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
