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biology of disease I > Exam 2 > Flashcards

Exam 2 Flashcards

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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
Q

Abscess

A

a local collection of pus (suppurative inflammation)

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26
Q

Empyema

A

accumulation of pus in the body cavity
(suppurative inflammation)
guttural pouch common site for this

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27
Q

Fibrinopurulent inflammation

A

acute inflammation is characterized by increased vascular permeability, this means there is a concurrent exudation of both fibrin and neutrophils leading to this.

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28
Q

Heterophils

A

the avian, reptile, rabbit, and amphibian equivalent of neutrophils
essentially lack the enzymes to liquify and therefore heterophilic lesions are caseated

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29
Q

Heterophilic lesions

A

often caseous because heterophils lack the enzymes to liquify

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30
Q

eosinophilic inflammation

A

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

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31
Q

What appearance do tissues with eosinophilic inflammation commonly have?

A

a greenish hue from major basic protein

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32
Q

Eosinophil granules

A

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

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33
Q

Mast. cells

A

associated with allergic and hypersensitivity reactions
-granules stain metachromatically with T. blue
mucosal surfaces and within parenchymal organs
mitotically active

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34
Q

Lymphocytic and Lymphoplasmacytic inflammation

A

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)

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35
Q

Macrophages

A

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

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36
Q

What is the function of macrophages?

A

modulate inflammation, immunty and repair processes (fibrogenic growth factors)
actively phagocytic and secretory
debride tissue debris
present antigen
primarily oxidative respiration

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37
Q

What is the outcome of acute inflammation?

A

1) Complete resolution (best option)
2) scarring
3) abscessation
4) chronic inflammation- if the innate response was not successful

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38
Q

What are the causes of chronic inflammation?

A

1) continuation of acute inflammation
2) chronic repeated injury
3) insidious onset without apparent acute inflammatory phase

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39
Q

chronic inflammation

A

prolonges course characterized by simulataneous inflammation, tissue destruction, and attempted healing
associated with persistent or recurrent stimulus of injury, often including persistent antigenic stimulus

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40
Q

What is the key cell type in chronic inflammation?

A

the macrophage

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41
Q

Chronic-active inflammation

A

esp. pyogranulomatous
characterized by recurrent bouts of reddening/obvious exudative change and periods of relative quiet
certain to be progressive injury and significant scaring

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42
Q

pyogranulomatous

A

chronic inflammation with responses from both neutrophils and macrophages (chronic active)

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43
Q

granulomatous inflammation

A

form of chronic inflammation in which “epithelioid” macrophages predominate
can be mixed with other cell types like pyogranulomatous (as in furunculosis)
eosinophilic granulomatous
lymphogranulomatous

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44
Q

Furunculosis

A

a deep infection of the hair follicle leading to abscess formation with accumulation of pus and necrotic tissue
pyogranulomatous

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45
Q

granuloma

A

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

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46
Q

foreign body granuloma

A

formed in response to indigestible material: keratin, hair, plant material

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47
Q

immune granuloma

A

persistent antigen with T-cell response

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48
Q

gossypiboma

A

or gauzoma where a textile or cotton substance is retained within the body following surgical procedures
becomes encapsulated by macrophages and fibrosis

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49
Q

Healing and repair

A

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

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50
Q

Labile populations

A

cells that have easy regenerative capacity of tissue (ex: gi tract, and primates with menstrual cycles)

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51
Q

stable population

A

cells with medium regenerative capacity
(smooth muscle, cartilage)

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52
Q

permanent cells

A

cells that do not have regenerative capacity
ex: neurons and cardiac muscles and red blood cells

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53
Q

growth factors (healing)

A

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

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54
Q

Phases of wound healing

A

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

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55
Q

granulation tissue

A

proliferation of fibrovascular tissue that fills tissue defect and provides framework for elaboration of fibrous tissue

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56
Q

Granulation tissue formation

A

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

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57
Q

What cells are involved in granulation tissue?

A

-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

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58
Q

Process of wound healing

A

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

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59
Q

Hypertrophic scar

A

a raised scar that remains within the wound margin. an outcome of healing

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60
Q

Keloid

A

a raised scar that extends beyond the original wound margin
a possible outcome of healing

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61
Q

ankylosis

A

a joint is fixed in place, can be septic or fibrous (fixed by CT)
an adverse possible outcome of healing

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62
Q

Stricture

A

lumen structure that is decreased
an adverse outcome of healing

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63
Q

cell proliferation

A

the mitotic division of stem cells or partially differentiated precursors

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64
Q

cell differentiation

A

progressive acquisition of specialized structure and function as cells mature
usually by altered/restricted gene expression
progressive loss of capacity to divide

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65
Q

cell turnover

A

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

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66
Q

Proto-oncogenes

A

normal genes where normal gene products involved in promotion of cell proliferation and tissue growth

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67
Q

oncogenes

A

abnormal forms with non-functional regulatory elements drive proliferation of cancer cells
drive proliferation bc they arent regulated

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68
Q

growth factors

A

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

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69
Q

Suppressor genes

A

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
Q

p53

A

policies cell cycle checkpoint to determine time for repair or induction of apoptotic pathways

71
Q

Developmental disorders of growth

A

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
Q

acquired disorders of growth

A

physiological responses to external stimuli (trauma to a growth plate) or internal altered demands (liver loss with regeneration)

73
Q

Normal embryological development

A

intricately timed balance between cell proliferation, differentiation, and cell death (apoptosis) within a tissue and timed development and or regression between different tissues

74
Q

agenesis

A

the complete failure of an organ or tissue to develop

75
Q

aplasia

A

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
Q

Hypoplasia

A

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
Q

Schistosomas reflexus

A

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
Q

atresia

A

congenital absence of an opening or normally patent lumen: body orifice or tubular organ

79
Q

atresia ani

A

an imperforate anus- absence of the opening or normally patent lumen
feces accumulates and leads to pot belly

80
Q

atresia coli

A

an imperforate colon- absence of the opening or normally patent lumen

81
Q

biliary atresia

A

common bile duct blocked or absent- absence of the opening or normally patent lumen

82
Q

choanal atresia

A

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
Q

esophageal atresia

A

esophagus ends before it connects to the stomach. absence of the opening or normally patent lumen

84
Q

intestinal atresia

A

malformation of the intestine, usually thought to be due to utero vascular accident- absence of the opening or normally patent lumen

85
Q

What developmental defect is the cleft palate and ventricular septal defects (VSD) an example of?

A

failure to fuse or separate

86
Q

Spina bifida

A

meningomyelocele
failure of vertebral closure leading to meninges/cord protrusion

87
Q

polydactyly

A

a congenital defect where there are more than the normal number of digits.
a defect of vestigial remnants, accessory or supernumerary tissues

88
Q

hamartoma

A

abnormal amounts of tissue in a normal location

89
Q

choristoma

A

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
Q

atrophy

A

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
Q

What are some causes of atrophy (decreased size of organ after it has reached normal size and diminished organ function?

A

decreased nutrition (starvation), denervation, reduced blood flow, local pressure, endocrine effects, drugs, toxins, aging, chronic inflammation, secretory duct occlusion

92
Q

Sweeney

A

a cause of muscle atrophy due to suprascapular nerve injury causing muscular atrophy of supraspinatis and infraspinatus muscles

93
Q

What are the causes of atrophy?

A

decreased nutrition, denervation, reduced blood flow, local pressure, endocrine effects, drugs, toxins, aging, chronic inflammation, secretory duct occlusion

94
Q

hydronephrosis

A

urolithiasis with obstructed ureter
tissue pressure builds up causing atrophy

95
Q

involution

A

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
Q

hypertrophy

A

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
Q

hyperplasia

A

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
Q

Hypertrophy vs hyperplasia

A

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
Q

Physiologic hyperplasia

A

-Compensatory regeneration (unilateral renal injury)
-Mammary gland, uterus in pregnancy
-Increased nutrition
-idiopathic- age associated change

100
Q

Pathologic hyperplasia

A

from excessive hormonal stimulation, chronic irritation, drugs/toxins

101
Q

Metaplasia

A

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
Q

Dysplasia

A

the disorganized growth of cells or tissues
can be developmental (abnormal formation of tissue/organ) or acquired (degenerative or proliferative

103
Q

Hip dysplasia

A

the disorganized growth of cells or tissues leading where the jip joint doesnt form correctly and subluxates

104
Q

dystrophy

A

faulty development or tissue maintenance or derived from defective or faulty nutrition

105
Q

osteodystrophy

A

a nutritional disease that can be caused by nutritional secondary hyperparathyroidism- high P or low Vitamin D leads to fibrous osteodystrophy

106
Q

neoplasia

A

new growth resulting in a neoplasm
can be benign (non-threatening or incapable of spread) or malignant neoplasm

107
Q

cancer

A

malignant neoplasia

108
Q

oncology

A

the study of neoplasm

109
Q

carcinogenic/oncogenesis

A

the process of becoming neoplastic

110
Q

transformation

A

induction of neoplastic cells

111
Q

what suffix is added to benign neoplasias

A

-oma

112
Q

What suffix is added to malignant neoplasias of epithelial orgins

A

carcinoma

113
Q

what suffix is added to malignant neoplasias of mesencymal origins

A

sarcoma

114
Q

Sarcoma or Carcinoma?
epidermis

A

carcinoma

115
Q

Sarcoma or Carcinoma?
nasal cavity

A

carcinoma

116
Q

Sarcoma or Carcinoma?
cutaneous glands

A

carcinoma

117
Q

Sarcoma or Carcinoma?
mouth

A

carcinoma

118
Q

Sarcoma or Carcinoma?
epithelium of kidneys

A

sarcoma

119
Q

Sarcoma or Carcinoma?
serous membranes

A

sarcoma

120
Q

Sarcoma or Carcinoma?
gonads

A

sarcoma

121
Q

Sarcoma or Carcinoma?
skeletal and cardiac muscle

A

sarcoma

122
Q

Sarcoma or Carcinoma?
smooth muscle, connective tissue, cartilage, bone, blood, lymphoid tissue, endothelium

A

sarcoma

123
Q

Sarcoma or Carcinoma?
epithelium of pharynx, thyroid, parathyroid, lens, thymus, larynx, trachea, lungs, digestive tube, bladder, vagina, urethra

A

carcinoma

124
Q

A malignant neoplasm of fibrous tissue

A

fibrosarcoma

125
Q

a benign neoplasm of fibrous tissue

A

fibroma

126
Q

A malignant neoplasm of bone

A

osteosarcoma

127
Q

A benign neoplasm of bone

A

osteoma

128
Q

A malignant neoplasm of cartilage

A

chondrosarcoma

129
Q

A malignant neoplasm of adipose (fat cells)

A

liposarcoma

130
Q

A malignant neoplasm of endothelium, blood vasculature

A

hemangiosarcoma

131
Q

a benign neoplasm of endothelium, blood vasculature

A

hemangioma

132
Q

A malignant neoplasm of stratified squamous

A

squamous cell carcinoma

133
Q

a benign neoplasm of stratified squamous

A

squamous papilloma

134
Q

A malignant neoplasm of basal epithelium

A

basal cell carcinoma

135
Q

A malignant neoplasm of glandular epithelium

A

adenocarcinoma

136
Q

A benign neoplasm of glandular epithelium

A

adenoma

137
Q

A malignant neoplasm of liver

A

hepatocellular carcinoma

138
Q

A benign neoplasm of liver

A

hepatocellular adenoma

139
Q

A malignant neoplasm of renal tubules

A

renal cell carcinoma

140
Q

A malignant neoplasm of mammary gland

A

mammary carcinoma or adenocarcinoma

141
Q

a benign neoplasm of mammary gland

A

mammary adenoma

142
Q

Can lymphocyte neoplasms ever be bengin

A

no they are always malignant, lymphoma does not exist despite everyone referring to it. Should be lymphosarcoma

143
Q

What are benign increases of hematopoietic neoplasms called?

A

they are called hyperplasia
ex: lymphoid hyperplasia

144
Q

What are malignant neoplasms of monocytes called

A

monocytic leukemia

145
Q

What are malignant neoplasms of plasma cells called

A

extramedullary plasmacytoma, myeloma plasmacytoid lymphoma

146
Q

What are malignant neoplasms of granulocytes called

A

granulocytic (myeloid) leukemia, granulocytic sarcoma

147
Q

Naming of neuroendrocrine and nervous tissue neoplasms

A

benign are simply named -oma while malignant tumors simply have malignant added before it

148
Q

Circumscribed

A

a characteristic of a benign tumor tumor where the growth limits are restricted

149
Q

Anaplastic

A

a characteristic of malignant tumors where there is poorly differentiated cells, lack of different characteristics

150
Q

desmoplasia

A

excessive connective tissue or support stroma around a malignant tumor

151
Q

How does the recurrence of bening vs malignant tumors differ?

A

benign- rare
malignant- frequent

152
Q

pleomorphism of malignant tumors

A

cellular and nuclear is mod-marked

153
Q

Nucleus/Cytoplasm ratio of benign vs malignant tumors

A

high in malignant tumors, increased nucleus size bc of rapid division

154
Q

leiomyosarcoma

A

malignant tumor of smooth muscle

155
Q

Nucleoli in malignant tumors

A

increased number/size/shape

156
Q

tumors of the vascular endothelium

A

benign- hemangioma
malignant- hemangiosarcoma

157
Q

liposarcoma

A

malignant tumor of fat but rarely metastasize

158
Q

tumors of cutaneous/subcutaneous soft tissues

A

benign- fibroma, bening peripheral nerve sheath tumor
malignant- soft tissue sarcoma

159
Q

epithelial neoplasm

A

benign: adenoma
malignant: adenocarcinoma

160
Q

Malignant mixed tumor carcinosarcoma

A

a malignant mammary gland tumor that has epithelium + myoepithelium with mesenchymal differentiation

161
Q

tumors of odontogenic epithelium

A

always benign
acanathomatous ameloblastoma
easy to treat, tooth making epithelium

162
Q

transmissible venereal tumor (TVT)

A

an immortalized cell line that can be transmissible through sniffing anus
develops buccal, anus, penis, and vulva,
can metastasis, luckily easily treatable

163
Q

teratoma

A

typically arise from the ovary
can be benign or malignant
large in appearance
multiple cell types present

164
Q

What are the properties between benign and malignant tumors?

A

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
Q

Do benign or malignant tumors have poor differentiation?

A

malignant are poor (anaplastic)

166
Q

How do you differentiate the cytological features of benign vs malignant tumors?

A

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
Q

What tissues does catarrhal inflammation take place at?

A

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
Q

zones of granulation tissue

A

basal to apical
zone of mature connective tissue
zone of capillary proliferation
zone of capillary sprouts and arches
zone of necrotic debris

169
Q

do animals get keloid scars?

A

No they do not, they get hypertrophic scars

170
Q

How does granuloma differ from granulation tissue

A

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

biology of disease I (3 decks)

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