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pathology > GP 3,4,5 > Flashcards

GP 3,4,5 Flashcards

1
Q

what are four causes of edema

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

what type of cell is dominated by acute inflammation

A

neutrophils

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3
Q

describe effusion

A

pyothorax

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4
Q

what is a critical growth factor in wound healing and what does it act on

A

-TGF-beta
-acts on keratinocytes, fibroblasts, endothelial cells, monocytes

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5
Q

describe effusion

A

chylothorax

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6
Q

von willebrand factor

A

protein in the blood that helps blood clot, like glue

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7
Q

describe this effusion

A

serosanguinous

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8
Q

what type of hypersensitivity is most common with atopic forms of allergens and what immunologic component is it associated with?

A

type I hypersensitivity and IgE

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9
Q

major determinants of thrombosis?

A

-virchows triad
-specifcally alterations in the endothelium which results in increased production of pro-coagulant substances and decreased production of anti-coagulant substances

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10
Q

what factors is the extrinsic pathway of the coagulation cascade consisted of?

A

tissue factor (III)
VII

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11
Q

what is secondary hemostasis

A

coagulation to form a meshwork of fibrin
-tissue factor that initiates extrinsic pathway of coagulation cascade

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12
Q

what is primary hemostasis

A

transient vasoconstriction and platelet aggregation to form platelet plug at the site of damage

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13
Q

what is an example of diffuse/lepromatous granuloma

A

Johne’s disease (cattle, sheep, and goats)
-lesion occurring in the ileum and colon

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14
Q

what are the major players of chronic fibrosis when looking histologically

A

-mononuclear inflammatory cells (macrophages, lymphocytes, plasma cells)
-fibroblasts

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15
Q

what type of hypersensitivity is most common with auto immune disorders and what immunologic component is it associated with?

A

type II hypersensitivity
IgG and IgM

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16
Q

pyo pus has neutrophils

A

:)

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17
Q

what is the most potent inhibitor to inhibit coagulation

A

antithrombin III

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18
Q

what are the two major causes of non-inflammatory edema and transudate

A

-hepatic failure, reduce production of albumin (reduce oncotic pressure bc albumin draw in fluid)
-heart failure (increase hydrostatic pressure)

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19
Q

what factor is the last enzyme in the coagulation cascade

A

thrombin (factor II)

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20
Q

what cytokines play a role in acute inflammation

A

IL 1, IL 6, TNF

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21
Q

what is the hemostatic process

A
  1. primary hemostasis
  2. secondary hemostasis
  3. fibrinolysis
  4. tissue/ vascular repair at damage site
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22
Q

where is albumin produced

A

liver

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23
Q

what inhibits phospholipases

A

steroids

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24
Q

fibrinolysis

A

removes platelet/fibrin plug
-cleavage of plasminogen to plasmin

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25
Q

what blocks cyclooxygenase

A

NSAIDs

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26
Q

hemostasis

A

physiological response to vascular damage and stop bleeding to prevent loss
-normal

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27
Q

what is diffuse (lepromatous) granuloma

A

poorly demarcated
widespread distribution
-non-caseating aggregates of macrophages, variable degree of fibrosis

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28
Q

when an animal has gout due to the lack of what enzyme? and how does the enzyme work

A

-gout is an accumulation of gout crystals (uric acid) in the joint or viscera
-due to lack of the enzyme uricase (that converts blood uric acid into allantoin which is normally excreted out

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29
Q

what are some examples of nodular (tuberculoid) granuloma

A

-mycobacterium bovis of mycobacterium tuberculosis
-valley fever

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30
Q

three major anticoagulant-antothrombotic systems on endothelial cells

A
  1. protein C-protein S thrombomodulin system
  2. antithrombin III (prevents coagulation from happening)
  3. tissue factor pathway inhibitor
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31
Q

hyperemia blood flow and perfusion

A

active
arteriole dilation (erythema in skin)

32
Q

ecchymosis hemorrhage

A

more extensive vascular damage

33
Q

steps of leukocyte adhesion cascade

A

margination
rolling
adhesion
diapedesis (migration)
chemotaxis

34
Q

what factors does the common pathway consist of in the coagulation cascade?

A

X
prothrombin (II) thrombin
fibrinogen (I)
fibrin clot (XIII)

35
Q

what are the 5 cardinal signs of inflammation

A

redness
swelling
heat
pain
loss of function

36
Q

what is FIP and its pathogenesis

A

-chronic-active inflammation

ingestion of feline enteric corona virus (fecal-oral)-> replication in enerocytes and peyers patches of intestine-> mutation and replication in macrophages and blood monocytes->virus infected macrophages disseminate to multiple organs-> host immune response -> pyograulomatous vascutlitis

37
Q

petechia hemorrhage

A

pinpoint
minor vascular damagee

38
Q

morphaologial diagnosis

A

fibrinosuppurative epidcarditis/pericarditis

39
Q

thrombus resolution

A
40
Q

transudate or serous

A

clear watery fluid

41
Q

how much loss of blood volume to be considered an exsanguination

A

40% loss of blood volume

42
Q

what factors are consisted of in the intrinsic pathway of the coagulation cascade?

A

XII, XI, IX, VIII
$12 no $11.98

43
Q

what is an example of a negative (decrease inflammation) acute phase protein

A

albumin

44
Q

what is the most potent and clinically significant coagulation inhibitor and is produced by endothelium and hepatocytes

A

antithrombin III

45
Q

give pathogenesis of hemoperricardium causing cardiac tamponade

A

ruptured right auricular hemanigosarcoma -> compression of heart from blood -> decreased diastolic filling time -> decreased cardiac output

46
Q

function of plasmin

A

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

47
Q

what type of infarct is this?

A

acute red infarct
-red and often swollen or slightly raised (hemorrhage)

48
Q

what is edema

A

abnormal accumulation of fluid in the interstitial and body cavities

49
Q

suffusive hemorrhage

A

larger
contiguous areas of tissue
paintbrush

50
Q

types of chronic inflammation

A

-abscess
-granuloma/granulomatous inflammation (nodular, diffuse)
-eosinophilic inflammation/granuloma (parasites, no specific antigen)
-lymphocytic to lymphoplasmacytic inflammation

51
Q

function of albumin

A

helps keep fluid from leaking out of blood vessels

52
Q
A
53
Q

what is a driver of fever

A

PGE2

54
Q

congestion blood flow and perfusion

A

passive
impaired/decreased outflow of blood

55
Q

what chemokine is big activator and chemotaxis for neutrophils

A

IL 8

56
Q

coagulation cascade

A
57
Q

what are 2 examples of positive (increase inflammation) acute phase proteins

A

C-reactive proteins
serum amyloid a

58
Q

what is vascular leakage

A

when fluid leaks idiot body cavities rather than tissues
-effusion

59
Q

what is disseminated intravascular coagulation (DIC)

A

when the coagulation cascade is inappropriately set off, causing massive coagulation which leads to consumption of platelets, coagulation factors, and increase fibrinolysis
-since the coagulation factors are exhausted any small trauma can lead to uncontrolled bleeding

60
Q

phases of wound healing

A
  1. HEMOSTASIS (immediately after injury) accumulation of platelets exposed collagen
  2. INFLAMMATION (acute)
  3. PROLIFERATION (granulation tissue, angiogenesis, epithelialization)
  4. MATUREATION (remodeling of collagen, blood vessels regress and collagen synthesis eventually stops then scar)
61
Q

what factors are vitamin K dependent?

A

II, VII, IX, X
1972

62
Q

what is the main outcome/goals of the activated complement cascade

A

-formation of C5a and C3a (inducing inflammation by attracting leukocytes)
-formation of C3b (opsonization)
-formation of the membrane attack complex (pore in microbial surface)

63
Q

phases of acute inflammation

A

1.fluidic (exudative), dilte and localize
2. cellular, deliverinig white blood cells
3. reparative

64
Q

process of granulation tissue to healing by fibrosis

A

necrosis of tissue framework–>dead tissue and acute inflammatory exudate are removed–> space fills with fibrovascualr tissue (granulation tissue)–> eventually gets replaced by immature fibrous connective tissue –> scar

65
Q

what is the function of von willebran factor vWF

A

protein in the blood that helps blood clot

66
Q

thrombosis

A

inappropriate activation of the hemostatic process in a blood vessel
-clotting blood too much
-abnormal

67
Q

what are some examples of eosinophilic granulomas

A

-eosinophilic dermatitis (cutaneous habronemiasis)
-oral eosinophilic granulomas

68
Q

educate

A

-thick and cloudy fluid
hemorrahagic
serosanguious
purulent
chylous fibrinous

69
Q

what type of infarct is this?

A

subacute pale infarction
-affect areas become pale and often still surrounded by zones of hyperemia
(necrosis–> swelling–> force blood out of infarcted region–> pale appearance)

70
Q

what type of infarct is this?

A

chronic infarct
-pale, shrunken, firm, fibrosis

71
Q

what is the Virchow triad

A

-factors that contribute to hemostasis and thrombosis
1. endothelia injury
2. alterations in blood flow
3. blood hypercoaglability

72
Q

what are the three distinct morphologic nodular (tuberculoid) granuloma areas

A

-inner most: macrophages, multinucleated giant cells caseating (central necrosis)
-middle: macrophages, epithelioid macrophages, multinucleate giant cells
-outermost: lymphocytes, plasma cells, fibroblasts with a fibrous capsule

73
Q

endotoxemia causing vasculitis would incite which mechanism of edema?

A

increased vascular permeability

74
Q

what is secondary immunodeficiency disease

A

acquired

75
Q

what helps activate fibrinogen (factor I) to turn into fibrin (XIII)?

A

thrombin (facrtor II)

76
Q

what is primary immunodeficiency disease

A

congenital or genetic defect

77
Q

what is granulation tissue

A

exposed connective tissue that forms within a healing wound

pathology (10 decks)

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