Gastrointestinal Flashcards
Define achalasia
An oesophageal motor disorder characterised by a LACK OF OESOPHAGEAL PERISTALSIS and failure of the lower oesophageal sphincter to relax in response to swallowing.
Explain the aetiology of achalasia
Degeneration of the ganglion cells of the myenteric plexus due to unknown aetiology
What are the risk factors for alchalasia?
Infection (herpes and measles virus), autoimmunity, genetics, allgrove syndrome
Epidemiology of achalasia
1 in 100,000.
Can occur at any age but peak in those over 60.
Equal incidence in men and women.
What are the presenting symptoms of achalasia?
Intermittent DYSPHAGIA of solids and liquids Difficulty belching Regurgitation of bland, undigested food or saliva (especially at night) - NOT ACIDIC Heartburn Chest pain Weight loss Nocturnal cough when lying down Pain relived by drinking cold water
What are the signs of achalasia on physical examination?
Nil signs of note
Any signs would be signs of complications eg aspiration pneumonia and malnutrition
What would be appropriate investigations for achalasia and what would their results be?
Upper GI endoscopy - normal, excludes malignancy
Barium swallow - Dilated oesophagus which smoothly tapers down to the sphincter (beak shaped)
Oesophageal manometry - high resting LOS pressure
CXR - absence of gastric gas bubble, widened mediastinum, double right heart border, air-fluid level in upper chest
Define acute cholangitis
Infection of the bile ducts
Explain the aetiology of acute cholangitis
Obstruction of bile duct by gallstones allows bacteria to ascend up the bile duct.
ERCP
Tumours (e.g. pancreatic, cholangiocarcinoma)
Bile duct stricture or stenosis
Parasitic infection
What are the risk factors for acute cholangitis?
Age >50 years
Cholelithiasis
Benign or malignant stricture
Post-procedure injury of bile ducts
What is the epidemiology of acute cholangitis?
Equal in males and females
Median age of presentation: 50-60 yrs
Racial distribution follows that of gallstone disease -
fair skinned people, fat, female, fertile, forty
What are the presenting symptoms of acute cholangitis?
CHARCOT’S TRIAD - RUQ pain, jaundice, fever +/- rigors
REYNOLD’S PENTAD - RUQ pain, jaundice, fever +/- rigors, mental confusion, septic shock
Pruritis (itchy skin)
What are the signs of acute cholangitis on examination?
Fever RUQ tenderness Mild hepatomegaly Jaundice Mental status changes Sepsis Hypotension Tachycardia
What would the appropriate investigations for acute cholangitis be and what would the results be?
Bloods: FBC - High WCC CRP/ESR - possibly raised LFTs - raised ALP + GGT U&Es - urea and creatinine raised, potassium and magnesium low Blood cultures - check for sepsis
Imaging:
ERCP
Abdo USS - see dilated bile duct and stones
If suspecting but negative: contrast-enhanced CT, MRCP or PTC
What is the management of acute cholangitis?
Intravenous antibiotics, intensive medical management and non-operative biliary decompression (ERCP or PTC) with endoscopic lithotripsy to fragment stones if necessary
Analgesics
Second line: surgical biliary decompression via cholecystectomy or choledochotomy (incision into CBD)
Identify the possible complications of acute cholangitis?
Hepatic abscess Liver failure Bacteraemia Gram-negative sepsis Septic shock AKI Organ dysfunction Complications of PTC or ERCP eg abdominal or percutaneous bleeding, sepsis, fistulae and bile leakage
Summarise the prognosis of patients with acute cholangitis
Rapid clinical improvement once adequate biliary drainage is achieved
Patients with significant underlying medical conditions or delayed decompression, poorer prognosis
Hyperbilirubinaemia, high fever, leukocytosis, older age, hypoalbuminaemia are predictive of poor prognosis
17-40% mortality
Define alcohol withdrawal
A syndrome which occurs in patients with chronic alcoholism or alcohol dependence 4-12 hours following the abrupt cessation or decrease of alcohol consumption.
Explain the aetiology of alcohol withdrawal
Chronic alcohol use:
- upregulates post-synaptic STIMULATORY NMDA receptors
- downregulates post-synaptic INHIBITORY GABA type A receptors.
- ethanol activates the inhibitory receptors.
On cessation there is an imbalance between GABA and NMDA stimulation - increased excitation of NMDA.
What are the risk factors for alcohol withdrawal syndrome?
History of alcohol withdrawal syndrome and delirium tremens.
Abrupt cessation of alcohol.
Summarise the epidemiology of alcohol withdrawal syndrome
50% of alcohol dependent patients will experience AWS on abrupt cessation of consumption.
8% of all patients admitted to hospital are at risk of alcohol withdrawal.
What are the presenting symptoms of alcohol withdrawal?
Change in mental status Hallucinations Seizures Delusions Nausea and vomiting Tremor
What are the signs of alcohol withdrawal?
Hypertension
Tachycardia
Hyperthermia
What are the investigations for alcohol withdrawal?
Serum urea and creatinine - check for dehydration
LFTs - if increased, alcoholic hepatitis
Ethanol - high = more severe AWS
Electrolytes - hypokalaemia = severe AWS, DT
FBC - rule out infection
CT head and CXR to rule out other cause.
Generate a management plan for alcohol withdrawal
First line = long acting benzodiazepines - diazepam (oral if mild, if moderate or severe then i.v.) or clomethiazole
Supportive treatment to prevent relapse and relieve symptoms.
Phenobarbital if patient needs large benzodiazepine dose
Vitamin supplementation (thiamine, magnesium).
If severe AWS with or without benziodiazepine-resistance, ICU admission.
What are the possible complications of alcohol withdrawal?
Oversedation from treatment
Delirium tremens
Alcohol-withdrawal seizures - less than 3% of these progress to status epilepticus
What is the prognosis of alcohol withdrawal?
Some patients experience persistent insomnia and autonomic symptoms for few months.
50% remain abstinent for a year.
Define alcoholic hepatitis
Inflammatory liver injury caused by chronic heavy alcohol intake.
Explain the aetiology of alcoholic hepatitis
Histopathology shows: Steatosis Ballooning and necrosis of hepatocytes Mallory bodies (cytoplasmic inclusions in hepatocytes). Neutrophilic inflammation Cholestasis Giant mitochondria
One of the THREE forms of liver disease caused by excessive alcohol intake - the spectrum consists of:
Alcoholic fatty liver (steatosis)
Alcoholic hepatitis
Chronic cirrhosis
What are the risk factors of alcoholic hepatitis?
Excessive alcohol intake for 10-15 years
Presence of hepatitis C
Summarise the epidemiology of alcoholic hepatitis
Occurs in 10-35% of heavy drinkers
What are the presenting symptoms of alcoholic hepatitis?
Rapid onset jaundice Nausea Malaise Anorexia RUQ pain Drowsiness, confusion Fever Abdominal distension (ascites) Swollen ankles GI bleeding
What are the signs of alcoholic hepatitis on examination?
Febrile Tachycardia Jaundice Bruising Encephalopathy Ascites Hepatomegaly Splenomegaly Palmar erythema Dupuytren’s contracture Spider naevi Gynaecomastia
What are appropriate investigations for alcoholic hepatitis?
Bloods
- FBC: low Hb, high MCV, high WCC, low platelets
- LFTs: high AST + ALT, high bilirubin, high ALP + GGT, low albumin
- U&Es: low urea and K+
- Clotting: prolonged PT
Ultrasound - exclude malignancy, abscess etc
Upper GI Endoscopy - investigate varices
Liver Biopsy
EEG - slow-wave activity indicates encephalopathy
Generate a management plan for alcoholic hepatitis
Acute:
- IV Thiamine, Vit C and multivitamins
- Monitor and correct K, Mg and glucose abnormalities
- Ensure adequate urine output
- Treat encephalopathy: oral lactulose and phosphate enemas
- Treat ascites: diuretics, paracentesis
- Treat hepatorenal syndrome: glypressin, N-acetylcysteine
Nutrition
- Oral or nasogastric feeding (high protein diet)
- Vitamin supplementation (IV then oral B vitamins, thiamine, folic acid)
Note: if have encephalopathy then protein restriction
Steroid therapy
- 40mg/day for 4 weeks
Long term
- Stop drinking/reduce alcohol intake
What is hepatorenal syndrome?
The development of renal failure in patients with advanced chronic liver disease
What are the possible complications of alcoholic hepatitis?
Hepatorenal syndrome
Cirrhosis
Acute liver decompensation
What is the prognosis for patients with alcoholic hepatitis?
Mortality in the first month = 10%
Mortality in the first year = 40%
If alcohol intake continues, most will progress to cirrhosis within 1-3 years.
Define amyloidosis
The accumulation of misfolded proteins known as amyloid in organs and tissues.
Amyloid demonstrates apple green birefringence under polarised light with Congo red stain.
Amyloid deposition is disruptive to tissues and so amyloidosis manifests its clinical sequelae by the dysfunction of those organs in which it deposits
What are the different types of amyloidosis?
Primary amyloidosis (AL): Produce immunoglobulin light chains that are inherently prone to misfolding into an insoluble beta-pleated sheet configuration. Primary target organ = kidney (disruption of glomerular basement membrane) Also deposits in heart (conduction abnormalities) and nerves (vasa nervorum)
Secondary amyloidosis (AA): Improper processing of serum amyloid A protein - not broken down enough. Affects kidney, GI tract, thyroid.
What are the risk factors/causes of amyloidosis?
AL: MGUS, Multiple myeloma. No underlying genetic, environmental or occupational risk factors.
AA:
Inflammatory polyarthropathies - RA, psoriatic arthritis, ankylosing spondylitis
Chronic infections - bronchiectasis, TB, osteomyelitis
IBD – Crohn’s
Malignancy - Hodgkin’s lymphoma, renal cell carcinoma
Castleman’s disease - lymphoproliferative disorder
