Gastroenterology Flashcards
Primary cause of pill oesophagitis
doxycycline
What causes zolliger ellison syndrome?
Secretion of gastrin from neuroendocrine tumours (gastrinoma)
Barrett;s eosphagus histo
metaplastic columnar epithelium
how long is barretts when it has higher risk of malignancy?
> 3cm
Characetistic findings of oesinophilic eosophagitis
stacked circular rings
strictures
linear furrows
Microscopy which is diagnostic of eosinophilic oedeophagitis
> 15 eosinophils on high power field
eosinophilic oesophagitis mangement
PPI for 8 weeks, if no improvement fluticasone or budesonide slurry
pathology of achalasia
progressive degeneration of ganglion cells in myenteric plexus -> failure of relaxation of lower oesophageal sphincter and loss of peristalsis in distal oesophagitis
secondary causes of achalasia
chagas disease
amyloidosis
sarcoidosis
investigation findings in achalasia
barium - oesophageal dilatation, bird beak oesophageal junction
manometry - failure of relation of LOS
Achalasia management
pneumatic dilatation of LOS
surgical myotomy
botox (elderly)
nitrates, CCB
POEM
risk of dilation of LOS
3% perforation
What pressure do varices occur and when do they bleed
Seen when presure gradient between portal and hepatic veins >12mmHg
Bleeding when >18
gastric varices bleed more than oesophageal varices
What causes risk of AKI and Na and fluid retention in liver disease
shunting of blood flow from cardiac circulation to splanchnic leads to relative renal hypoperfusion
Therapies in acute variceal bleeds
AIm Hb >80
antibiotic prophylaxis (oral norflox or IV cipro)
somatostatin or octreotide for 3-5 days
TIPS when not controlled bleeding or recurrent
can use balloon tamponade
Prevention of varicies
non-selective beta blockers (propranolol, carvedilol) and maximal tolerated dose
ligation (same outcomes)
Most common reason for inadequate treatment of H pylori
clarithromycin resistance
Virulence factor of H pylori
CagA
VacA
H pylori resistance in australia
clarithromycin resistance 10%
Metronidazole 30%
amox 10%
How to test for H pylori eradication
breath test 8 weeks after treatment
Which type of ulcer do you repeat endocopy after 8 weeks of PPI therapy?
Gastric not duodenal (higher risk of malignancy)
What does forrest classification predict
risk of rebleeding
and which lesions need therapy
Why PPI 72 hours post bleeding
helps prevent re-bleeding
Genetic associations with coeliac
HLA-DQ2 DQ8
Skin manifestations of coaelic
Dermatitis hepatiformis (itchy symmetrical blistering rash over scalp shoulders buttocks elbow and knees)
atrophic glossitis
Associated conditions with coeliac
Selective IgA deficiency (false negatives of EMA and TTG)
T1DM, thyroid disease
GORD, eosinophilic eosophagitis
IBD (UC more than CD)
Glomerular IgA deposition
Autoimmune myocarditis and idiopathic dilated cardiomyopathy
Diagnosis of coeliac
TTG is preferred
endomysial (EMA)
-ve result has high negative predictive value
Both serology and small bowel bx is required
If positive serology but -ve endoscopy do HLA testing, if positive then high gluten diet for 6-12 weeks then repeat scope
Histo findings for coeliac disease
atrophic mucosa, loss of folds on endoscopy
complete loss of villi, crypt hyperplasia, enhanced epithelial apoptosis
Malignancy associated with coeliac disease
enteropathy associated T cell lymphoma (EATL) - <5% of all GI lymphomas, gluten free prevents
Small bowel adenocarcinoma HR 3.05
Specific finding in Igg4 related disease
retroperitoneal fibrosis
Treatment of IGG4
corticosteriods
additional immunosuppressant (AZA, MMF) or biologic
Impaired synthetic function
INR >1.5
King’s college criteria
ABG pH <7.25 after fluid resus and NAC >24 hours
or all 3: PT >100/INR>6.5n Creat >300 or anuric, grade 3/4 encephalopathy
LFT pattern in alcohol hepatitis
AST:ALT>2
hallmark of alcoholic induced liver injury
neutrophil infiltration
NAFLD progression % to cirrhosis and then to decompensation
25% 7-8 years then 25% to 8-10%
Therapies for NASH
Only in those with fibrosis >2
If no DM vitamin E
If DM pioglitazone or GLP1
Type 1 vs T2 autoimmune hepatitis
T1: ANA, anti-smooth muscle, antiactin, antimitochondrial, anti-SLP, p-ANCA
T2: ALKM1 or ALC1 ab
primary biliary cholangitis ab
antimitochondrial ab
Condition associated with primary sclerosising cholangitis
UC
Liver Bx for autoimmune hepatitis
hepatitis with lymphoplasmacytic infiltrate
Autoimmune hepatitis treatment
Glococorticoids
- most improve in 4 weeks
Alt AZA
Histology findings in primary biliary cirrhosis
non-suoourative, granulomatous, lymphocytic small bile duct cholangitis
clinical manifestations of primary biliary cirrhosis
most asymptomatic
pruritis
hyperpigmentation
sjogrens 65%
scleroderma
Diagnosis of Primary biliary cirrhosis
adults with cholstasis, no systemic disease, elevated ALP and AMA >1:40 is diagnostic
Treatment of primary biliary cirrhosis
Ursodeoxycholic acid
2nd line obeticholic acid
Assess response with serial bx if AIH overlap
Characteristics of Primary sclerosing cholangitis
chronic progressive disorder
inflammation, fibrosis and stricturing of medium and large bile ducts
Conditions associated with primary sclerosing cholangitis
cholangiocarcinoma (10-20%)
70% with IBD (UC >CD)
Diagnosis of primary sclerosising cholangitis
cholstatic pattern LFTs
p-ANCA
MRCP >ERCP showing abnormalities in biliary tree
liver bx only if dx uncertain
Treatment for primary sclerosing cholangitis
UDCA can be beneficial
Liver tx
Primary scleorising cholangitis survival
median 1 year
Signficant fibrosis on fibroscan in cirrhosis
Low range has good negative predictive value
>7.5 signfiicant cirrhosis
>11 cirrhosis
SAAG
SAAG > 11 suggests portal HTN
Tap findings in SBP
Leuks >500
PMN >250
Mangement of SBP
Ceftriaxone for 5 days
IV albumin then daily for 3 days
Hish risk features for varicies
size
red wale marks
advanced liver disease
difference between T1 and T2 hepatorenal
T1 more rapid, x2 increase in creatinine in < 2 weeks
T2 less severe than type 1, major clinical feature is ascities which is resistant to diuretics
Difference between hepatopulmonary syndrome and portopulmonary syndrome
Hepatopulmonary -> pulmonary vascular dilatation -> hypoxia
Portopulomary -> pulmonary vasocontriction -> RHF
What serology indicates acute HCV infection
HCV RNA +ve with antiHCV Ab -ve which becomes positive in 12 weeks
or
HCV RNA +ve and antiHCV positive with neagtive tests 6 motnsh prior
Most common HCV genotype in australia
type 3
Treatment duration of hep C
8 weeks for glecaprevir and pibrentasvir, 12 weeks for others plus if cirrhosis
side effects of glecaprevir
elevation in bilirubin due to inhibition of bilirubin transporters
Usual sustained virological response to HCV treatment
SVR >95%
HCV treatment CYP and drug interactions
CYP3A4
PPIs
statins
OCP
amiodarone
When are protease inhibitors contraindicated
in decompensated cirrhosis (B and C)
What are the differences between genotypes of HBV
Genotype B - less active disease
Gene C - higher risk of HCC
Gene F - fulminant liver disease (rare)
aminotransferase indication of higher cirrhosis risk
ALT (not AST)
Extrahepatic manifestations of HBV
polyarteritis nodosa
membranous or MPGN
Lynch syndrome and mutations
autosomal dominant
MSH2 due to deletions in EPCAM gene
MLH1 MSH2 MSH6
PMS2 most common
increased right sided colorectal Ca, endometrial and prostate
Most common met site of HCC
Lungs
Then abdominal LN
Serum marker for hcc
AFP
Transplantation criteria for HCC
single lesion <5m or max 3 lesions <3cm
No vascular invasion
organ allocation based on MELD
Treatment for advanced stage HCC
1st: Atezolizumab and bavacizumab
2nd: TKI
Side effects of TKI
hand foot skin reaction
Fatal liver toxicity (rare)
Features of HCC on CT
arterial enchancement
portal venous washout
LIRADS 4-5
MRI characetistics of focal nocule hyperplasia
T2 hyperintense
central scar
Mutation which causes early surgeries due to stricturing disease
Nod2/CARD15
Extraintestinal manifestations associated with active GI disease in IBD
oral ulcers
erythema nodosa
large joint arthritis
episcleritis
Extraintestinal manifestations independent of active GI disease in IBD
primary scleorising cholangitis
ank spond
uveitis
pyoderma gangrenosum
renal stones
gall stones
What secetes faecal calprotectin
Neutrophils in the bowel
Histology of UC
confined to mucosa and submucosa
Goblet cell depletion
crypt abscesses
crypt branching
Endoscopy findings in crohns
apthous ulcers
longitudinal snail trail ulcer
cobblestoning
Crohns histology
transmural ulceration
goblets preserved
granulomas
parietal metaplasia
Treatment for mild/mod UC
Mesalazine
Corticosteriods
If poor prognostic features: other maintence (thiopurines and then biologics)
Moderate/severe disease for UC
Iv corticosteriods, reasses day 3
if response -> steriods
no response -< surgery or 2nd line, IV cephalosporin or infliximab
if still no response -> surgery
Treatment differences based off location in mild/mod crohns
if colonic use 5ASA or pred
If small bowel -> use pred
If persistant disease in mild/mod crohns despite initial therapy?
MTX or thiopurine
(MTX not useful in UC)
Management of mod/severe crohns
induction: systemic corticosteriods, biologics
Treatment of stricturing crohns disease
if inflammatory may respond to medical therapy
if fibrotic poor response to medical therapy, usually surgical options
Most common site of external fistula in fistulating crohns disease
perianal
Fistulating crohns disease medical treatment
Abx: cipro and metro
minimal evidence in immunomodulators
infliximab and adalimumab
Dose dependant thiopurine side effects
N+V
Leucopenia
Hepatotoxicity
Dose independant side effects of thiopurines
infection
pancreatitis
hepatosplenic T cell lymphoma
non-melanoma skin cancers
rare side effect of thiopurines
nodular regenerative hyperplasia
Infliximab moa
Anti-TNF
Adalimumab moa
anti-tNF
Golimumab moa
anti-TNF
Vedolizumab moa
anti-integrin
ustekinumab moa
anti IL12/23
tafacitinib moa
jak inihibitor
upadacitinib moa
JAK inhibitor
Ozanimod moa
S1p modulators
Associations with hep C
insulin resistance
essential mixed cryo
lymphoma
membranoproliferative
thyroiditis
porphyria cutanea tarda
lichen planus
