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Pathophysiology > Chapter 22 > Flashcards

Chapter 22 Flashcards

1
Q

Hemostasis

A

The stoppage of blood flow where fibrin strands glue the aggregated platelets together to form blood clot —> plasma becomes gel like and traps RBCs and formed elements in blood

regulated by activators and inhibitors to prevent blood from leaving the vascular compartment

Normal when it seals a blood vessel to prevent blood loss and hemorrhage and abnormal when it causes inappropriate blood clotting or when clotting is insufficient to stop blood from from the vascular compartments

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2
Q

Mechanisms of hemostasis

A

Vascular constriction, formation of the platelet plug, blood coagulation

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3
Q

What initiates vessel spasm?

A

Endothelial injury or local and humoral mechanisms

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4
Q

What factors contribute to vasoconstriction in blood coagulation/ hemostasis?

A

Neural reflexes and thromboxane A2, prostaglandin released from platelets

Most powerful: endothelial 1

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5
Q

What is used to seal small breaks in a vessel wall?

A

Platelet plugs, rather than blood clots

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6
Q

Platelets originate from

A

Thrombocytes or platelets arise from megakaryocytes

Eliminated by macrophages after 8-12 pages

Normal concentration: 150000-400000 platelets per microliter

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7
Q

Thrombopoeitin

A

Control protein production

Causes proliferation and maturation of magakaryocytes

Source: liver, kidneys, smooth muscle, bone marrow

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8
Q

Platelet granules

A

Release mediators for hemostasis

Types: alpha (vwb factors) and delta granules (adp and atp, ionize histamine, serotonin, vasoconstriction molecules)

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9
Q

Platelet plug formation

A

Activation, adhesion, and aggregation of platelets

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10
Q

Platelet activation

A

Platelets attracted to damaged vessel wall —> activated —> change from smooth disks to spiny spheres (expose glycoprotein receptors) —> platelet receptor binds to vWF at the injury site —> platelet and exposed collagen fibers are linked

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11
Q

vWF

A

Required for platelet adhesion

leaks into injured tissue from plasma

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12
Q

Platelet aggregation

A

Combine actions of ADP and TXA2 lead to expansion of the enlarging platelet aggregate —> becomes primary hemostasis plug

Coagulation pathway activated on platelet surface —> fibrinogen is converted to fibrin —> fibrin mesh work that cements platelets and other blood components together —> p selection binds leukocytes to heal vessel wall

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13
Q

What role does the platelet membrane play in the adhesion and coagulation process?

A

Glycoproteins: controls interactions with the vessel endothelium

Platelets interact with injured areas of the vessel wall and deeper exposed collagen

Glycoproteins receptors on membrane bind fibrinogen and link platelets together

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14
Q

Symptoms of defective platelet plug formation

A

Bleeding in people who are deficient in platelets or vWF

Usually superficial and localized

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15
Q

How do platelets play a role in marinating normal vascular integrity?

A

By supplying growth factors for endothelial and arterial smooth muscle cells

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16
Q

Platelet inhibitors

A

Pharmacological agents that work in different are of the adhesion-activation-aggregation progression

Eg: cyclooxygenase-1 (cox-1) like aspiring prevent clot formation in people who are at risk for MI, stroke, or peripheral artery disease

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17
Q

What does low dose aspirin therapy do to vascular pathophysiology?

A

Inhibits prostaglandin synthesis (TXA2)

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18
Q

Blood coagulation cascade

A

Converts soluble plasma protein, fibrinogen, into fibrin

Insolvable fibrin strands create a mesh work that cements platelets and other blood components together to form the clot

Results form the activation of the intrinsic and extrinsic pathways who form prothrombin activators

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19
Q

What regulate the coagulation process?

A

Procoagulation factors or anti coagulation factors

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20
Q

How does vitamin K play a role in the coagulation process?

A

Necessary for the synthesis of factors II, VII, IX, and X in the cascade, as well as prothrombin, and protein C

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21
Q

Why does a bleeding tendency develop when a person is low on vitamin K?

A

There is not enough prothrombin created

Typically due to deficiency or liver failure

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22
Q

Where is calcium involved in the coagulation cascade?

A

AKA factor IV

Required in all but the first two steps

Inactivation of calcium prevents blood from clotting when removed from the blood

23
Q

Intrinsic pathway

A

Slow process, clotting in 1-6 minutes

Termination: activation of factor X and conversion of prothrombin to thrombin

Activated: blood passes out of vascular system and comes into contact with collagen in injured vessel wall

Defects: lead to severe bleeding

24
Q

Extrinsic pathway

A

Faster process, clotting in 15 seconds

Begins with trauma to the BV or surrounding tissues

Termination: activation of factor X and conversion of prothrombin to thrombin

Activation: blood passes out of the vascular system and exposed to tissue extracts

Defects: bleeding is much less severe

25
Q

Action of thrombin

A

Acts as an enzyme to convert fibrinogen to fibrin (material that stabilizes a clot)

26
Q

What regulates blood coagulation?

A

Natural anticoagulants
Antithrombin III
Heparin

Provides protection against uncontrolled thrombus formation on the endothelial surface

27
Q

Protein C

A

Anticoagulation that inactivated factors V and VIII

28
Q

Protein S

A

Accolade rates action of protein C

A deficiency in protein C or protein S puts one at risk for thrombosis

29
Q

what are anticoagulant drugs used for?

A

warfarin and heparin

Prevent thromboembolic disorder

30
Q

Clot retraction

A

20-60 minutes after a clot has formed

Squeezes serum from clot and joins edges of broken vessel

Platelets are also involved

31
Q

What might cause a failure of clot retraction?

A

Low platelet count

32
Q

Clot dissolution

A

Begins shortly after blot clot formation to ensure blood flow can be reestablished and permanent tissue repair to take place

Plasminogen is activated into pals in —> digests fibrin strands of the clot and clotting factors —> limits fibrinolytic process to the local clot/ prevents from occurring in entire circulation

33
Q

Fibrinolysis

A

Process by which a blood clot dissolves

34
Q

Why would plasminogen activators be released?

A

In response to vasoactive drugs, venous occlusion, elevated body temperature, and exercise

35
Q

why does liver disease cause altered fibrinolytic activity?

A

Plasminogen actions are unstable and rapidly inactivated by inhibitors synthesized by the endothelium and the liver

36
Q

In high doses, what negative clinical implicates does plasminogen activator inhibitor 1 have?

A

Associates with DVT, coronary artery disease, and MI

37
Q

Hyper-coagulability States

A

Exaggerated form of hemostasis that predisposes thrombosis and blood vessel occlusion

Two forms: condition that create increased platelet function and conditions that cause accelerated activity of the coagulation system

38
Q

What conditions are associated with increased platelet function?

A 
Atherosclerosis
Diabetes mellitus
Smoking
Elevated blood lipid and cholesterol levels
Increased platelet levels
39
Q

What condition are associated with accelerated activity of the clotting system?

A 
Pregnancy and the puerperal
Use of oral contraceptives
Post surgical state
Immobility
Congestive heart failure
Malignant disease
40
Q

Pathophysiology of hypercoagulability associated with increased platelet function

A

Results in platelet adhesion, formation of platelet clots, and disruption fo blood flow

Eg: atherosclerotic plaques disturb blood flow —> endothelial damage —> prompt platelet adherence through growth factors —> proliferation of smooth muscle —> development of atherosclerosis

41
Q

Pathophysiology of hypercoagulability associated with increased clotting activity

A

Can result from primary (genetic) or secondary (acquired) disorders affecting coagulation components

42
Q

Thrombocytosis

A

Elevations in platelet count above 1,000,000 uL

Can be primary or secondary (caused by disease that stimulates thrombopoietin)

Clinical manifestation: thrombosis (portal and hepatic veins) and hemorrhage, DVT, PE

43
Q

Hereditary thrombopoeitin

A

Causes activated protein C resistance

Clinical manifestations: VTE (DVT and PE)

44
Q

What is a common cause of venous thrombosis in the immobilized or post surgical person?

A

Slow and disturbed flow that causes accumulation of activated clotting factors and platelet that are prevented from interacting with inhibitors

45
Q

Antiphospholipid syndrome

A

Cause of increased venous and arterial thrombosis

Associated with autoantibodies (igG) —> increased coagulation activity

Clinical manifestations: venous and arterial thrombi, recurrent fetal loss, thrombocytopenia

Can be primary or secondary

46
Q

Antiphospholipid syndrome treatment

A

Removal or reduction in factors that predispose to thrombosis, including advice to stop smoking and counseling against use of estrogen-containing oral contraceptive by women

Aspiring and anticoagulants and vitamin K anticoagulation’s may be used to prevent future thrombosis

47
Q

Consequence of bleeding disorders

A

Can result from defects in any of the factors that contribute to hemostasis

Eg: disorders associated with platelet number or function, coagulation factors, and blood vessel integrity

48
Q

Bleeding associated with platelet disorders

A

Due to decrease in platelet number due to decreased production, increased destruction, or impaired function of platelets

Petechiae is often seen in conditions of platelet deficiency, not dysfunction

49
Q

Thrombocytopenia

A

A reduction in platelet number often as a result of decreased platelet production, increased sequestration of platelets in the spleen, or decreased platelet survival; cause of generalized bleeding

Level less than 150,000 uL

50
Q

In what conditions is the decreased platelet production due to loss of bone marrow function?

A

Aplastic anemia

51
Q

Excessive pooling of platelets in the spleen

A

Splenomegaly; instead of sequestering 30-40 percent of platelets, the spleen holds onto way more, up to 90 percent

Leads to an enlarged spleen

52
Q

Drug-induced thrombocytopenia

A

Eg; aspiring, Astor a statin, antibiotics

Formation of immune complexes and induction of antigen-antibody response cause platelet destruction by complement-mediated lysis

53
Q

Heparin-induced thrombocytopenia (HIT)

A

Caused by an immune reaction against a complex of heparin and platelet factor 4

Activate remaining platelets leading to thrombosis

Promotion of coagulation

Treatment: immediate discontinuation of heparin

54
Q

Immune Thrombocytopenic Purpura

A

Platelet antibody formation and excess destruction of platelets

Primary ITP: autoimmune disease

Secondary forms of ITP: hemorrhagic symptoms might be absent

Platelet counts <20000 to 30000

Pathophysiology (9 decks)

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