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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
What are the effects of histamine and serotonin in inflammation?
early transient dilation of BV (15-30 mins) | increase permeability of BV
26
What are the 2 functions of plasmin in inflammation?
degrades fibrin | cleaves C3 of complement
27
What cells release heparin during inflammation and what effect does it have?
mast cells | prolongs exudation in acute phase
28
Which prostaglandins are involved in vasodilation?
PGE2 and PGI2
29
What are the 3 ways fibrin is removed?
fibrinolytic enzymes from leukocytes phagocytic leukocytes plasmin
30
What is the prostaglandin involved in hyperalgesia?
PGE2
31
What leukotriene is a powerful chemotactic?
Leuko-B4
32
What leukotrienes are involved in vascular permeability?
Leuko-C4, D4, E4
33
What is responsible for vascular dilation after histamine?
kinin system
34
Kinin activates hageman factor which results in what?
amplification mechanism in inflammation
35
What do prostaglandins and leukotrienes do to smooth muscles?
contract
36
What other chemical mediators of inflammation do the prostaglandins and leukotriens enhance?
histamine and kinin
37
What are the 4 ways that oxygen derived free radicals cause cell damage?
peroxidation of cell membrane lipids cross linking of proteins damage DNA cleaving glycoconjugates
38
What are the roles of nitric oxide during inflammation?
``` vasodilation inhibits platelets oxidizes lipids inhibits mast cells regulates chemotaxis ```
39
What do interleukins do?
regulate interactions between lymphocytes and other WBCs
40
What are the three types of cytokines?
interleukins tumor necrosis factors interferons
41
What cytokine produced by macrophages stimulates Th2 cells?
interleukin 1
42
What cytokine is produced by macrophages and promotes B cell maturation?
Interleukin 6
43
What cytokine is produced by macrophages and is a co-stimulator of Th1 cells?
interleukin 12
44
What are the major cytokines produced by macrophages?
IL 1, 6, 12, 18, and TNF
45
What 2 cytokines are produced by Th1 cells?
Interleukin 2 | Interferon-y (gamma)
46
What are the cytokines produced by Th2 cells?
IL-4,5,9,10, 13
47
What do interferons do?
inhibit virus replication by interfering with viral RNA and protein synthesis
48
What are type 1 interferons?
have antiviral activity, used in pregnancy signaling
49
What is the type 2 interferon?
IFNY
50
What are the 3 properties of neutrophils?
strong amoeboid movement phagocytic and killing of microbes and tumors intracellular digestion
51
How long do neutrophils survive in tissue?
1 to 4 days
52
What are the normal neutrophil percentages in different species?
Carnivores - 60-75% Ruminants - 20-30% Horse - 50%
53
What are the pHs of the smaller neutrophil granules? large ones?
small - acidic | large - alkaline
54
What does migration of neutrophils stimulate?
colony stimulating factor--> granulopoeisis
55
What is degenerative left shift?
band forms increase but number of mature neutrophils is normal or decreased
56
What are the 3 causes of neutropenia?
acute tissue demand (acute inflammation, sepsis) decreased marrow production increased margination
57
What 2 conditions increase margination of neutrophils leading to neutropenia?
anaphylaxis | endotoxemia
58
What are the 4 steps in neutrophil phagocytosis?
Chemotaxis, adherence, ingestion, digestion
59
What are the 2 ways neutrophils digest the material they phagocytize?
respiratory burst | lysosomes
60
What are the 4 fxns of eosinophils?
limited phagocytic activity cytotoxicity of parasites inflammatory rxn allergic rxn
61
What term is used for chronic inflammation that has dense infiltration of eosinophils?
eosinophilic granuloma
62
What are the 3 idiopathic eosinophilic granulomas in felines?
eosinophilic plaque linear granuloma eosinophilic ulcer
63
Where are eosinophilic granulomas usually seen in felines?
abdomen and inner thigh
64
Where are eosinophilic ulcers usually seen in felines?
upper lip
65
Where are Equine collagenolytic granulomas seen?
saddle area
66
Where is eosinophilic myositis seen in dogs?
muscles of mastication - special 2m myosin, test for antibodies to this
67
Where is eosinophilic myositis seen in cattle and sheep?
skeletal and cardiac muscle, allergy to own muscle is suspected
68
Where are mast cells found?
organs rich in connective tissue
69
What is the life span of mast cells in tissue?
4-12 weeks
70
What do basophils release?
IL4, IL13, and histamine
71
What immunoglobulin do basophils and mast cells have many receptors for?
IgE
72
What do B lymphocytes differentiate into and are not found in blood circulation?
plasma cells
73
Where are class 1 MHC molecules expressed?
all nucleated cells
74
Where are class 2 MHC molecules expressed?
specialized APC
75
What MHC class do CD4+ T cells react to?
class 2 on surface of APC
76
What MHC class do CD8+ T cells (CTLs) react to?
class 1
77
What do CD4+T cells differentiate into and do?
effector cells - help other immune cells
78
What are some reasons that monocytes are not present in large numbers during acute inflammation like neutrophils?
circulating pool is low production is lower different chemotaxis not as mobile
79
What can monocytosis indicate?
inflammation | tissue necrosis
80
What 3 things do macrophages secrete?
enzymes pro-inflammatory products growth factors
81
What conditions are epitheloid cells usually seen?
chronic inflammation - tuberculosis and johnes dz
82
What are epitheloid cells?
large foamy macrophages
83
What are giant cells?
2 or more fused macrophages
84
Where are the nuclei in Langhan's type of giant cell?
periphery
85
Where are the nuclei in foreign body giant cells?
clustered in center or distributed
86
What are the causes of serous inflammation and where are they found?
``` serous cavities - infection joints - trauma lungs - infection, poison skin - toxins, trauma, burn mucous membranes - viral infection ```
87
Where does fibrinous inflammation occur?
serous and mucous membranes (same as serous except not skin)
88
What are the causes of fibrinous inflammation?
same as serous
89
What is the microscopic appearance of fibrin inflammation?
dirty pink mixed with leukocytes
90
What are the effects of fibrin inflammation?
protection, chemotactin, regeneration of underlying tissue, organization
91
Where does the mucus come from in mucus inflammation?
the cells (instead of the blood)
92
What are the causes of catarrhal or mucus inflammation?
``` bacteria and low virulence viruses mild chemicals irritating food inhalation of dust/foreign protein parasite - chronic irritation ```
93
what does mucus stain with H&E?
pale blue
94
What are the effects of mucus inflammation?
protective | chronic - becomes purulent
95
Where does hemorrhagic inflammation occur?
organs of rich blood supply - lung, GI
96
How does hemorrhagic inflammation differ from hemorrhage?
inflammation - blood oozes from inflamed tissue by diapedesis
97
What are the causes of hemorrhagic inflammation?
microorganisms of high virulence | acute poisoning
98
What is the effect of hemorrhagic inflammation?
if cause is not removed, fatal
99
Where does purulent inflammation occur?
ALL TISSUES
100
What are the causes of purulent inflammation?
pyogenic bacteria | fungal infections
101
What color can the pus be in purulent inflammation?
yellow cream to bluish green to black
102
What is the microscopic hallmark of purulent inflammation?
neutrophils
103
What is the most effective method of defense against bacteria and fungi?
purulent inflammation
104
What happens if abscess ruptures on surface of organ or mucous membranes of respiratory, digestive or repro tract?
fatal
105
What happens if abscess ruptures in blood stream?
metastatic abscesses | toxemia/death
106
What is the definition of an abscess?
encapsulated area of inflammation
107
How is chronic inflammation different than acute?
infiltration of mononuclear cells, tissue destruction, attempt at repair
108
Is granulomatous inflammation chronic or acute?
chronic
109
What are the two types of granulomatous lesions?
diffuse and nodular
110
What does the composition of cells around the granuloma depend on?
causative agent
111
What causes lymphocytic inflitration seen in chronic inflammatory lesions?
``` 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
What is healing by repair?
damaged cells replaced by OTHER types of cells (connective tissue)
113
What are the 3 categories of cells being able to regenerate?
labile, stable, permanant
114
What are labile cells?
continuously dividing cells - epithelial cells, bone marrow, lymphoid organs
115
What are stable cells?
quiescent - parenchymatous organs such as liver, kidney, pancreas, adrenal, bone, tendon, nerve, smooth muscle (and mesenchymal?)
116
What does paranchymal mean?
many different types of cells - liver with blood vessels, etc
117
What are examples of permanent cells?
neurons, cardiac and skeletal muscle cells
118
What are the two examples of loss of specialized function during repair by connective tissue?
fibrous replacement of kidney | myocardial infarction
119
What are the steps of primary healing?
``` clot formation inflammatory response fibroblast response endothelial response epithelial regeneration collagen formation ```
120
What is the definition of healing by first intention?
healing of a clean wound where tissues are opposed
121
what are the 3 layers of a secondary union healing?
superficial layer of cell debris layer of newly formed BV at right angles to lesion deep layer of fibroblasts with collagen running parallel
122
What is the term used for large amounts of scar tissue?
cicatrization
123
What antibody is involved in Type 1 hypersensitivity?
IgE
124
What are the specific features of type 1 hypersensitivites?
need sensitization phase and re exposure transferable to normal animal genetic predisposition reaction time - 15 to 20 minutes
125
What does a lick granuloma look like grossly?
circumscribed, hairless, ulcerated | on carpal, metacarpal, metatarsal, tibia or radius areas
126
What are the 3 different antibody dependent mechanisms for type 2 hypersensitivity?
1. complement dependent reaction 2. antibody dependent cell mediated cytotoxicity (ADCC) 3. antibody mediated cellular dysfunction
127
What does complement dependent reaction usually involve?
blood cells - transfusion, hemolytic anemia of newborn auto immune hemolytic anemia, thrombo, certain drug rxns
128
What is antibody mediated cellular dysfunction?
antibodies directed against cell surface receptors impair or dysregulate function
129
What are characteristics of type 3 hypersensitivities?
immune complexes | tissue damage
130
What are the two categories of antigens and what are examples?
exogenous - foreign protein, bacteria, viruses | endogenous - nuclear antigen immunoglobulin, tumors
131
What are localized type 3 sensitivity reactions called?
arthus rxn
132
What is the pathogenesis of immune complex dzs? (type 3 hyper)
formation of antigen/antibody complex deposition of immune complex initiation of inflammatory rxn
133
What are 6 examples of system immune complex diseases
1. glomerulonephritis 2. systemic lupus erythomatousus 3. immune mediated arthropathies - RA 4. idiopathic poyarthritis 5. periarteritis nodosa,, necrotizing vasculitis 6. immune mediated meningitis
134
What are examples of localized immune complex diseases?
hypersensitivity pneuomonitis - alveoli deposition vasculitis - dogs and horses purpura hemorrhagica anterior uveitis - dogs, cats, horses,
135
What is another name for type 4 DTH?
cell mediated hypersensitivity
136
What are the features of DTH?
``` no antibody cellular reactions 24-48 hours intracellular organisims T lymphocytes ```
137
What are examples of type 4 hypersensitivity (DTH)?
tuberculin test contact dermatitis flea allergy dermatitis sweet itch in horses
138
What charcterisizes flea allergy dermatitis in dogs and cats?
dogs - alopecia, hyperkeratosis | cats - scabs on back
139
What are 3 examples of failure of normal development?
aplasia, atresia, hypoplasia
140
What are examples of cellular adaptation to change that results in growth disturbance?
aging, involution of thymus | atrophy, hypertrophy, metaplasia, dysplasia
141
What are the 3 factors that are stimuli to proliferate cells during repair?
cytokines and wound hormones chemical stimulants pressure gradients
142
What are the 3 systemic factors involved in adequacy of repair?
physioloical condition of animal nutrition endocrine factors
143
What are the local factors affecting adequacy of repair?
blood supply infection mobility of tissues site of injury
144
What is aplasia (agenesis)?
organ did not develop fully during embryogenesis
145
What is atresia?
absence of closure of organ opening
146
What are the 2 causes of hypoplasia (organ doesnt get full size)?
viral infections in mother | genetic
147
What are examples of viral hypoplasia?
BVD - cerebellar Blue tongue virus - cerebellar in lambs canine distemper - enamal
148
What are some known genetic effects of hypoplasia
familial renal hypoplasia in dogs | pancreatic hypoplasia - dogs and cattle
149
What is the difference between aplasia and hypoplasia?
hypoplastic structure shows normal architechture
150
What is atrophy?
decrease in tissue mass after achieving normal growth
151
What are some causes of atrophy?
physiologic - thymic ,uterine involution, mammary gland | pathologic
152
What are the 2 main causes of pathologic atrophy?
``` disuse atropy neurogenic vasculogenic nutritional endocrine inflammatory ```
153
What happens during sublethal injury?
autophagocytosis
154
What is hypertrophy?
increase tissue size due to increase in individual cell size
155
What are causes of hypertrophy?
physio - uterus, muscles | pathologic - cardiac, renal, hormone
156
What is hyperplasia?
much more common than hypertrophy | increase in cell number - reversible
157
What is metaplasia?
transformation of cell type to another of same germ layer
158
Where is metaplasia usually seen?
in epithelium and connective tissue
159
What are some causes of metaplasia?
chronic irritation, vit A def, estrogen, blockage of bile ducts, myeloid
160
What is dysplasia?
abnormal development
161
What is dystrophy?
progressive degenerating and atrophic changes | some nutritional, some inherited
162
What are examples of dystrophy?
osteodystrophies - rickets muscular - inherited neuroaxonal - sheep and dogs
163
What does "malignant" imply?
ability to invade locally | ability for metastasis
164
What is the suffix for benign?
oma
165
What is the suffix for malignant?
- carcinoma : epithelial tissue | - sarcoma : mesenchymal tissue
166
Malignant glandular-epithelium tumor
adenocarcinoma
167
benign surface protective epithelium tumor
papilloma
168
Malignant surface protective epithelium tumor
carcinoma
169
What layer do carcinomas come from
ANY layer of epithelium
170
What is a mixed tumor?
arises from cells normally found in the tissue
171
What can not be part of a mixed tumor?
bone and cartilage
172
What are teratomas/teratocarcinomas?
germ ccells - contain tissue from all embryonic cell layers
173
What is anaplasia
tumor cells do not resemble parent tissue (cell differentiation)
174
Are immature or mature anaplasias more malignant?
immature
175
Tumors of melanocytes
B - melanocytoma | M - melanoma
176
Tumors of lymphocytes
both malignant - lymphoma, lymphosarcoma
177
Tumors of mast cells
B- mast cell tumor | M - mast cell sarcoma, mastocytoma
178
Tumors of astroglia
both benign and malignant - astrocytoma
179
Bone marrow tumors
malignant - leukemia
180
Term for disorganize mass growing around nerve tissue after trauma
neuroma
181
Term for hyperplastic mass of mature tissue as a result of anomalous development, normal to location but not a tumor
hamartoma
182
Term for non neoplastic normal mature tissue that do not occur normally at that site (dermoid)
chriostoma
183
What is a leiomyoma
smooth muscle tumor
184
What is the exception that benign tumors grow slowly?
papillomas, hormone dependent mammary tumors in bitch
185
What are the most important criteria for benign tumors?
rarely invade | never metastasize
186
How do tumors metastasize in body cavities?
implantation - through serous membrane
187
What is the "paranchyma" of tumor cells?
the actual neoplastic cells
188
What is the stroma made of in tumors?
supporting tissue - host derived, ct, bv
189
What does vessel leakiness allow in tumors?
deposition of fibrin network that promotes formation of collagenous tumor stroma
190
What causes angiogenesis near tumor cells?
angiogenic factors hypoxia glucocorticoids interfere with angiogenesis
191
What is the term for fibrous capsule around benign tumors?
fibroplasia
192
What are the non specific host defenses against a tumor
inflammatory (not very protective) | phagocytosis
193
What is a specific mechanism of host defense against tumor?
tumor antigens - antibodies and cytotoxic T lympphos
194
What are the 2 parts of the innate immune response against tumors?
natural killer cells | macrophages
195
What are the parts of adaptive antitumor response?
lymphocytes - CTLs and CD8 T lymphos | B Lymphocytes - ADCC
196
What does failure of immunosurveilance mean?
if humoral and adaptive immune response fail
197
How are tumors able to evade the immune response?
no surface molecules, masking of antigens by glycolyx, fibrin or ab, tolerance of antigens, no MHC, immunosuppressive effects, apoptosis in T lymphos
198
What type of disease is cancer?
non lethal genetic damage
199
What are protooncogenes?
genes that promote cell grwoth
200
What antibodies are associated with type 2 hypersensitivity reactions?
IgG and IgM
201
What determines the extent of tissue damage in type 3 hypersensitivity?
size of immune complex | overload and intrinsc dysfunction of MPS
202
What bacteria genus is known to cause cancer?
Helicobacter spp
203
What parasite is known to cause cancer?
spirocerca lupi
204
What are the local effects of neoplasms?
compression, oobstruction, tissue damage, organ/tissue replacement
205
What are the systemic effects of tumors?
1. hormonal (indiginous) | 2. hormonal - ectopic, (PTH from anal sac adenoma)
206
What is the term for how tumors suppress appetite,, and cause wasting
cancer cackexia
207
What are the molecules that can hide tumor antigens on the surface?
glycalyx, fibrin, or antibodies
208
What is the term for systemic complications of neoplasia that are remote from the primary tumor?
paraneoplastic conditions
209
What are the 2 paraneoplastic syndromes affecting metabolism?
hypercalcemia - lymphosarcoma, anal sac adenocarcinooma, multiple myeloma hypoglycemia - insulinoma in dogs
210
What paraneoplastic syndrome affects bones?
hypertrophic (pulmonary) osteopathy
211
What are the 7 paraneoplastic syndromes affecting costituents of circulation?
Immunoglobulin production, altered coagulability, hyperheparinemia, neutrophilic leukocytosis, eosinophilia, anemia, polycythemia
212
What are the 2 paraneoplastic syndromes affecting neurologic system?
Peripheral nerve syndrome | mysthenia gravis
213
What are the 2 paraneoplastic syndromes affecting the skin?
Alopecia | nodular dermatofibrosis
214
What are the 2 important parts of histological diagnosis of tumors?
grading of tumor - differentiation | staging of tumor - indicates growth and spread
215
What are the 3 chemical mediators in vasodilation?
Nitric Oxide Histamine Protaglandins - PGD2
216
What 6 chemical mediators increase vascular permeability?
``` Leukotriens (LTB4) Histamine Complement factors - C5a, C3a Prostaglandins - PGE2 Leukotriens - LTC4, LTD4, LTE4 Platelet activating factor ```
217
What are the 5 chemical mediators of leukocyte activation and chemotaxis?
``` Complement factors C5a Leukotriens LTB4 Chemokines IL-8 Defensins Bacterial products ```
218
What are the 4 chemical mediators of fever?
Cytokines IL1, IL6 TNF PGE2
219
What are the 2 chemical mediators in nausea?
Cytokine IL-1 | TNF
220
What are the 2 chemical mediators of pain?
Bradykinin | PGE2
221
What are the principal mediators of tissue damage?
Neutrophils macrophages reactive oxygen species

Pathology (13 decks)

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