GI problems Flashcards
Crohns disease
- Any part of GI tract
- Discontinuous inflammation- Skip lesions!, may spare rectum
- Deep ulcers, cobblestone appearance
- Transmural inflammation
- Granulomas may form
- -Made worse by smoking
- Different behaviours due to transmural nature: fistulising, strictures (abdo pain distension, vomiting,bowels not opening), perianal (abcess, fistula, fissure, ca occur in isolation)
most common is ascending colon and terminal ileum, ileo-caecal valve
Ulcerative Colitis
Colon only Continuous inflammation, starts at rectum Shallow ulcers Mucosal inflammation Smoking is protective Inflammatory
Colectomy is curative
Complications is toxic megacolon: parlytic bowel, air is trapped and dilate- perforation
Extra intestinal manifestations of IBD
- Liver and bile ducts: Primary cholganing scleritis in Crohns
- UVEITIS
- Sore joints
Treatments of IBD
5-ASA’s (salazines)- maintenance due to anti-inflammatory properties
Steroids for flares
Immunsuppression: azathioprine
Anti-TNF: infliximab, adalimumab `
Causes of upper GI bleeding
- Peptic ulcers ( H.Pylori (stool antigen test (-ve when reslved), serology), medications (NSAIDs)
- Varices: Liver disease, varices: larger bleeding, haematemesis
- Stomach Cancer: iron deficiency, mild bleeding
- Oesophageal cancer: Dysphagia
- Oesophagitis: GORD, some haematemesis
- Angiodysplasia
- Mallory Weiss tear: retching, recurrent
Lower GI bleeding
- Angiodysplasia
- Diverticula
- Carcinoma
- Meckel’s diverticulum
- Anal fissure/haemorrhoids
- Rectal ulcer
- UC/Crohns
- Polyps
- Ischaemic colitis: inflammatory response and bleeding, older people
Coeliac serology
note gluten insensitivity, AI
Treat w gluten free diet, oats is okay, no gliadin (small numbers of people can not tolerate, be careful of cross contamination)
First test used to confirm coeliac, needs to be done while consuming gluten. If restricted before test, falsely negative
-TTG IgA Ab preffered
-Can do DGP
Can be falsely negative in IgA deficiency, NB common with coeliacs
NB most coelaic people have HLA-DQ2 or HLA-DQ8, +Ve is not indicative, as 50% of gen population have, -ve rules out
Coeliac duodenal biopsy finding
- Intra-epithelial lymphocytosis
- Crypt hyperplasia
- Villous blunting (most diagnostic)
proximal duodenum
Coeliac associations
Dermatitis herpertiformis- 100%* 1st degree relative with, should test* Type 1 diabetes- strong* AI-Thyroid disease (Graves?) Osteoporosis Infertility/recurrent miscarriage Unexplained neurological Unexplained liver disease Addisons
Terminology, Gallstones
Biliary Colic: RUQ pain associated with inflammation of gall bladder or common bile duct
Cholelithiasis: Gall stones, uncomplicated
Cholecystitis: Inflammation of gall bladder
Choledocholithiasis: Stone in bile duct
Cholangitis: Choledocholithiasis + inflammation (fever, rigors etc)
80% cholesterol stones, others are pigmented
Common causes of elevated GGT and ALP
Stones, biliary disease (PSC, Primary biliary Cirrhosis), drugs, tumour
Significance of pain and jaundice
Biliary colic would suggest gall stones, must confirm
Painless jaundice has list of differentials
Choledocholithiasis
Typically secondary stones, from GB
Rarely stones form inside, pigmented
GB removal will likely treat, however ca still be complicated by pigment stones
Typically a negative Murphys sign, but jaundice
Cholangitis
Charcots triad, of
fever
Pain (suggestive of biliary colic)
Jaundice
Complication of choledocholithiasis, bacteria enter from duodenum
MRCP vs ERCP
MRCP: if not seen on US, do this. Accurate visualisation of biliary tree. ADV: noninvasive, DISADV: non-therapeutic
ERCP: diagnostic and therapeutic way of curing choledocholithiasis. ADV: therapeutic. DISADV: risk of complications
PBC vs PSC
PBC: -Effects intra-hepatic bile ducts, no way to visage - Need biopsy -Associated with AMA (anti-mitochondrial antibody) Diagnosis PSC: -Intra and extra hepatic bile ducts -Diffuse stricturing on imaging -Associated with IBD -Diagnosed by biopsy or imaging
PBC presentation
Gradually increasing LFT’s
fatigue, pruritus, steatorrhea, fatigue
Long term cirrhosis
Associated with dyslipidaemia (high), ostopenia/osteoporosis
PSC presentation
Diffuse strictures in bile ducts
No antibody seen, maybe triggered by bacterial infection
Often seen with IBD, UC (If PSC, UC, if UC, not necessarily PSC)
Similar presentation to PBC (gradually increase in LFT’s(cholestasis)), pruritus, fatigue, steatorrhea
Can get jaundice, cirrhosis
Can get recurrent infections
PSC is likely going to need liver transplantation, maybe need stent, ERCP in large ducts
Tumours causing obstructive jaundice
Head of pancreas cancer
Cholangiocarcinoma
Signs of chronic liver disease
Jaundice Palmar erythema (redness on outer edges) Spider naevi (chest/upper back) Ascites (portal hypertension) Caput medusae
Basic break down of the LFT’s
GGT up alone: steatosis
ALP + GGT: Cholestasis
AST/ALT: hepatocellular pattern
Causes of steatosis
Alcohol
NAFLD: From metabolic syndrome, diabetes, dyslipidaemia, HT, increased BMI. Typically increased ALT
Most common causes of hepatitis
Viral; alcoholic; non-alcholic; auto-immune; ischaemic; haemochromatosis; drugs (bear in mind, also over the counter stuff. New drugs or long standing)
Alcoholic liver disease
Alcohol exposure over time can lead to steatosis, and abstinence can restore a normal liver
Severe exposure can cause a hepatitis, and abstinence can lead to steatosis
Steatotic livers continually exposed can cause hepatitis, and together can make liver cirrhosis
rehash on hepatitis risk factors and transmission
A: faecal oral, travel. Acute (also E)
B: Parenteral, sexual transmission, vertical transfusion. D comes with B
C: blood borne, IVDU
Read Char’s notes on AI hepatitis, ishchaemic and haemochromatosis
-
Handy hints reading LFT’s
- If AST/ALT are in thousands, either viral; ischaemia; paracetamol
- If in the hundreds, not so helpful
- If AST > 2 x ALT suggestive of alcoholic hepatitis (AST/ALT ratio reversed)
Hepb transmission
Perinatal (Asia)
Horizontal transmission
Sexual
Parenteral (IVDU/transfusion)
4 Phases of chronic Hep B
1) Child, HepB high in blood, body does not act against virus as immature
2) Body tries to clear virus, ALT goes up, HepB load drops, treatment considered. In 20s/30s. Most at risk, inflammation. Can last years
3) Body controls the virus, ALT lowers.
4) Virus never leaves, but stays suppressed. Can last years, and can reactivate and rise in virus, recurrent inflammation and liver damage
Encephalopathy stages
Confusion- drowsiness- coma
Can be incoordinated, tremor, asterixis, ataxia
Liver functions
- Removes toxins
- Metabolises nutrients from foods to produce energy
- helps fight infection by removing bacteria
- Prevents nutrient shortage by storage (vitamins, minerals, sugar)
- Produces most proteins needed by body
- Produces bile to digest and absorb fat and fat soluble vitamins
Hepatorenal disease
Can occur with ascites (cirrhosis, portal hypertension) associated with a loss of renal function due to RAAS activation
Tumour marker for HCC
AFP
