Gastrointestinal Flashcards
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.
What are the investigations for alcoholic hepatitis:
- LFTs- showing?
- AST/ALT- what do these show?
AST>ALT (2:1) - Elevated GGT
- Raised ALP
- Raised bilirubin
- Less albumin
- AST/ALT- what do these show?
- FBC- showing? (2)
- Non-megaloblastic macrocytic anaemia (sign of alcoholic liver disease)
- Thrombocytopaenia
- Increased PT- meaning?Sensitive marker of significant liver damageClotting factors 2, 7, 9, 10 are made by liver
- What scan is done?US to check for other causes of liver impairment e.g. malignancy
What is the acute management of alcoholic hepatitis:
IV Thiamine
or
Pabrinex as it contains:
- Thiamine (Vitamin B1) to prevent Wernicke’s encephalopathy
- Vitamin C
What is the management for severe alcoholic hepatitis:
- What steroid therapy is given and why?
- Corticosteroids- prednisolone
- Reduces short term mortality for severe alcoholic hepatitis
- What measurement is used to see who would benefit from steroid therapy in acute episodes?
Maddrey’s discriminant function (DF) calculated using prothrombin time and bilirubin concentration
How is the Maddrey’s discriminant function calculated?
It is 4.6 × [prothrombin time − control time (seconds)] + bilirubin in mg/dl. To calculate the DF using bilirubin in micromol/l divide the bilirubin value by 17.
What is the complication of alcoholic hepatitis:
Cirrhosis
- Describe the prognosis
- 10% mortality in 1st month
- 40% mortality in first year
- If alcoholic intake continues, will progress to cirrhosis in 1-3 years
Define anal fissures:
Anal fissures are linear tears or cracks in the distal anal canal, often causing severe pain and bleeding during or after bowel movements.
Causes of anal fissures:
Constipation: Hard stools can cause tearing in the distal anal canal.
Pregnancy: Increased risk during the third trimester and post-delivery.
Signs and symptoms of anal fissures:
Severe anal pain or a tearing sensation during bowel movements, lasting for hours afterward.
Anal spasms reported by about 70% of patients.
Bright red PR bleeding typically noticed on the stool or the toilet paper.
Over 90% of fissures are in the posterior midline, visible on parting the buttocks.
In chronic cases, a sentinel pile (skin tag) may be visible.
In severe cases, digital rectal examination may not be possible due to pain.
What are the investigations for anal fissures:
Investigation of anal fissures primarily involves a physical examination, including inspection of the anal area and potentially a digital rectal examination (if tolerable by the patient). Further investigations may be warranted in atypical cases or in those with potential signs of systemic disease like Crohn’s disease.
What is the management for anal fissures:
Treatment of constipation with the use of laxatives and dietary fiber.
Use of topical analgesics, such as lidocaine cream or jelly.
Application of topical vasodilators like nifedipine or nitroglycerine in patients with symptoms for longer than one week
Second-line treatments include topical calcium channel blockers (diltiazem), or oral nifedipine / diltiazem.
Patients with atypical anal fissures or symptoms/signs suggestive of Crohn’s disease should be referred to a gastroenterologist.
Define appendicitis:
Appendicitis refers to the inflammation of the appendix, a narrow, finger-like pouch extending from the caecum, the initial part of the large intestine.
What is the aetiology of appendicitis:
Acute appendicitis typically develops due to an obstruction within the appendix. This blockage can result from various factors, including fibrous tissue, a foreign body, or a hardened mass of stool (faecolith). Subsequent bacterial multiplication and infiltration of the appendix’s wall lead to tissue damage, pressure-induced necrosis, and the potential for perforation. In some cases, gangrene can develop due to thrombosis in the appendix’s arterial supply, specifically the ileocolic artery.
What are the symptoms of appendicitis:
Pain: Acute appendicitis manifests as progressively worsening periumbilical pain, which typically migrates to the right iliac fossa.
The initial dull, vague discomfort occurs due to irritation of the visceral afferent nerve fibres originating from the T8-T10.
When the inflammation and irritation of the appendix intensify, the pain becomes more localised. This transition from visceral pain to somatic pain occurs as the inflammation affects the parietal peritoneum covering the abdominal wall.
The parietal peritoneum is supplied by the somatic afferent nerve fibres derived from T10-L1. This results in the pain moving to the right iliac fossa, where the appendix is anatomically situated.
Gastrointestinal symptoms: These include nausea, vomiting, anorexia, and changes in bowel habits, such as constipation or diarrhea.
Systemic features: Patients may exhibit signs of infection, such as fever and tachycardia.
What are the signs of appendicitis:
Clinical examination may reveal localised tenderness and guarding in the right iliac fossa. McBurney’s point, located one-third of the way from the anterior superior iliac spine to the umbilicus, may be particularly tender.
Rovsing’s sign, eliciting right iliac fossa pain with palpation of the left iliac fossa, may also be present.
In cases of perforation, the abdomen may become rigid, and signs of peritonitis (rebound tenderness, percussion tenderness) may develop.
Additional signs, such as the Psoas sign (pain with passive extension of the right thigh), the Obturator sign (pain with passive internal rotation of the right hip), and the presence of a retrocecal appendix (which may not exhibit classical signs), can aid in diagnosis.
What are the investigations for appendicitis:
Bedside
VBG to check lactate levels
Pregnancy test (urine hCG) should be done in all females of reproductive age presenting with an acute abdomen
A urine dip may show the presence of leukocytes, indicative of appendicitis
Laboratory
FBC for white cell count to identify signs of infection
CRP to detect inflammation
U&Es to assess renal function if dehydration is suspected
LFTs and amylase to rule out biliary differentials
Clotting, G&S for theatre
Blood cultures if sepsis is suspected
Imaging
Erect chest x-ray to rule out perforation
CT of the abdomen and pelvis or ultrasound of the right iliac fossa (RIF) for further evaluation
Appendicitis is a clinical diagnosis and in most cases, imaging is not required before intervention.
What is the management for appendicitis:
Administer prophylactic antibiotics; initiate full septis 6 if appropriate
Laparoscopic appendicectomy is 1st line management following this
If there is evidence of perforation, open appendicectomy is preferred, with copius lavage in theatre
As per NICE guidelines, if there is negative imaging, a non-operative management strategy with IV fluids and antibiotics can be a safe and effective approach in selected patients with uncomplicated acute appendicitis
What are the complications of appendicitis:
Local abscess formation
Perforation
Gangrene
Postoperative wound infection
Peritonitis
Explain the signs and symptoms of a Appendicular abscess
The patient has presented with ongoing and worsening symptoms, signifying failed conservative management of appendicitis. She also has ‘swinging pyrexia’ which is a common finding in the presence of an abscess. An appendicular abscess is a common complication of acute appendicitis, particularly after a perforated appendix. Note that this patient’s observations are indicative of a SIRS response and she would benefit from an urgent appendicectomy
Define ascites?
Ascites is defined as the abnormal accumulation of fluid within the peritoneal cavity. This condition is typically associated with liver disease, particularly cirrhosis, but can also occur due to other medical conditions affecting the heart, kidneys, or peritoneum.
What is the epidemiology of ascites:
Ascites is a common complication of cirrhosis and represents a key landmark in the natural history of chronic liver disease. The prevalence and incidence of ascites depend significantly on the severity and duration of liver disease.
What is the aetiology of ascites?
The mechanism of ascites formation is complex and not fully understood. It is thought to involve portal hypertension causing increased hydrostatic pressure, leading to the transudation of fluid into the peritoneal cavity.
Name some causes of ascites?
Causes include liver disorders (cirrhosis, acute liver failure, liver metastases), cardiac causes (right heart failure) and others such as Budd-Chiari, Portal vein thrombosis etc. (see below).
Other types of ascites can form due to reduced oncotic pressure (nephrotic syndrome, Kwashiorkor), or due to malignancy (peritoneal carcinomatosis, or peritoneal metastasis), or infection (increased permeability – TB), and other causes of 3rd spacing (acute pancreatitis).
What are the signs and symptoms of ascites?
Abdominal distension
Abdominal discomfort or pain
Dyspnea
Reduced mobility
Anorexia and early satiety due to pressure on the stomach
Tense abdomen
Shifting dullness
Stigmata of the underlying cause (see below)
What are the investigations for ascites?
The primary investigation for ascites is an ascitic tap, which can provide valuable information about the content of the ascitic fluid. This is usually done under USS guidance to avoid e.g. perforating bowel.
The SAAG can help to determine the cause of ascites. It is calculated by subtracting the albumin concentration of the ascitic fluid from the serum albumin concentration.
Bloods (to help determine the underlying cause) - FBC, U+E, LFTs, CRP
Imaging - CT abdomen, CXR (looking for signs of right-sided heart failure)
A diagnosis of spontaneous bacterial peritonitis is suspected when ascitic fluid reveals a high neutrophil count with predominantly neutrophils and a negative gram stain.
How do you calculate the serum ascites albumin gradient (SAAG)
serum albumin concentration – ascites albumin concentration
Causes of a high SAAG (>11g/L)
Cirrhosis
Heart failure
Budd Chiari syndrome
Constrictive pericarditis
Hepatic failure
A high SAAG (>11g/L) suggests that the cause of the ascites is due to raised portal pressure. Raised hydrostatic pressure forces water into the peritoneal cavity whilst albumin remains within the vessels, thus resulting in a higher difference in the albumin concentration between the serum and ascitic fluid.
Causes of a low SAAG (<11g/L)
Cancer of the peritoneum, metastatic disease
Tuberculosis, peritonitis and other infections
Pancreatitis
Hypoalbuminaemia - nephrotic syndrome, Kwashiokor
Compare transudative ascites and exudative ascites:
What is the management for ascites?
Addressing the underlying cause
High SAAG - implementing a salt-restricted diet and fluid restriction
Administering spironolactone is first line. Providing adjunctive diuretic therapy such as furosemide if spironolactone is insufficient.
Spironolactone is an aldosterone-antagonist and is the first-line treatment for ascites in liver cirrhosis. Patients should be started on 100mg once daily and can be titrated up to 400mg once daily. Note: this is a much higher dose than when initiated in heart failure patients (12.5mg – 25mg once daily).
Conducting regular therapeutic paracentesis for patients with ascites refractory to medical management, whereby the fluid is drained from the abdomen over a few hours. These patients require replacement with human albumin solution (HAS) in order to avoid the ascites re-accumulating.
Patients with SBP are at increased risk of developing renal impairment, and this is one of the strongest predictors of mortality. These patients, particularly those with an increased serum creatinine, should be prescribed albumin to reduce this risk. The current British Society of Gastroenterology guidelines recommend infusing 1.5g albumin/kg in the first 6 hours, followed by 1g albumin/kg on day 3. One unit of HAS 20% contains 20g of albumin
If the ascitic tap shows neutrophils >250mm3, this is diagnostic of spontaneous bacterial peritonitis, a serious complication of ascites. This is treated with intravenous piperacillin-tazobactam.
Prophylactic antibiotics – 1st line = ciprofloxacin (indication if cirrhotic with ascites and ascites protein <15g/L, until ascites has resolved OR previous SBP OR hepato-renal syndrome OR child pugh C)
For refractory ascites in portal hypertension, a TIPS (transjugular intrahepatic portosystemic) shunt procedure can be considered.
Ovarian cancer with peritoneal metastases typically causes ascites with a low or high Serum Ascites Albumin Gradient (SAAG).
low
Define cholecystitis:
Cholecystitis refers to the acute or chronic inflammation of the gallbladder, which is commonly precipitated by cholelithiasis, or gallstones. Cholecystitis can be categorised into acute or chronic forms based on the duration and progression of inflammation, and into calculous or acalculous types based on the presence or absence of gallstones.
What is the epidemiology of cholecystitis:
Cholecystitis is a common gastrointestinal disease and one of the major causes of hospital admissions related to gastrointestinal disorders worldwide. It affects women more than men, with an estimated ratio of 2:1. Age is a significant risk factor, with incidence rising in individuals over 40 years of age. Other risk factors include obesity, ethnicity (higher prevalence in Hispanic and Native American populations), rapid weight loss, diabetes, pregnancy, and a family history of gallstones.
What is the pathophysiology of cholecystitis:
Cholecystitis predominantly results from the obstruction of the cystic duct by gallstones. This obstruction can lead to an infection in the gallbladder caused by organisms including:
E.coli (most common)
Klebsiella
Enterococcus
How can cholecystitis be classified:
acute and chronic. Additionally, cholecystitis can be further categorised based on the presence or absence of gallstones.
define acute cholecystitis:
This is characterised by the sudden onset of inflammation in the gallbladder. It is often associated with the presence of gallstones, particularly when one of these stones obstructs the cystic duct, leading to a buildup of bile and subsequent inflammation.
Define chronic cholecystitis :
This is a long-term, smoldering inflammation of the gallbladder, usually caused by the repeated irritation of gallstones. Over time, chronic cholecystitis can lead to thickening of the gallbladder wall and a decrease in its overall function. Unlike acute cholecystitis, chronic cholecystitis may have milder and more intermittent symptoms, including recurrent abdominal discomfort after meals.
Define calculous cholecystitis:
This type of cholecystitis occurs when gallstones are present in the gallbladder. These stones can obstruct the cystic duct, impair bile flow, and trigger an inflammatory response. Calculous cholecystitis is the most common form of cholecystitis.
Define Acalculous Cholecystitis
In contrast, acalculous cholecystitis develops without the presence of gallstones. It is often associated with other underlying medical conditions, such as critical illness, severe trauma, or prolonged fasting, which can lead to gallbladder stasis or ischaemia. Acalculous cholecystitis is less common but can be more severe and challenging to diagnose, as it may not present with the typical gallstone-related symptoms.
What are the signs and symptoms of cholecystitis:
Right upper quadrant/epigastric pain, which can radiate to the right shoulder tip if the diaphragm is irritated
Fever
Nausea and vomiting
Right upper quadrant tenderness
Positive Murphy’s sign
In cases with associated biliary obstruction, patients may exhibit jaundice, dark urine, and pale stools. However, these are not key features of cholecystitis.
What are the investigations for cholecystitis:
The first line investigation for suspected cholecystitis is an ultrasound examination of the abdomen, which can identify gallstones, gallbladder wall thickening, and pericholecystic fluid.
Alongside this, blood tests including FBC, U+Es, CRP and LFTs will help reveal if there is an underlying infection/evidence of sepsis, as well as any cholestasis
CT abdomen-pelvis (rarely MRI) is helpful to look for complications e.g. perforation, collections
What is the treatment for acute calculous cholecystitis:
Conservative Management: In mild cases, patients may be managed conservatively with bowel rest, fasting, and intravenous fluids to relieve symptoms.
Antibiotics: Antibiotics, often covering common pathogens like Escherichia coli and Klebsiella pneumoniae, are typically prescribed.
Cholecystectomy: The definitive treatment for acute calculous cholecystitis is laparoscopic cholecystectomy, which is recommended during the same hospital admission or within a week.
What is the treatment for Acalculous Cholecystitis
Prompt Surgery: Acalculous cholecystitis is considered a surgical emergency, and prompt cholecystectomy is typically recommended.
What is the treatment for Chronic Cholecystitis?
Elective Cholecystectomy: For patients with chronic cholecystitis, an elective laparoscopic cholecystectomy may be performed to prevent recurrent episodes and complications.
Symptomatic Management: In some cases, patients may initially receive symptomatic management and dietary modifications, but surgery is eventually recommended.
What is the difference in treatment between hot and cold elective cholecystectomy:
Hot Elective Cholecystectomy:
In cases of acute cholecystitis where the patient’s condition has improved with conservative management, but the inflammation is still present, an elective (“hot”) laparoscopic cholecystectomy should be performed within 6 weeks of the acute episode.
This approach balances the need to address the underlying cause with allowing the patient’s condition to stabilise.
Cold Elective Cholecystectomy:
In cases of chronic cholecystitis or asymptomatic gallstones, where there is no acute inflammation or infection, an elective (“cold”) laparoscopic cholecystectomy can be scheduled based on the patient’s convenience and availability.
This approach avoids the urgency associated with acute inflammation.
What are the complications of Laparoscopic Cholecystectomies?
Haemorrhage: Rapid hypotension or development of a retroperitoneal haematoma. May require surgical intervention if severe.
Post-cholecystectomy syndrome: Symptoms include colicky abdominal pain, diarrhea, vague abdominal pain, and jaundice. Management is symptomatic with e.g. anti-spasmodics for pain and nausea.
Bile duct injury: Presents with dark-colored urine and stools, potentially progressing to chemical peritonitis, causing abdominal pain and distension. Sometimes this requires surgical intervention.
Bile leak: The presence of bile in the drain with abnormal LFTs means a bile leak is the most likely diagnosis. Causes include slipped clips on the cystic duct remnant, missed distal common bile duct obstruction by a stone and subsequent ‘blowout’ higher up, and iatrogenic injury to common hepatic or bile duct. Endoscopic retrograde cholangiopancreatography (ERCP) may identify the site of the leak and allow simultaneous intervention with temporary stenting to allow biliary drainage
Pneumoperitoneum: Trapped air in the subcutaneous space can lead to subcutaneous emphysema, pneumothorax, or air embolism.
What are the complications of cholecystitis:
Empyema: This occurs when the gallbladder becomes filled with pus due to a severe infection. It can lead to systemic infection and sepsis if not treated promptly.
Gangrenous Cholecystitis: In severe cases of cholecystitis, the gallbladder tissue may become necrotic (dead) due to impaired blood flow. This condition is known as gangrenous cholecystitis and can lead to tissue perforation, abscess formation, or peritonitis.
Perforation: Prolonged inflammation can cause the gallbladder to rupture or perforate, leading to bile leakage into the abdominal cavity. This is a life-threatening emergency requiring immediate surgery.
Abscess Formation: A collection of pus can develop within or around the gallbladder, leading to an abscess. Abscesses may require drainage and antibiotic therapy.
Bile Duct Obstruction: Inflammation or gallstones can cause blockage of the common bile duct, leading to jaundice, pancreatitis, or cholangitis (bile duct infection).
Chronic Cholecystitis Complications: Long-term inflammation of the gallbladder may lead to scarring, thickening of the gallbladder walls, and impaired gallbladder function. This can result in chronic abdominal pain and discomfort.
What is the treatment for Empyema of the gallbladder?
necessitates urgent drainage, even in deteriorating patients, as antibiotics may be insufficient for treatment.
The source is his gallbladder which is obstructed and filled with pus, a condition called a gallbladder empyema. A gallbladder that is very distended is at risk of perforation and so should be drained urgently. If it was less distended it may be that he can wait for an urgent cholecystectomy, but to control his sepsis he need source control which means relieving the obstruction or draining the collection.
Define cirrhosis:
Cirrhosis refers to irreversible scarring of the liver with loss of normal hepatic architecture.
What is the epidemiology of cirrhosis:
The prevalence and incidence of cirrhosis are dependent on the underlying aetiological factors prevalent in the population. Alcohol and viral hepatitis, particularly Hepatitis B and C, are major contributors globally. Non-alcoholic fatty liver disease is increasingly becoming a significant cause due to rising obesity rates.
Name the common causes of cirrhosis:
Alcohol
Hepatitis B and C
Non-alcoholic fatty liver disease (NAFLD)
Name the less common causes of cirrhosis:
Autoimmune:
Autoimmune hepatitis
Primary biliary cirrhosis
Primary sclerosis cholangitis
Sarcoid
Genetic:
Haemochromatosis
Wilson’s disease
Alpha-1-antitrypsin deficiency
Drugs:
Methotrexate
Amiodarone
Isoniazid
Others:
Budd-Chiari Syndrome
Heart failure
Tertiary syphilis
What are the clinical features of cirrhosis divided on?
whether the cirrhosis is compensated or decompensated.
What are the signs and symptoms of compensated cirrhosis?
Fatigue and anergia
Anorexia and cachexia
Nausea or abdominal pain
Spider naevi
Gynaecomastia
Finger clubbing
Leuconychia
Dupuytren’s contracture
Caput medusae
Splenomegaly
In addition to the signs of compensated cirrhosis what does uncompensated cirrhosis present with:
Ascites and oedema
Jaundice
Pruritus
Palmar erythema
Gynaecomastia and testicular atrophy
Easy bruising
Encephalopathy/confusion
Liver ‘flap’
What initial blood tests should one do for liver cirrhosis:
Liver Function Tests: AST, ALT, ALP, GGT, Albumin, and Bilirubin
Full blood count to look for leucocytosis, thrombocytopaenia, and anaemia
Urea and electrolytes to establish baseline renal function and look for hepato-renal syndrome or any electrolyte abnormalities
INR to look for coagulopathy
A low platelet count, elevated aspartate aminotransferase (AST): alanine transaminase (ALT) ratio, high bilirubin, low albumin, or increased prothrombin time or international normalized ratio (INR) can suggest impaired liver function. Patients can however also present with normal blood tests which is why clinical examination findings are equally important.
Specific tests to determine the potential cause such as Hepatitis serology, cytomegalovirus serology, iron studies, α-1 anti-trypsin, caeruloplasmin level, and auto-antibodies
What imaging and invasive investigations should one do for liver cirrhosis:
Peritoneal tap for microscopy and culture if ascites is present
Doppler ultrasound to identify Budd-Chiari syndrome
Transient elastography (fibroscan) or acoustic radiation force impulse imaging should be done for patient groups at risk of cirrhosis: those with hepatitis C infection, increased alcohol intake (men who drink >50 units of alcohol/week, women who drink >35 units of alcohol/week), and those with known alcohol-related disease
If cirrhosis is not diagnosed on initial testing, these patients should have retesting for cirrhosis every 2 years
Liver biopsy for confirmation of diagnosis if in doubt
The severity of liver cirrhosis can be estimated by calculating the what score?
Child Pugh score
What is the scoring system for liver cirrhosis:
The scores are added and the degree of cirrhosis is classified as Child-Pugh A (<7 points), B (7-9 points) or C (>9 points). The score can be used as a predictor of mortality, and may also be used to predict the need for a liver transplant.
What is the MELD score used for?
The Model for End-Stage Liver Disease (MELD) score evaluates the severity of liver disease based on bilirubin, creatinine, and INR levels.
Higher scores indicate a greater risk of mortality within a three-month period. MELD scores are used to prioritise patients for liver transplantation.
In liver cirrhosis, MELD scores ≥15 typically indicate significant disease severity, with increased mortality rates and the need for liver transplantation consideration.
What is the conservative management for liver cirrhosis:
Ensuring good nutrition and total alcohol abstinence
Avoiding non-steroidal anti-inflammatory drugs, sedatives, and opiates
6 monthly ultrasound scans and serum α-fetoprotein tests for hepatocellular carcinoma detection
Upper gastrointestinal endoscopy surveillance for oesophageal varices may be needed at diagnosis (one-off) and every 3 years, unless the person is taking carvedilol or propranolol non-selective beta-blocker therapy for primary prevention of decompensation, or for primary prevention of bleeding from medium or large varices
What is the medical management for cirrhosis:
Using cholestyramine for pruritus
Managing ascites with fluid restriction, low-salt diet, pharmacological management with spironolactone; furosemide, therapeutic paracentesis, and albumin infusions in severe cases
Reducing recurrent episodes of encephalopathy through prophylactic lactulose and rifaximin
Using prophylactic antibiotics in patients at high-risk of spontaneous bacterial peritonitis
What is the surgical management for liver cirrhosis:
Liver transplantation is the only definitive management for liver cirrhosis, and different scoring criteria are used to assess severity and suitability for transplanation
What criteria is used in acute liver failure:
King’s criteria
Paracetamol Toxicity:
pH - < 7.3 at any time or < 7.30 - 7.35 after fluid resuscitation
Prothrombin time (INR) - > 100 seconds or > 6.5
Grade 3 or 4 encephalopathy
Non-Paracetamol-Induced Fulminant Hepatic Failure:
INR - > 50 seconds or > 3.5 despite Vitamin K treatment
Serum Creatinine - > 300 µmol/L
Grade 3 or 4 encephalopathy
If there is chronic liver failure leading to advanced cirrhosis, UK End-stage Liver Disease (UKELD) score is used to predict disease severity and is based on the MELD score but also includes sodium
What are the complications of acute liver failure:
Ascites
This results from portal hypertension and hypoalbuminaemia. It gives rise to other complications such as spontaneous bacterial peritonitis.
Spontaneous bacterial peritonitis (SBP)
Sudden peritonitis can occur in patients with ascites. It may present atypically (often with no abdominal tenderness or guarding) and should be suspected in patients who deteriorate suddenly with no other obvious cause. An ascitic tap with neutrophils >250mm³ indicates SBP. Patients with a low ascitic albumin are especially at risk and should be treated with prophylactic antibiotics.
Liver failure
With its sequelae of hepatic encephalopathy, jaundice and coagulopathy. The former can result in cerebral oedema progressing to raised intracranial pressure and death, and the latter can contribute to life-threatening bleeds in those with a source of bleeding due to thrombocytopaenia.
Hepatocellular carcinoma
Patients with cirrhosis are at significantly increased risk, especially those with Hepatitis B and C.
Oesophageal varices ± haemorrhage
The development of portal hypertension in cirrhosis leads to dilatation of oesophageal veins. These are liable to rupture and this can be fatal, especially in patients with coagulopathy. There can also be gastric varices, and caput medusae (dilatation of umbilical veins) – these are due to portosystemic collaterals trying to get around the cirrhotic liver.
Renal failure
Cirrhosis and ascites with renal failure is known as hepatorenal syndrome if other causes of acute kidney injury have been ruled out. Abnormal haemodynamics in liver disease cause renal vasoconstriction which makes the kidneys more susceptible to injury. It has a very poor prognosis.
What is the treatment for hepatic encephalopathy:
A key sign of this is asterixis
first line treatment for this is lactulose. Lactulose is a laxative which also helps by eliminating ammonia. Patients with hepatic encephalopathy should be prescribed regular lactulose and aim for 2-3 loose stools per day
In individuals with unexplained liver dysfunction, family history of liver disease and signs suggestive of chronic obstructive pulmonary disease you should consider investigating for
alpha-1 antitrypsin deficiency with a combination of liver function tests and pulmonary function testing including spirometry.
Patients with cirrhosis due to hepatitis B infection require 6-monthly screening for hepatocellular carcinoma with ?
ultrasound and alpha-fetoprotein measurement
What of the following is offered for prophylaxis of spontaneous bacterial peritonitis?
Prophylactic ciprofloxacin or norfloxacin is recommended as per NICE guidelines for those at high risk of spontaneous bacterial peritonitis, including those with cirrhosis and ascites with a level of ascitic protein of 15 g/L or less, until the resolution of ascites.
Define coeliac disease:
Coeliac disease is a T cell-mediated autoimmune disorder affecting the small intestine. The condition arises due to the production of an auto-antibody against gluten, specifically its component called prolamin, which results in inflammation and villous atrophy of the small bowel leading to malabsorption.
What is the epidemiology of coeliac disease:
Coeliac disease exhibits a bimodal age of onset, presenting either in infancy or between the ages of 50-60. It is notably more prevalent in individuals of Irish descent.
What is the aetiology of coeliac disease?
Coeliac disease is associated with a positive family history, the presence of the HLA-DQ2 allele, and other autoimmune diseases, including type 1 diabetes mellitus.
What are the gastrointestinal symptoms of coeliac disease?
Abdominal pain
Distension
Nausea and vomiting
Diarrhoea
Steatorrhoea (indication of severe disease)
What are the systemic symptoms of coeliac disease?
Fatigue
Weight loss or failure to thrive in children (indication of severe disease)
What may physical examination reveal in coeliac disease?
Pallor (secondary to anaemia)
Short stature and wasted buttocks (secondary to malnutrition)
Signs of vitamin deficiency due to malabsorption (e.g., bruising secondary to vitamin K deficiency)
Dermatological manifestations: dermatitis herpetiformis (pruritic papulovesicular lesions over the buttocks and extensor surfaces of the arms, legs, and trunk).
Abdominal distension
What are the investigations for coeliac disease?
Bedside:
Stool culture to exclude infectious causes. A faecal calprotectin may also be done as IBD is a differential.
Bloods:
Blood tests include FBC, U&E, bone profile, LFT, Iron, B12, and Folate levels.
It is important to screen for conditions related to malabsorption such as mixed anaemias, vitamin deficiencies.
First line serological tests such as anti-TTG IgA antibody and IgA level, followed by anti-TTG IgG, anti-endomyseal antibody, (anti-gliadin is not recommended by NICE.)
anti-endomysial antibodies
Imaging/Invasive:
Oesophago-gastroduodenoscopy (OGD) and duodenal/jejunal biopsy, is considered the gold standard for diagnosis.
Histology typically reveals sub-total villous atrophy, crypt hyperplasia, and intra-epithelial lymphocytes.
NB: in the context of antibody blood tests and OGDs looking for changes, the patient needs to have been eating gluten for 6 weeks prior to the investigation.
IgA deficiency can result in false negative results for Tissue Transglutaminase antibody tests in individuals with suspected coeliac disease.
What is the management of coeliac disease?
Primary management of coeliac disease is a lifelong commitment to a gluten-free diet. Patient education about food items containing gluten is crucial.
Common food items which contain gluten include bread, pasta, pastries and most beers.
Regular monitoring of the patient is necessary to ensure adherence to the diet and screen for potential complications. Serological tests can also be done to assess response to removing dietary gluten intake.
Dermatitis herpetiformis is managed with dapsone
What are the complications of coeliac disease:
Mixed anaemia
Hyposplenism (increasing susceptibility to encapsulated organisms). Patients with coeliac disease therefore require annual flu and one-off pneumovax vaccinations
Osteoporosis (a DEXA scan may be needed)
Enteropathy-associated T cell lymphoma (EATL; a rare type of non-Hodgkin lymphoma), the likelihood of which is proportional to the strength of adherence to a gluten-free diet.
NICE guidelines dictate that coeliac disease should be tested for in those with ? This is owing to the underlying autoimmune element to these diseases
a new diagnosis of autoimmune thyroid disease or type 1 diabetes.
Explain the blood results from coeliac disease?
Iron deficiency anaemia causes a microcytic anaemia whereas B12 and folate deficiency causes macrocytic anaemia. The MCV is an average value, so a normal MCV with a high red cell distribution width is suspicious for a mixture of large and small cells.
Explain this blood film in context of coeliac disease:
A blood film is performed, which identifies multiple small, round inclusions within her red blood cells. These appear basophilic (purple) on a hematoxylin and eosin (H&E) stain.
The red blood cell abnormality described is in keeping with Howell-Jolly bodies. On a blood smear stained with standard H&E, DNA stains purple (basophilic) and protein stains pink (eosinophilic). Thus, this patient has DNA inclusions within her red blood cells. Mature erythrocytes should have no nucleus, as it is eliminated during development. However, this process is not perfect and even in healthy individuals, some abnormal erythrocytes with a small amount of DNA remain. These imperfect cells should be recognised and destroyed by the spleen. The presence of the Howell-Jolly bodies is thus an indication of hyposplenism, which may be explained by underlying coeliac disease - around 30% of people with coeliac disease have hyposplenism.
Define colorectal cancer:
Colorectal cancer is a type of malignancy that starts in the colon or rectum. It is a result of uncontrolled cell growth in the lining of the colon or rectum. It may start as benign polyps, which can over time progress to cancerous tumours if not removed.
What are the risk factors for colorectal cancer:
Strong risk factors
Increasing age
Hereditary syndromes
Familial adenomatous polyposis
Hereditary nonpolyposis colorectal cancer (Lynch Syndrome)
Juvenile polyposis
Peutz-Jeghers syndrome
Increased alcohol intake
Smoking tobacco
Processed meat
Obesity
Previous exposure to radiation
Inflammatory bowel disease
Weak risk factors
Lack of dietary fibre
Limited physical activity
Asbestos exposure
Red meat (non-processed)
What are the types of colon cancer?
- Sporadic (95%)
- Hereditary non-polyposis colorectal carcinoma (HNPCC, 5%)- most common inheritable form
- Familial adenomatous polyposis (FAP, <1%)
Which part of the colon do colorectal cancers occur in most?
- 60% rectum and sigmoid
- 30% descending
- 10% rest of colon
What are the general signs and symptoms of colorectal cancers:
Rectal bleeding: Often noticed as blood in the stool.
Unexplained weight loss
Change in bowel habit: Patients might experience alterations in their bowel movements, such as diarrhea or constipation.
Abdominal pain: Persistent abdominal discomfort or pain may be present.
Iron-deficiency anaemia: This can result from chronic bleeding.
Bowel obstruction: advanced tumours can obstruct the bowel, resulting in abdominal pain, nausea and vomiting
What right-sided tumour signs are there (caecum, ascending and transverse colon)?
- Melaena (dark blood in stool). May be occult (not visible)
- Iron deficiency anaemia signs (e.g. lethargy)
- Diarrhoea
What left-sided tumour signs are there (splenic flexure, descending and sigmoid colon)? (3)
- Changes in bowel habits (size, consistency, frequency)
- Blood-streaked stools (mixed in)
- Colicky abdominal pain (due to obstruction because of narrower lumen)
What rectal tumour signs are there?
- Hematochezia (fresh, bright red blood in stool)
- Rectal pain
- Tenesmus (urge to empty rectum or bladder)
- Flatulence
- Faecal Incontinence
What is the staging for colorectal cancers:
T: Tis (carcinoma in situ/intramucosal cancer), T1 (extends through the mucosa into the submucosa), T2 (extends through the submucosal into the muscularis), T3 (extends through the muscularis into the subserosa), T4 (extends into neighbouring organs or tissues).
N: N0 (no regional lymph node involvement), N1 (metastasis to 1-3 regional lymph nodes), N2 (metastasis to 4 or more regional lymph nodes).
M: M0 (no distant metastasis), M1 (distant metastasis). Staging informs both the prognosis and the treatment plan.
Patients with Duke’s stage C or stage III (T1-4, N1-2, M0) colon cancer benefit from adjuvant chemotherapy. Note that patients without lymph node involvement but with high risk features (such as vascular or perineural invasion) also show improved survival with adjuvant chemotherapy.
What is the screening for colorectal tumours?
The aim of screening is to detect cancer at an earlier (asymptomatic) stage, when it is easier to treat and patients have a better chance of survival.
Current NHS screening programmes include:
Faecal immunochemical test (FIT) every 2 years for men and women age 60-74. If positive patients are referred for colonoscopy.
One-off flexible sigmoidoscopy has now been discontinued.
This screening programme reduces the risk of dying from bowel cancer by 16%.
What is the criteria for urgent 2 week wait pathway:
With an abdominal mass.
With a change in bowel habit.
With iron-deficiency anaemia.
Aged 40 years and over with unexplained weight loss and abdominal pain.
Aged under 50 years with rectal bleeding and either of the following unexplained symptoms:
Abdominal pain.
Weight loss.
Aged 50 years and over with any of the following unexplained symptoms:
Rectal bleeding.
Abdominal pain.
Weight loss.
Aged 60 years and over with anaemia even in the absence of iron deficiency.
If they have a FIT result of at least 10 micrograms, they should be referred for an urgent (within 2 weeks) colonoscopy.
FIT testing should be offered even if they have had a negative result from the screening programme previously.
Adults with a rectal mass should still be considered for a suspected cancer pathway referral (for an appointment within 2 weeks) and do not need a prior FIT test.
What are the investigations for colorectal tumours?
Bloods - FBC (anaemia), iron studies, and carcinoembryonic antigen (CEA) are useful initial investigations:
It would show - Microcytic anaemia with low ferritin in iron deficiency anaemia
CEA is not used as a diagnostic tool but is a tumour marker that can be used to monitor therapeutic response to interventions.
The gold standard investigation is a colonoscopy. It allows
Direct visualisation of the colon
Biopsies to be taken
Removal of any polyps seen
If colonoscopy cannot be performed, either due to technical difficulties, poor tolerance of bowel preparation or there is an increased risk of colonic perforation a CT colonoscopy is a suitable alternative but does not allow biopsy.
After a histological diagnosis is made, a CT chest, abdomen and pelvis should be performed to stage the disease, so an appropriate intervention can be planned.
In rectal disease, a pelvic MRI or endorectal ultrasound are preferred over CT scan, as are better for identifying locally invasive disease.
What is the management for colorectal tumours?
Surgical excision + adjuvant or neoadjuvant chemo/radiotherapy
What is the Duke’s staging for colorectal tumours?
What is the management of colon cancer:
Stage I-III disease: surgical resection ± adjuvant chemotherapy. The type of surgery depends on the tumour site: right hemicolectomy for tumours of the caecum and ascending colon, left hemicolectomy for tumours of the distal transverse colon and descending colon, and sigmoid colectomy for tumours of the sigmoid colon.
Stage IV disease (metastases): treatment is as above, but neoadjuvant chemotherapy may also be performed. The staged colectomy and resection of metastatic disease is performed after neoadjuvant chemotherapy.
In terms of specific surgical procedures, patients with caecal and ascending colon tumours undergo right hemicolectomy
What is the management of rectal cancer?
For patients with rectal cancer suitable for surgery: Anterior resection for tumours >8 cm from the anal canal or involving the proximal 2/3 of the rectum. Abdomino-perineal (AP) resection for tumours <8 cm from the anal canal or involving the distal 1/3 of the rectum.
Patients with stage III disease benefit from adjuvant chemotherapy.
Patients with stage IV disease benefit from adjuvant chemoradiotherapy
What is the non-surgical managememt of colon?
For patients unsuitable for surgery management is with chemotherapy (FOLFOX or FOLFIRI i.e. oxaliplatin/irinotecan plus folinic acid plus fluorouracil are the preferred regimens).
New monoclonal antibody therapies are becoming available. Note that NICE concluded that cetuximab (anti-EGFR), but not bevacizumab (anti-VEGF), is cost effective in combination with chemotherapy for metastatic colorectal cancer.
Note that stenting may be used as a palliative measure for patients with obstructing tumours of the sigmoid colon or rectum. If the patient presents with acute bowel obstruction, a Hartmann’s procedure may be required as an interim measure (resection of the rectosigmoid colon with formation of a temporary end colostomy and anorectal stump).
What is familial adenomatous polyposis (FAP)
Caused by a mutation in the adenomatous polyposis coli (APC) gene and has an autosomal dominant inheritance pattern.
Patients develop hundreds of adenomatous polyps in their teens and are virtually guaranteed to develop colorectal cancer by their 20s, unless they undergo prophylactic proctocolectomy.
Note that there is a high risk of developing duodenal cancer, so patients undergo regular endoscopic surveillance.
Gardener’s syndrome is a variant of FAP in which patients may also develop epidermal cysts, supernumerary teeth, osteomas, and thyroid tumours.
What is Hereditary non-polyposis colorectal cancer (HNPCC)/Lynch syndrome?
Is caused by a mutation in the mismatch repair genes MLH1/MSH2 and has an autosomal dominant inheritance pattern.
Patients have an 80% risk of developing colorectal cancer by their 30s.
There is increased risk of additional cancers such as gastric, endometrial, breast, and prostate cancer.
Patients are managed with regular endoscopic surveillance.
What is Peutz-Jeghers syndrome?
Is caused by a mutation in the STK11 gene and has an autosomal dominant inheritance pattern.
Patients typically present in their teens with mucocutaneous pigmentaiton and hamartomatous polyps.
Note that the risk of neoplastic transformation of hamartomatous polyps is low, but many polyps are present so patients are at increased risk of developing colorectal cancer. They are managed with regular endoscopic surveillance.
Define constipation:
Constipation may involve any or all of the following (Rome IV criteria):
Fewer than three bowel movements per week
Hard stool in more than 25% of bowel movements
Tenesmus (sense of incomplete evacuation) in more than 25% of bowel movements
Excessive straining in more than 25% of bowel movements
A need for manual evacuation of bowel movements
How can constipation be categorised:
Primary constipation: no organic cause, thought to be due to dysregulation of the function of the colon or anorectal muscles
Secondary constipation: due to factors such as diet, medications, metabolic, endocrine or neurological disorders or obstruction
What are the risk factors for constipation:
Advanced age
Inactivity
Low calorie intake
Low fibre diet
Certain medications
Female sex
Name some causes of constipation:
Dietary factors, such as inadequate fibre or fluid intake
Behavioural factors, like inactivity (common cause of constipation in inpatients) or avoidance of defecation
Electrolyte disturbances, like hypercalcaemia
Certain drugs, particularly opiates, calcium channel blockers and some antipsychotics
Neurological disorders, like spinal cord lesions, Parkinson’s disease, and diabetic neuropathy
Endocrine disorders, such as hypothyroidism
Colon diseases, like strictures or malignancies. Bowel obstruction can also cause complete constipation (obstipation)
Anal diseases, like anal fissures or proctitis
What are the signs and symptoms of constipation:
Infrequent bowel movements (less than 3 per week)
Difficulty passing bowel motions
Tenesmus
Excessive straining
Abdominal distension
Abdominal mass felt at the left or right lower quadrants (stool)
Rectal bleeding
Anal fissures
Haemorrhoids
Presence of hard stool or impaction on digital rectal examination
ALARMS features which may indicate gastrointestinal malignancy include: anaemia, weight loss, anorexia, recent onset, melaena/haematemesis/PR bleeding, swallowing difficulties
What is the two week wait pathway for constipation and what are they trying to rule out?
2-week-wait criteria
Constipation (or diarrhoea) with weight loss, 60 and over. Consider an urgent, direct access CT scan, or an urgent ultrasound scan if CT is not available, to rule out pancreatic cancer
If it a patient does not fit the 2-week-wait criteria above, and the cause is thought to be primary, then it is likely that no further investigations are needed.
What are the investigations for constipation?
Bedside:
PR exam
Stool culture – MC&S, ova,cysts,parasites
FIT testing (if accompanied with new rectal bleeding and signs suggestive of colorectal cancer), faecal calprotectin
Bloods:
Full blood count (may show an anaemia), U+Es (including calcium), TFTs
Imaging:
Abdominal x-ray if suspicious of a secondary cause of constipation such as obstruction (may reveal faecal loading)
Barium enema if suspicious of impaction or rectal mass
Colonoscopy if suspicious of lower GI malignancy
What is the conservative management for constipation?
Conservative:
Lifestyle modifications such as dietary improvements and increased exercise
What is the medical management for constipation:
Laxatives are the mainstay of treatment, please see summary table below.
Explain bulking agents:
MOA, Indications, side effects and contraindications
Explain stimulants:
MOA, Indications, side effects and contraindications
Explain stool softeners:
MOA, Indications, side effects and contraindications
explain osmotic laxatives:
MOA, Indications, side effects and contraindications
Explain phosphate enema:
MOA, Indications, side effects and contraindications
What is the surgical management of constipation
Surgical:
If suspicions of colorectal cancer, referral to lower GI/colorectal surgeons
If concerns over obstruction these patients need to go to A&E for urgent management and imaging
In older adults, tricyclic antidepressants can contribute to constipation by causing anticholinergic side effects.
Amitriptyline
Iatrogenic constipation is a common side effect of long-term levodopa treatment for Parkinson’s disease.
:)
Define diverticular disease:
is a term used to describe conditions related to the presence of diverticula, which are small, bulging pouches that can form in the lining of the digestive system, most commonly in the lower part of the colon (sigmoid colon).
What is the severity scale of c.difficile infections:
What is the severity scale of c.difficile infections:
What are the two main types of hiatus hernias:
Sliding hiatus hernia and rolling hiatal hernia
Compare Crohn’s disease and ulcerative colitis:
What does the truelove and Witt’s severity index measure:
What are the grades of encephalopathy?
