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General Pathology > Lecture 3: Circulatory Disturbances > Flashcards

Lecture 3: Circulatory Disturbances Flashcards

1
Q

__ accumulation of abnormal amounts of fluid in interstitial and extracellular spaces or body cavities

A

edema

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2
Q

5 pathogenic mechanisms for edema

A
  1. increased hydrostatic P
  2. increased vascular permeability
  3. decreased oncotic P (hypoalbuminemia)
  4. lymphatic obstruction
  5. sodium retention in renal dz
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3
Q

4 pathophysiologic significances of edema

A
  1. fluid compression of adjacent structures
  2. diffusion/transport barrier
  3. alter mechanical properties of tissue
  4. alter cell function in tissue
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4
Q

4 sequelae (after effect of a dz) of edema

A
  1. resolves/returns to normal
  2. cell/tissue dysfunction
  3. fibrosis/atrophy w/ chronic edema
  4. death (pulmonary or cerebral edema)
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5
Q

__ increased volume of blood in microvascular systems associated with increased arterial inflow and/or decreased venous outflow

A

hyperemia

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6
Q

__ is due to arterial dilation

A

active hyperemia

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7
Q

__ is due to decreased venous return

A

hyperemia (synonymous with congestion)

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8
Q

__ increased volume of blood in microvascular systems associated decreased venous outflow

A

congestion

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9
Q

2 pathophysiologic significances of congestion

A
  1. increased hydrostatic pressure

2. decreased tissue perfusion

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10
Q

3 sequelae (after effect of a dz) of congestion

A
  1. resolves/returns to normal
  2. edema and hemorrhaging
  3. local hypoxemia w/ cell damage
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11
Q

__ is the escape of blood from the CV system during life

A

hemorrhage

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12
Q

3 pathogenetic mechanisms of hemorrhaging

A
  1. trauma/injury
  2. diapedesis (movement of WBC out of circulation)
  3. hemorrhagic diatheses (vessel, platelet, coagulation abnormalities/tendency to bleed)
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13
Q

chronic congestion of liver and decreased flow/hypoxemia through the liver is an example of

A

diapedesis

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14
Q

__ hemorrhaging consists of very small (1-2cm) pinpoint lesions

A

petechiae (path mech: thrombocytopenia, vasculitis, cachexic, etc)

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15
Q

__ hemorrhaging consists of irregular (2-3cm) diameter lesions

A

ecchymoses

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16
Q

__ hemorrhage is intermediate to petechiae and ecchymoses lesions

A

purpura

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17
Q

__ is a 3D mass of hemorrhage in TISSUE.

A

hematoma

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18
Q

Hemorrhage in cavities is named for the region: heart = __, peritoneal cavity = ___, joints = __

A

hemopericardium, hemoperitoneum, hemarthroses

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19
Q

pathophysiologic significance of hemorrhaging is determined by

A

location, rate, and volume of hemorrhage

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20
Q

3 outcomes of hemorrhaging

A
  1. systemic hypovolemia/anemia = hypoxia
  2. tissue ischemic injury
  3. space occupying lesion with compression (like edema) - can cause death (brain hematoma, aortic rupture)
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21
Q

3 sequelae (aftermath) discussed for hemorrhaging

A
  1. hemorrhagic anemia and death
  2. chronic anemia
  3. hemostasis (reabsorption of blood, inflammation and organization of blood clot)
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22
Q

__ is the process of intravascular or intracardiac formation of a clot of fibrin and platelets during life

A

thrombosis

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23
Q

Thrombosis process involves what 3 things

A
  1. vessel wall
  2. platelet aggregation
  3. coagulation
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24
Q

__ is a mass carried from its site of origin in the vessel wall to a distant site

A

embolus

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25
Q

___ is a clot of blood formed intravascularly after death or extravascularly during life or death

A

blood clot

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26
Q

__ is a process resulting in the termination of hemorrhage (vasoconstriction, platelet plug formation, coagulation)

A

hemostasis

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27
Q

__ is the formation of a fibrin clot

A

coagulation

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28
Q

stallion that died during exercise via ruptured aorta which started clotting during the life of the animal (hemopericardium) is a __

A

blood clot (outside the vessel)

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29
Q

What is the appearance of a post mortem horse heart blood clot

A

RBC sedimentation making a gravity line dividing RBC “currant jelly clots” and yellow “chicken fat clots”

30
Q

Coagulation (formation of fibrin clot) requires what 4 things

A
  1. vessle wall
  2. plasma proteins
  3. platelets
  4. leukocytes
31
Q

Intrinsic coagulation cascade initiated by

A

hageman factor (XII)

32
Q

extrinsic coagulation cascade is initiated by

A

thromboplastin (III) - tissue factor

33
Q

__ converts soluble fibrinogen to insoluble firbin that undergoes further crosslinking for coagulation

34
Q

Factor __ initiates conversion of prothrombin to thrombin which acts on fibrinogen

35
Q

damage to blood vessel exposes collagen which activates __, damage to endothelial cells activates ___. Both can happen at the same time and produce __

A

hageman factor (XII), thromboplastin (III), fibrin.

36
Q

__ form platelet plugs at sites of vascular/endothelial injury and accelerate coagulation

37
Q

3 steps to forming platelet plug of thrombus

A
  1. adhesion
  2. release reaction
  3. platelet aggregation
38
Q

__ factors mediate the binding of platelets to the surface and __ is important for aggregation of platelets

A

von willebrand’s factor, fibrinogen

39
Q

__ is the ability of platelets to stick to non-platelet surfaces

40
Q

__ acts as a molecular bridge between platelets and collagen which stabilizes platelet adhesion against shear forces

A

von Wilebrand’s factor

41
Q

genetic defects in which factor are associated with bleeding disorders?

A

von willebrand’s factor

42
Q

synthesis and release of __ stimulates vasoconstriction and platelet aggregation

A

thromboxane A2

43
Q

platelet-platelet adherence causes release of __ which is an important accelerate of coagulation cascade.

A

platelet factor III (PF3)

44
Q

What are the 2 main roles of endothelial cells in thrombosis

A
  1. inhibit thrombogenesis

2. promote thrombogenesis

45
Q

3 ways endothelial cells inhibit thrombosis

A
  1. inhibit platelet aggregation
  2. binding and inhibition of thrombin
  3. promotion of fibrinolysis
46
Q

3 ways endothelial cells inhibit platelet aggregation

A
  1. prostacyclin (PGI2)
  2. ADPase
  3. nitric oxide
47
Q

3 ways endothelial cells inhibit thrombin

A
  1. antithrombin 3
  2. thrombomodulin
  3. alpha2 macroglobulin
48
Q

How do endothelial cells promote fibrinolysis

A

plasminogen activator

49
Q

Activation of procoagulation factors occur when tissue is damaged and collagen is exposed activating __ and releasing __ and __

A

factor XII (hageman’s), von Willebrand’s factor, platelet activating factor

50
Q

3 events of Virchow’s Triad!!!

A
  1. alterations in the vessel wall
  2. changes in blood flow
  3. changes in the blood that promote thrombosis (hypercoagulabilty)
51
Q

Low RBC content during initial platelet and fibrin deposition under __ flow

52
Q

High RBC content causes partial occulusion of vessel lumen with __ flow = thrombus tail

53
Q

__ thrombus is partially occlusive, a __ thrombus is occlusive, and a __ thrombus is not occlusive.

A

arterial, venous, cardiac mural

54
Q

__ are fibrous laminar sheets seen in some thrombus.

A

lines of Zahn

55
Q

Postmortem blood clots differ from thrombus grossly by

A

rubbery/gelatenous, soft (not friable), not attached to vessel wall

56
Q

Postmortem blood clots differ from thrombus microscopically by

A

No lines of Zahn (fibrin and RBC are not laminated due to lack of flow, but have some cross linking), leukocytes are not necrotic

57
Q

Occluded artery can lead to __ where an occluded vein can lead to -_

A

ischemia, increased hydrostatic pressure = edema and ischemia

58
Q

5 sequelae (aftermath) to thrombosis

A
  1. propagation
  2. infarction
  3. thromboembolism
  4. organization and recanalization
  5. fibrinolysis (breakdown of clot via plasmin)
59
Q

__ breaks down the thrombus and returns blood flow to normal

A

fibrinolysis (via plasmin)

60
Q

__ involves capillary vessel ingrowth (and enlargement) into a thrombus. Vessels eventually fuse and reestablish a blood flow however flow is not returned to normal.

A

recanalization

61
Q

when endothelial cells are damaged they release __ which initiates plasminogen conversion to plasmin for fibrinolysis (thrombus breakdown)

A

tissue plasminogen activator (tPA) (- there are others but this is most common activator. )

62
Q

3 things that activate fibrinolysis by converting plasminogen to plasmin

A
  1. Kallikrein (converted by hageman factor)
  2. streptokinase
  3. tissue plasminogen activator (tPA) - MOST NATURAL/COMMON
63
Q

__ is widespread thrombosis of microvascular beds with concurrent fibrinolysis. It can terminate with widespread hemorrhage due to consumptive coagulopathy (thrombocytopenia).

A

Disseminated Intravascular Coagulation (DIC)

64
Q

3 predisposing factors to DIC

A
  1. Massive release of factor 3 (bruns, sepsis, trauma, neoplasia)
  2. widespread microvascular damage (vasculitis, sepsis, virus)
  3. abnormal clotting/platelets (liver or kidney dz)
65
Q

Kidney dz: amyloidosis leads to protein losing nephromyopathy (hypoalbuminemia) and also lose a lot of __ and become prone to thrombosis predisposing them to DIC

A

antithrombin 3 (inhibits thrombosis)

66
Q

5 diagnostic features of DIC laboratory values

A
  1. thrombocytopenia
  2. hypofibrinogenemia (fibrinogen being consumed)
  3. prolonged clotting times
  4. fibrin degradation products (FDP, FSP)
  5. Increased D-dimers
67
Q

Fibrinogen is a large soluble protein. Thrombin cleaves it for thrombus mesh work. Plasmin also cleaves it making __, a good ddx indicator of wide spread fibrinolysis and thrombosis (DIC)

68
Q

2 features seen during necropsy of DIC

A
  1. microvascular thrombi (lung, adrenal kidney, heart, initial site)
  2. terminal widespread hemorrhaging
69
Q

__ is a localized area of ischemic necrosis resulting from occlusion of the arterial or venous supply

A

infarction

70
Q

2 sequelae to infarction

A
  1. fibrous c.t./scarring

2. death (heart, brain)

General Pathology (14 decks)

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