gastrointestinal Flashcards
treatment for H. Pylori
triple therapy PAC500 proton pump inhibitor amoxicillin 1g clarithromyocin 500 or PMC250 full dose PPI metronidazole 400mg, clarithromycin 250 mg
risk factors for peptic ulcer
H. pylori smoking alcohol NSAIDS and aspirin group O hypercalcaemia physiological stress burns (curling’s ulcers) or brain trauma (cushings ulcers)
different types of portosystemic shunts
caput medusae (umbilicus) oesophageal varices rectal varices diaphragm retropertineum
what is the child-Pugh score used for
liver cirrhosis
score 5-6 100% one year survival
10-15 points 45%
clotting cascade simplify
intrinsic APTT (34 sec) heparin prolongation caused by von willebrand disease haemophilias extrinsic PT (14 sec) Warfarin and liver disease
liver produces which clotting factors
II, VII, IX, X
treatment for achalasia
- pneumatic balloon dilatation 60% free at 5 years
- surgical (Heller’s) myotomy longitudinal incision of the muscle fibres of the distal oesophagus risk of GORd so sometimes occurs with funoplication
- botox injection
- drugs like ca channel blockers and nitrates but these are last and not very effective
risk factors for squamous cell carcinoma
drinking smoking nitrosamines (pickled moldy foods) and nitrates aflatoxins achalasia plummer vinson syndrome hereditary tylosis coeliac disease
risk factors for adenocarcinoma
barrett’s oesophagus
smoking and alcohol but not as imp as school
plummer vinson syndrome
strophic glossitis (smooth tongue) cheilosis (cracks at the mouth) koilonychia dysphagia post cricoid web of hyperkeratinization may require balloon dilatation and it is premalignant to cricopharyngeal carcinoma
what is the pathophysiology of achalasia?
absence of ganglion cells in the myenteric plexus which leads to failure of the relaxation of the lower esophageal sphincter and aperistalsis in the oesophageal body. ddx chagas disease or met carcinoma
vomit with undigested foods
oesophageal disorders achalasia, pharyngeal pouch
partially digested vomit
gastric outlet obstruction, gastroparesis
bile in the vomit
small bowel obstruction distal to the ampulla of vater
foul looking vomiting
distal intestinal or colonic obstruction
NB the only time you will see true faeces in the vomit is if there is a gastocolonic fistula or coprophagia
blood or coffee ground appearance
heamatemsis
long duration of vomiting
less likely it is a small bowel obstruction rules out acute pathologies
why should you always ask about constipation and flatus?
because an absolute constipation and flatus is a serious sign suggesting bowel obstruction
management of cholecystitis
nonoperative
clear fluids- avoiding food in the duodenum symptomatic relief to keep the gallbladder from contraction and also to prepare her for surgery.
IV fluids- vomiting
analgesics- WHO paracetamol and opioids given regular intervals.
antibiotics- according to local hospital guidelines gram neg
operative
laparoscopic cholecystectomy
urgent within 72 hours
or treating the acute episode and cholecystectomy 6-12 weeks later.
complications of cholecystitis
empyema
cholecystodoudenal fistula
gallbladder carcinoma
ascending cholangitis
what are the sings of ascending cholangitis?
charcots triad: RUQ pain jaundice fever with rigors swinging fever
management of ascending cholangitis
surgical emergency- blood culture fluids oxygen broad spectrum antibiotics lactate serum urine output endoscopic retrograde cholangiopancreatography drainage endoscope is placed in the esophagus through to the duodenum sphincter of oddi a fine catheter placed there pus drained and sent for culture. small basket collect any obstructing stone or sludge sphincterotomy
post drainage of CBD management
nil by mouth
monitoring and abx
definition mgx is cholecystectomy
bile is made up of what?
water
fats cholesterol and phospholipids
bile salts (help stabilise fats to ease digestion)
conjugated bilirubin (stool brown colour)
bile salts are reabsorbed in the terminal ileum
Give parental vitamin K due to what type of jaundice
if PT time is prolonged you can give vit K in obstructive jaundice
types of gallstone
bile pigment: heamolytic anaemia pictureor long term parental nutrition
cholesterol stone: the five fs fat, fair, fertile, female of forty.
complications of gallstones
anatomically
gallbladder ciliary colic, cholecystitis,mucocoele, empyema, cancer of gallbladder of CBD (cholangiocarcinoma)
CBD- obstructive jaundice, ascending cholangitis
acute pancreatitis
gallstones ileus
how do fatty foods cause pain in biliary colic and cholecystitis
CCK released in duodenum in response to fatty foods stimulating the gallbladder to contract.
what is calots triangle
top liver
inferior is cystic duct
medial side is common bile duct and right hepatic duct
cystic artery is a branch of the right hepatic artery which passes behind the common bile duct.
what is Mirizzi syndrome
stone in hartmann’s pouch pressing on the common bile duct
courvoisier’s law
if the gallbladder is palpable in the presence of jaundice then the jaundice is unlikely to be due to stones…
if stone in the CBD gallbladder thickened and fibrotic *shrivelled
CBD is obstructed due to carcinoma gallbladder is likely to be normal.
what is ERCP and how does it differ from MRCP
ERCP can be therapeutic and diagnostic
therapeutic * dormia basket and endoscopic sphinctectomy
MRCP purely diagnostic
risks of ERCP is bleeding, perforation of biliary tree, cholangitis, and pancreatitis.
if you think that your patient has pancreatitis what blood tests would you order?
FBC- leucocytosis and neutrophillia
LFT= hepatic involvement or obstructive picture (primary cause)
serum amylase- greater than 1000 Amylase or greater than 300 Lipase
modified Glasgow score for pancreatitis severity FBcm calcium, urea, liver enzymes, LDH, albumin, glucose, and arterial blood gas)
what can result in protienuria
UTI and appendicitis irritating the bladder
how should patient be follow up after acute diverticulitis
offered colonscopy 2-6 weeks after resolution of episode
extent and strictures
high fibre diet
when would surgery be considered in this patient
advise 1/3 remain well without symptoms 1/3 ocasional cramps 1.3 require hospital admission 2 episodes of hospital admission associated obstructive symptoms contrast leak during CT abdomen
emergency management of a perforated diverticulitis
- resus (fluids titrated in response to BP, HR, and urinary output)
oxygen keeping it greater than 94 Nil by mouth - blood tests: VBG, FBC, U&E, cross match
- analgesia
- antibiotics
- CT
emergency laparoscopy - normally Hartmanns procedure
when should a patient with renal stones (nephrolithiasis) be admitted?
evidence of an upper UTI
renal impairment (high creatinine, urea, high k)
refractory pain
bilateral obstructing stones
patient is elderly, child or systemically unwell
management for kidney stone
- regular multimodal analgesia (NSAIDS and paracetamol)
- encourage fluid intake
- tamsulosin (alpha blocker) or nifedipine (ca channel blockers)
both relax smooth muscle - active stone removal
stones less than 5mm can spontaneously 50% of time (keep the stone for analysis) - KUB x-ray before discharge to see if stone appears
- stones greater than 5 mm are unlikely to pass discuss with urology
methods of kidney stone removal
lithotripsy extracorporeal shock wave if stones are less than 2 cm
ureterorenoscopic removal = dormia basket, holmium laser and mechanical lithotripsy may require a post op ureteric stent
percutaneous nephrolithotomy= rarely
stenting or percutaneous nephrostomy may be performed in order to prevent hydronephrosis
antibiotic cover- given if their are invasive procedure.
what are the different causes of kidney stones
calcium- investigate for hyperparathyroidism
struvite- ammonium magnesium phosphate proteus infection, pseudomonas
urate- tx with potassium citrate
cystine
RF fro developing kidney stones
metabolic: hypercaliuria hyperuricosuria hypocitraturia hyperoxaluria gout (G6PDH deficiency, malignancy) cystinuria primary hyperparathyriodism crohn’s chronic urinary tract medullary sponge or polycystic kidneys sarcoidosis
jelly like or mucous stool what species?
salmonella or villious polyps
How do you diagnose IBS
ROME III
at least 3 months with onset at least 6 months previously of recurrent abdominal pain or discomfort associated with two or more of the following:
improvement with defecation
onset associated with a change is stool consistency
and also frequency of stooling
what is the definition of inflammatory bowel disease?
this is a spectrum of diseases including pouchititis and also have extraintestinal effects of the disease.
risk factors for IBD
white, european ancestry and jewish populations
prevalece
1: 500
1: 1000
which IBD is less likely in smokers
ulcerative colitis
which is more common in smokers?
crohns
what is the genetic component of IBD?
5-10% in siblings
50% in monozygotic twins
What are the gene variants that associated with Chrons?
NOD2
IBD pathogenesis
dysfunction of the bowel immune system.
pathology- acute (neutrophils) and chronic inflammation
gut flora- take away gut improves
Ulcerative colitis presentation
frequency
tenesmus
rectal bleeding
endoscopy UC
ulcers friability pseudopolyps variable extension proximal continous
histology hallmark UC
lumen of the crypt is lined with neutrophils
what is the differential for UC
crohn’s disease shingella salmonella e. coli campylobacter pseudomembranous colitis (severe C DIFF) non-steroidal anti-inflammatory drugs
How do you diagnose IBD- UC?
no gold standard- clinical ddx
diarrhoea and rectal bleeding for a couple weeks or months
neg. stool culture
neg C diff
colonoscopy showing continuous colitis from anal verge proximally absence of small bowel involvement
histology shows chronic inflammation with crypt abcesses.
extra-enteric manifestations
Uveitis
enteropathic arteritis
oligioartheritis = large joint single joint
ankolsing spondylitis - morning stiffness and back involvement
primary scelerosing cholangitis- irregular, narrow bile ducts greatly increased risk of cholangiocarcinoma. No effective treatment.
obstructive picture.
pyoderma gangrenosum
erythmatous nodusum= painful bumps on shins
UC treatment
aminosalicylates- mesalazine mild disease
corticosteroids= severe disease
azathioprine=
anti- TNF
UC complications
toxic megacolon- higher risk of perforation
if flare up= IV fluids and corticosteroids
normal X ray of colon even if symptomatic
2 daily physical examination for abdominal tenderness- peritonitis
toxic megacolon
indication for emergency surgery.
surgery ulcerative colitis
permanent illiotosmy
permanent J pouch= works well in young people but not older people= anal
6 bowel movements a day
crohn’s disease associated with which which gene change
NOD2 or CARD15
the more alleles the greater the risk
1= 3X risk
2= 40X
what are some of the traits associated with Crohns
mouth to anus
transmural disease
skip lesions
crohn’s presentation
diarrhoea
crampy pain
rectal
perianal disease
endoscopic chrons
deep ulcers
surgical chrons
fat proliferation
producing proinflammatory cytokines
perianal disease in crohns
abcess and fistula
How can you tell the air fluid level in a CT?
look up on radio pedía
treatment of crohn’s disease
do not use amiosalicyates
use coritcosteriods
immunosuppressants
inflixamab and other biologics
treatment of fistula and abcess
surgical drainage
metronidazole
should you do surgery in Crohns
recurrence in the illuim just above anastomosis
most patients don’t have granuloma
crypt abcess is the most
complications of Crohns
abcess and fistula and stricture formation
biologics
inflixamab- 1/5 of patients in remission
placebo = 10%
patients needed to treat- 13 patients
active crohns - combination of inflix and azothioprine is better
anti drug antibodies
trough inflixamab
can amount immune response against it.
vedolizumab
gut specific
anti intergrin= MS and UC
prevent rolling
historical treatment vs current treatment of crohns
currently based on severity of the disease and going with a strong therapy.
fecal calportectin
neg good for saying they don’t have the disease
also monitoring disease activity
