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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
Action of thrombin
Acts as an enzyme to convert fibrinogen to fibrin (material that stabilizes a clot)
26
What regulates blood coagulation?
Natural anticoagulants Antithrombin III Heparin Provides protection against uncontrolled thrombus formation on the endothelial surface
27
Protein C
Anticoagulation that inactivated factors V and VIII
28
Protein S
Accolade rates action of protein C A deficiency in protein C or protein S puts one at risk for thrombosis
29
what are anticoagulant drugs used for?
warfarin and heparin Prevent thromboembolic disorder
30
Clot retraction
20-60 minutes after a clot has formed Squeezes serum from clot and joins edges of broken vessel Platelets are also involved
31
What might cause a failure of clot retraction?
Low platelet count
32
Clot dissolution
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
Fibrinolysis
Process by which a blood clot dissolves
34
Why would plasminogen activators be released?
In response to vasoactive drugs, venous occlusion, elevated body temperature, and exercise
35
why does liver disease cause altered fibrinolytic activity?
Plasminogen actions are unstable and rapidly inactivated by inhibitors synthesized by the endothelium and the liver
36
In high doses, what negative clinical implicates does plasminogen activator inhibitor 1 have?
Associates with DVT, coronary artery disease, and MI
37
Hyper-coagulability States
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
What conditions are associated with increased platelet function?
``` Atherosclerosis Diabetes mellitus Smoking Elevated blood lipid and cholesterol levels Increased platelet levels ```
39
What condition are associated with accelerated activity of the clotting system?
``` Pregnancy and the puerperal Use of oral contraceptives Post surgical state Immobility Congestive heart failure Malignant disease ```
40
Pathophysiology of hypercoagulability associated with increased platelet function
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
Pathophysiology of hypercoagulability associated with increased clotting activity
Can result from primary (genetic) or secondary (acquired) disorders affecting coagulation components
42
Thrombocytosis
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
Hereditary thrombopoeitin
Causes activated protein C resistance Clinical manifestations: VTE (DVT and PE)
44
What is a common cause of venous thrombosis in the immobilized or post surgical person?
Slow and disturbed flow that causes accumulation of activated clotting factors and platelet that are prevented from interacting with inhibitors
45
Antiphospholipid syndrome
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
Antiphospholipid syndrome treatment
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
Consequence of bleeding disorders
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
Bleeding associated with platelet disorders
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
Thrombocytopenia
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
In what conditions is the decreased platelet production due to loss of bone marrow function?
Aplastic anemia
51
Excessive pooling of platelets in the spleen
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
Drug-induced thrombocytopenia
Eg; aspiring, Astor a statin, antibiotics Formation of immune complexes and induction of antigen-antibody response cause platelet destruction by complement-mediated lysis
53
Heparin-induced thrombocytopenia (HIT)
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
Immune Thrombocytopenic Purpura
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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