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Pathology > Hemodynamics > Flashcards

Hemodynamics Flashcards

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1
Q

artery or vein? label the layers from outer-most to inner-most

A
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2
Q

artery or vein? Label parts

A

vein

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3
Q

what structural components differentiates a vein and artery microscopically?

A

elastic lamina

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4
Q

define edema

A

abnormal accumulation of fluid in interstitium and tisssues

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5
Q

list the four main causes of edema

A
  1. increased microvascular permeability (leaky vessel)
  2. increased vascular hydrostatic pressure
  3. decreased intravascular osmotic pressure
  4. decreased lymphatic drainage
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6
Q

ID the pathologies and describe colors

A

edema

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7
Q

list the two main causes of non-inflammatory edema

A

hepatic failure
heart failure

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8
Q

describe the two pathologies that cause edema from liver failure

A

reduced albumin production > decreased oncotic pressure > edema

portal hypertension aka blocked blood from stomach/intestines to the liver > increased hydrostatic pressure > edema

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9
Q

how does heart failure (dec CO and RAAS) cause edema?

A

dec CO > dec BF to kidneys > kidney sense reduction in volume > inc fluid volume through Na and H20 by activating RAAS > inc reabsorption of sodium > water retention > inc hydrostatic pressure

renin production by RAAS > angiotensin converted to angiotensin II > angiotensin II causes vasoconstriction > inc hydrostatic pressure

angiotensin II stimulates secretion of ADH > inc water permeability in CD > inc water retention > inc hydrostatic pressure

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10
Q

define hyperemia. is it an active or passive process?

A

arteriolar dilation causing a local increase in volume of blood
active process

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11
Q

list ways in which hyperemia occurs

A

inflammation
physical activity
increased blood flow to GI after food
physiologic mechanism to dissipate heat

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12
Q

define congestion. is it active or passive?

A

passive
impaired/decreased outflow of blood

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13
Q

list ways in which congestion occurs

A

CHF
local venous obstruction
organ displacement

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14
Q

ID hyperemia or congestion

A

hyperemia - called erythema in the skin

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15
Q

ID hyperemia or congestion

A

congestion

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16
Q

ID hyperemia or congestion

A

CHRONIC congestion

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17
Q

define erythrophagocytosis

A

macrophages that contain whole RBCs

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18
Q

define hemosiderin-laden macrophages

A

brown, iron containing from breakdown of RBC
heart failure cells

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19
Q

define hemostasis

A

PHYSIOLOGICAL response to vascular damage and stops bleeding

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20
Q

define thrombosis

A

PATHOLOGIC activation of hemostatic process to induce clot

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21
Q

what is virchow’s triad?

A

factors that contribute to hemostasis and thrombosis
1. endothelial injury !!!
2. abnormal blood flow
3. blood hypercoaguability

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22
Q

describe the hemostatic process (4 steps)

A
  1. primary hemostasis - vasoconstriction and platelet aggregation to form platelet plug at damaged site
  2. secondary hemostasis - coagulation to form fibrin mesh
  3. fibrinolysis - remove platelet/fibrin plug
  4. tissue/vascular repair
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23
Q

what is von willebrand factor? what step of the hemostatic process is it involved in?

A

protein that helps blood clot - glue for platelets to bind to injury
primary hemostasis

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24
Q

what is tissue factor? what step of the hemostatic process is it involved in?

A

initiates extrinsic path of coagulation cascade
secondary hemostasis

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25
describe the intrinsic coagulation cascade
factors 12 11, 9, 8 -> common path, factor 10 -> (prothrombin to thrombin factor 2) -> fibrinogen (1) -> fibrin clot
26
describe the extrinsic coagulation cascade
tissue factor 3 -> factor 7 -> common path, factor 10 -> (prothrombin to thrombin factor 3) -> fibrinogen -> fibrin clot
27
list the vitamin k dependent coag factors
factors 2, 7, 9, 10 1972
28
define fibrinolysis
prevents blood clots from forming pathogenic condition
29
describe the role of plasmin in the fibrinolytic system
digests fibrin clots and releases fibrin degradation products inhibits additional fibrin formation
30
what's the most important/potent coagulation inhibitor?
antithrombin 3 - made by endothelium and hepatocytes
31
what are the 3 major anticoagulant-antithrombotic systems on endothelial cells?
1. protein C-protein S thrombomodulin system 2. antithrombin III 3. tissue factor pathway inhbitor
32
list the three hemorrhage descriptive terms
petechia ecchymosis suffusive
33
define petechia
pinpoint hemorrhage minor vascular damage
34
define ecchymosis
more extensive vascular damage than petechia
35
define suffusive
larger, contiguous area of tissue hemorrhage damage paintbrush
36
ID hemorrhage type
37
ID hemorrhage type
38
ID hemorrhage type(s)
1. petechia 2. ecchymosis
39
ID hemorrhage type
40
what does hemorrhage significance depend on?
amount, location, rate large amounts > hypovolemia > decreased tissue perfusion > hypovolemic shock
41
exsanguination is __% of blood loss volume
40%
42
in which organs is it worst to have hemorrhage?
brain and heart - very little room to expand
43
define thrombus
group of platelets, fibrin, and other blood in injured blood vessel
44
physiologic vs persistent thrombus
physiologic - normal, rapidly resolves after healing persistent - forms on wall of injured vessel (blood, lymphatic, or heart)
45
define thromboembolism
persistent thrombus that is free in a vessel lumen
46
list major determinants of thrombosis
VIRCHOWS TRIAD *** alterations of endothelium to cause increased production of pro-coag substances
47
describe cardiac and large arterial thrombi what is it initiated by?
firmly attached to vessel wall lamellated appearance from rapid flow and alternating layers of platelets tunucia intima is lost/damaged initiated by endothelial damage
48
ID this pathology
cardiac/large arterial thrombi
49
describe venous thrombus what is it initiated by?
dark red, gelatinous since large amount of erythrocytes loosely incorporated into thrombus from slow BF most are occlusive become molded to shape of lumen of vein and grow upstream from site of initiation initiated by areas of slow blood flow/stasis
50
ID pathology
venous thrombus
51
How are small thrombi resolved?
removed by thombolysis and BV returns to normal structure and function
52
How larger thrombi resolved?
removal of thrombotic debris by phagocytes > granulation tissue formation and fibrosis >regrowth of endothelium over surface of thrombi to incorporate the affected area into the vessel wall
53
How are large mural or occlusive thombi resolved?
growth of endothelial-lined blood channels through fibrotic area (recanalization)
54
what type of thrombus resolution is shown here?
recanalization
55
where do venous emboli typically lodge?
pulmonary circulation causes R sided HF or infarcts
56
where do arterial thromboemboli lodge?
in the tissue that depends on it ex: saddle thrombus
57
what two main things could occur due to occlusion of a vessel?
hypoxia infarct
58
what's occurring here?
infarct
59
define acute red infarct
red, often swollen or slightly raised cause: hemorrhage
60
define subacute pale infarct and pathogenesis
pale necrosis > swelling > forces blood out of infarcted region > pale appearance
61
define chronic infarct
pale, shrunken, firm, fibrosis
62
describe the concept of disseminated intravascular coagulation (DIC)
endothelial damage > microvascular thrombosis > too much clotting and usage of factors > ischemia in one organ/area > lack of clotting factors in rest of body so too much bleeding in other areas
63
describe the infarct
acute red infarct
64
describe the infarct
subacute pale infarct
65
describe the infarct
chronic infarct

Pathology (12 decks)

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