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pharm exam 2 > Topic 14 Platelet Blockers > Flashcards

Topic 14 Platelet Blockers Flashcards

1
Q

Aspirin &/or called?

A

Acetylsalicylic Acid

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2
Q

Many functions are mediated by aspirin’s ability to irreversibly bind (and inactivate) what enzyme ?

A

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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3
Q

once COX-2 has been modified by aspirin it produces what?

A

lipoxins

Lipoxins are anti-inflammatory

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4
Q

Lipoxins are what?

A

anti-inflammatory

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5
Q

Aspirin inhibits platelets ability to do what?

A

–Platelets’ release of ADP is inhibited

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

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6
Q

Thromboxanes produced by platelets tend to help what?

A

help induce clot formation while the Prostaglandins tend to be pro-inflammatory

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7
Q

Prostaglandins tend to be what?

A

Pro-inflammatory

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8
Q

Aspirin function - With Thromboxanes

blocked, platelets won’t aggregate for how long

A

for the life of the platelet

–a good thing in places like coronary or carotid arteries!

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9
Q

RBCs live how long?

A

100 days

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10
Q

Platelets live how long?

A

8-9 days

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11
Q

four major clinical applications for aspirin

A

fever
inflammation
joint pain
platelet aggregation/clot/thrombosis

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12
Q

when aspirin is given – platelets cant aggregate what 4 things can be prevented?

A

Thrombotic stroke
Deep MI
Pulmonary Emboli
Venous emboli

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13
Q

Aspirin side effects

A

bleeding
COMPLETE PLATELET ACTIVATION -occurs at a dose of 160mg
GI (like gastric ulcers)
Kidney damage

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14
Q

Aspirin dose that causes complete platelet activation

A

160mg

this has big variability/ not true but use

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15
Q

Aspirin GI side effects (like ulcers) are caused how (cellularly)?

A

-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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16
Q

PGF2 alpha also causes what in animals and can be ppl?

A

pus filled uterus

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17
Q

How does Aspirin cause kidney damage ?

A

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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18
Q

Prostaglandins are largely responsible for what in the kindeys?

A

for maintaining adequate RBF

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19
Q

Aspirin Clearance where? T1/2

A

Conjugated by the liver, cleared by the kidneys so the half-life is 3.5 hours

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20
Q

The conjugated stage of Aspirin in the liver is very saturable. what does this mean for T1/2?

A

so at higher doses over several days the half-life increases 4-5X

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21
Q

Ticlopidine

A

(Ticlid)

Thienopyidines (pts coming fromcath lab will be on these prob)
Like aspirin: Block platelet aggregation
Unlike aspirin: Different M.O.A

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22
Q

Clopidogrel

A

(Plavix)

Thienopyidines (pts coming fromcath lab will be on these prob)
Like aspirin: Block platelet aggregation
Unlike aspirin: Different M.O.A

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23
Q

Prasugrel

A

Effient

Thienopyidines (pts coming fromcath lab will be on these prob)
Like aspirin: Block platelet aggregation
Unlike aspirin: Different M.O.A

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24
Q

Thienopyidines - what do they inhibit/block ?

A

act by irreversibly inhibiting the ADP pathway of platelets…
•This blocks platelets’ GPIIb/IIIa receptors.
•Consequently, affected platelets can’t bind to each other or to fibrinogen

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25
Q

Which Thienopyidine is Approved for use in the prevention of TIAs and strokes
and for use with aspirin post-stent placement to prevent thrombi formation

A

Ticlopidine (Ticlid)

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26
Q

Ticlopidine (Ticlid) has what kind of warnings?

A

Black Box Warnings for hematological disorders

  • Aplastic anemia (not producing more cells)
  • Neutropenia
  • Thrombotic Thrombocytopenia Purpura (low levels of platelets bc you get these little clots that use up all the platelets and you get purple splotches)
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27
Q

what is Neutropenia

A

the presence of abnormally few neutrophils in the blood, leading to increased susceptibility to infection.

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28
Q

Clopidogrel (Plavix) is used more for what as compared to Ticlopidine

A

Used more for cardiac “issues” (MI prevention, ACS, post-PTCA etc.) than Ticlopidine

29
Q

Prasugrel’s (Effient) is more effective in treating what events than other thienopyridines!?

A

thrombotic-related events

30
Q

Prasugrel (effient) Black Box Warning?

A

for hemorrhagic stroke, excessive hemorrage and negative sequelae (a condition that is the consequence of a previous disease) resulting from sudden discontinuation

31
Q

Glycoprotein IIb/IIIa Blockers (3)

A

Abciximab (Reopro)
Eptifibatide (Integrilin)
Tirofiban (aggrastat)

32
Q

Abciximab

A

Reopro

Glycoprotein IIb/IIIa Blockers

33
Q

Reopro

A

Abciximab

Glycoprotein IIb/IIIa Blockers

34
Q

Epitifibatide

A

Integrilin

Glycoprotein IIb/IIIa Blockers

35
Q

Tirofiban

A

Aggrastat

Glycoprotein IIb/IIIa Blockers

36
Q

Integrilin

A

Eptifibatide

Glycoprotein IIb/IIIa Blockers

37
Q

Aggrastat

A

Tirofiban

Glycoprotein IIb/IIIa Blockers

38
Q

Glycoprotein IIb/IIIa Blockers are all used extensively for what?

A

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

39
Q

Dipyridamole

A

Persantine

primarily a coronary vasodilator

40
Q

Persantine

A

Dipyridamile

primarily a coronary vasodilator

41
Q

Dipryidamole (Persantine) how is it used?

A

Rarely (if ever) used by itself.
-Typically used as an adjunct with warfarin or aspirin for anticoagulation post-prosthetic heart valve implantation or for a-fib

42
Q

Dextrans what are they?

A

glucose based polymers - can be made positive or negative

43
Q

Dextrans - what are they used as? why

A

used as a volume expander

BC - One gram of dextran binds 20-25 ml of H2O (same effect as albumin)

44
Q

Two kinds of Dextrans?

A
  • Dextran 70 (Macrodex)
  • Dextran 40 (Rheomacrodex)

May be used as part of pump prime
Both mostly excreted by the kidneys over several hours and the rest metabolized

45
Q

Dextran – do what to RBCs? and do what to clots?

A

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.

46
Q

Dextran side effects ? (3) - (#2 is the most important)

A 
#1) Intra-op and post-op bleeding.
#2) Volume overload, particularly in heart failure and anuric renal failure patients.
#3) Anaphylaxis is not uncommon and occurs within minutes of administration
47
Q

Dextrans Typical MAX Dosage to put in prime

A

2g/kg (20ml/kg)

48
Q

Hespan is made with what?

A

a mixture of starch polymers (instead of glucose polymers - like dextrans)

49
Q

Hespan does waht?

A

volume expander

sig reduces FVIII causing elevated aPTT

50
Q

Hespan side effects?

A

Acute renal failure, coagulopathies and anaphylaxis

51
Q

Hespan MAX daily dosage

A

20ml/kg

52
Q

Alteplase/tPA

A

Activase

Thrombolytics

53
Q

Reteplase

A

Retevase

Thrombolytics

54
Q

Streptokinase

A

Streptase

Thrombolytics
Approved for pulmonary emboli, DVTs, aMIs, and thrombosed shunts

55
Q

Urokinase

A

Kinlytic

Thrombolytics
Approved for use in pulmonary emboli

56
Q

Thrombolytics - when will you give these?

Alteplase, Reteplase, Streptokinase, Urokinase

A

YOU WILL NEVER GIVE THESE! ESP NEVER ON BYPASS

57
Q

Thrombolytics end in what ?

A

ase

58
Q

What do Thrombolytics do?

A

they actually dissolve “lyse” clots that are already present. cant put in your reservoir

59
Q

Streptokinase (streptase) attaches to what ? to convert what?

A

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

60
Q

Urokinase (kinlytic) converts what to do what?

A

Directly converts plasminogen into plasmin to dissolve clots

61
Q

Altepase/tPA (activase) used for?

A

Used for aMIs, thombotic strokes, and pulmonary embolism

62
Q

Antithrombin III works with what to effect anticoagulation?

A

AT III works with heparin to effect anticoagulation

effect is multiplied by thousands to millions of times when combined with heparin

63
Q

ATIII is made where?

A

liver (its a small protein)

64
Q

Thrombate

A

Is a type of ATIII

Made from pooled human plasma

65
Q

Atryn

A

Is a type of ATIII

Made from the milk of genetically modified goats

66
Q

Differences btwn the two types of ATIII - Atryn and Thrombate?

A

Atryn 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
67
Q

Which ATIII do we use?

A

Recent perfusion trend is away from Thrombate use towards Atryn

68
Q

When do we administer ATIII?

A

AT III is used in the treatment of acquired or congenital AT III deficiency

pharm exam 2 (9 decks)

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