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%)
Identify the possible complications of an appendicectomy
Relatively uncommon, but presence reflects the degree of inflammmation or peritonitis:
e.g. ileus, haemorrhage, wound infection, more rarely local abscess or a pelvic abscess, perforation
Classic triad of Budd-chiari syndrome
No known cause in 50% of people
Remaining 50%- 75% have thrombosis of hepatic vein (primary), 25% have external compression of the hepatic vein (secondary budd-chiari)
- Hepatomegaly
- Ascites
- Abdo pain
What is the most sensitive investigation for gall stones?
Abdominal USS!
Which drugs cause cholestasis
Clavulanic acid Penicillins Oestroges Erythromycin Chlorpromazine
Explain how the relation of pain to eating can help distinguish gastric from duodenal ulcers?
Duodenal and gastric ulcers tend to be associated with pain. The pain caused by duodenal ulcers is often epigastric and before meals/at night and relieved by eating/milk. Gastric ulcers may cause pain related to meals.
Following an OGD successfully diagnosing gastric cancer, what would be done before surgery
Needs staging before surgery can be considered. This is done using a contrast enhanced chest, abdomen and pelvic CT scan.
(Note ndoscopic ultrasound has little role in staging gastric cancer, but is used to stage oesophageal cancer for local invasion)
What is the most common type of stomach cancer
Adenocarcinoma.
What are the risk factors for gastric carcinoma
ncreasing age
Male sex
Poor socio-economic status
Helicobacter pylori
A diet involving a high level of salt and preserved foods
Smoking
Atrophic gastritis, pernicious anaemia, post-gastrectomy, Ménétrier’s disease, adenomatous polyps
Familial risk: families with a very high incidence have been identified. There is a 2- to 3-fold increased risk to first-degree relatives of gastric cancer patients. There is a link between E-cadherin gene mutations and some familial gastric cancers.
Blood group A
Hypogammaglobulinaemia
T/F stomach cancers can prosent as an ovarian mass
T.
A Krukenberg tumor refers to a malignancy in the ovary that metastasized from a primary site, classically the gastrointestinal tract, although it can arise in other tissues such as the breast. Gastric adenocarcinoma, especially at the pylorus, is the most common source.
What are the most common causes of bowel obstruction
SBO:
- Intra-abdominal adhesions
- Hernias
- Crohn’s disease
- Malignancy
- Volvulus
LBO:
Colon carcinoma
Diverticilar disease
Volvulus
Where are common sites of metastasis for LBO
Pericolic lymph nodes
Liver and lung
Which side of the colon is more likely to obstruct when it has a tumour there and why
Left sided tumours are more likely to obstruct because the colonic diameter is smaller on the left side and the bowel content more solid.
“acute cramping pain and rectal bleeding” with obstruction
Consistent with ischaemia
When is a barium enema contraindicated
in patients who are at risk of perforation (can cause peritonitis)
Lack of gas in the rectum makes which type of obstruction less likely
Pseudo-obstruction.
Lack of gas in the rectum makes true obstruction more likely
Which AXR sign suggests ischaemic obstruction
Thumb printing
What is the management of a diverticular abscess
If small and walled off:
Conservatively in the first instance using rehydration, nil by mouth and broad spectrum intravenous antibiotics.
Follow-up CT to ensure abscess resolution – if enlarging consider percutaneous drainage.
Interval colonoscopy will be required once acute inflammation has resolved.
Faeculent vaginal discharge may suggest which disease?
Name other complications.
Diverticular disease is a common cause of fistula, either with small bowel, bladder or vagina and may present with pneumaturia, or faeculent vaginal discharge.
It is also a cause of profound rectal haemorrhage.
What is the cause of most diverticular disease
Most diverticula are acquired, secondary to low-fibre diet and they may occur throughout the bowel, although most arise in the sigmoid region.
Low-fibre diets and constipation are risk factors for the development of diverticulae.
Define primary biliary cirrhosis
PBC is a chronic inflammatory liver disease involving progressive destruction of INTRAHEPATIC bile ducts, leading to cholestasis and, ultimately, cirrhosis.
Explain the aetiology / risk factors of primary biliary cirrhosis
Which antibodies
T cells destroying cholangiocytes lining intrahepatic bile ducts
As the cholangiocytes are damaged, the tight junctions are impaired in the ducts, and bile can leak into
- blood –> jaundice and hypercholesterolaemia
- hepatocytes –> chronic liver disease
First you get CHOLANGITIS (inflammation of the bile ducts) which then advances to cirrhosis
DISEASE ASSOCIATION:
- Autoimmune hepatitis
- Sjorgens syndrome
Antibodies to mitochondria (anti-mitochondrial antibody, AMA) - 95% have this!
Summarise the epidemiology of primary biliary cirrhosis
9:1 female to male ratio! Affecting middle aged women
Recognise the presenting symptoms of primary biliary cirrhosis
Can be an incidental finding on blood tests (e.g. raised alk phos and cholesterol).
Fatigue, weight loss and pruritis
Discomfort in the RUQ rarely
May present with complication of liver decompensation: jaundice, ascites, variceal haemorrhage
Symptoms of associated conditions:
- Dry eyes and mouth (Sjorgens)
- Arthritis, raynaud phenomenon (rheumatoid)
Recognise the signs of primary biliary cirrhosis on physical examination
Early: might not be signs
Late:
Jaundice (once lots of the cholangiocytes are destroyed)
Xanthomas (cholesterol from the bile can leak into the blood too and then be deposited)
Pruritis (before jaundice sets in? But also because of bile salts in bile)
Joint pain and arthropathy–> linked to rheumatoid arthritis
Skin pigmentation
Hepatomegaly
Ascites
Signs of chronic liver disease (palmar erythema, clubbing, spider naevi)
Identify appropriate investigations for primary biliary cirrhosis and interpret the results
BLOOD:
- LFTs (raised AlkPhos, GGT, bilirubin can be normal or raised in later stages, transaminases initially normal, then inrease with disease progression and development of cirrhosis)
- AMAs
- Increased IgM and increased cholesterol typical
- TFTs (PBC associated with autoimmune thyroid disease)
- Plasma calcium, phosphate
USS: exclude biliary obstruction (gall stones and strictures)
Liver biopsy: chronic inflammatory cells and granulomas around the intrahepatic bile ducts, destruction of bile ducts, fibrosis and regenerating nodules of hepaticyte (repeat liver biopsies whilst on treatment)
Complications of PBC
Cirrhosis and associated complications:
- Jaundice
- Encephalopathy
- Ascites
- Variceal bleeding
- HCC!
- Hyperlipidaemia
- Malabsorption of fat soluble vitamins
What is the use of the erect abdominal radiograph
Abdominal radiographs are generally performed supine- erect films are RARELY undertaken, but can demonstrate air-fluid levels in dilated small bowel
So it is done only when there is strong clinical evidence of small bowel obstruction, but supine film is unhelpful
What is a respiratory complication of a subphrenic abscess
You can get a reactive pleural effusion in the lobe of the right lung
What is the imaging of choice for a subphrenic abscess
Chest x-ray and supine abdo xray
Then ultrasound. You can visualise the abscess and then USS can guide percutaneous drainage
What type of bacteria are usually the causative organisms of a subphrenic abscess
Causative pathogens tend to be anaerobes or Gram-ves.
Does a pleural effusion reactive to a subphrenic abscess require drainage
Pleural effusions are usually reactive and resolve with treatment of abscess – they do not usually need drainage unless impairing respiration.
Subphrenic abscess is a complication of which conditions
Perforation of hollow viscus (appendix, colon)
Inflammatory process (pancreatitis, cholecystitis)
Trauma of internal organs (stab, gunshot)
Complication of surgery (splenectomy, cholecystectomy, gastrectomy)
Idiopathic
Diverticulitis
If you are investigating the integrity of an anastomosis in the bowel, what investigation should you use
Contrast enema with WATER-SOLUBLE CONTRAST
Water-soluble contrast should be introduced via a Foley catheter
Barium contrast is contra-indicated in the presence of suspected bowel perforation – it can cause a medistinitis or peritonitis if it extravasates
What is the main cause of anastomotic breakdown.
What would need to be done usually in a failed recto-sigmoid anastamosis
Anastomotic breakdown is usually secondary to ischaemia (incidence of 5%) and the bowel usually needs to be defunctioned with preparation of a covering colostomy.
The anastomosis may then be repaired at a later date.
Define primary sclerosing cholangitis
Chronic cholestatic liver disease characterized by progressive inflammatory fibrosis and obliteration of intrahepatic and extrahepatic bile ducts.
(whereas PBC affects intrahepatic)
Explain the aetiology / risk factors of primary sclerosing cholangitis
HLA associations?
Antibody association, or none significant?
Don’t really know
ASSOCIATED WITH ULCERATIVE COLLITIS (and Crohn’s disease)- 70% of PSC patients have UC. About 5% of patients with UC develop PSC.
Thought to be an autoimmune disease due to T cells attacking bile duct cells
Associated with:
HLA-B8
HLA-DR3
HLA-DRw52a
pANCA is a very significant antibody association. As many as 80% of PSC patients have it
Summarise the epidemiology of primary sclerosing cholangitis
Usually presents between 25 and 40 years
Recognise the presenting symptoms of primary sclerosing cholangitis
May be asymptomatic, diagnosed after persistently raised AlkPhos.
May present with intermittent:
- Jaundice
- Pruritis
- RUQ tenderness
- Weight loss
- Fatigue
Hx of ulcerative colitis
Recognise the signs of primary sclerosing cholangitis on physical examination
May have no signs or have evidence of jaundice, hepatosplenomegaly, spider naevi, palmar erythema or ascites
Identify appropriate investigations for primary sclerosing cholangitis and interpret the results
BLOODS:
-LFTs: Raised ALP, GGT, mild raised transaminases. Later, raised bilirubin and reduced albumin
SEROLOGY:
- Elevated IgM in the serum
- Elevated pANCA (70%), raised ASM and ANA (~30%)
ERCP:
Stricturing and interspersed dilation (beading) of intrahepatic and, occasionally, extrahepatic bile ducts, small diverticula on the common bile duct may be seen.
MRCP: Enables non-invasive imaging of the biliary tree. Liver biopsy: Confirms diagnosis and allows staging of disease.
HISTOLOGY:
-Onion skin appearance of bile ducts, due to concentric rings of fibrosis
Complications of PSC
Recurrent cholangitis, biliary cirrhosis, cholangiocarcinoma (bile duct carcinoma,!15% of cases), portal hypertension (encephalopathy, ascites/oedema, variceal bleeding), metabolic bone disease.
What do the following AXR signs represent
Coffee bean sign
Embryo sign
A caecal volvulus produces a gas bubble on AXR that looks like an
embryo and, hence, is called ‘embryo sign’.
A sigmoid volvulus produces a gas bubble in the shape of a coffee bean – ‘coffee
bean sign’.
What are the 4 ways of detecting H Pylori infection`
1) Urea breath test
2) Blood antibody test
3) Stool antigen test
4) Rapid urease test/campylobacter like organism (CLO) test
Outline the urea breath test
The patient swallows urea labelled with radioactive carbon-14.
If CO2, containing the labelled carbon, is detected in the patient’s breath 10-30 minutes later, it suggests that the urea has been cleaved by urease produced by H. pylori.
Outlien the CLO test
A biopsy of stomach
mucosa is put into a medium containing urea and an indicator. The urease produced
by H.pylori hydrolyses urea to ammonia, which changes the pH of the medium and makes the indicator change colour.
What are diverticulae
Diverticulae are outpouchings of the mucosa and submucosa that have herniated through the muscularis.
What is the cause of rectal bleeding in divertciulitis
They most commonly occur in the sigmoid and
descending colon, particularly at the sites of nutrient artery penetration (hence, the
rectal bleeding).
What does cryptosporidium cause
diarrhoeal illness in immunocompromised patients
Define diverticular disease
Define: diverticulosis, divercular disease, diverticulitis.
How is it classified
Diverticulosis: The presence of diverticulae outpouchings of the colonic mucosa and submucosa through the muscular wall of the large bowel.
Diverticular disease: Diverticulosis associated with complications, e.g. haemorrhage, infection, fistulae.
Diverticulitis: Acute inflammation and infection of colonic diverticulae.
Hinchey classification of acute diverticulitis:
Ia: phlegmon,
IbandII: localizedabscesses,
III: perforation with purulent peritonitis or
IV: faecal peritonitis
Explain the aetiology / risk factors of diverticular disease
What causes diverticulitis
Anywhere in GI tract but most commonly colon.
Formed in areas of high pressure, this is why most common in the sigmoid colon (which has the lowest diameter in the colon, and thus the highest pressure)
Association with low fibre, thus constipation.
Symptoms may be worse when eating red meat
May be a secondary cause e.g. connective tissue disorders like Marfan and Ehlers Danlos
Often occurs where there is nutrient artery perforating the colon wall, making this part of the muscle weaker.
Diverticulitis is an inflamed diverticula, due to erosion from high pressures (more likely) or lodged faecolith (less common). This can lead to bacterial overgrowth, leading to: diverticulitis, perforation, pericolic phlegmon, abscess, ulceration, fistula or stricture (which can lead to obstruction)
Summarise the epidemiology of diverticular disease
COMMON!
60% of people living in industrialized countries will develop colonic diverticula, rare <40years. Right-sided diverticula are more common in Asia.
Recognise the presenting symptoms of diverticular disease
When does bleeding occur.
Hx for diverticulosis, diverticulitis and diverticular fistula please.
Diverticulosis- diverticula not infected or inflamed:
- Often asymptomatic (80-90%)
- Stomach pain
- Rectal bleeding (haematochezia) because the vessels are now only protected from the lumen by mucosa (no longer run in the muscle layer, as the mucosa has pouched into the muscle). Often found incidentally
Diverticulitis is NOT ASSOCIATED with rectal bleeding (haematochezia) because the blood vessels are scarred from bleeding:
- Ass with left lower quadrant pain
- Fever
Diverticular fistula with the bladder: pneumaturia, faecaluria, recurrent UTI.
Recognise the signs of diverticular disease on physical examination
Diverticulitis: tender abdomen + signs of local or generalised peritonitis if perforation has occurred
Identify appropriate investigations for diverticular disease and interpret the results
Acute setting?
Hb: FBC. High WCC and CRP in diverticulitis.
Barium enema (+/- air contrast)- NOT IN THE ACUTE SETTING: -Demonstrates presence of diverticulae with saw-tooth appearance of lumen. Contraindicated with diverticulitis in case there is perforation
Flexible sigmoidoscopy & colonoscopy:
-Diverticulae can be seen. Other pathology excluded.
IN ACUTE SETTING:
-CT scan for evidence of diverticular disease and complication
Generate a management plan for diverticular disease
Asymptomatic?
If diverticulitis?
Surgical options
Aysymptomatic (diverticulosis) :
-No treatment (maybe some more fibre in diet)
Symptomatic diverticular disease:
- Dietary modification and fibre supplements
- Oral Abx
Symptomatic diverticulitis (uncomplicated)
- Analgesia
- Oral Abx therapy
- Low residue diet
- Swtich to IV Abx if goes on >72hr
Symptomatic diverticulitis with acute rectal bleeding
- Endoscopic haemostasis, if fails then angiographic embolisation if fails then surgery
- Oral Abx
- Analgesia
Symptomatic diverticulitis unresponsive to IV Abx or with abscess >3cm diameter, perforation, fistulae or obstruction
- Radiological drain/surgery
- IV Abx
- Analgesia
Surgery (For patients with severe or diffuse peritonitis):
Open: hartmann’s procedure (resection and stoma) or one-stage resection and anastomosis (risk of leak and defunctioning stoma though)
Laparscopic (more recent): drainage, peritoneal lavage and drain placement
Identify the possible complications of diverticular disease and its management
Diverticulitis
Pericolic abscess
Perforation
Faecal peritonitis
Colonic obstruction
Fistula. The diverticulae may rupture and then form a fistula, e.g. with the bladder. Which can cause faecal matter OR AIR in the urine.
Haemorrahge
Summarise the prognosis for patients with diverticular disease
Ten to 25% of patients will have one or more episodes of diverticulitis. Of these, 30% will have a second episode.
What are the GI causes of clubbing
Inflammatory bowel disease (e.g. ulcerative colitis and Crohn’s disease) is
liver cirrhosis,
primary biliary cirrhosis,
oesophageal leiyomyoma,
coeliac disease and
achalasia.
Define gastritis
Inflammation of the gastric mucosa.
Acute: neutrophil invasion
Chronic: lymphocyte and plasma cell infiltration
Explain the aetiology / risk factors of gastritis
What causes acute gastritis
Acute gastritis is an imbalance between mucosal defenses and acidic environment of the stomach
Starts with gastric EROSIONS (which penetrate only into the mucosa). These are NOT gastric ulcers (which penetrate into the submucosa and deeper)
These can be caused by:
- XS alcohol, corticosteroids, meds
- NSAIDS
- H Pylori infection
- Extreme physiological stress (sepsis, shock, trauma)
Chronic gastritis is caused by chronic inflammation due to:
-H Pylori (most common type of gastritis), affects antrum. CagA is carcinogenic from H Pylori
-AI gastritis (type IV hypersensitivity)
It is characterised by chronic inflammation leading to gastric atrophy and metaplasia and dysplasia, and gastric adenocarcinoma
AI gastritis also associated with increased risk of neuroendocrine tumours
Summarise the epidemiology of gastritis
.
Recognise the presenting symptoms of gastritis
ACUTE GASTRITIS:
Epigastric pain
Nausea
Vomiting
Life threatening upper GI bleed (can cause melaena)
Symptoms:
Asymptomatic sometimes
Epigastric pain
Nausea
Vomiting
Identify appropriate investigations for gastritis and interpret the results
Diagnosis: Endoscopic biopsy Detection of H pylori using: -Serology -Stool antigen test -Urease breath test
Generate a management plan for gastritis
Treating the underlying cause (remove NSAIDs)
Antacids
Antibiotics to eradicate the H Pylori infection:
-Triple therapy: PPI + clari + amoxicillin for 2 weeks
Identify the possible complications of gastritis and its management
Chronic:
Infectious (H Pylori): Peptic ulcers, MALTomas
Autoimmune: Pernicious anaemia, iron deficiency anaemia, carcinoid tumour
Define peptic ulcer disease
Ulceration of areas of the GI tract caused by exposure to gastric acid and pepsin
Explain the aetiology / risk factors of peptic ulcer disease and gastritis
Where are the gastric ulcers and duodenal ulcers usually located
Imbalance between damaging action of acid and pepsin and mucosal protective mechanism.
STRONG CORRELATION with H. PYLORI.
RF:
- H pylori (95% of duodenal ulcer and 70-80% of gastric ulcer)
- NSAID use
- Zollinger Ellison (rare)
Gastric ulcers usually in gastric antrum
Duodenal usually in duodenal bulb
Summarise the epidemiology of peptic ulcer disease and gastritis
Common. Annual incidence is about 1–4/1000.
More common in males.
Duodenal ulcers have a mean age in the thirties, while gastric ulcers have a mean age in the fifties. H. pylori is usually acquired in childhood and the prevalence is roughly equivalent to age in years.
Recognise the presenting symptoms of peptic ulcer disease and gastritis
Epigastric abdominal pain, relieved by antacids
Variable relationship with food.
Worse when eating (or 30 minutes after) –> more likely to be gastric. (may lose weight as they avoid meals)
Worse several hours later (actually improves with eating, so may be weight gain??) –> duodenal
May present with complications (haematemesis, malaena)
Recognise the signs of peptic ulcer disease and gastritis on physical examination
May be none.
Epigastric tenderness
Signs of complicaations (anaemia, succession splash in pyloric stenosis)
Identify appropriate investigations for peptic ulcer disease and gastritis and interpret the results
BLOODS:
- Hb (anaemia)
- Amylase (exclude pancreatitis)
- U&Es
- Clotting screen (if GI bleeding)
- LFT
ENDOSCOPY:
- 4 quadrant gastric ulcer biopsies to rule out malignancy
- Duodenal ulcer need NOT be biopsies
ROCKALL SCORING:
-For severity of GI bleed. <3 is good prognosis. >8 have high mortality risk
H PYLORI TEST: C-Urea breath test Serology: IgG Ab against H Pylori Stool antigen test Campylobacter like organism test (YELLOW TO RED if present)
Histology of biopsy of limited value
Generate a management plan for peptic ulcer disease and gastritis
ACUTE
ACUTE:
-Resuscitation if perforated or bleeding (IV colloids/crystalloids), close monitoring of vital signs, and proceeding endoscopic or surgical treatment.
Acute meds:
-Patients with upper GI bleeding should be treated with IV PPI at presentation until cause of bleeding confirmed
-Patients with active bleeding peptic ulcer should continue IV PPI
-Swtich to oral PPI if there is no rebleeding within 24 hrs
Acute endoscopy:
-Haemostasis by injection sclerotherapy, laser or electrocoagulation
Acute surgery:
If perforated or ulcer-related bleeding cannot be controlled
NON-ACUTE: H. Pylori eradication: Triple therapy for 1-2 weeks 1 PPI and 2 Abx e.g. (clari + amox + omeprazole) or (metronidazole + tetra + omeprazole)
IF NOT associtated with H Pylori:
-PPIs for at least 8 weeks or H2 antagonists. Stop NSAID use (especially diclofenac, use misoprostol if NSAID use is necessary)
Identify the possible complications of peptic ulcer disease and gastritis and its management
Rate of major complication is 1% per year including:
1) Haemorrhage (haematemesis, melaena, iron-deficiency anaemia)
2) perforation (more common in anterior wall of duodenum)
3) obstruction/pyloric stenosis due to scarring, penetration, pancreatitis).
4) Malignant gastric ulcer (gastric MALT lymphoma, gastric adenocarcinoma)
Summarise the prognosis for patients with peptic ulcer disease and gastritis
Overall lifetime risk”10%.
Generally good as peptic ulcers associated with H. pylori can be cured by eradication.
How do NSAIDs affect the gastric musocsa
They block the COX enzyme, which reduces production of prostaglandin E2
Prostaglandin E2 protects gastric mucosa by increasing mucus production and suppressing gastric acid production
Outline stress ulcers
Sepsis, shock and trauma can lead to stomach erosions.
Specific types: curling’s ulcers (secondary to burns) and cushings ulcer (secondary to brain injuries)
What might point you towards zollinger ellison with a peptic ulcer
If the ulcer is in the DISTAl duodenum or another atypical place
What causes haemorrhage in gastric ulcer and duodenal ulcer
When gastric ulcer in lesser curvature of the stomach erodes into the left gastric artery
When duodenal ulcer erodes into posterior wall of duodenum and into the gastroduodenal artery
What is the most common cause of iron deficiency anaemia in men <50 vs men >50
under 50: peptic ulcer
over 50: colorectal carcinoma
How can perforated duodenal ulcer present
Referred pain to shoulder due to irritation of phrenic nerve and pneumoperitonuem (free air under diaphragm)
What is zollinger ellison syndrome
Gastrinoma (secretes gastrin –> hyperacidic environment)
What medications worse GORD
Drugs that damage the mucosa: NSAIDs, steroids, bisphosphinates, aspirin
Drugs that affect eosophageal motility: nitrates, TCAs and anticholinergics
Management of GORD
GORD is
managed with lifestyle interventions such as stopping smoking, avoiding spicy food,
losing weight, having small, regular meals and avoiding eating before bed.
Patients are usually started on a once daily PPI and patients who do not respond should be
offered twice daily PPIs.
Triad of features assocaited with acute mesenteric ischaemia
Severe abdominal pain, normal abdo examination and shock
Cause of acute mesenteric ischaemia
This is
characterised by vascular compromise of the small bowel due to occlusion of the
superior mesenteric artery
What is the cause of acute vs chronic mesenteric ischaemia
Acute disease
occurs due to arterial thrombosis (e.g. due to atherosclerosis) or embolism (e.g. due
to emboli from AF). Other causes of acute mesenteric ischaemia include venous
thrombosis (in hypercoagulable states) and non-occlusive disease (e.g.
hypotension). Chronic mesenteric ischaemia usually occurs due a combination of a
low-flow state, such as heart failure, and atherosclerotic disease.
How does chronic mesenteric ischaemia present
It presents with ‘gut
claudication’ (poorly localised, colicky, post-prandial abdominal pain), PR bleeding
and weight loss.
What are the x ray findings associated with severe mesenteric ischaemia
In advanced disease, it may show a gasless abdomen, thickening
of the bowel wall and pneumatosis (air within the bowel wall due to necrosis). If the
abdominal X-ray in inconclusive, a CT scan should be performed.
What is riglers sign and pneumoperitneum and what are they signs of
Rigler’- air present on both sides of the bowel wall, creating the impression of a double wall
Pneumoperitoneum (air under the diaphragm)
are signs of perforation.
T/F constipation can present with diarrhoea
T.
Faecal impaction in the distal colon can lead
to liquid stools leaking through the little space left in the lumen causing, what is known as, overflow diarrhoea. It can lead to faecal incontinence.
What are the cell types in the anus
Dentate line. separates the upper 2/3 from the lower 1/3 of the anus.
Upper: mucosa lined by simple columnar epithelium
Lower: Anoderm (squamous epithelium)
What are haemmarhoids
Now, hemorrhoids are normal vascular structures in the anal canal that act as cushions for the stool as it passes through.
What is haemarrhoidal disease
Hemorrhoidal disease is when hemorrhoids get swollen or inflamed; but the term “hemorrhoid” is often used to refer to the disease.
Aertiology and risk factors for haemarrhoids
Hemorrhoids are often caused by chronically or recurrently increased abdominal pressure, from a variety of causes. For example, straining during bowel movements, chronic diarrhea or constipation, obesity, pregnancy, and old age.
Classify haemarrhoids into 2 typesq
Internal hemorrhoids are ones above the dentate line, and external hemorrhoids are ones below the dentate line.
Grade internal haemorrhoids
Internal hemorrhoids are subclassified into four grades based on the degree of prolapse from the anal canal.
Grade I hemorrhoids don’t protrude outside the anal canal.
Grade II hemorrhoids protrude outside the anus during bowel movement, but they retract spontaneously.
Grade III are prolapsed hemorrhoids that don’t retract spontaneously, but they can be pushed back in manually.
Finally, grade IV hemorrhoids are prolapsed hemorrhoids that cannot be manually pushed back in.
History of haemorrhoids
Internal hemorrhoids usually don’t cause symptoms, but sometimes they get inflamed, causing itching and painless passage of bright red blood with a bowel movement.
On the other hand, external hemorrhoids are innervated somatically, and they’re typically painful, especially when associated with thrombosed hemorrhoids, which have no blood flow due to a blood clot in the vein, and swelling in the affected area.
Bright red bleeding on toilet paper or dripping into pan after passage of stool. NEVER MIXED WITHIN STOOL.
Itching, anal lumps
Signs of haemorrhoids
- Puruple/blue veins?
- Dark pink, glistening masses at the anal margin?
- Purplish hue?
A diagnosis is usually made based on a visual and digital exam of the anus (can see grade III and grade IV)
Internal hemorrhoids look like bulging purplish-blue veins, and prolapsed internal hemorrhoids appear dark pink, glistening, and are sometimes tender masses at the anal margin.
Thrombosed external hemorrhoids are tender and have a purplish hue.
Investigations for haemorrhouds
Diagnosis of stage III and IV internal haemmorhoids and external haemorrhoids can be made on examination, but grade I and II internal haemorrhouds can’t be seen or felt, and confirmation requires anoscopy
If there are haemrrhoids with changes in bowel habits?
Further testing with flexible sigmoidoscopy or colonoscopy is recommended if signs and symptoms suggest another digestive system disease and in individuals older than 40 years with symptoms of colorectal cancer, like weight loss and change in bowel habit
Management of haemorrhoids
Conservative: High fibre diet, fluid intake, topic creams containing LAs, corticosteroids on short term basis
Local therapy (for 1st and 2nd degree):
- Injection sclerotherapy (5% phenol injected into submucosa above a haemarrhoid)
- Banding proximal to haemorrhoid (higher cure, but more painful0
Surgical (3rd and 4th degree, symptomatic):
Open haemorrhoidectomy= incision of haemorrhoidal cushions with preservation of skin between the haemorrhoids to avoid stricturing.
Stapled haemorrhoidectomy.
Post op: laxatives, metronidazole
Complications of haemorrhoids
What about of slerotherapy and haemorrhoidectomy
Bleeding, prolapse, thrombosis
Slcero: prostatitis, perineal sepsis, rarely impotence
Haemorhoidectomy: pain, bleeding, incontinence
Anal fissure definition and causes
T/F the pathology of anal fissure just relates to the skin
Elongated ulcer in anal canal lower part
Trauma: constipation tears posterior anal lining. In pregnant women, anterior fissures more common as damaged pelvic floor elaves anterior anal tissues less supported
Inflammation: IBDs
Mechanical tear in anal mucosa + sphincter spasm
Age for anal fissure
Most common under age of 40.
Male=female
Hx of anal fissure
Severe burning pain on defaecation, can persist for hours
Patients may avoid bowel movements
Bright red bleeding per rectum, small amount
Itchy
Examination of anal fissure
Can see a sentinel pile.
DRE may not be possible due to pain
Chronic fissures –> firm, indurated ridge
Investigations of anal fissure
Diagnosis on history
Exclude other things
Management of anal fissure
ON PRESENTATION:
Conservative: ensure stools soft and easily passed
Medical: conservative GTN (but can cause headache), topical dilitiazem
RESISTANT:
Surgical: Botox/surgical sphincterotomy. Botox more recently
2nd line anal advancement flap
Complication of anal fissure
Chronic fissure and chronic pain
What is a pilonidal sinus
Abnormal epithelium line tract filled with hair that opens to the skin surface, most commonly into natal cleft
Cause of pilonidal sinus
Caused by sheared hairs penetrating the skin and inciting inflammatory reaction, with intermittent negative pressure drawing in more hair
Epidemiology of pilonidal sinus
Ass with hirsute individuals.
Occupations like hairdressors may develop interdigital pilonidal sinus
Hx of pilonidal sinus
Painful natal cleft, esppecially if inflamed/superimposed infection
Discharge and swelling
Examination of pilonidal sinus
Midline opening or pits seen between buttocks, hair may protrude
Tender swelling that may be fluctant/discharge etc. if assocaited infection/abscess
Investigation of pilonidal sinus
None needed for diagnosis,
If infection raised WCC
Glucose (diabetes)
Management of acute pilonidal sinus
Management of chronic pilonidal sinus
Incision and drainage under LA if small, for evaculation of pus and hair. Cavity irrigated and packed, dressings changed regualry to allow secondary closure. Not usually nececssary for Abx post op
Chronic: sinus tract excision under GA with exploration, laying open and removal of tract. Wound closure by primary closure, or left open and healing by secondary intention.
Wounds closed primarily heal more quickly, but higher risk of recurrence
Karydakis operation: asymmetric excision with lateral closure, flattnes nad lateralises midline cleft
Bascom technique
Define
Perianal abscess
Perianal fistula
Abscess: pus collection in perianal region
Fistula: abnormal chronically infected tract communicating between perianal skin and either anal canal or rectum
Types of perianal abscess
Classified according to location
What are the anatomical landmarks for discrubing a low anal vs high anal fistula
low- below puborectalis
high- at or above puborectalis
pelvirectal- involving levator ani
Pepperpot perineum sign?
Multiple perineal fistulae (Crohn’s disease)
What is perianal fistulae ass with
Crohn’s, diabetes, malignancy
History in perianal fistulae/absces
Constant throbbing pain in perineum
Intermittent discharge (blood stained/mucus) near anal region
Perianal fistula/abscess examination
Localised tender perianal swelling or small skin opening with discharge, corresponding to opening of fistula
PR an area of induration corresponding to abscess or fistula tract.
What is goodsall’s rule
Rule of tump to correlate location of internal fistula opening based on location of external fistula opening.
If external opening is anterior to anal canal, fistula runs radially and directly into the anal canal
If external opening is posterior to the anal canal, the fistula follows a curved path, opening internally in the posterior midline
Investigations for perianal fistula/abscess
Clinical examination, under anaesthetic if neccessary
Blood: FBC, CRP, ESR, blood cultures if pyrexial
Complex fistulae: MRI extremely useful to study tracts, and plan for surgical excision
Endoanal ultrasound: used by less useful
Management of perianal abscess/fistula
SURGICAL, under anaesthaesia.
Open drainage of abscess: incision and drainage.
ALL patients should be put on broad spectrum antibiotics with gram -ve cover. E.g. Ampicillin + metronidazole
Antibiotics useful if there is surrounding cellulitis
Rectal prolapse in a child which investigation
Sweat chloride test- 10% will have CF
Investigations for rectal prolapse
Proctosigmoidoscopy, defaecating proctogram or barium enema
Management of rectal prolapse
Conservative
Emergency
Chronic
Conservative: bulk laxatives. high fibre diet might be sufficient in kids
Emergency:
Acute prolapse may be manually reduced after adequate analgesia. Patients nursed with ice packs topically prior to attempted manual reduction to reduce swelling
If bowel is gangrenous, excision by rectosigmoidosicopy
Incomplete prolapse:
-Submucosal sclerotherapy with pnol, bandoing or haemorrhoidectomy
Complete prlapse:
- Operative repair using laparoscopic, abdominal or perineal approaches.
- E.g. ripstein rectopexy is
Prognosis of rectal prolapse
Sponatenosusly resolves usually in kids
15% recurrence in adults
What are the following surgical procedures used for
1) Hartmann’s
2) Left colectomy
3) Abdomino-perineal resection
4) Anterior resection
5) Delorme’s procedure
1) Removal of sigmoid (you remove the area, and then create a rectal stump and an end colostomy. You then perform primary anastamosis at a later date (if it’s an emergency at the time with inflammation etc.)
2) CaSncer localised to descending colon Remove from 2/3 along transverse colon down to the beginning of the sigmoid.
3) Low lying rectal cancers- removes anus, rectum and part of sigmoid. End colostomy
4) High lying rectal tumour. emoves upper 2/3 of rectum and part of sigmoid colon. Anal sphoncter remains in tact and an anastamosis formed
5) Delorme’s- full thickness rectal prolapse
Differentiating between anal fissure and haemorrhoids
An anal fissure is a painful tear in the squamous lining of the lower anal
canal, which causes pain on defecation and bright red blood streaked on the toilet
paper/stools but not mixed in with the stools. Anal fissures often occur in patients
with a low fibre diet and poor fluid intake who may be constipated and strain at the
stool.
Haemorrhoids are enlarged and engorged anal vascular cushions that can bleed.
They are very common and usually present with bright red rectal bleeding that is
separate to the stool and may drip into the pan after defecation.
Peutz-jehger syndrome
Diffuse GI polyp + mucocutanous pigmentation of lip and gum BENIGN but increased risk of cancer
Familial polyposis coli
Inheritence?
Multiple stomach, small and large bowel adenomas.
Autosomal dominant
premalignant
Gardner’s syndrome
Osteomas, soft tissue tumours, sebaceous cysts, congeital hypertrophy of RPE and multiple colonic adenomas.
Turcots syndrome
Glioblastomas or medulloblastomas with mutliple clonic adenomas. Premalignant
Turcot syndrome is a variant of familial adenomatous polyposis (FAP) that is characterized by extensive polyposis of the GI tract as well as CNS tumors, usually medulloblastoma .
Cronkhite canadas syndrome
Alopecia, nail atrophy, pigmentation, watery diarrhoea, multiple colnic adnomas, premalignant
What is receommended in familial polposis coli
Early subtotal colectomy
Aetiology of colorectal cancer
Sequence from epithelial dysplasia to adenoma and then carcinoma.
Accumulation of genetic changes, activation of oncogenes (APC, K-ras) and inactication of tumour suppresser genes (p53, DCC)
RF for colorectal cancer
Colorectal polyps
Previous CRC
IBD (particularly UC)
Genetic syndromes (FAP, lynch sydrome)
Gender specifics of colorectal cancer
Rectal, male>female
Colon female>male
History of colorectal cancer
Can be asymptomatic and present with faecal occult bloods.
Left sided: change in bowel habit, rectal bleeding or blood/mucus mixed with stools.
Right sided: Later presentation, symptoms of anaemia, weight loss and non-sepcifc malaise (more rarely lower abdo pain)
Rectal masses: tenesmus
What might CRC look like on barium enema
Apple core lesion, for annular tumours
Investigations for CRC
Screening: blood (FBC), stool (occult or frank)
Endoscopy: sigmoidoscopy and colonoscopy allows visualisation and biopsy.
Imaging: barium enema, CT scan, MRI, endorectal ultrasound.
State the operation for the following cancers:
- Caecal tumour
- Transverse colon tumours
- Descending colon tumours
- Sigmoid tumours
- High mid-rectal
- Low rectal
- Emergency
- Caecal tumour: right hemicolectomy
- Transverse colon tumours: extended right hemicolectomy
- Descending colon tumours: left hemicolectomy
- Sigmoid tumours: anterior resection
- High mid-rectal: Anterior resection with total mesorectal excision
- Low rectal: Abdominoperineal resection if unable to clear below tumour
- Emergency: Hartmann’s procedure
Chemo and radio for CRC?
Radio: neoadjucant
Chemo: FOLFOX (5-FU)
Dukes staging
A=confined to bowel wall B= breached serosa, no lymph nodes C1=breached serosa, lymph node involved but not apical C2=breached serosa, apical lymph nodes D=distant mets.
At what portal pressure might anastamoses become congested and dilated
When the portal pressure is > 12 mm Hg, these
anastomoses become congested and dilated, and are prone to bleeding.
Organisms commonly involved in SBP
The bacteria most commonly involved are E. coli and Klebsiella
pneumoniae
Which transaminase is higher in the serum with alcoholic hepatitis. What is the ratio
An AST to ALT ratio (AST:ALT) > 2 is suggestive
of liver damage secondary to alcohol abuse.
Chronic alcohol consumption also
induces a rise in serum GGT.
Symptomatic GORD, lower dysphagia and painless regurgitation of food. Likely diagnosis
Hiatus hernia
2 types of hiatus hernia
Sliding (80%): Gastro-oesophageal junction (GEJ) slides into
the thorax
Rolling: GEJ remains in place but a bulge of fundus herniates into
the chest alongside the oesophagus
Best investigation for hiatus hernia
Barium swallow is the best investigation to confirm the diagnosis
What might hiatus hernia show in chest x ray
If the hiatus hernia is very large, a CXR may show a retrocardiac mass with an airfluid level. `
Management of hiatus hernia
Management of a hiatus hernia comprises of lifes`tyle changes
(e.g. weight loss), treatment of reflux (PPIs) and surgery in refractory cases. Nissen
fundoplication is the most commonly used surgical procedure for hiatus hernias.
Criteria for acute severe colitis (in UC)
Frequency of stool >6 Overtly bloody stool Fever (>37.5) Tachycardia (>90) Anaemia (Hb<105) Raised ESR (>30)
Management of acutely presenting UC
1st line –>IV steroids
2nd line –> asporin
3rd line –> infliximab
(Bone protection also required, so give Adcal D3 with it)
Heparin is really important because patients with acute s evere ulcerative colitis are at high risk of thromboembolic events so unless they have significant haemorrhage, the risk of a clot is higher than the risk of bleeding.
What is a loop vs end ileostomy
End ileostomy is when everything distal to the stoma is cut out (i.e the whole colon)
Loop ileostomy is used when, there is still a colon, but, for example, you are waiting for a wound to heal further round the colon. So you cut the ileum open onto the skin, so that the faecal matter doesn’t pass through the colon to allow it to heal first
What is the faecal matter like that comes from an ileostomy
How to deal?
Faecal matter will be more liquid in nature
High output from this type of stoma can quickly lead to dehydration. Loperamide/ codeine may be needed to control the output
What does an ileostomy look like compared to a colostomy
the ileum will form a ‘spout’ at the skin surface (compared to a colostomy which will be flat)
Which 3 symptoms are diagnostic of acute cholangitis
The triad of acute pain, fever and jaundice is diagnostic of ascending cholangitis
Initial treatment of ascending cholangitis
The initial treatment is intravenous antibiotics and intravenous fluid (often a lot of i.v. fluid is needed for resuscitation). Analgesia may also be required.
Especially during these initial investigations the patient is likely to be kept nil by mouth, making IV fluids even more important.
T/F a bile duct always dilates after a cholecystecomy anyway
The common bile duct can dilate after cholecystectomy, although not usually much above 7mm in patients of this age.
So dilation >7mm might indcate a stone
Investigation if you suspect a stone given abdo USS
MRCP is a non-invasive tool which is good at evaluating the biliary tree.
The stone may already have passed so ERCP may not be necessary
However there can often be a delay in organising an MRCP and many clinicians would proceed with ERCP in a patient with evidence of ascending cholangitis and a dilated CBD
What procedure can be done to remove stones, what if it’s not possible
ERCP is the technique of choice although if this is not technically possible for some reason then these stones can be reached and stents inserted etc. at PTC performed by interventional radiology. (percutaneous transhepatic cholangiogram and stone retrieval)
Open bile duct exploration is a last resort due to a high mortality risk.
What is HCC
Primary malignancy of hepatocytes, usually occurring in a cirrhotic liver.
Aetiology of HCC
3 main causes
1) Chronic liver damage (e.g. alcoholic liver disease, hepatitis B, hepatitis C, autoimmune disease), .
2) Metabolic disease (e.g. haemochromatosis), and .
3) Aflatoxins (Aspergillus flavus fungal toxin found on stored grains or biological weapons).
T/F primary HCC is more common than secondary malignancy of the liver
Common making up 1–2% of all malignancies, but less common than secondary liver malignancies.
Hx of HCC
Symptoms of malignancy: Malaise, weight loss, loss of appetite.
Symptoms of chronic liver disease: Abdominal distension, jaundice.
History of carcinogen exposure: High alcohol intake, Hepatitis B or C, aflatoxins.
Examination HCC
Signs of malignancy: Cachexia, lymphadenopathy.
Hepatomegaly: Nodular (but may be smooth). Deep palpation may elicit tenderness. There may be bruit heard over the liver.
Signs of chronic liver disease: Jaundice, ascite (see Cirrhosis).
Investigation of HCC
Blood: raised AFP (high sensitivity). LFT can show biliary obstruction
Imaging:
- (1st imaging): Abdo USS, but it is not sensitive for tumours <1cm
- (superior imaging, but not 1st line) CT (CAP): to define structural lesion and spread
- Duplex scan of liver: for large vessel invasion
- Liver biopsy (usually NOT required for diagnosis) confirms histology of tumour, but risk of tumour seeding along biopsy tract
Staging:
-CXR, CT CAP, radionuclide bone scan
Screening: AFP and abdominal USS in at-risk individuals
What is a HCC in young people with no Hx of liver disease, and what tumour marker can be used
Vitamin B12-binding protein is a marker of fibrolamellar hepatocellular carcinoma
What is the management of gastroenteritis
Gastroenteritis is a self-limiting disease that can be managed with bed rest and oral
rehydration (to compensate for fluid and electrolyte losses from sweating, diarrhoea
and vomiting).
Admit if cannot retain oral fluids, has features of shock or is severely dehydrated.
Abx prescribed when causative organism identified by stool culture
Blistering rash on the elbows?
Dermatitis herpetiformis
Differentiate hiatus hernia sliding and rolling
Overall it’s herniation of contents of abdominal cavity into the mediastinum through the eosophageal hiatus in the diaphragm.
Sliding: GOJ is a above diaphragm
Rolling (or paraeosophageal): defect in phreno-eosophageal membrane. GOJ does not move but fundus is lead point of herniation
You can get a mixed type (=type III)
And type IV is when other abdo contents come through too
Aetiology of hiatus hernia
Congenital or acquired.
Thinning and increased laxity of the phreno-oesophageal ligament with age
Associated with obesity, GORD, chronic eosophagitis
Which hiatus hernia is more common
Type 1 (95%)
Increase in frequency with age
Hx of hiatus hernia
Many asymptomatic.
Reflux symptoms of heart burn, indigestion, postprandial fullness and regurg
No examination findings unless complications develop
Investigation for hiatus herna.
1st line: Upper GI series (i.e. barium x-ray), chest ray (retrosternal cardiac bubble)
OGD doesn’t rule out. But patients with reflux symptoms should have this to check for eosophagitis or dysplasia
CT/MRI when diagnosis not clear
Manometry and pH monitoring- double hump configuration seen due to gastric herniation above high pressure zone of the crura.
Management of hiatus hernia
Conservative: modification of lifestyle factors (weight loss, avoid late meals)
Medical management if there’s symptomatic GORD. PPIs
Surgical repair if refractory to medical therapy. Laparoscopic hernia reduction, crural repair combined with antireflux fundoplication (Nissen’s)
Complications of hiatus hernia
Eosophageal: eosophagitis, erosions/ulceration, stricutres, Barrett’s
Other: rarely, incarceration of para-eosophageal hernia, strangulation or peroration.
Can enlarge with time and sometimes progress to where the entire stomach lies in thoracic cavity.
Surgery: high recurrence rates in large hiatus hernias. If mesh repair is used, infections, stricturing and veisceral erosions are risks
T/F hypoglycaemia is a cause of pancreatitis
F.
hyperlipidaemia, hyperglycaemia, hypercaleamia
is the H in GET SMASHED!
C difficile causes what type of gut inflammation
Treatment
The release of toxins by C. difficile leads to extensive inflammation and
disruption of the brush border membrane of the colon, resulting in what is known as
pseudomembranous colitis.
Metronidazole or vancomycin
History of a subdiaphragmatic abscess
Upper abdominal pain radiating to the shoulder tip with a swinging fever in the
days/weeks following abdominal surgery is suggestive of a subphrenic abscess.
These are localised collections of pus, commonly underneath the right or left
hemidiaphragm, which usually occur following a breach in the integrity of the
peritoneum (e.g. perforated viscus, bowel surgery). Patients may also complain of
malaise, weight loss, nausea, hiccups (due to diaphragmatic irritation by the
abscess), a dry cough and shoulder tip pain (referred pain) on the affected side.
There may be an associated pleural effusion
How would a liver abscess present differently to subdiaphragmatic abscess
Liver abscesses can present similarly, but gastrointestinal signs such as
hepatomegaly and jaundice will be more prominent, and respiratory symptoms are
unlikely.
Imaging for suspected subdiaphragmatic abscess
affected side. The
patient’s respiratory symptoms are likely to be due to a pleural effusion. Abdominal
CT or ultrasound are the preferred imaging modalities for visualising an abscess.
FBC can aid diagnosis by showing leukocytosis and a chest X-ray will reveal a
raised hemidiaphragm and a pleural effusion.
T/F atelectasis can occur as a complication of subphrenic abscess
T
How would ascending cholangitis present differently to cholecystitis
In cholecytsitis you can get RUQ (as with ascending cholangitis), bit with chole, Signs of jaundice are not typical, as obstruction of the biliary tract is limited to the gallbladder .
Pruritis in pregnancy?
Intrahepatic
cholestasis
of pregnancy is a reversible form of
cholestasis
affecting some pregnant women in their second or third trimesters characterized by
hepatic dysfunction
and pruritus of the skin caused by elevated
bile acids
in the bloodstream, causing
bile salt
deposition in the skin, and secondary skin lesions due to scratching only (no primary lesions).
Define Wilson’s
Reduced biliary excretion of copper and accumulation of copper in teh liver and brain, cornea and kidneys
Hence it is aka hepatolenticular degeneration
Which area of the brain does copper accumulate in particuarly in wilsons
Basal ganglia
Cause of wilson’s
Mutation in gene on chromosome 13 that codes for copper-transporting ATPase in hepatocytes.
The mutation inferferes iwth the transport of copper into the INTRACELLULAR compartments for incorporation into caeuruloplasmin (and secretion into the plasma) or excretion in the bile.
XS copper damages hepatocyte mitocondria causing cell death and release of FREE copper into the plasma, which is subsequently deposited in other tiddues
T/F wilson’s can cause liver disease in young children, and neuro disease in young adults
T.
Liver disease may present in children (>5 years). Neurological disease usually presents in young adults.
Hx of Wilson’s disease
Liver: May present with hepatitis, liver failure or cirrhosis. Jaundice, easy bruising, variceal bleeding, encephalopathy.
Neurological signs: Dyskinesia, rigidity, tremor, dystonia, dysarthria, dysphagia, drooling, dementia, ataxia.
Psych: Conduct disorder, personality change, psychosis
Examination of wilson’s
Liver: Hepatosplenomegaly, jaundice, ascites/oedema, gynaecomastia.
Neurological: As above.
Eyes:Green or brown Kayser–Fleischer ring at the corneal limbus, sun flower cataract (copper accumulation in the lens, seen with slit lamp).
Investigations for wilsons
LFTs (raised AST, ALT and AlkPhos), serum caeruloplasmin and copper (LOW, but may provide false-negatives as caeurloplasmin is an acute phase protein)
24hr urinary copper levels increased
Liver biopsy: increased copper content
Genetic analysis. No simple genetic test
Kayser fleischer involves copper deposition in which layer of the cornea
Descemet’s membrane
What is the normal copper handling in the body
Normal copper is taken from the gut to the liver via the portal vein.
It is taken into hepatocytes. When inside hepatocytes, the copper-transporting ATPase (ATP7B) can move copper into either
1) Vesicles, where it can then be taken into the bile cannuliculi (major route)
2) Bind it to apoceruloplasmin, which is then called caeruloplasmin. This can be excerted by the urine.
With the defect in this enzyme, the copper creates free radicals, damaging hepatocytes and then spilling out into the blood to damage other tissues
What happens to blood caeruloplasmin in wilsons
IT REDUCES (counterintuitive)
This is because you need the ATP7B protein (which isn’t produced in wilson’s) to actually create caeruloplasmin from apoceruloplasmin.
So you won’t get caeruloplasmin being produced, the the level in the blood will be low.
Apocaeruloplasmin is realtively unstable and doesn’t last long in the plasma
What haem problem can wilsons cause
Haemolytic anaemia because copper can cause direct damage to circulating RBCs
What is the most likely cokmplication of crohns
Perianal fistulae
Triple therapy for peptic ulcers involving h pylori?
H. pylori is
eradicated using triple therapy: a 1 week treatment regimen consisting of a PPI (e.g.
omeprazole) and two antibiotics (most commonly amoxicillin and clarithromycin or
clarithromycin and metronidazole) – each drug is taken twice daily.
What if triple therapy fails in H pylori
Triple therapy is
effective in 80-85% of cases. If this fails second-line therapy involves using a
different combination of antibiotics or adding a bismuth compound (quadruple
therapy).
Pancreatic pseudocysts present with what
They are fluid filled round well demarcated dark circles in the pancreas on abdominal CT
What to pancreatic pseudocysts results from
Chronic pancreatitis or pancreatic trauma
What HLA is coeliac associated with
HLA-DQ2
Black pigmented gall stones?
The presence of pigmented stones, which are small darkly colored stones, indicates the presence of chronic hemolysis or cirrhosis . Chronic hemolysis and cirrhosis both create an internal environment of high heme turnover, leading to higher than normal concentrations of unconjugated bilirubin and subsequently crystallized calcium bilirubinate that precipitates from solution and form crystals.
What stones would you find in someone with small intestine resection
Reuced reabsorption of bile salts.
Leads to reduced hepatic bile acid secretion and deranged composition of hepatic bile
Saturation of bile and formation of CHOLESTEROL gall stones
Diabetes mellitus which type of gallstones
Diabetes mellitus
has been shown to be associated with an increased risk of
cholesterol
gallstones
Chronic Abx and gall stones?
Chronic antibiotic therapy, such as the use of ceftriaxone , can lead to the increase precipitation of ceftriaxone - calcium complexes. This supersaturation and crystal formation predisposes patients to increased cholesterol
gallstones
, not pigmented
gallstones
.
What is IBS
A functional bowel disorder defined as recurrent episodes (in the absence of detectable organic pathology) of abdominal pain/discomfort for >6 months of the previous year, associated with two of the following:
- Altered stool passage
- Abdominal bloating
- Symptoms made worse by eating
- Passage of mucous
Aetiology of IBS
Unknown. Visceral sensory abnormalities, gut motility abnormalities, psychosocial factors (particularly stress), food intolerance (e.g. lactose) are all implicated.
Investigations for IBS
Diagnosis mainly from history.
Blood:
FBC (anaemia), LFTs, ESR, CRP, TFT. Antibodies for coeliac (anti-endomysial or anti-transglutaminase antibodies)
Stool examination: Microscopy and culture for parasites, cysts and infection. Ultrasound: To exclude gallstone disease.
Hydrogen breath test: To exclude dyspepsia associated with Helicobacter pylori.
Endoscopy: Upper GI endoscopy, sigmoidoscopy or colonoscopy if other pathologies suspected.
Management of IBS
ALL CASES: lifestyle and dietary modification
-Constipation predominant: Add laxatives (lactulose) If there is bloating you can add antispasmodics or SSRI
-Diarrhoea predominant: Add antidiarrhoeals (loperamide) If there is bloating you can add antispasmodics or TCA
CBT may also be helpful
Complication of IBS
Increased risk of colonic diverticulae
What are mixed stones made of. What proportions of gall stones do they make up
What associations does it have
Contain cholesterol, calcium bilirubinate, phosphate and protein (80%).
Associated with older age, female, obesity, parenteral nutrition, drugs (OCP, octreotide), family history, ethnicity (e.g. Pima Indians), interruption of the entero hepatic recirculation of bile salts (e.g. Crohn’s disease), terminal ileal resection.
What are pure cholesterol stones made of. What proportions of gall stones do they make up
What associations does it have
Pure cholesterol stones (10%): Similar associations as mixed stones.
What are pigment stones made of. What proportions of gall stones do they make up
What associations does it have
Pigment stones (10%): Black stones made of calcium bilirubinate (“bilirubin secondary to haemolytic disorders, cirrhosis), brown stones due to bile duct infestation by liver fluke Clonorchis sinensis. Associated with haemolytic disorders (e.g. sickle cell, thalassemia, hereditary spherocytosis).
What % of gall stones are asymptomatic
90%!!!!
Biliary colic Hx and examination
Sudden onset, severe right upper quadrant or epigastric pain, constant in nature. May radiate to right scapula, often precipitated by a fatty meal. Can last hours, may be associated nausea and vomiting.
Right upper quadrant or epigastric tendernes
Acute cholecystitis Hx and examination
Patient systemically unwell, fever, prolonged upper abdominal pain that may be referred to the right shoulder (due to diaphragmatic irritation).
Tachycardia, pyrexia, RUQ/epigastric tenderness.
Guarding and rebound, Murphys sign.
Ascending cholangitis Hx and examination
Classical association between right upper quadrant pain, jaundice and rigors (Charcots triad). If combined with hypotension and confusion, it is known as Reynolds pentad.
Pyrexia, RUQ pain and jaundice
Investigations for gall stones
FBC, LFTs, lipase and amylase, ABDOMINAL USS
Abdominal ultrasound has low sensitivity for choledocholithiasis, but accuracy is better for any accompanying bile duct dilation.
Then, MRCP for suspected choledocholithiasis that is not confirmed by abdominal ultrasound.
Management of mild biliary colic symptoms
Conservaive, avoidance of fat in diet
Management of choledocholithiasis
Admit, IV fluids, analesia, antiemetics and Abx if signs of infection (cholecystitis or cholangitis)
If there is evidence of obstruction, urgent biliary drainage by ERCP or percutaneous transhepatic cholangiogram.
If symptoms worsen/don’t improve, suspect localised abscess or empyema. Drain percutaneously by cholecystostomy and pigtail catheter
Elective cholecystectomy if concurrent cholelithiasis or cholecystitis
Mangement of cholelithiasis (i.e. stones in gallbladder, but no infection)
Supportive care, analgesics
Elective cholecystectomy for:
Symptomatic cholelithiasis
Asymptomatic cholelithiasis only if at increased risk of gallbladder cancer
Management of acute cholecystitis
(cholelithiasis or biliary sludge leading to inflammation of gall bladder wall)
Supportive care, analgesics
IV antibiotics
Cholecystectomy (timing depends on severity)
Management of acute cholangitis
Supportive care, analgesics
IV antibiotics (Moderate to mild community acquired: cefuroxime. Severe community acquired: meropenem, pip-taz. Healthcare-associated: meropenem, pip-taz
SURGICAL:
If mild cases, do elective chole within 24-72hrs.
If complications (gangrene, perforation) or condition worsens, do emergency lap chole.
If there are high risk of surgical complications and/or they’re critically ill, do emergency percutaneous biliary drainage (e.g. cholecystostomy), follow up with interval surgery when possible.
In severe, high risk cases: delayed elective cholecystectomy (>2 weeks)
What is bouveret’s syndrome
gallstones causing gastric outlet obstruction
What is mirizzi syndrome
common hepatic duct obstruction by an extrinsic compression from an impacted stone in the cystic duct
What Abx are used for actue cholangitis
Cephalosporin and metronidazole
What is the commenest neurological manifestation of sarcoid
Sarcoidosis only rarely presents with neurologic complications. The most common neurological involvement that presents in this clinical situation is facial nerve palsy - either unilateral or bilateral.
T/F patients should refrain from a gluten-free diet until biopsy
True, kind of.
A tTG antibody test will be done on everybody first, then preferably a small bowel biopsy
If patients have put themselves onto a gluten free diet before small bowel biopsies were obtained, and feel so much better that they are not able to go back to gluten for the required 6-8 weeks before the biopsies are taken, then they can have HLA genotyping.
Same goes for children (anti-tTG and HLA genotyping is enough, so they don’t have to have biopsy)
What are the complication of coeliac disease
Coeliac disease is associated with lymphocytic colitis
Small bowel lymphoma in the context of coeliac disease, although in all the text books, is vanishingly rare and certainly not something that we would screen all newly diagnosed patients for.
What should you screen for for newly diagnosed patients with coeliac
osteopenia / osteoporosis is very common in patients who are newly diagnosed with coeliac disease and screening is recommended.
Patient with coeliac disease diagnosis but after 6 months diarroea hasn’t resolved, still hasn’t put on much weight
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.
Even trace gluten like on utensils, or using the same toaster, can cause inflammation
Progressive dysphagia for food and GORD?
Peptic stricture needs to be excluded, along with oesophageal carcinoma
Management for symptomatic, benign peptic stricture
Balloon dilatation is the treatment of choice for symptomatic, benign peptic strictures. Endoscopy and biopsy confirmation of benign disease must be undertaken prior to dilatation.
Temporary oesophageal stenting can be considered for patient’s refractory to repeated balloon dilatation.
Investigation of eosophageal perforation
CT scan with WATER SOLUBLE oral contrast
Which extra-intestinal manifestations of UC are related to the activity of the colitis
Pyoderma gangrenosum Erythema nodosum Episcleritis Aphthous ulcers Anterior uveitis Acute arthropathy
Which extra-intestinal manifestations of UC are NOT related to the activity of the colitis
Sacroiliitis/ank spond
PSC
Acute severe UC management
Intravenous hydrocortisone is first-line management for acute severe colitis. Antibiotics would only be started if there was concern about toxic megacolon and risk of perforation or signs of infection which are not apparent in this case.
What if you’ve give IV corticosteroids for acute severe UC and it doesn’t work
NICE guidance recommends the use of intravenous ciclosporin for patients who are not responding to intravenous hydrocortisone or where hydrocortisone treatment is not appropriate.
TNF-alpha and should only be considered if intravenous ciclosporin is contra-indicated or inappropriate.
Contraindications for ciclosporin
Hypertension and renal impairment
Best long term management for eosophageal varicies
Non-cardioselective beta blockers
Non-cardioselective beta-blokers are the first line treatment of prevention of variceal bleeding. Where a beta-blocker is not tolerated or if there is a singificant contra-indication to their usage, then regular endoscopy with variceal band ligation would be the second-line managment.
T/F TIPSS is a prophylactic treatment for variceal bleeding
F….
A TIPSS may also be considered with an acute presentation of variceal bleeding not managed by endscopy but is not used as prophylactic management.
T/F pabrinex is best given as a rapid IV bolus in wernicke’s
F
Wernicke’s encephalopathy is reversible but needs prompt treatment with thiamine (B1) to prevent progression to Korsakoff’s psychosis (permanent loss of short-term memory).
IV Pabrinex however needs to be given at a controlled rate as giving too quickly increases the risk of anaphylaxis
T/F you should treat wernicke’s with glucose infusion
F
It may be precipitated by glucose infusion
T/F chronic alcoholism is assocaited with chronic kidney disease
F
Chronic alcohol intake is not associated with pulmonary fibrosis or chronic kidney disease
T/f alcohol is associated with diabetes
F.
Pancreatic damage can precipitate diabetes
Who are benign liver tumours especially frequent in
Young women
What types of bening liver tumours are there. What is most to least common
hepatic hemangioma (most common) > focal nodular hyperplasia (FNH) > hepatocellular adenoma (rare)
Epidemiology of hepatic benign tumors
Sex: women to men (∼ 6:1)
Age: can appear at any age, but mostly affects young women
Most often an incidental finding on imaging tests
Cause of liver benign tumour:
Hepatocellular adenoma
oral contraceptives and anabolic steroids
Cause of liver benign tumour:
Hepatic haemangioma
possible hormonal component; estrogen therapy associated with increased growth in size
Symptoms/clinical findings of benign liver tumours
Usually asymptomatic
Large tumors –> upper abdominal pain, fullness, and nausea
Best initial test for liver tumour, further test to reach definitive diagnosis , and if unsure
Best initial test: ultrasound Further imaging Contrast-enhanced CT MRI Biopsy: to confirm diagnosis if imaging is inconclusive
Where are hepatocellular adenomas more commonly located
Right lobe
Ultrasound of a suspected liver benign tumour shows a central stellate scar
Focal nodular hyperplasia
Histology of a hepatocellular benign tumour:
Cavernous vascular spaces of variable size, lined by flat endothelial cells
Hepatic hemangioma
Histology of a hepatocellular benign tumour:
Enlarged hepatocytes, with small and regular nuclei, cytoplasmic glycogen and lipid deposits
Arranged in sheets or 2-cell thick cords
Normal hepatic lobular architecture is absent
Hepatocellular adenoma
What are the types of liver cysts
Simple cyst (congenital, usually asymptomatic- USS and CT)
Congenital polycystic liver (associated with PKD)
Hyatid echinococcal cysts
What is crohn’s
A chronic granulomatous inflammatory bowel disease resulting in destruction of the GI wall anywhere along the GI tract.
Aetiology of crohn’s
Genetic and environmental factors
Hx of crohn’s
Crampy abdominal pain (caused by inflammation, fibrosis or bowel obstruction).
Diarrhoea (can be bloody, but typically not/steathorrhoea)
Fever, malaise, weight loss
Symptoms of complications
Exam of crohn’ss
Weight loss, clubbing, signs of anaemia.
Aphthous ulceration of the mouth.
Perianal skin tags, fistulae and abscesses.
Signs of complications (eye disease, joint disease, skin disease).
Commmon locations for crohns
CD may involve any or all parts of the entire GI tract from mouth to perianal area, although it is usually seen in the terminal ileal and perianal locations.
What is the association between IBD and smoking
Smokers are more than twice as likely to develop Crohn’s as non-smokers.
This is in contrast to ulcerative colitis, in which smoking reduces the risk of developing the disease by up to 40%.
T/F OCC and NSAIDS increase the risk of crohns
Yes
Which organism, which casues an acute ileitis, is a differential for crohn’s
Yersnia enterocolitica (an alternative differential)
Investigations for crohns
BLOOD:
FBC (anaemia, leukocytosis)
Iron studies (normal, or iron deficient, due to GI bleeding or malabsorption of iron)
b12 and folate (normal of low)- b12 deficiency most common in ileocaecal CD/post-ileocaecal resection
STOOL MICROSCOPY AND CULTURE (exclude infective colitis)
AXR- toxic megacolon
Erect CXR- IF RISK OF PERFORATION
USS- GI wall thickening/may detect abscesses/fistulas
Plain radiography with barium swallow
Colonoscopy/ OGD and biopsy
Why do a plain radiography with barium swallow in crohn’s?
What might be found
To detect fistulas or stenoses.
Creeping fat- Proliferated mesenteric fat between the intestinal loops is pathognomonic for CD.
String sign- fibrotic bits look like string
Why do endoscopy in crohns? What might you find
Endoscopy confirms the diagnosis, assesses the extent of the disease, differentiates CD from other diseases (e.g., ulcerative colitis, peptic ulcers, etc.), and may also be used as a therapeutic tool (e.g., dilatation of ducts, intestinal loops).
Segmental involvement
MACROSCOPIC findings:
- Linear ulcers (snail trails)
- Other apththous haemorrhagic mucosa defects (pinpoint lesions)
- Cobblestone sign
- Fissures/fistulas
- Ertyhema and transumral inflammation
What might you find in crohns histology
Skip lesions (discontinuous inflammation)
Hypertrophic lymph nodes
Transmural inflammation:
Non-caseating granulomas
Giant cells
Distinct lymphoid aggregates of the lamina propria
Management of ACUTE exacerbation of crohns
Fluid resuscitation, IV or oral corticosteroids, 5-ASA analogues (e.g. mesalazine, sulfasalazine) may induce a remission in colonic Crohn’s disease
Elemental diet may induce remission (more often used in children). Parenteral nutrition may be necessary. Monitor markers of activity (fluid balance, ESR, CRP, platelets, stool frequency, Hb and albumin). Assess for complications.
Conservative management of crohns
Stop smoking, dietician referral. Education and advice (e.g. from inflammatory bowel disease nurse specialists).
Long term medical management of crohn’s disease
Steroids for acute exacerbation
5-ASA to reduced relapses (mild to moderate disease)
Steroid sparing agents for immunosuppression (azathioprine, methotrexate). Reduces relapse
Anti-TNF (infliximab). Only for refractory cases
Long term surgical managemnet of crohns
Indicated for failure of medical treatment, failure to thrive in children or the presence of complications.
This involves resection of affected bowel and stoma formation, although there is a risk of disease recurrence.
Complications of crohn’s
GI: haemorrhage, bowel strictures, perforation, fistulae (between bowel, bladder, vagina), perianal fistulae and abscess, GI carcinoma (5% risk in 10 years), malabsorption
Extraintestinal features of crohns
Uveitis, episcleritis, gallstones, kidney stones, arthropathy, sacroiliitis, ank spond, erythema nodosum, pooferman gangrenosum, amyloid!!!!!
Prognosis of crohn’s
Chronic relapsing condition. Two-thirds will require surgery at some stage and two-thirds of these >1 surgical procedure.
Which type of hernia has the highest rate of incarceration of the small bowel
Femoral hernias protrude below the inguinal ligament through the femoral canal . This type of hernia most commonly occurs in women and has the highest rate of incarceration of the small bowel
What tube is used for short term vs long term enteral nutrition
Short-term: nasogastric tube
Long-term (> 2–3 weeks):
Gastrostomy tube: gastric feeding tube inserted endoscopically through a small incision through the abdomen into the stomach or
Jejunostomy tube: feeding tube inserted through a small incision through the abdomen into the jejunum to bypass the distal small bowel and/or colon
Contraindications for parenteral nutrition
Enteral nutrition is feasible Serum hyperosmolality Severe hyperglycemia Severe electrolyte abnormalities Volume overload
What is the route of administration for short and long term parenteral nurtition
arenteral nutrition is required for < 2 weeks: peripheral venous line, or peripherally inserted central catheter
Parenteral nutrition is required for > 2 weeks: tunneled central venous catheter or a port
Metabolic complications associated with specialised nutritional support
Electrolyte imbalances:
hypocalcemia, hypomagnesemia, hypophosphatemia
Hyperglycaemia
Refeeding syndrome
Gallstone disease
NAFLD
Renal damage
Acalculous cholecystits
What causes refeeding syndrome
If there has been poor nutrition, then giving someone good nutrition will suddenly increase the insulin
This will switch on protein, fat synthesis in the liver and elsewhere, which will use up the already depleted reserves of phosphate, magnesium, and thiamine in chronically malnourished patients. A drop in thiamine levels can cause Wernicke’s encephalopathy.
Additionally, insulin causes an intracellular shift of potassium, phosphate, and magnesium. The resulting drop in these serum levels can trigger cardiac arrhythmias
What is vitamin b1 (thiamine) needed for
Thiamine enables the body to use carbohydrates as energy. It is essential for glucose metabolism, and it plays a key role in nerve, muscle, and heart function
Multiple hamartous polyps on the colon of a young person
Juvenile polyposis syndrome is a rare, autosomal dominant condition that involves hamartomatous polyps of the GI tract, especially the colorectum. Patients should be regularly screened for colorectal cancer .
hamatomatous
polyps
of the GI tract, mucosal
hyperpigmentation
Peutz-Jeghers syndrome (PJS) is an autosomal dominant syndrome associated with hamatomatous polyps of the GI tract, mucosal hyperpigmentation , and increased risk of cancer` . Though this patient has hamartomatous lesions of the GI tract, he does not have the pigmented macules seen in more than 95% of PJS.
Cause of acute cholecystits
It develops in up to 10% of patients with symptomatic gallstones.
In most cases (90%), it is caused by complete cystic duct obstruction usually due to an impacted gallstone in the gallbladder neck or cystic duct, which leads to inflammation within the gallbladder wall.
In 5% of cases, bile inspissation (due to dehydration) or bile stasis (due to trauma or severe systemic illness) can block the cystic duct, causing an acalculous cholecystitis.
Investigations for cholecystitis
- USS (if no sepsis suspected)
- MRCP
- Endoscopic ultrasound
(CT or MRI of abdomen if septic and you suspect gangrenous cholecystitis/gallbladder perforation)
Management of acute cholecystitis
See booklet
What are the causes of GI perforation
- Gastroduodenal:
- Ruptured peptic ulcers
- Rarely gastric carcinoma - Large bowel (most common) :
- Diverticulitis and colorectal carcinoma (80%)
- Crohn’s
- Acute appendicitis
- Volvulus, UC (Toxic megacolon, trauma, complication of colonoscopy - Small bowel:
- Trauma, infection (typhoid, TB), Crohn’s
- Obstruction due to adhesions - Eosophagus:
- Boorhaeve’s
- Iatrogenic perforation in OGD (more commonly during dilation of strictures)
Signs of GI perforation on examination
Unwell, signs of localised and generalised peritonitis with abdominal rigidity and guarding
Reduced/absent bowel sounds
Loss of liver dullness due to overlying gas
Shock, pyrexia, pallor and dehydration
Investigations for GI perforation. First imaging?
Blood: FBC, U&E, LFT, amylase (can be raised in perforation)
Erect CXR (gas under diaphragm)
AXR can show abnormal gas shadows in tissue….. Riglers sign referes to gfas on either side of the bowel wall. Lateral decubitas film best for intraperitoneal gas though
CT very sensitive for free intraperitnoeal gas
What is a liver abscess
A pyogenic liver abscess is a rare disease characterized by solitary/multiple collections of pus within the liver.
Can be due to bacterial, fungal or parasitic infection
What is the cause of a pyogenic liver abscess
Polymicrobial commonly.
Escherichia coli, Klebsiella, enterococcus, bacteroides, streptococci, staphylococci
Which other organisms can cause liver cysts
Amoebic (amboeba histolytica)
Hyatid cyst (tapeworm Echinococcus granulosis)
Hx of liver abscesses
Fever, malaise, nausea, anorexia, night sweats, weight loss
RUQ or epigastric pain, which may be referred to shoulder (diaphragmatic irritation)
Jaundice, diarrhoea, pyrexia of unknown origin.
Foreign travel
Risk factor for developing a liver abscess
Diabetes
Examination of liver absceses
Fever (continuous/spiking), jaundice
Tender hepatomegaly, R lobe affected more commmonly than left
Dullness to percussion and breath sounds at right base of lung, caused by reactive pleural effusion.
Liver abscess with raised eosinophils
Hyatid cyst
Investigations of liver abscesses
FBC, LFTs, blood culture,, PT and aPTT
IMAGING:
USS
Gram stain and culture of aspirated abscess fluid
CT
What are the LFT findings with liver abscess
High Alk Phos, mildly elevated AST/ALT and bili, hypoalbuminaemia
Why is clotting profile used in liver abscesses
Indicated to check that blood clotting is within normal limits before aspiration is performed
When would you not aspirate a liver abscess
If there is abnormal clotting or if you suspect hyatid
What is oesophageal carcinoma
Malignant tumour arising in the oesophageal mucosa.
Two major histological types: squamous cell carcinoma and adenocarcinoma
What is the cause of squamous cell carcinoma in oesophagus
Alcohol, tobacco, nutritional deficiency, HPV infection, achalasia, Plummer-Vinson syndrome, tylosis, scleroderman, coecliac disease, lye stricture, previous thoracic radiotherapy , dietary nitrosamines
What is the cause of adenocarcinoma
GORD, Barrett’s oesophagus (intestinal metaplasia of the distal oesophageal mucosa with “0.5–0.7% incidence of adenocarcinoma per year).
Where is squamous cell carcinoma vs adenomcarcinoma more common within the oesophagus
Squamous cell carcinomas are more common in the mid-upper oesophagus. Adenocarcinoma usually develops in the lower oesophagus or, increasingly, the gastrooesophageal junction
How do oesophageal cancers spread
Spread is typically initially direct (oesophagus has no serosa) and longitudinal via an extensive network of submucosal lymphatics to tracheobronchial, mediastinal, coeliac, gastric or cervical nodes
Hx of eosophageal cancer
Early: symptomatic/symptoms of reflux.
Later: dysphagia, initially worse for solids, regurgitation, cough or choking after food, pain (odynophagia), weight loss, fatigue, voice hoarseness (may indicate recurrent laryngeal nerve palsy).
Examination of oesophageal cancer
No physical signs may be evident, signs of weight loss. With metastatic disease there may be supraclavicular lymphadenopathy, hepatomegaly. Respiratory signs may be due to aspiration or direct tracheobronchial involvement
Which investigations would you do for oesophageal cancer
1st test?
Staging
1st test: OGD + biopsy
OGD is the first test in patients with severe dysphagia, odynophagia, or weight loss. This will differentiate oesophageal cancer from benign causes of dysphagia
Staging: CT thorax and abdo
What metabolic disturbance might present in oesophageal obstruction
patients may become severely volume-depleted and hypokalaemic because of their inability to swallow fluids and their own potassium-rich saliva.
What investigation might be done prior to treatment once a diagnosis of oesophageal cancer is confirmed
Endoscopic ultrasound (EUS) is now a standard pre-treatment test
It can identify all the histological layers of the oesophagus and thereby confirm the T-stage with 90% accuracy. It can also identify abnormal or enlarged mediastinal and coeliac axis lymph nodes, and enable cytological examination by fine needle aspiration (FNA).
Crucial prior to surgery
Where do inguinal hernias appear with respect to the pubic tubercle?
Superior and MEDIAL! (I know it’s confusing but this is correct)
Why are right sided indirect inguinal hernias more common?
They are more common on the right side in males, because the right testis descends later and there is an increased incidence of failed closure of the processus vaginalis (thus predisposing to hernias)
A 35-year-old Indian man presents with a swelling lateral to the femoral artery. On examination it is tender and fluctuant, but cannot be reduced. He also describes a recent history of weight loss and night sweats.
TB.
A known complication of intraabdominal TB is abscess formation in the lumbar vertebrae (Pott’s disease).
Such an abscess may track down the psoas sheath and into the groin, forming a psoas abscess. Psoas abscesses are described as ‘cold’, as they are painless and not warm to touch.
A 35-year-old Indian man presents with a swelling lateral to the femoral artery. On examination it is tender and fluctuant, but cannot be reduced. He also describes a recent history of weight loss and night sweats.
TB.
A known complication of intraabdominal TB is abscess formation in the lumbar vertebrae (Pott’s disease).
Such an abscess may track down the psoas sheath and into the groin, forming a psoas abscess. Psoas abscesses are described as ‘cold’, as they are painless and not warm to touch.
