Disorders of Hemostasis Flashcards

(38 cards)

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

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 =

24
Q

Too little vitamain K=

25
Where is vitamin k stored
in the liver
26
Liver disease causes
defects in coagulation fibrinolysis platelet number and function
27
NASH
non alcoholic fatty liver
28
Hypercoaguability states
Inherited genetically and acquired | Increased platelet function
29
Inheritated hypercoagulation
usually associated with venous thrombosis C protein down will create DVT S protein down will create arterial thrombosis
30
C breaks down
clots
31
Factor V leiden AKA activated protein resistance (Inherited hypercoaguability)
resists protein c from breaking down a clot due to genetic mutation
32
Most common acquired increased clotting
``` Smoking Disseminated Cancer Obesity sickle cell Most common female aquired oral contriceptives ```
33
Hemophilia
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
DIC
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
What would you expect to see if your patient had widespread thrombosis followed by widespread bleeding?
symmetrical blue fingers and toes
36
Anticoagulant drugs
Heparin- Binds to ATP | Coumadin- interfere with vit K (oral)
37
Antiplatelet drugs
Inhibits platelet formation | Asprin plavix
38
Thrombocytic drugs
tissue plasminagin actorvator tPA plasmin to plasmin