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pharmocology > platelet blockers > Flashcards

platelet blockers Flashcards

1
Q

aspirin inactivates

A

the enzyme cyclooxygenase-1 (COX-1) and modify the activities of COX-2.
• This inhibition lasts for the entire life of the platelet!!!

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2
Q

since aspirin inhibits cox1 and 2

A

latelets’ release of ADP is inhibited

– Platelets’ ability to synthesize Thromboxane A2 and Prostaglandin E2 from Arachadonic Acid is inhibited.

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3
Q

thrromboxanes and prostaglandins

A

The Thromboxanes produced by platelets tend to help induce clot formation while the Prostaglandins tend to be pro-inflammatory.

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4
Q

cOX-2 produces

A

lipoxins once its been modified by aspirin. Lipoxins are anti- inflammatory.

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5
Q

With Thromboxanes blocked

A

platelets won’t aggregate for the life of the platelet (a good thing in places like coronary or carotid arteries!)

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6
Q

*Why don’t platelets just make more Thromboxane???

A

dont have a nucleus

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7
Q

With Prostaglandins blocked, inflammation

A

(such as occurs in arthritis) is decreased, nerve endings’ thresholds for pain is increased, the anterior pituitary’s “thermostat” is reset at a lower level (hence aspirin’s antipyretic effect).

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8
Q

four clinical apps for aspirin

A

anti inflammatory, anti platelet, anti arthritic, anti pyrrittic or fever

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9
Q

since platelets cant aggregate cuz of aspirin it reduces

A

acute MI, thrombotic stroke,DVT, and pulmonary emboli

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10
Q

side effects of aspirin #1

A

1 bleeding (hemmorhagic strokes at high doses)

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11
Q

complet platelet inactivation occurs at

A

160mg

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12
Q

side effect #2 of aspirin

A

GI (such as gastric ulcers) -PGI2 prevents gastric parietal cells from
secreting HCL.
-PGE2 and PGF2-alpha cause the stomach and SI to creative surface-protective mucus.
*This happens on a cellular biochemical level, therefore things like “coated” and “enteric”
aspirin don’t actually accomplish much!

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13
Q

aspirin side effect #3

A

Kidney damage -Prostaglandins are largely responsible
for maintaining adequate renal blood flow.
-By blocking Prostaglandin synthesis, salts and fluid start to be retained, potassium isn’t excreted properly, and the kidneys are “scarred” (interstitial nephritis.)

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14
Q

aspirin clearance

A

Conjugated by the liver, cleared by the kidneys so the half-life is 3.5 hours.
• The conjugation stage is very saturable, so at higher doses over several days the half- life increases 4-5X.
• This increased half-life dramatically increases renal toxicity causing a vicious cycle.

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15
Q

thyenopydines

A

Like aspirin: Block platelet aggregation Unlike aspirin: Different M.O.A. All act by irreversibly inhibiting the ADP pathway of platelets..• This blocks platelets’ GP IIb/IIIa receptors.
• Consequently, affected platelets can’t bind to each other or to fibrinogen.

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16
Q

ticlopidine use

A

(ticlid) thyenopydine Approved for use in the prevention of TIAs and strokes
• Approved for use with aspirin post-stent placement to prevent thrombi formation

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17
Q

ticlopidine black box warning

A

hematological disorders:

– Aplastic anemia – Neutropenia – Thrombotic Thrombocytopenia Purpura

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18
Q

clopidogrel. uses

A

(plavix) thyenopydine Like Ticlopidine, but less side effects (although thrombotic thrombocytopenia purpurea still can occur).
• Used more for cardiac “issues” (MI prevention, ACS, post-PTCA etc.) than Ticlopidine.

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19
Q

prasugrel

A

(effient) thyenopydine. The GOOD news:
-Prasugrel’s is more effective in treating thrombotic-related events than the other thienopyridines!
⦁ The BAD news:
-Black Box Warning for hemorrhagic stroke, excessive hemorrhage, and negative sequelae resulting from sudden discontinuation of Prasugrel therapy.

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20
Q

used to monitor thyenopydines AND Antiplatelet Therapy Resistance

A

TEG

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21
Q

Glycoprotein IIb/IIIa Blockers USES

A

All given parenterally
• All used extensively for ACS and in cath labs to make your life more miserable when they finally decide to send the patient to surgery.

22
Q

Glycoprotein IIb/IIIa Blockers DRUGS

A

Abciximab (Reopro) - Eptifibatide (Integrilin) - Tirofiban (Aggrastat)

23
Q

Dypridamole how it works and used

A

(persantine) primarily used as a coronary vasodilator • Blocks cyclic AMP (cAMP) which
is a ubiquitous intracellular “messenger” chemical derived from that ubiquitous cellular energy currency, ATP.

24
Q

dypyridamole end result

A

After a chain of intracellular miracles, Thromboxane A2 synthesis is blocked (no prostaglandin effect).

25
Q

Dipyridamole

-Rarely (if ever)

A

sed by itself.
-Typically used as an adjunct with warfarin or aspirin for anticoagulation post-prosthetic heart valve implantation or for a-fib.

26
Q

Dextrans are

A

heavily- branched complex glucose-based polymers.

27
Q

Dextrans

• Used as a

A 
volume expander (particularly when albumin is unavailable!)
Besides acting as a volume expander/blood viscosity reducer it has anti-thrombotic functions that are sort of ill-defined.
• Dextrans bind RBCs, platelets, and vascular endothelium making them all less “sticky”.
• Decreases Factor V, VIII, and IX functionality.
• Clots formed in the presence of dextrans are “less sturdy” and more easily lysed.
28
Q

why dextran

A

One gram of dextran binds 20-25 ml of H2O.

29
Q

dextran side effect

A 
#1) Intra-op and post-op bleeding.
#2) Volume overload, particularly in heart failure (why?) and anuric renal failure patients.
#3) Anaphylaxis is not uncommon and occurs within minutes of administration!
30
Q

dextran 70

A

macrodex bigger osmotic effect than 40

31
Q

dextran 40

A

rheomacrodex

32
Q

dextran excreted

A

by kidneys over several hours

33
Q

Dextrans max dosage

A

*MAXIMUM 2g/kg (20ml/kg)

34
Q

hespan

A

Like Dextrans, but made with a mixture of starch polymers instead of glucose polymers.
• A volume expander like Dextran. • Significantly reduces Factor VIII causing
elevated aPTT values
• Hespan usage is associated with acute renal failure, coagulopathies, and anaphylaxis.

35
Q

hespan clearance

A

Cleared similarly to Dextrans but has a real tendency to “hand around”.
• Hespan is found in the plasma months after administration.

36
Q

max daily hespan dose

A

Maximum daily dosage listed as 20ml/kg

*…but this seems to be more dogma than evidence-based.

37
Q

thrombolytics drugs

A

• Alteplase/tPA: (Activase) • Reteplase(Retavase) • Streptokinase (Streptase) • Urokinase(Kinlytic)

38
Q

thrombolytic drugs on bypass

A

never!!!

39
Q

*Unlike all the anticoagulants thrombolytics

A

hese drugs actually dissolve (“lyse”) clots that are already present in a critter.

40
Q

Streptokinase

• Not really an enzyme,

A

Streptase. but attaches to plasminogen and this complex acts to convert plasminogen into plasmin.
• This complex also destroys fibrinogen and Factors V and VII

41
Q

streptokinase used for

A

pulmonary emboli(might not work cuz of shunts), DVTs, aMIs, and thrombosed shunts

42
Q

streptokinase half life

A

less than 30 minutes

43
Q

streptokinase monitored by

A

thrombin time from bugs

44
Q

urokinase half life and what it does

A

Kinlytic. Directly converts plasminogen into plasmin to dissolve clots.
• Very short half life (~20 minutes) • Approved for use in pulmonary emboli • Made from urine (well, it could be…)

45
Q

Alteplase

A

Activase.naturally occurring enzyme from human cancer cells, tPA selectively and directly binds with plasminogen that is bound to fibrin (as in a clot.)
• In low doses, free plasminogen is hardly affected but bound fibrinogen is selectively targeted, so you get more clot lysis and less diffuse hemorrhagic problems as compared to streptokinase.

46
Q

alteplase used for/half life

A

aMIs, thombotic strokes, and pulmonary embolism.

• Very short half-life (5-30 minutes)

47
Q

Reteplase

A

Retavase. A synthetic close-relative of tPA. • Cheaper than tPA. • Less fibrin-specific than tPA.

48
Q

AT 3 half life

A

0.5-~3 days.

49
Q

types of AT 3

A

1) Made from pooled human plasma
and called Thrombate*
2) Made from the milk of genetically modified goats (I’m not making this up!) and called Atryn.

50
Q

Antithrombin

*Other major differences:

A
  • Atryn is ~40% cheaper to use than Thrombate.
  • Atryn’s half-life is ~9 hours vs. Thrombate’s ~3 days.
  • Atryn must be refrigerated, Thrombate’s stored at room temperature.. TREND TOWARDS ATRYN
51
Q

AT III is used in the treatment of

A

acquired or congenital AT III deficiency!

pharmocology (20 decks)

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