Gastroenterology & Hepatology Flashcards
(167 cards)
1
Q
What is the definition, aetiology and epidemiology of Achalasia?
A
Achalasia is the failure of relaxation of the lower oesophageal sphincter accompanied by loss of peristalsis in the distal oesophagus. This is due to progressive degeneration of ganglion cells in the myenteric plexus in the oesophageal wall.It is quite an uncommon disorder (10 in 100,000). Achalasia is usually diagnosed between the ages of 25 and 60.
2
Q
What are the clinical features of Achalasia?
A
Diagnosed after years (mean of 4.7) of symptoms, as the symptoms are often misdiagnosed for GORD. These symptoms include:
• Dysphagia (difficulty swallowing) for solids (91%) and liquids (85%).
• Regurgitation of bland undigested food
○ This may result in aspiration
• Difficulty belching
• Substernal chest pain and heartburn
3
Q
How is Achalasia investigated?
A
An oesophageal manometry is primarily used if achalasia is suspected.
A barium oesophagram can also be used, however, it is not a sensitive test for achalasia (up to 1/3 patients interpreted as normal)
4
Q
What is the management of Achalasia?
A
• Drugs are not very effective. Nitrates and calcium-channel blockers provide short-lived effects on the lower oesophageal sphincter and have side effects.
○ Botulinum toxin can be injected into the sphincter, which reduces sphincter pressure and relieves symptoms. However, the effects are short-lived, and repeat injections are necessary every 6-12 months.
- Endoscopic dilatation is where a balloon is inflated for 1-2 minutes over the sphincter. This produces good results, but patients may need more than one procedure.
- Surgical myotomy is effective in 90% of cases, but causes reflux in 10%.
5
Q
What is the definition, aetiology and epidemiology of Anal Fissure?
A
An anal fissure is a tear in the anoderm distal to the dentate line. It may be acute or chronic.
Acute fissures can be due to trauma (stretching of the anal mucosa due to hard stool, prolonged diarrhoea, vaginal delivery or anal sex) or may be due to an underlying pathology.
6
Q
What are the clinical features of Anal fissure?
A
Patients present with a tearing/burning pain accompanying stool passage. Patients may also describe bright red rectal bleeding.On examination, the patient may have a laceration (like a papercut) indicating an acute fissure, or if chronic, the edges will be raised and [looks like its been there for a while]. You may have to use a proctoscope and pain on digital rectal examination.
7
Q
What is the management of Anal fissure?
A
Medical treatment involves ensuring the patient has proper fibre intake, to loosen stools (fibre supplements and laxatives can also be given). This is coupled with proper hygiene and preventing further trauma.You can also prescribe an ointment/cream to relax the internal sphincter. This cream can be Nitrite or CCB.Chronic anal fissures often require surgery, but are started on medical treatment, with vasodilators. Surgery is usually an lateral internal sphincterotomy.
8
Q
What is the definition and epidemiology of Appendicitis?
A
Appendicitis is the inflammation of the appendix. Occurs most commonly in 20’s and 30’s.It is one of the most common causes of the acute abdomen and one of the most frequent indications for an emergent abdominal surgical procedure worldwide.
9
Q
What is the pathophysiology of Appendicitis?
A
Appendiceal obstruction has been proposed as the primary cause of appendicitis. This may be due to foecaliths (hard foecal masses), calculi, infectious processes or tumors. Obstruction leads to inflammation due to increased intraluminal pressure and occlusion of small vessels. This causes localised ischemia (and later necrosis) and perforation if not treated. Bacterial overgrowth occurs within the diseased appendix, resulting in stimulation of somatic nerves, causing pain at the side of peritoneal irritation.
10
Q
What are the clinical features of Appendicitis?
A
- Right iliac fossa pain at McBurney’s point (one-third of the distance from the anterior superior iliac spine to the umbilicus). Usually starts in the periumbilical region, with subsequent migration to the right iliac fossa. However, this migration only happens in up to 60% of patients.
- Nausea and vomitting
- Anorexia
- Other atypical symptoms include indigestion, flatulence, bowel irregularity, diarrhoea, generalised malaise.
On examination, may find low-grade fever and right lower quadrant tenderness.
11
Q
How is Appendicitis investigated?
A
- FBC may show mild leukocytosis.
- CT may show enlarged appendiceal diameter or wall thickening- Ultrasound may also show a dilated appendix (>6cm)
12
Q
What is the definition, aetiology and epidemiology of Barrett’s Oesophagus?
A
Barrett’s oesophagus is when columnar epithelium replaces the normal stratified squamous epithelium of the distal oesophagus. The condition develops as a consequence of chronic GORD, and is a premalignant adenocarcinoma.The mean age of diagnosis is 55.
13
Q
What are the clinical and diagnostic features of Barrett’s Oesophagus?
A
Most patients are initially seen for the symptoms of GORD (heartburn, regurgitation and dysphagia).
To diagnose Barrett’s oesophagus, two diagnostic criteria must be fulfilled:
- The endoscope must reveal that columnar epithelium lines the distal oesophagus. Squamous epithelium has a pale, glossy appearance, while columnar epithelium has a reddish velvet-like texture on endoscopic examination.
- Histologic examination of the biopsy specimens from that columnar epithelium must reveal intestinal metaplasia.
14
Q
What is the management of Barrett’s Oesophagus?
A
Although risk of cancer is increased x30, the absolute risk is still very low. Whether to screen for Barrett’s oesophagus is controversial.
The principles of management include:
• Management of acid reflux - aggressively with indefinite PPI (studies show might prevent cancer)
• Chemoprevention - apirin and other NSAID use decreases risk of oesophageal cancer from Barrett’s oesophagus. This is because the epithelium in the Barrett’s oesophagus have higher expression of COX-2, so inhibiting this has been shown to have anti-proliferative and pro-apoptotic effects.
Patients with low-grade dysplasia are usually only monitored, while patients with high-grade dysplasia undergo RFB (radiofrequency ablation) which removes all Barrett’s epithelium with favourable safety profile.
15
Q
What is the definition, aetiology and epidemiology of Coeliac disease?
A
Coeliac disease is an autoimmune disease resulting in enteropathy due to a gluten-insensitivity. Like many autoimmune diseases, it is triggered by an environmental agent (the gliadin competent of gluten) in a genetically predisposed individual.
Coeliac disease is not uncommon, affecting from 1:70 - 1:300.
16
Q
What are the clinical features of Coeliac disease?
A
Gastrointestinal manifestations:
Classically, patients present with:
• Diarrhoea
• Steatorrhea (floating stools) that may be foul smelling
• Flatulence
• Consequences of malabsorption such as growth restriction in children, weight loss, severe anaemia, neurological disorders due to vitamin B deficiencies and osteopenia from vitamin D deficiencies.
However, there is a shift (around 38% of patients) to atyipical symptoms, which may present as irritable bowel-like symptoms.As coeliac disease can come in mild forms, patients may have mild and unspecific symptoms, such as fatigue, borderline iron deficiency. These patients are only diagnosed thanks to serological tests and increased clinician awareness.
Non-Gastrointestinal manifestations:
In some patients, these are the presenting complaints:
• Neuropsychiatric diseases such as depression (10%), epilepsy (3.5%), migraine headaches (3%) anxiety and other conditions. Peripheral neuropathies have been described in up to 50% of patients, and may precede the coeliac diagnosis.
• Osteoarthritis
• Metabolic bone diseases (decrease in BMD) are mainly due to secondary hyperparathyroidism due to vitamin D deficiency. Osteomalacia can also result due to vitamin D deficiency.Risk of malignancy and mortality
The risk of malignancy has been found to be 30% higher in those with coeliac disease. The risk was highest for lymphoproliferative disease and gastrointestinal cancer.
There is also an increase in overall mortality in those with coeliac disease; even worse if undiagnosed.
17
Q
How is Coeliac disease investigated?
A
- Serological evaluation is done first, looking at TTG IgA. However, this is not perfect, and with patients who have a high probability of coeliac disease, a tissue biopsy should be done even after a negative serological test.
- Testing on a gluten-free diet: Coeliac disease should be differentiated from nonceliac gluten sensitivity
- Small bowel biopsy
18
Q
What is the definition and pathophysiology of Alcoholic Hepatitis?
A
Hepatitis is the inflammation of the liver (can be acute or chronic). It results from a combination of fatty liver and inflammation with necrosis of the hepatocytes, after long period of drinking. Hepatocytes develop a swollen and granular cytoplasm. There is also deposition of fibrillar protein and clumping of organelles in the cytoplasm.
19
Q
What are the clinical features of Alcoholic Hepatitis?
A
- Acute onset of malaise
- Jaundice
- Anorexia
- Diarrhoea
- Nausea
- Tender hepatomegaly
- Signs of decompensated liver disease (such as ascites or hepatic encephalopathy)
- Malnutrition is common as they consume a large amount of their calories through the alcohol.
20
Q
How is Alcoholic Hepatitis investigated?
A
Investigations can be done through bloods:
• FBC:
○ Elevated white cell count (in 50% of cases)
○ Decreased platelets why??
○ Increased MCV why??
• U&Es:
○ May show decreased electrolytes (Na+, K+, Ca2+ and Mg2+)
○ Renal failure may be due to dehydration, sepsis or hepatorenal syndrome
• LFTs:
○ AST/ALT raised (with AST usually > ALT)
○ Increased billirubin
• Acute phase markers (CRP and Ferritin)
A liver biopsy is diagnostic, as it excludes underlying cirrhosis.
21
Q
How can Alcoholic Hepatitis be managed?
A
The management of alcoholic hepatitis includes:
• General supportive measures (with diligent care of IV lines to prevent sepsis)
• Insert urinary catheter to monitor urinary output.
• Vitamin K for 3 days
• Thiamine (prophylaxis against Wernicke’s encephalopathy)
• Protein supplements
• Corticosteroids in severe disease
Also treat ascites, hepatic encephalopathy etc.
Alcohol withdrawal can be treated effectively with benzodiazepines such as chlordiazepoxide.
22
Q
What is the definition, aetiology and pathophysiology of Cholangitis?
A
Acute cholangitis is inflammation of the biliary tree usually due to stasis and infection in the tract. Cholangitis is also called ascending cholangitis as bacteria from the duodenum are allowed to climb up the blocked biliary tree, and can take residence in the stone (or whatever is causing the stasis, such as malignancy).
Causes of obstruction include:
• Gall stones (cholelithiasis)
• Biliary strictures (as in primary sclerosing cholangitis,
• pancreatic cancer and cholangiocarcinoma)
• Following an ERCP
23
Q
What are the clinical features of Cholangitis?
A
Charcot's triad: • Fever (>90%) • Jaundice (65%) • Right upper quadrant pain (>40%) • Septic shock • Confusion
24
Q
What are the complications of Cholangitis?
A
Secondary complications include acute renal failure, disseminated intravascular coagulation and liver abscess formation.
25
How can Cholangitis be investigated?
Acute cholangitis should be suspected if the patient has a fever and is jaundiced. Diagnosis is confirmed by abdominal ultrasound or x-ray showing biliary dilation or evidence of aetiology (e.g stone or stent).
* FBC shows increased WCC and neutrophils
* U&Es may show renal failure associated with septic shock
* LFTs are elevated (increased bilirubin) but also increased ALS/ALT
* Blood cultures may be positive in 50% of cases
26
How is Cholangitis managed?
Treat and monitor for sepsis. This often involves fluid resuscitation. Place on antibiotics for colonic bacteria, but importantly drain the obstruction with an ERCP.
27
What is the prognosis of Cholangitis?
Mortality for moderate cholangitis is around 11%, while for severe/complicated cholangitis is up to 30%.
28
Define Appendiectomy
An appendectomy is the surgical removal of the appendix. It is the mainstay treatment for acute appendicitis.
29
Identify the possible complications of an Appendiectomy
The most common complication is infection. This is can either be a wound/incisional infection (which is more common in the open operation), or an intraabdominal abscess (which is slightly more common after the laparoscopic approach)
30
What is the definition, aetiology and epidemiology of Autoimmune hepatitis?
Autoimmune hepatitis is quite rare, affecting up to 100 people per million. Affects females more than males, in a ratio 4:1.
Strongly associated with HLA genes:
• DR3 (manifests in younger patients, with a more severe disease)
• DR4 (later on in life, with a more benign disease)
31
What are the clinical features of Autoimmune hepatitis?
- Presents with acute hepatitis in up-to 40%. Gradual onset of jaundice, fatigue, abdominal pail, and fever.
- 30-80% have cirrhosis at presentation-
Associated with other autoimmune conditions in 48% of cases: thyroid disease, arthritis, vitiligo, ulcerative colitis, diabetes mellitus, mixed connective tissue disease.
- Overlap syndromes with cholangitis, and cirrhosis occurs.
32
How can Autoimmune hepatitis be investigated?
Definitive investigation involves measuring circulating autoantibodies that are greater than the ULN (Upper Limit of Normal), while excluding all other causes of chronic liver disease. ALT/AST are only 1.5x ULN elevated. Highly elevated points to hepatitis due to drugs or viral
33
How is Autoimmune hepatitis managed?
1. Corticosteroids is the mainstay of treatment for remission
2. Azathioprine is useful only in combination with corticosteroids to maintain remission
New immunosuppressants may be used, and if all else fails, consider liver transplant.
34
Describe the symptom of Biliary Colic
Biliary colic is used to describe pain associated with the temporary obstruction of the cystic or common bile duct. Despite the term 'colic' the pain is not colicky, and is of sudden onset and severe.
Some patients relate the symptoms to over-indulgence with food (particularly fatty food). The most common time of day for such an episode therefore is in the mid-evening, lasting until the early hours of the morning. The pain may start in the epigastrium, but there may be a right upper quadrant component. Radiation may occur over the right shoulder and subscapular region. Can be treated by opiate analgesia.
Nausea and vomiting may accompany more severe attacks.
35
What can Biliary Colic point to?
Temporary obstruction of gallbladder. Pain that lasts longer, especially when associated with fevers and rigors, suggests a secondary complication such as cholecystitis or cholangitis or gallstone-related pancreatitis.
36
Define Cholecystectomy
A cholecystectomy is the surgical removal of the gallbladder. Can be done openly or laparoscopically (gold standard). It is one of the most commonly performed abdominal surgical procedures.
37
Summarise the indications for a Cholecystectomy
* Cholelithiasis (gall stones), causing biliary colic or pancreatitis
* Cholecystitis
* Gall bladder cancer
38
Identify the possible complications of a Cholecystectomy
* Gallbladder perforation which results in the spillage of bile and/or stones. Stones left in the abdomen can later become a site of infection.
* Vascular injury
* Bowel injury
* Bile duct injuries can lead to the leaking of bile and cause a painful and potentially dangerous infection.
39
What is the definition and aetiology of Cholecystitis?
Cholecystitis is the inflammation of the gall bladder usually secondary to an obstruction of the cystic duct. This is usually due to gallstones (95%), but can also be due to a cholangiocarcinoma.
40
What are the clinical features of Cholecystitis?
Most patients have a history of biliary colic, (epigastric to RUQ pain, nausea and vomiting) but with the pain becoming more severe and localised to the right upper quadrant.
On examination, the patient presents with tenderness and muscle guarding or rigidity. A positive Murphy's sign can also be elicited.
41
How Cholecystitis can be investigated?
An abdominal ultrasound is the single most useful investigation when taken with a history of fever and a positive Murphy's sign.
The US can show a biliary stone, but also gallbladder wall thickening and oedema. Blood test can be done:
• FBC may show moderate leucocytosis
• Raised inflammatory markers (CRP, ESR)
• Marginally raised bilirubin, ALT and AST may also be seen.
42
How is Cholecystitis managed?
It is first critical to stabilise the patient with I.V fluids (keeping them nil by mouth). I.V antibiotics is also administered to prevent sepsis although cholecystitis (in comparison to cholangitis) is primarily an inflammatory and only secondarily an infective process. Opiates can be given to help with pain.
Once the patient is stabilised, a cholecystectomy is the treatment of choice for virtually all patients to prevent recurrence. This can be done laparoscopically.
43
What is the definition, aetiology and epidemiology of Cirrhosis?
Cirrhosis is the end-stage of chronic liver damage, where the architecture of normal liver is replaced by diffuse fibrosis and nodules of regenerating hepatocytes.Common causes include: alcoholic liver disease (most common cause in UK), hepatitis C/B (most common causes worldwide), hemochromatosis, non-alcoholic fatty liver disease. It is amongst the top 10 leading cause of death worldwide.
44
What is the pathophysiology of Cirrhosis?
The fibrosis takes place around regenerating nodules. These bands of collagen are formed by stellate cells. Normally these stellate cells are quiescent and store vitamin A, living in the perisunosidal space.When hepatocytes become injured, they release paracrine factors that activate these stellate cells. In response, the stellate cells lose their vitamin A, and secrete TGF-b which causes them to produce collagen. It is thought that in the normal state, this promotes wound healing, but when the hepatocytes are constantly injured, this leads to fibrosis.As this fibrotic tissue builds up, it starts to compress the sinusoids. This leads to some of the complications seen in end-stage liver disease caused by portal hypertension.
45
What are the clinical features of Cirrhosis?
Initially patients have non-specific symptoms such as anorexia, nausea and fatigue as well as weakness and weight loss.
Symptoms caused by portal hypertension:
- Ascites
- Splenomegaly
- Haematemesis, PR bleeding, melena
Symptoms caused by decreased liver function:
- Jaundice
- asterixis, personality change, altered sleep patterns
- gynaecomastia, spider nevi, hair loss and amenorrhoea
- easy brusing
On examination you may find:
• Asterixis, Bruises, Clubbing, Dupuytren's contracture, Erythema.
• Jaundice, gynaecomastia, testicular atrophy, stretch marks, spider nevi, caput medusae (dilated superficial abdominal veins) and Splenomegaly.
Leukonychia
46
What are the complications of Cirrhosis?
Portal hypotension:
- ascites
- splenomegaly
- varicel bleeding
Decreased hepatocyte function:
- jaundice
- coagulopathy
- encephalopathy
- increased oestrogen
47
How is Cirrhosis managed?
Treat the cause if possible. Avoid alcohol and drugs that affect liver. Ultimately, a liver transplant is the definitive treatment.Nutrition is very important, and so dietician should get involved. They should give supplements and ensure adequate nutrition (as if due to alcoholism, they obtain calories through drinks). May be placed in a salt-restricted diet.
Most treatment is symptomatic:
• Treating ascites is important as can be uncomfortable. This is done by diuretics (spironolactone and frusemide). Fluid restriction and therapeutic paracentesis (with human albumin replacement) can also be done.
• Treating encephalopathy with lactulose and phosphate enemas (to relieve constipation)
• Consider insertion of TIPS (Transjugular Intrahepatic Portosystemic Shunt) to treat portal hypertension.
48
How is Cirrhosis diagnosed? What further investigations would we do after diagnosis?
History, coupled with laboratory and examination findings is enough to understand the presence of cirrhosis. However, an abdominal ultrasound is useful in visualising the extent of cirrhosis, and a liver biopsy is the definitive investigation. Blood tests:
• ↓ Hb
• ↓ Platelets due to hypersplenism
• LFTs may be normal or increased. ↑ bilirubin and ↓ albumin
• Prolonged PT due to decreased synthesis of clotting factors
• Viral serology to look for viral cause
• Iron studies (hemochromatosis)
• Autoimmune antibodies
An ascitic tap microscopy, culture and sensitivity. If neutrophils is above 250mm, this indicates spontaneous bacterial peritonitis.
Other imaging modalities includes abdominal MRI (often used to assess complications such as hepatocellular carcinoma) and CT.
49
What is the prognosis of Cirrhosis?
5-year survival is 50% without ascites2-year survival is 50% with ascites
50
Define Colonoscopy
Colonoscopy is the endoscopic examination of the colon and distal part of the small bowel. It can provide visual diagnosis and allows for biopsy and removal of polyps.
Laxatives are given before the examination so that the doctor can see properly.
51
Summarise the indications for a Colonoscopy
* To investigate cause of GI bleeding such as from a tumour or diverticulosis
* Investigate changes in bowel habit and if malignancy is suspected.
* To diagnose inflammatory bowel disease
* Colon cancer screening
52
Identify the possible complications of colonoscopies.
1 in 200 people have a serious complication:
• Bowel preformation is the most serious, and often requires immediate surgery to fix.
• Complications involving the anaesthesia
• Dehydration due to the laxatives given before the test.
53
What is the definition, aetiology and epidemiology of Chron's Disease?
A granulomatous inflammatory bowel disease that affects all layers of the bowel from the mouth to the anus.
Fewer genes implicated than UC
Found worldwide, but incidence varies. In high incidence areas (UK, USA, northern Europe) the incidence is about 4–8 in 100,000. Low-incidence areas include Asia, Japan, and South America, with estimates of 0.05–0.8 in 100,000 per year.
54
What is the pathophysiology of Chron's Disease?
Th1 Mediated autoimmune disorder.
Involves INF-y, TNF-a, IL-17, and IL-23.
Florid T-cell expansion with defective apoptosis.
Causes uncontrolled patchy inflammation of all layers of the gastrointestinal tract.
55
What are the symptoms of Chron's Disease?
- Classical symptoms of abdominal pain and diarrhoea.
- Weight loss, anorexia and fever may be seen.
- Growth restriction in children is important.
- Anaemia is a common presentation (30%), mainly as a result of iron deficiency but sometimes as a result of vitamin B12 deficiency.
- Can also present with small bowel obstruction or helicobacter-negative peptic ulcer disease.
56
What should you always look for when examining a patient with Crohn's Disease?
On examination, look carefully for signs of obstruction, tenderness, or a mass. Always examine the perianal region.
57
What are the extraintestinal manifestations of Chron's Disease?
- Pauci-articular arthropathy usually sacroillitis
- Metabolic bone disease is common with osteopenia
- Thromboembolic disease
- Pyoderma gangrenosum and erythema nodosum
- Clubbing
58
What are the complications of Chron's Disease?
* Small bowel obstruction
* Toxic dilatation
* Abscess formation
* Fistulae
59
How can Chron's Disease be investigated?
* Laboratory tests such as FBC (anaemia), ESR, CRP. Faecal calprotectin.
* Stool sample to exclude C.difficile and Campylobacter infection
* Endoscopy is the gold standard in diagnosing CD. It also permits biopsy. This can also be a capsule endoscopy or a colonoscopy.
60
How is Chron's Disease managed?
Patients with mild symptoms should be treated symptomatically. I.e treating pain and diarrhoea during flare-ups.
The benefits of aminosalicylates in the management of Crohn's seems marginal at best.
Instead, corticosteroids (such as prednisolone) play the central role in treating mild (oral) and severe attacks (IV). However, they are not affective long-term.
Azathioprine and methotrexate are used in patients with active Crohn's disease who fail to respond to first-line therapies or who fail to taper steroids.
Biological treatments such as infliximab and adalimumab have been approved by NICE to decrease disease activity and maintenance therapy.
61
What is the definition, epidemiology and risk factors of Diverticulosis?
Diverticular disease/diverticulosis is the presence of diverticula. A diverticulum is a sac-like protrusion of the colonic wall.
The prevalence of diverticulosis is related to age. Around 50% of 60year olds have diverticula.
* Low dietary fibre and high red meat diets have been shown to predispose to diverticular disease
* Vigorous physical activity has been shown to reduce the risk of diverticular disease
62
What is the pathophysiology of Diverticulosis?
Diverticula occur at sites of weakness in the colonic wall, where the vasa recta penetrate the circular smooth muscle. Over time, pressure can cause the little cul-de-sac pouches.
63
What are the clinical features of Diverticulosis?
Diverticular disease is asymptomatic, but the common complications are not.
64
What is the definition and epidemiology of Diverticulitis?
Diverticulitis is the acute inflammation and infection of a diverticular sac. Diverticulitis occurs in 4-15% of patients with diverticulosis.
65
What is the pathophysiology of Diverticulitis?
Diverticulitis occurs due to the bacteria that sit in the pouches producing noxious chemicals, which leads to an inflammatory response.
66
What are the clinical features of Diverticulitis?
Diverticulitis classically presents with:
• Lower left quadrant pain (due to the involvement of the sigmoid colon). Patients may also have lower right quadrant pain or suprapubic pain.
• Nausea and vomiting in 20-62% of patients
• Change in bowel habit
On examination, there may be lower abdominal tenderness and an abdominal mass (in 20%). They may also have a low-grade fever.
67
What are the potential complications of Diverticulitis?
Complications of diverticulitis include:
- Abscess, which may be notes in a CT scan.
- Obstruction due to relative narrowing of the lumen due to pericolonic inflammation or from compression from abscess.
- Fistulas occur due to inflammation from acute diverticulitis.
68
How can Diverticulitis be investigated?
Diverticulitis is diagnosed by exclusion of other causes of abdominal pain, usually using a CT scan. This is because a CT can identify complications including peritonitis, fistula formation, obstruction and abscess formation.
69
How is Diverticulitis managed?
Patients with diverticulitis are advised to go on a low fibre diet until the diarrhoea clears up. They are given antibiotics, especially metronidazole as this targets anaerobes, which are present in the gut. Complications of diverticulitis are dealt with in hospital.
Patients with complicated diverticular disease (at least two episode of diverticulitis or perforation) can be considered for surgery.
70
What are the complications of Diverticulosis?
- Diverticulitis
| - Diverticular Bleeds
71
What are the clinical features of Diverticular bleeds?
A diverticular bleed presents as painless haematochezia (blood through anus that is fresh, as opposed to melena) that is self-limited, or (in 30%) massive and persistent. Blood from the left colon is bright red, while blood from the right colon (most common, even though most diverticula are from the left) are darker maroon and may be mixed with stool. Patients typically have few abdominal symptoms, reflecting the noninflammatory pathogenesis of the bleeding.
72
How are diverticular bleeds investigated?
Diverticular bleeds are diagnosed by colonoscopy after initial resuscitation, and upper GI source of bleeding has been excluded.
Diverticular bleeds are treated by fluid resuscitation, and if the bleed is active during investigative endoscopy, can be treated by endoscopic therapy. In this case, adrenaline is injected into the site to stop bleeding.
73
Define an ERCP
An Endoscopic Retrograde Cholangiopancreatography is a technique that uses endoscopy and fluroroscopy (X-rays in real time) to primarily diagnose and treat conditions of the bile ducts and main pancreatic duct.
74
Summarise the indications for an ERCP
Indicated in diagnostic and therapeutic cases.
```
Common diagnostic uses include to help in the diagnosis of:
• Obstructive jaundice
• Gallstones
• Bile duct tumours
• Sphincter of Oddi dysfunction
• Chronic pancreatitis
```
Therapeutic uses include:
• Endoscopic sphincterotomy (of the biliary or the pancreatic duct sphincter)
• Stone removal
• Insertion of bile duct stents
• Dilation of strictures (e.g in primary sclerosing cholangitis)
75
Identify the possible complications of an ERCP
The major risk of an ERCP is the development of pancreatitis, which can occur in 5% of all patients.
Smaller risks includes of intestinal perforation (especially if a sphincterotomy is performed). There is also risk of an allergic reaction to the contrast dye which contains iodine.
76
Define Endoscopy
Endoscopy is looking at an organ through an endoscope. Often the term alone is used to describe endoscopy of the upper gastrointestinal tract.
77
Summarise the indications for Endoscopy
Help in diagnosis of:
• Unexplained anaemia (looking for bleeds)
• Upper GI bleeding (haematemesis or melena)
• Persistent dyspepsia
• Heartburn and chronic acid reflux (check for Barrett's oesophagus)
• Persistent vomiting or nausea
• Dysphagia or odynophagia (indicative of GORD or oesophageal cancer)
• Inflammatory Bowel Disease
Can be used in the treatment of:
• Oesophageal varices
• Cutting off larger pieces of tissue with a snare device (for polyps)
• Cauterising tissues
• Removal of foreign bodies
• Endoscopic drainage of pancreatic pseudocyst
• Tightening the lower esophageal sphincter
• Dilating or stenting of stenosis or achalasia
• Percutaneous endoscopic gastrostomy (feeding tube placement)
• ERCP
78
Identify the possible complications of Endoscopy
The complication rate is about 1 in 1000. Common complications include:
• Aspiration causing aspiration pneumonia
• Bleeding
• Perforation
• Cardiopulmonary problems
79
What is the definition, aetiology and epidemiology of GORD?
GORD is the inflammation of the oesophagus caused by reflux of the gastric acid and/or bile. It is caused by a disruption of mechanisms that prevent reflux including:
• Physiological loss of Lower Oesophageal Sphincter tone
• Mucosal rosettes
• Acute angle of junction
• Intra-abdominal portion of oesophagus (Hiatus Hernia)
Obesity is an important risk factor.
It is common, affecting 5-10% of adults.
80
What are the clinical features of GORD?
* Patients may present with sub sternal burning or 'heartburn' aggravated by lying supine, bending or large meals and drinking alcohol. Pain is relieved by antacids.
* Odynophagia (pain when swallowing)
* Patients typically regurgitate acidic material with small amounts of undigested food
* Dysphagia is commonly attributable to reflux esophagitis but potentially indicative of a stricture which is a sign of long-standing GORD.
Examination is usually normal. Occasionally may find epigastric tenderness, wheeze on chest auscultation and dysphonia (caused when acid reaches trachea and vocal chords).
81
How can GORD be investigated?
* An endoscopy and biopsy is done to confirm the presence of eosophagitis in patients over 45 years, to exclude malignancy.
* A barium swallow can also be used to detect a hiatus hernia, peptic stricture, and any extrinsic compression.
* A 24h oesophageal pH and manometry is the gold standard
82
What are the Differential Diagnoses for GORD symptoms?
* Infective esophagitis
* Peptic-ulcer disease
* Non-ulcer dyspepsia
* Biliary tract disease
* Cardiac causes (coronary artery disease)
83
How is GORD managed?
Patient is given lifestyle advice such as to avoid high fat meals, avoid eating late in the evenings, weight loss and avoid smoking.
Antacids, H2 antagonists (Ranitidine) or a proton pump inhibitor are usually enough for most patients.
If this does not work, surgery may be needed, such as a Nissen fundoplication (fundus of the stomach is wrapped around the lower oesophagus and held with seromuscular sutures).
84
What is the definition, epidemiology and aetiology of Gastroenteritis?
Gastroenteritis is the inflammation of the lining of the GI tract, manifested by nausea, vomiting, diarrhoea and abdominal discomfort. It is common and under-reported, and a serious cause of morbidity and mortality in the developing world.
Causes include:
• Viral (most common): rotavirus, adenovirus, norovirus etc. Spread from surface to surface, and when food is prepared.
• Bacterial: Campylobacter jejuni and Listeria (from milk and cheeses), Salmonella (from eggs and poultry), Shigella, Vibrio chloreae, E. coli, etc.
• Toxins: S. aureus and Clostridium species (from improperly cooked meat), Bacillus species (from old rice), mushrooms, heavy metals and seafood can also cause gastroenteritis.
85
What are the clinical features of Gastroenteritis?
Patients present with sudden onset nausea, vomiting and anorexia. They also may present with diarrhoea (may be bloody or watery), abdominal pain or discomfort, fever and malaise.
When taking a history, enquire about recent travel, antibiotic use, and recent food intake (including how cooked and if anyone else sick).
On examination, patients show diffuse abdominal tenderness, abdominal distention, and often increased bowel sounds. If severe, patients are also dehydrated, may have pyrexia, hypotension and peripheral shutdown.
86
How can Gastroenteritis be investigated?
* Bloods: FBC, blood cultures (helps identify if bacteraemia is present), U&Es (dehydration)
* Stool MSC (microbiology, culture and sensitivity) and analysis for toxins (particularly for psuedomembranous colitis due to C. difficile).
* AXR or ultrasound to rule out other causes of abdominal pain.
* Sigmoidoscopy is only needed if IBD needs to be excluded.
87
How is Gastroenteritis managed?
Is often just bed rest, fluid and electrolyte replacement with oral rehydration solution. IV rehydration may only be necessary in those with severe vomiting.
Most infections are self-limiting. Antibiotics are only needed if severe, or causative agent has been identified.
88
What is the definition, aetiology and epidemiology of Haemorrhoids?
Haemorrhoids are inflamed vascular structures that are normally present in the anal canal. It is very common, affecting 10-25% of the adult population, and is the most common cause of rectal bleeding.
89
What are the clinical features of Haemorrhoids?
Symptoms include:
• Bright red blood in stool, or when wiping
• Pruritis ani (itchy bottom)
• Discomfort
90
How can Haemorrhoids be investigated?
Diagnosis is made by inspection, rectal examination and proctoscopy.
91
How are Haemorrhoids managed
If symptoms are mild, no treatment is necessary. Patient should be advised to eat fibre to prevent constipation.
Suppositories containing a local anaesthetic and corticosteroids are helpful. An haemorrhoidectomy can be performed if it is severe.
92
What is the definition, aetiology and epidemiology of a Hiatus Hernia?
A hiatus hernia occurs when the diaphragm is lax, allowing the fundus of the stomach to herniate into the posterior mediastinum.
93
What are the clinical features of a Hiatus Hernia?
Mild hiatus hernias do not cause symptoms, apart from occasional acid reflux. More severe hiatus hernias can cause GI bleeding or iron deficiency anaemia.
94
How is a Hiatus Hernia managed?
Hiatus hernias do not need treatment.
95
What is the definition, aetiology and epidemiology of Intestinal Ischaemia?
Intestinal ischaemia is caused by a reduction of blood flow to a level that is insufficient for the delivery of oxygen and nutrients required for cellular metabolism. This can lead to inflammation causing intestinal colitis. More common in the elderly (60-80 years)
It can be caused by arterial occlusion (due to embolus or thrombus, which has an increased risk by atherosclerosis or AF), or hypoperfusion of the mesenteric vasculature. In younger patients may be caused by small vessel vasculitis, vasospasm (e.g. cocaine) or hypercoagulable states.
It particularly affects the 'watershed' area of the splenic flexure which is between the superior and inferior mesenteric artery territories.
96
What are the clinical features of Intestinal Ischaemia?
Colonic ischaemia can present acutely or chronically, with varying symptoms based on onset, duration and extent of ischaemia.
Patients usually present with crampy abdominal pain that may be post-prandial (after eating), and may have be nausea. Patients also have fever and rectal bleeding which can be bloody diarrhoea.
On examination:
There may not be many signs. But can include: abdominal distention and tenderness. Fever and tachycardia depending on the severity of insult. Proctoscopy shows normal rectal mucosa (and thus blood from a higher source)
97
How can Intestinal Ischaemia be investigated?
```
Blood tests:
• ↑WBC
• ↑CRP
• ↑LDH
• ↑CK
• ↑Lactate
• ABG can show metabolic acidosis
```
Stool samples for cultures, looking for Salmonella, Shigella, Campylobacter, Yersinia, E. Coli, and assay for Clostridium toxins.
Abdominal x-ray can show large-bowel dilation or thickening, air in bowel wall, and thumb-printing (mucosal oedema). A CXR may show air underneath diaphragm in case of perforation. CT, angiography and colonoscopy can also be used.
98
How is Intestinal Ischaemia managed?
Start patient on I.V fluids, broad-spectrum antibiotics, nil-by-mouth.
Treat the cause of the vascular insufficiency. The majority of cases settle after this. This can involve antithrombotic therapy.
Colonic resection may be required in case of gangrenous or perforated bowel.
99
What is the definition and aetiology of IBS?
```
Irritable Bowel Syndrome is a functional bowel disorder (as opposed to an inflammatory one) defined as recurrent episodes (in the absence of detectable organic pathology) of abdominal pain/discomfort for >6 months of the previous year, associated with two of the following:
• Altered stool passage
• Abdominal bloating
• Symptoms made worse by eating
• Passage of mucous
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It's aetiology can be unknown but also due to visceral sensory abnormalities, gut motility abnormalities, psychosocial factors (particularly stress), and food intolerance (e.g lactose).
100
What is the epidemiology of IBS?
It is a fairly common condition affecting 10-20%. It is more common in females than males (2:1).
101
What are the clinical features of IBS?
```
Patients can present with:
• >6 month history of abdominal pain
• Altered bowel frequency (can be constipation or diarrhoea)
• Change in stool consistency
• Passage with urgency or staining
• Tenesmus
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It is important to screen for 'red flag' symptoms which warrant referral to exclude malignancy.
On examination, abdomen may be distended and mildly tender on palpation.
102
How can IBS be investigated?
Diagnosis is mainly from history, but it may be vital to exclude organic pathology. If they have diarrhoea, ask if it is nocturnal: people with IBS do not wake up for diarrhoea, while people with IBD do wake up in the middle of the night.
Bloods tests to look for anaemia and antibodies to exclude coeliac disease. Stool examination microscopy and culture for parasites, cysts and infection. Ultrasound to exclude gallstone disease. Hydrogen breath test to exclude dyspepsia from H. pylori. An endoscopy can be done if other pathologies are suspected.
103
How is IBS managed?
Management involves giving advice about dietary modification.
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Medical treatment should be given according to the predominant symptoms:
• Antispasmodics
• Prokinetic agents
• Antidiarrhoeals
• Laxatives
• Low-dose tricyclic antidepressants
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Psychological therapies may often be beneficial (e.g CBT, relaxation and psychotherapy.
104
What are the types of liver abscesses/cysts?
1. Pyogenic (bacterial): commonly caused by E. coli, Klebsiella, enterococcus, bacteroides, streptococci etc. 60% of theses are due to biliary tract disease (cholangitis with underlying biliary obstruction).
2. Amoebic is caused by Entamoeba histolytica
3. Hydatid cyst caused by Tapeworm Echinococcosis granulosis
4. Other, such as from tuberculosis
105
What are the epidemiology of liver abscesses/cysts?
Pyogenic abscesses are the most common in the industrialised world affecting 0.8 in 100,000 (still pretty rare). But amoebic bacteria are the most common in the world as 10% are infected. Hydatid disease is more common in sheep-rearing countries
106
What are the clinical features of Liver abscesses/cysts?
* Patients present with a history of fever, malaise, nausea, anorexia, night sweats and weight loss
* They also present with RUQ abdominal or epigastric pain, which may be referred to the shoulder.
* May also have diarrhoea
On examination, patients would be jaundiced, have a fever, and have tender hepatomegaly (right lobe tends to be affected more commonly than left). There can also be a dullness to percussion and decreased breath sounds at right base of the lung, caused by reactive pleural effusion.
107
What are the complications of liver abscesses/cysts?
Main complication arises due to abscess rupture, which is rare, but can cause septic shock.
108
How can liver abscesses/cysts be investigated?
A CT scan is the imaging modality of choice, though MRI and US can also be done to confirm diagnosis by localising cysts/abscesses. Tumours may appear similar, so can be challenging. The abscess should be aspirated, followed by the culturing of the material.
Blood tests:
• FBC will show leukocytosis; ↑ eosinophils in hydatid disease; may have mild anaemia
• LFTs will show ↑ Alkaline Phosphatase, and ↑ Bilirubin
• ↑ ESR and CRP
• Conduct blood cultures, amoebic and hydatid serology.
Stool MC&S for E. hystolytica
109
How are liver abscesses managed?
Pyogenic abscesses need aspiration or percutaneous catheter drainage. I.V Broad Spectrum antibiotics.
Amoebic abscesses metronidazole and diloxandine
110
What is the definition of Liver Failure?
Acute liver failure refers to the development of severe acute liver injury with encephalopathy and impaired synthetic function in a patient without cirrhosis or pre-existing liver disease.
When it occurs as a result of decompensation of a chronic liver disease, it is called acute-onset-chronic liver failure.
111
What is the aetiology of Liver Failure?
* Vascular: Budd-Chiari syndrome and veno-occlusive disease
* Infective: viral hepatitis (especially hepatitis, A and B, and CMV), yellow fever and leptospirosis.
* Alcohol
* Toxins: Amanita phalloides mushroom, carbon tetrachloride
* Wilson's disease
* Drugs: paracetamol overdose (most common cause of hepatic failure), halothene, isoniazid.
* Primary biliary cirrhosis
* Haemochromatosis
* Autoimmune hepatitis
* Malignancy
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What are the potential complications of Liver Failure?
* Metabolic abnormalities: commonly include acid-base (usually alkalosis) and electrolyte disorders.
* Hepatic encephalopathy: one of the defining characteristics, although precise mechanism remains unclear, though widely accepted to be due to increased production of ammonia.
* Acute renal failure is a complication in 30-50% of patients. Once renal failure develops, it is usually progressive and is associated with a poor prognosis without liver transplantation.
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What are the clinical manifestations of Liver Failure?
Patients present with:
• Jaundice (due to decreased bilirubin conjugation)
• Hepatic encephalopathy (due to decreased detoxification of gut-derived products)
• Fetor hepaticus
• Asterixis
• Bleeding from GI tract (due to coagulopathy)
• Fatigue, lethargy, anorexia
• Right upper quadrant pain
• Abdominal distention from ascites
114
How can Liver Failure be investigated?
Blood tests:
• FBC (to see whether there is infection or GI bleed), also should have low platelet count
• LFTs should be elevated
• Clotting (should have raised PT/INR)
• U&Es may show hepatorenal failure
• Paracetamol level
• Viral serologies for hepatitis viruses and CMS and EBV.
Ultrasound and CT can be used to image the liver.
Microbiological tests on blood, urine and ascitic fluid (to pick up spontaneous bacterial peritonitis)
115
How is Liver Failure managed?
1. Acute presentation needs ABC resuscitation with ITU care or specialist unit care.
2. Treat the cause if possible (e.g N-acetylcysteine for paracetamol overdose)
3. Treat/prevent the complications: invasive ventilator and cardiovascular support is often required.
○ Monitor vital signs, pH, PT, createnine, encephalopathy
○ Manage encephalopathy with lactulose and phosphate enemas
○ Treat hypoglycaemia
○ Coagulopathy treatment: vitamin K, FFP, platelet infusions
4. Treat renal failure
5. Surgery is required for liver transplant
116
What is the definition, aetiology and epidemiology of Mallory-Weiss tears?
A Mallory-Weiss tear is a laceration in the gastro-oesophageal junction caused by retching. They account for 5-10% of upper GI bleed cases.
Predisposing conditions that contribute to risk of a Mallory-Weiss tear include:
• Hiatus hernia
• Alcoholism
• Age
117
What are the clinical features of Mallory-Weiss tears?
Patients present with acute GI bleeding often with a history of vomiting before haematemesis. Bleeding is usually accompanied by epigastric pain or back pain.
The amount of bleeding is usually self-limiting, but massive haemorrhages leading to death can occur.
118
How are Mallory-Weiss tears investigated?
Endoscopy is the best way to visualise and confirm diagnosis, though not always needed.
119
How are Mallory-Weiss tears treated?
Resuscitate patient, often requiring blood transfusions.
Endoscopy can be used to stop the bleed (by injecting adrenaline or by electrocoagulation)
Surgery is rarely needed.
120
Define Nasogastric Tube Insertion
A nasogastric tube is a plastic tube that is inserted through the nose, past the throat, and into the stomach.
121
Summarise the indications for Nasogastric Tube Insertion
* Feeding
* Administering drugs and other oral agents such as activated charcoal
* Aspiration (suction) of gastrointestinal secretions and swallowed air
122
What is the definition and epidemiology of acute pancreatitis?
Acute pancreatitis is an acute inflammatory process of the pancreas. It should be suspected in patients with severe acute upper abdominal pain but requires further evidence for diagnosis. It is a relatively common (1 in 1000) acute condition.
123
What are the causes of acute pancreatitis?
* Idiopathic
* Gallstones (most common)
* Ethanol (most common)
* Trauma
* Steroids
* Mumps and Malignancy
* Autoimmune
* Scorpion/Spider bites
* Hyperlipidaemia/hypercalcaemia/hyperparathyroidism
* ERCP
* Drugs (azathioprine, thiazides, valproate)
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What is the pathophysiology of acute pancreatitis?
These insults can cause acute pancreatitis through injury to the pancreatic acinar cells or preventing the proenzymes from reaching the small intestine. This results in activation of digestive proenzymes in the acinar or duct, leading to inflammation and tissue damage, and therefore autodigestion of the pancreas.
125
What are the clinical features of acute pancreatitis?
The patient may present with severe epigastric or abdominal pain that may radiate to the back. This pain also tends to be relieved by sitting forward, and exacerbated by movement. The pain is also often associated with nausea, vomiting and anorexia.
PMH may indicate alcohol abuse or previous gallstones.
On examination, the patient would have epigastric tenderness, fever, shock, tachycardia, tachypnoea. There may also be decreased bowel sounds due to ileus.
If pancreatitis is severe and haemorrhagic, there may be Turner's sign (flank bruising) and Cullen's sign (periumbilical bruising).
126
What are the potential complications of acute pancreatitis?
* Local complications include: pancreatic necrosis, pseudocyst formation, abscess, ascites, pseudoaneurysm, or venous thrombosis.
* Systemic complications are severe and often fatal (70%): multiorgan failure, sepsis, renal failure, ARDS (Acute Respiratory Distress Syndrome), DIC, hypocalcaemia and diabetes.
* Long-term complications include chronic pancreatitis (with diabetes and malabsorption)
127
How can acute pancreatitis be investigated?
The first clue is acute onset severe pain in the epigastric region, radiating to the back, with tenderness on palpation (history and examination). To secure a diagnosis, two of the three criteria are needed:
• Pain as described above
• ↑ in serum lipase and amylase (usually x3 normal)
• Characteristic findings of acute pancreatitis on imaging; US used if gallstones suspected, AXR, and CT also used.
Other blood tests can show ↑WBC, ↑CRP, ↑Glucose, ↓Ca2+, deranged LFTs.
128
How is acute pancreatitis managed?
* Fluid and electrolyte resuscitation, with analgesia and blood sugar control. Meta-analysis shows decreased mortality with enteral feeding.
* ERCP and sphincterotomy for gallstone pancreatitis within 72h
* Early detection of signs of necrosis or sepsis. Necrosis can be removed by debridement in a specialised unit.
129
What is the definition, aetiology and epidemiology of chronic pancreatitis?
Chronic pancreatitis is a syndrome that involves chronic inflammatory changes to the pancreas, resulting in fibrosis and parenchymal atrophy. This causes impaired endocrine and exocrine function. 70% of cases are due to alcohol while 20% are idiopathic.
130
What are the clinical features of chronic pancreatitis?
Clinical Presentation
Patient may complain of recurrent severe epigastric pain that may radiate to the back, and may be alleviated by sitting forward. It may also be exacerbated by drinking alcohol or eating meals. Over many years, they may experience bloating, weight loss, and steatorrhea.
On examination, may find epigastric tenderness and signs of complications, such as weight loss and malnutrition.
131
What are the potential complications of chronic pancreatitis?
Complications:
• Local: Pancreatic pseudocysts, biliary duct stricture, duodenal obstruction, pancreatic ascites, pancreatic carcinoma.
• Systemic: Diabetes, chronic pain, steatorrhea, reduced QoL.
132
How can Chronic Pancreatitis be investigated?
Diagnosis can be difficult because laboratory results may be fairly normal.
Blood tests:
• ↑Glucose (due to improper insulin control)
• ↑/normal Lipases and Amylase enzymes. Not as raised as in acute pancreatitis. (Not used to test chronic pancreatitis)
• ↑Immunoglobulins if autoimmune picture.
A 72-hour foecal fat test can be done to confirm steatorrhea.
Imaging is a better way to confirm diagnosis using US, CT (may show calcification), MRI, ERCP.
133
How is chronic pancreatitis managed?
General treatment is mainly symptomatic and supportive. This may involve, dietary advice, chronic pain management.
Endoscopic therapy may involve a sphincterotomy, stone extraction. Surgical procedures include drainage and resection procedures.
134
What is the definition and epidemiology of peptic ulcer disease?
Peptic ulcer disease is a defect in the gastric or duodenal mucosa that extends through the muscularis mucosa into the deeper layers of the wall. It can be a gastric ulcer or duodenal ulcer.
Common. Incidence is 1-4/1000 annually.
135
What is the aetiology of Peptic Ulcer Disease?
Factors that contribute to damaging the GI barrier:
• Helicobacter pylori infection. 100% of patients with duodenal ulcers have H. Pylori, and 80-90% of people with gastric ulcers have the infection. 50-80% of the world is chronically infected by H. pylori, 10% of these go on to produce peptic ulcers of neoplasias.
• Genetic predisposition with a history of alcohol, diet and smoking leads to a loss of prostaglandin production.
136
What is the pathophysiology of Peptic Ulcer Disease?
Imbalance of protective (mucus and bicarbonate secretion) and damaging (acid and pepsinogen secretion) factors.
This leads to damage of the gastric lining.
137
What are the clinical features of Peptic Ulcer Disease?
* Asymptomatic (around 70% of peptic ulcers are asymptomatic), however may later present with complications
* Dyspepsia . Classically, a gastric ulcer causes pain at mealtimes, and a duodenal ulcer two to five hours after a meal when acid is secreted in the absence of a food buffer, and at night (between about 11 PM and 2 AM) when the circadian stimulation of acid secretion is maximal. Duodenal ulcers can also radiate to the back.
* Acid reflux
* Feeling full quickly when eating
* Nausea and vomiting
* Melena
138
How can Peptic Ulcer Disease be investigated?
An upper endoscopy can diagnose peptic ulcers. Tissue biopsies should also be taken to investigate change of malignancy.
In some cases, a barium swallow can be done.
Anyone confirmed with a peptic ulcer should be tested for H. pylori so that the infection can be treated.
139
How is Peptic Ulcer Disease managed?
Initial management involves eradication of Helicobacter pylori, withdrawal of offending/contributing factors and antisecretory therapy (PPIs or H2R antagonists).
Eradication of helicobacter pylori is done by triple therapy - consisting of amoxicillin (can be substituted for metronidazole) and clarithromycin + PPI such as lansoprazole and omeprazole. Or a quadruple therapy where a bismuth chelate is added as a cytoprotective drug.
Patients with pepetic ulcers should avoid NSAIDs and given the benefits of smoking cessation as well as advising alcohol limitation.
140
What is the definition and aetiology of Gastritis?
Gastritis is the inflammation of the gastric mucosa. However, histopathological findings do not necessarily correlate with endoscopic or clinical symptoms.
Gastritis is usually caused by infectious agents (such as Helicobacter pylori) or autoimmune and hypersensitivity reactions, although in many cases the cause of the gastritis is unknown.
141
What is the definition and epidemiology of Primary Biliary Cirrhosis?
Primary Biliary Cholangitis/Cirrhosis is a chronic inflammatory liver disease involving progressive destruction of intrahepatic bile ducts, leading to cholestasis (hence why called cholangitis) and ultimately cirrhosis. It affects 10-20 per 100,000 people, affecting middle-aged women more (9:1).
142
What is the aetiology of PBC?
Like PSC, PBC is of unknown aetiology; thought to have a genetic background, and an environmental trigger that causes bile duct epithelial injury. This leads to a T-cell mediated response against bile duct epithelial cells in the liver. This causes leakage of bile contents (such as bilirubin, cholesterol and bile salts) to the blood and liver inflammation.
143
What are the symptoms of Primary Biliary Cirrhosis?
A person may be asymptomatic, and only be diagnosed due to ↑AlkPhos and ↑Cholesterol levels. Alternatively, they may present with vague symptoms of fatigue and weight loss. They may also present with pruritus, which helps narrow down the cause. Rarely (8%), patient's complain of RUQ pain.
Patients may have symptoms of hepatic complications:
• Jaundice
• Ascites
• Variceal bleeds
Other complications include malabsorption of fat-soluble vitamins and hyperlipidaemia (due to cholesterol in blood).
History may also show symptoms, or presence of associated autoimmune diseases such as Sjorgen's syndrome, Rheumatoid arthritis, and Reynaud's phenomenon.
144
What are the examination features of PBC?
* Skin: Xanthomas, jaundice, skin pigmentation, scratch marks.
* Hepatomegaly, ascites and other signs of liver disease
* Spider nevi, palmar erythema and clubbing as a sign of chronic liver disease.
145
How can Primary Biliary Cirrhosis be investigated?
PBC should be considered in patients with elevated AlkPhos levels without extrahepatic biliary obstruction, and women with unexplained pruritus, with other features of the history.
* Blood tests: ↑AlkPhos, ↑GGT, ↑Bilirubin, ↑PTT, ↑cholesterol
* Serology: Anti-Mitochondrial antibodies (AMA), ↑IgM
* Ultrasound to exclude biliary obstruction (gallstones or strictures)
* Liver biopsies
146
How is PBC managed?
UDCA (Urodeoxycholic Acid) may improve symptoms and survival. Rest of treatment is symptomatic:
• Treat pruritus with Cholestyramine
• Treat metabolic bone disease with Calcium and Vitamin D supplements
• Vitamin replacement
• Portal hypertension, treated with B-blockers and banding of varices.
Ultimately, liver transplantation for end-stage liver disease.
147
What is the definition and epidemiology of Primary Sclerosing Cholangitis?
PSC is a condition resulting in the progressive inflammatory fibrosis and obliteration of the intrahepatic and extrahepatic bile ducts. It is of unknown aetiology, though has an immune and genetic predisposition. 70% of patients with PSC also have ulcerative colitis, though 5% of UC patients go on to develop PSC.
Like many autoimmune conditions, PSC presents around 25-40 years of age, affecting 2-7 per 100,000 people.
148
What is the pathophysiology of PSC?
It is thought that an autoimmune response leads to periductal inflammation and subsequent fibrosis. This causes obstruction of bile, but also areas of dilation in the bile duct, which allows bile to move into the blood.
149
What are the clinical features of PSC?
Patients can be asymptomatic and are only diagnosed because of consistently ↑AlkPhos in the blood (50%).
Pruritis (due to bile in blood)is a common symptom that can be extremely disabling. Patients may also have RUQ pain, weight loss and fatigue. Episodes of fevers and rigors are less common. They may also have symptoms of PSC complications.
Patients also tend to have a PMHx of Ulcerative Colitis (70%).
On examination, patient may be/have jaundiced, hepatosplenomegaly, spider nevi, palmar erythema or ascites.
150
How can PSC be investigated?
* Blood tests show ↑AlkPhos and GGT, and mildly ↑AST/ALT.
* Serology shows ↑immunoglobulin levels (IgM in adults, IgG in children); ASM and ANA present in 30%, pANCA present in 70%
* ERCP can show structuring and dilatation (bead-like). MRCP can also be helpful
* A liver biopsy can confirm the diagnosis, and allows for staging.
151
How is PSC managed?
There is no curative treatment, management is focused on symptom control.
• Pruritus to be treated using cholestyramine or phototherapy.
• Fat-soluble vitamins and dietary calcium
• Endoscopic or percutaneous transhepatic stenting to relieve biliary obstruction.
Ultimately a liver transplant is needed
152
What is the definition and epidemiology of Ulcerative Colitis?
Ulcerative colitis (UC) is a type of inflammatory bowel disease that characteristically involves the rectum and extends proximally to affect a variable length of the colon. Not uncommon, affects 1 in 1000.
153
What are the clinical features of Ulcerative Colitis?
Usually present with diarrhoea with blood in stools. Bowel movements are frequent with small volume as a result of rectal inflammation. Associated symptoms include:
• Colicky (starts and stops abruptly) abdominal pain
• Urgency
• Tenesmus
• Incontinence
Onset of symptoms are usually gradual and progressive over several weeks.
Patients may have systemic symptoms including fever, fatigue, and weight loss. Patients may also have dyspnoea and palpitations due to anaemia secondary to iron deficiency from blood loss, anaemia of chronic disease, or autoimmune haemolytic anaemia.
Severity can be assessed by the Truelove and Witts' severity index.
Abdominal examination is normal in patients with mild disease. Patients with moderate to severe disease may have abdominal tenderness, fever, hypotension, tachycardia and pallor.
154
What are the potential complications of Ulcerative Colitis?
* Perforation (usually as a consequence of Toxic Megacolon) leads to 50% mortality!
* Severe bleeding may necessitate urgent colectomy
* Toxic megacolon (or dilatation of colon above >6cm)
155
How can UC be investigated?
• Laboratory test checking for anaemia or iron deficiency. Thrombocytosis, eosinophilia, and Leukocytosis may all reflect active disease. Hypo-kalaemia, hypoalbuminemia, and abnormal liver blood tests may be associated with severe disease.
○ Faecal Calprotectin test on stools is a good indicator of IBD. Stool sample to also exclude infectious colitis.
○ Blood cultures to exclude Campylobacter, C. difficile, Salmonealla, Shigella, E.coli.
* Colonoscopy is not usually necessary for the diagnosis, but can be helpful in determining the extent of the disease. Also allows biopsy which can show inflammatory infiltration.
* An abdominal X-ray useful to exclude perforation, assessing the amount of faecal loading, excluding toxic dilatation, and giving some evidence of extent of disease.
156
How is UC managed?
5-aminosalicylates such as sulfalazine, mesalazine or olsalazine are the preferred way to induce remission in mild UC. Corticosteroids such as prednisolone, fluticasone and budesonide may be used to induce remission (treat acute colitis).
5-aminosalicylates are safer and more efficacious in maintaining remission. Combining topical (suppositories) and oral 5-ASAs is most effective.
Immunosuppressive drugs such as azathioprine/6-mercaptopurine, metho-trexate are useful in the treatment of chronically active UC. Nearly 10% of patients need to stop treatment because of side effects, which include pancreatitis, bone-marrow suppression, hepatotoxicity and a 4x increased risk of lymphoma and skin cancer.
Surgery (proctocolectomy + terminal ileostomy) is indicated (and needed in around 20% of patients) for perforation, massive haemorrhage, toxic dilatation and failed medical therapy.
Antibodies such as infliximab may be used to treat UC though not currently approved for UC by NICE
157
Which microorganisms cause gastroenteritis with diarrhoea (not blood), and what are their risk factors?
- Campylobacter (from uncooked poultry)
- C. difficile (ESCAPE organism associated with hospitalisation and antibiotic use)
- Staphylococcus aureus (2-6h after eating, lasts less than 12h)
- Vibrio cholarae (causes rice water diarrhoea, common in developing countries with poor sanitation, leads to hypovolaemic shock)
- E. Coli (leafy vegetables)
- Salmonella (from eggs)
- Bacillus cereus (from reheated rice causes cerebral abscess)
158
Which microorganisms cause gastroenteritis with dysentery (diarrhoea with blood), and what are their risk factors?
Campylobacter (from uncooked poultry)
C. difficile (ESCAPE organism associated with hospitalisation and antibiotic use)
Haemorrhagic E. Coli (leafy vegetables) if also causes haemolytic uraemia then it is EHIC.
Entamoeba histolica (poor sanitation, tropical places, MSM)
Shigella (person-person contact, travel to areas with poor sanitation and MSM)
Salmonella (from eggs)
159
What is the definition and epidemiology of Small Bowel Obstruction?
SBO is the mechanical disruption in the patency of the GI tract, resulting in a combination of emesis (that may be billous), obstipation, and abdominal pain. It is not uncommon in patients who have undergone previous surgery.
160
What is the aetiology of Small Bowel Obstruction?
```
In adults:
• Previous abdominal surgery (that causes adhesions)
• Irreducible inguinal hernia
• Crohn's Disease
• Intestinal malignancy
• Appendicitis
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In children:
• Appendicitis
• Intussusception (when part of the intestine folds into itself)
• Intestinal atresia
• Volvulus
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Rare causes include radiation enteritis, intra-abdominal abscess (from perforated appendicitis/ diverticulitis), gallstone ileus, foreign body, and intestinal bezoar.
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What are the clinical features of Small Bowel Obstruction?
Patients present with severe gripping colicky pain located in the central abdomen. This often precedes frequent vomiting which may contain bile (appears greenish). The patient also has obstipation (complete or severe constipation) not even passing flatus or just constipation.
On Examination:
• There is abdominal distention with an increased pitch of bowel sounds (tinkling in character).
• Abdominal tenderness is indicative of intestinal ischemia.
• You may feel a palpable mass which indicates malignant cause of the SBO or intussusception,
• Guarding and rebound tenderness is suggestive of peritonitis
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How can SBO be investigated?
Abdominal X-Ray (erect and supine) assists in diagnosis. SBO causes central dilated loops with valvulae conniventes (mucosal folds seen).
FBC, U&Es to identify signs of volume depletion.
Barium follow-through can also identify the stricture.
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What is the definition and epidemiology of Large Bowel obstruction?
LBO is a surgical emergency where a mechanical interruption occurs to the flow of intestinal contents, with multiple potential causes. The most common cause is malignant colorectal disease but less than one third of colorectal cancer patients actually present with LBO.
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What is the aetiology of LBO?
Aetiology
- 90% of cases are caused by underlying colorectal malignancy
- 5% are caused by colonic volvulus
- 3% are caused by benign stricture
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What are the clinical features of Large Bowel Obstruction?
Patients present with severe gripping colicky pain located in the lower abdomen. The patient also complains of a change in bowel habbits:
• Complete obstruction would lead to failure to pass faeces
• Partial obstruction would allow some flatus or faeces
There is commonly rectal bleeding indicative of an underlying malignancy. Patient may also report recent weight loss due to malignancy.
Unlike SBO, nausea and vomiting is a late sign.
On Examination:
• There is abdominal distention with an increased pitch of bowel sounds (tinkling in character).
• You more commonly feel a palpable abdominal or rectal mass which indicates malignancy.
• DRE may reveal faecal impaction (hard faeces) or empty rectum (implies proximal obstruction).
• Guarding and rebound tenderness is suggestive of peritonitis
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How can LBO be investigated?
Abdominal X-Ray (erect and supine) assists in diagnosis. LBO causes gaseous distention of the large bowel proximal to obstruction. May be a kidney-bean shape in volvulus.
FBC shows anaemia and elevated WBC count. U&Es may show problems with renal function.
Serum amylase/lipase and coagulation studies may indicate perforation.
A water soluble contrast enema can show the location of the obstruction.
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How is Intestinal Obstruction managed?
General:
Gastric aspiration by NG tube if the patient is vomiting. Resuscitation with I.V fluids and electrolyte replacement.
Ensure close monitoring of vital signs and fluid balance, urine output and clinical status.
Conservative measures may settle an obstruction, however if not resolving or there are signs of complications, operative intervention should be carried out. Surgery is usually indicated.
Surgical:
Emergency laparotomy in acute obstruction. Usually resect perforated bowel and treat underlying cause. May require Hartmann's operation or hemicolectomy with refunctioning stoma in LBO.
Post-op care in a HDU ot ITU setting may be required.
