Gastrointestinal Flashcards

(356 cards)

1
Q

Define ascending cholangitis:

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the causes of ascending cholangitis:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the aetiology of ascending cholangitis:

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is Charcot’s triad in ascending cholangitis:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

In severe cases of ascending cholangitis what is Reynolds pentad:

A

Right upper quadrant pain
Fever
Jaundice
Hypotension
Mental confusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the key clinical features between ascending cholangitis, cholecystitis and biliary colic:

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the investigations for ascending cholangitis:

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Define acute pancreatitis

A

Acute pancreatitis refers to an inflammatory process affecting the pancreas as well as local or distant tissues and organs in some cases.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the epidemiology of acute pancreatitis:

A

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%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Name some causes of acute pancreatitis: GET SMASHED

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What do we use to classify acute pancreatitis:

A

Glasgow-imrie score

each of the following scores 1 point and a score of 3 or more predicts severe pancreatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the criteria of the Glasgow score:

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the signs and symptoms of acute pancreatitis:

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the bedside tests for acute pancreatitis:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the blood tests for acute pancreatitis:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the imaging for acute pancreatitis:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the conservative management for acute pancreatitis:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the medical management for acute pancreatitis:

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the surgical management for acute pancreatitis:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the local complications of acute pancreatitis:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the systemic complications of acute pancreatitis:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Name some drugs that cause acute pancreatitis: FAT SHEEP

A

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).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the pathophysiology of alcoholic hepatitis:

A

Inflammation and necrosis of liver cells, characterised by tender hepatomegaly, jaundice, and systemic symptoms.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the signs and symptoms of alcoholic hepatitis:

A

Jaundice, fever, tender hepatomegaly, nausea, vomiting, malaise.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
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 - FBC- showing? **(2)** - Non-megaloblastic macrocytic anaemia (sign of alcoholic liver disease) - Thrombocytopaenia - Increased PT- meaning? Sensitive marker of significant liver damage Clotting 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
26
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
27
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
28
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.
29
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
30
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.
31
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.
32
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.
33
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.
34
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.
35
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.
36
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.
37
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.
38
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.
39
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.
40
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
41
What are the complications of appendicitis:
Local abscess formation Perforation Gangrene Postoperative wound infection Peritonitis
42
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
43
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.
44
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.
45
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.
46
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).
47
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)
48
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.
49
How do you calculate the serum ascites albumin gradient (SAAG)
serum albumin concentration – ascites albumin concentration
50
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.
51
Causes of a low SAAG (<11g/L)
Cancer of the peritoneum, metastatic disease Tuberculosis, peritonitis and other infections Pancreatitis Hypoalbuminaemia - nephrotic syndrome, Kwashiokor
52
Compare transudative ascites and exudative ascites:
53
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.
54
Ovarian cancer with peritoneal metastases typically causes ascites with a low or high Serum Ascites Albumin Gradient (SAAG).
low
55
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.
56
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.
57
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
58
How can cholecystitis be classified:
acute and chronic. Additionally, cholecystitis can be further categorised based on the presence or absence of gallstones.
59
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.
60
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.
61
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.
62
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.
63
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.
64
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
65
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.
66
What is the treatment for Acalculous Cholecystitis
Prompt Surgery: Acalculous cholecystitis is considered a surgical emergency, and prompt cholecystectomy is typically recommended.
67
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.
68
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.
69
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.
70
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.
71
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.
72
Define cirrhosis:
Cirrhosis refers to irreversible scarring of the liver with loss of normal hepatic architecture.
73
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.
74
Name the common causes of cirrhosis:
Alcohol Hepatitis B and C Non-alcoholic fatty liver disease (NAFLD)
75
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
76
What are the clinical features of cirrhosis divided on?
whether the cirrhosis is compensated or decompensated.
77
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
78
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'
79
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
80
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
81
The severity of liver cirrhosis can be estimated by calculating the what score?
Child Pugh score
82
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.
83
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.
84
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
85
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
86
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
87
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
88
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.
89
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
90
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.
91
Patients with cirrhosis due to hepatitis B infection require 6-monthly screening for hepatocellular carcinoma with ?
ultrasound and alpha-fetoprotein measurement
92
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.
93
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.
94
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.
95
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.
96
What are the gastrointestinal symptoms of coeliac disease?
Abdominal pain Distension Nausea and vomiting Diarrhoea Steatorrhoea (indication of severe disease)
97
What are the systemic symptoms of coeliac disease?
Fatigue Weight loss or failure to thrive in children (indication of severe disease)
98
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
99
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.
100
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
101
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.
102
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.
103
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.
104
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.
105
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.
106
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)
107
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%)
108
Which part of the colon do colorectal cancers occur in most?
- 60% rectum and sigmoid - 30% descending - 10% rest of colon
109
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
110
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
111
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)
112
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
113
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.
114
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%.
115
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.
116
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.
117
What is the management for colorectal tumours?
Surgical excision + adjuvant or neoadjuvant chemo/radiotherapy
118
What is the Duke's staging for colorectal tumours?
119
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
120
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
121
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).
122
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.
123
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.
124
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.
125
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
126
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
127
What are the risk factors for constipation:
Advanced age Inactivity Low calorie intake Low fibre diet Certain medications Female sex
128
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
129
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
130
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.
131
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
132
What is the conservative management for constipation?
Conservative: Lifestyle modifications such as dietary improvements and increased exercise
133
What is the medical management for constipation:
Laxatives are the mainstay of treatment, please see summary table below.
134
Explain bulking agents: MOA, Indications, side effects and contraindications
135
Explain stimulants: MOA, Indications, side effects and contraindications
136
Explain stool softeners: MOA, Indications, side effects and contraindications
137
explain osmotic laxatives: MOA, Indications, side effects and contraindications
138
Explain phosphate enema: MOA, Indications, side effects and contraindications
139
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
140
In older adults, tricyclic antidepressants can contribute to constipation by causing anticholinergic side effects.
Amitriptyline
141
Iatrogenic constipation is a common side effect of long-term levodopa treatment for Parkinson's disease.
:)
142
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).
143
Define Diverticulosis:
refers to the simple presence of diverticula. In many cases, diverticulosis is asymptomatic, and individuals may not even be aware that they have these diverticula as they are typically discovered incidentally during tests for other conditions.
144
Define diverticulitis:
a subset of diverticular disease, occurs when these diverticula become inflamed or infected. This condition is typically characterized by severe abdominal pain, fever, and nausea. Diverticulitis often requires treatment, which can include antibiotics, pain relievers, and, in severe cases, surgery.
145
What are the risk factors for diverticular disease:
The primary risk factor for diverticular disease is age, with the condition being more prevalent in individuals over the age of 50. Other risk factors include consuming a low-fibre Western diet, obesity, lack of exercise, and certain medications such as nonsteroidal anti-inflammatory drugs (NSAIDs) and opiates.
146
What are the signs and symptoms of diverticular disease:
Diverticular disease typically presents with: Constipation Left lower quadrant abdominal pain Possible rectal bleeding Physical examination may be normal or may demonstrate tenderness in the left lower quadrant on digital rectal examination. pain relieved by defecation
147
What are the signs and symptoms of diverticulitis:
Left lower quadrant abdominal pain Fever Nausea/vomiting Pyrexia and left lower quadrant tenderness/guarding on physical examination Diffuse abdominal tenderness suggestive of perforation or generalised peritonitis.
148
What are the investigations for diverticular disease:
Abdominal imaging (CT scan or ultrasound): Thickening of the sigmoid colon wall and pericolonic fat stranding Blood tests demonstrating inflammation (leukocytosis) Colonoscopy/endoscopy
149
What is the management of asymptomatic diverticulosis:
No treatment is required if diverticula are seen incidentally on imaging or endoscopy.
150
What is the management of Symptomatic diverticular disease?
Patients should be advised to increase dietary fibre intake and hydration. If there is evidence of diverticulitis (leukocytosis, fever), patients are initially managed with oral antibiotics (e.g. 7 days co-amoxiclav). Analgesia may also be required, prescribed in a step-wise fashion, starting with oral paracetamol. A low residue diet is also advised.
151
What is the Management of diverticulitis:
Patients unresponsive to antibiotics, or presenting with an abscess, perforation, stricture, or obstruction may require surgical intervention. A localised abscess may be drained under CT/ultrasound guidance, with surgery considered if this fails.
152
What are the short term complications of diverticular disease:
Abscess formation: Initially managed with bowel rest, broad-spectrum antibiotics ± CT-guided percutaneous drainage. Surgical management is considered if medical management fails. Perforation: A surgical emergency suspected in cases of generalised peritonitis. Free air on the abdominal x-ray and high clinical suspicion necessitate urgent exploratory laparotomy.
153
What are the long term complications of diverticular disease:
Fistula formation: Most commonly colovesical fistulas, presenting with pneumaturia, faecaluria, and recurrent UTIs. Diagnosed with cystoscopy or cystography and require surgical repair. Colovaginal, coloenteric, colouterine, and colourethral fistulas may also occur. Fibrosis: Secondary to inflammation, resulting in strictures and large bowel obstruction.
154
Define gallstones:
Gallstones are solid deposits, often of cholesterol or bilirubin (a pigment), that form within the gallbladder, a small organ responsible for storing bile. These stones may range from the size of a grain of sand to larger than a golf ball.
155
What three things cause gallstones:
Super-saturation of bile with cholesterol Gallbladder dysmotility leading to stasis Excessive bilirubin excretion
156
What are the three types of gallstones:
Pigment (<10%) Associated with haemolysis, stasis and infection. Haemolysis increases the amount of pigment productions thereby increasing the risk of pigment stone formation Cholesterol (90%) Associated with female sex, increasing age and obesity. Mixed
157
Name some risk factors for gallstones:
Obesity Female sex Diabetes Family history Chronic loss of bile salts (e.g., terminal ileal disease, Crohn's disease) Combined oral contraceptive pill Pregnancy Rapid weight change (e.g., bariatric surgery) Chronic haemolysis (e.g., sickle cell anaemia, G6PD deficiency) Increasing age ileal resection - Bile salts are reabsorbed in the terminal ileum; thus its resection increases the risk of stone formation The mnemonic 'fair, fat, female and forty' is often used to remember these risk factors.
158
What are the signs and symptoms of gallstones:
Biliary colic: Colicky right upper quadrant pain, worse after eating, no fever, negative Murphy's sign. Acute cholecystitis: Right upper quadrant/epigastric pain (radiating to right shoulder tip if the diaphragm is irritated), fever, nausea and vomiting, right upper quadrant tenderness, positive Murphy's sign. Ascending cholangitis: Right upper quadrant pain, fever, jaundice, hypotension, and confusion if sepsis is severe. Mirizzi's syndrome: Chronic right upper quadrant pain, intermittent jaundice due to extrinsic compression of the common hepatic duct by an impacted stone in the cystic duct or gallbladder neck. Chronic cholecystitis: Flatulent dyspepsia, vague abdominal pain, nausea, bloating, symptoms worsening after a fatty meal, occasional colicky pain. Gallstone ileus: Signs of small bowel obstruction due to gallstone migration. Cholangiocarcinoma: Abdominal pain, jaundice, anorexia, weight loss, possible right upper quadrant mass.
159
What are the investigations for gallstones:
Basic blood panel: Raised liver function tests and C-reactive protein. Ultrasound: First-line imaging; detects bile duct dilatation but less effective for mid/distal stones. CT scan: Provides detailed anatomy of the biliary tree, better visualization of radiopaque stones. MRCP: Most accurate for detecting gallstones or strictures, provides detailed view of biliary blockage. ERCP: Used for therapeutic intervention once aetiology is confirmed.
160
What is the management of gallstones:
Resuscitation: Intravenous fluids and antibiotics, critical care if necessary. Biliary drainage: Via endoscopic (ERCP), percutaneous (PTC), or surgical means. Addressing the underlying cause: e.g., cholecystectomy for gallstones, further investigation and treatment for malignant strictures.
161
What are the features of gallstone ileus:
Gallstone ileus causes symptoms of small bowel obstruction, pneumobilia (air within the biliary tree) on imaging is a hallmark feature. It typically occurs in older patients and is due to a gallstone passing into the intestinal system via a biliary-enteric fistula causing a distal obstruction. Most common site for gallstone erosion is into the duodenum. The name is a misnomer and can cause confusion; this pathology is one of a mechanical intraluminal obstruction by the stone lodging, most commonly, in the narrow terminal ileum, it is not a paralytic ileus. CT may show air in the biliary tree. Treatment is to 'milk' the stone proximal to the obstruction site and remove via enterotomy. In the acute setting the gallbladder and fistula should be left alone and not interfered with
162
A palpable mass in the right upper quadrant associated with inflammatory signs and symptoms suggests gallbladder empyema, requiring urgent intervention to manage infection.
The presence of a palpable tender mass in the right upper quadrant alongside a strong inflammatory response (hypotension, rigors, swinging pyrexia, tachycardia and tachypnoea) makes this the most likely diagnosis. It can be a complication of cholecystitis and will require drainage in order to control the infection
163
Define gastric cancer:
Gastric cancer, or stomach cancer, is a malignancy that begins in the tissues lining the stomach. The most common type of gastric cancer is adenocarcinoma, which originates from the glandular cells that line the stomach's mucosal layer.
164
What are the risk factors for gastric cancer:
Smoking Pernicious anaemia H. pylori infection High alcohol intake (> 6 units per day) Dietary nitrosamines (found in smoked foods and gastric cancer has higher incidence in Japan) Atrophic gastritis Blood group A Adenomatous polyps Achlorhydria (as seen in Menetrier's disease) Gastric cancer can also result from pre-cancerous conditions such as Menetrier's disease. GORD does not increase the risk of gastric cancer, but does increase the risk of oesophageal adenocarcinoma via Barrett's oesophagus (metaplastic changes which occur with longstanding GORD).
165
Signs and symptoms of gastric cancer:
Anaemia (iron deficient) Weight loss Anorexia (early satiety) Recent onset/progression of symptoms Melaena/haematemesis Swallowing difficulty (dysphagia) Lymphadenopathy - may suggest early spread Left supraclavicular lymph node (Virchow's node) An enlarged node here is known as Troisier's sign, which suggests the presence of a gastric malignancy Periumbilical nodule (Sister Mary Joseph's node) If a patient is presenting with dyspepsia along with ALARM symptoms, these red flag symptoms should prompt investigation into upper GI malignancy: anaemia, loss of weight, anorexia, recent onset of symptoms, malaena/haematemesis
166
What are the investigations for gastric cancer:
If there is evidence of dyspepsia and ALARM symptoms, first line investigation is OGD under the 2 week-wait pathway. This will enable histological diagnosis as biopsies are taken at the same time. Staging: Endoscopic USS can be used to determine if there has been muscle wall invasion. CT chest, abdomen and pelvis to assess the size of the tumour, local spread, and lymph node spread. It also identifies any visceral metastases to the liver or lungs. MRI for identifying metastatic spread to the liver and advanced local disease. gastric adenocarcinoma, which is confirmed by the presence of signet ring cells in a biopsy
167
What is the management for gastric cancer:
Management strategies for gastric cancer depend on the stage of the disease: Locally invasive disease is managed with partial or total gastrectomy. Neoadjuvant chemotherapy improves outcomes for patients undergoing surgery. Advanced cases are managed palliatively through surgery to relieve obstruction or haemorrhage, or chemotherapy to improve quality of life. Prognosis is generally poor, with a 10-year survival rate of 11%.
168
Menetrier's disease, a rare condition is characterised by
hypertrophy of the gastric mucosa and achlorhydria
169
Define gastro-oesophageal reflux disease:
Gastro-oesophageal reflux disease (GORD) is a clinical diagnosis based on the presence of typical symptoms (dyspepsia, ""heartburn"" or ""acid reflux"") resulting from the reflux of gastric contents into the oesophagus caused by a defective lower oesophageal sphincter.
170
What are the risk factors for GORD:
Risk factors contributing to the development of GORD include obesity, alcohol use, smoking, and intake of specific foods (e.g. coffee, citrus foods, spicy foods, fat).
171
What are the typical symptoms of GORD:
Dyspepsia (""heartburn"") Sensation of acid regurgitation
172
What are the atypical symptoms of GORD:
Epigastric or chest pain Nausea Bloating Belching Globus Laryngitis Tooth erosion
173
What are the alarm symptoms of GORD:
Weight loss Anaemia Dysphagia Haematemesis Melaena Persistent vomiting
174
What are the investigations for GORD:
Urea (13C) breath test, Stool Helicobacter Antigen Test (SAT), or laboratory-based serology if symptoms suggestive of H.pylori infection. Oesophagogastroduodenoscopy (OGD) if alarm features or atypical, persistent or relapsing symptoms are present. Oesophageal manometry
175
What is the referral criteria for an urgent OGD to investigate oesophageal and gastric cancer?
Aged 55 years and over with weight loss + dyspepsia/reflux Referral criteria for non-urgent OGD: Aged 55 years and over plus Treatment-resistant dyspepsia OR Raised platelet count + dyspepsia/reflux Nausea/vomiting + dyspepsia/reflux
176
What is the management for gastro-oesophageal reflux disease:
Lifestyle interventions - weight loss, dietary changes, elevation of the head of the bed at night, avoidance of late-night eating. Proton pump inhibitor therapy. For patients <40 years old who present with typical symptoms and no red flags, commence treatment with a standard-dose PPI for 4 weeks in combination with lifestyle changes. If the patient meets criteria for urgent OGD, they should only be commenced on PPI therapy after this has been done Antacids for symptomatic relief. Anti-reflux surgery for refractory cases. Treatment for H.pylori infection if confirmed (PPI + antibiotics), with retesting using the urea breath test It should not be performed within 2 weeks of treatment with a proton pump inhibitor or within 4 weeks of antibacterial treatment, as this can lead to false negatives.
177
What are the complications of GORD:
Oesophageal ulcer Oesophageal stricture Barrett's oesophagus Adenocarcinoma of the oesophagus
178
Define haemorrhoids:
Haemorrhoids are a pathological condition where the vascular cushions within the anal canal abnormally expand and can protrude outside the anal canal.
179
What are the grades of haemorrhoids:
Grade 1 - no prolapse Grade 2 - prolapse on straining which spontaneously reduces Grade 3 - prolapse on straining and require manual reduction Grade 4 - prolapse on straining and can't be manually reduced, external haemorrhoids, or lower grade haemorrhoids failing to respond to less invasive measures
180
What causes haemorrhoids:
Constipation Pregnancy Increased intra-abdominal pressure due to causes like obesity, chronic cough or space-occupying lesions Portal hypertension, particularly secondary to cirrhosis, due to increased pressure at the rectal porto-systemic anastomosis
181
What are the signs and symptoms of haemorrhoids:
Bright red PR bleeding, often associated with defecation and on wiping Absence of pain, unless the patient has a thrombosed external haemorrhoid or another condition such as an anal fissure Anal pruritus A palpable or protruding mass in the anal region during examination, suggestive of prolapsing haemorrhoids
182
What are the investigations for haemorrhoids:
The primary investigation for haemorrhoids is an anoscopic examination, which allows direct visualisation of the anal canal and rectum. This is however rarely done in practice as the first 'investigation' you would do is a digital rectal exam (i.e. PR).
183
What is the management of haemorrhoids according to the grade:
Grade 1: Conservative management, including potential use of topical corticosteroids to alleviate pruritus Grade 2: Management may involve rubber band ligation (preferred), sclerotherapy, or infrared photocoagulation Grade 3: Rubber band ligation is the treatment of choice Grade 4: Surgical haemorrhoidectomy may be necessary In all cases, patients should be advised to maintain a diet rich in fibre and fluids to reduce the risk of constipation, thereby limiting exacerbation of haemorrhoids.
184
What is the treatment for thrombosed haemorrhoids:
For thrombosed haemorrhoids, which present as painful, purple protrusions, conservative measures such as ice packs, laxatives, and lidocaine gel are first-line treatments. If these measures fail, haemorrhoidectomy may be required.
185
Define autoimmune hepatitis:
Autoimmune hepatitis is a chronic, inflammatory disease of the liver that occurs when the body's immune system attacks liver cells leading to inflammation and damage. It is classified into three main types based on the presence of specific antibodies.
186
What causes autoimmune hepatitis and how many types are there:
Autoimmune hepatitis occurs due to an abnormal autoimmune reaction against hepatocyte surface antigen, with HLA-B8 and DR3 most frequently implicated. Specifically, there are 3 different types of autoimmune hepatitis
187
Name the three types of autoimmune hepatitis:
Type 1) ANA positive, with anti-smooth muscle antibodies Type 2) anti-liver/kidney mitochondrial type 1 antibodies (LKM1) – can be remembered as ‘Little Kids’ – children predominantly get Type 2 Type 3) Antibodies directed against soluble liver-kidney Antigen
188
what are the signs and symptoms of autoimmune hepatitis:
Can present as an acute hepatitis - fever, jaundice, malaise, abdominal pain urticarial rash, polyarthritis, pulmonary infilitration, glomerulonephritis It can also present as chronic liver disease - ascites, jaundice, leuconychia, spider naevi Other signs and symptoms include: Fatigue Anorexia Hepatomegaly Splenomegaly
189
What are the investigations for autoimmune hepatitis:
Bloods: Abnormal liver function tests often indicate autoimmune hepatitis, showing a hepatic pattern of disease, such as raised ALT and bilirubin with normal or mildly raised ALP. Additionally, patients may present with an IgG predominant hypergammaglobulinemia. The presence of specific antibodies helps to differentiate between the three types of autoimmune hepatitis: Type I: Characterised by raised levels of anti-smooth muscle antibodies (80%) and possibly positive antinuclear antibodies (10%). Type II: Less common and often more severe, typically positive for anti liver/kidney microsomal antibodies type 1. Type III: Also less common, often positive for anti-soluble liver antigen.
190
Management for autoimmune hepatitis:
Management of autoimmune hepatitis is largely dependent on the severity of symptoms and the severity of disease, as determined by blood results and liver biopsy. Initial treatment of acute episodes involves steroid (prednisolone) induction therapy, followed by maintenance therapy with azathioprine, which is effective in most cases. For patients who do not respond to standard treatment, second-line treatment with other immunosuppressants can be considered. In patients presenting with chronic liver disease with decompensated cirrhosis or those who have failed to respond to immunosuppression, liver transplantation is the only management option.
191
Define inguinal hernia:
Inguinal hernias refer to protrusions of intra-abdominal contents through a defect in the abdominal wall, specifically in the groin region.
192
What can hernias be divided into:
Indirect inguinal hernias: These hernias follow the path of the descent of the testes, which occurs via the processus vaginalis during fetal development. They are typically congenital and often observed in young males. Direct inguinal hernias: These hernias protrude through a weakness in the abdominal wall, specifically the inguinal triangle (Hesselbach's triangle). They are usually acquired and more common in elderly males. Incarcerated hernias are those which cannot be reduced, and strangulation is when the blood supply to the affected bowel is compromised, leading to ischaemia and necrosis. Strangulation is a surgical emergency.
193
What causes indirect and direct inguinal hernias:
Indirect inguinal hernias are generally congenital, resulting from a patent processus vaginalis. Direct inguinal hernias are typically acquired, caused by factors that raise intra-abdominal pressure such as chronic cough (e.g., in smokers), constipation, heavy lifting, or obesity.
194
What are the signs and symptoms of indirect inguinal hernias:
may descend into the scrotum and potentially strangulate. Clinical signs include groin swelling, pain, and a palpable mass that can be pushed back or reduces with lying down.
195
What are the signs and symptoms of direct inguinal hernias:
rarely descend into the scrotum or strangulate. Similar to indirect hernias, they also present with groin swelling, pain, and a palpable mass, but it typically cannot be pushed back.
196
What are the signs of a strangulated hernia:
more painful (due to ischaemia), and present with nausea and vomiting and fever. They may present with bowel obstruction, and there can be reduced/absent bowel sounds.
197
Investigations for hernias:
The diagnosis of inguinal hernias is primarily clinical, with physical examination being the key investigative tool. Blood tests may reveal a raised lactate in a blood gas (suggestive of ischaemia) and raised white cells/CRP can suggest inflammation due to necrosis if there is strangulation Imaging may be used if the diagnosis is uncertain, with ultrasonography being the first-line choice. CT scans may be used for further characterization if needed. If obstruction/perforation is suspected all patients should have an abdominal x-ray and erect chest x-ray
198
What is the management of hernias:
All hernias, irrespective of whether they are symptomatic or asymptomatic, should be referred for surgical repair. This typically involves open or laparoscopic mesh repair. Indirect hernias particularly require intervention due to the risk of strangulation. Strangulated hernias are a surgical emergency and require prompt treatement with laparoscopic/open repair to avoid necrosis (death of bowel tissue). Open mesh repair is the preferred management for reducing recurrence in uncomplicated cases of direct inguinal hernias in low-risk candidates.
199
Define femoral hernias:
A femoral hernia is a type of hernia that develops in the femoral canal, a space near the groin and thigh. It is often marked by the presence of an irreducible lump in the groin area located inferior to the inguinal ligament and inferior and lateral to the pubic tubercle.
200
causes of femoral hernias:
Femoral hernias are often caused by increased intra-abdominal pressure, which can result from activities such as lifting heavy objects, chronic cough, constipation, obesity, or pregnancy. They may also develop due to age-related weakening of the abdominal and pelvic muscles.
201
Signs and symptoms of femoral hernias:
Groin lump: Located inferior to the inguinal ligament and inferior and lateral to the pubic tubercle. Irreducibility: The lump is often irreducible, making it persistently visible and palpable. Inflammation: Patients may present with an inflamed lump. Bowel obstruction features: In severe cases, symptoms may manifest as nausea, vomiting, abdominal pain, and constipation.
202
what are the investigations for femoral hernias?
Physical examination: To identify and assess the lump. Ultrasound: Useful for differentiating between a femoral hernia and other potential diagnoses. CT scan: In complex or uncertain cases, a CT scan may provide more detailed imaging.
203
What is the management of femoral hernias:
Given the high risk of strangulation, which can lead to bowel ischemia and necrosis, urgent surgical management of femoral hernias is generally required. Surgical options may include open repair or laparoscopic repair, often involving the placement of a synthetic mesh to reinforce the area. Postoperative care involves pain management, activity modifications, and monitoring for potential complications.
204
What does a cough impulse mean?
cough impulse is a key diagnostic sign for hernias, helping differentiate reducible hernias from more serious conditions like incarceration or strangulation. Its presence or absence provides vital clues in determining the nature and urgency of the condition.
205
Define infectious colitis:
Infectious colitis refers to inflammation of the colon due to infection by pathogenic organisms. It is typically caused by bacteria, viruses, or parasites.
206
Name the common bacteria and viral culprits for infectious colitis:
ommon bacterial culprits include Campylobacter, Salmonella, and Shigella. Viruses such as rotavirus or norovirus are also frequent offenders, while parasites like Giardia lamblia can also cause this condition.
207
What is the clinical manifestation of infectious colitis:
diarrhoea, abdominal pain and sometimes fever. The patient may also present with bloody stools if the infection is severe
208
What are the investigations for infectious colitis:
Diagnosis involves stool culture and sensitivity tests to identify the causative organism and guide antibiotic therapy. Endoscopy may be required in severe cases or when diagnosis is uncertain.
209
What is the treatment for infectious colitis:
Treatment generally involves fluid rehydration and antibiotics for bacterial infections. Antiviral or antiparasitic drugs may be used depending on the identified pathogen. In severe cases, hospitalisation for intravenous fluids and antibiotics may be necessary.
210
What is the MOA of clostridioides difficile:
Gram positive rod often encountered in hospital practice. It produces an exotoxin which causes intestinal damage leading to a syndrome called pseudomembranous colitis. anaerobic gram-positive, spore-forming, toxin-producing bacillus transmission: via the faecal-oral route by ingestion of spores releases two exotoxins (toxin A and toxin B) that act on intestinal epithelial cells and inflammatory cells resulting in colitis
211
What causes c.difficle pseudomembranous colitis:
. difficile develops when the normal gut flora are suppressed by broad-spectrum antibiotics. Clindamycin is historically associated with causing C. difficile but the aetiology has evolved significantly over the past 10 years. Second and third-generation cephalosporins are now the leading cause of C. difficile. Other than antibiotics, risk factors include: proton pump inhibitors
212
What are the features of a c.difficile infection:
diarrhoea abdominal pain a raised white blood cell count (WCC) is characteristic if severe toxic megacolon may develop
213
What is the severity scale of c.difficile infections:
214
What is the severity scale of c.difficile infections:
215
What is the diagnosis for c.difficile:
is made by detecting C. difficile toxin (CDT) in the stool C. difficile antigen positivity only shows exposure to the bacteria, rather than current infection
216
What is the management for first episodes of c.difficile infections:
First episode of C. difficile infection first-line therapy is oral vancomycin for 10 days second-line therapy: oral fidaxomicin third-line therapy: oral vancomycin +/- IV metronidazole
217
What is the treatment for recurrent episodes of c.difficile reactions:
recurrent infection occurs in around 20% of patients, increasing to 50% after their second episode within 12 weeks of symptom resolution: oral fidaxomicin after 12 weeks of symptom resolution: oral vancomycin OR fidaxomicin
218
What is the treatment for life-threatening c.difficile infection:
oral vancomycin AND IV metronidazole specialist advice - surgery may be considered
219
How does one prevent the spread of c.difficile infections:
Preventing the spread of C. difficile infection isolation in side room: the patient should remain isolated until there has been no diarrhoea (types 5-7 on the Bristol Stool Chart) for at least 48 hours all staff should wear disposable gloves and an apron during any contact with patients known to have C. difficile hand washing is also essential - alcohol gel does not kill the spores of C. difficile
220
In individuals with Clostridium difficile infection, persistent diarrhoea may indicate pseudomembranous colitis. This is characterised by
raised yellow plaques across the colonic mucosa.
221
Define a hiatus hernia:
A hiatus hernia is a medical condition that occurs when abdominal contents protrude through an enlarged oesophageal hiatus in the diaphragm.
222
What are risk factors for hiatus hernias:
Obesity Prior hiatal surgery Increased intra-abdominal pressure, such as from chronic cough, multiparity, or ascites
223
What are the two main types of hiatus hernias:
Sliding hiatus hernia and rolling hiatal hernia
224
Explain a sliding hiatus hernia:
Here, the gastro-oesophageal junction slides up into the chest. This results in a less competent sphincter and consequent acid reflux. Treatment is similar to Gastroesophageal reflux disease (GORD).
225
Explain a rolling hiatus hernia:
In this type, the gastro-oesophageal junction stays in the abdomen, but part of the stomach protrudes into the chest alongside the oesophagus. This type requires more urgent treatment since volvulus can lead to ischemia and necrosis.
226
What are the symptoms of a hiatus hernia:
Heartburn Dysphagia Regurgitation Odynophagia Shortness of breath Chronic cough Chest pain
227
What are the investigations for a hiatus hernia:
Barium swallows (upper GI series), which is the most sensitive method Endoscopy Oesophageal manometry
228
What is the conservative management for hiatus hernias:
Weight loss Elevating the head of the bed Avoidance of large meals and eating 3-4 hours before bedtime Avoidance of alcohol and acidic foods Smoking cessation as nicotine relaxes the lower oesophageal sphincter. Other substances and medications that can relax the lower oesophageal sphincter include chocolate, peppermint, caffeine, fatty foods, and medications such as calcium-channel blockers, nitrates, and beta-blockers
229
Define Crohn's disease:
Crohn's disease (CD) is a chronic relapsing inflammatory bowel disease (IBD). It is characterised by transmural granulomatous inflammation which can affect any part of the gastrointestinal tract ('from mouth to anus', most commonly the terminal ileum, leading to fistula formation or stricturing.
230
Risk factors for Crohn's disease:
Family history - 10-25% of patients have a first-degree relative who also suffers from Crohn's disease Smoking - x3 increased risk Diets high in refined carbohydrates and fats have been implicated
231
What is the epidemiology of Crohn's disease:
Crohn's disease has a bimodal age of onset: the most common age of onset is between 15 and 40 years old, but there is a smaller secondary peak between 60-80 years. Crohn's disease is more common in Caucasian people than in Asian and black people. Ashkenazi Jews have a 2-4 fold higher risk of Crohn's disease.
232
What are the signs and symptoms of Crohn's disease:
Symptoms: Gastrointestinal symptoms (crampy abdominal pain and non-bloody diarrhoea) Up to 50% have perianal disease Systemic symptoms (weight loss and fever) Signs: General appearance: cachectic and pale (secondary to anaemia), clubbing. Abdominal examination: aphthous ulcers in the mouth, right lower quadrant tenderness and a right iliac fossa mass. PR examination to check for perianal skin tags, fistulae, or perianal abscess.
233
What are the Extra-gastrointestinal manifestations of Crohn's disease:
Dermatological manifestations: Erythema nodosum (painful erythematous nodules/plaques on the shins) Pyoderma gangrenosum (a well-defined ulcer with a purple overhanging edge) Ocular manifestations: Anterior uveitis (painful red eye with blurred vision and photophobia) Episcleritis (painless red eye). Musculoskeletal manifestation: Enteropathic arthropathy (symmetrical, non-deforming) Axial spondyloarthropathy (sacro-iliitis), Hepatobiliary manifestations: Gallstones (these are more common in Crohn's disease than in ulcerative colitis) - reduced bile acid reabsorption and increased calcium loss predisposes to gallstones Haematological and renal manifestations: AA amyloidosis (secondary to chronic inflammation) and renal stones (more common in Crohn's disease than in ulcerative colitis)
234
What are the bedside investigations for crohn's disease:
Stool culture is necessary to exclude infection (MC&S and ovas/cysts/parasite). Faecal calprotectin (an antigen produced by neutrophils) will be raised (this helps distinguish inflammatory bowel disease from irritable bowel syndrome).
235
What are the blood tests for Crohn's disease:
Raised white cell count Raised ESR/CRP Thrombocytosis Anaemia (secondary to chronic inflammation) Low albumin (secondary to malabsorption) Haematinics and iron studies including (B12, folate) due to terminal ileum involvement
236
What is the imaging for Crohn's disease:
Endoscopy with imaging is required for diagnosis. Small bowel video capsule endoscopy can be used for proximal disease MRI can be used for suspected small bowel disease. Upper GI series may show the 'string sign of Kantour'. This is used to describe the string-like appearance of contrast-filled narrowed terminal ileum, and is suggestive of Crohn's disease. Colonoscopy with biopsy will reveal: Intermittent inflammation ('skip lesions') Cobblestone mucosa (due to ulceration and mural oedema) Rose-thorn ulcers (due to transmural inflammation), ± fistulae or abscesses. Non-caseating granulomas
237
What is the initial management for Crohn's disease:
As a general management point, it is paramount to advise patients with Crohn's who are smokers to stop smoking as this is known to strongly impact disease activity Inducing remission The first step of treatment is inducing remission in patients having a flare Patients should be offered monotherapy with glucocorticoids (oral prednisolone, or IV hydrocortisone if first presentation is severe flare necessitating admission). There is an increasing role for biologics for acute management of severe flares
238
How does one maintain remission in Crohn's disease:
Azathioprine or mercaptopurine may be added on to induce remission if there are 2 or more exacerbations in a 12-month period or the glucocorticoid cannot be tapered. It is important to assess for thiopurine methyltransferase (TPMT) activity before offering azathioprine or mercaptopurine. If there is underactivity, this greatly increases the risk of profound bone marrow suppression if the above medications are given Methotrexate may be considered in patients who are intolerant/have a contraindication to azathioprine or mercaptopurine or who do not respond to azathioprine or mercaptopurine monotherapy. Biological agents (such as infliximab or adalimumab) are recommended in patients with severe Crohn's disease who fail to respond to the above. These patients should have a CXR before treatment initiation due to the risk of re-activation of latent TB
239
What is the surgical management for Crohn's disease:
Surgical management is rarely curative in Crohn's disease (unlike in ulcerative colitis) because disease can occur anywhere along the GI tract, however 50-80% of Crohn’s patients end up requiring surgery at some point. Surgical options will depend on the part of the GI tract that is affected, and is indicated in those who have failed medical therapy or in those with severe stricturing or fistulating disease: Control fistulae Resection of strictures Rest/defunctioning of the bowel
240
What is the management of peri-anal fistulae in crohn's disease:
Drainage seton is the management of choice for high (trans-sphincteric) fistulae. A seton is a thread passed through the fistula tract, forming a ring between the internal and external openings. It is used in the management of high trans-sphincteric fistulae, to prevent division of the anal sphincter muscles and incontinence. Closure of the fistula occurs by the formation of granulation tissue. Fistulotomy is the management of choice for low (submucosal) fistulae. Fistulotomy involves dissecting the superficial tissue and opening the fistula tract. This is not a treatment option for high fistulae due to the risk of incontinence. 'Sphincter saving' methods include fibrin glue and fistula plug - these are still under investigation and have not yet been approved in mainstream management.
241
What is the management of peri-anal abscess in Crohn's disease:
The patient should be started on intravenous antibiotics e.g. ceftriaxone + metronidazole. Patients typically require examination under anaesthetic and incision and drainage. An incision is made in the affected region, the pus is broken up, the infected tissue material is excised, and anti-septic soaked packs are inserted. Healing occurs by secondary intention.
242
Name some complications of Crohn's disease:
Fistulas: Formation of abnormal connections between different parts of the digestive tract or between the digestive tract and other organs. Commonly involves the small intestine and other structures like the bladder or skin. Strictures: Narrowing or tightening of the intestinal walls. Can lead to bowel obstruction and difficulties with the passage of stool. Abscesses: Collection of pus within the abdomen, often near areas of inflammation. Presents with localized pain, swelling, and may require drainage. Malabsorption: Impaired absorption of nutrients due to inflammation and damage to the intestinal lining. Can lead to nutritional deficiencies and weight loss. Perforation: Formation of a hole or tear in the intestinal wall. Can result in peritonitis, a serious and potentially life-threatening condition. Nutritional Deficiencies: Chronic inflammation can affect nutrient absorption. Common deficiencies include vitamin B12, vitamin D, and iron. Increased Risk of Colon Cancer: Prolonged inflammation may elevate the risk of developing colorectal cancer, particularly in long-standing disease involving the colon. Osteoporosis: Reduced bone density due to chronic inflammation and corticosteroid use. Increases the risk of fractures. Intestinal Obstruction andToxic Megacolon: Severe inflammation can lead to the dilation of the colon. Presents as abdominal distension, fever, and can be a medical emergency.
243
Compare Crohn's disease and ulcerative colitis:
244
In Crohn's disease patients with prior ileal resection, diarrhoea and fatty stools may be indicative of bile acid malabsorption.
:)
245
Which drug interacts with azathioprine?
allopurinol due to increased risk of bone marrow toxicity
246
Define ulcerative colitis:
Ulcerative colitis (UC) is a chronic relapsing-remitting inflammatory disease that primarily affects the large bowel. It usually affects the rectum first, then can extend to the part of the colon (left-hand-side colitis) or the entire colon (pancolitis). It does not spread beyond the ileocaecal valve or to the small bowel, except where backwash ileitis can occur.
247
What causes ulcerative colitis:
The exact cause of UC is unknown, but it is believed to result from a combination of genetic predisposition, environmental factors, and dysregulation of the immune system. There is also a higher incidence of UC among non-smokers and ex-smokers.
248
What are the gastro-intestinal symptoms of ulcerative colitis:
Diarrhoea often containing blood and/or mucus Tenesmus or urgency Generalised crampy abdominal pain in the left iliac fossa
249
What are the systemic symptoms of ulcerative colitis:
Weight loss Fever Malaise Anorexia Physical examination may reveal general signs such as pallor due to anaemia and clubbing. Abdominal examination may reveal distension or tenderness, and a PR examination may show tenderness, and blood/mucus.
250
What are the extra-intestinal symptoms of ulcerative colitis:
Dermatological manifestations: erythema nodosum, pyoderma gangrenosum Ocular manifestations: anterior uveitis, episcleritis, conjunctivitis Musculoskeletal manifestations: clubbing, non-deforming asymmetrical arthritis, sacroiliitis Hepatobiliary manifestations: jaundice due to primary sclerosing cholangitis (PSC). 80% of those with PSC have ulcerative colitis. Other features include AA amyloidosis
251
What are the bedside and bloods for ulcerative colitis:
Bedside: Microbiological investigations: Stool microscopy (for ova/cysts/parasites), culture and sensitivity, and stool C. difficile toxin to exclude infective colitis Faecal calprotectin: Distinguishes between inflammatory bowel syndrome (normal) and inflammatory bowel disease (raised) Bloods: Blood tests: FBC (anaemia and a raised white cell count), ESR/CRP is typically raised, LFTs may show a low albumin
252
What is the Imaging/Invasive investigations for ulcerative colitis:
Radiological investigations: Abdominal X-ray and erect chest x-ray in acute settings to exclude toxic megacolon and perforation. Long-standing UC will show 'lead-pipe' colon on AXR Endoscopic investigations: Colonoscopy, barium enema, and biopsy are used to confirm the diagnosis. Colonoscopy will reveal shows continuous inflammation starting at the rectum that does not go beyond the submucosa with an erythematous mucosa, loss of haustral markings, and pseudopolyps. Biopsy: loss of goblet cells, crypt abscess, and inflammatory cells (predominantly lymphocytes) Barium enema will reveal lead-piping inflammation (secondary to loss of haustral markings), thumb-printing (a marker of bowel wall inflammation), and pseudopolyps (due to areas of ulcerating mucosa adjacent to areas of regenerating mucosa). This is less commonly used nowadays due to the increasing availability of endoscopic investigations
253
An acute exacerbation of ulcerative colitis should be assessed using what criteria:
the Truelove and Witt's severity index.
254
What does the truelove and Witt's severity index measure:
255
What is the treatment for mild/moderate ulcerative colitis:
Mild-moderate disease The aim of step 1 treatment is to induce remission. If this does not work after 4 weeks, or symptoms worsen, move to step 2. The first step in management for a moderate first presentation is to offer a topical aminosalicylate as first-line treatment. If remission is not achieved within 4 weeks, consider adding an oral aminosalicylate. In acute moderate disease if all other measures haven't worked then a trial of Etrasimod (also known as Velsipity). This is a selective sphingosine 1-phosphate (S1P) receptor modulator. Proctitis and proctosigmoiditis: Step 1: Topical ASA or oral ASA. Step 2: Consider adding oral prednisolone. If this does not help after 2-4 weeks or symptoms worsen, consider adding oral tacrolimus. Left sided or extensive disease Step 1: High dose oral ASA. Step 2: Consider adding oral prednisolone. If this does not help after 2-4 weeks or symptoms worsen, consider adding oral tacrolimus.
256
What is the treatment for severe ulcerative colitis:
Step 1: IV corticosteroids (if contraindicated or not tolerated, use IV ciclosporin). Step 2: If no improvement in 72 hours or worsening symptoms, add IV ciclosporin or consider surgery (if IV ciclosporin contraindicated or not tolerated, consider infliximab). Step 3: A trial of Etrasimod (also known as Velsipity). This is a selective sphingosine 1-phosphate (S1P) receptor modulator. Indications for emergency surgery: Surgery should be considered in patients with: Acute fulminant ulcerative colitis Toxic megacolon who have little improvement after 48-72 hours of intravenous steroids Symptoms worsening despite intravenous steroids Note that an alternative is to initiate rescue therapy (with ciclosporin or infliximab) if the patient has a sub-optimal response to intravenous steroids but is stable enough to delay surgery. Surgery should be considered if patients fail to respond to rescue therapy within 3 days.
257
What is the surgical treatment for ulcerative colitis:
Surgical options Panproctocolectomy with permanent end ilesotomy Colectomy with temporary end ileostomy (approximately 3 months later the ileostomy can be reversed by forming an ileorectal anastomosis, an alternative option is completion proctectomy with a permanent end ileostomy or ileal pouch anal anastomosis (IPAA)). Indications for elective surgery This can be considered in patients in which there is failure to induce remission by medical means. Surgical options include: panproctocolectomy with permanent end ileostomy or IPAA. An alternative is a total colectomy with ileorectal anastomosis (i.e. no stoma).
258
What are some short term acute complications of ulcerative colitis:
Toxic megacolon: this describes a severe form of colitis, and is seen in around 15% of ulcerative colitis patients. Massive lower gastrointestinal haemorrhage: this occurs in up to 3% of patients.
259
What are some long term complications of ulcerative colitis:
Long-term complications Colorectal cancer: this occurs in 3-5% of patients. There is a higher risk with disease duration, severity and extent of colitis, and concomitant primary sclerosing cholangitis (PSC). NICE guidance suggests offering colonoscopy surveillance to high risk patients. Cholangiocarcinoma: ulcerative colitis approximately doubles the risk of cholangiocarcinoma. Colonic strictures: these can cause large bowel obstruction. Variable-term complications Primary Sclerosing Cholangitis: this is characterised by inflammation and fibrosis of the extra- and intra-hepatic biliary tree and affects 3-7% of patients with ulcerative colitis. LFTs should be monitored yearly to check for the presence of PSC. Inflammatory pseudopolyps: these are areas of normal mucosa between areas of ulceration and regeneration. Increased risk of VTE - as with any inflammatory disease, but in the acute and chronic context, patients have an increased risk of developing blood clots, especially during flares
260
Define liver failure:
Liver failure refers to the loss of liver function and the development of complications including coagulopathy, jaundice or encephalopathy. It can occur acutely if onset of symptoms in less than 26 weeks with a previously healthy liver and subdivided into hyperacute (< 7 days), acute (8-21 days), or subacute (4-26 weeks) liver failure. Chronic liver failure occurs on a background of liver cirrhosis.
261
Name some causes of acute liver failure:
Viral Hepatitis: Hepatitis A, B, and E infections can lead to acute liver failure, particularly in cases of fulminant hepatitis. Drug-Induced Liver Injury: Overdose or adverse reactions to medications like paracetamol (acetaminophen), halothane, isoniazid, and certain antibiotics can precipitate acute liver failure. Toxic Exposures: Exposure to hepatotoxic substances such as Amanita phalloides mushrooms or industrial chemicals like carbon tetrachloride can cause acute liver damage. Vascular Disorders: Conditions like Budd-Chiari syndrome, characterised by hepatic vein obstruction, can result in rapid liver failure.
262
Name some causes of chronic liver failure:
Alcohol Misuse: Chronic alcohol consumption is a leading cause of liver cirrhosis and subsequent liver failure. Chronic Viral Hepatitis: Persistent infection with hepatitis B or C viruses can progress to cirrhosis and liver failure if left untreated. Non-Alcoholic Fatty Liver Disease (NAFLD): Accumulation of fat in the liver, often associated with obesity and metabolic syndrome, can lead to inflammation, fibrosis, and ultimately liver failure. Autoimmune Liver Diseases: Conditions such as autoimmune hepatitis, primary biliary cholangitis (formerly primary biliary cirrhosis), and primary sclerosing cholangitis can cause chronic inflammation and scarring of the liver. Hereditary Conditions: Genetic disorders like haemochromatosis, Wilson's disease, and alpha-1 antitrypsin deficiency can result in progressive liver damage and failure over time.
263
What are the signs and symptoms of liver failure:
Hepatic encephalopathy Abnormal bleeding Jaundice If the cerebral oedema is severe, raised intracranial pressure may develop. This is more common in fulminant hepatic failure and has a high mortality rate. It is important to separate the signs of liver failure from the signs of chronic liver disease. The presence of both indicates a de-compensation of chronic liver disease.
264
What is the Pathophysiology of Hepatic Encephalopathy?
In liver failure, nitrogenous waste (ammonia) accumulates in the circulation. This small molecule is able to cross the blood-brain barrier, and once in the cerebral circulation it is detoxified by astrocytes which form glutamine through the amidation of glutamate. The excess glutamine disrupts the osmotic balance and the astrocytes begin to swell, giving rise to cerebral oedema.
265
What are the Four stages of hepatic encephalopathy?
Altered mood and behaviour, disturbance of sleep pattern and dyspraxia Drowsiness, confusion, slurring of speech and personality change Incoherency, restlessness, asterixis Coma
266
What are the investigations for liver failure:
Blood tests assessing synthetic function of the liver: INR to look for coagulopathy and establish a diagnosis of liver failure Liver Function Tests including albumin to check liver enzymes, bilirubin levels and to further assess synthetic function of the liver Full blood count to look for leucocytosis (possible infective cause), thrombocytopaenia (in chronic liver disease) and anaemia (normocytic could indicate haemolytic anaemia as in Wilson's or a GI bleed from oesophageal varices, macrocytic could indicate B12 and folate deficiency as in alcohol excess) Urea and electrolytes to establish baseline renal function and to look for hepato-renal syndrome or any electrolyte abnormalities (such as hypokalaemia which can worsen encephalopathy and should be corrected) Tests to determine cause such as: Paracetamol level (paracetamol overdose) Hepatitis Epstein-Barr virus Cytomegalovirus serology (viral infection) Iron studies (haemochromatosis) α-1 anti-trypsin (α-1 antitrypsin deficiency) Caeruloplasmin level (Wilson's disease) Iron studies (hereditary haemochromatosis) Auto-antibodies (autoimmune hepatitis, primary biliary cirrhosis, primary sclerosing cholangitis) If ascites is present, a peritoneal tap should be taken for microscopy and culture to look for spontaneous bacterial peritonitis. Abdominal ultrasound Doppler ultrasound would be of use in identifying Budd-Chiari syndrome OGD may be required if concerns over varices/variceal bleeding
267
What is the treatment for hepatic encephalopathy?
firstly, the stage of encephalopathy should be graded (see table below) Lactulose is given to help nitrogenous waste loss through the bowels (reducing encephalopathy). Constipation is an important precipitant of encephalopathy in patients with chronic liver disease. Rifaximin is a 2nd line antibiotic which reduces nitrogen forming micro-organisms in gut IV mannitol can be given to reduce cerebral oedema in encephalopathy
268
What are the grades of encephalopathy?
269
What is the treatment for coagulopathy?
Vitamin K may need to be given IV - helps production of coagulation factors Fresh frozen plasma can be given if patient is bleeding
270
What is the treatment for Spontaneous bacterial peritonitis?
Broad spectrum antibiotics - IV Piperacillin-Tazobactam is usually first-line
271
What is the treatment for portal hypertension?
leads to release of vasoactive mediators which leads to splanchnic vasodilation, which reduces perfusion to kidneys, sensed by macula densa cells in JGA and leads to the activation of RAS. There are two types: 1. Rapidly progressive, often managed with terlipressin 2. Slowly progressive, usually managed with Midodrine May require haemofiltration If patient required fluid resuscitation, human albumin solution rather than crystalloid fluid. A TIPSS procedure may be necessary but note immediately after this can worsen hepatic encephalopathy Liver transplantation may be necessary as this is the only definitive management for chronic liver failure - indications are set out below.
272
What is the king's college hospital criteria for paracetamol induced liver failure liver transplant?
Arterial pH <7.3 24h after ingestion OR Pro-thrombin time >100s AND creatinine >300µmol/L AND grade III or IV encephalopathy.
273
What is King's College Hospital Criteria for Liver Transplant (non-paracetamol liver failure):
Prothrombin time >100s OR Any three of: Drug-induced liver failure Age under 10 or over 40 years 1 week from 1st jaundice to encephalopathy Prothrombin time >50s Bilirubin ≥300µmol/L.
274
What are the complications of liver failure:
The most common complication of acute liver failure is infection. Bacterial infection occurs in up to 80% of patients, and fungal infection in around 30%. This is thought to result from decreased phagocyte action, reduced complement levels and multiple medical interventions which are often invasive. Patients often present atypically, with no fever or raised white cell count. Other complications include: Cerebral oedema ± raised intracranial pressure Bleeding (where there is a source, for example during the introduction of intracranial pressure monitors) Hypoglycaemia (easily treated with glucose) Multi-organ failure
275
Severe hypotension can cause ischaemic hepatitis, characterised by??
characterised by marked elevation of alanine aminotransferase (ALT) with normal alkaline phosphatase (ALP) and bilirubin levels. Additionally, it may be associated with acute kidney injury.
276
Define Malabsorption:
is a clinical syndrome characterised by impaired absorption of nutrients, vitamins, or minerals from the diet, resulting in nutritional deficiencies and associated symptoms. The absorption process can be disrupted at any point along the gastrointestinal tract, with the small intestine being most commonly affected.
277
What are gastric causes of malabsorption?
Post-gastrectomy (dumping syndrome)
278
What are small bowel causes of malabsorption?
Coeliac disease Crohn's disease Small bowel resection
279
What are pancreatic causes of malabsorption?
Chronic pancreatitis Pancreatic cancer Cystic fibrosis
280
What are Hepatobiliary pathway causes of malabsorption?
Primary biliary cirrhosis Ileal resection (failure of bile acid absorption at the terminal ileum) Post-cholecystectomy (bile acids go into the intestines leading to malabsorption and diarrhoea)
281
What are infective causes of malabsorption?
Infective causes are less easily categorised anatomically but should also be considered. These include giardiasis, Whipple's disease, and bacterial overgrowth (which can occur in post-operative patients or patients with diabetes mellitus, for example).
282
What are the signs and symptoms of malabsorption?
Diarrhoea Steatorrhoea (pale, foul-smelling, greasy stools that can be difficult to flush) Weight loss Nutritional deficiencies leading to symptoms such as anaemia, osteoporosis, and peripheral neuropathy
283
What are the investigations for malabsorption?
Bedside Stool analysis: To detect the presence of fat (steatorrhoea) and assess for infective causes. Bloods: Full blood count, electrolytes, liver function tests, coeliac serology, and vitamin levels to identify specific nutrient deficiencies. Imaging/Invasive: Abdominal ultrasound, CT scan, or MRI to identify any structural abnormalities. Endoscopy and biopsy: To evaluate for conditions like coeliac disease and Crohn's disease.
284
What is the management for malabsorption?
Treating the underlying cause: This may involve medication, surgery, or other interventions depending on the specific cause. Dietary modifications: These may include a gluten-free diet for coeliac disease, or fat-restricted diet in cases of pancreatic insufficiency. Supplementation of deficient nutrients: This can involve oral or intravenous supplementation of vitamins, minerals, proteins, or calories as needed. Bile acid malabsorption can be managed with cholestyramine
285
Define irritable bowel syndrome
Irritable Bowel Syndrome (IBS) is a common, chronic gastrointestinal disorder characterised by abdominal pain or discomfort associated with altered bowel habits, without any identifiable structural or biochemical abnormalities.
286
What is the criteria for irritable bowel syndrome?
The Manning criteria for diagnosis of IBS includes: Abdominal discomfort or pain relieved by defecation OR associated with altered bowel frequency or stool form At least two of the following: Altered stool passage (e.g., straining or urgency) Abdominal bloating Symptoms worsened by eating Passage of mucus Additional symptoms such as lethargy, nausea, backache, and bladder symptoms may also be present. Physical examination typically reveals no abnormalities.
287
What are the investigations for irritable bowel syndrome?
The following investigations are often performed to rule out other organic diseases: Faecal calprotectin (raised in IBD, not IBS) Full Blood Count (FBC), and Erythrocyte Sedimentation Rate/C-Reactive Protein (ESR/CRP) (also raised in IBD, not IBS) Coeliac serology As per NICE guidelines, abdominal ultrasound, sigmoidoscopy/colonoscopy, Thyroid Function Tests (TFTs), Faecal Occult Blood Test (FOBT), faecal ova and parasite test, and hydrogen breath test are not required for diagnosis.
288
What is the management for irritable bowel syndrome:
Management of IBS primarily involves: Dietary and lifestyle modifications: Including regular exercise, stress management, and dietary changes (such as low-FODMAP diet). Pharmacotherapy: Medications such as antispasmodics such as mebeverine, laxatives, or anti-diarrhoeal agents may be used depending on the predominant symptoms. 2nd-line medications include low-dose tricyclic antidepressants Refractory IBS - symptoms not improving for 12 months; psychotherapy advised, including: cognitive-behavioral therapy, hypnotherapy, and mindfulness-based therapy
289
Define malnutrition:
Malnutrition is defined as a state of nutrition in which a deficiency, excess, or imbalance of energy, protein, and other nutrients causes measurable adverse effects on tissue/body form (body shape, size, composition), function, and clinical outcome.
290
How does Nice define malnutrition:
NICE define malnourishment as: A body mass index (BMI) of less than 18.5 kg/m2. Unintentional weight loss greater than 10% within the last 3–6 months. A BMI of less than 20 kg/m2 and unintentional weight loss greater than 5% within the last 3–6 months.
291
Name some causes of malnutrition:
Inadequate intake: Poor dietary intake due to socio-economic factors, poor appetite, or food availability. Physical difficulties in eating, such as dysphagia or dental issues. Increased requirements: Growth in children and adolescents. Pregnancy and lactation. Acute or chronic illnesses that increase metabolic demands. Malabsorption: Gastrointestinal diseases such as Crohn’s disease, coeliac disease, and chronic pancreatitis. Post-surgical states affecting the gut. Chronic diseases: Cancer, chronic kidney disease, heart failure, and chronic obstructive pulmonary disease (COPD). Socioeconomic factors: Poverty, lack of access to nutritious food, and social isolation.
292
Malnutrition can be classified into two types:
Undernutrition: Protein-energy malnutrition: Includes conditions such as marasmus and kwashiorkor. Micronutrient deficiencies: Deficiencies in vitamins and minerals, such as iron, iodine, vitamin A, and zinc. Overnutrition: Obesity and related conditions such as metabolic syndrome.
293
What are the signs and symptoms of malnutrition:
General signs: Weight loss or failure to gain weight (in children). Fatigue, weakness, and lethargy. Poor concentration and mental function. Decreased immunity and frequent infections. Specific signs: Muscle wasting. Oedema (in cases of protein deficiency). Brittle hair and nails. Dry, scaly skin. Delayed wound healing. Growth retardation in children.
294
What are the investigations for malnutrition:
Bedside: Nutritional screening tools (e.g., MUST – Malnutrition Universal Screening Tool). Anthropometric measurements (height, weight, BMI, mid-arm circumference). Bloods: Full blood count (FBC) to check for anaemia. Serum albumin and prealbumin levels. Electrolytes, urea, and creatinine. Liver function tests. Vitamin and mineral levels (e.g., iron studies, vitamin D, vitamin B12, folate). Imaging: Dual-energy X-ray absorptiometry (DEXA) scan for body composition analysis. Invasive: Endoscopy and biopsy for suspected malabsorptive disorders.
295
What is the management for malnutrition:
General measures: Nutritional support: Oral nutritional supplements, fortified foods, and dietary modifications. Treat underlying causes: Addressing chronic illnesses, infections, or socioeconomic issues. Specific interventions: Enteral nutrition: Tube feeding for those unable to eat adequately by mouth. Parenteral nutrition: Intravenous feeding for severe cases where the gastrointestinal tract cannot be used. Micronutrient supplementation: Specific vitamins and minerals based on identified deficiencies. Monitoring and follow-up: Regular assessment of nutritional status and dietary intake. Adjustments to the nutritional plan based on progress and any new medical issues.
296
What are the complications of malnutrition:
Increased risk of infections due to impaired immune function. Delayed wound healing and recovery from illnesses. Muscle weakness and decreased functional capacity. Developmental delays in children. Increased morbidity and mortality.
297
Define mesenteric adentitis
Mesenteric adenitis is an inflammatory condition that primarily involves the mesenteric lymph nodes in the abdomen and is a common mimic of appendicitis.
298
What is the epidemiology of mesenteric adentitis:
While mesenteric adenitis can affect individuals of any age, it is more prevalent in children and adolescents. The condition typically follows an upper respiratory tract infection, suggesting a link with viral pathogens.
299
What causes mesenteric adentitis:
it is commonly associated with viral or bacterial infections that trigger an immune response, leading to inflammation of the mesenteric lymph nodes. Here are some common pathogens known to be linked with the condition: Viruses: A significant proportion of cases occur following viral infections, especially of the upper respiratory tract. Epstein-Barr virus (EBV), responsible for causing infectious mononucleosis, is among the most common viral triggers. Other viral aetiologies include adenoviruses and enteroviruses. Bacteria: Certain bacterial infections, particularly those caused by Yersinia and Campylobacter species, are known to be associated with mesenteric adenitis. Yersinia enterocolitica and Yersinia pseudotuberculosis are often implicated and are typically contracted through contaminated food or water. Campylobacter infections usually occur due to ingestion of undercooked poultry or unpasteurized milk. Other Causes: Rarely, other pathogens such as Mycobacterium, Salmonella, and Streptococcus have been linked to the condition. It's important to note that mesenteric adenitis often occurs after the initial infection has resolved, indicating a reactive process rather than an ongoing infection of the mesenteric lymph nodes themselves
300
What are the signs and symptoms of mesenteric adentitis
Diffuse abdominal pain, often mistaken for appendicitis Low-grade fever Generalized abdominal tenderness Pharyngitis or sore throat Nausea Diarrhoea
301
What are the key investigations in mesenteric adentitis:
Full blood count: Typically normal, unlike the elevated white cell count seen in appendicitis/inflammatory causes of abdominal pain. US abdomen: Reveals mesenteric lymph nodes which are enlarged, clustered and hypervascular. A normal appendix may also be visualised, but it is sometimes difficult to image using ultrasound, and such careful clinical correlation is needed.
302
What is the management of mesenteric adentitis:
Conservative management including analgesia and ensuring sufficient fluid intake. Monitoring for any worsening of symptoms is essential, and patients should be advised to return if any concerns arise. Surgical intervention should be considered with caution, as it is typically unnecessary for this condition. However, it may be needed if appendicitis cannot be definitively ruled out.
303
Which bacteria is the most common cause of mesenteric adentitis:
Yersinia enterocolitica
304
Define oesophageal cancer:
Oesophageal carcinoma is a type of cancer that originates from the epithelial cells lining the oesophagus, primarily categorised into adenocarcinoma or squamous cell carcinoma.
305
What is the epidemiology of oesophageal cancer:
Squamous cell carcinoma of the oesophagus is the most prevalent type globally, often seen in the upper two-thirds of the oesophagus. Conversely, adenocarcinoma has become the most common cause of oesophageal carcinoma in the Western world, owing to the increasing prevalence of GORD, and is often seen in the lower one-third of the oeseophagus.
306
What are the risk factors for oesophageal cancer:
Smoking: The most significant risk factor for both adenocarcinoma and squamous cell carcinoma. High alcohol intake Obesity and gastro-oesophageal reflux disease: Linked specifically to adenocarcinoma, as recurrent reflux leads to metaplastic formations of mucin-producing glandular tissue known as Barrett's oesophagus, which can further develop into neoplasia. Achalasia Zenker diverticulum Oesophageal web High intake of hot beverages Dietary intake of: Increased dietary nitrosamines Areca or betel nuts
307
What are the signs and symptoms of oesophageal carcinoma?
Progressive dysphagia: Initially for solids, and later for liquids. Dysphagia typically occurs when there is obstruction of more than two-thirds of the lumen. Weight loss: This symptom, the second most common, results from a combination of anorexia and dysphagia. Odynophagia: Pain on swallowing can occur. Hoarseness: Can develop if there is local invasion of the recurrent laryngeal nerve.
308
What is the NICE 2 week referral pathway for oesophageal carcinoma?
NICE 2-week-wait criteria: Offer urgent direct access upper gastrointestinal endoscopy (to be performed within 2 weeks) to assess for oesophageal cancer in people with dysphagia or those aged 55 years and over with weight loss and any of the following: upper abdominal pain, reflux, or dyspepsia. Consider non-urgent direct access upper gastrointestinal endoscopy to assess for oesophageal cancer in people with haematemesis.
309
What are the investigations for oesophageal carcinoma?
Investigations for oesophageal carcinoma encompass: Initial investigation: Upper GI endoscopy is performed to visualise and grade the tumour via biopsy. Staging: CT chest, abdomen and pelvis: Assesses the size of the tumour, local and lymph node spread, and any visceral metastases. MRI: Identifies metastatic spread to the liver and advanced local disease. Endoscopic ultrasound: Assesses whether a tumour is amenable for resection. FDG-PET scan: Identifies distant and nodal metastases. Laparoscopy: Used to identify intra-abdominal metastases if all other imaging has been negative.
310
What is the management for oesophageal carcinoma?
Management of oesophageal carcinoma is based on the stage of the disease and may include: Surgical resection: The primary choice for localised disease. Endoscopic therapies: Such as endoscopic mucosal resection or endoscopic submucosal dissection for early-stage disease. Non-surgical options: Such as radiotherapy, chemotherapy or chemoradiotherapy for advanced disease, or as neoadjuvant or adjuvant therapy with surgery.
311
Define pancreatic cancer:
Pancreatic cancer is a malignant neoplasm originating from the pancreatic tissue. The pancreas is a glandular organ involved in both the digestive and endocrine systems of vertebrates. The most prevalent type of pancreatic cancer is pancreatic adenocarcinoma, which usually originates from the head of the pancreas.
312
Name some risk factors for pancreatic cancer:
Age: Pancreatic cancer is more prevalent in elderly individuals. Smoking: The risk significantly increases with tobacco use. Obesity: Overweight and obese individuals have a higher risk. Diabetes: Long-standing diabetes may increase risk. Chronic pancreatitis: Chronic inflammation of the pancreas can lead to cancer. Family history: Having a first-degree relative with pancreatic cancer increases the risk. Certain genetic syndromes: Genetic mutations linked to pancreatic cancer include BRCA2, Lynch syndrome, and familial atypical mole and melanoma (FAMMM) syndrome.
313
What are the early signs of pancreatic cancer:
Malaise Abdominal pain Nausea Weight loss Painless jaundice Courvoisier's sign - painless jaundice with a palpable gallbladder is usually indicative of a pancreatic or gallbladder malignancy (and less likely due to e.g. gallstones)
314
What are the signs of advanced pancreatic cancer:
Obstructive jaundice, often due to blockage of the common bile duct by a tumour in the pancreatic head. It may present with Courvoisier's sign. Diabetes mellitus, typically in an elderly patient with newly diagnosed diabetes and weight loss, may suggest a tumour in the body/tail of the pancreas. Pancreatic infiltration can lead to unexplained pancreatitis and pancreatic exocrine dysfunction with steatorrhoea. Paraneoplastic syndromes, such as Trousseau's syndrome (migratory thrombophlebitis), or marantic endocarditis. Disseminated intravascular coagulation (DIC)
315
What is the NICE 2 week wait referral pathway for suspected pancreatic cancer:
NICE 2-week-wait criteria: Refer people using a suspected cancer pathway referral (for an appointment within 2 weeks) for pancreatic cancer if they are aged 40 years and over and have jaundice. Consider an urgent CT scan (to be performed within 2 weeks), or an urgent ultrasound scan if CT is not available, to assess for pancreatic cancer in people aged 60 years and over with weight loss and any of the following: diarrhoea, back pain, abdominal pain, nausea, vomiting, constipation, or new-onset diabetes.
316
What are the investigations for pancreatic cancer?
Initial assessment with abdominal ultrasound to detect tumours (>2cm), potential liver metastases and any dilation of the common bile duct. CT abdomen/pelvis for patients with a high clinical suspicion. This can predict surgical resectability and enables disease staging. Magnetic resonance cholangiopancreatography (MRCP) for details about the biliary ducts. Endoscopic ultrasound to detect small lesions (2-3mm) and for biopsy if needed. PET-FDG and MRI as adjuncts.
317
What is the definitive management for pancreatic cancer:
The only potentially curative treatment for pancreatic cancer is surgical resection. However, due to late presentation, only 15-20% of patients present with resectable disease. Criteria for resection include: No evidence of superior mesenteric artery (SMA) or coeliac arteries involvement. No evidence of distant metastases. The common surgical procedure for tumours in the head of the pancreas is the Kausch-Whipple procedure (radical pancreaticoduodenectomy). Adjuvant chemotherapy is offered post-surgery to patients who have recovered well.
318
What is the management for pancreatic cancer if it is locally advanced or there are signs of metastatic disease:
In cases of locally advanced or metastatic disease, palliative therapy is the only option. This includes: Endoscopic stent insertion into the common bile duct. Palliative surgery if endoscopic stent insertion fails. Chemotherapy. Radiotherapy (only for localised advanced disease). It is crucial to refer these patients to palliative care services for pain management and psychological support.
319
What tumour marker is a sign for pancreatic cancer?
The tumour marker CA 19-9 has a sensitivity and specificity of 90% for pancreatic cancer
320
Define peptic ulcer disease:
Peptic ulcer disease refers to painful sores or ulcers in the lining of the stomach or the first part of the small intestine, known as the duodenum. The frequency of duodenal ulcers is four times higher than that of gastric ulcers. It is an endoscopic diagnosis (NB: dyspepsia is a clinical diagnosis). Peptic ulcer disease can be uncomplicated, or complicated (perforation, bleeding).
320
What causes peptic ulcers?
The primary cause of duodenal ulcers is the infection by H. Pylori. Other factors contributing to the development of these ulcers include: NSAIDs Chronic use of steroids SSRIs Increased secretion of gastric acid Smoking Blood group O Accelerated gastric emptying For gastric ulcers, the risk factors include: NSAIDs H. Pylori infection Smoking Delayed gastric emptying Severe stress
321
What are the signs and symptoms of peptic ulcers?
Patients with peptic ulcer disease may present with: Abdominal pain Nausea Vomiting Loss of appetite Unexplained weight loss Patients with complicated peptic ulcer disease may present with coffee ground vomiting (bleeding), and can be haemodynamically unstable due to perforation
322
What are the signs and symptoms that distinguish between a duodenal ulcer and a gastric ulcer?
Duodenal ulcers typically present with epigastric pain typically relieved on eating (closure of pyloric sphincter, less acid irritating ulcerated surface). Symptoms of gastric ulcers on the other hand are often worsened by eating - stomach increases acid production in response to food and irritates ulcerated surface.
323
What are the investigations for peptic ulcers?
Patients >55 with weight loss and dyspepsia should be referred for an urgent OGD (within 2 weeks) to investigate for oesophageal and gastric cancer Patients should be investigated for H.pylori infection with C-13 urea breath test (ensure the person has not taken a PPI in the past 2 weeks, or antibiotics in the past 4 weeks) Investigation tools for peptic ulcer disease primarily include endoscopy, which allows a direct visual inspection of the ulcers. Biopsies may be taken to rule out malignancy.
324
What is the Management of H. Pylori-negative peptic ulcer disease:
involves a 4-8 week course of full-dose PPI treatment in conjunction with lifestyle advice, such as: Smoking cessation Reducing alcohol intake Regular, small meals and avoiding eating 4 hours before bedtime Avoidance of acidic, fatty or spicy foods, and coffee Weight loss if overweight Stress management Avoidance of NSAIDs, steroids, bisphosphonates, potassium supplements, SSRIs, and crack cocaine Over-the-counter antacids
325
What is the management if the patient is H.pylori positive:
If the patient is H.pylori positive with a proven gastric/duodenal ulcer which is: Associated with NSAID use: 8 week PPI therapy followed by first-line eradication therapy - PPI (omeprazole/lansoperazole) + amoxicillin + clarithromycin/metronidazole for 7 days If penicillin allergic, offer: PPI + clarithromycin + metronidazole for 7 days Not associated with NSAID use: eradication therapy with PPI (omeprazole/lansoperazole) + amoxicillin + clarithromycin/metronidazole for 7 days If the person is allergic to pencillin and has had previous exposure to clarithromycin, offer a 7-day quadruple therapy regimen of: PPI + metronidazole + tetracycline hydrochloride + bismuth subsalicylate For patients with gastric ulcers, a repeat endoscopy 6-8 weeks following the start of PPI treatment is recommended to ensure ulcer healing and rule out malignancy, as well as H.pylori re-testing (C-13 urea breath test first-line, stool antigen test second line) if appropriate.
326
What is the management for Complicated peptic ulcer disease?
Requires urgent surgical intervention with OGD for underunning of ulcers and haemostasis Perforated peptic ulcers present initially with localised epigastric pain which later becomes generalised and peritonitic. These patients require an AXR and erect CXR to look for pneumoperitoneum.
327
Define perianal abscess:
a pus collection in the perianal region
328
Define perianal fistula:
an abnormally chronically infected tract communicating between the rectum and the perineum
329
What’s the difference between anal abscesses and anal fistulae?
Anal abscesses are the acute manifestation of a purulent infection in the perirectal area, while anal fistulas are the chronic manifestation of such infections Anal abscesses can progress into fistulas
330
What causes perianal abscess and fistulae?
Anorectal abscesses are often secondary to conditions that cause a breach in the integrity of the intestinal barrier. Key factors include: Anal fistulae: These are abnormal connections between the surface of the anal canal and the exterior skin. Crohn's disease: This chronic inflammatory bowel disease can lead to the formation of abscesses due to constant irritation and inflammation of the bowel wall.
331
What are the signs and symptoms of perianal abscess and fistulae?
Patients with anorectal abscesses typically present with the following: Perianal pain: Often severe and aggravated by sitting or bowel movements. Perianal swelling: This may be fluctuant and tender upon examination. Systemic symptoms: Low-grade pyrexia, tachycardia, and potentially sepsis if the infection spreads, leading to haemodynamic compromise.
332
What are the investigations for perianal abscess and fistulae?
Evaluation of suspected anorectal abscesses involves a thorough examination and potentially additional diagnostic studies: Physical examination: Inspection is performed to detect perianal swelling, and a digital rectal examination (if tolerated) is conducted to assess the size of the swelling. Assessment of vital signs: Detecting systemic symptoms such as fever and tachycardia is crucial, as these can indicate the spread of the abscess causing sepsis. Laboratory investigations: Full blood count, CRP, and ESR can aid in detecting systemic inflammation and infection. Blood cultures may be necessary if sepsis is suspected. Imaging: MRI pelvis is the gold standard for definitive diagnosis of an anorectal abscess. If unavailable ultrasound may be of benefit.
333
What is the management for perianal abscess and fistulae?
The mainstay of treatment for anorectal abscesses is early surgical intervention to prevent sepsis. Management options include: Drainage: Perianal abscesses can be drained in A&E under local anaesthesia. Incision and drainage under general anaesthetic: This is necessary when the degree of tissue damage is unknown or in the case of deep perirectal abscesses with sphincter extension. Antibiotics are used if there is an underlying condition such as diabetes or immunosuppression. If on presentation the patient is already septic, intravenous antibiotics will be needed.
334
Define peritonitis:
Peritonitis is defined as inflammation of the peritoneum, which is the serous membrane lining the cavity of the abdomen and covering the abdominal organs.
335
What are the causes of peritonitis:
Perforation of a hollow viscus: This can be from a perforated oesophagus (Boerhaave syndrome), a perforated duodenal or gastric ulcer, a perforated intestine (secondary to conditions such as appendicitis, diverticulitis, intestinal infarction, colorectal cancer, or inflammatory bowel disease). Perforation may also occur due to trauma, such as the ingestion of a foreign body. Perforation can lead to diffuse or faeculent peritonitis. Infection: Infections leading to peritonitis include spontaneous bacterial peritonitis and peritoneal infection secondary to peritoneal dialysis. Uncomplicated appendicities can cause local peritonitis due to inflammation of the surrounding peritoneum. Remember, sterile fluids can also leak into and irritate the peritoneum. This can occur with leakage of blood (e.g. in blunt abdominal trauma), bile (e.g. in liver biopsy), and pancreatic fluids (e.g. in acute pancreatitis).
336
What are the signs and symptoms of peritonitis:
Severe abdominal pain. Patients will often be lying completely still so as to not trigger/exacerbate pain Systemic signs of illness such as fever, haemodynamic instability, tachycardia Nausea and vomiting Abdominal rigidity/Involuntary abdominal guarding: Involuntary tensing of the abdominal wall muscles in response to pressure on the abdomen (to protect inflamed abdominal organs). Rebound tenderness: Pressing on the abdomen elicits less pain than releasing the hand (as the peritoneum bounces back into place). Percussion tenderness
337
What are the investigations for peritonitis:
Patients presenting with peritonitis can be very systemically unwell and the SEPSIS 6 should be initiated in these situation. Laboratory tests: Blood tests to assess for elevated white blood cell count and markers of inflammation (e.g. C-reactive protein), kidney function, and liver function. Imaging: Abdominal x-ray, ultrasound, or CT scan to identify fluid collections or perforations (looking for free gas - pneumoperitoneum, rigler’s sign and football sign). Peritoneal fluid analysis: If feasible, an analysis of peritoneal fluid obtained by paracentesis can help identify the causative organism and guide treatment.
338
What is the management for peritonitis:
Management of peritonitis is guided by the underlying cause but may include: Surgical intervention: For conditions such as a perforated viscus, appendicitis, or diverticulitis, surgical intervention is often required to control the source of infection or inflammation. Antibiotics: Empirical antibiotic therapy should be initiated as soon as possible and then tailored according to culture results. Supportive care: Fluid resuscitation, pain management, and monitoring of vital signs are crucial in the management of peritonitis.
339
What does vitamin b12 do?
RBC formation and myelination of NS
340
Where is vitamin B12 absorbed?
Terminal ileum and requires intrinsic factor (IF)
341
When do we get a deficiency of B12?
- pernicious anaemia- autoantibodies against IF or gastric parietal cells and increases risk of gastric cancer- may have history of autoimmune disease - Post gastrectomy - Vegan diet - Terminal ileum affected e.g. Crohn’s or ileocaecal resection
342
What is the purpose of folate?
DNA synthesis and amino acid metabolism
343
What is the source of folate?
- Green leafy vegetables - Fruits - Liver - Bread - Cereal
344
What causes a deficiency of folate?
- Malabsorption e.g. small bowel disease due to IBD or Coeliac - Malnutrition e.g. chronic alcohol use - Increased requirement e.g. pregnancy - Drug related e.g. methotrexate or antiepileptics
345
What are the clinical features of a Vitamin B12 deficiency?
- Signs of anaemia- fatigue, pallor, SOB - Glossitis - Peripheral neuropathy- describe this **(3)** - tingling, numbness, paraesthesia in hands and feet - Weakness in legs - diminished proprioception and vibration sensation in feet - Dementia
346
What are the clinical features of a folate deficiency?
- Signs of anaemia- fatigue, pallor, SOB - Glossitis - Foetal spina bifida (neural tube defects) if maternal deficiency
347
What investigations do we do for a B12 and folate deficiency?
- What would a blood film show? Macrocytic megaloblastic anaemia- decreased Hb, increased MCV, hyperchromic RBCs, hypersegmented neutrophils - How do we test for pernicious anaemia? Test for autoantibodies- anti-IF (more specific) or antiparietal cell - What does homocysteine show in both deficiencies? Elevated in both - What does methylmalonic acid show in both deficiencies? Elevated in B12 deficiency and normal in folate deficiency
348
What is the management for B12 and folate deficiency?
- For vit B12 deficiency? IM supplementation of B12 (hydroxycobalamin) - For folate deficiency? Oral folate supplementation, nutritional counselling to increase folate intake - Why is it given to pregnant women? Risk of neural tube defects e.g. spina bifida and anencephaly 400mcg of folic acid until 12th week of pregnancy - Why do we always replace B12 before folate (**B**e**F**ore)? Protects against subacute combined degeneration of spinal cord - What are the signs of this? **(5)** - Hyperreflexia - absent ankle jerks/extensor plantars - Distal sensory loss, impaired proprioception and vibration - tingling - gait abnormalities/Romberg's positive
349
Define gastrointestinal perforation:
A gastrointestinal perforation refers to a hole in the wall of the bowel, stomach or oesophagus that allows the contents of the GI tract to leak out.
350
Causes of upper GI tract perforation:
Oesophageal or gastric malignancies Peptic ulcer disease Boerhaave syndrome (oesophageal rupture secondary to forceful vomiting) Ingestion of sharp or caustic materials Iatrogenic e.g. during surgery or endoscopy
351
Causes of lower GI tract perforation include:
Diverticulitis Colorectal cancer Bowel obstruction Colitis (e.g. inflammatory bowel disease) Appendicitis Infection (e.g. toxic megacolon secondary to C. difficile infection) Iatrogenic (e.g. abdominal surgery or colonoscopy) Mesenteric ischaemia Invasion of the bowel by other tumours
352
Signs and symptoms of gastrointestinal perforation:
Symptoms include: Abdominal pain, which is sudden in onset and severe Nausea and vomiting Malaise Lethargy Signs: Peritonism e.g. guarding, rebound tenderness, rigidity on palpation of the abdomen Hypotension Tachycardia Tachypnoea Fevers
353
What are the investigations for gastrointestinal perforation:
Bedside tests: Blood gas to measure lactate and acid-base status which may be deranged due to bowel ischaemia or sepsis Pregnancy test in women of childbearing age to rule out obstetric causes of abdominal pain such as ectopic pregnancy Blood tests: FBC and CRP for inflammatory markers LFTs and U&Es which may be deranged in sepsis Clotting screen and group and saves to prepare for possible surgery; a coagulopathy may develop secondary to sepsis Blood cultures if febrile or other signs of infection to help target antibiotic treatment Imaging: CT with contrast looking for free air (confirming perforation) and the site of perforation; an underlying cause may also be seen (e.g. an obstructing tumour) - Oral contrast may be used as well as IV in order to better identify the site of perforation Chest X-ray may show air under the diaphragm (pneumoperitoneum) but is significantly less sensitive than CT Abdominal X-ray may show Rigler's sign (where gas outlines both sides of the bowel wall as it is in the peritoneal cavity as well as the lumen) - also not a first-line test due to limited sensitivity
354
Management for gastrointestinal perforation:
Conservative: Make the patient nil by mouth Urgent surgical review May require critical care input e.g. in cases of organ failure secondary to sepsis Consider nasogastric tube insertion e.g. in severe vomiting Medical: Start IV broad spectrum antibiotics IV fluid resuscitation as required Give analgesia and antiemetics - may need to be parenteral Certain cases of perforation may be managed with medical treatment only, for example a localised diverticular perforation in a well patient Surgical: Most cases of perforation will require surgical management with a laparotomy This usually involves a thorough washout, identifying the cause of perforation and repairing the defect For example, cases of bowel perforation would usually be managed with a bowel resection and formation of a temporary stoma to protect the site of repair
355