Gastro Flashcards
Define coeliac disease
A systemic autoimmune disease triggered by dietary gluten peptides found in wheat, rye, barley, and related grains
Atrophy of the intestinal villi, hypertrophy of the crypts and increased numbers of lymphocytes in the epithelium and lamina propria
Leads to GI symptoms and malabsorption
Explain the aetiology / risk factors of coeliac disease
Aetiology:
The requirement for DQ2 (95% of coeliac) or DQ8 (the rest) (both MHCII variants) is a major factor in the genetic predisposition to coeliac disease. However, most DQ2- or DQ8-positive people never develop coeliac disease despite daily exposure to dietary gluten.
Hypothesised environmental factors include initial exposure to gluten peptides, GI infection (mimicry) and damage to the intestinal-epithelial barrier leading to abnormal exposure of the mucosa to gluten peptides
- Loss of immune tolerance to peptide antigens derived from prolamins (e.g gliadin, secalin etc.) is central abnormality.
- These peptides are resistant to human proteases, so persist into the small intestine
- They get through to intestinal submucosa in coeliac patients, trigger innate and adaptive immune response
- Innate: stimulate IL-15
- Adaptive: tTG deamidates gliadin, allowing high affinity binding only to DQ2 and DQ8 HLA found on APCs and Th cells.
- This leads to Th1-derived cytotoxic T lymphocytes (–> villous atrophy and crypt hypertrophy) AND Th2 triggers plasma cell maturation and anti-gliadin and anti-tTG Ab production.
Risk factors (strong): family history of coeliac disease immunoglobulin A deficiency type 1 diabetes autoimmune thyroid disease
Summarise the epidemiology of coeliac disease
Recognise the presenting symptoms of coeliac disease
1% of population, can present at any age (peaks childhood and 50-60y/o)
Stinking stools/steatorrhoea;
Diarrhoea;
Abdo pain and bloating;
nausea &
vomiting;
and failure to thrive,
to iron-deficiency anaemia or osteoporosis.
1/3 asymptomatic
RECURRENT MOUTH ULCERS!
Recognise the signs of coeliac disease on physical examination
Signs of anaemia
angular stomatitis
weight loss
RASH (intensely itchy)!!!! Dermatitis herpetiformis (vesicular rash, chronic AI skin condition ass with coeliac disease, often on elbows)
Apthous ulcers
Clubbing
Identify appropriate investigations for coeliac disease and interpret the results
Bloods: Reduced Hb (causes iron deficiency anaemia), b12, ferritin.
FIRST LINE INVESTIGATION: Anti-transglutaminase is single perferred test (but is an IgA Ab, so check IgA levels to exclude subclass deficiency)
Anti-endomysial (95% specific unless patient is IgA deficient) is most specific
Anti-gliadin antibodies
THEN,
DEFINITIVE DIAGNOSTIC: OGD and duodenal biopsy. The classic histological
appearance of bowel affected by coeliac disease is the presence of ‘subtotal villous
atrophy with crypt hyperplasia’.
Where doubt persists, hla dq2 and dq8 genotyping may help.
Generate a management plan for coeliac disease
- Referral to dieticians for gluten free diet advice
Lifelong gluten-free diet—patients become experts. Rice, maize, soya, potatoes, and sugar are ok. Limited consumption of oats (≤50g/d) may be tolerated in patients with mild disease.
Gluten-free biscuits, flour, bread, and pasta are prescribable.
Monitor response by symptoms AND repeat serology! (If coeliac disease is not getting better on a gluten free diet it is nearly always because the patient is not being strict enough about their diet and the TTG is a good way to screen for this without putting them back through the OGD and biopsy.)
- Referral for gastroscopy and duodenal biopsy
- Screening of 1st degree relatives!
- Bone density scan (osteopaenia)
Summarise the prognosis for patients with coeliac disease
higher overall mortality than in the general population.
Summarise the complications for patients with coeliac disease
higher overall mortality than in the general population.
Anaemia; dermatitis herpetiformis (ohcs);
osteopenia/osteoporosis (lack of absorption of calcium, vit D, vit K)
hyposplenism (offer ‘flu and pneumococcal vaccinations);
gi t-cell lymphoma (rare; suspect if refractory symptoms or ↓weight);
↑risk of malignancy (lymphoma, gastric, oesophageal, colorectal)…Celiac disease (CD) is associated with intestinal lymphoma and other forms of cancer, especially adenocarcinoma of the small intestine, of the pharynx, and of the esophagus.
neuropathies.
Define alcoholic hepatitis
Inflammatory liver injury caused by chronic heavy intake of alcohol
Explain the aetiology / risk factors of alcoholic hepatitis
what diseases is it part of
(histopathalogical features)
Part of a spectrum of ARLD:
o Alcoholic fatty liver (steatosis)
o Alcoholic hepatitis
o Chronic cirrhosis
Steatosis happens when lack of NAD+ and increased NADH (due to the alcohol metabolism to acetaldehyde) mean there is less fat metabolism and increased fat production in the liver= fatty changes/steatosis. On histology you see the circles of fat.
Alcoholic hepatitis occurs because there is a build up of ROS (due to metabolism of alcohol). The ROS can damage DNA and proteins too. The acetaldehyde can also form adducts with macromolecules like cell membrane, enzymes etc. Acetyaldehyde adducts can be recognised by your immune system, causing neutrophil infiltration. There are mallory bodies on histology, which are located in the cytoplasm and are damaged intermediate filaments
DEFINING HISTO FEATURES FOR ALCO HEP:
- liver cell damage
- inflammation
- fibrosis
ASSOCIATED HISTO FEATURES FOR ALCO HEP:
- fatty change
- mega mitochondria
• Histopathological features of alcohol hepatitis:
o Centrilobular ballooning
o Degeneration and necrosis of hepatocytes
o Steatosis – fatty change
o Neutrophilic inflammation
o Cholestasis – condition in which bile cannot flow from liver to the duodenum
o Mallory-hyaline inclusions (eosinophilic intracytoplasmic aggregates of cytokeratin intermediate filaments)
o Giant mitochondria
Summarise the epidemiology of alcoholic hepatitis
In long-term heavy alcohol consumers, about 90% to 100% develop fatty liver, 20% to 35% develop alcoholic hepatitis, and 8% to 20% develop alcoholic cirrhosis.
The risk of ALD is at least 2 times higher in patients who are overweight
Recognise the presenting symptoms/signs of alcoholic hepatitis
General ARLD symptoms:
Fatigue, anorexia, weight loss, jaundice, fever, N&V, RUQ discomfort
In advanced liver disease:
Abdo distension and weight gain (ascites), asterix, leg swelling
on examination:
Signs of portal HTN +
ascites, splenomegaly, venous collateral circulations
Identify appropriate investigations for alcoholic hepatitis and interpret the results
Bloods:
- LFTs: AST, ALT, Alk Phos, bili, protein, albumin, GGT
- FBC
- Basic metabolic panel (Na+, K+, Cl-, HCO3-, urea, creatinine)
- Coagulation profile (PT, INR)
Imaging:
- Ultrasound should be performed among patients with harmful alcohol use, as it helps diagnose alcoholic fatty liver disease in patients with hepatic steatosis.
- USS/CT of abdo useful to exclude cholecystitis, biliary obstruction and liver mass
- Liver biopsy only indicated in patients with atypical presentation to evaluate co-existing liver disease like haemochromatosis, AI hepatitis or if it is very very severe
Generate a management plan for acute management of alcoholic hepatitis
Acute management:
-Nutrition, electrolyte, ascites, hepatorenal syndrome?
Acute:
- Thiamine, vit C and other multivitamins (initially parenterallly)
- Monitor and correct K+, Mg2+ and glucose
- Treat encephalopathy with oral lactulose and phosphate enemas
- Treat ascites with spironolactone with or without frusemide (furosemide) or therapeutic paracentesis.
- Glypressin and N-acetylcysteine for hepatorenal syndrome.
Continue nutritional support with eneteral nutrition ASAP (nasogastric tube). Protein restriction only in encephalopathy.
Steroids reduce short term mortality in severe alcogholic hepatitis patients
[SEE ALCOHOL DEPENDENCE FOR LONG TERM MANAGEMENT)
Identify the possible complications of alcoholic hepatitis and its management
Hepatic encephalopathy Coagulopathy GI bleeds Portal HTN Hepatorenal failure HCC Sepsis
Summarise the prognosis for patients with alcoholic hepatitis
Alcoholic fatty liver (steatosis) usually reverts to normal with alcohol
The 5-year survival rate for people with cirrhosis who stop drinking is about 90%, compared with 70% of those who do not stop drinking. However, for late-stage cirrhosis (e.g., jaundice, ascites, or gastrointestinal bleeding), the survival rate is only 60% for those who stop drinking and 35% for those who do not.abstinence
How is alcohol metabolised in the liver
Alcohol is metabolised mainly in the liver, through 2 main pathways: alcohol dehydrogenase and cytochrome P-450 2E1.
Why might ALT/AST be normal in advanced liver disease
AST and ALT can be normal either in the absence of significant liver inflammation (a reassuring sign) or in advanced cirrhosis in which there are few viable hepatocytes left to produce the transaminases (a sign of end-stage disease).
Which transaminase is usually raised higher in ARLD
AST level is almost always elevated (usually above the ALT level). The classic ratio of AST/ALT >2 is seen in about 70% of cases.
The presence of which cell type is prognostic in severe alcoholic hepatitis
The presence of polymorphonuclear cells on liver biopsy may be prognostic for survival of patients with severe alcoholic hepatitis
Which drugs are used to treat alcohol withdrawal syndrome
Benzodiazepines are the most commonly used drugs to treat AWS
Long acting protect against seizures and deliurum,
Shorter acting safer in older adults/those with hepatic dysfunction
How are liver transplants decided
MELD score
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Define portal HTN
- What is portal vein formed of
- Normal pressure in the portal vein, what about in portal HTN
- 4 common sites of porto-systemic anastamoses
- How to distinguish rectal varices from haemarrhoids
Portal veins formed by joining of the splenic with the superior mesenteric vein
Normal pressure is 5–8 mmHg with only a small gradient across the liver to the hepatic vein, in which blood is returned to the heart via the inferior vena cava
If pressure rises to 10-12mmHg, the compliant venous system dilates and collaterals form within the systemic venous system.
The main sites of collaterals are the gastro-oesophageal junction, rectum, left renal vein, diaphragm, retroperitoneum and the anterior abdominal wall via the umbilical vein. The collaterals at the gastro-oesophageal junction (varices) are superficial and tend to rupture.
Rectal varices are found frequently (30%) if looked for and can be differentiated from haemorrhoids, which are lower in the anal canal.
Explain aetiology/risk factors of portal HTN
- Liver injury, fibrogenesis and activated myofibroblasts increase resistance to flow, leading to portal HTN. This can happen in pre-cirrhotic and cirrhotic livers.
- The hyperdynamic circulation of cirrhosis causes peripheral and splanchnic vasodilation (–>splenomegaly and ascites), and sodium retention (related to ascites) increases plasma volume expansion
Causes:
Prehepatic: portal vein thrombosis
Intrahepatic:
Presinusoidal-schistosomiasis/sarcoidosis
Sinusoidal- chirrhosis
Postsinusoidal- venoocclusive disease, budd-chiari syndrome
Posthepatic: Right heart failure, constrictive pericarditis, IVC obstruction
Summarise epidemiology of portal HTN
…
Recognise presenting symptoms of portal HTN
Patients are often asymptomatic, the only clinical evidence being splenomegaly, although features of chronic liver disease may exist
GI haemmorahage may be the initial presenting symptom
Those patients with more advanced liver disease often
present with ascites, hepatic encephalopathy , jaundice, coagulopathy, or spider angiomata.
splenomegaly and dilated abdominal wall veins
Recognise the signs of portal HTN on physical examination
caput medusae, splenomegaly, edema of the legs, and gynecomastia
Identify appropriate investigations for portal HTN and interpret the results
Gold standard investigation
Clinical diagnosis can be made in the setting of end-stage liver disease and in the presence of ascites and/or varices
Splenomegaly can result in sequestration of platelets from the systemic circulation, and low platelet counts may be the earliest
abnormal laboratory finding.
Imaging:
Duplex doppler ultrasonography-provides specifics regarding the
direction and velocity of portal flow. CT/MRI not that useful.
Pressure measurement studies generally not indicated (The gold standard for determining if there is portal hypertension is obtaining a hepatic venous pressure gradient measurement, where a catheter is inserted inside the inferior vena cava, and then inside the portal vein to measure the difference between both pressures.)
Endoscopic diagnosis (in patients with acute gastrointestinal hemorrhage after initial resuscitation)
Generate a management plan for portal HTN
i. Ascites
ii. Acute variceal bleed.
Treatment of portal hypertension is aimed at prevention of complications. The main goal of therapy is to decrease portal pressures
- Ascites. Diuretics (spironolactone and furesomide). Restrict sodium to <2g/day (or restrict fluid if hyponatraemia). Monitor weight. Therapeutic paracentesis with IV human albumin if difficult to control
- Varices.
Medical. Any upper GI bleed: ABC, IV access, fluids, G&S, cross match blood, OGD. For variceal bleed you need to give Abx (CEFTRIAXONE or CIPROFLOXACIN) and TERLIPRESSIN OR VASOPRESSIN OR OCTREOTIDE too. Then, within 12 hrs do OGD (once haemodynamically stable) to perform endoscopic variceal ligation (EVL)= banding.
Sclerotherapy 2nd line if EVL not possible
A TIPS should then be performed in high risk patients 72hrs after EVL. If it’s not performed, the patient should be put on a beta blocker (nadalol/propanalol) after the vasoactive drug has been stopped.
Nonsurgical Transjugular Intrahepatic Portal-Systemic Shunt (TIPSS)- radiologic procedure in patients who have had recurrent bleeding despite medical or endoscopic management. Contraindicated in severe liver dysfunction, renal failure and heart failure
AT ANY STAGE, IF THE BLEEDING IS UNCONTRLLABLE, USE BALLOON TAMPONADE OR SELF EXPANDING METAL MESH STENT
Identify the possible complications of portal HTN and its management
Bleeding varices, ascites, gastropathy, spenomegaly,
Summarise the prognosis for patients with portal HTN
Variceal haemorrhages have a 1-year mortality of 40%
Define acute pancreatitis
(mild vs severe)
An acute inflammatory process of the pancreas with variable involvement of other regional tissues or remote organ systems.
Mild: Associated with minimal organ dysfunction and uneventful recovery.
Severe: Associated with organ failure and/or local complications such as necrosis, abscess or pseudocyst
Explain the aetiology / risk factors of acute pancreatitis
Insult results in activation of pancreatic proenzymes within the duct/acini resulting in tissue damage and inflammation.
Most common: Gallstones, alcohol (80% cases).
Others: Drugs (e.g. steroids, azathioprine, thiazides, valproate), trauma, ERCP or abdominal surgery, infective (e.g. mumps, EBV, CMV, coxsackie B, mycoplasma), hyperlipidaemia, hyperparathyroidism, anatomical (e.g. pancreas divisum, annular pancreas), idiopathic.
Or you can use the mnemonic
I: idiopathic
G: gallstones, genetic - cystic fibrosis
E: ethanol (alcohol)
T: trauma
S: steroids
M: mumps (and other infections)/malignancy
A: autoimmune
S: scorpion stings/spider bites
H: hyperlipidaemia/hypercalcaemia/hyperparathyroidism (metabolic disorders)
E: ERCP
D: drugs (tetracyclines, furosemide, azathioprine, thiazides and many others)
Summarise the epidemiology of acute pancreatitis
Common. Annual UK incidence 10/10 000. Peak age is 60 years; in males, alcohol-induced is more common while in females, principal cause is gallstones.
Recognise the presenting symptoms of acute pancreatitis
Severe epigastric or abdominal pain (radiating to back, relieved by sitting forward, aggravated by movement).
Associated with anorexia, nausea and vomiting.
There may be a history of gallstones or alcohol intake.
Recognise the signs of acute pancreatitis on physical examination
Epigastric tenderness, fever. Shock, tachycardia, tachypnoea.
Reduced bowel sounds (due to ileus, mechanism unclear).
If severe and haemorrhagic, Turner’s sign (flank bruising) or Cullen’s sign (periumbilical bruising).
Identify appropriate investigations for acute pancreatitis and interpret the results
Bloods: Increase amylase (usually >3 x normal but does not correlate with severity); FBC (raised WCC), U&Es, raised glucose, raised CRP, reduced Ca2+, LFTs (maybe deranged if gallstone pancreatitis or alcohol), ABG (for hypoxia or metabolic acidosis)
USS: for gallstones/biliary dilation, pancreatic inflammation, calcification and free fluid
Erect CXR: There may be pleural effusion. Mainly for excluding other causes.
AXR: To exclude other causes of acute abdomen. Psoas shadow may be lost. May show a sentinel loop of bowel (localised ileus caused by intra-abdominal inflammation)
CT scan: If diagnostic uncertainty or if persisting organ failure, signs of sepsis or deterioration for severe cases. Can be used for staging pancreatitis and detecting complications (e.g. necrosis)
MRCP: Can be used instead of CT in patients with renal insufficiency who cannot tolerate IV contrast.
Scoring system (Balthazar score): combination of grade of pancreatitis and degree of necrosis.
Generate a management plan for acute pancreatitis
When operate, when FNA
- Assessment of severity. Modified glasgow scale combined with CRP (>210mg/L):
P- PO2 (<8kPa) A- Age >55 N- WCC (>15*10^9/L) C- Ca2+ <2mmol/L uR- Urea >16mmol/ E- Enzymes (LDH>600) A- Albumin >32g/L S- glucose >10mmol
(REMEMBER AMYLASE DOES NOT INDICATE SEVERITY!)
- Medical:
- Fluid and electrolyte rescusitation, urinary catheter and NG tube if vomiting
- Analgesia and blood sugar control
- Reduced infective complications and mortality with enteral as opposed to parenteral feeding
- Prophylactic Abx only reduce mortality if infective pancreatic necrosis develop - ERCP and sphincterotomy
- For gallstone pancreatitis, cholangitis, jaundice or dilated common bile duct, ideally within 72 h. All patients should undergo definitive management of gallstones during same admission or within 2 weeks. - Early detection and treatment of complications
- e.g. if persistent symptoms and > 30% pancreatic necrosis or signs of sepsis should undergo image guided fine needle aspiration for culture - Surgical: Patient with necrotizing pancreatitis should be managed in a specialist unit. Minimal access or open necresectomy (drainage and debridement of all necrotic tissue).
Identify the possible complications of acute pancreatitis and its management
What is a pseudocyst
Local: Pancreatic necrosis; pseudocyst (peripancreatic fluid collection persisting >4 weeks); abscess; ascites; psuedoaneurysm or venous thrombosis
Systemic: Multiorgan dysdunction, sepsis, renal failure, ARDS, DIC, hypocalcaemia, diabetes
Long term: Chronic pancreatitis (with diabetes and malabsorption)
Summarise the prognosis for patients with acute pancreatitis
Twenty percent follow severe fulminating course with high mortality (infected pancreatic necrosis associated with 70% mortality), 80% run milder course (but still 5% mortality).
Define chronic pancreatitis
Chronic inflammatory disease of the pancreas characterized by irreversible parenchymal atrophy and fibrosis leading to impaired endocrine and exocrine function and recurrent abdominal pain.
Explain the aetiology / risk factors of chronic pancreatitis
Pathophysiology. Important cell type?
Alcohol (70%). Idiopathic in 20%.
Rare: Recurrent acute pancreatitis, ductal obstruction, pancreas divisum, hereditary pancreatitis, tropical pancreatitis, autoimmune pancreatitis, hyperparathryroidism, hypertriglyceridemia.
From rapid medicine:
Disruption of normal pancreatic glandular architecture due to chronic inflammation and fibrosis, calcification, parenchymal atropy, ductal dilatation, cyst and stone formation. Pancreatic stellate cells are thought to play a role, converting from quiescent fat storing cells to myofibroblast-like cells forming extracellular matrix, cytokines and growth factors in response to injury. Pain is associated with raised intraductal pressures and inflammation.
Summarise the epidemiology of chronic pancreatitis
Annual UK incidence ~ 1/100 000; prevalence ~ 3/100 000.
Mean age 40– 50 years in alcohol-associated disease.
Recognise the presenting symptoms of chronic pancreatitis
Recurrent, severe epigastric pain, radiating to th eback, relived by sitting forward, can be exacerbated by eating or drinking alcohol.
Over many years, weight loss, bloating and pale offensive stools (steatorrhoea).
Recognise the signs of chronic pancreatitis on physical examination
Epigastric tenderness. Signs of complications e.g. weight loss, malnutrition
Identify appropriate investigations for chronic pancreatitis.
1st investigation: blood glucose and CT scan (pancreatic calcifications, focal or diffuse enlargement of the pancreas, ductal dilation, and/or vascular complications).
USS can be done if CT not available but is not as good.
Bloods: Glucose (raised may indicate endocrine dysfunction); Amylase and lipase (usually NORMAL); raised immunoglobulins, especially IgG4 in autoimmune pancreatitis
USS: percutaneous or endoscopic: can show hyperechoic foci with post acoustic shadowing
ERCP or MRCP: Early changes include main duct dilatation and stumping of branches. Late manifestations are duct strictures with alternating dilatation ( chain of lakes appearance).
AXR: Pancreatic calcification may be visible.
CT scan: Pancreatic cysts, calcification.
Tests of pancreatic exocrine function: Faecal elastase.
Generate a management plan for chronic pancreatitis
General:
- Treatment mainly symptomatic and supportive, e.g. dietary advice, abstinence from alcohol and smoking, treatment of diabetes, oral pancreatic enzyme replacements, e.g. Creon, analgesia for exacerbations of pain.
- Chronic pain management may need specialist input. The sensory nerves to the pancreas transverse the coeliac ganglia and splanchnic nerves, coeliac plexus block (CT or EUS-guided neurolysis) and transthoracic splanchnicectomy offer variable degrees of pain relief.
Endoscopic therapy: Sphincterotomy, stone extraction, dilatation or stenting of strictures. Extracorporeal shock-wave lithotripsy is sometimes used for fragmentation of larger pancreatic stones prior to endoscopic removal.
Surgical: May be indicated if medical management has failed. Options include lateral pancreaticojejunal drainage (modified Puestow procedure), resection (pancreaticoduodenectomy or Whipple’s) or limited resection of the pancreatic head (Beger procedure) or combined opening of the pancreatic duct and excavation of the pancreatic head (Frey procedure).
Identify the possible complications of chronic pancreatitis and its management
Local: Pseudocysts, biliary duct stricture, duodenal obstruction, pancreatic ascites, pancreatic carcinoma.
Systemic: Diabetes, steatorrhoea, reduced quality of life, chronic pain syndromes and dependence on strong analgesics.
Summarise the prognosis for patients with chronic pancreatitis
PROGNOSIS Difficult to predict as pain may improve, stabilize or worsen.
Surgery improves symptoms in 60– 70% but results are often not sustained. Life expectancy can be reduced by 10– 20 years.
Define Barrett’s oesophagus
Pre-malignant condition
Metaplastic change in the eosophagus, from stratified squamous epithelium to simple columnar epithelium (which is usually native to lower GI tract)
Explain the aetiology / risk factors of Barrett’s oesophagus
2 types of barretts and which is worse
Chronic acid exposure –> reflux esophagitis (chronic irritation) –> metaplasia
Bile acids –> intestinal differentiation –> promotes cancer growth
2 types depending on z line:
-If z-line and GEJ coincide then there’s intestinal metaplasia at the GEJ. This is associated with H Pylori.
Short-segment Barrett’s esophagus (< 3 cm of columnar epithelium between Z-line and GEJ)
Long-segment Barrett’s esophagus (> 3 cm of columnar epithelium between Z-line and GEJ). Higher risk of adenocarcinoma!
Risk factors:
Bulimia Central obesity Previous chemical damage to esophageal epithelium (e.g. swallowing lye) Smoking Hiatal hernia Angle of His >60 (newborns) Scleroderma!
Triggers for GORD
Bending down, supine position
Habits: smoking and/or alcohol consumption
Psychological factors: especially stress
Recognise the presenting symptoms of Barrett’s oesophagus
Often asymptomatic,
Frequent, prolonged heartburn, dysphagia, haematemesis, epigastric pain, weight loss
Recognise the signs of Barrett’s oesophagus on physical examination
Often asymptomatic,
Frequent, prolonged heartburn, dysphagia, haematemesis, epigastric pain, weight loss
Identify appropriate investigations for Barrett’s oesophagus and interpret the results
OGD + biopsy and histological corroboration using the prague criteria (C&M, look up if time). IHC staining assists.
Histologically: Histological appearance of the squamocolumnar junction in a case of Barrett’s esophagus. The underlying glandular epithelium contains goblet cells, indicating intestinal metaplasia.
Generate a management plan for Barrett’s oesophagus
Medical management with PPIs
Endoscopy with 4-quadrant biopsies at every 2cm of the suspicious area.
If no dysplasia: repeat endoscopy every 3-5 years
If indefinite for dysplasia: repeat endoscopy with biopsies after 3–6 months of optimized PPI therapy
If low-grade dysplasia: Endoscopy therapy of the irregularity (Usually including endoscopic mucosal resection and radiofrequency ablation)
OR
surveillance every 12 months with biopsies every 1cm
If high grade dysplasia:
Endoscopy therapy of the irregularity (Usually including endoscopic mucosal resection and radiofrequency ablation)
Identify the possible complications of Barrett’s oesophagus and its management
Eosophageal adenocarcinoma
Annual endoscopic observation for nondysplastic/low-grade lesions
Management of acid reflux:
Avoid/reduce intake of foods known to worsen refl ux: chocolate, coffee, tea, peppermint, alcohol, fatty/spicy/acidic foods. High dose long term PPIs.
Summarise the prognosis for patients with Barrett’s oesophagus
.
Define acute cholangitis
Ascending cholangitis, also known as acute cholangitis or simply cholangitis, is inflammation of the bile duct (cholangitis), usually caused by bacteria ascending from its junction with the duodenum (first part of the small intestine). It tends to occur if the bile duct is already partially obstructed by gallstones.
Explain the aetiology / risk factors of acute cholangitis
Most common causative organism
- Gallstone blocking flow of bile through the CBD
Bile usually flushes out the bacteria going from the gut into the biliary system via the ampulla of vater, but when this flow is obstructed, a bacterial infection can move up the CBD, called ascending cholangitis.
Remember the risk factors for gallstones are the 4 Fs:
Female, Fertile (aka PREGNANT), Fat (obese) or Forty (age)
- Strictures= type of abnormal narrowing in a passage in the body. (e.g due to a nearby cancerous growth OR injury from a procedure)
Note that the bacteria can colonise distal to the blockage in the CBD, but also migrate beyond the blockage and infect the stagnant bile and surrounding tissue
Most common causative organisms= mixture of enteric organisms e.g. E Coli, klebsiella and enterococcus.
Summarise the epidemiology of acute cholangitis
..
Recognise the symptoms/signs of acute cholangitis on physical examination
Fever, RUQ pain, jaundice*
These 3 are called charcot’s triad
*ONLY if there is high pressure proximal to the obstruction such that the spaces between cells lining the CBD have bigger gaps between them, allowing bile (and bacteria!) to leak into the blood stream
Reynolds pentag=
Fever, RUQ pain, jaundice, hypotension and confusion
Identify appropriate investigations for acute cholangitis and interpret the results
BMJ best practice:
- USS
- CT (if USS non diagnostic)
- MRCP (if USS non diagnostic)
Then go to ERCP
If high suspicion of acute cholangitis (e.g. charcto traid +ve)–> straight to diagnostic and therapeutic ERCP
If acute cholangitis suspected but without charcot triad –> RUQ USS (–>CT/MRI if nondiagnostic–>MRCP if still non-diagnostic but suspicion is high)
Generate a management plan for acute cholangitis
Manage symptoms: rehydration and Abx
To definitively treat, you need to remove the blockage, e.g. using ERCP to suck out the gallstone + sphincterotomy
For larger gall stones, can use shockwave lithrotripsy
Percutaneous transhepatic cholangiography (PTC) if ERCP is unsuccessful or unavailable
Interval cholecystectomy if gallstones present/concurrent cholecystitis
Identify the possible complications of acute cholangitis and its management
Proximal to the obstruction (e.g. gallstone or stricture), there can be openings in the gaps between the cells lining the CBD, allowing bile AND the bacteria to leak out into the bloodstream. –> septic shock (leading to hypotension and confusion due to leaky blood vessels
Summarise the prognosis for patients with acute cholangitis
Septic shock
Define haemochromatosis
A condition of iron overload- the body absorbs too much iron
Explain the aetiology / risk factors of haemochromatosis
Primary (Hereditary haemochromatosis- RECESSIVE):
-Gene mutation in the HFE gene causes duodenal cells to bring too much iron into the bloodstream perhaps due to hepcidin deficiency
Secondary haemochromatosis
-Repeat blood transfusions. The RBCs in the transfusion are broken down after 120 days, but the iron is not
It causes damage because iron can undergo the fenton reaction which leads to free radical production.
Free radicals cause cellular damage, cell death and tissue fibrosis over many years.
Summarise the epidemiology of haemochromatosis
Why do men experience early haemochromatosis?
Presents in men age 50
And in women around 10-20 years after the menopause
Later in women because they have better opportunity to get rid of iron due to menstrual bleeding
But it is NOT a gender specific disease
Recognise the presenting symptoms of haemochromatosis
May be asymptomatic
Non specific:
-Weakness, fatigue, lethargy, abdo pain
Later:
-Small/large joints pains (most commonly 2nd/3rd metacarpophalangeal joints), degenerative joint disease (involves calcium crystals)
- Liver disease symptoms (those with cirrhosis at increased risk of HCC)
- DM (type 1 due to destruction of beta islet cells)
- Hypogonadism (amenorrhoea in women/testic atrophy in men) due to pituitary dysfunction
- Cardiac failure (can lead to arrhythmia)
- Skin pigmentation
Recognise the signs of haemochromatosis on physical examination
WITH SEVERE iron overload:
- Bronze skin (iron deposition and increased melanin production)
- Liver: hepatosplenomegaly
- Heart: signs of HF/ arrhythmia
- Hypogonadism: testic atrophy, loss of hair, gynaecomastia
Identify appropriate investigations for haemochromatosis and interpret the results
Iron: High
Transferrin saturation: high
Total iron binding capacity: low
Increased ferritin (usually signals to decrease transferrin production)
BIOPSY
Brown spots inside cells can represent iron, but htedse can be be confused with a pigment called lipofuscin which is part of normal wear and tear of cells.
To confirm it’s iron you can use Prussian blue stain, which shows iron as blue.
What is iron critical for in the body
o2 transport
Oxidative phosphorylation
Outline how iron is usually handled in the body
We only absorb about 10% of the iron we ingest per day, because the body has no mechanism to actively excrete iron
Fe 2+ and haem can be absorbed across the luminal membrane of the intestinal enterocytes (Fe3+ must be converted to Fe2+ to be absorbed, and this is catalysed by Vit C)
Once inside, one of two things can happen to the Fe2+:
- It can be transferred into the blood stream by ferroportin. After than it is then transferred back to Fe3+ and carried by transferrin
- It can be transferred back to Fe3+ in the cytosol and bound to apoferritin, which holds the Fe3+, inert. This is useful when there’s enough iron in the body, because the apoferritin just gets excreted into the faeces.
Hepcidin inhibits ferroportin to reduce iron intake.
Iron is stored as ferritin intracellulary in the body
Treatment for haemochromatosis
Phlebotomy!
Deferoxamine
-this drug binds free iron in the blood and allows it to be excreted in the urine
T/F acute cholecystits is a risk factor for cholangiocarcinoma
F.
Neither cholelithiasis nor cholecystitis is associated with increased risk of cholangiocarcinoma. Risk factors include Primary sclerosing cholangitis, chronic duct inflammation, infections, and ulcerative colitis.
T/F acute cholecystitis is a risk factor for gall bladder carcinoma
Acute cholecystitis is not a risk factor for carcinoma of the gallbladder, but multiple stones increase the risk of GBC.
It should be noted that the vast majority of patients with cholelithiasis will not develop carcinoma of the gallbladder.
T/F acute cholcystitis and high alcohol consumption are risk factors for pancreatic cancer
F. Acute cholecystitis/ alcohol does not increase the risk of pancreatic cancer.
Pancreatic cancer risk factors include smoking, a high-fat diet, and chemical exposures. Of note, alcohol consumption is not a demonstrated risk factor.
T/F acute cholcystitis is a risk factor hepatocellular carcinoma
T, but while patients who have gallstones or have undergone cholecystectomy may have an increased risk of hepatocellular carcinoma (HCC), the biggest risk factors for HCC are hepatitis B, hepatitis C, and cirrhosis.
What is rigler triad
pneumobilia (air in the biliary tract),
low small bowel obstruction with distended small bowel loops
and an impacted gallstone in the terminal ileum
=GALL STONE ILEUS
What is gallstone ileus
A mechanical small bowel obstruction secondary to gallstone impaction in the terminal ileum
The gallstone passes through a cholecystoduodenal fistula, travels the length of the small bowel, and obstructs proximal to the ileocecal valve.
It is an unusual complication of cholecystolithiasis and chronic cholecystitis.
Gallstone ileus is an uncommon cause of small bowel obstruction, however, in the elderly, it accounts for up to 25% of non-strangulated bowel obstructions. Females are more frequently affected.
Which antibodies are associated with each of the following conditions:
- Primary biliary cirrhosis
- Primary sclerosing cholangitis
Which type of biliary ducts are affected in each case
PBC. Your typical AI conditions. Associated with RA, sjorgen. Sero positive- AMA antibodies. Intrahepatic ducts affected.
PSC. Associated with UC. Concentric rings of fibrosis on MCRP. Perinuclear antineutrophil cytoplasmic antibody. Extrahepatic ducts
Define achalasia
Eosophageal motility disorder characterised by loss of peristalsis and failure of relaxation of the LOS
Explain the aetiology / risk factors of achalasia
Which cells are affected?
Which infection causes a similar effect?
Degeneration of ganglion cells of the myenteric plexus in the oesophagus due to an unknown cause.
Oesophageal infection with Trypanosoma cruzi seen in Central and South America produces a similar disorder (Chagas’ disease).
Summarise the epidemiology of achalasia
present 25-60 years
Recognise the presenting symptoms of achalasia
Insidious onset/gradual progression of:
- intermittent dysphagia involving solids and liquids;
- difficulty belching;
- regurgitation (particularly at night);
- heartburn;
- chest pain (atypical/cramping, retrosternal);
- weight loss.
Recognise the signs of achalasia on physical examination
Signs of complications
Clubbing
Identify appropriate investigations for achalasia and interpret the results
Best test is MANOMETRY:
- Elevated resting LOS pressure
- Incomplete LOS relaxation
- Absence of peristalsis in the distal smooth muscle portion of the oesophagus
Barium swallow:
- dilated eosophagus which smoothly tapers down to the sphincter (beak-shaped)
- tertiary peristalsis waves (multiple, disorganised contractions appear as dilations and constrictions through a portion or the entire length of the oesophagus- not triggered by swallowing)
CXR:
- widened mediastinum/double right heart border (dilated eosophagus),
- air-fluid level in the upper chest (due to stasis in a thoracic oesophagus filled with retained secretions and food) and
- absence of the normal gastric air bubble
Endoscopy: only to exclude malignancy which can mimic achalasia
Serology for antibodies against T. cruzi if chaga’s is suggested by epidemiology and symptoms. Blood film might show parasites
What causes each of the following types of peristalsis:
- primary
- secondary
- tertiary
- primary: normal! Peristalsis triggered by swallowing, followed by deglutitive inhibition.
- secondary: Secondary peristaltic waves occur after swallowing to clear the esophagus of food, reflux, or gas. They are triggered by esophageal distention.
- tertiary: caused by esophageal spasm or by achalasia
bulky and foul smelling stools?
This is classic description of steatorroeah (doesn’t have to be diarroeah like!)
What is D-xylose and what is it used for
It is a monosaccharide that is absorbed through small intestines and excreted through the kidneys.
It helps to distinguish structural from functional causes of steatorrhoeah (which is due to fat malabsorption).
If the level of D-xylose excretion is low, it suggests there is a structural problem with absorption (so the excreted sugar is low as well as the fat would be). E.g. Coeliac and crohn’s
But if D-xylose is normal then it suggests this is an issue affecting fats only, and thus is a functional problem (e.g. exocrine pancreatic insufficiency leading to lack of lipase and thus lack of absorption of fats, leading to steatorroeah)
What will the excretion of D-xylose show in the following conditions:
- Coeliac disease
- Crohn’s
- Small intestinal bacterial overgrowth
- Pancreatic insufficiency
Coeliac: reduced excretion
Crohn’s: normal excretion (i don’t get why but think this test is old anyway)
Pancreatic insufficiency: normal
Small intestinal bacterial overgrowth: decreased urinary excretion of D-xylose
What is mackler’s triad
Boerhaave syndrome is characterized by the Mackler triad (vomiting, chest pain, and subcutaneous emphysema) in just 14% of patients.
What does an upturned U shape on abdominal radiograph represent
grossly dilated loop of sigmoid colon, secondary to volvulus.
Ischaemic colitis usually involves which part of the colon, and what sign do you get on abdominal radiograph
Ischaemia tends to involve the splenic flexure and is associated with mucosal oedema (“thumbprinting”)
Initial management of patient with sigmoid volvulus.
What if it recurs?
Passage of a decompressing flatus tube will relieve symptoms and is relatively non-invasive.
For some patients this treatment may suffice.
Volvulus may be recurrent however, requiring sigmoid colectomy and obtunded patients, or those with associated perforation, may require surgery also.
What is the management of caecal volvulus
.These patients usually require a right hemicolectomy.
Initial management of patient with sigmoid volvulus.
What if it recurs?
Passage of a decompressing flatus tube will relieve symptoms and is relatively non-invasive.
For some patients this treatment may suffice.
Volvulus may be recurrent however, requiring sigmoid colectomy and obtunded patients, or those with associated perforation, may require surgery also.
Sigmoid volvulus is due to twisting of the bowel on what mesentery, what about caecal volvulus
Both lax
What is splenic injruy associated with
Rib fractures (40%), left kidney injury (25%) and less commonly diaphragmatic rupture (2%)
T/F most splenic lacerations are self limiting
T
The majority of splenic lacerations are self limiting and can be managed conservatively avoiding the need for a splenectomy
What would an US be used for in an emergency with presumed splenic injury
Just to assess for free air/fluid (not looking at solid organs)
What is splenic injruy associated with
Rib fractures (40%), left kidney injury (25%) and less commonly diaphragmatic rupture (2%)
T/F most splenic lacerations are self limiting
T
The majority of splenic lacerations are self limiting and can be managed conservatively avoiding the need for a splenectomy
What vaccines and prophylaxis are to be given following splenectomy
Post-splenectomy, patients are at increased risk of severe bacterial infections in particular:
- Pneumococcus,
- Meningococcus and
- Haemophilus influenzae,
all of which can be vaccinated against.
Also at risk of malaria, so they should take caution when travelling to affected countries
Long term penicillin for prophylaxis (it’s controversial but still done)
How would you differentiate small bowel obstruction from small bowel ileus on examination
In paralytic ileus, bowel sounds are usually absent on auscultation, whereas a high-pitched tinkling sound would be heard in the early phase of a mechanical bowel obstruction (i.e. bowel sounds increased).
Why do you insert a NG tube in ileus/obstruction
Patients will be much more comfortable if you insert a nasogastric tube to decompress the stomach and upper small bowel.
What must you consider when giving analgesia for patients with ileus?
The distension of bowel loops found in ileum will cause abdominal pain and therefore the patient is likely to need analgesia, although be aware that opiate analgesia slows the gut and may then contribute to ongoing ileus. Review chart for other drugs that might be contributing.
What causes electrolyte abnormalities and dehydration in ileus/mechanical obstruction
Bowel distention leads to third-space volume loss, resulting in dehydration and electrolyte abnormalities.
And
Vomiting
Which electrolytes are particualrly important to correct in ileus
Correct electrolytes in particular K and Mg, aiming for a K of greater than 4 to maximise the chance of the gut getting moving again.
What do you need to monitor when giving TPN
- Daily inspection of line & dressing
- 4hr temp and observations
- Blood glucose
- Daily electrolytes
- Accurate recording of fluid balance
What are the complications of TPN
- Infection of the central line
- TPN has high sugar content (sugar derangement can develop in even those w/o diabetes- it also increases the risk of infection if blood sugar high)
- Fluid balance problems (either becauses losses from NG, fistula, high output stoma etc are not adequately corrected on top of the TPN volume, or because people forget that TPN contains a lot of fluid and then give standard IV fluids in addition)
- Electrolyytes need to be watched as TPN patients often have difficult fluid balance with high losses and GI fluid contains a lot of electrolytes in particular Na, K and Mg. Additionally electrolytes can be dramatically affected by refeeding syndrome
What should TPN patients be given before they begin this form of nutrition and why
Pabrinex
Pabrinex contains a mixture of B vitamins and vitamin C. The reason we give it is to make sure that the patient has plenty of thiamine available to them as they start feeding. Thiamine is required to process the food which has been given and if you have been in a state of starvation then thiamine levels will be low with a risk that it could be used up as feeding commences.
This results in Wernicke’s encephalopathy which is reversible if thiamine is given rapidly. If it is not identified and thiamine administered then it will rapidly progress to Korsakoff’s Psychosis an irreversible dementia.
Why are alcoholics given pabrinex/thiamine
Because they frequently have a very poor quality diet in the community and so can develop Wernicke’s when they are give proper meals in the hospital, it is nothing to do with the withdrawal itself.
What is a typical history for bowel ischaemia
Cramping pain and bleeding
Megacolon is usually associated with what
It leads to sepsis (fever and high WCC)
Air absent vs present in the rectum when querying bowel obstruction?
Air absent in the rectum is consistent with left sided obstruction e.g. sigmoid stricture
If air is present in the rectum it makes left sided obstruction unlikely. It is more likely to be pseudo- obstruction, or possibly a low lying lesion in the rectum
What is the difference between ileus and pseudoobstruction
Pseudo-obstruction is defined as acute, marked distention of the large bowel.
As with ileus, it occurs in the absence of a definable mechanical pathology.
Pseudo-obstruction is clearly limited to the colon alone, whereas ileus involves both the small bowel and colon.
How is pseudo-obstruction usually managed
Conservatively.
Exclusion of a mechanical obstruction is needed in a proportion of patients, either via CT scan or colonscopy.
Colonscopic decompression is useful in acute cases
Neostigmine treatment is useful in acute cases
Which electrolyte imbalance is a cause of pseudo-obstruction
Hypokalaemia
Which surgery is assocaited with pseudo-obstruction
There is an association with recent surgery, particularly orthopaedic
Differentiate the broad management of ileus vs mechanical obstruction
It is important to differentiate the two, as ileus can often be resolved by conservatively managing the physiological upset that caused it in the first place. In contrast the causes of mechanical obstruction are often surgical, as in our case.
If you ‘cant get above’ a scrotal lump, what does this indicate
You should be able to do so with any such lump that is confined solely to the scrotum. If you can’t, the lump must be originating from the abdomen
What is the differentials for a lump that you can’t “get above”
How do you differentiate the two
It will be either be a hydrocele of the spermatic cord (which transilluminates and is found in babies and infants) or an inguinal hernia.
Define hernia
An abnormal protrusion of a viscus from one cavity into another.
Outline 2 classic features of hernia
Two classic features of hernias are that they have a cough reflex (owing to transmitted pressure from the abdomen) and that they can be reduced (pushed back) into the abdomen.
When will you see a loss of classic features of hernia
If however, the loop of bowel or mesentery passing through them should get stuck, from narrowing of the hernial orifices for example, these two features will not be elicited.
How do you differentiate a narrowed hernial orifice from hernia incarceration.
How do you differentiate this from infarction (due to strangulation)
Narrowed orifice –> loss of classic features
Incarcerated –> hard hernia
Infarcted –> The latter is typified by severe tenderness over the hernia and signs and symptoms of peritonitis caused by bacteria and intestinal/colonic material escaping from necrotic bowel.
What is hernial incarceration
If the impingement is tight enough, gastrointestinal contents will not be able to pass through any loops of bowel involved, and intestinal obstruction will ensue.
What is hernial strangulation
Blood supply to the incarcerated protruding viscus can also be compromised, leading to ischaemia and infarction. This is called strangulation.
How do you differentiate large from small bowel in abdominal x ray
A more reliable means of telling small from large bowel is to look at their respective bowel markings; small bowel has valvulae conniventes (bands which go all the way round the bowel circumferentially – see Fig 1) while large bowel has haustra (lines which do not quite go all the way around).
Also, large bowel more peripheral and small bowel more central (but not reliable as things are mobile)
Main causes of mechanical obstruction (in small and large bowel) and of functional obstruction (ileus)
Mechanical
Small bowel: incarcerated hernia and adhesions
Large bowel: strictures (e.g. secondary to diverticular disease) and intra-luminal cancers
Ileus
variety of reasons that interfere with the normal physiology of the bowel, eg. immediately following bowel surgery, during electrolyte disturbances, and sepsis
How does bowel obstruction cause shock
Up to 9L are secreted into the GI tract everyday (as wll as whatever fluid has come from food and drinking).
The body usually reabsorbs this in the large bowel, so it’s easy to understand how bowel obstruction and the accumulation of fluid in the third space can result in severe hypovolaemia and then shock
Indirect inguinal hernias are associated with which developmental variation
Indirect inguinal hernias are associated with a patent processus vaginalis, an invagination of the embryonic parietal peritoneum into the scrotum. This results in the formation of the inguinal canal which permits the testes to subsequently enter the scrotum from the abdomen.
The processus vaginalis usually close within 18 months of birth, but persists in a significant proportion of individuals into adulthood. In such people, there is a potential pathway by which bowel can gain entry into the scrotum via the inguinal canal, just like the testes did in utero.
Differentiate the path of direct and indirect inguinal hernias into the scrotum
Whereas indirect inguinal hernias exit both the deep and superficial inguinal orifices (or ‘rings’) before entering the scrotum, direct hernias exit the abdomen via the superficial ring only. This occurs as a result of weakening of the abdominal muscles that make up the superficial ring, and is unsurprisingly more common in older patients.
What are incisional hernias
Muscle weakening can also explain why hernias are also more common at the sites of surgical incisions, ie. surgical scars. These are known as incisional hernias, and can easily be demonstrated on the abdomen, if present, by asking a patient to lift their torso off the examination couch without using their hands (almost as if they are doing a sit-up).
What structures in the gut can herniate
In terms of which viscera is involved, anything that is relatively mobile can herniate.
This includes the small bowel (by way of the mesentery), transverse and sigmoid colon (by way of their respective mesocolons), omentum, and even the ovaries and fallopian tubes (as result of the mesovarium). Any of theses viscera could become incarcerated and eventually, strangulate within a hernia.
T/F toxic megacolon results from obstruction
Not correct.
Toxic megacolon is a consequence usually of ulcerative colitis (more rarely crohns disease).
It CAUSES an ileus (so reduced bowel sounds)
T/F an incompetent ileocaecal valve is actually good in the case of left colonic obstruction
T!
A competent ileocaecal valve will stop bowel contents moving from the obstructed colon back into the small intestine so will actually increase risk of colonic perforation
What abdominal sign might suggest colonic carcinoma on barium enema
Apple core lesion
What imaging modality is best way to investigate colonic carcinoma
In cases of large and small bowel obstruction, especially if no history to suggest adhesions, CT has largely become the technique of choice for further assessment.
Air distension of the bowel is not employed (as per colonography) as this may precipitate perforation.
CT will identify the cause of obstruction non-invasively in most cases and will also provide staging information etc (liver, lungs, regional nodes).
Use contrast enhanced
How would you manage small bowel obstruction
What are the indications for surgery
In what proportion of cases do you think the obstruction resolves spontaneously with conservative management
Standard things first:
1) Assess ABC
2) NBM
3) IV fluids and NG tube to aspirate gastric contents
4) Analgesia
Then referral to surgical team, who will probably trial conservative management first:
A sensible approach would be:
1) A trial of conservative management, i.e. fl uids and NG aspiration (‘drip and
suck’), to see if the obstruction resolves of its own accord. He should be reviewed
regularly to ensure he does not deteriorate (e.g. bowel strangulation).
2) Surgery, if:
− there are signs of strangulation or peritonism;
− after ~48 hours the obstruction has not resolved; or
− there is no history of abdominal surgery, making adhesions less likely and
more sinister causes more likely (virgin abdomen)
In 75% of cases,
adhesions resolve spontaneously with conservative management.
Differentiate a pancreatic pseudocyst and a pancreatic abscess, both complications of acute pancreatitis
The pseudocyst is defined as a localized collection of pancreatic juices confine to a retroperitoneal area by a fibrous membrane without epithelium; an abscess is a collection of pus and necrotic tissue.
A pancreatic abscess would present with pain, and features of sepsis.
2 methods of pseudocyst drainage?
The pseundocyst can also be drained percutaneously or through the stomach wall at EUS.
A blind attempt at gastroscopy is not generally advocated due to the increased risks.
Which blood test is a measure of pancreatic exocrine function
Faecal elastase
What is the treatment of pancreatic exocrine insufficiency
Oral enzyme replacement e.g. creon
What is the tumour marker for pancreatic carcinoma
(CA19-9)
if you suspect pancreatic cancer and feel a mass in the right upper quadrant, what is this likely to represent
Not the tumour itself!
The right upper quadrant mass is likely to represent a distended gallbladder (due to biliary obstruction)
When is MRCP most useful
MRCP is a useful diagnostic tool only and is best suited for assessment of suspected choledocholithiasis.
What is the technique of choice for staging pancreatic carcinoma
CT is the technique of choice for staging pancreatic carcinoma (look for local invasion of duodenum and vessels, enlarged regional nodes and liver metastases).
What will be found in malignant vs inflammatory causes of biliary obstruction on ercp
Malignant: shouldered and irregualar
Inflammaotry: smooth
Risk factors for pancreatic cancer
Cigarette, diabetes
What are the complications of ERCP
Perforation Aspiration pneumonia Haemorrhage Acute pancreatitis Ascending cholangitis
What is the best modality for each of the following in the adbomen:
- air
- calcification
CT for both
What is porcelain gallbladder
Calcification in the wall of the gallbladder
It is associated with gallstones and chronic inflammation of the gallbladder
There is an association with gallbladder carcinoma
Surgery is indicated
What is emphysematous cholecystits
A type of cholecystitis more common in diabetics
Air arises in the wall of the gallbladder due to gallbladder ischaemia and infection with gas-forming organisms (clostridium)
Symptoms and signs are initially minor but mortality is high due to sepsis
Risk factors for gallstones
‘fair, fat, female, fertile and forty’
pregnant
T/F lap chole has lower complication that open chole
F
A Cochrane review comparing the two methods of surgery found no differences in mortality, complications, or operative time. There was however, clear evidence of a shorter stay in hospital with quicker convalescence.
Which two organisms can mimic ileo-caecal chrohns disease?
Yersinia and TB!
t/f patients with ileocaecal tuberculosis present with pulmonary TB in the vast majority of cases
F….
A chest radiograph should be performed to demonstrate previous or active pulmonary tuberculosis, although half of all patients do not present with a previous history of pulmonary TB.
T/F onset of achalasia is usually slower than malignancy
What else might help you differentiate
T.
benign pathologies e.g. peptic stricture and achalasia tend to have longer histories
Achalasia commonly just as bad for liquids as it is for solids
What would the best investigations for dysphagia be?
Upper GI endoscopy opy first if you suspect cancer
If this is normal then a barium swallow can give important information on oesophageal motility and is better at picking up achalasia.
Which investigation is used to confirm achalasia after barium swallow
Manometry is used to confirm the diagnosis of achalasia
T/F achalasia is a risk factor for oesophageal carcinoma
T!
Progressive dysphasia with aspiration and difficulty swallowing solids and liquids from the atart?
Achalasia /motility disorder
What is an infectious cause of dysphagia, and who might present with it
Oesophageal candidiasis generally occurs in patients who are frail and immunosuppressed, particularly those on steroids, including inhaled steroids. It tends to present with odinophagia and dysphagia and oral plaques are usually present.
What could be the chest xray findings in achalasia
A chest x-ray may show a dilated oesophagus in achalasia with absence of the gastric air bubble
Look on google images for “
VCU Department of Radiology
Esophageal Dilatation with “Air Esophogram Sign”
What would the barium swallow show for achalasia vs malignancy
Achalasia: There is a tight, smooth narrowing of the distal oesophagus
Malignancy: irregular stricture (usually happens on a background of GORD)
What are the possible interventions for achalasia
Balloon dilation
Surgical cardiomyotomy
Anti-reflux medication
Define volvulus
Colonic volvulus:
Rotation of a loop of bowel around the axis of its own mesentery that results in bowel obstruction and potential ischaemia.
65% sigmoid colon, 30% caecum
Explain the aetiology / risk factors of volvulus
Anatomical factors:
- Long sigmoid mesentery
- Mobile caecum
- Chronic constipation and debility
- Age
- Very high residue diet
- Tumour
- Adhesions
- Chagas’ disease of the colon
Rotation of the segment of bowel results in partial or complete closed loop obstruction. With a 360 degree twist, the veins tot he bowel are compressed and occluded, leading to circulatory impairment and, if not relieved, gangrene and perforation
Summarise the epidemiology of volvulus
5-10% of large bowel obstructions, more common in elderly
Recognise the presenting symptoms of volvulus
Abdo pain and swelling, absolute constipation and later vomiting
May be previous episodes with spontaneous resolution
Recognise the signs of volvulus on physical examination
Signs of bowel obstruction:
- Distension
- Tenderness
- Tinkling bowel sounds
Identify appropriate investigations for volvulus and interpret the results
Abdominal xray:
-Massively dilated loop of bowel, may have a
-Coffee bean shape:
In caecal valvulus it points towards the lower right quadrant
In sigmoid it points to the left.
-May be associated with proximally dilated loops of bowel and collapse
Water soluble contrast enema:
-Demonstrates the site of obstruction. In sigmoid volvulus there is “bird beak” or “ace of spades” deformity with spiral narrowing of the distal bowel at the site
CT scan: identifiies mesentery and bowel as well as signs of bowel ischaemia
Define ulcerative colitis
Most common type of IBD.
Chronic RELAPSING and REMITTING inflammatory bowel disease affecting the LARGE bowel (including the rectum)
Flare (new damage has happened)
Affects mucosa and submucosa or large intestine ONLY
Explain the aetiology / risk factors of ulcerative colitis
Which antibody is it associated with? What condition?
Genetic suceptibility + environmental trigger (sulfide producing bacteria?)
Autoimmune in origin (stress and diet are secondary meaning they worsen it)
T cells destroy the lining of the large instestine leaving ulcers.
Associated with increased serum pANCA (antibodies that attach neutrophils), which may result from cross-reactivity with antigens from gut bacteria.
UC patients seem to have higher proportion of bacteria that produce sulfides, and high sulfide is correlated with active periods of destruction.
Associated with primary sclerosing cholangitis.
Summarise the epidemiology of ulcerative colitis
What is the pattern of ulceration in UC
15% positive family history
Young women in teens-30s have high prevalence
Caucasions and eastern european jews high prevalence
Pattern tends to be circumferentiala and continuous (goes all the way around the surface of the lumen, and then it progressively works itway back CONTINUOUSLY from the rectum around the large bowel
Recognise the presenting symptoms of ulcerative colitis
Pain in left lower quadrant (correspond to rectum)
More severe and frequent bouts of diarrhoea + BLOOD/mucus in stool
Did you know: stool frequency is related to severity of disease!
Tenesmus and urgency
(the destruction of epithelium and mucosa causes bleeding into the stools, and the destruction also means that the colon can’t perform its important function of reabsorbing water, leading to diarrhoea)
Recognise the signs of ulcerative colitis on physical examination
EXTRA-GI manifestations?
- Fe deficiency anaemia, dehydration
- Clubbing
- Abdo terderness, tachycardia
- Blood, mucus and tenderness on PR.
Extra GI manifestations (uveitis, renal calculi, arthropathy, sacroiliitis, ankylosing spondylitis, erythema nodosum (BUT MORE COMMON IN CROHNS rash on anterior shin) , pyoderma gangrenosum (on leg, non-infectious painful pustules or nodules become ulcers), oesteoporisis (due to steroid treatment), amyloidosis)
Identify appropriate investigations for ulcerative colitis and interpret the results
T/F faecal calprotectin is a measure of disease severity in UC
When is barium enema/colonoscopy dangerous
Blood: FBC (reduced Hb, increased WCC), increased ESR/CRP. Reduced albumin. LFT
Stool: culture as infectious colitis is a differential. FAECAL CALPROTECTIN- marker for disease severity
AXR: rule out toxic megacolon
Diagnosis requires colonoscopy/flexible sig- take biopsy: severity, histological confirmation, detects dysplasia
Barium enema: mucosal ulceration with granular appearance and filling defects (pseudopolyps), featureless narrow colon, loss of haustral pattern (LEAD PIPE/HOSEPIPE APPEARANCE).
Radiological imaging:
CT scan, MRI barium enema, X-ray
COLONOSCOPY AND BARIUM ENEMA DANGEROUS IN ACUTE EXACERBATION
Generate a management plan for ulcerative colitis
Identify the possible
Acute exacerbation?
Acute exacerbation: IV rehydration, IV corticosteroids, Abx, bowel rest, pareneteral feeding may be necessary, DVT prophylaxis. Monitor fluid balance and vital signs. -If toxic megacolon develops, low threshold for proctocolectomy and ileostomy as perforation has 30% mortality.
Chronic management
DEPENDS ON SEVERITY, which is determined by: low Hb, low albumin, increased ESR/CRP, bleeding, fever and diarrhoea frequency (<4/day mild, 4-6 moderate, >6 severe)
MILD DISEASE:
Anti-inflammatory medications: oral/rectal 5-ASA derivatives (sulfasalazine) +/- rectal steroids
MODERATE-SEVERE DISEASE:
Anti-inflammatory medications: oral/rectal 5-ASA derivatives (sulfasalazine)
+
Immunosupressants (corticosteroids, azathioprine, cyclosporin)
Biological treatments -Infliximab -Adalimumab -Golimumab (these 3 are all anti-TNFa)
SURGICAL (inicated for failure of treatment, presence of complications or prevention of colonic carcinoma):
-Proctocolectomy (generally curative) with ileostomy OR ileoanal pouch formation
complications of ulcerative colitis and its management
See extra GI manifestations
GI complications:
- Haemorrhage
- Toxic megacolon
- Perforation
- Colonic carcinoma (extensive disease >10 years of UC)
- Gallstones
- PSC
- Large joint arthritis
- Anterior uveitis
- Apthous ulceration
Summarise the prognosis for patients with ulcerative colitis
What are the poor prognostic factors (ABCDEF)
Relapsing and remitting, normal life expectancy
Poor prognostic factors:
-Albumin (<30g/L), Blood PR, CRP raised, Dilated loops of bowel, Eight or more bowel movements per day, Fever (>38 degrees in first 24hrs)
Obturator hernia is associated with which sign
Obturator hernias occur through the obturator canal and
they present with inner thigh pain when the hip is internally rotated (Howship-
Romberg sign).
How does the coughing test distinguish direct and indirect inguinal hernia
When you ask them to cough you place your hand over the midpoint of the inguinal ligament (where the deep ring is).
An indirect inguinal hernia enters the inguinal canal through the deep ring. So when they cough, the hernia will not protrude.
But a direct hernia enters the inguinal canal through a weakening in the posterior wall of the inguinal canal, medial to the deep ring. So covering over the deep ring will not stop protrusion of direct hernia when intra-abdominal pressure is increased through a cough
What is a spigelian hernia
Spigelian hernias occur when
abdominal contents herniate through the linea semilunaris, typically occurring inferior
and lateral to the umbilicus.
What do each of the following signs represent:
Psoas sign Rovsing's sign Cope's sign Aaron's sign Murphy's sign
Psoas: passive extension of right leg. Pain represents a retrocaecal inflammed appendix
Rovsing’s: palpation of the LIF causes pain in the RIF.
Cope’s sign: pain on flexion and internal rotation of the hip and indicates that the appendix lies close to the obturator inernus
Aarons sign: referred epigastric pain when pressure is applied over mcburney’s point
Murphy’s sign (cholecystitis): cessation of inspiraton when two fingers are placed below the right costal margin in the MCL and the patient is asked to take a deep breath in.
Grade haemorrhoids
Grade 1: no prolapse
Grade 2: prolapse on defecation but reduces spontaneously
Grade 3: prolapse requires manual reduction
Grade 4: remain persistently prolapsed and cannot be reduced
Differentiate type 1 and type 2 rectal prolapse
Type 1 (incomplete) rectal prolapse occurs when only the rectal mucosa protrudes through the anus. Seein in children and adults, associated with straining, constipation and haemorrhoids
type 2 (complete) occurs when all layers of the rectum protrude through the anus, creating a mass which has palpable, concentric muscular rings. Mainly in adults, associated with constipation, advanced age, chronic straining, neurologic conditions like MS, CF in kids
Symptoms of rectal prolapse
Protrutding anal mass, may need digital replacemnet.
Some patients report constipation, but fecal
incontinence is more common due to the lax anal tone.
Passing mucus or blood PR.
Can present as emergency with irreducible or strangulated prolapse
2 main causes of rectal prolapse
1 Lax anal tone due to pundendal nerve damage
2) Prolonged straining
When would metronidazole be used
Metronidazole is effective against anaerobes,
and, so, is used to treat several GI infections (e.g. C. difficile colitis), pelvic
inflammatory disease and aspiration pneumonia.
What is the typical presentation of right vs left sided colorectal cancers?
Left-sided colorectal cancer tends to present earlier with a change in bowel habit and PR bleeding, whereas right-sided tends to present later with abdominal pain and symptoms of anaemia (e.g. shortness of breath, fatigue).
There is a degree of overlap between these presentations as left-
sided colorectal cancers are also associated with symptoms of anaemia.
Where is colorectal cancer most commonly found
Colorectal cancer most commonly occurs in the rectum (27%) followed by the sigmoid colon (20%) and caecum (14%).
Which tumour marker is most specific for colorectal cancer
Serum carcinoembryonic antigen
CEA – the most specific tumour marker for colorectal cancer
Virchow’s node is commonly associated with which type of cancer
Don’t get caught out by the enlargement of Virchow’s node (Troisier’s sign)
described in this SBA. Although this is most often associated with gastric cancer, it
can also be found in other abdominal malignancies.
What is the typical presentation of gastric cancer
Gastric cancer is also more
likely to present with dyspepsia, vomiting, early satiety, bloating and melaena.
Define appendicitis
Acute inflammation and infection of the vermiform appendix, which is the little closed-ended hollow tube attached to the caecum
Explain the aetiology / risk factors of appendicitis
What are the specific causes
Which is more common in children
What then causes pain
Which bacteria
Usually, appendicitis occurs because something obstructs the appendix:
- Faecalith (hardened faecal matter)
- Lymphoid follicle growth (lymphoid hyperplasia)= more common in children
- Caecal carcinoma
- Undigested material (gum, seeds)
- Intestinal parasites (pinworms)
The mucosa in the appendix will secrete fluid and mucous, which build up behind the obstruction in the appendix. This increases pressure, making appendix grow in size and it will physically push on the nearby afferent visceral nerve fibers, causing abdominal pain.
Along with that, the flora and bacteria in the gut, usually E. coli and Bacteroides fragilis, will multiply in the appendix.
This triggers the immune system to recruit white blood cells and pus starts to accumulate, resulting in full-blown inflammation of the appendix.
As the pressure keeps growing and the appendix continues to swell up, it will push on and compress nearby small blood vessels causing ischemia and local necrosis.
As a result, inflammation extends to the serosa of the appendix, where it begins to spread to the parietal peritoneum, irritating it.
The growing colony of bacteria can then invade the wall of the appendix causing more inflammation, and the wall becomes weaker and weaker, to the point where the appendix can rupture.
Summarise the epidemiology of appendicitis
Any age, most common 2nd and 3rd decade.
One of commonest surgical diagnoses with 7% lifetime risk
Recognise the presenting symptoms of appendicitis
Acute appendicitis typically starts with nausea, vomiting, fever and periumbilical abdo pain (due to visceral nerve irritation, due to the enlarged appendix)
Within 24-48hrs, the appendix becomes more swollen and inflamed, irritating the abdominal wall, causing the pain to get more severe and migrate to right lower quadrant and causing fever
Recognise the signs of appendicitis on physical examination
McBurney’s sign (tenderness at McBurney’s point- located one-third of the distance from the anterior superior iliac spine to the belly button.)
Another sign is Rovsing’s sign, which is palpation of the left lower quadrant and moving along the path of the large intestine towards the right.
The obturator sign is when the person flexes the hip and knees to 90 degrees while lying down, and the clinician rotates the hip internally.
The psoas sign where the person lies on their left side and the clinician extends the right hip. Since the appendix borders the psoas muscle, when it’s stretched by hip extension, the friction will lead to pain.
SIGNS OF PERITONITIS (I.E. RUPTURED APPENDIX)
Guarding
Then there’s the Blumberg’s sign, also known as rebound tenderness, where a deep palpation and quick release causes pain during the release.
Identify appropriate investigations for appendicitis and interpret the results
Lab and imaging tests.
Increased WCC with NEUTROPHIL DOMINANCE of around 85%
Dehydration and electrolye imbalances
Urinalysis to rule out genitourinary condition:
- slight WCC elevation: rritation of the bladder or ureter by an inflamed appendix
- significant WCC elevation: suggests UTI
ULTRASOUND IS THE IMAGING OF FIRST CHOICE:
- Shows enlarged appendix with diameter of more than 6mm, as well as tenderness over the appendix with compression of the USS probe
- If there’s an abscess, there might be increased echogenicity of inflamed periappendiceal fat, and may an appendicolith (a calcified deposit within the appendix)
A CT scan is done as a follow-up if the ultrasound is inconclusive.
MRI is recommended over CT in pregnant women and children who can cooperate, to minimize radiation exposure.
CT findings:
enlarged appendix, appendiceal wall thickening of more than 2 millimeters, periappendiceal fat stranding, appendiceal wall enhancement, and there may also be evidence of an abscess.
CT has 94% sensitivity and 95% specificity so is gold standarf
Generate a management plan for appendicitis
Management:
-General: IV fluids, broad spectrum antibiotics pre- and perioperatively if signs of sepsis.
- Surgical: appendicectomy, open or laproscopic
- Post op: Abx may be continued in cases of gangernous or perforated appendix
The standard treatment for appendicitis is surgical removal of the appendix, or appendectomy. The goal is to operate early, before appendiceal rupture and peritonitis develop.
Identify the possible complications of appendicitis and its management
Inflammatory mass, appendiceal abscess, perforation and peritonitis, rarely portal pyaemia.
Management of appendicieal abscess:
-Drainage percutaneously (USS/CT guided) or itnraoperatively (with appendicectomy)
Summarise the prognosis for patients with appendicitis
Appendicectomy is curative. If untreated, can be life threatening. Diagnosis can be difficult in the very young, elderly and pregnant.
Morbidity and mortality in these groups are higher
The following atypical presentations suggest which anatomical position of the appendix:
Pain in the right flank
Pain in the RUQ
Plain in the lower abdomen
Pain in the right flank= retrocaecal
Pain in the RUQ= long appendix
Plain in the lower abdomen=pelvic appendix
A pelvic appendix may be associated with urinary frequency or loose stools due to bladder of bowel irritation
Summarise the indications for an appendicectomy
1) Acute appendicitis
2) Interval proceudre following management of an appendix mass with IV antibitoics
Which anatomical position can the appendix lie in
Retrocaecal (70%)
Pelvic (20%)
Subcaecal (2%)
Pre- or post-ileal (5%)