Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathology > Hemodynamics > Flashcards

Hemodynamics Flashcards

1
Q

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

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

artery or vein? Label parts

A

vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what structural components differentiates a vein and artery microscopically?

A

elastic lamina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

define edema

A

abnormal accumulation of fluid in interstitium and tisssues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

ID the pathologies and describe colors

A

edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

list the two main causes of non-inflammatory edema

A

hepatic failure
heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

define hyperemia. is it an active or passive process?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

list ways in which hyperemia occurs

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

define congestion. is it active or passive?

A

passive
impaired/decreased outflow of blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

list ways in which congestion occurs

A

CHF
local venous obstruction
organ displacement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

ID hyperemia or congestion

A

hyperemia - called erythema in the skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

ID hyperemia or congestion

A

congestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

ID hyperemia or congestion

A

CHRONIC congestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

define erythrophagocytosis

A

macrophages that contain whole RBCs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

define hemosiderin-laden macrophages

A

brown, iron containing from breakdown of RBC
heart failure cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

define hemostasis

A

PHYSIOLOGICAL response to vascular damage and stops bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

define thrombosis

A

PATHOLOGIC activation of hemostatic process to induce clot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

describe the intrinsic coagulation cascade

A

factors 12 11, 9, 8 -> common path, factor 10 -> (prothrombin to thrombin factor 2) -> fibrinogen (1) -> fibrin clot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

describe the extrinsic coagulation cascade

A

tissue factor 3 -> factor 7 -> common path, factor 10 -> (prothrombin to thrombin factor 3) -> fibrinogen -> fibrin clot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

list the vitamin k dependent coag factors

A

factors 2, 7, 9, 10

1972

28
Q

define fibrinolysis

A

prevents blood clots from forming pathogenic condition

29
Q

describe the role of plasmin in the fibrinolytic system

A

digests fibrin clots and releases fibrin degradation products
inhibits additional fibrin formation

30
Q

what’s the most important/potent coagulation inhibitor?

A

antithrombin 3 - made by endothelium and hepatocytes

31
Q

what are the 3 major anticoagulant-antithrombotic systems on endothelial cells?

A
  1. protein C-protein S thrombomodulin system
  2. antithrombin III
  3. tissue factor pathway inhbitor
32
Q

list the three hemorrhage descriptive terms

A

petechia
ecchymosis
suffusive

33
Q

define petechia

A

pinpoint hemorrhage
minor vascular damage

34
Q

define ecchymosis

A

more extensive vascular damage than petechia

35
Q

define suffusive

A

larger, contiguous area of tissue hemorrhage damage
paintbrush

36
Q

ID hemorrhage type

A
37
Q

ID hemorrhage type

A
38
Q

ID hemorrhage type(s)

A
  1. petechia
  2. ecchymosis
39
Q

ID hemorrhage type

A
40
Q

what does hemorrhage significance depend on?

A

amount, location, rate

large amounts > hypovolemia > decreased tissue perfusion > hypovolemic shock

41
Q

exsanguination is __% of blood loss volume

A

40%

42
Q

in which organs is it worst to have hemorrhage?

A

brain and heart - very little room to expand

43
Q

define thrombus

A

group of platelets, fibrin, and other blood in injured blood vessel

44
Q

physiologic vs persistent thrombus

A

physiologic - normal, rapidly resolves after healing
persistent - forms on wall of injured vessel (blood, lymphatic, or heart)

45
Q

define thromboembolism

A

persistent thrombus that is free in a vessel lumen

46
Q

list major determinants of thrombosis

A

VIRCHOWS TRIAD
*** alterations of endothelium to cause increased production of pro-coag substances

47
Q

describe cardiac and large arterial thrombi

what is it initiated by?

A

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
Q

ID this pathology

A

cardiac/large arterial thrombi

49
Q

describe venous thrombus

what is it initiated by?

A

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
Q

ID pathology

A

venous thrombus

51
Q

How are small thrombi resolved?

A

removed by thombolysis and BV returns to normal structure and function

52
Q

How larger thrombi resolved?

A

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
Q

How are large mural or occlusive thombi resolved?

A

growth of endothelial-lined blood channels through fibrotic area (recanalization)

54
Q

what type of thrombus resolution is shown here?

A

recanalization

55
Q

where do venous emboli typically lodge?

A

pulmonary circulation
causes R sided HF or infarcts

56
Q

where do arterial thromboemboli lodge?

A

in the tissue that depends on it
ex: saddle thrombus

57
Q

what two main things could occur due to occlusion of a vessel?

A

hypoxia
infarct

58
Q

what’s occurring here?

A

infarct

59
Q

define acute red infarct

A

red, often swollen or slightly raised
cause: hemorrhage

60
Q

define subacute pale infarct and pathogenesis

A

pale
necrosis > swelling > forces blood out of infarcted region > pale appearance

61
Q

define chronic infarct

A

pale, shrunken, firm, fibrosis

62
Q

describe the concept of disseminated intravascular coagulation (DIC)

A

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
Q

describe the infarct

A

acute red infarct

64
Q

describe the infarct

A

subacute pale infarct

65
Q

describe the infarct

A

chronic infarct

Pathology (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions