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Pharm 3 > Clotting System > Flashcards

Clotting System Flashcards

1
Q

What receptors are found on a platelet

A

Thrombin

ADP

TXA2

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2
Q

Platelet aggregation mechanism

A
  1. Collagen disrupted at injury site
  2. Platelet release ADP and TXA2, which then further activate platelet
  3. ADP binds to other platelets and activates glycoprotein receptors (GPIIB/IIIA)
  4. Fibrinogen binds to activated GPIIB/IIIA receptors forming crosslink btw platelets
  5. Platelet aggregation
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3
Q

Clotting cascade mechanism

A

XII→XIIa

XI→(Ca)→XIa

IX→IXa

VIII→VIIIa OR X→(Ca)→Xa

VII→VIIa also facilitates X→(Ca)→Xa

Prothrombin (II)→(Ca)→Thrombin (IIa)→activates platelets, factors VII, VIII, XIII

Fibrinogen→(Ca)→Fibrin→Forms clot

*Fibrinogen cross links platelets*

XIII→(Ca)→XIIIa→Stabilizes clot

As we go down, the enzymes get more significant

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4
Q

Once a clot forms what can happen?

A
  1. Can be dissolved
  2. Can be stabilized
  3. Can be permanent fibrin seal
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5
Q

What class of molecules are clotting factors? Once they are activated?

A

Factors-circulating proteins (they are enzymes)

Activated factors-Proteolytic enzymes

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6
Q

What molecule is required for synth of certain clotting factor synth?

Which factors?

A

Vit K

Factors 7, 9, 10, and Prothrombin

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7
Q

Clot formation reversal

A

Plasminogen→Plasmin→Clot lysis

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8
Q

To localize clotting:

A

Antithrombin III→Inactivation of thrombin factors IX, X, XI, XII

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9
Q

Hemophilia

A

Inadequate clotting

Genetic disorder

More likely to bleed

More likely to get joint replacement

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10
Q

Too much clotting

Thrombi in arteries

A

Results in formation of thrombus-clot that adheres to vessel wall

White thrombi-associated w/ atherosclerotic plaque

Consists of Platelets and fibrin

Ischemic damage to tissues whose blood supply is compromised

Worst case scenario: Thromoboembolis

Piece of thrombus breaks off and travels until it can’t anymore

Clog vessel→stroke, heart attack

or cause lung damage

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11
Q

Too much clotting

Thrombi in veins

A

Results in formation of thrombus-clot that adheres to vessel wall

Red thrombi-associated w/ pooling of blood in extremities

Consists of RBC and fibrin

​Ischemic damage to tissues whose blood supply is compromised

Worst case scenario: Thromoboembolis

Piece of thrombus breaks off and travels until it can’t anymore

Clog vessel→stroke, heart attack

or cause lung damage

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12
Q

When are anticoagulants used?

A
  • Thromboembolic disease
    • Prevent formation and extension of clot in venous system
    • Thrombophlebitis-If you have deep venous thrombosis
  • After surgery
    • Esp. abdominal or orthopedic surgeries
    • Or for traumatic injury repair
  • During transfusions
  • In pts w/ heart disease
    • Arrythmias (AFib)
    • MI
    • Damaged or replaced heart valves
    • Any operation on cardiovascular syst. is associated w/ increased risk of stroke
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13
Q

Calcium chelators

A

Citric acid (in blood transfusion bags(

EDTA

EGTA

Tx: Anticoagulants

Mech: Chelate Ca

Remove Ca from clotting cascade (5 steps need Ca)

We don’t give these to people b/c Ca is involed w/ lots of mechanisms

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14
Q

Heparin

A

Tx: Anticoagulant

Mech:

  • Heparin activates anti-thrombin (protease inhib) and increases its affinity for clotting factors by 1000x
    • Low doses: inhibits Xa
    • High doses: inhibits thrombin, IXa, XIa, and XIIa
  • Strong neg charge

Effects:

  • Heparin inhibits clotting in vivo and in vitro
  • Activates lipoprotein lipases in blood

Where we get it:

  • located in mast cells
  • Harvest it from cow lung and pig intestines
  • Not synthetic-each batch tested individually

Pharmacokinetics: IV or subQ

  • Too large to be absorbed in GI tract or pass placenta
    • Immediate onset–T1/2=1 hour
  • Not risk free in pregnancy though
  • Degradation via heparinase
  • Can bind to variety of proteins so dose response in unpredictable

_Toxicity: _

  • Generally non toxic
  • Major danger is bleeding
  • Overdose treated w/ protamine sulfate
    • Strong pos charge binds w/ strong neg of heparin
  • Long term use can lead to
    • Osteoporosis-act. osteoclasts
    • Thrombocytopenia-loss of platelets
      • HIT-heparin induced thrombocytopenia
      • Fibrinogen receptor inhibitors also cause thrombocytopenia
    • Hypersensitivity-rare but we are injecting animal products

Remember HAT HOT

Heparin

Anti-

Thrombin

Hypersensitivity

Osteoporosis

Thrombocytopenia

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15
Q

“-parin” drugs excluding heparin

A

Enoxaparin

Dalteparin

Tx: Anticoagulant

Low molecular wt heparins-Partially purified heparin

Activates anti-thrombin III but…

More effect on Xa than thrombin

Less osteoporosis and HIT

Longer T1/2=4 hrs

More predictable dose-response

(Smaller so don’t bind as readily to lots of proteins)

More expensive

Not readily reversed by protamine sulfate

SE: spinal hematoma in pts who have had spinal tap or anesth.

-Xabans and other -parins inhibit Xa and can cause spinal bleeding

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16
Q

Fondaparinux

A

Tx: Anticoagulant

Synthetic heparin like drug

Activates anti-thrombin III but…

Mech: only on Xa

Longest T1/2=17 hrs

Can cross placenta (heparin could not)

Can’t bind protamine

Given SubQ

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17
Q

Hirudin

A

Tx: Anticoagulant–found in leech saliva

Mech: Directly inhibits thrombin

  • Enzyme inhibitor*
  • Careful: *
  • Hirudin inhibits thrombin*
  • Heparin activates anti-thrombin*
18
Q

“-rudin”s

Other than hirudin

A

Bivalirudin

Desirudin

Tx: Anticoagulant

Synthetic analogs of hirudin

Clinical use: when patient has HIT

Skin grafts and reattaching body parts

Route: Injection

19
Q

Argatroban

A

Tx: Anticoagulant

Peptide from hirudin-diff structure, similar mech

Clinical use: when patient has HIT

Skin grafts and reattaching body parts

Route: Injection

20
Q

Warfarin

A

Tx: Anticoagulant

Mech:

  • Vit K analog–*Koagulation*
  • Inhibits enzyme that allows vit K to be recycled
    • Leads to vit K deficiency
  • Vit K is essential for factors 7, 9, 10 and prothrombin
  • Works indirectly-doesn’t directly block clotting cascade

Route: Oral

Pharmacokinetics:

  • Factor T1/2s (hrs)
    • VII–6
    • IX–24
    • X–40
    • II–60
  • So 5-6 T1/2s for 99% to be gone
    • 30-36 hrs
    • So initial onset is 24+ hours–Long half life!
  • Metabolism
    • P450
    • Lots of drug interactions
      • Phenytoin/barbituates vs grapefruit juice, etc.
    • Diet interactions
      • Lots of Vit K in green veggies

Toxicity:

  • Overdose-tx w/ Vit K
  • Hemorrhage
  • Can pass placenta-preg. category X
21
Q

Dabigatran

A

Tx: Anticoagulant

Dabigatran

Mech: Direct thrombin inhibitor

Enzyme inhibitor

Route: Oral

Kinetics:

  • Prodrug
  • Onset w/in 1 hr
  • P450 inhibitor may impact (same w/ warfarin)

SE-hemorhhage

  • What else directly inhibits thrombin?*
  • Hirudin*
22
Q

“-xaban”s

A

Tx: Anticoagulant

Mech: Factor Xa inhibitor

Think -xaban=_Ban_s factor Xa

Route: Oral

Kinetics: Rapid onset

SE: Bleeding after spinal tap or spinal injury

*Spinal bleeding with -xabans and other -parins *

23
Q

Vorapaxar

A

Tx: Anticoagulant

Mech: Platelet inhibitor

Thrombin receptor blocker on platelet

SE: Use carefully w/ pts w/ history of intracranial bleeding (like Aaron who runs into trees)

  • Intracranial pressure/bleeding contraindication for vorapaxar and opiates*
  • Mannitol decreases intracranial pressure*
24
Q

Ticlopidine

A

Tx: Anticoagulant

Mech: Platelet inhibitor

ADP receptor blocker on platelet

SE:

  • Neutropenia-loss of neutrophils
  • Agranulocytosis

“ADP receptor blocker=_Ticl_opidinde and -grels”

_A_aron’s _D_elicious _P_enis _Tic_kles the _Girls_ (Grels)

or _A_aron’s _D_ick _P_ubes (if you prefer that image)

25
Q

“-grel”s

A

Tx: Anticoagulant

Mech: Platelet inhibitor

ADP receptor blocker on platelet

Same as ticlopidine-diff is pharmacokinetics: rapid onset, shorter T1/2

“ADP receptor blocker=_Ticl_opidinde and -grels”

_A_aron’s _D_elicious _P_enis _Tic_kles the _Girls_ (Grels)

or _A_aron’s _D_ick _P_ubes (if you prefer that image)

26
Q

Abciximab

A

Tx: Anticoagulant

Mech: Platelet inhibitor

Fibrinogen receptor blocker on platelet (GPIIB/IIIA receptor)

Monoclonal antibody

Clinical use: Decrease white thrombi

Used for coronary operation

Route: IV

SE: Thromobocytopenia

Heparin and the fibrinogen receptor blockers→thrombocytopenia

27
Q

Tirofiban

A

Tx: Anticoagulant

Mech: Platelet inhibitor

Fibrinogen receptor blocker on platelet (GPIIB/IIIA receptor)

Clinical use: Decrease white thrombi

Used for coronary operation

Route: IV

SE: Thromobocytopenia

Heparin and the fibrinogen receptor blockers→thrombocytopenia

28
Q

Eptifibatide

A

Tx: Anticoagulant

Mech: Platelet inhibitor

Fibrinogen receptor blocker on platelet (GPIIB/IIIA receptor)

Clinical use: Decrease white thrombi

Used for coronary operation

Route: IV

SE: Thromobocytopenia

Heparin and the fibrinogen receptor blockers→thrombocytopenia

29
Q

Aspirin

A

Tx: Anticoagulant

Mech: Platelet inhibitor

COX (enzyme) inhibitor

Inhibits TXA2 synth

Decreases platelet aggregation

30
Q

Cilostazol

A

Tx: Anticoagulant

Mech: Platelet inhibitor

Inhibits phosphodiesterase

Inh. enzyme that breaks down cAMP

Increased cAMP→Decrease platelet agg.

  • Methyl xanthines also increase cAMP by inhibiting phosphodiesterase*
  • Opiates decrease cAMP by binding to a receptor *
31
Q

Dipryridamole

A

Tx: Anticoagulant

Mech: Platelet inhibitor

Inhibits phosphodiesterase

Inh. enzyme that breaks down cAMP

Increased cAMP→Decrease platelet agg.

  • Methyl xanthines also increase cAMP by inhibiting phosphodiesterase*
  • Opiates decrease cAMP by binding to a receptor *
32
Q

Anagrelide

A

Tx: Anticoagulant

Mech: Platelet inhibitor

Platelet count reducer

Decreases platelet formation, maturation, and #

  • Careful: This is also a -grel*
  • It’s a nag that this one is also a grel*

_A_-_na__gre_lide

33
Q

Contraindications for all anticoagulants

A
  • Anyone w/ bleeding disorder
    • Bleeding in GI tract
      • 25% of the time this goes unoticed
  • Severe hypertension
    • Start sprouting leaks
  • After surgery on eye, brain, or spinal cord
34
Q

“-kinase”s

A

Streptokinase

Urokinase

Tx: Thrombolytic agent

(dissolve formed clots)

Mech:

  • Urine plasminogen activator=Enzyme activator
  • Plasminogen→plasmin
  • Plasmin:
    • hydrolyzes fibrin
    • degrades fibrinogen
    • degrades factors V and VII

Route: IV

SE: May prolong bleeding time

35
Q

Tissue plasminogen activator (TPA)

A

Tx: Thrombolytic agent

(dissolve formed clots)

Mech:

  • Urine plasminogen activator=Enzyme activator
  • Plasminogen→plasmin
  • Plasmin:
    • hydrolyzes fibrin
    • degrades fibrinogen
    • degrades factors V and VII

Route: IV

SE: May prolong bleeding time

36
Q

Aminocaproic acid

A

Tx: Hemostatic agent (enhance clotting)

Mech: Inhibits plasminogen activation

Enzyme inhibitor

Binds to plasminogen in plasma

Route: Oral or injection

37
Q

Tranexamic acid

A

Tx: Hemostatic agent (enhance clotting)

Mech: Inhibits plasminogen activation

Enzyme inhibitor

Binds to plasminogen in plasma

38
Q

Can we make clotting factors?

A

Yes

Can be synthetically made

39
Q

What are the oral anticoagulants?

A

Warfarin (K analog–enz. inh)

-Xabans (inh Xa)

Dabigatran (direct thrombin inh)

40
Q

What anticoagulants should pregnant pts avoid?

A

Warfarin-preg risk X

Heparin-doesn’t cross placenta but not risk free

Pharm 3 (6 decks)

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