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Pathophysiology 1 > Hemostasis and Coagulation > Flashcards

Hemostasis and Coagulation Flashcards

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1
Q

What happens with excessive hemostasis?

A

Inappropriate clotting and/or thrombosis

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2
Q

What are the three stages of hemostasis?

A

Primary hemostasis
Secondary hemostasis
Clot retraction

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3
Q

What is in primary hemostasis?

A

vascular spasms (clamping down on damaged blood vessel)
Interaction b/w platelets and vessel
Formation of platelet plug (temp solution)
occurs in 3-7 minutes

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4
Q

Secondary hemostasis components

A

Formation of fibrin clot (coagulation)
Involves clotting factors
3-10 minutes

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5
Q

What happens during clot retraction?

A

Compression of fibrin to form firm clot

within a hour

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6
Q

what is the primary cell type in a clot?

A

Red blood corpuscle

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7
Q

Where are platelets (thrombocyte) produced from?

A

Megakaryocytes (mature cell in bone marrow) that flake apart to form these fragment cells

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8
Q

What do platelets adhere to?

A

Collagen exposed by trauma

then they degranulate

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9
Q

After degranulate- what granules are released by platelets?

A

Alpha granules and Dense granules

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10
Q

What is inside alpha granules?

A

Platelet thrombospondin, fibrinogen, fibronectin, von Willebrand factor, coagulation factors V & VIII

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11
Q

What is found in dense granules?

A

ADP, ATP, Serotonin

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12
Q

What causes the formation of thromboxane A2 (TxA2) and what does it do?

A

ADP + collagen;

TxA2 stimulates glycoprotein llb/llla receptor expression which promote platelet adhesion

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13
Q

what do platelets do in secondary hemostasis?

A

Catalyze interaction between activated coagulation factors

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14
Q

what blood coagulation factors are not plasma proteins?

A

Factor lll and calcium

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15
Q

All blood coagulation factors are synthesized by the

A

Liver (except part of factor VIII)

some synthesized by megakaryocytes and endothelial cells

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16
Q

Viktamin K helps for the synthesis and future activity of

A

Factors II, VII, IX, X, prot C, Prot S

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17
Q

What does Protein C do?

A

Inactivates Factors V and VIII- prevents clot formation

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18
Q

What does protein S do?

A

Stimulates with release of TPA (tissue plasminogen activator)

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19
Q

What is involved in intrinsic pathway of fibrin clot?

A

Factors XII, HMWK, prekallikrien, XI- formation of Xa (factor ten activated) and initiation of common pathway

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20
Q

Extrinsic pathway is triggered by…

A

Trauma of vascular wall (from outside)

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21
Q

What is the end result of intrinsic and extrinsic pathways?

A

Activation of Factor X and initiates of common final pathway

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22
Q

Factor Xa initiation the conversion of

A

Prothrombin to thrombin

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23
Q

What does thrombin do?

A

Cleaves fibrinogen to fibrin and activates factor XIII

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24
Q

What does factor XIII do?

A

forms insoluble clot- aid in clot retraction

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25
What does fibrinolysis aid in?
Clot dissolution; initiated along with clot formation
26
What do the factors in Fibrinolysis result in ?
release of plasminogen activators (TPA) | Cleave plasminogen to plasmin
27
What does plasmin do?
DIgests fibrinogen and fibrin- inactivates factors V and VIII
28
What do you need to know to evaluate for evaluation of clotting factor disorders?
Family history, location, severity, duration, med history
29
Where are the most signs of clotting factor disorders?
Skin and mucous membranes (but they can happen in the internal organs as well)
30
how will individuals with clotting disorders often look?
Pale or jaundice
31
2 types of vascular disorders
Vascular purpura | Hereditary hemorrhagic Telangiectasia
32
What is vascular pupura?
When purpura presents on skin | Abnormality of vessels or tissues that support them
33
What are some types of vascular pupura
Allergic form, drug induced, abnormality of vessels or tissues that support them
34
What two types of vascular purpura are caused by Decreased and poor quality collagen and elastin
Ehlers-Danlos syndrome, osteogenesis imperfecta
35
Why does scurvy lead to vascular purpura?
Defective collagen due to lack of Vitamin C
36
Do vascular purpura lesions blanch?
No
37
In allergic vascular purpura- where do the lesions show up?
Proximal extremities (thigh and buttocks)
38
Where do you find hemorrhagic telangiectasia?
Any mucosal surface (most severe in lung, liver, brain); bright red or purple lesions on nose, lips. palate, etc.
39
What type disorder is hereditary hemorrhagic telangiectasia?
Autosomal dominant (also know as Osler-Weber-Rendu disease)
40
What is the most common clinical problem with hereditary hemorrhagic telangiectasia?
Epistaxis
41
What are 2 main platelet disorders?
Thrombocytopenia | Thrombocytosis
42
What is thrombocytopenia?
Lack of platelets | most common cause of generalized bleeding
43
What type of purpura is found in thrombocytopenia?
Idiopathic thrombocytopenic purpura (ITP)- immune mediated
44
What causes acute ITP?
An actue viral infection
45
What is chronic ITP caused by?
Probably autoimmune, found most often in women
46
Four mechanisms of thrombocytopenia
Decreased platelet production, decreased platelet survival, splenic sequestration, platelet dilution
47
What is thrombocytosis?
Excessive platelet numbers
48
What is thrombocytosis secondary to?
Hemorrhage, inflammatory disease, malignancy, infection, hemolysis, splenectomy
49
What is the transatory form of thrombocytosis?
Due to stress or exercise- there is a release of preformed platelets
50
What is the primary form of thrombocytosis?
Abnormal megakaryoctye proliferation
51
What are the complications with the primary form of thrombocytosis?
Hemorrhaging and thrombotic complications (create clots where they don't belong- suck up all coagulation factors)
52
What are three inherited qualitative platelet disorders?
Bernard-Soulier syndrome Von Willebrand disease Glanzmann disease (these are rare)
53
What are some causes of acquired platelet disorders?
Drug, with uremia, coexisting with hematolgic disease
54
What causes hemophilia A?
Factor VIII deficit X-linked recessive (males) (classic)
55
What causes hemophilia B?
Factor IX deficit | Classified by extend coagulation factor deficit
56
How is hemophilia diagnosed neonatally?
following circumcision | Following vitamin K injection (hematoma forms at stie)
57
Three classifications of hemophilia
<1 % severe case 1-5% normal- moderate 5-25% normal- mild
58
Biggest problem w/ hemophilia
Intracranial hemorrhage and serious bleeding episodes
59
With the mild form of hemophilia- when do symptoms occur?
When stressed (ex- surgery)
60
What is von Willebrand Disease caused by?
Autosomal disorder of factor VIII carrier protein- also includes platelet dysfunction (affects both sexes)
61
What is the connection between von Wilebrand (VW) factor and Factor VIII
Normally circulate as a complex VW stabilized factor VIII- normal platelet adherance Disease VW- depression of factor VIII
62
When does Vitamin K Deficiency appear?
Newborns 48-72 hours to 6 months | more common in breast-fed infants
63
What factors are Vitamin K dependent?
II, VII, IX, X (meaning with vitamin K deficiency- will not be able to properly form a blot clot)
64
Where is Vit K absorbed?
Small intenstine; Store in liver Fat soluble
65
Why do bile problems possibly lead to vitamin K deficiency?
Bile problems- no fat dissolved- so no fat soluble vitamins are absorbed
66
What happens in DIC (disseminated intravascular coagulation)
Will have clotting in some parts of the body and bleeding in another part of the body (similar to not having enough platelets- but much more severe)
67
Where does chronic form of DIC show up?
Malignant cancer patients
68
What types of events are more common in chronic DIC?
Thromboses
69
What type of DIC is secondarily to other disorders?
Actue DIC
70
What is acrocyanosis? and where is it seen?
Cold, mottled, fingers, & toes | DIC (disseminated intravascular coagulation)
71
What does hepatic disease alter?
Function and production of factors | bile production and transport

Pathophysiology 1 (11 decks)

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