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GP 3,4,5 Flashcards

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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
what blocks cyclooxygenase
NSAIDs
26
hemostasis
physiological response to vascular damage and stop bleeding to prevent loss -normal
27
what is diffuse (lepromatous) granuloma
poorly demarcated widespread distribution -non-caseating aggregates of macrophages, variable degree of fibrosis
28
when an animal has gout due to the lack of what enzyme? and how does the enzyme work
-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
29
what are some examples of nodular (tuberculoid) granuloma
-mycobacterium bovis of mycobacterium tuberculosis -valley fever
30
three major anticoagulant-antothrombotic systems on endothelial cells
1. protein C-protein S thrombomodulin system 2. antithrombin III (prevents coagulation from happening) 3. tissue factor pathway inhibitor
31
hyperemia blood flow and perfusion
active arteriole dilation (erythema in skin)
32
ecchymosis hemorrhage
more extensive vascular damage
33
steps of leukocyte adhesion cascade
margination rolling adhesion diapedesis (migration) chemotaxis
34
what factors does the common pathway consist of in the coagulation cascade?
X prothrombin (II) thrombin fibrinogen (I) fibrin clot (XIII)
35
what are the 5 cardinal signs of inflammation
redness swelling heat pain loss of function
36
what is FIP and its pathogenesis
-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
petechia hemorrhage
pinpoint minor vascular damagee
38
morphaologial diagnosis
fibrinosuppurative epidcarditis/pericarditis
39
thrombus resolution
40
transudate or serous
clear watery fluid
41
how much loss of blood volume to be considered an exsanguination
40% loss of blood volume
42
what factors are consisted of in the intrinsic pathway of the coagulation cascade?
XII, XI, IX, VIII $12 no $11.98
43
what is an example of a negative (decrease inflammation) acute phase protein
albumin
44
what is the most potent and clinically significant coagulation inhibitor and is produced by endothelium and hepatocytes
antithrombin III
45
give pathogenesis of hemoperricardium causing cardiac tamponade
ruptured right auricular hemanigosarcoma -> compression of heart from blood -> decreased diastolic filling time -> decreased cardiac output
46
function of plasmin
digests fibrin clots and releases fibrin degradation products and inhibits additional fibrin formation
47
what type of infarct is this?
acute red infarct -red and often swollen or slightly raised (hemorrhage)
48
what is edema
abnormal accumulation of fluid in the interstitial and body cavities
49
suffusive hemorrhage
larger contiguous areas of tissue paintbrush
50
types of chronic inflammation
-abscess -granuloma/granulomatous inflammation (nodular, diffuse) -eosinophilic inflammation/granuloma (parasites, no specific antigen) -lymphocytic to lymphoplasmacytic inflammation
51
function of albumin
helps keep fluid from leaking out of blood vessels
52
53
what is a driver of fever
PGE2
54
congestion blood flow and perfusion
passive impaired/decreased outflow of blood
55
what chemokine is big activator and chemotaxis for neutrophils
IL 8
56
coagulation cascade
57
what are 2 examples of positive (increase inflammation) acute phase proteins
C-reactive proteins serum amyloid a
58
what is vascular leakage
when fluid leaks idiot body cavities rather than tissues -effusion
59
what is disseminated intravascular coagulation (DIC)
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
phases of wound healing
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
what factors are vitamin K dependent?
II, VII, IX, X 1972
62
what is the main outcome/goals of the activated complement cascade
-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
phases of acute inflammation
1.fluidic (exudative), dilte and localize 2. cellular, deliverinig white blood cells 3. reparative
64
process of granulation tissue to healing by fibrosis
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
what is the function of von willebran factor vWF
protein in the blood that helps blood clot
66
thrombosis
inappropriate activation of the hemostatic process in a blood vessel -clotting blood too much -abnormal
67
what are some examples of eosinophilic granulomas
-eosinophilic dermatitis (cutaneous habronemiasis) -oral eosinophilic granulomas
68
educate
-thick and cloudy fluid hemorrahagic serosanguious purulent chylous fibrinous
69
what type of infarct is this?
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
what type of infarct is this?
chronic infarct -pale, shrunken, firm, fibrosis
71
what is the Virchow triad
-factors that contribute to hemostasis and thrombosis 1. endothelia injury 2. alterations in blood flow 3. blood hypercoaglability
72
what are the three distinct morphologic nodular (tuberculoid) granuloma areas
-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
endotoxemia causing vasculitis would incite which mechanism of edema?
increased vascular permeability
74
what is secondary immunodeficiency disease
acquired
75
what helps activate fibrinogen (factor I) to turn into fibrin (XIII)?
thrombin (facrtor II)
76
what is primary immunodeficiency disease
congenital or genetic defect
77
what is granulation tissue
exposed connective tissue that forms within a healing wound

pathology (10 decks)

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