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Gastroenterology Flashcards

1
Q

What are the causes of diarrhoea?

A
  • Acute
    • Suspect gastroenteritis
    • Travel, diet, contacts?
  • Chronic
    • Diarrhoea alternating with constipation: IBS
    • Anorexia, ↓wt., nocturnal diarrhoea: organic cause
  • Bloody
    • Vascular: ischaemic colitis
    • Infective: campylobacter, shigella, salmonella, E. coli, amoeba, pseudomembranous colitis
    • Inflammatory: UC, Crohn’s
    • Neoplastic: CRC, polyps
  • Mucus
    • IBS, CRC, polyps
  • Pus
    • IBD, diverticulitis, abscess
  • Assoc. c¯ medical disease
    • ↑ T4
    • Autonomic neuropathy (e.g. DM)
    • Carcinoid
  • Assoc. c¯ drugs
    • Abx
    • PPI, cimetidine
    • NSAIDs
    • Digoxin
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2
Q

What investigations would you perform in a patient presenting with diarrhoea?

A
  • Bloods
    • FBC: ↑ WCC, anaemia
    • U+E: ↓K+, dehydration
    • ↑ESR: IBD, Ca
    • ↑CRP: IBD, infection
    • Coeliac serology: anti-TTG or anti-endomysial Abs
  • Stool
    • MCS and C. diff toxin
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3
Q

How would you manage a patient with diarrhoea?

A
  • Treat cause
  • Oral or IV rehydration
  • Codeine phosphate or loperamide after each loose stool
  • Anti-emetic if assoc. with n/v: e.g. prochlorperazine
  • Abx (e.g. cipro) in infective diarrhoea → systemic illness
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4
Q

What is the pathogen, epidemiology and risk factors for C. diff diarrhoea?

A

Pathogen

  • Gm+ve spore-forming anaerobe
  • Release enterotoxins A and B
  • Spores are v. robust and can survive for >40d

Epidemiology

  • Commonest cause (25%) of Abx assoc. diarrhoea
    • 100% of Abx assoc. pseudomembranous colitis
  • Stool carriage in 3% of healthy adults and 15-30% of hospital pts.

Risk Factors

  • Abx: e.g. clindamycin, cefs, augmentin, quinolones
  • ↑ age
  • In hospital: ↑ c¯ length of stay, ↑ c¯ C. diff +ve contact
  • PPIs
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5
Q

How can C. diff infection present?

A
  • Asymptomatic
  • Mild diarrhoea
  • Colitis w/o pseudomembranes
  • Pseudomembranous colitis
  • Fulminant colitis
  • May occur up to 2mo after discontinuation of Abx
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6
Q

What are the features of Pseudomembranous Colitis?

A
  • Severe systemic symptoms: fever, dehydration
  • Abdominal pain, bloody diarrhoea, mucus PR
  • Pseudomembranes (yellow plaques) on flexi sig
  • Complications
    • Paralytic ileus
    • Toxic dilatation → perforation
    • Multi-organ failure
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7
Q

What investigations would you perform in a patient presenting with suspected C. diff?

A
  • Bloods: ↑↑CRP, ↑↑WCC, ↓albumin, dehydration
  • CDT ELISA
  • Stool culture
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8
Q

What markers of severe disease are there for C. diff infection?

A

Severe Disease: ≥1 of

  • WCC >15
  • Cr >50% above baseline
  • Temp >38.5
  • Clinical / radiological evidence of severe colitis
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9
Q

How would you manage a patient with C. diff infection?

A

General

  • Stop causative Abx
  • Avoid antidiarrhoeals and opiates
  • Enteric precautions

Specific

  • 1st line: Metronidazole 400mg TDS PO x 10-14d
  • 2nd line: Vanc 125mg QDS PO x 10-14d
    • Failed metro
  • Severe: Vanc 1st (may add metro IV)
    • ↑ to 250mg QDS if no response (max 500mg)
    • Urgent colectomy may be needed if
      • Toxic megacolon
      • ↑ LDH
      • Deteriorating condition
  • Recurrence (15-30%)
    • Reinfection or residual spores
    • Repeat course of metro x 10-14d
    • Vanc if further relapse (25%)
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10
Q

What are the causes of constipation?

A

OPENED IT

  • Obstruction
    • Mechanical: adhesions, hernia, Ca, inflamatory strictures, pelvic mass
    • Pseudo-obstruction: post-op ileus
  • Pain
    • Anal fissure
    • Proctalgia fugax
  • Endocrine / Electrolytes
    • Endo: ↓T4
    • Electrolytes: ↓Ca, ↓K, uraemia
  • Neuro
    • MS
    • Myelopathy
    • Cauda equina syndrome
  • Elderly
  • Diet / Dehydration
  • IBS
  • Toxins
    • Opioids
    • Anti-mACh
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11
Q

How would you manage a patient with constipation?

A
  • General
    • Drink more
    • ↑ dietary fibre
  • Bulking: ↑ faecal mass → ↑ peristalsis
    • CI: obstruction and faecal impaction
    • Bran
    • Ispaghula husk (Fybogel)
    • Methylcellulose
  • Osmotic: retain fluid in the bowel
    • Lactulose
    • MgSO4 (rapid)
  • Stimulant: ↑ intestinal motility and secretion
    • CI: obstruction, acute colitis
    • SE: abdo cramps
    • Bisacodyl PO or PR
    • Senna
    • Docusate sodium
    • Sodium picosulphate (rapid)
  • Softeners
    • Useful when managing painful anal conditions
    • Liquid paraffin
  • Enemas
    • Phosphate enema (osmotic)
  • Suppositories
    • Glycerol (stimulant)
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12
Q

What is the definition of IBS?

A

Disorders of enhanced visceral perception → bowel symptoms for which no organic cause can be found

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13
Q

What are the diagnostic criteria for IBS?

A

ROME Criteria

  • Abdo discomfort / pain for ≥ 12wks which has 2 of:
    • Relieved by defecation
    • Change in stool frequency (D or C)
    • Change in stool form: pellets, mucus
    • 2 of:
      • Urgency
      • Incomplete evacuation
      • Abdo bloating / distension
      • Mucous PR
      • Worsening symptoms after food
  • Exclusion criteria
    • >40yrs
    • Bloody stool
    • Anorexia
    • Wt. loss
    • Diarrhoea at night
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14
Q

How would you investigate and manage a patient with IBS?

A

Investigations

  • Bloods: FBC, ESR, LFT, coeliac serology, TSH
  • Colonoscopy: if >60yrs or any features of organic disease

Management

  • Exclusion diets can be tried
  • Bulking agents for constipation and diarrhoea (e.g.
  • fybogel).
  • Antispasmodics for colic/bloating (e.g. mebeverine)
  • Amitriptyline may be helpful
  • CBT
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15
Q

What are the causes of dysphagia?

A
  • Inflammatory
    • Tonsillitis, pharyngitis
    • Oesophagitis: GORD, candida
    • Oral candidiasis
    • Aphthous ulcers
  • Mechanical Block
    • Luminal
      • FB
      • Large food bolus
    • Mural
      • Benign stricture
        • Web (e.g. Plummer-Vinson)
        • Oesophagitis
        • Trauma (e.g. OGD)
      • Malignant stricture
        • Pharynx, oesophagus, gastric
        • Pharyngeal pouch
    • Extra-mural
      • Lung Ca
      • Rolling hiatus hernia
      • Mediastinal LNs (e.g. lymphoma)
      • Retrosternal goitre
      • Thoracic aortic aneurysm
  • Motility Disorders
    • Local
      • Achalasia
      • Diffuse oesophageal spasm
      • Nutcracker oesophagus
      • Bulbar / pseudobulbar palsy (CVA, MND)
    • Systemic
      • Systemic sclerosis / CREST
      • MG
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16
Q

What are the different ways in which dysphagia can present?

A
  • Dysphagia for liquids and solids at start
    • Yes: motility disorder
    • No, solids > liquids: stricture
  • Difficulty making swallowing movement: bulbar palsy
  • Odonophagia: Ca, oesophageal ulcer, spasm
  • Intermittent: oesophageal spasm
  • Constant and worsening: malignant stricture
  • Neck bulges or gurgles on drinking: pharyngeal pouch
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17
Q

What clinical signs would you look for when examining a patient with dysphagia?

A
  • Cachexia
  • Anaemia
  • Virchow’s node (+ve = Troisier’s sign)
  • Neurology
  • Signs of systemic disease (e.g. scleroderma)
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18
Q

What investigations would you like to perform in a patient with dysphagia?

A
  • Bloods: FBC, U+E
  • CXR
  • OGD
  • Barium swallow ± video fluoroscopy
  • Oesophageal manometrry
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19
Q

What is the pathophysiology, cause, presentation and complication of achalasia?

A
  • Pathophysiology
    • Degeneration of myenteric plexus (Auerbach’s)
    • ↓ peristalsis
    • LOS fails to relax
  • Cause
    • 1O / idiopathic: commonest
    • 2O: oesophageal Ca, Chagas’ disease (T. cruzii)
  • Presentation
    • Dysphagia: liquids and solids at same time
    • Regurgitation
    • Substernal cramps
    • Wt. loss
  • Comps
    • Chronic achalasia → oesophageal SCC
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20
Q

How would you investigate and manage a patient with achalasia?

A
  • Investigations
    • Ba swallow: dilated tapering oesophagus (Bird’s beak)
    • Manometry: failure of relaxation + ↓ peristalsis
    • CXR: may show widended mediastinum
    • OGD: exclude malignancy
  • Management
    • Med: CCBs, nitrates
    • Int: endoscopic balloon dilatation, botulinum toxin injection
    • Surg: Heller’s cardiomyotomy (open or endo)
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21
Q

What should you know about a pharyngeal pouch?

A

AKA Zenker’s Diverticulum

  • Outpouching of oesophagus between upper boarder of cricopharyngeus muscle and lower boarder of inferior constrictor of pharynx
    • Weak area called Killian’s dehiscence.
  • Defect usually occurs posteriorly but swelling usually bulges to left side of neck.
  • Food debris → pouch expansion → oesophageal compression → dysphagia.
  • Pres: regurgitation, halitosis, gurgling sounds
  • Rx: excision, endoscopic stapling
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22
Q

What is diffuse oesophageal spasm?

A
  • Intermittent dysphagia ± chest pain
  • Ba swallow shows corkscrew oesophagus
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23
Q

What is nutcracker oesophagus?

A

↑ contraction pressure with normal peristalsis

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24
Q

What worrying associated features might there be with dyspepsia?

A

ALARM Symptoms

  • Anaemia
  • Loss of wt.
  • Anorexia
  • Recent onset progressive symptoms
  • Melaena or haematemesis
  • Swallowing difficulty
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25
Q

What are the causes of dyspepsia?

A
  • Inflammation: GORD, gastritis, PUD
  • Ca: oesophageal, gastric
  • Functional: non-ulcer dyspepsia
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26
Q

How would you manage a patient with new onset dyspepsia?

A
  • OGD if >55 or ALARMS
  • Try conservative measures for 4 wks
    • Stop drugs: NSAIDs, CCBs (relax LOS)
    • Lose wt., stop smoking, ↓ EtOH
    • Avoid hot drinks and spicy food
    • OTC
      • Antacids: magnesium trisilicate
      • Alginates: gaviscon advance
  • Test for H. pylori if no improvement: breath or serology
    • +ve → eradication therapy
      • Consider OGD if no improvement
    • -ve → PPI trial for 4wks
      • Consider OGD if no improvement
      • PPIs can be used intermittently to control symptoms.
  • ​​Proven GORD
    • Full dose PPI for 1-2mo
    • Then, low-dose PPI PRN
  • Proven PUD
    • Full dose PPI for 1-2mo
    • H. pylori eradication if positive
    • Endoscopy to check for resolution if GU
    • Then, low-dose PPI PRN
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27
Q

What is H. pylori eradication therapy?

A
  • 7 days Rx
  • NB. PPIs and cimetidine → false –ve C13 breath tests and antigen tests so stop >2wks before.
  • PAC 500
    • PPI: lansoprazole 30mg BD
    • Amoxicillin 1g BD
    • Clarithromycin 500mg BD
  • PMC 250
    • PPI: lansoprazole 30mg BD
    • Metronidazole 400mg BD
    • Clarithromycin 250mg BD
  • Failure
    • 95% success
    • Mostly due to poor compliance
    • Add bismuth
    • Stools become tarry black
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28
Q

What are the causes of peptic ulcer disease?

A
  • Acute: usually due to drugs (NSAIDs, steroids) or “stress”
  • Chronic: drugs, H. pylori, ↑Ca, Zollinger-Ellison
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29
Q

What are the features of duodenal ulcers?

A
  • Pathology
    • 4x commoner than GU
    • 1st part of duodenum (cap)
    • M>F
  • Risk factors
    • H. pylori (90%)
    • Drugs: NSAIDs, steroids
    • Smoking
    • EtOH
    • ↑ gastric emptying
    • Blood group O
  • Presentation
    • Epigastric pain:
      • Before meals and at night
      • Relieved by eating or milk
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30
Q

What are the features of gastric ulcers?

A
  • Pathology
    • Lesser curve of gastric antrum
    • Beware ulcers elsewhere (often malignant)
  • Risk factors
    • H. pylori (80%)
    • Smoking
    • Drugs
    • Delayed gastric emptying
    • Stress
      • Cushing’s: intracranial disease
      • Curling’s: burns, sepsis, trauma
  • Presentation
    • Epigastric pain:
      • Worse on eating
      • Relieved by antacids
    • Wt. loss
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31
Q

What are the complications of peptic ulcer disease?

A
  • Haemorrhage
    • Haematemeis or melaena
    • Fe deficiency anaemia
  • Perforation
    • Peritonitis
  • Gastric Outflow Obstruction
    • Vomiting, colic, distension
  • Malignancy
    • ↑ risk c¯ H. pylori
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32
Q

How would you investigate a patient with peptic ulcer disease?

A
  • Bloods: FBC, urea (↑ in haemorrhage)
  • C13 breath test
  • OGD (stop PPIs >2wks before)
    • CLO / urease test for H. pylori
    • Always take biopsies of ulcers to check for Ca
  • Gastrin levels if Zollinger-Ellison suspected
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33
Q

What are the conservative and medical management options for peptic ulcer disease?

A
  • Conservative
    • Lose wt.
    • Stop smoking and ↓ EtOH
    • Avoid hot drinks and spicy food
    • Stop drugs: NSAIDs, steroids
    • OTC antacids
  • Medical
    • OTC antacids: Gaviscon, Mg trisilicate
    • H. pylori eradication: PAC500 or PMC250
    • Full-dose acid suppression for 1-2mo
      • PPIs: lansoprazole 30mg OD
      • H2RAs: ranitidine 300mg nocte
    • Low-dose acid suppression PRN
34
Q

What are the surgical management options for peptic ulcer disease?

A
  • Concepts
    • No acid → no ulcer
    • Secretion stimulated by gastrin and vagus N.
  • Vagotomy
    • Truncal: ↓ acid secretion but prevents pyloric sphincter relaxation so must be combined with pyloroplasty or gastroenterostomy.
    • Selective: vagus nerve only denervated where it supplies lower oesophagus and stomach
      • Nerves of Laterjet (supply pylorus) left intact
  • Antrectomy with vagotomy
    • Distal half of stomach removed + anastomosis:
      • Directly to duodenum: Billroth 1
      • To small bowel loop with duodenal stump oversewn: Billroth 2 or Polya
  • Subtotal gastrectomy with Roux-en-Y
    • Occasionally performed for Zollinger-Ellison
35
Q

What complications can there be following surgical management for peptic ulcer disease?

A
  • Physical
    • Stump leakage
    • Abdominal fullness
    • Reflux or bilious vomiting (improves c¯ time)
    • Stricture
  • Metabolic
    • Dumping syndrome
      • Abdo distension, flushing, n/v
      • Early: osmotic hypovolaemia
      • Late: reactive hypoglycaemia
    • Blind loop syndrome → malabsorption, diarrhoea
      • Overgrowth of bacteria in duodenal stump
      • Anaemia: Fe + B12
      • Osteoporosis
    • Wt. loss: malabsorption of ↓ calories intake
36
Q

What are the risk factors for GORD?

A
  • Hiatus hernia
  • Smoking
  • EtOH
  • Obesity
  • Pregnancy
  • Drugs: anti-AChM, nitrates, CCB, TCAs
  • Iatrogenic: Heller’s myotomy
37
Q

What are the symptoms of GORD?

A
  • Oesophageal
    • Heartburn
    • Related to meals
    • Worse lying down / stooping
    • Relieved by antacids
    • Belching
    • Acid brash, water brash
    • Odonophagia
  • Extra-oesophageal
    • Nocturnal asthma
    • Chronic cough
    • Laryngitis, sinusitis
38
Q

What complications can occur with GORD?

A
  • Oesophagitis: heartburn
  • Ulceration: rarely → haematemesis, melaena, ↓Fe
  • Benign stricture: dysphagia
  • Barrett’s oesophagus
    • Intestinal metaplasia of squamous epithelium
    • Metaplasia → dysplasia → adenocarcinoma
  • Oesophageal adenocarcinoma
39
Q

What is the differential diagnosis for GORD?

A
  • Oesophagitis
    • Infection: CMV, candida
    • IBD
    • Caustic substances / burns
  • PUD
  • Oesophageal Ca
40
Q

What investigations would you order for a patient presenting with GORD?

A
  • Isolated symptoms don’t need Ix
  • Bloods: FBC
  • CXR: hiatus hernia may be seen
  • OGD if:
    • >55yrs
    • Symptoms >4wks
    • Dysphagia
    • Persistent symptoms despite Rx
    • Wt. loss
    • OGD allows grading by Los Angeles Classification
  • Ba swallow: hiatus hernia, dysmotility
  • 24h pH testing ± manometry
    • pH <4 for >4hrs
41
Q

What are the conservative treatment options for GORD?

A
  • Lose wt.
  • Raise head of bed
  • Small regular meals ≥ 3h before bed
  • Stop smoking and ↓ EtOH
  • Avoid hot drinks and spicy food
  • Stop drugs: NSAIDs, steroids, CCBs, nitrates
42
Q

What are medical and surgical treatment options for GORD?

A
  • Medical
    • OTC antacids: Gaviscon, Mg trisilicate
    • 1: Full-dose PPI for 1-2mo
      • Lansoprazole 30mg OD
    • 2: No response → double dose PPI BD
    • 3: No response: add an H2RA
      • Ranitidine 300mg nocte
    • Control: low-dose acid suppression PRN
  • Surgical: Nissen Fundoplication
    • Indications: all 3 of:
      • Severe symptoms
      • Refractory to medical therapy
      • Confirmed reflux (pH monitoring)
43
Q

What is a Nissen Fundoplication?

A
  • Aim: prevent reflux, repair diaphragm
  • Usually laparoscopic approach
  • Mobilise gastric fundus and wrap around lower oesophagus
  • Close any diaphragmatic hiatus
  • Complications:
    • Gas-bloat syn.: inability to belch / vomit
    • Dysphagia if wrap too tight
44
Q

How are hiatus hernias classified?

A
  • Sliding (80%)
    • Gastro-oesophageal junction slides up into chest
    • Often assoc. with GORD
  • Rolling (15%)
    • Gastro-oesophageal junction remains in abdomen but a bulge of stomach rolls into chest alongside the oesophagus
    • LOS remains intact so GORD uncommon
    • Can → strangulation
  • Mixed (5%)
45
Q

What investigations would you order for a patient with a suspected hiatus hernia?

A
  • CXR: gas bubble and fluid level in chest
  • Ba swallow: diagnostic
  • OGD: visualises the mucosa but can’t exclude hernia
  • 24h pH + manometry: exclude dysmotility or achalsia
46
Q

What are the management options for a hiatus hernia?

A
  • Lose wt.
  • Rx reflux
  • Surgery if intractable symptoms despite medical Rx.
    • Should repair rolling hernia (even if asympto) as it may strangulate.
47
Q

What is the differential diagnosis for haematemesis?

A

VINTAGE

  • Varices
  • Inflammation
    • Oesophago-gastro-duodenitis
    • PUD: DU is commonest cause
  • Neoplasia
    • Oesophageal or gastric Ca
  • Trauma
    • Mallory-Weiss Tear
      • Mucosal tear due to vomiting
    • Boerhaave’s Syndrome
      • Full-thickness tear
      • 2cm proximal to LOS
  • Angiodysplasia + other vascular anomalies
    • Angiodysplasia
    • HHT
    • Dieulafoy lesion: rupture of large arteriole in stomach or other bowel
  • Generalised bleeding diathesis
    • Warfarin, thrombolytics
    • CRF
  • Epistaxis
48
Q

What is the differential diagnosis for rectal bleeding?

A

DRIPING Arse

  • Diverticulae
  • Rectal
    • Haemorrhoids
  • Infection
    • Campylobacter, shigella, E. coli, C. diff, amoebic dysentery
  • Polyps
  • Inflammation
    • UC, Crohn’s
  • Neoplasia
  • Gastic-upper bowel bleeding
  • Angio
    • Ischaemic colitis
    • HHT
    • Angiodysplasia
49
Q

What important points should you ask in the history for a patient presenting with an upper GI bleed?

A
  • Previous bleeds
  • Dyspepsia, known ulcers
  • Liver disease or oesophageal varices
  • Dysphagia, wt. loss
  • Drugs and EtOH
  • Co-morbidities
50
Q

What should you look for in your examination of a patient presenting with an upper GI bleed?

A
  • Signs of CLD
  • PR:melaena
  • Shock?
    • Cool, clammy, CRT>2s
    • ↓BP (<100) or postural hypotension (>20 drop)
    • ↓ urine output (<30ml/h)
    • Tachycardia
    • ↓GCS
51
Q

What are the common causes of an upper GI bleed?

A
  • PUD: 40% (DU commonly)
  • Acute erosions / gastritis:20%
  • Mallory-Weiss tear: 10%
  • Varices: 5%
  • Oesophagitis: 5%
  • Ca Stomach / oesophagus:<3%
52
Q

What is the Rockall score?

A

Rockall Score: (Prof T Rockall, St. Mary’s)

  • Prediction of re-bleeding and mortality
  • 40% of re-bleeders die
  • Initial score pre-endoscopy
    • Age
    • Shock: BP, pulse
    • Comorbidities
  • Final score post-endoscopy
    • Final Dx + evidence of recent haemorrhage
      • Active bleeding
      • Visible vessel
      • Adherent clot
  • Initial score ≥3 or final >6 are indications for surgery
53
Q

What is the pathophysiology and prognosis of oesophageal varicies?

A
  • Portal HTN → dilated veins @ sites of porto-systemic anastomosis: L. gastric and inferior oesophageal veins
  • 30-50% with portal HTN will bleed from varices
  • Overall mortality 25%: ↑ with severity of liver disease.
54
Q

What are the causes of protal HTN?

A
  • Pre-hepatic: portal vein thrombosis
  • Hepatic: cirrhosis (80% in UK), schistosomasis (commonest worldwide), sarcoidosis.
  • Post-hepatic: Budd-Chiari, RHF, constrictive pericarditis
55
Q

What treatment is used to try and prevent oesophageal varicial bleeds?

A
  • 1º: β-B, repeat endoscopic banding
  • 2º: β-B, repeat banding, TIPSS

Transjugular Intrahepatic Porto-Systemic Shunt (TIPSS)

  • IR creates artificial channel between hepatic vein and portal vein → ↓ portal pressure.
  • Colapinto needle creates tract through liver parenchyma which is expand using a balloon and maintained by placement of a stent.
  • Used prophylactically or acutely if endoscopic therapy fails to control variceal bleeding.
56
Q

What is the acute management of an upper GI bleed?

A
  • Resuscitate
    • Head-down
    • 100% O2, protect airway
    • 2 x 14G cannulae + IV crystalloid infusion up to 1L.
    • Bloods: FBC, U+E (↑ urea), LFTs, clotting, x-match 6u, ABG, glucose
  • Blood if remains shocked
    • Group specific or O- until X-matched
  • Variceal Bleed
    • Terlipressin IV (splanchnic vasopressor)
    • Prophylactic Abx: e.g. ciprofloxacin 1g/24h
  • Maintenance
    • Crystalloid IVI, transfuse if necessary (keep Hb≥10)
    • Catheter + consider CVP (aim for >5cm H2O)
    • Correct coagulopathy: vit K, FFP, platelets
    • Thiamine if EtOH
    • Notify surgeons of severe bleeds
  • Urgent Endoscopy
57
Q

What is the endoscopic management of an acute upper GI bleed?

A
  • Haemostasis of vessel or ulcer:
    • Adrenaline injection
    • Thermal / laser coagulation
    • Fibrin glue
    • Endoclips
  • Variceal bleeding:
    • 2 of: banding, sclerotherapy, adrenaline, coagulation
    • Balloon tamponade with Sengstaken-Blakemore tube
      • Only used if exsanguinating haemorrhage or failure of endoscopic therapy
    • TIPSS if bleeding can’t be stopped endoscopically
  • After endoscopy
    • Omeprazole IV + continuation PO (↓s re-bleeding)
    • Keep NBM for 24h → clear fluids → light diet @ 48h
    • Daily bloods: FBC, U+E, LFT, clotting
    • H. pylori testing and eradication
    • Stop NSAIDs, steroids et.c.
58
Q

What are the indications for surgery for an acute upper GI bleed?

A
  • Re-bleeding
  • Bleeding despite transfusing 6u
  • Uncontrollable bleeding at endoscopy
  • Initial Rockall score ≥3, or final >6

Open stomach, find bleeder and underrun vessel.

59
Q

What type of fluid replacement should be used for an upper GI bleed in a patient with uncompensated liver disease?

A

Avoid 0.9% NS in uncompensated liver disease (worsens ascites). Use blood or albumin for resus and 5% dex for maintenance.

60
Q

What is the normal bilirubin physiology?

A
  • Normal BR = 3-17uM
  • Jaundice visible @ 50uM (3 x ULN)
  • Hb → unconjugated BR by splenic macrophages
  • uBR → cBR by BR-UDP-glucuronyl transferase in liver
  • Secreted in bile then cBR → urobilinogen (colourless)
    • Some urobilinogen is reabsorbed, returned to liver and re-excreted into bile.
    • Some reabsorbed urobilinogen is excreted into the urine
    • The urobilinogen that remains in the GIT is converted to stercobilin (brown) and excreted.
61
Q

What are the causes of jaundice?

A
  • Pre-Hepatic
    • Excess BR production
      • Haemolytic anaemia
      • Ineffective erythropoiesis e.g. thalassaemia
  • Hepatic
    • Unconjugated
      • ↓ BR Uptake
        • Drugs: contrast, RMP
        • CCF
      • ↓ BR Conjugation
        • Hypothyroidism
        • Gilbert’s (AD)
        • Crigler-Najjar (AR)
      • Neonatal jaundice is both ↑ production + ↓ conjug.
    • Conjugated
      • Hepatocellular Dysfunction
        • Congen: HH, Wilson’s, α1ATD
        • Infection: Hep A/B/C, CMV, EBV
        • Toxin: EtOH, drugs
        • AI: AIH
        • Neoplasia: HCC, mets
        • Vasc: Budd-Chiari
      • ↓ Hepatic BR Excretion
        • Dubin-Johnson
        • Rotor’s
  • Post-Hepatic
    • Obstruction
      • Stones
      • Ca pancreas
      • Drugs
      • PBC
      • PSC
      • Biliary atresia
      • Choledochal cyst
      • Cholangio Ca
62
Q

What drugs can cause jaundice and by what different mechanisms?

A
  • Haemolysis
    • Antimalarials (e.g. dapsone)
  • Hepatitis
    • Paracetamol OD
    • RMP, INH, PZA
    • Valproate
    • Statins
    • Halothane
    • MOAIs
  • Cholestasis
    • Fluclox (may be wks after Rx)
    • Co-amoxiclav
    • OCP
    • Sulfonylureas
    • Chlopromazine, prochlorperazine
63
Q

What are Gilbert’s and Crigler-Najjar?

A
  • Gilbert’s
    • Autosomal dominant partial UDP-GT deficiency
    • 2% of the population
    • Jaundice occurs during intercurrent illness
    • Dx: ↑ uBR on fasting, normal LFTs
  • Crigler-Najjar
    • Rare autosomal recessive total UDP-GT deficiency
    • Severe neonatal jaundice and kernicterus
    • Rx: liver Tx
64
Q

What investigations would you do for a patient with suspected pre-hepatic jaundice?

A
  • Urine
    • No BR (acholuric)
    • ↑ urobilinogen
    • ↑Hb if intravascular haemolysis
  • LFTs
    • ↑ uBR
    • ↑ AST
    • ↑ LDH
  • Other
    • FBC and film
    • Coombs Test
    • Hb electrophoresis
65
Q

What investigations would you do for a patient with suspected hepatic jaundice?

A
  • Urine
    • ↑BR
    • ↑ urobilinogen
  • LFTs
    • ↑ cBR (usually)
    • ↑AST:↑ALT
      • > 2 = EtOH
      • < 1 = Viral
    • ↑ GGT (EtOH, obstruction)
    • ↑ ALP
    • Function: ↓ albumin, ↑ PT
  • Other
    • FBC: anaemia
    • Anti- SMA, LKM, SLA, ANA
    • α1AT, ferritin, caeruloplasmin
    • Liver biopsy
66
Q

What investigations would you do for a patient with suspected post-hepatic jaundice?

A
  • Urine
    • ↑↑ BR
    • No urobilinogen
  • LFTs
    • ↑↑ cBR
    • ↑ AST, ↑ ALT
    • ↑↑ ALP
    • ↑ GGT
  • Other
    • Abdo US: ducts >6mm
    • ERCP, MRCP
    • Anti- AMA, ANCA, ANA
67
Q

What are the causes of liver failure?

A
  • Acute
    • Infection: Hep A/B, CMV, EBV, leptospirosis
    • Toxin: EtOH, paracetamol, isoniazid, halothane
    • Vasc: Budd-Chiari
    • Other: Wilson’s, AIH
    • Obs: eclampsia, acute fatty liver of pregnancy
  • Cirrhosis
68
Q

What are the signs of liver failure?

A
  • Jaundice
  • Oedema + ascites
  • Bruising
  • Encephalopathy
    • Aterixis
    • Constructional apraxia (5-pointed star)
  • Fetor hepaticus
  • Signs of cirrhosis / chronic liver disease
69
Q

What investigations should you do for a patient with suspected liver failure?

A
  • Blood
    • FBC: infection, GI bleed, ↓ MCV (EtOH)
    • U+E
      • ↓U, ↑Cr: hepatorenal syndrome
      • Urea synth in liver thus poor test of renal function
    • LFT
      • AST:ALT > 2 = EtOH
      • AST:ALT < 1 = Viral
      • Albumin: ↓ in chronic liver failure
      • PT: ↑ in acute liver failure
    • Clotting: ↑INR
    • Glucose
    • ABG: metabolic acidosis
    • Cause: Ferritin, α1AT, caeruloplasmin, Abs, paracetamol levels
  • Microbiology
    • Hep, CMV, EBV serology
    • Blood and urine culture
    • Ascites MCS + SAAG
  • Radiology
    • CXR
    • Abdo US + portal vein duplex
70
Q

What is the pathophysiology, classification and treatment for hepatorenal syndrome?

A
  • Hepatorenal syndrome
    • Renal failure in pts. with advanced CLF
    • Dx of exclusion
  • Pathophysiology: “Underfill theory”
    • Cirrhosis → splanchnic arterial vasodilatation → effective circulatory volume → RAS activation → renal arterial vasoconstriction.
    • Persistent underfilling of renal circulation → failure
  • Classification
    • Type 1: rapidly progressive deterioration (survival <2wks)
    • Type 2: steady deterioration (survival ~6mo)
  • Rx
    • IV albumin + splanchnic vasoconstrictors (terlipressin)
    • Haemodialysis as supportive Rx
    • Liver Tx is Rx of choice
71
Q

How do you manage liver failure generally and what should be monitored?

A
  • Management
    • Manage in ITU
    • Rx underlying cause: e.g. NAC in paracetamol OD
    • Good nutrition: e.g. via NGT with high carbs
    • Thiamine supplements
    • Prophylactic PPIs vs. stress ulcers
  • Monitoring
    • Fluids: urinary and central venous catheters
    • Bloods: daily FBC, U+E, LFT, INR
    • Glucose: 1-4hrly + 10% dextrose IV 1L/12h
72
Q

What complications can occur in patients with liver failure and how shoud they be managed?

A
  • Bleeding: Vit K, platelets, FFP, blood
  • Sepsis: tazocin (avoid gent: nephrotoxicity)
  • Ascites: fluid and salt restrict, spiro, fruse, tap, daily weight
  • Hypoglycaemia: regular BMs, IV glucose if <2mM
  • Encephalopathy: avoid sedatives, lactulose ± enemas, rifaximin
  • Seizures: lorazepam
  • Cerebral oedema: mannitol
73
Q

What do you need to remember when prescribing in liver failure?

A
  • Avoid:
    • opiates
    • oral hypoglycaemics
    • Na-containing IVI
  • Warfarin effects ↑
  • Hepatotoxic drugs:
    • paracetamol
    • methotrexate
    • isoniazid
    • salicylates
    • tetracycline
74
Q

What are poor prognostic factors in liver failure?

A
  • Grade 3/4 hepatic encephalopathy
  • Age >40yrs
  • Albumin <30g/L
  • ↑INR
  • Drug-induced liver failure
75
Q

What types of liver transplant are there and what are the criteria?

A
  • Types
    • Cadaveric: heart-beating or non-heart beating
    • Live: right lobe
  • Kings College Hospital Criteria in Acute Failure
    • Paracetamol-induced
      • pH< 7.3 24h after ingestion
      • Or all of:
        • PT > 100s
        • Cr > 300uM
        • Grade 3/4 encephalopathy
    • Non-paracetamol
      • PT > 100s
      • Or 3 out of 5 of:
        • Drug-induced
        • Age <10 or >40
        • >1wk from jaundice to encephalopathy
        • PT > 50s
        • BR ≥ 300uM
76
Q

What are the causes of cirrhosis?

A
  • Common
    • Chronic EtOH
    • Chronic HCV (and HBV)
    • Non-alcoholic fatty liver disease / Non-alcoholic steatohepatitis
  • Other
    • Genetic: Wilson’s, α1ATD, HH, CF
    • AI: AH, PBC, PSC
    • Drugs: Methotrexate, amiodarone, methyldopa, INH
    • Neoplasm: HCC, mets
    • Vasc: Budd-Chiari, RHF, constrictive pericarditis
77
Q

What are the clinical signs of cirrhosis?

A
  • Hands
    • Clubbing (± periostitis)
    • Leuconychia (↓ albumin)
    • Terry’s nails (white proximally, red distally)
    • Palmer erythema
    • Dupuytron’s contracture
  • Face
    • Pallor: ACD
    • Xanthelasma: PBC
    • Parotid enlargement (esp. c¯ EtOH)
  • Trunk
    • Spider naevi (>5, fill from centre)
    • Gynaecomastia
    • Loss of 2º sexual hair
  • Abdo
    • Striae
    • Hepatomegaly (may be small in late disease)
    • Splenomegaly
    • Dilated superficial veins (Caput medusa)
    • Testicular atrophy
78
Q

What complications can occur with cirrhosis?

A
  • Decompensation → Hepatic Failure
    • Jaundice (conjugated)
    • Encephalopathy
    • Hypoalbuminaemia → oedema + ascites
    • Coagulopathy → bruising
    • Hypoglycaemia
  • SBP (spontaneous bacterial peritonitis)
  • Portal Hypertension: SAVE
    • Splenomegaly
    • Ascites
    • Varices
      • Oesophageal varices (90% of cirrhotics)
      • Caput medusa
      • Worsens existing piles
    • Encephalopathy
  • ↑ risk of HCC
79
Q

What investigations would you order for a patient with cirrhosis?

A
  • Bloods
    • FBC: ↓WCC and ↓ plats indicate hypersplenism
    • ↑LFTs
    • ↑INR
    • ↓Albumin
  • Find Cause
    • EtOH: ↑MCV, ↑GGT
    • NASH: hyperlipidaemia, ↑ glucose
    • Infection: Hep, CMV, EBV serology
    • Genetic: Ferritin, α1AT, caeruloplasmin (↓ in Wilson’s)
    • Autoimmune: Abs (there is lots of cross-over)
      • AIH: SMA, SLA, LKM, ANA
      • PBC: AMA
      • PSC: ANCA, ANA
      • Ig: ↑IgG – AIH, ↑IgM – PBC
    • Ca: α-fetoprotein
  • Abdo US + PV Duplex
    • Small / large liver
    • Focal lesions
    • Reversed portal vein flow
    • Ascites
  • Ascitic Tap + MCS
    • PMN >250mm3 indicates SBP
  • Liver biopsy
80
Q

How should a patient with cirrhosis be managed?

A
  • General
    • Good nutrition
    • EtOH abstinence: baclofen helps ↓ cravings
    • Colestyramine for pruritus
    • Screening
      • HCC: US and AFP
      • Oesophageal varices: endoscopy
  • Specific
    • HCV: Interferon-α
    • PBC: Ursodeoxycholic acid
    • Wilson’s: Penicillamine
  • Complications
    • Varices: OGD screening + banding
    • HCC: US + AFP every 3-6mo
  • Decompensation
    • Ascites: fluid and salt restrict, spiro, fruse, tap, daily wt
    • Coagulopathy: Vit K, platelets, FFP, blood
    • Encephalopathy: avoid sedatives, lactulose ± enemas, rifaximin
    • Sepsis / SBP: tazocin (avoid gent: nephrotoxicity)
    • Hepatorenal syndrome: IV albumin + terlipressin
81
Q

What grading system is used for cirrhosis?

A

Child-Pugh Grading of Cirrhosis

  • Predicts risk of bleeding, mortality and need for Tx
  • Graded A-C using severity of 5 factors
    • Albumin
    • Bilirubin
    • Clotting
    • Distension: Ascites
    • Encephalopathy
  • Score >8 = significant risk of variceal bleeding
82
Q
A

Medicine AS (16 decks)

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