Gastro Flashcards
What is the most common cause of cryoglobulinemia?
Hep C
- cryoglobulins are present in 25% of those with Hep C, but clinical features only present in 15% of cases
When choosing between tenofovir and entecavir for hep B, what factors would affect your decision?
Tenofovir: pregnant, previous resistance to lamivudine
Entecavir: osteoporosis
Hepatitis B
Risk factors for developing HCC and cirrhosis
Male
family hx
co infection with HCV, HIV, HDV
older age
habitual alcohol consumption
HBV genotype C
core promoter mutation
Indication for starting treatment in HepB
- If HBeAg positive, DNA >20,000 and persistently elevated ALT or fibrosis
- If HbeAg negative, DNA >2000 and persistently elevated ALT or fibrosis
- 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
Tenofovir
IS A: NRTI
TAF > TDF
preferred in HBV-HIV co infection
reduced renal SE
H. pylori tx resistances
Metronidazole (30%)>Clarithromycin (10%)>Amoxicillin> levofloxacin
Microscopic colitis
More common than coeliac disease (50-70x)
Mean age 65, FEMALE
Aggravated by: NSAIDs, aspirin, PPIs
3 subtypes: collagenous, lyphocytic, incomplete
why is hep B antiviral not effective in treating hep D
the antivirals will suppress viral DNA, but won’t clear the surface antigen. Hep D uses the surface antigen for virulence
PSC
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
Suffix of Hep C drugs
previr
asvir
buvir
- proteasome inhibitor
- NS5a inhibitors
- NS5b inhibitors
Factors that have been associated with a higher likelihood of spontaneous clearance of HCV include:
●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
MELD score
Stratifies severity of end-stage liver disease, for transplant planning
Dialysis
Creat
Na
INR
Bilirubin
> 15 would benefit from transplant
Liver transplant
Complications
**- 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
- Chronic (rare)
> months to years
> Vanishing bile duct syndrome (cholestatic LFTs)
> tx: increase immunosuppression
Recurrence: essentially all except metabolic sx confined to liver
VBDS
Complication of drug induced liver injury
**Chronic cholestatis **and loss of intrahepatic bile ducts
Manifests as chronic liver rejection
IBD
Extraintestinal manifestation associated with disease activity
Oral ulcers
erythema nodosum
large joint arthritis
episcleritis
IBD
Extraintestinal manifestation independent to disease activity
Ankylosing spondylitis
Uveitis
PSC
pyoderma gangrenosum
Kidney stones
gallstones
Common mutation in haemochromatosis
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
Common mutation in haemochromatosis
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
5-ASA
used in UC
rectal+oral>rectal alone > oral alone
potential benefit in reducing risk of CRC
Can weight loss cause improvement in liver histology
yes
Gastric vs oesophageal varices
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
What’s the treatment for Hep D
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.
Which class of HepC treatment is CI in decompensated cirrhosis
Protease inhibitors
What is the mechanism of increased resistance in portal HTN?
increased fibrosis
decreased NO
Autoimmune hepatitis
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
SBP primary prophylaxis indication
bili >50 with impaired renal function
Low protein <10g/L in ascites
When should you test HCV antibodies after birth?
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.
RF for hepatotoxicity in paracetamol overdose
age >40
malnutrition
CYP2c1 inducers (carbamazepine, phenytoin)
Hypophosphataemia is protective
Which medical therapy has shown to reduce mortality in variceal bleed?
Terlipressin
Contraindication for TIPSS?
portal vein thrombosis, hepatic encephalopathy, advanced HCC, pulm HTN
Notable HepB genotypes
B: slow, low activity of disease
C: associated with higher rates of HCC and cirrhosis
F: associated with fulminant liver disease
VIPoma
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.
Which of the following is associated with higher risk of variceal bleeding?
- Childs Pugh C
- Alcohol use
- Red wale sign present endoscopically
- high portal pressures >12mmHg
- Hx of prev variceal bleed
What is PNPLA3 mutation associated with?
alcoholic disease and NAFLD
Hep B immune tolerance /clearance/control/Escape
- High HBV DNA, HBeAg +ve, normal LFTs
- High HBV DNA, HBeAg +ve, Abnormal LFTs
- Low HBV DNA, HBeAg -ve, normal LFTs
- High HBV DNA, HBeAg -ve, Abnormal LFTS
Which phase of Hep B should you start treatment?
Immune clearance and Immune escape
Comment on the use of betablockers in SBP
associated with reduced survival and increased rate of hepatorenal syndrome
eosinophilic esophagitis
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
RF for developing oesophageal adenocarcinoma?
Being male, elderly, caucasian and obese
Gastric acid secretion from parietal cells is regulated by
endocrine (gastrin)
paracrine (locally delivered histamine and somatostatin)
neural (acetylcholine)
autocrine (transforming growth factor-alpha) factors
PG tx
What’s in Child Pugh score?
Albumin28-35
Bilirubin 20-30
PT/INR
Ascites
Encephalopathy
1 year survival:
A: 100%
B: 80%
c: 45%
NOD2/CARD15
Associated in IBF (crohn’s)
- early surgery due to stricturing disease
Use of combination Aza/Infliximab in mod-sev UC
- increased CS free survival
- Better mucosal healing
- Improvement in mayo score
- Reduction in faecal calprotectin
REDUCED serious infection cf. aza alone
Anti IF vs anti parietal
Anti IF 100% specific, low sensitivity
Anti parietal: high sensitivity, less specific
MMA
Homocystein
MMA is elevated in B12 def, not folate
HomoC is elevated in both
What kind of LFTs does Cotrim induced liver injury produce?
Cholestatic
RF for severe crohns at diagnosis
- steroids at diagnosis
- perianal dx
- <40
- Smoking
- high ASCA titre
- NOD2
- UGI involvement
- strictures
- deep ulcers
RF for severe UC
<40
extensive disease
PSC
high pANCA titre
deep ulcers
What does itraepithelial lymphocytosis a feature of
microscopic colitis
- chornic diarrhoea
- tx: budesonide, may need MTx for maintenance)
MTX should never be used in which type of IBD
UC
Which IBD tx is likely to cause acute pancreatitis?
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
What’s the treatment choice for perianal fistula in CD
Infliximab
Indications for colectomy in UC
dysplasia
fluminant colitis/toxic megacolon
failure of medical therapy
Common complication of colectomy
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
Barrett’s
Precursor to oesophageal adenocarcinoma
- metaplasia of squamous to columnar
- RF: chronic GORD, Age>50, overweight, high SES, alcohol, smoking
- after initial dx –> repeat scope in 1 year to check for dysplasia
- 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