  • NSAIDS are reversible and only inhibit COX-2
  • NSAIDS not indicated for anti-platelet action
  • NSAIDS reduce inflammation (and pain) by reducing Pg’s in damaged tissue
23
Q

Two examples of ADP antagonists
How long they are used for?

A

Clopidogrel
Ticagrelor

Typically 1 year

24
Q

Clopidogrel

A
  • ADP antagonist
  • Prodrug that requires liver metabolism for activation
  • Inhibits ADP receptor
  • Irreversible inhibitor
25
Q

Ticagrelor

A
  • Reversible inhibitor of ADP receptor
  • Not a prodrug
  • Common in Post-Mi setting
26
Q

How do ADP antagonists work?

A
  • Prevent the consequences following artherosclerotic rupture. Prevents coagulation cascade. Does not reduce the risk of plaque rupture.
27
Q

What is the role of ADP antagonists?

A
  • Used in people at high risk for MI or stroke primarily as secondary prevention
28
Q

Glycoprotein IIb/IIIa Inhibitors MOA

A
  • Hopsital use only
  • Receptor that prmotes platlet aggregation
  • Fibrinogen is the principle target
29
Q

What other drug is commonly used in coronary artery disease?

A

Nitroglycerin
- Used to manage or prevent angina
- Angina is pain or discomfort resulting from inadequate blood supply to cardiac muscle
- Can occur in heart attack or when cardiac workload increases

30
Q

What is the difference between unstable angina and stable angina?

A
  • Unstable angina is due to an unstable plaque and pertains to an ischemic part of the heart.
  • Stable angina is a fixed obstruction angina where at rest no angina, but increase cardiac output, angina develops as need for more oxygen and energy. Ischemic pain will go away if decrease workload
31
Q

How is nitroglycerin used for stable angina?

A
  • Works on veins more than arteries
  • By dilating veins, reduce pre-load on heart (filling pressure) by allowing blood to pool in veins
  • Decrease preload, decrease workload and decrease pain from angina.
32
Q

Drugs that can be used to manage/prevent angina?

A
  • Nitroglycerin spray (prn use)
  • Nitroglycerin patch
  • Beta-blockers and Non-DHP CCB
  • DHP CCB

PHAR 121 (6 decks)

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