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RACP > Gastro > Flashcards

Gastro Flashcards

1
Q

What is the most common cause of cryoglobulinemia?

A

Hep C
- cryoglobulins are present in 25% of those with Hep C, but clinical features only present in 15% of cases

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2
Q

When choosing between tenofovir and entecavir for hep B, what factors would affect your decision?

A

Tenofovir: pregnant, previous resistance to lamivudine
Entecavir: osteoporosis

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3
Q

Hepatitis B

Risk factors for developing HCC and cirrhosis

A

Male
family hx
co infection with HCV, HIV, HDV
older age
habitual alcohol consumption
HBV genotype C
core promoter mutation

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4
Q

Indication for starting treatment in HepB

A
  1. If HBeAg positive, DNA >20,000 and persistently elevated ALT or fibrosis
  2. If HbeAg negative, DNA >2000 and persistently elevated ALT or fibrosis
  3. Any pt with Cirrhosis and any detectable DNA –> treat regardless of ALT

High risk chemo (Rituxumab):
- if evidence of previous infection, then needs treatment for at least 18 mo after chemotherapy

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5
Q

Tenofovir

A

IS A: NRTI

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6
Q

TAF > TDF

A

preferred in HBV-HIV co infection
reduced renal SE

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7
Q

H. pylori tx resistances

A

Metronidazole (30%)>Clarithromycin (10%)>Amoxicillin> levofloxacin

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8
Q

Microscopic colitis

More common than coeliac disease (50-70x)

A

Mean age 65, FEMALE
Aggravated by: NSAIDs, aspirin, PPIs
3 subtypes: collagenous, lyphocytic, incomplete

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9
Q

why is hep B antiviral not effective in treating hep D

A

the antivirals will suppress viral DNA, but won’t clear the surface antigen. Hep D uses the surface antigen for virulence

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10
Q

PSC

A

MALE
75% cases associated with IBD
HLA A1, B8 and DR 3
Average age of onset 40
pANCA, hypergammaglobulinemia

measure IgG4 in new PSC, as IgG4 associated cholangitis can be indistinhuishable from PSC

Complications of PSC:
-cholangiocarcinoma
GB cancer
Cirrhosis
DEKA def
Metabolic bone dx
Colon ca if UC present
Cholangitis

Tx:
Stent
Screen
Liver Tx

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11
Q

Suffix of Hep C drugs

previr
asvir
buvir

A
  1. proteasome inhibitor
  2. NS5a inhibitors
  3. NS5b inhibitors
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12
Q

Factors that have been associated with a higher likelihood of spontaneous clearance of HCV include:

A

●The presence of specific HLA-DRB1 and DQB1 alleles
●High titers of neutralizing antibodies against HCV structural proteins
●Host neutralizing responses that target viral entry after HCV binding
●The persistence of an HCV-specific CD4 T-cell response
●White patients with relatively low peak levels of HCV viremia during acute infection
●Female sex
●Infection during childhood
●Symptomatic acute infection

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13
Q

MELD score

Stratifies severity of end-stage liver disease, for transplant planning

A

Dialysis
Creat
Na
INR
Bilirubin

> 15 would benefit from transplant

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14
Q

Liver transplant

Complications

A

**- Acute cellular rejection:
30%, portase based inflammation. obstructive LFTs

Immunosuppression:
CNI: tac/CyA - nephrotoxic, HTN, DM (Tac), Lipids, Neuro (Tac), Tremor, hirsutism
MMF - GI upset, leucopenia
Steroid wean

Failure:
Early (<3/12):
-** Infection (bacterail, CMV, fungal)**
> leading cause of death post-tx
- Biliary stricture
- Graft failure (rare)
- Renal/diabetes/cosmetic

*CMV risk is higher +/- (Proph: oral valganciclovir)
*PCP proph: Co-trim

Late (>3/12)
- Cancer: skin, PTLD
- Vascular (AMI)
- Renal
- Recurrent disease
- Osteoporosis

Rejection:
1. Acute (30%): portal based inflammation (cholestatic LFTs)
>7-10 days
>tx with steroids

  1. Chronic (rare)
    > months to years
    > Vanishing bile duct syndrome (cholestatic LFTs)
    > tx: increase immunosuppression

Recurrence: essentially all except metabolic sx confined to liver

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15
Q

VBDS

A

Complication of drug induced liver injury
**Chronic cholestatis **and loss of intrahepatic bile ducts
Manifests as chronic liver rejection

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16
Q

IBD

Extraintestinal manifestation associated with disease activity

A

Oral ulcers
erythema nodosum
large joint arthritis
episcleritis

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17
Q

IBD

Extraintestinal manifestation independent to disease activity

A

Ankylosing spondylitis
Uveitis
PSC
pyoderma gangrenosum
Kidney stones
gallstones

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18
Q

Common mutation in haemochromatosis

A

C282Y (homozygous)
it accounts for 90% of the disease, but only 10% develop clinical iron overload

Hepcidin: iron brake
upregulated by IL-6

Manifestation of haemochromatosis:
Bronzing of skin
Hypogonadism (improves)/hypothyroidism
CM (improves)
Cirrhosis/HCC
Arthritis/arthropathy (pseudogout -does not improve)
Diabetes - does not improve with phleb

Transferrin saturation >45% is indicative of disease. Most sensitive screening tool

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18
Q

Common mutation in haemochromatosis

A

C282Y (homozygous)
it accounts for 90% of the disease, but only 10% develop clinical iron overload

Transferrin saturation >45% is indicative of disease. Most sensitive screening tool

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19
Q

5-ASA

A

used in UC
rectal+oral>rectal alone > oral alone
potential benefit in reducing risk of CRC

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20
Q

Can weight loss cause improvement in liver histology

A

yes

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21
Q

Gastric vs oesophageal varices

A

Gastric is harder to treat
Medical therapy with betablocker is less effective
banding and injection do not work for gastric
Cyanoacrolyte glue is mixed with lipiodiol to manage gastric varices endoscopically using a super glue mixture

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22
Q

What’s the treatment for Hep D

A

IF for 48wks

  • hepatitis D is unlike hepatitis B in the sense that patients may be surface antigen negative. VIral load therefore must always be tested.
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23
Q

Which class of HepC treatment is CI in decompensated cirrhosis

A

Protease inhibitors

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24
Q

What is the mechanism of increased resistance in portal HTN?

A

increased fibrosis
decreased NO

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25
Q

Autoimmune hepatitis

A

HLA DR3 and DR4/8
very steroid sensitive
associated with hypergammaglubulinemia (2x IgG level)
AST >10x or AST >5x

Type 1: ANA, Anti smooth muscle, Anti actin b (adults/children), 99% specific, sens 43%
Type 2: Anti LKM 1 (children only), 99% specific
Type 3: Soluble liver-kidney antigen - middle age adults

Raised IgG level

liver biopsy: inflammation extending beyond limiting plate ‘piecemeal necrosis’, bridging necrosis

Tx:
1. steroids if symptomatics
2. +/- Azathiopurines

Normalisation of lab takes >12months

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26
Q

SBP primary prophylaxis indication

A

bili >50 with impaired renal function
Low protein <10g/L in ascites

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27
Q

When should you test HCV antibodies after birth?

A

15-18 months after

  • Hepatitis C antibody testing should not be done immediately after birth due to maternal transmission of antibodies
  • Whilst hepatitis C RNA is transmitted via breast milk this does not cause an increased risk of transmission.
  • Hepatitis b and HIV have much higher rates of vertical transmission compared to hepatitis C.
  • the risk of hepatitis C transmission is higher in patients who have HIV co-infection.
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28
Q

RF for hepatotoxicity in paracetamol overdose

A

age >40
malnutrition
CYP2c1 inducers (carbamazepine, phenytoin)
Hypophosphataemia is protective

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29
Q

Which medical therapy has shown to reduce mortality in variceal bleed?

A

Terlipressin

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30
Q

Contraindication for TIPSS?

A

portal vein thrombosis, hepatic encephalopathy, advanced HCC, pulm HTN

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31
Q

Notable HepB genotypes

A

B: slow, low activity of disease
C: associated with higher rates of HCC and cirrhosis
F: associated with fulminant liver disease

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32
Q

VIPoma

A

This is a rare neuroendocrine tumor typically of the pancreas and with high malignant potential.

The clinical syndrome of watery diarrhea, hypokalemia, acidosis, hypochlorhydria, and hypercalcemia.

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33
Q

Which of the following is associated with higher risk of variceal bleeding?

A
  • Childs Pugh C
  • Alcohol use
  • Red wale sign present endoscopically
  • high portal pressures >12mmHg
  • Hx of prev variceal bleed
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34
Q

What is PNPLA3 mutation associated with?

A

alcoholic disease and NAFLD

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35
Q

Hep B immune tolerance /clearance/control/Escape

A
  1. High HBV DNA, HBeAg +ve, normal LFTs
  2. High HBV DNA, HBeAg +ve, Abnormal LFTs
  3. Low HBV DNA, HBeAg -ve, normal LFTs
  4. High HBV DNA, HBeAg -ve, Abnormal LFTS
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36
Q

Which phase of Hep B should you start treatment?

A

Immune clearance and Immune escape

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37
Q

Comment on the use of betablockers in SBP

A

associated with reduced survival and increased rate of hepatorenal syndrome

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38
Q

eosinophilic esophagitis

A

For patients who opt for a PPI, the clinical response should be evaluated after an eight-week course of treatment with repeat endoscopy.

PPIs and corticosteroid therapy are effective therapy with similar efficacy.

six-food elimination diet can improve symptoms and esophageal eosinophilia and help identify causative foods. As a result, a six-food elimination diet is a reasonable primary option for adults

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39
Q

RF for developing oesophageal adenocarcinoma?

A

Being male, elderly, caucasian and obese

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40
Q

Gastric acid secretion from parietal cells is regulated by

A

endocrine (gastrin)
paracrine (locally delivered histamine and somatostatin)
neural (acetylcholine)
autocrine (transforming growth factor-alpha) factors

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41
Q

PG tx

A
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42
Q

What’s in Child Pugh score?

A

Albumin28-35
Bilirubin 20-30
PT/INR
Ascites
Encephalopathy

1 year survival:
A: 100%
B: 80%
c: 45%

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43
Q

NOD2/CARD15

A

Associated in IBF (crohn’s)
- early surgery due to stricturing disease

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44
Q

Use of combination Aza/Infliximab in mod-sev UC

A
  • increased CS free survival
  • Better mucosal healing
  • Improvement in mayo score
  • Reduction in faecal calprotectin

REDUCED serious infection cf. aza alone

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45
Q

Anti IF vs anti parietal

A

Anti IF 100% specific, low sensitivity
Anti parietal: high sensitivity, less specific

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46
Q

MMA
Homocystein

A

MMA is elevated in B12 def, not folate
HomoC is elevated in both

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47
Q

What kind of LFTs does Cotrim induced liver injury produce?

A

Cholestatic

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48
Q

RF for severe crohns at diagnosis

A
  • steroids at diagnosis
  • perianal dx
  • <40
  • Smoking
  • high ASCA titre
  • NOD2
  • UGI involvement
  • strictures
  • deep ulcers
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49
Q

RF for severe UC

A

<40
extensive disease
PSC
high pANCA titre
deep ulcers

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50
Q

What does itraepithelial lymphocytosis a feature of

A

microscopic colitis
- chornic diarrhoea
- tx: budesonide, may need MTx for maintenance)

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51
Q

MTX should never be used in which type of IBD

A

UC

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52
Q

Which IBD tx is likely to cause acute pancreatitis?

A

Azathiopurine
- usually around 3 weeks from starting tx

Other aza related:
Serum like sickness
Myelosupression - dependent on 6TG level
Hepatitis (related to 6MMP, dose dependent)

Non-melanoma skin cancer
Lymphoma: >65, young male w EBV neg

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53
Q

What’s the treatment choice for perianal fistula in CD

A

Infliximab

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54
Q

Indications for colectomy in UC

A

dysplasia
fluminant colitis/toxic megacolon
failure of medical therapy

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55
Q

Common complication of colectomy

A

Pouchitis
- 1/3 will develop it
- 2/3 of above will develop recurrent pouchitis
- of that, 1/4 will develop chronic pouchitis
Criteria: Diarrhoea >6/da, endoscopic: oedema, granularity, friability, loss of vascular pattern, mucosal haem, or ulceration (4)
Polymorphonuclear leucocyte infiltrate and percetnage of ulceration

Female infertility
Incontinence
Pouch failure

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56
Q

Barrett’s

A

Precursor to oesophageal adenocarcinoma
- metaplasia of squamous to columnar
- RF: chronic GORD, Age>50, overweight, high SES, alcohol, smoking

  1. after initial dx –> repeat scope in 1 year to check for dysplasia
  2. if no dysplasia on 2 scope biopsies: 3 year FU
    -> if no dysplasia –> long term PPI

If low grade dysplasia: repeat scope in 1 year
if high grade dysplasia –> surgical resection
if not medically fit: 3 monthyl scope or endoscopic ablative therapy

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57
Q

Oesophageal varices

Endoscopic band ligation vs sclerotherapy

A

Rapid onset of benefit
Lower rate of complications
reduced mortality and rebleeding

58
Q

Which gastric varices have higher tendency to bleed?

A

IGV 1 (Fundus)
>GOV1 or GOV2 or IGV2

59
Q

What is the difference in efficacy between nonselective beta blockers and endoscopic band ligation in med - large varices?

60
Q

Contraindication to liver transplant

A
  1. cardiopulm disease that cannot be corrected
  2. Malignancy outside of the liver <5yrs - not including superficial skin cancers
  3. Active alcohol or drug use (must be abstinent for 6 months)
  4. raised ICP in acute liver failure

AIDS/Age/Obesity are relative CI

61
Q

PRSS1 - what is it associated with

A

Chronic pancreatitis

62
Q

Pancreatic cysts that are precursor to pancreatic cancer

A

Mucinous cystic neoplasm
IPMN
NET

pseudocyst
serous cystoadenoma are both benign

63
Q

RF for pancreatic cancer

A

Smoking
Chronic pancreatitis
CF
BRCA2 >BRCA1
LYNCH sx
Peitz-Jeghers syndrome
Hereditary pancreatitis
FAMMM
FDR - MORE = HIGHER RISK

9% SURVIVE 5 YEARS

64
Q

H. pylori

A

gram negative curved rod with flagella

  • duondenal ulcers
  • worse gastritis
  • CagA= more virulent, produces VacA cytotoxin *antiCagA ab can cross react with platelet antigen –> ITP)
  • reduced oesophageal cancer
  • Eradication ==> long term remission of PUD
  • Resistance:
  • Clarithromycin 94%, Metronidazole 68%
  • Tx: Amoxil, tetracycline, bismuth +/- levofloxacin

only give triple therapy if clarithro resistance is <15% and known

in the absence of knowledge about resistance, USE QUADRUPLE THERAPY for 14 days

65
Q

TXA in pts with acute GI bleed

A

no change in death, transfusion, intervention, but increased risk of venous events

66
Q

Should you change aspirin to clopidogrel if somone bled on aspirin

A

NO
A + clopi is safer than clopi alone
weird right!

67
Q

PUD: bleeding risk based on endoscopic finding

A

Spurler > NBVV> clot > dot > clean base

68
Q

Benefits of therapeutic endoscopy

A
  • control active bleeding (90%)
  • Reduce rebleeding
  • improve morbidity
  • reduce mortality

Adrenaline + Endoscopic secondary haemostatic modality (any) –> improves all outcomes

69
Q

Post endoscopic PPI

A

High dose PPI infusion for 72hr:
improves rebleeding in 3 days, 30 days, morbidity, surgery, mortality at 30d
LOS
transfusion need

70
Q

PO vs IV PPI

A

similar rebleeding rate and transfusion requirements, and mortality

71
Q

what should you do with aspirin if you are using it for secondary prevention CVD and you have a GI bleed?

A

start aspirin within a week
There is a increase risk of bleed at 4 weeks, but higher death if you don’t

72
Q

eradication testing

A

atleast 4 weeks after tx
WH abx and bismuth >28 days
WH PPI >14 days

Tests: urea breath test, faecal antigen test
serology takes 2 years to clear

73
Q

Antiplatelet agents in high risk pts with GI bleed

A
  • restart APA on day 3
  • if onDAPT:
  • continue aspirin
  • if low risk stigmata (Forrest 2c/3) continue DAPT
74
Q

OAC and GI bleed

A

Dabi and Riva (not Apixaban) has higher bleeding cf warfarin

INR <2.5 can scope with warfarin

Best cumulative survival data would recommend restarting 1-2 weeks

75
Q

Coeliac disease

A

Histology: villous atrophy
intraepithelial lymphocytosis
Cryot hyperplasia

Anti TTG is test of choice (but check IgA level)
Anti-endomysial IgA (is also specific)

IgG test: Anti-DGP, Antiendomysial IgG, Anti TTG IgG

Associated with T1DM and other autoimmune
HLA DQ2/DQ8
Down’s syndrome, Turner’s, William’s
Pancreatitis

There is an increases risk of SB adenocarcinoma

76
Q

Coeliac disease

Diet

A

Avoid wheat, rye, barley
Oat crossreactivity is rare

77
Q

Coeliac disease

Vitamin/element deficiency

A

Fe deficiency
Fat soluble vitamin DEKA
B12
Folate
Copper def
Vitamin def –> bone dx in 25%

78
Q

Coeliac disease

Monitoring

A

Anti-TTG 3-6 monthly, then annually
histological can take years

Non-responsive:
- persistent sx, lab despite 6-12 gluten avoidance
- causes:
>inadvertent gluten ingestion
>other food
>SIBO
>Microscopic colitis
>IBS
>refractory CD

79
Q

Eosinophilic esophagitis

A

sx: dysphagia and food impaction, CP, heartburm, abdominal pain, refractory GERD

Solid>fluid

Common in young men
Assoc:
with CBZ hypersensitivity syndrome

Histology:
>15 intraepithelial eos/HPF
>Basal zone hyperplasia
>dilated intercellular spaces

Endoscopic:
Longitudinal furrows
Oedema
reduce vasculature
excudate
concentric rings
strictures

Tx:
> 6 food elimination diet: Milk, wheat, eggs, soy, nuts, fish/shellfish
> then reintroduce one at a time

> Elemental diet: 93% response

> most respond to PPI (?NERD vs antiinfl effect of PPI)
Topical steroids: fluticasone, budesonide, ciclesonide
Dilation: 7% risk of perf, 75% risk of CP, bleed

80
Q

Achalasia

Post op GORD - which surgical procedure has higher rates

81
Q

Barrett’s

Risk factors

A

Male, caucasian, age, overweight, chronic heartburn GORD sx for 1 week, increases risk of adeno by 7x, smoking, FHx

82
Q

Barrett’s

Treatment

A

**PPI: **reduces progression to HDG or OAC. by 71%

High dose PPI +aspirin reduces progression

Surgical therapy is no more beneficial than high dose PPI

83
Q

Whipple’s disease

A

rare multi-system disorder caused by Tropheryma whippelii infection

HLA-B27 +ve and middle aged men

Features
malabsorption: diarrhoea, weight loss
large-joint arthralgia
lymphadenopathy
skin: hyperpigmentation and photosensitivity
pleurisy, pericarditis
neurological symptoms (rare): ophthalmoplegia, dementia, seizures, ataxia, myoclonus

Investigation
jejunal biopsy shows deposition of **macrophages **containing Periodic acid-Schiff (PAS) granules

Management
guidelines vary: **oral co-trimoxazole **for a year is thought to have the lowest relapse rate, sometimes preceded by a course of IV penicillin

84
Q

Hepatic encephalopathy

Prognostic implication is not associated with the amount of ammonia

any rise >2xULN doesn’t contribute to worsening HE

A

Ammonia is produced by enterocyte from glutamine. Healthy liver clears the ammonia by converting it to glutamine
muscle can also remove ammonia peripherally

hypokalaemia increases renal ammonia production

85
Q

Hepatic encephalopathy

Treatment:

A

Lactulose
Rifaximin

Protein restriction is not recommended - can substitute to vegetable protein

86
Q

SAAG

A

> 11 g/L or 1.1
= portal HTN, alcoholic hepatitis, HF etc

<11 or 1.1
- malignancy
- TB
- serositis
- nephrotic sx
- pancreatitis

87
Q

Ascitic fluid

A

WCC >500 = abnormal
Nt >250/mm3 = peritonitis
if bloody, subtract 1 nt for 250 RBC

TP <10g/L = high risk for SBP
Low glucose: bacteria, WCC, malignant cell consumption

Perforation: if 2/3
TP >10
Gluc <2.8
LDH >ULN for serum

Cytology: 100% positive in peritoneal carcinomatosis

88
Q

SBP

A

> 250 PMN/mm3
Bacteria: E.coli and Klebsiella are the most common

Tx:
Cefotaxime 2gram Q8H for 5/7, fluoroquinolones - Early abx saves lives

Hold NSBB in frail, hypotensive pts

prophylaxis:
- Hx of SBP: Cotrim or fluroquinolone
- IP with ascites with TP <10-15: only during hospitalisation
- Cirrhosis with GI bleed: Ceftriaxone 1g, then Cotrim or cipro for 7 days

Use of PPI in pts with liver disease - increases risk of SBP slightly

88
Q

SBP

A

> 250 PMN/mm3
Bacteria: E.coli and Klebsiella are the most common

Tx:
Cefotaxime 2gram Q8H for 5/7, fluoroquinolones - Early abx saves lives

Hold NSBB in frail, hypotensive pts

prophylaxis:
- Hx of SBP: Cotrim or fluroquinolone
- IP with ascites with TP <10-15: only during hospitalisation
- Cirrhosis with GI bleed: Ceftriaxone 1g, then Cotrim or cipro for 7 days

Use of PPI in pts with liver disease - increases risk of SBP slightly

89
Q

What’s the normal portal pressure?

90
Q

Portal pressure and complications

A

10: GO varices
12: Variceal bleed
16: decomp-> mortality
20: faillure to control bleed -> low 1 year survival
22: marked increase in mortality

91
Q

Gastroesophageal varices

A

30% mortality with each bleed, 70% will rebleed in 1 year
40% of pts with cirrhosis will have varices
Porto-hepatic pressure grad >12mmHg

Tx:
1. Primary prevention: Screen yearly
>NSBB or endoscopic variceal ligation

  1. Secondary prevention: Endoscopic ligation + NSBB
    > STOP BB in pt with SBP <90, AKI or hyponatraemia <130

Risk of variceal bleed: 5-15%/year
- related to** variceal size **
- risk amplified in progression of Child-pugh score and red wale marks, red sign
- alcohol abuse
-** HVPG >12mmHg**
previous bleed 60-70%

92
Q

Variceal bleed

A
  1. Resuscitation
    >Hb 70-80
  2. Antibiotic prophylaxsis - reduces mortality
  3. Lower the portal pressure
    >Terlipression (only one to improve mortality) cf. octreotide, sandostatin
    >TIPSS
    >Surgical shunt
  4. Occlude the varix
    - **Glue **is superior to banding (only if experienced)
    < pitfall: too quick or too much –> embolisation, too slow = needle in varix
    - Ligation is superior to sclerotherapy
    - Other: balloon tamponade (Sengstaken Blakemore tube), esophageal
  5. PPI post banding (reduce post banding ulcers)

aim endoscopy withnin 12hr

93
Q

Haemostasis in bleed in liver disease

A

IV vit K
Treat infection
Optimise renal function
Consider DIC (dem. FVIII)
Cryoprecipitate (fibrinogen, VIII, XIII, vWF)
PCC and rcom activated FVII has not proven to improve outcomes
Plt >50,000
Hyperfibrynolysis: TXA and epsilon aminocaproic acid

94
Q

UGIB

A
  • most common is Non-variceal bleed and most is PUD
  • Aim Hb 70-90 (improves survival, reduce further bleed, and AE), unless high risk (IHD) aim >90

Endoscopy: <24hr –> reduce LOS, and transfusion requirement

95
Q

Blatchford score

A

Urea, Hb, SBP, other (syncope, heaptic disease, HF, melena, HR >100)
<1: can be OP

96
Q

Forrest score

A

1a: active arterial bleeding

2a: NB visible vessel
2b: adherent clot
1b: oozing without visible vessel (risk of rebleeding on medical management is lower (10-20), better than 2a, 2b)
2c: flat spot
3. clean ulcer base

97
Q

Rockall

A

Predict rebleeding and mortality
Age, haemodynamics, comorbidities, dx, Recent haemorrhage

98
Q

AIM 65

A

Albumin <30
INR >1.5
Altered mental state
SBP
Age >65

99
Q

Endoscopic tx:

A

PUD:
- dual therapy (Inject adrenaline + clip or cauterise): reduction in rebleed, surgery, and mortality

Glue/powder: allow platelet adherence -> only used as salvage therapy as high risk of rebleeding

Salvage therapy: failed haemostatis on 2nd attempt:
- hemostatic spray/OTSC
- TAE or surgery

100
Q

HRS

A

Progressive rise in creatinine >150mg/L
Normal urine sediment, no proteinuria
Absence of shock
Urine Na <10-20
Cirrhosis with ascites
No response to fluid or no nephrotoxins

Reduced cardiac reservce increases the risk of developing HRS

Prevention:
1. Precent SBP
2. IV albumin for pt with SBP at diagnosis and on day 3

101
Q

HRS 1

A

HRS with AKI
BAD
- double creat to >226umol/L or 50% reduction in 24h CrCl to <20ml/min) in < 2 weeks
- requiring RRT increases mortality significantly

Reversal of HRS prior to OLTx affects survival post tx

Tx:
1. Volume expansion: Albumin or blood
> 1g/kg/d up 100g/d
2. WH NSBB
3. Terlipression (V1 receptor agonist - vasoconstrict 1-2mg IV q4-6h with albumin
<SE: arrhythmias, cyanotic digits, splanchnic ischaemia, increased pulm. odema
> higher reversal of HRS
> improved survival in responders
> reduced Na retention

4: Hb >80

  • median survival 1 month
102
Q

PBC

A

T-lymphocytic autoimmune dx of small intralobular bile duct
- non-obstructive cholestatic disease
- Femal 30-60
- 100x increase in FDR
- Fatigue and pruritis (worse at night) are the most common sx

  • elevated ALP
  • Elevated **GGT, 5’nucleotidase **
  • eosinophilia (early)
  • AMA (95% pf pt with PBC and 98% specific)

May have:
elevated ANA, lipids
Other AI:
- sjogrens, RA, thyroid dx
- metabolic bone dx

Tx:
Ursodeoxycholic acd
- improves liver test
- improves disease progression
- improves tx free survival
- no effect on pruritis or fatigue

103
Q

King’s college criteria for liver transplant referral

A

Paracetamol induced liver failure:
- Arterial pH<7.30 or Grade 3 or 4 encephalopathy with PT >100sec/INR>6.5 and Cr >340mg/L

Non-paracetamol:
PT>100sec or any three:
- age <10 or >40
- Non A and non-B viral hepatitis, idiosyncratic drug reaction, Wilson
- Jaundice >7days prior to encephalopathy
- PT>50sec or INR >3.5
- Bili >180mg/L

104
Q

Viral Hep A

A

Vax high risk groups
Post exp prophylaxis:
- 1 dose of vax within 2 weeks if <40
- if >40, <1, frail or immunocompromised or liver dx: Vax and Ig

105
Q

HCC

Transplant indication

Milan criteria

A

Single lesion <5cm or 3 separate lesion<3cm
no evidence of vascular invasion
no evidence of regional nodal or met sx

UCSF:
<6.5cm
cumulative tumour size < 8cm
*sum of tumour size and the number of nodules and Log10 AFP are significant;y associated with HCC specific death *

106
Q

Alcoholic hepatitis

A

AST/ALT >2
Mod leucocytotis
eleavated AST, ALT <300

Steroids and diet are the only tx that improves mortality

Maddret discrominant score
- >32: give steroids
- uses PT and bilirubin

MELD >11, high mortality

pentoxifyline: inhibitor of TNF as an alterantive to steroids

107
Q

Wilson disease

CLinical

A

ATP7B mutation
AR
low ceruloplasmin

Liver: steotosis, fulminant hepatic failure, Coombs neg HA, cirrhosis (not HCC)
ALP usually normal

Neuro:
- behaviour
- tremor
- speech
- PD sx
- Ataxia
- drooling
- dystonia
- 98% will have KF rings
- MRI: basal ganglia hyperintensity on T2
elevated copper in CSF

Psych:
- psychosis, depression anxiety

Age of dx: 5-35

Tx:
1. D-penicillamine:
> not good for neuro sx (may worsen)

  1. Trientine
  2. Tetrathiomolybate

Diet: AVOID:
- liver, kidney, shellfish, nut, fruits, beans, peas, unprocess wheat, chocolate, cocoa, mushroom
- Oral zinc –> interferes with Cu absorption

108
Q

NAFLD/MAFLD

RF

A
  • Obesity (80%)
    • type 2 diabetes mellitus (60%)
      ○ T2DM is associated with 2 fold increase in Advance liver fibrosis, HCC, liver mortality
    • Hyperlipidaemia
    • Metabolic syndrome
    • PCOS
    • jejunoileal bypass
      * sudden weight loss/starvation

Other conditions that are associated:
Hypothyroidism, OSA, hypopituitarism, Hypogonadism, Pancreatoduodenal resection, Psoriasis

109
Q

minimum steatosis required for dx of NAFLD

110
Q

enhanced liver fibrosis (ELF) blood test

A

hyaluronic acid + procollagen III + tissue inhibitor of metalloproteinase 1

111
Q

NAFLD activity score

A

§ Steotosis (0-3)
§ Lobular inflammation (0-3)
** § Hepatocellular ballooning (0-2)**
>=5 = NASH (fibrosis may or may not be seen

FIBROSIS IS THE MAJOR DETERMINANT OF ADVERSE OUTCOMES

112
Q

NAFLD

FIB4

A

FIB 4 Score: Age, AST, ALT, Plt

113
Q

Fibroscan:

A

○ <6 kPa = low liver stiffness, clinically significant fibrosis is very low (NPV 90%)
○** >12.5 kPa** = High working dx of advanced fibrosis or cirrhosis (PPV 80%)
○ To note: fibroscan cannot differentiate between fibrosis and inflammation

114
Q

Can steatosis cause HCC without becoming NASH?

115
Q

What is the most common cause of death in NAFLD pt

A
  • CVD is the most common cause of death in NAFLD pts
    NAFLD is an independent RF for CVD
116
Q

NAFLD

management

A
  • Histological resolution of NASH (90% of pts) can occur with10% weight loss
  • 10% weight loss can result in fibrosis regression (45% of pts)
      ○ Exercise independent of weight loss may reduce hepatic disease (reduce HS and improve insulin sensitivity)

  ○ Mediterranean diet (**high monounsaturated fatty acids)**
      § Reduce liver fat, improve insulin resistance
      § Reduce risk of developing metabolic syndrome 
      § Reduce death from CVD in NAFLD pts Coffee reduced progression of fibrosis in patients with NAFLD
117
Q

Statins in NAFLD

A
  • STATINS:
    ○ Reduce fibrosis and incidence of cirrhosis decompensation and HCC
    ○ Statin may be used to reduce LDL cholesterol and reduce risk of CVD
    **○ No proven benefit or harm to liver disease **
118
Q

NAFLD

insulin-sensitising drugs (e.g. metformin, pioglitazone)

A
  • Metformin improved LFTs and insulin sentivity but NOT HISTOLOGY
  • Pioglitazone: IMPROVES histology including fibrosis

VitE: NASH resolution in non-diabetic pt
- ADR: haemorrhagic stroke, prostate cancer

118
Q

NAFLD

insulin-sensitising drugs (e.g. metformin, pioglitazone)

A
  • Metformin improved LFTs and insulin sentivity but NOT HISTOLOGY
  • Pioglitazone: IMPROVES histology including fibrosis

VitE: NASH resolution in non-diabetic pt
- ADR: haemorrhagic stroke, prostate cancer

119
Q

Pancreatic cancer

RF

A
  • smoking
  • high BMI, low physical activity
  • Non-hereditary chronic pancreatitis
  • FAmilial cause
  • BRCA 2, BRCA 1, PALP2
  • pancreatic cysts

CA19-9 is senstitive/specific 70-90%; needs lewis blood group antigen (absent in 10%)

Usually ductal adenoca

120
Q

What is the 5 year survival of metastatic CRC

121
Q

CRC

FAP

A

AD
Tumour suppressor gene, APC
100-1000 colonic adenomas
100% penetrance
adenoma at 16, carcinoma at 39
Duodenal malignancy 12%

Clinical syndrome:
Gardner’s: osteomas, odontomas, epidermoid cyst, desmoid tumour

Turcot’s: CNS malignancies
Attenuated FAP: less polyps, present later in life, 100% penetrance

122
Q

MAP

MYH associated polyposis

A

AR
MutY - codes MYH, OGG1, MTH1
80% penetrance
Clinical: multiple adenoma (>15)
Age <50
Accounts for 40% of attenuated FAP without APC mutation

123
Q

Hamartomatous polyposis syndrome

Peutz-Jeghers Syndrome

A
  • AD
  • numerous hamartomatous polyp in the GI tract - these polyps don’t have malignant potential
  • pigmented freckles on the lips, face, palms, soles
    • around 50% of patients will have died from another gastrointestinal tract cancer by the age of 60 years.
  • gene encodes serine threonine kinase LKB1 or STK11

Can cause SBO or GI bleed

Associated with:
- pancreatic ca
- CRC
- sex-cord tumours

124
Q

Hamartomatous polyposis syndrome

A

Familial juvenile polyposis
Cowden’s disease
Bannayan-Ruvalcaba-Riley

125
Q

HNPCC

A

Mostly sporadic - MLH1
MSH 2 (60% of Lynch, MLH1 30% of Lynch)
MSI - 100% of HNPCC
<15% of sporiadic CRC
80% penetrance

RIGHT SIDED
Generally <10 adenoma
OTher than GI:
- endometrial 40-60%
- - ovarian 10-12%
- Gastric 10-20%

126
Q

histological features that predict dMMR

A
  • mucinous
  • poor differentiation
  • R) sided
  • Lymphocytic infiltrate
  • Expanding growth pattern

IHC:
MLH1/PSM2
MSH2/MSH6

Methylation: somatic variant
Germ line is only 3%

127
Q

CRC

Surveillance and Screening

A

FAP:
- sigmoidoscopy annually from 12 until 35, then 3 yearly
- Gastroscopy: 1-3 yearly, starting 30-35
- Colonoscopy if polyp found

HNPCC:
- colonoscopy biennually from 25 or 5 years earlier than the youngest cancer in family
- Annually in mutation carrier
- Pelvic exam/TVUSS yearly from 25
- Gastroscopy every 2 years, in mutation carriers

128
Q

Family hx and CRC screening

A

FDR x 1 >55: not recommended

**1 FDR <55 or 2 FDR any age: **5 yearly from 50 or 10 years earlier than the youngest person with can

  • FHx of FAP/HNPCC or other
  • ## 1 FDR + >2 FDR/SDR on same side of family
129
Q

Chronic paracetamol overdose

A

chronic paracetamol overdose in an alcohol user is characterised by markedly elevated aminotransferase (>3000 IU/l), combined with hypovolemia, jaundice, coagulopathy, hypoglycaemia, acute renal failure in over 50%

130
Q

Whats the AST/ALT ratio in alcoholic liver disease

131
Q

H. pylori and CagA-ve or +ve

A

+ve: Duodenal
-ve: Gastric

132
Q

Clopidogrel has a higher risk of bleeding cf A + C, VKA alone

133
Q

Rank the forrest classication in terms of rebleeding risk

A

1a - Spurter
2a - NBVV
2b - clot
2c - dot
3: clean base

134
Q

UGIB:
second endoscopic method with adrenaline - is it better than adrenaline alone?

A

combination reduces rebleeding and need for surgery

obsviously mre ADR:
- perforation
- gastric wall necrosis

135
Q

Post endoscopic PPI for 72hrs

A

SS in reduction in rebleeding in 3 days and in 30days

no SS in need for surgery or 30 day mortality

136
Q

Antiplatelet therapy (secondary prevention) post endoscopy

A

Mortality risk increases >7days off aspirin

137
Q

H. pylori:

Reason for treatment failure

A
  • clarithromycin +/- metronidazole resistance
  • clarithromycin resistance rate is increasing
  • ONLY for triple therapy if clarithromycin resistances known AND is < 15%

Otherwise use: quadruple tx for 14 days
1. Clarithro + metronidazole + amoxicillin + PPI
2. Bismuth + metronidazole + tetracycline + PPI

or sequential therapy

138
Q

H. pylori: post eradication testing

A
  • EVERYONE
  • no sooner than 4 weeks from treatment completion
  • breath test:
    > abx/bismuth needs to be WH for 28 days
    > WH PPI for 7-14 days
  • Pre-faecal antigen test:
    > JUST PPI WH for 14 days
139
Q

Wafarin and scope

A

Scope when INR <2.5

140
Q

is PAS positive Macrophage in duodenum, what should you consider?

A

Whipple’s disease

Whipple’s disease is a rare multi-system disorder caused by Tropheryma whippelii infection. It is more common in those who are HLA-B27 positive and in middle-aged men.

Features
malabsorption: diarrhoea, weight loss
large-joint arthralgia
lymphadenopathy
skin: hyperpigmentation and photosensitivity
pleurisy, pericarditis
neurological symptoms (rare): ophthalmoplegia, dementia, seizures, ataxia, myoclonus

Investigation
jejunal biopsy shows deposition of macrophages containing **Periodic acid-Schiff (PAS) granules
**
Management
guidelines vary: oral co-trimoxazole for a year is thought to have the lowest relapse rate, sometimes preceded by a course of IV penicillin

RACP (20 decks)

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