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PCOL2 > Fibrinolytics > Flashcards

Fibrinolytics Flashcards

1
Q

What are the three things in Virchow’s triad?

A
  1. endothelial injury
  2. altered blood flow (low movement, e.g. DVT)
  3. abnormal coagulability (e.g. pregnancy)
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2
Q

Venous thromboses are usually associated with ___________ and have many ___________, whereas arterial thromboses are most often caused by __________ and _______ are predominant.

A

Venous (red thrombus): stasis; RBCs

Arterial: atherosclerosis (white thrombus); platelets (and leukocytes).

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3
Q

What is the significance of thrombin (factor IIa) in the coagulation cascade?

A

Active thrombin catalyses the conversion of fibrinogen to fibrin - the insoluble fibre mesh that stabilises clots.

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4
Q

What is the ultimate goal of coagulation cascade?

A

The conversion of fibrinogen to fibrin.

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5
Q

What active factor activates thrombin from prothrombin? (i.e. IIa from II)
What is the meeting point of the intrinsic and extrinsic pathways?

A

Xa (activated from X)

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6
Q

What can activate factor X?

A

VII:TF, XII and IX.

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7
Q

Which factor is synonymous with “prothrombin activator?”

A

Xa

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8
Q

What complex in the intrinsic pathway activates factor X?

A

IXa:XIIa

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9
Q

What complex in the intrinsic pathway activates factor X?

A

IXa [:XIIa]

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10
Q

Which of the three main groups of anti-clotting drugs is good for arterial thrombi? Why?

A

Antiplatelets (e.g. aspirin) because platelets predominate in white thrombi.

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11
Q

What kind of thrombi are warfarin and heparin used to treat? Red or white?

A

RED.

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12
Q

Seems we just have to know that prostaglandins [and calcium] are essential to the overall process. Where do the prostaglandins come from?

A

PLATELETS provide the prostaglandins.

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13
Q

What is the main endogenous anticoagulant mentioned in this lecture?

A

Antithrombin III (ATIII)

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14
Q

What factors depend on vitamin K for synthesis?

A

II, VII, IX, X also protein C and S

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15
Q

Which factors are serine proteases (easy to remember)?

- ATIII neutralises serine proteases.

A

XII, XI, X, XI and II

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16
Q

[These factors depend on vitK for synthesis]

[These factors are neutralised by ATIII/heparin]

A

VitK: II, VII, IX, X also proteins C and S.
ATIII: XII, XI, X IX, II

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17
Q

What DOESN’T heparin help to neutralise?

A

VII.

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18
Q

What’s the exam example of a LMWH?

A

Dalteparin

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19
Q

Does unfractionated heparin have zero or first order kinetics?

A 
Zero
Half life (40-90mins) increases with dose.
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20
Q

How do you administer heparin? 3 steps.

A
  1. Give IV bolus
  2. maintain with constant rate IV
  3. Use in vitro APTT to adjust dose.

half life 40-90mins

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21
Q

What can unfractionated heparin neutralise that LMWH can’t?

A

Factor IIa.

So UFH: IIa and Xa (mainly), and
LMWH: Xa only

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22
Q

3 risky patients for heparin

ARL be sure to watch out for heparin side effect.

A

Aspirin
Liver problems
Renal failure

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23
Q

What’s the antidote to pull the breaks on heparin?

basic bitch being like “these protons are mine”

A

Protamine

binds ACIDIC UFH.

24
Q

UFH would come in a ______ and LMWH would come in a _______.

A

UFH: tubey needle to go into the canula
MFWH: hyperdermic needle for SC.

25
Q

List the 3 pros of LMWH compared to UFH?

A
  1. predictable FIRST ORDER kinetics.
  2. they DON’T PROLONG APTT (no need to monitor)
  3. just as effective, and self administerable
26
Q

Renal problems are risky when administering heparin. If the patient said yes to renal problems, could you hook him up or just jab him?

A

Hook him up.

That is, IV UFH, not subcutaneous LMWH.
Because LMWH is renally excreted.

27
Q

Why is it patients get so much heparin they could bleed spontaneously?

A

Because thrombotic IIa is less susceptible to heparin than circulatory IIa, we need to dose the person up until we can deal with the thromus.
Hence, resolving the clot with heparin leaves us with very IIa-poor blood.

28
Q

What is an γ-carboxyglutamic acid residue?

A

That the PTM that requires vitamin K for factors II, VII, IX and X.

29
Q

What is the actual target of warfarin?

A

Vitamin K reductase.

30
Q

Briefly explain how warfarin prevents

A

Vitamin K is needed for essential post modifications of factors II, VII, IX, X and proteins C and S. In the PTM reaction, vitamin K is consumed by the process in a 1:1 fashion.
o By consumed, we mean oxidised.
Normally, vitamin K reductase replenishes the pool of vitamin K, allowing normal production to take place.
vitamin K reductase is inhibited by warfarin.

31
Q

What are those other things in addition to factors II VII IX and X that warfarin prevents?
Imagining poisoning CS Lewis slowly with warfarin until he bleeds to death.

A

Anticoagulant proteins C and S.

32
Q

Two reasons why warfarin needs so long to set on?

Bonus: is warfarin absorbed slowly or rapidly?

A

Staggering plasma binding
Mode of action (we need to wait for all existing targets to deplete naturally).

Bonus: rapid absorption

33
Q

What’s responsible for the initial hypercoagulability brought on by warfarin?

A

Reduction in anticoagulant protein C.

34
Q

What’s the International Normalised Ratio (INR)?

A

(Patient’s prothrombin time)(control prothrombin time)

35
Q

What IFN is a risk of clotting?
What IFN is a risk of bleeding?
What’s normal?

A
  1. 5
  2. 0
  3. 9-1.3
36
Q

Warfarin. Hepatic or liver clearance?
It’d be hard to clear CS Lewis from this earth in a darstardly way because he’s so distant. Hard to kill someone when they LIVE FAR away.

A

HEPATIC.

37
Q

When do we switch from heparin to warfarin?

A

Once the INR is back to normal for at least 48 hours.

38
Q

A lot of things can potentiate warfarin activity. What are 4?

A

Liver disease (clotting factor synthesis)
Antiplatelet drugs
CP450 inhibitors (there are MANY)
Warfarin albumin-displacers

39
Q

What 4 factors reduce warfarin effect?

A

Pregnancy
Hyperthyroidism (lowers factor degradation)
CP450 inducers (many)
Absorption inhibition (cholestyramine)

Bonus: vitamin K obviously

40
Q

What’s cholestyramine?

A

That’s a drug that inhibits warfarin binding in the stomach.
Not of high importance.

41
Q

Be familiar with areas you’d use use oral anticoagulants as a prophylactic.

A 
Deep vein thrombosis
Coronary embolism
Cardiac prostheses
Stable angina
During haemodialysis
42
Q

What two things do platelets do once they adhere to a vessel wall that sets off coagulation?

A

Release granular contents

Expose acidic phospholipids

43
Q

Aspirin inhibits COX, so no TXA2 or TXA2. Normally these cause vasoconstriction, but what’s the main thing they do that precipitates the coagulation?

A

Induce surface expression of GPIIb/IIIa.

This GP IIb/IIIa provides the anchor point for fibrinogen..

44
Q

Clopidogrel is pretty damn expensive. Who is it reserved for? Where else?

A

Patients who can’t tolerate aspirin.

In combination with aspirin for a cardiac emergency.

45
Q

What does copidogrel bind to? What does that prevent?

A

P2Y12 receptors on platelets - that’s the protein with which platelets adhere to each other.

46
Q

What P450 CV doctors hate?

A

P2C19.

Lotta polymorphisms.

47
Q

What P450 metabolises clopidogrel?

A

2C19

48
Q

Why is it difficult to predict clopedigrel metabolism interpersonally?

A

Because it’s metabolised by 2C19, which is infamous for its many polymorphisms.

49
Q

What is the only anti-GPIIb/IIIa Ken would use in a question?
Let’s ban tire fires. When they stack up like that it just causes problems.

A

Tirofiban

Platelet piles look like tire piles.

50
Q

Which TWO drugs in this lecture can’t be given with renal failure (or have to be dose adjusted?)

A

LMWH (contraindicated)

Tirofiban

51
Q

Be aware, because we don’t trust Francis, that another antiplatelet is…
Highly fancy plates are used by this one really rich mole who lives in a pyramid rather than a hill. He needs to die for wealth to redistribute.

A

dipyridamole.

52
Q

Plasminogen sits on fibrin and waits to be activated by _________, whereupon it will cleave up the fibrin.

A

Plasminogen activators. Easy.

Bonus: e.g. tPA

53
Q

T or F: Tenecteplase (and all the -teplases) are recombinant streptokinase.

A

FALSE

The -teplases are recombinant tPA.

54
Q

What is tPA?

A

A plasminogen activator

55
Q

What are the -teplases?

A

They are recombinant tPA.

56
Q

Everyone who presents within 12h or STEMI gets fibrinolytics. T or F?

A

True

57
Q

When could you use PCI [+ fibrinolytics] instead of fibrinolytic monotherapy?

A

When you’re a big rich hospital and you can afford to do it and you have someone on hand who can perform it.

PCI first choice wherever possible.

PCOL2 (24 decks)

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