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pharmocology > blood 2 direct and indirect thrombin inhibitors > Flashcards

blood 2 direct and indirect thrombin inhibitors Flashcards

1
Q

anticoagulants

A

inhibit one or more steps in the clotting cascade that lead to fibrin formation…
*They do NOT dissolve clots!

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2
Q

heparin why so acidic?

A

indirect thrombin inhibitormany carboxyl and sulfate groups are attached (and virtually all critters produce heparin, even ones lacking “traditional blood”, so it’s an ancient molecule on the evolutionary tree.)

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3
Q

Heparin “lives” in

A

mast cells (basophils)

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4
Q

mast cells produce

A

histamine

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5
Q

Unfractionated heparin size

A

5000-30,000 Daltons h2o is 10

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6
Q

heparin is measure in

A

units

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7
Q

What’s One (1) Unit of Heparin?

A

The quanTiTy of heparin required to keep 1 milliliter of caT’s blood fluid for 24 hours at 0° C”
“No way!”
• This is ~~0.002 mg of heparin/unit.

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8
Q

porcine intestinal derived heparin better in avoiding

A

HIT

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9
Q

TWO MAIN SOURCES OF HEPARIN

A

PORCINE INTESTINE, BOVINE LUNG

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10
Q

heparin always given

A

parentally

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11
Q

fractionated heparin weight

A

5500 daltons

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12
Q

fractionated heparin onlt works on___ but

A

one part of coag. t’s much more uniform, contains less “contaminants” and inactive forms of heparin.

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13
Q

heparin increase at3 activity by

A

1000

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14
Q

unfractionated heparin accelerates both

A

AT3 INTERACTION WITH BOTH THROMBIN AND FACTOR Xa

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15
Q

fractionated heparin accelerates

A

at3 interaction with Xa

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16
Q

only reason we dont use LMWH is

A

(lovenox) because it is not as efficaious in anticoagulatin

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17
Q

IV half life of heparin

A

2 hours. 4 hours for LMWH

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18
Q

SETTING OF THERAPY FOR TWO TYPES OF HEPARIN

A

HOSPITAL. hospital and outpatient for LMWH

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19
Q

MAJOR EFFECT OF BOTH HEPARIN

A

TOO MUCH BLEEDING AND TOO LITTLE FOR LMWH

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20
Q

BIOAVAILABILITY OF BOTH HEPARIN

A

20 for unfractionated, 90 for LMWH

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21
Q

PREDCTABILITY OF BOTH HEPARIN

A

lmwh more predictable

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22
Q

heparin uses

A

lab samples,orthopedic surgery, pregnancy, flush for cell savers/lines, dialysis machines,circuits

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23
Q

heparin pharmokinetics time to effect:

A

Time to effect: – Intravenous (IV): a few minutes – Subcutaneous (SQ): 1-2 hours
• Heparin is cleared by binding to macrophages and being depolymerized and desulfonated in the liver…
• …and the metabolites • are excreted in the • urine.

24
Q

half life of heparin is prolonged

A

by either renal &/or liver dysfunction. Unfractionated heparin’s half-life is ~1-2 hours (a source of constant controversy amongst perfusionists).
*Fractionated (LMWH) has a much longer half-life (3-7 hours).

25
Q

Lower doses of heparin are cleared at a

A

faster rate than higher higher doses (implying that the process is saturable).

  • Since it’s a metabolic process, heparin clearance is (naturally) slower at lower temps and accelerated at higher temps.
  • Heparin is chemically reversed with Protamine
26
Q

side effects of heparin

A

bleeding,HIT,

27
Q

fondaparinux half life

A

(arixtra) A synthetic LMWH (a pentasaccharide). • Half-life of ~20 hours and eliminated
unchanged in the urine.

28
Q

major advantage of fondaparinux

A

major advantage is the elimination of the risk of “bad” (Type II) HIT.

29
Q

warfarin what it is and how it works

A

(coumadin) indirect thrombin inhibitor. widely prescribed orally administered anticoagulant.
* Works by inhibiting Vitamin K (phytonadione/Mephyton) slow acting because you have ton use all vitamin k

30
Q

warfarin how it inhibits vitamin k

A

blocks an enzyme (creatively named Vitamin K epoxide reductase)
• Vitamin K epoxide reductase is required to allow the liver to “recycle” spent (oxidized) Vitamin K so eventually stores of Vitamin K are simply depleted.

31
Q

Warfarin is NOT

A

Vitamin K antagonist (it doesn’t have antagonist kinetics)…
…so giving the critter Vitamin K readily reverses the effects of warfarin.

32
Q

liver requires vitamin k to produce

A

II: Prothrombin VII: Proconvertin
IX: Plasma Thromboplastin Component X: Stuart-Prower Factor

33
Q

warfarin and protein c +s

A

(which are also anticoagulants via their ability to block factors Va and VIIIa).
– Consequently, the liver produces incomplete, biologically inactive molecules instead of functioning clotting factors.

34
Q

akes a while for Warfarin to exert its clinical effect (8-24 hours) since

A

hose Vitamin K stores have to be depleted.

• Peak effects occur ~2-4 days (once those stores are completely empty)

35
Q

warfarin half life and duration is

A

nsanely variable! PLUS it’s highly protein-bound (SO what?)
• Drugs, genetics, foods, spices (!), etc. all effect how long it lasts!
-”Normally” ~ 40 hrs

36
Q

warfarin used to

A

prevent pulmonary embolism, VAD,DVT,artificial valves,afib,

37
Q

warfarin side effects

A

bleeding#1,Birth/fetal deformities &/or death. • Warfarin necrosis (typical in obese women)

38
Q

Warfarin Dosing

A

typical dose is 5-7mg/day with adjustments made after ∽ one week.

39
Q

warfarin monitoring

A

Warfarin typically monitored via the prothrombin time (PT).

  • So, the PT measures the activity of which factors? intrinsic activity
  • ”Normal” PTs vary from lab to lab (due to reagent variability, mostly)
40
Q

added to warfarin when monitoring

A

tissue Factor (Factor III) and Calcium (Factor IV) are added to the critter’s plasma.

41
Q

normal pt range

A

80-120%

42
Q

INR

A

INTERNATIONAL NORMALIZED RATIO. INR = critters PT/LAB NORMAL PT MEAN

43
Q

lepirudin

A

(refludon). direct thrombin inhibitor. bivalently and irreversibly to thrombin. no reversible agent

44
Q

lepirudin cleared

A

by kidneys

45
Q

leprrudin half life…..

A

1 hour but can increase because antibodies can decrease clearance especially in kidney failure

46
Q

monitoring lepirudin

A

heir aPTTs and renal functions monitored.

47
Q

bivalirudin

A

angiomax. completely synthetic yet chemically smaller
“cousin” of hirudin.
• Like hirudin, it’s also a bivalent direct thrombin inhibitor, operates independent of AT III, and is given parenterally.
Relatively expensive!

48
Q

bivalirudin clearance

A

less renal clearance than lepirudin (20%)

49
Q

bivalirudin half life depending on kidney function

A

– Mod. renal dysfunction: half-life ~35 minutes – Severe renal dysfunction: half-life ~1 hour – Dialysis patient: half-life ~3.5 hours. can be removed with hemoconcentrators

50
Q

Bivalirudin

• Very commonly used during PTCAs to prevent

A

platelet activation.

*Also commonly used for anticoagulation for patients with HIT (we’ll discuss this more later.)

51
Q

bivalirudin Monitoring

*Ideally, anticoagulation (as on bypass) is measured with the

A

ecarin clotting time” (ECT)

52
Q

argatroban half life,clearance, monitoring

A 
parenterally-administered small molecule
direct thrombin inhibitor.
• Shorthalf-life(~40-50minutes).
• Clinical use similar to Angiomax but monitored with aPTTs.
•
*Eliminated by hepatic clearance
53
Q

Angiomax vs. Argatroban

A

Essentially, the choice is made by whether the patient has intact renal or hepatic function (which drug with which condition?)
…and ease of monitoring the anticoagulation

54
Q

Dabigatran etexilate

A

pradaxa. An oral anticoagulant cleared by the kidneys that also acts as a direct thrombin inhibitor
– A possible future replacement for oral warfarin (don’t need to test INRs, fewer drug interactions, less variable half- life)
– Currently used for a-fib (why?) cood place for clots

55
Q

apixiban and rivaroxaban

A

eliquis, xarelto. Both are oral anticoagulants that directly
inhibit Factor Xa
– Both are cleared renally and used for a-fib

pharmocology (20 decks)

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