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Pharmacology III > Coagulation Disorders > Flashcards

Coagulation Disorders Flashcards

1
Q

What do disorders of clotting result from?

A

Decreased number of platelets
Decreased function of platelets
Deficiency/ abnormality of coagulation factors
Enhanced fibrinolytic activity

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2
Q

How many plasma proteins are there?

A

12 plasma proteins

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3
Q

What is the function of the plasma proteins?

A

Circulate as inactive precursors (zymogens)
This is what gets activated upon injury and stimulates the cascade.
Proteolytic rxns activate in cascade
Contribute to platelet aggregation and clot strength

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4
Q

What are the vitamin K dependent factors in the coagulation cascade?

A

II (prothrombin), VII, IX, and X

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5
Q

What are the contact activation factors in the coagulation cascade?

A

XI, XII, prekallekrein, high molecular weight (HMW) kinogen

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6
Q

What are the thrombin sensitive factors in the coagulation cascade?

A

I (fibrinogen), V, VIII, XIII

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7
Q

What is the function of the fibrinolytic system?

A

-Regulatory mechanism for maintaining blood flow
-Prevents excessive clotting
-Dissolves fibrin clots
-Plasminogen activated by tissue and urokinase plasminogen activators– Released in response to thrombin, venous stasis (big risk factor for clot development), exercise, and ischemia
Convert plasminogen to plasmin, disolve fibrin clot locally
Occurs at the location of the clot

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8
Q

What are the coagulation labs?

A

PT
INR
aPTT
D-Dimer

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9
Q

What is the PT?

A

Prothrombin time
Extrinsic clotting pathway
Time to fibrin formation after addition of thromboplastin (phospholipids and tissue factor) to plasma
Activity of Vit K dep proteins, Proteins C and S, and Factors V and XIII
Measured in seconds (~12-15)
Used with INR

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10
Q

What is INR?

A

International normalized ration
Ratio of PT patient/ PT normal
Measures extrinsic clotting along with PT

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11
Q

What is INR elevated with?

A 
Hypocoagulability
Liver disease
Vit K deficiency
Warfarin 
Normal is 0.8-1.2
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12
Q

What is aPTT?

A

Activated partial thromboplasin time.
Intrinsic and common pathways
Time to fibrin formation following addition of partial thromboplastin , calcium, and activating agent to plasma
Assesses activity of factors I, II, V, VIII, IX, X, XI, XII, prekallekrein, HMW kininogen
Measured in seconds (23-37)- varies by institution

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13
Q

When is aPTT elevated?

A

Hypocoaguability
Liver disease
Heparin

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14
Q

What is the D-Dimer?

A

A fibrin degredation product

Presence indicates plasmin is at work

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15
Q

What will the D-dimer be positive in?

A

DVT/PE

Disseminated intravascular coagulation (DIC)

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16
Q

What are the natural anticoagulants?

A 
Tissue factor pathway inhibitor (TFPI)
Protein C- inactivates Va and VIIIa
Protein S- activates protein C
Both are Vit K dep
Antithrombin III inactivates Iia, VIIa, Ixa, Xa, Xia, XIIa
Heparin potentiates this action
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17
Q

What does deficiency of the natural anticoagulants result in?

A

A hypercoagulable state

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18
Q

What is the most common congenital bleeding disorder?

A

Von Willebrand Disease

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19
Q

What is Von Willebrand Disease?

A

Decreased quantity and quality of von Willebrand factor (VFW)
Stabilizes Factor VIII, deficiency reduces half life of Factor VIII
Affects Intrinsic pathway

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20
Q

What are the three types of Von Willebrand Disease?

A
  1. Mild to moderate- most common
  2. Functionally abnormal- more severe than type 1
  3. Nearly undetectable- autosomal recessive, rare, VERY SEVERE bleeding
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21
Q

What is acquired VW disease associate with?

A

Rare, similar to disease
Associated with autoimmune disease
Mild to severe bleeding

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22
Q

What are the drug causes of acquired VW disease?

A

Valproic acid, griseofulvin, hydroxyethyl starch, ciprofloxacin

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23
Q

What is the treatment of acquired VW disease?

A

Resolves with treatment of causative disease / removal of agent

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24
Q

What are the sign and sx of acquired VW disease?

A

Mucocutaneous bleeding
Easy bruising
Postoperative bleeding

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25
Q

How do you diagnose acquired VW disease?

A 
Diagnosis based off labs and S+S
PT – normal
aPTT – prolonged: Reflection of the extrinsic pathway not working like it should. 
Platelets – normal
VWF low
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26
Q

What is the treatment of acquired VW disease for mild bleeding?

A

Goal- prevent bleeding episode

Mild bleeding: pressure, ice, apply topical thrombin

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27
Q

What is the treatment of acquired VW disease for moderate- severe bleeding?

A

Goal- prevent bleeding episode
Moderate- Severe bleeding / Prevention of bleeding(surgery)
Stimulate release of endogenous VWF/factor VIII Inhibit clot breakdown
Give exogenous VWF and Factor VIII

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28
Q

Desmopressin (DDAVP)- MOA and ROA

A

Synthetic angalog of vasopressin
Stimulates endothelial cell release of VFW and factor VIII
Intranasal and SubQ injection

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29
Q

Desmopressin (DDAVP)- ADRs

A

Tachycardia, headache, flushing, hyponatremia, transient thrombocytopenia, tachyphylaxis

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30
Q

Desmopressin (DDAVP)- monitoring

A

During infusion: pulse, BP
Factor VIII levels (increased levels 3-5X above baseline)
aPTT
Bleeding time

31
Q

What are the antifibrinolytic therapies?

A

Aminocaprioic acid

Tranexamic Acid

32
Q 
Antifibrinolytic therapy (Aminocaprioic acid
Tranexamic Acid)- MOA
A

Used alone or as adjunct for management of mucosal bleeding

Prevent lysis of clots by saturating binding sites of plasminogen- fibrin stays intact

33
Q 
Antifibrinolytic therapy (Aminocaprioic acid
Tranexamic Acid)- ADRs
A

Reduce doses in renal dysfunction
ADR:
Diarrhea, N/V, Hypotension, Thrombosis / DVT

34
Q

VWF/Factor VIII concentrates- MOA

A

Used to control severe bleeding in all patients with VW
Used in patients unresponsive to DDAVP
Replenishes VWF, and factor VIII

35
Q

VWF/Factor VIII concentrates- ADRs

A

Chills, Fever, Hypotension, Headache, Edema, THROMBOSIS/DVT, Viral infection (should have Hep A and B vaccines) (plasma> recombinant products), Anaphylaxis

36
Q

VWF/Factor VIII concentrates- monitoring

A

Factor levels

S+S bleeding

37
Q

What is hemophilia?

A

Bleeding disorder resulting from congenital deficiency of a coagulation factor

38
Q

What coagulation factor is hemophilia type A deficient in?

A

Factor VIII

39
Q

What coagulation factor is hemophilia type B deficient in?

A

Factor IX

40
Q

What type of disease is hemophila?

A

Recessive X linked diseaes ( males have it and females carry with the exception of females having deficits in both factors VIII and IX.)

41
Q

What are the signs and sx of hemophila?

A

-Palpable ecchymoses
-Hemarthroses: Joint pain, swelling, erythema, Decreased joint range of motion
-Muscle Hemorrhage: Swelling, Pain
-Hematuria
-Excessive bleeding after surgery or trauma
I-ntraccranial hemorrhage

42
Q

How is hemophila diagnosed?

A 
Suspicious in any male with unusual bleeding
Genetic testing
Labs:
Prolonged aPTT
Normal PT
Normal platelet count
Normal VWF
Reduced factor VIII or IX level
43
Q

What is the treatment for hemophilia?

A

Goal- stop bleeding
Mainstay is infusion of missing factors
Factor VIII in type A, Factor IX in type B

All patients should receive Hepatitis A and B vaccines due to risk of viral infection from products

Recombinant product < plasma product risk

44
Q

What can be used in the treatment of mild bleeding episodes in those with hemphilia A?

A

DDAVP

45
Q

What can be used as an adjunctive treatment for prevention of bleeding with dental procedures in patients with hemophilia?

A

Antifibrinolytic therapy–
Aminocaproic acid
Tranexamic acid

46
Q

Factors VIII and IX

A

Require long term prophylaxis to prevent arthropathy and complications

High cost and inconvenient due to infusion, also increased infection risk

47
Q

When is primary prophylaxis indicated with factors VIII and IX?

A

Age < 2 years, no prior bleeding events

Any age following 1 bleed and no evidence of damage

48
Q

When is secondary prophylaxis indicated with factors VIII and IX?

A

Started after onset of joint bleeding and evident damage

49
Q

Plasma derived factor VIII products

A

-From plasma of thousands of pooled donors
-Lower risk of antibody formation than recombinant
-Small risk of viral transmittance
Donor screening, plasma testing, viral reductions through purification, pasteurization to reduce risk
-No HIV since 1986
-However Hep A, Hep C, Parvovirus

50
Q

Recombinant factor VIII products

A

-Produced with recombinant DNA technology
-Low risk of transmitting disease
Small risk of viral infection from cell lines (Parvovirus) Factor VIII
No human products used to make Factor IX
-As effective as plasma-derived products
28-33% risk of developing antibodies to product

51
Q

Are human products used to make recombinant factor IX products?

A

No

52
Q

Plasma Derived Factor IX products

A
  • From plasma of thousands of pooled donors
  • Lower risk of antibody formation than recombinant
  • Small risk of viral transmittance
  • Donor screening, plasma testing, viral reductions through purification, pasteurization to reduce risk
53
Q

Recombinant Factor IX products

A
  • Produced with recombinant DNA technology
  • Very low risk of transmitting disease
  • No human products used to make Factor IX
  • Less effective than plasma-derived products
  • Require higher doses
  • Treatment of choice for hemophilia B
54
Q

What is the treatment choice for hemophilia B?

A

Recombinant Factor IX products

55
Q

Infusable factors (VIII and IX)- ADRs

A 
Chills
Fever
Hypotension
Edema
THROMBOSIS/DVT
Viral infections (plasma products > recombinant)
Anaphylactic reactions
Development antibodies
56
Q

Infusable factors (VIII and IX)- Monitoring

A

Factor Levels

S+S of bleeding/thrombosis

57
Q

Antibodies

A

-Inhibitor to Factor
-Patients may produce IgG antibodies to factors following multiple infusions
Up to ½ of patients with Hemophilia A
<5% with B
More common in severe patients
-Suspect if post-infusion factor levels are lower than predicted
-If low, antibodies can be overcome by giving higher doses of factors more frequently
If cannot overcome must give concentrated containing ACTIVATED factors

58
Q

What are the activated factors?

A

Prothrombin complex concentrates (PCC)

Recombinant activated factor VII

59
Q

Prothromin Complex Concentrates (PCC)- MOA

A

Plasma derived

Contain vit K dep factors

60
Q

Prothromin Complex Concentrates (PCC)- ADRs

A

Dizziness, nausea, hives, flushing

Serious thrombotic complications- PE, DVT, MI

61
Q

Recombinant activated factor VII- indications

A

For bleeding episodes or prophylaxis before surgery

62
Q

Recombinant activated factor VII- ADRs and monitoring

A

Monitor clinically- no labs to measure effect

ADR- hypertension, fever, thrombosis

63
Q

What other medications are used in hemophilia?

A

Hemophiliacs may need pain medications for acute or chronic pain

Intraarticular dexamethasone for joint pain

Acetaminophen or narcotics
ASA/NSAIDs may increase bleeding risk

64
Q

What is disseminated intravascular coagulation (DIC)>

A

Acquired homeostatic disorder
Due to underlying condition or illness

Inappropriate systemic thrombosis followed by massive bleeding

Severe cases require extensive supportive care

65
Q

What is the hypercoagulability pathophysiology behind DIC?

A

Hypercoagulability
Initial insult (such as sepsis) causes widespread inflammation
Leads to excessive formation of thrombin (in response to inflammation)

66
Q

What is the thrombosis pathophysiology behind DIC?

A

Thrombosis
Extensive, widespread micro and macrovascular clotting- causes ischemia and tissue damage and death
Consumes platelets and coagulations factors (due to clotting everywhere.)(Start to have no blood flow to places)

67
Q

What is the bleeding pathophysiology behind DIC?

A

Bleeding
Concomitant excessive production of plasmin cleaves fibrin in clots
Plasmin also causes RBC and platelet lysis (get purple spots all over the body)

68
Q

What are the causes of DIC?

A 
SEPSIS
CANCER
Head trauma
Serious burns
Serious crushing injuries
Amniotic fluid embolism
Aortic aneurysm
MI
Giant hemangiomas
Anaphylaxis
Transfusion reactions
Transplant rejections
Snake venom
IV drugs
69
Q

What are the signs and sx of DIC?

A 
Bleeding/oozing
Thrombosis
Petichiae/purpura
Peripheral cyanosis
Gangrene of distal extremities
Hemorrhagic bullae
70
Q

How is DIC diagnosed?

A
  • Underlying illness is present
  • May have primarily bleeding or thrombotic symptoms, or both

Labs (vary depending on stage- check serially- regularly either will improve or worsen)
Elevated PT and aPTT (usually)
Thrombocytopenia (rapid)
Elevated D-dimer and fibrin degradation products (FDP)
Decreased antithrombin III
Decreased proteins C and S
Decreased fibrinogen
Evidence of end-organ damage/failure
Must distinguish from Liver disease!
Liver disease usually has normal fibrinogen

71
Q

What is the treatment goal for DIC?

A

Prevent death and end organ damage

72
Q

What is the treatment involved with DIC?

A

Treat underlying condition
Supportive care
If serious bleeding- platelet infusion, Fresh Frozen Plasma, cryoprecipitate can be used to replace fibrinogin
Anticoagulation- only consider in thrombotic case, will not dissolve thrombi only will prevent further formation (heparin or LMWH– need to monitor D-dimer, fibrinogen, clinical signs of bleeding)
Antifibrinolytics- only consider in phase of fibronolysis/bleeding (aminocaproic acid/tanexamic acid) DO NOT COADMINISTER WITH HEPARIN)

73
Q

What treatment do you give to a patient with DIC in the bleeding phase?

A

Antifibrinolytics

74
Q

What treatment can you consider in the clotting phase of DIC?

A

Anticoagulation.

Pharmacology III (19 decks)

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