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Path Midterm Flashcards

0
Q

what are the 5 changes in the vascular system during inflammation?

A 
dilation of bv by chemicals
increased permeability- loss of protein
change in rate of blood flow
change in blood stream
margination and immigration of leukocytes
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1
Q

what are the 5 clinical signs of inflammation?

A 
redness
swelling
heat
pain
loss of fxn
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2
Q

what are the 3 mechanisms of extravasation?

A

endothelial cell contraction - most common
vascular leakage from direct endothelial cell injury
vascular leakage resulting from leukocyte injury adhesion cascade

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3
Q

which mechanism of extravasation acts on arterioles?

A

direct injury to endothelial cells leading to vascular leakage

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4
Q

in mild injury, what vessels become permeable?

A

post capillary venules

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5
Q

in moderate injury, what blood vessels become permeable?

A

capillaries and small venules

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6
Q

in severe injury, what vessels become permeable?

A

venules and arterioles

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7
Q

what vessels does the immediate transient response to injury occur?

A

post capillary venules

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8
Q

how long does immediate transient response (monophasic) last?

A

15 to 30 minutes

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9
Q

what vessels are involved in immediate prolonged response (biphasic) and how long did it last?

A

capillaries and venules

lasts minutes to days

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10
Q

what is immediate prolonged response mediated by in the early phase?

A

kinin

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11
Q

what is it called when many rbcs exit bv by diapedesis?

A

hemorrhagic inflammation

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12
Q

which response of vascular permeability lasts the longest?

A

sustained response - direct injury to endothelial cells

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13
Q

what are the 3 causes of slowing down of blood during inflammation?

A

loss of fluid - high viscosity of blood
passive congestion
stasis of lymph flow

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14
Q

what is leukocyte adhesion mostly determined by in margination?

A

complementary adhesion molecules (cam)

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16
Q

what are the 4 different types of adhesion molecules?

A

selectins
immunoglobins
integrins
mucus like glycoproteins

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17
Q

What are the 4 beneficial effects of exudation during inflammation?

A

dilutes toxin
brings antibodies
fibrin supports leukocyte mobility
fibrin localizes inflammation

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18
Q

What species are prone to leukocyte adhesion deficiencies?

A

Cows and dogs (irish setters)

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19
Q

What are the symptoms in cattle that have leukocyte adhesion deficiency?

A

severe gingivitis, tooth loss
oral and enteric ulcers
abcesses and pneumonia
=lethal

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20
Q

What are the 2 vasoactive amines?

A

histamine and serotonin

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21
Q

What are the 2 vasoactive proteases?

A

plasmin and globulin factors

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22
Q

What are the 3 preformed chemical mediators of inflammation?

A

histamine
serotonin
lysosomal enzymes

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23
Q

What are the 2 parts of the plasma chemical mediators in inflammation?

A

complement activation

hageman factor activation

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24
Q

What cells store histamine in their granules?

A

basophils
mast cells
blood platelets

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25
Q

What are the effects of histamine and serotonin in inflammation?

A

early transient dilation of BV (15-30 mins)

increase permeability of BV

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26
Q

What are the 2 functions of plasmin in inflammation?

A

degrades fibrin

cleaves C3 of complement

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27
Q

What cells release heparin during inflammation and what effect does it have?

A

mast cells

prolongs exudation in acute phase

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28
Q

Which prostaglandins are involved in vasodilation?

A

PGE2 and PGI2

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29
Q

What are the 3 ways fibrin is removed?

A

fibrinolytic enzymes from leukocytes
phagocytic leukocytes
plasmin

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30
Q

What is the prostaglandin involved in hyperalgesia?

A

PGE2

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31
Q

What leukotriene is a powerful chemotactic?

A

Leuko-B4

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32
Q

What leukotrienes are involved in vascular permeability?

A

Leuko-C4, D4, E4

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33
Q

What is responsible for vascular dilation after histamine?

A

kinin system

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34
Q

Kinin activates hageman factor which results in what?

A

amplification mechanism in inflammation

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35
Q

What do prostaglandins and leukotrienes do to smooth muscles?

A

contract

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36
Q

What other chemical mediators of inflammation do the prostaglandins and leukotriens enhance?

A

histamine and kinin

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37
Q

What are the 4 ways that oxygen derived free radicals cause cell damage?

A

peroxidation of cell membrane lipids
cross linking of proteins
damage DNA
cleaving glycoconjugates

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38
Q

What are the roles of nitric oxide during inflammation?

A 
vasodilation
inhibits platelets
oxidizes lipids
inhibits mast cells
regulates chemotaxis
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39
Q

What do interleukins do?

A

regulate interactions between lymphocytes and other WBCs

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40
Q

What are the three types of cytokines?

A

interleukins
tumor necrosis factors
interferons

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41
Q

What cytokine produced by macrophages stimulates Th2 cells?

A

interleukin 1

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42
Q

What cytokine is produced by macrophages and promotes B cell maturation?

A

Interleukin 6

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43
Q

What cytokine is produced by macrophages and is a co-stimulator of Th1 cells?

A

interleukin 12

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44
Q

What are the major cytokines produced by macrophages?

A

IL 1, 6, 12, 18, and TNF

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45
Q

What 2 cytokines are produced by Th1 cells?

A

Interleukin 2

Interferon-y (gamma)

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46
Q

What are the cytokines produced by Th2 cells?

A

IL-4,5,9,10, 13

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47
Q

What do interferons do?

A

inhibit virus replication by interfering with viral RNA and protein synthesis

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48
Q

What are type 1 interferons?

A

have antiviral activity, used in pregnancy signaling

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49
Q

What is the type 2 interferon?

A

IFNY

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50
Q

What are the 3 properties of neutrophils?

A

strong amoeboid movement
phagocytic and killing of microbes and tumors
intracellular digestion

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51
Q

How long do neutrophils survive in tissue?

A

1 to 4 days

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52
Q

What are the normal neutrophil percentages in different species?

A

Carnivores - 60-75%
Ruminants - 20-30%
Horse - 50%

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53
Q

What are the pHs of the smaller neutrophil granules? large ones?

A

small - acidic

large - alkaline

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54
Q

What does migration of neutrophils stimulate?

A

colony stimulating factor–> granulopoeisis

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55
Q

What is degenerative left shift?

A

band forms increase but number of mature neutrophils is normal or decreased

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56
Q

What are the 3 causes of neutropenia?

A

acute tissue demand (acute inflammation, sepsis)
decreased marrow production
increased margination

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57
Q

What 2 conditions increase margination of neutrophils leading to neutropenia?

A

anaphylaxis

endotoxemia

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58
Q

What are the 4 steps in neutrophil phagocytosis?

A

Chemotaxis, adherence, ingestion, digestion

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59
Q

What are the 2 ways neutrophils digest the material they phagocytize?

A

respiratory burst

lysosomes

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60
Q

What are the 4 fxns of eosinophils?

A

limited phagocytic activity
cytotoxicity of parasites
inflammatory rxn
allergic rxn

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61
Q

What term is used for chronic inflammation that has dense infiltration of eosinophils?

A

eosinophilic granuloma

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62
Q

What are the 3 idiopathic eosinophilic granulomas in felines?

A

eosinophilic plaque
linear granuloma
eosinophilic ulcer

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63
Q

Where are eosinophilic granulomas usually seen in felines?

A

abdomen and inner thigh

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64
Q

Where are eosinophilic ulcers usually seen in felines?

A

upper lip

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65
Q

Where are Equine collagenolytic granulomas seen?

A

saddle area

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66
Q

Where is eosinophilic myositis seen in dogs?

A

muscles of mastication - special 2m myosin, test for antibodies to this

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67
Q

Where is eosinophilic myositis seen in cattle and sheep?

A

skeletal and cardiac muscle, allergy to own muscle is suspected

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68
Q

Where are mast cells found?

A

organs rich in connective tissue

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69
Q

What is the life span of mast cells in tissue?

A

4-12 weeks

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70
Q

What do basophils release?

A

IL4, IL13, and histamine

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71
Q

What immunoglobulin do basophils and mast cells have many receptors for?

A

IgE

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72
Q

What do B lymphocytes differentiate into and are not found in blood circulation?

A

plasma cells

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73
Q

Where are class 1 MHC molecules expressed?

A

all nucleated cells

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74
Q

Where are class 2 MHC molecules expressed?

A

specialized APC

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75
Q

What MHC class do CD4+ T cells react to?

A

class 2 on surface of APC

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76
Q

What MHC class do CD8+ T cells (CTLs) react to?

A

class 1

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77
Q

What do CD4+T cells differentiate into and do?

A

effector cells - help other immune cells

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78
Q

What are some reasons that monocytes are not present in large numbers during acute inflammation like neutrophils?

A

circulating pool is low
production is lower
different chemotaxis
not as mobile

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79
Q

What can monocytosis indicate?

A

inflammation

tissue necrosis

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80
Q

What 3 things do macrophages secrete?

A

enzymes
pro-inflammatory products
growth factors

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81
Q

What conditions are epitheloid cells usually seen?

A

chronic inflammation - tuberculosis and johnes dz

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82
Q

What are epitheloid cells?

A

large foamy macrophages

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83
Q

What are giant cells?

A

2 or more fused macrophages

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84
Q

Where are the nuclei in Langhan’s type of giant cell?

A

periphery

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85
Q

Where are the nuclei in foreign body giant cells?

A

clustered in center or distributed

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86
Q

What are the causes of serous inflammation and where are they found?

A 
serous cavities - infection
joints - trauma
lungs - infection, poison
skin - toxins, trauma, burn
mucous membranes - viral infection
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87
Q

Where does fibrinous inflammation occur?

A

serous and mucous membranes (same as serous except not skin)

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88
Q

What are the causes of fibrinous inflammation?

A

same as serous

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89
Q

What is the microscopic appearance of fibrin inflammation?

A

dirty pink mixed with leukocytes

90
Q

What are the effects of fibrin inflammation?

A

protection, chemotactin, regeneration of underlying tissue, organization

91
Q

Where does the mucus come from in mucus inflammation?

A

the cells (instead of the blood)

92
Q

What are the causes of catarrhal or mucus inflammation?

A 
bacteria and low virulence viruses
mild chemicals
irritating food
inhalation of dust/foreign protein
parasite - chronic irritation
93
Q

what does mucus stain with H&E?

94
Q

What are the effects of mucus inflammation?

A

protective

chronic - becomes purulent

95
Q

Where does hemorrhagic inflammation occur?

A

organs of rich blood supply - lung, GI

96
Q

How does hemorrhagic inflammation differ from hemorrhage?

A

inflammation - blood oozes from inflamed tissue by diapedesis

97
Q

What are the causes of hemorrhagic inflammation?

A

microorganisms of high virulence

acute poisoning

98
Q

What is the effect of hemorrhagic inflammation?

A

if cause is not removed, fatal

99
Q

Where does purulent inflammation occur?

A

ALL TISSUES

100
Q

What are the causes of purulent inflammation?

A

pyogenic bacteria

fungal infections

101
Q

What color can the pus be in purulent inflammation?

A

yellow cream to bluish green to black

102
Q

What is the microscopic hallmark of purulent inflammation?

A

neutrophils

103
Q

What is the most effective method of defense against bacteria and fungi?

A

purulent inflammation

104
Q

What happens if abscess ruptures on surface of organ or mucous membranes of respiratory, digestive or repro tract?

105
Q

What happens if abscess ruptures in blood stream?

A

metastatic abscesses

toxemia/death

106
Q

What is the definition of an abscess?

A

encapsulated area of inflammation

107
Q

How is chronic inflammation different than acute?

A

infiltration of mononuclear cells, tissue destruction, attempt at repair

108
Q

Is granulomatous inflammation chronic or acute?

109
Q

What are the two types of granulomatous lesions?

A

diffuse and nodular

110
Q

What does the composition of cells around the granuloma depend on?

A

causative agent

111
Q

What causes lymphocytic inflitration seen in chronic inflammatory lesions?

A 
infections of CNS - perivascular cuffing
portal triad of liver and in cortex of kidney
mucous membranes - lamina propria
bronchi - peribronchial cuffing
effect and significance not clear
112
Q

What is healing by repair?

A

damaged cells replaced by OTHER types of cells (connective tissue)

113
Q

What are the 3 categories of cells being able to regenerate?

A

labile, stable, permanant

114
Q

What are labile cells?

A

continuously dividing cells - epithelial cells, bone marrow, lymphoid organs

115
Q

What are stable cells?

A

quiescent - parenchymatous organs such as liver, kidney, pancreas, adrenal, bone, tendon, nerve, smooth muscle (and mesenchymal?)

116
Q

What does paranchymal mean?

A

many different types of cells - liver with blood vessels, etc

117
Q

What are examples of permanent cells?

A

neurons, cardiac and skeletal muscle cells

118
Q

What are the two examples of loss of specialized function during repair by connective tissue?

A

fibrous replacement of kidney

myocardial infarction

119
Q

What are the steps of primary healing?

A 
clot formation
inflammatory response
fibroblast response
endothelial response
epithelial regeneration
collagen formation
120
Q

What is the definition of healing by first intention?

A

healing of a clean wound where tissues are opposed

121
Q

what are the 3 layers of a secondary union healing?

A

superficial layer of cell debris
layer of newly formed BV at right angles to lesion
deep layer of fibroblasts with collagen running parallel

122
Q

What is the term used for large amounts of scar tissue?

A

cicatrization

123
Q

What antibody is involved in Type 1 hypersensitivity?

124
Q

What are the specific features of type 1 hypersensitivites?

A

need sensitization phase and re exposure
transferable to normal animal
genetic predisposition
reaction time - 15 to 20 minutes

125
Q

What does a lick granuloma look like grossly?

A

circumscribed, hairless, ulcerated

on carpal, metacarpal, metatarsal, tibia or radius areas

126
Q

What are the 3 different antibody dependent mechanisms for type 2 hypersensitivity?

A
  1. complement dependent reaction
  2. antibody dependent cell mediated cytotoxicity (ADCC)
  3. antibody mediated cellular dysfunction
127
Q

What does complement dependent reaction usually involve?

A

blood cells - transfusion, hemolytic anemia of newborn auto immune hemolytic anemia, thrombo, certain drug rxns

128
Q

What is antibody mediated cellular dysfunction?

A

antibodies directed against cell surface receptors impair or dysregulate function

129
Q

What are characteristics of type 3 hypersensitivities?

A

immune complexes

tissue damage

130
Q

What are the two categories of antigens and what are examples?

A

exogenous - foreign protein, bacteria, viruses

endogenous - nuclear antigen immunoglobulin, tumors

131
Q

What are localized type 3 sensitivity reactions called?

A

arthus rxn

132
Q

What is the pathogenesis of immune complex dzs? (type 3 hyper)

A

formation of antigen/antibody complex
deposition of immune complex
initiation of inflammatory rxn

133
Q

What are 6 examples of system immune complex diseases

A
  1. glomerulonephritis
  2. systemic lupus erythomatousus
  3. immune mediated arthropathies - RA
  4. idiopathic poyarthritis
  5. periarteritis nodosa,, necrotizing vasculitis
  6. immune mediated meningitis
134
Q

What are examples of localized immune complex diseases?

A

hypersensitivity pneuomonitis - alveoli deposition
vasculitis - dogs and horses
purpura hemorrhagica
anterior uveitis - dogs, cats, horses,

135
Q

What is another name for type 4 DTH?

A

cell mediated hypersensitivity

136
Q

What are the features of DTH?

A 
no antibody
cellular reactions
24-48 hours
intracellular organisims
T lymphocytes
137
Q

What are examples of type 4 hypersensitivity (DTH)?

A

tuberculin test
contact dermatitis
flea allergy dermatitis
sweet itch in horses

138
Q

What charcterisizes flea allergy dermatitis in dogs and cats?

A

dogs - alopecia, hyperkeratosis

cats - scabs on back

139
Q

What are 3 examples of failure of normal development?

A

aplasia, atresia, hypoplasia

140
Q

What are examples of cellular adaptation to change that results in growth disturbance?

A

aging, involution of thymus

atrophy, hypertrophy, metaplasia, dysplasia

141
Q

What are the 3 factors that are stimuli to proliferate cells during repair?

A

cytokines and wound hormones
chemical stimulants
pressure gradients

142
Q

What are the 3 systemic factors involved in adequacy of repair?

A

physioloical condition of animal
nutrition
endocrine factors

143
Q

What are the local factors affecting adequacy of repair?

A

blood supply
infection
mobility of tissues
site of injury

144
Q

What is aplasia (agenesis)?

A

organ did not develop fully during embryogenesis

145
Q

What is atresia?

A

absence of closure of organ opening

146
Q

What are the 2 causes of hypoplasia (organ doesnt get full size)?

A

viral infections in mother

genetic

147
Q

What are examples of viral hypoplasia?

A

BVD - cerebellar
Blue tongue virus - cerebellar in lambs
canine distemper - enamal

148
Q

What are some known genetic effects of hypoplasia

A

familial renal hypoplasia in dogs

pancreatic hypoplasia - dogs and cattle

149
Q

What is the difference between aplasia and hypoplasia?

A

hypoplastic structure shows normal architechture

150
Q

What is atrophy?

A

decrease in tissue mass after achieving normal growth

151
Q

What are some causes of atrophy?

A

physiologic - thymic ,uterine involution, mammary gland

pathologic

152
Q

What are the 2 main causes of pathologic atrophy?

A 
disuse atropy
neurogenic
vasculogenic
nutritional
endocrine
inflammatory
153
Q

What happens during sublethal injury?

A

autophagocytosis

154
Q

What is hypertrophy?

A

increase tissue size due to increase in individual cell size

155
Q

What are causes of hypertrophy?

A

physio - uterus, muscles

pathologic - cardiac, renal, hormone

156
Q

What is hyperplasia?

A

much more common than hypertrophy

increase in cell number - reversible

157
Q

What is metaplasia?

A

transformation of cell type to another of same germ layer

158
Q

Where is metaplasia usually seen?

A

in epithelium and connective tissue

159
Q

What are some causes of metaplasia?

A

chronic irritation, vit A def, estrogen, blockage of bile ducts, myeloid

160
Q

What is dysplasia?

A

abnormal development

161
Q

What is dystrophy?

A

progressive degenerating and atrophic changes

some nutritional, some inherited

162
Q

What are examples of dystrophy?

A

osteodystrophies - rickets
muscular - inherited
neuroaxonal - sheep and dogs

163
Q

What does “malignant” imply?

A

ability to invade locally

ability for metastasis

164
Q

What is the suffix for benign?

165
Q

What is the suffix for malignant?

A
  • carcinoma : epithelial tissue

- sarcoma : mesenchymal tissue

166
Q

Malignant glandular-epithelium tumor

A

adenocarcinoma

167
Q

benign surface protective epithelium tumor

168
Q

Malignant surface protective epithelium tumor

169
Q

What layer do carcinomas come from

A

ANY layer of epithelium

170
Q

What is a mixed tumor?

A

arises from cells normally found in the tissue

171
Q

What can not be part of a mixed tumor?

A

bone and cartilage

172
Q

What are teratomas/teratocarcinomas?

A

germ ccells - contain tissue from all embryonic cell layers

173
Q

What is anaplasia

A

tumor cells do not resemble parent tissue (cell differentiation)

174
Q

Are immature or mature anaplasias more malignant?

175
Q

Tumors of melanocytes

A

B - melanocytoma

M - melanoma

176
Q

Tumors of lymphocytes

A

both malignant - lymphoma, lymphosarcoma

177
Q

Tumors of mast cells

A

B- mast cell tumor

M - mast cell sarcoma, mastocytoma

178
Q

Tumors of astroglia

A

both benign and malignant - astrocytoma

179
Q

Bone marrow tumors

A

malignant - leukemia

180
Q

Term for disorganize mass growing around nerve tissue after trauma

181
Q

Term for hyperplastic mass of mature tissue as a result of anomalous development, normal to location but not a tumor

182
Q

Term for non neoplastic normal mature tissue that do not occur normally at that site (dermoid)

A

chriostoma

183
Q

What is a leiomyoma

A

smooth muscle tumor

184
Q

What is the exception that benign tumors grow slowly?

A

papillomas, hormone dependent mammary tumors in bitch

185
Q

What are the most important criteria for benign tumors?

A

rarely invade

never metastasize

186
Q

How do tumors metastasize in body cavities?

A

implantation - through serous membrane

187
Q

What is the “paranchyma” of tumor cells?

A

the actual neoplastic cells

188
Q

What is the stroma made of in tumors?

A

supporting tissue - host derived, ct, bv

189
Q

What does vessel leakiness allow in tumors?

A

deposition of fibrin network that promotes formation of collagenous tumor stroma

190
Q

What causes angiogenesis near tumor cells?

A

angiogenic factors
hypoxia
glucocorticoids interfere with angiogenesis

191
Q

What is the term for fibrous capsule around benign tumors?

A

fibroplasia

192
Q

What are the non specific host defenses against a tumor

A

inflammatory (not very protective)

phagocytosis

193
Q

What is a specific mechanism of host defense against tumor?

A

tumor antigens - antibodies and cytotoxic T lympphos

194
Q

What are the 2 parts of the innate immune response against tumors?

A

natural killer cells

macrophages

195
Q

What are the parts of adaptive antitumor response?

A

lymphocytes - CTLs and CD8 T lymphos

B Lymphocytes - ADCC

196
Q

What does failure of immunosurveilance mean?

A

if humoral and adaptive immune response fail

197
Q

How are tumors able to evade the immune response?

A

no surface molecules, masking of antigens by glycolyx, fibrin or ab, tolerance of antigens, no MHC, immunosuppressive effects, apoptosis in T lymphos

198
Q

What type of disease is cancer?

A

non lethal genetic damage

199
Q

What are protooncogenes?

A

genes that promote cell grwoth

200
Q

What antibodies are associated with type 2 hypersensitivity reactions?

A

IgG and IgM

201
Q

What determines the extent of tissue damage in type 3 hypersensitivity?

A

size of immune complex

overload and intrinsc dysfunction of MPS

202
Q

What bacteria genus is known to cause cancer?

A

Helicobacter spp

203
Q

What parasite is known to cause cancer?

A

spirocerca lupi

204
Q

What are the local effects of neoplasms?

A

compression, oobstruction, tissue damage, organ/tissue replacement

205
Q

What are the systemic effects of tumors?

A
  1. hormonal (indiginous)

2. hormonal - ectopic, (PTH from anal sac adenoma)

206
Q

What is the term for how tumors suppress appetite,, and cause wasting

A

cancer cackexia

207
Q

What are the molecules that can hide tumor antigens on the surface?

A

glycalyx, fibrin, or antibodies

208
Q

What is the term for systemic complications of neoplasia that are remote from the primary tumor?

A

paraneoplastic conditions

209
Q

What are the 2 paraneoplastic syndromes affecting metabolism?

A

hypercalcemia - lymphosarcoma, anal sac adenocarcinooma, multiple myeloma
hypoglycemia - insulinoma in dogs

210
Q

What paraneoplastic syndrome affects bones?

A

hypertrophic (pulmonary) osteopathy

211
Q

What are the 7 paraneoplastic syndromes affecting costituents of circulation?

A

Immunoglobulin production, altered coagulability, hyperheparinemia, neutrophilic leukocytosis, eosinophilia, anemia, polycythemia

212
Q

What are the 2 paraneoplastic syndromes affecting neurologic system?

A

Peripheral nerve syndrome

mysthenia gravis

213
Q

What are the 2 paraneoplastic syndromes affecting the skin?

A

Alopecia

nodular dermatofibrosis

214
Q

What are the 2 important parts of histological diagnosis of tumors?

A

grading of tumor - differentiation

staging of tumor - indicates growth and spread

215
Q

What are the 3 chemical mediators in vasodilation?

A

Nitric Oxide
Histamine
Protaglandins - PGD2

216
Q

What 6 chemical mediators increase vascular permeability?

A 
Leukotriens (LTB4)
Histamine
Complement factors - C5a, C3a
Prostaglandins - PGE2
Leukotriens - LTC4, LTD4, LTE4
Platelet activating factor
217
Q

What are the 5 chemical mediators of leukocyte activation and chemotaxis?

A 
Complement factors C5a
Leukotriens LTB4
Chemokines IL-8
Defensins
Bacterial products
218
Q

What are the 4 chemical mediators of fever?

A

Cytokines IL1, IL6
TNF
PGE2

219
Q

What are the 2 chemical mediators in nausea?

A

Cytokine IL-1

TNF

220
Q

What are the 2 chemical mediators of pain?

A

Bradykinin

PGE2

221
Q

What are the principal mediators of tissue damage?

A

Neutrophils
macrophages
reactive oxygen species

Pathology (13 decks)

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