Intro Vet Path (1-11) Flashcards
1
Q
this is the mechanism of disease development i.e. the sequence of events occurring following exposure to the inciting agent/event
A
pathogenesis
2
Q
this diagnosis is based on the predominant lesions and refers to the structural changes that are seen in cells or tissues in association with the disease process
A
morphologic diagnosis
3
Q
this diagnosis specifically identifies the etiology
A
etiological diagnosis
4
Q
how much volume of buffered formalin should be used to fix tissues?
A
10x their volume
5
Q
this is the stain routinely used in diagnostic pathology
A
Hematoxylin & Eosin (H&E)
6
Q
this is a special histological stain that stains for fat
A
Oil Red-O (red)
7
Q
this is a special histological stain that stains for glycogen
A
PAS (Periodic acid-Schiff) (pink)
8
Q
this is a special histological stain that stains for Haemosiderin
A
Perl’s Prussian Blue Reaction (blue)
9
Q
this is a special histological stain that stains for connective tissue
A
Massons Trichrome (green)
10
Q
this is a special histological stain that stains for basement membranes
A
Jones’ stain (black)
11
Q
this is the incomplete or underdevelopment of tissue or organ
A
hypoplasia
12
Q
this is an increase in number of cells
A
hyperplasia
13
Q
this is when one adult cell type is replaced by another adult cell type
A
metaplasia
14
Q
this is when there is alteration in the size, shape or organization of a tissue
A
dysplasia
15
Q
this is when an organ does not develop at all - rudimentary tissue only present
A
aplasia
16
Q
this is failure to develop due to lack of embryonic primordial tissue
A
agenesis
17
Q
this is an increase in the size of cells resulting in an increase in the size of the organ (no new cells, just bigger cells)
A
hypertrophy
18
Q
cellular swelling appears as this in the cytoplasm which do not stain for fat or glycogen
A
clear vacuoles
19
Q
this type of necrosis is when basic cell outlines are preserved due to delayed proteolysis - acute
A
coagulative necrosis
20
Q
this type of necrosis has a friable ‘cheese’ like appearance, chronic lesion, may develop dystrophic calcification
A
caseous necrosis
21
Q
this type of necrosis has cavity/cavities filled with liquefied debris
A
liquefactive necrosis
22
Q
specific necrosis of fat
A
fat necrosis
23
Q
destructive fragmentation of the nucleus; chromatin is distributed regularly throughout the cytoplasm
A
karyorrhexis
24
Q
disintegration and dissolution of the nucleus of a necrotic cell
A
karyolysis
25
this is the shrinkage or condensation of a cell with increased nuclear compactness or density
pyknosis
26
what's another term for fatty change
lipidosis
27
this is the accumulation of intracytoplasmic lipid
lipidosis
28
what does lipidosis look like with H&E stain?
punched out holes (fat doesnt stain. with H&E)
29
list 3 examples of situations where glycogen accumulation might occur
1. Corticosteroid therapy
2. diabetes mellitus
3. glycogen storage disease
30
this is when serum calcium levels are normal but the calcium is deposited in tissue that is already dead or dying
dystrophic calcification
31
this is when the primary problem is hypercalcemia causing damage to intracellular organelles
metastatic calcification
32
these inflammatory cells have condensed, dark purple chromatin that is segmented into lobes connected by filaments
neutrophils
33
these inflammatory cells have a segmented nucleus and granules (orange/pink) in the cytoplasm
eosinophils
34
these inflammatory cells are small round cells with a round nucleus, dense chromatin, and scant rim of clear cytoplasm
lymphocytes
35
these inflammatory cells are a round cell with abundant deep blue cytoplasm with a pale area next to the nucleus (Golgi apparatus)
plasma cells
36
these inflammatory cells are oval/irregularly shaped cells with dense granular cytoplasm often obscuring the nucleus and other organelles
mast cells
37
these inflammatory cells have an ovoid/irregular nucleus and the cytoplasm contains vacuoles and granules
macrophages
38
clear or yellow watery fluid occurring early in most inflammatory lesions
serous exudate
39
thick and gelatinous consistency inflammatory response in respiratory and GI tract where mucus secreting cells are prominent
catarrhal exudate
40
this occurs where damage is more severe allowing larger molecular weight proteins to leak through endothelium; causes surfaces of organs to be red and covered by white/yellow exudate
fibrinous exudate
41
thick white/yellow material often bacterial in origin
suppurative/purulent exudate
42
this is when a lesion involves the whole organ or whole of a specified area
diffuse
43
this is when multifocal lesions 'join up' with each other
multifocal to coalescing
44
this is used for describing a portion of a tubular organ
segmental
45
this is used to describe multiple small lesions
miliary
46
what 3 things must you know in order to draw conclusions about a lesion?
1. how the animal died
2. when the animal died
3. conditions post mortem
47
this is when a lesion is characteristic or indicative of a particular disease
pathognomic
48
multifocal lesions usually imply this type of spread
systemic/hematogenous spread
49
a raised lesion implies this
something has been added
50
a depressed lesion implies this
something has been lost
51
a flat lesion can imply this
acute process or incidental color change
52
a lesion of this color is due to an increase in amount of blood (hemorrhage, congestion)
red to red/black
53
a lesion of this color indicates melanin, exogenous carbon, putrefactive bacteria, or hemosiderin
black to brown/black
54
a lesion of this color is usually bile pigment (seen in PM areas of liver and intestine); some fungal pathogens
green
55
a lesion of this color may indicate fat, bile pigment (bilirubin), fibrin, cellular exudates, neoplasms
yellow
56
a lesion of this color may indicate exudates, neoplasia, connective tissue (cartilage, bone)
white
57
a hard lesion implies this
mineral density (cartilage, bone, mineral salt deposition)
58
list the 10 steps of the PM prosection
1. external examination
2. initial dissection
3. neck region
4. open abdomen and thorax
5. removal of thoracic viscera
6. removal of abdominal viscera
7. musculoskeletal systems
8. nervous system
9. special senses
10. individual organ dissections
59
name the organs incised/examined in the neck region during a PM prosection
tongue, soft palate, hyoid apparatus, tonsils, R/P lymph nodes, thyroids, oesophagus, trachea
60
name the thoracic viscera removed during a PM prosection
heart, lungs (leave oesophagus connected to stomach)
61
name the abdominal viscera removed during a PM prosection
(intestines, stomach, liver and spleen), adrenals, (kidneys, ureters, bladder)
62
how should tissue samples for histopathology be stored from a PM
fixed in 10x 10% buffered formalin
63
this is the cooling of body after death (can aid in estimating time of death)
algor mortis
64
this is an effect of gravity, often evident in lungs and kidneys - PM change
hypostatic congestion
65
Blood coagulation in vessels; careful not to mistake for thrombosis - PM change
postmortem clotting of blood
66
this is when pigment from bile is absorbed by liver/other organs in contact with gall bladder (ex. GI tract) - PM change
biliary imbibition
67
this is a green/black discoloration due to conversion of iron to iron sulphide by GI bacteria - PM change
pseudomelanosis
68
this is invasion by gas producing bacteria - PM change
emphysema
69
this PM change begins approximately 2-4 hours after death; rigidity of skeletal muscles due to lack of ATP (sustained contraction)
rigor mortis
70
this is the process whereby the release of intracellular lytic enzymes results in self digestion of tissues
autolysis
71
this PM change occurs when dead tissue is invaded by anaerobic organisms such as Clostridia; tissue turns green/brown
putrefaction
72
these changes occur around the time of death/time of irreversible circulatory failure and often leads to vascular congestion
agonal changes
73
this PM change may result in food material being present in the airways and possibly alveoli
agonal regurgitation of GI contents
74
name 3 PM changes that may be associated with administration of barbiturates
1. local reaction
2. barbiturate crystals
3. splenomegaly
75
this incidental finding occurs when hyperplastic nodules of tissue develop in organs but can be mistaken for genuine neoplasms
nodular hyperplasia
76
this PM change occurs due to inhaled carbon particles being phagocytose by alveolar macrophages which can become visible as multiple small black foci in lung tissue
anthracosis
77
this is the degeneration and proliferation in the arterial wall resulting in loss of elasticity and hardening; common PM change but usually incidental
arteriosclerosis
78
long time steroid use can lead to this where glucocorticoids induce glycogen synthetase to increase storage of glycogen within hepatocytes, can be up to 20x the normal size
steroid-induced hepatopathy
79
Total Body Water (TBW) comprises this percent of body weight
60%
80
Intracellular Fluid (ICF) makes up this much of total body water
40%
81
Extracellular Fluid (ECF) makes up this much of total body water
20%
82
interstitial fluid (component of ECF) makes up this much of total body water
15%
83
plasma (component of ECF) makes up this much of total body water
5%
84
this is extracellular fluid around cells
interstitial fluid (ISF)
85
this is extracellular fluid within blood vessels
intravascular fluid (IVF)
86
this is extracellular fluid produced by specialized cells (ex: CSF, synovial fluid)
transcellular fluid (TSF)
87
this is a proteolytic enzyme that is produced by specialized juxtaglomerular cells in the glomerular afferent arteriole in response to decr. renal profusion
renin
88
this is a serum globulin produced by the liver which is converted by renin into angiotensin I
angiotensinogen
89
this is produced by RAAS and increases aldosterone production which enhances renal Na+ and water reabsorption
angiotensin II
90
this controls permeability of distal tubules and collecting ducts. when it's present, water permeability is high, allowing water to follow Na into the blood stream so urine output is low
ADH (anti-diuretic hormone)
91
this is a group of diverse peptide hormones released by the heart in response to stretching of the heart & reduce cardiac output and blood pressure
ANF (atrial natriuretic factor) or ANP (peptide)
92
these are vital in most of life's processes and affect the volume of fluid present in each body fluid compartment
electrolytes
93
this is when the ratio of total body Na to total body water is increased (may be caused by water deficiency or sodium excess)
hypernatremia
94
what is the overall effect of hypernatremia
cell dehydrates and eventually dies
95
this is when the ratio of total body Na to total body water is decreased (may be caused by sodium deficit or water excess)
hyponatremia
96
this is the overall effect of hyponatremia caused by a sodium deficit
hemoconcentration and circulatory failure
97
this is the overall effect of hyponatremia caused by water excess
CNS convulsions and death
98
water distribution between plasma and interstitium is mainly determined by these 2 forces acting against each other
hydrostatic pressure and oncotic pressure
99
this force tends to pull water out of the vessels into the interstitium
hydrostatic pressure
100
this force is the osmotic pressure created by the plasma proteins that pulls water from the interstitium into the vessels
oncotic pressure
101
this is an accumulation of excess interstitial fluid. it can be generalized or localized
oedema
102
this is a type of generalized oedema where the fluid tends to sink with gravity so that the ventral abdomen and limbs are mainly affected
dependent oedema
103
this is severe diffuse subcutaneous oedema, where a finger pushed into the expanded interstitium leaves an indentation
pitting oedema
104
this is severe, generalized oedema
anasarca
105
this is when excessive fluid leaks into a body cavity lined by mesothelial cells (peritoneum, pleural, pericardium)
effusion
106
name 4 causes of excessive fluid leakage from the vasculature (that may lead to oedema or effusion formation)
1. incr hydrostatic pressure
2. decr oncotic pressure
3. incr microvascular permeability
4. decr lymphatic drainage
107
right heart failure can lead to this type of oedema
peripheral oedema
108
left heart failure can lead to this type of oedema
pulmonary oedema
109
generalized heart failure can lead to this type of oedema
generalized oedema
110
oedema caused by lymphatic obstruction if often this type
localized
111
pulmonary oedema is mainly caused but these 2 mechanisms
increased hydrostatic pressure and increased vascular permeability
112
this type of effusion is a clear/pale yellow fluid characterized by low protein and cellular content
transudate
113
this effusion type has <25 g/l protein and <1 cell x10^9/l cellular content
transudate
114
this effusion type has >30 g/l protein and >5 cell x10^9/l cellular content
exudate
115
pleural transudate is called this
hydrothorax
116
abdominal transudate is called this
hydroperitoneum or ascites
117
pericardial transudate is called this
hydropericardium
118
this type of effusion is a turbid, deep yellow/orange to brown fluid characterized by high protein and cellular content
exudate
119
cytological analysis of exudates reveals high numbers of this type of cell
neutrophils (& other inflammatory cells)
120
effusion due to neutrophilic inflammation in the pleura is called this
pyothorax
121
this type of effusion can vary from clear to mild turbid with variable color (yellow to pink)
modified transudate
122
name some cell types that might be seen in low lumbers in transudate effusion
macrophages, mesothelial cells, neutrophils, occasional lymphocytes
123
this type of effusion is caused by leakage or rupture of lymphatic vessels and is usually turbid and white in color
chylous
124
this type of effusion is caused by leakage of blood into a body cavity and has a bloody appearance
hemorrhagic
125
this type of effusion is caused by urinary tract rupture and leakage of urine in the abdomen
uroperitoneum
126
this is another word for cardiac collapse
shock
127
name 3 life-threatening events that can lead to shock
1. severe hemorrhage
2. extensive trauma or burns
3. sepsis
128
name the 3 categories of shock
1. cardiogenic
2. hypovolemic
3. blood maldistribution
129
this type shock results from failure of the heart to adequately pump blood
cardiogenic shock
130
this type of shock is due to reduced circulating volume resulting from blood or fluid loss (hemorrhage, vomiting, diarrhea, extensive burns)
hypovolemic shock
131
if volume reduction is around this percent in hypovolemic shock, then return to normal can occur
10%
132
if volume reduction is around this percent in hypovolemic shock, then BP and CO fall dramatically
35-45%
133
this type of shock is characterized by decreased peripheral vascular resistance and pooling of blood peripheral tissues
blood maldistribution
134
name the 3 main types of maldistribution shock
1. neurogenic shock
2. anaphylactic shock
3. septic shock
135
this is a life-threatening reaction to an infection which causes the immune system to overreact and damage the body's own tissues and organs
sepsis
136
this occurs when a bacterial infection enters the bloodstream
septicemia
137
this is the most common cause of septic shock; it is a lipopolysaccharide (LPS) in the wall of gram negative bacteria
endotoxin
138
name the 3 stages of shock
1. non-progressive stage
2. progressive stage
3. irreversible stage
139
during this stage of shock, mechanisms aimed at vasoconstriction are overcome leading to widespread vasodilation and multi organ failure/DIC
irreversible stage
140
during this stage of shock, compensatory mechanisms are overcome and there is blood pooling, tissue hypoperfusion and cellular injury leading to necrosis
progressive stage
141
during this stage of shock, the body compensates and blood flow is maintained to critical organs (heart, kidney, brain)
non-progressive stage
142
name some clinical features of shock
hypotension, weak pulse and tachycardia, hyperventilation, decr. urine production, hypothermia
143
name some morphologic features of shock
congestion and pooling of blood, oedema and hemorrhage, thrombosis, cellular necrosis
144
this occurs when arteriolar dilation increases blood flow to the tissue (active process) which leads to tissue redness
hyperemia
145
this is due to reduced outflow of blood from a tissue (passive process)
congestion
146
hyperemia is an active or passive process?
active process
147
congestion is an active or passive process?
passive process
148
this is the escape of blood from vessels due to vascular rupture or damage which may lead to loss of blood from the body or blood accumulating within surrounding tissue/body cavity
hemorrhage
149
this is a massive accumulation of blood within a tissue
hematoma
150
this is an accumulation of blood within the thorax
hemothorax
151
this is a 1-2mm hemorrhage in the skin, mucus membranes and serial surfaces
petechiae
152
this is a 3mm+ hemorrhage in the skin, mucus membranes and serial surfaces
purpura
153
this is a 1-3cm hemorrhage in the skin, mucus membranes and serial surfaces
ecchymoses
154
this is a hemorrhage in the skin, mucus membranes and serial surfaces that affects large contiguous areas of tissue
suffusive hemorrhage
155
the significance of hemorrhage depends on these 3 factors of blood loss
volume, rate, and location
156
this is the physiological process which stops hemorrhage and is a highly regulated, complex interrelationship between blood vessels, platelets and coagulation factors
hemostasis
157
name the 4 steps/processes of hemostasis
1. vascular response (transient effect)
2. platelet response (primary hemostasis)
3. coagulation cascade (secondary hemostasis)
4. fibrinolysis (tertiary hemostasis)
158
this step of hemostasis is when vascular injury causes arteriolar vasoconstriction
vascular response
159
this step of hemostasis includes platelet adherence, activation, and aggregation to form a hemostatic plug
platelet response (primary hemostasis)
160
this step of hemostasis is when clotting factors are activated to form thrombin which converts fibrinogen to fibrin to stabilize primary hemostatic plug and stop further hemorrhage
coagulation cascade (secondary hemostasis)
161
this step of hemostasis is to prevent over-production or persistence of fibrin and to control hemostatic plug formation
fibrinolysis (tertiary hemostasis)
162
these act as weak anticoagulants and can be measured to diagnose pro-thrombin states
fibrin degradation products (FDPs)
163
this is a cause of primary hemostasis disorders and is decreased platelet numbers in peripheral blood
thrombocytopenia
164
this is the most common cause of thrombocytopenia
platelet clumping (pseudothrombocytopenia)
165
name 4 causes of true thrombocytopenia
1. decreased production
2. increased destruction or utilization of platelets
3. sequestration of platelets
4. inherited causes
166
this is an inherited disorder of a specific adhesion molecule between platelets and endothelial cells essential for primary homeostasis
von Willebrands disease (vWD)
167
this type of hemostasis disorder is due to coagulation factor deficiencies
disorders of secondary hemostasis
168
Hemophilia A is a deficiency of this coagulation factor
VIII (8)
169
Hemophilia B is a deficiency of this coagulation factor
IX (9)
170
these are sex-linked coagulation factor disorders with a recessive inheritance pattern where males are affected (disorders of secondary hemostasis)
hemophilia A and B
171
this type of hemostasis disorder is mostly associated with disseminated intravascular coagulation/DIC which results in clot formation in the microvasculature
disorders of tertiary hemostasis
172
primary hemostasis can be evaluated by these 3 tests
1. platelet count
2. platelet function
3. buccal mucosal bleeding time (BMBT)
173
secondary hemostasis can be evaluated by these 5 tests
1. prothrombin time (PT)
2. activated partial thromboplastin time (aPTT)
3. activated clotting time (ACT)
4. whole blood clotting time (WBCT)
5. thrombin clot time (TCT)
174
tertiary hemostasis can be evaluated by these 2 tests
evaluation of FDPs and D-dimers
175
this is a mass of platelets, fibrin, red and white blood cells, which is attached to the wall of the cardiovascular system
thrombus
176
what is the difference between an ante-mortem thrombus and a post-mortem clot surface
thrombus: granular, dry, dull
clot: smooth, moist, shiny
177
what is the difference between an ante-mortem thrombus and a post-mortem clot texture
thrombus: firm or friable
clot: elastic or gelatinous
178
what is the difference between an ante-mortem thrombus and a post-mortem clot structure
thrombus: variegated (maybe laminated)
clot: homogenous
179
what is the difference between an ante-mortem thrombus and a post-mortem clot color
thrombus: white (arterial), OR red (veins), OR red/white laminate (arteries, large veins, heart)
clot: dark red OR "chicken fat"
180
what is the difference between an ante-mortem thrombus and a post-mortem clot shape
thrombus: ovoid, flat, or pear-shape
clot: conforms to vessel shape
181
which is easier to remove: an ante-mortem thrombus or a post-mortem clot?
post-mortem clot (thrombus is attached to vessel wall or chord tendinae)
182
name the 3 main factors that predispose to thrombus formation (Virchow's Triad)
1. damage to epithelium
2. altered blood flow
3. hypercoagulability of blood
183
venous thrombi tend to have this appearance
red, soft, loose vascular attachment
184
thrombi in heart or arteries often have this appearance
pale (red-grey), firm, attached to wall, striated/laminar
185
the clinical significance of thrombosis depends on these 3 factors
size, location, rate of formation
186
name the 4 possible fates of a thrombus
1. dissolution
2. propagation
3. organization and recanalization
4. embolization
187
this is when the thrombus is completely removed by fibrinolysis
dissolution
188
this is when additional platelets and fibrin accumulate and extend/elongate the thrombus along the vessel wall toward the heart
propagation
189
this is when the thrombus is invaded by endothelial cells and fibroblasts forming granulation tissue with subsequent fibrosis
organization
190
this is when capillary channels in a large organizing thrombus anastomose and allow blood flow to be re-established
recanalization
191
this is when fragments of the thrombus break off and travel to other sites in the body via the vasculature
embolization
192
this is a solid or gaseous mass carried by the bloodstream from its point of origin to a distant site within the circulation
embolus
193
this is the most common type of embolism, where fragments of thrombi detach and spread throughout circulation
thromboembolism
194
this type of embolus occurs if a large enough volume of air is injected into the circulation - can accumulate in pulmonary trunk and form a fatal airlock
gas embolism
195
adipocytes from bone marrow may be released into circulation following bone fractures leading to this type of embolus
fat embolism
196
this is due to reduction or failure of blood flow to or from a tissue/organ and results in tissue hypoxia and reduced nutrient supply
ischemia
197
name 3 possible causes of ischemia
1. arterispasms
2. compression of vessels
3. thromboembolism
198
extent and consequences of ischemia depend on these 4 factors
1. degree of occlusion
2. speed of occlusion
3. presence of collateral circulation
4. vulnerability of tissues/cells to ischemia
199
this is a segmental or localized area of coagulative necrosis due to occlusion of the blood supply
infarction
200
macroscopic appearance of an infarction
red or pale, wedge-shaped
201
a venous occlusion will give this color infarction
red
202
an arterial occlusion will give this color infarction
pale
203
this is widespread pathologic activation of hemostasis within the vascular system resulting in generalized intravascular thrombosis
DIC (disseminated intravascular coagulation)
204
the intrinsic pathway of the coagulation cascade involves these coagulation factors
12, 11, 9, 8
205
the extrinsic pathway of the coagulation cascade involves this coagulation factor
7
206
the common pathway of the coagulation cascade involves these coagulation factors
10, 5, 2 (13)
207
what is hemoptysis?
coughing up blood
208
what is epistaxis?
nose bleed
209
what is hematochezia?
fresh blood in feces
210
this is the increased tendency to hemorrhage after minor injury
hemorrhagic diathesis
211
this is a prolonged/persistent inflammatory response that comprises varying combinations of inflammation, tissue injury and repair
chronic inflammation
212
name 4 infectious causes of chronic inflammation
1. Mycobacterium spp.
2. fungi
3. parasites
4. viruses
213
name the 3 main components of chronic inflammation
1. inflammation
2. tissue destruction
3. tissue repair attempts
214
215
these inflammatory cells play a huge role in adaptive immunity against infectious agents and produce cytokines that influence other inflammatory cell types
lymphocytes (B & T)
216
these inflammatory cells produce antibodies and often accompany lymphocytes in chronic inflammation
plasma cells
217
name the 3 main functions of macrophages in chronic inflammation
1. phagocytosis
2. secrete cytokines
3. initiation of repair
218
inflammation mediated by IgE (hypersensitivity) or parasitic infections will be dominated by this type of cell
eosinophils
219
persistence of infectious agents in chronic inflammation can lead to the continues presence of these cells
neutrophils
220
this is a distinct form of inflammation which is always chronic with macrophages predominate
granulomatous inflammation
221
this is discrete clusters/nodules of macrophages separated by host tissue
granulomas
222
this is discrete clusters of macrophages AND neutrophils
pyogranulomas
223
this is a type of chronic inflammation where macrophages are predominate but neutrophils are also present
pyogranulomatous
224
these are macrophages that become activated to the extent that they develop abundant cytoplasm
epithelioid macrophages
225
name 5 systemic effects of chronic inflammation
1. leucocytosis (mediated by IL-1 and TNF-alpha)
2. low grade pyrexia
3. acute phase response
4. cachexia (mediated by TNF-alpha)
5. anemia
226
these are the two types of reactions of repair
regeneration and scar formation
227
this is when surviving cells have the capacity to proliferate and to replace damaged components
regeneration
228
name the three groups of cells in regeneration based on proliferative capacity
labile, stable, permanent
229
this group of regenerative cell is continually lost and replaced by maturation of stem cells and proliferation of mature cells
labile
230
this group of regenerative cell are quiescent cells in G0 phase of cell cycle or will divide in response to injury to loss
stable
231
this group of regenerative cell is terminally differentiated and non-proliferative in postnatal life
permanent
232
this type of repair happens if tissue injury results in damage to parenchymal or epithelial cells, if it destroys the connective tissue framework or if non-dividing cells are damaged
scar formation
233
name the 3 main steps in scar formation
angiogenesis, formation of granulation tissue, remodeling
234
this step of scar formation is the formation of new blood vessels
angiogenesis
235
this step of scar formation is migration and proliferation of fibroblasts and deposition of collagen, together with new blood vessels
formation of granulation tissue
236
this step of scar formation is when the connective tissue matures and reorganizes to produce a stable fibrous scar
remodeling
237
this type of scar is due to exuberant formation of granulation tissue; most common in distal limbs of horses
hypertrophic scars
238
this is the abnormal growth of a tissue into a mass; usually recognized by the fact its cells have abnormal growth patterns, are no longer under the control of normal homeostatic growth controlling mechanisms and have no functional value
neoplasia
239
this literally means "swelling" and is not necessarily neoplastic
tumor
240
these tumors arise in any of the tissues of the body and grow locally; they can grow to a large size but are not invasive
benign tumors
241
what is the clinical significance of benign tumors
can cause local pressure, cause obstruction, or form a space-occupying lesion
242
these are often small tumors that arise in the epithelium; appears to contain cancer but tumor remains in epithelial layer
in-situ tumors
243
this is any malignant growth or tumor caused by abnormal and uncontrolled cell division, able to invade tissues locally and able to spread to other parts of the body through the lymphatic system or blood stream
cancer
244
a severe lack of differentiation in malignant tumors is referred to as this
anaplasia
245
what is the growth rate of benign tumors
slow & periods of dormancy
246
what is the mode of growth of benign tumors by?
expansion
247
what is the mode of growth of malignant tumors by?
initially expansion then invasion
248
# name the tissue/cell of origin for the benign tumor
suffix -oma (fibroma, lipoma, chondroma)
mesenchymal or nervous tissue
249
# name the tissue/cell of origin for the benign tumor
referred to as adenoma
glandular epithelium
250
# name the tissue/cell of origin for the benign tumor
referred to as papilloma
protective epithelium
251
# name the tissue/cell of origin for the malignant tumor
addition of 'sarcoma' (fibrosarcoma, liposarcoma, chondrosarcoma)
mesenchymal
252
# name the tissue/cell of origin for the malignant tumor
referred to as adenocarcinoma
glandular epithelium
253
name the 5 types of round cell tumors
1. Lymphoma
2. Transmissible Venereal Tumor (TVT)
3. Mast Cell Tumor
4. Plasmacytoma and multiple myeloma
5. Histiocytoma
254
round cell tumors tend to form this histiological pattern
solid sheets
255
epithelial tumors form these histiological patterns
nests, cords, islands, acini, tubules, or trabeculae
256
mesenchymal tumors form these histiological patterns
interlacing streams, bundles, fascicles
257
this means variation in cell size
anisocytosis
258
this means variation in nuclear size
anisokaryosis
259
this means variation in cell shape
pleomorphism
260
this means the distant spread of a neoplasm and is often the cause of death in most patients
metastasis
261
name the 3 different routes od metastasis
1. hematogenous
2. lymphatic
3. transcoelomic
262
name the 5 steps/stages of metastasis
1. subset of cells detaches from main mass and breaches the basement membrane
2. cells pass thrugh ECM and enter a nearby vessel
3. tumor cells form embolus that travels to distant site in blood or lymph
4. adhesion of tumor cells to endothelial cells
5. metastatic deposit forms and grows with help of angiogenesis
263
this is a cellular oncogene that does not have transforming potential to form tumors in its native state but can be altered to lead to malignancy
proto-oncogene
264
most proto-oncogenes are key genes involved in these two things
1. cell growth
2. proliferation
265
name the 6 possible modes of action of proto-oncogenes in the normal cell (oncogene classes)
1. growth factors
2. growth factor receptors
3. protein kinases
4. signal transducers
5. nuclear proteins
6. transcription factors
266
name the 4 possible mechanisms of oncogene activation
1. chromosomal translocation
2. gene amplification
3. point mutations
4. viral insertions
267
mutations or translocations of these genes produce positive signals leading to uncontrolled growth
oncogenes
268
mutations or translocations of these genes leads to a loss of inhibitory functions leading to tumor formation
tumor supressor genes
269
this was the first gene to inform mechanisms of tumor suppressor genes
retinoblastoma gene (Rb)
270
this is the most frequently inactivated gene in human neoplasia
p53
271
name the 7 hallmark capabilities of cancer/alterations in cellular physiology that collectively dictate malignant growth
1. self-sufficiency in growth
2. insensitivity to anti-growth signals
3. ability to evade programmed cell death (apoptosis)
4. limitless replicative potential
5. ability to sustain angiogenesis
6. ability to invade and metastasize
7. ability to evade host immunity
272
name the 3 broad categories of cancer causing agents
1. oncogenic viruses
2. chemical carcinogens
3. physical agents (radiation)
273
what viruses are included as oncogenic viruses
DNA viruses and Retroviruses
274
# name the oncogenic virus group
important oncogenic virsuses of cats, cattle and chickens;
can promote carcinogenesis through activation of cellular oncogenes by integrating adjacent to them;
FeLV (lymphomas and leukemia
retroviruses
275
# name the oncogenic virus group
ex: papilloma virus (esp. Bovine PV), lifecycle of virus tightly coupled with differentiation process of epithelial cell & can transform benign wart to a squamous cell carcinoma;
also herpes viruses (known to cause Marek's disease in chickens)
DNA viruses
276
name 4 chemical carcinogens involved with veterinary cancers
1. bracken fern (with papilloma viruses in cattle)
2. herbicides (canine lymphoma)
3. Aflatoxin
4. cyclophosphamide (chronic inflammation and transitional carcinoma)
277
what 2 ways can radiation cause cancer
1. cause errors in DNA replication
2. cause production of oxygen free radicals
