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Pathology Exam 2 > Chapter 4.2 > Flashcards

Chapter 4.2 Flashcards

1
Q

Thrombin

A

Most important coagulation factor
Converts plasma protein fibrinogen into fibrin monomers that polymerize into an insoluble gel
Gel encases platelets and other circulating cells in Secondary Hemostatic plut
Cross linked and stabilized by factor XIIIa

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2
Q

PT Assay

A

Function of factors 7, 10, 2 and 5 and fibrinogen
Add tissue factor and phospholipids to citrated plasma (prevents spontaneous clotting)
Initiated by exogenous Ca2+ and the time for fibrin clot formation is recorded

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3
Q

PTT

A

Screens 12, 11, 9, 8, 10, 5, II and fibrinogen
Clotting initiated through the addition of negatively charged particles
Activates factor 12 Hageman factor, phospholipids and Ca2+, time to fibrin clot formation is recorded

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4
Q

PARs

A

Protease Activated Receptors
7 Transmembrane G protein coupled receptor family
Expressed on endothelium, monocytes, dendritic cells, T-lymphocytes, etc

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5
Q

Antithrombin III

A

Inhibits activity of thrombin and other serine proteases, IXa, Xa, XIa and XIIa
Activated by binding to heparin-like molecules on endothelial cells
Administer heparin to minimize thrombosis

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6
Q

Protein C and S

A

Vitamin K-dependent proteins

Act in complex that proteolytically inactivates Va and VIIIa

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7
Q

TFPI:

A

protein produced by endothelium

Inactivates tissue factor-factor VIIa complexes

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8
Q

PAI

A

Plasminogen activator inhibitor PAI
Blocks fibrinolysis by inhibiting t-PA binding to fibrin
Confers an overall procoagulant effect
Production is increased by thrombin as well as other cytokines

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9
Q

Virchows Triad

A
  1. Endothelial injury
  2. Stasis or turbulent blood flow
  3. Hypercoagulability of blood
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10
Q

Endothelial injury

A

Any perturbation in the dynamic balance of prothombic and antithrombotic activities of endothelium can influence local clotting events

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11
Q

Turbulance

A

Contributes to arterial and cardiac thrombosis by causing endothelial injury or dysfunction
Countercurrents and local pockets of stasis
Stasis contributes to development of venous thrombi
Enhance pro-coagulant activity

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12
Q

Hypercoagulability

A

Less frequent contributor to thrombotic states

Alteration of coagulation pathways, predispose to thrombosis

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13
Q

Inherited Hypercoagulability

A

Most common
Pt mutations in factor V gene
Prothrombin gene

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14
Q

Elevated Homocysteine

A

Contirubtes to arterial and venous thrombosis

Thioester linkages occur between homocysteine metabolites and a variety of proteins

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15
Q

Causes of Venous Thrombosis or Recurrent Thromboembolism

A

Deficiencies of anticoagulants

Antithrombin III, protein C or protein S

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16
Q

Heparin-induced thrombocytopenia

A

Occurs after administratoin of unfractionated heparin
Can induce appearence of ABs
Recognize complexes of heparain and platelet factor 4 on platelet surface
Will see low platelet counts

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17
Q

Anti-phospholipid syndrome

A

Recurrent thromboses, repeated miscarriages, cardiac valve vegetations, thrombocytopenia
Pulmonary embolism, pulmonary hypertension, stroke, bowel infarction, renovascular hypertension
Autoantibodies can induce hypercoagulable state
Cause endothelial injury

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18
Q

Secondary Anti-Phospholipid Syndrome

A

Individuals with well defined autoimmune disease

Systemic lupus erythematosus

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19
Q

Primary Anti-Phospholipid Syndrome

A

Only manifestations of hypercoagulable state
Lack evidence of other autoimmune disorders
Associate with certain drugs or infections

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20
Q

Arterial thrombi

A

Grow retrograde from pt of attachment
Begin at sites of turbulence or endothelial injury
Occlusive
Common in coronary, cerebral, femoral arteries
Meshwork of platelets, fibrin, red cells, degenerating leukocytes
Superimposed on ruptures atherosclerotic plaque

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21
Q

Venous Thrombi

A 
extend in direction of blood flow
Occur at sites of stasis
Invariably occlusive
Long cast of lument
Sluggish venous circulation
More enmeshed red cells
90% cases veins in LE
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22
Q

Lines of Zahn

A

Alternating lines of platelet and fibrin deposits
Indicate that a thrombus has formed in flowing blood
Can be distinguished from antemortem thrombosis from bland nonlaminated clots

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23
Q

Postmortem thrombus

A

Dark red dependent protion
RBCs settled by gravity
Yellow chicken fat upper protion
Not underlying wall

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24
Q

Red Thrombi

A

Firmer
Focally attached
Lines of Zahn

25
Q

Mural Thrombi

A

abnormal myocardial contraction
Occur in heart chambers or aortic lumen
Abnormal myocardial contraction

26
Q

Vegetations

A 
Thrombi on heart valves
Blood-borne bacteria or fungi
Adhere to previously damaged valves
Directly cause valve damage
Infective endocarditis
27
Q

Sterile vegetations

A

Nonbacterial thrombotic endocarditis

28
Q

Sterile, verrucous endocarditis

A

Libman-Sacks endocarditis

29
Q

4 Steps of the Life of a Thrombus

A

Propagation
Embolization
Dissolution
Organization and recanalization

30
Q

Thrombus propagation

A

Thrombi accumulate additional platelets and fibrin

31
Q

Thrombus Embolization

A

Thrombi dislodge and travel to other sites in vasculature

32
Q

Thrombus Dissolution

A

Result of fibrinolysis

Shrinkage and total disappearance of recent thrombi

33
Q

Thrombus Organization/Recanalization

A

Older thrombi

Ingrowth of endothelial cells, smooth muscle cells, fibroblasts

34
Q

DVT

A

larger leg veins at or above knee
Thrombi often embolize to lungs (pulmonary infarct)
Offset with collateral channels
Asymptomatic in 50% of individuals
Recognized retrospectively after embolization

35
Q

Disseminated Intravascular Coagulation

A

Obstetric complications to advanced malignancy
Sudden or insidious onset of widespread fibrin thrombi in micro-circulation
Not grossly visible
Diffuse circulatory insufficiency, particular in brain, lungs, heart and kidney
Widespread microvascular thrombosis results in platelet and coagulation protein consumption
Initially thrombotic, evolves into bleeding catastrophe as platelets used up

36
Q

Pulmonary Embolism

A

Embolic occlusions
95% from deep leg veins
Indwelling central venous lines
50,000 deaths/year in US

37
Q

Large emboli

A

Lodged in major branches of pulmonary arteries
Emboli from leg or pelvic veins
Saddle emboli–>V-shaped spanning pulmonary arteries

38
Q

Small emboli

A

Minimal symptoms
Exception: inadequate bronchial circulation
Can be caused by immobilization, hypercoagulable state, heart failure

39
Q

Pulmonary Embolism Issues

A 
Respiratory compromise
Hemodynamic compromise
Bronchial artery compensation, hemorrhage without infarction
Inadequate circulation
Rare in young
40
Q

Electromechanical dissociation pulmonary embolism

A

ECG has a rhythm but no pulses are detected

41
Q

Pulmonary embolism diagnosis

A

Spiral CT

Hamptom’s hump, non-specific for PE

42
Q

Pulmonary Embolism Prevention

A

Prophylactic therapy-early ambulation, stockings, anticoagulation, filter

43
Q

Treatment Pulmonary Embolism

A

Thrombolysis

Anticoagulation

44
Q

Pulmonary Embolism

A 
Most infarcts in lower lobes
>50% multiple lesions
Wedge shaped
hemorrhagic
Fibrinous pleural exudate
Scar
Embolus
45
Q

Pulmonary embolism Microscopic Appearance

A

Ischemic necrosis

Infected embolus

46
Q

Septic Infarct

A

Pulmonary embolus that is infected, modified by a more intense neutrophilic inflammatory reaction

47
Q

Fat embolism

A 
microscopic fat globules
Hematopoietic marrow elements
After fracture of long bones
Soft tissue trauma/burns
Incidental findings after vigorous CPR
No clinical issues
48
Q

Air Embolism

A 
Gas bubbles within circulation
Frothy mass
Obstruct vascular flow
More than 100 CC air for clinical effect
Decompression sickness
49
Q

Bends

A

Rapid formation of gas bubbles within skeletal muscles and supporting tissues in and about joints

50
Q

The Chokes

A

Gas bubbles in vasculature

Causes edema, hemorrhage, focal atelectasis or emphysema, leads to respiratory distress

51
Q

Caisson disease

A

chronic depcompression sickness
Persistence of gas emboli in skeletal system (multiple foci of ischemic necrosis, common at femoral heads, tibia, humerus)

52
Q

Amniotic Fluid Embolism

A

Complication of labor and immediate postpartum period
Severe dyspnea, cyanosis, shock
Neurologic impairment, headache, seizures, coma
PE along with DIC (50%)
Infusion of amniotic fluid/fetal tissue into maternal circulation (tear in placental membrane or rupture of uterine veins)
Presence of squamous cells, lanugo, hair, fat, mucin

53
Q

Septic Infarction

A

When infected cardiac valve vegetations embolize or when microbes seed necrotic tissue
Infarct is converted into abscesses with great inflammatory response

54
Q

Bland Infarction

A

Uninfected infarct

Replaced by scar

55
Q

Cardiogenic shock

A

Low cardiac output due to pump failure (infarction, ventricular arrhythmia, extrinsic compression, outflow obstruction)

56
Q

Hypovolemic shock

A

Low cardiac output due to loss of blood or plasma volume (massive hemorrhage, severe burns)

57
Q

Septic shock

A

Vasodilation and peripheral pooling of blood as part of systemic immune reaction
Skin initially warm and flushed because of peripheral vasodilation

58
Q

Clinical consequences of shock

A

Impaired tissue perfusion and cellular hypoxia (systemic hypotension)
Cardiac, cerebral, pulmonary changes secondary to shock worsen the problem
Electrolyte disturbances and metabolic acidosis

Pathology Exam 2 (6 decks)

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