Intro Vet Path (1-11) Flashcards
this is the mechanism of disease development i.e. the sequence of events occurring following exposure to the inciting agent/event
pathogenesis
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
morphologic diagnosis
this diagnosis specifically identifies the etiology
etiological diagnosis
how much volume of buffered formalin should be used to fix tissues?
10x their volume
this is the stain routinely used in diagnostic pathology
Hematoxylin & Eosin (H&E)
this is a special histological stain that stains for fat
Oil Red-O (red)
this is a special histological stain that stains for glycogen
PAS (Periodic acid-Schiff) (pink)
this is a special histological stain that stains for Haemosiderin
Perl’s Prussian Blue Reaction (blue)
this is a special histological stain that stains for connective tissue
Massons Trichrome (green)
this is a special histological stain that stains for basement membranes
Jones’ stain (black)
this is the incomplete or underdevelopment of tissue or organ
hypoplasia
this is an increase in number of cells
hyperplasia
this is when one adult cell type is replaced by another adult cell type
metaplasia
this is when there is alteration in the size, shape or organization of a tissue
dysplasia
this is when an organ does not develop at all - rudimentary tissue only present
aplasia
this is failure to develop due to lack of embryonic primordial tissue
agenesis
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)
hypertrophy
cellular swelling appears as this in the cytoplasm which do not stain for fat or glycogen
clear vacuoles
this type of necrosis is when basic cell outlines are preserved due to delayed proteolysis - acute
coagulative necrosis
this type of necrosis has a friable ‘cheese’ like appearance, chronic lesion, may develop dystrophic calcification
caseous necrosis
this type of necrosis has cavity/cavities filled with liquefied debris
liquefactive necrosis
specific necrosis of fat
fat necrosis
destructive fragmentation of the nucleus; chromatin is distributed regularly throughout the cytoplasm
karyorrhexis
disintegration and dissolution of the nucleus of a necrotic cell
karyolysis
this is the shrinkage or condensation of a cell with increased nuclear compactness or density
pyknosis
what’s another term for fatty change
lipidosis
this is the accumulation of intracytoplasmic lipid
lipidosis
what does lipidosis look like with H&E stain?
punched out holes (fat doesnt stain. with H&E)
list 3 examples of situations where glycogen accumulation might occur
- Corticosteroid therapy
- diabetes mellitus
- glycogen storage disease
this is when serum calcium levels are normal but the calcium is deposited in tissue that is already dead or dying
dystrophic calcification
this is when the primary problem is hypercalcemia causing damage to intracellular organelles
metastatic calcification
these inflammatory cells have condensed, dark purple chromatin that is segmented into lobes connected by filaments
neutrophils
these inflammatory cells have a segmented nucleus and granules (orange/pink) in the cytoplasm
eosinophils
these inflammatory cells are small round cells with a round nucleus, dense chromatin, and scant rim of clear cytoplasm
lymphocytes
these inflammatory cells are a round cell with abundant deep blue cytoplasm with a pale area next to the nucleus (Golgi apparatus)
plasma cells
these inflammatory cells are oval/irregularly shaped cells with dense granular cytoplasm often obscuring the nucleus and other organelles
mast cells
these inflammatory cells have an ovoid/irregular nucleus and the cytoplasm contains vacuoles and granules
macrophages
clear or yellow watery fluid occurring early in most inflammatory lesions
serous exudate
thick and gelatinous consistency inflammatory response in respiratory and GI tract where mucus secreting cells are prominent
catarrhal exudate
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
thick white/yellow material often bacterial in origin
suppurative/purulent exudate
this is when a lesion involves the whole organ or whole of a specified area
diffuse
this is when multifocal lesions ‘join up’ with each other
multifocal to coalescing
this is used for describing a portion of a tubular organ
segmental
this is used to describe multiple small lesions
miliary
what 3 things must you know in order to draw conclusions about a lesion?
- how the animal died
- when the animal died
- conditions post mortem
this is when a lesion is characteristic or indicative of a particular disease
pathognomic
multifocal lesions usually imply this type of spread
systemic/hematogenous spread
a raised lesion implies this
something has been added
a depressed lesion implies this
something has been lost
a flat lesion can imply this
acute process or incidental color change
a lesion of this color is due to an increase in amount of blood (hemorrhage, congestion)
red to red/black
a lesion of this color indicates melanin, exogenous carbon, putrefactive bacteria, or hemosiderin
black to brown/black
a lesion of this color is usually bile pigment (seen in PM areas of liver and intestine); some fungal pathogens
green
a lesion of this color may indicate fat, bile pigment (bilirubin), fibrin, cellular exudates, neoplasms
yellow
a lesion of this color may indicate exudates, neoplasia, connective tissue (cartilage, bone)
white
a hard lesion implies this
mineral density (cartilage, bone, mineral salt deposition)
list the 10 steps of the PM prosection
- external examination
- initial dissection
- neck region
- open abdomen and thorax
- removal of thoracic viscera
- removal of abdominal viscera
- musculoskeletal systems
- nervous system
- special senses
- individual organ dissections
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
name the thoracic viscera removed during a PM prosection
heart, lungs (leave oesophagus connected to stomach)
name the abdominal viscera removed during a PM prosection
(intestines, stomach, liver and spleen), adrenals, (kidneys, ureters, bladder)
how should tissue samples for histopathology be stored from a PM
fixed in 10x 10% buffered formalin
this is the cooling of body after death (can aid in estimating time of death)
algor mortis
this is an effect of gravity, often evident in lungs and kidneys - PM change
hypostatic congestion
Blood coagulation in vessels; careful not to mistake for thrombosis - PM change
postmortem clotting of blood
this is when pigment from bile is absorbed by liver/other organs in contact with gall bladder (ex. GI tract) - PM change
biliary imbibition
this is a green/black discoloration due to conversion of iron to iron sulphide by GI bacteria - PM change
pseudomelanosis
this is invasion by gas producing bacteria - PM change
emphysema
this PM change begins approximately 2-4 hours after death; rigidity of skeletal muscles due to lack of ATP (sustained contraction)
rigor mortis
this is the process whereby the release of intracellular lytic enzymes results in self digestion of tissues
autolysis
this PM change occurs when dead tissue is invaded by anaerobic organisms such as Clostridia; tissue turns green/brown
putrefaction
these changes occur around the time of death/time of irreversible circulatory failure and often leads to vascular congestion
agonal changes
this PM change may result in food material being present in the airways and possibly alveoli
agonal regurgitation of GI contents
name 3 PM changes that may be associated with administration of barbiturates
- local reaction
- barbiturate crystals
- splenomegaly
this incidental finding occurs when hyperplastic nodules of tissue develop in organs but can be mistaken for genuine neoplasms
nodular hyperplasia
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
this is the degeneration and proliferation in the arterial wall resulting in loss of elasticity and hardening; common PM change but usually incidental
arteriosclerosis
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
Total Body Water (TBW) comprises this percent of body weight
60%
Intracellular Fluid (ICF) makes up this much of total body water
40%
Extracellular Fluid (ECF) makes up this much of total body water
20%
interstitial fluid (component of ECF) makes up this much of total body water
15%
plasma (component of ECF) makes up this much of total body water
5%
this is extracellular fluid around cells
interstitial fluid (ISF)
this is extracellular fluid within blood vessels
intravascular fluid (IVF)
this is extracellular fluid produced by specialized cells (ex: CSF, synovial fluid)
transcellular fluid (TSF)
this is a proteolytic enzyme that is produced by specialized juxtaglomerular cells in the glomerular afferent arteriole in response to decr. renal profusion
renin
this is a serum globulin produced by the liver which is converted by renin into angiotensin I
angiotensinogen
this is produced by RAAS and increases aldosterone production which enhances renal Na+ and water reabsorption
angiotensin II
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)
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)
these are vital in most of life’s processes and affect the volume of fluid present in each body fluid compartment
electrolytes
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
what is the overall effect of hypernatremia
cell dehydrates and eventually dies
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
this is the overall effect of hyponatremia caused by a sodium deficit
hemoconcentration and circulatory failure
this is the overall effect of hyponatremia caused by water excess
CNS convulsions and death
water distribution between plasma and interstitium is mainly determined by these 2 forces acting against each other
hydrostatic pressure and oncotic pressure
this force tends to pull water out of the vessels into the interstitium
hydrostatic pressure
this force is the osmotic pressure created by the plasma proteins that pulls water from the interstitium into the vessels
oncotic pressure
this is an accumulation of excess interstitial fluid. it can be generalized or localized
oedema
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
this is severe diffuse subcutaneous oedema, where a finger pushed into the expanded interstitium leaves an indentation
pitting oedema
this is severe, generalized oedema
anasarca
this is when excessive fluid leaks into a body cavity lined by mesothelial cells (peritoneum, pleural, pericardium)
effusion
name 4 causes of excessive fluid leakage from the vasculature (that may lead to oedema or effusion formation)
- incr hydrostatic pressure
- decr oncotic pressure
- incr microvascular permeability
- decr lymphatic drainage
right heart failure can lead to this type of oedema
peripheral oedema
left heart failure can lead to this type of oedema
pulmonary oedema
generalized heart failure can lead to this type of oedema
generalized oedema
oedema caused by lymphatic obstruction if often this type
localized
pulmonary oedema is mainly caused but these 2 mechanisms
increased hydrostatic pressure and increased vascular permeability
this type of effusion is a clear/pale yellow fluid characterized by low protein and cellular content
transudate
this effusion type has <25 g/l protein and <1 cell x10^9/l cellular content
transudate
this effusion type has >30 g/l protein and >5 cell x10^9/l cellular content
exudate
pleural transudate is called this
hydrothorax
abdominal transudate is called this
hydroperitoneum or ascites
pericardial transudate is called this
hydropericardium
this type of effusion is a turbid, deep yellow/orange to brown fluid characterized by high protein and cellular content
exudate
cytological analysis of exudates reveals high numbers of this type of cell
neutrophils (& other inflammatory cells)
effusion due to neutrophilic inflammation in the pleura is called this
pyothorax
this type of effusion can vary from clear to mild turbid with variable color (yellow to pink)
modified transudate
name some cell types that might be seen in low lumbers in transudate effusion
macrophages, mesothelial cells, neutrophils, occasional lymphocytes
this type of effusion is caused by leakage or rupture of lymphatic vessels and is usually turbid and white in color
chylous
this type of effusion is caused by leakage of blood into a body cavity and has a bloody appearance
hemorrhagic
this type of effusion is caused by urinary tract rupture and leakage of urine in the abdomen
uroperitoneum
this is another word for cardiac collapse
shock
name 3 life-threatening events that can lead to shock
- severe hemorrhage
- extensive trauma or burns
- sepsis
name the 3 categories of shock
- cardiogenic
- hypovolemic
- blood maldistribution
this type shock results from failure of the heart to adequately pump blood
cardiogenic shock
this type of shock is due to reduced circulating volume resulting from blood or fluid loss (hemorrhage, vomiting, diarrhea, extensive burns)
hypovolemic shock
if volume reduction is around this percent in hypovolemic shock, then return to normal can occur
10%
if volume reduction is around this percent in hypovolemic shock, then BP and CO fall dramatically
35-45%
this type of shock is characterized by decreased peripheral vascular resistance and pooling of blood peripheral tissues
blood maldistribution
name the 3 main types of maldistribution shock
- neurogenic shock
- anaphylactic shock
- septic shock
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
this occurs when a bacterial infection enters the bloodstream
septicemia
this is the most common cause of septic shock; it is a lipopolysaccharide (LPS) in the wall of gram negative bacteria
endotoxin
name the 3 stages of shock
- non-progressive stage
- progressive stage
- irreversible stage
during this stage of shock, mechanisms aimed at vasoconstriction are overcome leading to widespread vasodilation and multi organ failure/DIC
irreversible stage
during this stage of shock, compensatory mechanisms are overcome and there is blood pooling, tissue hypoperfusion and cellular injury leading to necrosis
progressive stage
during this stage of shock, the body compensates and blood flow is maintained to critical organs (heart, kidney, brain)
non-progressive stage
name some clinical features of shock
hypotension, weak pulse and tachycardia, hyperventilation, decr. urine production, hypothermia
name some morphologic features of shock
congestion and pooling of blood, oedema and hemorrhage, thrombosis, cellular necrosis
this occurs when arteriolar dilation increases blood flow to the tissue (active process) which leads to tissue redness
hyperemia
this is due to reduced outflow of blood from a tissue (passive process)
congestion
hyperemia is an active or passive process?
active process
congestion is an active or passive process?
passive process
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
this is a massive accumulation of blood within a tissue
hematoma
this is an accumulation of blood within the thorax
hemothorax
this is a 1-2mm hemorrhage in the skin, mucus membranes and serial surfaces
petechiae
this is a 3mm+ hemorrhage in the skin, mucus membranes and serial surfaces
purpura
this is a 1-3cm hemorrhage in the skin, mucus membranes and serial surfaces
ecchymoses
this is a hemorrhage in the skin, mucus membranes and serial surfaces that affects large contiguous areas of tissue
suffusive hemorrhage
the significance of hemorrhage depends on these 3 factors of blood loss
volume, rate, and location
this is the physiological process which stops hemorrhage and is a highly regulated, complex interrelationship between blood vessels, platelets and coagulation factors
hemostasis
name the 4 steps/processes of hemostasis
- vascular response (transient effect)
- platelet response (primary hemostasis)
- coagulation cascade (secondary hemostasis)
- fibrinolysis (tertiary hemostasis)
this step of hemostasis is when vascular injury causes arteriolar vasoconstriction
vascular response
this step of hemostasis includes platelet adherence, activation, and aggregation to form a hemostatic plug
platelet response (primary hemostasis)
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)
this step of hemostasis is to prevent over-production or persistence of fibrin and to control hemostatic plug formation
fibrinolysis (tertiary hemostasis)
these act as weak anticoagulants and can be measured to diagnose pro-thrombin states
fibrin degradation products (FDPs)
this is a cause of primary hemostasis disorders and is decreased platelet numbers in peripheral blood
thrombocytopenia
this is the most common cause of thrombocytopenia
platelet clumping (pseudothrombocytopenia)
name 4 causes of true thrombocytopenia
- decreased production
- increased destruction or utilization of platelets
- sequestration of platelets
- inherited causes
this is an inherited disorder of a specific adhesion molecule between platelets and endothelial cells essential for primary homeostasis
von Willebrands disease (vWD)
this type of hemostasis disorder is due to coagulation factor deficiencies
disorders of secondary hemostasis
Hemophilia A is a deficiency of this coagulation factor
VIII (8)
Hemophilia B is a deficiency of this coagulation factor
IX (9)
these are sex-linked coagulation factor disorders with a recessive inheritance pattern where males are affected (disorders of secondary hemostasis)
hemophilia A and B
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
primary hemostasis can be evaluated by these 3 tests
- platelet count
- platelet function
- buccal mucosal bleeding time (BMBT)
secondary hemostasis can be evaluated by these 5 tests
- prothrombin time (PT)
- activated partial thromboplastin time (aPTT)
- activated clotting time (ACT)
- whole blood clotting time (WBCT)
- thrombin clot time (TCT)
tertiary hemostasis can be evaluated by these 2 tests
evaluation of FDPs and D-dimers
this is a mass of platelets, fibrin, red and white blood cells, which is attached to the wall of the cardiovascular system
thrombus
what is the difference between an ante-mortem thrombus and a post-mortem clot surface
thrombus: granular, dry, dull
clot: smooth, moist, shiny
what is the difference between an ante-mortem thrombus and a post-mortem clot texture
thrombus: firm or friable
clot: elastic or gelatinous
what is the difference between an ante-mortem thrombus and a post-mortem clot structure
thrombus: variegated (maybe laminated)
clot: homogenous
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”
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
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)
name the 3 main factors that predispose to thrombus formation (Virchow’s Triad)
- damage to epithelium
- altered blood flow
- hypercoagulability of blood
venous thrombi tend to have this appearance
red, soft, loose vascular attachment
thrombi in heart or arteries often have this appearance
pale (red-grey), firm, attached to wall, striated/laminar
the clinical significance of thrombosis depends on these 3 factors
size, location, rate of formation
name the 4 possible fates of a thrombus
- dissolution
- propagation
- organization and recanalization
- embolization
this is when the thrombus is completely removed by fibrinolysis
dissolution
this is when additional platelets and fibrin accumulate and extend/elongate the thrombus along the vessel wall toward the heart
propagation
this is when the thrombus is invaded by endothelial cells and fibroblasts forming granulation tissue with subsequent fibrosis
organization
this is when capillary channels in a large organizing thrombus anastomose and allow blood flow to be re-established
recanalization
this is when fragments of the thrombus break off and travel to other sites in the body via the vasculature
embolization
this is a solid or gaseous mass carried by the bloodstream from its point of origin to a distant site within the circulation
embolus
this is the most common type of embolism, where fragments of thrombi detach and spread throughout circulation
thromboembolism
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
adipocytes from bone marrow may be released into circulation following bone fractures leading to this type of embolus
fat embolism
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
name 3 possible causes of ischemia
- arterispasms
- compression of vessels
- thromboembolism
extent and consequences of ischemia depend on these 4 factors
- degree of occlusion
- speed of occlusion
- presence of collateral circulation
- vulnerability of tissues/cells to ischemia
this is a segmental or localized area of coagulative necrosis due to occlusion of the blood supply
infarction
macroscopic appearance of an infarction
red or pale, wedge-shaped
a venous occlusion will give this color infarction
red
an arterial occlusion will give this color infarction
pale
this is widespread pathologic activation of hemostasis within the vascular system resulting in generalized intravascular thrombosis
DIC (disseminated intravascular coagulation)
the intrinsic pathway of the coagulation cascade involves these coagulation factors
12, 11, 9, 8
the extrinsic pathway of the coagulation cascade involves this coagulation factor
7
the common pathway of the coagulation cascade involves these coagulation factors
10, 5, 2 (13)
what is hemoptysis?
coughing up blood
what is epistaxis?
nose bleed
what is hematochezia?
fresh blood in feces
this is the increased tendency to hemorrhage after minor injury
hemorrhagic diathesis
this is a prolonged/persistent inflammatory response that comprises varying combinations of inflammation, tissue injury and repair
chronic inflammation
name 4 infectious causes of chronic inflammation
- Mycobacterium spp.
- fungi
- parasites
- viruses
name the 3 main components of chronic inflammation
- inflammation
- tissue destruction
- tissue repair attempts
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)
these inflammatory cells produce antibodies and often accompany lymphocytes in chronic inflammation
plasma cells
name the 3 main functions of macrophages in chronic inflammation
- phagocytosis
- secrete cytokines
- initiation of repair
inflammation mediated by IgE (hypersensitivity) or parasitic infections will be dominated by this type of cell
eosinophils
persistence of infectious agents in chronic inflammation can lead to the continues presence of these cells
neutrophils
this is a distinct form of inflammation which is always chronic with macrophages predominate
granulomatous inflammation
this is discrete clusters/nodules of macrophages separated by host tissue
granulomas
this is discrete clusters of macrophages AND neutrophils
pyogranulomas
this is a type of chronic inflammation where macrophages are predominate but neutrophils are also present
pyogranulomatous
these are macrophages that become activated to the extent that they develop abundant cytoplasm
epithelioid macrophages
name 5 systemic effects of chronic inflammation
- leucocytosis (mediated by IL-1 and TNF-alpha)
- low grade pyrexia
- acute phase response
- cachexia (mediated by TNF-alpha)
- anemia
these are the two types of reactions of repair
regeneration and scar formation
this is when surviving cells have the capacity to proliferate and to replace damaged components
regeneration
name the three groups of cells in regeneration based on proliferative capacity
labile, stable, permanent
this group of regenerative cell is continually lost and replaced by maturation of stem cells and proliferation of mature cells
labile
this group of regenerative cell are quiescent cells in G0 phase of cell cycle or will divide in response to injury to loss
stable
this group of regenerative cell is terminally differentiated and non-proliferative in postnatal life
permanent
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
name the 3 main steps in scar formation
angiogenesis, formation of granulation tissue, remodeling
this step of scar formation is the formation of new blood vessels
angiogenesis
this step of scar formation is migration and proliferation of fibroblasts and deposition of collagen, together with new blood vessels
formation of granulation tissue
this step of scar formation is when the connective tissue matures and reorganizes to produce a stable fibrous scar
remodeling
this type of scar is due to exuberant formation of granulation tissue; most common in distal limbs of horses
hypertrophic scars
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
this literally means “swelling” and is not necessarily neoplastic
tumor
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
what is the clinical significance of benign tumors
can cause local pressure, cause obstruction, or form a space-occupying lesion
these are often small tumors that arise in the epithelium; appears to contain cancer but tumor remains in epithelial layer
in-situ tumors
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
a severe lack of differentiation in malignant tumors is referred to as this
anaplasia
what is the growth rate of benign tumors
slow & periods of dormancy
what is the mode of growth of benign tumors by?
expansion
what is the mode of growth of malignant tumors by?
initially expansion then invasion
name the tissue/cell of origin for the benign tumor
suffix -oma (fibroma, lipoma, chondroma)
mesenchymal or nervous tissue
name the tissue/cell of origin for the benign tumor
referred to as adenoma
glandular epithelium
name the tissue/cell of origin for the benign tumor
referred to as papilloma
protective epithelium
name the tissue/cell of origin for the malignant tumor
addition of ‘sarcoma’ (fibrosarcoma, liposarcoma, chondrosarcoma)
mesenchymal
name the tissue/cell of origin for the malignant tumor
referred to as adenocarcinoma
glandular epithelium
name the 5 types of round cell tumors
- Lymphoma
- Transmissible Venereal Tumor (TVT)
- Mast Cell Tumor
- Plasmacytoma and multiple myeloma
- Histiocytoma
round cell tumors tend to form this histiological pattern
solid sheets
epithelial tumors form these histiological patterns
nests, cords, islands, acini, tubules, or trabeculae
mesenchymal tumors form these histiological patterns
interlacing streams, bundles, fascicles
this means variation in cell size
anisocytosis
this means variation in nuclear size
anisokaryosis
this means variation in cell shape
pleomorphism
this means the distant spread of a neoplasm and is often the cause of death in most patients
metastasis
name the 3 different routes od metastasis
- hematogenous
- lymphatic
- transcoelomic
name the 5 steps/stages of metastasis
- subset of cells detaches from main mass and breaches the basement membrane
- cells pass thrugh ECM and enter a nearby vessel
- tumor cells form embolus that travels to distant site in blood or lymph
- adhesion of tumor cells to endothelial cells
- metastatic deposit forms and grows with help of angiogenesis
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
most proto-oncogenes are key genes involved in these two things
- cell growth
- proliferation
name the 6 possible modes of action of proto-oncogenes in the normal cell (oncogene classes)
- growth factors
- growth factor receptors
- protein kinases
- signal transducers
- nuclear proteins
- transcription factors
name the 4 possible mechanisms of oncogene activation
- chromosomal translocation
- gene amplification
- point mutations
- viral insertions
mutations or translocations of these genes produce positive signals leading to uncontrolled growth
oncogenes
mutations or translocations of these genes leads to a loss of inhibitory functions leading to tumor formation
tumor supressor genes
this was the first gene to inform mechanisms of tumor suppressor genes
retinoblastoma gene (Rb)
this is the most frequently inactivated gene in human neoplasia
p53
name the 7 hallmark capabilities of cancer/alterations in cellular physiology that collectively dictate malignant growth
- self-sufficiency in growth
- insensitivity to anti-growth signals
- ability to evade programmed cell death (apoptosis)
- limitless replicative potential
- ability to sustain angiogenesis
- ability to invade and metastasize
- ability to evade host immunity
name the 3 broad categories of cancer causing agents
- oncogenic viruses
- chemical carcinogens
- physical agents (radiation)
what viruses are included as oncogenic viruses
DNA viruses and Retroviruses
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
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
name 4 chemical carcinogens involved with veterinary cancers
- bracken fern (with papilloma viruses in cattle)
- herbicides (canine lymphoma)
- Aflatoxin
- cyclophosphamide (chronic inflammation and transitional carcinoma)
what 2 ways can radiation cause cancer
- cause errors in DNA replication
- cause production of oxygen free radicals
