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!Final Year > Gastrointestinal (1) > Flashcards

Gastrointestinal (1) Flashcards

1
Q

What is achalasia?

A

Failure of oesophageal peristalsis and of relaxation of the lower oesophageal sphincter (LOS) due to degenerative loss of ganglia from Auerbach’s plexus

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2
Q

What is the epidemiology of achalasia?

A

Typically presents in middle-age and is equally common in men and women

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3
Q

What is the aetiology of achalasia?

A

1.Degenerative loss of ganglia from Auerbach’s (myenteric) plexus in the oesophagus
2. This leads to failure of the LOS to relax

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4
Q

What are the clinical features of achalasia?

A
  1. Dysphagia of BOTH liquids and solids
  2. Typically variation in severity of symptoms
  3. Heartburn
  4. Regurgitation of food
  5. May lead to cough, aspiration pneumonia
  6. Malignant change in small number of patients
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5
Q

What are the investigations for achalasia?

A
  1. Oesophageal manometry
  2. Barium swallow
  3. Chest x-ray
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6
Q

What is the most important diagnostic test for achalasia?

A

Oesophageal manometry
Shows excessive LOS tone which doesn’t relax on swallowing

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7
Q

What are the findings of achalasia on barium swallow and chest x-ray?

A

Barium swallow:
1. shows grossly expanded oesophagus, fluid level
2. ‘bird’s beak’ appearance
Chest x-ray
1. wide mediastinum
2. fluid level

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8
Q

What are the management options for achalasia?

A
  1. Pneumatic (balloon) dilation
  2. Surgical intervention with a Heller cardiomyotomy - considered if recurrent or persistent symptoms
  3. Itra-sphincteric injection of botulinum toxin - for high surgical risk patients
  4. Dug therapy (e.g. nitrates, calcium channel blockers) has a role but is limited by side-effects
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9
Q

What is the preferred management for achalasia?

A

Pneumatic (balloon) dilation
Less invasive and quicker recovery time than surgery
Patients should be a low surgical risk as surgery may be required if complications occur

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10
Q

What are some of the complications of achalasia?

A

Aspiration pneumonia
Malnutrition
Weight loss

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11
Q

What is acute cholangitis?

A

A bacterial infection of the biliary tree
The most common predisposing factor is gallstones

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12
Q

What is the most common bacterial infection in acute cholangitis?

A

E.coli, most commonly predisposed by gallstones

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13
Q

What is the main difference between acute cholangitis and acute cholecystitis?

A

Cholangitis = inflammation (and infection) of the biliary tree
Cholecystitis = the gallbladder

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14
Q

What is the triad in acute cholangitis and what is it known as?

A

Charcot’s triad:
1. Right upper quadrant pain
2. Fever/ riggers
3. Jaundice
Occurs in 20-50% of patients

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15
Q

What are the features of acute cholangitis?

A

Charcot’s triad: fever, jaundice and RUQ pain
Hypotension
Confusion
Together these five are known as Reynolds’ pentad

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16
Q

What are the appropriate investigations for acute cholangitis?

A

Ultrasound is first choice:
1. Bile duct dilatation
2. Bile duct stones (from gallstones)
Also see raised inflammatory markers

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17
Q

What is the management for acute cholangitis?

A
  1. IV antibiotics
  2. Endoscopic retrograde cholangiopancreatography (ERCP) after 24-48 hours to relieve any obstruction
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18
Q

What are the complications of acute cholangitis?

A

Acute pancreatitis (from ERCP?)
Inadequate biliary drainage from intervention
Hepatic abscess

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19
Q

What is the difference between laparotomy and laparoscopy?

A

Laparoscopy: ‘keyhole’/ minimally invasive
Laparotomy: open

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20
Q

What is alcohol withdrawal?

A

A patient who is alcohol dependent and has stopped or reduced their alcohol intake within hours or days of presentation

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21
Q

What is the mechanism of alcohol withdrawal?

A
  1. Chronic alcohol consumption enhances GABA mediated inhibition in the CNS (similar to benzodiazepines) and inhibits NMDA-type glutamate receptors
  2. Alcohol withdrawal is thought to be lead to the opposite (decreased inhibitory GABA and increased NMDA glutamate transmission)
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22
Q

What is alcohol dependence?

A

Characterized by three or more of:
. Withdrawal on cessation of alcohol
. Tolerance
. Compulsion to drink, difficulty controlling termination or the levels of use
. Persistent desire to cut down or control use
. Time is spent obtaining, using, or recovering from alcohol
. Neglect of other interests (social, occupational, or recreational)
. Continued use despite physical and psychological problems

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23
Q

What are the features of alcohol withdrawal?

A

Symptoms start at 6-12 hours: tremor, sweating, tachycardia, anxiety
Peak incidence of seizures at 36 hours
Peak incidence of delirium tremens is at 48-72 hours: coarse tremor, confusion, delusions, auditory and visual hallucinations, fever, tachycardia

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24
Q

What are the presenting symptoms of alcohol withdrawal?

A

HAD A PINT
Headache
Anxiety/ agitation
Depression
Anorexia
Palpitations
Insomnia
Nausea
Tremor

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25
Q

What are the signs of chronic alcohol misuse?

A

Dupuytren’s contracture
Palmar erythema
Bruising
Spider naevi
Telangiectasia- widened venules cause threadlike red lines or patterns on the skin
Bilateral parotid enlargement
Gynaecomastia
Smell of alcohol

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26
Q

What are the appropriate investigations for alcohol withdrawal?

A

A to E approach
VBG: respiratory alkalosis with delirium tremens
Bloods: Increased MCV, thrombocytopenia, hypomagnesaemia, hypokalaemia, hypophosphataemia, elevated AST, ALT, and GGT
Coagulation studies: prolonged INR and prothrombin time
Drug screen: barbiturates, paracetamol

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27
Q

What is the management plan for a patient with alcohol withdrawal?

A

First-line: long-acting benzodiazepines e.g. chlordiazepoxide or diazepam (lorazepam may be preferable in patients with hepatic failure) with a reducing dose protocol
B1 thiamine, pabrinex
Carbamazepine also effective in treatment of alcohol withdrawal
Patients with a history of complex withdrawals from alcohol (i.e. delirium tremens, seizures, blackouts) should be admitted to hospital for monitoring until withdrawals stabilised

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28
Q

What are the possible complications of alcohol withdrawal?

A

Seizures (generalised tonic-clonic) - cause of fatality
Delirium tremens

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29
Q

What are the complications of chronic alcohol use?

A

Cerebral atrophy and dementia
Cerebellar degeneration
Optic atrophy
Peripheral neuropathy
Myopathy
Indirect effects include hepatic encephalopathy, thiamine deficiency, causing Wernicke’s encephalopathy or Korsakoff’s psychosis

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30
Q

What is the prognosis for patients with alcohol withdrawal?

A

Depends on complications.
Alcoholic fatty liver is reversible on abstinence from alcohol
In general, 5-year survival rates in those with alcoholic cirrhosis who stop drinking are 60–75%, but < 40% in those who continue

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31
Q

What is Wernicke’s encephalopathy?

A

A neuropsychiatric disorder caused by thiamine deficiency which is most commonly seen in alcoholics

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32
Q

What is the triad seen in Wernicke’s encephalopathy?

A
  1. Oculomotor dysfunction: nystagmus (the most common ocular sign) or ophthalmoplegia: lateral rectus palsy, conjugate gaze palsy
  2. Gait ataxia
  3. Encephalopathy: confusion, disorientation, indifference, and inattentiveness
    (May also see peripheral sensory neuropathy)
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33
Q

What are the appropriate investigations for Wernicke’s encephalopathy?

A
  1. Bloods: decreased red cell transketolase
  2. MRI
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34
Q

What is the treatment for Wernicke’s encephalopathy?

A

Urgent replacement of thiamine

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35
Q

What are the complications of not treating Wernicke’s encephalopathy with thiamine?

A

Development of Korsakoff’s syndrome:
Triad of ataxia, oculomotor dysfunction and encephalopathy plus antero- and retrograde amnesia and confabulation (creation of false memories)

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36
Q

What is the aetiology of Wernicke- Korsakoff syndrome?

A
  1. Untreated thiamine deficiency
  2. This causes damage and haemorrhage to the mammillary bodies of the hypothalamus and the medial thalamus
  3. Therefore inability to acquire new memories (anterograde) and retrograde amnesia plus confabulation
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37
Q

What is alcoholic liver disease?

A

A spectrum of conditions:
1. Alcoholic fatty liver disease
2. Alcoholic hepatitis
3. Cirrhosis

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38
Q

What is Alcoholic hepatitis?

A

Inflammatory liver injury and necrosis caused by chronic heavy intake of alcohol

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39
Q

What is the aetiology of alcoholic hepatitis?

A

The middle stage between fatty liver disease and liver cirrhosis
Inflammatory liver injury with:
1. Centrilobal ballooning degeneration
2. Necrosis of hepatocytes
3. Steatosis: abnormal retention of lipids
4. Neutrophilic inflammation
5. Cholestasis: impaired secretion of bile

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40
Q

What is the epidemiology of alcoholic hepatitis?

A

10-35% of heavy drinkers develop this stage of liver disease

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41
Q

What are some of the features of alcoholic hepatitis?

A

Signs of alcohol liver disease: palmar erythema, telangiectasia, parotid enlargement, spider navei, gynaecomastia, bruising
More severe signs: hepatomegaly, encephalopathy, ascites

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42
Q

What are the most important investigations in alcoholic hepatitis?

A

LFTs:
1. gamma-GT (GGT) is characteristically elevated
2. Ratio of AST:ALT of > 3 is strongly suggestive of acute alcoholic hepatitis (>2 is normal)

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43
Q

What are some other investigations for alcoholic hepatitis?

A

FBC: macrocytic anaemia
Impaired renal and liver function tests including raised bilirubin and abnormal clotting: Prolonged PT
Ultrasounds to exclude other causes of liver impairment e.g. malignancy

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44
Q

What is the general management for alcoholic hepatitis?

A
  1. A to E approach
  2. Thiamine and other vitamins
  3. Treat encephalopathy with oral lactulose and phosphate enemas
  4. Treat ascites with diuretics (spironolactone ± furosemide)
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45
Q

What is the specific management of alcoholic hepatitis?

A
  1. Glucocorticoids e.g. prednisolone used during acute episodes
  2. Pentoxyphylline is sometimes used
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46
Q

What are the complications of alcoholic hepatitis?

A
  1. Acute liver decompensation
  2. Hepatorenal syndrome: renal failure secondary to advanced liver disease
  3. Cirrhosis
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47
Q

What are the two types of hepatorenal syndrome?

A
  1. Rapidly progressive, doubling of serum creatinine to > 221, ver poor prognosis
  2. Slow progression, patients may live for longer
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48
Q

What is the management for hepatorenal syndrome?

A

Ideal treatment = liver transplantation
1. Vasopressin analogues by causing vasoconstriction of the splanchnic circulation
2. 20% albumin
3. Transjugular intrahepatic portosystemic shunt

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49
Q

What are the two prognostic scores used in alcoholic hepatitis?

A
  1. Maddrey’s discriminant function (DF):
    - used during acute episodes
    - determines who would benefit from steroid therapy
    - calculated using prothrombin time and bilirubin concentration
  2. Glasgow alcoholic hepatitis score:
    - looks at age, white cell count, urea, PT ratio and bilirubin
    - >9 indicates >50% 30-day mortality
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50
Q

What is the prognosis for patients with alcoholic hepatitis?

A

Mortality in the first month = 10%
Mortality in the first year = 40%
If alcohol intake continues → most progress to cirrhosis within 1-3 years

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51
Q

What is amyloidosis?

A

A (heterogenous) group of diseases characterised by extracellular deposition of insoluble amyloid fibrils

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52
Q

What are the two types of amyloidosis?

A
  1. AL amyloid = primary, immunoglobulin light chain amyloidosis, associated with Myeloma
  2. AA amyloid = secondary, non-familial and familial
    2a. Non- familial AA = Inflammatory polyarthropathies account for 60% of cases, then chronic infections, IBD
    2b. Familial AA = familial periodic Mediterranean fever syndrome
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53
Q

What are the risk factors for amyloidosis?

A

PMH of inflammatory conditions (AA)
Chronic infections (AA)
Positive FH

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54
Q

What are the features of primary amyloidosis (AL)?

A

Dependent on organ involvement:
1. Kidneys: glomerular lesions—proteinuria and nephrotic syndrome
2. Heart: restrictive cardiomyopathy (looks ‘sparkling’ on echo), arrhythmias, angina
3. Nerves: peripheral and autonomic neuropathy; carpal tunnel syndrome
4. GI: macroglossia (big tongue), malabsorption/weight, perforation, haemorrhage, obstruction, and hepatomegaly
5. Vascular: purpura, especially periorbital—a characteristic feature

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55
Q

What are the features of secondary non-familial amyloidosis (AA)?

A

PMH of chronic inflammation (e.g. RA/ IBD) or chronic infection (e.g. TB)
Affects the kidneys, liver, and spleen, and may present with proteinuria, nephrotic syndrome, or hepatosplenomegaly
Macroglossia is not seen; cardiac involvement is rare

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56
Q

What are the appropriate investigations for amyloidosis?

A

Diagnosis made with biopsy of affected tissue: positive Congo Red staining with apple-green birefringence under polarized light microscopy
The rectum or subcutaneous fat are relatively non-invasive sites for biopsy and are positive in 80%
Can also use serum amyloid precursor (SAP) scan

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57
Q

What is the management of amyloidosis?

A

AL: optimize nutrition; PO melphalan + prednisolone extends survival
High-dose IV melphalan with autologous stem cell transplantation may be better
AA: manage the underlying condition optimally

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58
Q

What is the prognosis of patients with amyloidosis?

A

Median survival is 1–2 years
Patients with myeloma and amyloidosis have a shorter survival than those with myeloma alone

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59
Q

What is an anal fissure?

A

Longitudinal or elliptical tears of the squamous lining of the distal anal canal

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60
Q

What are the characteristic features of anal fissures?

A
  1. Pain on defecation
  2. Rectal bleeding
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61
Q

How can anal fissures be categorised?

A

Acute: present for less than 6 weeks
Chronic: present for more than 6 weeks

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62
Q

What are the risk factors for anal fissures?

A
  1. Constipation
  2. Inflammatory bowel disease
  3. STIs, e.g. HIV, syphilis, herpes
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63
Q

What are the features of anal fissures?

A
  1. Painful, bright red rectal bleeding
  2. Around 90% of anal fissures occur on the posterior midline (if alternative location consider Crohn’s disease)
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64
Q

How are anal fissures investigated?

A

Usually clinical diagnosis
If resistant fissures: anal manometry = low resting pressure
If suspected anal sphincter deficits = anal ultrasound

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65
Q

How is the management for anal fissures divided?

A

Split into acute anal fissure and chronic

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66
Q

What is the management of an acute anal fissure (<1 week)?

A
  1. Soften stool: high fibre diet with bulk-forming laxatives (lactulose is 2nd line)
  2. Lubricants e.g. petroleum jelly
  3. Topical anaesthetics
  4. Analgesia
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67
Q

What is the management of a chronic anal fissure?

A
  1. High fibre diet + bulk forming laxatives
  2. Lubricants
  3. Topical anaesthetics
  4. Analgesia
    PLUS:
  5. First line = Topical glyceryl trinitrate (GTN)
    If not effective after 8 weeks = secondary care referral should be considered for surgery (sphincterotomy) or botulinum toxin
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68
Q

What are the complications of anal fissures?

A

Most acute anal fissures heal spontaneously
A proportion if untreated can become chronic
Recurrence is more likely is a patient stops treatment too early
Risk of incontinence after surgical management?

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69
Q

What is the prognosis of anal fissures?

A

Around 60% of patients will heal after 6-8 weeks

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70
Q

What is an Appendicectomy?

A

The removal of the appendix either laparoscopically (mainly) or open surgery with general anaesthesia

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71
Q

What are the indications for an Appendicectomy?

A
  1. Appendicitis: indicated in all cases of suspected nonperforated appendicitis
  2. Carcinoid tumors are the most common malignancy of the appendix; most of these are small (<1 cm)
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72
Q

What are the possible complications of an Appendicectomy?

A
  1. Wound infection- prophylactic antibiotics may be given
  2. Haematoma
  3. Scarring
  4. Abscess
  5. Hernia – at the site of incision
  6. Bowel obstruction
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73
Q

What advancement in surgery has shown to decrease the risk of complications in an appendicectomy?

A

Laparoscopic appendicectomy

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74
Q

What is appendicitis?

A

An acute inflammation of the vermiform appendix, most likely due to obstruction of the lumen of the appendix

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75
Q

What is the pathophysiology of appendicitis?

A
  1. Lymphoid hyperplasia or a faecolith
  2. Obstruction of appendiceal lumen
  3. Gut organisms invading the appendix wall
  4. Resulting in oedema, ischaemia +/- perforation
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76
Q

What is the epidemiology of appendicitis?

A

Can occur at any age but is most common in young people aged 10-20 years

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77
Q

What are the main features of appendicitis?

A
  1. Abdominal pain:
    - Peri-umbilical pain radiating to the RIF due to localised parietal peritoneal inflammation
    - Often worse on coughing or going over speed bumps
  2. Vomiting (only once or twice)
  3. Mild pyrexia (higher temperatures are more typical of mesenteric adenitis)
  4. Anorexia
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78
Q

What are the signs of appendicitis on examination?

A
  1. If perforated or localised peritonism:
    1a. Generalised peritonitis
    1b. Rebound and percussion tenderness
    1c. Guarding and rigidity
  2. If retrocaecal appendicitis: psoas sign = pain on extending hip
  3. Rovsing’s sign = palpation in the LIF causes pain in the RIF
  4. DRE: may reveal boggy sensation if pelvic abscess is present, or even right-sided tenderness with a pelvic appendix
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79
Q

What are the investigations for appendicitis?

A
  1. Bloods:
    - Raised inflammatory markers coupled with compatible history and examination findings
    - Neutrophil- predominant leucocytosis
  2. Urine analysis: exclude pregnancy, renal colic and UTI
  3. Imaging:
    - Ultrasound is useful in females to exclude pelvic pathology
    - Not always needed depending on patient’s age, body habitus and the likelihood of appendicitis
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80
Q

What is the management for appendicitis?

A
  1. Appendicectomy: laparoscopic is now treatment of choice
  2. Prophylactic IV antibiotics
  3. If peroration = require copious abdominal lavage
  4. Be wary in older patients who may have either an underlying caecal malignancy or perforated sigmoid diverticular disease
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81
Q

How does the management for appendicitis differ without peritonitis?

A

Patients may receive broad-spectrum antibiotics and consideration for an interval appendicectomy around 6 weeks later

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82
Q

What are the complications of appendicitis?

A
  1. Perforation → generalised peritonitis
  2. Appendicular mass (usually due to delay in medical treatment)
  3. Appendicular abscess: usually occurs as a progression of the disease process, particularly after perforation
  4. Surgical wound infection
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83
Q

What is autoimmune hepatitis?

A

A chronic inflammatory disease of the liver of unknown aetiology, which is most commonly seen in young females

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84
Q

What are some associations of autoimmune hepatitis?

A
  1. Other autoimmune disorders
  2. Hypergammaglobulinaemia
  3. HLA B8, DR3
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85
Q

What is the aetiology of autoimmune hepatitis?

A
  1. Unknown
  2. Genetically predisposed person exposed to an environmental agent e.g. virus/ drug → hepatocyte expression of HLA agents
  3. T-cell mediated autoimmune attack
  4. Chronic inflammatory changes are similar to those seen in chronic viral hepatitis:
    - lymphoid infiltration of the portal tracts and hepatocyte necrosis, leading to fibrosis and, eventually, cirrhosis
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86
Q

What are the three types of autoimmune hepatitis?

A

Type 1: Anti-nucelar and/or anti-smooth muscle antibodies (ANA and/or SMA), affects both adults and children
Type 2: Anti-liver/kidney microsomal type 1 antibodies (LKM1), affects children only
Type 3: Soluble liver-kidney antigen, affects adults in middle-age

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87
Q

What are the features of autoimmune hepatitis?

A
  1. may present with signs of chronic liver disease
  2. Acute hepatitis: fever, jaundice etc (only 25% present in this way)
  3. Amenorrhoea (common)
  4. On investigation = ANA/SMA/LKM1 antibodies, raised IgG levels
  5. On liver biopsy: inflammation extending beyond limiting plate ‘piecemeal necrosis’, bridging necrosis
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88
Q

What are some of the common symptoms of autoimmune hepatitis?

A

Fatigue/ malaise
Anorexia
Pruritus
Arthralgia
Nausea
Fever
Amenorrhoea

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89
Q

What signs might you seen on examination in autoimmune hepatitis?

A

Hepatomegaly
Signs of chronic liver disease
Jaundice and fever
Spider angioma: dilation of vessels below the skin

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90
Q

What is the management of autoimmune hepatitis?

A
  1. Steroids
  2. Immunosuppressants such as azathioprine
  3. Liver transplantation
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91
Q

What are the causes of raised GGT levels?

A
  1. Alcohol abuse
  2. Intra or extra hepatic cholestasis and biliary obstruction
  3. Hepatocellular disease e.g. malignancy
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92
Q

What are the causes of raised Alk Phosphate?

A

Intra or extra hepatic cholestasis
Bone diseases e.g. fracture, paget’s
Placenta e.g. last trimester of pregnancy

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93
Q

What are the causes of low albumin?

A
  1. Most forms of chronic liver disease, especially cirrhosis
  2. Nephrotic syndrome
  3. Malnutrition/ malabsorption
  4. Chronic infection
  5. Loss from bloodstream: haemorrhage, burns
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94
Q

What is bariatric surgery?

A

A management option for obesity in patients who fail to lose wight with lifestyle and drug interventions

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95
Q

What are the NICE recommendations for bariatric surgery?

A

Very obese patients (e.g. BMI 40-50 kg/m^2 etc) should be referred early for bariatric surgery
This is particularly if they have other conditions that may be caused by it (e.g. type 2 DM, HTN), rather than it being a ‘last resort’

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96
Q

What are the different types of bariatric surgery?

A

Divided into:
1. Primarily restrictive operations
2. Primarily malabsorptive operations
3. Mixed operations

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97
Q

What are the primarily restrictive operations in bariatric surgery?

A
  1. Laparoscopic-adjustable gastric banding (LAGB)
    - normally the first-line intervention in patients with a BMI of 30-39kg/m^2
    - produces less weight loss than malabsorptive or mixed procedures but has fewer complications
  2. Sleeve gastrectomy= stomach is reduced to about 15% of its original size
  3. Intragastric balloon = balloon can be left in the stomach for a maximum of 6 months
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98
Q

What are the primarily malabsorptive operations in bariatric surgery?

A

Biliopancreatic diversion with duodenal switch
Usually reserved for very obese patients (e.g. BMI > 60 kg/m^2)

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99
Q

What are the mixed operations in bariatric surgery?

A

Roux-en-Y gastric bypass surgery = both restrictive and malabsorptive in action

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100
Q

What are the complications of bariatric surgery?

A

Acid reflux
Chronic nausea and vomiting
Dilation of oesophagus
Infection
Obstruction of stomach
Weight gain/ failure to lose weight

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101
Q

What is barrels oesophagus?

A

Metaplasia of the lower oesophageal mucosa, with the usual squamous epithelium being replaced by columnar epithelium

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102
Q

What is the aetiology of Barrett’s oesophagus?

A

The single strongest risk factor is gastro-oesophageal reflux disease (GORD)

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103
Q

What are the risk factors for barret’s oesophagus?

A

1st = GORD
Male gender (7:1)
Smoking
Central obesity

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104
Q

What is the role of alcohol in Barret’s oesophagus?

A

Alcohol is not an independent risk factor for barrels oesophagus but is associated with GORD and oesophageal cancer

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105
Q

What are the features of Barret’s oesophagus?

A

Symptoms of GORD: heartburn, nocturnal cough
Nausea
Chest pain
Dysphagia: difficulty swallowing

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106
Q

What is the investigation of choice for Barret’s oesophagus?

A

OGD and biopsy
Abnormal epithelium proximal to the gastro-oesophageal junction
Send for histology

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107
Q

What are the histological features of Barret’s oesophagus?

A

Columnar epithelium may resemble that of either the cardiac region of the stomach or that of the small intestine (e.g. with goblet cells, brush border)

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108
Q

What is the management for Barret’s oesophagus?

A
  1. High dose proton pump inhibitor
  2. Endoscopic surveillance with biopsies for patient with metaplasia every 3-5 years
  3. If dysplasia of any grade = identified endoscopic intervention
    - 1st line: Radiofrequency ablation for low-grade
    - Endoscopic mucosal resection
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109
Q

What is the difference between metaplasia and dysplasia?

A

Metaplasia: transforms a cell from one form to another- can be reversible
Dysplasia: transforms a cell into an abnormal version of itself- is not reversible

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110
Q

What is barret’s oesophagus?

A

Replacement of squamous epithelium by metaplastic columnar epithelium, usually from chronic GORD

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111
Q

What are the complications of Barret’s oesophagus?

A
  1. Oesophageal stricture (abnormal narrowing)
  2. Dysplasia and adenocarcinoma
    (and effect of quality of life)
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112
Q

What is the role of proton pump inhibitors in Barret’s oesophagus?

A

Commonly used to treat symptoms of GORD but does not lead to regression of barret’s oesophagus

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113
Q

What is the prognosis of Barret’s oesophagus?

A

Patients are at a greater risk of developing adenocarcinoma
Anti-reflux (and surgery) lower the risk of progression to cancer

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114
Q

What are cholangiocardinomas?

A

Cancer of the bile ducts

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115
Q

How can cholangiocarcinomas be divided?

A

On their location in the biliary tree:
1. Intrahepatic
2. Extrahepatic (perihilar or distal)

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116
Q

What is the main risk factor for cholangiocarcinoma?

A

Primary sclerosing cholangitis

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117
Q

What are some of the other risk factors for cholangiocarcinomas?

A

Main is primary sclerosis cholangitis
Worm infections
Liver cirrhosis

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118
Q

What is Primary sclerosing cholangitis?

A

Biliary disease of unknown aetiology characterised by inflammation and fibrosis of intra and extra-hepatic bile ducts
Closely associated with Ulcerative Colitis

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119
Q

What are the risk factors for Cholangiocarcinoma other than PSC?

A

Age > 50 years
Cholangitis
Choledocholithiasis (gall stones)
Structural disorders of the biliary tract e.g. bile duct adenoma
Ulcerative colitis
Non-specific cirrhosis
Alcoholic liver disease
HIV
Hepatitis B and C

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120
Q

What are the features of cholangiocarcinoma?

A
  1. Persistent biliary colic symptoms
  2. Associated with anorexia, jaundice and weight loss
  3. A palpable mass in the right upper quadrant (Courvoisier sign)
  4. Periumbilical lymphadenopathy (Sister Mary Joseph nodes) and left supraclavicular adenopathy (Virchow node) may be seen
  5. Obstructive jaundice = dark urine and pale stools
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121
Q

What is the triad seen in Acute Cholangitis?

A

Charcot’s triad:
Fever, jaundice and right upper quadrant pain

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122
Q

What are the appropriate investigations for cholangiocarcinomas?

A
  1. Raised CA 19-9 levels (often used for detecting cholangiocarcinoma in patients with PSC)
  2. Bloods e.g. bilirubin, LFTs
  3. Abdominal USS: intrahepatic cholangiocarcinoma may be seen as a mass lesion
  4. ERCP: filling defect or area of narrowing will be seen if a tumour is present
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123
Q

What is the management plan for cholangiocarcinoma?

A
  1. Surgical resection offers the only potential cure for early-stage disease
  2. Chemotherapy may have a positive effect on overall survival of patients following resection of intrahepatic cholangiocarcinoma
  3. Liver transplant is indicated in a small subset of patients
124
Q

What is a cholecystectomy?

A

The surgical removal of the gallbladder

125
Q

What are the indications of a cholecystectomy?

A
  1. Symptomatic gallstones (cholethiasis)
  2. Acute cholecystitis
  3. Cholangiocarcinoma
  4. Gallbladder trauma
126
Q

What are the main types of cholecystectomy?

A

Main way: laparoscopic cholecystectomy
In frail patients, can consider use of ultrasound guided cholecystectomy

127
Q

What other procedures can be used during a cholecystectomy?

A
  1. Some surgeons may routinely do intraoperative cholangiography or laparoscopic ultrasound to exclude common bile duct stones
  2. If CBD stones are found, an ERCP can be offered or immediate surgical exploration of the bile duct via trans cystic route or choledochotomy
128
Q

What are the complications of cholecystectomy?

A
  1. Bleeding and infection
  2. Bile leak- post cholecystectomy syndrome: abdominal pain, indigestion, diarrhoea, jaundice, fever
  3. Injury to nearby structures bile duct, liver, small intestine
  4. Greater risk of DVT
129
Q

What is cholecystitis?

A

Inflammation of the gallbladder

130
Q

What is the aetiology of cholecystitis?

A
  1. Secondary to gallstones (90%)
  2. 10% typically seen in hospitalised and severely ill patients:
    - multifactorial pathophysiology: gallbladder stasis, hypoperfusion, infection
    - in immunosuppressed patients it may develop secondary to Cryptosporidium or CMV
    - associated with high morbidity and mortality rates
131
Q

What is the epidemiology of cholecystitis?

A

Follows that of gallstones (cholelithiasis)
More common in women

132
Q

What are the features of cholecystitis?

A
  1. RUQ pain
  2. May radiate to the right shoulder
  3. Fever and signs of systemic upset
  4. Murphy’s sign on examination: inspiratory arrest upon palpation of the right upper quadrant
133
Q

What are the LFTs findings of cholecystitis?

A

Typically normal
Mirizzi syndrome: deranged LFTs may mean there is a gallstone impacted in the distal cystic duct causing extrinsic compression of the common bile duct

134
Q

What are the investigations for cholecystitis?

A
  1. Investigation of choice = ultrasound
  2. If diagnosis is unclear then cholescintigraphy (HIDA scan) may be used
135
Q

What would the findings of cholecystitis be on a cholescintigraphy (HIDA scan)?

A

Cystic duct obstruction (secondary to odema associated with inflammation or an obstructing stone) and hence the gallbladder will not be visualised

136
Q

What is the management for cholecystitis?

A
  1. IV antibiotics
  2. Cholecystectomy - NICE recommend early laparoscopic cholecystectomy, within 1 week of diagnosis (incl. pregnant women)
137
Q

What is a positive Murphy’s sign?

A
  1. Firmly place a hand at the costal margin in the RUQ and ask the patient to breathe deeply
  2. If the gallbladder is inflamed, the patient will experience pain and catch their breath (inspiration) as the gallbladder descends and contacts the palpating hand
138
Q

What are the complications of cholecystitis?

A
  1. Gangrenous cholecystitis: ischaemic necrosis of the wall
  2. Perforation of the gallbladder (10%)
  3. Suppurative cholecystitis: Thickened wall with white cell infiltration, intra-wall abscesses, and necrosis → perforation or pericholecystic abscess formation
  4. Bile duct injury due to surgery
  5. Gallstone ileus: gallstone passing from the biliary tract into the intestinal tract (through a fistula), leading to small-intestinal obstruction. (Rx: enterotomy and stone extraction)
139
Q

What is the prognosis of cholecystitis?

A

Surgical removal prevents risk of developing cholecystitis again
If gallbladder perforation → mortality is 30%
If untreated → mortality is up to 50%

140
Q

What is Liver Cirrhosis?

A
  1. End stage of chronic liver damage
  2. Replacement of normal liver architecture with diffuse fibrosis and nodules of regenerating hepatocytes
141
Q

What are the three main causes of cirrhosis?

A
  1. Alcohol
  2. Non-alcoholic fatty liver disease
  3. Viral hepatitis B and C
142
Q

What are some of the other causes of cirrhosis?

A
  1. Chronic biliary disease e.g. PSC, PBC, biliary atresia
  2. Autoimmune hepatitis
  3. Drugs e.g. methotrexate
  4. Inherited diseases e.g. alpha-1 anti-trypsin deficiency, haemochromatosis, Wilson’s disease
  5. Budd-chiari syndrome: occlusion of the hepatic veins that drain the liver
143
Q

What is the triad seen in Budd-chiari syndrome?

A
  1. Abdominal pain
  2. Ascites
  3. Hepatomegaly
144
Q

What is decompensated liver cirrhosis?

A

When there are complications e.g. ascites, jaundice, encephalopathy or GI bleeding (oesophageal varices)

145
Q

What are the precipitating factors for liver decompensation?

A
  1. Infection
  2. Constipation
  3. GI bleeding
  4. Electrolyte imbalances
  5. Alcohol and drug use
  6. Tumour development
  7. Portal vein thrombosis
146
Q

What are the early features of liver cirrhosis?

A

Anorexia
Nausea
Fatigue
Weakness
Weight loss

147
Q

How can the features of liver cirrhosis be divided?

A

Reduced liver synthetic function:
1. Easy bruising
2. Abdominal swelling
3. Ankle oedema
Reduced detoxification:
1. Jaundice
2. Personality change → encephalopathy
3. Altered sleep pattern
4. Amenorrhoea

148
Q

What are some of the features of portal hypertension in liver cirrhosis?

A
  1. Abdominal swelling
  2. Haematemesis
  3. PR bleeding or malaena
149
Q

What are the signs of chronic liver disease on examination?

A
  1. Asterixis (liver flap)
  2. Bruises
  3. Clubbing
  4. Dupuytren’s contracture
  5. Erythema (palmar)
150
Q

What are the signs of decompensated liver disease on examination?

A
  1. Jaundice
  2. Gynaecomastia,
  3. Leukonychia (hypoalbuminaemia)
  4. Parotid enlargement
  5. Spider naevi
  6. Scratch marks (due to pruritus)
  7. Ascites: shifting dullness and fluid thrill
  8. Enlarged liver (shrunken and small in later stage)
  9. Testicular atrophy
  10. Caput medusae: dilated superficial abdominal veins
  11. Splenomegaly (indicating portal hypertension)
151
Q

What are the investigations for liver cirrhosis alongside bloods, and ultrasound?

A

Transient elastography and acoustic radiation force impulse imaging

152
Q

What is transient elastography in the investigation of liver cirrhosis?

A
  1. Also known as ‘fibroscan’
  2. Uses a 50-MHz wave passed into the liver from a small transducer on the end of an ultrasound probe
  3. Measures the ‘stiffness’ of the liver which is a proxy for fibrosis
153
Q

According to NICE, who should be offered a transient elastography for suspected cirrhosis?

A
  1. People with hepatitis C virus infection
  2. Men who drink over 50 units of alcohol per week and women who drink over 35 units of alcohol per week and have done so for several months
  3. People diagnosed with alcohol-related liver disease
154
Q

What are some other investigations offered to patients with suspected liver cirrhosis?

A
  1. Upper endoscopy: to check for varices in patient’s with a new diagnosis of cirrhosis
  2. Liver ultrasound every 6 months (+/- alpha-feto protein) to check for hepatocellular cancer
155
Q

What is the scoring system for liver cirrhosis?

A
  1. Child-Pugh
  2. In recent years: Model for End-Stage Liver Disease (MELD) has been increasingly used
156
Q

What does the Model for End-Stage Liver Disease (MELD) scoring system use to predict survival in patient’s with cirrhosis?

A

Uses a combination of a patient’s bilirubin, creatinine, and the international normalized ratio (INR) to calculate a three month mortality risk

157
Q

What is the management for Cirrhosis?

A
  1. Treat the cause if possible such as such as hepatitis B and C virus infections
  2. Avoid alcohol, sedatives, opiates, NSAIDs and drugs that affect the liver
  3. Nutrition is very important and if intake is poor, dietitian review and enteral supplements should be given; nasogastric feeding may be indicated
  4. Treatment of the complications
  5. Liver transplantation is the only curative measure!
158
Q

What are the possible complications of Cirrhosis and their management?

A
  1. Encephalopathy
  2. Potral hypertension and ascites
  3. Spontaneous bacterial peritonitis
  4. Hepatocellular carcinoma
  5. Hepatorenal syndrome
  6. Hepatopulmonary syndrome: pulmonary hypertension
159
Q

What is the management on encephalopathy in cirrhosis?

A
  1. Treat infections
  2. Exclude a GI bleed
  3. Lactulose, phosphate enemas and avoid sedation
160
Q

What is the management of portal hypertension and ascites in cirrhosis?

A
  1. Diuretics (spironolactone/ furosemide)
  2. Dietary sodium restriction (88meq or 2g/day),
  3. Therapeutic paracentesis (with human albumin replacement IV)
  4. Monitor weight daily
  5. Fluid restriction in patients with plasma sodium <120mmol/L
  6. Avoid alcohol and NSAIDs.
161
Q

What is the management of spontaneous bacterial peritonitis?

A

Features: ascites, abdominal pain and fever
Diagnosis: paracentesis: neutrophil count > 250 cells/ul, most commonly E. coli
Treatment: IV cefotaxime

162
Q

What do NICE recommend to patients with liver cirrhosis and ascites?

A

Offer prophylactic oral ciprofloxacin or norfloxacin for people with cirrhosis and ascites with an ascitic protein of 15 g/litre or less until the ascites has resolved

163
Q

What is the prognosis of Cirrhosis?

A

Depends on the aetiology and complications
Generally poor:
1. Overall 5-year survival is 50%
2. In the presence of ascites, 2-year survival of 50%
3. Alcoholic liver disease is a marker of poor prognosis in SBP

164
Q

What is Coeliac disease?

A

Autoimmune disease caused by intolerance to gluten, causing chronic intestinal malabsorption

165
Q

What is the pathophysiology of coeliac disease?

A
  1. Caused by sensitivity to the protein gluten
  2. Almost all people with coeliac disease carry one of two major histocompatibility complex class-II molecules (HLA-DQ2 or -DQ8) that are required to present gluten peptides in a manner that activates an antigen-specific T cell response
  3. Repeated exposure leads to villous atrophy which in turn causes malabsorption
166
Q

What conditions are associated with coeliac disease?

A
  1. Dermatitis herpetiformis (a vesicular, pruritic skin eruption)
  2. Autoimmune disorders: type 1 diabetes mellitus and autoimmune hepatitis, thyroid diseases
  3. IBS
  4. First-degree relatives with coeliac disease
167
Q

What is the epidemiology of coeliac disease?

A

It is thought to affect around 1% of the UK population

168
Q

What are the signs and symptoms of coeliac disease?

A
  1. Chronic or intermittent diarrhoea
  2. Failure to thrive or faltering growth (in children)
  3. Persistent or unexplained GI symptoms including nausea and vomiting
  4. Prolonged fatigue (‘tired all the time’)
  5. Recurrent abdominal pain, cramping or distension
  6. Sudden or unexpected weight loss
  7. Unexplained iron-deficiency anaemia, or other unspecified anaemia
169
Q

What are the signs of Coeliac disease on physical examination?

A
  1. Signs of anaemia: Pallor
  2. Signs of malnutrition: Short stature, abdominal distension (bloating) and wasted buttocks in children
  3. Triceps skinfold thickness gives an indication of fat stores
  4. Signs of vitamin or mineral deficiencies (e.g. osteomalacia, easy bruising)
  5. Intense, itchy blisters on elbows, knees or buttocks (dermatitis herpetiformis)-this is uncommon
170
Q

What is the first choice investigation for coeliac disease?

A

Serology:
1. Tissue transglutaminase (TTG) antibodies (IgA) (first choice)
2. Endomyseal antibody (IgA)

171
Q

What is the gold standard test for coeliac disease?

A

Endoscopic intestinal biopsy: traditionally done in the duodenum but jejunal biopsies are also sometimes performed

172
Q

What are the findings on endoscopic intestinal biopsy for coeliac disease?

A
  1. Villous atrophy
  2. Crypt hyperplasia
  3. Increase in intraepithelial lymphocytes
  4. Lamina propria infiltration with lymphocytes
173
Q

What is important regarding patients who require coeliac disease testing but are already on a gluten-free diet?

A

Villous atrophy and immunology normally reverses on a gluten-free diet: patients should be asked, if possible, to reintroduce gluten for at least 6 weeks prior to testing

174
Q

What is the management of coeliac disease?

A

Advice:
1. Strict lifelong gluten-free diet with avoidance of all wheat, rye and barley products
2. Education and expert dietary advice is essential- the Coeliac Society offers patient support and advice
Medical:
-Vitamin and mineral supplements
-Oral corticosteroids (may be considered)
Immunisation:
1. Patients have a degree of functional hyposplenism
2. All patients should be offered the pneumococcal vaccine and given a booster every 5 years

175
Q

What are the complications of coeliac disease?

A
  1. Anaemia: iron, folate and vitamin B12 deficiency (folate deficiency is more common than vitamin B12 deficiency in coeliac disease)
  2. Hyposplenism
  3. Osteoporosis, osteomalacia
  4. Lactose intolerance
  5. Enteropathy-associated T-cell lymphoma of small intestine
  6. Subfertility, unfavourable pregnancy outcomes
  7. Rare: oesophageal cancer, other malignancies
176
Q

What is the prognosis of coeliac disease?

A
  1. With strict adherence to gluten-free diet, most patients make a full recovery
  2. Symptoms usually resolve within weeks but histological changes may take longer to resolve
  3. A gluten-free diet needs to be followed for life
177
Q

What is colorectal carcinoma?

A
  1. Malignancy of the large bowel
  2. The third most common type of cancer in the UK and the second most cause of cancer deaths
178
Q

What is the aetiology of colorectal carcinoma?

A

Currently thought to be three types:
1. Sporadic (95%)
2. Hereditary non-polyposis colorectal carcinoma (HNPCC, 5%)
3. Familial adenomatous polyposis (FAP, <1%)

179
Q

What are the most common risk factors for colorectal carcinoma?

A
  1. Age
  2. Genetics (even in sporadic cases, FH is important)
  3. Inflammatory bowel disease
  4. Lifestyle/ environmental factors
180
Q

What is hereditary non-polyposis colorectal carcinoma (HNPCC)?

A
  1. An autosomal dominant condition: most common form of inherited colon cancer
  2. Around 90% of patients develop cancers, often of the proximal colon, which are usually poorly differentiated and highly aggressive
  3. At risk of other cancers: endometrial cancer
181
Q

What is familial adenomatous polyposis (FAP)?

A
  1. A rare autosomal dominant condition which leads to the formation of hundreds of polyps by the age of 30-40 years
  2. Patients inevitably develop carcinoma
  3. It is due to a mutation in a tumour suppressor gene called adenomatous polyposis coli gene (APC), located on chromosome 5
  4. Also at risk from duodenal tumours
  5. A variant of FAP called Gardner’s syndrome can also feature osteomas of the skull and mandible, retinal pigmentation, thyroid carcinoma and epidermoid cysts on the skin
182
Q

What are the common locations for colorectal carcinomas?

A
  1. Rectal: 40%
  2. Sigmoid: 30%
  3. Ascending colon and caecum: 15%
  4. Transverse colon: 10%
  5. Descending colon: 5%
183
Q

What are the features of a left sided colon and rectum carcinoma?

A
  1. Change in bowel habit: increased frequency, looser stools
  2. Rectal bleeding or blood/mucous mixed in with stools
  3. Rectal masses may also present as tenesmus: sensation of incomplete emptying after defecation
184
Q

What are the features of a right sided colon carcinoma?

A

Later presentation:
1. Symptoms of anaemia
2. Weight loss and non- specific malaise
2. More rarely, lower abdominal pain

185
Q

How can colorectal carcinoma present in an emergency?

A
  1. 20% of cases
  2. Pain and distension caused by large bowel obstruction, haemorrhage or peritonitis as a result of perforation
186
Q

What are the signs of colorectal carcinoma on examination?

A
  1. Left sided: abdominal mass, low-lying rectal tumours may be palpable on rectal examination
  2. Right sided: anaemia may be only sign
  3. Metastatic disease: hepatomegaly, shifting dullness of ascites
187
Q

What are the referral guidelines for colorectal carcinoma for the 2 week pathway?

A
  1. Patients ≥ 40 years with unexplained weight loss AND abdominal pain
  2. Patients ≥ 50 years with unexplained rectal bleeding
  3. Patients ≥ 60 years with iron deficiency anaemia OR change in bowel habit
188
Q

When else should a patient be referred to the 2WW pathway for colorectal carcinoma?

A

Tests show occult blood in their faeces (FIT)

189
Q

When should a referral to the 2WW pathway be considered?

A
  1. There is a rectal or abdominal mass
  2. There is an unexplained anal mass or anal ulceration
  3. Patients < 50 years with rectal bleeding AND any of the following unexplained symptoms/findings:
    a. abdominal pain
    b. change in bowel habit
    c. weight loss
    d. iron deficiency anaemia
190
Q

What is the faecal immunochemical test (FIT)?

A

National screening programme offering screening every 2 years to everyone aged 60 to 74 years in England (if over 74 years may request screening)
1. Eligible patients are sent the tests through the post
2. A type of faecal occult blood (FOB) test which uses antibodies that specifically recognise human haemoglobin (Hb)
3. Used to detect, and can quantify, the amount of human blood in a single stool sample
4. Patients with abnormal results are offered a colonoscopy

191
Q

When is a FIT test recommended to patients outside of the screening programme?

A

If patients have new symptoms but do not fit the 2WW referral criteria:
1. Patients ≥ 50 years with unexplained abdominal pain OR weight loss
2. Patients < 60 years with changes in their bowel habit OR iron deficiency anaemia
3. Patients ≥ 60 years who have anaemia even in the absence of iron deficiency

192
Q

What is the investigation that all patients with suspected colorectal cancer receive?

A

Colonoscopy (alongside further blood tests and stool tests

193
Q

What is the sign of colorectal carcinoma on barium enema?

A

Apple core stricture (stenosing annular carcinoma)

194
Q

What are the staging investigations for colorectal carcinoma?

A
  1. CT of the chest/ abdomen and pelvis: may show colonic wall thickening, enlarged lymph nodes, liver metastases, ascites, lung secondaries
  2. The entire colon should have been evaluated with colonoscopy or CT colonography
  3. Patients whose tumours lie below the peritoneal reflection should have their mesorectum evaluated with MRI
195
Q

What is the management of colorectal carcinoma?

A

MDT approach- nearly always treated with surgery:
1. Stents, surgical bypass and diversion stomas may all be used as palliative adjuncts
2. Resectional surgery is the only option for cure in patients with colon cancer
3. When a colonic cancer presents with an obstructing lesion; the options are to either stent it or resect

196
Q

What is the management of rectal cancer?

A

Tumours located in the rectum can be surgically resected with either an anterior resection or an abdomino-perineal excision of rectum (APER), involvement of the cirumferential resection margin carries a high risk of disease recurrence

197
Q

What are the types of resection for colorectal cancer depending on the site of the tumour?

A
  1. Caecal, ascending or proximal transverse colon:
    a. Right hemicolectomy
    b. Ileo-colic anastamosis
  2. Distal transverse, descending colon:
    a. Left hemicolectomy
    b. Colo-colon anastamosis
  3. Sigmoid colon:
    a. High anterior resection
    b. Colo-rectal anastamosis
  4. Upper rectum:
    a. Anterior resection (TME)
    b. Colo-rectal anastamosis
  5. Low rectum:
    a. Anterior resection (Low TME) b. Colo-rectal anastamosis
    (+/- Defunctioning stoma)
  6. Anal verge:
    a. Abdomino-perineal excision of rectu
    b. No anastamosis needed
198
Q

What is Hartmann’s procedure and when is it used in the management of colorectal carcinoma?

A

Defintion: when resection of the sigmoid colon is performed and an end colostomy is fashioned
Indication:
1. In an emergency setting where the bowel has perforated
2. The risk of an anastomosis is much greater, particularly when the anastomosis is colon-colon
3. In this situation, an end colostomy is often safer and can be reversed later

199
Q

What is a colorectal resection?

A
  1. The only option for cure in patients with colon cancer
  2. Is tailored to the patient and the tumour location
  3. The lymphatic drainage of the colon follows the arterial supply and therefore most resections are tailored around the resection of particular lymphatic chains (e.g. ileo-colic pedicle for right sided tumours)
  4. Some patients may have confounding factors that will govern the choice of procedure, e.g. a tumour in a patient from a HNPCC family may be better served with a panproctocolectomy rather than segmental resection
200
Q

What decision must be made following colorectal resection regarding restoration of continuity?

A

Anastamosis (surgical connection between two structures) or end stoma

201
Q

What are the technical factors regarding anastamosis healing in colorectal resections?

A

Adequate blood supply, mucosal apposition and no tissue tension
In certain situations (e.g. surrounding sepsis, unstable patients, inexperienced surgeons) it may be better to opt for an end stoma

202
Q

What are stomas?

A

Involve bringing the lumen or visceral contents onto the skin, most commonly the bowel

203
Q

What stoma should be used for the right side of the abdomen, specifically the RIF?

A
  1. Ileostomy: can be loop or end depending on location
  2. Should be spouted so that their irritant contents are not in contact with the skin
  3. Output = liquid
204
Q

What stoma should be used for the left side of the abdomen?

A
  1. Colostomy: end or loop, again depends on location and colonic segment used
  2. Should be flushed (no need for spouted because contents are less irritant)
  3. Output = solid
205
Q

What is important regarding stoma siting?

A
  1. Will ultimately influence the patient’s ability to manage their stoma and the risk of leakage
  2. Leakage of stoma contents and subsequent maceration of the surrounding skin can rapidly progress into a spiralling loss of control of stoma contents
  3. Ideally, the site of the stoma should be discussed with the patient prior to surgery
206
Q

What is Crohn’s disease?

A
  1. A form of inflammatory bowel disease
  2. Chronic granulomatous transmural inflammatory disease that can affect any part of the gastrointestinal tract
207
Q

What is the pathology of Crohn’s disease?

A
  1. Cause is unknown but there is a strong genetic susceptibility
  2. Inflammation occurs in all layers, down to the serosa
  3. This is why patients with Crohn’s are prone to strictures, fistulas and adhesions
  4. Can occur anywhere along the GI tract, with inflamed segments of bowel interspersed with normal segments: skip lesions
208
Q

What is the epidemiology of Crohn’s disease?

A

Typically presents in late adolescence or early adulthood (15-40 years)

209
Q

What are the common presenting symptoms of Crohn’s disease?

A
  1. May be non-specific symptoms such as weight loss and lethargy
  2. Diarrhoea: the most prominent symptom in adults (may cause bloody diarrhoea)
210
Q

What is the most common presenting symptom of Crohn’s disease in children?

A

Abdominal pain

211
Q

What are the other features of Crohn’s disease?

A
  1. Non-specific: lethargy, malaise
  2. Diarrhoea
  3. Abdominal pain
  4. Perianal disease: e.g. Skin tags or ulcers
  5. Extra-intestinal features: eye disease, joint disease, skin disease
212
Q

What are the signs of Crohn’s disease on examination?

A
  1. Weight loss
  2. Clubbing
  3. Signs of anaemia (pallor)
  4. Aphthous ulceration of the mouth
  5. Perianal skin tags, fistulae and abscesses
  6. Signs of complications (eye disease, joint disease, skin disease)
213
Q

What are the extra-intestinal features of inflammatory bowel disease?

A

Related to disease activity:
1. Arthritis (most common in UC and CD)
2. Erythema nodosum
3. Episcleritis (more common in CD)
4. Osteoporosis
Unrelated to disease activity:
1. Uveitis (more common in UC)
2. Pyoderma gangrenosum
3. Clubbing
4. Primary sclerosing cholangitis (UC)

214
Q

What are the investigations for Crohn’s disease?

A
  1. Bloods: FBC, inflammatory markers (CRP correlates well with disease activity)
  2. Stool culture (exclude infective colitis), faecal calprotectin
  3. Colonoscopy: investigation of choice
  4. Histology
  5. Small bowel enema
215
Q

What is the investigation of choice for crohn’s disease?

A

Colonoscopy: deep ulcers and skip lesions

216
Q

What are the histological findings of Crohn’s disease?

A
  1. Inflammation in all layers from mucosa to serosa
  2. Goblet cells
  3. Granulomas
217
Q

What are the findings on small bowel enema for Crohn’s disease?

A

High sensitivity and specificity for examination of the terminal ileum:
1. Strictures: ‘Kantor’s string sign’
2. Proximal bowel dilation
3. ‘rose thorn’ ulcers
4. Fistulae

218
Q

What is the management of Crohn’s disease divided into?

A
  1. General (smoking cessation, lifestyle)
  2. Inducing remission
  3. Maintaining remission
  4. Surgery
219
Q

What is the management for inducing remission in Crohn’s disease?

A
  1. Glucocorticoids (oral, topical or IV)
  2. Enteral feeding with an elemental diet may be used in addition to or instead of other measures to induce remission, particularly if there is concern regarding the side-effects of steroids (for example in young children)
  3. 5-ASA drugs (e.g. mesalazine) are used second-line to glucocorticoids but are not as effective
  4. Azathioprine or mercaptopurine (but assess TPMT before) may be used as an add-on medication to induce remission but is not used as monotherapy
  5. Methotrexate is an alternative to azathioprine
220
Q

What is the management for maintaining remission in Crohn’s disease?

A
  1. Stopping smoking is a priority (may be protective in UC)
  2. Azathioprine or mercaptopurine is used first-line to maintain remission
221
Q

What is the surgical management of Crohn’s disease?

A

Around 80% of patient’s with Crohn’s disease will have surgery for one of the following:
1. Stricturing terminal ileal disease → ileocaecal resection
2. Segmental small bowel resections
3. Stricturoplasty
4. Perianal fistulae: an inflammatory tract or connection between the anal canal and the perianal skin, perform MRI
5. Perianal abscess: requires incision and drainage combined with antibiotic therapy

222
Q

What is the management for an acute exacerbation of Crohn’s disease?

A
  1. Fluid resuscitation
  2. IV or oral corticosteroids
  3. Immunmodulators (azathioprine and methotrexate) may induce a remission in colonic Crohn’s disease
  4. Analgesia
  5. Elemental diet may induce remission (more often used in children)
  6. Parenteral nutrition may be necessary
  7. Monitor markers of activity (fluid balance, ESR, CRP, platelets, stool frequency, Hb and albumin)
  8. Assess for complications
223
Q

What are the complications of Crohn’s disease?

A

Can be GI and extra-intestinal:
1. Haemorrhage
2. Bowel strictures
3. Toxic megacolon (colon expands, dilates, and distends- high risk of rupture which is life threatening)
4. Perforation
5. Fistulae (between bowel, bladder, vagina)
6. Perianal fistulae and abscess
7. Malabsorption
8. Osteoporosis, uveitis, pyoderma gangrenosum

224
Q

What is the risk of malignancy for patient’s with Crohn’s disease?

A
  1. Small bowel cancer (standard incidence ratio = 40)
  2. Colorectal cancer (standard incidence ratio = 2, i.e. less than the risk associated with UC)
225
Q

What is the prognosis for Crohn’s disease?

A
  1. Chronic relapsing condition
  2. 80% will require surgery
226
Q

What is Diverticular disease?

A

The herniation (outpouchings) of colonic mucosa through the muscular wall of the colon (almost always in the sigmoid colon)

227
Q

What is the difference between diverticular disease and diverticulosis?

A

The more accurate term for diverticula being present, diverticular disease is reserved for patient who have symptoms

228
Q

What are the risk factors for diverticulosis?

A
  1. Increasing age
  2. Low fibre diet
229
Q

How can diverticulosis present?

A
  1. Diverticular disease
  2. Diverticulitis (infected diverticular)
230
Q

What are the symptoms of diverticular disease?

A
  1. Altered bowel habit
  2. Rectal bleeding
  3. Abdominal pain
    (or presence of complications)
231
Q

What are the complications of diverticular disease?

A
  1. Diverticulitis
  2. Haemorrhage
  3. Development of fistula
  4. Perforation and faecal peritonitis
  5. Perforation and development of abscess
232
Q

What is the pathophysiology of diverticular disease?

A
  1. A low-fibre diet leads to loss of stool bulk
  2. Consequently, high colonic intraluminal pressures must be generated to propel the stool, leading to herniation of the mucosa and submucosa through the muscularis
  3. Proposed diverticular obstruction by inspissated faeces can lead to bacterial overgrowth, toxin production and mucosal injury and diverticulitis: development of complications
233
Q

What are the investigations for diverticular disease?

A

Patients presenting in clinic will typically undergo either a colonoscopy, CT cologram or barium enema as part of their diagnostic work up (all can confirm diagnosis)

234
Q

What is the management of diverticular disease?

A
  1. Increase dietary fibre intake
  2. Mild attacks of diverticulitis may be managed conservatively with antibiotics
  3. Peri colonic abscesses should be drained either surgically or radiologically
  4. Recurrent episodes of acute diverticulitis requiring hospitalisation are a relative indication for a segmental resection
235
Q

What is diverticulitis?

A

Infection of a diverticulum, an out-pouching of the intestinal mucosa

236
Q

What is the epidemiology of diverticular disease and diverticulitis?

A
  1. Diverticula are incredibly common and it is thought that 30% of Westerners will have diverticula by the age of 60
  2. Only about 25% of people with diverticulosis will experience symptoms but 75% of these will experience an episode of diverticulitis
237
Q

What are the risk factors for diverticulitis?

A
  1. Increasing age
  2. Lack of dietary fibre
  3. Obesity: especially in younger patients
  4. Sedentary lifestyle
238
Q

What is the chronic history in patients with diverticulitis?

A
  1. Intermittent abdominal pain: particularly in the left lower quadrant
  2. Bloating
  3. Change in bowel habit: constipation or diarrhoea
239
Q

What are the features of acute diverticulitis?

A
  1. Severe abdominal pain: LIF (may be right in some Asians)
  2. Nausea and vomiting: this may be due to ileus or complicated diverticulitis with colonic obstruction
  3. Change in bowel habit: constipation is more common
  4. Urinary frequency, urgency or dysuria: due to irritation of the bladder by the inflamed bowel
  5. PR bleeding
240
Q

What are the signs of diverticulitis on examination?

A
  1. Low-grade pyrexia
  2. Tachycardia
  3. Tender LIF
  4. In 20% there will be a tender palpable mass due to inflammation or an abscess
  5. Possibly reduced bowel sounds
  6. Guarding, rigidity and rebound tenderness may suggest complicated diverticulitis with perforation
241
Q

What finding may suggest the presence of an abscess in diverticulitis?

A

Lack of improvement with treatment in seemingly uncomplicated diverticulitis

242
Q

What are the investigations for diverticulitis?

A
  1. Bloods: raised WCC, elevated CRP
  2. Imaging:
    a. Erect CXR: may show pneumoperitoneum in cases of perforation
    b. Abdominal XR: may show dilated bowel loops, obstruction or abscesses
    c. CT (best modality in suspected abscesses): bowel wall thickening, oedema and mesenteric fat stranding
243
Q

What investigation should be avoided in diverticulitis?

A

Avoided initially due to the increased risk of perforation in diverticulitis

244
Q

What is the management of diverticulitis?

A
  1. Mild cases: may be managed with oral antibiotics, liquid diet and analgesia
  2. More severe cases or if the symptoms don’t settle within 72 hours: patient should be admitted to hospital for IV antibiotics
245
Q

What are the typical IV antibiotics used in more severe diverticulitis?

A

A cephalosporin + metronidazole

246
Q

What are the complications of diverticular disease?

A
  1. Abscess formation
  2. Peritonitis
  3. Obstruction
  4. Perforation
247
Q

What is Endoscopic retrograde cholangiopancreatography (ERCP)?

A
  1. A procedure that combines upper gastrointestinal (GI) endoscopy and x-rays to treat problems of the bile and pancreatic ducts
  2. During an ERCP, stents can be inserted into the bile ducts, to allow drainage of bile into the intestine and biopsies can be taken
248
Q

What are the indications for Endoscopic retrograde cholangiopancreatography (ERCP)?

A

When your bile or pancreatic ducts have become narrowed or blocked:
1. Jaundice
2. Choledocholithiasis (gallstones)
3. Infection
4. Acute/chronic pancreatitis
5. Abnormal LFTs
6. Trauma or surgical complications in your bile or pancreatic ducts
7. Suspected malignancy of the bile ducts or pancreas
More used as a treatment rather than diagnostic test as it is invasive (MRCP is preferred)

249
Q

What are the possible complications of Endoscopic retrograde cholangiopancreatography (ERCP)?

A

Pancreatitis (most common)
Infection
Bleeding
Perforation
Prolonged pancreatic stenting is associated with stent occlusion, pancreatic duct obstruction and pseudocyst formation

250
Q

What is Enteral feeding?

A

The administration of feed and/or fluid via a tube going into the gastrointestinal tract. Can also be used:
1. To administer medication
2. For gastric aspiration
3. For gastric decompression (in bowel obstruction)

251
Q

What is Parenteral feeding?

A

The administration of specialist nutritional products to a person intravenously, bypassing the usual process of eating and digestion (GI tract)

252
Q

What are the indications for Feeding (enteral & parenteral)?

A
  1. Stroke, which may impair ability to swallow
  2. Malignancy which may cause fatigue, nausea, and vomiting that make it difficult to eat
  3. Critical illness or injury, which reduces energy or ability to eat
  4. Failure to thrive or inability to eat in young children or infants
  5. Serious illness, which places the body in a state of stress, making it difficult to take in enough nutrients
  6. Neurological or movement disorders that increase caloric requirements while making it more difficult to eat
    GI dysfunction or disease
253
Q

What are the possible complications of Feeding (enteral & parenteral)?

A
  1. Aspiration
  2. Refeeding syndrome: dangerous electrolyte imbalances that may occur in people who are very malnourished and start receiving enteral feeds
  3. Infection of the tube or insertion site
  4. Nausea and vomiting that may result from feeds that are too large or fast, or from slowed emptying of the stomach
  5. Skin irritation at the tube insertion site
  6. Diarrhoea due to a liquid diet or possibly medications
  7. Tube dislodgement or blockage, which may occur if not flushed properly
254
Q

What type of feeding is preferred?

A

Enteral (although sometimes parenteral is the life-saving option)

255
Q

What are the different types of Enteral Feeding?

A
  1. Nasogastric tube (NGT) starts in the nose and ends in the stomach
  2. Orogastric tube (OGT) starts in the mouth and ends in the stomach
  3. Nasoenteric tube starts in the nose and ends in the intestines (subtypes include nasojejunal and nasoduodenal tubes)
  4. Oroenteric tube starts in the mouth and ends in the intestines
  5. Gastrostomy tube is placed through the skin of the abdomen straight to the stomach (subtypes include PEG, PRG, and button tubes)
  6. Jejunostomy tube is placed through the skin of the abdomen straight into the intestines (subtypes include PEJ and PRJ tubes)
256
Q

What are the recognised complications of enteral feeding?

A
  1. Diarrhoea
  2. Apsiration
  3. Metabolic: hyperglycaemia, refeeding syndrome
257
Q

What is dyspepsia?

A

Pain after eating (indigestion)

258
Q

What is the referral criteria for a 2WW urgent endoscopy for dyspepsia?

A
  1. All patients with dysphagia
  2. All patients who’ve got an upper abdominal mass consistent with stomach cancer
  3. Patients aged ≥ 55 years who’ve got weight loss, AND any of the following:
    a. upper abdominal pain
    b. reflux
    c. dyspepsia
259
Q

What is the non-urgent referral criteria for an endoscopy for dyspepsia?

A
  1. Patients with haematemesis
  2. Patients aged ≥ 55 years who’ve got:
    a. treatment-resistant dyspepsia or
    b. upper abdominal pain with low haemoglobin levels or
    c. raised platelet count with any of the following: nausea, vomiting, weight loss, reflux, dyspepsia, upper abdominal pain
    d. nausea or vomiting with any of the following: weight loss, reflux, dyspepsia, upper abdominal pain
260
Q

What is the management for those patients who do not meet the referral criteria for dyspepsia?

A
  1. Review medications for possible causes of dyspepsia
  2. Lifestyle advice
  3. Trial of full-dose proton pump inhibitor for one month OR a ‘test and treat’ approach for H. pylori
    (if symptoms persist after either of the above approaches then the alternative approach should be tried)
261
Q

What is the test for H. pylori?

A
  1. Initial diagnosis: NICE recommend using a carbon-13 urea breath test or a stool antigen test, or laboratory-based serology ‘where its performance has been locally validated’
  2. Test of cure:
    a. there is no need to check for H. pylori eradication if symptoms have resolved following test and treat
    b. however, if repeat testing is required then a carbon-13 urea breath test should be used
262
Q

What is Functional dyspepsia?

A
  1. A term to describe a symptom or a combination of symptoms where UGI endoscopy did not reveal a potential cause for the dyspepsia
  2. (It is generally reserved for patients with a normal endoscopy whose symptoms do not suggest GORD)
263
Q

What is the aetiology of Functional dyspepsia?

A
  1. Post-prandial distress syndrome (PDS): meal-induced dyspeptic symptoms e.g. discomfort, pain, nausea, and fullness
  2. Epigastric pain syndrome (EPS): epigastric pain or burning, that does not occur exclusively post-prandially, can occur during fasting, and can even be improved by meal ingestion
  3. Overlapping PDS and EPS
264
Q

What is the epidemiology of Functional dyspepsia & irritable bowel syndrome (IBS)?

A

There is much overlap between functional dyspepsia and IBS
Patients who have both disorders have a substantially greater symptom burden and are more likely to consult a physician

265
Q

What is Irritable bowel syndrome (IBS)?

A

A chronic condition characterised by abdominal pain associated with bowel dysfunction, the pain is often relieved by defecation and is sometimes accompanied by abdominal bloating

266
Q

When should a diagnosis of IBS be considered in a patient?

A

If the patient has had the following for at least 6 months:
a. Abdominal pain, and/or
b. Bloating, and/or
c. Change in bowel habit
*abdominal pain relieved by defecation

267
Q

What are some of red flag features in a history of IBS that should be investigated?

A
  1. Rectal bleeding
  2. Unexplained/unintentional weight loss
  3. FH of bowel or ovarian cancer
  4. Onset after 60 years of age
268
Q

What are the presenting symptoms/signs of Functional dyspepsia?

A
  1. Epigastric pain or burning
  2. Early satiety and post-prandial fullness
  3. Belching
  4. Bloating
  5. Nausea
  6. Discomfort in the upper abdomen
269
Q

What are the appropriate investigations for Functional dyspepsia & irritable bowel syndrome (IBS)?

A

Exclude other causes:
1. FBC: normal, anaemia may suggest another cause
2. Stool studies: normal
3. Anti-endomysial antibodies/anti-tissue transglutaminase: if coeliac disease is suspected
4. Plain abdominal x-ray: normal no abnormal bowel pattern to suggest obstruction
5. Endoscopy: colonoscopy/sigmoidoscopy or gastroscopy are normal

270
Q

What is the pharmacological management of IBS?

A

First-line pharmacological treatment: according to predominant symptom:
1. Pain: antispasmodic agents
2. Constipation: laxatives but avoid lactulose
3. Diarrhoea: loperamide is first-line

271
Q

What is the general dietary advice for IBS?

A
  1. ave regular meals and take time to eat
  2. Avoid missing meals or leaving long gaps between eating
  3. Drink at least 8 cups of fluid per day, especially water or other non-caffeinated drinks such as herbal teas
  4. Restrict tea and coffee to 3 cups per day
  5. Reduce intake of alcohol and fizzy drinks
  6. Consider limiting intake of high-fibre food (for example, wholemeal or high-fibre flour and breads, cereals high in bran, and whole grains such as brown rice)
  7. For diarrhoea, avoid sorbitol
    for wind and bloating consider increasing intake of oats (for example, oat-based breakfast cereal or porridge) and linseeds (up to one tablespoon per day)
272
Q

What is the second-line pharmacological treatment for IBS?

A

Low-dose tricyclic antidepressants (e.g. amitriptyline 5-10 mg)

273
Q

What should be offered to patients if symptoms of IBS have not responded despite pharmacological treatment?

A

Psychological interventions e.g. CBT

274
Q

What are gallstones?

A
  1. Also known as cholelithiasis, is the presence of solid concretions in the gallbladder
  2. Gallstones form in the gallbladder but may exit into the bile ducts (choledocholithiasis)
275
Q

What is biliary colic?

A

A dull pain in the middle to upper right quadrant of the abdomen and occurs when a gallstone passes through the biliary tree

276
Q

What are the risk factors for gallstones and biliary colic?

A

4F’s:
1. Fat: obesity is thought to be a risk factor due to enhanced cholesterol synthesis and secretion
2. Female: gallstones are 2-3 times more common in women, oestrogen increases activity of HMG-CoA reductase
3. Fertile: pregnancy is a risk factor
4. Forty (> 40 increased risk)

277
Q

What conditions are associated with gallstones?

A
  1. Diabetes mellitus
  2. Crohn’s disease
  3. Rapid weight loss e.g. weight reduction surgery
  4. COCP
278
Q

What is the aetiology of gallstones?

A
  1. 90% are composed of cholesterol
  2. Different type of stones:
    a. Mixed stones: Contain cholesterol, calcium bilirubinate, phosphate and protein
    b. Pure cholesterol stones
    c. Approximately 2% of all gallstones are black pigment stones: elevated bilirubin secondary to haemolytic disorders, cirrhosis
279
Q

What is the aetiology of biliary colic?

A

Colicky right upper quadrant pain occurs due to the gallbladder contracting against a stone lodged in the cystic duct

280
Q

What are the main presentations of gallstones?

A
  1. Asymptomatic (90%): found incidentally
  2. Biliary colic
  3. Acute cholecystitis
  4. Acute cholangitis
281
Q

What are the features of biliary colic?

A
  1. Colicky right upper quadrant abdominal pain:
    a. worse postprandially, worse after fatty foods
    b. the pain may radiate to the right shoulder/interscapular region
  2. Nausea and vomiting are common
282
Q

What is the key difference between biliary colic and the other presentations of gallstones?

A

In biliary colic there is no fever and liver function tests/inflammatory markers are normal

283
Q

What is the investigation of choice for gallstones/ biliary colic?

A

Ultrasound

284
Q

What is the management of gallstones/ biliary colic?

A

Asymptomatic gallstone: only dietary advice
Biliary colic: Elective laparoscopic cholecystectomy

285
Q

When could gallstones cause obstructive jaundice?

A

If gallstones block the common bile duct (choledocholithiasis)

286
Q

What are the possible complications of gallstones?

A
  1. Acute cholecystitis: the most common complication
  2. Ascending cholangitis
  3. Acute pancreatitis
  4. Gallstone ileus
  5. Gallbladder cancer
287
Q

What is the management of severe biliary colic?

A
  1. Admission, IV fluids, analgesia, antiemetics and antibiotics if there are signs of infection (cholecystitis or cholangitis)
  2. If symptoms fail to improve or worsen, a localized abscess or empyema should be suspected
  3. This can be drained percutaneously by cholecystostomy and pigtail catheter
  4. If there is evidence of obstruction, urgent biliary drainage by ERCP
288
Q

What is the prognosis for gallstones?

A
  1. In most cases gallstones are (asymptomatic) benign and do not cause significant problems
  2. If they become symptomatic, surgery is an effective treatment
  3. Risk factors for recurrent problems: bile duct dilatation to >15mm, gallbladder being left intact, diverticulum, brown pigmented stones
289
Q

What is gastrectomy?

A

Partial or total surgical removal of the stomach

290
Q

When is gastrectomy indicated?

A

Usually for the management. of gastric cancer (depend on extent and size)
Can be used in the management of perforated peptic disease if a large lesion

291
Q

What are the complications of a gastrectomy?

A
  1. Dumping syndrome: fluid shift and rebound hypoglycaemia
  2. Weight loss and early satiety
  3. Anaemia: Vitamin B12 deficiency, iron deficiency
  4. Osteoporosis/ osteomalacia
292
Q

What are the more rarer complications of a gastrectomy?

A

Increased risk of gallstones and gastric cancer

293
Q

What is gastric cancer?

A

A neoplasm that can develop in any portion of the stomach and may spread to the lymph nodes and other organs

294
Q

What is the epidemiology of gastric cancer?

A
  1. Accounts for around 2% of all cancer diagnoses in the developed world
  2. Much less common than colorectal and slightly less common than oesophageal cancer
  3. It is a cancer of older people (half of patients are > 75 years) are has a male predominance (2:1)
295
Q

What are the risk factors for gastric cancer?

A
  1. Helicobacter pylori
  2. Atrophic gastritis
  3. Lifestyle: diet and smoking
296
Q

How does Helicobacter pylori increase the risk of gastric cancer?

A
  1. Triggers inflammation of the mucosa
  2. Leads to atrophy and intestinal metaplasia
297
Q

What are the symptoms of gastric cancer in the early stages?

A

Often asymptomatic

298
Q

What are the features of gastric cancer?

A
  1. Abdominal pain: typically vague, epigastric pain, may present as dyspepsia
  2. Weight loss and anorexia
  3. Nausea and vomiting
  4. Dysphagia: particularly if the cancer arises in the proximal stomach
  5. Overt upper gastrointestinal bleeding is seen only in a minority of patients
299
Q

What are the features of lymphatic spread in gastric cancer?

A
  1. Left supraclavicular lymph node: Virchow’s node
  2. Periumbilical nodule: Sister Mary Joseph’s node
300
Q

What is the investigation of choice to diagnose gastric cancer?

A

Oesophago-gastro-duodenoscopy with biopsy

301
Q

What are the findings of gastric cancer on biopsy?

A

Signet ring cells:
1. They contain a large vacuole of mucin which displaces the nucleus to one side
2. Higher numbers of signet ring cells are associated with a worse prognosis

302
Q

What investigation is used for staging in gastric cancer?

A

CT

303
Q

What is the management of gastric cancer?

A
  1. Surgery: options depend on the extent and site but include:
    a. Endoscopic mucosal resection
    b. Partial gastrectomy
    c. Total gastrectomy
  2. Chemotherapy
304
Q

What is a gastric MALT lymphoma?

A
  1. Associated with H. pylori infection in 95% of cases
  2. Good prognosis
  3. If low grade then 80% respond to H. pylori eradication
305
Q

What is H. pylori eradication therapy?

A

A 7-day course of:
1. A proton pump inhibitor + amoxicillin + (clarithromycin OR metronidazole)
2. If penicillin-allergic: a proton pump inhibitor + metronidazole + clarithromycin

!Final Year (26 decks)

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