Exam 2 Flashcards

(170 cards)

1
Q

Inflammation

A

reaction to living tissue to injury
innate defensive mechanism. stereotyped response, blood derived components, may be more harmful than inciting injury
important to control inflammation through drugs NSAID or steroids
most things that can injure tissues, living or inanimate, endogenous or exogenous
it is a steotypical and defensive response to rid tissue of injury, reove damaged tissue, initiate healing and repair

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2
Q

What are the cardinal signs of inflammation?

A

Hemodynamic changes, increase in vascular permeability, and efflux of WBC

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3
Q

Arteriolar constriction

A

a hemodynamic event of inflammation that is a direct action of injurious stimulation on vessel wall and local neurogenic reflex with epinephrine release

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4
Q

Hemodynamic events of inflammation

A

arteriolar constriction, vasodilation and opening of capillary beds, increased hydrostatic pressure, and slowing/stasis of blood flow

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5
Q

Vasodilation in inflammation

A

a hemodynamic event where arterioles, pre-capillaries, and effluent veins dilute
histamine acts on venules
bradykinin and some prostaglandins relax vascular smooth muscle

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6
Q

Edema with inflammation

A

hyperemia and venous engorgement lead to increased hydrostatic pressure
increased hydrostatic pressure favors fluid efflux. from the vessel (edema) this fluid loss from vasculature leads to hemo-concentration and decreases blood flow

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7
Q

permeability changes with inflammation

A

primarily venular leakage but arterioles and capillaries leak in more severe injuries
increased vascular permeability- low protein with mild injurt
with further damage, protein rich exudate, leakage of proteins enhances osmotic pull of fluid into interstitium

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8
Q

Chemical mediators of vascular permeability

A

vasoactive amines (esp released by mast cells), kinins, complement fragments, arachidonic acid mediators, cytokines, platelet activating factor

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9
Q

serous inflammation

A

exudation of thin watery fluid
most apparent on body or organ surfaces
may be perceived in tissue as edema
functions to dilute or wash away injurious agent
common causes are environmental, irritants, trauma, early infectious process

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10
Q

Catarrhal inflammation

A

can only occur in tissues containing goblet cells, appears as shiny mucoid material coating mucosal surfaces
serves to dilute, wash away injurious agent (provide a barrier)
caused by irritants, infectious processes affecting mucus membrane
called an exudate but is a glandular secretory product, not a product of increased vascular permeability.

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11
Q

fibrinous inflammation

A

the increased vascular permeability results in exudation of fibrinogen from the blood which polymerizes into fibrin polymer.
visible exudate which polymerized fibrin is present
fibrin forms adherent strands and sheet which can be stripped off surfaces
most visible on serosal surfaces and in response to infectious disease
functions to wall off the agent and serves as a matrix for migration of WBC, endothelial cells and fibroblasts into the injured area

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12
Q

Neutrophils

A

first line of defense in response to any injury but often associated with foci of bacterial infection
circulating and marginated pools
short lived
actively phagocytic
glycolytic metabolism
produce oxidative species in response to phagocytic stimulus
release enzymes, antimicrobial molecules and secrete pro-inflammatory mediators
granule contents expelled by degranulation

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13
Q

Suppurative/Purulent Inflammation

A

dominated by neutrophils, marked by vascular exudation
tissue at site is typically liquified with thick creamy to yellow exudate
usually in response to infectious agent
immediate defensive reaction
acute Stimulus

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14
Q

WBC emigration

A

neutrophils emigrate within 1 hour, short lifespan in the tissue
macrophages enter after 12-48 hours, capable of long life in tissue, may undergo mitosis
lymphocytes slow to enter tissue, capable of mitosis in tissue

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15
Q

How do neutrophils cross endothelial cells with activation?

A

Neutrophils in the blood roll, adhesion, and transmigrate across endothelial cells
selectins allow neutrohpils to roll and slow across the surface and integrins
stimulus: endothelial activation, leukocyte activation and chemotaxis activation

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16
Q

Chemotaxis

A

a direct motion up concentration gradient
surface receptors sense gradient
cell rearranges its cytoplasm
molecules: C5a, bacterial products, leukotrienes, fibrin degradation products, WBC products (IL-8, MCP-1, PAF)

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17
Q

Phagocytosis

A

uptake and destruction of particulate matter
macrophages and neutrophils most important
purpose:
1) destroy injurious agent
2) clean up tissue debris

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18
Q

Opsonization

A

surface of particle coated with material that aids recognition by phagocytes and needed for phagocytosis–> allows binding
C3b and C3bi, immunoglobin, lysozyme, fibronectin

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19
Q

What happens once bacteria is opsonized?

A

It gets engulfed, a phagocytic vacuole is formed which fuses with the lysosome (phagolysosome) , this kills the bacteria and it is digested to later have debris extruded

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20
Q

Oxygen-dependent killing

A

tremendous oxygen uptake by neutrophils
NADPH oxidase reduces oxygen to super-oxide and subsequent reactions form to produce hydrogen peroxide, hydroxyl radical, singlet oxygen, secondary reactive nitrogen oxides, hydroxyl radical, singlet oxygen, secondary reactive nitrogen oxides, hypohalous species

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21
Q

How can neutrophils damage tissues?

A

destructive enzymes can be released into the tissue upon cell death and membrane rupture

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22
Q

Cellulitis

A

purulent inflammation of connective tissues
(suppurative inflammation)
contained to the skin

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23
Q

Phlegmon

A

suppurative inflammation where there is a fluctuant pocket of pus in the subcutis

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24
Q

Fasciitis

A

purulent inflammation of fascia (suppurative inflammation)

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25
Abscess
a local collection of pus (suppurative inflammation)
26
Empyema
accumulation of pus in the body cavity (suppurative inflammation) guttural pouch common site for this
27
Fibrinopurulent inflammation
acute inflammation is characterized by increased vascular permeability, this means there is a concurrent exudation of both fibrin and neutrophils leading to this.
28
Heterophils
the avian, reptile, rabbit, and amphibian equivalent of neutrophils essentially lack the enzymes to liquify and therefore heterophilic lesions are caseated
29
Heterophilic lesions
often caseous because heterophils lack the enzymes to liquify
30
eosinophilic inflammation
exudate that contains many eosinophils, lesions are often edematous may give tissues greenish hue associated with allergic, hypersensitivity reactions, fungal infections, and parasitic infestations mucosal tissues respond to eotaxisn from mast cells weakly phagocytic secretory cells
31
What appearance do tissues with eosinophilic inflammation commonly have?
a greenish hue from major basic protein
32
Eosinophil granules
secretory products inactivate mast cell-derived mediators major basic protein - disrupts helminth cuticle arylsulfatase- inactivates LtC4, D4, and E4 enzymes- histiminase inactivates histamine, phospholipase D inactivates PAF
33
Mast. cells
associated with allergic and hypersensitivity reactions -granules stain metachromatically with T. blue mucosal surfaces and within parenchymal organs mitotically active
34
Lymphocytic and Lymphoplasmacytic inflammation
the accumulation of lymphocytes and plasma cells, may form aggregates, follicles, cuff vessels processes with immune component, esp. viral infection may be describe as subacute or non-suppurative seldom visible grossly, except on mucosal surfaces (ex: cherry eye)
35
Macrophages
circulate for 24-72 hours activation and differentiation into macrophage occurs upon emigration modulate inflammation, immunity, and repair processes, actively phagocytic, and secretory, debride tissue debris, present antigen, primarily oxidative respiration Subtypes: alveolar, pulmonary intravascular, microglia, kuppfer, epithelioid, and multinucleate giant cells can survive in tissue and undergo mitosis
36
What is the function of macrophages?
modulate inflammation, immunty and repair processes (fibrogenic growth factors) actively phagocytic and secretory debride tissue debris present antigen primarily oxidative respiration
37
What is the outcome of acute inflammation?
1) Complete resolution (best option) 2) scarring 3) abscessation 4) chronic inflammation- if the innate response was not successful
38
What are the causes of chronic inflammation?
1) continuation of acute inflammation 2) chronic repeated injury 3) insidious onset without apparent acute inflammatory phase
39
chronic inflammation
prolonges course characterized by simulataneous inflammation, tissue destruction, and attempted healing associated with persistent or recurrent stimulus of injury, often including persistent antigenic stimulus
40
What is the key cell type in chronic inflammation?
the macrophage
41
Chronic-active inflammation
esp. pyogranulomatous characterized by recurrent bouts of reddening/obvious exudative change and periods of relative quiet certain to be progressive injury and significant scaring
42
pyogranulomatous
chronic inflammation with responses from both neutrophils and macrophages (chronic active)
43
granulomatous inflammation
form of chronic inflammation in which "epithelioid" macrophages predominate can be mixed with other cell types like pyogranulomatous (as in furunculosis) eosinophilic granulomatous lymphogranulomatous
44
Furunculosis
a deep infection of the hair follicle leading to abscess formation with accumulation of pus and necrotic tissue pyogranulomatous
45
granuloma
discrete aggregate of epithelioid macrophages with mantle of lymphoid cells and peripheral fibrosis may also have: central necrotic debris or a foreign body, dystrophic mineralization (caseation), multinucleate giant cells
46
foreign body granuloma
formed in response to indigestible material: keratin, hair, plant material
47
immune granuloma
persistent antigen with T-cell response
48
gossypiboma
or gauzoma where a textile or cotton substance is retained within the body following surgical procedures becomes encapsulated by macrophages and fibrosis
49
Healing and repair
occurs by parenchymal regeneration regeneration and fibrosis (scarring) replacement by fibrous tissue, occurs when: stomal framework destroyed, permanent cell population damaged, exudate cannot be reabsorbed
50
Labile populations
cells that have easy regenerative capacity of tissue (ex: gi tract, and primates with menstrual cycles)
51
stable population
cells with medium regenerative capacity (smooth muscle, cartilage)
52
permanent cells
cells that do not have regenerative capacity ex: neurons and cardiac muscles and red blood cells
53
growth factors (healing)
proteins that regulate growth and regeneration. they are also involved in neoplasia mitogenic and chemotactic Ex: epidermal growth factor, platelet-derived growth factor, macrophage-derived growth factors, vascular endothelial growth factors, transforming growth factor, fibroblast growth factor
54
Phases of wound healing
1) inflammation (+ blood clot and neutrophil) 2) cell migration (macrophage, fibroblast, endothelial) 3) matrix deposition (collagen from fibroblast) 4) vascular proliferation (to support cells) 5) collagen synthesis 6) remodeling - scar becomes smaller with remodeling
55
granulation tissue
proliferation of fibrovascular tissue that fills tissue defect and provides framework for elaboration of fibrous tissue
56
Granulation tissue formation
1) inflammatory phase- inflammatory response initiates healing process 2) proliferative phase- rapid growth of delicate fibrovascular tissue 3) remodeling phase- collagen fibers are replaced and reorganized, vascular regresses
57
What cells are involved in granulation tissue?
-macrophages remove exudate, secrete fibrogenic and angiogenic factors to influence healing -fibroblasts- lay down collagen matrix. myofibroblasts have contractile activity reducing wound volume -endothelial cells provide vascular supply to new connective tissue
58
Process of wound healing
wound edges opposed, rapid healing with minimal scar tissue delayed first intention- the wound is left open to clean up tissue debris/infection before surgical closure second intention- defect filled with granulation tissue, there is a prolonged course and potential for significant scarring
59
Hypertrophic scar
a raised scar that remains within the wound margin. an outcome of healing
60
Keloid
a raised scar that extends beyond the original wound margin a possible outcome of healing
61
ankylosis
a joint is fixed in place, can be septic or fibrous (fixed by CT) an adverse possible outcome of healing
62
Stricture
lumen structure that is decreased an adverse outcome of healing
63
cell proliferation
the mitotic division of stem cells or partially differentiated precursors
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cell differentiation
progressive acquisition of specialized structure and function as cells mature usually by altered/restricted gene expression progressive loss of capacity to divide
65
cell turnover
loss and renewal to maintain organ mass appropriately replacement of cells lost during normal tissue function adult- usually individual cell loss, DNA double strand breaks, toxins, etc. development- tissue/organ shifts
66
Proto-oncogenes
normal genes where normal gene products involved in promotion of cell proliferation and tissue growth
67
oncogenes
abnormal forms with non-functional regulatory elements drive proliferation of cancer cells drive proliferation bc they arent regulated
68
growth factors
drive cell differentiation and proliferation inhibit cell death (apoptosis) the same growth factor may cause both proliferation and differentiation TGF-beta stimulates proliferation and differentiation of epithelial cells
69
Suppressor genes
anti-proto-oncogenes that control and inhibit cell proliferation as well as act by inhibiting cell cycle progression and/or shunt cells to apoptosis or into resting phase (G0)
70
p53
policies cell cycle checkpoint to determine time for repair or induction of apoptotic pathways
71
Developmental disorders of growth
alterations of normal development, may affect a single site, causing a specific developmental disorder or several resulting in many defect often hereditary (germline) or somatic (non-germline) cause is usually unknown- genetic, toxic, infection, trauma results in decreased function or functional reserve may be subclinical or result in fetal/neonatal morbidity or neonatal/fetal mortality typically irreversible
72
acquired disorders of growth
physiological responses to external stimuli (trauma to a growth plate) or internal altered demands (liver loss with regeneration)
73
Normal embryological development
intricately timed balance between cell proliferation, differentiation, and cell death (apoptosis) within a tissue and timed development and or regression between different tissues
74
agenesis
the complete failure of an organ or tissue to develop
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aplasia
failure of an organ or tissue to grow -resulting in a rudimentary organ or failure of a tissue to renew itself ex: aplastic anemia in the adult
76
Hypoplasia
failure of organ or tissue to reach normal size -during development or decreased renewal of an adult tissue, incomplete development ex: erythroid hypoplasia in the adulty
77
Schistosomas reflexus
multiple abnormalities including failure of the body wall to close, resulting in a calf that is essentially inside out with exposure of abdominal organs a congenital structural defect
78
atresia
congenital absence of an opening or normally patent lumen: body orifice or tubular organ
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atresia ani
an imperforate anus- absence of the opening or normally patent lumen feces accumulates and leads to pot belly
80
atresia coli
an imperforate colon- absence of the opening or normally patent lumen
81
biliary atresia
common bile duct blocked or absent- absence of the opening or normally patent lumen
82
choanal atresia
bony or soft tissue blockage, common in camelids absence of the opening or normally patent lumen of the choana. can be unilateral or bilateral
83
esophageal atresia
esophagus ends before it connects to the stomach. absence of the opening or normally patent lumen
84
intestinal atresia
malformation of the intestine, usually thought to be due to utero vascular accident- absence of the opening or normally patent lumen
85
What developmental defect is the cleft palate and ventricular septal defects (VSD) an example of?
failure to fuse or separate
86
Spina bifida
meningomyelocele failure of vertebral closure leading to meninges/cord protrusion
87
polydactyly
a congenital defect where there are more than the normal number of digits. a defect of vestigial remnants, accessory or supernumerary tissues
88
hamartoma
abnormal amounts of tissue in a normal location
89
choristoma
ectopic tissue where there is normal tissue in an abnormal location ex: ectopic pancreas that is in duodenum or ectopic intestine in heart ectopic spleen very common
90
atrophy
decreased size of an organ or tissue: occurring after it has reached its normal size due to loss of cells or decreased size of individual cells: rate of loss exceeds rate of production diminishes organ function can be pathologic or physiologic
91
What are some causes of atrophy (decreased size of organ after it has reached normal size and diminished organ function?
decreased nutrition (starvation), denervation, reduced blood flow, local pressure, endocrine effects, drugs, toxins, aging, chronic inflammation, secretory duct occlusion
92
Sweeney
a cause of muscle atrophy due to suprascapular nerve injury causing muscular atrophy of supraspinatis and infraspinatus muscles
93
What are the causes of atrophy?
decreased nutrition, denervation, reduced blood flow, local pressure, endocrine effects, drugs, toxins, aging, chronic inflammation, secretory duct occlusion
94
hydronephrosis
urolithiasis with obstructed ureter tissue pressure builds up causing atrophy
95
involution
decrease in the size of a tissue or organ due to decease in number of cells -physiological: mammary gland and uterus after pregnancy, thymus in the young adult an example of endocrine effected atrophy
96
hypertrophy
increased size of an organ or tissue due to increased size of cells often a compensatory response occurs in organ whose cells are fully differentiated and have lost mitotic capacity initial response before mitotically active cells undergo hyperplasia response to some forms of injury rarely results in increased organ size
97
hyperplasia
increased size of an organ or tissue due to an increase in the number of cells requires cells capable of mitotic division: fully differentiated post0mitotic cells can only hypertrophy (ex: skeletal muscle)
98
Hypertrophy vs hyperplasia
hypertrophy is an increased size of a tissue due to increased cell size while hyperplasia is an increase in tissue due to the increase in number of cells
99
Physiologic hyperplasia
-Compensatory regeneration (unilateral renal injury) -Mammary gland, uterus in pregnancy -Increased nutrition -idiopathic- age associated change
100
Pathologic hyperplasia
from excessive hormonal stimulation, chronic irritation, drugs/toxins
101
Metaplasia
an adaptive change from one adult differentiated cell type to another which is not normally present in that organ or tissue, always occurs within, and is limited to, a given germ cell line, metaplasia is a change in differentiation typically from highly specialized to less specialized
102
Dysplasia
the disorganized growth of cells or tissues can be developmental (abnormal formation of tissue/organ) or acquired (degenerative or proliferative
103
Hip dysplasia
the disorganized growth of cells or tissues leading where the jip joint doesnt form correctly and subluxates
104
dystrophy
faulty development or tissue maintenance or derived from defective or faulty nutrition
105
osteodystrophy
a nutritional disease that can be caused by nutritional secondary hyperparathyroidism- high P or low Vitamin D leads to fibrous osteodystrophy
106
neoplasia
new growth resulting in a neoplasm can be benign (non-threatening or incapable of spread) or malignant neoplasm
107
cancer
malignant neoplasia
108
oncology
the study of neoplasm
109
carcinogenic/oncogenesis
the process of becoming neoplastic
110
transformation
induction of neoplastic cells
111
what suffix is added to benign neoplasias
-oma
112
What suffix is added to malignant neoplasias of epithelial orgins
carcinoma
113
what suffix is added to malignant neoplasias of mesencymal origins
sarcoma
114
Sarcoma or Carcinoma? epidermis
carcinoma
115
Sarcoma or Carcinoma? nasal cavity
carcinoma
116
Sarcoma or Carcinoma? cutaneous glands
carcinoma
117
Sarcoma or Carcinoma? mouth
carcinoma
118
Sarcoma or Carcinoma? epithelium of kidneys
sarcoma
119
Sarcoma or Carcinoma? serous membranes
sarcoma
120
Sarcoma or Carcinoma? gonads
sarcoma
121
Sarcoma or Carcinoma? skeletal and cardiac muscle
sarcoma
122
Sarcoma or Carcinoma? smooth muscle, connective tissue, cartilage, bone, blood, lymphoid tissue, endothelium
sarcoma
123
Sarcoma or Carcinoma? epithelium of pharynx, thyroid, parathyroid, lens, thymus, larynx, trachea, lungs, digestive tube, bladder, vagina, urethra
carcinoma
124
A malignant neoplasm of fibrous tissue
fibrosarcoma
125
a benign neoplasm of fibrous tissue
fibroma
126
A malignant neoplasm of bone
osteosarcoma
127
A benign neoplasm of bone
osteoma
128
A malignant neoplasm of cartilage
chondrosarcoma
129
A malignant neoplasm of adipose (fat cells)
liposarcoma
130
A malignant neoplasm of endothelium, blood vasculature
hemangiosarcoma
131
a benign neoplasm of endothelium, blood vasculature
hemangioma
132
A malignant neoplasm of stratified squamous
squamous cell carcinoma
133
a benign neoplasm of stratified squamous
squamous papilloma
134
A malignant neoplasm of basal epithelium
basal cell carcinoma
135
A malignant neoplasm of glandular epithelium
adenocarcinoma
136
A benign neoplasm of glandular epithelium
adenoma
137
A malignant neoplasm of liver
hepatocellular carcinoma
138
A benign neoplasm of liver
hepatocellular adenoma
139
A malignant neoplasm of renal tubules
renal cell carcinoma
140
A malignant neoplasm of mammary gland
mammary carcinoma or adenocarcinoma
141
a benign neoplasm of mammary gland
mammary adenoma
142
Can lymphocyte neoplasms ever be bengin
no they are always malignant, lymphoma does not exist despite everyone referring to it. Should be lymphosarcoma
143
What are benign increases of hematopoietic neoplasms called?
they are called hyperplasia ex: lymphoid hyperplasia
144
What are malignant neoplasms of monocytes called
monocytic leukemia
145
What are malignant neoplasms of plasma cells called
extramedullary plasmacytoma, myeloma plasmacytoid lymphoma
146
What are malignant neoplasms of granulocytes called
granulocytic (myeloid) leukemia, granulocytic sarcoma
147
Naming of neuroendrocrine and nervous tissue neoplasms
benign are simply named -oma while malignant tumors simply have malignant added before it
148
Circumscribed
a characteristic of a benign tumor tumor where the growth limits are restricted
149
Anaplastic
a characteristic of malignant tumors where there is poorly differentiated cells, lack of different characteristics
150
desmoplasia
excessive connective tissue or support stroma around a malignant tumor
151
How does the recurrence of bening vs malignant tumors differ?
benign- rare malignant- frequent
152
pleomorphism of malignant tumors
cellular and nuclear is mod-marked
153
Nucleus/Cytoplasm ratio of benign vs malignant tumors
high in malignant tumors, increased nucleus size bc of rapid division
154
leiomyosarcoma
malignant tumor of smooth muscle
155
Nucleoli in malignant tumors
increased number/size/shape
156
tumors of the vascular endothelium
benign- hemangioma malignant- hemangiosarcoma
157
liposarcoma
malignant tumor of fat but rarely metastasize
158
tumors of cutaneous/subcutaneous soft tissues
benign- fibroma, bening peripheral nerve sheath tumor malignant- soft tissue sarcoma
159
epithelial neoplasm
benign: adenoma malignant: adenocarcinoma
160
Malignant mixed tumor carcinosarcoma
a malignant mammary gland tumor that has epithelium + myoepithelium with mesenchymal differentiation
161
tumors of odontogenic epithelium
always benign acanathomatous ameloblastoma easy to treat, tooth making epithelium
162
transmissible venereal tumor (TVT)
an immortalized cell line that can be transmissible through sniffing anus develops buccal, anus, penis, and vulva, can metastasis, luckily easily treatable
163
teratoma
typically arise from the ovary can be benign or malignant large in appearance multiple cell types present
164
What are the properties between benign and malignant tumors?
Benign: slow, circumscribed, expand/compress, good (well-differentiated), abundant support stroma, no matastasis, rare recurrence Malignant: rapid growth rate with unrestricted growth limits, expand/compress/invade, anaplastic- poorly differentiated, excessive support stroma (desmoplasia), frequent metastasis, frequent recurrence
165
Do benign or malignant tumors have poor differentiation?
malignant are poor (anaplastic)
166
How do you differentiate the cytological features of benign vs malignant tumors?
Benign: well differentiated cells, minimal cellular/nuclear pleomorphism, low N/C ratio, low mitotic figures, normal numbers of nucleoli, minimal necrosis, distinct demarcation Malignant: low differentiation (anaplasia), mod-marked, high N/C ratio, high mitotic index with atypical mitotic figures, increases size and shape of nucleoli, minimal-adundant necrosis, invasive demarcation
167
What tissues does catarrhal inflammation take place at?
only tissues where there are goblet cells serves to dilute and wash away injurious agent, appears as shiny mucoid material coating mucosal surfaces, irritants, infectious processes affecting mucus membranes
168
zones of granulation tissue
basal to apical zone of mature connective tissue zone of capillary proliferation zone of capillary sprouts and arches zone of necrotic debris
169
do animals get keloid scars?
No they do not, they get hypertrophic scars
170
How does granuloma differ from granulation tissue
granuloma is a discrete aggregate of epitheloid macrophages with a mantle of lymphoid cells and peripheral fibrosis granulation tissue is the proliferation of fibrovascular tissue that fills a tissue defect and lays the framwork for the elaboration of fibrous tissue