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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
what is hemophilia B?
- similar to hemophilia A but affecting factor IX | - treated with factor transfusion when severe
26
what are the hypercoagulatable coagulation diseases?
- protein C deficiency, protein S deficiency | - factor V leiden
27
what is the link between coagulation and liver disease?
- 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
what is the best way to determine if your liver is diseased?
model for end-stage liver disease score *may be more useful predictor of bleeding complications than INR alone
29
what is the link between coagularion and renal disease?
- 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
what are the anti-platelet drugs?
- aspirin - clopidogrel (plavix) - Dipyramidole - glycoprotein receptor IIb/IIIa inhibitors
31
how does aspirin work?
- irreversible inhibitor of platelet membrane associated cyclooxygenase - may be associated with sig impairment of primary hemostasis and mild enhancement of bleeding
32
what are the adverse effects of aspirin?
- 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
how does clopidogrel work?
- 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
how does dipyramidole work?
- antiplatelet effect by inhibition of phosphodiesterase | - a potent inhibitor of platelet aggregation but has not seen many clinical trials
35
how does glycoprotein receptor IIb/IIIa inhibitors work?
- MOST POTENT inhibitor of platelet aggregation - competitive inhibitor of fibrinogen binding to the IIb/IIIa site - intravenous forms more effective than oral
36
what are the anticoagulation drugs/
- coumadin - factor Xa inhibitors - heparin - low molecular weight heparins - pentasaccharides
37
how does coumadin work?
- 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
what is used to monitor coumadin?
PT/INR
39
what is the most important side effect of coumadin?
bleeding *it is rare but coumadin induced skin necrosis may occur
40
how do factor Xa inhibitors work? NOACs, TSOACs, DOACs = synonyms
- 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
how does heparin work?
- 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
how do low molecular weight heparins work?
- given parenterally - in some situations have a more favorable antithrombitic effects and induce fewer bleeding complications - more predicatable and longer half-life
43
how do pentsaccharides work/
- parenteral - indicated DVT prophy or DVT/PE tx - synthetic compounds that exert antithrombin-dependent exclusive inhibition of factor Xa - Xa inhibition is indirect
44
what are the complications with heparin and its derivatives?
- BLEEDING - heparin induced thrombocytopenia - long term use of heparin has been associated with osteocytopenia
45
what are the steps to ID a pt with a risk of bleeding
- 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
what does a prolonged PTT time indicate?
- use of heparin - antiphospholipid antibody, which inc the risk of thrombosis - coagulation factor (hemophilia) - sepsis - presence of antibodies agains coagulation factors
47
what is the deal with measuring platelet function - bleeding time
- 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
what is considered the GOLD STANDARD for platelet function analysis?
-platelet affregometry

Pharm II (16 decks)

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