GI 2 Flashcards
discuss autoimmune hepatitis presentaiton, Ix
presents with longstanding non specific symptoms - fatigue, wt loss, mild RUQ pain, mild jaundice or joint pain.
no specific evidence of cause
strongly associated with anti-smooth muscle antibodies.
clincial, lab and histological investigation needed to diagnose
biopsy: lots of non specific findings seen
blood- to look for specific autoantibodies- antinucelar + smooth muscle.
discuss the two types of autoimmune hepatitis and the autoantibody findings within
type 1- anti smooth muscle andibotides +/- ANA
type 2 - positive anti- liver/ anti-kidney microsome antibodies
80% of cases are type 1
discuss management of autoimmune hepatitis
if untreated will develop chirrosis and die within 2 year of diagnosis
therapy should begin when ast + ALT are 10x upper limit of normal.
gamma globulins 2x normal
bridging necrosis + mmultilobular necrosis
steroids is Rx- usually leads to complete remission- pred + azathioprine
discuss drug induced hepatitis, risk factors, epiidaemiology, the mechansism of disease
an acute or chronic response to herb or drug- leading cause of liver flaiure in uk + us
RF: female, older, inc bmi
epidaemiology difficult to report.
2 mechanisms- intrinsic and idiosynchratic
intrinsic is predictable dose depenant- the metabolites produced are toxic. (paracetammol)
idiosynchratic- unpredictable cause. not reproducable. delayed 7-14 days.
Ix + Rx of Drug induced liver hepatitis + S+S
very varied presentation- good history essential
jaundice, weakness, abdo pain, dark stool/ urine, nausea, pruritis.
Ix: no specific tests available. transaminases 3x ALP.
Rx: remove offending agent,
NAC (regenerates glutatione)
steroids if it loos a bit inflammatory
low threshold for admission.
discuss liver metastases
one of the most common sites for mets. 25% of cases.
majority are adenocarcinomas.
very suseptable from the GI tract due to portal vein. 20-50% of bowel Ca will met to liver.
most remain confined to the liver.
becaue tumours are throught to get their blood supply from the hepatic artery not the portal vein, you can target them uniquely without affecting hepatocites.
Ix of liver mets
bopsy- diagnosis can be made on morphology alone. other stuff can help
S+S are just classic liver signs really.
triple phase Ct + MRI
Rx: surgica resection- cant take up to 80% and it will regenerate to normal function in a few weeks.
aim for margin of 1mm at least.
types of GI bleed, where is the dividing line and symptoms of each
upper and lower
ligament of treitz - distal to duodenum
upper: haematamesis, melena (greater digestion)
lower: haematochezia.
causes and investigations of upper and lower GI bleeds
upper : oespohagitis, cancer, mallory-weiss tear, varices, ulcer, erosive gastritis, aortoenteric fistula
lower: diverticulitis, haemorrhoids, fissures, ulcers.
neoplasm (polyp/ cancer)
inflammation- cholitis, chrons etc.
upper Gi bleeds more common.
Ix: Upper: NG lavage, oesophago-gastro-duodenoscopy.
lower: R/O upper Gi bleed
DRE, CT + contrast, bloods,
if younger than 45- sigmoidoscopy
if stable flexi/ colonoscopy
if unstable–> colonocsopy —> laproscopy
scoring systems for Gi bleeds
all patients with upper gi bleeds need glasgow-blatchford score on admission
if scores higher than 0 needs medical intervention 6 or more assoc with greater than 50% risk of needing an intervent.
based on blood urea, Hb level, BP, pulse, history/ comorbidities.
urea goes up when blood is digested.
management of GI bleeds
upper: ABCDE - 2 large bore cannulas
protect airway
high dose PPI
non-variceal- adrenaline + cauterisation/ clipping
variceal- terflipressin + Abx
lower:
ABCDE
check amylase/lipase
await Hb before crossmatching
calculate shock index
if >1 - active bleed- CT angio- interventional radiography
<1 admit for lower gi endoscopy if major bleed
if minor f/u as OP
major / minor bleed is calculated off a oakland score
discuss gastric cancer
most commonly adenocarcinoma- columnar glandular epithelium - this can be intestinal or diffuse.
(lymphoid, carcinoid, leiomyosarcoma other types)
risk factors-
Fhx, smoking, alcohol, obesity, age.
germline mutations- CDH1
type A blood, nitrates in diet, H pylori, male,
fibre is protective.
common in japan, eastern europe, china and south america.
causes of intestinal and diffuse adenocarcinoma
intestinal:
H-pylori –> Cag A released–> damage –> immune response –> chronic gastritis –> metaplasia –> resemble intestinal cells more–> dysplasia–> malignancy
Diffuse–> can occur any park or stomach mutation in E-cadherin which menas cells dont stick to each other much –> easy spreadsee signet ring cells + stomach goes hard/ leathery.
signs and symptoms of gastric cancer
usually asymptomatic.
can get anaemia, B symptoms, dyspepsia, N+V, haematamesis/ coffie ground, enlarged belly button, troisiers sign (virchows node)
Ix:
gastroscopy+ multiple biopsy
USS
Ct/MRI
lap + peritoneal washings.
Rx:
easly gastric cancers- small resection
advanced + distal–> partial gastrectomy
proximal–> total gastrectomy
combine with chaemo
complications and prognosis of gastric cancer
5 year survival is less than 10 %
pseudoachalasia syndrome
can met to many places- petironeym, lymph, liver, can get bilateral mets to ovaries
trousseaus syndrome- migratory clots caused by cancer stimmed coagulation
brown spots on skin
polyarteritis nodosa, inflamm and necrosis of med sized arteries.
