Exam 7 L. 4 Flashcards

1
Q

Primary hemostasis

A

The formation of the platelet plug

-sufficient for small vessel injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Secondary hemostasis

A

The formation of the fibrin clot through the coagulation cascade
-fibrin clot is needed for medium/large vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Tertiary hemostasis

A

Fibrinolysis to reestablish blood flow through vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Normal vessel

A

Platelet adhesion prevented by:

  • negatively charged endothelium (repels platelets)
  • nitric oxide
  • prostacyclin
  • ADPase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Endothelial damage

A

1) vasoconstriction: platelets are slowed, giving them time to interact with subendothelium
2) subendothelium exposed: vWF visible
3) platelets tether to vWF ==> activates platelets to bind to fibrinogen
- fibrinogen allows platelets to bind together
4) activated platelets attract and activate more platelets (ADP and Thromboxane A2)
5) activated platelets set the stage for secondary hemostasis (provide docking site for clotting factors need)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What can go wrong with primary hemostasis?

A

1) platelet: function and number

2) von Willebrand factor: number and function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Primary hemostatic disorders

A

1) thrombocytopenia
- use, destruction, decreased production
2) acquired
- immune mediated, infectious disease, DIC, drugs
- thrombocytopenia is the most common acquired disorder of primary hemostasis!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Primary hemostatic disorder: von Willebrand’s disease

A

Inherited: Doberman!

-Most common inherited primary hemostatic disorder is von Willebrand’s disease!**

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Platelet count

A

1) estimate from a blood smear
- 1 per 100x field = 20,000 platelets/ul
- check the feathered edge!!
- A normal dog has between 8 to 10 platelets per high-powered field
2) spontaneous bleeding will not occurring last count is under 30,000 platelets/ul

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How do you test platelet function?

A

1) Buccal mucosal bleeding time
- a test for a defect in primary hemostasis
- makes an incision of standard depth and width in buccal mucosa
2) will be abnormal (>4 minutes) if:
- thrombocytopenic, thrombopathic, vWF deficient/abnormal, abnormal vasculature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Immune-mediated thrombocytopenia (ITP)

A

1) can be primary or secondary
2) secondary: drugs, infectious agents (especially vectorborne diseases), neoplasia
- for some reason there is antibody versus platelets, and macrophages are gobbling up the platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Treatment for ITP

A

1) Vincristine
- a 1 time shot! (It works or it doesn’t)
- prevents microtubule polymerization
- accelerated megakaryocyte fragmentation and platelet release from bone marrow
- no place for vincristine in IMHA treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

When to transfuse platelets?

A

1) Severe thrombocytopenia
2) suspect pulmonary or CNS hemorrhage
3) acquired or hereditary thrombopathia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What products contain viable platelets??

A

1) fresh whole blood
2) platelet rich plasma
- generated from a soft spin of blood
3) platelet concentrate (fresh or cryopreserved)
- PRP that has been spun hard to concentrate platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

ITP prognosis

A

1) good!
2) 10-30% mortality rate
3) like IMHA, does require long-term immunosuppressive therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Inhibitors of primary hemostasis

A

1) endothelial cells!*
- Physical barrier: separates platelets and vWF unless there is an injury
2) ADPase, prostacyclin, nitric oxide
- inhibit platelet activation

17
Q

Pathological inhibitors of primary hemostasis

A

1) disease:
- DIC
- metabolites in liver and kidney disease inhibit platelet function

18
Q

Therapeutic inhibitors of primary hemostasis

A

1) platelet inhibitors
- aspirin, NSAID’s: inhibit TxA2 production ==> platelets don’t activate their neighbors!
- Clopidogrel: inhibit platelets by binding to their ADP receptor (platelets cannot be activated by ADP)

19
Q

Remember

A

1) platelets do a lot!
- 1st to site of injury, essential for platelet plug formation, and platelet membranes are needed for secondary hemostasis
2) vWF
- the glue for platelet adhesion to the vessel wall: stops bleeding
3) thrombocytopenia is the most common acquired cause of defective primary hemostasis
4) von Willebrand’s disease is the most common cause of inherited defective primary hemostasis