Pathology Semester 2 part 2 Flashcards
Explain a neurogenic disease of the oral cavity
hypoglossal nerve damage in horses with guttoral pouch disease. cause lingual muscle atrophy.
give 3 colour changes to the oral mucosa and the reason
pallor (anaemia/CHF), cyanosis (toxic, uraemia, hypoxia), petechiae/haemorrhages
term for inflm of gums and of palate structures
gingivitis and stomatitis.
necrobacillosis GI disease… type of inflm
Fusobacterium necrophorum. Calf diptheria or hepatic necrosis. Fibrino-necrotising laryngitis.
Wooden tongue
Actinobacillus ligniersi. pyogranulomatous inflm with fibrosis and abscessating glossitis. Splendore-Hoepli figures on histo.
Give 2 bacterial inflm infections of mouth
wooden tongue and necrobacillosis
Bluetongue virus GI path… vector, virus, pathogenesis
culicoides vector, orbivirus. viraemia, endothelial damage, microthrombi, haemorrhages, ischaemic necrosis. oedema and hyperaemia of oral/nasal mucosa, ischaemic necrosis of mucosa.
two types of stomatitis
vesicular and erosive/ulcerative
oral vesicles are caused by what process
ballooning degeneration of epithelial cells.
FMD
aerosol/oropharyngeal transmission. ulcers on tongue, lips, mouth, coronary band. ballooning degeneration, cells detach from BM, oedema and fibrin fill vesicle, bullae forms, ulcerates/ruptures
2 other causes of vesicular stomatitis (except FMD)
Rhabdovirus vesicular stomatitis and Picorne-viridae-enterovirus in pigs (swine vesicular disease)
Erosive and ulcerative stomatitis (2)
BVD/Mucosal Disease (MD) - Pestivirus, BVDV1. Malignant catarrhal fever (ovine herpes virus 2).
‘Mucosal Disease’
seen in PI calves with cytopathic form of BVDV. sharply delineated flat ulcers on mouth, tongue, oeseophagus and GI tract.
malignant catarrhal fever
Ovine herpes virus 2, Allcephaline herpes virus 1. Bison most susceptible. Oral and GI erosions with conjunctival and keratitis lesions (unlike MD).
2 agents of feline erosive and ulcerative stomatitis
feline herpes virus and feline calicivirus
fungi causing oral disease in suckling animals
candida albicans. white, fluffy chalky plaque on oral structures. poor hygiene or immunocompromised.
lingual muscle can harbour which kind of parasite
metacestode cyst of tapeworms (Taenia saginata/solium)
eosinopihlic granuloma complex 3 parts
indolent ulcer, oral eosinophilia granuloma, eosinophilic plaque.
tonsilitis bacteria
haemolytic streptococci, coliforms.
aujeskys disease
necrotising tonsillitis, swine herpes virus type 1.
oral benign tumour
papilloma, epulides
epulides, 3 types
benign tumour in dog/cat. derive from periodontal ligament or connective tissue. fibrous, ossifying and acanthomatous
most common oral tumour in cats, how about dogs?
squamous cell carcinoma. melanoma.
tonsillar squamous carcinoma what species and how malignant
spreads early, found in dogs. characteristic keratin pearls.
which neoplasm derives from connective tissue of oral cavity, is malignant and second most common in cats?
fibrosarcoma
sialoadenitis and sialolith
inflm of salivary gland and calculi in ducts
ranula
cyst formation in salivary gland duct.
how could the oes be obstructed, strictured or compressed?
obstruct with foreign body, neoplasm, parasites. compressed by LN, abscess or neoplasm. stricture with persistant RAA.
2 types of megaoesaphagus
congenital (GSD, great dane, irish setter) or acquired secondary to neural reflex disorder. can be due to distemper, botulism, myaesthenia gravis.
thymoma and myaesthenia gravis are assoc with which disease
megaoesophagus
spirocerca lupi
intermediate host is beetle, dogs/canids DH. ingested beetle, L3 migrate to oes, cause granulomatous oesophagitis and related to fibro and ossifying sarcoma
oesophageal papilloma in cattle
BPV type 4.
abnormality of ruminal mucosa
parakeratosis, hyperkeratosis. due to high concentrate diet.
2 types of ruminal tympany
frothy and gassy bloat. decrease venous return and hypovolaemic shock. frothy due to lots of legumes, gassy due to physical obstruction.
Saponaria officinalis (saponins) are responsible for what
cause of bloat in cattle
Lactobacillus acidophilus causes what
ruminal acidosis. Over ingestion of CHO - increase VFA - atony - drop in ruminal pH - proliferation of L. acidophilus - death when pH reaches below 4.5.
what is the risk to survivors of ruminal acidosis
secondary necrobacillosis, peritonitis and pericarditis.
3 viruses that can induce ruminal ulceration
FMD, MD, MCF
5 areas of the stomach
cardia, fundus, body, antrum, pylorus
which cells produce pepsinogen and gastric acid?
pepsinogen = chief cells. acid = parietal cells. ECL cells stimulate acid cells via histamine.
GDV is assoc w/
excess eating and aerophagia. small food particles and weak hepatogastric ligament is predisposition.
what displacements occur in gastric volvulus
pylorus and duodenum compressed between oes and dilated stomach, spleen moves with gastrosplenic ligament, oes can be completely occluded
results of displacements of gut (GDV)…
gastric haemorrhagic infarction, decreased venous return, decreased CO, hypotension, decrease renal function, shock.
what is the cattle equivalent of GDV
left or right abomasal displacement. similar results as in GDV.
Horse stomach parasites. pathogenic?
Gastrophilus intestinalis, nasalis and haemorrhoidalis, no link with ulcers
ruminant gut parasite causing hypoproteinaemic oedema and anaemia
haemonchus contortus (problem when moving cattle off and moving sheep on)
allotriophagia term for? assoc w/ 3 conditions
pica. encephalitis, starvation, boredom.
which species get gastroliths
reptiles and horses.
acute catarrhal gastritis patho and causes
serous inflm of mucosa and serosa, thickened and red. poisons, Helicobacter spp, parasites.
Ollulanus tricuspis causes what condition
parasitic catarrhal gastritis in felids. transmission via vomit. small <1mm worm.
acute haemorrhagic gastritis
poisons, swine erysipelas, braxy, NSAID overuse
Braxy
sheep/calves in cold climates. Clostridium septicum enterotoxin, severe odema and emphysema in submucosa, haemorrhage and venous thrombosis.
haemorrhagic gastritis causal agents
CSF virus, anthrax, leptospirosis (with uraemia)
uraemic gastritis
endothelial degeneration, necrosis, thrombosis, infarction. excretion of ammonium (in saliva and gastric juices) causing coagulative necrosis. assoc w/ chronic renal failure.
stomach ulcers cattle
in pylorus, assoc w/ transport or diet
pig stomach ulcers
in squamous epithelial part, due to hyperacidity, fine grain diet or stress.
horse stomach ulcers
in non-glandular portion
dog/cat stomach ulcers
pylorus or proximal duodenum. associated highly with mast cell tumours! histamine over stimulation
outcome of stomach ulcers
haemorrhage, perforation, peritonitis
stomach ruptures common in
horses due to dilation. First serosal tear, then musclaris. can occur post-mortem, see fine borders with less haemorrhages.
horse stomach rupture types (2)
primary (over ingestion of CHO, excess water intake). secondary (due to blockage in colic or dysautonomia).
most common gastric neoplasia of dogs
adenocarcinoma. arises from glandular mucosa, can metastasise.
benign stomach tumour
adenoma/benign adenomatous polyp
stomach epithelial tumour common in large proventricular area
squamous cell carcinoma. yellow-brown colour due to keratin production
cats, FeLV negative, B cell tumour in older patient
lymphosarcoma
which tumour would be originating from tunica muscularis of stomach
leiomyoma
common congenital GI finding
atresia. anal/rectal or intestinal
aplasia of neurons in large intestinal myenteric ganglia would give rise to
megacolon - lack of peristaltic movement
which gut herniation is common in horses
epiploic herniation
RF for intussusception in small animals and horses
hyperactive bowel movements, parvo, distemper enteritis. in horses, ileum into caecum due to tapeworm.
horse volvulus causes
pedunculated lipoma in mesentery, usually at jejunum or ileum
intestinal misalignment consequences
misalignment of bowel, occlusion of veins, persistence of arterial supply, hyperaemia, hypoxia, capillary fragility, haemorrhage and necrosis and infarction
necrosis and aplasia of neurones in sympathetic ganglia (coeliac)… in horses
Clostridium botulinum type C. Horse grass sickness (primary dysautonomia)
4 MOA of enteritis
maldigestion, malabsorption, hypersecretion, increase motility
maldigestive enteritis
impaired villous enzymatic digestion (rota virus, coronavirus, enteropathogenic e. coli)
malabsorptive enteritis
loss of villous SA
hypersecretive enteritis
secretion of electrolytes due to enterotoxin damage (Enterotoxic E. coli, Yersinia enterocolitica)
common TYPE of enteritis inflm
catarrhal. hyperaemic, lymphocytic infiltrates and loss of villi.
corona and rota virus pathogenesis
need lactases so damage the tip of villi. crypts are spared of damage, recovery is possible.
canine parvovirus type 2 pathogenesis
need highly replicating cells with DNA polymerase, attack crypts of mucosa, poor ability to repair
fibrinous enteritis often caused by
feline parvovirus (panleukopenia virus)
Enterotoxic E. coli causes
<1w old catarrhal enteritis. adheres to enterocytes, produces toxin and toxin causes secretory diarrhoea
Enteropathogenic E. coli
catarrhal enteritis by adhering loosely and leading to destruction of villi
E. coli septicaemia
first few days of life, oral/umbilical infection in immunocompromised animals.
‘oedema disease’ in pigs
STEC (shiga-like toxins) produced by E. coli. occurs mainly post weaning. oedema in sub-cutis of face, stomach wall, mesenteric LN. toxin damages vessel integrity.
fibrinous/fibrino-necrotising enteritis feeatures
fibrinous exudate, deep mucosal damage and the vessel integrity is poorer cf. catarrhal.
viral causes of fibrinous/fibrino-necrotising enteritis
Classical swine fever / ‘Hog cholera’ - fibrinonecrotising typhlo-colitis or just colitis (‘boutons’). not in UK.
why do boutons form in inflm conditions
lymphoid patches in gut, contain fibrin and lymphoid aggregates. In CSF they are raised, in parvo they are depressed.
bacterial causes of fibrinous/fibrinonecrotising enteritis
Salmonella, PPE
Salmonella enteritis
S. choleraesuis or S. typhimurium. SI colonisation, adhere, penetrate, proliferate and survive in Mp, trojan horse effect. In young animals septicaemia, adults can cause typhlocolitis or sub-clininical carry.
pig form of salmonellosis
necrotising enteritis (S. cholerasuis) or ulcerative proctitis with rectal stricture (S. typhimurium) - stricture is due to lack of blood supply at one point in rectum where if damaged, scar-like tissue forms.
Porcine Proliferative Enteritis
intestinal adenomatosis complex. L. intracellularis. Infects crypt cells, spreads in epithelium by cell proliferation. Has variable disease forms.
PPE forms (4)
1) PPE - lesions in ileum, post weaning pigs, mucosal hyperplasia, hypertrophic mucosa with large crypts.
2) Proliferative haemorrhagic enteropathy - older animals, more lethal.
3) necrotic enteritis - mucosal necrosis, pigs.
4) terminal ilietis - chronic, related to healing of necrotic enteritis.
haemorrhgaic enteritis cause
Bacillus anthracis. ACUTE and ZOONOTIC.
granulomatous enteritis
Johne’s (paratuberculosis). ileal lamina propria macrophages contain acid fast bacteria.
lymphoproliferative and eosinophilic enteritis (IBD)
idiopathic IBD with lymphoplasmacytic proliferation most common. Chronic vomiting and diarrhoea. possible hypersensitivity to dietary antigens or bacterial antigens in intestinal flora.
malabsorption syndrome causes
V+/D+. Weight loss, steatorrhoea. caused by pancreatic enzyme insufficiency or acute/chronic enteritis.
malabsorption syndrome gross
dilated white villi (lymphangiectasia), small granulomas in subserosa and mucosa (lipid granules, Mp try to clear), dilated sub-serosal and mesenteric lymph vessels.
passive hyperaemia, oedema and haemorrhagic infarction are seen with what condition of bowel
misalignment
Strongylus vulgaris associated with which 2 lesions of gut
ischaemic intestinal infarction and haemomelasma ilei (dark nodules on subserosa along vessels). can be incidental and sub-clinical.
4 MOA of parasites causing damage
deprive host nutrients, blood sucking, mechanical blockage, toxic/allergic metabolites
chronic catarrhal enteritis caused by protozoa is commonly. what histo finding?
Eimeria or Isospora. hypertrophic crypt cells.
sheep, cattle, goat, horse coccidia species
E. crandallis/bakuensis/ahsata. E. bovis/zuerni. E. arloingi. E. leuckarti.
pig, rabbit, cat coccidia spp
Isospora suis. E. irresidua/magna/piriformis/perforans. Isospora felis.
ruminant cestodes where ruminant is DH
Moniezia expansa/benedeni
horse cestodes
anoplocephala perfoliate, A. magna.
thrombotic verminous endoarteritis in horses caused by… what about L3 induced granulomas in wall of colonic mucosa/caecum?
large strongyles - small stronglyes
Oesophagostomum dentatum
swine follicular ulcers in lymphatic follicles.
colorectal polyps seen in
dogs, benign neoplasm.
malignant tumour of caudal GI tract
adenocarcinoma. severe fibrous tissue proliferation (scirrhous reaction). can invade and metastasise.
cats mainly get which GI tumour
malignant lymphoma. diffuse/nodular thickening of intestinal wall. usually older cats.
Congenital defects of the liver
Intrahepatic cysts (Persian cats), portosystemic shunt (intra or extra hepatic)
Intra v extra hepatic shunts
Intra - ductus venosus does not close, left umbilical connection to VC (Irish wolfhound). Extra - portal vein connection to VC/azygous, more severe. (Maltese, Yorkshire terriers). Get microhepatia, ultimately hepatic encephalopathy.
2 dislocations of liver
Diaphragmatic hernia or lobe torsion
RF for liver rupture
Trauma, neoplasia (haemangiosarc), amyloidosis. Get haemoperitoneum.
Passive hyperaemia of liver
“Congestion”. ++hepatic vein pressure. Occurs near central vein first.
Chronic congestion of liver, causes? Gross?
CHF, endocardiosis, reticuloperitonitis. Sinusoids pressure increase, thick capsular surface and nodular texture. ‘Nutmeg liver’
Histo of backwards congestion
Centrolobular necrosis, fibrosis at central vein. Hypoxia leads to necrosis and fibrosis.
Explain acquired portosystemic shunt.
Chronic liver diseases causes increased pressure/flow in usually non functional veins, bypass liver to give route with better flow. Many small connections instead of one large shunt.
Teleangiectasis
Dilation of functional blood vessels. In liver see dilation of sinusoids. Unknown pathogenesis.
Peliosis hepatis
Irregular blood filled cysts in liver parenchyma. Mainly cats due to focal necrosis of hepatocytes.
hydropic degeneration occurs where and why
in hepatocytes, due to high metabolic rate and prone to hypoxic change. looks like ‘cloudy swelling’. It is a non-specific change due to Na+ influx into the cell. expanding organelles.
atrophy of hepatocytes looks like
reduction in size of cells. due to pressure from other organ or reduced blood supply.
what fatty change occurs in the liver? what is the normal mechanism for fat?
lipidosis. accumulation of triglycerides in hepatocytes. usually FFA (from adipose tissue and food) go into liver and esterified to form triglycerides which then are sent to form apoproteins and lipoproteins (in times of energy deficits).
4 pathogenesis methods of lipidosis
nutritional lipidosis (too much fat in diet). excessive FFA release (energy demand too high). hypoxic lipidosis (decreased oxidation of FA, accumulation of FFA), toxic lipidosis (impaired synthesis of apoproteins, destruction of cellular membranes).
gross and histo of hepatic lipidosis
enlarged, round edges, pale yellow and friable. small vacuoles which distend cell and displace nucleus to periphery.
stain used to highlight fat in lipidosis
oil-red-orange.
5 diseases that may cause lipidosis
hyperlipidaemia (diabetes etc), ketosis (twin lamb etc), hypoglycaemia (puppies starvation or stress), hyperadrenocorticism, tension lipidosis (cattle liver ligament area of hypoxia)
4 examples of depositions in liver cells
lipidosis, glycogen, amyloidosis, pigment storage
glycogen accumulation histo
swelling, hydropic degeneration appearance, feathery, central nucleus. can stain with PAS.
4 causes of glycogen accumulation
1) diabetes mellitus (hyperglycaemia) 2) glycogen storage disease (enzyme lacking which breaks down glycogen) 3) iatrogenic steroid induced 4) cushings
4 reasons for high cortisol and therefore glycogen storage overload
increased gluconeogenesis overall. 1) idiopathic adrenal cortical hyperplasia 2) primary adrenal cortex tumour 3) iatrogenic cortisol 4) pituitary tumour
where is amyloid usually depositd in liver
in space of Disse, between sinusoid and hepatocytes.
types of amyloidosis
AA (amyloid associated), Reactive amyloidosis (immunoglobulin)
amyloidosis gross and histo
pale, enlarged, rounded liver edges. perisinusoidal proteinaceous material compressing hepatocytes and acting as barrier to exchange.
5 pigments stored in liver
bile, lipofuscin/ceroid, haemosiderin, melanin, iron porphyrin
kupffer cells have higher levels of which pigment? how can this be diseased in ruminants?
Haemosiderin, due to RBC breakdown. in rmns get ‘‘haemochromatosis’’, iron overload due to high intake. hepatomegaly, haemosiderin accumulation (Perl’s stain)
Defect in porphyrin metabolism may cause what type of disease
liver-related skin photosensitisation
bovine congenital EPO porphyria
red-brown pigment in bone, dentin and liver. excretion of compounds in skin. Uroporphyrins absorbing UV-A in skin creating radicals and causing skin damage. mainly in white skin.
Intoxication related photosensitisation
St.John’s Wort, buckweat, spring parsley causing photodermatitis.
common hepatic necrosis type and histo appearance
coagulative. outline of cell is present, cell is shrunken and cell contents are hypereosinophilic and nuclei is fragmented.
focal necrosis in liver due to…
EHV1/Toxoplasmosis - disseminated infections such as septicaemia. aggregates of necrotic hepatocytes.
zonal necrosis in liver 3 types
centrolobular, mid-zonal, periportal
phosphorous poisoning causing what zone of necrosis
periportal.
Tyzzer’s disease
Clostridium piliforme, focal necrosis in liver.
Rabbit viral haemorrhagic disease
Calicivirus, focal necrosis in liver.
massive (diffuse) hepatic necrosis
whole lobe necrosis. often infarction. Hepatosis dietetica (Mulberry’s Heart Disease) in pigs. Also get oedema of gall bladder wall.
outcomes of necrosis in liver
resolution by regeneration or replacement of parenchyma with fibrous scar. if destruction of reticular framework then scar formation more likely (non-functional).
4 patterns of fibrosis
periportal, centrolobular, diffuse or bridging, post-necrotic scarring.
types of bridging fibrosis
central-central, porto-portal, porto-central.
hepatic cirrhosis
end stage liver disease, irreversible.
3 features of hepatic cirrhosis
degeneration (disruption of liver architecture), regeneration (nodules), repair (bridging fibrosis, central pathogenic process).
attempts of compensation in liver disease
nodule formation, bile duct proliferation, fibrosis, anastasmoses of vascular tissue.
hepatic cirrhosis infectious causes
idiopathic, CAV-1 or leptospirosis persistence.
2 parasitic causes of cirrhosis
fluke and ascarids.
4 causes of cirrhosis with no infectious agent
chronic congestion (CHF), post-necrotic cirrhosis (toxin/infectious insult), pigment cirrhosis (haemochromatosis), biliary cirrhosis (chronic cholangitis)
cirrhosis results (3)
jaundice, ascites, hepatoencephalic syndrome (hyperammonia in blood)
3 types of jaundice
pre-hepatic, hepatic and post-hepatic
pre-hepatic jaundice
'’haemolytic jaundice’’. high UNCONJUGATED bilirubin in blood.
causes of pre-hepatic jaundice
infectious (EIA, lepto, haemolytic streps, anthrax, snake venom), internal haemorrhage, icterus neonatum (lack of glucornyl transferase)
hepatic jaundice
intrinsic liver damage. toxic substances or infectious agents. high unconjugated bilirubin usually, can get bile blockage so possibly some bilirubin high.
post-hepatic jaundice
obstructed bile flow. high conjugated bilirubin in blood.
2 major groups of hepatic failure
1) synthesis, catabolism, detoxifying, secretion/excretion 2) CHO, proein and lipid metabolism.
results of hepatic failure
jaundice, hypoalbuminaemia, coagulopathy, hyperammonia, hepatic encephalopathy, portal hypertension and ascites.
hepatic encephalopathy pathogenesis
metabolites passing the BBB. ammonia can inhibit generation of excitatory/inhibitory post-synaptic signals as well as altering amino acid, water and electrolyte transit in neuronal membranes. e
hepatic encephalopathy lesions
cerebral oedema (status spongiosa), neuronal necrosis and swelling, degeneration of astrocytes. Alzheimer type 2 microglia, indicate damae to brain. liver can lack portal triad veins.
3 acute characterstics of hepatitis
degeneration and necrosis of hepatocytes, leukocyte infiltration in periportal CT or sinusoids, if septicaemia related then kupffer activation.
periportal inflammation often also presents with
ductular hyperplasia
chronic hepatitis characteristics
periportal infiltration with lymphocytes and plasma cells.. progressive periportal fibrosis, hepatocyte apoptosis and necrosis.
chronic active hepatitis
dobermans commnonly. determined by quantity of inflm and hepatocellular death. possible assoc w/ lepto, canine hepatitis, aflatoxicosis and copper. Can lead to cirrhosis.
cholangitis/cholangiohepatitis/pericholangitis
biliary tree inflm, bile duct and liver inflm, inflm around around bile duct.
cats commonly get what inflm condition associated with IBD
‘triaditis’… ascending inflm via common bile duct and pancreatitis. happens because pancreatic and biliary ducts fuse before entering duodenum.
triaditis histo lesions
1) suppurative cholangitis 2) lymphocytic and plasmacytic periportal infiltration, bile duct hyperplasia, periportal fibrosis 3) biliary cirrhosis
viral hepatitis causes (6), usually are secondary to…
CAV-1, EHV-1, CaHV1, RVHD, FCV, FIP. viraemia.
infectious canine hepatitis
CAV-1. invades via tonsils + LN, travels to blood, tropism for endothelial cells. infects liver, eye, kidney and blood vessels. in liver causes a necrotising hepatitis. if survive acute phase, can recover.
CAV-1 liver histo
intranuclear inclusion bodies, hepatic necrosis (centrilobular), oedema, haemorrhage.
equine herpes virus hepatitis
EHV-1 (rarely EHV-4). Abortion (necrosis of placental attachment). Can infect foetus, get multifocal miliary necrosis, inclusion bodies seen occasionally.
Canine herpes virus 1 hepatitis
(CaHV1). multifocal necrosis and haemorrhage/DIC in young puppies. infection can occur intra-uterine, during birth or soon after. in adults causes venereal and respiratory infection.
neonate puppy CaHV1 infection
if >2w localised infection and replication as adult form. If <1w get epithelial replication, mucosal invasion… leads to leukocyte associated viraemia.
foetal puppy CaHV1 infection
in utero, leukocyte associated viraemia: lymphoid hyperplasia, generalised infection, diffuse necrotising vasculitis, multifocal haemorrhagic necrosis of many orgnas and can lead to CNS damage or death
Rabbit haemorrhagic disease
Calicivirus. Massive hepatocyte necrosis, DIC (in lungs and renal glomeruli). death rapid.
Feline systemic calicivirus
FCV. systemic disease, necrotising dermatitis and oedema, bronchointerstitial pneumonia and hepatic, pancreatic and splenic necrosis.
Feline infectious peritonitis
Feline coronoavirus (FeCoV). viraemia, granulomatous periphlebitis, serositis and hepatitis. sometimes granulomatous-fibrinous perihepatitis. Due to immune-complex deposition.
abscess and granuloma causing organisms of the liver
Francisella tularensis, Nocardia asteroids, Actinobacillus spp, Mycobacterium spp, Fusobacterium necrophorum.
necrobacillosis in liver
F. necrophorum. Rmns with rumenitis-liver-syndrome. ulcerative rumenitis followed by transmission to liver via blood.
Tularaemia
Francisella tularensis (ZOONOTIC). vector is ticks. localised infection, lymphadenitis, bacteraemia, ulceration of LN, peyer’s patches, hepatitis.
Yersiniosis
Yersinia pseudotuberculosis (ZOONOTIC). enteric infection, invasion of peyer’s patches, microabscesses, liver/kidney/spleen dissemination.
Tuberculosis in liver
M. bovis/M. tuberculosis/M. avium. Miliary hepatic necrosis with multifocal granulomatous inflammation.
Leptospirosis agents (3)
L. canicola, L. icterohaemorrhagica, L. grippotyphosa. (ZOONOTIC).
leptospirosis patho
mucosa or skin wound, replication in blood, dissemination. antibody clears systemic infection but remains in kidneys. when systemic, cause liver damage by toxins causing necrosis. see hepatocellular dissociation.
leptospirosis histo
rounded hepatocytes, eosinophilic granular cytoplasm, dark shrunken nuclei, loss of cords (dissociation).
Clostridium piliforme
zoonotic. proliferative intestinal ulcerations and necrotising colitis/typhilitis. if immunosuppressed can spread to liver and cause necrosis. important in foals.
protozoal infections of liver
toxoplasma, coccidiosis, leishmaniasis
toxoplasma hepatitis
T. gondii. tachyzoites seen in hepatocytes. multifocal necrosis with no cysts in liver.
coccidiosis hepatitis
Eimeria stiedai (hare/rabbit). replicate in bile duct, cause bile duct proliferation
leishmaniasis hepatitis
replication in Mp, rupture of cells, infect new. Granulomatous hepatitis.
metazoan hepatitis
flukes (F. gigantic, hepatica) tapeworm (Dicrocoelium dendriticum). eosinophil/granulomatous hepatitis and fibrinous peritonitis.
consequences of parasitic hepatitis
hepatic dysfunction, hypoproteinaemia, debilitation and death. 1) heal by granulation tissue, fibrosis 2) black disease (latent spores of Cl. novyi activate). 3) chronic fascioliasis.
chronic hyperplastic cholangitis with peribiliary fibrosis and calcification may indicate what disease
fluke
hepatophilic and serosophilic cysts differ in the liver because…
serosophilic are on the serosal surface (e.g. T. hydatigena), hepatic are within (e.g. E. granulosus).
milk spot liver
ascaris suis. chronic eosinophil-dominated periportal infiltration.
difference btw obligate or idiosyncratic toxins
obligate lead to predictable toxic effects. idiosyncratic are unpredictable and differ btw individuals.
direct effects of liver toxins
oxidation of membrane lipids, denaturing of structural proteins, inhibition of enzymes.
indirect effect of liver toxins
blocking of receptor or transport protein, modification of proteins, free radical production.
overall effects of liver toxins
cellular membrane damage, leakage of enzymes and inactivation of Na+ pump, loss of control of intracellular calcium, mitochondrial dysfunction, phospholipase release, cytoskeletal abnormalities, loss of compartmentalisation, leakage of mitochondrial enzymes and lysozymes.
site of damage for toxic liver injury
zone 3 - highest levels of CP450 and lowest levels of oxygenated blood.
hepatocyte detoxification methods (3)
1) biotransformation (conjugated and hydroxylation) 2) carrier systems (biliary excretion) 3) kupffer activation`
zone 1 domination toxin
direct acting e.g. metal salts. centriacinar location.
acute toxic hepatosis gross and histo
gross - ascites, oedema of gall bladder wall, petechial haemorrhage in serosa (DIC). histo - centrilobular to massive necrosis, often with fatty or hydropic change.
early v late stage acute toxic hepatosis
early = degenerate/necrotic hepatocytes. later = dilated, blood-filled sinusoids.
one time submassive necrosis due to toxins in liver…
regeneration is possible
one time massive nerosis with reticular framework disruption
fibrosis (repair)
chronic or recurrent toxins effects…
chronic active hepatitis, cirrhosis.
copper toxicosis which species
sheep, cattle (holstein/jersey), pigs, bedlington terriers
3 MOA for copper toxicosis
excess intake, reduced excretion or familial disposition.
sheep copper toxicosis
low dietary intolerance, reduced excretion apparatus.
pasture problem with copper
contamination with poultry/swine slurry or slug/snail pellets.
problem with giving pig/cattle feed to sheep
copper levels too high.
Mo/Sulphur levels in soil can cause
usually bind to copper and form complexes.
pyrrololizidine alkaloids in Aus can cause
hepatotoxic problems
Sheep breeds most susceptible
Merino, Texel, North Ronaldsay
pathogenesis of copper intoxication and histo
> 150-400ug/g starts at pre-haemoloytic stage. progress into haemolytic crisis, release of copper from necrotic hepatocytes. made worse by hepatotoxicosis or stress. histo = zone 3 necrosis and renal tubular Hb casts.
familial copper toxicosis
bedlington terrier, Cu accumulates in zone 3, progressive hepatitis and cirrhosis. focal hepatitis, chronic active hepatitis, fibrosis.
stain for copper
Rhodanine
which sheep breed is most susceptible (<5ppm) to copper
North Ronaldsay
Senecio, crotolaria, heliotropium all contain
pyrrolizidine alkaloids
pyrrolizidine alkaloids MOA of disease
converted to pyrrolic esters - interact with DNA/RNA bases -> cause hepatic fibrosis and cirrhosis.
histo of pyrrolizidine alkaloids. why do you get megalocytosis?
single cell necrosis, megalocytosis, inflm + fibrosis, bile duct proliferation, hepatoencephalopathy. Megalocytosis is regenerative attempt, due to inhibition of mitosis, but not of protein synthesis.
Aflatoxicosis toxin and species. pathogenesis?
Aspergillus flavus/parasiticus and Penicillium puberculum. toxin is furanocumarin. toxic, carcinogenic, teratogenic, mitosis inhibiting, immunosuppressive. liver changes are similar to seneciosis.
blue-green algae poisoning
Microcystis aeruginosa (cyanobacteria). acute hepatoxicity, centrilobular to massive necrosis with haemorrhage.
Non-neoplastic benign nodular hyperplasia
common in old dogs, usually multiple, expanding compressing adjacent tissue.
non-neoplastic regenerative nodules
common in old dogs. adjacent tissue often fibrotic, loss of lobular architecture.
hepatocellular adenoma
single, sharply delineated, no portal areas or lobular structure. compressing normal tissue.
hepatocellular carcinoma
compression and invasion of adjacent tissue, metastasis into portal vessels. growth either trabecular, acinar or solid.
bile duct adenoma
often cystic, single, sharply delineated.
bile duct carcinoma
commonly spread along biliary tracts, metastasis common to hepatic serosa, LN and lungs. induces desmoplasia and so get scirrhous reaction.
which tumour commonly metastasises to liver?
mammary carcinoma.
how can tumours spread to liver commonly?
serosal contact, blood spread.
which blood vessels supply the pancreas? which ducts does the pancreas use to secrete enzymes?
cranial mesenteric and coeliac arteries. drained by portal veins. major and minor pancreatic ducts, differ btw species.
sheep and goats pancreatic arrangement
ONLY have MAJOR duct
pigs, cattle and dog pancreatic arrangment
ONLY have MINOR duct
cats pancreatic arrangement
MOST have MAJOR but SOME have BOTH
horses pancreatic arrangement
BOTH MAJOR and MINOR
what opens into the major duodenal papilla?
major pancreatic duct AND bile duct
cholecystokinin and secretin stimulate - where are they produced?
secretion of enzymes from pancreas and water/bicarbonate. produced in duodenum in response to acid and distension.
how does the pancreas prevent itself from autodigestion (6)
stores inactive proenzymes, in zymogen granules. only activated when away from pancreas. mucoid layer produced to protect. secretes trypsin inhibitors and protease inhibitors produced by the liver.
what is the major protease produced by the pancreas, where and how does it become active?
trypsin - in gut becomes activated by trypsinogen.
which cells are present in the islets of langerhans? (6)
alpha, beta, delta, PP, D1, ECL cells.
juvenile pancreatic atrophy occurs in? how does it look in histo?
young dogs (eg GSD). true atrophy not hypoplasia, only affecting exocrine tissue. islets are fine. causes EPI (exocrine pancreatic insufficiency)
what may cause pancreatic haemorrhages
coagulation disorder, CAV-1 in dogs, toxins e.g. Dicumarol (rat poison).
3 infectious causes of pancreatitis
CAV-1, FIP, FMD.
parasitic pancreatitis cause
migrating strongyles
zinc poisoning in cattle and sheep can cause
pancreatitis
what may cause a difference in necrotising or fibrosing pancreatitis?
acute (necrotising) or chronic (fibrosing) disease.
acute necrotising pancreatitis
mainly dogs. activation of enzymes within pancreas. trypsin becomes active, activates other enzymes. low pH the inhibitors stop working. possible cause is lysosomes fusing with zymogen granules.
necrosis of what tissue is common with acute necrotising pancreatitis?
fat necrosis.
histo of acute necrotising pancreatitis and clinical signs
focal necrosis, haemorrhage, thrombosis, oedema. inflm infiltrates and fat necrosis in omentum, mesentery and pancreas. acute V+/D+, dullness, thirst, abd pain.
what is common cause of death in acute necrotising pancreatitis?
DIC due to consumption of please protease inhibitors.
chronic fibrosing pancreatitis
result of survival of acute pancreatitis or in cats without cause. fibrous tissue replacing damaged tissue.
why are cats at risk of pancreatitis
bile duct duses with pancreatic ducts.
what is EPI? when does it occur? 4 causes?
exocrine pancreatic insufficiency. >80% of tissue lost. causes: hypoplasia in calves, juvenile atrophy in dogs, chronic pancreatitis in cats, neoplasia.
clinical signs of EPI
Diarrhoea, weight loss, pancreatogenic maldigestion (pale, soft, voluminous malodorous faeces/steatorrhea).
serum trypsin-like immunoreactivity (TLI) assay is used to diagnose
EPI
non-neoplastic growth of pancreas
nodular hyperplasia. older patients.
what is more common in the glandular tumours of pancreas?
adenocarcinoma more common. arise in centre of pancreas. grey/scirrhous tissue. aggressive and metastatic.
if islet is amyloid filled and secreting multiple hormones it is usually
endocine tumour.
insulinoma present as
hyperinsulinaemia, hypoglycaemia, neuro signs
gastrinoma present as
hypergastrinaemia, Zollinger-Ellison syndrome (mucosal ulceration of stomach)
glucagonoma present as
hyperglycaemia, diabetes mellitus
primary diabetes mellitus could be caused by
neoplastic destruction of pancreatic tissue, necrosis following inflammation.
cats with primary diabetes mellitus…
islet amyloidosis (associated w/ obesity).
cattle with primary diabetes mellitus
chronic FMD/BVD
how is sex differentiation controlled
chromosomal, gonadal, hormonal. SRY most important.
which ducts form in males and females for repro
mullerian (paramesonephric) for female. wolffian (mesonephric) for male.
Turner’s syndrome
XO (or XXX) = hypoplastic females
Klinefelter’s syndrome
XXY = hypoplastic males
freemartinism
ovarian dysgenesis. male/female twins, testis determining factor and anti-mullerian hormone shared between both - hypoplastic female calf.
reasons for intrafollicular or traumatic ovarian haemorrhage
physioogical (can be lethal in mares) or manual enucleation of CL
follicular cysts arise from
non-ovulated follicle. cause excess oestrogen secretion
ovarian surface epithelium tumours
papillary cystadenoma and papilary cystadenocarcinoma
ovarian stroma tumour
granulosa cell tumour
ovarian germ cell tumours
dysgerminoma and teratoma
terms for fallopian condtions
hydrosalpinx, salpingitis, pyosalpinx
post-partum hypocalcaemia often associated with
uterine prolapse
difference between endometrial hyperplasia in ungulates and dog/cat
ungulates mainly oestrogen reliant, dog/cat is progresterone acting on oestrogen-primed endometrium.
terms for inflm of uterus
metritis, endometritis, perimetritis, panmetritis.
suppurative endometritis another name for
pyometra
pyometra bitch/queen
bacterial infection following hyperplastic endometrium. E.coli, Proteus, Staphs and Streps
pyometra cows
persistant CL. Tritrichomonas foetus subsp. venerealis, Arcanobacterium pyogenes, E.coli, Pseudomonas aeruginosa, Streps and Staphs
pyometra mares
indepenent of persistent CL. Strep zooepidemicus, E.coli, Pseudomonas aeruginosa, Klebsiella pneumoniae, Pasteurella
uterine tumours (3)
leimyoma, leimyosarcoma, adenocarcinoma
rabbits get which common uterine tumour
adenocarcinoma
foetal mummification occurs when
no infection, fluids are resorbed.
foetal maceration and emphysema due to
infection - campylobacter foetus and tritrichomonas foetus
why is gravid uterus prone to infection
progesterone influence, secretions and immuno-privelaged
Brucellosis cattle
Brucella abortus. notifiable. oedema and necrosis of cotyledons.
brucellosis pigs, sheep/goat, dog
Brucella suis, Brucella melitensis and Brucella ovis, Brucella canis
campylobacter cattle and sheep
C. foetus sbsp. venerealis (Cattle), C. foetus sbsp. feotus or C. jejuni (sheep).
chlamydia abortion
chlamydia psittaci/abortus
protozoal abortions
toxoplasma and neospora
viral abortions cattle and horses
BVDV, BDV, EHV1
viral abortions swine
porcine parvovirus, porcine reproductive and respiratory virus, porcine circovirus 2
infectious pustular vulvovaginitis 3 agents
IBR, EH3 (ECE), Trypanosoma equiperdum
necrotising vaginitis and vulvitis agent
F. necrophorum
3 vaginal/vulval tumours
leimyoma, fibroma, transmissible venereal tumour
haematogenous mastitis agents
Brucella and TB
which organism does cows immunity decrease with age for mastitis?
streptococcuus agalactiae
3 streptococcal mastitis
strep agalactiae, strep dysgalactiae, strep uberis
S. aureus, S. intermedius, S. hyicus are all
mastitis causing, coagulase positive staphs
gangrenous mastitis is caused usually by
staphylococcal organisms
toxic mastitis usually
coliforms e.g. e coli. see bloody milk discharge due to endotoxin microvasculature damage
Summer mastitis agents
Truperella pyogenes. Combined with S. dysgalactiae, Peptococcus indolicus, Bacterioides melaninogenicus, Fusobacterium necrophorum
sheep/goat galactogenic entry mastitis
s. aureus or p. haemolytica
sheep/goat wound entry mastitis
C. pseudotuberculosis or Arcanobacterium pyogenes
contagious agalactiae in goats mainly
Mycoplasma agalactiae
types of mammary tumours
simple (one cell type) or complex (2 cell type) adenomas.
mixed mammary tumour
epithelial and mesenchymal components (e.g. bone, cartilage, fat).
the most and least malignant mammary tumours
most = anaplastic carcinoma. least = non-infiltrating carcnoma
feline mammary hypertrophy + hyperplasia
fibroadenomatous change. bening. oedema and fibrous stroma.
2 testicular developmental disorders
hypoplasia and cryptorchidism
orchitis/epididymitis causes
streps, staphs, e.coli, arcanobacterium.
horses testicular inflm
equine viral arteritis and salmonella abortus equi
sheep testicular inflm
C. pseudotuberculosis, Y. pseudotuberculosis and Brucella ovis
Dogs testicular inflm
E.coli, Proteus, Brucella canis
cattle testicular inflm
brucella abortus, mycobacterium bovis
testicular tumours (4)
seminoma (germ cell - white/grey), Sertoli cell tumour (white/grey - feminisation), Leydig cell tumour (yellow/orange - vacuolated histo), teratoma
prostatic tumours
adenocarcinoma or non-differentiated carcinoma
prostatic hyperplasia
bilateral and symmetrical. can impede defaecation
phalloposthitis and balanoposthitis
penis + prepuce , glans penis and prepuce
penis tumours in bulls
fibropapilloma (BPV1)
penis tumours stallions
squamous cell papilloma, sarcoid (BPV1), squamous cell carcinoma
dog penis tumours
transmissible venereal tumour
