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237 Cards in this Set
- Front
- Back
5 definitive features of a neoplasm (tumor)
|
- Mass of tissue
- Arises from and resembles normal tissue - Poorly regulated cell division that's irreversible - Serves no beneficial physiologic purpose - Usually harmful, sometimes lethal |
|
Benign (define)
|
'Kind'
- Lacks ability to metastasize |
|
Key characteristic of a malignant tumor
|
Has ability to metastasize
|
|
Anaplasia (define)
|
Loss of structural/functional characteristics in a differentiated cell (de-differentiation)
|
|
How does the cause of neoplasia differ from hyperplasia?
|
Hyperplasia is a physiologic response to increased demand on an organ
- Neoplasia is a non-physiologic response of genetically abnormal cells |
|
Suffix for a benign, glandular neoplasm
|
- adenoma
|
|
Suffix for a malignant, glandular neoplasm
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- adenocarcinoma
|
|
Suffix for a benign, non-glandular neoplasm
|
- oma
|
|
Suffix for a malignant, non-glandular neoplasm
|
- carcinoma
|
|
Suffix for a benign, mesodermal neoplasm
|
- oma
|
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Suffix for a malignant, mesodermal neoplasm
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- sarcoma
|
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5 characteristics of benign tumors
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- Never metastasizes
- Tends to resemble origin tissue - Relatively slow-growing - Expansile, encapsulated - Some benign tumors can be quite lethal |
|
5 characteristics of a malignant tumor
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- Metastatic
- Rapid growth (numerous mitotic fragments) - Invasive - May not resemble tissue of origin - Large and variable nuclei |
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Initiation (define)
|
Rapid, permanent, inherited change to a cell
- 'Sets the stage' for tumor development |
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Promotion (define)
|
Occurs when an initiated cell is stimulated to divide via continuous or frequently repeated stimulations to the promotor
- Establishes neoplastic cell line and causes formation of a mass |
|
What substance has both an initiator and a promoter?
|
Complete carcinogen
|
|
Oncogene (define)
|
'Cancer gene'
- Region of eukaryotic genome with a homologous region on retroviral RNA genome |
|
Oncogene (function)
|
Regulatory substances in the cell
|
|
Proto-oncogene (function)
|
Plays a critical role in regulation of cell growth
- AKA as a 'cellular oncogene' |
|
Tumor-suppressor gene (function)
|
Creates normal gene products that regulate or inhibit cell proliferation
|
|
Two tumor suppression gene examples
|
- Rb
- p53 |
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Viral pathogenesis of neoplasia
|
Involves either oncogenic DNA or RNA viruses
|
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Which oncogenic virus integrates with host cell's genome?
|
DNA oncogenic viuses
|
|
Which oncogenic virus is retroviral?
|
RNA
|
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Two 'types' of DNA oncogenic viruses
|
- Productive
- Transforming |
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3 characteristics of productive DNA viruses
|
- Cause cell death
- Spread of infection - Non-oncogenic |
|
3 characteristics of transforming DNA viruses
|
- Integration
- No spread - Tumor cells formed |
|
3 physical ways to cause neoplasia
|
- Radiation
- Trauma - Bone fixation hardware |
|
Two types of cancer that UV light is associated with
|
- Squamous cell carcinoma
- Melanoma |
|
What carcinogen type actually converts a cell into cancer?
|
Proximate carcinogen
|
|
What is a procarcinogen?
|
A carcinogen that has to be metabolized to be active
|
|
3 examples of chemical carcinogens
|
- Hydrocarbons
- Azo dyes - Aflatoxins |
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Metastasis (define)
|
Distant spread of tumors
|
|
Two mechanisms of metastasis
|
- Vascular spread
- Implantation |
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What is paraneoplastic syndrome?
|
Systemic effect of tumor secretions on a body
- Unrelated to the physical characteristics of the tumor itself |
|
Mechanism for Type I HS (2)
|
AG binds with AB on mast cell or basophil, causing degranulation
- Causes edema and vasodilation Simultaneously, ARA is metabolized into PG and SRSA - Causes bronchoconstriction, vasodilation, and edema |
|
Mechanisms for Type II HS (2)
|
AB mediated cyto-toxicity
- AB binds to AG --> complement cascade activated AB mimicry of ligand - AB binds to cell-associated receptor --> mimics natural ligand --> induces cell to perform function of normal ligand binding (alternatively, can inhibit cell as well) |
|
Mechanism for Type III HS
|
Immune complex deposition under endothelium
- Causes 'frustrated phagocytosis' where leukocytes get pissed off at inaccessible complexes --> large deposition of lysosomal contents --> necrosis and inflammation of tissue |
|
Mechanism for Type IV HS
|
Cell mediated response of cytotoxic lymphocytes to abnormal cells in the body (due to injury, transplantation, etc.)
|
|
3 similarities between immune mediated injury and inflammation
|
- Use of vasoactive amines
- Recruitment of inflammatory cellls - Production of secondary tissue damage |
|
Clinical example of Type I HS rxn
|
Allergic reactions
|
|
Clinical example of Type II HS rxn (3)
|
- Myasthenia gravis
- Blood transfusion reactions - IMHA |
|
Clinical example of Type III HS rxn (2)
|
- Lupus
- FIP |
|
Clinical example of Type IV HS rxn (2)
|
- Contact dermatitis
- Tuberculin |
|
What is 'Type V HS'?
|
Antibody mimicry of a ligand
|
|
What is the term for a hepatic stellate cell?
|
Ito cell
|
|
Ito cell function (3)
|
- Stores vitamin A
- Stores fat - Sinusoidal blood flow |
|
What can an Ito cell turn into?
|
Myofibroblast during fibrosis following injury
|
|
What is a Kupffer cell?
|
MP of the liver
|
|
Bile circulation pattern (4)
|
Canaliculi --> bile ductules --> portal triads --> common bile duct
|
|
Lobule model (define)
|
Polygonal shape centered ona central vein that's bound by portal triads
|
|
Acinus model (define)
|
Diamond shape centered on triad and bounded by central veins
|
|
What zone of acini is exposed to blood containing highest amount of nutrients?
|
I
|
|
What zone of acini is exposed to blood containing lowest amount of nutrients?
|
III
|
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What zone of acini is the most metabolically active?
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I
|
|
What zone of acini has the most fatty acid synthesis?
|
I
|
|
What zone of acini has the highest levels of mixed function oxidase enzymes?
|
III
|
|
Metabolism of drugs, toxins, and environmental chemicals to render them harmless and facilitate their excretion from the body
|
Hepatic biotransformation (define)
|
|
What's involved with phase I biotransformation?
|
Cleavage of parent compounds and insertion of reactive groups
|
|
What's involved with Phase II biotransformation?
|
Conjugation of Phase I metabolites
|
|
Can biotransformation lead to toxicity?
|
Yup
- Phase I metabolites may be more reactive than their parent molecules |
|
How can the liver cause ascites? (3)
|
- Hypoalbuminemia
- Portal hypertension - CHF (though indirectly) |
|
How can the liver cause coagulopathies?
|
Fails to produce the necessary coagulation factors
|
|
How does pre-hepatic hyperbillirubinemia occur?
|
Hemolysis
|
|
How does hepatic hyperbillirubinemia occur?
|
Hepatocellular or cholestatic liver disease impairing uptake, conjugation, or excretion of billirubin into bile
|
|
How does post-hepatic hyperbillirubinemia occur?
|
Obstruction of common bile duct
|
|
How does intrahepatic cholestasis occur?
|
Functional reduction in bile outflow due to impairment of bile flow within the liver
|
|
How does extrahepatic cholestasis occur?
|
Functional reduction in bile outflow due to obstruction of extrahepatic bile duct
|
|
Mechanism of photosensitization
|
Chlorophyl metabolite phylloerythrin accumulates in tissue
- Happens due to cholestasis, because phylloerythrin is excreted in the bile |
|
Liver doesn't synthesize urea correctly, so NH4 levels rise causing CNS signs and toxicity. What condition is this?
|
Hepatic encephalopathies
|
|
What is hepatic encephalopathy related to in dogs?
|
Portosystemic shunts
|
|
What is hepatic encephalopathy related to in horses?
|
Acute liver disease
|
|
What is hepatic encephalopathy related to in cattle?
|
Chronic liver disease
|
|
Two histologic features of reversible hepatocellular injury
|
- Vacuolation
- Atrophy |
|
3 causes of intracellular vacuolation
|
- Hydropic
- Glycogen accumulation - Triglyceride accumulation |
|
Two general causes of atrophy of hepatocytes
|
- Lack of growth factors reaching liver
- Pressure from surrounding viscera |
|
Four types of necrosis
|
- Single cell
- Coagulative - Liquefactive - Caseous |
|
What defines a coagulative necrosis?
|
Cells maintain outline
|
|
What defines a liquefactive necrosis?
|
Rapid digestion of dead cells by hydrolytic enzymes
- Loss of cellular architecture |
|
What defines a caseous necrosis?
|
Friable material with cheese-like consistency within a wall of granulomatous inflammation
|
|
Six patterns of necrosis of the liver
|
- Focal/multifocal
- Centrilobular - Midzonal - Periportal - Massive - Piecemeal |
|
What causes centrilobular necrosis? (2)
|
- Hepatocytes furthest from portal vein are susceptible to hypoxia
- Viral infections |
|
What causes periportal necrosis?
|
Unmetabolized toxins
|
|
What causes midzonal necrosis?
|
High enough [enzyme] to perform phase I but not enough to perform phase II, so reactive intermediates from phase I are just hanging around and start messing up the joint
|
|
2 causes of massive necrosis
|
- Nutritional disease
- Toxic disease |
|
What differs piecemeal necrosis from multifocal?
|
Not sure actually, but it sounds like the distribution pattern (periportal --> lobule) and symptoms (lymphocytic inflammation, fibrosis)
|
|
What generally causes focal/multifocal necrosis?
|
Infectious agents
|
|
Why is Zone 3 predisposed to necrosis? (2)
|
- Hypoxia (furthest away from portal vein)
- Highest concentration of mixed function oxidase enzymes (CYP450; prone to highly reactive metabolites from toxin digestion) |
|
Two types of hepatic cell classifications in Zone 3
|
- Centrilobular
- Periacinar |
|
Hepatitis (define)
|
Inflammation of liver parenchyma
|
|
Inflammation of bile ducts
|
Cholangitis
|
|
Inflammation of bile ducts with extension into periportal parenchyma
|
Cholangiohepatitis
|
|
Inflammation of gall bladder
|
Cholecystitis
|
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Why might the liver be mistaken for being neoplastic?
|
After liver regeneration, it may appear to be multinodular
|
|
Scarring of the liver (word)
|
Cirrhosis
|
|
What is a sign of a liver in liver failure?
|
Cirrhosis
|
|
3 sequelae of hepatic fibrosis
|
- Portal hypertension
- Ascites - Biliary hyperplasia |
|
2 things that portal hypertension may result in
|
- Acquired portosystemic shunts
- Ascites |
|
Gross appearance of acquired portosystemic shunts
|
Multiple smaller vessels
|
|
Gross appearance of congenital shunts
|
One, large vessel
|
|
Most common congenital shunt
|
Persistent fetal ductus venosus
|
|
4 reasons hepatic rupture might occur
|
- Trauma
- Amyloidosis - Fatty change - Neoplasia |
|
Multifocal, cavernous, blood-filled dilations of groups of hepatic sinusoids
|
Telangiectasis
|
|
What two species does Telangiectasis usually occur in?
|
- Cattle
- Cats |
|
How does CHF cause ascites?
|
Increase hydrostatic pressureat
|
|
How does CHF affect the liver? (4)
|
- Induces chronic passive congestion
- Atrophy - Fatty change - Necrosis |
|
Morphological term for liver changes caused by chronic passive congestion
|
Nutmeg liver
|
|
Why does portal hypertension occur?
|
Increases resistance to portal blood flow (pre-, hepatic, or post-)
|
|
Sequelae of portal hypertension (2)
|
- Ascites
- Acquired portosystemic shunts |
|
What occurs in portal hypertension that does not occur in CHF?
|
Acquired portosystemic shunts
|
|
What substance accumulates in hepatocytes during corticosteroid-induced hepatopathy?
|
Glycogen
|
|
Mechanism for cortico-steroid induced hepatopathy
|
Glucocorticoids induce glycogen synthetase, which increases glycogen production
|
|
5 mechanisms for increased TRIG accumulation in hepatocytes
|
- Increase entry of fatty acid
- Increase synthesis of fatty acids - Decreased oxidation of fatty acids - Decreased synthesis of apoproteins - Decreased synthesis and excretion of lipoproteins |
|
Clinical conditions characterized by hepatic lipidosis (9)
|
- Starvation
- Equine hyperlipidemia - Feline hepatic lipidosis - Bovine fatty liver syndrome (Pregnancy toxemia) - Bovine ketosis - Diabetes mellitus - Hypoxia - Toxicosis - Tension lipidosis |
|
How does primary copper accumulation occur?
|
Genetic defect in copper excretion
|
|
What causes secondary copper accumulation to occur?
|
Cholestasis
|
|
Breed predisposed to primary copper accumulation
|
Bedlington Terriers
|
|
4 breeds that may have variable copper levels
|
- Dalmation
- Dobermans - West Highland White Terriers - Sky Terriers |
|
Three causes of liver abscesses in ruminants
|
- Grain overload
- Rumenitis - Parasites |
|
How does grain overload cause liver abscesses? (5)
|
Increase in vFAs --> Acidosis --> increase in anaerobes --> rumen mucosal necrosis --> bacteria enter portal circulation
|
|
What are multifocal lesions of fibrosis and chronic inflammation of the liver caused by larval ascarid migration called?
|
Milk spots
|
|
Two types of cholangiohepatitis
|
- Suppurative
- Lymphocytic |
|
What causes suppurative cholangiohepatitis? (3)
|
- Ascending bacterial ifnection
- Choleliths - Bile duct obstruction |
|
Two possible causes of lymphocytic cholangiohepatitis
|
- Advanced suppurative cholangiohepatitis
- Immune mediated |
|
Two types of hepatotoxins
|
- Idiosyncratic
- Dose dependent |
|
Which hepatotoxin type is unpredictable?
|
Idiosyncratic
|
|
Two examples of idiosyncratic toxins
|
- Carprofen (dogs)
- Diazepam (cats) |
|
Two examples of dose-dependent hepatotoxins
|
- Xylitol (dog)
- Acetiminophen (cats) |
|
What is dose-dependent hepatotoxin outcome dependent on? (3)
|
- Toxin factors
- Time factors - Animal factors |
|
3 Toxin factors
|
- Dose
- Chemical form - Source |
|
2 timing factors
|
- Time over which toxin was introduced
- Frequency of toxin introduction |
|
7 animal factors
|
- Age
- Sex - Species - Physiologic status - Nutritional status - Genetics - Exposure to other chemicals |
|
Morphology of acute hepatotoxicity (3)
|
- Enlarged liver
- Accentuated lobular pattern - Edema of gallbladder wall |
|
Morphology of chronic hepatoxicity
|
Small, shrunken, nodular
|
|
Gross appearance of hyperplastic liver nodules
|
Spherical, sharply demarcated nodules
- Benign - Affects older dogs |
|
Gross appearance of Hepatocellular carcinoma
|
Massive enlargement of single lobe or diffuse involving multiple lobes
|
|
Gross appearance of bilary adenomas (cholangiomas)
|
White, solid, or cystic masses of well-differentiated bile ductules
- Benign - Affects older cats |
|
Gross appearance of Biliary carcinomas (cholangiocarcinomas)
|
Multifocal, solid, white/tan, depressed
- Locally invasive - Malignant - Affects older dogs |
|
Gross appearance of cystic mucinous hyperplasia of the gall bladder
|
Numerous clear to yellow/green nodules
|
|
Clinically significant form of cystic mucinous hyperplasia
|
Biliary mucocele
|
|
Pathogenesis of pancreatic acinar atrophy
|
Progressive loss of exocrine pancreatic function
|
|
3 clinical signs of pancreatic acinar atrophy
|
- Diarrhea
- Weight loss - Polyphagia |
|
Gross morphology of acute pancreatitis (4)
|
- Swollen
- Edematous - Variable hemorrhage - Fibrinous adhesions |
|
Chalky white areas of necrosis in peripancreatic fat
|
Saponification
|
|
Pathogenesis of acute pancreatitis
|
Premature activation of pancreatic enzymes
|
|
Gross morphology of chronic interstitial pancreatitis of cats
|
Smaller, firm, gray, irregular pancreas
|
|
Morphology of chronic interstitial pancreatitis of cats
|
- Small, firm, irregular pancreas
- Atrophy of acinar tissue - Fibrosis |
|
Morphology of exocrine pancreatic hyperplasia
|
Multiple small, firm, white/tan, slightly raised nodules within pancreas
- Should not be confused as a neoplasm |
|
Aggressive malignant neoplasms of acinar or ductular origin that implant on peritoneal surface or metastasize to other organs
|
Exocrine pancreatic carcinomas
|
|
What should exocrine pancreatic carcinomas be differentiated from?
|
Insulin producing islet cell neoplasms (insulinomas)
|
|
Primitive tissue that is the source of pleuripotential tissue
|
Mesenchyme
|
|
Which bones develop entirely by intramembranous ossification?
|
Flat bones of the head
|
|
What part of a long bone develops by intramembranous ossification?
|
Shaft (diaphysis)
|
|
Environmental factor influencing development of bone tissue from mesenchyme in fetuses
|
Presence of vascular bed with adequate oxygen
|
|
Which CT tissue cell doesn't exhibit mitotic activity?
|
Osteoblast
|
|
Membranes that cover bone
|
Periosteum
|
|
Membranes that cover cartilage
|
Perichondrium
|
|
Location of bone fluid in bone tissue that participates in Ca++ homeostasis
|
Canalicular-lacunar system
|
|
Mechanism responsible for osteocyte nutrition
|
Bone fluid of the canalicular-lacunar system
|
|
Barrier that separates bone fluid from ECF adjacent to bone tissue
|
Bone lining cells
- Usually bone-lining osteoblasts |
|
Name given to the initial bone matrix deposited prior to mineralization
|
Osteoid
|
|
Two ways the periosteum located on outer surface of skull plate and perosteum located on inner surface of skull plate differ
|
- Inner surface has less osteogenic layer producing bone
- Adhered to dura mater |
|
Term given to cancellous bone that connects outer and inner cortices of skull plates
|
Diploe
|
|
Two major types of collagen in bone and cartilage
|
Bone: Type I
Cartilage: Type II |
|
From what stem cell line do osteoclast precursor cells arise?
|
mononuclear-MP cell line
|
|
What cell type has a plasmalemma with a 'striated' or 'ruffled' border?
|
Osteoclast
|
|
Mediators tha tattract osteoclast precursor cells
|
Osteoclast Activating Factor
|
|
Density measurement that differs compact from cancellous bone
|
Compact has greater density (>30%) than cancellous
|
|
Differences between woven and lamellar bone tissue (2)
|
- Woven bone is rapidly laid down by osteoblasts with uneven distribution
- Lamellar bone is quite orderly |
|
Process by which osteoclasts and osteoblasts change the observable shape of a bone
|
Bone modeling
|
|
Area of the metaphysis where Osteoclasts progressively reduce diameter of the metaphysis as it blends into the diaphysis
|
'Cutback zone'
|
|
What is the biomechanical effect of racing on the shape of Metacarpal III?
|
Bone thickens over the dorsomedial cortex to respond to increased weight bearing
|
|
Mechanism used by bone organs to shift trabecular systems of cancellous bone in order to resist mechanical forces?
|
Bone micromodeling
|
|
Conversion of primary to secondary trabecular bone is result of which of the bone mechanisms?
|
Bone micromodeling
|
|
In which bone mechanism does osteoclastic activity always occur before osteoblastic activity?
|
Bone remodeling
|
|
Which type of bone tissue is always deposited by osteoblasts that are part of a bone-remodeling unit?
|
Lamellar bone tissue
|
|
No change in shape occurs following bone remodeling
|
No change in shape occurs following bone remodeling
|
|
Cutting cone function
Filling cone function |
Removal of focal areas of bone tissue fatigue
Formation and replacement of new packets of bone tissue that participate in calcium homeostasis |
|
Name of the bone-remodeling unit of compact bone
|
BMU (bone metabolic unit)
|
|
Pattern of orientation of collagen fibers deposited in lamellar bone tissue deposited in a BMU of cancellous bone
|
Collagen fibers in adjacent lamellae are oriented and lie in different planes
|
|
What type of bone tissue is deposited by the filling cone?
|
Osteonal lamellar bone
|
|
Interstitial lamellae (define)
|
Remnant of the old osteon of the cortical compact
|
|
How are interstitial lamellae formed?
|
Cutting cones of bone remodeling units as they cut longitudinal canals in cortical bone
|
|
What layer of periosteum is absent in endosteum?
|
Fibrous layer
|
|
What does osteogenic mesnechyme form when under tension?
|
Fibrous tissue
|
|
What does osteogenic mesnechyme form in a hypoxic environment?
|
Cartilage
|
|
Four possible functions of endosteal peritrabecular mesenchymal cellular envelope
|
- Produce hematopoietic growth factors
- Progenitor cells of osteoblasts - Stimulate osteoclasts and lining cells to form a crude fibro-osseous matrix - Act as strain gauges to activate bone remodeling |
|
Two major categories of muscle disease
|
- Neurogenic
- Myopathic |
|
Myopathy (define)
|
Muscle disease
|
|
Muscular dystrophy is what type of muscle disease?
|
Myopathic
|
|
Cause of muscular dystrophy in males
|
Defective X-linked gene causing dystrophin to not form or form abnormally
|
|
Five requirements for repair of segmental necrosis in skeletal muscle fiber
|
- Source of regenerative myoblasts
- Guidance system - Small gap - Adequate blood supply - Nerve innervation of motor endplate |
|
What differentiates steatosis from fatty degeneration?
|
Fatty degeneration is potentially serious metabolic disorder, while steatosis is a clinically insignificant deposition of fat
|
|
What is important about steatosis?
|
Impacts economic gain from slaughter
|
|
Two common causes of disuse atrophy in muscles
|
- Immobilization
- Pain |
|
What muscle disease is characterized by Serous atrophy of fat?
|
Cachectic atrophy
|
|
What type of muscular atrophy is characterized by angular atrophy?
|
Neurogenic
|
|
What type of atrophy produces compensatory hypertrophy?
|
Neurogenic
|
|
In what type of atrophy is one likely to encounter an animal exhibiting psuedohypertrophy?
|
Chronic neurogenic atrophy
|
|
Muscle is (more or less) resistant to hematagenous spread of bacteria compared to other tissues
|
More
|
|
Diffuse spread of infection through CT and along fascial planes of muscle
|
Phlegmon
|
|
Pathology of malignant edema
|
Clostridial myositis
- Characterized by gas formation, cellulitis, and rapid death |
|
Malignant edema is AKA?
|
Gas gangrene
|
|
Pathology of Blackleg in cattle
|
Cattle disease caused by ingestion of bacterial spores during grazing.
- Awaits activation during hypoxic episode |
|
What is a distinctive external ID method of blackleg in cattle?
|
Smell of rancid butter on necropsy
|
|
Which disease irreversibly binds presynaptic nerve terminals?
|
Botulism
|
|
What domestic mammal is most susceptible to botulism?
|
Horses
|
|
What morphologic change does botulism cause in tissue?
|
The toxin doesn't cause any
|
|
Pathogenesis of myasthenia gravis
|
Attachment of circulating AB to ACH receptors on post-synaptic endplates to prevent nerve transmission
|
|
4 clinical signs of myasthenia gravis
|
- Weakness
- Dysphagia - Megaesophagus - Laryngeal paralysis |
|
What is the cause of eosinophillic myositis?
|
HS to degenerating sarcocysts in skeletal muscle
|
|
Clinical significance of eosinophilic myositis in livestock
|
None, but does have economic significance
|
|
Location of lesions of eosinophilic myositis in dogs
|
Masticatory muscles
|
|
Histolopathology of eosinophilic myositis in dogs (acute, subacute)
|
Acute:
- Edema - Necrosis - Muscle fiber degeneration Subacute: - Moderate loss of fiber tissue embedded into a exudate of lymphocytes and plasma cells |
|
Why are only the masticatory muscles affected by Eosinophilic myositis in dogs?
|
Unique myosin type in masticatory Type-II muscles that acts as a foreign antigen that antibodies attack
|
|
How to differentiate atrophic myositis from eosinophilic myositis?
|
Atrophic myositis is not accompanies by pain like eosinophilic myositis
|
|
Underlying pathologic mechanism for nutritional myopathy of cattle
|
Deficiency in:
- Vitamin E - Selenium which causes lipid membranes of striated muscle to be prone to free radicals |
|
What is nutritional myopathy of cattle AKA?
|
White muscle disease
|
|
Benign muscle tumor that arises in wall of pylorus of stomach and gradually obstructs the passage of ingesta into SI
|
Leiomyoma
|
|
Malignant striated muscle tumor that may arise in skeletal, cardiac, and smooth muscle
|
Rhabdomyosarcoma
|
|
Which is stronger, lamellar or woven bone?
|
Lamellar
|
|
What bone type is formed secondary to irritation, trauma, or infection?
|
Woven and lamellar both can be formed dependent on circumstances
|
|
What histologic type of bone tissue is formed by normal bone modeling or remodeling mechanisms of the skeleton?
|
Lamellar
|
|
Bone collagen's bending ability
|
Poor
- Acts as a homogenous brittle substance |
|
Bone's ability to withstand torsion/bending, tension, and compression from greatest to least
|
- Compression
- Tension - Torsion/bending |
|
Which way does blood flow in long bones?
|
Centrifugal
|
|
4 things that epiphyseal blood vessels supply nutrients to in immature animals
|
- Subchondral capillary bed
- Epiphyseal cancellous bone - Epiphyseal bone marrow - Metaphyseal physis |
|
Which two species have transphyseal blood vessels?
|
- Foals
- Calves |
|
4 features of direct bone healing
|
- Requires complete stability
- Anatomic alignment at fracture ends - Fracture line set under dynamic compression - Primary osteonal remodeling required |
|
4 features of indirect bone healing
|
- Hematoma formation
- Internal callus - External callus - Good vascular supply and tissue support |
|
Description of Blood supply to external callus in primary bone healing
|
Vessels emerge from traumatized soft tissues that supply the external callus in a centripetal direction
|
|
Blood flow in a stable, external callus near completion of the secondary healing process
|
Centrifugal
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Where do repair cells in an external callus come from in a secondary fracture healing? (2)
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Damaged soft tissue
Periosteum |
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Where do repair cells in the internal callus come from in secondary fracture healing? (2)
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Reticular marrow stroma
Endosteum |
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4 locations where blood supply comes from in a long bone
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- Multiple nutrient arteries
- Reversal of normal blood flow direction in periosteum and cortex - Metaphyseal vessels - Transphyseal vessels if present |
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What differs gap healing from contact healing?
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Gap healing uses woven bone to form small gaps to fill up.
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What's the primary thing that differs primary and secondary osteonal reconstruction of bones?
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Stabilization
- If a 'primary' osteonal reconstruction site has mobility, it's secondary, period. |