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Systemics- GI > Fungi and miscellaneous > Flashcards

Fungi and miscellaneous Flashcards

1
Q

Histoplasma capsulatum is a _____________; When does histoplasma capsulatum cause GI disease?

A

Dimorhic intracellular fungus; Usually granulomatous pneumonia, spreads to GI if systemic

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2
Q

Key histo with histoplasma

A

Oval yeast with basophilic center and clear halo

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3
Q

Histoplasma virulence factors

A

Melanin
Surface polysaccharides
Inhibit phagosome acidification

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4
Q

Three presentations of eosinophilic granulomas in cats

A
  1. Eosinophilic granuloma (linear)
  2. Eosinophilic plaque- pruritic, no flame figures
  3. Indolent ulcer *** classic gross
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5
Q

Who gets chronic eosinophilic enteritis? Often part of what syndrome?

A

Horses; Multisystemic epitheliotropic syndrome

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6
Q

Other lesions associated with multisystemic epitheliotropic disease in horses?

A

Eosinophilic granulomatous pancreatitis and eosinophilic dermatitis

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7
Q

Key gross with hypertrophic gastritis

A

Thickened rugal folds

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8
Q

Key histo with hypertrophic gastritis

A

Epithelial hyperplasia with parietal cell loss and replacement by mucus cells, lymphoplasmacytic inflammation

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9
Q

Who is affected by mucoid enteropathy; presentation?

A

Rabbits, weanlings; gastric bloat, mucus discharge, cecal impaction

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10
Q

Key histo with mucoid enteropathy

A

Goblet cell hyperplasia in ileum and colon, luminal mucin, no inflammation

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11
Q

What layer is primarily affected by emphysema intestinalis? In who?

A

Submucosa, gas filled lymphatics; In pigs, rabbits, manatees, turtles, lemurs

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12
Q

What is the suspected cause of Theilers disease? Classic gross?

A

Equine parvovirus (EqPV-H); Dish rag liver

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13
Q

Key histo with Theiler’s Disease

A

Hepatocyte loss and stromal collapse (no inflammation)

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14
Q

Key histo with lymphocytic cholangiohepatitis

A

Lymphocytic portal inflammation, ductular reaction, fibrosis
Periportal inflammation- piecemeal necrosis

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15
Q

Where does tissue mineralization occur in renal failure? At what concentration

A

Intercostal, middle/deep gastric mucosa (vessels, BMs); CaxP>70

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16
Q

Clin path findings with uremic gastropathy

A

Hyperphosphatemia, increased PTH, anemia, and azotemia

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17
Q

Key histo with uremic gastropathy

A

Mineralization, necrotizing colitis, glossitis, gastric ulceration

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18
Q

Effects of vitamin A deficiency

A

Impaired immunity
Photoreceptor atrophy
Odontodystrophy
Defective bone remodeling
Teratogenic

19
Q

Key histo with vitamin A deficiency

A

Squamous metaplasia of mucous membranes and glands

20
Q

Syndromes associated with vitamin E/selenium imbalance

A

Hepatosis dietetica
Yellow fat disease
White muscle disease
Mulberry heart disease
Exudative diathesis (serous effusions)
Brown dog gut (intestinal ceroidosis)
Avian encephalomal.

21
Q

Key histo with hepatosis dietetica

A

Acute centrilobular to massive hepatic necrosis, fibrinoid arteriolar necrosis, cardiac necrosis

22
Q

Predisposed animals to hepatic lipidosis

A

Shetland ponies (VLDL) with insulin resistance due to increased lipolysis
Rabbits with gastric trichobezoars
Watanabe rabbits

23
Q

What is hepatic lipidosis associated with in small ruminants?

A

Vitamin B12 and cobalt deficiency

24
Q

Who gets necrotizing sialometaplasia; which gland is affected

A

Small breed terriers and cats; mandibular salivary gland

25
Q

Key histo with necrotizing sialometaplasia

A

Coagulative necrosis, ductal hyperplasia, vascular thrombosis

26
Q

Which types of shunts are more common in large breed dogs? small breed dogs?

A

Intrahepatic; extrahepatic

27
Q

Difference between portosystemic shunt and other vascular anomalies

A

No portal hypertension or ascites

28
Q

Key histo with portosystemic shunt

A

Hepatic hypoplasia, absent portal veins, arteriole reduplication, lipidosis, lipogranulomas

28
Q

Predisposed animals to acute pancreatic necrosis

A

Cocker spaniels, obese animals, females

29
Q

What are the sequela to acute pancreatic necrosis

A

EPI and DM

30
Q

Pathogenesis of acute pancreatic necrosis

A

Lysosyme and zymogen granules fuse–>increased Ca–>trypsin activation–>autodigestion–>necrosis

31
Q

Who gets congenital/idiopathic lymphangiectasia? What are the two other parts of the syndrome in the lundehund?

A

Yorkies, Norwegian Lundehund; PLE and IBD

32
Q

Clin path findings with lymphangiectasia

A

Panhypoproteinemia, lymphopenia, hypocalcemia, and hypocholesterolemia

33
Q

Key histo with lymphangiectasia

A

Lacteal dilation and lipogranulomas

34
Q

Key histo with chronic-active hepatitis

A

Hepatocellular necrosis, degeneration, regeneration, fibrosis, mixed inflammation, piecemeal necrosis

35
Q

Who gets sialocele? Where?

A

GSD and poodles; sublingual gland, then zygomatic, then parotid

36
Q

Key histo with sialocele

A

Pseudocyst (wall of granulation tissue)

37
Q

A cat with a mass at the pylorus or ileocecocolic junction likely has; key histo

A

Eosinophilic sclerosing fibroplasia; Coarse collagen trabeculae, large spindle cells, eosinophilic inflammation

38
Q

Who gets hemochromatosis

A

Salers cattle and Mynah birds

39
Q

Clin path findings with hemochromatosis

A

Hyperferremia, hemolysis

40
Q

Stains for hemochromatosis; key histo

A

Prussian blue and Perl’s; fibrosis, hemosiderin laden macrophages, hepatic degeneration and necrosis, nodular regeneration

41
Q

Who gets FEPLOs most? Where do FEPLOs occur?

A

Boxers; Rostral maxilla and caudal mandible

42
Q

Key histo with FEPLOs

A

Odontogenic mesenchyme (periodontal ligament-like stroma with kite-shaped stellate mesenchymal cells) +/- cemento-osseous matrix and odontogenic epithelium

Systemics- GI (8 decks)

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