Lecture 3: Circulatory Disturbances Flashcards
1
Q
__ accumulation of abnormal amounts of fluid in interstitial and extracellular spaces or body cavities
A
edema
2
Q
5 pathogenic mechanisms for edema
A
- increased hydrostatic P
- increased vascular permeability
- decreased oncotic P (hypoalbuminemia)
- lymphatic obstruction
- sodium retention in renal dz
3
Q
4 pathophysiologic significances of edema
A
- fluid compression of adjacent structures
- diffusion/transport barrier
- alter mechanical properties of tissue
- alter cell function in tissue
4
Q
4 sequelae (after effect of a dz) of edema
A
- resolves/returns to normal
- cell/tissue dysfunction
- fibrosis/atrophy w/ chronic edema
- death (pulmonary or cerebral edema)
5
Q
__ increased volume of blood in microvascular systems associated with increased arterial inflow and/or decreased venous outflow
A
hyperemia
6
Q
__ is due to arterial dilation
A
active hyperemia
7
Q
__ is due to decreased venous return
A
hyperemia (synonymous with congestion)
8
Q
__ increased volume of blood in microvascular systems associated decreased venous outflow
A
congestion
9
Q
2 pathophysiologic significances of congestion
A
- increased hydrostatic pressure
2. decreased tissue perfusion
10
Q
3 sequelae (after effect of a dz) of congestion
A
- resolves/returns to normal
- edema and hemorrhaging
- local hypoxemia w/ cell damage
11
Q
__ is the escape of blood from the CV system during life
A
hemorrhage
12
Q
3 pathogenetic mechanisms of hemorrhaging
A
- trauma/injury
- diapedesis (movement of WBC out of circulation)
- hemorrhagic diatheses (vessel, platelet, coagulation abnormalities/tendency to bleed)
13
Q
chronic congestion of liver and decreased flow/hypoxemia through the liver is an example of
A
diapedesis
14
Q
__ hemorrhaging consists of very small (1-2cm) pinpoint lesions
A
petechiae (path mech: thrombocytopenia, vasculitis, cachexic, etc)
15
Q
__ hemorrhaging consists of irregular (2-3cm) diameter lesions
A
ecchymoses
16
Q
__ hemorrhage is intermediate to petechiae and ecchymoses lesions
A
purpura
17
Q
__ is a 3D mass of hemorrhage in TISSUE.
A
hematoma
18
Q
Hemorrhage in cavities is named for the region: heart = __, peritoneal cavity = ___, joints = __
A
hemopericardium, hemoperitoneum, hemarthroses
19
Q
pathophysiologic significance of hemorrhaging is determined by
A
location, rate, and volume of hemorrhage
20
Q
3 outcomes of hemorrhaging
A
- systemic hypovolemia/anemia = hypoxia
- tissue ischemic injury
- space occupying lesion with compression (like edema) - can cause death (brain hematoma, aortic rupture)
21
Q
3 sequelae (aftermath) discussed for hemorrhaging
A
- hemorrhagic anemia and death
- chronic anemia
- hemostasis (reabsorption of blood, inflammation and organization of blood clot)
22
Q
__ is the process of intravascular or intracardiac formation of a clot of fibrin and platelets during life
A
thrombosis
23
Q
Thrombosis process involves what 3 things
A
- vessel wall
- platelet aggregation
- coagulation
24
Q
__ is a mass carried from its site of origin in the vessel wall to a distant site
A
embolus
25
___ is a clot of blood formed intravascularly after death or extravascularly during life or death
blood clot
26
__ is a process resulting in the termination of hemorrhage (vasoconstriction, platelet plug formation, coagulation)
hemostasis
27
__ is the formation of a fibrin clot
coagulation
28
stallion that died during exercise via ruptured aorta which started clotting during the life of the animal (hemopericardium) is a __
blood clot (outside the vessel)
29
What is the appearance of a post mortem horse heart blood clot
RBC sedimentation making a gravity line dividing RBC "currant jelly clots" and yellow "chicken fat clots"
30
Coagulation (formation of fibrin clot) requires what 4 things
1. vessle wall
2. plasma proteins
3. platelets
4. leukocytes
31
Intrinsic coagulation cascade initiated by
hageman factor (XII)
32
extrinsic coagulation cascade is initiated by
thromboplastin (III) - tissue factor
33
__ converts soluble fibrinogen to insoluble firbin that undergoes further crosslinking for coagulation
thrombin
34
Factor __ initiates conversion of prothrombin to thrombin which acts on fibrinogen
10
35
damage to blood vessel exposes collagen which activates __, damage to endothelial cells activates ___. Both can happen at the same time and produce __
hageman factor (XII), thromboplastin (III), fibrin.
36
__ form platelet plugs at sites of vascular/endothelial injury and accelerate coagulation
platelets
37
3 steps to forming platelet plug of thrombus
1. adhesion
2. release reaction
3. platelet aggregation
38
__ factors mediate the binding of platelets to the surface and __ is important for aggregation of platelets
von willebrand's factor, fibrinogen
39
__ is the ability of platelets to stick to non-platelet surfaces
adhesion
40
__ acts as a molecular bridge between platelets and collagen which stabilizes platelet adhesion against shear forces
von Wilebrand's factor
41
genetic defects in which factor are associated with bleeding disorders?
von willebrand's factor
42
synthesis and release of __ stimulates vasoconstriction and platelet aggregation
thromboxane A2
43
platelet-platelet adherence causes release of __ which is an important accelerate of coagulation cascade.
platelet factor III (PF3)
44
What are the 2 main roles of endothelial cells in thrombosis
1. inhibit thrombogenesis
| 2. promote thrombogenesis
45
3 ways endothelial cells inhibit thrombosis
1. inhibit platelet aggregation
2. binding and inhibition of thrombin
3. promotion of fibrinolysis
46
3 ways endothelial cells inhibit platelet aggregation
1. prostacyclin (PGI2)
2. ADPase
3. nitric oxide
47
3 ways endothelial cells inhibit thrombin
1. antithrombin 3
2. thrombomodulin
3. alpha2 macroglobulin
48
How do endothelial cells promote fibrinolysis
plasminogen activator
49
Activation of procoagulation factors occur when tissue is damaged and collagen is exposed activating __ and releasing __ and __
factor XII (hageman's), von Willebrand's factor, platelet activating factor
50
3 events of Virchow's Triad!!!
1. alterations in the vessel wall
2. changes in blood flow
3. changes in the blood that promote thrombosis (hypercoagulabilty)
51
Low RBC content during initial platelet and fibrin deposition under __ flow
high
52
High RBC content causes partial occulusion of vessel lumen with __ flow = thrombus tail
decreased
53
__ thrombus is partially occlusive, a __ thrombus is occlusive, and a __ thrombus is not occlusive.
arterial, venous, cardiac mural
54
__ are fibrous laminar sheets seen in some thrombus.
lines of Zahn
55
Postmortem blood clots differ from thrombus grossly by
rubbery/gelatenous, soft (not friable), not attached to vessel wall
56
Postmortem blood clots differ from thrombus microscopically by
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
Occluded artery can lead to __ where an occluded vein can lead to -_
ischemia, increased hydrostatic pressure = edema and ischemia
58
5 sequelae (aftermath) to thrombosis
1. propagation
2. infarction
3. thromboembolism
4. organization and recanalization
5. fibrinolysis (breakdown of clot via plasmin)
59
__ breaks down the thrombus and returns blood flow to normal
fibrinolysis (via plasmin)
60
__ involves capillary vessel ingrowth (and enlargement) into a thrombus. Vessels eventually fuse and reestablish a blood flow however flow is not returned to normal.
recanalization
61
when endothelial cells are damaged they release __ which initiates plasminogen conversion to plasmin for fibrinolysis (thrombus breakdown)
tissue plasminogen activator (tPA) (- there are others but this is most common activator. )
62
3 things that activate fibrinolysis by converting plasminogen to plasmin
1. Kallikrein (converted by hageman factor)
2. streptokinase
3. tissue plasminogen activator (tPA) - MOST NATURAL/COMMON
63
__ is widespread thrombosis of microvascular beds with concurrent fibrinolysis. It can terminate with widespread hemorrhage due to consumptive coagulopathy (thrombocytopenia).
Disseminated Intravascular Coagulation (DIC)
64
3 predisposing factors to DIC
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
Kidney dz: amyloidosis leads to protein losing nephromyopathy (hypoalbuminemia) and also lose a lot of __ and become prone to thrombosis predisposing them to DIC
antithrombin 3 (inhibits thrombosis)
66
5 diagnostic features of DIC laboratory values
1. thrombocytopenia
2. hypofibrinogenemia (fibrinogen being consumed)
3. prolonged clotting times
4. fibrin degradation products (FDP, FSP)
5. Increased D-dimers
67
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)
D-Dimers.
68
2 features seen during necropsy of DIC
1. microvascular thrombi (lung, adrenal kidney, heart, initial site)
2. terminal widespread hemorrhaging
69
__ is a localized area of ischemic necrosis resulting from occlusion of the arterial or venous supply
infarction
70
2 sequelae to infarction
1. fibrous c.t./scarring
| 2. death (heart, brain)
