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General Pathology (Fall 2014) > Lecture 5: Disturbances of Circulation > Flashcards

Lecture 5: Disturbances of Circulation Flashcards

1
Q

Edema

A

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

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2
Q

Anasarca

A

severe diffuse edema of the subcutis

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3
Q

hydrothorax

A

edema in pleural cavity

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4
Q

Starling Equilibrium

A

hydrostatic pressure drives fluid and electrolytes into perivascular space towards lymphatics on arterial end to supply nutrients to tissues, while oncotic P drives fluid back in on venous end. Any excess fluid that drains can also drain out of lymphatics

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5
Q

Pathogenic mechs. of edema and what they are assoc. with (5)**

A

1) increased hydrostatic P –> CV dz
2) increased vascular permeability –> inflammation
3) decreased oncotic pressure (hypoalbuminemia) –> protein-losing enteropathies, renal/liver dz
4) lymphatic obstruction –> malformations of lymphatic system or lumenal blockage from tumors
5) sodium retention in renal dz
* *listed in order of important. First 2 most important**

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6
Q

4 consequences of edema

A

1) fluid compression of adjacent structures
2) diffusion/transport barrier
3) alter mechanical properties of tissue
4) alter cell fx in tissue

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7
Q

Sequelae of edema (4)

A

1) resolution
2) cell and tissue dysfunction
3) fibrosis/atrophy in areas of chronic edema
4) death

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8
Q

Congestion

A

indicates a passive process characterized by decreased venous outflow resulting in increased volume of blood in microvascular systems

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9
Q

Hyperemia

A

more general term than congestion. Refers to either active arteriolar dilation OR passive decreased venous outflow resulting in increased volume of blood in microvascular systems

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10
Q

Clicker Q: which of the following mechanisms most likely explains edema fluid with high protein content?

A

increased vascular permeability

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11
Q

Clicker Q: 3D masses of hemorhage in tissue are:

A

hematomas

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12
Q

active vs. passive hyperemia

A 
active = due to arterial dilation
passive = due to decreased venous return (aka congestion)
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13
Q

pathophysiologic consequences of congestion

A

1) increased hydrostatic P

2) decreased tissue perfusion

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14
Q

3 Congestion sequelae

A

1) resolution
2) edema and hemorrhage
3) local hypoxemia with cell damage

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15
Q

Hemorrhage

A

escape of blood from the CV system during life

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16
Q

diapedesis

A

blood cells squeeze b/w epithelial cells in a high P capillary. Often occurs in lungs when there is congestion assoc. with L-sided heart failure. Can lead to hemorrhage

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17
Q

things that lead to hemorrhage

A
  • trauma
  • diapedesis
  • hemorrhagic dz
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18
Q

Common descriptive terms of hemorrhage, in order or size

A

petechiae < ecchymoses < purpura < hematoma < hemorrhage in cavities.
(side note: petechiae can be assoc. with thrombocytopenia)

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19
Q

pathophysiologic significance of hemorrhage is determined by:

A

location, rate, and volume of hemorrhage

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20
Q

Possible outcomes of hemorrhage

A
  • systemic hypovolemia/anemia –> hypoxia
  • tissue ischemic injury
  • space occupying lesion with compression
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21
Q

Sequelae of hemorrhage

A
  • hemorrhagic anemia and death
  • chronic anemia
  • hemostasis (leading to either reabsorption of blood, or inflammation and organization of blood clot by specialized connective tissue)
22
Q

Thrombosis

A

the process of intravascular or intracardiac formation of a clot of fibrin and platelets during life.
Involves vessel wall, platelet aggregation, and coagulation Is different from a blood clot!

23
Q

Thromboembolysis

A

when thrombus forms, breaks off, travels and lodges somewhere else

24
Q

Thrombus

A

an intravascular clot of fibrin and platelets attached to the CV wall formed during life

25
Q

embolus

A

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

26
Q

blood clot

A

clot of blood formed IV after death or EV during life or death

27
Q

hemostasis

A

process resulting in the termination of hemorrhage (vasoconstriction, platelet plug form, coag)

28
Q

coagulation

A

the formation of a fibrin clot. Requires complex interaction of:

  • vessel wall: endothelium/wall components
  • plasma proteins
  • platelets
  • leukocytes
29
Q

2 pathways of coagulation. what is their end result?

A

intrinsic and extrinsic. End result = activation of thrombin which converts fibrinogen to fibrin which is further polymerized to form a cross-linked visible network

30
Q

activation of intrinsic coag pathway is via:

A

activation of factor XII (results from vascular damage, exposure to collagen/endotoxin, virus, parasites, etc.)

31
Q

activation of extrinsic coag pathway is via:

A

release of thromboplastin (Tissue Factor III) from damaged endothelial cells

32
Q

T/F: initiation of cag. often involves interaction of intrinsic and extrinsic pathways

A

T

33
Q

Clicker: A thrombus carried from its site of vascular origin to a more distant vessel is a:**

A

embolus and/or thromboembolus

34
Q

Role of platelets in thrombosis

A

form platelet plugs at sites of vascular/endothelial injury and accelerate coag.
3 main steps: adehesion –> release reaction –> platelet aggregation

35
Q

von Willebrand’s factor

A

released from endothelial cells to help platelets interact with vessel wall to form a platelet plug. Serves as a molecular bridge betwen platelets and collagen, and stabilizes platelet adhesion against shear forces. (As aggregation process develops, there is intra-leaking of platelets by fibrinogen and it forms a stable plug and an aggregation)

36
Q

adhesion

A

the ability of platelets to stick to non-platelet surfaces

37
Q

cytoplasmic granules released in platelet release reaction

A

alpha granules: fibrinogen, fibronection, Factor 5 and 7, platelet factor 4, PDGF, TGF-beta
electron dense bodies: ADP, Ca, serotonin, EP

38
Q

role of thromboxane in platelet release rxn

A

stimulates vasoconstriction and platelet aggregation

39
Q

platelet-platelet adherence results in the exposure of:

A

platelet factor III (PF3). Provides a surface to accelerate many coag. sequences.

40
Q

PF3 is promoted by:

A

collagen, ADP, thromboxane, thrombin, PAF, endotoxin

41
Q

T/F: endothelial cells both inhibit and promote thrombogenesis

A

T

42
Q

How do endothelial cells inhibit platelet aggregation (and therefore thrombosis)?

A

release of prostacyclin, ADPase, NO

43
Q

How do endothelial cells promote binding and inhibition of thrombin?

A

binding of antithombin III, thrombomodulin, and alpha-2 macroglobulin

44
Q

How do endothelial cells promote fibrinolysis?

A

release plasminogen activator

45
Q

antithrombin III can be depleted in animals with what dz conditions?

A

glomerular nephritis/amyloidosis

46
Q

t-PA =

A

tissue plasminogen activator. Breaks down clot

47
Q

Endothelial inhibition of coag.

A

endothelial cells bind thrombomodulin/thrombin on the surface –> Protein S and C activation. Also bind to antithrombin III, which acts to inhibit thrombin. t-PA also promotes breakdown of clot.

48
Q

Endothelial cell promotion of thrombosis

A
  • production/activation of procoag factors
  • tissue factor release
  • factor 12 activation
  • von Willebrand factor release
  • PAF release
49
Q

Virchow’s Triad**

A

1) alterations in the vessel wall
2) changes in blood flow
3) changes in the blood that promote thrombosis (hypercoagulability)

50
Q

main role of PF3

A

accelerates coag.

51
Q

Descriptive terms of hemorrhage

A

petechiae < ecchymoses < purpura < hematoma < hemorrhage in cavities
(side note: petechiae can be assoc. with thrombocytopenia)

52
Q

morphogenesis of an arterial thrombus

A

1) initial platelet and fibrin deposition under high flow (low RBC content)

General Pathology (Fall 2014) (6 decks)

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