GI Flashcards
What is GORD
Gastro-Oesophageal Reflux Disease
Common condition caused by stomach acid entering the oesophagus
Causes of Gastro-Oesophageal Reflux Disease
Lax Oesophageal Sphincter
Reduced oesophageal motility (E.g. caused by systemic sclerosis)
Hiatus Hernia
Reduced stomach emptying
What is systemic sclerosis
Overproduction of collagen thought to result from an autoimmune dysfunction
Characterised by thickening of the skin caused by accumulation of collagen, and by injuries to small arteries
What are the risk factors for GORD
Smoking Alcohol Various Drugs Pregnancy Obesity Hiatus Hernia
Signs and Symptoms of GORD
Burning pain in abdomen/chest
Precipitated by having a meal
Often worse on lying down
Trouble swallowing/pain swallowing
Complications of GORD
Barrets Oesophagus Oesophageal Ulcers Oesophagitis Oesophageal stricture due to scar tissue build up Aspiration on regurgitated contents/acid
What is Barrett’s Oesophagus
Metaplasia of normal stratified squamous epithelium lining of the oesophagus by simple columnar epithelium (with goblet cells).
Thus can lead to oesophageal adenocarcinoma.
Treatment for Barrets Oesophagus
Oesophageal Resection
Oesophageal mucosectomy
Oesophageal mucosal ablation
Signs and Symptoms of Oesophageal Ulcers
Bleeding
Anaemia
Haemoptesis
Differential Diagnosis for GORD
Oesophagitits from a swallowed corrosive material or drug, that has then become stuck in the oesophagus
Infection
Peptic Ulcer
GI cancer
Non-Ulcer Dyspepsia - meaning that no known cause can be found for the symptoms
Oesophageal spasms
Investigations in suspected GORD
May be none necessary if patient has a very typical history
Endoscopy - Assess level of dysplasia in Barrets and will differentiate between any gastric ulcers
Barium Swallow - Diagnose any hiatus hernia
Monitor Oesophageal pH - Monitors acid reflux level
Urea breath test - Rule out H.Pylori infection
Treatment of GORD
Lifestyle Factors
o Reduce Weight
o Stop Smoking
o Reduce alcohol intake
o Raise head in bed at night to prevent reflux
o Eat smaller meals more frequently
o Avoid food and hot drinks 3 hours before bed
Stop drugs that can precipitate GORD
o Drugs that affect oesophageal motility e.g. nitrates, anticholinergics, tricyclic antidepressants
o Drugs that damage mucosa e.g. NSAIDS, potassium, bisphosphonates
Pharmacological Treatment
o PPI e.g. Omeprazole
o H2 receptor Antagonist e.g. Ranitidine
Surgery - in patients who are not responding to medical treatment
o Insert artificial sphincter made of magnetic beads
o Fix Hiatus Hernia
o Nissen Fundoplication - Wrap stomach fundus around lower oesophageal sphincter
What are Oesophageal Varices
Dilated Veins in the oesophagus due to portosystemic hypertension which can lead to haemorrhage or heavy bleeds
What are the causes of Oesophageal Varices
Caused by portosystemic hypertension, and thus chronic liver disease is the main cause
Pre Hepatic
o Portal Vein Thrombosis
o Fistula leading to increased portal blood flow
o Increased splenic blood flow
o Portal Vein Occlusion e.g. stenosis/atresia
Hepatic o Cirrhosis o Idiopathic Portal Hypertension o Acute hepatitis o Congenital Hepatic Fibrosis o Myelosclerosis
Post Hepatic
o Compression e.g. from tumour
o Constrictive Pericarditis
Signs and Symptoms of Oesophageal Varices
Haematemisis Melaena Epigastric Pain Dysphagia Odonyphagia (pain swallowing) Pallor and low blood pressure due to bleeding/anaemia Patient may have other bleeds e.g. Rectal Varices Other features of chronic Liver Disease
What are some examples of signs of chronic liver disease
Palmar erythema Hepatomegally Caput Medusa Spider Naevi Jaundice
Differential Diagnosis of Oesophageal Varices
Gastric/Peptic Ulcer
Mallory-Weiss Tear
Oesophagitis and Barrets Oesophagus
Malignancy
Investigations for Oesophageal Varices
Bloods
o FBC - To check for any anaemia or raised WCC
o Clotting screen and INR
o U&E
o LFT - to look for chronic liver disease
o Group and save/Cross Match as patient is at high risk of bleed
Chest X-Ray - To check for Aspiration Pneumonia
Liver Ultrasound
Endoscopy to confirm varices
Treatment of Oesophageal Varices
Fluid resuscitation (consider blood transfusion)
Vasoactive drugs e.g. omatostatin that reduce rate of bleeding
Prophylactic Antibiotics
Endoscopic band ligation
Transjugular intrahepatic portosystemic shunting - reduces portosystemic hypertension
Emergency endoscopic sclerotherapy
What is a Peptic Ulcer
Loss of mucosa of the stomach/duodenum leading to damage to the lining below, leading to epithelial damage and ulceration
Causes of Peptic Ulcer
H.Pylori infection
Long term NSAID use
Signs and symptoms of peptic ulcers
Epigastric Pain - Worse after eating, worse after spicy food
GORD type symptoms due to increased chance of reflux
Tender epigastrum
Melaena/Haematemsis in severe ulceration
Differential Diagnosis of Peptic Ulcers
Abdominal Aortic Aneurysm - Pain pattern in similar place but not similar pattern
GORD - In GOrd pain is worse on lying down
Gallstones - Normally much more painful
Pancreatitis - Pain in pancreatitis is normally in a different location
Irritable Bowel Syndrome
Hepatitis
Zolinger Ellison syndrome - Excess Acid Produced due to a gastrin secreting gastrinomas
How to differentiate gastric vs duodenal ulcers
Pain shortly after meals with gastric ulcer and 2-3 hours afterwards with duodenal ulcer.
Investigations for Peptic Ulcers
FBC - looking for any iron deficiency anaemia
Urea breath test to look for H.Pylori
Endoscopy - IN some cases or to see extent of ulceration and bleeding
What are the indications for the use an endoscopy in Peptic Ulcers investigations
First presentation
Over 55 years old
Warning signs - ALARMS
Treatment of Peptic Ulcers
Eradication of H.Pylori (Triple Therapy)
o 2x Antibiotics - Clarithromycin and Metranidazole
o PPI - Omeprazole
Stop Smoking
Stop NSAIDS
Possible ablation of bleeding vessels
Repeat endoscopy post treatment to confirm resolution
What is dyspepsia
Indigestion
Epigastric Pain related to hunger, certain food and time of day. A bloating and fullness after meals. Associated with heartburn
Differential Diagnosis of dyspepsia
Non-ulcer dyspepsia GORD Oesophagitis Peptic Ulcer Duodenitis Gastritis
When would you perform an endoscopy on a patient
When showing ALARM signs
Anaemia Loss of weight Anorexia Recent onset/progression Melaena/Haematemsis Swallowing Difficulty
What is decompensated Liver Failure
When the liver loses the ability to regenerate/repair and thus fails to function
What are the causes of liver failure
Tuberculosis - But anti TB drugs can also cause hepatitis Alcoholic liver disease Primary Biliary Cirrhoisis Haemachromatosis - Accumulation of iron in the body Autoimmune hepatitis Alpha 1 anti trypsin deficiency Wilsons Disease Fatty liver disease HELLP Syndorme (Haemolysis, Elevated liver enzymes Infections o Viral Hepatitis - Hep B,C and Cytomegalovirus, Epstein-Barr o Yellow fever o Leptospirosis Drug Induced Causes o Paracetamol Overdose o Halothane - a GA o Isoniazid - TB treatment Toxins o Deathcap Mushrooms o Carbon Tetrachloride Venous Occlusion o Occlusion of hepatic portal vein o Occlusion of hepatic veins
Signs and Symptoms of Live Failure
Nausea
Loss of appetite
Fatigue
Diarrhoea
Bruising - Coagulation factors 1,2,5,7,8,9,10 made in liver
Jaundice and pruritis - Unconjugated bilirubin and bile salt build up in skin
Hepatic Encephalopathy
Sweet, faecal smell on breath
Leuconycia - hypoalbuminaemia
Clubbing
Palmar erythema
Dupuytrens contracture - Alcoholic liver disease
Hyper-dynamic circulation - increased circulatory volume
Spider Naevi - >5 for indication of cirrhosis
Hepatomegaly - Shrunk liver in late disease
Ascites and peripheral oedema - Hypoalbuminaemia
Kayser-Fleicsher rings - Copper rings around eyes in Wilson’s disease
Bronzed skin - caused by Haemachromatosis (iron overload)
Polyuria
Polydipsia
How do you examine for Hepatic Encephalopathy
Do hepatic flap test and do a mini mental state examination
What is Hepatic Encephalopathy
Ammonia build up in circulation as normally cleared by the liver. This enters the brain where it is converted to glutamine by astrocytes. This causes an osmotic imbalance. Fluid shifts into the brain causing cerebral oedema and causing the confusion.
Differential Diagnosis of Liver Disease
Lesions in the brain/ cerebral infarction Intoxication Wernickes Encepalopathy Hypoglycemia Ketoacidosis Electrolyte imbalance Hypoxia Hypercapnia Renal failure/Heart failure - Oedema and Ascites
Investigations for Liver Failure
Bloods
o FBC - Anaemia. signs of infection
o U&E - Check for mineral levels (malnutrition) and renal function
o LFTs and Serum Albumin - Raised ALP, AST, ALT, Gamma GT, bilirubin are indicative of liver disease and albumin will be low
o Clotting - INR and PT will be prolonged due to deranged clotting factors
o Paracetamol Levels - Check for an overdose
o Virology - CMV, Hepatitis, Epstein Barr, HIV
o Ferritin for Haemochromatosis
o Copper for Wilson’s Disease
o Alpha 1 anti trypsin
o Caeruloplasmin - Copper transport for Wilson’s Disease
o Autoantibodies - Primary Biliary Cirrhosis and autoimmune hepatitis
o Immunoglobulins
o Metabolic Syndromes - Thyrotoxicosis ()T3,4) and diabetes (Glucose)
Coeliac Disease - Tissue Transglutaminase
Test for parasites
Blood Cultures
Urine Cultures
Paracentesis - take out peritoneal fluid, then culture and check neutrophil level
Radiology
o Chest X-ray
o Abdominal Ultrasound
o Doppler of portal vein and hepatic vein to check for block or Budd-Chaiari syndrome
o Fibroscan to assess cirrhosis
EEG for neurological Abnormalities
General Treatment for Liver Failure
Lactulose - Keeps gut motility up and prevent ammonia from building up, reducing risk of encephalopathy
Treat bleeds with fresh frozen plasma, platelet concentrates, antifibrinolytic drugs, prothrombin complex concentrates and/or recombinant factor 7
Ascites must be drained and collected for testing - and treat fluid build ups with spirinolactone (aldosterone antagonist)
Monitor bloods
Monitor weight - See how fast weight is coming off
Liver transplant may be necessary depending on degree on encephalitis, age, and cause of liver disease.
If caused by drug damage, may consider stopping some drugs
Treatment for Alcoholic Liver DIsease
Stop alcohol intake - Treat withdrawal symptoms (Chlordiazepoxide), stop cravings (Acamprosate) and cause unpleasant drinking effects (Disulfaram)
CBT and help groups for alcohol
Vitamin and mineral replacement - Vit K and Pabrinex IV (contains important vitamins)
Optimise nutrition - 40kcal/kg/day and >1.2g protein/kg/day
Monitor bilirubin as a marker for improvement
Prednisalone 40mg/day over 5 days
Signs and symptoms of primary Biliary cirrhosis
Normal Liver disease signs and symptoms
Chronic Cholestasis (no bile flow through bile duct leading to gallstones)
Patients more likely to have pruritits due to deposition of bile in the skin
Right upper quadrant pain
Very fatigued
Steatorhea
Dark urine (increased conjugated bilirubin in urine)
Investigations for Biliary Cirrhosis
LFT’s - ALP will be raised due to cholestasis
Auto-antibody tests - Antimicrobial antibodies in >95% cases, Raised serum IGM, anti smooth muscle antibodies and antinuclear may be present
Thyroid function tests - Patients often develop thyrotoxicsis (autoimmune)
Ultrasound and Possible CT of gall bladder and liver
Treatment of Biliary Cirrhosis
Sedating Antihistamines to treat pruritis
Cholestryamine/Colestipol to sequester bile salts and also help with pruritits
Ursodeoxycholic acid to slow disease progression
Steroid to suppress autoimmune process of damage
What is Biliary Cirrhosis
A kind of cirrhosis caused by damage to the bile ducts in the liver. Unknown cause but thought to be autoimmune
What is Haemochromatosis
Autosomal recessive disease that commonly presents in over 30’s
Patients have a deficiency in hepcidin (an iron regulatory hormone) which leads to increased intestinal iron absorption
This increased iron then accumulates in tissues
o Skin and pancreas often affected (bronzed diabetic)
o Heart,gonads and joints may also be affected
Signs and Symptoms of Haemochromatosis
Early Symptoms o Fatigue/Weakness o Arthropathy o Erectile dysfunction o Amenorrhoea - Absence of period o Heart Problems
Advanced Symptoms o Diabetic Symptoms o Bronzed skin o Hepatomgeally o Cirrhosis o LIver Failure
Investigations for Haemochromatosis
Fasting transferrin saturation and serum ferritin
Genetic screening for human haemochromatosis protein
Treatment of Haemochromatosis
Venesection - Bleed the patient (500ml) every week to keep iron levels low and to prevent deposit (maintain ferritiin at <50Mg/L)
Low iron diet may help
Tea, coffee and red wine with meals to reduce absorption
Serum Ferritin >1000ml risks cirrhosis
What is Wilson’s Disease
Autosomal recessive disorder, where copper is deposited in the liver. Leading to hepatitis and cirrhosis. Normally present and young age (early adult)
Patients may also have psychiatric, neuro, renal problems, or rheumatoid pathologies as well a others.
Signs and Symptoms of Wilson’s disease
Kayser-Fleicher rings - Copper deposits in the eyes, leading to a copper ring around iris (sign may also occur in bile excretion disorders as copper removed this way) Neurological Problems - Depression, Psychosis. Asymmetrical tremor (resting, postural or kinetic) Osteopaenia - Low bone density Osteoarthritis Myopathy, including cardiomyopathy Pancreatitis - Hypoglycemia Hypoparathyroidism Kidney Dysfunction Symptoms of liver failure
Differential Diagnosis for Wilson’s Disease
Primary biliary cirrhosis and other disease of cholestasis - Lead to copper build up as copper is excreted in bile Depression/anxiety disorders Hypothyroidism Diabetes Hepatitis and cirrhosis Huntington's/Parkinson's/MS
Investigations for Wilson’s DIsease
Caeruloplasmin (copper binding protein) level <0.1g/l diagnostic
Check urine for copper excretion
Liver Biopsy if other tests inconclusive
Tests of exclusion for other causes of liver damage, renal impairment,hypothyroidism etc
Treatment of Wilson’s Disease
Avoid alcohol and hepatotoxic drugs
Low copper diet - Liver, chocolate, nuts mushrooms,. legumes and shellfish avoided
annual examination of KF rings to see them disappear
Chelating agents prevent copper absorption in the gut e.g. Zinc Acetate
Test first degree family members as chance they have it too
What is autoimmune hepatitis
Hepatitis caused by autoimmune antibodies. There are two types caused by different antibodies, With type 1 being most common (75%)
Investigations for autoimmune hepatitis
Screen for antibodies that cause autoimmune hepatitis
Antinuclear antibodies(ANA)
Anti smooth muscle antibodies (ASMA),
Anti liver kidney miscrosmal 1 antibody(Anti-LKM-1)
Antibodies against soluble liver antigen (Anti-SLA)
Anti-mitochondrial antibody (AMA)
Antiphospholipid antibodies
Type 1 is associated with ASMA or ANA (75% patients). Type 2 is associated with presence of either anti-LKM-1 or anti-LC-1
Treatment of autoimmune hepatitis
Oral corticosteroids (prednisalone) to treat acute presentation Azathioprine to maintain remission
What is Alpha-1-antitrypsin deficiency (In the Liver)
Autosommal recessive inherited disease, with a mutation in the SERPINA1 gene leading to reduced production of Alpha-1-Antitrypsin
Signs and symptoms of Alpha-1-antitrypsin deficiency (In the Liver)
Neonatal jaundice and hepatitis
Older children develop hepatitis, cirrhosis and liver failure
Obviously will have lung symptoms (symptoms of COPD)
Investigations for Alpha-1-antitrypsin deficiency (In the Liver)
Serum levels of Alpha-1-antitrypsin measured
LFT’s and liver biopsy to see level of liver damage
Treatment of Alpha-1-antitrypsin deficiency (In the Liver)
Lower alcohol consumption and quit smoking Treat lung disease the same as COPD Give recombinant Alpha-1-antitrypsin May need liver transplant Screen for hepatocellular carcinoma
What is Fatty liver disease
Accumulation of lipid in and around the liver due to impaired fatty acid metabolism in hepatocytes - may be due to G^PD or NAD+ deficiency
There are two main categories - Alcoholic or non alcoholic fatty liver disease
Signs and symptoms of Fatty liver disease
Majority Asymptomatic Fatigue and malaise Right upper quadrant pain Advanced disease may present with cirrhotic symptoms such as jaundice and ascites Hepatomegally Splenomgally
Investigations for Fatty liver disease
Liver biopsy histopathology for diagnosis
LFT’s - show raised ALT in early disease (but normal in late). Also may be raised gamma GT if alcohol is the cause
Fasting lipids are often raised
Rule out other causes of hepatitis and liver failure by blood tests
Treatment of Fatty liver disease
Treat any alcoholism by abstaining and good healthy diet
Treat withdrawal symptoms (Chlordiazepoxide), stop cravings (Acamprosate) and cause unpleasant drinking effects (Disulfaram)
Lose weight
Insulin sensitisers may give some benefit e.g. Metformin
Consider stain therapy
What is Viral Hepatitis
Hepatitis caused by one of many different viruses including Cytomegalovirus. Epstein-Barr, Adenovirus, Herpes Simplex and Hepatitis ABCDE
When would you consider viral hepatitis more commonly
In patients at higher risk of getting a viral infection
Anyone who has pierced skin o IV Drug Abuse o Tattoos with non sterile needles o Body piercings o Needle stick injury o Shared razors/toothbrushes Hepatitis A has faecal-oral transmission, raw shellfish from polluted water can cause problems Sexual transmission Vertical Transmission Insect bites
Signs and Symptoms of Viral Hepatitis
Signs of hepatitis and cirrhosis
Diarrhoea with Hepatitis A
Investigations for Viral Hepatitis
Virology study on bloods when looking for cirrhosis and hepatitis
Treatment of Viral Hepatitis
Symptom control Interferon Alpha may work in early disease - Antiviral Agent Antivirals/Retrovirals o Ribvarin for Hep C o Entecovir or Tenofovir for Hep B
Causes of Pre Hepatic Jaundice
Haemolysis - Increased RBC breakdown
Gilbert’s Syndrome - Congenital cause of occasional raised bilirubin
Crigler-Najjar - Decreased conjugation due to enzyme defects
Causes of Hepatic Jaundice
Viral Hepatitis
Alcoholic Hepatitis
Drug induced - NSAID, Steroid, amiodarone, some antibiotics
Cirrhosis
Causes of post hepatic Jaundice
Gallstones
Biliary Strictures
Tumours/Malignancy
What are the different LFT results for different types of jaundice
Pre Hepatic
o Raised LDH and unconjugated bilirubin
o Low haemoglobin
o Normal AST, ALT, ALP
Hepatic
o Raised ALT, ALP and Bilirubin
o ALP>ALT
Post Hepatic
o Raised ALP, ALT and conjugated bilirubin
o ALP>ALT
What are the possible causes of a low Albumin level in LFT’s
Liver Disease Nephrotic Syndrome (lost in urine) Poor long term nutrition
How do you interpret ALT and AST blood results in LFT’s
Raised levels indicate liver hepatocyte damage
ALT is more specific to the live
AST is a general muscle damage marker - Check Creatinine Kinase to exclude this as a cause for a raised result
ALT>AST = Chronic Liver Disease
AST>ALT = Cirrhosis
AST:ALT>2 = Alcoholic Liver Disease
How do you interpret Gamma GT in LFT’s
Liver disease causes increased Gamma GT
Often more associated with bile duct disease
o Cholescytits and ascending cholangitis
o Gallstones
How do you interpret ALP in LFT’s
Alkaline Phosphatase is a marker of damage to the bile ducts
May be elevated in bone disease - check gamma GT as well to rule out this as the cause of raised ALP
How do you interpret prothrombin in LFT’s
The liver is the site of production for many clotting factors
Raised prothrombin time/high INR is a good indicator of liver disease
Obviously not useful if patient is on Warfarin/blood thinning drugs
Describe a Paracetamol Overdose
Paracetamol is very toxic to the liver when taken in high doses and can cause acute liver failure
A dose of >150mg/kg tends to have fatal effects
Normally the liver metabolises paracetamol to NAPQI and then on to inactive metabolites by glutathione. However in high paracetamol doses glutathione is depleted and so NAPQI levels rise, leading to hepatocellular damage.
What are the signs and symptoms of a paracetamol overdose
Asymptomatic for first 24 hours - May have non specific abdominal symptoms Hepatic necrosis begins at 24hrs Right upper quadrant pain Jaundice Encephalopathy Oliguria Hypoglycemia Renal failure Lactic acidosis
Investigations in paracetamol overdose
Paracetamol level - done >4hrs after overdose
o Will not work for a staggered overdose
o Results inaccurate <4hrs after taking
Blood Tests
o U&E, eGFR, Creatinine - Get baseline renal function and check for failure
o LFT’s - Generally raised specifically ALT
o Glucose - Hypoglycemia is common
o Clotting Screen - Prothrombin time is a good indicator of liver failure
o ABG - Acidosis
Treatment of Paracetamol Overdose
Activated Charcoal
o if <1hr since ingestion
N-Acetyl Cysteine - Basically use the treatment graph
o If paracetamol level is >100mg/l at 4hrs or >15mg/l at 10 hrs
o If patient has had no bloods after 8hrs
o Keep giving till paracetamol is under treatment level
If patient arrives after 24hrs, necrosis has already begun and so very hard to treat
What are Gallstones (Cholelithiasis)
Stones formed in the gallbladder of many patients, not always symptomatic. Stones can be cholesterol, pigment or mixed.
What are the risk factors for Gallstones
Fat - BMI>30 Female Fertile Fair - White Forty+
Increased cholesterol (excreted in bile) leads to increased bile formation, stasis occurs, and the bile becomes concentrated into crystals that form the stones.
Signs and symptoms of Gallstones
Biliary Colic - RUQ pain that comes in waves due to transient obstruction of cystic duct - Exacerbated b y foods (especially fatty foods) as this causes the bile duct to contract against the stone while trying to release bile.
Nausea and vomiting
Steatorhea - Lack of bile salts entering intestine
What is acute cholecystitis
Inflammation of the gall bladder due to stasis of bile and therefore infection. Inflammation may spread to the parietal peritoneum, leading to more generalised pain and peritonitis.
E.coli and Klebsiella most common infective organism
What are the signs of acute cholecystitis
Palpable Gall Bladder Positive Murphy's Sign Associated systemic response o Fever o Raised WCC o Nausea and Vomiting
What is ascending cholangitis
Infection and inflammation of the bile duct, ascending from a point of bile stasis (caused by stones, tumours, strictures, stenosis, parasites, ERCP damage etc) .
E.coli and Klebsiella most common infective organism
What are the symptoms and signs of ascending cholangitis
Charcots Triad - Jaundice, Fever, RUQ pain
Mental confusion
Septic Shock
What are the Diagnostic Criteria of ascending cholangitis
Diagnostic Criteria - 1 of each letter
A: Signs of systemic infection
o Fever/Shaking/Chills
o Evidence of inflammatory response - Raised CRP
B: Signs of Cholestasis
o Jaundice
o Abnormal LFT
C: Evidence on imaging
o Biliary Dilation
o Evidence of causative factor - stone, stricture, stenosis etc
Investigations for ascending cholangitis
Raised Bilirubin
Raised CRP/ESR (erythrocyte sedimentation rate) and Leukocyte levels (WCC)
Abnormal LFT’s - increased ALP, AST, ALT and Gamma GT
Imaging to show biliary dilation
Differential diagnosis for gallstones
Acute pancreatitis Appendicitis Bile duct strictures and tumours Pancreatic and hepatic tumours Courvoisers Law - In the presence of jaundice, a palpable, non tender gall bladder is unlikely to be gallstones
Investigations for Gallstones
Bloods
o FBC - Check for raised WCC
o U&E, LFT and amylase -To rule out other differentials and gallstones can block the pancreatic and hepatic ducts leading to damage - raise ALP is common and does not necessarily indicate obstruction
o Blood cultures in cases of fever
o Send of any already taken bile drains for culture
Ultrasound scan - Very sensitive and specific
o View any cholestasis and see some causative factors
o Allows evaluation of common bile and intrahepatic duct dilation
MRCP - Shows static fluid and therefore cholecystitis, cholangitis and choledocholithiasis
Treatment of Gallstones
Analgesia
ECRP - Visualise and remove stones
Cholecystectomy - Without removal likely to return
Treatment of cholangitis and choledocholithiasis after normal Gallstone treatment
IV antibiotics - Co-amoxiclav for cholecystitis and cholangitis
Endoscopic Biliary Drainage for cholestasis #May require resuscitation if Septic
What are the local complications of Gallstones
Mucocele (cyst) - Failure to relive cystic duct obstruction leads to formation and may lead to necrosis if untreated (leading to perforation, peritonitis, sepsis and death)
Empyema - Similar to mucocele but with a systemic response as infected
Fistula Formation - May fistula between duodenum or colon - this may progress to gallstone ileus if a large stone enters lumen of either
Mirrizi syndrome - Compression of common bile duct by large stone in Hartman’s pouch ( junction of the neck of the gallbladder and the cystic duct) - leads to obstructive jaundice
What are the more distal complications of Gallstones
Choledochlithiasis - Stone lodged in common bile duct - can lead to cholecystitis, obstructive jaundice, or cholangitis.
Pancreatitis - Deranged LFT’s and raised serum amylase (3x upper limit diagnostic)
How do you differentiate between Gall stones, Cholecystitis and Cholangitis
Gall Stones - RUQ pain
Cholecystitis - RUQ pain, Fever and Leucocytosis
Cholangitis - RUQ pain, Fever and Leucocytosis and Jaundice +/- septic shock and confusion
What are the causes of acute pancreatitis
GET SMASHED
Gallstones Ethanol Trauma Steroids Mumps and Malignancy Autoimmune Scorpion bite Hyperlipidaemia, Hypercalcaemia, Haemochromatosis ERCP Drugs - Thiazides, Valproate, Azathioprine, Corticosteroids
Signs and symptoms of Pancreatitis
Left upper quadrant pain/Epigastric pain radiating to the back
Nausea and vomiting
Fever, tachycardia and malaise
Jaundice may be present depending on cause (gallstones, malignancy or alcohol related)
Paralytic Ileus may develop
What is a scoring system used for Pancreatitis Prognosis
Glasgow Criteria - PANCREAS
1 point for each, scores >2 mean severe pancreatitis
PO2 <8kpa Age > 55yrs Neutrophil count >15x10^9cells/l Calcium <2mmol/L Renal - Serum urea nitrogen >16mmol/L Enzymes - Serum Lactate dehydrogenase >600 or AST/ALT>200 Albumin <32g/l Sugar - Blood Glucose >mmol/l
Acute Pancreatitis Investigations
Serum Amylase - 3x diagnostic
Serum Lipase - Better than amylase in late presentation as amylase has short half life
FBC, U&E, Glucose, CRP, LFT’s, ABG - Used to assess prognosis - Raise ALT suggestive of gallstone cause, Hypocalcaemia is common
Plain Abd Xray to exclude other causes
CT scan - Diagnostic
Ultrasound - Swelling, dilation of common bile duct indicates gallstone cause
Treatment of acute appendicitis
Mild cases
o Pain relief - Opiate>NSAID as NSAID can cause damage
o NBM and IV fluids
o Nasogastric tube/Anti Emetics for severe vomiting
Antibiotics for specific infection
Cather to monitor urine output
Correct electrolyte imbalances
o Hourly Obs - BP, urine output, RR, Blood sugar - EWS scoring
o Alcohol withdrawal prophylaxis - Patients may have lied
o Treat cause
Severe Pancreatitis
o IV antibiotics for pancreatic necrosis
o Enteral Nutrition bypassing the duodenum to avoid pancreas
o ERCP for removal of any stones/obstructive causes
o Surgical debriment in infection/necrosis
o Drain any pancreatic abscesses
What is chronic Pancreatitis
Pancreatitis as a result of chronic inflammation of the pancreas leading to irreversible damage.
Causes of Chronic Pancreatitis
Chronic blockage of the outflow tract - leads to damage to the pancreas by its own enzymes
Alcohol - can lead to protein precipitation in the pancreas, leading to damage, plus direct damage if alcohol
Hereditary/familial
Autoimmune disease
Signs and symptoms of chronic pancreatitis
Severe abdominal pain - Epigastric radiating to back
Nausea and vomiting
Reduced appetite
Exocrine dysfunction - malabsorption wit weight loss, diarrhoea, steatorrhea, and protein deficiency
Endocrine dysfunction - diabetes in 30% patients (fatigued, polyuria, polydipsia, glycosuria on urine dip)
Differential diagnosis for chronic pancreatitis
Cholecystitis or Cholelithiasis Peptic ulcer Acute Hepatitis Abdominal Aortic Aneurysm Pyelonephritis Acute Pancreatitis MI Pneumonia
Investigations for chronic pancreatitis
Blood Tests - FBC, U&E, Creatinine, LFT’s, Calcium, Amylase (normally normal in chronic, glucose, HBA1C
Secretin Stimulation test - Give secretin IV and monitor fluids passed into the duodenum via NasoDuodenal tube - NBM 12hrs before, and a 60% reduction in pancreatic exocrine function if positive
Imaging - Ultrasound first line, CT and Abdominal X-ray to show calcification, ERCP and MRCP for stones
Pancreatic biopsy - Can confirm inflammation and fibrosis but high risk
Reduced faecal elastase levels show pancreatic endocrine insufficiency
Treatment for Chronic Pancreatitis
Analgesia - Opiates>NSAIDS as NSAIDS can cause damage
Assess alcohol intake and counsel patient
Psychiatric evaluation for depression if heavy drinker
Treat any malabsorption by replacing pancreatic enzymes with CREON supplements
Appropriate diabetic control
Surgery
o Pancreatic duct stenting in stricture
o Resection to remove abnormal/damaged parts of pancreas
Whipple’s Procedure (Pancreatoduodectomy) for head involvement
Distal pancreatectomy if tail involvement
Total pancreatectomy if entire pancreas diseased
What is Ulcerative Colitis
An inflammatory disorder of the large intestine (including rectum and anus) affecting the mucosa. The disease is continuous throughout the colonic mucosa and will never extend passed the ileocaecal valve, except in the case of a backwash ileitis where i can spread backwards.
The disease goes through stages of relapse and remission, and is thought to be of immune origin, triggered by colonic bacteria so most treatments involve immunosuppresion
Signs and symptoms of Ulcerative Colitis
Diarrhoea - Many times per day, associated with urgency and tenesmus, often blood and mucous in the stool.
If the disease is limited to the rectum and anus then you may have constipation and rectal bleeding instead
Systemically unwell - Fever, malaise, weight loss, anorexia etc
Tender, distended abdomen
Tachycardia
Dehydrated
Anaemia
Extra-intestinal Symptoms Joint pain Mouth ulcers Clubbing Erythema nodosum - inflammation of fat cells under skin (commonly in shin) Pyoderma Gangrenousum - necrotic ulcer (often on legs) Fatty liver Primary Sclerosing Cholangitis Amyloidosis Conjunctivitis/Iritis and episcleritis
Differential Diagnosis for Ulcerative Colitis
Crohns - Biopsy to differentiate Prolonged use of laxatives Infective colitis - Schistosomiasis, amoebiasis, tuberculosis C.Diff Irritable bowel syndrome - Mild colitis can mimic IBS Diverticulitis Colorectal Cancer Polyposis syndrome and colonic polyps Ischaemic and radiation colitis
Investigations for Ulcerative Colitis
Bloods
o FBC - Looking for anaemia due to bleeding and looking for inflammation with raised WCC
o CRP/ESR - Check for inflammation
o U&E + eGFR - Check kidney function and electrolytes as patient may be malnourished or dehydrated
o LFT’s
o Blood and stool cultures - Rule out pseudo membranous colitis (C.Diff)
Faecal Calprotectin can help detect colonic inflammation - substance released in colonic inflammation
Stool Microscopy, culture, and sensitivities to exclude any infective cause of diarrhoea e.g. E.coli, Camplyobacter, Shigella, C.Diff, salmonella
Abdominal X-ray - Look for faecal shadows, mucosal thickening, colonic dilation or for perforation
Barium enema - Shows ulceration and loss of haustra pattern
Colonoscopy or flexible sigmoidoscopy - Shows extent of disease and allows for biopsy (also looks for inflammation, ulceration, crypt abscess)
Complications of Ulcerative Colitis
Perforation and bleeding - sepsis and death
Toxic Mega colon - Toxic dilation of colon (mucosal islands and colonic diameter >6cm on xray)
Venous thrombosis (unknown cause) - Prophylactic Dalteparin
Increased risk of colon cancer
Medical Treatment of Ulcerative Colitis
Mild
o 5-ASA preparations - such as sulfasalazine or mesalazine
o Oral or topical steroid (prednisalone) to induce remission
o Possible oral tacrolimmus to induce remission
Moderate
o Same as mild
o Increase steroid dose (Prednisalone)
o 2x daily steroid enemas
Severe - In hospital o NBM with IV Hydration o IV steroids (hydrocortisone) o Rectal steroids o If still not improving consider Colectomy or Rescue therapy (ciclosporin/infliximab)
Maintaining remission
o 5-ASA preparation such as mesalazine and sulfasalazine will reduce relapse rate
What are the common surgical treatments for Ulcerative Colitis
Colectomy - Curative treatment
Restorative Proctolectomy with ileal pouch-anal anastamosis is the usual common procedure
What is Crohns disease?
Chronic inflammation of the bowel, including large and small intestine. It can be found anywhere in the bowels, from mouth to anus, and is not always continuos in nature. It goes through stages of remission and relapse.
Some infectious agents have been implicated, though it is thought to be autoimmune and triggered by bacteria
Signs and Symptoms of Crohns Disease
Diarrhoea - With blood, urgency and tenesmus, patient may wake up night needing to empty bowels (not seen in UC)
Patients may have constipation if proctitis
Systemic symptoms - fever, malaise, night sweats, anorexia and weight loss
Abdominal Pain and tenderness
Vomitting
Mouth Ulcers
Anal and Perianal lesions - Abscess, skin tags and fistulae
Extra GI symptoms
Clubbing
Erythema nodosum and pyoderma gangrenosum
Conjunctivitis, episcleritis and iritis
Large joint arthritis, sacroilitis, ankylosing spondylitis
Fatty liver disease, primary sclerosing colangitis and cholangiocarcinoma
Granulomata in many organs
Renal Stones
Osteomalacia
Amyloidosis
Differential Diagnosis of Crohns Disease
Ulcerative Colitis - differentiated by possibility of inflammation in area’s other than the large intestine and on biopsy
Tuberculosis
Gastroenteritis
Bowel Carcinoma
Diverticulitis
Mild cases may be mistaken for Irritable bowel syndrome
Ischaemic, radiation or drug induced colitis
Investigations for Crohns Disease
Bloods
o FBC - To check for anaemia, and white cells for inflammation
o CRP - To check for inflammation
o U&Es - Kidney Function (To check for dehydration) and to check for any mineral deficiency (as malnourishment is likely)
o LFT’s
o Blood cultures to rule out infective causes
Stool culture and Faecal calpotetctin
Colonsocpopy to assess areas affected and take biopsies
MRI can help to assess pelvic disease
How is Crohns Disease Staged
The Crohns Disease Activity Index (CDAI)
Complications of Crohns Disease
Small Bowel Obstruction Toxic Dilation of colon - rarer than in UC Abscess formation Fistulae - Colovesical, Colovaginal, Perianal, Enterocutaneous Perforated bowel - Leading to peritonitis Rectal Haemorrhage Colon Cancer Fatty Liver Disease Primary Sclerosing Cholangitis Cholangiocarcinoma Renal Stones Osteomalacia Malnutrition Amyloidosis
Medical Treatment of Crohns Disease
Smoking Cessation
Induce Remission
o Prednisalone in mild attacks
o Mesalazine (Can be used as enema if left sided colonic Crohns)
o IV corticosteroids - Budesonide for Crohns in terminal ileum and ascending colon, Hydrocortisone for rectal Crohns
o Azathioprine used as steroid sparing agent, but takes 6-8 weeks - so often used in combination with steroids
o Methotrexate
o Infliximab and anti-TNFa
Maintenance of Remission
o 5-ASA preparations such as sulfasalazine
o Antibiotics (e.g. Rifaximin) used to prevent infections in abscesses and fistulae
o Corticosteroids can be used in place of 5-ASA if ineffective
Difference in smoking between Crohns and Ulcerative Colitis
Smoking is a risk factor for Crohns
Smoking is preventive in UC (UC = Use cigarettes)
Difference in area of effect between Crohns and Ulcerative Colitis
Crohns can affect entire GI tract and is non-continuos (skip lesions)
Ulcerative Colitis can only affects the colon and is continuous
Difference in appearance between Crohns and Ulcerative Colitis
In ulcerative colitis the mucous lining of the colon may have ulcers , but they do not extend below the inner lining.
In Crohns the colon wall may be thickened and will have a cobblestone appearance. Ulcers are deep and extend into all layers of the bowel - transmural lesions
Difference in symptoms between Crohns and Ulcerative Colitis
In Ulcerative colitis patients are less likely to wake in the night to empty bowels, and blood. and mucus in the stools are much more likely
In Crohns patients are more likely to vomit, they are also more likely to develop anal fistulae, skin tags and abscesses. Crohns is more likely to develop granulomas.
What is Pseudomembranous Colitis
An infection with Clostridium Difficile normally following removal of any other bacteria by antibiotic therapy
What are the main causes of Clostridium Difficile infection?
The 4 C’s
Co-amoxiclax
Clindamycin
Cephalosporin - Ceftriaxone, Cefotaxime
Ciprofloxacin
Signs and Symptoms of Clostridium Difficile infection
Tends to be after antibiotic therapy More common in older patients Water Diarrhoea - 3+ stools within 24 hours and may contain mucous or blood Lower abdominal pain and cramping Low grade fever Nausea Anorexia Dehydration
What are the differential diagnosis for Clostridium Difficile infection (Pseudomembranous Colitis)
Crohns and Ulcerative Colitis Ischaemic Colitis Other infections o Gastroenteritis o Camplylobacter o Salmonella o Shigella o Cholera o Amoebiasis
Investigations for Clostridium Difficile infection
Bloods
o FBC - Check for an elevated WCC and to check for CRP (as better marker in elderly patients)
o LFTs - Hypoalbuminemia may be present
Stool Sample/Culture - Look for C.Diff cytotoxin and can check faecal calpotetctin for UC and Crohns
Sigmoidoscopy or Colonsocpopy with biopsy can confirm a diagnosis however fairly invasive so not normally performed
Plain X-Rays to look for Toxic Megacolon (Septic) - Thumb printing and loss of Haustra/Valvulae seen as precursors
Treatment of Pseudomembranous Colitis
Isolate the patient and practice barrier nursing - Very infective spores
Fluid resuscitation with an IV crystalloid
Stop the causative antibiotics if possible - in 20% of patients this alone is curative, and if not possible to stop, replace with an alternative
Use metronidazole or Vancomycin to treat the C.Diff infection
Surgery to treat patients with toxic Megacolon or acute severe colitis (Basically if patient is septic)
What is a toxic Megacolon
Colonic dilation and distension, commonly caused by inflammatory bowel disease (More commonly Ulcerative Colitis) and some infections of the colon e.g. Clostridium Difficile
Signs and Symptoms of a Toxic Megacolon
Abdominal pain and tenderness on palpation Distension of the abdomen Fever Tachycardia Dehydration Septic Shock Bowie Perforation Sepsis
Investigations for a Toxic Megacolon
X-Ray to show dilation of the bowel due to Megacolon - >6cm is diagnostic
Treatment for Toxic Megacolon
Fluid Replacement and broad spectrum Antibiotics IV to treat any sepsis
IV Hydrocortisone to reduce inflammation
Decompress the bowel using long nasogastric tube to receive pressure
NBM
Subtotal colectomy if decompression is not possible within 2-3 days
What is Irritable Bowel Syndrome
A Bowel disorder with no known cause, leading to abdominal discomfort and GI symptoms. It is thought to be a disorder in smooth muscle activity and visceral hypersensitivity.
Signs and symptoms of Irritable Bowel Syndrome
Boating and Distension
Abdominal Pain or discomfort - May be relieved by defecating, and may have tender abdomen on examination
Changes in bowel habit - Straining, tenesmus, urgency, and patient may have constipation, diarrhoea or a mix of the two
Symptoms tend to be worse on eating
Patients may have mucus in their stool
Generalised symptoms - lethargy, nausea, heartburn, dysphagia, backache and bladder symptoms
Relapses commonly in times of stress
Differential Diagnosis of Irritable Bowel Syndrome
Colon Cancer
Inflammatory bowel disease - UC and Crohns
Coeliac disease
Gastroenteritis
Diverticular disease
Gynaecological problems with abdominal pain - Ovarian Torsion, Ovarian Cancer (Bloating and altered bowel habit) and endometriosis (cyclical pain on defecation and urination)
Investigations for Irritable Bowel Syndrome
Bloods
o FBC and CRP
o Coeliac Screen
o CA-125 in women if symptoms could be due to ovarian cancer
Faecal calprotectin to rule out IBD
Can use radiology and Colonsocpopy/Flexible sigmoidoscopy in order to confirm there is no other diagnosis
Treatment of Irritable Bowel Syndrome
Lifestyle Factors
o Healthy Diet
o Fibre, lactose, fructose, wheat, starch, caffeine, sorbitol, alcohol and fizzy drinks may make it worse
o Low fibre diet can cause other problems, so try water soluble fibre rather than more solid fibre types.
o Drink lots of fluid
Drug Therapy
o Laxatives and bulking agents - Ispaghula, Bisacodyl and sodium picosulfate to treat constipation and Loperamide to treat diarrhoea
o Antispasmodics may help with abdominal pain/discomfort - Mebeverine, alverine citrate, sometime, buscapon
Cognitive Behavioural Therapy may help if the symptoms gets worse with stress
What is Coeliac Disease
An adverse reaction to gluten leading to a range of symptoms and poor absorption in the intestines
What are the signs and symptoms of Coeliac Disease
Diarrhoea with steatorrhoea Bloating and flatulence Nausea and Vomitting Abdominal pain Weight loss Feeling tired all the time (Due to malnutrition and thus anaemia - so get signs of anaemia) Failure to thrive in children
What are the differential diagnosis for Coeliac Disease
Irritable Bowel Syndrome
Lactose Intolerance
Inflammatory bowel disease
General Malabsorption
Investigations for Coeliac Disease
Blood tests for auto-antibodies (Tissue transglutaminase, endomyseal and anti-casein antibodies) - Give gluten diet for a week before test is taken
Gene testing - HLA-DQ2 and HLA-DQ8
Biopsy of Jejenum as confirmation (While on gluten diet) - Will show subtotal villous atrophy compensated by crypt hyperplasia and lamina propria infiltration with lymphocytes and an increase in intraepithelial lymphocytes)
FBC - To check for Anaemia
Treatment for Coeliac Disease
Eat a gluten free diet
Remove Wheat, rye, barley and possibly oats should be cut
What is Diverticular Disease
Diverticulum form - Outpouchings forming in the gut wall (congenital or acquired). These can occur anywhere in the gut, but are most common in the ascending, descending and sigmoid colon.
These outpouchings can act like mini appendicitis’s and become inflamed (diverticulitis)
Signs and Symptoms of Diverticular Disease
Most often asymptomatic (unless patient develops diverticulitis) and thus found on screening for other conditions e.g. colon cancer
Lower left quadrant pain if diverticulae are on the left side of the colon (most common) and right lower quadrant pain if they are on the right hand side (more common in Asians) - Colic type pain relieved by defecation of flatulence.
Fever and tachycardia
Anorexia
Nausea and Vomiting
Localised tenderness possibly with mass on palpation
PR Bleeding (fresh blood on stools)
Complications of Diverticulitis
Strictures - will cause an obstruction
Abscesses - can cause peritonitis and sepsis
Fistulae - can cause infection elsewhere in the body and will likely cause problems for the patient
Haemorrhage is common in the lower GI tract (colon) – patient usually has abrupt, painless bleeding, often with the urge to defaecate beforehand
Differential diagnosis for Diverticular disease
Other causes of acute abdominal pain, including acute appendicitis
Irritable bowel syndrome
Inflammatory bowel disease – Crohn’s disease, ulcerative colitis
Colorectal cancer
Other forms of colitis – ischaemic, pseudomembranous, amoebic
Investigations for Diverticular disease
Barium enema can be used to confirm diagnosis, rather than go all invasive with a colonoscopy
Colnoscopy is usually the best way to look for diverticulae
CT abdomen (CT colonoscopy) is best in the acute setting as a colonoscopy or enema may perforate the bowel - Can also be used to find out where a fistula leads to
Treatment of Diverticular disease
Patient should be advised to eat more fibre in future, as a low fibre diet is thought to be the cause of diverticulum formation
Mild attacks can be treated with a fluid diet and antibiotics
Analgesia and NBM may be necessary if patients can’t tolerate liquids
IV antibiotics and fluids
Surgery may be necessary for abscesses and for diverticulitis
Resection of affected area of colon
What is Appendicitis
Inflammation of an out pouching of the ascending colon, leading to epigastric pain
Usually caused by obstruction, such as a faecolith which leads to obstruction thus stasis and bacterial colonisation. Causing infection and inflammation
If the appendix ruptures it can lead to life threatening peritonitis
Signs and symptoms of Appendicitis
Acute, severe abdominal pain - Early periumbilical pain which moves over a period of hours/days towards the right iliac fossa. This pain wakes patient up and is aggravated by movement, deep breathing and coughing
Tender to the touch in right iliac fossa
Nausea, vomiting and anorexia
Fever
May have diarrhoea
Tachycardia indicates peritonitis
Palpation of left lower quadrant may increase pain in the right lower quadrant (Rovsing’s sign)
Extend hip and abduct thigh with patient on left side, if this causes pain then it indicates appendicitis (psoas sign)
Appendicitis can present in many atypical ways. In what ways can this occur?
Appendix may be abnormally positioned – Pain may therefore be located on the left rather than on the right, may be generalised or may be back pain.
Also children may have abdominal pain that is milder than expected, they may not want to eat
When should appendicitis be considered as a differential diagnosis?
All instances of acute abdominal pain
Differential diagnosis for appendicitis
GI obstruction Constipation Diverticulitis Strangulated hernia Crohn's or Ulcerative Colitis Cholecystitis Peptic ulcer Gastroenteritis Pancreatitis Testicular torsion Renal calculi UTI Ectopic pregnancy – always pregnancy test in fertile women Ovarian cyst – rupture or torsion Pelvic inflammatory disease
Investigations for appendicitis
Normally a clinical diagnosis
Urinalysis – exclude UTI or stone
Pregnancy test – exclude ectopic pregnancy
Bloods
Full blood count – may show leukocytosis, exclude bleed if no anaemia
CRP – marker for inflammation
Laparoscopic investigation and treatment tends to be the first line of investigation in suspected appendicitis
Ultrasound may aid diagnosis however CT scanning is better
X-ray can show if there has been any perforation of the peritoneum
Treatment for appendicitis
Laparoscopic appendicectomy - with Pre-operative antibiotics to reduce risk of infection
What is Peritonitis
Inflammation of the peritoneum, can be primary or secondary
Primary peritonitis is inflammation of the peritoneum itself – bacterial infection from intraperitoneal dialysis is an example
Secondary peritonitis occurs due to inflammation of an organ adjacent to the peritoneum – perforation of the viscera can cause secondary peritonitis
Signs and symptoms of Peritonitis
Abdominal pain - May be localised or widespread dependent on whether it is a local or general peritonitis
Nausea and vomiting
Anorexia
Fever
Tenderness on palpation, guarding, rigidity and rebound tenderness - Maximum tenderness over the area of pathology
Bowel sounds might be absent
Differential diagnosis for Peritonitis
Neoplasms Perforation of the viscera Splenosis Peritoneal cysts Other causes of acute abdominal pain e.g. Appendiciti or Diverticulitis Abdominal aortic aneurysm Ectopic pregnancy Inflammation of other abdominal viscera - e.g. Pancreatitis, Pyelonephritis or Hepatitis
Investigations for Peritonitis
Bloods
o FBC – leukocytosis, white blood cells
o CRP
o Liver function tests – ALP, AST, ALT, amylase and lipase, rule out pancreatitis or hepatitis causing peritoneal inflammation
o U+Es – Rule out kidney inflammation as the cause of peritonitis
Peritoneal fluid – culture and get amylase level
Urinalysis to exclude renal pathology
May want to do imaging studies – look for any areas of intestinal perforation or air under diaphragm
Pregnancy test to rule out ectopic pregnancy
Treatment of Peritonitis
IV antibiotics – broad spectrum (cefotaxime) or a combination of two are normally used
May want to drain ascites if present
Monitor and protect renal function
Surgery to close any perforations
Treat any cause of secondary peritonitis
Antibiotic treatment
Removal of inflamed appendix, diverticula, etc.
What are the causes/risk factors for Hepatic cancer
Hepatocellular carcinoma most often caused by chronic liver disease o Hepatitis B and C viruses o Alcoholic liver disease and cirrhosis o Haemochromatosis o Primary biliary cirrhosis o Alpha-1-antitrypsin deficiency Diabetes Smoking Steroids
Signs and symptoms of Hepatic cancer
Right upper quadrant pain Pruritis (itching) and jaundice Hepatomegaly and splenomegaly Oesophageal and anorectal varices Spider naevi and caput medusae Abdominal distension – ascites Confusion – hepatic encephalopathy Weight loss
Who is screening for Hepatic cancer
Those at high risk should be offered surveillance
Cirrhotic patients
Hep B, Alcohol related or Hep C cirrhosis
Patients with high Hepatitis B virus concentration
How do you screen for Hepatic cancer
Ultrasonography at 6-12 monthly intervals
Alphafetoprotein testing – high levels may be indicative of carcinoma, >400ng/mL may be regarded as diagnostic
Investigations for Hepatic cancer
Ultrasound scan for focal lesions (>2cm) with raised Alpha-Fetoprotein is diagnostic
CT chest, abdo, pelvis for local spread or for evidence of primary cancers in case hepatocellular cancer is a secondary metastasis (which is fairly common)
Fine needle aspiration or biopsy can be used in unclear diagnosis
LFTs will be consistent with cirrhosis, clotting may be deranged
Differential diagnosis for Hepatic cancer
Secondary metastasis to liver (30x more common than primary hepatocellular carcinoma) - Likely from colon, breast, pancreas, stomach, lung, ovary or melanoma
Cirrhosis and its causes
Lymphoma of liver
Treatment of Hepatic cancer
Treat complications of cirrhosis/liver failure
Surgical resection – more viable in patients without cirrhosis
Transplantation
Ablation in early stage cancer
Chemotherapy direct to tumour via hepatic artery
Investigate for primary tumour
What is the main type of Pancreatic Cancer
Exocrine tumours (infiltrating ductal adenocarcinoma) make up ~90% of pancreatic cancer
What are the Risk factors for Pancreatic Cancer
Smoking
High BMI
Low fruit and veg intake
Diabetes
High alcohol intake
Chronic pancreatitis gives a 5-15x increased risk - Hereditary pancreatitis gives an up to 70x increased risk
Family history of pancreatic cancer, as well as known BRCA1 or BRCA2 mutations (breast cancer oncogenes)
FAP/gardner’s syndrome and peutz-jegher in family are risk factors
Multiple endocrine neoplasia type 1 is a risk factor, especially for insuloma development
History of IBD and peptic ulcer disease
Signs and symptoms of Pancreatic Cancer
Early symptoms are very non-specific
o Epigastric pain and dull backache - Often worse lying down and eased by sitting forward, however pain may be felt solely as a dull back-ache
o Painless, progressive, obstructive jaundice – RED FLAG
o Pale stools (lack of bilirubin), dark urine (high bilirubin) and pruritis – due to conjugated bilirubin in urine (and not being present in stool)
o Courvoisier’s sign – palpable, non-tender gall bladder with painless jaundice is very unlikely to be gallstone pathology
o Patients may develop an acute pancreatitis thus showing signs (Fever, nausea, vomiting, epigastric pain, etc.)
o Unexplained weight loss and anorexia
o Steatorrhoea due to malabsorption – lack of pancreatic enzymes
o Patients may have constipation, nausea and vomiting due to obstruction at the duodenum - More likely to be constipated due to lack of pancreatic enzymes leading to sticky stool and thus distal intestinal obstruction syndrome (DIOS)
In late disease, an epigastric mass will be palpable,
Virchow’s node may also be palpable (troisier’s sign)
Palpable gall bladder (see courvoisier’s law/sign)
Paraneoplastic signs/symptoms such as thrombotic events and hypercalcaemia
Differential diagnosis of Pancreatic Cancer
Abdominal pain
o Gallstones (but remember courvoisier’s non-tender gall bladder)
o Peptic ulcers – will be exacerbated by feeding
o Gastric or colorectal cancers – haemoptysis and melaena likely
o Oesophagitis, gastritis
o Hepatitis
o Liver abscess
o Liver tumours
o Chest pathology – pneumonia or PE – would have dyspnoea
o Abdominal aortic aneurysm (also radiates to back)
Obstructive jaundice
o Bile duct stricture – will tend to follow previous pathology, eg. gallstones
o Gallstones – only if lodged in the common bile duct
o Ascending cholangitis
o Pancreatitis
o Cancer of gallbladder
Investigations for Pancreatic Cancer
Blood tests
o Full blood count for anaemia and thrombocytosis – to rule out haemolytic anaemia as jaundice cause
o LFTs to confirm jaundice and look for potential cause - ALT/AST up in liver pathology or ALP and Gamma-GT up in bile duct pathology
o Tumour markers if we suspect cancer - CA19-9 for pancreatic cancer, CEA for colorectal cancer, Alpha-fetoprotein for hepatocellular carcinoma
o Ultrasound of the abdomen
o ERCP may aid in biopsy
o High resolution/helical CT with contrast chest, abdo, pelvis for staging
o Remember to take U+Es to check renal function is OK before administering contrast
Treatment for Pancreatic Cancer
Surgical resection of tumour and regional lymph nodes in low stage cancer (only 10-20% suitable for resection)
o Whipple’s procedure – proximal pancreaticoduodenectomy, with (modified Whipple’s) or without pylorus preservation
o Distal pancreatectomy for tumours of body and tail
Adjuvant chemotherapy commonly recommended following surgery
Palliative care for non-resectable disease - Stenting of any ducts blocked by the cancer, however surgical bypass may be needed in severe obstruction
Palliative chemotherapy and radiotherapy
Pain management – opiates or coeliac plexus nerve block for severe cases
Creon supplements to treat malabsorption
Antiemetics for nausea and vomiting
What are the main types of Oesophageal cancer
Most commonly squamous cell or adenocarcinoma
Risk factors for Oesophageal cancer
Tobacco and alcohol increase risk
Barrett’s oesophagus (and GORD before it) is likely to progress to adenocarcinoma
Achalasia is a risk factor for squamous cell carcinoma
Chronic inflammation – oesophagitis
Family history of oesophageal cancer
Family history of hiatus hernia also shows correlation with increased risk
Signs and symptoms of Oesophageal cancer
Think ALARMS Anaemia Loss of weight Anorexia Rapid onset/progression Melaena/haematemesis Swallowing difficulty – dysphagia (difficult swallowing), odynophagia (painful swallowing)
+++
Hoarseness
Retrosternal or epigastric pain
Intractable hiccups
Lymphadenopathy
Differential diagnosis of Oesophageal cancer
Oesophageal stricture
Compression of oesophagus from external (extramural) source – lung/bronchial carcinoma, aortic aneurysm, lymph gland enlargement
Achalasia – oesophageal muscles unable to relax leads to blockage
Gastric cancer
Investigations for Oesophageal cancer
Bloods
o Full blood count – look for anaemia, iron deficiency especially (hypochromic, microcytic)
o U+Es, eGFR and LFTs for metastatic disease
o CRP for inflammation – oesophagitis or Crohn’s disease could be cause of haematemesis
Urgent endoscopy in patients >55years old with dyspepsia or those with ALARMS symptoms
Barium swallow may be more viable in high risk patients
Chest X-ray or chest, abdo, pelvis staging CT to look for metastatic disease
PET scan can help
Endoscopic ultrasound can increase accuracy of staging
Treatment of Oesophageal cancer
Endoscopic mucosal resection and submucosal dissection
Photodynamic therapy or laser treatment via endoscope
Oesophagectomy (Ivor Lewis procedure) for advanced cancer - Will remove lymph nodes and maybe even part of the stomach, then affected oesophagus is removed and stomach is moved up through diaphragm to allow for anastamosis with proximal oesophagus
Abdominal lymphadenectomy may be beneficial
Pre-operative chemoradiotherapy may be beneficial in adenocarcinoma
Palliative care in late stage disease
o Radiotherapy and chemotherapy or ablation to reduce tumour bulk and bleeding
o Stenting to assist swallowing
o Pain relief
Risk factors for Gastric cancer
Increasing age
Male gender
Low socio-economic status
H. pylori infection can double the risk of gastric cancer
A history of ulceration is likely to increase the risk
Diet – diets with low fruit and veg intake or high levels of salt or preserved food intake
Smoking
Gastritis
Family history
Hypogammaglobulinaemia
Signs and symptoms of Gastric cancer
Often patients only have symptoms of uncomplicated dyspepsia (indigestion)
ALARMS likely to only occur in late disease
Anaemia
Loss of weight
Anorexia
Rapid onset/progression
Melaena/haematemesis
Swallowing difficulty – dysphagia (difficult swallowing), odynophagia (painful swallowing)
In Late DIsease o Epigastric mass o Hepatomegaly o Jaundice o Ascites o Enlarged Virchow's node (Troisier's sign)
Differential diagnosis for Gastric cancer
GORD
Peptic ulceration
Acute gastritis
Gastroenteritis
Investigations for Gastric cancer
Urgent endoscopy referral within 2 weeks if ALARMS symptoms or 55+ with dyspepsia
Full blood count for anaemia and LFTs for possible liver mets
Endoscopy and biopsy of the stomach and possibly the duodenum
Staging CT of chest and abdomen or PET scan
Treatment of Gastric cancer
Treat pain, nausea and vomiting
Surgical resection of stomach – more useful in palliative care
Total gastrectomy may be necessary
Lymphadenectomy often necessary
Palliative care
o Remove obstruction through chemo/radio-therapy or resection
o Manage pain
o Subtotal gastrectomy or gastroduodenectomy may be relevant
o Endoscopic laser therapy may be of some use
What are the symptoms of Colon Cancer
Vague ill health and weight loss Acute or chronic obstruction of the intestine – patient not passing faeces or flatus Perforation and peritonitis Bleeding Anaemia Tenesmus (feel of incomplete voiding)
What are the symptoms of rectal cancer
Bleeding Change in bowel habit Urgency Incomplete evacuation Wet wind Tenesmus Colic Sacral root pain
What are the differences between right and left sided Colorectal cancer
Right sided cancer
Less likely to be obstructive in nature due to the faeces in that part of the colon being more liquid
Blood in the stools is less likely to be fresh and is more often mixed in with the faeces
Faecal occult blood screen will pick it up
Often painless
Left sided cancer
Bowel obstruction common, tenesmus and change in bowel habit likely
Bleeds are more likely to coat the stool rather than being mixed with it
Colicky pain common
Examination for Colorectal cancer
Feel for abdominal masses
PR/DRE to feel for a mass
Inspect finger for any blood after exiting anus
Investigations for Colorectal cancer
Chest/abdominal x-ray to look for:
o Gas build-up in intestine due to obstruction, proximal to the obstruction
o Gas under diaphragm, suggesting perforation
CT colonography
Bloods – FBC for anaemia, LFTs to check for metastatic liver damage - Colon cancer likely to metastasise to liver and lungs
Endoscopy/Colonoscopy/Flexible Sigmoidoscopy and biopsy
Liver ultrasound and CT or MRI are useful in staging
Chest/Abdo/Pelvis staging CT to look for colonic cancer as well as liver and lung mets
How does Colorectal cancer spread
Direct, through bowel wall
Lymphatic, based on stage
Blood stream – to liver via hepatic portal vein
What staging system is used for Colorectal cancer
Dukes classification
What is Dukes classification/staging of Colorectal cancer
A = confined to muscle (94% 5 year survival)
B = through muscle (76% 5 year survival) C = into lymph nodes (32% 5 year survival)
C1 is into the lymph nodes, but the highest (apical node) is not involved
C2 is into the lymph nodes, with involvement of the apical node
D = distant metastases (liver and lungs likely, 6.6% 5 year survival)
Treatment of Colorectal cancer
Surgery
Right hemicolectomy for right sided cancer, left hemicolectomy for left
Rectum cancer can be removed with an anterior resection (if >5cm from the anus) or an abdomino-perineal resection with end colostomy if <5cm from anus
Must take blood supply from whatever part of colon is taken as well
Radiotherapy
Adjuvent – after surgery in an attempt to reduce recurrence
Neo-adjuvent – before surgery in an attempt to shrink the tumour before removal
What Screening is used for colorectal cancer
A one off flexible sigmoidoscopy is currently being trialled and is offered to everyone aged 55
Men and women aged 60-74 are screened every 2 years - Patients wipe a sample of poo onto the sample kit, send it off and it is tested for faecal occult blood
What is the most common types of Anorectal cancer
Cancer below dentate line will often be squamous cell carcinoma
Above the dentate line the epithelium is mucosal
What are the different lymph node drainages of Anorectal cancer and why is this important to know?
Lymph drainage from squamous cells is to the inguinal, femoral and external iliac nodes
Lymph drainage above the pectinate line (mucosa) is to the internal iliac lymph nodes
Lymph drainage below the pectinate line (skin) is to the superficial inguinal lymph nodes
It is important to know the difference in lymph drainage for sentinel node biopsy in staging
What are the Risk factors for Anorectal cancer
Human papillomavirus – genital warts - 50% of tumours contain viral DNA, also Anal intercourse and promiscuity increase the risk
Increased risk in HIV patients – 2x as common in HIV+ homosexual men
Other forms of immune suppression such as in transplant patients
Smoking
Previous malignancy
Signs and symptoms of Anorectal cancer
Perianal pain and bleeding Palpable lesion Faecal incontinence Tenesmus Rectovaginal fistula in women Weight loss and malaise
Differential diagnosis of Anorectal cancer
Piles/Haemorrhoids – especially non-reducible (grade 4)
Large rectal cancers or cervical cancers
Fissure or Fistula in anorectal area -
However Both are more likely to form in anal cancer anyway
Investigations for Anorectal cancer
DRE and proctoscopy to see the size of the mass
Sigmoidoscopy or flexisig to take a Biopsy to confirm this is cancer, sentinel node biopsy is also helpful
CT, MRI or PET can be used for staging
Test for relevant infections such as HIV - If HPV or HIV are suspected causes then you may want to test for other blood-borne viruses
Treatment of Anorectal cancer
Chemotherapy and radiotherapy are recommended as first line treatments
o 5-fluorouracil and mitomycin C
o Chemotherapy allows for reduced dose of radiation, allowing for reduced radio-load
o Radiotherapy to both tumour and affected lymph nodes
o If unsuccessful consider surgery
Surgery – Anterior resection - excision of anus, rectum and part of the large bowel with insertion of a colostomy
What is Hereditary Non-polyposis Colorectal Cancer (Lynch syndrome)
An autosomal dominant genetic condition that has a high risk of colon cancer. It is a type of cancer syndrome.
What types of cancer does Hereditary Non-polyposis Colorectal Cancer predispose
Colorectal cancer – seen most commonly (80% lifetime risk) - 2/3rds appear in the proximal colon (right sided cancer)
Endometrial carcinoma
Digestive adenoma – gastric, pyloric and duodenal adenomas
Ovarian serous cystadenocarcinoma
How do you diagnose Hereditary non-polyposis colorectal cancer
Genetic Testing in patients who met the Amsterdam criteria (identifies high risk patients)
Treatment of Hereditary non-polyposis colorectal cancer
Other first degree relatives should also be tested
Colonoscopy at least every 2 years from age 25 onwards
Consider prophylactic total colectomy
Patient should be made aware of how other (non-colon) cancers will present, so that they can be tested should any red flag symptoms arise
What is Familial adenomatous polyposis (FAP)
A polyp within the colon is an abnormal growth of cells forming from the mucosa of the colon. Each polyp holds a small risk of becoming malignant – most patients will develop cancer by age 30
In familial adenomatous polyposis (also known as Gardner’s syndrome), patients have many polyps (adenoma=benign tumour) and therefore the risk of malignancy is greatly increased
Signs and symptoms of singular GI polyps
Singular polyps are normally asymptomatic
Patients who do present, most commonly present with rectal bleeding or iron deficiency anaemia
Occult blood may be detected in the stools
Signs and symptoms of Familial adenomatous polyposis (FAP)
In FAP, due to the increased amount of polyps, patients are more likely to be symptomatic
Obstruction and constipation
Diarrhoea, abdominal pain and mucous discharge
Gastric polyps may form, leading to epigastric pain, dyspepsia, vomiting and haemoptesis
Duodenal polyps may cause obstructive jaundice
Rectal polyps may be detectable by the patient, feeling similar to haemorrhoids -May lead to blood on wiping or tenesmus
Patients with FAP are more likely to have extra teeth, odontomas and non-erupted teeth
Thyroid carcinoma is more common in patients with FAP
Epidermoid cysts are more common in patients with FAP
Differential diagnosis of Familial adenomatous polyposis (FAP)
Any Causes of lower GI bleeds
Haemorrhoids Ulcerative colitis and Crohn's Colorectal cancer Anorectal cancer Diverticulitis
Investigations for Familial adenomatous polyposis (FAP)
Bloods
o Full blood count for anaemia and white cells (to rule out infection/inflammation) o LFTs to look for damage caused by liver metastases
o Carcinoembryonic antigen (CEA) testing for colorectal carcinoma
Faecal occult blood (microscopic blood, not normally seen by patient in stool)
CT chest, abdomen and pelvis to look for tumours and metastases
Colonoscopy and endoscopy with biopsies of any polyps viewed
Genetic testing for the adenomatous polyposis coli gene and the mutY DNA glycosylase (MUTYH) gene
Non-bowel manifestations of FAP
o Thyroid function tests
o Dental X-rays, chest x-rays and skull x-rays to look for osteomas, jaw lesions and supernumary teeth
Treatment for Familial adenomatous polyposis (FAP)
FlexiSig every 1-2 years in early cases of FAP (at ages 10-12) to document the onset of any polyp formation
Children will require colonoscopic polyp removal in early disease until they are old enough to handle a colectomy both physically and emotionally/psychologically
If no polyps are found by age 20 then patients will have colonoscopy every 5 years after that
Curative treatments normally involve resection of the colon or parts of the colon-This will likely require ileostomy or ileo-rectal anastomosis and Restorative proctolectomy with ileal pouch anal anastomosis is most often used
Patients will still need to be reviewed every 3-6 months for rectal or ileal pouch polyps following surgery - These polyps will need ablation
Endoscopy every 1-3 years following surgery to look for upper GI polyps - Can ablate these if necessary
COX2 inhibitors such as aspirin or calecoxib can help to reduce rates of recurrence
Causes of Haematemesis
Could be epistaxis (nose bleed) cause
Oesophageal causes – mallory-weiss tear, tumour, varices (from liver pathology)
Stomach pathology – tumour, ulcer, ingestion of foreign object (especially batteries)
Duodenum – ulcers, haemobilia (bleeding into biliary tree)
Causes of Rectal bleeding
Small bowel Tumours Ulceration Inflammatory bowel disease (Crohn's) Meckel's diverticulum
Large bowel/anus
Tumours
Diverticular disease
Radiation damage – eg. Prostate, ovary or bladder radiotherapy
AV malformation/angiodysplasia
Inflammatory bowel disease – Crohn’s or Ulcerative colitis
Varices (liver pathology)
Haemorrhoids (piles) – much less blood than in other conditions
How do you Examine a patient that has had a GI bleeds
Always look for signs of liver disease as this can easily lead to varices (oesophageal or colonic/rectal)
Always do a PR exam to assess the anus, rectum and whether the patient has any melaena or blood in their stools
Investigations for Upper GI bleeds
Oesophago-gastro-duodenoscopy/endoscopy to look for ulceration and upper GI tumours in patients: o Presenting 1st time over age 55 o Showing ALARMS symptom o In patients with warning signs - Iron deficiency anaemia - Chronic blood loss - Weight loss - Progressive dysphagia - Persistent vomiting - Epigastric mass felt on examination Urea breath tests for H pylori infection to see if present and causing ulceration FBC for iron deficiency anaemia LFTs for hepatic cause of varices
Treatment of an upper GI ulcer that is causing an upper GI bleed
Endoscopic ulcer intervention – ablation of bleeding ulcer
Resuscitation and stabilisation of patients who may have lost a lot of blood and are therefore in shock
Treatment for mallory weiss tears
Resection
Resuscitation and stabilisation of patients who may have lost a lot of blood and are therefore in shock
Treatment for Oesophageal Varices that are bleeding
Endoscopic variceal ligation or sclerosis
Resuscitation and stabilisation of patients who may have lost a lot of blood and are therefore in shock
What scoring systems can be used for an Acute upper GI bleed
Blatchford score for risk assessment
Rockall score can be calculated post-endoscopy
If a patient comes in with very minute lower GI bleeding what do you need to do?
Minute bleeding can give way to a major haemorrhage very quickly, therefore it is important to get early IV access and take blood for group and save/crossmatch
Investigations for Lower GI bleeds
FBC, U+Es, clotting and cross match
Endoscopy or sigmoidoscopy (left bowel only but takes less prep) or colonoscopy. Can use Capsule endoscopy instead – camera in a non-digestible capsule is swallowed, allowing visualisation of entire bowel to look for cause of bleed
Radiology mesenteric angiogram (a Radiolabelled red scan) red blood cells are taken, radiolabelled and re-infused, we then wait to see where they pool in the bowel after they bleed into it, telling us the location of the bleed
Treatment for Lower GI bleeds
Resuscitation o 2 large bore cannulae o IV fluids, have blood on hand o Urinary catheterisation o Oxygen
Non-operative – best to treat conservatively until a cause is found
Operative – only once a cause of the bleeding has been found
Causes of GI perforations
Upper GI – ulcers, tumours
Small bowel – tumours, foreign bodies, obstruction, trauma
Large bowel – diverticular disease, cancer, obstruction, inflammatory bowel disease, iatrogenic
Presentation of GI perforations
Abdominal pain
Peritonitis – generalised excruciating abdominal pain with guarding on examination (If a patient has peritonitis, always be aware that it may be perforate)
Shock
Investigations for GI perforations
FBC, U+Es, clotting, crossmatch
Arterial blood gas
ECG – monitor heart function due to shock and SIRS
Chest X-ray to look for gas under the diaphragm
CT scan abdomen for similar
Management of GI perforations
Resuscitation
o IV fluids – have blood on hand
o Oxygen
o Urinary catheterisation
o IV antibiotics (peritoneal cavity likely to become infected)
o Analgesia – analgesic ladder (probably opiates though)
Conservative management is indicated in patients without generalised sepsis/peritonitis
o Omentum may cover the perforation, preventing leak of contents and major contamination
o Treat with antibiotics and rest the bowel (parenteral feeding)
o Give PPIs in upper GI perforations to reduce acid damage and leak
Surgical management
o Possible to sew omentum over the area of perforation, stitching it to the perforated structure (upper GI generally)
o Resection of areas of perforated small bowel or colon – generally leads to stoma being necessary
What is a Stoma
A stoma is an opening made in the bowel to allow faecal material out into a stoma bag in patients for whom the bowel distal to that point has been removed due to its inviability
What are the different types of stoma
Colostomy – opening made in the large intestine (colon), bypassing the anal canal
Ileostomy – opening in the ileum of the small intestine, bypassing the large intestine
Gastrostomy and jejunostomy are used for enteral feeding tubes
What are the conditions stomas are often used in
Inflammatory bowel disease
Neoplasia (cancer)
Diverticular disease
How can you tell the difference between a Colostomy and an Ileostomy
Colostomies are flat to the skinand are fairly big, like the large intestine (colon)
Whereas ileostomies are spouted and comparatively small (like the small intestine)
What are the signs of a Healthy stoma
Above skin level
Red and moist – pallor suggests anaemia, dark suggests ischaemia
No separation between musculocutaneous edge and skin
No erythema, rash, ulceration or inflammation (obviously should not be present)
How often will faeces be present in a stoma
Ileostomy
Produce faeces roughly 4 hours after a meal
Increased output over normal defaecation
Colostomy will produce faeces roughly 8-12 hours after a meal
What dietary changes will patients with an ileostomy have to make
Patients may need to change their diet to reduce output rate or reduce output of flatus (flatus filters available)
Risk of dehydration, best for patients to avoid fizzy drinks and alcohol and drink more fluid than normal (roughly an extra litre a day)
What are the complications of a stoma
Possibility of prolapse, narrowing or blockage of the stoma - Stenosis can be recognised by thin, ribbon-like stools and high pitched flatus and will require surgical correction
Mucocutaneous junction may become detached, partially or fully - However good wound care will lead to reattachment
Parastomal hernias which may need surgery to resolve
What are the main cause of Loose stools
Tend to be caused by mucosal problems e.g. Inflammation – infection, diverticulitis, inflammatory bowel disease
If a patient arrives with new loose stools, what will you do?
The bowel should be scoped –
colonoscopy best
What are the main cause of Constipation
Tends to be obstructive
If a patient arrives with new constipation, what will you do?
CT to look for obstructed areas of bowel
If a patient arrives with blood in stools what will you do?
Assessment of the anus and rectum for haemorrhoids, etc.
Patient will likely need colonoscopy
Take bloods to look for anaemia
Signs and Symptoms of Intestinal Obstruction
Abdominal pain – colicky, every 4-5 minutes (with contractions, longer wait in large bowel)
Faeculant vomiting – brown, offensive smelling vomit that has been caused by stasis of bowel material and bacterial partial breakdown of digested material. This is different from faecal vomiting, which will occur in long-standing large bowel obstruction where peristalsis will work the material back up
Vomiting is less conspicuous in large bowel obstruction as there is more bowel for the faeculent material to build up in
Obstipation – severe or complete constipation, not passing motions for dayswith an inability to pass flatus
Abdominal distention and bloating
Abdominal tenderness
Visible peristalsis
Visible hernias
Rectal examination may reveal a mass in large bowel/rectal obstruction
High pitched, tinkling bowel sounds
Dehydration and hypotension with tachycardia
Fever
Causes of Primary Bowel Obstruction
Slow gut – can be present from birth, some patients may always be constipated
Neurological deficit or muscle weakness
Issues with the pelvic floor muscles
Secondary causes of Extramural Bowel Obstruction
Adhesions (fibrous tissue from previous surgery, trauma or intra-abdominal infection)
Herniae (external and internal)
Compression by tumour of another structure
Liver, pancreas, gall bladder, ovary, uterus
Secondary causes of Intramural Bowel Obstruction
Inflammation + oedema eg. Crohn’s
Polyp or tumour of the intestine – carcinoma, lymphoma, carcinoid tumour
Left sided carcinoma is more likely to cause constipation
Strictures
Diverticular disease
Ileus – Non-mechanical obstruction caused by paralysis of the intestine and therefore a lack of peristalsis
Secondary causes of Intraluminal Bowel Obstruction
Faecal impaction
Foreign bodies and bezoars (hair or fibre balls)
Large gallstone
Volvulus – The transverse colon, sigmoid colon and caecum are non-retroperitoneal (intraperitoneal) sections of the large bowel, allowing movement and therefore twisting on their mesenteries (Elderly patient, chronic constipation, megacolon are risk factors)
What are the possible tumours causing Bowel Obstruction
Gastrointestinal stromal tumours (GIST) Carcinoid tumours Lymphomas Metastatic o Ovarian o Colorectal (metastasises to small bowel) o Stomach o Most likely malignant cause of small bowel obstruction is a carcinoma of the large bowel at the ileocaecal junction Large polyps
Investigations for Bowel Obstruction
Blood tests
o Full blood count, clotting screen and group and save (in case surgery is needed)
o Urea and electrolytes (patient may be malnourished)
o Liver function tests
o Arterial blood gas
Radiology
o Abdominal/chest x-ray – look for evidence of perforation (air under diaphragm)
o Look for where gas ends in bowel – will show the rough area of obstruction
o CT scan
o Barium meal and follow-through and MRI in patients with chronic symptoms
Management of Small Bowel Obstruction
Resuscitation
Urinary catheter
Nasogastric tube placement may help to relieve some pressure
Non-operative may be fine as adhesional obstructions will resolve most of the time
Operative to remove non-adhesional obstruction or to resolve adhesional obstruction which has caused:
o Fever
o Tenderness and guarding, indicative of peritonitis
o Evidence of a perforation on imaging
o Failure of resolution
Management of Large Bowel Obstruction
Resuscitation
Urinary catheter
Sigmoid volvulus can normally be resolved via colonoscopy to give it a nudge back into position
Operative removal of lesion causing blockage or stenting of strictures
What are the main types of Hernia
Inguinal (groin)
o direct (through hesselbach’s triangle in the inguinal canal)
o ndirect (through deep inguinal ring)
Femoral
Incisional – from incisions, likely from previous abdominal surgery
Umbilical
Hiatal
What is a Direct inguinal hernia
A hernia arising from a defect in the posterior wall of the inguinal canal and then passes through the superficial inguinal ring
Inguinal hernias may enter the scrotum, especially indirect hernias
What is an Indirect inguinal hernia
A hernia that passes through the deep inguinal ring, along the inguinal canal and out through the superficial inguinal ring
Inguinal hernias may enter the scrotum, especially indirect hernias
What are the Boundaries of the inguinal canal
Anterior wall – external oblique aponeurosis and internal obliques
Posterior wall – transversalis fascia
Roof – transversalis fascia, internal oblique and transversus abdominis
Floor – inguinal ligament, lacunar ligament and iliopubic tract
Why are femoral hernias more prone to obstruction?
Due to narrowness of the femoral ring
What are the Boundaries of the femoral ring and canal
Medial – Lacunar ligament
Lateral – Femoral vein
Anterior – Inguinal ligament
What is an Incisional hernia
A hernia that develops along the scar tissue of a surgical incision, most often due to weakness in the abdominal wall due to incisions in the muscles
What is an Umbilical hernia
A hernia protruding through the umbilicus, most often due to congenital malformation
What is an Epigastric hernia
A Hernia in the epigastric region, more commonly congenital than acquired
Where is The mid-inguinal point
Half-way between the ASIS and the pubic symphysis - Femoral pulse should be palpable here
Where is the Femoral pulse palpable
The mid-inguinal point
What is The mid-point of the inguinal ligament
Half-way between ASIS and pubic tubercle
The deep inguinal ring is roughly half an inch superior to this point and so helps to determine a direct or indirect inguinal hernia
Where does the superficial inguinal ring lie
Superior and medial to the pubic tubercle
Investigations for a hernia
Ultrasound or X-rays with contrast agent injected into the peritoneum will help to be sure of the type of hernia
A CT scan may need to be performed to see what is going on in abdominal herniae and in obese patients
Treatment of a hernia
Strangulated herniae are a medical emergency and require immediate surgery
Lichtenstein technique – Mesh can be inserted to cover the weakness in the abdominal wall and prevent re-perforation once reduced
Bassini’s technique – Apposition of the surrounding musculature, transversus abdominis and transversalis fascia and lateral rectus sheath, to the inguinal ligament, closing off openings through which hernias in the groin could perforate
Femoral sacs surrounding femoral hernias may need to be dissected to allow for reduction followed by closure between the inguinal and pectineal ligaments
Laparoscopic repair is possible
Patients can wear a truss if surgery is inadvisable or refused
How to differentiate femoral from inguinal (direct or indirect) herniae
Differentiating femoral from inguinal (direct or indirect) herniae is a matter of location
Femoral herniae are found infero-lateral to the pubic tubercle (below inguinal ligament)
Femoral hernia are firmer than inguinal hernias
More common in women (but still less common in women than inguinal)
Inguinal herniae are found supero-medial to the pubic tubercle (above inguinal ligament) Inguinal herniae (especially indirect) may enter the scrotum whereas femoral herniae will not
How to differentiate direct and indirect inguinal herniae
Direct pass through only the superficial inguinal ring
A reduced indirect inguinal hernia will protrude on coughing even if the deep inguinal ring is blocked by an examiner’s finger
Indirect pass through the deep and superficial inguinal canal
A reduced indirect inguinal hernia will not become apparent again on coughing if a finger is used to block the deep inguinal ring (at the midpoint of the inguinal ligament)
Differential Diagnosis of a hernia
Saphena varix – varices of the saphenous vein however Often patients will have other varicoso veins, leading to a raised suspicion for saphena varix, a history of DVT will also support diagnosis
Femoral aneurysm
Inguinal lymphadenopathy
What is a Saphena varix
Varices of the saphenous vein
As with herniae, a saphena varix will become uncomfortable after prolonged periodsand a saphena varix will reduce on lying down as this will remove gravity from the equation, allowing for ease of draining
What are the characteristics of a saphena varix:
Non-tender
Fluctuant
Has a cough impulse
Infero-lateral to the pubic tubercle – Like a femoral hernia
Bluish tinge
Easily reducible and will reappear as soon as a finger is removed
Disappears as soon as the patient lies flat – only seen on standing examination
Often patients will have other varicose veins, leading to a raised suspicion for saphena varix
History of DVT will also support diagnosis
What are the characteristics of a Femoral aneurysm
The lump will be felt best at the mid-inguinal point (midway between ASIS and pubic symphisis)
The lump will be pulsatile
A fluctuant lump
What are the characterisitcs of an Inguinal lymphadenopathy
A solid lump – this differentiates it from other groin lump pathologies
May be pulsatile if overlying an artery
May be warm and tender
Causes of an inguinal lymphadenopathy
Infective causes – HIV, tuberculosis, lower limb infection
Neoplastic causes
o Lymphomas
o Leukaemias
o Metastases from lower limb and external genitalia
- Scrotum, skin of penis, vulva, anus (below pectinate line), perineum and buttocks - But remember that the testes drain to para-aortic nodes
What are Haemorrhoids (Piles)
Vascular cushions at the rectal boundary, that have a sensory function in feeling when the rectum is full and whether it contains gas, liquid or solid – allows us to fart without worry of following through. In low residue diets with straining to evacuate hard and solid faeces,damage to the haemorrhoids can occur, causing bleeding and possible prolapse
Constipation is a big risk factor
Piles lead to a lot of pain and discomfort for the patient
How do you Grade Piles
Grade 1 – Small swellings in the lining of the anal canal
Can’t be seen or felt from outside of the anus
Grade 2 – larger, may slightly protrude from the anus when passing motions
Reduce spontaneously on finishing defaecation
Grade 3 – hang out of the anus when passing motions
Felt as small, hard lumps hanging from the anus
Can be pushed back up with a finger
Grade 4 – permanently hang from the anus, unable to be pushed back in
Signs and symptoms of Piles
Patients may notice fresh blood in the bowl or on the paper when they wipe -
Bleeding may be painless
Anal itching and irritation due to irritation of the perianal skin by mucous discharge
Patients may feel the prolapsed haemorrhoids
Patients may have tenesmus
Patients may have impaired continence
External haemorrhoids may be painful due to strangulation or thrombosis
On PR examination, the swollen haemorrhoids will be felt
Can ask patient to strain to see if their haemorrhoids prolapse to help with grading and confirm diagnosis
Differential diagnosis of Piles
Anal carcinoma Colorectal cancer Inflammatory bowel disease Rectal prolapse Adenomatous polyps Anal fissure Anorectal abscess Anal fistula
Investigations for Piles
Proctoscopy – may need referral to secondary care
If nothing seen on proctoscopy, consider other differentials, patient may need colonoscopy
Treatment of Piles
Improve stool consistency
o Increase fluid and fibre intake and reduce intake of refined foods (eat wholemeal instead)
o Bulk forming laxatives (eg. Ispaghula husk) or fibre supplements may be needed to treat constipation
Pain and symptom relief
o Simple analgesia (paracetamol, NSAIDs) – avoid opiates as they will lead to worse constipation
o Topical anaesthesia can also be used and topical corticosteroids will help to reduce inflammation
Non-surgical treatments
o Rubber band ligation of haemorrhoids – haemorrhoid will necrose and drop off
o Injection sclerotherapy – phenol injection at base of haemorrhoids, leading to atrophy due to fibrosis of the blood vessels
Surgical treatments – reserved for large haemorrhoids that will not respond to other treatments
o Haemorrhoidectomy – painful but effective long-term
o Haemorrhoidal arterial ligation – cut off blood supply so they necrose and drop off
What are Anal fissures
Tears in the anus normally caused by constipated patients passing big motions which stretch the anus and lead to tears
Tears lead to pain and can become infected leading to further problems
Tears will take a long time to heal, as repeated defecation will lead to inflammation and anal spasm and therefore slowed healing
Blood supply to area reduced by spasms
Signs and symptoms of Anal fissures
Pain on defecation, often described as feeling like passing nails or glass
A visible fissure on examination of the anus
Look for any signs of infection
Ask the patient about constipation as this is likely the underlying cause and must be treated
Acute fissures will be extremely painful to the touch and will lead to anal spasm
Treatment of Anal fissures
Advice on fibre, liquids and fewer refined foods (more whole grain) to soften stools
Consider prescription of laxatives (bulk forming)
Simple oral analgesia (avoid opiates as they will cause constipation) or topical analgesia
Consider GTN ointment which will relax the anal sphincter, preventing spasm and improving healing
Botox can also be used to relax the anus
Surgery – Lateral sphincterotomy
What are the Cuases of Secondary Anal fissures
Patients with multiple fissures may have formed them due to Crohn’s disease
Large, non-healing fissures may have been caused by anal cancer
What is a Perianal (anorectal) abscess
A collection of pus in the anal/rectal region caused by infection of an anal fissure, as a result of STIs or blocked anal glands
If left untreated they can lead to necrotising fasciitis, which is a medical emergency
What are the signs and symptoms of a Perianal (anorectal) abscess
Painful, hardened tissue in the perianal area -Pain is usually constant, throbbing and worse on sitting down
Discharge of pus from the rectum and tenderness around the anus
Lumps and nodules
Fever, constipation or pain associated with bowel movements
Investigations for a Perianal (anorectal) abscess
DRE usually enough for diagnosis – pus on finger
STI screen may be relevant
Proctoscopy/sigmoidoscopy to rule out malignant cause
MRI will show location of fistulae and locations of deep abscesses
What is a Anorectal fistulae
Connection between anus or rectum and the skin allowing a leak of faeces to the skin
Associated with diverticular disease, IBD, malignancies, tuberculosis and actinomycosis
Patients will have faecal leak without feeling that they are defaecating
Treatment of a Perianal (anorectal) abscess
Surgical drainage of abscesses
Analgesia
Antibiotics only relevant if the patient is diabetic or immunosuppressed
Best treatment for anal fistulae is to lay them open by cutting between them and the skin- This can lead to problems with continence as the anus and rectum may have to be cut
What are the Surgical treatments of obesity
Gastric band surgery
Gastric bypass
What is Gastric band surgery
Reduction of stomach capacity leads patients to feel fuller, sooner and therefore reduces their overall calorie intake
Creates an additional stomach pouch, which acts as a smaller stomach which will hold much less food
Size can easily be adjusted to allow for more or less of an effect
Fewer complications than gastric bypass
What is Gastric bypass surgery
Reducing length of small bowel – Leads to malabsorption of food, thus reducing overall calorie intake, also has a hand in reducing the total concentration of gut peptides, thought to lead to reduced hunger response
A loop of jejunum is attached to the stomach allowing food to bypass the duodenum and proximal jejunum
Greater weight loss than gastric band but greater risk of complications
Patients will likely require multivitamin supplementation due to the reduce absorption of key vitamins from their small bowel
When should surgery for weight loss be considered?
BMI≥40 or ≥35 with significant comorbidity that could improve with reduced weight e.g. Type 2 diabetes or Severe hypertension
Failure of non-surgical management to achieve and maintain any clinically beneficial weight loss for 6 months
Patient must be fit enough for surgery and anaesthesia
Patient must have shown willingness to lose weight by following previous guidance on diet and exercise regimes
Patient must be willing to continue these regimes
The patient must be well informed and motivated to lose weight
