Gastrointestinal Flashcards
(356 cards)
Define ascending cholangitis:
Ascending cholangitis is a severe, acute infection and inflammation of the biliary tree, often resulting from a blockage that facilitates bacterial ascent from the duodenum.
What are the causes of ascending cholangitis:
Biliary calculi (stones) – accounting for approximately 50% of cases
Benign biliary stricture – 20%. These can be congenital, post-infectious, or due to an inflammatory process
Malignancy – 10-20%. This can originate from the gallbladder, bile duct, ampulla, duodenum, or pancreas
What is the aetiology of ascending cholangitis:
Ascending cholangitis is typically caused by the ascending infection of the biliary tree due to obstruction, commonly by a gallstone lodged in the common bile duct. The obstruction leads to bile stasis (resulting in jaundice), bacterial overgrowth, and ascending infection, often with enteric organisms. This results in inflammation and oedema of the bile ducts, leading to characteristic clinical symptoms such as fever, right upper quadrant pain, and jaundice. In severe cases, bacterial translocation into the bloodstream can lead to sepsis and multi-organ dysfunction, making early diagnosis and intervention crucial.
What is Charcot’s triad in ascending cholangitis:
Patients with ascending cholangitis often present with Charcot’s triad, which is observed in around one-third of patients:
Right upper quadrant pain
Fever
Jaundice
In severe cases of ascending cholangitis what is Reynolds pentad:
Right upper quadrant pain
Fever
Jaundice
Hypotension
Mental confusion
What are the key clinical features between ascending cholangitis, cholecystitis and biliary colic:
What are the investigations for ascending cholangitis:
Basic blood panel showing raised liver function tests (LFTs) and elevated inflammatory markers such as white cell count (WCC) and C-reactive protein (CRP).
1st line imaging with an ultrasound of the abdomen, which can detect bile duct dilatation but may not reliably identify stones in the mid/distal biliary duct. After this CT/MRCP/ERCP can be considered (see below).
Computed tomography (CT) scan provides a detailed anatomical view of the biliary tree and may visualize radiopaque stones. However, it is less effective at viewing radiolucent cholesterol stones, which are more common.
Magnetic resonance cholangiopancreatography (MRCP) offers the highest accuracy in determining the disease, including detection of gallstones or strictures, and visualizes nearly all causes of biliary tree obstruction.
Endoscopic retrograde cholangiopancreatography (ERCP) may be used therapeutically once the aetiology has been determined.
Define acute pancreatitis
Acute pancreatitis refers to an inflammatory process affecting the pancreas as well as local or distant tissues and organs in some cases.
What is the epidemiology of acute pancreatitis:
Acute pancreatitis has an incidence of approximately 30 cases per 100,000 people per year
There are many causes as detailed below
Half of cases are caused by gallstones, and around a quarter of cases by alcohol
10% of cases are idiopathic
The majority of cases (around 80%) are mild and self-limiting, with low mortality rates (1-3%)
The 20% of patients with moderate or severe disease have a higher risk of death (estimated at 13-35%)
Name some causes of acute pancreatitis: GET SMASHED
Gallstones
Ethanol (alcohol)
Trauma
Steroids
Mumps
Autoimmune disease (e.g. systemic lupus erythematosus, Sjogren’s syndrome)
Scorpion stings
Hypercalcaemia, hypertriglyceridemia, hypothermia
ERCP
Drugs (e.g. thiazides, azathioprine, sulphonamides)
Other causes include blunt abdominal trauma or local surgery, microlithiasis (tiny gallstones and biliary sludge), pancreatic tumours and cholangiocarcinomas and congenital abnormalities such as pancreas divisum.
What do we use to classify acute pancreatitis:
Glasgow-imrie score
each of the following scores 1 point and a score of 3 or more predicts severe pancreatitis
What are the criteria of the Glasgow score:
PaO2 < 8kPa
Age > 55 years
Neutrophils > 15
Calcium < 2
Renal i.e. Urea > 16
Enzymes i.e. LDH > 600 or AST > 200
Albumin < 32
Sugar i.e. Glucose > 10
This should be calculated on admission and at 48 hours.
What are the signs and symptoms of acute pancreatitis:
The main symptom of acute pancreatitis is epigastric pain which may radiate to the back
Nausea and vomiting are also common symptoms
Diarrhoea can occur
On examination, signs may include:
Abdominal tenderness
Peritonism, rebound tenderness and guarding may be seen
Abdominal distension
Fevers (which may be due to inflammation or superadded infection)
Tachycardia and hypotension if shocked
Haemorrhagic pancreatitis may present with Grey-Turner’s sign (bruising in the flank area), Cullen’s sign (bruising around the umbilicus) or Fox’s sign (bruising over the inguinal ligament)
What are the bedside tests for acute pancreatitis:
ABG if low oxygen saturations to help with risk stratification (the pO2 is needed for the Glasgow criteria)
ECG to rule out acute coronary syndrome as a cause of pain
Pregnancy test in women of child-bearing age to rule out causes of abdominal pain such as ectopic pregnancy
Capillary blood glucose as hyperglycaemia indicates severe pancreatitis
What are the blood tests for acute pancreatitis:
FBC and CRP for inflammatory markers
U&Es to look for kidney injury; urea is part of the Glasgow imrie criteria
LFTs are often deranged; a low albumin and high AST indicate severe pancreatitis
Amylase is the key diagnostic test, with levels over 3x the upper limit of normal indicating acute pancreatitis
Lipase is not usually measured but can also be used to diagnose pancreatitis - it is more sensitive and specific than amylase
LDH and a bone profile for calcium are also required for the Glasgow criteria with hypocalcaemia being a poor prognostic factor
Blood cultures in patients with fevers or other signs of infection
Coagulation screen as a baseline - may be deranged in severe illness
Lipid profile if hypertriglyceridaemia is suspected as a cause of pancreatitis
Autoimmune markers if the cause of pancreatitis is unclear
What is the imaging for acute pancreatitis:
Abdominal ultrasound looking for gallstones and duct dilation
Chest X-ray for complications such as pleural effusions or acute respiratory distress syndrome
CT pancreas with contrast should be done in patients who are deteriorating or have signs of sepsis or organ failure after 6-10 days - may detect complications such as pseudocysts or necrotising pancreatitis
Magnetic Resonance Cholangiopancreatography (MRCP) may be required in cases of pancreatitis secondary to gallstones
What is the conservative management for acute pancreatitis:
Ensure patients with severe pancreatitis (e.g. Glasgow score 3+, hypotension, oliguria, respiratory distress) are referred for intensive care assessment and input
Catheterise and monitor input-output
Insert an NG tube if significant vomiting
If the patient can eat, encourage oral intake as tolerated - they should not be made nil by mouth unless there is another reason for this
Enteral nutrition should be started within 72 hours of presentation (e.g. NG feeding) - if this fails parenteral nutrition should be considered
What is the medical management for acute pancreatitis:
IV fluid resuscitation is the mainstay of treatment - crystalloids should be used and should be titrated to achieve an adequate urine output given 4-6 hourly
Ensure adequate analgesia is given - opioids may be required
Antiemetics for nausea and vomiting
Antibiotics should not be given routinely - in some cases (e.g. confirmed pancreatic necrosis) broad-spectrum antibiotics should be given
Monitor for and treat any complications
For alcohol-related pancreatitis, alcohol withdrawal treatment may be required (i.e. benzodiazepines and pabrinex)
What is the surgical management for acute pancreatitis:
The underlying cause of pancreatitis should be treated; an ERCP may be required for gallstones in cases of jaundice, cholangitis or a dilated common bile duct on imaging
Laparoscopic cholecystectomy for gallstone pancreatitis should ideally be done in the same admission unless the patient is not fit for surgery
Surgical or interventional management may be required for complications e.g. drainage of large pancreatic pseudocysts or debridement of pancreatic necrosis
What are the local complications of acute pancreatitis:
A pancreatic pseudocyst is a fluid-filled sac that lacks a true epithelial lining (the wall is vascular and fibrotic); typically these form weeks after an episode of acute pancreatitis and can become infected, rupture, haemorrhage or cause compression of surrounding structures
Pancreatic necrosis occurs due to ischaemia of the pancreas and may become infected causing systemic inflammation and multi-organ failure
Peripancreatic fluid collections may occur, which can get infected leading to abscess formation
Haemorrhage from local vessels (e.g. pancreatic or splenic arteries or veins) can occur due to inflammation and enzyme release
Pancreatic fistulae may form due to pancreatic duct disruption, causing these to communicate with for example the skin, the abdominal cavity or the pleural space
What are the systemic complications of acute pancreatitis:
Acute Respiratory Distress Syndrome (ARDS) which is a severe lung injury with non-cardiogenic pulmonary oedema and respiratory failure
Acute kidney injury is a common complication which may require renal replacement therapy; often secondary to intravascular volume depletion due to third spacing
Disseminated intravascular coagulation
Sepsis for example secondary to infected pancreatic necrosis
Multi-organ failure which may lead to death
Hypocalcaemia occurs due to free fatty acids reacting with serum calcium to form salts, a process called saponification; this can cause tetany if severe
Hyperglycaemia due to disruptions in insulin production due to pancreatic destruction as well as systemic inflammation
Name some drugs that cause acute pancreatitis: FAT SHEEP
F: Furosemide (loop diuretic) and other diuretics like thiazides.
A: Azathioprine (and 6-mercaptopurine, immunosuppressants).
T: Tetracyclines.
S: Steroids (corticosteroids).
H: Hydrochlorothiazide (and other thiazides), Heparin.
E: Estrogens (oral contraceptives, hormone replacement therapy).
E: Ethanol (alcohol; while not a drug, it’s a common cause of pancreatitis).
P: Protease inhibitors (e.g., ritonavir, antiretrovirals used in HIV treatment).
What is the pathophysiology of alcoholic hepatitis:
Inflammation and necrosis of liver cells, characterised by tender hepatomegaly, jaundice, and systemic symptoms.
What are the signs and symptoms of alcoholic hepatitis:
Jaundice, fever, tender hepatomegaly, nausea, vomiting, malaise.