GI Flashcards
What is the most common micro organism is amoebic liver abscess?
Entamoeba histolytica
What happens in ascites?
Fluid leaks out of capillaries due to build up of pressure in the portal vein so fluid leaks out into abdominal cavity, increasing chance on infection.
What does the secretion of TGF do in cirrhosis?
Further stimulates stellate cells for a cascade of myofibroblasts proliferation which eventually produce matrix causing fibrosis.
What are the two types of gallstone?
Cholesterol and Bile pigment stones
How would IBD investigations differentiate between UC and Crohns?
Serology shows Crohns pANCA negative and UC is pANCA positive. Colonoscopy would show the different ulceration.
What is the treatment of a fistula in ano?
Drainage, antibiotics, fistulotomy and excision. May need a seton suture to maintain continence.
What causes refractory ascites?
Occurs secondary to metastatic malignancy caused by peritoneal infiltration by tumour, liver metastases and lymphatic obstruction, heart failure, advanced liver disease
What is treatment for hydatid abscess?
Albendazole and percuatnous aspiration, injection of scolicidal agent and re aspirate. (PAIR), surgery.
What is a 1st degree haemorrhoid and its treatment?
It remains in the rectum an treated with fluids, fibre, stool softener and topical analgesic.
What happens in hepatic pulmonary syndrome?
Endothelin 1 is secreted and binds to capillary cells and cause NO secretion for vasodilation, so not all will be replenished by o2 due to increase pressure, leucocytes also migrate to pulmonary capillaries to further stimulate NO secretion, causing insufficient o2 supply throughout the body, causing difficulty breathing
What causes an abscess?
Gut organisms, mainly in women, in the perianal area.
What are the ulcer management risk scales?
Pre endoscopy - Rockall score / Glasgow Blatchord Post endoscopy - Forest scale
What is extracorporeal shock wave uthotripsy?
A shock wave directed radio-logically or by US onto gallstones.
What are the causes of peritonitis?
blood borne or genital tract organisms, cirrhosis with ascites, ruptured appendicitis or diverticulitis, IBD, perforation, pancreatitis, surgery, spontaneous, PID, TB
What is midgut dysmotility and its symptoms?
Disordered motility and visceral sensation after the SI, causing abdominal pain from eating which is not relieved by opening the bowels, abdominal distension, postprandial fullness, nausea, anorexia, weight loss
Treatment of gastritis?
H. pylori - PPI, amoxicillin and clarithromycin, metronidazole Antacids or H2 receptor antagonists, PPI, Ranitidine
What main bacteria can cause infective diarrhoea?
salmonella (reptiles), shigella, campylobacter (puppies), Yersinia, E.coli, C.diff (antibiotics, in hospitals, community acquired, antimicrobials), mycobacterium avium complex (watery)
Symptoms of acute pancreatitis?
epigastric pain radiating to the back, nausea, vomiting, peri-umbilical and flank bruising
What symptoms are specific to amoebic liver abscess?
Diarrhoea, cough (anchovy paste suggesting broncho pleura fistula formation), history of travel to endemic areas in 5 month
What is an incisional hernia?
Weakness caused by a surgical repair that has not fully healed
What is used to detect scleroderma and what is the treatment?
Manometry or barium swallow, treat the reflux and the benign stricture.
How is fibrosis caused in liver cirrhosis?
Stellate cells and Kupffer cells are activated by cytokines and their receptors, reactive oxygen intermediates and paracrine and autocrine signals causing stellate cells to become swollen, lose retinoids, secrete cytokines (TNF-a, IL-6, IL-1B, TGF) and up regulate receptors for proliferative and fibrogenic cytokines via the CCL2 receptor e.g. PDGF and TGFB1.
What is diverticulitis and the symptoms?
When diverticulum in the intestines become inflamed from infection, LI pain, fever, constipation, diarrhoea, and decreased appetite. May be due to accumulation of pus from an abscess leading to perforation.
What is the treatment of Crohns disease?
Continued monitoring of complications, diet, TNF-a antagonists, methotrexate, colectomy, B12 and folate supplements, thrombosis prophylaxis, stop smoking, corticosteroids, antibiotics
What is an anal fissure and what is it caused by?
A tear in the sensitive skin liner lower anal canal, distal to the dentate line, causing pain on defecation. Caused by hard faeces or secondary to Crohn’s or ulcerative colitis. Spasm could also constrict the inferior rectal artery causing ischemia, making it difficult to heal.
Symptoms of ischaemic colitis?
Sudden abdominal pain, passage of bright red blood, shock, distended and tender abdomen, thumb printing seen a splenic flexure on x-ray
Symptoms of gastritis?
functional dyspepsia, red mucosa, epigastric pain, vomiting, haematemesis
What does Ranson’s criteria measure on admission of acute pancreatitis?
glucose, AST, LDH, Age, WBC
What are the investigations and results for peptic ulcer?
H.pylori test is a 13C urea breath test, stool antigen test, serological test and biopsy urease test. If younger than 55yrs and is H.pylori positive due to the tagged CO2 being present, start treatment immediately. If older than 55, may need endoscopic diagnosis and cancer exclusion.
What is ulcerative colitis called if it reaches the transverse colon?
Extensive colitis (20%)
What happens in hepatorenal syndrome?
No damage to kidney, but reduced kidney perfusion due to insufficient blood supply to kidneys from portal hypertension
What causes a peptic ulcer?
Can be caused by H.pylori infection, NSAIDs or corticosteroids as they reduce mucosal protection and cause mucosal ischaemia. This causes the mucosa to appear inflamed and friable with a fibrous base and increase in inflammatory cells. (rarer causes are hyperparathyroidism, Zollinger Ellison syndrome, vascular insufficiency, sarcoidosis and Crohn’s disease.)
Treatment of diffuse oesophageal spasm?
PPIs for reflux e.g. omeprazole, antispasmodics, nitrates, CCBs, GABA receptor agonists e.g. baclofen. Balloon dilation of longitudinal oesophageal myotmy.
What is the treatment for chronic pancreatitis?
Stop smoking, no alcohol, avoid high fat foods, analgesics, insulin therapy for diabetes, membrane stabalising agents e.g. pregabalin, duct drainage, pancreatic enzyme replacement therapy (PERT), multivitamin supplements, tricyclic antidepressants
What would liver biochemistry show in cirrhosis?
As severity increases, PT and creatinine increase and sodium decreases due to defect in free water clearance. Increase in ALP and aminotransferase. Look for viral markers, seum autoantibodies, immunoglobulins, iron, ferritin, coper, a, antitrypsin.
What causes varices?
Liver cirrhosis
Symptoms of varice?
Massive upper GI bleed (much more than Mallory Weiss tear)
Features of C.diff which make it suitable for infection?
Gram positive with terminal bulge due to spore, some hyper virulent strains e.g. ribotype 027, glucosyltransferases that target Rho family GTPases blocking their activation, toxin and b induce actin depolymerisation and cytoskeletal arrangement effecting epithelial tight junctions and permeability, spores allow persistence in environment, ingested by faeces-oral route, germinate in colon on exposure to bile salts
What would investigations show in IBD?
increased WBC, platelets, ESR, CRP, stools and c.diff toxin test to exclude infection, US shows inflammations and free fluid in abdominal wall
Which hiatus hernia is more painful?
Rolling due to volvulus and strangulation formed, so must be treated surgically.
Why dose liver cirrhosis cause itching?
Due to high levels of uric acid that can’t be cleared by the liver?
DD for diarrhoea?
Malaria, sepsis, IBD, IBS, mal absorption (coeliac), malignancy, overflow with constipation, medicine (PI as antivirals), throtoxicosis
What is acute cholangitis?
A bile duct duct infection mostly from gall stone obstruction, causing biliary sepsis and septicaemia
What is the treatment of primary biliary cirrhosis?
Ursodeoxycolic acid which improves bilirubin and ATL. Cholestyramine to control pruritus. Steroids improve biochemical and histological disease Fat soluble vitamin supplements Bisphosphonates for osteoporosis Rifampicin and naloxone hydrochloride for opioid antagonists Liver transplant.
What is a 4th degree haemorrhoid and its treatment?
It remains persistently prolapsed. Treated with excisional haemorrhoidectomy or a stapled haemohhoidopexy.
What causes hydatid liver abscess?
Food or water contaminated with dog faeces causing a multi-layered cyst with daughter cysts tat can calcify
What is acute pancreatitis?
inflammation of the pancreatic gland and parenchyma due to acute injury
What are the 3 types of liver abscess?
Pyogenic, amoebic and hydatid
Signs and symptoms of IBD?
diarrhoea, rectal bleeding, abdominal pain, tenesmus, weight loss, fever, vomiting, cramps, muscle spasms
Signs and symptoms of liver cirrhosis?
Astrexis (hepatic flap), parotid gland swelling, spider naevi, jaundice, gynocomastia, hepatomegaly, splenomegaly, ascites, caput medusa, testicular atrophy, nail changes, clubbing, pulmonary empyema, hypertrophic osteoarthropathy
What are the symptoms of chronic
epigastric pain radiating to back, relieved on sitting forward and worse when eating and heavy drinking, weight loss, mal absorption, diabetes, jaundice, oily foul smelling stools
Chronic pancreatitis causes malnutrition, what are some complication of this?
osteoporosis, vision loss, difficulty maintaining weight
What are the two types of hiatus hernia?
Sliding (95%) and rolling
What causes a rectal prolapse and how?
Straining excessively and constipation leading to ulceration of anterior rectal wall so that it bleeds and produces mucus on defaecation.
How are cholesterol stones formed?
By cholesterol crystallization, when there is an excess of cholesterol in the bile duct as there is reduced bile salt and phospho lipids which normally keep cholesterol soluble to form micelles and vesicles
Epidemiology of IBD?
Crohns is more common than UC, and females are more likely to get Crohns, whereas both are equally predisposed in UC. Onset occurs usually around 15-40 years.
What is primary biliary cirrhosis?
An autoimmune illness where T cells are destroying the bile ducts leading to impaired bile formation and impaired bile secretion causing cholestasis causing retained toxic material leading to cirrhosis
What is the treatment for diverticulosis?
Increased fibre, stool softeners
What is a fistula in ano?
Blockage of deep intramuscular gland ducts between the skin and the anal /rectal canal causing a abscess with discharge.
What is gastritis?
Inflammation of the stomach lining due to decreased prostaglandin production causing mucosal damage.
Complications of ulcerative colitis?
severe bleeding, toxic megacolon, rupture of bowel, colon cancer, osteoporosis, haemorrhage, primary sclerosing cholangitis
What is peritonitis?
Inflammation of the peritoneum and endothelial lining of the abdominal cavity and can be localised or generalised.
How does a rolling hiatus hernia occur?
Part of the fundus prolapses through the hiatus, alongside the oesophagus so the sphincter remains competent and below the diaphragm
What does Achalasia cause dysphagia for from onset and what other symptoms occur?
Solids and liquids. and regurgitation of food from dilated oesophagus, mainly at night, with spontaneous chest pains due to oesophageal spasm.
What does TNF-a do in cirrhosis?
Attract more neutrophils and T cells for inflammation causing necrosis and fibrosis.
What are factors influencing IBD?
antimicrobial peptide problems, autophagy, handling of bacteria, cytokines, diet, infection, stress, NSAIDs, smoking, antibiotics
What is a toxin mediated cause of infective diarrhoea?
Shiga toxin (bloody), B cereus and S aureus
What do clonochis sinensis and opisthorchis spp. cause?
relapsing cholangitis and cholangiocarcinoma
What happens in hepatic carcinoma and the symptoms?
Causes pain, sweating, hepatomegaly and weight loss. Cell apoptosis and uncontrolled multiplication of liver cells.
What are probiotics?
Live or attenuated bacteria or bacterial products for a significant health benefit in the host e.g. bifidobacterium infancts 35624
What is the difference between a micro and macro nodular in the liver and in what diseases would you see them?
Micro -
What is an appendicitis and what does if present with?
Inflammation of the appendix, causing umbilical pain, migrating to the right iliac fossa and tenderness with guarding, nausea, vomiting, anorexia and diarrhoea
What are the symptoms of peritonitis?
Generalised acute abdominal pain that can become localised, abdominal tenderness and muscle guarding, fever, decreased peristalsis, abdominal distension, pyrexia, chills, dizziness, inability to pass stool, nausea, anorexia, vomiting, sinus tachycardia, lie still with shallow breaths
Describe stage 1-4 of ascites
1 - detectable after careful examination/US 2 - easily detectable but of relatively small volume 3 - obvious but not tense 4 - tense and large
What is toxic megacolon?
dilated thin walled colon with >6cm diameter, gas filled and contains mucosal islands, risk or perforation and mortality
Complications of cirrhosis?
Increase in pressure from portal hypertension causes ascites, hepatic encelopathy, variceal haemorrhage, bacterial peritonitis, hepatic renal syndrome, portal hypertension gastropathy, hepatic hydrothorax, hepatopulmonary syndrome, portopulmonary hypertension, cirrhotic cardiomyopathy.
What is the treatment of an appendicitis?
laparoscopic surgery, IV fluids, antibiotics if mass, interval appendictectomy prevents further acute episodes
What causes intra hepatic portal hypertension and what investigation is needed?
Can be mild fibrosis if non cirrhotic portal hypertension or schistomsomiasis with extensive fibrosis or congenital hepatic fibrosis or nodular regenerative hyperplasia. Need a wedge liver biopsy.
What is a complication of biliary colic if it is not treated?
Acute pancreatitis
Complication of TIPS and variceal banding?
hepatic encephalopathy
Complications of primary biliary cirrhosis?
cirrhosis, osteoporosis, osteomalacia, polyneuropathy
What is the difference in histology between acute and chronic gastritis?
Acute has neutrophil infiltration and chronic has mononuclear cells, chiefly lymphocytes, plasma cells and macrophages.
Complications of gastritis?
Gastric outlet obstruction, pernicious anaemia, peptic ulcers, stricture formation, mucosa associated lymphoid tissue (MALT) lyphoma
What is Achalasia and how is it caused?
degeneration of the lower oesophageal sphincter and the nerves controlling the muscles causing impaired relaxation of the LOS, difficulty swallowing, chest pain and regurgitation of food. Thought to be caused by inflammation of myentreric plexus of the oesophagus with reduced ganglion cell number, reduced NO containing neurons and loss of inhibitory nitregic neurones.
What is biliary pain and what causes it?
Pain associated with temporary obstruction of the cystic duct and common bile duct, caused by a stone. Pain is in the RUQ and spreads to the right shoulder and scapula area.
What investigations would you conduct for liver cirrhosis?
Liver biopsy, liver function test, ultrasound, metabolic breath test (assesses functional reserve of the liver), hepatic venous pressure gradient, transient elastography (measure liver stiffness of fibrosis and oedema), CT shows hapatosplenomegaly and dilated collaterals, endoscopy detects varicies and portal hypertensive gasrtopathy
What is chronic cholecystitis, the signs and symptoms?
Chronic inflammation of the gall bladder wall associated with gallstones and IBD, causing flatulence, nausea, discomfort in right hypercondrium, fatty food intolerance and US shows small sunken gall bladder, Treat with cholecystectomy.
What is a common micro organism in peritonitis?
s.pneumoniae and other streptococci, staph aureus, E.coli, P.aeruginosa
What is portal hypertension?
Blockage of blood flow through the liver, causing a portal vein bypass, increasing portal vein pressure, resulting in backflow towards the gastro oesophageal vein and cause oesophageal-gastric varicies causing bleeding.
What is a pilonidal sinus?
An abscess near the anus caused by an obstructed hair follicle which has excited a foreign body reaction causing secondary tracks to open laterally forming foul smelling discharge.
What is shown in investigations for chronic pancreatitis?
raised serum amylase and lipase, decreases faecal elastase, mutations in genes, CT shows calcification, US and MRI, pancreatic stimulation test using secretin
What main viruses can cause infective diarrhoea?
Norovirus (contact with other cases) and rotavirus (small children), CMV (transplant)
What is the treatment of diverticulitis?
Drainage of abscess, surgery to remove affected colon segment (may need stoma), clear liquid diet, oral antibiotics (amoxicillin-clavulinic acid)
What is classed as diarrhoea?
6 loose bowel movements a day. More than 1 month is chronic. Less than 1 month means it could be infection.
What happens in the space of Disse in cirrhosis?
Collagen replaces the matrix and loss of endothelial fenestrations (openings) cause impairment of liver function. Increase in tissue inhibitors of metalloproteinases cause inhibition of collagen degradation.
What is the function of mucus in the stomach?
Acts as a barrier to acid
What are systemic complications of IBD?
conjunctivitis, iritis, mouth ulcer, fatty liver, liver abscess, thrombosis, large joint arthritis, erythema nodosum and pyodema gangrenosum due to cytokine release
How do gallstones cause acute pancreatitis?
They block the ampulla drainage, causing ductular hypertension and increase in ca2+, causing early activation of trypsinogen
How can bacteria get into the liver in pyogenic abscess?
Via portal vein (appendicitis, diverticulitis), biliary tract (cholangitis), hematogenous (bacteramia), trauma or infection of tumour/cyst
What do COX 1 enzymes do in the stomach?
Make prostaglandins in the mucosal lining of the stomach to protect it from the stomach
What are the main two types IBD and their main differentiation?
Crohns (discontinuous and patchy with skip lesions, transmura, granulomasl) and ulcerative colitis (continuous and restricted to the mucosa, moving distal to proximal with pseudopolyps, petichae exudates oedema, crypt abscesses, mucin depletion, goblet cell depletion)
What do investigations show in acute pancreatitis?
increased serum amylase and lipase, US and CT to look for cause, LFTs, FBC, MRI to assess pancreatic damage
DD for upper GI bleeds?
oesophageal varices, gastritis, peptic ulcers, malignancy, Mallory Weiss tear
What is gastropathy?
injury to gastric mucosa, associated with epithelial damage and regeneration with little of no accompanying inflammation
What is systemic sclerosis (scleroderma) and what does it cause?
Dimished peristalsis and oesophageal clearance caused by smooth muscle replacement with fibrous tissue. This decreases LOS pressure, causing reflux and mucosal damage, so deep strictures develop with dysphagia and heartburn.
What are parasitic causes of infective diarrhoea?
Giardia (well water), cryptosporidium (HIV or transplant or flooding), entamoeba (travellers)
Investigations in ascites?
serum ascites albumin gradient (SAAG), microscopy, diagnostic aspiration of ascitic fluid, cytology for malignant cells, amylase to exclude pancreatic ascites, neutrophil count, US and CT, protein count, sodium
Where are the most common places for ischaemic colitis to occur?
In watershed areas, in the splenic flexure and caecum
Complications of acute pancreatitis?
haemorrhage, DIC, ARDS, multi organ failure, necrosis
What is the treatment of an amoebic liver abscess?
Metronidazole and luminal agent, aspirate if large
What causes chronic pancreatitis?
CF, alcohol, malnourishment, pancreatic duct obstruction, genetic, autoimmune, smoking, elevated triglycerides, hereditary pancreatitis
What cause post hepatic portal hypertension?
Prolonged severe heart failure with tricuspid incompetence and constrictive pericarditis.
What does IL-8 do in the formation of peptic ulcers?
It is a cytokine that promotes inflammation
Treatment of acute cholangitis?
MRCP and ERCP for further assessment, biliary drainage and biopsy cultures. IV antibiotics (cefotaxime, metronidazole, amoxicillin, and gentamicin) and bile duct drainage with cholecystectomy, remove stones via balloon or basket catheter, if it can’t be removed, place a stent in the biliary tree. Mechanical lithotripsy.
Investigations for gastritis?
H.pylori urea breath test, endoscopy with biopsy of stomach lining, stool microscopy, urinalysis, blood, H.pylori antibody
What is a peptic ulcer?
A break in the superficial epithelial cells, penetrating down to the muscularis mucosa of the stomach or duodenum (mainly in duodenal cap or lesser curvature near incisura)
What is a Mallory-Weiss tear and what is it caused by?
A linear mucosal tear at the oesophageal junction caused by a sudden increase in intra abdominal pressure. Occurs after a bout of coughing, retching and after an alcohol dry heaves. It is the cause of 10% of upper GI bleeds.
Complications of ascites?
Spontaneous bacterial peritonitis e.g. E.coli, treat with antibiotics and liver transplant
What is the treatment of ulcerative colitis in a flare up?
5-AminoSalicylicAcid therapy e.g. sulfasalazine if mild, IV fluids, IV corticosteroids to reduce flare, IV antibiotics if all unresponsive
What are causes of acute pancreatitis and how?
Gallstones, alcohol (trauma, mumps, autoimmune disease, drugs, hyperlipidaemia, steroids) - an acute increase in pancreas intracellular calcium ions, causing an early activation of trypsinogen to trypsin and an impairment of trypsin degradation by chymotrypsin C, leading to cellular necrosis and haemorrhage.
Treatment of peptic ulcer if H.pylori negative?
PPIs to stop excess gastric secretion, stop the initiating factors, use selective COX2 inhibitors instead of NSAIDs in future to prevent recurrence, follow up with endoscopy and biopsy. Surgery of vagotomy or partial gastrectomy if uncontrolled haemorrhage, antacids
How do you diagnose infective diarrhoea?
Stool culture (SSYC and Shiga toxin), ova and parasite, Cryptosporidium and Giardia antigen, C.diff toxin A and B PCR, faecal leukocytes (inflammation), BMP and electrolytes if dehydrated., CT scan, colonoscopy, biopsy
What is 5-ASA?
It treat UC and is activated by bacteria in the colon as it breaks down azo bonds to release 5-ASA. Released in the microsphere and acts via PPAR-Y signalling pathway to induce and retain remission and reduce inflammation.
Treatment of dyspepsia?
Stop smoking and alcohol, reduce weight around stomach and gaviscon in the day to reduce reflux. PPI before dinner and breakfast. Stop NSAIDs. Check for red flags (weight loss, dysphagia, mass, vomiting) for malignancy. Anti-reflux surgery. If functional (non ulcer) have diet review and antidepressants.
How do you diagnose primary biliary cirrhosis?
Positive anti mitochondrial antibody (AMA), positive antigen M2 and increased GGT and alkaline phosphatase, liver biopsy shows portal tract infiltration of lymphocytes and pasma cells and granulomas in zone 1, increased IgM as failure to switch to IgG, increased serum cholesterol, US shows diffuse alteration in liver architecture
What is acute cholecytitis and its symptoms and signs?
Severe pain in the RUQ following the impaction of a stone in the cystic duct or neck of gall bladder causing fever, raised WCC, abnormal liver biochemistry, focal tenderness, muscle guarding and thicken gall bladder wall
Treatment of anal prolapse?
Increase fluids and fibre, stool softeners, and if severe, surgical rejection rectopexy.
What microorganisms commonly causes biliary disease?
E.coli, K.pneumoniae, Bacterioides (anaerobes), Enterococci, clonorchis sinensis, opisthorchis spp., fasciola hepatica
What is the treatment of pruritus ani?
Enhanced toilet hygiene, capsaicin, no spicy food, anaesthetic cream keeping the area dry, avoid perfumed soaps and moisturised creams..
Signs and symptoms of acute cholangitis?
Causes RUQ pain radiating to LUQ and epigastrium, fever, jaundice (dark urine, pal stools, itchy skin), rigors and can be tachycardia during an attack. Increased WBC, leucocytosis, abnormal liver biochemistry, increased serum bilirubin and alkaline phosphatase. U/S shows dilated common bile duct and the cause of obstruction. ATL and PTT increased, decreased potassium absorption
Treatment of cirrhosis?
Avoid alcohol, aspirin, NSAIDs, reduce salt intake, adjust medications, manage symptoms e.g. cramps, hernias, treat complications, liver transplant.
What is a hiatus hernia?
Part of the stomach herniating through the oesophageal hiatus of the diaphragm caused by obesity and constipation
Treatment of a pilonidal sinus?
Excision of sinus tract with pre op antibiotics, complex tracts can be laid open and packed individually or skin flap can be used to cover the defect, keep clean, remove hair, drain pus.
DD for appendicitis pain?
IBD, inflamed Meckels diverticulum, acute salpingitis in women, terminal ileitis from Crohn’s, mesenteric lymphadenitis
Treatment of peptic ulcer if H.pylrori positive?
Eradicate H.pylori with antibiotics, to increase healing and reduce recurrence, anti-secretary treatment if haemorrhage or perforation, antacids
What part is mainly affected in ulcerative colitis?
inflammation of rectal and sigmoid colon in 50% (proctitis)
What is a problem with probiotics?
Quality control and formulation restrict the clinical availability.
DD for RI pain?
Appendicitis, ectopic pregnancy, ovarian torsion, inguinal or femoral hernia
What makes up brown pigment stones, where are they found and when?
Calcium, salts of fatty acids and calcium bilirubinate. Found in bile stasis and biliary infection and cause recurrent bile duct stones post cholecystectomy.
In the presence of abdominal pain, what constitutes functional diarrhoea?
Passage of several stools in rapid succession, usually first thing in the morning A formed first stool, later ones are more mushy and watery Urgency of defecation Anxiety about bowel movement Exhaustion after defecation
What causes a fistula in ano?
Perianal sepsis, abscesses, Chron’s disease, TB, diverticular disease, rectal carcinoma, immunocompromised
DD for RL pain?
kidney stones, UTI, constipation
What is diffuse oesophageal spasm and its symptoms?
Severe oesophageal dysmotility causing retrosternal chest pain and dysphagia, can accompany GORD. Can cause marked contractions on swallowing in oesophagus, but can be asymptomatic.
Epidemiology of DU?
in 10% of adults, 2.3x more common than GU, more common in elderly and developing countries.
What does Ranson’s criteria measure after 48 hours of acute pancreatitis?
calcium, Hct, paO2, BUN, base defecit, sequestration of fluids (CHOBBS)
What are potential complications of hernias?
strangulation, incarceration, fistula formation, femoral are irreducible
How dose a mechanical lithotripsy work?
it facilitates fragmentation by increasing bile salt content to solubilise stones, uses oral chendeoxycholic acid and ursodeoxycholic acid
What would Achalasia show on investigations?
CXR - dilated pesophagus, fluid behing heart and absent fundal gas shadow Manometry - aperistalsis of oesophagus and failure of lower sphincter relaxation Oesophagoscopy and CT scan exclude carcinoma Barium swallow - lack of peristalsis and synchronous contractions inn oesophagus body with dilatation. Lower end shows bird beak due to lack of relaxation.
Treatment of varice?
IV Octreotide inhibits vasodilation and decreased bloodflow. IV Terlipressin restricts portal inflow by splenic arterial constriction (CI if IHD), somatostatin is similar Endoscopic banding around large veins to cut off blood supply. Transjugular intrahepatic porto systemic shunting to create a bypass with a metal stent between portal and hepatic venous circulation to relieve hypertension. Balloon tamponade with sengstaken Blakemore tube to prevent blood flow to bleeding point Injection sclerotherapy produces vessel thrombosis Endoscopic haemostasis by dilute adrenaline injection with coagulation of vessel, thermal therapy and mechanical dips to the vessel.
DD for RUQ pain?
Pancreatitis, Gastric ulcer, gallstones, biliary colic, acute cholangitis, acute cholecystitis
Treatment of biliary colic?
Analgesia, rehydrate, elective laproscopic cholecystectomy, may need a MRCP before if the liver biochemistry is abnormal
What is the treatment of functional diarrhoea?
Loperamide and an tricyclic antidepressant e.g. clomipramine
What part is mainly affected in crohns?
caecum and ileum (40%) SI (30%) - has skip lesions
Symptoms of ascites?
painful abdominal distension, SOB, nausea, vomiting, loss of appetite, constipation, cachexia, weight loss, jaundice
What causes diverticulosis?
low fibre, constipation, straining with bowel movements due to increased pressure causing the mucosa and sub mucosa to herniate through the weakened part, forming a diverticulum
What are common micro organisms in a pyogenic liver abscess?
E.coli, K.pneumoniae, Streptococcus milleri, bacterioides spp.
What causes pre hepatic portal hypertension?
Blockage of the portal vein due to thrombosis caused by secondary congenital portal venous abnormality.
How does H.pylori cause a peptic ulcer?
It is adapted to live in gastric mucus (antrum) as it has urease which generates ammonium to buffer acidity and neutralise it so H.pylori can move down to the epithelial cells and adhere. It then excretes Cag A and Vac A, breaking down the tight junctions of epithelial cells and induces inflammation by mononuclear and neutrophil cellular infiltrate in lamina propria so the HCl acid layer can reach the epithelial cells and damage them causing an ulcer. This promotes gastric acid secretion and spread to the duodenum.
What is the treatment for midgut dysmotility?
avoid narcotics, FODMAP diet, SSRI paroxetine and smooth muscle relaxant
What are the symptoms of a liver abscess?
Fever, weight loss, nausea, vomiting, leucocytosis, RUQ pain radiating to right shoulder and scapula, jaundice (more severe than in cholencytitis, tender hepatomegaly
What makes up black pigment stones and in what kind of patient would you find them?
Calcium biliruibinate, mucin glycoproteins and calcium carbonate, in haemolytic patients
What causes calcification in chronic pancreatitis?
The prolonged intra pancreatic enzyme activity, leads to precipitation of proteins forming plugs and a nidus for calcification and ductal obstruction and hypertension
Epidemiology of primary biliary cirrhosis?
90% are female, aged 35-55years
If H.pylori decreases gastric acid in a patient, what does this suggest?
Gastric cancer
What is a varice?
Elevated pressure in the portal renal system causes dilated veins to become engorged which can rupture if the pressure becomes more than >12mmHG, leading to haemorrhage
What is haemorrhoids and what is it caused by?
Disruption and dilation of the 3 anal cushions which line the anus to help with anal closure. Caused by gravity, pregnancy, pelvis tumour, CCF, portal hypertension, increased anal tone and straining at the stool.
What causes an amoebic liver abscess?
From food contaminated with faeces in endemic areas, swallow cyst into intestines, reaches caecum and grows and goes into mesenteric vein, portal vein and liver
Complications of diverticulosis?
Diverticulitis, abscess in pelvis from spreading pus which can erode into the urinary bladder causing bladder infection and passing of intestinal gas in the urine, colon obstruction, bacterial peritonitis, bleeding into colon, fistula formation
What factors would lead you to do surgery in varice treatment?
Severe bleeding or bleeding despite transfusing 6U if >60. Active of uncontrollable bleeding at endoscopy. Initial Rockall score >=3 or final Rockall score >6.
What can cause a false positive result in a Heliobactor test?
Previous Heliobacter treatment
What does the rate of cholesterol stone formation depend on?
Cholesterol supersaturation of bile, crystallization promoting factors in bile (mucus and calcium) and motility of gall bladder.
What is pruritus ani and what are its primary and secondary causes?
Itching and scratching of the perianal due to haemorrhoids or overactive sweat glands or secondary to threadworm, a fungal infection or perianal eczema.
What is type B chronic gastritis?
Caused by H.pylori infection, and is the most commo chronic cause
Treatment of hepatic encephalopathy?
Nursing, NBM, ranitidine to reduce acid secretion, sucralfate to decrease oesophageal ulceration post endoscope
What test would differentiate between amoebic and pyogenic liver abscess?
Stool microscopy, antigen (fresh), culture, serology EIA
What investigations would be used for a hernia?
Endoscopy, barium swallow, ultrasound
Diagnosis of peritonitis?
CXR shows free air and fluid under diaphragm and perforation, increased WBC, US and CT show location, peritoneal aspiration, serum amylase for pancreatitis
What are the symptoms specific to hydatid abscess?
asymptomatic until 5cm. The symptom depends on where the cyst is. Diagnose by serology ELISA
Treatment of acute cholecystitis?
NBM, IV fluids, opiate analgesia, IV antibiotics (Cefotaxime), drain if empyema, delayed cholecystectomy to allow symptoms to settle.
What are complications of Achalasia?
Aspiration pneumonia, increased risk of oesophagus squamous carcinoma and reflux esophagitis risk.
DD for lower GI bleeds?
haemorrhoids, diverticulitis, IBD, malignancy, polyps. angiodysplasia, infectious diarrhoea, anal fissure
What is a femoral hernia?
Weakness in the femoral canal, lateral and inferior to the pubic tubercle, more common in females, presenting with a mass in the groin.
Treatment of a Mallory-Weiss tear?
Can heal spontaneously, or can use surgery to over sew the tear. IV omeprazole to reduce re-bleeding rates and reduce the need for surgery.
Treatment of peritonitis?
NPO status, nasogastric tube to suction and decompress stomach, IV fluids, antibiotics, analgesics, oxygen and electrolyte replacement, surgery to identify cause and repair, drain peritoneal fluid, colon resection, antimicrobials, ascitic tap if >250PMN/uL and positive culture
What are some complications of acute cholecystitis?
Empyema (pus), perforation and peritonitis
What is the management of ulcerative colitis when there is not a flare up?
5-ASA therapy via rectal or oral and then oral prednisolone, colectomy
Treatment of infective diarrhoea?
Bacterial - fluoroquinolones, azithromycin, susceptibility testing C.diff - metronidazole or oral vancomycin Giardia - metronidazole or tinidazole Cryptosporidium - nitazoxanide Virus - self limited Amoebiasis - metronidazole and intraluminal agent e.g. paromycin or diloxanide
What do investigations show with diverticular disease?
Increased WCC, ESR, CRP and leucocytosis. CT shows paracolic abscess, colonic wall thickening, US shows thickened bowel and large pericolic collections
What is the difference between 2nd and 3rd degree haemorrhoids and what is their treatment?
2nd is prolapse through anus on defecation but spontaneously reduces and 3rd degree is the same but needs digital reduction. Treatment via rubber band ligation, scerolsant injection, infrared coagulation or cryotherapy.
How does smoking affect the two IBD?
Aggravates Crohns but protects against ulcerative colitis
DD for LUQ pain?
gastric ulcer, pancreatitis
DD for LI pain?
diverticular disease, IBD, ectopic pregnancy, ovarian torsion, inguinal or femoral hernia
What is an umbilical hernia?
Weakness in the umbilicus, mainly in males, and is self resolving.
What is skip lesions in the colon referred as?
Crohn’s colitis
Causes of liver cirrhosis?
Chronic viral hepatitis, alcoholic liver disease, hemochromatosis, autoimmune hepatitis, Wilson’s disease and coeliac disease
What is the pathogenesis behind genetic chronic pancreatitis?
There is a mutation in the PRSSI gene which codes for cationic trypsinogen (the main trysinogen produced by the pancreas).
How does the sliding hiatus hernia occur?
The sphincter and top part of the stomach push upwards into the chest and cause heart burn due to reflux. They can slide back and forth through the hiatus, so symptoms can come and go.
Where is fasciola acquired from and what does it cause?
Fluke acquired from livestock in wetlands. Larvae picked up from plants, leads to hepatitis followed by biliary tract infestation with eoisinophilia
What is the treatment of acute pancreatitis?
IV fluids, nasogastric suction prevents abdominal distension and vomit, analgesics, prophylactic antibiotics, NBM, LMW heparin for DVT, ERCP for gallstone extraction, low fat diet
What are some acute causes of gastritis?
stress, NSAIDs, uraemia, Curling’s ulcer, alcohol, spicy food
What type of cell produce HCl acid in the stomach?
Parietal cells
What are prebiotics?
non-digestible food supplements that are fermented by host bacteria, altering the microbiota of the host, stimulating the growth of healthy bacteria.
Symptoms of primary biliary cirrhosis?
Fatigue, pruritus, dry mouth and eyes, RUQ discomfort, hepatomegaly, hyperpigmentation of skin, jaundice, pigmented xathelasma, association with other autoimmune diseases
Apart from UC and Crohns, what are other IBDs?
infective colitis, diverticulitis, ischaemic colitis
What is chronic pancreatitis?
structural integrity of the pancreas permanently altered due to chronic inflammation
Diagnosis of varice?
EGD to confirm diagnosis, identify bleeding site, estimate risk of bleeding , stop NSAIDs and start PPI post endoscope
Investigations in liver abscess?
LFT, elevated AST/ALT/ALP/bilirubin, low albumin, US shows hypo echoic mass and CT scan shows huge abscess, CXR shows pneumonia and air under diaphragm from complications
What causes black pigment stones?
A decrease in bile salts causes an increase in solubilization, colonic reabsorption of bilirubin, enterohepatic circulation and therefore an increase in biliary bilirubin secretion and increased stones
Complications of portal hypertension?
Gastro-oesophageal varicies, splenomegaly, thrombocytopenia, low platelet count, anaemia, leucopoenia, haemorrhoids, hepatic encephalopathy due to excess ammonia, loss of memory, confusion, coma, hepatic pulmonary syndrome,
DD for hypogastrium pain?
UTI, appendicitis, IBD, diverticular disease
What are mixed gallstones made up of?
Calcium salts, cholesterol and pigment
Questions to ask in a diarrhoea presentation?
times per day, blood, mucus, recent travel, pets, day care exposure, children, food exposure, sexual history, immunosuppressed, diabetes, medications, dehydrated, generalised tenderness, hyperactive bowel sounds
What is dyspepsia and what does it present with?
Postprandial fullness or early satiation or epigastric pain or burning for >4weeks a year. Presents with reflux, indigestion, heartburn, acid taste, boating.
What is the difference between a direct and indirect inguinal hernia?
Direct is due to weakness in abdominal wall, medial to inferior epigastric vessels Indirect is due to congential weakness of the internal inguinal ring, lateral to the inferior epigastric vessel (more common)
DD for LL pain?
kidney stones, UTI, constipation, IBD, diverticular disease
Complications of peptic ulcer?
Perforation, peritonitis, pancreatitis, gastric outlet obstruction from surrounding oedema or scarring which can lead to projectile vomiting and metabolic alkalosis, haemorrhage
How is gastric obstruction caused in gastritis?
There is increased inflammation which extends into the muscle lining of the stomach at the gastro duodenal sphincter so it cannot empty leading to severe vomiting, hypokalemia due to electrolyte loss and metabolic alkalosis, treat with pylori plathy
Treatment of ischaemic colitis?
Treat the symptoms, but surgery may be needed if gangrene, perforation or stricture formation
What is the scoring system called for acute pancreatitis and when do you do it?
The Ranson and Glasgow scoring system, on admission and 48hrs post presentation, The acute physiology and chronic health evaluation score (APACHE) assesses the severity based on physiological lab values.
Why does liver cirrhosis cause oedema?
Due to ascites, not all fluid will be returning to the heart, so the heart will think it has not got enough blood (hypovalaemia) so will cause vasodilation to increase blood flow to organs so the kidney will active RAAS system to increase sodium and water reabsorption leading to oedema. It is also encouraged by hypoalbuminaemia.
Prevention of recurrent variceal bleeding?
Non-selective BB e.g. propanol to reduce pulse rate and lower portal pressure Repeated Variceal banding if CI to BB TIPS if all else fails
What do panneth cells secrete?
Antimicrobial peptides to keep the microbes in the intestine in check
Treatment of pyogenic liver abscess?
Antibiotics e.g. amoxicillin-clavulinic acid, percutaneous aspiration US/CT guided, surgery to drain or remove abscess
Risk factors for gallstones?
age, female, obesity, Scandinavian, South America, smoking, parity
Symptoms of peptic ulcer?
Recurrent, burning epigastic pain, worse when hungry, nausea, vomiting, anorexia, weight loss, heartburn, flatulence. Back pain suggests penetrating posterior ulcer, severe ulceration can be symptomless and persistent and severe pain suggests penetration into other organs.
Treatment of achalasia?
Palliative treatment, nifedipine or sildenafil for durable relief, intrasphincteric injection with botulin toxin A, surgical division of LOS (Heller operation laproscopically), endoscopic dilation of LOS with hydrostatic balloon under x-ray control to weaken sphincter
What are the two main problems caused by cirrhosis?
Liver damage and portal hypertension
Management of refractory ascites?
Repeated paracentesis, diuretics (oral spironolactone and furosemide), intra peritoneal chemo, transjugular intrahepatic porto systemic shunt, peritoneovenous shunt, sodium restriction, albumin replacement, lose weight
Signs and symptoms of pre hepatic portal hypertension?
Bleeding at young age, normal liver function, blockage seen on US. Treat with anticoagulation.
What do M cells do in the intestine?
M cells sample antigens in the lumen for translocation of microbial peptide to activate immune cells resulting in chronic inflammation
Risk factors of a pilonidal sinus?
Male, obese, Caucasian, Asian, Middle East, sitting down a lot, lots of body hair
In who is ischaemic colitis common?
The young with contraceptives, thrombophilia and vasculitis.
Factors that help H.pylori infect?
Gram negative rod bacteria, flagella for motility, lipopolysaccharides for adherence, urease to convert urea and water to CO2 and ammonia, has VacA which causes apoptosis of cells, CagA disrupts cellular integrity and structure and promotes inflammation.
What is the most common micro organism is hydatid abscess?
Echinococcus granylosis (tapeworm)
What is diverticular disease?
Pouches of mucosa in large intestine extruding through the colonic muscular wall via weakened areas near blood vessels to form a diverticular (mainly in the sigmoid).
Complications of peritonitis?
dehydration, abscess formation, multi organ failure, toxaemia, septicaemia, septic shock, ARDS, bowel obstruction
How would you treat an anal fissure?
Local anaesthetic gel, fluids, fibre, stool softener, glyceryl titrate, diltiazem ointments, lidocaine ointment, GTN ointment or Botulin toxin or internal spichterectomy if severe.
Treatment of hernias?
Surgery
What causes pernicious anaemia?
Burning to the stomach, destroys parietal cells which make intrinsic factor which produces B12, essential for red blood cell formation, causing low blood count and pernicious anaemia
What do investigations of an appendicitis show?
raised WCC, ESR and CRP, US shows inflamed appendix or mass, pregnancy test to rule it out
What would a SI biopsy show in midgut dysmotility?
alpha actin staining deficiency in the inner circular layer of smooth muscle
Symptoms of an inguinal hernia?
mass in groin, pain, more painful on coughing
Which two main arteries become occluded in ischaemic colitis?
The superior and inferior mesenteric arteries
What is type A chronic gastritis?
Autoimmune cause, where autoantibodies attack parietal cells in the fundus/body of the stomach leading to atrophic gastritis and loss of parietal cells with achorhydria and intrinsic factor deficiency causing pernicious anaemia
DD for epigastic pain?
heartburn, pancreatitis, epigastric hernia, gall stones, gastric ulcer
Complications of Crohns?
stenosis, abscess formation, fistula, colon cancer, perforation (more severe than UC), pyoedma gangrenous, anaemia, osteoporosis
Symptoms and signs of biliary colic?
RUQ pain spreading to right shoulder and right scapula, can cause nausea and vomiting. Pain subsides after a few hours. U/S shows gallstones, there is an increased serum alkaline phosphatase and bilirubin during an attack.
What is cirrhosis?
Necrosis and apoptosis of liver cells followed by fibrosis and nodule formation, causing liver architecture to become abnormal, interfering with blood flow causing portal hypertension.
What are the causes of ascites?
cirrhosis (75%), malignancy (10%), heart failure, TB, pancreatitis, increased sodium, abdominal surgery, selective protein deficiency e.g. albumin (as reduces plasma oncotic pressure), obesity
What is GORD?
Gastro oesophageal reflux disease - abdnorma reflux from the stomach to oesophagus
What 5 mechanisms prevent GORD?
- Folds of gastric mucosa forming mucosa roulette
- crural diaphram contraction
- secondary peristalsis
- gravity
- NaHCO3
What risk factors causes failure of LOS relaxtion causing GORD?
obesity, fatty foods, caffeine, carbonated bevarages, alcohol, smoking, pregancy, CCB, antimuscarinic drugs, tricyclic antidepressants, oesophagitis, sliding or rolling hiatus hernia, genetic inheritance of angle of LOS
How does acid reflux cause damage and what two complications can this lead to?
Acid has prolonged contact with the squamous oesophageal lining, causing it discomfort which can lead to a peptic stricure of Barrett’s oesopahgus
What clinical features does GORD present with?
heartburn (worse with bending over, lying down, heavy meal, alcohol), regurgitated acid in mouth, water brash (excess salivation), dysphagia, nocturnal asthma, chronic cough, iron deficient anaemia
In GORD, what is the correlation like between heartburn and severity of disease?
Poor correlation
What are the investigations for GORD?
If younger than 55 and no alarm symptoms (weight loss, haematemesis, anorexia) - precede straight to treatment
If older than 55, do an EGD and a 24 hour pH monitor
What is the treatment of GORD?
- lifetsyle management e.g. stop drinking, smoking, no fatty foods, raise bed head
- anatacids e.g. aluminium hydroxide - reduces reflux
- PPI e.g. omeprazole - inhibit gastric hydorgen/potassium ATPase and reduce 90% of gastric secretion
- H2 blockers e.g. ranitidine - for acid suppression if anatacids fail
- dopamine anatagnoist prokinetic agents e.g. metoclopramide - enhance peristalsis and increase gastric emptying
- endolumincal gastroplication making multiple plications and pleats in the GO juntion to reduce symptoms
- Niseens fundoplicaton if all else fails
Side effects of Mg and Al antacids in GORD?
Mg - cause diarrhoea
Al - cause constipation
What is Barretts oesophagus?
metaplasaia of oesophagus squamous epithelieum to columnar epithelieum
What will investigations show on Barretts oesophagus?
- endoscopy shoes proximal displacement of squamous coloumnar junction
- biopsy shows columnar lining above proximal gastric folds in all four quadrants
- continual circumferential sheet or finge like projections extending upwards from squamocolumnar junction
What is the treatment of Barretts esophagus?
PPIs, endoscopic surveillance every 2 years, multiple oesophageal biopsies to look for carnicoma, oesophagectomy in young, endoscopic muscosal resection, screening if longterm heart burn, endoscopic ablative therapies to ablate dysplasstic tissue, radiofrequency ablation
What does a peptic stricture present with?
intermittent dysphagia for solids, getting worse over time
What is treatment of a peptic stricture?
PPI, surgery if that fails
If what age group do peptic strictures normally occur?
over 60s
What is coeliac disease also known as?
Gluten sensitive enteropathy with a heightened immunological response or coeliac spure
What is coeliac disease?
An immune repsonse to gliadin.
Gliadin has a high glutamine and proline content and can be resistant to digestion from pepsin and chymotrypsin so remains in a high content in the intestine causing an immune T cell response, causing injury to villus
What is gliadin?
A component of gluten which is a protein found in wheat, rye and barley
What is the epidemiology of coeliac disease?
occurs in 1% of the population, more common in females and adults, mainly occurs in 40-60years and 10-15% genetics in 1st degree relatives
What does the histology of the intestine show in coeliac disease?
- abnormal villus architecture
- hyperplastic crypts
- chronic inflammatory cells in lamina propria
- villus atrophy
- cuboidal enterocytes
- increased lymphocytes
- increased EILS
What symptoms would present in coeliac disease?
anaemia, folate/B12 deficiency, diarrhoea, steatorrhoea, weight loss, failure o thrive, IBS, chronic fatigue, osteomalacia, osteoporosis, dermatitis herpetiformis
What would investigations show in coeliac diease?
- HLA-DQ2 positive (even if on GF diet)
- 4-6 2nd part duodenum biopsy show histological changes (must be eating gluten still)
- reduced folds in duodenum
- thick bowel folds
- dilation of small bowel
- mosaic pattern on surface
- scalloping of mucosal folds
- more damage in proximal small bowel than ileum as gluten would have been digested into smalller non toxic fragments
- serology if family history and persistant symptoms
Treatment of coeliac disease?
GF diet, dietician, educate, DEXA scan for osteoporosis, replace minerals and vitamins
Complications of coeliac disease?
persistant symptoms, osteoporosis, osteomalacia, small bowel lymphoma, oesophageal and ENT malignancy, decreased QoL, refractory coeliac disease, EATCL, ulcerative jejunitis
What does the acronym “these will cause devastating absorption problems” mean in malabsorption disease?
tropical sprue, Whipples, coeliac, dissacharide deficiency/defective bil secretion, a-beta-lipoproteinaemia, pancreatic insufficiency/parasite
What is tropical sprue and when can it occur?
A malabsorption disease from the tropics, cause malabsorption of 2 or more substances with unknown cause, can effect all of the small intestine. Can be a few days or a few years after being in the tropics.
What are the symptoms of tropical sprue?
diarrhoea, anorexia, abdominal distension, weight loss, malabsorption
What is the treatment of tropical sprue?
leave tropical area, antibiotics, fluids and electrolytes, vitamin B12 and folic acid, tetracycline antibodies
What is Whipples disease caused by?
Is caused by Tropheryma Whipplei bacteria (gram positive)
What are the symptoms of Whipples disease?
weight loss, peripheral lymphodenopathy, neuro conditions. arthritis, athralgia
What will investigations show in Whipples disease?
- endoscopy shows - pale shaggy duodenal mucosa and eroded, red, friable patches
- pas positive macrophages
- gram positive bacteria
- T.whipplei antibodies present
- Trilaminar cell wall have T.whipplei seen with macrophages
- confirmatory PCR
- small bowel biopsy
What is the treatment of Whipples disease?
antibiotics for 1-2 years e.g. trimethoprim and sulphamethoxaole
Who mainly gets Whipples disease?
87% are white, male and middle ages
What is dermatitis herpetiformis and what is it treated with?
Uncommon blistering and subepidermal eruption of the skin which can be associated with malabsorption similar to coeliac, treat with a gluten free diet
What is pancreatic insufficiency and what is it caused by?
Indeficiency of absorption of vitmain A, D, E and K (fat soluble vitmamins), caused by CF, cancer and pancreatitis
What is the treatment for pancreatic insufficiency?
pancrelipase (creon)
What are the causes of bile acid malabsorption?
secondary to ileal resection/inflammtion, idiopathic (primary) or secondary to GI disease
What are the symptoms of bile acid malabsorption?
diarrhoea
What is the pathology of bile acid malabsorption?
There is a defect in the bile acid absorption in the ileum or patients have increased bile acid pool size so have too much bile. Lower levels of the FGF19 hormone, cause bile acid overproduction too, more than the ileum can absorb eading to diarrhoea. Increased bile salt leads to malabsoprtion of water and electrolyes causing diarrhoea.
What is A-beta-lipoproteinaemia and what is its treatment?
An autosomal recessive disorder cusing the inability to synthesise chylomicrons, treat with vitmain E.
What is dissacharide deficiency? Give an example of this disease and its treatment?
a deficiency in enzymes required for digestion and absorption of dissacharides e.g. beta glycosidase complex
causes lactose intolerance, as cant break down lactose so it absorbs the bacteria, producing co2, wind and diarrhoea, treat with a restricted diet
What is radiation enteritis?
Radiation of >40Gy1 causes damage to intestine causing muscle fibre atrophy and ulcerative changes form ischaemia and obstruction due to radiation induced fibrotic structures. Mainly occurs in the ileum and rectum.
In what kind of patient would you see radiation enteritis?
In patients post radiotherapy, especially of the gyanecological and urinary tract malignancy
What are the symptoms of radiation enteritis and when does it become chronic?
increased bowel frequency and for more than 3 months
What is the treatment of radiation enteropathy?
treat symptoms, try and avoid surgery, local steroids, argon plasma coagulation to treat persistant bleeding from mucosal telanicastesies
What parasite causes malabsorption?
Giarda intestinalis
What are the symptoms and signs of a parasite causing malabsorption?
diarrhoea, stearrhoea, malabsorption, minor changes to jejunal mucosa, erytospondosis
How does bacterial overgrowth cause malabsorption?
It is associated with structural abnormality of the small intesine meaning that gastric acid and intestina motility are not making it sterile.
Bacteriodies deconjugatee and dehydroxylate bile salts so can be detected in small bowel aspirates
What are the symptoms of bacterial overgrowth in the gut?
diarrhoea, stearrhoea, B12 deficiency, neurological deficit, high serum folate
What investigations and treatment is needed for bacterial overgrowth?
cofirm with a hydrogen breath test, coreect the underlying lesions, rotating course of antibiotics e.g. metrondazole and tetracycline and correct brush border damage
How does intestinal resection of the ileum affect malabsorption?
Removal of the ileum can lead to decreased bile salt and vitamin B12 absorption and increased diarrhoea.
Increased bile salts in the colon causes increased oxalate absorption with oxaluna leading to urinary stone formation
Decreased bile salt absorption can also cause decreased micelle formation, steatorrhoea, lithogenic bile and gall stone formation
Decreased B12 absorption leads to macrocytosis
How does the body respond to intestinal resection causing decreased bile salt absorption?
Increasd bile salt retention and synthesis which can compensate for about 1/3 of the loss
What investigations can you do to see the effect of ileum resection?
small bowel follow through test, B12 measurements, bile salt retention test, H2 breath test
What is the treatment for ileum resection malabsorption?
B12 replacement, low fat diet
Cholestryamine - binds bile salts and reduces diarrhogenic bile salts
How does the body respond to jejunum resection?
Increased gastric hypersecretion with incrrased gastrin
Structural and functional intestinal adaptation for increased absorption
What does a massive intestinal resection cause?
Short bowel syndrome and inabillity to maintain protein energy, fluid electrolytes and micronutrient balance
When may you require a massive intestinal resection?
Crohns, mesenteric vessel occlusion, radiation enteritis, trauma, congential defect
What is the treatment for short bowel syndrome that ends in a stoma bag?
- Parental supplements of fluids, electrolyes and nutrients
- increased salt uptake and decrease hypotonic fluids between meals
- oral glucose electrolye mixtures
- octrotide with PPI, loperamide and codeine phosphate to increase jejunal transit time and decrease stomal effluent loss
What is the treatment of short bowel syndrome in continuity with the colon?
- Less parental supplements needed
- low fat diet and increase carb intake
- cholestryamine to reduce diarrhoea and colonic oxalate absorption
What is the main cause of liver disease?
Alcohol
What causes the accumlation of fat in the liver?
Increased uptake and synthesis of lipids, more than the rate of fatty acid oxidation and secretion of lipids
What controls the balance of fatty acid in the liver?
lipogenenisis in the liver,
hepatic free fatty acid uptake,
fatty acid oxidation in the liver and
fatty acid export with VLDL
How does the liver take up fatty acids and then control the balance of free fatty acids?
Hepatocytes have lipase which hydrolyses triglycerides, from lipoproteins in the blood, into fatty acids so they can be brought into the hepatocyte.
Hepatocytes can then either reform the triglycerides or can break fatty acids down again by oxidation.
(Adipose tissue also contains lipoproteins)
What happens in steatosis?
Steatosis is when hepatic cells become swollen with fat due to more triglycerides being reformed than broken down in the heptocytes, does not cause damage and this is reversible
What does the accumalation of fat in fatty liver cause?
The formation of fatty venules and less oxidation
Why is there less oxidation in fatty liver?
When there is excess energy, the liver goes through a sensing process in the liver, the PPAR alpha is a nulcear receptor protein and is regulalator of lipid metabolism in the liver and will increase fat oxidation to get rid of excess energy and get rid of excess fat, but if sensing is defective, decrease fat oxidation leading to steatosis.
What is the effect of PPAR gamma in the liver?
stimulates the decreased fat oxidation process, leading to steatosis.
What are the two types of fatty liver disease?
Alcoholic and non alcoholic
How does alcohol cause alcoholic fatty liver disease?
An increase in ethanol causing an increased volumes of acetylaldehye through the enzyme alcohol dehydrogenase and the conversion of NAD+ to NADH.
This then converts to acetic acid with the enzyme aldehyde dehydrogenase, forming another NADH.
This then converts to acetyle co A which is the main precursor to fatty acids in the liver
How does the excess of NADH in with alcohol cause fatty liver disease?
It causes shunting of normal substrate away from metabolism and towards lipid synthesis as NADH are needed to make fatty acids
How does ethanol affect carb and protein metabolism and what does this cause?
Impairs their metabolism and causes centrilobular necrosis of the hepatic acinus
How does ethanol effect drug metabolism?
Increases the toxic effects of drugs on the liver and induces microsomal metabolism via microsomal etahol oxidasing system (MEOS)
How does ethanol affect stellate cells?
Transforms them into collagen round central hepatic veins, producing myofibroblast cells leading to perivenicular fibrosis and cirrhosis
What is the cause of non alcoholic fatty liver disease?
Increased intake of dietry fats and fructose leading to high fat uptake, reduced fat secretion, increased storafe and reduced secretion of lipoproteins
How does fructose cause non alcoholic liver disease?
Fructose converts to fructose 1 phosphate by the fructose kinase, then into glyceryl aldehyde and dihydroxyacetone phosphate by F1P aldolase.
dihydroxyacetone phosphate can covert to glycerol 3 phosphate and the become phospocidic acid once 2 acteyl co a are added to then form diacyglycerols and triacyglycerols.
glyceryl aldehyde can form glyceraldehdye 3 phosphate to then form pyruvate and acetyle co a
What is metabolic syndrome in terms of liver diease?
made up of at least 3 of :
central obesiy, hypertenison, dyslipidaemia, impaired glucose tolderance and insulin resistance
How does steatosis lead to steatohepatitis?
more fat accumalation leading to heptocyte necrosis and inflammation, mallory bodies and giant mitochondria then lead to fibrosis and alcohol cirrhosis
What are the sign and symptoms of fatty liver?
No major signs, vague nausea and vomiting and diarrhoea,, and slight hepatomegaly
What are the signs and symptoms of alcholic hepatitis?
ill health, mild jaundice, signs of chronic liver diease, abnormal liver biochemistry, ascites, abdominal apin, high fever, liver necrosis, hepatomegaly, splenomegaly, ankle oedema
What is the treatment of alcoholic liver diease?
- stop drinking alcohol
- bed rest
- increased protein and vitamin supplements
- alcohol cessation programme
- diazepam for delirieum tremors
- steroid therapy and acetycysteine to reduce reflammatory process (CI if renal failure)
- supportive treatment
What is jaundice?
The yellow discolouration of mucus membranes, sclera and skin due to accumalation of bilirubin seen at >2.5-3mg/dL (>42.8-51.3mmol/L)
How is bilirubin formed and excreted?
Formed by the breakdown of Hb in the spleen by macrophages.
The heme is broken down into unconjugated biliruin and iron.
The UCB binds to albumin in the blood to be taken to the liver to be conjugated by glucuronyl transferase to bilirubin glucorinade
This is excreted by the bile duct into intestine to be converted into urobilinogen in the terminal ileum
Then reabsorbed by blood (10%) to be excreted in the urine (5%) or reused in the enterohepatic cycle (5%) or oxidised into stercobulin (90%) to excreted by faeces
What are the causes of prehepatic jaundice?
haemolytic, malaria, sickle cell, Gilberts syndrome
What causes intrahepatic jaundice?
viral hepatitis, drugs, cirrhosis, pregnancy, alcoholic hepatitis
what are the causes of extrahepatic jaundice?
duct stones, carcinoma, biliary stricture, pancreatitis, schistosomiasis
What are the symptoms acute liver disease?
Yellowing of tissue of the sclera of the eye and yellowing of the skin.
Changes in urine and stool colour
malasie, fever, anorexia, spider naevi, palmar erythema
What happens in pre hepatic jaundice?
there is an icreased break down of RBCs or ineffective haematopoesis so macrophages have to break down the RBC.
This causes hepatocytes can not keep up with the excess UCB being produced so that some UCB stays in the blood and then excess CB in bile leading to risk of increased pigmented bilirubin gallstones
Once the CB is converted to urobilinogen this causes urine to become darker?
What happens in Gilbert syndrome?
Genetic Mutation in the HUG-Br1 gene which encodes UDP glucerynol activity
So not enough UCB can become CB due to low glucorynal transferase enzyme activity
Causes a build up of UCB in blood
What happens in Crigler Najjar syndrome?
Where there is virtually no glucerynol transferase enzyme so not conversion of UCB to CB
Leads to very high UCB levels which can build up in the brain, leading to kernicterus
This can be fatal, so would need transplant
What happens in Dubin Johnson syndrome?
An autosomal recessive disorder
Defect in the MRP2 transporter gene that transports CB from hepatocytes to bile duct so CB builds up in liver
MRP3 is then unregulated and move CB into blood, causes dark urine and a black liver due to melanin deposits
What happens in post hepatic jaundice?
The bile duct has been blocked causing a build up of pressure in the bile canaliculus and bile ducts
This causes bile to leak through the tight junctions between hepatocytes that line the bile duct into the blood
This means, bile salts, acids and cholestrol get into the blood and lead to pruritis (itchy skin) and cholesterolemia and xanthomas
CB is excreted in the urine again causing dark urine
Excrete a lot of fat due to lack of bile salts (steatorrhea) and decreased vitamins
How does viral hepatitis cause jaundice?
Hepatocytes become infected and lose the ability to convert UCB to CB leading to excess UCB.
Hepatocytes also lose the ability to line to bile ducts, so CB leaks into the blood causing dark urine and steatorrhoea
What happens in physiologic jaundice of the newborn?
Already low UGT levels at birth, and after birth UCB can be high due to macrophages breaking down fetal RBC.
This can cause a build up of UCB in the basal ganglia of the brain (kernicterus) leading to brain damage and death
What is the treatment of kernicterus?
Phototherapy which uses light to induce structural and configurational changes in biliruibin molecule, so is more soluble and can be excreted in the urine
What are the signs and symptoms of chronic liver disease?
RUQ pain fro liver distension, ankle oedema, ascites, haemotamesis, prurtis, breast swelling, loss of libido, confusion, drowsiness, spider naevi, haemochromatosis, slate grey skin, palmar erythma on hands, clubbing, dupuytress contraction, Xanthomas in palmar creases, hepatomegaly, splenomegaly, gynaecomasha and testitulcar atropy, loss of body hair
What is alpha 1 antitrypsin and its function?
Enzyme produced in the liver to protect the lung from damage neutrophil elastase (a protease produced by WBC)
What is Wilson’s disease and what happens in it?
A rare, autosomal inherited mutation in the ATP7B gene on chromosome 13 causing a defect in copper metabolism so it cannot be moved out the hepatocyte by ceruloplasmin or by vesicles.
So coppe builds up and forms free radicals causing damage to the hepatocyte so free copper spills out into interstitial space and blood supply, reaching other tissues, causing more damage, especially the brain
How does excess copper cause damage of the tissues?
Reacts with H2O2 to form the hydroxyl radical which is a ROS that damages tissue
How is copper usually excreted in the body?
Copper absorbed into stomach and SI via enterocytes and passed into portal vein to liver.
Sent to ATP7B to bind to it to form ceruloplasmin to hold 6 molecules of copper.
The rest of copper is packaged into vesicles for exocytosis into bile
Where are the main places in the body damaged by Wilsons disease and what diseases can this cause?
- Basal ganglia - Parkinsons
- Cerebral cortex - dementia
- Descemets membrane in cornea (between stroma and endothelial layer of cornea) - Kayser Fleicher Rings
- Liver failure
What would investigations show in Wilsons disease?
- Decrease in ceruloplasmin
- Increase apoceruloplasmin
- Increased free copper levels in blood and urine
- Hepatosplenomegaly
- Renal disease from damaged proximal tubules
- Haemolytic anaemia due to dmaage to red blood cells
- Liver problems present in childhood
- Young adults will have neurological problems
What is the treatment of Wilson’s disease?
- penicillamine or trieritene - a copper chelate agent that binds to copper allowing easier excretion
- zinc and ammonium tetrathiomolybdate decrease copper reabsorption so increase copper excretion
- liver transplant
- screening of first degree relatives
What causes alpha 1 antitrypsin deficiency and what does it lead to?
An autosomal recessive mutation in the alpha 1 antitrypsin gene on chromosome 14
causing alpha 1 antitrypsin to be stuck in the liver, causing liver damage
and lack of it in the lung leads to lung disease e.g. copd and empyema
What are the symptoms and complications of alpha 1 antitrypsin deficiency?
jaundice, cirrhosis, increased liver cancer risk, emphysema, copd, chronic bronchitis
dyspnoea, chough, wheeze, recurrent infections
How do you diagnose alpha 1 antitrypsin deficiency?
Difficult diagnosis, so low diagnosis rate
Blood test for alpha 1 antitrypsin - low
Emphysema at
Emphysema non smoker at any age
Unexplained liver disease
What is the treatment of alpha 1 antitrypsin deficiency?
Weekly alpha 1 antitrypsin injection
Treat complications with bronchodialators, steroids, transplant, stop smoking, no alcohol
What are the genetic variants for alpha 1 antitrypsin deficiency?
Characterised by electrophoretic mobilities:
medium (M), slow (S), very slow (Z)
Normal = PiMM, Very slow = PiZZ, Slow = PiSZ, Medium = PiMZ
Most are PIZZ
What is hereditary haemochromatosis and what does it lead to?
Gene mutation in the HFE gene on chromosome 6 which regulates iron absorption - either C282Y (more common) or H63D mutation
Enterocytes then absorb an unusually large amount of iron as it can’t regulate the absorption, so then deposited in organs and tissue (haemosiderosis)
Iron is broken down by H2O2 into free radicals (fenton reaction), causing damage to the tissues and tissue necrosis
What are the two possible gene mutations in hereditay hemochromatosis and which is more common?
C282Y mutation is more common
H63D mustation
What is a cause of secondary haemochromatosis?
Frequent blood transfusions
In hereditary haemochromatosis, why is the liver most prone to damage?
Hepcidin is normally synthesised by the liver to control iron absorption.
But hepcidin is reduced, causing iron overload leading to fibrosis
What complications and hereditary haemochromatosis lead to?
cirrhosis, liver cancer, type 1 diabetes, malabsorption from exocrine pancreas damage, bronze pigment skin, restrictive cardiomyopathy, arrhythmias, amenorrhea and testicular atrophy, degenerative joint disease
What do investigations show in hereditary haemochromatosis?
- Increased iron in blood
- increased transferrin % saturation as more binding sites occupied by iron
- total iron binding capacity is decreased
- increased serum ferritin as it stores iron
- liver biopsy shows brown spots from iron with a prussian blue stain
- MRI shows decreased signal intensity of liver and pancreas due to paramagnetic effect of ferritin and haemosiderin
What is the treatment of hereditary haemochromatosis?
- A phlebotomy to remove blood to reduce ferritin and blood saturation and iron load
- Deferoxamine - binds to free iron in the blood to aid excretion of iron
- Screening in 1st degree relatives
- Venesection prolongs life and reverse tissue dmaage - 2x a week
- testosterone replacement
What is a volvulus and what causes it?
A twist/rotation of bowel segment caused by a caecal rotation, congenital or adhesional band, has a narrow base and wide apex, cutting off the blood supply
What is an intessuption and what is it caused by?
Telescoping of intestine into one another, caused by an imbalance of longitudinal forces along intestinal wall with a mass acting as a lead point or a disorganised pattern of peristalsis
What is atriesia?
Abscence of opening of hollow structure
What are causes of mechanical small bowel obstruction?
adhesions, incarcerated hernia, cancers, appendicitis, atresia, hypertrophic pyloric stenosis, Crohns, radiation, gall stones, diverticulitis, previous surgery
What are functional causes of small bowel obstruction?
paralytic ileus, bacterial and virus infection, analgesics and irritable bowel disease
What are clinical features of small bowel obstruction?
vomiting, (projectile if high obstruction, faeculent if bacteria), colicky pain, constipation, distension (more distal causes more distension), localised tenderness, tachycardia, fever, diffuse perforation, tympanic is gas filled, bowel sounds in early stage
What do investigations show in small bowel obstruction?
imaging show gas throughout if partial or no distal gas if complete, if complicated there will be air under the diaphram and perforation, high pitched bowel sounds at the start (paralytic ileus has no sounds)
Who does a intessuption usually affect?
infants and toddlers
what does an intesussuption usually present with?
vomiting, abdominal pain, blood, mucus, palpable sausage shaped mass in RUQ
What is the management for small bowel obstruction?
- aggressive fluid resuscitation
- bowel decompression
- analgesics and antimetrics
- early surgical consultation
- antibiotics
- surgery
When would you want to do immediate surgery in small bowel obstruction?
if signs of strangulation or perforation seen clinically or radiologically with free air
what is the treatment for intessusption?
non operative for air/contrast enema and operative for open/laparoscopic reduction
How does large bowel obstruction cause complications?
The colon proximal to the obstruction dilates and increases with pressure and decreased mesenteric blood flow causing mucosal ulceration with full thickness necrosis and perforation
Causes mucosal oedema and transudation of fluid and electrolytes
Bacterial translocation can cause sepsis
How does a colonic volvulus cause damage?
Causes a closed loop obstruction with a fluid and electrolyte shift in closed loop. There is increased pressure and tension, impairing blood flow leading to ischaemia, necrosis and perforation of bowel loop.
70% of obsturctions are due to colorrectal cancers. Where are tumours in the colon most and least likely to cause an obsturction?
Most likely in the left and least likely at flexures
How does a large bowel obstruction present and its investigations?
abdominal discomford, pain, fullness, bloating , nausea, altered bowel habit, vomiting in late stages, weight loss, palpable mass, rigidity, blood in rectum, decreased Hb, chronic occulu blood loss, sigmoidoscopy
How does a sigmoid, caecal and barium enema sigmoid volvulus appear?
sigmoid = concavity towards left
caecal = concavity towards right
barium enema sigmoid = bird of prey sign
What is the management of a large bowel obstruction?
- fast the patient
- give supplement o2
- Iv fluids and electrolytes
- urinary catheterisation and monitor urinary output
- nasogastirc decompression
- antibiotics
- treat underlying cause
- surgery
- wash out contaminant
- colostomy
What is the treatment of bowel cancer surgery?
empty bowel, remove tumour, lymphadenectomy, neo adjuvant chemo
What are the causes of non mechanical bowel obstruction?
post operative, increased sympathetic discharge, toxins, metabolic disturbance, electrolyte imbalance, MI, spesis, pancreatitis
What are the symptoms of non mechanical bowel obsturction?
painless distension, vomiting, minimal bowel sounds
what is the treatment of non mechanical bowel obstruction?
NBM, iv fluids, NG tube, treat underlying cause, avoid opiates, support nutrition
What are complications of bowel obstruction?
electrolyte imbalances, infection, jaundice, perforation of the intestine, necrosis and death of bowel tissue
What are the 3 types of benign liver tumour and which is most common?
Cavernous hemangiomas (most common)
Focal nodular hyperplasia
Hepatocellular adenomas
What are cavernous hamangiomas?
The most common form of benign liver cancer
Masses of the endothelial cells in the liver causing large vasuclar spaces (seen on histology)
usually around 1.5cm
Can be larger and rarely lead to rupture and bleeding
What are focal nodular hyperplasia tumours, how are they formed and in who do they occur?
localised aggregates of rapidly reproducing liver cells
could be response to vascular injury due to the abnormally large blood vessels in the centre and centralised fibrous scar tissue made by stellate cells, can also see fibrous septae
found incidentally
more common in women, occur at any age
What is a hepatic adenoma, a potential cause, associations, complications and treatment?
Made up of liver epithelial cells, englarged and non functional and contain increased amount of glycogen and lipids, highly vascularised, absent bile ducts and portal areas
highly associated with oestrogen based drugs and other anabolic steroids and increased on increased dose
associated with von Gierkes disease
complications are rupture and bleeding
treatment with adjusted diet
How common are liver tumours?
3rd leading cause of cancer deaths
the most common is a secondary metastase
the 5th most common cancer worldwide
more common in males
What causes hepatic tumours?
alcoholic hepatitis, haemochromatosis, primary biliary cirrhosis, alpha 1 antitrypsin deficiency, hepatitis c and b, exposure to aflatoxins
What is a common distiction between a primary and secondary hepatic tumour on examination?
Secondary has multiple focal points
Symptoms and investigations of hepatic tumour?
ascites, heptomegaly, Budd-chiari syndrome, abdominal pain, fever, (can be asymptomatic), bile in hepatocytes
increase in alpha fetoprotein which is produced by tumour cells
increased alp and ggt which are released in liver cell damage
increase in erythropoietin, insulin like growth fatcor and parathyroid hormone related protein
angiogrpahy shows vascularity of tumour
What is the treatment of hepatic cancer?
surgical removal gives better survival rate
radiation and chemo
liver transplant
Why do gallstones increase the risk of gallbladder cancer?
Gallstones increase the inflammtion of the glandular tissue in the gallbladder wall (cholecystitis) causing increase of cell turnover and increased risk of cancer
What does increased inflammation of the gallbladder lead to?
calcification and fibrosis and porcelain gallbladder
What is a complication of porcelain gallbladder and its treatment?
50% increased risk of progressing to gallbladder cancer
cholecystectomy and potential radiation
what are the causes of gallbladder cancer?
constant inflammation, infection of salmonella and helicobacter, Garner syndrome, neurofibromatosis, gallstones, abnormal pancreaticobiliaryduct junction
What is the prognosis of gall bladder adenomacarcinoma?
usually caught in the late stages due to the slow process of inflammation and calcification
found incidentally when thought to have cholecystitis
poor prognosis
What are examples of benign small bowel tumours?
Peutz-Jeghers syndrome
Adenomas, leiomyomas and lipomas
Familial adenomatous polyposis
What is Peutz-Jeghers syndrome?
An autosomal dominant benign small bowel tumour, with mucocutanous pigmentation (circumoral, hands and feet) and hamartomatous gastrointestinal polyps that can bleed or cause intussusception and may undergo malignant change
How do tumours of the small intestine present?
abdominal pain, diarrhoea, anorexia and anemia
How do carcinoid tumours of the small intestine originate from and how do they occur?
They originate from enterochromaffin cells (serotonin producing) and result from serotonin, kinins, histamine and prostagladins, released into the circulation by the tumour
What are the symptoms of a small intestine carcinoid syndrome and why?
They always have liver metastases
So the tumour directly drains into the hepatic vein and into the circulation
Causes flushing, wheezing, diarrhoea, abdominal pain, right sided cardiac valvular fibrosis causing stenosis and regurgitation
What investigation is used to diagnose small intestine carcinoid syndrome?
increase in urinary 5-hydroxyindoleacetic acid (5-HIAA) which is the breakdown product of serotonin
liver US confirms
What is the treatment of small intestine carcinoid syndrome?
5-HT antagonists, somatostatin analogues
surgical resection, hepatic artery embolisation,
radiofrequency ablation or chemotherapy
What conditions increase the risk of a malignant adenocarcinoma of the small intestine and what is its treatment?
coeliac disease, Crohn’s disease
surgery and chemo and radiotherapy
How common is squamous carcinoma of the oesophagus?
5-10 per 100,000 in the UK
This increases in china, africa and iran
and most common in 60-70 years
What are risk factors for oesophageal cancer?
smoking, alcohol, high intake of salted fish and pickled vegetables, intake of very hot food, pre existing oesophageal disease
Where does adenocarcinoma of the oesophagus arise from?
Barretts oesophagus
What are the symptoms and investigations for squamous carcinoma of the oesophagus?
progressive dysphagia for solids then liquids
weight loss
bolus food impaction or local infiltration causing chest pain
OGD and biopsy for diagnosis
barium swallow shows strictured area
CT and PET scan for staging
What is the management for oesophageal cancer?
Surgical resection if it hasn’t infiltrated oesophageal wall.
Pre op Chemo and radiotherapy
Endoscopic insertion of an expanding metal stent across the tumour, or laser and alcohol injections to cause tumour necrosis
treat dysphagia
poor prognosis
How common is gastric cancer and where abouts in the world is it most common?
4th most common cancer worldwide
2nd leading cause of cancer mortality
increased in men and as you get older
more likely in japan, chile, and less common in usa
incidence is decreasing worldwide but increased in west
What are potential causes and risk factors for gastic cancer?
H.pylori infection, smoking, alcohol, poor diet, high salt or smoked diet, pernicious anaemia, family history, after a partial gastrectomy
Where abouts in the stomach do gastric cancers normally occur?
in the antrum
How do gastric tumours differ on appearnce in comparson to diffuse or localised?
localised = ulcerated lesions with rolled edges
diffuse = extensive submucosal spread - linitis plastica
What are the symptoms of gastric cancer?
nausea, vomiting, anorexia, weight loss, vomiting, dysphagia
50% have palapable epigastric mass
lymph node is sometimes flet in the supraclavicular fossa (Virchows node)
metastases can cause ascites and hepatosplenemagly, dermatomyositis, acanthosis nigrcans
What is the management for gastic cancer?
surgery
post operative chemoradotherapy
palliative chemotherapy
What is the prognosis like for gastric cancer?
Poor, 10% for 5 years
50% after curative surgery
screening programme in japan which has increased 5 year survival to 90%
What is a gastrointestinal stromal tumour?
A tumour of the stromal or mesenchymal Gi in the stomach and proximal SI, they are benign but progress to malignant, found incidentally
What are the symptoms and treatment of a gastrointestinal stromal tumour?
dyspepsia, ulceration and bleeding
treat with surgical resection or imatinib for advanced
What is another name for a gastric lymphoma?
mucosa associated lymphoid tissue tumour (MALToma)
How common is pancreatic cancer and who is most at risk?
The 5th most common cause of cancer death in the Western world
Incidence increase with age and male
Hereditary and enviromental risks
Most are over 60years with an adenocarcinoma
What symptoms does pancreatic cancer of the head cause?
painless jaundice, weight loss, scratch marks and distended palpable gall bladder
What symptoms does pancreatic cancer of the tail or body cause?
abdominal pain, weight loss and anorexia, diabetes can occur, increase thrombophilebitis risk, change in bowel habit, dyspepsia
What do investigations of pancreatic cancer show?
dilated bile duct and mass lesion
mri and endoscope for staging
tumour marker CA19-9 is sensitive
serial measurements monitor treatment
What is the management of pancreatic cancer?
MDT and palliative care
surgical resection
combined chemo and radiotherapy
5 flurairacil and gencitabine improve survival
poor prognosis
What are the symptoms of colorectal cancer?
rectal bleeding, mucus, thin stool, tenesmus, altered bowel habit, altered bleeding, anaemia, late presentation, mass
What are the risk factors for colorectal cancer?
fibre, red meat, alcohol, smoking, family history, increased age, IBD, streptococcus bovis bacteramia, congenital polyposis syndromes, familial adenomatous polyposis, hereditary nonpolyposis colorectal carcinorma
What do investigations show in colorectal cancer?
iron deficiency anaemia, carcinoembryonic antigen tumour marker, colonoscopy, double contrast barium enerma study shows apple core sign, MDT meeting, bloods for staging, CT
What two systems assess staging for colorectal cancer?
TNM and Dukes staging
What are Dukes 4 stages for colorectal cancer and the expected 5 yr survival?
a - confined to muscularis mucosa - 90%
b - extends through muscularis mucosa - 65%
c - lymph node involvement - 30%
d - distant metastases -
What is the treatment for colorectal cancer?
education, Macmillan nurses, chemotherapy, oxaliplatin, folinic acid and 5-flurouracil, radiotherapy, surgical rsection, stent to relieve obstruction, surgery
What is viral hepatitis and how does this occur?
Inflammation of the liver caued by a virus that infect hepatocytes causing them to present abnormal proteins via their MHC1 molecules causing T cells to cause apoptosis
What is a councilman body?
A sign of hepatitis in the liver, occurs in the portal tracts and lobules, when apoptosis of the liver occurs
What are the symptoms of viral hepatitis?
fever, malaise, nausea,, hepatomegaly, RUQ pain, increased blood transaminase from leakage from the liver, so increase ALT and AST, increased atypical lymphocytes, jaundice,
How long does it take for hepatitis to become chronic and then where does this inflammation mainly occur?
6 months
In the portal tract
How is hepatitis A transmitted?
Via the faecal-oral route
Where is hepatitis A mainly acquired from?
travellers, contaminated shellfish, water and infected food handlers
What virus is in hepatitis A?
The RNA picornavirus
What do investigations show in hepatitis A?
HAV IgM antibody is active
HAV IgG antibody shows body is in recovery or has vaccination
leucopaenia and lymphocytosis
increased prothrombin and ESR
How long is the incubation period for hepatitis A?
2-3 weeks
What are the two stages in hepatitis A?
prodromal and icteric stages
In which stage in hepatitis A is there the max AST and decreased ALP?
Icteric
What is the treatment of hepatitis A?
good hygiene, boil water for 10 minutes, vaccination (2 jabs, 6months between with a 10yr booster), Ig for post exposure of less than 2 weeks, supportive treatment
What is the main route of transmission of hepatitis E?
faecal-oral
How is hepatitis E normally acquired?
Through contaminated sea food and water
What is the virus in hepatitis E?
A single strand RNA virus similar to HAV
What do investigations for hepatitis E show?
IgM antibody in active disease and IgG antibody in recovery disease
HEV RNA detected by PCR in stools/serum
What are the two biggest issues in hepatitis E?
no vaccination available
very dangerous in pregnant women due to leading to fulminant hepatitis
What is the treatment and prognosis of hepatitis E?
good sanitation and hygiene
supportive treatment
10-20% mortality if pregnant
How is hepatitis C transmitted?
through childbirth, sex or blood
What is the virus in hepatitis C?
single stranded RNA of the flavivirus family, and there is a rpid change in envelope proteins
How long is the incubation period for hepatitis C?
6-9 weeks
What do investigations show in hepatitis C?
HCV IgG antiobody after 8 weeks
HCV RNA detected seen with PCR - can show recovery or chronic progression
negative HAV and BBV markers
recombinant immunoblot assay
How does recombinant immunoblot assay compare with enzyme immunoassay in specificity and sensitivity in HCV?
increased specificity and decreased sensitivity in HCV
What is the treatment of acute hepatitis C?
educate and prevent
antiviral meds e.g. interferon
What precautions can be done to prevent hepatitis C?
screen blood products
lifestyle modifications
universal precautions of bodily fluids
Side effects of ribavirin antiviral meds?
haemolysis, pruritis, nasal congestion
Side effects of teloprevir antiviral meds?
rash and anaemia
What causes acute hepatitis C to lead to chronic?
Prolonged virus
Cytokines are profibrotic and lead to fibrosis
can be asymptomatic increased ALT and positibe HCV antibodies
How is hepatitis B transmitted?
childbirth, sex and blood
What is the virus causing hepatitis B and what is it made of?
a partially stranded, enveloped DNA virus with an e-antigen
outer surface protein of HBsAg with mutations that can lead to chronic
inner nucleocapsid
surface coat produced by infected hepatocyes
what percentage of acute hepatitis B develop to chronic and what does it largely depend on?
20%
depends on what age you get the virus - the younger, the more likely
what is a major complication of hepatitis B?
liver cancer
What do investigation show in acute hepatitis B virus and what do these mean in its progression?
HBsAg = hepatitis B surface antigen
HBcAg = core antigen
e-antigen = marker of infected cells
IgM antibodies and IgG antibodies in window stage
HBV DNA in serum
serum sicklenesslike immunological syndrome - rashes, polyartitis, fever, arteritis
What is the incubation period for hepatitis B?
1-5months
What is the treatment of acute hepatitis B?
treat symptoms, monitor markers
antiviral meds - entecavir and tenofovir
vaccine at 0, 1 and 6 years, 5 year booster
How do investigations of hepatitis B differ in acute and chronic?
chronic won’t have IgM or IgG present
How do investigations in an active and inactive hepatitis B differ?
active - increased ATL, HBV DNA in serum
inactive - normal ATL, decreased HBV DNA in serum
What is the treatment of chronic hepatitis B?
- seroconversion of HBeAG to antiHBe and reduce HBV DNA to
- anitviral agents e.g. interferon, adefovir, entercavir, lamivuidine
- daily tablet to stop replications of undetectable DNA
- vaccination
- post exposure prophylaxis
- increases survival and reduces progression
What scoring system is used in chronic hepatitis B?
Knodell scoring system
What virus is in hepatitis D?
single stranded defective RNA that needs HBV, in the deltaviridae family
What is the difference between coinfection and superinfection in hepatitis D?
coinfection = B and D infect at the same time
superinfection = D infects after B which is more severe
What do investigations show in hepatitis D?
HDV IgM and IgG (but not a protective antibody is this casein active
How is hepatitis D transmitted?
sex, bloods, IV drug users
What is the treatment of hepatitis D?
pergulated alpha 2a IFN
adifovir
What is the Rome III criteria for diagnositic IBS?
Recurrant abdominal pain at least 3 days a month with 2 or more of:
improvement of pain with defecation, change in stool frequency, change in form of stool
What are the symptoms of IBS?
abdominal pain, bloating, gas, cramping, change in stool form and frequency
what are the diagnostic behavioural features of IBS?
- symptoms for >6 months
- frequent consultations for non GI symptoms
- previously medically unexplained symptoms
- stress aggravates symptoms
What is the manning criteria for IBS?
- pain relieved by defecations
- more frequent stools at pain onset
- visibe abdominal distension
- passage of mucus per rectum
- sense of incomplete evacuation
What are the 7 parts of the Bristol stool chart?
1 - separate hard lumps
2 - sausage shape with lumps
3 - sausage with cracks
4 - smooth sausage
5 - soft blobs with clear cut edges
6 - fluffy pieces with ragged edges and mushy stools
7 - entirely liquid
DD for IBS?
colonic cancer, IBD, bile acid malabsorption, coeliac, gastroenteritis, diverticultis, gynological problems, anxiety
What causes IBS?
stress, post GI infection, genetic, autoimmune nervous dysfunction, visceral hypersensitivity, altered gut microbiota
What is the epidemiology of IBS?
more common in females
in 3.6-15% of western population
What is the Carnetts test for IBS?
ask the patient to fold arms across the chest and raise head off pillow with resistance from doctor
Investigations for IBS?
Carnetts test, examine perianal region and rectum, ask location of pain, endoscopic examination, hospital anxiety and depression scale, hydrogen breath test, cap refil, faecal calprotein coeliac screen
What is the treatment of IBS?
FODMAP diet, antispasmodics, laxatives, anti motility medicines (loperamine), low dose tricyclic antidepressants, exercise, education and reassurances, regular mealls, gluids, avoid caffiene and alcohol, increase soluble fibre, CBT
