Sys Path Trivia Flashcards

1
Q

Phylloerythrins

A

Phylloerythrins are green photoactive catabolites of plant porphyrins that are normally excreted in bile. Retention of phylloerythrins = photosensitive dermatitis.
iii) Inherited: abnormalities in porphyrin metabolism

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2
Q

Glucuronic acid

A

Conjugated by the enzyme UDP-glucuronyl transferase to substances such as drugs, pollutants, bilirubin, androgens, estrogens, mineralocorticoids, glucocorticoids, fatty acid derivatives, retinoids, and bile acids - conjugation (acts like a detergent to make toxic substances soluble so they can be excreted by the kidneys).

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3
Q

Superficial necrolytic dermatitis

A

unique cutaneous manifestation of some forms of chronic liver dx (hepatocutaneous syndrome) in dogs. Crusting, ulceration and necrosis of epidermis. Mechanism is thought to be related to an abnormal metabolic state due to hepatic insufficiency.

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4
Q
Liver colour changes
White/pale yellow
Yellow-orange
Black (diffuse focal)
Red (diffuse focal)
Pale tan/brown
A

white or pale yellow =fat; necrosis; cellular infiltrate; fibrosis

  • yellow-orange (turns green in formalin) = BILE
  • Black – diffuse = hemosiderin or melanin-like pigments
    • focal = melanosis or liver fluke
  • red- diffuse = congestion
    - focal = telangiectasis(capillary dilation) or hemorrhage
  • pale tan/brown = diffuse inflammatory or neoplastic infiltrate; amyloid
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5
Q

cytochrome P450

A

enzyme that metabolizes lipids, drugs etc

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6
Q

cytochrome reductase

A

It catalyzes the reduction of cytochrome c by oxidation of coenzyme Q (CoQ) and the concomitant pumping of 4 protons from the mitochondrial matrix to the intermembrane space

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7
Q

Hepatic glycogenosis

A

buildup of glycogen in hepatocytes (?)
(glucocorticoid-induce or “steroid” hepatopathy): Common in dogs, associated with exposure to glucocorticoids (hyperadrenocorticism).

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8
Q

Cirrhosis pathogenesis - Process

A

Pathogenesis: initiated by “reparative” processes following episodes of hepatocellular necrosis and inflammation

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9
Q

Space of Disse

A

The space of Disse (or perisinusoidal space) is a location in the liver between a hepatocyte and a sinusoid. It contains the blood plasma. Microvilli of hepatocytes extend into this space, allowing proteins and other plasma components from the sinusoids to be absorbed by the hepatocytes.

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10
Q

periacinar

A

Zone 3,hepatocytes are furthest from the portal triad (afferent oxygen rich blood) & nearest the outflow

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11
Q

Intrahepatic arterivenous fistula

A

= usually multiple, dilated vessels on capsular surface, atrophy of adjacent parenchyma.

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12
Q

Amanita mushrooms

A

toxic cyclopeptides; dogs; massive hepatic necrosis

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13
Q

Alsike clover

A

Consumption as pasture or hay is associated with biliary fibrosis/cholangiohepatitis. Pathogenesis unknown.

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14
Q

Pathogenesis for chronic copper toxicosis in the liver of a Bedlington terrier

A
  • accumulation of Cu in hepatocyte lysosomes; cytoplasmic Cu overflow toxic to cell
  • leads to the production of free-radicals
  • diffuse single cell necrosis over time → chronic hepatitis
  • icterus, ascites, weight loss
  • occasional copper release and haemolytic crisis
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15
Q

Primary liver neoplasms

A

⇒ Hepatocellular adenoma (benign), hepatocellular carcinoma (malignant): often solitary. Carcinoma = local invasion; may metastasize to local LNs, lung, peritoneal cavity.
⇒ Bile duct adenoma, bile duct carcinoma: uncommon (older dogs) = locally invasive, may metastasize widely. Must be differentiated from metastatic carcinomas of extrahepatic origin
⇒ Primary mesenchymal tumors –RARE

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16
Q

Most common cardiac anomalies

A
  • DOG: PDA, pulmonic stenosis, aortic/subaortic stenosis
  • CAT: left AV valvular dysplasia
  • CATTLE: VSD, aortic transposition
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17
Q

Viral/bacterial/protozoal causes of heart disease

A

Viral causes: Parvo, Distemper, Foot & mouth
Protozoal: Toxoplasma, Neospora, Trypanosoma cruzi (Chaga’s disease)
Bacterial:
1. H. somni (cattle: animals partially immune don’t have pneumonia or encephalitic form – instead myocaridis)
Bacteremic/septicaemia – localized in left interventricular septum (in papillary muscle) → septic infarct and arrhythmia and death; vasculitis w/ infarction
2. Clostridium chauvoei (blackleg)
Only a couple significant bacterial causes – keep in mind at PM
3. Immune mediated causes -> Human – rheumatic fever

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18
Q

Vascular disease
Cattle
Cats
Horses

A
  • Infectious agents (direct: H. somni)
  • Cattle: Acute BVD, MCF
  • Cats: FIP (wet form: fibrinoid necrosis & vasculitis)
  • Horses: African horse sickness (ddx: equine viral arteritis)
  • Direct attack of vascular endo cells via the virus (not a true 1˚ vasculitis)
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19
Q

Causes of arterial mineralization

A
  1. Metabolic: VitD toxicity, Johne’s disease
    • HyperCa states ↑ VitD (which → ↑ Ca)
  2. ‘Dystrophic’: vascular injury of many causes -> 2˚ to necrosis of tissue e.g. Strongyles valargearis in horses
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20
Q

Neoplasia

A

Hemangiosarcoma - dogs

Lymphangiosarcoma - cats

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21
Q

What cells do detox in the lungs?

A

Clara cells & type II pneumocytes convert drugs into highly reactive intermediates, which are detoxified and excreted.

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22
Q

Pulmonary IV macrophages – present in alveolar septal wall – w/n capillaries in what species?

A

• Mo in blood vessels of cat, horse, ruminants, pigs; NOT in dogs, rodents, humans

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23
Q

Innate factors in the lungs

A

o Surfactant pr A & D
o Defensins (host-defense peptides)
o Lactoferrin – binds iron away from pathogens
o Lactoperoxidase (natural antibacterial agent)

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24
Q

Examples of failure of lung defences (6 examples)

A

o Overwhelm defences – VERY large amt of agents introduced
o Viral and mycoplasma infection → impair function of cilia, secretory epithelium, PAM
o Stress impairs macrophage function and impairs immune response
o Neutropenia: parvoV, BVDV, chemotherapy etc
o Air-borne pollutants → may ↓ m-a-c
o Genetic disorders: ciliary dyskinesia (congenital; seen in some breeds of dog, cats, pigs) → chronic resp disease etc

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25
Q

3 examples of pathogens in bronchitis

A

Bacterial (heaves), viral (influenza), allergy

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26
Q

Exception to the cranio-ventral broncho-alveolar pattern

A
  • Actinobacillus pleuropneumoniae (middle/caudal) -> pigs
  • In small animals may look patchy
  • BRSV- viral bronchopneumonia
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27
Q

Bronchiolitis obliterans fibrosa

A

intrabronchial polyps
a. If exudate can’t be removed- organized by fibroblast infiltration, collagen production, neovascularization, re-epithelialization→ airway obstruction

28
Q

Primary lung tumours

A
o	Primary pulmonary carinomas (cats, sometimes dogs)
o	Granular cell tumours (horses)
o	Lymphoma (all species)
29
Q

Cats resp diseases
Primary:
Secondary:
Other:

A
Cats resp diseases
Primary: • Viral respiratory infections
• Bacterial pneumonia
• FIP
• Paragonimus
Secondary:  
• Aleurostrongylus abstrusus
• Empyema
• Cryptococcosis
• Calicivirus
• Bordetella
Other: 
• Mycoplasma felis 
• Toxoplasmosis
30
Q

Cattle resp diseases
Primary:
Secondary:
Other:

A
Primary: 
• Pneumonic pasteurellosis
• Mycoplasma bovis
• Bovine respiratory syncytial virus
• Infectious bovine rhinotracheitis
• 3-MI toxicity
• Aspiration pneumonia
Secondary:• Parainfluenza, coronavirus
• Embolic pneumonia
• Dictyocaulus
• Tuberculosis
• Interstitial pneumonia of feedlot cattle
• Histophilus
pleuritis 
Other: • Ascaris suum larval migration
• Contagious bovine pleuropneumonia
31
Q

Swine resp diseases
Primary:
Secondary:
Other:

A

Primary:
• Porcine reproductive and respiratory syndrome
• Mycoplasma hyopneumoniae
• Swine influenza
• Actinobacillus pleu-
ropneumoniae
• Polyserositis
Secondary: Porcine circovirus (PMWS), atopic rhinitis (Bordetella bronchiseptica and Pasteurella multocida?), pasteurellosis
Other: Pseudorabies (herpes), Porcine respiratory coronavirus, Inclusion body rhinitis(herpes), Metastrongylus, Actinobacillus suis

32
Q

Horses resp diseases
Primary (5):
Secondary:
Other:

A
Primary: 
• Rhodococcus equi
• Strangles/ Streptococcus equi
• Equine influxenza
• Equine viral rhinotracheitis
• Heaves 
Secondary: • Interstitial pneumonia of foals
• Guttural pouch mycosis
• Exercise-induced pulmonary hemorrhage
• Pleuropneumonia
Other: 
• Equine rhinoviruses
• Equine adenovirus
• Dictyocaulus arnfieldi
• Pneumocystis carinii
33
Q

Sheep resp diseases
Primary:
Secondary:
Other:

A
Primary: 
• Maedi-visna/ ovine progressive pneumonia
• Muellerius capillaris
• Pasteurellosis
Secondary: 
• Respiratory syncytial viruses
• Mycoplasma spp.
• Oestrus ovis
• Transmissible nasal carcinoma
Other:  Pulmonary adenomatosis, pestes de petites ruminants
34
Q

Dog resp diseases
Primary:
Secondary:
Other:

A
Primary: • Blastomycosis
• Pulmonary neoplasia
• Bacterial pneumonia
• Aspergillosis
• Nasal carcinoma
• Herpesvirus
Secondary:  
• ARDS
• Pulmonary thromboembolism
• Pyothorax
Other: 
• Eosinophilic lung disease
• Kennel cough
• Tracheal collapse
• Oslerus oslerii
• Crenosoma vulpis
• Canine distemper
35
Q

Pneumoconiosis

A

Chronic inhalation of inorganic substance causing pulmonary fibrosis

36
Q

Most common primary lung tumour in cats

A

Adenocarcinoma, metastasizes to footpads

37
Q

3 sites for blasto other than lungs

A

Bone, eyes, skin

38
Q

Paragonimus kellicotti

A

Causes cyst-like nodules in the lungs of cats. From crayfish. Mistaken for tumours “Kill a cat-e”

39
Q

Aleurostrongylous abstrusus

A

soft nodules, generalized or dorso-caudal region. Common in cats, usually not causing serious disease.

40
Q

What are the 3 important features of Wallerian degeneration? (3 marks)

A
Axonal swelling (spheroids)
Myelin swelling
Digestion chambers (myelin macrophages
41
Q

Leiomyoma

Leiomyosarcoma

A

Erector pili muscle tumour (smooth muscle)

42
Q

Grading scheme for mast cell tumours

A
Anisocytosis
Anisokeriosis
Mitotic Rate
Granularity
Location
(I is best with 90% survival at 3-4 years)
43
Q

What is a common site of predilection for squamous cell carcinoma in horses & cats?

A
  1. Horses: 3rd Eyelid, penis prepuce, white areas, scars
  2. Cats: Ear tips, nasal planum, lower palpebrae, oral mucosa
  3. Dogs: pharynx, subalveolar gingiva (?)
44
Q

Non-agressive canine mouth lesions

A

Epulis, fibromatous epulis, gingival hyperplasia, inflammatory other benign lesions of the oral cavity.

45
Q

Aggressive canine mouth lesions

A

Squamous cell carcinoma
Acanthomatous ameloblastoma
Malignant melanoma
Fibrosarcoma (basically any malignant neoplasm)

46
Q

Causes of hypercalcemia - tumour

A

Secretion of calcium-­mobilizing substance (ex: PTH-­rP, IL-­1, TNF) by tumor cells
• Example ­‐ Anal sac carcinoma, apocrine gland carcinoma, lymphoma
• This would also ↓ P dt renal excretion (mimics PTH)

Lymphoma, adenocarcinoma of apocrine glands in anal sac, plasma cell myeloma, malignant bone
tumors, mammary adenocarcinomas, etc.
Early: ↑ Ca, ↓ P
Later: ↑Ca, ↑ P

47
Q

What causes Pyelonephritis in pigs? in cats?

A
Eubacterium suis (sows, porine contagious pyelonephritis)
Decending e.coli infection
48
Q

Hypercalcemia nephropathy - what is it? what if it is chronic?

A

Hypercalcemia→ inactivates adenylate cyclase→ disrupts Na transport in the loop of henle. Also interferes with ADH receptor

Chronic hypercalcemia→ renal mineralization of the tubular BM, epithelial cells, interstitium→ blood vessels and glomeruli.

49
Q

Vasopressin control (ADH)

A

Secreted if:

  1. reduced plasma volume is activated by pressure receptors in the veins, atria, and carotids.
  2. increases in plasma osmotic pressure is mediated by osmoreceptors in the hypothalamus.
  3. increases in plasma CCK (released after eating) is mediated by an unknown pathway.
50
Q

Aldosterone control/activity

A

Aldosterone release causes sodium and water retention

Controlled via renin/angiotensin by baroreceptor MAP and sodium content

51
Q

Pituitary gland - what is made where?

A
Anterior lobe (pars distalis) (adenohypophysis) = hormones: GH, ACTH, prolactin, FSH, LH, TTH, TSH
Posterior lobe (pars nervosa) (neurohypophysis): ADH, oxytocin
52
Q

Causes of hyperadrenocorticoidism in dogs

A

Most often a functional Corticotroph (pituitary) adenoma – 85%

15% primary functional Adrenal Tumors
• Carcinomas and Adenomas
• Adrenal Cortical Hyperplasia- chronic stimulation of ACTH
–> Can be due to long term Cortisol administration

53
Q

Urine cortisol to creatinine ration

A

Used as a screening test for hyperadrenocorticism. Only useful if no renal disease.

54
Q

Hirsuitism

A

excessive hairiness

55
Q

Horses with hyperadrenocorticism - most common cause? Test?

A

Adenoma in the pars distal secreting ACTH.
Dex test contraindicated due to laminitis risk
ACTH is better test.

56
Q

Clinical signs of addisons:

A

o hyperkalemia (therefore CV dysfunction)
o hyponatremia and hypochloremia (less Na and Cl absorbed)
o hypovolemia/ dehydration and hemoconcentration due to increased water excretion by kidneys, because of increased Na loss
o vomiting/diarrhea because of electrolyte imbalance
o muscle weakness because of inability to utilize glucose

57
Q

a) Indicate 2 abnormalities typically found on the routine biochemistry profile of hyperthyroid cats.
b) Indicate 2 abnormalities typically found on the routine biochemistry profile of dogs with hyperadrenocorticsm.

A

a) Increased urea, creatinine, ALP, ALT, P (producing more waste products, PU/PD so sodium loss, phosphorus retention?)
b) Increased ALP, ALT, cholesterol, glucose
(steroid damage to the liver, more fats & sugars)

58
Q

Serum Na:K ration in hypoadrenocorticism

A

o Serum Na:K of <23:1 indicative (less Na absorbed - less aldosterone)
Note: need to rule out renal failure, diarrhea, vomitting, and other Ddx

59
Q

Phaeochromocytomas

A

o chromaffin cell tumors (the cells that secrete epi and norepi)
o most common in dogs and cattle
o can be invasive or metastatic
o rarely functional tumors
o if are→edema, CV collapse and arrhythmic episodes

60
Q

What decreases T4? Increases

A

Decreases: GCs, NSAIDs, Phenobarbital, Androgens, Sulfonamides
Increases: Halothane, Insulin, Narcotic analgesics, prostaglandins

61
Q

Pancreas - secrete what from these endocrine cells in the islets of langerhans? A, B, D, F, G

A

A cells: glucagon (stim GNG and lipolysis, increases blood glucose)
B cells: insulin (stim liver, muscle and adipose storage of glycogen and fat, dec blood glucose)
D cells: somatostatin-regulates the release of other islet hormones
F cells: pancreatic polypeptide (inhibition of pancreatic exocrine secretion)
G cells: gastrin (stim of acid secretion)

62
Q

Steps in muscle degeneration & death (5?)

A
  1. Myofiber swelling, hypereosinophilia
  2. loss of striation, coagulation, fragmentation
  3. tension bands
  4. mineralization
  5. Macrophages come in to clean up mess/necrotic tissue
63
Q

Process in muscle atrophy

A

Myofibres become smaller by loosing myofibrils→eventual loss→ fat replacement→ fibrosis

64
Q

Muscle regeneration process

A

Involves sarcolemmal tube and satellite cells.
Satellite cells divide→ myoblasts→ myoblasts proliferate→ form myotube→ enlarge and differentiate (central nuclei)→ nuclei peripheralize and reposition

65
Q

Bacterial myosities causes for various species

A

o Streptococcus equi in horses,
o Arcanobacterium pyogenes in cattle
o Corynebacterium pseudotuberculosis (CLA) in sheep,
o Streptococcus canis (necrotizing fasciitis) in dogs,
o Actinobacillosis (wooden tongue, lumpy jaw) in cattle are but a few of the more common.
Clostridial myositis is very important in ruminants
• Clostridium chauvoei- blackleg.

66
Q

Causes of primary axonopathy & demyelination

A
1. Primary Axonopathy
•	Organophospate toxicosis
•	Laryngeal hemiplegia in horses
•	Diabetes mellitus
2. Primary Demyelination
•	Lead toxicosis
•	Immune mediated (MS)
•	Acute polyadiculoneuritis (coonhound paralysis)
•	Vaccine induced from H1N1
•	Hypothyroidism 
•	Myelin loss affects spinal cord causing ataxia in neonates