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ECVIM Certifier > Hepatobiliary and Pancreatic > Flashcards

Hepatobiliary and Pancreatic Flashcards

1
Q

Amino acid changes in PSS?

A

Increased aromatic: tyrosine, phenylalanine

Decreased branched chain: leucine, isoleucine, valine

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2
Q

MicroRNAs in hepatic disease?

A

Chronic hepatitis - miR-126/122/29a. 122 corr with fibrosis. Increase ET1 too
miR-200 hepatocell carc
mrR21/122 mucocoele
mrR122 gen hepatic dz (

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3
Q

Dermatological presentation of hepatic disease?

A

Superficial necrolytic dermatitis

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4
Q

Compounds associated with hepatic encephalopathy?

A

Increased: ammonia, aromatic AAs, endogenous benzodiazepines, gamma-aminobutyric acid (GABA), glutamine, phenol. short chain FAs, tryptophan, false NTs

Decreased: alpha-ketoglutarate

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5
Q

What is the half life of ALT, ALP and AST in dogs and cats?

A

ALT: 48-60/6
AST: 22h/77m (nb 20 % in mitochondria)
ALP: 70/6

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6
Q

What links ALP to cell membranes? Why is it released in cholestasis?

A

Glucosyl phosphatidyl inositol linkage

Cholestasis - bile acids detergent, increased glucosylphosphatidylinositol phospholipase activity

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7
Q

When is GGT increased?

A

Zone 1 peri portal disease

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8
Q

When do steroids start increasing ALP?

A

mRNA 24-48h, expression gene 10d

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9
Q

Mechanism of RBC changes in hepatobiliary disease?

A

Microcytosis - impaired iron transport
Target cells/poikilocytes - altered RBC cell membrane lipoprotein content/deformability
Anaemia - chronic dz, haemorrhage
Thrombocytopenia - sequestration, decreased thrombopoietin

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10
Q

Why do dogs have bilirubin in urine?

A

Can conjugate it renal - have enzymes - esp males, plus low renal threshold

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11
Q

Mechanism of ammonium biurate stones?

A

No uric acid conversion to allantoin (uricase)

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12
Q

Low USG?

A

Loss medullary hypertonicity, decreased cortisol metabolism, psychogenic

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13
Q

Glucose?

A

Decrease when 75 % liver gone - decreased glycogen stores, gluconeogenesis, insulin clearance and glucagon response

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14
Q

Increase in globulin?

A

Decreased filtration and clearance of toxins and bacteria

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15
Q

How is ammonia incorporated into the urea cycle?

A

Carbamoyl phosphate synthesise 1 (helped with nacetylglutamate)

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16
Q

What is more sens/spec - single BA, fasting NH3, pre and post BA PSS?

A

Sens - pre + post BA then ammonia then single BA

Spec - ammonia > BA

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17
Q

Urine versus serum BAs?

A

Increased specificity lower sens HEPATOBILIARY
Equivalent serum in cats

Lower sens PSS

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18
Q

Values of ammonia for PSS?

A

> 45 - 98/89 % sens/spec

Don’t do tolerance test if > 150 basal

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19
Q

What clotting factor does the liver not produce?

A

vonWB subtype of VII

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20
Q

Protein C?

A

Binds protein S to degrade V and VIII clotting factors

Decreased in PSS vs PVH

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21
Q

What is used to conjugate bile acids?

A

Glycine/taurine

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22
Q

Bile salt hepatocyte export and import?

A

Bile salt export pump (multi drug resistance associated protein 2)

Sodium dependent taurochlorate cotransporter

Ileum - apical sodium bile acid cotransporter

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23
Q

What transports bilirubin and bile acids in blood?

A

Organic ion transporting polypeptide

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24
Q

Top end normal CBD cat/dog?

A

< 4 <3

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25
Q

Sensitivity of AUS for PSS? CT?

A

80 - 100 epss, 100 IPSS

Portal vein:aorta < 0.8 v sensitive, < 0.65 - PSS

CT - 96 sens 89 spec - 5.5 x more likely than AUS

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26
Q

AUS with MAPSS? Sensitivity?

A

Left dorsal renal, 60 %, splenorenal

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27
Q

Contrast enhanced hepatic ultrasonography?

A

Decreased perfusion in malignant

Increased enhancement benign lesions esp late phase

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28
Q

MRI more sens PSS than CT?

A

No - less - but more specific

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29
Q

Incidence of haemorrhage after tru cut bx?

A

Cat - probably around half major haemorrhage but not corr with coags

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30
Q

Stains for liver?

A

Rubeanic acid/rhodanine - copper
Sudan - lipid
PAS - glycogen
Masson’s trichrome/sirius red fibrosis

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31
Q

Utility of FNA for liver disease?

A

Highest sens vac change and neoplasia (50 % each)

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32
Q

Tru cut liver?

A

NB vagotonic shock with autofire
Discordant with wedge half the time (better if neoplasia)

Increased concordance 14 G - more portal triads

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33
Q

Goals of therapy in liver dz?

A

Address underlying cause
Decrease or prevent inflammation, oxidative damage, fibrosis and copper accumulation
Provide nutrition
Manage complications

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34
Q

Major bile acids?

A

Chenodeoxycholic acid and cholic acid from cholesterol hydroxylation form trihydroxy bile acid taurocholate

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35
Q

Mechanism of action SAM-e

A

Synthesis of glutathione via homocysteine transmethylation and transsulfuration pathway

Prevent hepatic glutathione depletion

Modulate apoptosis, anti-inflammatory, anti carcinogenic, improve membrane structure, fluidity and function

Inhibits pro-inflamm cytokine production, prevents development of oxidative stress, improved redox status

Increases hepatic GSH (and amount of reduced GSH), decrease oxidised glutathione disulphide form

Does not prevent vacuolar hepatopathy

Decrease level of hepatic enzymes and amount of tx delay when combined with silymarin in dogs tx lomustine

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36
Q

N-acetylcysteine?

A

Formation L-cysteine, precursor of glutathione

Stabilises glutathione conc, improves redox status

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37
Q

Silymarin?

A

Flavanoligans including silybin - most biologically active around 50 - 70 %

Antiox: free radical scavenger, decreased lipid per oxidation, suppress hydrogen peroxide/superoxide/lipoxygenase, increase glutathione

Anti-inflamm: decrease TNFalpha/IL1beta/NFkappabeta, inhibit kuppffer cells

Anti-fibrotic: decrease hepatic stellate cell activity and decrease hepatic collagen expression

Might be choleretic

Increase bioavailability if give with phosphatidylcholine

Amanita phalloides tox, lomustine

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38
Q

What enzyme conjugates bilirubin?

A

UDP glucuronosyltransferase

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39
Q

Vit E mechanism?

A

Alpha tocopherol most biologically active

Antioxidant: protect phospholipid from oxidant injury, scavenge free radicals, minimise lipid peroxidation

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40
Q

Ursodeoxycholic acid?

A

Hydrophilic bile acid - displace toxic hydrophobic ones from circulating pool. Increase fluidity of bile.
Choleretic (protonated UCDA absorbed by biliary epithelial cells and leaves bicarb - bicarb draws water)
Inhibit hepatocyte apoptosis
Decrease IL1/2, B lymph AB, (immunomodulatory)
Stabilise mitochondrial function
Increase glutathione (increase methionine adenosyl transferase activity to generate SAMe)
Anti-fibrotic - NAFKB

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41
Q

D-penicillamine?

A

Copper chelator and anti-fibrotic (prevents collagen molecule cross linking)

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42
Q

Zinc?

A

Increase metallothionein synthesis by enterocytes to bind copper

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43
Q

How to manage fibrosis in hepatic disease?

A

Caused by increase in stellate cell and fibroblast activity - steroids for latter, decrease ox injury for former as increases stellate cell activity

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44
Q

What precipitates hepatic encephalopathy?

A

Increased ammonia production in the GI tract:
Poor quality poorly digestible protein, or excess protein in diet - reaches colon for bacterial degradation
Constipation
GI haemorrhage
Azotaemia (increases systemic ammonia generation)
Blood transfusion of stored blood
Protein calorie deficiency and catabolism

Factors influencing the CNS uptake or metabolism of ammonia:
Alkalosis
Hypokalaemia
Hypoglycaemia (potentiates activity and production of neurotoxins)
Inflammation (cytokines are neurotoxic and potentiate ammonia)
Sedative and GA drugs

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45
Q

What effect does ammonia have in the CNS?

A

Inhibitory. Depletes glutamate and alters glutamate receptors, impairs mitochondrial function.

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46
Q

Taurine defiency?

A

Important in cats - conjugation of bile acids, take from muscle if depleted
NB neck ventroflexion!

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47
Q

Important amino acids in cats?

A

Taurine, arginine, methionine, cysteine

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48
Q

Cell cycle inhibitors in chronic hepatitis?

A

Increase p21, cell senescence, correlated with survival.

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49
Q

Evidence for immune mediated aetiology in chronic hepatitis?

A

Lymphocytic inflammation
MHC Class II haplotype association (ESS/Dobermann)
Positive serum autoABs, antihistone ABs (Doberman)
Familial association (Dob, lab, westie)
Assoc with other immune disorders (lab)
Female (dob, lab, ess, acs)
Response to immunosuppressives

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50
Q

Age CH in diff breeds?

A

Dalmatian, dobermann and ESS younger
Lab, ECS, Cairn older

ACS younger than ECS

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51
Q

Signalment for lobular dissecting hepatitis?

A

Younger
Standard poodle, ACS, rottie, GSD, Gret
80 % have ascites

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52
Q

Best screening test for CH?

A

Increased ALT more than 2 months

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53
Q

Indicators of portal hypertension?

A

GI/gall bladder/pancreatic oedema, decreased portal vein velocity, hepatofugal flow

Decreased protein C, PV:aorta <0.65, anaemia, microcytosis, increased ammonia and bile acids

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54
Q

Difference between chronic hepatitis and lobular dissecting hepatitis on histopath?

A

Minimal inflamm in latter

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55
Q

Cirrhosis

A

Fibrosis with nodules

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56
Q

Factors to consider when predicting bleeding risk in CH?

A 
PT/aPTT 1.5 x upper RI
plt <50
PCV < 30
Fibrinogen < 100
vWF < 50 %
BMBT > 5min
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57
Q

Where should a sample for copper be collected from?

A

Least affected region

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58
Q

How many portal triads do you need to make dx?

A

12 - 15 (but sometimes don’t need that many if v obvious widespread disease)

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59
Q

Evidence for immunosuppressive tx in CH?

A

Pred:
Increased length of survival time dobermans
Complete remission around 1/3
ESS - imp enzyme bili and survival
Labs increased survival cf historic controls with combo aza - MST 630 d

Ciclosporin:
Remission in 76 %

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60
Q

What to do if granulomatous inflammation on hepatic bx?

A

Search infectious dz

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61
Q

CH survival time?

A

Around 600 d

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62
Q

Negative CH px factors?

A

Ascites (not cockers) cirrhosis, lobular dissecting hepatitis, hypoglycaemia, hypoalphaglobulin, hyperbili, decreased plt, increased coags, fibrosis, necrosis, bridging/marked fibrosis, small liver, portal lymphadenopathy, SIRS, clinical score

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63
Q

How often is copper the cause of CH?

A

Around a third depending on breed (cupric oxidation state Cu2+ is hepatotoxic, gen O2 free radicals)

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64
Q

How might copper accumulate?

A

Increased diet, primary defect in metabolism, altered biliary excretion

Toxicity depends on concentration, molecular association and sub cellular localisation

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65
Q

Bedlington?

A

Copper metabolism gene MURR1 containing domain 1) - auto recessive

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66
Q

Labrador copper mutation?

A

ATP7B/A (copper excretor, COMMD1 acts on it) ALSO DOBERMAN ATP7B

ATP7B = ceruloplasmin - biliary excretion - Wilson’s dz

NB COMMD1 NOT described in dobermans/lab
Cat - ATP7A/B

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67
Q

How often is copper accumulation detected in feline liver biopsies?

A

12 %, NB lower RI for cats

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68
Q

Major copper assoc CH breeds?

A

Bedlington, Dalmatian
Lab, doberman (female predip)
Westie, skye terrier

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69
Q

What is ATP7A?

A

Basolateral enterocyte copper transporter - upreg = more Cu absorb

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70
Q

What transports copper from the GI lumen?

A

Copper transporter 1

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71
Q

Stages of bedlington terrier copper disease?

A

Cu accum begins from 8-12w
Cu 400 - 1500, no clin/HP abn, poss Cu granules
Cu 1500 - 2000, HP inflamm
> 2000, clin signs

Could get haemolysis if copper released from hepatocytes

NB heterozygotes might start to accumulate copper then resolve at 15m

Huge amounts of copper > other breeds

72
Q

Measurement of hepatic copper?

A

< 400 normal, > 2000 required for morph/func change and clin dz

Non copper CH, copper up to 1500

Take from least affected areas, might be falsely low in regenerative nodules or fibrotic areas

Atomic absorption spectrometry needs less liver than spectrophotometric

73
Q

Copper hepatic histopath?

A

Centrilobular copper zone 3, adjacent and distant hepatocytes

Grading system (none solitary cells small groups large groups large areas diffuse) corr well with measurement - 3+

74
Q

When to use diet for copper? Chelation? Zinc?

A 
Diet:
> 600 
Chelate:
D-penicillamine, if > 1500 overall or if > 750 plus centrilobular
Zinc:
no additional benefit cf diet?

If severe lymphocytic w/ less macrophages consider immunosupp

75
Q

What collagen is increased in hepatic fibrosis?

A

I and III - cross linking
I - Masson’s trichrome
III - reticulin

Stellate cells unregulated by endothelin from sinusoidal epithelial cells and PDGF/ROS/TGFbeta from macrophages, s endothelial cells and platelets

76
Q

WSAVA classification of liver histopath in cats?

A

Acute/chronic neutrophilic cholangitis
Lymphocytic cholangitis
Destructive cholangitis
Chronic cholangitis assoc with liver fluke

77
Q

What is lymphocytic portal hepatitis?

A

Poss aging change or secondary to extra hepatic dz - NO BILE DUCT INVOLVEMENT!

80 % of cats > 10

78
Q

Most common bacteria in neutrophilic cholangitis?

A

E coli

Salmonella enterica, Klebsiella, Strep

Majority one species, more likely to culture from bile

Higher numbers of E coli on FISH cf lymphocytic. 25 % bacteria around bile ducts.

79
Q

Number of IBD and pancreatitis in NC cases?

A

83% and 50 %

FISH pos pancreas?

80
Q

Most consistently increased hepatic enzyme in feline liver disease?

A

AST

Bile acids more sensitive than any enzyme

81
Q

Clotting factor changes in feline liver disease?

A

Decreased 7 and 13

82
Q

Vitamin D in feline liver disease?

A

Decreased cholestatic liver disease, corr with WBC, most decreased in hepatic lipidosis, PTH higher

83
Q

What distinguishes cholangitis from cholangiohepatitis

A

Extension of inflammatory cells beyond the limiting plate

84
Q

Acute neutrophilic cholangitis versus chronic?

A

Minimal biliary hyperplasia and fibrosis

Bacteria may only be in larger bile ducts if very acute

Chronic - biliary hyperplasia, periductal sclerosing fibroplasia, bridging. fibrosis, bile duct rupture, bile leakage, necrosis, abscess

Can be non supp or mixed lymph/plas with variable neuts

85
Q

What feline cholestatic liver disease is most likely to be associated with pancreatitis?

A

NC, but other studies have found equal

86
Q

Chronicity feline cholestatic liver disease on imaging?

A

Hyperechoic periportal and tortuous bile ducts

87
Q

What lymphocytes in feline LC?

A

Predominance of T cells

Is Helicobacter or bartonella involved?

Persians? Older than NC?

88
Q

Most consistent LC clin path?

A

Globulins

Icterus, ascites, HE as advanced

Variable increased hepatic enzymes

89
Q

LC histopath?

A

Small lymphocytes around bile ducts, mostly periportal, often portal fibrosis/bridging fibrosis

May infiltrate bile duct and hepatic parenchyma

May get plasma cells and eosinophils

Portal lipogranulomas, portal B cell aggregates

Maybe have less intense lymph if chronic mono lobular fibrosis

90
Q

What embryonic veins form the portal vein?

A

Cranial and caudal mesenteric

80 % blood and 50 % O2 supply to the liver

91
Q

What is the cause of intrahepatic PSS?

A

Abnormal vitelline venous system development

92
Q

What is the difference between PVH with and without portal hypertension?

A

More severe or more diffuse intrahepatic vascular malformations?

93
Q

Consequences of hepatic vascular malformations?

A

No trophic factors (insulin/glucagon) for hepatic growth
Poor hepatic development, deficient protein production reticuloendothelial dysfunction, altered fat/protein metabolism, hepatic atrophy and failure

94
Q

Pathophys of hepatic encephalopathy?

A

Ammonia:
Increases brain tryptophan and glutamine - decreased ATP availability, increased excitability, increased glycolysis, oedema, decreased microsomal NaK ATPase

Tryptophan:
Direct neurotox, increased serotonin, inhibitory

Glutamine:
Altered blood brain barrier ammonia transport

SCFAs:
Decreased microsomal NaKATPase, uncouple oxphos, impair O2 utilisation, increase free tryptophan by displacing from albumin

Aromatic AAs:
Decrease DOPA neurotransmitter synthesis, altered neuroreceptors, increase false neurotransmitter synthesis

False NTs:
Tyrosine > octopamine > phenylalanine > methionine > mercaptans
Impair norepi action, synergism with ammonia and SCFA, decrease brain urea cycle, decrease ammonia detox, decrease microsomal NaK ATPase

Phenol:
From phenylalanine and tyrosine, decrease cell enzymes, neuro/hepatotox

GABA:
Inhibitory

Bile acids:
Membranocytolytic effects, alter membrane permeability, BBB more permeable to toxin, impaired cellular metabolism and cytotoxic

Endogenous benzodiazepines:
Neural inhibition, hyperpolarise neuronal membrane

Alpha ketoglutarate:
Goes down, this reduces ATP avail and less ammonia detox

95
Q

Breed feline PSS?

A

DSH Persian siamese himalayan Burmese, males maybe overep

96
Q

Inheritance of PVH?

A

Autosomal inherited Cairn

97
Q

NCPH?

A

Doberman, rottie, cocker

98
Q

Clinical signs and shunt morphology?
CNS signs most common with…?
Urinary signs most common with?

A

More caval than right azygous and more if insertion caudal to liver vs diaphragm
Most CNS splenocaval
Urinary right gastric (also older, male, hx medical management)

99
Q

Older dog EHPSS?

A

Splenonephric and splenoazygous

100
Q

Role of microcytic anaemia in PSS?

A

Defective iron transport, decreased TIBC/iron, increased Kupffer cell iron stores

Target cell dog poikilocyte cat

101
Q

Difference NCPH vs PSS?

A

Former increased bilirubin

102
Q

Clotting factor changes in PSS?

A

Decreased II, V, VII, X

103
Q

Ascites and vascular malformation?

A

AEPSS
HAVM
NCPH

104
Q

AUS sens/spec PSS?

A

74-95/67 - 100

105
Q

How to distinguish intra from extra hepatic PSS on portovenography?

A

Portal vein divergence T13

106
Q

Name some branched and aromatic amino acids

A

Aromatic - tyrosine, phenylalanine

Branched - valine, leucine, isoleucine

107
Q

Where are most HAVMs?

A

right/central, 25 % 2 lobes

108
Q

When should you suspect insufficient ligation post PSS surg (bile acids)?

A

< 50 fine, > 94 pre/post to investigate

Protein C helpful too, coags helpful too

109
Q

Hepatic function test diagnosis PSS

A

BA: postprandial up to 100 % sens, NB maltese

Ammonia: pre prand up to 88 %, post prand 6h 91 %, ammonia tolerance 95 - 100 % NB ornithine transcarbomylase deficiency

Protein C: < 70 % PSS not MVD

Hyaluronic acid: increased PSS, decreased with surg

110
Q

Factors which would raise concern for development of postoperative PH?

A

Ascites, vomiting, pain, hypotension, DIC, shock

111
Q

Problem with PSS and hypoglycaemia?

A

periop, 1/3 don’t respond to dextrose

112
Q

Incidence of PSS post op seizures?

A

12 % dogs, around half recovery

1/3 cats, half central blindness (transient)

113
Q

Surgical versus medical management for shunts?

A

Medical - half pts with MST 9m, 1/3 long term survival MST 5y
88 % dead medical versus 22 % surg

More poor px IHPSS with medical

114
Q

Histopath steroid hepatopathy?

A

Vacuolated cytoplasm and sometimes nucleus, glycogen, zone 3, generalised with chroniticty

115
Q

UCCR in scottie glycogen vac hep?

A

UCCR normal 75 %. Adrenals enlarged 25 %. GBM 16 %

116
Q

What lipoprotein is changes in feline hepatic lipidosis?

A

Increased LDL decreased HDL

117
Q

Prognostic factors in feline hepatic lipidosis?

A

Negative - old, anaemic, secondary cause

No assisted feeding

118
Q

Acetominophen tox?

A

NAPQI (bioactivated by cp450 and detox by glutathione conjugation - acute centrilobular hepatic necrosis

Dose dependent

Cats - absence of VGTI16 and ABCG2 transport export

119
Q

Phenobarbital tox?

A

Poss secondary bio activation/hepatotox other drugs as induce cp450?

Dose dependent, cumulative

Bridging portal fibrosis bile duct hyperplasia nodular degeneration.

Serum conc = risk factor

120
Q

Azole antifungals?

A

N-deacetylketoconazole = tox metabolite, covalent bind liver protein, deplete glutathione

Fluconazole and decrease dose less tox

121
Q

Azathioprine?

A

Oxidative metabolites, depletion antiox, gen by xanthine oxidase

GSD at risk?

122
Q

Amiodarone?

A

MDSA ox metabolite, uncouple oxphos

123
Q

Lomustine

A

Mech?

Median 4 dose and 350mg/m2 - cumulative

Boxers and young dogs

Portal haemosiderin Kupffer cells

124
Q

Tetracycline?

A

Inh beta oxidation of FAs in mitochondria and inhibit lipoprotein secretion

125
Q

Potentiated sulphonamide?

A

Idiosyncratic - nitroso metabolites, covalent protein binding, haptens

Hepatic necrosis

126
Q

Caprofen

A

Always ALT increase, never ALP, idiosyncratic

Bridging necrosis

Lab

127
Q

Methimazole

A

Ox metabolite Nmethylthiourea gen flavin monooxygenases, glutathione depletion

Centrilobular necrosiis

128
Q

Diazepam?

A

> 5d use, centrilobular necrosis/biliary hyperplasia

129
Q

What might impair phenobarbital clearance?

130
Q

Amanita phalloides tox?

A

Inh RNA polymerase, decreased protein synthesis and necrosis of metabolically active cells, hepatic and renal tubular necrosis

Silybin decreases uptake by OATP1B3, prevents fatality

131
Q

Blue green algae?

A

Microcystin and nodularin, inhibit serine/threonine protein phosphatase, hyperphosphorylation, cytoskeletal disruption

Hepatic necrosis, glutathione depletion

Cholestyramine might bind the toxins

Nodularin does renal tubular necrosis

132
Q

Cycad palm

A

Seeds most tox but all parts of plant.

Cyasin bioact to methylazoxymethanol by gut bacteria

Cycad AAs neuro toi

Centrilobular necrosis and neut inflamm

133
Q

Cholelithasis in dogs and cats?

A

Dogs - calcium rare are canine GB can absorb free calcium. Cholesterol/bilirubin

Cat - cholesterol, bilirubin, calcium

134
Q

Risk factors for cholelithiasis?

A

increased hydrophobic cholesterol in bile, bile stasis, hypertrig/bili, endocrine dz, cholesterol transportation/absorption defects

135
Q

Timing of biliary tree dilation in cholelithiasis?

A

GB 24h, extrahepatic bile ducts 24-48h, intrahepatic 5-7d

136
Q

Common bacteria in canine cholangitis?

A

E coli, enterococcus, clostridium, bacteroides, strep

Bile culture pos 60 %

137
Q

How well do cyto/culture agree with gall bladder aspirate?

A

Almost perfect if no AB, 85 % otherwise

138
Q

Gall bladder abnormalities and culture?

A

Sensitive but not specific

139
Q

Bacteria associated with emphysematous cholecystitis?

A

E coli, clostridium perfringens

140
Q

Leptin?

A

Increased in GBM dogs

141
Q

Causes of GBM?

A

Hyperplasia of mucus secreting glands and mucous accumulation
Impaired GB motility - accumulation of bile salts (stim mucous), DM/hT4/HAC decrease gall bladder emptying
Increased unconjugated bile acids - HAC, hydrophobic, epithelial injury and mucin secretion
Impaired relaxation sphincter of Oddi - hT4, impaired relaxation. Also altered cholesterol metabolism and. decreased bile secretion
Sheltie and imidacloprid
ABCB4 transporter mutation (phosphaditylcholine across canalicular membrane) - alter bile composition?

142
Q

Bile acids and GBM?

A

Taurochenodeoxycholic acid and deoxycholic acid stim mucin secretion

Unconjugated chenodeoxycholic acid and deoxycholic acid increased in HAC

Taurocholic acid/taurodeoxycholic acid/taurochenodeoxycholic acid conjugated

2 primary bile acids = cholic acid and chenodeoxycholic acid

Secondary BAs (unconjugated) - deoxycholic acid, ursodeoxycholic acid, lithocolic acid

143
Q

Positive culture in GB mucocoele cases?

A

9 - 66 %

Enterococcus, enterobacter, E coli, staph, strep

144
Q

UCDA in GBM?

A

Might increase canalicular transporters which could be helpful in gene defect

Decreases mucin formation and decreases formation cholesterol crystals

145
Q

Negative prognostic factors GBM?

A

Clinical for disease, increased ALT, hyperbili, decreased alb, phosphate, ALP, azotaemia , rupture

146
Q

Best place to culture in GBM?

A

FISH GB wall most sens

147
Q

Border terrier GBM?

A

Transglutaminase 21gA autoABs

148
Q

Cobalamin half life in dogs?

149
Q

Components of cobalamin receptor in ileum?

A

Cubam, amnionleess

150
Q

Where do GI bacteria produce cobalamin?

A

Colon - after receptors

151
Q

Cobalamin biliary recycling?

A

Bile haptocorrin

152
Q

Cobalamin storage?

A

Liver and kidney

153
Q

Renal cobalamin handling?

A

Cobalamin reabsorbed by megalin PCT - cobalamin/transcobalamin II complex

Cubam - renal resorption of albumin, transferrin and vit D binding protein

154
Q

Consequences of cobalamin deficiency?

A

Lack of methylmalonyl CoA mutase activity increases methylmalonic acid and decreased n-acetyl glutamate therefore decreased carbomyl phosphate synthetase activity

Lack of methionine synthase activity - decrease methionine, increase homocysteine, decrease tetrahydrofolate, increase 5 methyl tetra hydrofolate

Homocysteine - neurotox, hepatic degeneration and fibrosis, Heinz body anaemia

Methylmalonic acid - neuro, and ammonia neuro

CBC - anaemia neutropenia hyperseg neut megaloblastic

155
Q

What might increase homocysteine or methylmalonic acid in the absence of cobalamin deficiency?

A

Renal cardiac disease, decreased alb, delayed serum separation

Renal insufficiency dehydration SIBO URINE - bacterial contamination

156
Q

What is holotranscobalamin?

A

Cobalamin plus TCII - measured in humans

157
Q

Immerslund grasbeck syndrome?

A

Hypoglycaemia, hyperammonaemia, ketoacidosis, oral lesions, anaemia, proteinuria (renal cubam for reabsorption)

158
Q

Beagles and cobalamin?

A

Cubulin mutation

May get degenerative liver disease (hyperhomocystinaemia?)

Immunosupressed - ?decreased phagocytic activity

159
Q

Border collie and cobalamin?

A

Cubulin, less severe beagle, delayed onset

160
Q

Giant schnauzer and cobalamin?

A

Amnionless mutation (more like border collie than beagle)

161
Q

Aussie shephard cobalamin?

A

Their own amnionless mutation (border collie more than beagle presentation)

162
Q

Komondor cobalamin?

A

Autosomal recessive cubulin splice variant

163
Q

Other causes of B12 deficiency

A

Hyperthyroidism (not functional), hAC, multi centric lymphoma, dysbiosis

NB Bacteroides can use cobalamin bound to intrinsic factor

164
Q

What cobalamin supplementation is thought to be most effective?

A

Hydroxycobalamin

165
Q

Risk factors for pancreatitis?

A 
Hypertriglyceridemia
Maybe SPINK (contraversial) no CFTR or PRSSI
Endocrine - hAC hT4 DM
166
Q

What is cathepsin B?

A

Activator of trypsinogen

167
Q

Effect of feeding in pancreatitis?

A

Decreased hospitalisation time (may not decrease mortality?)

168
Q

Does organophosphate toxicity cause pancreatitis?

A

In dogs but probably not cats (experimental)

169
Q

Low fat feline pancreatitis?

A

Not necessary - they need arachidonic acid from omega 6 FAs

170
Q

Mode of inheritance in EPI

A

Not simple auto recessive

171
Q

Pathophys canine EPI

A

Atrophy - probably subclin immune med first - T lymph infiltration

172
Q

Breeds?

A

GSD, rough collie, eurasian

chow, ckcs, whwt

173
Q

Alternative EPI diagnosis?

A

Faecal pancreatic elastase 1 (resistant to GI absorb) - nb false pos

174
Q

Why might bacterial overgrowth decrease fat absorption?

A

Deconjugate bile salts, decrease activity

175
Q

Cobalamin and EPI?

A

Decreased survival if marked decrease

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