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Pharm Exam 2 > Topic 14 > Flashcards

Topic 14 Flashcards

1
Q

Plasma response to vascular injury: 1

Healthy, intact endothelium releases _____ into plasma

A

prostacyclin

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2
Q

Plasma response to vascular injury: 2

Prostacyclin binds to platelet membrane receptors, causing synthesis of

A

cAMP

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3
Q

Plasma response to vascular injury: 3

cAMP stabilizes inactive ______ receptors and inhibits release of granules containing ______ or _____

A

GP IIb/IIIa

platelet aggregation agents or Ca++

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4
Q

Plasma response to vascular injury: 4

Activated platelets cover/adhere to exposed ____ of damaged endothelium

A

subendothelial surface

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5
Q

Plasma response to vascular injury: 5

Activated platelets release what chemical mediators

A

Thromboxane A2
Serotonin
ADP
PAF

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6
Q

Plasma response to vascular injury: 6

Platelets are recruited to the ______

A

platelet plug

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7
Q

Plasma response to vascular injury: 7
After platelets go to the platelet plug- the chemical mediators that are bound to collagen from the subendothelium cause an increase in ____

A

Ca++ levels

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8
Q

Plasma response to vascular injury: 8

The elevated Ca++ causes what (3)

A
  1. release of platelet granules
  2. Activation of thromboxane A2 synthesis
  3. Activation of the GP IIb/IIIa receptors
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9
Q

Plasma response to vascular injury: 9

Fibrinolysis =

A

plaminogen –> plasmin —> Fibrin peptides

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10
Q

Plasma response to vascular injury: 10

formation of platelet fibrin plug =

A

prothrombin –> thrombin –> fibrinogen –> fibrin

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11
Q

Many functions mediated by aspirin’s ability to

A 
irreversibly bind (and inactivate) 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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12
Q

Aspirin inhibits (2)

A
  1. Platelets’ release of ADP is inhibited

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

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13
Q

Aspirin: The Thromboxanes produced by platelets

tend to help induce _______ while the Prostaglandins tend to be ________.

A

clot formation

pro-inflammatory

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14
Q

Aspirin: COX-2 produces _____ once its been modified by aspirin.

A

lipoxins

– Lipoxins are anti-inflammatory

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15
Q

Aspirin: With Thromboxanes blocked, platelets won’t

A

aggregate for the life of the platelet (a good thing in places like coronary or carotid arteries!)
–RBC live for 100 days and platelets only live a week

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16
Q

Aspirin: With Prostaglandins blocked, inflammation (such
as occurs in arthritis) is _____, nerve endings’ thresholds for pain is _____, the anterior pituitary’s “thermostat” is _______

A

decreased
increased
reset at a lower level (hence aspirin’s antipyretic effect).
*These effects are all mediated through Prostaglandins

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17
Q

Aspirin side effects:

A
  1. bleeding
  2. GI (gastric ulcers)
  3. kidney damage
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18
Q

So while it helps prevent Transient Ischemic Attacks (TIAs) and embolic strokes, it can increase the incidence of

A 
hemorrhagic strokes (particularly when given at high
levels).
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19
Q

complete platelet inactivation occurs at a dose of

A

160 mg

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20
Q

Aspirin side effects (GI gastric ulcer)=
-PGI₂ prevents gastric parietal cells from secreting ___.
-PGE₂ and PGF₂-alpha cause the stomach
and SI to create

A

HCL
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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21
Q

Aspirin side effects (kidney damage)=
Prostaglandins are largely responsible for maintaining adequate renal blood flow.
-By blocking Prostaglandin synthesis:

A

salts and fluid start to be retained, potassium isn’t excreted properly, and the kidneys are “scarred” (interstitial nephritis.)

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22
Q

Aspirin Clearance: Conjugated by the ____, cleared by the ______ so the half-life is ______

A

liver
kidneys
3.5 hours

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23
Q

Aspirin Clearance: The conjugation stage is very
______, so at higher doses over several days the half-life increases ______.
•This increased half-life dramatically increases ______

A

saturable
4-5x
renal toxicity causing a vicious cycle

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24
Q

Aspirin: other drug name

A

Acetylsalicylic Acid

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25
Q

Thienopyidines: drugs

A

Ticlopidine (Ticlid)
Clopidogrel (Plavix)
Prasugrel (Effient)

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26
Q

Thienopyidines:
like aspirin…
unlike aspirin…

A 
like= blocks platelet aggregation
unlike= different MOA
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27
Q

Ticlopidine

A

(Ticlid)

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28
Q

Clopidogrel

A

(Plavix)

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29
Q

Prasugrel

A

(Effient)

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30
Q

Thienopyidines All act by

A

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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31
Q

Ticlopidine Approved for use in the prevention of

A

TIAs and strokes

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32
Q

Ticlopidine Approved for use with aspirin post-stent placement to prevent

A

thrombi formation

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33
Q

Ticlopidine BLACK BOX WARNING for hematological disorders:

A

Aplastic anemia
Neutropenia
Thrombotic Thrombocytopenia Purpura

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34
Q

Clopidogrel: Like Ticlopidine, but less

A

side effects (although thrombotic thrombocytopenia purpurea still can occur).

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35
Q

Clopidogrel: Used more for _____ than Ticlopidine

A

cardiac “issues” (MI prevention, ACS, post-PTCA etc.)

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36
Q

Prasugrel (good news): Prasugrel’s is more effective in treating

A

thrombotic-related events than the other thienopyridines!

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37
Q

Prasugrel (bad news): Black Box Warning for

A
  • hemorrhagic stroke
  • excessive hemorrhage
  • negative sequelae resulting from sudden discontinuation of Prasugrel therapy
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38
Q

Glycoprotein IIb/IIIa Blockers: drugs

A

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

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39
Q

Abciximab

A

(Reopro)

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40
Q

Eptifibatide

A

(Integrilin)

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41
Q

Tirofiban

A

(Aggrastat)

42
Q

Glycoprotein IIb/IIIa Blockers: are all given

A

parenterally

43
Q

Glycoprotein IIb/IIIa Blockers: all used extensively for

A

CS and in cath labs

44
Q

Glycoprotein IIb/IIIa Blockers:
drug with highest death or nonfatal MI=
drug with lowest death or nonfatal MI=

A 
highest= Abciximab
lowest= Tirofiban
45
Q

Dipyridamole (Persantine) Primarily used as a

A

coronary vasodilator

46
Q

Dipyridamole

A

(Persantine)

47
Q

Dipyirdamole blocks

A 
cyclic AMP (cAMP) which is a ubiquitous intracellular
“messenger” chemical derived from that ubiquitous cellular energy currency, ATP
48
Q

Dipyirdamole: After a chain of intracellular miracles

A

Thromboxane A₂ synthesis is blocked (no prostaglandin effect).

49
Q

Dipyridamole: Rarely (if ever) used by itself-Typically used as an adjunct with

A

warfarin or aspirin for anticoagulation post-prosthetic

heart valve implantation or for a-fib.

50
Q

Dextrans are heavily-branched complex

A

glucose-based polymers.

51
Q

Dextrans: First discovered by

A

Louis Pasteur as a component of wine.

52
Q

Dextrans: Used as a volume expander- particularly when

A

albumin is unavailable

53
Q

One gram of dextran binds to

A

20-25 ml of H₂O

54
Q

Dextrans= Two kinds:

A 
Dextran 70 (Macrodex)
Dextran 40 (Rheomacrodex)
55
Q

Dextran 70

A

(Macrodex)

56
Q

Dextran 40

A

(Rheomacrodex)

57
Q

how are dextrans given

A

parenterally

58
Q

dextrans may be used as part of a

A

pump prime protocol

59
Q

Dextran 70 has somewhat ________ than Dextran 40

A

greater osmotic capabilities

60
Q

Both dextran 40 and 70 are mostly excreted by the

A

kidneys over several hours and the rest metabolized

61
Q

Dextrans: Besides acting as a volume expander/blood viscosity reducer it has

A

anti-thrombotic functions that are sort of ill-defined

62
Q

Dextrans bind ___, ___, and ___ making them all less “sticky”.

A

RBCs, platelets, and vascular endothelium

63
Q

dextrans decrease what factors functionality

A

Factor V, VIII, and IX (5, 8, 9)

64
Q

Clots formed in the presence of dextrans are

A

“less sturdy” and more easily lysed.

65
Q

Dextrans Concerns & Side Effects (3)

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!
66
Q 
Dextrans Typical Dosages:
Infants
Children
Adults
Max
A

Infants: 0.5g/kg (5ml/kg)
Children: 1.0g/kg (10ml/kg)
Adults: 1-2g/kg (10-20ml/kg)
*MAXIMUM 2g/kg (20ml/kg)

67
Q

Hespan: Like Dextrans, but made with a

A

mixture of starch polymers instead of glucose polymers.

68
Q

hespan is a ________ like Dextran

A

volume expander

69
Q

hespan significantly reduces Factor ___ causing elevated ______

A

VIII

aPTT values

70
Q

Hespan usage is associated with

A

acute renal failure, coagulopathies, and anaphylaxis

71
Q

Hespan: Cleared similarly to Dextrans but has a

A

real tendency to “hand around”.

72
Q

Hespan is found in the plasma _____ after administration

A

months

73
Q

Hespan *Maximum daily dosage listed as

A

20ml/kg

74
Q

Thrombolytics: drug names

A

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

75
Q

Alteplase/tPA

A

(Activase)

76
Q

Reteplase

A

(Retavase)

77
Q

Streptokinase

A

(Streptase)

78
Q

Urokinase

A

(Kinlytic)

79
Q

You will never give Thrombolytics, particularly on

A

bypass

80
Q

Thrombolytics *Unlike all the anticoagulants mentioned so far, these drugs actually dissolve

A

(“lyse”) clots that are already present in a critter. [but you dont give them if you see a clot form in the VR]

81
Q

Streptokinase: Not really an enzyme, but attaches to plasminogen and this complex acts

A

to convert plasminogen into plasmin.

and to destroy fibrinogen and Factors V and VII

82
Q

Streptokinase: Approved for

A

pulmonary emboli, DVTs, aMIs, and thrombosed shunts

83
Q 
Streptokinase:
Half life:
Given how:
Monitored by the:
Made from:
A

Half life: short (<30 minute)
Given how: given within 4 hours of an MI via slow infusion
Monitored by the: Thrombin Time (TT)
Made from: bugs

84
Q

Urokinase: Directly converts

A

plasminogen into plasmin to dissolve clots

85
Q

Urokinase:
Half life:
Approved for:
Made from:

A

Half life: Very short (~20 minutes)
Approved for: pulmonary emboli
Made from: urine (well, it could be…)

86
Q

Urokinase: Certain malignant tumors produce

urokinase to help “invade” tissues=

A

“Mesupron” acts as a urokinase Plasminogen Activator (uPA) Inhibitor non-cyto toxic chemotherapeutic

87
Q

Alteplase: A naturally occurring enzyme from human cancer cells, tPA…

A

selectively and directly binds with plasminogen that is bound to fibrin (as in a clot.)

88
Q

Alteplase: In low doses, free plasminogen is hardly affected but bound fibrinogen is

A

selectively targeted, so you get more clot lysis and less diffuse hemorrhagic problems as compared to streptokinase

89
Q

Alteplase:
Used for:
Half Life:

A

Used for: aMIs, thombotic strokes, pulmonary embolism.

Half life: Very short (5-30 minutes)

90
Q

Reteplase: A synthetic close-relative of

A

tPA

  • -Cheaper than tPA
  • -Less fibrin-specific than tPA
91
Q

Out of Alteplase, Streptokinase and Urokinase- which has the highest antigenicity

A

Streptokinase

92
Q

Out of Alteplase, Streptokinase and Urokinase- which has the highest fibrin specificity

A

Alteplase and Urokinase equally

93
Q

Out of Alteplase, Streptokinase and Urokinase- list them in order of longest half life to the shortest

A

Streptokinase
Urokinase
Alteplase

94
Q

Antithrombin (AT): [AT III]
Made in the:
Half live:
Works with:

A

Made in the: small protein made in the liver.
Half live: 0.5 ~3 days
Works with: heparin to effect anticoagulation

95
Q

Normal AT III has a mild effect on

A

Thrombin and Factors IXa and Xa. That effect is multiplied by thousands to millions of times when combined with
heparin.

96
Q

Antithrombin: Two types available:

A

1) Made from pooled human plasma and called Thrombate*
Antithrombin
2) Made from the milk of genetically modified goats and called Atryn*

97
Q

Atryn is ___% cheaper to use than Thrombate

A

~40%

98
Q

Atryn’s half-life is ___ vs. Thrombate’s ______

A

Atryn ~9 hours

Thrombate ~3 days

99
Q

Atryn must be ______, Thrombate’s stored at _____

A

Atryn: refrigerated
Thrombate: room temperature

100
Q

Recent perfusion trend is away from Thrombate use and towards

A

Atryn

101
Q

AT III is used in the treatment of

A

acquired or congenital AT III deficiency!

Pharm Exam 2 (9 decks)

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