Disorders of Hemostasis Flashcards

1
Q

Hemostasis

A

stopping blood flow, literally taking blood from a liquid state into a solid state
-Either inappropriate clotting or insufficient clotting

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2
Q

Platelets (Thrombocytes)

A
  • Platelets live 8-10 days in circulation
  • Many stored in the spleen
  • are disc shaped
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3
Q

What is the normal value for platelets

A

150,000 - 400, 000

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4
Q

What are mediators hemostasis

A

Chemicals produced by platelets that are released at an injury to start the clotting process

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5
Q

What is the blood vessels role in clotting

A

The prevent and control the formation of blood clots. Blood vessels are lined with epithelial cells that either promote blood flow by blocking platelet adhesion and lysing blood clots

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6
Q

How is the endothelium activated?

A

by infectious agents
hemodynamic factors
plasma mediators
and cytokines that are liberated during the inflammatory process

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7
Q

Epithelium cells elaborate and enzyme called

A

adenosine diphosphatase

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8
Q

Phase 1 of hemostasis

A

Vessel spasm
vasoconstricton
formation of soft plug
short lived

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9
Q

Phase 2 of hemostasis

A

Release of Von Willebrand Factor by endothelial cells

ADP helps stick together

Release of factor 3 which constricts the vessel so that the platelet doesn’t get kicked off

platelet plug

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10
Q

Phase 3 of hemostasis

A

Coagulation phase

Extrinsic pathways, Intrinsic Pathways start 30 seconds to several min after phase 1 and 2

which both end in x factor (common pathway) prothombin to thrombin (without this it cannot occur)

Fibrinogen to fibrin

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11
Q

Extrinsic Pathway (tissue factor)

A

much faster
begins with trauma to the tissue to release
very rapid, 12-15 seconds (smaller clots)
chemical shortcut
Ends in factor x

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12
Q

factor x

A

prothombin activator

Without this, you cannot clot

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13
Q

Intrinsic Pathway (Blood Vessel injury)

A

slow (5-10 min)
collagen in the blood vessel wall activates
Larger amounts of thrombin= larger clots
ends in factor x

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14
Q

Ptt

A

Intrinsic- heparin, already have a clot

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15
Q

aPt

A

Extrinsic- coumadin- to avoid a clot

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16
Q

factor v complex

A

prothombin to thrombin, without this you cannot clot

17
Q

Prothombin to thrombin ——–>

A

fibrogenogen to fibrin =clot

18
Q

Clot retraction IV

A

pulls tight on top of injury site in order to reduce further hemorrhage

19
Q

Fibrinolysis V

A

and enzyme plasmin digests or degrades the clot

T-PA tissue plasminogen activator converts plasminogen into plasmin and eats the clot

then plasmin digests the clot

20
Q

All but 2 of the hemostasis phases require calcium to clot except for stages

A

1 and 2

21
Q

Thrombocytopenia

A

Platelet count less than 150,000

Less than 50,000 means hemorrhage
Less than 15,000 means spontaneous bleeding
less than 10,000 means severe bleeding

22
Q

What causes thrombocytopenia

A

Hyperspleenism,
autoimmune disease
hypothermia
viral or bacterial infections that cause DIC

23
Q

Too much vitamin K =

A

clot

24
Q

Too little vitamain K=

A

bleed

25
Q

Where is vitamin k stored

A

in the liver

26
Q

Liver disease causes

A

defects in coagulation
fibrinolysis
platelet number and function

27
Q

NASH

A

non alcoholic fatty liver

28
Q

Hypercoaguability states

A

Inherited genetically and acquired

Increased platelet function

29
Q

Inheritated hypercoagulation

A

usually associated with venous thrombosis

C protein down will create DVT

S protein down will create arterial thrombosis

30
Q

C breaks down

A

clots

31
Q

Factor V leiden AKA activated protein resistance (Inherited hypercoaguability)

A

resists protein c from breaking down a clot due to genetic mutation

32
Q

Most common acquired increased clotting

A
Smoking
Disseminated Cancer
Obesity
sickle cell
Most common female aquired
oral contriceptives
33
Q

Hemophilia

A

most common x linked genetic disease (female carrier)

Hemophilia A or classic, factor 8 most common and is a lack of factor 8

Hemophilia b is a lack of factor 9 and is called christmas disease

34
Q

DIC

A

is acquired

is where clotting and bleeding at the same time

Caused by sepsis, cancer, trauma, blood transfusion

causes tissue damage and has 85% mortality rate

35
Q

What would you expect to see if your patient had widespread thrombosis followed by widespread bleeding?

A

symmetrical blue fingers and toes

36
Q

Anticoagulant drugs

A

Heparin- Binds to ATP

Coumadin- interfere with vit K (oral)

37
Q

Antiplatelet drugs

A

Inhibits platelet formation

Asprin plavix

38
Q

Thrombocytic drugs

A

tissue plasminagin actorvator tPA plasmin to plasmin