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Pathophysiology 1 > Hemostasis and Coagulation > Flashcards

Hemostasis and Coagulation Flashcards

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
Q

What does fibrinolysis aid in?

A

Clot dissolution; initiated along with clot formation

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26
Q

What do the factors in Fibrinolysis result in ?

A

release of plasminogen activators (TPA)

Cleave plasminogen to plasmin

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27
Q

What does plasmin do?

A

DIgests fibrinogen and fibrin- inactivates factors V and VIII

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28
Q

What do you need to know to evaluate for evaluation of clotting factor disorders?

A

Family history, location, severity, duration, med history

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29
Q

Where are the most signs of clotting factor disorders?

A

Skin and mucous membranes (but they can happen in the internal organs as well)

30
Q

how will individuals with clotting disorders often look?

A

Pale or jaundice

31
Q

2 types of vascular disorders

A

Vascular purpura

Hereditary hemorrhagic Telangiectasia

32
Q

What is vascular pupura?

A

When purpura presents on skin

Abnormality of vessels or tissues that support them

33
Q

What are some types of vascular pupura

A

Allergic form, drug induced, abnormality of vessels or tissues that support them

34
Q

What two types of vascular purpura are caused by Decreased and poor quality collagen and elastin

A

Ehlers-Danlos syndrome, osteogenesis imperfecta

35
Q

Why does scurvy lead to vascular purpura?

A

Defective collagen due to lack of Vitamin C

36
Q

Do vascular purpura lesions blanch?

A

No

37
Q

In allergic vascular purpura- where do the lesions show up?

A

Proximal extremities (thigh and buttocks)

38
Q

Where do you find hemorrhagic telangiectasia?

A

Any mucosal surface (most severe in lung, liver, brain); bright red or purple lesions on nose, lips. palate, etc.

39
Q

What type disorder is hereditary hemorrhagic telangiectasia?

A

Autosomal dominant (also know as Osler-Weber-Rendu disease)

40
Q

What is the most common clinical problem with hereditary hemorrhagic telangiectasia?

A

Epistaxis

41
Q

What are 2 main platelet disorders?

A

Thrombocytopenia

Thrombocytosis

42
Q

What is thrombocytopenia?

A

Lack of platelets

most common cause of generalized bleeding

43
Q

What type of purpura is found in thrombocytopenia?

A

Idiopathic thrombocytopenic purpura (ITP)- immune mediated

44
Q

What causes acute ITP?

A

An actue viral infection

45
Q

What is chronic ITP caused by?

A

Probably autoimmune, found most often in women

46
Q

Four mechanisms of thrombocytopenia

A

Decreased platelet production, decreased platelet survival, splenic sequestration, platelet dilution

47
Q

What is thrombocytosis?

A

Excessive platelet numbers

48
Q

What is thrombocytosis secondary to?

A

Hemorrhage, inflammatory disease, malignancy, infection, hemolysis, splenectomy

49
Q

What is the transatory form of thrombocytosis?

A

Due to stress or exercise- there is a release of preformed platelets

50
Q

What is the primary form of thrombocytosis?

A

Abnormal megakaryoctye proliferation

51
Q

What are the complications with the primary form of thrombocytosis?

A

Hemorrhaging and thrombotic complications (create clots where they don’t belong- suck up all coagulation factors)

52
Q

What are three inherited qualitative platelet disorders?

A

Bernard-Soulier syndrome
Von Willebrand disease
Glanzmann disease
(these are rare)

53
Q

What are some causes of acquired platelet disorders?

A

Drug, with uremia, coexisting with hematolgic disease

54
Q

What causes hemophilia A?

A

Factor VIII deficit
X-linked recessive (males)
(classic)

55
Q

What causes hemophilia B?

A

Factor IX deficit

Classified by extend coagulation factor deficit

56
Q

How is hemophilia diagnosed neonatally?

A

following circumcision

Following vitamin K injection (hematoma forms at stie)

57
Q

Three classifications of hemophilia

A

<1 % severe case
1-5% normal- moderate
5-25% normal- mild

58
Q

Biggest problem w/ hemophilia

A

Intracranial hemorrhage and serious bleeding episodes

59
Q

With the mild form of hemophilia- when do symptoms occur?

A

When stressed (ex- surgery)

60
Q

What is von Willebrand Disease caused by?

A

Autosomal disorder of factor VIII carrier protein- also includes platelet dysfunction
(affects both sexes)

61
Q

What is the connection between von Wilebrand (VW) factor and Factor VIII

A

Normally circulate as a complex
VW stabilized factor VIII- normal platelet adherance
Disease VW- depression of factor VIII

62
Q

When does Vitamin K Deficiency appear?

A

Newborns 48-72 hours to 6 months

more common in breast-fed infants

63
Q

What factors are Vitamin K dependent?

A

II, VII, IX, X (meaning with vitamin K deficiency- will not be able to properly form a blot clot)

64
Q

Where is Vit K absorbed?

A

Small intenstine;
Store in liver
Fat soluble

65
Q

Why do bile problems possibly lead to vitamin K deficiency?

A

Bile problems- no fat dissolved- so no fat soluble vitamins are absorbed

66
Q

What happens in DIC (disseminated intravascular coagulation)

A

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
Q

Where does chronic form of DIC show up?

A

Malignant cancer patients

68
Q

What types of events are more common in chronic DIC?

A

Thromboses

69
Q

What type of DIC is secondarily to other disorders?

A

Actue DIC

70
Q

What is acrocyanosis? and where is it seen?

A

Cold, mottled, fingers, & toes

DIC (disseminated intravascular coagulation)

71
Q

What does hepatic disease alter?

A

Function and production of factors

bile production and transport

Pathophysiology 1 (11 decks)

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