GI Flashcards
What is Crohn’s disease?
form of inflammatory bowel disease. It commonly affects the terminal ileum and colon but may be seen anywhere from the mouth to anus
Healthy tissue destroyed, initially around crypts in ulceration of sup mucosa, involves deeper, non caseating granulomas. All layers of intestinal wall, mesentery, LN.
20-40 peak 20-30 + 60-70
RF for Crohn’s disease?
FH, abnormal gut flora, smoking, NSAIDs, pill, diet in refined sugar, nutritional def, acute gastritis, measles, paratuberculosis, pseudomonas, listeria, white, not BF.
Sx of Crohn’s disease?
Flares + remission
Abdo pain: RLQ, peri-umbilical, partially relieved by defecation
Diarrhoea ± blood, urgency, mucus + pus.
FTT, weight loss, anorexia
Inflam skin, eye, joint lesions, uveitis, erythema nodosum, pyoderma gangrenosum, arthritis
Episcleritis
Aphthous ulcers, angular stomatitis, glossitis
Clubbing
Fatigue + malaise
Temp
Complications of Crohn’s disease?
Strictures Fistulas Adhesions Bowel obstruction Perianal disease: abscess, phlegmon, skin tags Toxic dilation/ megacolon (rarer than in UC) Abscess Sepsis, perf Cancer: colon, anal SCC, small bowel, lung, lymphoma Fatty liver PSC Cholangiocarcinoma Osteomalacia, osteoporosis (CS), Malabsorption, anaemia, vit/ min def, dehydration, steatorrhoea Renal stones Amyloidosis Short bowel syndrome after resection
Investigations for Crohn’s?
Colonoscopy: early hyperaemia + oedema, discrete deep ulcers, cobblestone, skip lesions. Thickened bowel wall (fibrosis), all layers, goblet cells, granulomas, fat wrapping
FBC: normochromic normocytic anaemia.
Leukocytosis, thrombocytosis.
Iron studies
B12, folate
↓Mg + P due to diarrhoea.
↑CRP + ESR
↑faecal calprotectin
Histology - inflammation in all layers from mucosa to serosa, goblet cells, granulomas
Small bowel enema: strictures (Kantor’s string sign), proximal bowel dilation, rose thorn ulcers, fistulae
MRI for suspected perianal fistulae
Treatment of Crohn’s disease?
Stop smoking
Perianal fistula: metronidazole, infliximab
Inducing remission
1st - Glucocorticoids
2nd - Amino salicylates eg sulfasalazine
Resistant: azathioprine, mercaptopurine, methotrexate, infliximab
Metronidazole: isolated perianal disease
Maintaining
- Azathioprine/ mercaptopurine
- TPMT activity assessed before starting methotrexate 2nd line
Attacks
Mild: oral pred
Severe: admit, IV steroids, NBM. Infliximab, adalimumab.
Surgery
Resection of affected tissues
Stricturing terminal ileal disease → ileocaecal resection
Balloon dilation of stricture
Draining seton for complex fistulae
Perianal fistulae - oral metronidazole, infliximab, draining seton if complex
Perianal abscess: incision + drainage.
What is Ulcerative colitis?
is a form of inflammatory bowel disease.
Inflammation always starts at rectum (hence it is the most common site for UC), never spreads beyond ileocaecal valve and is continuous.
The peak incidence of ulcerative colitis is in people aged 15-25 years and in those aged 55-65 years.
CD8 activation, destruction of cells in mucosa/ submucosa
Ulcerated areas covered by granulatuion tissue > inflam pseudopolyps
Protective: smoking, appendectomy
AI reaction against colonic flora, molecular mimicry, XS sulphide producing bacteria, HLA-B27, NSAIDS, F>M
Relapses: stress + diet, infections.
Features of UC?
usually following insidious and intermittent symptoms. Features include:
bloody diarrhoea
urgency
tenesmus
abdominal pain, particularly in the left lower quadrant
extra-intestinal features - PSC, uveititis, erythema nodosum pyoderma gangrenous, arthritis
Complications of UC?
Arthritis, uveitis, iritis, uveitis, episcleritis Erythema nodosum Pyoderma gangrenosum PSC Conjunctivitis Sacroiliitis, ankylosing spondylitis Cholangiocarcinoma Toxic megacolon VTE Anal fissures Perirectal abscess Fulmant colitis Colonic adenocarcinoma Benign stricture Osteoporosis Flares: stress, NSAIDs Abx, cessation of smoking Amyloidosis
Investigations of UC?
Colonoscopy + biopsy: not in severe attacks as can perf, flexible sigmoidoscopy. Mucosa red + bleeds easily. No inflammation beyond submucosa. Widespread ulceration with appearance of polyps (pseudo polyps). Inflammatory cell infiltrate in lamina propria. Crypt abscesses, branching or sparsity, loss of goblet cells and mucin from gland epithelium. Granulomas are infrequent. Sup ulcer/ inflam, whole lumen, starts in rectum, continuous, bowel wall thin/ normal, oedema, fat accumulation + hypertrophy of muscles. Inflam cells in lamina propria
in patients with severe colitis colonoscopy should be avoided due to the risk of perforation - a flexible sigmoidoscopy is preferred
↑faecal calprotectin, ESR, CRP, pANCA/ ASCA may be pos, leucocytosis, thrombocytosis, anaemia.
AXR: assess colonic dilation = lead piping, thumbprinting (large bowel oedem)
Barium enema: loss of haustra, superficial ulceration, pseudopolyps, drain pipe colon in long standing (narrow + short)
Management of UC?
Mild to moderate UC:
Topical amino salicylate (mesalazine), + high dose oral AS if extensive
If remission not in 4 wks add oral AS, if more extensive than proctitis, offer high dose topical/ oral CS.
If still not remission > oral CS
Severe colitis: hosp, IV steroids, if 72hrs no improvement, IV ciclosporin or surgery.
Colectomy: only if localised, curative.
Maintenance
Mild/mod flare: topical AS OR oral AS + topical AS OR oral AS.
Left-sided and extensive UC - low maintenance dose of an oral aminosalicylate
Severe/>2 relapses in yr: oral azathioprine/ mercaptopurine
Methotrexate not recommended for management of UC (in contrast to Crohn’s disease)
Severity of UC?
The severity of UC is usually classified as being mild, moderate or severe:
mild: < 4 stools/day, only a small amount of blood
moderate: 4-6 stools/day, varying amounts of blood, no systemic upset
severe: >6 bloody stools per day + features of systemic upset (pyrexia, tachycardia, abdo tenderness, distension, decreased bowel sounds, anaemia, raised inflammatory markers, hypoalbuminaemia)
What is microscopic colitis?
an inflammation of the large intestine (colon) that causes persistent watery diarrhea.
Idiopathic chronic inflam of colon.
Associated w: celiac, AI, PPIs, NSAIDs, statins, smoking, infection, bile acid not absorbed + irritating lining of colon
Trigger, abnormal collagen met, epithelium dysfunctional, altered barrier function mucosal inflam > ↓Na absorption, ↑Cl secretion > secretory diarrhoea.
Triggers: damage to gut, genes, smoking, age, F>M. Immune system attack healthy cells lining colon.
Lymphocytic or collagenous
Sx of microscopic colitis?
Watery diarrhoea, sudden explosive, urgency, incontinence
Abdo pain
Bloating
Weight loss, nausea, dehydration
Anaemia
Investigations for microscopic colitis?
Endoscopy: non-specific, normal mucosa
Biopsy: inflam changes in lamina propria, IE lymphocytic infiltration, dense subepithelial collagenous layer.
↑ESR, myeloperoxidase
Management of microscopic colitis?
Avoid NSAIDs
Antidiarrheals: loperamide
CS: budesonide, prednisone
Bile acid sequestrants: cholestyramine, if bile acid malabsorption
PPIs: omeprazole
Surgical resection: ileostomy
Biological: infliximab
IS: azathioprine +
mercaptopurine
Cut down caffeine, cut down alcohol, stop smoking
What is ischaemic colitis?
occurs when blood flow to part of the large intestine (colon) is temporarily reduced, usually due to constriction of the blood vessels supplying the colon or lower flow of blood through the vessels due to low pressures.
Large bowel watershed areas eg splenic flexure borders of territory suppled by SMA/IMA
Occlusive (embolic/ thrombotic), ↓mesenteric circulation (↓BP, vasospasm)
RF: ↑age, hypercoag (F5 leiden), vasculopathy drugs eg vasopressors, AF, endocarditis, cocaine, HTN, DM, malignancy
Features of ischaemic colitis?
May be self limiting
Localised abdo cramping/ tender (usually L side)
Loose, bloody stool
Haematochezia
↓bowel sounds
Guarding, rebound tenderness
Fever
Hypotension
Transient, less severe Sx
Complications of ischaemic colitis?
Perf, peritonitis, septic shock, met acidosis, organ failure
Gangrenous bowel
Stricture
Pancolitis
Reperfusion injury
Fatal
Gangrenous mucosa promotes fluid/ electrolyte loss, dehydration, shock
Investigations for ischaemic colitis?
XR/CT: obstruction, perf, pneumonitis, thumb printing, (bowel oedema, thickening), double halo, pneumatosis coli, pneumoperitoneum
Colonoscopy: ischaemia (oedema, erythema, friable mucosa), single stripe line (linear, ulcer longitudinal axis), submucosa haem: bluish nodules.
Biopsy: transmural infllam, mucosal atrophy
↑lactate, CK, amylase
Management of ischaemic colitis?
Bowel rest, O2, IV fluids, electrolytes
Most recover
Abx
Gangrenous: resus, resection of affected bowel, stoma formation
What is mesenteric ischaemia?
decreased or blocked blood flow to your large or small intestine. It can be chronic, due to plaque buildup over time, or acute, due to a blood clot. It can also happen from certain drugs and cocaine.
Acute: embolism, classically have AF
Chronic: rarely clinical Dx, intestinal angina
Paralytic: if ischaemic continues
RF: AF, ^ age, hypercoag, vasopressors, endocarditis, HTN, DM, malignancy, arrhythmias, cardiac catheterisation, cardiopul bypass, vasoconstrictors
Sx of mesenteric ischaemia?
Severe sudden
Abdo pain, out of keeping with PE, often postprandial
Rectal bleeding
Diarrhoea
Fever, N/V
Chronic: colicky intermittent abdo pain, post prandial, weight loss, abdo bruit.
Paralytic: more diffuse abdo pain, tenderness, bowel movements ↓, absent BS.
Distension
Fever, tachycardia, tachypnoea
Feculent breath
Complications of mesenteric ischaemia?
High mortality
Peritonitis
Gangrenous bowel promotes fluid/electrolyte loss, dehydration, shock
Sepsis: break in epithelial line, bacteria in lumen to get into BV wall + peritoneal space + lymphatics.
Reperfusion injury: influx of O2 into already damaged cell overwhelming, oxidative stress, worsens cell damage.
Ileus
Shock
Organ failure
Investigations for mesenteric ischaemia?
↑WBCC, lactic acidosis
CT/MR angiography
Metabolic acidosis
Abdo XR/CT: dilated bowel loops, bowel wall thickening thumbprinting, pneumatosis free intraperitoneal air
Leucocytosis, L shift, ↑ haematocrit (dehydration) ↑WCC, Hb, serum lactate, amylase, ALP
Laparotomy: abdo exploration
Management for mesenteric ischaemia?
Urgent surgery
Abx: gentamicin, metronidazole
IV fluids, electrolytes, inotropic meds
surgery resection of infarcted tissue
pain management, bowel rest with decompression
Restabilising blood flow through surgery, thrombolytic if clot suspected
Causes of upper GI bleed?
Peptic ulcer Dx Oesophageal varices Oesophagitis. Mallory-Weiss tear Gastritis/ gastric erosions Drugs: NSAIDs, aspirin, steroids, thrombolytics, anticaog Boerhaave syndrome Gastric varices AVM Dieulafoy’s lesions Upper GI tumours Aortoenteric fistulae Coagulopathy
Sx of upper GI bleed?
Haematemesis
Melena
Unaltered blood per rectum > massive GI bleed
Glasgow-Blatchford Bleeding score - UGIB need medical intervention - Hb, BUN, initial systolic BP, sex, HR, melena, recent scope, hepatic disease history, cardiac failure present
Rockall score - assesses risk of death in UGIB - age, shock, co-morbidities, diagnosis, major stigmata of recent haemorrhage
Investigations for upper GI bleed?
FBC: Hb, LFTs, ↑urea (bleed in upper GIT has gone through whole digestive tract + RBCs broken into urea, protein meal)
Clotting: INR, PTT
Urgent endoscopy
Glasgow Blatchford: >6 need endoscopic intervention + transfusion. Blood urea, Hb↓, SBP ↓
Rockall score: after endoscopy, risk of rebleed, mortality
Forest classification: T1 spurting/oozing, 100% chance rebleed if no intervention, T2 visible vessel, adherent clot or black spot 50% chance rebleed with no intervention, T3 clean based lesion, no stigmata of bleeding 5-10% chance rebleed if no intervention
What is the management of UGIB?
Head down, prevent aspiration, 100% O2
2 large bore cannulas
Hb <80 give packed cells
Plt <50 transfusion
FFP: fibrinogen <1g/L, prothrombin >1.5X than normal
Prothrombin complex if warfarin + actively bleeding
Rebleed: ↑HR, falling JVP, ↓UO, haematemesis/ melaena (normal to pass decreasing amount of melaena 24hrs post haemostasis)
Ocreotide
Pts Blatchford 0 considered for early discharge
Endoscopy within 24 hrs
PPIs if non-variceal bleed
Causes of lower GI bleed?
Common: diverticula, colonic angiodysplasia, ischaemic colitis, IBD, infectious colitis, CRC, internal haemorrhoids, anal fissure, colonic polyps, dysentery
Uncommon: Meckel’s, radiation induced telangiectasia, Dieufaloy’s lesion, aorto-enteric fistula, vasculitis, hereditary haemorrhagic telangiectasia, blue rubber bleb nevus, anal cancer, rectal ulcer, rectal varices, post-polypectomy bleed, NSAID
What is an Aorto enteric fistulae?
A fistula is an abnormal, tubelike connection between two structures inside the body. When the connection is between the aorta and a loop of bowel that is near the aorta it is known as an aortoenteric fistula (AEF)
Hx of vascular graft or aortic aneurysm
Sx of aorto enteric fistulae?
Herald bleed (self limiting) before massive Haematochezia Haematemesis Abdo/ back pain Fever
Can cause septic shock
Can hear Abdo bruits/ feel pulsatile masses O/E
What is peptic ulcer?
Break in sup epithelial cells, penetrate to muscularis mucosa fibrous base, inflam cells
RFs for peptic ulcer?
h pylori, NSAIDs, SSRIs, corticosteroids, bisphosphonates, stress (cushing’s ↑ICP, curling severe burns), hyperchlorhydria, smoking, COPD, chronic gastritis, hypergastrinemia (Zollinger Ellison syndrome, neuroendocrine tumour in duodenal wall/ pancreas)
Sx of peptic ulcer?
Small punched out hole in mucosa
Asymptomatic 70%
Epigastric burning, night worse
Radiate to back/ L/RUP
Antacids/PPI relieve
N/V, coffee ground emesis
Bloating, belching
ALARM S: anaemia, loss of weight, anorexia, recent onset/ progressive, melaena/ haematemesis, swallowing difficulty
Abdo guarding, peritonitis
Complications of peptic ulcer?
Bleed if erosion into BVs
Perf: DU>GU, peritonitis, irritates phrenic N, referred shoulder pain.
Gastric outflow obstruction: active ulcer + surrounding oedema or healing ulcer + scarring, vomiting, ingested fluid + food
Fistula formation
Investigations for peptic ulcer?
Abdo CT: perf pneumoperitoneum, site of perf (discontinuity of wall)
Barium meal: fill crater, oedematous collar of swollen mucosa, radiating folds of mucsoa away from ulcer.
Endoscopy: gastric (biopsy, 6 from edge + 1 from removed region for H pylori), CLO test (biopsy mixed with urea + pH indicator = colour change if urease activity), white punched out lesion, surrounding hyperaemic mucosa
13C urea breath test: off PPI 14 days prior, urea labelled with carbon-13, after 13 mins, measure 13-CO2 production (by urea producing bacterium).
Stool test.
Gasrtrin levels
Management of peptic ulcer disease?
Discontinue NSAIDs, avoid smoking, alcohol, caffeine e
Loose weight
if H. Pylori negative - PPIs under healed > Lansoprazole, 30mg BD, ↑PH, better plt activity, pepsin requires acid to be active ↓chance clots digested
H pylori triple eradication: 1PPI, 2 Abx metro, clarithro, amox
Endoscopic ligation/ coag of bleeding ulcer, adrenaline injection (around vessel, not into vessel, causes vasoconstriction in vessels, prevent fluid absorbed allow time for clotting), clipping
Misoprostol in NSAID induced ulcers
Erythromycin: ↑gastric mobility, enhances stomach emptying, get rid of blood/ clot
What are duodenal ulcers?
Most in duodenal cap, more common than gastric
Brunner gland hypertrophy
Major RF: H pylori, NSAIDs, steroids, SSRIs
Minor: 🡩gastric secretion + gastric emptying, blood group O, smoking.
Sx of duodenal ulcers?
Epigastric pain, before meals, or at night, worse when hungry
Relieved by eating/ drinking milk
Weight gain
Pain 2-3hrs after meals
Complications of duodenal ulcers?
Post wall ulcers more common to bleed due to proximity to vessel (gastroduodenal artery)
Gastroduodenal a can be source of significant GI bleed
Investigation of duodenal ulcer?
Infection of antrum: causes hyper section if gastrin release, damages duoneal mucosa
If suspect perf: upright erect CXR
Tests for peptic ulcers
Causes of gastric ulcer?
Elderly
More common lesser curve near incisura
RF: h pylori, NSAIDs, reflux of duodenal contents, delayed gastric emptying, stress
Sx of gastric ulcer?
Asymptomatic
Epigastric pain - worsened by eating
Weight loss
Whilst eating or shortly after
Complications of gastric ulcer?
Infection of body of stomach: release of urea, inflam response, gastritis, cellular apoptosis > loss of parietal cells, decrease acid production > get 2° hypergastrinaemia
Summary of peptic ulcer disease perforation?
Sx - epigastric pain, later becomes generalised, patients may describe syncope
Ix - largely clinical diagnosis, upright chest x-ray (free air under diaphragm)
Management of acute bleeding of peptic ulcer disease?
ABC approach as with any upper gastrointestinal haemorrhage
IV proton pump inhibitor
the first-line treatment is endoscopic intervention
if this fails (approximately 10% of patients) then either:
urgent interventional angiography with transarterial embolization or
surgery
What is gastritis?
Inflammation of the lining of the stomach.
Acute: inflam of gastric mucosa. CS, NSAIDs, uraemia, H pylori, alcohol, smoking, caffeine, physiological stress.
Atrophic gastritis: chronic inflame of gastric mucosa, epithelial metaplasia, mucosal atrophy, gland loss. infections (80%): h pylori, AI against intrinsic factor, H+/K+ ATPase, inhib gastric acid secretion. Damage limited to fundus. HLA-DR3, B8.
Sx of gastritis?
Asymptomatic
Epigastric pain
N/V
Loss of appetite
Heartburn
Haemorrhage, haematemesis, melena.
Complications of gastritis?
AI: iron def anaemia,
Pernicious anaemia - gastric parietal cells
Bleeding
Stomach ulcers
Gastric AC
Neuroendocrine Ca
Investigations for gastritis?
Infection: normal gastrin level, no hypochloridria, no anti-parietal cell/ anti IF Ig
AI: hypergastrinemia, hypochloridria, ↓IF
Endoscopic biopsy: nonspecific, mucosal erosions, erythema, lack of rugae.
Infectious atrophic: multifocal atrophy, ulcers, erythematous, nodular mucosa, thickened rugae early, loss of rugae late damage limited to antrum. AI: diffuse atrophy, absent rugae, mucosal thinning, visible submucosal BVs.
H pylori detection: urea breath test, stool antigen test, biopsy
Management of gastritis?
Remove offending agents
Eradicate H pylori - triple eradication
PPIs, antacids, H2 blocker
Correct vit def, for AI
What is oesophagitis?
is an inflammation of the lining of the gullet (oesophagus). In most people it is caused by the digestive juices from the stomach, repeatedly moving upwards (reflux) into the lower oesophagus producing redness and ulceration.
GORD
Infection: candida
Eosinophilic infiltration: food allergies,
Corrosive meds: NSAIDs, tetracycline, doxy, bisphosphonates.
Radiotherapy, NG tube
Sx of oesophagitis?
Heartburn
Lump in throat
Hoarseness
Chest discomfort
Odynophagia
Dysphagia
N/V abdo pain
Associated with haitus hernia, 80% sliding hernias, 20% rolling hernias.
Investigations for oesophagitis?
FBC: ↑eosinophils
Endoscopy
Management of oesophagitis?
PPIs
Avoid cause
Treat infection
What are oesophageal varices?
are enlarged veins in the esophagus. They’re often due to obstructed blood flow through the portal vein, which carries blood from the intestine, pancreas and spleen to the liver.
Usually a large volume of fresh blood. Swallowed blood may cause melena. Often associated with haemodynamic compromise. May stop spontaneously but re-bleeds are common until appropriately managed.
Dilated veins at junction between portal + systemic venous system. Distal oesophagus ± prox stomach, can be distal stomach + S+L intestine.
Blocked flow to liver, collat circulation in lower oesophagus to areas of lower pressure, veins distended + thinner walls
Portal HTN
Prehepatic: portal vein thrombosis/obstruction (atresia/ stenosis), decreased portal blood flow (fistula), decreased splenic flow.
Intrahepatic: cirrhosis, idiopathic portal HTN, acute hepatitis, schistomiasis, congen hepatic fibrosis, myelosclerosis
Posthepatic: compression Budd-Chiari syndrome, constrictive pericarditis
Sx of oesophageal varices?
Haematemesis
Melaena
Abdo pain
Features of LD
Dysphagia/ odynophagia
Confusion 2° to encephalopathy
Pallor
↓BP ↑HR ↓UO
↓GCS
Complications of oesophageal varices?
^ risk of bleed: decompensation of LD, malnourishment, alcohol, physical exercise, circadian rhythms, ↑abdo pressure, aspirin, NSAIDs, bacterial infection.
Large varices with red spots are at highest risk of rupture.
TIPs: exacerbation of hepatic encephalopathy is common complication
Investigations of oesophageal varices?
FBC: low Hb + platelets, MCV high, normal or low. WCC low
Clotting including INR
Renal function, LFTs
Endoscopy
Management of oesophageal varices?
Prophylaxis of haem: propranolol, endoscopic variceal band ligation at 2 wk intervals until all varices eradicated.
Terlipressin
Octreotide
Prophylactic IV Abx: quinolones
Endoscopy: variceal band ligation, Sengstaken-Blakemore tube if uncontrolled haem, TIPS (connects hepatic vein to portal vein), balloon tamponade salvage Tx for uncontrolled haem
What is Mallory Weiss tear?
Typically brisk small to moderate volume of bright red blood following a bout of repeated vomiting. Malena rare. Usually ceases spontaneously.
Tear of mucosa + submucosa (not muscular), commonly at point where oesophagus + stomach meet.
Severe vomiting, straining coughing, seizures, blunt abdo injury, NG tube placement, gastroscopy.
RF: alcoholism, bulimia, food poisoning, hiatal hernia, NSAIDs, M>F, hyperemesis gravidarum
Sx of Mallory Weiss tear?
Haematemesis after ep of violent retching/ vomiting
Bright red
Melena
Bleeding may cease after 24-48 hrs
Epigastric
Back pain
↑HR ↓BP (not usually)
Investigation of Mallory Weiss tear?
Endoscopy: red longitudinal break in mucosa, may be covered y clot
Hb, haematocrit
Management of Mallory Weiss tear?
Supportive: IV PPIs, antiemetics
Surgery: endoscopy, cauterisation, haemoclips, endoscopic band ligation, arterial embolization
What is Boerhaave’s syndrome?
a spontaneous rupture of the oesophagus that occurs as a result of repeated episodes of vomiting, ↑ intraoesophageal pressure + neg intrathoracic pressure.
The rupture is usually distally sited and on the left side.
Causes - Vomiting/ retching, caustic ingestion, infectious ulcers, Barrett’s, eosinophilic oesophagitis, stricture dilation
Sx of Boerhaave’s syndrome?
Sudden onset of severe chest pain that may complicate severe vomiting.
Subcutaneous emphysema may be observed on the chest wall.
Retrosternal pain, radiate to L shoulder or abdo
Odynophagia
Dysphonia
Back pain
Inability to lie supine
Tachypnoea/ dyspnoea
Cyanosis, fever
Mackler’s triad: CP, vomiting, subcut emphysema
Hamman’s sign: crunching/ rasping sound syncronus with HB, heard over precordium
Diagnosis of Boerhaave’s syndrome?
CXR: free mediastinal air, pleural effusion, pneumothorax, widened mediastinum, SC emphysema
CT contrast swallow - oesophageal wall oedema/ thickening, extraoesophageal air, periesophageal fluid, mediastinal widening, pneumothorax.
Spillage of barium sulfate contrast leads to inflam + fibrosis. Water soluble contrast
Endoscopy avoided
Hb, haematocrit
Treatment of Boerhaave’s syndrome?
thoracotomy and lavage, if less than 12 hours after onset then primary repair is usually feasible,
surgery delayed beyond 12 hours is best managed by insertion of a T tube to create a controlled fistula between oesophagus and skin.
Supportive care
Prophylactic Abx
IV PPI
Complications of Boerhaave’s syndrome?
Delays beyond 24 hours are associated with a very high mortality rate.
Chemical mediastinitis
Severe sepsis occurs secondary to mediastinitis
Pleural effusion
Summary of gastric erosions?
Spots of damage on lining of stomach. Mucous membrane inflamed
lamina propria.
NSAIDs, alcohol, virus, gastritis, radiation, IS
Dyspepsia
N+V
Blood in vomit/ stool
Damage limited to mucosa: epithelium, basement membrane
Stop causative agent
Most erosions heal on their own once cause removed
Surgery
PPIs to ↓ acid
What is angiodysplasia?
a vascular deformity of the gastrointestinal tract which predisposes to bleeding and iron deficiency anaemia.
There is thought to be an association with aortic stenosis, although this is debated.
Angiodysplasia is generally seen in elderly patients
Usually caecum or ascending colon
Age + ↑ strain on bowel wall from chronic + intermittent contraction of colon.
Sx of angiodysplasia?
Capillaries of mucosa gradually dilate, precapillary sphincter becomes incompetent.
Complications of angiodysplasia?
Bleeding, ↑ in coag disorders + prescribed anticoag
Iron def anaemia
Obstructs venous drainage of mucosa
Investigations of angiodysplasia?
Colonoscopy
Mesenteric angiography if acutely bleeding
Management of angiodysplasia?
Blood transfusions + endoscopic Tx, where cauterisation or argon plasma coag Tx can be used
If Tx fails resection of affected bowel
antifibrinolytics e.g. Tranexamic acid
oestrogens may also be used
What is Barrett’s oesophagus?
metaplasia of the lower oesophageal mucosa, with the usual squamous epithelium being replaced by columnar epithelium. There is an increased risk of oesophageal adenocarcinoma, estimated at 50-100 fold.
There are no screening programs for Barrett’s - it’s typically identified when patients have an endoscopy for evaluation of upper gastrointestinal symptoms such as dyspepsia.
can be subdivided into short (<3cm) and long (>3cm). The length of the affected segment correlates strongly with the chances of identifying metaplasia.
The overall prevalence of Barrett’s oesophagus is difficult to determine but may be in the region of 1 in 20 and is identified in up to 12% of those undergoing endoscopy for reflux.
the columnar epithelium may resemble that of either the cardiac region of the stomach or that of the small intestine (e.g. with goblet cells, brush border)
RFs for Barrett’s oesophagus?
gastro-oesophageal reflux disease (GORD) is the single strongest risk factor
male gender (7:1 ratio)
smoking
central obesity
hiatal hernia
previous damage to oesophageal epithelium (e.g., swallowing lye)
Management of Barrett’s oesophagus?
endoscopic surveillance with biopsies. for patients with metaplasia (but not dysplasia) endoscopy is recommended every 3-5 years
high-dose proton pump inhibitor: whilst this is commonly used in patients with Barrett’s the evidence base that this reduces the change of progression to dysplasia or induces regression of the lesion is limited
If dysplasia of any grade is identified endoscopic intervention is offered. Options include:
endoscopic mucosal resection,
radiofrequency ablation
NSAIDs may prevent progression
Avoid chocolate, coffee, tea, peppermint, alcohol, fatty spicy acidic foods.
Features of Barrett’s oesophagus?
Asymptomatic
Frequent, prolonged heart burn, dysphagia, haematemesis, epigastric pain, weight loss
Long: more severe reflux, upright/ supine reflux
Short: asymptomatic, upright reflux
Complications of Barrett’s oesophagus?
Oesophageal adenocarcinoma, sig more likely if long
Investigation for Barrett’s oesophagus?
Oesophagastro duodenoscopy
Screening: M>F, >60, long standing reflux, life expectancy >5 yrs
Biopsy: goblet cells, intestinal metaplasia.
What is refeeding syndrome?
describes the metabolic abnormalities which occur on feeding a person following a period of starvation.
It occurs when an extended period of catabolism ends abruptly with switching to carbohydrate metabolism.
The metabolic consequences include: hypophosphataemia hypokalaemia hypomagnesaemia: may predispose to torsades de pointes abnormal fluid balance
can lead to organ failure
↓ carb intake, ↓ insulin when carb intake ↑, insulin secreted, ↑cellular uptake of electrolytes
Who is at risk of refeeding syndrome?
Patients are considered high-risk if one or more of the following:
BMI < 16 kg/m2
unintentional weight loss >15% over 3-6 months
little nutritional intake > 10 days
hypokalaemia, hypophosphataemia or hypomagnesaemia prior to feeding (unless high)
If two or more of the following:
BMI < 18.5 kg/m2
unintentional weight loss > 10% over 3-6 months
little nutritional intake > 5 days
history of: alcohol abuse, drug therapy including insulin, chemotherapy, diuretics and antacids
NICE recommend that if a patient hasn’t eaten for > 5 days, aim to re-feed at no more than 50% of requirements for the first 2 days.
Complications of refeeding syndrome?
Abnormal fluid balance
Organ failure
Investigations for refeeding syndrome?
Hypophosphatemia: rhabdomyolysis, resp failure, leucocyte dysfunction, coma
↓K: cardiac issues,
↓Mg, TdP
Management of refeeding syndrome?
Start at no more than 50% target energy + protein needs
Build up to meet full needs over 1st 24-48 hrs
Provide full amounts of electrolytes, vits, minerals from outset of feeding.
Causes of malabsorption?
IBD, lactase def, tropical sprue, Whipple’s disease, giardiasis, pancreatic (chronic pancreatitis, CF, pancreatic cancer) Biliary: obstruction, PBC Bacterial overgrowth Short loop syndrome Lymphoma Bile acid malabsorption Orlistat Thyrotoxicosis Diabetic induced neuropathy Meckel’s diverticulum
Features of malabsorption?
Fats: steatorrhoea
Protein: dry hair, hair loss, fluid retention, oedema
Sugars: bloating, gas, explosive diarrhoea
Carpopedal spasm: Ca, Mg
Glossitis: B12, folate, iron, niacin
Diarrhoea
Flatulence + abdo distension: bacterial fermentation of unabsorbed foods
↓BS
Complications of malabsorption?
Anaemia
Bleeding, bruising, petechiae: vit K + C
Night blindness: vit A
Amenorrhoea
Oedema: hypoalbuminaemia, chronic protein malabsorption
Orthostatic hypotension
Dermatitis herpetiformis, erythema nodosum + pyoderma gangrenosum, pellagra, alopecia, seborrheic dermatitis.
What is coeliac disease?
is an autoimmune condition caused by sensitivity to the protein gluten
It is thought to affect around 1% of the UK population.
Repeated exposure leads to villous atrophy which in turn causes malabsorption.
Conditions associated with coeliac disease include dermatitis herpetiformis (a vesicular, pruritic skin eruption) and autoimmune disorders (type 1 diabetes mellitus and autoimmune hepatitis).
It is strongly associated with HLA-DQ2 (95% of patients) and HLA-DQ8 (80%).
Features of coeliac disease?
Chronic or intermittent diarrhoea
Failure to thrive or faltering growth (in children)
Persistent or unexplained gastrointestinal symptoms including nausea and vomiting
Prolonged fatigue (‘tired all the time’)
Recurrent abdominal pain, cramping or distension
Sudden or unexpected weight loss
Unexplained iron-deficiency anaemia, or other unspecified anaemia
Complications of coeliac disease?
anaemia: iron, folate and vitamin B12 deficiency (folate deficiency is more common than vitamin B12 deficiency in coeliac disease)
hyposplenism
osteoporosis, osteomalacia
lactose intolerance
enteropathy-associated T-cell lymphoma of small intestine
subfertility, unfavourable pregnancy outcomes
rare: oesophageal cancer, other malignancies
Investigations for coeliac disease?
Serology
- TTG antibodies (IgA)
- endomyseal antibody (IgA)
Endoscopic intestinal biopsy - traditional duodenum, show villous atrophy, crypt hyperplasia, increase in intraepithelial lymphocytes, lamina propria infiltration with lymphocytes
Management of coeliac disease?
Gluten free diet (avoid wheat, barley, rye, oats)
Can have rice, potatoes, corn
Immunisation - due to functional hyposplenism, pneumococcal infection every 5 years + influenza
Summary of coeliac disease in children?
Children normally present before the age of 3 years, following the introduction of cereals into the diet
failure to thrive diarrhoea abdominal distension older children may present with anaemia many cases are not diagnosed to adulthood
What is lactose intolerance?
Lactase def/inactive, ↑undigested lactose > fermentation by colonic flora, gas, osmotically active substances produced, osmotic pressure decreases (water moves into bowels)
Most often acquired due to physiological weaning off milk, after weaning lactase levels tend to decrease
RF: non-european, congen (autosomal recessive), underlying intestinal disease.
Symptoms of lactose intolerance?
Congen: diarrhoea starting from birth as can’t digest breast milk
Abdo pain
Cramping in lower quadrants
Abdo distension
Flatulence
V/D
Those with lactase persistence can develop bouts of lactose intolerance in response to infection. Inflame
Diagnosis of lactose intolerance?
↑osmotic stool gap: unabsorbed carbs
Bacterial lactose fermentation: acidic stool
Hydrogen breath test: drink lactose solution, test every 15 mins. If breath contains low H2 after consuming lactose = LI.
Lactose tolerance test: drink lactose solution, blood sugar tested, if LI blood sugar rise slowly or not at all as body can’t break down lactose into glucose.
Diagnosis of lactose intolerance?
↑osmotic stool gap: unabsorbed carbs
Bacterial lactose fermentation: acidic stool
Hydrogen breath test: drink lactose solution, test every 15 mins. If breath contains high H2 after consuming lactose = LI.
Lactose tolerance test: drink lactose solution, blood sugar tested, if LI blood sugar rise slowly or not at all as body can’t break down lactose into glucose.
Management of lactose intolerance?
Optimise Ca + Vit D intake
Lactose free diet
Compensate with lactase
What is diverticulosis?
common disorder characterised by multiple outpouchings of the bowel wall, most commonly in the sigmoid colon (as has smallest diameter so ^ pressure)
True - is all organ layers
False - most common in colonic diverticula mucosa and submucosa
Abnormal/ exaggerated smooth muscle contraction, unequal intraluminal pressure distribution, ↑pressure pushes wall out.
Risk factors
increasing age
low-fibre diet
Can present as painful diverticular disease (altered bowel habit, colicky left sided abdominal pain) and diverticulitis
Sx of diverticulitis?
asymptomatic
left iliac fossa pain and tenderness
anorexia, nausea and vomiting
diarrhoea
features of infection (pyrexia, raised WBC and CRP)
left sided colic relieved by defection
rectal bleeding
rectal mass tenderness
Fever, malaise, tachycardia
Urinary urgency, freq, dysuria (inflamed sigmoid colon, bladder irritation)
Acute: abdo pain, severe, localising to LLQ, rectal bleed, rectal mucus
Management of diverticulitis?
mild attacks can be treated with oral antibiotics. Uncomplicated: co-amox, 2nd cefalexin + metro
Liquid diet, analgesia
If Sx don’t resolve within 72 hrs or pt present with severe Sx IV Abx (metro + ceftriaxone)
more significant episodes are managed in hospital. Patients are made nil by mouth, intravenous fluids and intravenous antibiotics (typical a cephalosporin + metronidazole) are given
Surgical resection
Avoid NSAIDs/ opiods as can ↑risk of diverticula perf
If no improvement with Tx with seemingly uncomplicated diverticulitis may suggest abscess
Complications of diverticulitis?
abscess formation
peritonitis
obstruction
perforation - guarding, rebound tenderness
sepsis
fistula - faecaluria, pneumaturia, vaginal passage of faeces or flatus
Complications of diverticulosis?
BV separated from wall lumen by mucosa so vulnerable to injury + rupture
Diverticulitis
Segmental colitis
If diverticula distended enough, can rupture + form fistula
Found in R colon in Asian pts
Investigations of diverticulosis?
Often found incidentally
XR with barium enema: directly shows pouches
CT: visualise colonic diverticula bowel wall thickening (>4mm), ^ soft tissue density with pericolonic.
Low fibre diet, constipation, fatty food, red meat, inactivity, smoking, ↑age, M>F, FH, obesity. CT disorders (Marfans, EDS, AD polycystic kidneys)
Management of diverticulosis?
Resection
↑fibre, avoid constipation, ↑physical activity, smoking cessation
Adequate fluid intake
Bulk forming laxatives eg isphagula + methylcellulose
What is diverticulitis?
Inflamed/ perf of diverticula
Lodged fecalith, obstructs neck of diverticula, stagnation + bacterial multiplication.
Erosion of diverticula wall from higher luminal pressures, inflam, focal necrosis, perforation
Sx of diverticulosis?
Asymptomatic
Vague abdo tenderness
Bloating
Left sided colic relieved by defecation
Nausea
Flatulence
Diarrhoea/ constipation
Rectal bleeding
Palpable mass tenderness
Investigations of diverticulitis?
CT w contrast: inflam hyperdense tissue, thickened bowel wall, abscess, mass, streaky mesenteric fat, gas in bladder in case of fistula
AXR: bowel obstruction, perf, pneumoperitoneum, ileus, soft tissue densitieis, dilated bowel loops
Avoid colonoscopy initially as may perf
Leucocytosis, ↑WCC, CRP + ESR
Symptoms of haemorrhoids?
No sensory fibres above dentate line, aren’t painful unless thrombose when protrodue + gripped by anal sphincter, blocking venous return
Bright red blood, on toilet paper, dripping into pan
Itching
Mucous discharge
Thrombosed: pain, purplish oedematous tender SC perianal mass
Soiling: 3rd/4th deg
Complications of haemorrhoids?
Vulnerable to trauma eg hard stools, bleed
Prolapse
Severe anaemia
Incarceration. Strangulation
Hygiene difficulties
External prone to thrombosis
Investigation of haemorrhoids?
Proctoscopy for internal haemorrhoids
PR, internal haemorrhoids not palpable
Internal 1 - Bleed but no prolapse 2 - Prolapse on straining, reduce spont 3 - Prolapse on straining, manual reduction 4 - Spontaneous irreducible prolapse
Management of haemorrhoids?
1st deg: 🡩 fluid + fibre. Analgesics, stool softener.
Topical anaesthetics + steroids
2nd/3rd deg: rubber band ligation, sclerotherapy, infra-red coag, cryotherapy
Excisional haemorrhoidectomy
Summary of anal fissure?
Painful tear in squamous lining of lower canal.
Hard bowel movement, anal mucosa stretches, acute fissure, internal anal sphincter spasms, blood flow ↓, diff healing chronic fissure
Low fibre, C/D, prev anal surgery, anal trauma, anal cancer, psoriasis, abnormalities in internal anal sphincter, STIs, IBD
Features:
Midline tear
Pain during bowel movement, fear of defecation, constipation, harder stool, more pain
Blood on toilet paper/ stool
Complication:
Faecal bacterial infection
Investigation:
Hx + exam
<6wks acute, >6wks chronic
90% on post midline, if fissures found in alternative locations other causes should be considered
Management:
Stool softeners, fibre, fluid
Bulk forming laxatives if not tolerated try lactulose
Chronic: topical nitrates (GTN ointment), CCB (diltiazem), lidocaine ointment
Referral for botox, if fail internal sphincterotomy
Proper anal hygiene, warm sitz bath
What is an anal fistula?
Abnormal communication between anal canal + perianal skin
Goodsall’s rule: determines path if ant straight line, if post, internal ooening always at 6 o clock, curved
Cause: perianal sepsis, abscess, CD, TB, diverticular disease, rectal carcinoma, IC.
What is an anal fistula?
Abnormal communication between anal canal + perianal skin
Goodsall’s rule states that a fistula with the external opening anterior to an imaginary transverse line across the anus has its internal opening at the same radial position and for an external opening posterior to this line, the internal opening is in the midline posteriorly with a horse-shoe track.
Cause: perianal sepsis, abscess, CD, TB, diverticular disease, rectal carcinoma, IC.
Features of an anal fistula?
Skin excoriations
Itching
Pus/ serous fluid/ faeces draining from skin opening, pass pus/ blood when poo
Pain: constant, throbbing, worse when sit, move, poo or cough
Red, swelling
Investigation and management of anal fistula?
Anal exam, delineate course of fistula
Drain infection, eradicate fistulous tract, preserve anal sphincter function
Require seton suture tightened over time to maintain continence
Summary of rectal prolapse?
Partial/ total slip of rectal tissue through anal orifice, due to lax sphincter, prolonged straining, chronic neurological + psychological disorders
RF: C/D, pregnancy, pelvic floor damage, rectal intussception, child birth
Features: Mass protruding through anus after defecation, when sneezing/ coughing Pain Rectal bleeding Incontence
Management:
High fibre diet, enemas,
Kegel exercises
Sutures/ slings to anchor rectum to sacrum
Proctosigmoidectomy, reanastomosis of remaining rectum to colon, severe prolapse
Anal encirclement with Thiersch wire
What is Familial adenomatous polyposis?
is a genetic condition. It is diagnosed when a person develops more than 100 adenomatous colon polyps
Autosomal dominance, 100% penetrance
Classic: most aggressive, >100 polyps at diagnosis, early onset
Attenuated: <100 polyps at diagnosis, later onset.
Adenomatous polyps, usually pedunculated or sessile, either tubular, villous or tubulovillous
APC gene on chromosome 5q.
Gardner’s syndrome: variant with extracolonic manifestations. Malig in colon, thyroid, liver, kidney.
Features of Familial adenomatous polyposis?
Asymptomatic til malig
If big enough to obstruct, intestines abdo pain + constipation
Palpable abdo mass, pain
Haematochezia
Diarrhoea
Polyps begin in puberty, by 20 can have 100-1000s, more descending colon + rectum
Complications of Familial adenomatous polyposis?
Malig = mean age 35, by age 50 all do
Congen hypertrophy of retinal pigment epithelium
Fundic gland polyps
Duodenal adenomas
Abdo mesenchymal desmoid tumour
Thyroid, pancreas, brain, liver Cs
Sebaceous cysts
Osteomas
Epidermal cysts
Compression of adjacent structures
Investigations of Familial adenomatous polyposis?
Endoscopy, colonoscopy, flexible sigmoidoscopy
Barium enema: filling defects
Abdo CT: hyperdense outpouchings of colonic wall into lumen
Fe def anaemia
Digital rectal exam: palpable mass
Ophthalmic exam: CHRPE
Annual flexible sigmoidoscopy from 15, if no polyps found then 5 yrly colonoscopy from 20.
Management of Familial adenomatous polyposis?
NAIDs
EGFR inhib: erlotinib
Sulindac + celecoxib
Freq endoscopic check ups every 1-2yrs, if polyps detected > removal
Subtotal colectomy with ileorectal anastomosis. Total proctocolectomy with ileoanal anastomosis
What is Lynch syndrome?
Hereditary non-polyposis colon Ca
a type of inherited cancer syndrome associated with a genetic predisposition to different cancer types.
most common cause of hereditary colorectal cancer
mostly at younger age (<50), plus other cancers (uterine, ovarian, bladder, stomach, liver, kidney, brain and certain skin cancers)
Colonic tumours likely to be R sided + mucinous
Autosomal dominant mutation in DNA mismatch repair genes, hMSH2, hPMS1, MSH6, hMLH1, HPMS2
Features of Lynch syndrome?
Blood in stool
Diarrhoea
Long periods in constipation
Crampy pain in abdo
Persistent ↓in size or calibre of stool
Freq feeling of distension in abdo or bowel region (gas pain, bloating, fullness)
Vomiting + continual lack of energy
Investigations and management of Lynch syndrome?
Amsterdam criteria: typical (R sided, mucinous, dense lymphocytic infiltrate), 3 individuals (1 1st degree/ 2 sucessive generations), 1 must have Ca diagnosed <50
Colonoscopy: every 1-2 yrs starting by age 25 or 5-10 yrs before age of earliest CRC diagnosed in family. At 40 annual colonsocpy
Women: yrly pelvic exam, Pap test. Transvaginal USS starting at 25, annually
Upper endoscopy in families with gastric Ca
Polyp removal
Colectomy
