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.
discuss hiatus hernia and GORD + the types of it
hole in diaphragm at the hiatus- allows stomach through
this compromises the lower oesophageal sphincter- allowing stomach contents into the oesophagus
type 1- sliding- 95% of hiatus hernias- gastroeosophageal junction displaced upwards
2: stomah migrates into mediastium parallel to esophagus
3: type 1 and 2 together
4: stomach + another organ go into the chest.
causes symptoms and investigations of hiatus hernias
causes- congenital
aquired- age + muscle weakness is a big factor. – elevated intraabdominal pressure (preg, chronic constipation)
refux is a typical presentation - can get cough or asthma
Ix: endoscopy
manometry
Ph monitoring- 24 hours- gold standard
esophagogaraphy
treatment of hiatus hernia and GORD
double dose of PPI- both therapeutuic and diagnostic.
if have mroe than 8 years life expectancy OR (and) ulcer, stricture or barrets — surgery
need a thorough work up prior to surgery as differential diagnosis is broad.
at least 90% will have no symptoms at 10 years after surgery.
discuss ulers of the stomach and duodenum- how prevalent they are etc.
prone to ulceration after breakdown of mucosa.
duodenal ulcers 2-3x more common
more prevalent in older women.
mucosa broken down by- steds, nsaids, ssri, H pylori
increaced acid can be due to- stress, alcool, caffeine, smoking, spicy foods.
signs and symptoms of ulcers
DU- pain when hungry + at night + in the day
Gastric- pain when eating- usually in the antrum
nausea, weight loss
relapse and remit cause, restosternal pain
ALARM
Anaemia
Loss of weight
Anorexia
Recurrent symptoms
Melena
Ix or ulcers of the gastric area
urea breath test- checks for H pylori
stool test- for H pylori
OGD- +/- biopsy- gold standard for H pylori
FBC for anaemia
erect Cxr- for perf (air under diaphragm)
if over 55 go streight to endoscopy
if under- try management of disease first before invasive procedures.
Rx of gastric ulcers
lifestyle modifications- stop alcohol and smoking.
H pylori- triple therapy ppi, clarithromycin metronidazole
if bleeding from them- argon heat therapy or inject adrenaline into them or clip surgically
laproscopic for the big ones
strictures if left untreated
can develop pyloric stenosis- upper abdo pain, vom, distention.
discuss gastritis
poorly defined term- inflammation in the stomach
or any redness seen of the mucosa at endoscopy
causes: Hpylori
nsaids
discuss oesophageal cancer
9 in 100 000 uk. iran 100
RF: diet, alcohol, smoking, achalasia, reflux, barretts, obesity, hot drinks,
20% upper, 50% middle, 30% lower 30% lower. if proximal- squamous cell, if distal adenocarcinomas
S+S: wt loss, retrosternal chest pain, , hoarseness, cough, dysphagia
Ix: oesophagoscopy + biopsy CT/MRI for staging.
Rx: oesophagectomy may be tried. pre op chaemo
Staging- in situ
invading submucose
invading muscularis
nvading adventitia
invastion of adjacent structures.
