Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathology Semester 1 > Pathology Semester 2 part 2 > Flashcards

Pathology Semester 2 part 2 Flashcards

1
Q

Explain a neurogenic disease of the oral cavity

A

hypoglossal nerve damage in horses with guttoral pouch disease. cause lingual muscle atrophy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

give 3 colour changes to the oral mucosa and the reason

A

pallor (anaemia/CHF), cyanosis (toxic, uraemia, hypoxia), petechiae/haemorrhages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

term for inflm of gums and of palate structures

A

gingivitis and stomatitis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

necrobacillosis GI disease… type of inflm

A

Fusobacterium necrophorum. Calf diptheria or hepatic necrosis. Fibrino-necrotising laryngitis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Wooden tongue

A

Actinobacillus ligniersi. pyogranulomatous inflm with fibrosis and abscessating glossitis. Splendore-Hoepli figures on histo.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Give 2 bacterial inflm infections of mouth

A

wooden tongue and necrobacillosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Bluetongue virus GI path… vector, virus, pathogenesis

A

culicoides vector, orbivirus. viraemia, endothelial damage, microthrombi, haemorrhages, ischaemic necrosis. oedema and hyperaemia of oral/nasal mucosa, ischaemic necrosis of mucosa.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

two types of stomatitis

A

vesicular and erosive/ulcerative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

oral vesicles are caused by what process

A

ballooning degeneration of epithelial cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

FMD

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

2 other causes of vesicular stomatitis (except FMD)

A

Rhabdovirus vesicular stomatitis and Picorne-viridae-enterovirus in pigs (swine vesicular disease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Erosive and ulcerative stomatitis (2)

A

BVD/Mucosal Disease (MD) - Pestivirus, BVDV1. Malignant catarrhal fever (ovine herpes virus 2).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

‘Mucosal Disease’

A

seen in PI calves with cytopathic form of BVDV. sharply delineated flat ulcers on mouth, tongue, oeseophagus and GI tract.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

malignant catarrhal fever

A

Ovine herpes virus 2, Allcephaline herpes virus 1. Bison most susceptible. Oral and GI erosions with conjunctival and keratitis lesions (unlike MD).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

2 agents of feline erosive and ulcerative stomatitis

A

feline herpes virus and feline calicivirus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

fungi causing oral disease in suckling animals

A

candida albicans. white, fluffy chalky plaque on oral structures. poor hygiene or immunocompromised.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

lingual muscle can harbour which kind of parasite

A

metacestode cyst of tapeworms (Taenia saginata/solium)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

eosinopihlic granuloma complex 3 parts

A

indolent ulcer, oral eosinophilia granuloma, eosinophilic plaque.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

tonsilitis bacteria

A

haemolytic streptococci, coliforms.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

aujeskys disease

A

necrotising tonsillitis, swine herpes virus type 1.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

oral benign tumour

A

papilloma, epulides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

epulides, 3 types

A

benign tumour in dog/cat. derive from periodontal ligament or connective tissue. fibrous, ossifying and acanthomatous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

most common oral tumour in cats, how about dogs?

A

squamous cell carcinoma. melanoma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

tonsillar squamous carcinoma what species and how malignant

A

spreads early, found in dogs. characteristic keratin pearls.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

which neoplasm derives from connective tissue of oral cavity, is malignant and second most common in cats?

A

fibrosarcoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

sialoadenitis and sialolith

A

inflm of salivary gland and calculi in ducts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

ranula

A

cyst formation in salivary gland duct.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

how could the oes be obstructed, strictured or compressed?

A

obstruct with foreign body, neoplasm, parasites. compressed by LN, abscess or neoplasm. stricture with persistant RAA.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

2 types of megaoesaphagus

A

congenital (GSD, great dane, irish setter) or acquired secondary to neural reflex disorder. can be due to distemper, botulism, myaesthenia gravis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

thymoma and myaesthenia gravis are assoc with which disease

A

megaoesophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

spirocerca lupi

A

intermediate host is beetle, dogs/canids DH. ingested beetle, L3 migrate to oes, cause granulomatous oesophagitis and related to fibro and ossifying sarcoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

oesophageal papilloma in cattle

A

BPV type 4.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

abnormality of ruminal mucosa

A

parakeratosis, hyperkeratosis. due to high concentrate diet.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

2 types of ruminal tympany

A

frothy and gassy bloat. decrease venous return and hypovolaemic shock. frothy due to lots of legumes, gassy due to physical obstruction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Saponaria officinalis (saponins) are responsible for what

A

cause of bloat in cattle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Lactobacillus acidophilus causes what

A

ruminal acidosis. Over ingestion of CHO - increase VFA - atony - drop in ruminal pH - proliferation of L. acidophilus - death when pH reaches below 4.5.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what is the risk to survivors of ruminal acidosis

A

secondary necrobacillosis, peritonitis and pericarditis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

3 viruses that can induce ruminal ulceration

A

FMD, MD, MCF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

5 areas of the stomach

A

cardia, fundus, body, antrum, pylorus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

which cells produce pepsinogen and gastric acid?

A

pepsinogen = chief cells. acid = parietal cells. ECL cells stimulate acid cells via histamine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

GDV is assoc w/

A

excess eating and aerophagia. small food particles and weak hepatogastric ligament is predisposition.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what displacements occur in gastric volvulus

A

pylorus and duodenum compressed between oes and dilated stomach, spleen moves with gastrosplenic ligament, oes can be completely occluded

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

results of displacements of gut (GDV)…

A

gastric haemorrhagic infarction, decreased venous return, decreased CO, hypotension, decrease renal function, shock.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what is the cattle equivalent of GDV

A

left or right abomasal displacement. similar results as in GDV.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Horse stomach parasites. pathogenic?

A

Gastrophilus intestinalis, nasalis and haemorrhoidalis, no link with ulcers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

ruminant gut parasite causing hypoproteinaemic oedema and anaemia

A

haemonchus contortus (problem when moving cattle off and moving sheep on)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

allotriophagia term for? assoc w/ 3 conditions

A

pica. encephalitis, starvation, boredom.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

which species get gastroliths

A

reptiles and horses.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

acute catarrhal gastritis patho and causes

A

serous inflm of mucosa and serosa, thickened and red. poisons, Helicobacter spp, parasites.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Ollulanus tricuspis causes what condition

A

parasitic catarrhal gastritis in felids. transmission via vomit. small <1mm worm.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

acute haemorrhagic gastritis

A

poisons, swine erysipelas, braxy, NSAID overuse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Braxy

A

sheep/calves in cold climates. Clostridium septicum enterotoxin, severe odema and emphysema in submucosa, haemorrhage and venous thrombosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

haemorrhagic gastritis causal agents

A

CSF virus, anthrax, leptospirosis (with uraemia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

uraemic gastritis

A

endothelial degeneration, necrosis, thrombosis, infarction. excretion of ammonium (in saliva and gastric juices) causing coagulative necrosis. assoc w/ chronic renal failure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

stomach ulcers cattle

A

in pylorus, assoc w/ transport or diet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

pig stomach ulcers

A

in squamous epithelial part, due to hyperacidity, fine grain diet or stress.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

horse stomach ulcers

A

in non-glandular portion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

dog/cat stomach ulcers

A

pylorus or proximal duodenum. associated highly with mast cell tumours! histamine over stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

outcome of stomach ulcers

A

haemorrhage, perforation, peritonitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

stomach ruptures common in

A

horses due to dilation. First serosal tear, then musclaris. can occur post-mortem, see fine borders with less haemorrhages.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

horse stomach rupture types (2)

A

primary (over ingestion of CHO, excess water intake). secondary (due to blockage in colic or dysautonomia).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

most common gastric neoplasia of dogs

A

adenocarcinoma. arises from glandular mucosa, can metastasise.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

benign stomach tumour

A

adenoma/benign adenomatous polyp

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

stomach epithelial tumour common in large proventricular area

A

squamous cell carcinoma. yellow-brown colour due to keratin production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

cats, FeLV negative, B cell tumour in older patient

A

lymphosarcoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

which tumour would be originating from tunica muscularis of stomach

A

leiomyoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

common congenital GI finding

A

atresia. anal/rectal or intestinal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

aplasia of neurons in large intestinal myenteric ganglia would give rise to

A

megacolon - lack of peristaltic movement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

which gut herniation is common in horses

A

epiploic herniation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

RF for intussusception in small animals and horses

A

hyperactive bowel movements, parvo, distemper enteritis. in horses, ileum into caecum due to tapeworm.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

horse volvulus causes

A

pedunculated lipoma in mesentery, usually at jejunum or ileum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

intestinal misalignment consequences

A

misalignment of bowel, occlusion of veins, persistence of arterial supply, hyperaemia, hypoxia, capillary fragility, haemorrhage and necrosis and infarction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

necrosis and aplasia of neurones in sympathetic ganglia (coeliac)… in horses

A

Clostridium botulinum type C. Horse grass sickness (primary dysautonomia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

4 MOA of enteritis

A

maldigestion, malabsorption, hypersecretion, increase motility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

maldigestive enteritis

A

impaired villous enzymatic digestion (rota virus, coronavirus, enteropathogenic e. coli)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

malabsorptive enteritis

A

loss of villous SA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

hypersecretive enteritis

A

secretion of electrolytes due to enterotoxin damage (Enterotoxic E. coli, Yersinia enterocolitica)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

common TYPE of enteritis inflm

A

catarrhal. hyperaemic, lymphocytic infiltrates and loss of villi.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

corona and rota virus pathogenesis

A

need lactases so damage the tip of villi. crypts are spared of damage, recovery is possible.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

canine parvovirus type 2 pathogenesis

A

need highly replicating cells with DNA polymerase, attack crypts of mucosa, poor ability to repair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

fibrinous enteritis often caused by

A

feline parvovirus (panleukopenia virus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Enterotoxic E. coli causes

A

<1w old catarrhal enteritis. adheres to enterocytes, produces toxin and toxin causes secretory diarrhoea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Enteropathogenic E. coli

A

catarrhal enteritis by adhering loosely and leading to destruction of villi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

E. coli septicaemia

A

first few days of life, oral/umbilical infection in immunocompromised animals.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

‘oedema disease’ in pigs

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

fibrinous/fibrino-necrotising enteritis feeatures

A

fibrinous exudate, deep mucosal damage and the vessel integrity is poorer cf. catarrhal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

viral causes of fibrinous/fibrino-necrotising enteritis

A

Classical swine fever / ‘Hog cholera’ - fibrinonecrotising typhlo-colitis or just colitis (‘boutons’). not in UK.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

why do boutons form in inflm conditions

A

lymphoid patches in gut, contain fibrin and lymphoid aggregates. In CSF they are raised, in parvo they are depressed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

bacterial causes of fibrinous/fibrinonecrotising enteritis

A

Salmonella, PPE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Salmonella enteritis

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

pig form of salmonellosis

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Porcine Proliferative Enteritis

A

intestinal adenomatosis complex. L. intracellularis. Infects crypt cells, spreads in epithelium by cell proliferation. Has variable disease forms.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

PPE forms (4)

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

haemorrhgaic enteritis cause

A

Bacillus anthracis. ACUTE and ZOONOTIC.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

granulomatous enteritis

A

Johne’s (paratuberculosis). ileal lamina propria macrophages contain acid fast bacteria.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

lymphoproliferative and eosinophilic enteritis (IBD)

A

idiopathic IBD with lymphoplasmacytic proliferation most common. Chronic vomiting and diarrhoea. possible hypersensitivity to dietary antigens or bacterial antigens in intestinal flora.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

malabsorption syndrome causes

A

V+/D+. Weight loss, steatorrhoea. caused by pancreatic enzyme insufficiency or acute/chronic enteritis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

malabsorption syndrome gross

A

dilated white villi (lymphangiectasia), small granulomas in subserosa and mucosa (lipid granules, Mp try to clear), dilated sub-serosal and mesenteric lymph vessels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

passive hyperaemia, oedema and haemorrhagic infarction are seen with what condition of bowel

A

misalignment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Strongylus vulgaris associated with which 2 lesions of gut

A

ischaemic intestinal infarction and haemomelasma ilei (dark nodules on subserosa along vessels). can be incidental and sub-clinical.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

4 MOA of parasites causing damage

A

deprive host nutrients, blood sucking, mechanical blockage, toxic/allergic metabolites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

chronic catarrhal enteritis caused by protozoa is commonly. what histo finding?

A

Eimeria or Isospora. hypertrophic crypt cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

sheep, cattle, goat, horse coccidia species

A

E. crandallis/bakuensis/ahsata. E. bovis/zuerni. E. arloingi. E. leuckarti.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

pig, rabbit, cat coccidia spp

A

Isospora suis. E. irresidua/magna/piriformis/perforans. Isospora felis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

ruminant cestodes where ruminant is DH

A

Moniezia expansa/benedeni

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

horse cestodes

A

anoplocephala perfoliate, A. magna.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

thrombotic verminous endoarteritis in horses caused by… what about L3 induced granulomas in wall of colonic mucosa/caecum?

A

large strongyles - small stronglyes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Oesophagostomum dentatum

A

swine follicular ulcers in lymphatic follicles.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

colorectal polyps seen in

A

dogs, benign neoplasm.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

malignant tumour of caudal GI tract

A

adenocarcinoma. severe fibrous tissue proliferation (scirrhous reaction). can invade and metastasise.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

cats mainly get which GI tumour

A

malignant lymphoma. diffuse/nodular thickening of intestinal wall. usually older cats.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

Congenital defects of the liver

A

Intrahepatic cysts (Persian cats), portosystemic shunt (intra or extra hepatic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

Intra v extra hepatic shunts

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

2 dislocations of liver

A

Diaphragmatic hernia or lobe torsion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

RF for liver rupture

A

Trauma, neoplasia (haemangiosarc), amyloidosis. Get haemoperitoneum.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

Passive hyperaemia of liver

A

“Congestion”. ++hepatic vein pressure. Occurs near central vein first.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Chronic congestion of liver, causes? Gross?

A

CHF, endocardiosis, reticuloperitonitis. Sinusoids pressure increase, thick capsular surface and nodular texture. ‘Nutmeg liver’

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

Histo of backwards congestion

A

Centrolobular necrosis, fibrosis at central vein. Hypoxia leads to necrosis and fibrosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

Explain acquired portosystemic shunt.

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

Teleangiectasis

A

Dilation of functional blood vessels. In liver see dilation of sinusoids. Unknown pathogenesis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

Peliosis hepatis

A

Irregular blood filled cysts in liver parenchyma. Mainly cats due to focal necrosis of hepatocytes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

hydropic degeneration occurs where and why

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

atrophy of hepatocytes looks like

A

reduction in size of cells. due to pressure from other organ or reduced blood supply.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

what fatty change occurs in the liver? what is the normal mechanism for fat?

A

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).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

4 pathogenesis methods of lipidosis

A

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).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

gross and histo of hepatic lipidosis

A

enlarged, round edges, pale yellow and friable. small vacuoles which distend cell and displace nucleus to periphery.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

stain used to highlight fat in lipidosis

A

oil-red-orange.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

5 diseases that may cause lipidosis

A

hyperlipidaemia (diabetes etc), ketosis (twin lamb etc), hypoglycaemia (puppies starvation or stress), hyperadrenocorticism, tension lipidosis (cattle liver ligament area of hypoxia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

4 examples of depositions in liver cells

A

lipidosis, glycogen, amyloidosis, pigment storage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

glycogen accumulation histo

A

swelling, hydropic degeneration appearance, feathery, central nucleus. can stain with PAS.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

4 causes of glycogen accumulation

A

1) diabetes mellitus (hyperglycaemia) 2) glycogen storage disease (enzyme lacking which breaks down glycogen) 3) iatrogenic steroid induced 4) cushings

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

4 reasons for high cortisol and therefore glycogen storage overload

A

increased gluconeogenesis overall. 1) idiopathic adrenal cortical hyperplasia 2) primary adrenal cortex tumour 3) iatrogenic cortisol 4) pituitary tumour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

where is amyloid usually depositd in liver

A

in space of Disse, between sinusoid and hepatocytes.

134
Q

types of amyloidosis

A

AA (amyloid associated), Reactive amyloidosis (immunoglobulin)

135
Q

amyloidosis gross and histo

A

pale, enlarged, rounded liver edges. perisinusoidal proteinaceous material compressing hepatocytes and acting as barrier to exchange.

136
Q

5 pigments stored in liver

A

bile, lipofuscin/ceroid, haemosiderin, melanin, iron porphyrin

137
Q

kupffer cells have higher levels of which pigment? how can this be diseased in ruminants?

A

Haemosiderin, due to RBC breakdown. in rmns get ‘‘haemochromatosis’’, iron overload due to high intake. hepatomegaly, haemosiderin accumulation (Perl’s stain)

138
Q

Defect in porphyrin metabolism may cause what type of disease

A

liver-related skin photosensitisation

139
Q

bovine congenital EPO porphyria

A

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.

140
Q

Intoxication related photosensitisation

A

St.John’s Wort, buckweat, spring parsley causing photodermatitis.

141
Q

common hepatic necrosis type and histo appearance

A

coagulative. outline of cell is present, cell is shrunken and cell contents are hypereosinophilic and nuclei is fragmented.

142
Q

focal necrosis in liver due to…

A

EHV1/Toxoplasmosis - disseminated infections such as septicaemia. aggregates of necrotic hepatocytes.

143
Q

zonal necrosis in liver 3 types

A

centrolobular, mid-zonal, periportal

144
Q

phosphorous poisoning causing what zone of necrosis

A

periportal.

145
Q

Tyzzer’s disease

A

Clostridium piliforme, focal necrosis in liver.

146
Q

Rabbit viral haemorrhagic disease

A

Calicivirus, focal necrosis in liver.

147
Q

massive (diffuse) hepatic necrosis

A

whole lobe necrosis. often infarction. Hepatosis dietetica (Mulberry’s Heart Disease) in pigs. Also get oedema of gall bladder wall.

148
Q

outcomes of necrosis in liver

A

resolution by regeneration or replacement of parenchyma with fibrous scar. if destruction of reticular framework then scar formation more likely (non-functional).

149
Q

4 patterns of fibrosis

A

periportal, centrolobular, diffuse or bridging, post-necrotic scarring.

150
Q

types of bridging fibrosis

A

central-central, porto-portal, porto-central.

151
Q

hepatic cirrhosis

A

end stage liver disease, irreversible.

152
Q

3 features of hepatic cirrhosis

A

degeneration (disruption of liver architecture), regeneration (nodules), repair (bridging fibrosis, central pathogenic process).

153
Q

attempts of compensation in liver disease

A

nodule formation, bile duct proliferation, fibrosis, anastasmoses of vascular tissue.

154
Q

hepatic cirrhosis infectious causes

A

idiopathic, CAV-1 or leptospirosis persistence.

155
Q

2 parasitic causes of cirrhosis

A

fluke and ascarids.

156
Q

4 causes of cirrhosis with no infectious agent

A

chronic congestion (CHF), post-necrotic cirrhosis (toxin/infectious insult), pigment cirrhosis (haemochromatosis), biliary cirrhosis (chronic cholangitis)

157
Q

cirrhosis results (3)

A

jaundice, ascites, hepatoencephalic syndrome (hyperammonia in blood)

158
Q

3 types of jaundice

A

pre-hepatic, hepatic and post-hepatic

159
Q

pre-hepatic jaundice

A

'’haemolytic jaundice’’. high UNCONJUGATED bilirubin in blood.

160
Q

causes of pre-hepatic jaundice

A

infectious (EIA, lepto, haemolytic streps, anthrax, snake venom), internal haemorrhage, icterus neonatum (lack of glucornyl transferase)

161
Q

hepatic jaundice

A

intrinsic liver damage. toxic substances or infectious agents. high unconjugated bilirubin usually, can get bile blockage so possibly some bilirubin high.

162
Q

post-hepatic jaundice

A

obstructed bile flow. high conjugated bilirubin in blood.

163
Q

2 major groups of hepatic failure

A

1) synthesis, catabolism, detoxifying, secretion/excretion 2) CHO, proein and lipid metabolism.

164
Q

results of hepatic failure

A

jaundice, hypoalbuminaemia, coagulopathy, hyperammonia, hepatic encephalopathy, portal hypertension and ascites.

165
Q

hepatic encephalopathy pathogenesis

A

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

166
Q

hepatic encephalopathy lesions

A

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.

167
Q

3 acute characterstics of hepatitis

A

degeneration and necrosis of hepatocytes, leukocyte infiltration in periportal CT or sinusoids, if septicaemia related then kupffer activation.

168
Q

periportal inflammation often also presents with

A

ductular hyperplasia

169
Q

chronic hepatitis characteristics

A

periportal infiltration with lymphocytes and plasma cells.. progressive periportal fibrosis, hepatocyte apoptosis and necrosis.

170
Q

chronic active hepatitis

A

dobermans commnonly. determined by quantity of inflm and hepatocellular death. possible assoc w/ lepto, canine hepatitis, aflatoxicosis and copper. Can lead to cirrhosis.

171
Q

cholangitis/cholangiohepatitis/pericholangitis

A

biliary tree inflm, bile duct and liver inflm, inflm around around bile duct.

172
Q

cats commonly get what inflm condition associated with IBD

A

‘triaditis’… ascending inflm via common bile duct and pancreatitis. happens because pancreatic and biliary ducts fuse before entering duodenum.

173
Q

triaditis histo lesions

A

1) suppurative cholangitis 2) lymphocytic and plasmacytic periportal infiltration, bile duct hyperplasia, periportal fibrosis 3) biliary cirrhosis

174
Q

viral hepatitis causes (6), usually are secondary to…

A

CAV-1, EHV-1, CaHV1, RVHD, FCV, FIP. viraemia.

175
Q

infectious canine hepatitis

A

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.

176
Q

CAV-1 liver histo

A

intranuclear inclusion bodies, hepatic necrosis (centrilobular), oedema, haemorrhage.

177
Q

equine herpes virus hepatitis

A

EHV-1 (rarely EHV-4). Abortion (necrosis of placental attachment). Can infect foetus, get multifocal miliary necrosis, inclusion bodies seen occasionally.

178
Q

Canine herpes virus 1 hepatitis

A

(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.

179
Q

neonate puppy CaHV1 infection

A

if >2w localised infection and replication as adult form. If <1w get epithelial replication, mucosal invasion… leads to leukocyte associated viraemia.

180
Q

foetal puppy CaHV1 infection

A

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

181
Q

Rabbit haemorrhagic disease

A

Calicivirus. Massive hepatocyte necrosis, DIC (in lungs and renal glomeruli). death rapid.

182
Q

Feline systemic calicivirus

A

FCV. systemic disease, necrotising dermatitis and oedema, bronchointerstitial pneumonia and hepatic, pancreatic and splenic necrosis.

183
Q

Feline infectious peritonitis

A

Feline coronoavirus (FeCoV). viraemia, granulomatous periphlebitis, serositis and hepatitis. sometimes granulomatous-fibrinous perihepatitis. Due to immune-complex deposition.

184
Q

abscess and granuloma causing organisms of the liver

A

Francisella tularensis, Nocardia asteroids, Actinobacillus spp, Mycobacterium spp, Fusobacterium necrophorum.

185
Q

necrobacillosis in liver

A

F. necrophorum. Rmns with rumenitis-liver-syndrome. ulcerative rumenitis followed by transmission to liver via blood.

186
Q

Tularaemia

A

Francisella tularensis (ZOONOTIC). vector is ticks. localised infection, lymphadenitis, bacteraemia, ulceration of LN, peyer’s patches, hepatitis.

187
Q

Yersiniosis

A

Yersinia pseudotuberculosis (ZOONOTIC). enteric infection, invasion of peyer’s patches, microabscesses, liver/kidney/spleen dissemination.

188
Q

Tuberculosis in liver

A

M. bovis/M. tuberculosis/M. avium. Miliary hepatic necrosis with multifocal granulomatous inflammation.

189
Q

Leptospirosis agents (3)

A

L. canicola, L. icterohaemorrhagica, L. grippotyphosa. (ZOONOTIC).

190
Q

leptospirosis patho

A

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.

191
Q

leptospirosis histo

A

rounded hepatocytes, eosinophilic granular cytoplasm, dark shrunken nuclei, loss of cords (dissociation).

192
Q

Clostridium piliforme

A

zoonotic. proliferative intestinal ulcerations and necrotising colitis/typhilitis. if immunosuppressed can spread to liver and cause necrosis. important in foals.

193
Q

protozoal infections of liver

A

toxoplasma, coccidiosis, leishmaniasis

194
Q

toxoplasma hepatitis

A

T. gondii. tachyzoites seen in hepatocytes. multifocal necrosis with no cysts in liver.

195
Q

coccidiosis hepatitis

A

Eimeria stiedai (hare/rabbit). replicate in bile duct, cause bile duct proliferation

196
Q

leishmaniasis hepatitis

A

replication in Mp, rupture of cells, infect new. Granulomatous hepatitis.

197
Q

metazoan hepatitis

A

flukes (F. gigantic, hepatica) tapeworm (Dicrocoelium dendriticum). eosinophil/granulomatous hepatitis and fibrinous peritonitis.

198
Q

consequences of parasitic hepatitis

A

hepatic dysfunction, hypoproteinaemia, debilitation and death. 1) heal by granulation tissue, fibrosis 2) black disease (latent spores of Cl. novyi activate). 3) chronic fascioliasis.

199
Q

chronic hyperplastic cholangitis with peribiliary fibrosis and calcification may indicate what disease

A

fluke

200
Q

hepatophilic and serosophilic cysts differ in the liver because…

A

serosophilic are on the serosal surface (e.g. T. hydatigena), hepatic are within (e.g. E. granulosus).

201
Q

milk spot liver

A

ascaris suis. chronic eosinophil-dominated periportal infiltration.

202
Q

difference btw obligate or idiosyncratic toxins

A

obligate lead to predictable toxic effects. idiosyncratic are unpredictable and differ btw individuals.

203
Q

direct effects of liver toxins

A

oxidation of membrane lipids, denaturing of structural proteins, inhibition of enzymes.

204
Q

indirect effect of liver toxins

A

blocking of receptor or transport protein, modification of proteins, free radical production.

205
Q

overall effects of liver toxins

A

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.

206
Q

site of damage for toxic liver injury

A

zone 3 - highest levels of CP450 and lowest levels of oxygenated blood.

207
Q

hepatocyte detoxification methods (3)

A

1) biotransformation (conjugated and hydroxylation) 2) carrier systems (biliary excretion) 3) kupffer activation`

208
Q

zone 1 domination toxin

A

direct acting e.g. metal salts. centriacinar location.

209
Q

acute toxic hepatosis gross and histo

A

gross - ascites, oedema of gall bladder wall, petechial haemorrhage in serosa (DIC). histo - centrilobular to massive necrosis, often with fatty or hydropic change.

210
Q

early v late stage acute toxic hepatosis

A

early = degenerate/necrotic hepatocytes. later = dilated, blood-filled sinusoids.

211
Q

one time submassive necrosis due to toxins in liver…

A

regeneration is possible

212
Q

one time massive nerosis with reticular framework disruption

A

fibrosis (repair)

213
Q

chronic or recurrent toxins effects…

A

chronic active hepatitis, cirrhosis.

214
Q

copper toxicosis which species

A

sheep, cattle (holstein/jersey), pigs, bedlington terriers

215
Q

3 MOA for copper toxicosis

A

excess intake, reduced excretion or familial disposition.

216
Q

sheep copper toxicosis

A

low dietary intolerance, reduced excretion apparatus.

217
Q

pasture problem with copper

A

contamination with poultry/swine slurry or slug/snail pellets.

218
Q

problem with giving pig/cattle feed to sheep

A

copper levels too high.

219
Q

Mo/Sulphur levels in soil can cause

A

usually bind to copper and form complexes.

220
Q

pyrrololizidine alkaloids in Aus can cause

A

hepatotoxic problems

221
Q

Sheep breeds most susceptible

A

Merino, Texel, North Ronaldsay

222
Q

pathogenesis of copper intoxication and histo

A

> 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.

223
Q

familial copper toxicosis

A

bedlington terrier, Cu accumulates in zone 3, progressive hepatitis and cirrhosis. focal hepatitis, chronic active hepatitis, fibrosis.

224
Q

stain for copper

A

Rhodanine

225
Q

which sheep breed is most susceptible (<5ppm) to copper

A

North Ronaldsay

226
Q

Senecio, crotolaria, heliotropium all contain

A

pyrrolizidine alkaloids

227
Q

pyrrolizidine alkaloids MOA of disease

A

converted to pyrrolic esters - interact with DNA/RNA bases -> cause hepatic fibrosis and cirrhosis.

228
Q

histo of pyrrolizidine alkaloids. why do you get megalocytosis?

A

single cell necrosis, megalocytosis, inflm + fibrosis, bile duct proliferation, hepatoencephalopathy. Megalocytosis is regenerative attempt, due to inhibition of mitosis, but not of protein synthesis.

229
Q

Aflatoxicosis toxin and species. pathogenesis?

A

Aspergillus flavus/parasiticus and Penicillium puberculum. toxin is furanocumarin. toxic, carcinogenic, teratogenic, mitosis inhibiting, immunosuppressive. liver changes are similar to seneciosis.

230
Q

blue-green algae poisoning

A

Microcystis aeruginosa (cyanobacteria). acute hepatoxicity, centrilobular to massive necrosis with haemorrhage.

231
Q

Non-neoplastic benign nodular hyperplasia

A

common in old dogs, usually multiple, expanding compressing adjacent tissue.

232
Q

non-neoplastic regenerative nodules

A

common in old dogs. adjacent tissue often fibrotic, loss of lobular architecture.

233
Q

hepatocellular adenoma

A

single, sharply delineated, no portal areas or lobular structure. compressing normal tissue.

234
Q

hepatocellular carcinoma

A

compression and invasion of adjacent tissue, metastasis into portal vessels. growth either trabecular, acinar or solid.

235
Q

bile duct adenoma

A

often cystic, single, sharply delineated.

236
Q

bile duct carcinoma

A

commonly spread along biliary tracts, metastasis common to hepatic serosa, LN and lungs. induces desmoplasia and so get scirrhous reaction.

237
Q

which tumour commonly metastasises to liver?

A

mammary carcinoma.

238
Q

how can tumours spread to liver commonly?

A

serosal contact, blood spread.

239
Q

which blood vessels supply the pancreas? which ducts does the pancreas use to secrete enzymes?

A

cranial mesenteric and coeliac arteries. drained by portal veins. major and minor pancreatic ducts, differ btw species.

240
Q

sheep and goats pancreatic arrangement

A

ONLY have MAJOR duct

241
Q

pigs, cattle and dog pancreatic arrangment

A

ONLY have MINOR duct

242
Q

cats pancreatic arrangement

A

MOST have MAJOR but SOME have BOTH

243
Q

horses pancreatic arrangement

A

BOTH MAJOR and MINOR

244
Q

what opens into the major duodenal papilla?

A

major pancreatic duct AND bile duct

245
Q

cholecystokinin and secretin stimulate - where are they produced?

A

secretion of enzymes from pancreas and water/bicarbonate. produced in duodenum in response to acid and distension.

246
Q

how does the pancreas prevent itself from autodigestion (6)

A

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.

247
Q

what is the major protease produced by the pancreas, where and how does it become active?

A

trypsin - in gut becomes activated by trypsinogen.

248
Q

which cells are present in the islets of langerhans? (6)

A

alpha, beta, delta, PP, D1, ECL cells.

249
Q

juvenile pancreatic atrophy occurs in? how does it look in histo?

A

young dogs (eg GSD). true atrophy not hypoplasia, only affecting exocrine tissue. islets are fine. causes EPI (exocrine pancreatic insufficiency)

250
Q

what may cause pancreatic haemorrhages

A

coagulation disorder, CAV-1 in dogs, toxins e.g. Dicumarol (rat poison).

251
Q

3 infectious causes of pancreatitis

A

CAV-1, FIP, FMD.

252
Q

parasitic pancreatitis cause

A

migrating strongyles

253
Q

zinc poisoning in cattle and sheep can cause

A

pancreatitis

254
Q

what may cause a difference in necrotising or fibrosing pancreatitis?

A

acute (necrotising) or chronic (fibrosing) disease.

255
Q

acute necrotising pancreatitis

A

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.

256
Q

necrosis of what tissue is common with acute necrotising pancreatitis?

A

fat necrosis.

257
Q

histo of acute necrotising pancreatitis and clinical signs

A

focal necrosis, haemorrhage, thrombosis, oedema. inflm infiltrates and fat necrosis in omentum, mesentery and pancreas. acute V+/D+, dullness, thirst, abd pain.

258
Q

what is common cause of death in acute necrotising pancreatitis?

A

DIC due to consumption of please protease inhibitors.

259
Q

chronic fibrosing pancreatitis

A

result of survival of acute pancreatitis or in cats without cause. fibrous tissue replacing damaged tissue.

260
Q

why are cats at risk of pancreatitis

A

bile duct duses with pancreatic ducts.

261
Q

what is EPI? when does it occur? 4 causes?

A

exocrine pancreatic insufficiency. >80% of tissue lost. causes: hypoplasia in calves, juvenile atrophy in dogs, chronic pancreatitis in cats, neoplasia.

262
Q

clinical signs of EPI

A

Diarrhoea, weight loss, pancreatogenic maldigestion (pale, soft, voluminous malodorous faeces/steatorrhea).

263
Q

serum trypsin-like immunoreactivity (TLI) assay is used to diagnose

A

EPI

264
Q

non-neoplastic growth of pancreas

A

nodular hyperplasia. older patients.

265
Q

what is more common in the glandular tumours of pancreas?

A

adenocarcinoma more common. arise in centre of pancreas. grey/scirrhous tissue. aggressive and metastatic.

266
Q

if islet is amyloid filled and secreting multiple hormones it is usually

A

endocine tumour.

267
Q

insulinoma present as

A

hyperinsulinaemia, hypoglycaemia, neuro signs

268
Q

gastrinoma present as

A

hypergastrinaemia, Zollinger-Ellison syndrome (mucosal ulceration of stomach)

269
Q

glucagonoma present as

A

hyperglycaemia, diabetes mellitus

270
Q

primary diabetes mellitus could be caused by

A

neoplastic destruction of pancreatic tissue, necrosis following inflammation.

271
Q

cats with primary diabetes mellitus…

A

islet amyloidosis (associated w/ obesity).

272
Q

cattle with primary diabetes mellitus

A

chronic FMD/BVD

273
Q

how is sex differentiation controlled

A

chromosomal, gonadal, hormonal. SRY most important.

274
Q

which ducts form in males and females for repro

A

mullerian (paramesonephric) for female. wolffian (mesonephric) for male.

275
Q

Turner’s syndrome

A

XO (or XXX) = hypoplastic females

276
Q

Klinefelter’s syndrome

A

XXY = hypoplastic males

277
Q

freemartinism

A

ovarian dysgenesis. male/female twins, testis determining factor and anti-mullerian hormone shared between both - hypoplastic female calf.

278
Q

reasons for intrafollicular or traumatic ovarian haemorrhage

A

physioogical (can be lethal in mares) or manual enucleation of CL

279
Q

follicular cysts arise from

A

non-ovulated follicle. cause excess oestrogen secretion

280
Q

ovarian surface epithelium tumours

A

papillary cystadenoma and papilary cystadenocarcinoma

281
Q

ovarian stroma tumour

A

granulosa cell tumour

282
Q

ovarian germ cell tumours

A

dysgerminoma and teratoma

283
Q

terms for fallopian condtions

A

hydrosalpinx, salpingitis, pyosalpinx

284
Q

post-partum hypocalcaemia often associated with

A

uterine prolapse

285
Q

difference between endometrial hyperplasia in ungulates and dog/cat

A

ungulates mainly oestrogen reliant, dog/cat is progresterone acting on oestrogen-primed endometrium.

286
Q

terms for inflm of uterus

A

metritis, endometritis, perimetritis, panmetritis.

287
Q

suppurative endometritis another name for

A

pyometra

288
Q

pyometra bitch/queen

A

bacterial infection following hyperplastic endometrium. E.coli, Proteus, Staphs and Streps

289
Q

pyometra cows

A

persistant CL. Tritrichomonas foetus subsp. venerealis, Arcanobacterium pyogenes, E.coli, Pseudomonas aeruginosa, Streps and Staphs

290
Q

pyometra mares

A

indepenent of persistent CL. Strep zooepidemicus, E.coli, Pseudomonas aeruginosa, Klebsiella pneumoniae, Pasteurella

291
Q

uterine tumours (3)

A

leimyoma, leimyosarcoma, adenocarcinoma

292
Q

rabbits get which common uterine tumour

A

adenocarcinoma

293
Q

foetal mummification occurs when

A

no infection, fluids are resorbed.

294
Q

foetal maceration and emphysema due to

A

infection - campylobacter foetus and tritrichomonas foetus

295
Q

why is gravid uterus prone to infection

A

progesterone influence, secretions and immuno-privelaged

296
Q

Brucellosis cattle

A

Brucella abortus. notifiable. oedema and necrosis of cotyledons.

297
Q

brucellosis pigs, sheep/goat, dog

A

Brucella suis, Brucella melitensis and Brucella ovis, Brucella canis

298
Q

campylobacter cattle and sheep

A

C. foetus sbsp. venerealis (Cattle), C. foetus sbsp. feotus or C. jejuni (sheep).

299
Q

chlamydia abortion

A

chlamydia psittaci/abortus

300
Q

protozoal abortions

A

toxoplasma and neospora

301
Q

viral abortions cattle and horses

A

BVDV, BDV, EHV1

302
Q

viral abortions swine

A

porcine parvovirus, porcine reproductive and respiratory virus, porcine circovirus 2

303
Q

infectious pustular vulvovaginitis 3 agents

A

IBR, EH3 (ECE), Trypanosoma equiperdum

304
Q

necrotising vaginitis and vulvitis agent

A

F. necrophorum

305
Q

3 vaginal/vulval tumours

A

leimyoma, fibroma, transmissible venereal tumour

306
Q

haematogenous mastitis agents

A

Brucella and TB

307
Q

which organism does cows immunity decrease with age for mastitis?

A

streptococcuus agalactiae

308
Q

3 streptococcal mastitis

A

strep agalactiae, strep dysgalactiae, strep uberis

309
Q

S. aureus, S. intermedius, S. hyicus are all

A

mastitis causing, coagulase positive staphs

310
Q

gangrenous mastitis is caused usually by

A

staphylococcal organisms

311
Q

toxic mastitis usually

A

coliforms e.g. e coli. see bloody milk discharge due to endotoxin microvasculature damage

312
Q

Summer mastitis agents

A

Truperella pyogenes. Combined with S. dysgalactiae, Peptococcus indolicus, Bacterioides melaninogenicus, Fusobacterium necrophorum

313
Q

sheep/goat galactogenic entry mastitis

A

s. aureus or p. haemolytica

314
Q

sheep/goat wound entry mastitis

A

C. pseudotuberculosis or Arcanobacterium pyogenes

315
Q

contagious agalactiae in goats mainly

A

Mycoplasma agalactiae

316
Q

types of mammary tumours

A

simple (one cell type) or complex (2 cell type) adenomas.

317
Q

mixed mammary tumour

A

epithelial and mesenchymal components (e.g. bone, cartilage, fat).

318
Q

the most and least malignant mammary tumours

A

most = anaplastic carcinoma. least = non-infiltrating carcnoma

319
Q

feline mammary hypertrophy + hyperplasia

A

fibroadenomatous change. bening. oedema and fibrous stroma.

320
Q

2 testicular developmental disorders

A

hypoplasia and cryptorchidism

321
Q

orchitis/epididymitis causes

A

streps, staphs, e.coli, arcanobacterium.

322
Q

horses testicular inflm

A

equine viral arteritis and salmonella abortus equi

323
Q

sheep testicular inflm

A

C. pseudotuberculosis, Y. pseudotuberculosis and Brucella ovis

324
Q

Dogs testicular inflm

A

E.coli, Proteus, Brucella canis

325
Q

cattle testicular inflm

A

brucella abortus, mycobacterium bovis

326
Q

testicular tumours (4)

A

seminoma (germ cell - white/grey), Sertoli cell tumour (white/grey - feminisation), Leydig cell tumour (yellow/orange - vacuolated histo), teratoma

327
Q

prostatic tumours

A

adenocarcinoma or non-differentiated carcinoma

328
Q

prostatic hyperplasia

A

bilateral and symmetrical. can impede defaecation

329
Q

phalloposthitis and balanoposthitis

A

penis + prepuce , glans penis and prepuce

330
Q

penis tumours in bulls

A

fibropapilloma (BPV1)

331
Q

penis tumours stallions

A

squamous cell papilloma, sarcoid (BPV1), squamous cell carcinoma

332
Q

dog penis tumours

A

transmissible venereal tumour

Pathology Semester 1 (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions