GI Flashcards
Define GORD
Reflux of gastric contents into oesophagus or beyond -> symptoms due to loss of lower oesophogeal sphinchter tone, delayed and impaired gastric emptying.
commonest cause of oesophagitis
Typical GORD presentation
Heartburn post meals, not usually exertional, worse after lying down/bend over/night
Sour taste in mouth
Rf for GORD
- Obesity
- Hiatus hernia
- FH
- Older age
- Drugs: nitrates, calcium channel blockers, alpha- and beta-adrenergic agonists, theophylline, and anticholinergics
- Other: stress, asthma, NSAIDs etc!
How is GORD diagnosed
Clinical
- trial PPI with px
Define eosinophilic oesophagitis
infilitration of oesophageal epithelium with eosinophils => immune mediated oesophageal dysfunction
Presentation of eosinophilic oesophagitis
- Long term dysphagia
- Food avoidance and behaviour modification
+ - heartburn, chest discomfort
- N+V
- Acid regurg
- Abdo pain
RF of eosinophilic oesophagitis
- FH
- kids. young
- Men
- White
- Atopic diseases
What is Barrett’s oesophagus
COLUMNAR METAPLASIA = Normal squamous cell epithelium lining oesophagus is replaced with columnar
INTESTINAL METAPLASIA = develop glands too
Changes are usually secondary to chronic GORD
Biggest concern -> oesophageal/barrets adenocarcinoma
Hepatitis A
- Cause
- Timescale
- Route transmission
- Diagnosis
- Complications
- Prevention
pretty chill average 1 month incubation
RNA virus
Time: Only acute not chronic carrier
Route: Faecal-oral = close contact, contaminated food/water
Diagnosis: HAV-IgM for recent and IgG for ever
CAN -> fulminant, cholestatic/relapsing hep but NOT Chronic or HCC
Prevention: vaccine
Who gets hep A`
Large communities , children resevoir
-> travelers
+ gay men
+ IVDU
Hepatitis E
- Cause
- Timescale
- Route transmission
- Diagnosis
- Complications
- Prevention
Cause: 4 genotypes
Timescale: acute only, v similar to hep A
Route: faecal-oral BUT very little person to person (vs A)
Diagnosis: igM and igG
Complications: chronic + HCC (vsA)
Prevent: no vaccine, water clean
Hepatitis B
- Cause
- Timescale
- Route transmission
- Diagnosis
- Complications
- Prevent
Cause DNA virus
Time: acute and chronic carriers
Route: vertical, close contact, sexual and blood: health workers, IVDA, sex workers and gay
Diagnosis: many blood tests inc HBV DNA in serum and HBsAg
Complications: chronic asymptomatic, active, cirrhosis, HCC
Prevent: vaccine
Hepatitis D
- Cause
- Timescale
- Route transmission
- Diagnosis
- Complications
- Prevent
CAN ONLY GET WITH HEP B and it works harder, limited tx options, quite uncommon
Timescale: coinfect with hep B= severe acute or superinfect= chronic HDV but may present as acute hep
Route: skin + Sex
Diagnosis: Abs
Complications:cirrhosis, failure, HCC
Prevent: no vaccine, avoidance
Hepatitis C
- Cause
- Timescale
- Route transmission
- Diagnosis
- Complications
- Prevent
Cause: RNA virus Timescale: acute or chronic carriers Route: BLOOD tissue donor, skin, sex, (mother - baby)less than hep b Diagnosis: anti hcv Complications: cirrhosis, HCC Prevent- no vaccine Aim to eradicate 2030
Treatments of hepatitis
- Interferon = chronic hep b
- Ribavirin= hep A
- Direct antivirals ending -vir = entecavir, tenofovir for hep B suppress progression to liver disease. Hep C too.
How does hepatitis B cause liver damage
Not via infection/replication
Liver damage is immune mediated: inflammation -> scarring -> cirrhosis
What is NAFLD/NASH
Range of severity but defined as histological steatosis of liver in individuals without alcohol xs
Pathophysiology of NAFLD
Obesity, metabolic syndrome -> insulin resistance -> circulating carbs/fats ->lipogenesis and lysis -> free FA in liver
free FA -> reactive ox species -> inflammation -> fibrosis -> cirrhosis
NB main cause of mortality is CV effect
Treatment of NAFLD
Lifestyle modification
Target metabolic syndrome
Treat end stage cirrhosis
Investigations to identify fibrosis
Raised AST:ALT ratio Raised AST: platelet (splenomegaly secondary to cirrhosis) FIB-4 estm severity criteria NAFLD fibrosis score IMAGING: fibroscan follow up w biopsy = gold
Alcohol metabolism
Relies on NAD not being saturated otherwise get toxic acetaldehyde build up
Overstimulating pathway -> met change = ketogenesis + FA production -> steatosis w impaired oxidation -> inflammation -> fibrosis + cirrhosis
What is alcoholic hepatitis
Clinical syndrome characterised by: Jaundice Enlarged, painful liver Ascites Very sick px
Treatment of alcoholic liver disease
- stop drinking
- manage complications of portal hypertension
- Manage nutrition and sometimes use steroids
- Liver transplant
Complications of cirrhosis
- Portal hypertension
- varisces + haem
- ascites + SBP + HRS - Liver failure
- encephalopathy
- jaundice - HCC
NB also more permeable gut -> sepsis
Causes of ascites
- Portal hypertension eg secondary to cirrhosis
- Malignancy
- Infection eg tb
- Nephrotic syndrome
- HF
Management of ascites
- Salt control
- Diuretics (can -> hyponatraemia, renal failure, enceph)
- Paracentesis (+ fluid replace, albumin)
- Definitive = liver transplant or TIPS
NB prophylactic abx considered esp prev SBP
Blood supply to gut
Celiac trunk: foregut (oes->D1/2)
SMA: midgut (D3-> prox 2/3 of transverse)
IMA: hindgut (distal 1/3 of transvere -> anal canal)
Signs of upper GI haemmorhage
- Haematemesis- red, emesis to inc coffee ground
- Malaena - black tar stool
- Collapse/anameic
- Abdo pain
Causes of upper GI bleed
- Gastric erosions/ ulcer
- Duodenal ulcer
NB PERFORATED ULCER PRESENT W PAIN NOT HAEM - Varices
- Mallory weiss syndrome
- Oesophagitis secondary to gord
- Rarer causes inc cancer
Mallory Weiss Tear
Tear of gastro-eosophageal junction
History of forecful vomiting = superficial tears
NB these are not full thickness tears = Boerhaaves v diff pres
Management of upper GI bleed
Airways- NBM Breathing - Oxygen C- 2 x large cannula, IV fluids G+S, CM. May need to transfuse FFP, beriplex vit k etc Reassess Endoscopy PPI is only post endoscopy NB RESUS IS SAME FOR LOWER GI will just have colonscopy/angiography/surgery
Rockhall scoring system
Identify patients risk of adverse outcome post upper GI bleed therefore whether to discharge
NB to decide if endscopy is urgent - blatchford score
Management of varisces
same resus protocol \+ ABX Terlipressin to reduce portal pressure even BEFORE endoscopy THEN OGD \+ band ligation if fail balloon tamponade, rescue tipss
6 causes of cirrhosis
3 acquired: 1. AFLD 2. NAFLD 3. Hepatitis AND 3 AI: 1. AIH 2. PBC 3. PSC
What is autoimmune hepatitis
chronic inflammatory liver disease of unknown aetiolofy that leads to T cell mediated destruction of hepatocytes involving B+plasma cells
Diagnosis of AIH
No single test
Abnormal LFT - always screen for igG and autoantibodies
Treatment of AIH
Immunosuppresion(IS)
- induced with high dose steroids
- maintain with azathioprine(IS)and maybe low dose steroids
What is fulminant hepatitis
Can develop from hepatitis
Rapid acute liver failure = decreased synthetic function and rapid onset encephalopathy
-
What is primary biliary cholangitis
Autoimmune destruction of INTRA hepatic bile ducts by T cells
Most common autoimmune liver disease but still rare
Morbidity and mortality of PBC
UNMET CLINICAL NEED - no cure, re-transplantation
1. constant fatugue
2. intense itch
PBC can be managed with oxicolic acid
What is primary sclerosing cholangitis
Autoimmune destruction of EXTRA hepatic bile ducts
Men with UC> crohns
Gold standard diagnosis MRCP
Extra hepatic manifestations of PSC when assd with IBD
Pyoderma gangrenosum
Erythema nodosum
Episcleritis
PSC treatment
None, same as PBC (oxycolic acid)
NB treat the IBD and recurring cholangitis
IT IS THE MOST LIKELY ONE OF THREE AID TO RECUR POST TRANSPLANT
Define fistula
Abnormal connection between two epithelial lined viscera
Causes of PR bleed
FATTHUD
- Haemorrhoids (H)
- Anal fissure (F)
- IBD (U) + other colitis
- colorectal cancer (T)
- Diverticulitis (D)
- Telangectasia (A)
Haemorrhoids presentation
Pain/less rectal bleeding
- bright red on tissue paper/loo
- pruritis
- tenesmus
- peri/anal mass
Anal fissure presentation
Severe pain on defecation - passing glass, can be burning
Fresh blood on stool or papers
- anal spasm
- sentinel pile
Haemorrhoids define
tear/protrusion of enlarged anal cushions (3,7,11)
Anal fissure define
Split of skin of distal anal canal due to repeated hard stool
Define UC
Inflammatory bowel disease involving the mucosal layer of rectum and variable lengths of colon but continuous in nature.
Multifactorial disease, aetiology ? smoking protective
Presentation of UC
Bloody diarrhoea Abdo pain Rectal bleeding Arthritis/spondylarthropathy Malnutrition NB can get weight loss,fever, constipation etc
Diagnosing UC
- Stool sample
- negative c diff culture
- WBC
- elevated faecal calprotectin = Inflam - FBC
- LFT to check for PSC
- ESR/CRP
- Imaging: x ray (TOXIC MEG), flex signoidoscopy, colonoscopy = BIOPSY
Management of UC
Severe: IV steroid, IV IS cyclosporin or surgery toxic meg/failing
Mild: 5-ASA IS like drugs eg mesalazine, oral and rectal steroids
Maintain: 5 ASA, no steroids
Define crohns
Granulomatous transmural inflammation of GIT anywhere from mouth ->anus, skip lesion.
Most common at terminal ileum.
Transmural -> fibrosis, fistulas, perforations
Crohns presentation
Same as UC
+ bowel obstruction(bloat,distend,vomit, constipation, pain)
Management of varices
- A to E
including fluid resus, may give packed RBC transfusion, will give prophylactic abx - Vasoconstriction drug PRE endoscopy+ endoscopic variceal ligation
Terlopressin, Vasopression or Octreotide - If this fails = TIPS rescue OR balloon tamponade
- beta blockers as secondary prophylaxis
Management of uc
- mild = mesalazine
- moderate = prednisolone induction + mesalazine
- severe - hospital, rescue ciclosporin or infliximab (TB) then maintain azathioprine or infliximab
+ surgery
Manage Crohns
- smoking cessation, nutrition
- mild oral steroids(budesonide)
- worse - steroids + immunomodulator (methotrexate, azathioprine)
- even worse + biologic infliximab (TB)
severe - admit hospital
+ surgery
Complications of UC
- colorectal cancer
- toxic megacolon -> bowel perforation -> IAS
- PSC
Complications of Crohns
- anaemia, malnutrition
- Colorectal cancer
- Toxic megacolon
- Small bowel obstruction
- abscesses
