GASTROINTESTINAL Flashcards
(37 cards)
Define Achalasia
Normal muscular activity of oesophagus is absent or uncoordinated.
Due to FAILURE/INCOMPLETE RELAXATION OF LOWER OESOPHAGEAL SPHINCTER.
=> delay in passage of swallowed material into stomach.
Aetiology of Achalasia
Degeneration of ganglion cells of myenteric plexus in oesophagus.
Unknown cause.
CHAGAS DISEASE
Epidemiology of Achalasia
May occur at any age
Affects both sexes equally
Annual incidence - 1/100,000
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 (because they are eating less)
Signs of Achalasia on examination
Aspiration pneumonia
Malnutrition
Weight loss
Investigations for Achalasia
CXR: Widened mediastinum Double right heart border (dilated oesophagus) Air-fluid level in the upper chest Absence of the normal gastric air bubble
Barium swallow:
Dilated oesophagus which smoothly tapers down to the sphincter (beak-shaped)
Endoscopy: exclude malignancy
Manometry:
Elevated resting LOS pressure (> 45 mm Hg).
Incomplete LOS relaxation.
Absence of peristalsis in the smooth muscle portion of the oesophagus.
Serology for antibodies against T. cruzi if CHAGAS DISEASE
Define Acute Cholangitis
Infection of the bile duct.
Aetiology of Acute Cholangitis
Obstruction of the gallbladder or bile duct due to stones.
ERCP.
Tumours (e.g. pancreatic, cholangiocarcinoma).
Bile duct stricture or stenosis
Parasitic infection (e.g. ascariasis).
Epidemiology of Acute Cholangitis
9% of patients admitted to hospital with gallstone disease will have acute cholangitis.
M=F.
50-60yrs.
Racial distribution = fair-skinned ppl (same as gallstone disease).
Presenting symptoms of Acute Cholangitis
CHARCOT’S TRIAD:
RUQ
Jaundice
Fever with rigors
Suppurative = REYNOLD’S PENTAD:
Mental confusion
Septic shock - hypotension
May complain of pruritus
Signs of Acute Cholangitis on examination
Fever RUQ tenderness Murphy’s sign positive Mild hepatomegaly Jaundice Mental status changes Sepsis Hypotension Tachycardia Peritonitis (uncommon - check for alternative diagnosis)
Investigations for Acute Cholangitis
Bloods:
FBC - high WCC.
CRP/ESR: possibly raised.
LFTs: typical pattern of obstructive jaundice (raised ALP + GGT).
U&Es: may be signs of renal dysfunction.
Blood cultures: check for sepsis.
Amylase: may be raised if the lower part of the common bile duct is involved.
Imaging: X-ray KUB: for stones. Abdominal ultrasound: for stones/dilation of common bile duct. Contrast-enhanced CT/MRI MRCP: to detect non-calcified stones.
Management plan for Acute Cholangitis
Resuscitation if in septic shock.
Broad-spectrum antibiotics: once blood cultures have been taken (select drugs that are effective against anaerobes and Gram-negative organisms: e.g. cefuroxime + metronidazole).
Endoscopic biliary drainage usually required to treat underlying obstruction.
Depends on severity:
Stage 1 (Mild)
- Antimicrobial therapy
- Percutaneous, endoscopic or operative intervention for non-responders.
Stage 2 (Moderate)
- Early percutaneous/ endoscopic drainage.
- Endoscopic biliary drainage recommended.
Stage 3 (Severe)
NOTE: severe cholangitis counts as including shock, conscious disturbance, acute lung injury, AKI, hepatic injury or DIC.
- Treatment of organ failure with ventilatory support, vasopressors etc.
- Urgent percutaneous or endoscopic drainage.
- Definitive treatment required once the clinical picture improves.
Possible complications of Acute Cholangitis
Liver abscesses Liver failure Bacteraemia Gram-negative sepsis Septic shock AKI Organ dysfunction Percutaneous or endoscopic drainage can lead to: Intra-abdominal or percutaneous bleeding, sepsis, fistulae and bile leakage.
Prognosis for patients with Acute Cholangitis
Mortality between 17-40%
Define Alcoholic Hepatitis
Inflammatory liver injury caused by chronic heavy intake of alcohol
Aetiology of Alcoholic Hepatitis
THREE forms of liver disease caused by excessive alcohol intake:
Alcoholic fatty liver (steatosis)
Alcoholic hepatitis
Chronic cirrhosis
Severe exposure to alcohol = hepatitis (reversible with abstinence)
Repeated attacks = cirrhosis
Exposure to alcohol = steatosis (reversible with abstinence)
Continued exposure = cirrhosis
Centrilobular ballooning
Degeneration and necrosis of hepatocytes
Steatosis – fatty change
Neutrophilic inflammation
Cholestasis – condition in which bile cannot flow from liver to the duodenum
Mallory-hyaline inclusions (eosinophilic intracytoplasmic aggregates of cytokeratin intermediate filaments)
Giant mitochondria
Epidemiology of Alcoholic Hepatitis
Occurs in 10-35% of heavy drinkers
Presenting symptoms of Alcoholic Hepatitis
May remain asymptomatic and undetected May be mild illness with: Nausea Malaise Epigastric pain Right hypochondrial pain Low-grade fever More severe presenting symptoms include: Jaundice Abdominal discomfort or swelling Swollen ankles GI bleeding
Long history of heavy drinking is required for development of alcoholic hepatitis (around 15-20 years)
Events may trigger the disease (e.g. aspiration pneumonia, injury)
Signs of Alcoholic Hepatitis on examination
Signs of Alcohol Excess Malnourished Palmar erythema Dupuytren's contracture Facial telangiectasia – red lines appear due to widened venules Parotid enlargement Spider naevi Gynaecomastia Testicular atrophy Hepatomegaly Easy bruising
Signs of Severe Alcoholic Hepatitis Febrile (in 50% of patients) Tachycardia Jaundice Bruising Encephalopathy (e.g. liver flap, drowsiness, disorientation) – caused by build up of ammonia in blood (which is normally removed by the liver) – crosses blood-brain barrier Ascites Hepatomegaly Splenomegaly
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:
Urea and K+ tend to be low
Clotting: prolonged PT is a sensitive marker for significant liver damage
Ultrasound - check for other causes of liver impairment (e.g. malignancy)
Upper GI Endoscopy - investigate varices
Liver Biopsy - can help distinguish from other causes of hepatitis
EEG - slow-wave activity indicates encephalopathy
Management plan for Alcoholic Hepatitis
Acute:
Thiamine
Vitamin C and other multivitamins (can be given as Pabrinex)
Monitor and correct K+, Mg2+ and glucose
Ensure adequate urine output
Treat encephalopathy with oral lactulose/phosphate enemas – decrease ammonia generation by bacteria
Ascites - manage with diuretics (spironolactone with/without furosemide)
Therapeutic paracentesis (removing fluid)
Glypressin and N-acetylcysteine for hepatorenal syndrome
Nutrition:
Via oral or NG feeding is important
Protein restriction should be avoided unless the patient is encephalopathic
Nutritional supplementation and vitamins (B group, thiamine and folic acid) should be started parenterally initially, and continued orally
Steroid Therapy:
reduce short-term mortality for severe alcoholic hepatitis
Possible complications of Alcoholic Hepatitis
- Acute liver decompensation
- Hepatorenal syndrome
= cirrhosis + ascites + renal failure (if other causes of renal impairment excluded) - Abnormalities in blood vessel tone kidneys = vessels constrict
because of dilatation of blood vessels in the splanchnic circulation (supplying the intestines), which is mediated by factors released by liver disease – e.g. nitric oxide, prostaglandins
Splanchnic vasodilation = reduced effective volume of blood detected by the juxtaglomerular apparatus = activation of RAS and vasoconstriction of vessels in the kidney -> kidney failure.
-Cirrhosis
Prognosis for patients with Alcoholic Hepatitis
Mortality:
First month = 10%
First year = 40%
If alcohol intake continues, most will progress to cirrhosis within 1-3 years
Maddrey’s discriminant function/Glasgow alcoholic hepatitis score to calculate prognostic score
