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Pharm II > (3-08-17) Bleeding Disorders and Assessments > Flashcards

(3-08-17) Bleeding Disorders and Assessments Flashcards

1
Q

what makes up the hemostasis tripod?

A
  • Primary hemostasis (platelets)
  • coagulation (chemical process)
  • vasoconstriction (mechanical process)

*all of these are balanced by ANTIcolagulant activity which prevents excessive coagulation and keeps blood flowing appropriately

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2
Q

what occurs in primary hemostasis?

A
  • platelets adhere to disrupted vessel wall (glycoprotein receptor Ib)(von willebrand factor)
  • platelets adhere to one another (glycoprotein IIb/IIIa)(fibrinogen)
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3
Q

what factors allow platelets to adhere to disrupted vessel wall in primary hemostasis?

A

glycoprotein IB

von willebrand factor

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4
Q

what factors allow platelets to adhere to each other ?

A

glycoprotein IIb/IIIa

fibrinogen

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5
Q

what two things do arachidonic acid vasoconstrictors release?

A
  • thromboxane A2

- prostaglandins (PGs)

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6
Q

what two things do platelets surfaces provide?

A
  • generation of thrombin

- subsequent fibrin formation

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7
Q

what is the extrinsic system of the coagulation cascade?

A
  1. TF exposed to blood
  2. TF then binds and activates factor VII to factor VIIa
  3. TF-VIIa then activates X to Xa
  4. Xa then converts prothrombin(II) to thrombin (IIa)

*this is most effective in the presence of phospholipid surface

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8
Q

what is the instrinsic (secondary) system of the coagulation cascade

A
  1. TF exposed to blood
  2. TF then binds and activates factor VII to factor VIIa
  3. TF-VIIa activate IX to IXa
  4. IXa uses cofactor VIII to activate X to Xa
  5. Xa then converts prothrombin (II) to thrombin (IIa)

*only small differences from extrinsic system

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9
Q

what is the 3rd pathway for the coagulation cascade?

A
  • thrombin itself activates XI to XIa
  • XIa activates IX to IXa
  • IXa goes back into intrinsic pathway to make additional thrombin

*postitive feedback

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10
Q

what is essential for the conversion of fibrinogen to fibrin?

A

thrombin

  • activates coagulation factors and cofacgtors, facilitating its own formation
  • mediates fibrinogen cleavage
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11
Q

what are the 3 natural anticoagulation mechanisms?

A
  • tissue factor pathway inhibitor (TFPI)
  • protein C
  • antithrombin III
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12
Q

what is the mechanism for the natural anticoagulation mechanism protein C?

A
  • protein C activated by endothelial cell-bound enzyme thrombinomodulin
  • activated protein C degrades the important co factors V and VIII
  • activation requires cofactor protein S
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13
Q

what is the mechanism for the natural anticoagulation mechanism antithrombin III

A
  • forms complex and inactivates thrombin and factor Xa

- strongly enhanced by presence of HEPARIN

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14
Q

what is fibrinolysis?

A

turning plasminogen into plasmin…. breaks down clots

-mediated by tPA and uPA (found in endothelial cells)

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15
Q

what two levels is fibrinolysis inhibited by?

A
  • activator inhibitors (PAIs)

- circulating protease inhibitors

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16
Q

what is the most common congenital coagulation disease?

A

von Willebrand Disease

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17
Q

what is the prevalence of von Willebrand disease?

A
  • mild (5:1,000)

- severe (1:25,000)

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18
Q

what are the 3 subtypes of von Willebrand disease?

A
  • type 1: reduced conc (10-45% normal levels)
  • type 2: dysfunctional vWF
  • type 3: absent vWF (homozygous for gene defect)
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19
Q

what is used to correct types one and IIa vWB disease?

*mild

A

DESMOPRESSIN

  • promotes release of vWF stored in endo cells
  • inc vWF circulating 2-3x
  • CONTRAINDICATED in type IIb vWB
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20
Q

what is used to correct type IIb and type III vWB disease?

A

replacement with transfused factors

*tx must continue for 4-7 days after surgery

21
Q

what is the most commonly inherited coagulation disorder?

A

hemophilia A

deals with factor VIII deficientcy

22
Q

what is mild and severe hemophilia?

A 
mild = 40% of normal
severe = less than 1%

*pts with factor VIII levels greater than 5% rarely bleed spontaneously, but will have bleeding problems after surgery or trauma

23
Q

what is the treatment for mild to moderate hemophilia A?

A

Desmopressin

  • releases endogenous factor VIII from liver and endo cells
  • releases vWF which inc VIII levels
24
Q

what is the treatment for severe hemophilia A

A

factor VIII transfusion

-very expensive

25
Q

what is hemophilia B?

A
  • similar to hemophilia A but affecting factor IX

- treated with factor transfusion when severe

26
Q

what are the hypercoagulatable coagulation diseases?

A
  • protein C deficiency, protein S deficiency

- factor V leiden

27
Q

what is the link between coagulation and liver disease?

A
  • liver is the source of coagulation factors
  • liver is also the source of protein C, protein S, and fibringogen
  • if diseases, thrombocytopenia may exist
  • thrombocyte function is impaired in cirrhotic pts
28
Q

what is the best way to determine if your liver is diseased?

A

model for end-stage liver disease score

*may be more useful predictor of bleeding complications than INR alone

29
Q

what is the link between coagularion and renal disease?

A
  • renal failure pts often present with coagulation abnormalities and are at risk for inc bleeding
  • low hematocrit in pts with renal failure may contribute to impaaired fxn of primary hemostasis

*desmopressin has been shown to correct prolonged bleeding time in pts with uremia

30
Q

what are the anti-platelet drugs?

A
  • aspirin
  • clopidogrel (plavix)
  • Dipyramidole
  • glycoprotein receptor IIb/IIIa inhibitors
31
Q

how does aspirin work?

A
  • irreversible inhibitor of platelet membrane associated cyclooxygenase
  • may be associated with sig impairment of primary hemostasis and mild enhancement of bleeding
32
Q

what are the adverse effects of aspirin?

A
  • excess bleeding and the occurrence of hemorrhagic gastritis or even gastric ulceration
  • for most dental procedures, discontinuing aspirin is NOT indicated and may pose greater risks than benefits
33
Q

how does clopidogrel work?

A
  • blocks the ADP receptor on the platelet
  • more expensive than aspirin
  • results in more clinical bleeding than aspirin
  • generally safe to continue through oral surgery like aspirin
34
Q

how does dipyramidole work?

A
  • antiplatelet effect by inhibition of phosphodiesterase

- a potent inhibitor of platelet aggregation but has not seen many clinical trials

35
Q

how does glycoprotein receptor IIb/IIIa inhibitors work?

A
  • MOST POTENT inhibitor of platelet aggregation
  • competitive inhibitor of fibrinogen binding to the IIb/IIIa site
  • intravenous forms more effective than oral
36
Q

what are the anticoagulation drugs/

A
  • coumadin
  • factor Xa inhibitors
  • heparin
  • low molecular weight heparins
  • pentasaccharides
37
Q

how does coumadin work?

A
  • given orally
  • blocks the essential vit K-dependent carboxylation of coagulation factors II, VII, IX, and X
  • dose effect relationship vaires considerably between pts and in individuals
38
Q

what is used to monitor coumadin?

A

PT/INR

39
Q

what is the most important side effect of coumadin?

A

bleeding

*it is rare but coumadin induced skin necrosis may occur

40
Q

how do factor Xa inhibitors work?

NOACs, TSOACs, DOACs = synonyms

A
  • first new drugs for stroke or DVT prophy since coumadin
  • do not require lab monitoring
  • reatively rapid onset (2-3 hrs) and short half-life
  • STROKE prevention comparable to coumadin
  • risk of extracranial bleeding same (or possibly higher)
41
Q

how does heparin work?

A
  • given parenterally
  • binds to antithrombin III which potentiates inhibition of factors IIa and Xa more than 1000 fold
  • effect after IV admin is immediate
  • heparin has a dose depentdent half life
42
Q

how do low molecular weight heparins work?

A
  • given parenterally
  • in some situations have a more favorable antithrombitic effects and induce fewer bleeding complications
  • more predicatable and longer half-life
43
Q

how do pentsaccharides work/

A
  • parenteral
  • indicated DVT prophy or DVT/PE tx
  • synthetic compounds that exert antithrombin-dependent exclusive inhibition of factor Xa
  • Xa inhibition is indirect
44
Q

what are the complications with heparin and its derivatives?

A
  • BLEEDING
  • heparin induced thrombocytopenia
  • long term use of heparin has been associated with osteocytopenia
45
Q

what are the steps to ID a pt with a risk of bleeding

A
  • med history (ask about previous surgeries)
  • NEVER advise a pt to hold or discontinue any prescribed anticoagulation, even aspirin, without consulting the prescriber first
  • physical exam (look for abnormal bruising, petechiae, splenomegaly)
  • lab exam
  • PT/INR (normal is 12 +/- 2 seconds
  • activated partial thromboplastin time (PTT)(measures “intrinsic” pathway
46
Q

what does a prolonged PTT time indicate?

A
  • use of heparin
  • antiphospholipid antibody, which inc the risk of thrombosis
  • coagulation factor (hemophilia)
  • sepsis
  • presence of antibodies agains coagulation factors
47
Q

what is the deal with measuring platelet function - bleeding time

A
  • was the standard method for assessing primary hemostasis for many years
  • is subject to many problems
  • is not sensitive and poorly reproducible
  • can be affected by aspirin

IT SUCKS

48
Q

what is considered the GOLD STANDARD for platelet function analysis?

A

-platelet affregometry

Pharm II (16 decks)

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