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GI Flashcards

1
Q

Causes of bloody diarrhoea

A 
 ischaemic colitis
 campylobacter, shigella, salmonella, E. coli,
amoeba, pseudomembranous colitis
 UC, Crohn’s
 CRC, polyps
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2
Q

Causes of pus in stools

A

IBD, diverticulitis, abscess

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3
Q

Management for diarrhoea

A

Treat cause

Oral or IV rehydration

Codeine phosphate or loperamide after each loose stool

Anti-emetic if assoc. n/v: e.g. prochlorperazine

Abx (e.g. cipro) in infective diarrhoea → systemic illness

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4
Q

What is C.diff

A

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

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5
Q

Risk factors for c.diff infection

A

 Abx: clindamycin, cefs, co-amox, ciprofloxacin
- up to 2m after
 ↑age
 In hospital: ↑ ̄c length of stay, ↑ ̄c C. diff +ve contact
 PPIs

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6
Q

Clinical presentation of infection with c.diff

A 
 Asymptomatic
 Mild diarrhoea
 Colitis 
 Pseudomembranous colitis
- fever, dehydration, abdo pain, bloody diarrhoea, mucus PR
 Fulminant colitis
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7
Q

Investigations for c.diff

A

 Bloods: ↑↑CRP, ↑↑WCC, ↓albumin, dehydration
 CDT ELISA -toxin A&B
 Stool culture

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8
Q

Complications of c.diff infection

A

 Paralytic ileus
 Toxic dilatation → perforation
 Multi-organ failure

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9
Q

Management of c.diff

A

Barrier nursing - put in side room
 Stop causative Abx
 Avoid antidiarrhoeals and opiates
 Enteric precautions

1st line: Metronidazole 2wk 2nd line: Vanc 125mg
Severe: Vanc 1st

Urgent colectomy may be needed if
 Toxic megacolon
 ↑ LDH
 Deteriorating condition

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10
Q

Causes of constipation

A 
OPENED IT
Obstruction - mechanical (adhesion/hernia/ca) or post op ileus
Pain - fissure
Endocrine/ electrolytes - ↓T4, ↓Ca, ↓K, uraemia
Neuro - MS, Myelopathy, Cauda Equina
Elderly
Diet/ Dehydration
IBS
Toxins - opiods
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11
Q

Management of constipation

A

 Drink more
 ↑ dietary fibre

Bulking: ↑ faecal mass → ↑ peristalsis - fybogel (Ispaghula husk)
 CI: obstruction and faecal impaction

Osmotic: retain fluid in the bowel - Lactulose

Stimulant: ↑ intestinal motility and secretion - Senna
 CI: obstruction, acute colitis
 SE: abdo cramps

Softeners
 For painful anal condition - Liquid paraffin

Phosphate enema (osmotic)

Suppositories
 Glycerol (stimulant)

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12
Q

Diagnosis of IBS

A

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

 \+2of:
 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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13
Q

Management of IBS

A

Bloods - incl Coeliac and TSH
+/- colonoscopy

  • Exclusion diets can be tried
  • Fybogel for constipation and diarrhoea
  • Antispasmodics for colic/bloating (e.g. mebeverine)
  • Amitriptyline may be helpful
  • CBT
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14
Q

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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15
Q

Presentation of dysphagia

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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16
Q

Signs that dysphagia could present with

A 
 Cachexia
 Anaemia
 Virchow’s node (+ve = Troisier’s sign)
 Neurology
 Signs of systemic disease (e.g. scleroderma)
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17
Q

Investigations for dysphagia

A

URGENT upper GI endoscopy +- biopsy (if >55, with weight loss, abdo pain, dyspepsia)

 Bloods: FBC, U+E
 Barium swallow ± video fluoroscopy
 Oesophageal manometrry
 +- USS/EUS/CT thorax

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18
Q

Pathophysiology of achalasia

A

 Degeneration of myenteric plexus (Auerbach’s)
 ↓ peristalsis
 LOS fails to relax
- most commonly idiopathic

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19
Q

Presentation of achalasia

A

 Dysphagia: liquids and solids at same time
 Regurgitation
 Substernal cramps
 Wt. loss

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20
Q

Investigations for achalasia

A

 Ba swallow: dilated tapering oesophagus (Bird’s beak)
 Manometry: failure of relaxation + ↓ peristalsis
 CXR: may show widended mediastinum
 OGD: exclude malignancy

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21
Q

Rx of achalasia

A

 Med: CCBs, nitrates
 Int: endoscopic balloon dilatation, botulinum toxin injection
 Surg: Heller’s cardiomyotomy (open or endo)

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22
Q

Pharyngeal pouch pathophysiology

A

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.

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23
Q

Presentation and rx of a pharyngeal pouch

A

Pres: regurgitation, halitosis, gurgling sounds

Rx: excision, endoscopic stapling

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24
Q

Diffuse oesophageal spasm presentation

A

 Intermittent chest pain ± dysphagia

 Ba swallow shows corkscrew oesophagus

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25
Q

Nutcracker oesophagus presentation

A

 Intermittent dysphagia ± chest pain

↑ contraction pressure ̄c normal peristalsis

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26
Q

Causes of an oesophageal rupture

A
  • Iatrogenic - endoscopy, biopsy, dilatation
  • violent emesis (boerhaave’s syndreom)
  • carcinoma
  • Trauma (surgical emphysema ±pneumothorax)
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27
Q

Features of oesophageal rupture

A
  • Odonophagia
  • Mediastinitis (tachypnoea, dyspnoea, fever, shock)
  • surgical emphysema
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28
Q

management of oesophageal rupture

A

PPI, Abx, NGT

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29
Q

Symptoms of dyspepsia

A 
 Epigastric pain
 Bloating
 Heartburn
ALARM
 Anaemia
 Loss of wt.
 Anorexia
 Recent onset progressive symptoms
 Melaena or haematemesis
 Swallowing difficulty
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30
Q

Causes of dyspepsia

A

 Inflammation: GORD, gastritis, PUD
 Ca: oesophageal, gastric
 Functional: non-ulcer dyspepsia

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31
Q

Management of new onset dyspepsia

A 
OGD if >55 or ALARMS
- Try conservative for 4 weeks 
> stop NSAIDS, CCBS
> Lose wt., stop smoking, ↓ EtOH
>  Avoid hot drinks and spicy food
>  OTC - Antacids/gaviscon
  • Test for H. pylori if no improvement: breath or serology
     +ve → eradication therapy
     -ve → PPI trial for 4wks

OGD if no improvement

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32
Q

Eradication therapy for H.Pylori

A

Triple therapy for 1 week

  • PPI
  • Amoxicillin
  • Clarithromycin
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33
Q

Presentation of Duodenal Ulcers v gastric ulcers

A 
DU
Epigastric pain:
 Before meals and at night 
 Relieved by eating or milk
GU
 Epigastric pain:
 Worse on eating
 Relieved by antacids 
 Wt. loss
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34
Q

Risk factors for PUD

A 
H. pylori (90%)
 Drugs: NSAIDs, steroids
 Smoking
 EtOH
 gastric emptying (↑ DU, ↓GU)
 Blood group O (PU)
 Stress -->  Cushings, burns, sepsis, trauma
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35
Q

Complications of PUD

A

Haemorrhage
 Haematemeis or melaena
 Fe deficiency anaemia

Perforation
 Peritonitis and distension, vomiting

Gastric Outflow Obstruction
 Vomiting, colic, distension, succission splash

Malignancy
 ↑ risk ̄c H. pylori

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36
Q

Investigations for PUD

A

 Bloods: FBC, urea (↑ in haemorrhage)
 C13 breath test
 OGD (stop PPIs >2wks before)
 Campylobacter-like organism test (CLO) / urease test for H. pylori (urea –> CO2 + ammonia - neutralises stomach acid)
 Biopsy ulcer to check for Ca
 Gastrin levels if Zollinger-Ellison suspected

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37
Q

Conservative Management of PUD

A 
 Lose wt.
 Stop smoking and ↓ EtOH
 Avoid hot drinks and spicy food
 Stop drugs: NSAIDs, steroids
 OTC antacids
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38
Q

Medical management of PUD

A 
 OTC antacids: Gaviscon, Mg trisilicate
 H. pylori eradication
 Full-dose acid suppression for 1-2mo
 PPIs: lansoprazole 30mg OD
 H2RAs: ranitidine 300mg nocte
 Low-dose acid suppression PRN
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39
Q

Surgical management of PUD

A

 No acid → no ulcer
 Acid secretion
stimulated by gastrin and vagus N.

Vagotomy +/- antrectomy ( distal half of stomach removed)

Subtotal gastrectomy

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40
Q

Complications of gastric surgery

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

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41
Q

Pathophysiology of GORD

A

LOS dysfunction → reflux of gastric contents → oesophagitis.

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42
Q

Risk factors for GORD

A 
 Hiatus hernia
 Smoking
 EtOH
 Obesity
 Pregnancy
 Drugs: anti-AChM, nitrates, CCB, TCAs
 Iatrogenic: Heller’s myotomy
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43
Q

Symptoms of GORD

A 
Oesophageal
 Heartburn
 Related to meals
 Worse lying down / stooping
 Relieved by antacids
 Belching
 Acid brash, water brash
 Odonophagia
 Hoarseness

Extra-oesophageal
 Nocturnal asthma
 Chronic cough
 Laryngitis, sinusitis

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44
Q

Anti- reflux mechanisms

A
  • LOS
  • Angle of His
  • Pressure in abdominal cavity higher than thoracic
  • R crus of diaphragm acts as a sling around oesophagus
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45
Q

Complications of GORD

A

 Oesophagitis: heartburn
 Ulceration: rarely → haematemesis, melaena, ↓Fe
 Benign stricture: dysphagia
 Barrett’s oesophagus
- metaplasia of squamous to gastric columnar epithelium and goblet cell
 Oesophageal adenocarcinoma
- Metaplasia → dysplasia → adenocarcinoma

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46
Q

Differential diagnosis of GO reflux

A 
Oesophagitis
 Infection: CMV, candida
 IBD
 Caustic substances / burns
PUD 
Oesophageal Ca
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47
Q

Investigations for GORD

A 
Isolated - no 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 (A-D)
Classification
Ba swallow: hiatus hernia, dysmotility 24h pH testing ± manometry
 pH <4 for >4hrs (demeester score)
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48
Q

Conservative management of 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
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49
Q

Medical management of GORD

A 
 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
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50
Q

Surgical management, indications and complications of GORD

A 
Nissen Fundoplication - Mobilise gastric fundus and wrap around lower
oesophagus
- Indications: all 3 of:
 Severe symptoms
 Refractory to medical therapy
 Confirmed reflux (pH monitoring)
Complications 
- Gas-bloat syn.: inability to belch / vomit
- Dysphagia if wrap too tight
OTHER
Radiofrequency ablation. magnetic beads
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51
Q

Classifications of hiatus hernias

A

Sliding (80%)
 GOJ slides up into chest
 assoc.GORD

Rolling (15%)
 GOJ remains in abdomen but a bulge of stomach rolls into chest alongside the oesophagus
 LOS remains intact so GORD uncommon
 Can → strangulation

Mixed (5%)

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52
Q

Gastric volvulus symptoms

A

Borchardt’s triad

  • severe epigastric pain
  • retching without vom
  • inability to pass NG tube
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53
Q

Ix for hiatus hernia

A

OGD: assess for oesophagitis and upwards displacement GOJ

CXR: gas bubble and fluid level in chest

24h pH + manometry: exclude dysmotility or achalsia

Ba Swallow

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54
Q

Rx of hiatus hernias

A

Lose wt.

Rx reflux

Surgery if intractable symptoms despite medical Rx OR rolling
- funoplication/ curoplasty

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55
Q

Risk factors for hiatus hernia

A 
Age (reduced diaphragm tone)
raised intra-abdo pressure
0 pregnancy
0 obesity 
0 ascites
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56
Q

Differentials of Haematemesis

A

VINTAGE

Varices
Inflammation (PUD/ oesopha/gastr- itis)
Neoplasia (oesoph/gastric)
Trauma (Mallory-weiss/ Boerhavve)
Angiodysplasia/ HHT/ Dieulafoy lesion
Generalised bleeding diathesis - warfarin, thrombolytics, CRF
Epistaxis
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57
Q

Difference between mallory-weiss and boerhaave’s

A

Mallory-Weiss - mucosal Tear
Boerhaave’s Syndrome - Full-thickness tear
 2cm proximal to LOS

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58
Q

Signs on examination after an Upper GI bleed

A 
 Signs of CLD - telangectasia, purpura, jaundice 
 PR:melaena
 Shock?
 - Cool, clammy, CRT>2s
-  ↓BP (<100) or postural hypotension (>20 drop)
-  ↓ urine output (<30ml/h)
- Tachycardia
-  ↓GCS
- ↓ JVP
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59
Q

What is the Rockall score

A 
Prediction of re-bleeding and mortality after Upper GI bleed
- 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

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60
Q

Pathology of oesophageal varices

A

Portal HTN → dilated veins @ sites of porto-systemic anastomosis: L. gastric and inferior oesophageal veins

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61
Q

Causes of portal hypertension

A

Pre-hepatic: portal vein thrombosis

Hepatic: cirrhosis (80% in UK), schisto (commonest
worldwide), sarcoidosis.

Post-hepatic: Budd-Chiari, RHF, constrict pericarditis

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62
Q

Management of oesophageal varices

A
  • bleed prevention
     1: β-B, repeat endoscopic banding
     2: β-B, repeat banding, TIPSS (Transjugular Intrahepatic Porto-Systemic Shunt)
  • IR creates artificial channel between hepatic vein and portal vein → ↓ portal pressure.
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63
Q

Management of an Upper GI bleed

A
  • Head-down
  • High flow oxygen + protect airway
  • 2 x 14G cannulae + IV bolus
  • Bloods: FBC, U+E (↑ urea), LFTs, clotting, x-match 6u, ABG, glucose
  • if remains shocked - o- blood
  • notify surgeons if severe

IF VARICEAL BLEED - Terlipressin IV (splanchnic vasopressor)
 Prophylactic Abx: e.g. ciprofloxacin 1g/24h

Urgent endoscopy
- Haemostasis of vessel or ulcer:
 Adr injection; Thermal coagulation; Fibrin glue; Endoclips

Variceal bleeding:
 2 of: banding, sclerotherapy, adrenaline,
coagulation
 Balloon tamponade  ̄c 
 TIPSS
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64
Q

Indications for surgery after Upper GI bleed

A

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

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65
Q

Risk factors for oesophageal cancer

A
  • alcohol
  • smoking
  • achalasia
  • GORD
  • Fatty diet
  • Low vit A/C
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66
Q

Pathophysiology of oesophageal cancer

A
  • 65% adenocarcinoma - lower 3rd

- 35% SCC - upper and middle 3rd

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67
Q

Presentation of oesophageal cancer

A
  • Progressive dysphagia
  • weight loss
  • retrostrenal chest pain and dyspepsia
  • lymphadenopathy
  • hoarseness (recurrent laryngeal n invasion)
  • cough +/- aspiratino pneumonia
  • odonophagia
  • mets - jaunice, hepatomegaly, ascites
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68
Q

Ix for oesophageal cancer

A

OGD + biopsy
- Bloods
- Staging CT
EUS - t stage

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69
Q

Staging used for oesophageal cancer

A 
TMN 
T1 - submucosa
T2 - muscularis propria
T3 - adventitia
T4 - adjacent structures
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70
Q

Causes of perforation

A

Inflammatory

  • chemical - PUD, Foreign body
  • infection - appendicitis, diverticulitis, meckels, cholecystitis,
  • ischaemia - mesenteric,, obstructive Ca, Bezoar, faeces
  • colitis - fistula, toxic megacolon

Traumatic

  • iatrogenic - surgery. endoscopy
  • penetrating force
  • direct rupture - booerhavve/ mallory weiss
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71
Q

Ix for perforated GIT

A
  • Blood - FBC, Amylase, CRP, clotting, ABG
  • urine dipstick
  • Erect CXR (erect 15min)
  • AXR - (riglers and psoas sign)
  • CT scan
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72
Q

Mx of Perforated PU

A
  • A-E
  • NBM
  • fluid resuscitation
  • catheter +/- CVP line
  • analgesia
  • Abx
  • NGT

+/- surgery is systemically unwell - abdominal washout and repair (patch - DU); may require gastrectomy

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73
Q

Ix for gastric outflow obstruction

A
  • ABG - hypercholraemic hypokalaemic met alkalosis
  • AXR (dilated gastric air bubble air fluid level, collapsed distal bowel)
  • OGD
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74
Q

Rx for gastric outflow obstruction

A
  • correct metabolic abnormalities
  • benign –> endscopic ballow dilation/ gastroenterostomy
  • malignant - stent/ resection
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75
Q

Risk factors for gastric cancer

A
  • atrophic gastritis - pernicious anaemia, h.pylori)
  • diet high nitrates
  • smoking and alcohol
  • blood group A
  • low social class
  • familial - E cadherin abnormality
  • partial gastrectomy
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76
Q

Pathology of gastric cancer

A

Mainly adenocarcinomas, located on gastric antrum

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77
Q

Symptoms of gastric cancer

A
  • weight loss + anorexia
  • dyspepsia
  • dysphagia
  • n + v
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78
Q

Signs of gastric cancer

A
  • anaemia
  • epigastric mass
  • jaundice
  • ascites
  • hepatomegaly
  • virchow’s node
  • acanthosis nigricans
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79
Q

Complications of gastric cancer

A
  • perforation
  • upper Gi bleed - haematemesis, melaena
  • gastric outlet obstruction
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80
Q

Ix for gastric cancer

A

URGENT OGD + biopsy
- CXR/USS/ CT - mets
Staging - CT CAP

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81
Q

Complications of gastrectomy

A
  • death
  • anastomotic leak
  • poor QoL
  • Vit B12 def
  • re-operation
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82
Q

describe the excretion of bilirubin

A

Hb → unconjugated to 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.

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83
Q

Causes of pre-hepatic jaundice

A

Excess BR production
 Haemolytic anaemia
 Ineffective erythropoiesis
 e.g. thalassaemia

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84
Q

Causes of Hepatic jaundice

A 
Unconjugated 
↓ BR Uptake
 Drugs: contrast, RMP  CCF
↓ BR Conjugation
 Hypothyroidism
 Gilbert’s (AD)
 Crigler-Najjar (AR)
Neonatal jaundice is both ↑ production + ↓ conjug.
Hepatocellular Dysfunction
 Congen: HH, Wilson’s, α1ATD
 Infection: Hep A/B/C, CMV, EBV
 Toxin: EtOH, drugs
 AIH
 Neoplasia: HCC, mets
 Vasc: Budd-Chiari1
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85
Q

Causes of post-hepatic jaundice

A 
Obstruction
 Stones
 Ca pancreas
 Drugs - OCP, sulfonylureas
 PBC
 PSC
 Biliary atresia
 Choledochal cyst
 Cholangio Ca
Inflammatory LN at porta hepatis - TB/ Ca
Mirizzi's syndrome
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86
Q

Ix for Jaundice

A
  • Urine
     pre - No BR (acholuric); ↑ urobilinogen; ↑Hb if intravascular haemolysis
     hepatic - ↑BR; ↑ urobilinogen
     post- ↑↑BR; No urobilinogen
  • LFTs
     pre - ↑uBR; ↑AST; ↑LDH
     hepatic - ↑ cBR (usually); ↑AST:↑ALT; >2=EtOH/ <1=Viral; ↑ GGT (EtOH, obstruction); ↑ALP; Function: ↓ albumin, ↑ PT
     post- ↑↑cBR; ↑AST,↑ALT; ↑↑ALP; ↑GGT
  • Other
     pre - FBC and film, Coombs, Hb electrophoresis
     hepatic - FBC, Ab, a1AT, Liver biopsy
     post - Abdo US (dilated ducts >6mm), ERCP/MRCP; Ab
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87
Q

Causes of liver failure

A
  • cirrhosis
  • 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
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88
Q

Signs of liver failure

A 
 Jaundice
 Oedema + ascites
 Bruising
 Encephalopathy
 Aterixis
 Constructional apraxia (5-pointed star)
 Fetor hepaticus
Signs of cirrhosis / chronic liver disease
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89
Q

Ix for liver failure

A 
Blood
 FBC: infection, GI bleed, ↓ MCV (EtOH)
 U+E - ↓U, ↑Cr: hepatorenal syndrome. Urea synth in liver -->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

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90
Q

Pathophysiology and classification of hepatorenal syndrome

A

 Cirrhosis → splanchnic arterial vasodilatation → effective circulatory volume → RAS activation → renal arterial vasoconstriction.
 Persistent underfilling of renal circulation → failure

 Type 1: rapidly progressive deterioration (survival
<2wks)
 Type 2: steady deterioration (survival ~6mo)

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91
Q

Rx of hepatorenal syndrome

A

 IV albumin + splanchnic vasoconstrictors (terlipressin)
 Haemodialysis as supportive Rx
 Liver Tx is Rx of choice

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92
Q

Mx of liver failure

A

 Manage in ITU
 Rx underlying cause: e.g. NAC in paracetamol OD
 Good nutrition: e.g. via NGT ̄c high carbs
 Thiamine supplements
 Prophylactic PPIs vs. stress ulcers

Monitor - fluids, bloods, glucose

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93
Q

Complications of liver failure

A

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

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94
Q

Drugs to avoid prescribing in liver failure

A

opiates, oral hypoglycaemics, Na-containing IVI

  • Warfarin effects ↑
  • Hepatotoxic drugs: paracetamol, methotrexate,
    isoniazid, salicylates, tetracycline
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95
Q

Poor prognostic factors in liver failure

A 
 Grade 3/4 hepatic encephalopathy
 Age >40yrs
 Albumin <30g/L
 ↑INR
 Drug-induced liver failure
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96
Q

Criteria for liver transplant

A

Kings college

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
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97
Q

Pathophysiology of cirrhosis

A

Irreversible loss of hepatic architecture with bridging fibrosis and nodular regeneration

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98
Q

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 due to dehydration increasing salvia production)

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

Hyperdynamic circualtion

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99
Q

Complications of cirrhosis

A
  • Decompensation –> heptatic failure (jaundice, encephalopathy, ↓Albumin, bruising (↑INR), hypoglycaemia)
  • Spontaneous bacterial peritonitis
- Portal hypertension 
Splenomegaly
Ascites
Varices - oeosphgeal, caput medusa, piles
Encephalopathy
  • ↑ risk of HCC
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100
Q

Ix to find cause of cirrhosis

A 
 EtOH: ↑MCV, ↑GGT
 NASH: hyperlipidaemia, ↑ glucose
 Infection: Hep, CMV, EBV serology
 Genetic: Ferritin, α1AT, caeruloplasmin (↓ in Wilson’s) 
 Abs 
 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

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101
Q

Different Ab in cirrhosis

A

 AIH: SMA, SLA, LKM, ANA
 PBC: AMA
 PSC: ANCA, ANA
 Ig: ↑IgG – AIH, ↑IgM – PBC

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102
Q

Mx of cirrhosis

A 
Good nutrition
EtOH abstinence 
Colestyramine for pruritus
Screening
 HCC: US &amp; AFP every 3-6 m
 Oesophageal varices: endoscopy +/- banding

Specific
 HCV: Interferon-α
 PBC: Ursodeoxycholic acid
 Wilson’s: Penicillamine

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

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103
Q

What is the Child-Pugh Grading score

A

Grades 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

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104
Q

Where are the portosystemic anastomoses

A

Oesophageal varices
- Left and short gastric veins
and Inf. oesophageal veins

Caput medusae
Peri-umbilical veins and Superficial abdo wall veins

Haemorrhoids
Sup. rectal veins and Inf. and mid. Rectal veins

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105
Q

Pathophysiology of Encephalopathy

A

 ↓Hepatic metabolic function
 Diversion of toxins from liver directly into systemic
system.
 Ammonia accumulates and pass to brain where
astrocytes clear it causing glutamate → glutamine
 ↑ glutamine → osmotic imbalance → cerebral oedema

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106
Q

Classification of Encephalopathy

A

 1: Confused – irritable, mild confusion, sleep inversion
 2: Drowsy – ↑ disorientated, slurred speech, asterixis
 3: Stupor – rousable, incoherence
 4: Coma – unrousable, ± extensor plantars

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107
Q

Presentation of encephalopathy

A 
 Asterixis, ataxia
 Confusion
 Dysarthria
 Constructional apraxia
 Seizures
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108
Q

Precipitants of encephalopathy

A 
HEPATICS
 Haemorrhage: e.g. varices
 Electrolytes: ↓K, ↓Na
 Poisons: diuretics, sedatives, anaesthetics
 Alcohol
 Tumour: HCC
 Infection: SBP , pneumonia, UTI, HDV
 Constipation (commonest cause)
 Sugar (glucose) ↓: e.g. low calorie diet
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109
Q

Management of encephalopathy

A

20 degrees head up
- Correct any precipitants
 Avoid sedatives
 Lactulose ± PO4 enemas to ↓ nitrogen-forming bowel
bacteria → 2-4 soft stools/d
 Consider rifaximin PO to kill intestinal microflora

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110
Q

Pathophysiology of ascites

A

Back-pressure → fluid exudation
 ↓ effective circulating volume → RAS activation
 (In cirrhosis: ↓ albumin → ↓ plasma oncotic pressure
and aldosterone metabolism impaired)

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111
Q

Symptoms of ascites

A

Distension → abdominal discomfort and anorexia
 Dyspnoea
 ↓ venous return

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112
Q

Ix for ascites

A

Bloods: FBC, U+E, LFTs, INR, chronic hepatitis screen

US: confirm ascites, liver echogenicity, PV duplex

Ascitic tap
 MCS and AFB
 Cytology
 Chemistry: albumin, LDH, glucose, protein 
 SAAG = serum albumin – ascites albumin

Liver biopsy

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113
Q

Management of ascites

A

 Daily wt. aiming for ≤0.5kg/d reduction
 Fluid restrict <1.5L/d and low Na diet
 Spironolactone + frusemide (if response poor)
 Therapeutic paracentesis ̄c albumin infusion (100ml
20% albumin /L drained)
- Respiratory compromise
- Pain / discomfort
- Renal impairment
 Refractory: TIPSS

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114
Q

Spontaneous bacterial peritonitis

  • causative organisms
  • Ix
  • management
A
  • ascites and peritonitic abdomen
     E. coli, Klebsiella, Streps

Complicated by hepatorenal syn. in 30%

 Ix: ascitic PMN > 250mm3 + MC+S
 Rx: Tazocin or cefotaxime until sensitivities known
 Prophylaxis: high recurrence - cipro long-term

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115
Q

Presentation of an alcoholic

A

 Fatty liver → hepatitits → cirrhosis
 AST:ALT >2, ↑ GGT

GIT
 Gastritis, erosions
 PUD
 Varices
 Pancreatitis
 Carcinoma

CNS
 Poor memory / cognition
 Peripheral polyneuropathy (mainly sensory)
 Wernicke’s encephalopathy
- Confusion; Ophthalmoplegia (nystagmus, LR palsy); Ataxia
 Korsakoff’s: amnesia → confabulation
 Fits, falls

Heart
 Arrhythmias: e.g. AF
 Dilated cardiomyopathy
 ↑BP

Blood
 ↑MCV
 Folate deficiency →anaemia

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116
Q

Screening tool for alcoholics

A 
CAGE
 Cut down?
 Annoyed by people’s criticisms
 Guilty about drinking
 Eye opener?
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117
Q

Features of alcohol withdrawal

A

0-72h after last drink
 Consider in new ward pt (≤3d) ̄c acute confusion

signs

  • Confusion, fits, hallucinations: esp formication (DTs)
  • ↑HR, ↓BP, tremor
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118
Q

Management of alcohol withdrawal

A

Tapering regimen of chlordiazepoxide PO / lorazepam IM

Thiamine

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119
Q

Management of alcholism

A

 Group therapy or self-help (e.g. AA)
 Baclofen: ↓ cravings
 Acamprosate: ↓ cravings
 Disulfiram: aversion therapy

120
Q

Presentation of alcoholic hepatitis

A 
 Anorexia
 D/V
 Tender hepatomegaly
 Ascites
 Severe: Jaundice, bleeding, encephalopathy
121
Q

Ix findings in alcoholic hepatitis

A

 Bloods: ↑MCV, ↑GGT, AST:ALT>2
 Ascitic tap
 Abdo US + PV duplex

122
Q

Management of alcoholic hepatitis

A 
 Stop EtOH
 Rx withdrawal
 High dose B vitamins: Pabrinex
 Optimise nutrition
 Daily wt., LFT, U+E, INR
 Mx complications of failure
123
Q

Score that predicts mortality in alcoholic hepatitis

A

Maddrey score predicts mortality
 Mild: 0-5% 30d mortality
 Severe: 50% 30d mortality
 1yr after admission: 40% mortality

124
Q

Describe the different HBV Ab

A

 HBsAg +ve = current infection
(>6mo = chronic disease)

 HBeAg +ve = high infectivity

 Anti-HBc IgM = recent infection

 Anti-HBc IgG = past infection

 Anti-HBs = cleared infection or vaccinated

125
Q

Presentation of hepatitis B

A

Prodromal phase
 Fever, malaise, arthralgia, nausea, anorexia
 Distaste for cigarettes

Icteric phase
 Jaundice, HSM, lymphadenopathy, cholestasis

Extra-hepatic features due to immune complexes
 Urticaria or vasculitic rash 
 Cryoglobulinaemia
 PAN
 GN
 Arthritis
126
Q

Types of viral hepatitis, causes and how they are spread

A 
A- FO
Seafood, especially abroad
B- IV
Blood, body fluids, babies (vertical)
C- IV
Mainly blood. Less vertical cf. HCV
D- IV
Dependent on prior HBV infection
E- FO
Developing world
127
Q

Management of viral hepatitis

A

A & E - supportive, avoid alcohol, +/- IFN α (fulminant hepatitis)
B - supportive, avoid alcohol, +/- PEGinterferon α2b (chronic disease)
C - PEGinterferon α2b + ribavirin

128
Q

Risk factors for non-alcoholic fatty liver disease

A

 Obesity
 HTN
 T2DM
 Hyperlipidaemia

129
Q

Presentation of NAFLD

A

 Mostly asymptomatic

 Hepatomegaly and RUQ discomfort may be present.

130
Q

Ix and Mx for NAFLD

A

 BMI
 Glucose, fasting lipids
 ↑ transaminases: AST:ALT <1  Liver biopsy

Mx -
 Lose wt.
 Control HTN, DM and lipids

131
Q

Pathophysiology of NAFLD

A 
↑ Fat diet and ↓ exercise 
                   ↓
hepatic steatosis 
                   ↓
↓ FAA ox and ↑ lipogenesis and ↑ lipid export 
                   ↕
Insulin resistance
132
Q

What is Budd-Chiari syndrome and causes

A

Hepatic vein obstruction → ischaemia and hepatocyte damage → liver failure or insidious cirrhosis.

  • hypercoagulable - myeloproliferative, OCP, Anti-PL
  • Local tumour - HCC
133
Q

Presentation of Budd-Chiari syndrome

A

 RUQ pain: stretching of Glisson’s capsule
 Hepatomegaly
 Ascites: SAAG ≥1.1g/dL
 Jaundice (and other features of liver failure)

134
Q

Rx of Budd-Chiari syndrome

A

 Anticoagulate unless there are varices
 Ascites: fluid and salt restrict, spiro, fruse, tap, daily wt
 Other options: thrombolysis, angioplasty, TIPSS
 Transplant if fulminant hepatic failure or cirrhosis
 Rx underlying cause

135
Q

Presentation of AI hepatitis

A 
 Cushingoid: hirsute, acne, striae
 HSM
 Fever/ malaise
 Amenorrhoea
 Polyarthritis
 Pulmonary infiltration 
 Pleurisy
136
Q

Presentation of PBC

A 
 Pruritus and fatigue
 Pigmentation of face
 Bones: osteoporosis, osteomalacia (↓ vit D)
 Big organs: HSM
 Cirrhosis and coagulopathy (↓ vit K)
 Cholesterol ↑: xanthelasma, xanthomata
 Steatorrhoea

Jaundice often occurs late

137
Q

Pathology of PBC

A

Intrahepatic bile duct destruction by chronic

granulomatous inflammation → cirrhosis

138
Q

Rx of PBC

A

Symptomatic
 Pruritus: colestyramine, naltrexone
 Diarrhoea: codeine phosphate
 Osteoporosis: bisphosphonates

Specific
 ADEK vitamins
 Ursodeoxcholic acid: ↓LFTs but no effect on mortality or need for transplant

Liver transplant
 End-stage disease or intractable pruritus
 Recurrence occurs in ~20% but doesn’t usually
→ graft failure.

139
Q

Pathophysiology of PSC

A

Inflammation, fibrosis and strictures and intra- and
extra-hepatic ducts.

Chronic biliary obstruction → secondary biliary cirrhosis → liver failure

140
Q

Presentation of PSC

A

Symptoms
 Jaundice
 Pruritus and fatigue
 Abdo pain

Signs
 Jaundice: dark urine, pale stools
 HSM

141
Q

Complications and associations of PSC

A

 Bacterial cholangitis
 ↑ Cholangiocarcinoma
 ↑ CRC

ASSOCIATED UC
- pANCA +ve

142
Q

Rx of PSC

A

NEED TRANSPLANT
 Pruritus: colestyramine, naltrexone
 Diarrhoea: codeine phosphate

 ADEK vitamins
 Ursodeoxycholic acid improves cholestasis only
 Abx for cholangitis
 Endoscopic stenting for dominant strictures
 Screening - Cholangiocarcinoma: US + Ca19-9 and CRC: colonoscopy

143
Q

Signs and Symptoms of liver tumours

A

Symptoms
 Benign tumours are usually asymptomatic
 Systemic: fever, malaise, wt. loss, anorexia
 RUQ pain: stretching of Glisson’s capsule
 Jaundice is often late, except in cholangiocarcinoma
 May rupture → intraperitoneal haemorrhage

Signs
 Hepatomegaly: smooth or hard and irregular
 Signs of chronic liver disease
 Abdominal mass
 Hepatic bruit (HCC)
144
Q

Pathology of liver tumours

A

90% of liver tumours are 2O metastases
 stomach, lung, colon, breast, uterus

90% of primary tumours are HCC.

145
Q

Causes and Mx of HCC

A

 Viral hepatitis
 Cirrhosis: EtOH, HH, PBC
 Aflatoxins (produced by Aspergillus)

  • resection
  • chemo, percutaneous ablation and embolization
146
Q

Causes of Cholangiocarcinoma

A

 Flukes (Clonorchis)
 PSC
 Congenital biliary cysts
 UC

147
Q

Presentation and Mx of Cholangiocarcinoma

A

 Fever, malaise
 Abdominal pain, ascites, jaundice
 ↑BR, ↑↑ALP

Mx - resect; pallative stent

148
Q

Indications for liver transplant in CLD

A

 Advanced cirrhosis

 HCC

149
Q

Contra- indications for liver transplant in CLD

A 
 Extra-hepatic malignancy
 Severe cardiorespiratory disease
 Systemic sepsis
 HIV infection
 Non-compliance  ̄c drug therapy
150
Q

Complications of liver transplant

A 
Acute rejection (T-cell mediated) 
 50% @ 5-10 days
 Pyrexia, tender hepatomegaly
 ↑ or change immunosuppressants
 Sepsis
 Hepatic artery thrombosis
 CMV infection
 Chronic rejection (6-9mo): shrinking bile ducts 
 Disease recurrence (e.g. HBV)
151
Q

Epidemiology of UC v CD

A

UC - 30s
Smoking protective TH2-mediated
CD - 20s
Smoking ↑ risk TH1/TH17-mediated

152
Q

Macroscopic features of UC v CD

A

> UC
Rectum + colon ± backwash ileitis
Contiguous
No Strictures

> CD
Mouth to anus esp. terminal ileum
Skip lesions
Strictures

153
Q

Microscopic features of UC v CD

A 
> CD
Transmural Inflammation 
Ulcers - Deep, thin, serpiginous → cobblestone mucosa
Marked Fibrosis
Granulomas
Fistulae

> UC
Mucosal Inflammation and Crypt Abscesses
Ulcers - Shallow, broad
Pseudoplyps

154
Q

Presentation of UC v CD

A

Fatigue, anorexia, malaise
 +/- fever
 Abdominal tenderness

UC
 Diarrhoea
 Blood ± mucus PR
 Abdominal discomfort
 Tenesmus, faecal urgency
CD
 Diarrhoea (not usually bloody)
 Abdominal pain
 Wt. loss
 RIF mass, 
 Perianal abscess, fistulae, tag
 anal/rectal stricture
155
Q

Extra-intestinal features of IBD

A 
Apthous ulcers
Pyoderma gangrenosum
Iritis
Erythema nodosum
Sacroilitis
Arthralgia/AS
Clubbing, Ca - Cholang, gall/renal stones
156
Q

Complications of UC

A 
 Toxic megacolon
- Diameter >6cm
-  Risk of perforation
 Bleeding
 Malignancy
- CRC and Cholangiocarcinoma
 Strictures → obstruction
 Venous thrombosis
157
Q

Complications of CD

A

Fistulae

  • Entero-enteric/colonic → diarrhoea
  • Enterovesical → frequency, UTI
  • “pepperpot” anus

Strictures → obstruction
Abscesses
 Abdominal
 Anorectal

Malabsorption
 Fat → Steatorrhoea, gallstones 
 B12 → megaloblastic anaemia 
 Vit D → osteomalacia
 Protein → oedema

Toxic megacolon and Ca may occur (< cf. UC)

158
Q

Ix findings in UC

A

 FBC: ↓Hb, ↑WCC
 LFT: ↓albumin
 ↑CRP/ESR
 Blood cultures

Stool
 MCS: exclude Campy, Shigella, Salmonella, C.diff

Imaging
 AXR: megacolon (>6cm), wall thickening 
 CXR: perforation
 CT
 Ba / gastrograffin enema
- Lead-pipe: no haustra
- Thumbprinting: mucosal thickening
- Pseudopolyps: regenerating mucosal island

Ileocolonoscopy + regional biopsy (at least 2 from 5 sites)

159
Q

Classification of UC severity

A

Mild
Fewer than 4 motions/ day; small amount of blood

Moderate
4-6 motions/ day; mild-severe blood

Severe
6 + motions a day. Visible blood
\+ 1 of: 
Pyrexia
HR >90
Anaemia
Erythrocyte sedimentation rate (mm/hour) > 30
160
Q

Management of acute severe UC

A 
 Resus: Admit, IV hydration, NBM
 Hydrocortisone: IV 100mg QDS + PR; switch to oral when improve then taper
(IV ciclosporin if CI)
 Transfuse if required
 Thromboprophylaxis: LMWH
 Monitoring
-  Bloods: FBC, ESR, CRP, U+E 
- Vitals + stool chart
- Twice daily examination
-  ± AXR
161
Q

Medical management of UC

A 
Inducing Remission 
- 5- ASAs (Mesalasine
- Prednisolone
\+/- suppositories/enemas 
- Infliximab if steroid sparing

Maintaining remission

1) Sulfasalazine/mesalasine (PO/ Topical)
2) Azathioprine/ Mercaptopiurine PO
3) Inflixmab

162
Q

Indications for emergency and elective surgery in UC/CD

A

 Toxic megacolon
 Perforation
 Massive haemorrhage
 Failure to respond to medical Rx

Elective - Chronic symptoms despite medical therapy
- Carcinoma or high-grade dysplasia

163
Q

Surgical management of UC

  • emergency
  • elective
A

Total / subtotal colectomy –> end ileostomy ± mucus fistula

After ~3mo
 Completion proctectomy + Ileal-pouch anal anastomosis (IPAA) or end ileostomy
 Ileorectal anastomosis (IRA)

Elective
 Panproctocolectomy –> end ileostomy or IPAA
 Total colectomy –> IRA

164
Q

Complications after UC surgery

A 
Abdominal
 SBO
 Anastomotic stricture
 Pelvic abscess
Stoma: retraction, stenosis, prolapse, dermatitis 
Pouch
 Pouchitis (50%) (abdo pain, bloody diarrhoea, nausea)
metronidazole + cipro 
 ↓ female fertility
 Faecal leakage
165
Q

Ix for CD

A 
Bloods 
 FBC: ↓Hb, ↑WCC
 LFT: ↓albumin
 ↑CRP/ESR
 Haematinics: Fe, B12, Folate
 Blood cultures

Stool
 MCS: exclude Campy, Shigella, Salmonella, C.diff

Imaging
 AXR: obstruction, sacroileitis
 CXR: perforation
 MRI - severity, pelvic disease and fistula
 Small bowel follow-through or enteroclysis
- Skip lesions
- Cobblestoning: ulceration + mural oedema
- String sign of Kantor: narrow terminal ileum

Endoscopy
 Ileocolonoscopy + regional biopsy

166
Q

Management of a severe CD attack

A

↑temp, ↑HR, ↑ESR, ↑CRP, ↑WCC, ↓albumin

 Resus: Admit, NBM, IV hydration
 Hydrocortisone: IV + PR if rectal disease (switch oral when can)
 Abx: metronidazole PO or IV
 Thromboprophylaxis: LMWH
 Dietician Review - Elemental diet;  Consider parenteral nutrition
 Monitoring
-  Vitals + stool chart
- Daily examination

No improvement –> methotrexate +/- infliximab

167
Q

Medical management of CD

A

Inducing remission

1) Sulfasalazine
2) prednisolone
3) methotrxate
4) infliximab

Maintaining remission

1) azathioprine or mercaptopurine
2) methotrexate
3) Infliximab / adalimumab

168
Q

Indications for surgery in CD

A

Emergency
 Failure to respond to medical Rx
 Intestinal obstruction or perforation
 Massive haemorrhage

Elective
 Abscess or fistula
 Perianal disease
 Chronic ill health  Carcinoma

169
Q

Surgical management of CD

and its complications

A

 Limited resection: e.g. ileocaecal
 Stricturoplasty
 Defunction distal disease ̄c temporary loop ileostomy

Complications
 Stoma complications
 Enterocutaneous fistulae
 Anastomotic leak or stricture
 Short gut syndrome (Steatorrhoea
; ADEK and B12 malabsorption; Bile acid depletion → gallstones; Hyperoxaluria → renal stones)
170
Q

Presentation of coeliac disease

A

GLIAD

GI malabsorption - fatigue and weakness
- n/v/d, abdo distension, colic, flatus, weight loss, steatorrhoea, vit def

Lymphoma and carcinoma
Immune associations - T1DM, IgA def
Anaemia
Dermatitis herpetiformis and apthous ulcers

171
Q

Ix findings in coeliac disease

A
  • Anaemia, ↓alb, vitamin def

- Anti-endomysial IgA Ab and anti-TTG IgG, Anti-gliadin

172
Q

Definition of true and false diverticulum

A

Diverticulum is an outpouching of tubular structure

  • true - composed of complete wall
  • false - composed of only mucosa
173
Q

Pathophysiology of diverticular disease

A
  • Associated with raised intraluminal pressure (low fibre diet, no osmotic effect keeping stool wet)
  • mucosa herniates through muscularis propria at points of weakness where perforating arteries enter
  • most often sigmoid
174
Q

Symptoms of diverticular disease

A
  • altered bowel habit +/- left sided colic (relieved by defecation)
  • nausea
  • flatulence
175
Q

Presentation of diverticulitis

A
  • abdominal pain and tenderness (often LIF, localised peritonitis)
  • pyrexia
176
Q

Pathophysiology of diverticulitis

A
  • inspissated faeces –> obstruction of diverticulum
177
Q

Complications of diverticulitis

A
  • perforation (sudden onset chest pain, peritonitis and shock - air under diaphragm)
  • haemorrhage (PR bleed)
  • abscess (swinging fever, leukocytosis)
  • fistulae
  • strictures
178
Q

Management of acute diverticulitis

A
  • mild - bowel rest (fluids only) + co-amox
  • admit if unwell, cant tolerate fluids and uncontrolled pain

medical

  • NBM
  • IV fluids
  • Analgesia
  • Abx - cefuroxime and metronidazole

Surgery - if perforation haemorrhage, stricture/ obstruction
- hartmanns / resection

179
Q

Hinchley grading of perforation due to diverticulitis

A

1) small confined pericolic abscess
2) large abscess extending into pelvis
2) generalised purulent peritonitis
3) generalised faecal peritonitis

180
Q

Symptoms of B3 (niacin) deficiency

A

Diarrhoea, Dermatitis, Dementia

181
Q

Different types of gallstones

A 
Cholesterol Stones: 20%
 Large
 Often solitary
 Formation ↑ according to Admirand’s Trangle
- ↓ bile salts
- ↓ lecithin
- ↑ cholesterol

Pigment Stones: 5%
 Small, black, gritty, fragile
 Calcium bilirubinate
 Associated c¯ haemolysis

Mixed Stones: 75%
 Often multiple
 Cholesterol is the major component

182
Q

Risk factors for gallstones

A 
 Female
 OCP, pregnancy
 ↑ age
 High fat diet and obesity
 Racial: e.g. American Indian tribes
 Loss of terminal ileum (↓ bile salts)
183
Q

Complications of gallstones

A

In the Gallbladder

  1. Biliary Colic
  2. Acute cholecystitis ± empyema
  3. Chronic cholecytsitis
  4. Mucocele
  5. Carcinoma
  6. Mirizzi’s syndrome

In the CBD

  1. Obstructive jaundice
  2. Pancreatitis
  3. Cholangitis

In the Gut
1. Gallstone ileus

184
Q

Pathogenesis and presentation of biliary colic

A

Gallbladder spasm against a stone impacted in the neck of the gallbladder – Hartmann’s Pouch.

 RUQ pain radiating → back (scapular region)
 Assoc. c¯ sweating, pallor, n/v
 Attacks may be ppted. by fatty food and last <6h
 o/e may be tenderness in right hypochondrium
 ± jaundice if stones passes in to CB

185
Q

Differentials of biliary colic

A

Pancreatitis

Cholecystitis

Bowel Perforation

186
Q

Ix for gallstone disease

A

 Urine: bilirubin, urobilinogen, Hb
 Bloods: FBC, U+E, amylase, LFTs, G+S, clotting, CRP

Imaging
 AXR: 10% of gallstones are radio-opaque
- pneumobilia - gas froming infection
 eCXR: look for perforation
 US:
- Stones: acoustic shadow
- Dilated ducts: >6mm
- Inflamed GB: wall oedema

 If Dx uncertain after US - HIDA cholescintigraphy: shows failure of GB filling
(requires functioning liver)

 If dilated ducts seen on US → MRCP

187
Q

Management of biliary colic

A

Conservative
 Rehydrate and NBM
 Opioid analgesia: morphine 5-10mg/2h max
 High recurrence rate - surgical Rx favoured

Surgical
 As for conservative + either:
 Urgent lap chole (same admission)
 Elective lap chole @ 6-12wks

188
Q

Differences between biliary colic, acute cholecystitis and Ascending cholangitis

A

All - RUQ
Fever - Acute cholecystitis and ascending cholangitis
Jaundice - Ascending cholangitis

189
Q

Pathogenesis of acute cholecystitis

A

Stone or sludge impaction in Hartmann’s pouch

 → chemical and / or bacterial inflammation

190
Q

Complications of acute cholecystitis

A
  1. recurrence
  2. Gangrene and rarely perforation
  3. Chronic cholecystitis
  4. Empyema
191
Q

Symptoms and signs of Acute Cholecystitis

A 
Symptoms
 Severe RUQ pain
-  Continuous
- Radiates to right scapula and epigastrium
 Fever
 Vomiting 
Signs
 Local peritonism in RUQ
 Tachycardia c¯ shallow breathing
 ± jaundice
 Murphy’s sign
- 2 fingers over the GB and ask pt. to breath in → pain and breath catch. Must be –ve on the L
192
Q

Management of acute cholecystitis

A 
Conservative
 NBM
 Fluid resuscitation
 Analgesia: paracetamol, diclofenac, codeine
 Abx: cefuroxime and metronidazole
 80-90% settle over 24-48h
 Deterioration: perforation, empyema

Surgical
 May be elective surgery @ 6-12wks (↓ inflam)
 If <72h, may perform lap chole in acute phase

Empyema
 High fever
 RUQ mass
 Percutaneous drainage: cholecystostomy

193
Q

Symptoms of chronic cholecystitis

A 
Flatulent Dyspepsia
 Vague upper abdominal discomfort
 Distension, bloating
 Nausea
 Flatulence, burping
 Symptoms exacerbated by fatty foods
- CCK release stimulates gallbladder
194
Q

Differentials of chronic cholecystitis

A

 PUD
 IBS
 Hiatus hernia
 Chronic pancreatitis

195
Q

Ix findings from chronic cholecystitis

A

 AXR: porcelain gallbladder

 US: stones, fibrotic, shrunken gallbladder

196
Q

Mx of chronic cholecystitis

A

 Medical - Bile salts (not very effective)
 Surgical
- Elective cholecystectomy
- ERCP first if US shows dilated ducts and stones

197
Q

What is a mucocele

A

Neck of gallbladder blocked by stone but contents
remains sterile
 Can be very large → palpable mass
 May become infected → empyema

198
Q

What is Mirizzi’s syndrome

A

Large stone in GB presses on the common hepatic duct
→ obstructive jaundice.
 Stone may erode through into the ducts

199
Q

Pathogenesis, symptoms and mx of gallstone ileus

A 
Large stone (>2.5cm) erodes from GB → duodenum
through a cholecysto-duodenal fistula secondary to chonic inflam.
 May impact in distal ileum → obstruction
Symptoms
Rigler’s Triad:
 Pneumobiliia
 Small bowel obstruction
 Gallstone in RLQ

Mx - stone removal via enterotomy

200
Q

management of gallstones

A 
Conservative
 Monitor LFTs: passage of stone may → resolution
 Vitamins ADEK
 Analgesia
 Cholestyramine

Interventional
 If: no resolution, worsening LFTs or cholangitis
 ERCP c¯ sphincterotomy and stone extraction

Surgical
 Open / lap stone removal c¯ T tube placement
 T tube cholangiogram 8d later to confirm
stone removal.
 Delayed cholecystectomy to prevent recurrence

201
Q

Features of ascending cholangitis

A

Charcot’s triad: fever/rigors, RUQ pain, jaundice

Reynolds pentad: Charcot’s triad + shock + confusion

202
Q

Management of ascending cholangitis

A

 Cef and met
 1st: ERCP
 2nd: Open or lap stone removal c¯ T tube drain

203
Q

Risk factors for pancreatic carcinoma

A 
 Smoking
 Inflammation: chronic pancreatitis
 Nutrition: ↑fat diet
 EtOH
 DM
204
Q

Pathology of pancreatic carcinoma

A 
90% ductal adenocarcinomas
 Present late, metastasise early
- Direct extension to local structures
- Lymphatics
- Blood → liver and lungs
 60% located in head, 25% body, 15% tail
205
Q

Presentation of pancreatic carcinoma

A

 Typically male >60yrs
 Painless obstructive jaundice: dark urine, pale stools
 Epigastric pain: radiates to back, relieved sitting
forward
 Anorexia, wt. loss and malabsorption
 Acute pancreatitis
 Sudden onset DM in the elderly

206
Q

Signs of pancreatic carcinoma

A

 Palpable gallbladder
 Jaundice
 Epigastric mass
 Thrombophlebitis migrans (Trousseau Sign)
 Splenomegaly: PV thrombosis → portal HTN
 Ascites

207
Q

Courvoisier’s Law

A

In the presence of painless obstructive jaundice, a

palpable gallbladder is unlikely to be due to stones.

208
Q

Ix for pancreatic carcinoma

A

Bloods: cholestatic LFTs, ↑Ca19-9 (90% sens), ↑Ca

Imaging
 US: pancreatic mass, dilated ducts, hepatic
mets, guide biopsy
 EUS: better than CT/MRI for staging
 CXR: mets
 Laparoscopy: mets, staging

ERCP
 Shows anatomy
 Allows stenting
 Biopsy of peri-ampullary lesions

209
Q

Rx of pancreatic carcinoma

A 
Surgery
 Fit, no mets, tumour ≤3cm (≤10% of pts)
 Whipple’s pancreaticoduodenectomy
 Distal pancreatectomy
 Post-op chemo delays progression
 5ys = 5-14%

Palliation
 Endoscopic / percutaneous stenting of CBD
 Palliative bypass surgery:
– cholecystojejunostomy + gastrojejunostomy
 Pain relief – may need coeliac plexus block

210
Q

Pathophysiology of acute pancreatitis

A

Pancreatic enzymes released and activated in vicious
circle → multi-stage process.

  1. Oedema + fluid shift + vomiting → hypovolaemic
    shock while enzymes → autodigestion and fat necrosis
  2. Vessel autodigestion → retroperitoneal haemorrhage
  3. Inflammation → pancreatic necrosis
  4. Super-added infection: 50% of pts. c¯ necrosis
211
Q

Causes of acute pancreatitis

A

Aetiology
 Gallstones (45%)
 Ethanol (25%)
 Trauma

 Steroids
 Mumps + Coxsackie B
 Autoimmune: e.g. PAN
 Scorpion (Trinidadian)
 Hyperlipidaemia (I and V), ↑Ca, Hypothermia
 ERCP: 5% risk
 Drugs: e.g. thiazides, azathioprine

 Idiopathic (20%): ?microstones

212
Q

Symptoms and signs of acute pancreatitis

A 
Symptoms 
 Severe epigastric pain → back
- May be relieved by sitting forward
 Vomiting 
Signs
 ↑HR, ↑RR
 Fever
 Hypovolaemia → shock
 Epigastric tenderness
 Jaundice
 Ileus → absent bowel sounds
 Grey Turners: flank
 Cullens: periumbilical (tracks up Falciform)
213
Q

Criteria used for acute pancreatitis

A

Glasgow (IMRIE)
- assess severity and predict mortality
1 = mild; 2 = mod; 3 = severe

PaO2 <8kPa 
 Age >55yrs
 Neutrophils >15 x109/L
 Ca2+ <2mM
 Renal function U>16mM
 Enzymes LDH>600iu/L
AST>200 iu/L
 Albumin <32g/L
 Sugar >10mM
214
Q

Criteria for diagnosis of acute pancreatitis

A
  • 2/3
    1) CT
    2) Amylase x 3
    3) epigastric pain radiatating to back
215
Q

Ix findings in acute pancreatitis

A 
Bloods
 FBC: ↑WCC
 ↑amylase (>1000 / 3x ULN) and ↑lipase - ↑ in 80%
- Returns to normal by 5-7d
 U+E: dehydration and renal failure
 LFTs: cholestatic picture, ↑AST, ↑LDH
 Ca2+: ↓
 Glucose: ↑
 CRP: monitor progress, >150 after 48hrs = sev
 ABG: ↓O2 suggests ARDS

Urine: glucose, ↑cBR, ↓urobilinogen

Imaging
 CXR: ARDS, exclude perfed DU
 AXR: sentinel loop, pancreatic calcification
 US: Gallstones and dilated ducts, inflammation
 Contrast CT: Balthazar Severity Score

216
Q

Conservative Mx of acute pancreatitis

A

Manage @ appropriate level: e.g. ITU if severe
 Constant reassessment is key
 Hrly TPR, UO
 Daily FBC, U+E, Ca2+, glucose, amylase ABG

Fluid Resuscitation
- Aggressive fluid resus: keep UO >30ml/h
- Catheter ± CVP
Pancreatic Rest
 NBM
 NGT if vomiting
 TPN may be required if severe to prevent catabolism
Analgesia
- Pethidine via PCA
- Or morphine 5-10mg/2h max
Antibiotics
 Not routinely given if mild
 Used if suspicion of infection or before ERCP
 Penems often used: e.g. meropenem, imipenem

OTHER

  • ARDS: O2 therapy or ventilation
  • EtOH withdrawal: chlordiazepoxide
217
Q

Interventional and surgical management for pancreatitis

A

ERCP + spincheterotomy –> If pancreatitis c¯ dilated ducts 2O to gallstones

Surgery
 Laparotomy + necrosectomy (pancreatic debridement)
 Laparotomy + peritoneal lavage
 Laparostomy: abdomen left open c¯ sterile packs in ITU

218
Q

Indications for surgery in acute pancreatitis

A

 Infected pancreatic necrosis
 Pseudocyst or abscess
 Unsure Dx

219
Q

Early complications of acute pancreatitis

A 
Systemic
 Respiratory: ARDS, pleural effusion
 Shock: hypovolaemic or septic
 Renal failure
 DIC
 Metabolic
 ↓ Ca2+
 ↑ glucose
 Metabolic acidosis
220
Q

Late complications of acute pancreatitis

A

> 1wk: Local
 Pancreatic necrosis
 Pancreatic infection
 Pancreatic abscess
- May form in pseudocyst or in pancreas –> Open or percutaneous drainage
 Bleeding: e.g. from splenic artery –> May require embolisation
 Thrombosis –> Splenic A., GDA or colic branches of SMA
= May → bowel necrosis
- Portal vein → portal HTN
 Fistula formation –> Pancreato-cutaneous → skin breakdown

221
Q

What is a pancreatic pseudocysts and how is it managed

A

Collection of pancreatic fluid in the lesser sac surrounded by granulation tissue
 4-6wks after acute attack
 Persisting abdominal pain
 Epigastric mass → early satiety

Complications
 Infection → abscess
 Obstruction of duodenum or CBD
Ix -->  Persistently ↑ amylase ± LFTs
 DO US / CT

Rx
 <6cm: spontaneous resolution
 >6cm - Endoscopic cyst-gastrostomy OR Percutaneous drainage under US/CT

222
Q

Causes of Chronic Pancreatitis

A 
AGITS
 Alcohol (70%)
 Genetic - CF
 Immune - Lymphoplasmacytic sclerosing pancreatitis (↑IgG4)
 Triglycerides ↑
 Structural - Obstruction by tumour
223
Q

Presentation of Chronic Pancreatitis

A

Epigastric pain
 Bores through to back
 Relieved by sitting back or hot water bottle → erythema ab igne
 Exacerbated by fatty food or EtOH

Steatorrhoea and wt. loss
DM: polyuria, polydipsia
Epigastric mass: pseudocyst

224
Q

Ix for chronic pancreatitis

A

↑ glucose

↓ faecal elastase: ↓ exocrine function

US: pseudocyst

AXR: speckled pancreatic calcifications

CT: pancreatic calcifications

225
Q

Management of acute pancreatitis

A 
Diet
 No EtOH
 ↓ fat, ↑ carb
Drugs
 Analgesia: may need coeliac plexus block
 Enzyme supplements: pancreatin (Creon)
 ADEK vitamins
 DM Rx
Surgery
- Indications
 Unremitting pain
 Wt. loss
 Duct blockage
--> Whipple’s/ endoscopic stenting
226
Q

Complications of chronic pancreatitis

A 
 Pseudocyst
 DM
 Pancreatic Ca
 Pancreatic swelling → biliary obstruction
 Splenic vein thrombosis → splenomegaly
227
Q

Differentials of upper abdominal pain

A
  • cholecystitis (R)
  • pyelonephritis
  • uteric colic
  • hepatitis (R)
  • pneumonia
  • gastric ulcer (L)
228
Q

Differentials of RIF pain

A 
 appendicitis
 Cholecystitis
 Diverticulitis
 Meckel’s diverticulitis
 Cyst accident: torsion, rupture, haemorrhage
 testicular torsion
 Salpingitis / PID
 Ruptured ectopic
 Mesenteric adenitis
 UTI
 Crohn’s 
 Inguinal hernia
229
Q

Causes of LLQ pain

A
  • ureteric colic
  • inguinal hernia
  • IBD
  • UTI
  • Gynaecological
  • testicular torsion
  • diverticulitis
230
Q

Causes of epigastic pain

A
  • PUD
  • Cholecystitis
  • Pancreatitis
  • MI
231
Q

Causes of Peri-umbilical pain

A
  • SI obstruction
  • LI obstruction
  • Appendicitis
  • AAA
232
Q

Features of carcinoid syndrome

A

FIVE HT
 Flushing: paroxysmal, upper body ± wheals
 Intestinal: diarrhoea
 Valve fibrosis: tricuspid regurg and pulmonary stenosis
 whEEze: bronchoconstriction
 Hepatic involvement: bypassed 1st pass metabolism
 Tryptophan deficiency → pellagra (3Ds)

233
Q

Pathogenesis of acute appendicitis

A 
Obstruction of the appendix
 Faecolith most commonly
 Lymphoid hyperplasia post-infection
 Tumour (e.g. caecal Ca, carcinoid)
 Worms (e.g. Ascaris lumbicoides, Schisto)

Gut organisms → infection behind obstruction → oedema → ischaemia → necrosis → perforation
 Peritonitis
 Abscess
 Appendix mass

234
Q

symptoms of acute appendicitis

A

Colicky abdo pain
 Central (visceral irritation)→ localised in RIF ) parietal irritation)
 Worse on movement

 Anorexia
 Nausea (vomiting is rarely prominent)
 Constipation / diarrhoea

235
Q

Signs of appendicitis

A 
 Low-grade pyrexia: 37.5 – 38.5
 ↑HR, shallow breathing
 Foetor oris
 Guarding and tenderness: @ McBurney’s point
- +ve cough / percussion tenderness
 Appendix mass may be palpable in RIF
 Pain PR suggests pelvic appendix. 
Rovsing’s Sign
 Pressure in LIF → more pain in RIF
Psoas Sign
 Pain on extending the hip: retrocaecal appendix
236
Q

Management of acute appendicitis

A
  • Urine dip - Pregnancy test and exclude UTI
  • US - exclude gynae and visialise appendix
  • fluids
  • abx - cef + met
  • analgesia

If uncertain - observe
If certain - appendicetomy

237
Q

Complications of acute appendicitis

A

> Appendix Mass - Abx + NBM
 Resolution of mass → interval appendicectomy
 Exclude a colonic tumour: colonoscopy

> Appendix Abscess
 Mass enlarges, pt. deteriorates - Abx + NBM
 CT-guided percutaneous drainage
 If no resolution, surgery may involve right hemicolectomy.

> Perforation - peritonitis

238
Q

Commonest causes of Small and Large bowel obstruction

- + a non-mechanical cause

A 
SBO
 Adhesions: 60%
 Hernia
 Neoplasm - mets/ lymphoma
LBO
 Colorectal Neoplasia: 60%
 Diverticular stricture: 20%
 Volvulus: 5%
  • paralytic ileus
239
Q

Causes of paralytic ileus

A 
 Post-op - bowel handling/ anesthesia
 Peritonitis
 Pancreatitis/ localised inflammation
 TCAs
 Pseudo-obstruction
 Metabolic: ↓K, ↓Na, ↓Mg, uraemia
 Mesenteric ischaemia
240
Q

Presentation of SB v LB obstruction

A

SBO
Early - Vom and mild distension.
Late - Absolute constipation
Colicky pain every 2-3 minutes

LBO
Early - Abdo pain and distension with absolute constipation
Late - Vomiting and can be faeculant
Colicky Pain every 10-15 minutes

  • constant pain –> strangulation
241
Q

Signs of bowel obstruction

A 
 ↑HR: hypovolaemia, strangulation
 Dehydration, hypovolaemia
 Fever-  inflam disease or strangulation
 Surgical scars
 Hernias
 Mass: neoplastic or inflammatory
 Bowel sounds
- ↑: mechanical obstruction
- ↓: ileus
 PR
- Empty rectum; Rectal mass; Hard impacted stool; Blood from higher pathology
242
Q

Ix for bowel obstruction

A

Bloods
 FBC: ↑WCC
 U+E: dehydration, electrolyte abnormalities
 Amylase: ↑↑ if strangulation/ perforation
 VBG: ↑ lactate - strangulation
 G+S, clotting: ?surgery

Imaging
 Erect CXR
 AXR: ± erect film for fluid levels
 CT: can show transition point

Gastrograffin studies
 Look for mechanical obstruction: no free flow
 Follow through or enema
 Follow through may relieve mild mechanical
obstruction: usually adhesional

Colonoscopy
 Can be used in some cases
 Risk of perforation
 May be used therapeutically to stent

243
Q

Findings on AXR of SBO v LBO

A

SBO
≥3cm; central; Valvulae coniventes; many loops, and many, short fluid levels; LB Gas Absent

LBO
≥6cm (caecum ≥9- emergency if ileocaecal valve working); Peripheral;
Haustra; LB Gas Present; few loops; Few, long fluid levels

244
Q

medical management of bowel obstruction

A

 NBM
 IV fluids: aggressive as pt. may be v. dehydrated
 NGT: decompress upper GIT, stops vomiting, prevents
aspiration
 Catheterise: monitor UO

 Analgesia: may require strong opioid
 Antibiotics: cef+met if strangulation or perforation
 Gastrograffin study: oral or via NGT
 Consider need for parenteral nutrition

 Regular clinical examination is necessary to ensure that
the pt. is not deteriorating.
- ↑ distension/ pain/ tenderness/ ↑ HR/ ↑RR
 Repeat imaging and bloods

245
Q

Indications for surgery in bowel obstruction

A

 Closed loop obstruction
 Obstructing neoplasm
 Strangulation / perforation → sepsis, peritonitis
 Failure of conservative Mx (up to 72h)

246
Q

Surgical management of. bowel obstruction

A

SBO: adhesiolysis

LBO
 Hartmann’s (proctosigmoidectomy)
 Colectomy + 1° anastomosis + on table lavage
 Palliative bypass procedure
 Transverse loop colostomy or loop ileostomy
 Caecostomy

247
Q

Types of stoma

A

Colostomy - flush to skin; LIF

  • loop –> entire loop of colon exteriorised and both proximal and distal end open into common stoma opening and are not transected
  • end –> created from proximal end of colon, distal end stapled/ sewn shut and remains as blind pouch

Ileostomy; RIF; spout as enzymes toxic to skin

  • loop - Loop SI brought out, colon ann rectum removed
  • end - colon and rectum removed, and of ileum brought out
248
Q

Pathophysiology of a sigmoid volvulus and sign on AXR

A

 Long mesentery c¯ narrow base predisposes to torsion
 Usually due to sigmoid elongation 2° to chronic
constipation
 ↑ risk in neuropsych pts.: MS, PD, psychiatric
 Disease or Rx interferes c¯ intestinal motility
→ closed loop obstruction

  • coffee bean sign on AXR
249
Q

Mx of sigmoid volvulus

A

Sigmoidoscopy and flatus tube
insertion

2) Sigmoid colectomy if Failed endoscopic decompression/ Bowel necrosis

250
Q

Presentation and Prevention of paralytic ileus

A

Presentation
 Distension
 Constipation ± vomiting
 Absent bowel sounds

Prevention
 ↓ bowel handling
 Laparoscopic approach
 Peritoneal lavage after peritonitis
 Unstarched gloves
251
Q

Mx of paralytic ileus

A

 NBM
 IV fluids: aggressive as pt. may be v. dehydrated
 NGT: decompress upper GIT, stops vomiting, prevents
aspiration
 Catheterise: monitor UO

Correct any underlying causes
 Drugs
 Metabolic abnormalities
+/- parenteral nutrition

252
Q

What is obstruction and mx

A

Clinical signs of mechanical obstruction but no
obstructing lesion found
 Usually distension only: no colic
- assoc elderly, CR disorders, hip arthroplasty and trauma

Mx - neostigmine and colonoscopic decompressino

253
Q

Pathology and. Presentation of L v R colorectal carcinoma

A

ADENOCARCINOMA

Left
 Altered bowel habit
 PR mass (60%)
 Obstruction (25%)
 Bleeding / mucus PR
 Tenesmus
Right
 Anaemia
 Wt. loss
 Abdominal pain
Either
 Abdominal mass
 Perforation
 Haemorrhage
 Fistula
254
Q

Ix for colorectal carcinoma

A

Bloods
 FBC: Hb - anaemia
 LFTs: mets
 Tumour Marker: CEA (carcinoembryonic Ag) (to monotor disease progression)

Imaging
 CXR: lung mets
 US liver: mets
 CT and MRI (rectal and liver)- staging 
 Endoanal US: staging rectal tumours

Endoscopy + Biopsy
 Flexi sig: 65% of tumours accessible
 Colonoscopy

255
Q

Staging and grading of colorectal carcinomas

A 
Dukes 
A Confined to bowel wall 
B Through bowel wall but no LNs
C Regional LNs 
D Distant mets
TNM
 TIS: carcinoma in situ
 T1: submucosa
 T2: muscularis propria
 T3: subserosa
 T4: through the serosa to adjacent organs
 N1: 1-3 nodes
 N2: >4 nodes

Grade - low - high based on Dysplasia, mitotic index, hyperchromatism

256
Q

Surgical management of colorectal carcinomas

A

o R Hemicolectomy
o Left Hemicolectomy
o Sigmoidcolectomy (Sigmoid colon tumours)
o Anterior Resection (High rectal tumours >5cm from the anus)
o Abdominoperineal (AP) Resection (Low rectal tumours <5cm from the anus)

257
Q

Screening for colorectal carcinoma

A

FOB Testing
 60-75yrs -  Home FOB testing every 2yrs: ~1/50 have +ve FOB
 Colonoscopy if +ve: ~1/10 have Ca

Flexi Sig
 55-60yrs
 Once only flexi Sig

258
Q

Risk factors for CRC

A
  • FAP
  • age (>60yrs)
  • Fhx
  • IBD
  • ↓ fibre diet; ↑processed meat intake
  • smoking
  • ↑ alcohol intake.
259
Q

Presentation of mesenteric ischaemia

A

 Triad
 Acute severe abdominal pain ± PR bleed
 Rapid hypovolaemia → shock
 No abdominal signs

260
Q

Causes of mesenteric ischaemia

A

 Arterial: thrombotic (35%), embolic (35%)
 Non-occlusive (20%)
 Splanchnic vasoconstriction: e.g. 2O to shock
 Venous thrombosis (5%)
 Other: trauma, vasculitis, strangulation

261
Q

Management of mesenteric ischaemia

A
  • Fluids
  • Abx
  • LMWH
  • Laparotomy to resect necrotic bowel
262
Q

Presentation of Chronic Small Bowel Ischaemia

A 
 Severe, colicky post-prandial abdo pain
 “gut claudication”
 PR bleeding
 Malabsorption
 Wt. loss

Mx –> angioplasty

263
Q

Causes of Lower GI bleed

A

 Rectal: haemorrhoids, fissure
 Diverticulitis
 Neoplasm

Other
 Inflammation: IBD
 Infection: shigella, campylobacter, C. diff
 Polyps
 Large upper GI bleed (15% of lower GI bleeds)
 Angio: dysplasia, ischaemic colitis, HHT

264
Q

Mx of Lower GI bleed

A

 Resuscitate
 Urinary catheter
 Abx: if evidence of sepsis or perf
 PPI: if upper GI bleed possible
 Keep bed bound: need to pass stool may be large bleed
→ collapse
 Stool chart
 Diet: keep on clear fluids (allows colonoscopy)
 Surgery: only if unremitting, massive bleed

265
Q

Pathophysiology of Haemorrhoids

A

Anal cushion: mass of spongy vascular tissue - Positioned @ 3, 7 and 11 O’clock
 Where the 3 major arteries that feed the vascular plexuses enter the anal canal

 Gravity, straining (+pregnancy, portal HTN) → engorgement and enlargement of
anal cushions

 Hard stool disrupts CT around cushions.
 Cushions protrude and can be damaged by hard stool → bright red (capillary) bleeding.

266
Q

Classification of haemorrhoids

A

 1st degree: never prolapse
 2nd: prolapse on defecation but spontaneously reduce
 3rd: prolapse on defecation but require digital reduction
 4th: remain permanently prolapsed

267
Q

Symptoms of haemorrhoids

A 
 Fresh painless PR bleeding
- Bright red
 Pruritis ani
 Lump in perianal area
 Severe pain = thrombosis
268
Q

Mx of haemorrhoids

A

 ↑ fibre and fluid intake
 Stop straining @ stool

Medical
 Anusol: hydrocortisone
 Topical analgesics
 Laxatives: lactulose, Fybogel

Interventional
 Injection c¯ sclerosant - above dentate line - SE: impotence, prostatitis
 Barron’s banding → thrombosis and separation - SE: bleeding, infection
 Cryotherapy - SE: watery discharge post-procedure
 Infra-red coagulation

Surgical:  Haemorrhoidectomy
 Excision of piles + ligation of vascular pedicles
 Lactulose + metronidazole 1wk pre-op
 Discharge c¯ laxatives post-op
-  SE: bleeding, stenosis
269
Q

Definition and causes of anal fissures

A

Tear of squamous epithelial lining in lower anal canal

 Mostly trauma 2 ° to the passage of hard stool
- Assoc. c¯ constipation
- Spasm of internal anal sphincter contributes to
pain and → ischaemia + poor healing
 Crohn’s
 Herpes
 Anal Ca

270
Q

Presentation of anal fissures

A 
 Intense anal pain
-  Especially on defecation
-  May prevent pt. from passing stools
- PR impossible
 Fresh rectal bleeding
271
Q

Mx of anal fissures

A

 Soaks in warm bath
 Toileting advice
 Dietary advice: ↑ fibre and fluids

Medical
 Laxatives: lactulose + fybogel
 Topical → resolution in 75%
 Lignocaine/ GTN/ Diltiazem
 Botulinum injection

Surgical: Lateral partial sphincterotomy
 Division of internal anal sphincter @ 3 O’clock
- Complications
 Minor faecal/flatus incontinence (= GTN)/ Perianal abscess

272
Q

Pathogenesis of Fistula in Ano

A

Abnormal connection between ano-rectal canal and the
skin.
- Usually occur 2° to perinanal sepsis
- Blockage of intramuscular glands → abscess → discharges to form a fistula
 Associations
CD, Diverticular disease, Rectal Ca, Immunosuppression

273
Q

Goodsall’s rule for Fistula’s in Ano

A

Fistula anterior to anus track in a straight line (radial)

Fistula posterior to anus always have internal opening
at the 6 o’clock position → curved track

274
Q

Presentation, Rx and Mx of Fistula in Ano

A

Persistent anal discharge
Perianal pain or discomfort

  • Endoanal USS/ MRI

Mx - Low - Fistulotomy and excision –> Laid open to heal by 2° intention
- High - a seton – passed through fistula and gradually
tightened over months

275
Q

Pathogenesis of peri-anal abscess

A

 Anal gland blockage → infection → abscess
E.g. coli, bacteroides
 May develop from skin infections
E.g. sebaceous gland or hair follicle OR Staphs

276
Q

Presentation of peri-anal abscess

A

Throbbing perianal pain - Worse on sitting

Occasionally a purulent anal discharge

Fluctuant mass on PR

Septic signs: fever, tachycardia

277
Q

Rx of peri-anal abscess

A

Abx may suffice if Rx instigated v. early in course

Most cases require EUA - I&D
 Wound packed
 Heals by 2O intention
 Daily dressing for 7-10d

278
Q

Pathophysiology and risk factors of pilonidal sinus

A

Hair works its way beneath skin → foreign body
reaction → formation of abscess
 Usually occur in the natal cleft.

Risk Factors
 M>F=4:1
 Geo: Mediterranean, Middle east, Asians
 Often overweight c¯ poor personal hygiene (sweaty)
 Occupations c¯ lots of sitting: e.g. truck drivers

279
Q

Presentation and Rx of pilonidal sinus

A

 Persistent discharge of purulent or clear fluid
 Recurrent pain
 Abscesses

Rx
 Hygiene advice
 Shave / remove hair from affected area
 Incision and drainage of abscesses
 Elective sinus excision
280
Q

Pathology and Presentation of anal carcinoma

A

 80% SCCs
 Spread
 Above dentate line → internal iliac nodes
 Below dentate line → inguinal nodes

Associated HPV

Presentation
 Perianal pain and bleeding
 Pruritis ani
 Faecal incontinence

281
Q

Ix and Rx of anal carcinoma

A 
Ix
 ↓ Hb (ACD)
 Endoanal US
 Rectal EUA + biopsy
 CT / MRI: assess pelvic spread

Rx
 Chemoradiotherapy: most pts
 Surgery: reserved for
 Tumours that fail to respond to radiotherapy
 GI obstruction
 Small anal margin tumours w/o sphincter involvement

282
Q

Rectal prolapse classification

A

Protrusion of rectal tissue through the anal canal.

Type 1: Mucosal Prolapse
 Partial prolapse of redundant mucosa
Type 2: Full Thickness Prolapse ( elderly)

283
Q

Presentation of rectal prolapse

A

Mass extrudes from rectum on defecation
 May reduce spontaneously or require manual reduction
 May become oedematous and ulcerated → pain and bleeding
 Faecal soiling
 Assoc. c¯ vaginal prolapse and urinary incontinence
↓ sphincter tone on PR

284
Q

Rx of rectal prolapse

A 
Partial Prolapse
 Phenol injection
 Rubber band ligation
 Surgery: Delorme’s Procedure
Complete Prolapse
 Pelvic floor exercises/ Stool softeners
 Rectopexy or Delorme’s Procedure
285
Q

Define a hernia

A

Protrusion of a viscus or part of a viscus through the walls of its containing cavity into an abnormal position

286
Q

Classification of Inguinal hernias

A 
Indirect
 80%: commoner in young
 Congenital patent processus vaginalis
 Emerge through deep ring
 Same 3 coverings as cord and descend into the scrotum
 Can strangulate

Direct
 20%: commoner in elderly
 Acquired ( ↑IAPe.g. Chronic cough/ constipation/ obesity)
 Emerge through Hesselbach’s triangle
 Can acquire internal and external spermatic fascia
 Rarely descend into scrotum
 Rarely strangulate

287
Q

Clinical features of Inguinal hernias

A

Children
 Lump in groin which may descend into scrotum
 Exacerbated by crying
 Commonly obstruct

Adults
 Lump in groin, exacerbated by straining/cough
 May be clear ppting event: e.g. heavy lifting
 Dragging pain radiating to groin
 May present c¯ obstruction/strangulation

288
Q

Mx of Inguinal hernia

A

Non-surgical
 Rx RFs: cough, constipation
 Lose weight
 Truss

Surgical
 Tension-free mesh and suture repair

289
Q

Complications of inguinal hernias

A 
Early
 Haematoma / seroma formation: 10%
 Intra-abdominal injury (lap)
 Infection: 1%
 Urinary retention

Late
 Recurrence (<2%)
 Ischaemic orchitis: 0.5%
 Chronic groin pain / paraesthesia: 5%

290
Q

Femoral hernia pathology

A

Protrusion of viscus through femoral canal (bounded by femoral vein and lacunar ligament) into femoral triangle (inguinal ligament, adductus longus and sartorius)

  • more common in females due to shape of pelvis
  • acquires - increased intra-abdominal pressure
291
Q

Clinical features of a femoral hernia

A

Painless groin lump
 inferior (and lateral) to the pubic tubercle.
 Cough impulse.
 Often irreducible (tight boarders)

Commonly present - obstruction or strangulation
 Tender, red and hot
 Abdo pain, distension, vomiting, constipation

292
Q

Mx of femoral hernia

A

High risk of strangulation

Rx - herniotomy and heniorrhaphy

293
Q

Differntials of femoral hernia

A
  • low inguinal hernia
  • femoral canal lipoma
  • femoral LN
  • saphena varix ( compressible, disappears when flat)
294
Q

Definition and risk factors for incisional hernia

A

Hernia arises through a previously acquired defect
- non- pulsatile, reducible soft and non-tender swelling near site of previous wound

Pre-operative
 ↑ age
 Obesity or malnutrition
 Comorbidities: DM, renal failure, malignancy
 Drugs: steroids, chemo, radio
Intra-operative
 Surgical technique/skill (major factor)
-Too small suture bites
- Inappropriate suture material
 Incision type (e.g. midline)
 Placing drains through wounds

Post-operative
 ↑ IAP: chronic cough, straining, post-op ileus
 Infection
 Haematoma

295
Q

Mx of incisional hernia

A

Conservative
 Manage RFs: e.g. constipation, cough
 Weight loss
 Elasticated corset or truss

Surgical
 Pre-Op
- Optimise cardiorespiratory function
- Encourage wt. loss
 Nylon mesh repair: open or lap

IPE (9 decks)

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