Gastrointestinal Flashcards
(508 cards)
Define achalasia
An oesophageal motor disorder characterised by a loss of oesophageal peristalsis and failure of the lower oesophageal sphincter (LOS) to relax in response to swallowing
Explain the aetiology of achalasia
The degeneration of ganglion cells of the myenteric plexus in the oesophagus
Summarise the epidemiology of achalasia
Annual incidence is about 1 in 100000. Usual presentation age: 25–60 years.
What are the presenting symptoms of achalasia?
Insidious onset and gradual progression of:
. intermittent dysphagia involving solids and liquids;
. difficulty belching;
. regurgitation (particularly at night);
. heartburn;
. chest pain (atypical/cramping, retrosternal);
. weight loss.
What are the signs of achalasia on physical examination?
May reveal signs of complications: aspiration pneumonia, malnutrition and weight loss may result
What are the appropriate investigations for achalasia?
1st line:
Upper gastrointestinal endoscopy- mucosa obscured by retained saliva (and to exclude malignancy)
Barium swallow: Dilated oesophagus which smoothly tapers down to the sphincter (beak- shaped). Loss of peristalsis and delayed oesophageal emptying
Oesophageal Manometry:
. incomplete LOS relaxation
. Elevated resting LOS pressure (>45 mmHg);
. absence of peristalsis in the distal (smooth muscle portion) of the oesophagus.
CXR:may show a widened mediastinum and double right heart border (dilated oesophagus), an air-fluid level in the upper chest and absence of the normal gastric air bubble.
What is acute cholangitis?
Also known as ascending Cholangitis
- Infection of the biliary tree, most commonly caused by obstruction
- In its less severe form, there is biliary obstruction with inflammation and bacterial seeding and growth in the biliary tree
What is the aetiology of acute cholangitis?
- Most commonly gallstones leading to choledocholithiasis (gallstones in the bile duct) and biliary obstruction.
- Iatrogenic biliary tract injury, most commonly caused via surgical injury cholecystectomy, can lead to benign strictures, which in turn can lead to obstructions
- Acute prancreatitis
- Malignant strictures (restricts flow)
What is the epidemiology of acute cholangitis?
Relatively uncommon
Male: female ratio is equal
Median age of presentation is 50-60
What are the presenting signs of acute cholangitis?
Pale stools
Pruritus
Hypotension
Mental status changes
What are the investigations for acute cholangitis?
FBC: Raised WBC, decreases platelets
Serum urea: Raised in severe cases
Serum creatinine: Raised in severe cases
ABG: Metabolic acidosis
LFT: Hyperbilinuraemia
CRP: Raised
Serum K & Mg: May be decreased
Blood cultures: Bacteria usually gram negative, but gram positive bacteria and anaerobes are also implicated in cholangitis
Tansabdominal USS: dilated bile duct, common bile duct stones- order CT with contrast if USS is negative
ERCP: best first intervention, can assist in the diagnosis of cholangitis by finding stones causing obstruction and is also therapeutic, as the procedure can be used for biliary stone extraction
What are the presenting symptoms of acute cholangitis?
Jaundice
Fever
Upper abdominal pain
Right upper quadrant tenderness
How is acute cholangitis managed?
Initial stabilisation:
-borad spectrum IV antibiotics
-correct any electrolyte imbalances and coagulation abnormalities
- give adequate analgesia
Biliary decompression:
-ERCP
-surgical incision of the common bile duct (choledochotomy with a T tube replacement)
- cholecystectomy
Consider endoscopic lithotripsy- physical destruction of gallstones
What are the possible complications of acute cholangitis?
- Acute prancreatitis
- Inadequate biliary drainage following performance of endoscopy, radiology or surgery
- Hepatic abscess
What is the prognosis of acute cholangitis?
If adequate biliary drainage is quickly obtained, most patients experience rapid clinical improvement
Outcome worse for patient’s with underlying medical conditions
What is Alcoholic hepatitis?
Inflammatory liver injury and necrosis caused by chronic heavy intake of alcohol
What are the three stages of Alcoholic liver disease?
- Fatty liver (steatosis)
- Alcoholic Hepatitis
- Alcoholic Liver Cirrhosis
What is the aetiology Alcoholic hepatitis?
The middle stage between fatty liver (steatosis) and alcoholic liver cirrhosis.
Inflammatory liver injury, liver histopathology shows:
-centrilobar ballooning degeneration
-necrosis of hepatocytes
-steatosis (abnormal retention of lipids)
-neutrophilic inflammation
-cholestasis (impaired secretion of bile from hepatocytes and so decrease flow of bile)
-Mallory hyaline inclusions and giant mitochondria
What is the epidemiology of Alcoholic hepatitis?
10-35% of heavy drinkers develop this form of liver disease
What are the presenting symptoms of Alcoholic hepatitis?
May remain asymptomatic and undetected unless they present for other reasons May be mild illness with: -Nausea -Malaise -Epigastric or right hypochondrial pain -Low-grade fever May be more severe with: -Jaundice -Abdominal discomfort or swelling -Swollen ankles -GI bleeding
Women tend to present with more florid (fully complete) illness than men
There is a history of heavy alcohol intake (15–20 years of excessive intake necessary for development of alcoholic hepatitis)
There may be trigger events (e.g. aspiration pneumonia or injury)
What are the signs of Alcoholic hepatitis on physical examination?
Signs of alcohol excess: -Malnourished -Palmar erythema -Dupuytrens contracture -Facial telangiectasia -Parotid enlargement -Spider naevi -Gynaecomastia -Testicular atrophy -Hepatomegaly -Easy bruising Signs of severe alcoholic hepatitis: -Febrile (50% of patients) -Tachycardia -Jaundice (>50% of patients) -Bruising -Encephalopathy (e.g. hepatic foetor-breath has a strong, musty smell, liver flap, drowsiness, unable to copy a five-pointed star, disoriented) -Ascites (30–60% of patients) -Hepatomegaly (may be tender on palpation) -Splenomegaly
What are the appropriate investigations for Alcoholic hepatitis?
Bloods:
-FBC: reduced Hb, raised MCV, raised WCC, reduced platelets
-LFT (raised transminases, raised bilirubin, reduced albumin, raised AlkPhos, raised GGT)
-U&Es: Urea and K+ levels tend to be low, unless significant renal impairment
*Clotting: Prolonged PT is a sensitive marker of significant liver damage
Ultrasound scan: For other causes of liver impairment (e.g. malignancies)
Upper GI endoscopy: To investigate for varices
Liver biopsy: Percutaneous or transjugular (in the presence of coagulopathy) may be helpful
to distinguish from other causes of hepatitis
Electroencephalogram: For slow-wave activity indicative of encephalopathy
What is the management of Alcoholic hepatitis?
Acute:
- Thiamine, Vitamin C and other multivitamins (initially parenterally)
- Monitor and correct K+ , Mg2+ and glucose abnormalities
- Ensure adequate urine output
- Treat encephalopathy with oral lactulose and phosphate enemas
- Ascites is managed by diuretics (spironolactone with or without furosemide) or therapeutic paracentesis
- Glypressin and N-acetylcysteine for hepatorenal syndrome (treatment of bleeding oesophageal varices)
Nutrition:
-Nutritional support with oral or nasogastric feeding is important with increased caloric intake
-Protein restriction should be avoided unless the patient is encephalopathic
-Total enteral nutrition may also be considered as this improves mortality rate
Nutritional supplementation and vitamins (B group, thiamine, folic acid) should be started parenterally initially and then continued orally after
Steroid therapy: Meta-analyses show that steroids reduce short-term mortality for severe alcoholic hepatitis
What are the complications of Alcoholic hepatitis?
Acute liver decompensation
Hepatorenal syndrome (renal failure secondary to advanced liver disease)
Cirrhosis