Gastroenterology Flashcards
What does faecal urgency suggest?
Rectal Pathology
Most likely causes of acute diarrhoea? <14 days.
Suspect Gastroenteritis and ask about travel history, their diet and any sick contacts.
- Rotavirus
- Norovirus
- Enteric Adenovirus
Could also be Diverticulitis, antibiotic therapy, constipation overflow.
Cause of a chronic diarrhoea alternating with constipation?
> 14 days.
> 3 loose stools per day for more than 4 weeks.
IBS
Causes of bloody diarrhoea?
Vascular: Ischaemic Colitis
Infection: Camyplobacter jejuni, Shigella, Salmonella, E.coli (enterotoxigenic E.coli).
Inflammatory: UC, Crohn’s
Neoplastic: Colorectal Cancer, Polpys
Causes of mucus with diarrhoea?
IBS
Colorectal Cancer
Polyps
Causes of pus mixed with diarrhoea?
IBD
Diverticulitis
Abscess
Medical causes of diarrhoea?
Increased T4
Autonomic Neuropathy (DM)
Carcinoid
Pancreatic Insufficiency
Drug causes of diarrhoea?
Lactulose abuse Antibiotics PPI, Cimetidine (H2 Antagonist) NSAIDS Digoxin
Investigations for diarrhoea?
Bloods:
- FBC: Increased WWC, Anaemia
- U+E: Decreased K, Dehydration (raised urea)
- Increased ESR: IBD, Oncological
- Increased CRP: IBD, Infection
- Coeliac Serology: Anti-TTG or Anti-Endomysial Abx
Stools:
- MCS and C.Diff
Causes of Chronic Diarrhoea
- Ulcerative Colitis
- Crohns
- Drug Effect
- Coeliac Disease
- Faecal Impaction (overflow Diarrhoea)
Duration of chronic diarrhoea?
- More than 4 weeks
- > 3 loose stools per day
- Waking at night with symptoms (less likely to be functional)
Management of diarrhoea?
- Treat Cause
- Oral or IV rehydration
- Codeine Phosphate or Loperamide (4mg orally, then 2mg after each unformed stool) after each loose stool
- Anti-emetic if associated with n/v e.g prochlorperazine
- Abx (e.g ciprofloxacin 750mg) in infective diarrhoea –> systemic illness
What is C.Diff?
- Gram Positive Spore-forming anaerobe
- Releases enterotoxins A and B
- Spores are V.robust and can survive for >40d
The majority of C.dff infections are caused by what?
- Abx associated Diarrhoea
- 100% of Abx associated pseudomembranous colitis
What are the risk factors of C diff diarrhoea?
Abx:
- Clindamycin
- Cephalosporins
- Augmentin
- Quinolones
- Increased Age
- Increased length of stay at hospital
- Increased contact with C.diff - +ve contact
- PPIs
What is the presentation of C.difficile? diarrhoea?
- Can be asymptomatic
- Mild Diarrhoea
- Colitis w/o pseudomembanes OR
- Pseudomembranous colitis
- Fulminant colitis
- May occur up to 2months after discontinuation of Abx
- May be due to post-surgery where patients are given antibiotics
- Clean surgery involving placement of prosthesis or implant
- clean-contaminated surgery
- contaminated surgery
- Dirty or infected wounds.
What is pseudomembranous colitis?
- Severe systemic symptoms: fever, dehydration.
- Abdominal pain, bloody diarrhoea, mucus PR
- Evidence of pseudomembranes (yellow plaques) on a flexible sigmoidoscopy
- Pseudomembranous colitis is a nonspecific pattern of injury resulting from decreased oxygenation, endothelial damage, and impaired blood flow to the mucosa that can be triggered by a number of disease states.
- Whilst most patients will have this due to C.diff, there may be other causes.
Complications of pseudomembranous colitis?
- Paralytic Ileus (obstruction of the intestine due to paralysis)
- Toxic Dilatation –> Perforation
- Multi-organ failure
Investigations for pseudomembranous colitis/C.diff?
Bloods
- FBC (increased WCC), U+E (increased CRP, dehydration), LFTs (decreased Albumin).
- Stool Culture/PCR
- Abdo X-ray
- Sigmoidoscopy (consider)
What are the categories defining severe C.Diff Diarrhoea?
> 1 of
- Shock
- WCC > 15
- Creatinine >50% above baseline
- Temp >38.5
- Clinical / Radiological evidence of severe colitis.
What is the management of C.diff Diarrhoea?
General
- STOP causative Abx
- Avoid antidiarrhoeals and opiates
- Precautions in the ward
Medical
- 1st line non-severe: metronidazole 500mg 3x OD.
- 1st line severe: Vancomycin 125mg orally 4x daily. Up to 250mg QDS if no response. (Max = 500mg). 2nd line = Van 125mg
May require urgent colectomy if toxic megacolon, Increased LDH, Deteriorating condition.
Repeated
- Repeat Vanc on a tapered and pulsed regimen.
What is the definition of constipation?
- Infrequent bowel motions less than 3/week.
OR - Less often than normal or with difficulty, straining or in pain.
What is the mnemonic to remember the causes of constipation?
OPENED IT
- Obstruction: Mechanical (adhesions, hernia, Ca inflammatory) or Pseudo-obstruction: post-op ileus.
- Pain - Anal Fissure or Proctalgia fugax (sporadic pain)
- Endocrine/Electrolytes: Endo (hypothyroidism), electrolytes (decreased Ca, Decreased K, Uraemia).
- Neuro: MS, Myelopathy (injury to the spinal cord), Cauda equina syndrome.
- Elderly
- Diet/Dehydration
- IBS
- Toxins: Opiods, Anti-mACh
What is the management of constipation < 3 months?
< 3 months?
- Treat underlying cause (medication induced/malignancy).
- Diet + lifestyle + laxatives or prunes/stool softeners.
- Consider Evacuation measures: Enemas, suppositories, macrogols, stimulant laxatives or disimpaction.
Management of constipation > 3 months?
> 3 months
- Treat underlying cause
- Diet + lifestyle advice (fibre and water)
Medical laxatives
- Bulk Laxatives (ispaghula) or methylcellulose.
- 2nd line - Osmotic Laxatives (lactulose, macrogols, magnesium citrate)
- 3rd line - Osmotic laxatives + diet + lifestyle + stimulant laxatives (senna or bisacodyl)
What is the mechanism of action of bulking laxatives?
Increases faecal mass –> Increased peristalsis.
Contraindications to bulking laxatives?
Obstruction or faecal impaction.
Examples of bulking laxatives?
Bran
Ispaghula husk (Fybogel)
Methylcellulose
Examples of Osmotic laxatives?
Lactulose
MgSO4 (rapid)
Mechanism of action of osmotic laxatives?
Retain fluid in the bowel
Examples of stimulant laxatives?
Senna
Bisacodyl PO or PR (10mg)
Sodium picosulphate
Examples of stool softeners?
Docusate sodium (500mg daily)
Indication for a phosphate enema?
Preparation for a flexible sigmoidoscopy
Constipation
Example of a suppository?
Glycerol (stimulant)
Enema Procedure?
- 1 hr before leaving home for day of examination
- Place unopened enema bottle into jug of warm water for 5 mins.
- Lie down on bed with knees to chest
- Insert length of nozzle into your bottom, and squeeze bottle until it is empty.
- Hold for 15 min until urge to open bowels.
What is IBS?
Enhanced visceral perception giving bowel symptoms for which no organic cause can be found.
IBS Diagnostic criteria?
ROME criteria
- At least 1 day per week in the last 3 months, with onset at least 6 months previously, of recurrent abdominal pain or discomfort.
- Associated with 2 or more of the following:
- 1) Improvement with defecation
- 2) Onset associated with change in frequency of stool;
- 3) Onset associated with a change in form of stool
NICE Diagnosis of IBS?
Consider in anyone who has 6 months of:
- Abdo pain
- Bloating OR
- Change in bowel habit.
Diagnosis if a person has abdo pain which is:
- related to defection
- Associated with altered stool frequency (more or less)
- Altered stool form or appearance.
Exclusion criteria for IBS
>40 yrs Bloody stool Anorexia Weight loss Diarrhoea at night
Investigations for IBS?
- Bloods: FBC, ESR, LFTs, Coeliac serology, TSH
- Colonoscopy: if >60yrs or any features of organic disease.
Management for IBS?
- Exclusion diet can be tried (low FODMAP). Try to have regular meals, avoid missing meals, drink 8 cups of water, restrict tea + coffee to 3 cups a day.
According to predominant symptom
pain: antispasmodic agents (merebavine)
constipation: laxatives but avoid lactulose (Linaclotide)
diarrhoea: loperamide is first-line. An opioid receptor agonist which does not have systemic effects.
2nd line:
- Amitriptyline may be helpful. (abdo pain)
- CBT
Definition of dysphagia?
Difficulty swallowing
Inflammatory causes of dysphagia?
Tonsilitis, pharyngitis, oesophagitis (GORD), Oral candidiasis, Aphthous ulcers.
Mechanical luminal causes of dysphagia?
Mechanical block:
- Luminal: (FB, Large food bolus),
Benign mechanical mural causes of dysphagia?
Plummer-Vinson (Web),
Oesophagitis
Trauma (GORD)
Pharyngeal pouch
Malignant mechanical mural causes of dysphagia?
Malignant stricture:
1) Pharynx
2) Oesphagus
3) Gastric
Extra-mural mechanical causes of dysphagia?
Lung Cancer Rolling hiatus hernia Mediastinal LN (Lymphoma) Retrosternal goitre Thoracic aortic aneurysm
Motility disorders causing dysphagia?
Local:
- Achalasia
- Diffuse oesophageal spasm
- Nutcracker oesophagus
- Bulbar/pseudobulbar palsy (CVA, MND)
Systemic:
- Systemic sclerosis/CREST
- MG
What is the presentation of dysphagia?
- Dysphagia for liquids and solids at start? Motility disorder
- If not: solids > liquids: Stricture
- Difficulty making swallowing: bulbar palsy
- Odynophagia: Ca, oesphageal ulcer, spasm
- Intermittent: oesophageal spasm
- Constant and worsening: malignant stricture
- Neck bulges or gurgles on drinking: pharyngeal pouch
Signs of dysphagia?
Cachexia Anaemia Virchow's node (+ve = Troisier's sign) Neurology Signs of systemic disease
Investigations for dysphagia?
Bloods: FBC, U+E
CXR
OGD (Upper GI Endoscopy) - Stop PPI 2 weeks before an upper GI endoscopy.
Barium Swallow ± Video fluroscopy
What is the pathophysiology of achalasia?
- Degeneration of the myenteric plexus (Auerbach’s)
- Decreased peristalsis
- Lower oesophageal sphincter fails to relax
What are the causes of Achalasia?
Primary/Idiopathic: commonest
Secondary: oesophageal Ca, Chagas’ disease (T.cruzii)
What is the presentation of achalasia?
Dysphagia: Liquids and solids at the same time
Arching of neck/standing sitting up straight
Regurgitations
Substernal cramps
Wt Loss
Complications of achalasia
Chronic achalasia –> Oesophageal primary squamous cell carcinoma.
Investigations for achalasia (BBBBM)
Bedside Obs: HR, O2, BP, RR.
Bloods: FBC (Anaemia), U+E (Electrolytes), (TFTs)
Barium swallow: See a dilated tapering oesophagus (Bird’s Beak). Better in older patients.
Manometry: Checking functioning of the oesophageal valve
CXR: Widened mediastinum
OGD: To exclude malignancy and is usually first line.
Management for achalasia?
Intra-sphincteric injection of botulinum toxin
First line: Pneumatic dilation - - Air inflated balloons are used to apply mechanical stretch to the lower oesophageal sphincter to tear its muscle fibres (Rigiflex or Witzel)
- Surgical cardiomyotomy (open or endo)
Poor surgical candidate?
- Medical - CCB (nifedipine or verapamil) or nitrates. (to lower oesophageal sphincter pressure.
- Botox - inhibits the release of acetylcholine from nerve terminals. Done endoscopically
What is a pharyngeal Pouch/ Zenker’s Diverticulum
Outpouching of the oesophagus
- Between borders of cricopharyngeus and lower border of inferior constrictor of pharynx.
- Weakness in muscle wall termed Killian’s dehiscence
Management is with Surgery
Mechanism of Zenker’s Diverticulum?
Defect usually posteriorly, but swelling usually bulges to left side of neck.
Therefore food debris, then pouch expansion and dysphagia.
Upper GI endoscopy is potentially hazardous and may result in iatrogenic perforation.
What is diffuse oesophageal spasm?
Intermittent dysphagia ± chest pain.
What do you see on barium swallow with diffuse oesophageal spasm?
Ba Swallow shows corkscrew oesophagus.
What is nutcracker oesophagus?
Increase contraction of smooth muscle with normal peristalsis.
What is the definition of dyspepsia?
Non-specific group of symptoms:
- Epigastric discomfort
- Bloating
- Heartburn
What symptoms alongside dyspepsia are red flags?
Urgent - All patients who’ve got dysphagia, all patients who have an upper abdo mass consistent with stomach cancer. Patients aged >55 years who’ve got weight loss, and any of the following: upper abdo pain, reflux, dyspepsia.
Non-urgent: Patients with haematemesis
Patients aged >= 55 years who’ve got:
treatment-resistant dyspepsia or
upper abdominal pain with low haemoglobin levels or
raised platelet count with any of the following: nausea, vomiting, weight loss, reflux, dyspepsia, upper abdominal pain
nausea or vomiting with any of the following: weight loss, reflux, dyspepsia, upper abdominal pain
Managing patients who do not meet referral criteria:
This can be summarised at a step-wise approach
- Review medications for possible causes of dyspepsia
- Lifestyle advice
- Trial of full-dose proton pump inhibitor for one month OR a ‘test and treat’ approach for H. pylori
Ensure you rule out coronary artery disease.
Consider ECG, Serum Troponin, exercise stress testing.
ALARM: Anaemia/bleeding/Abdo Mass Loss of Weight Anorexia (Appetite) Recent onset progressive symptoms Melaena or haematemesis/vomiting Swallowing Difficulty
What are the causes of dyspepsia?
Inflammation: GORD, Gastritis, PUD
Malignancy: Gastric or Oesophageal
Functional: Non-ulcer dyspepsia
How would you manage new onset dyspepsia?
- OGD >60 or ALARMS
- Consider conservative measures for 4 weeks - stopping NSAIDS/CCBs, stop smoking/ decrease ETOH, weight loss.
Try OTC Antacids/Alginates (Gaviscon).
1st line: If no alarming features do breath test or stool test for H/Pylori. Breath test = drink C12, measure level of urea as it is broken down by H.pylori.
Ensure patient has not had any antibiotics, no antisecretory drugs (PPI) in past 2 weeks.
Other: Rapid urease test (CLO test) - biopsy with urea + pH indicator.
Serum antibody: positive after eradication.
Culture of gastric bipsy
Gastric biopsy
+ve H.Pylori = 7 day 2x daily Amoxicillin and Clarithromcyin or Metronidazole.
-ve Result = PPI (Esomeprazole/Omeprazole/Lansoprazole
Management for proven GORD causes dyspepsia?
Lansoprazole 30mg, Omeprazole (20-40mg), Rabeprazole 20mg.
- Full dose PPI 1 -2months.
- Then, low dose PPI PRN.
Adverse effects
- Hyponatraemia
- Osteoporosis
- Microscopic Colitis
- Increased risk of C.diff
Management for proven PUD?
- Full dose PPI for 1-2 months?
What is that again?
- H.pylori eradication if positive
- Endoscopy to check for resolution if GU
- Then, low-dose PPI PRN
What is first line eradication therapy for H.pylori? (NKDA)
PAC 500 (Penicillin)
- PPI: Lansoprazole 30mg BD
- Amoxicillin 1g BD
- Clarithromycin 500mg BD
Post eradication investigation is breath test.
H.pylori eradication therapy (penicillin allergic)
- PPI: Lansoprazole 30mg BD
- Metronidazole 400mg BD
- Clarithromycin 250mg BD
Note that PPIs cause hyponatraemia, osteoporosis (increased risk of fractures), microscopic colitis. Increased risk of C.diff infections.
Success rate of eradication therapy?
95%.
Failure due to poor compliance.
Bismuth can be used for resistance to clarithromycin but gives stools tarry black colour.
What is the classification of peptic ulcer disease? (PUD)
Acute: Usually due to drugs (NSAIDs, Steroids) or Stress.
Chronic:
Drugs, H.pylori, Hypercalcaemia
Zollinger-Ellison - 1/3 have MEN-1. Parathyroid, pituitary and pancreas.
Zollinger-Ellison is too much gastrin - 30% have MEN-1.
Causes multiple gastroduodenal ulcers, diarrhoea, malabsorption.
Diagnosed with fasting gastrin and secretin.
What is more common, a duodenal ulcer or a gastric ulcer?
Duodenal are 4x more common
Where do you find duodenal ulcers?
First part of the duodenum (cap)
More common in males than females.
What are the risk factors of duodenal ulcers?
Lifestyle: ETOH, Smoking, increased gastric emptying (damage to duodenum)
Infection: H.pylori (90%)
Drugs: NSAIDS (COX-1 blocks prostaglandins needed for gastric mucosa), Steroids
Also SSRI, steroids, bisphosphonates.
What is the presentation of a duodenal ulcer?
Epigastric pain: BEFORE meals, after meals and at NIGHT. Cause pen when hungry and are relieved by eating. Pyloric sphincter contracts when eating.
Relieved by: eating or milk
What is the pathology of gastric ulcers?
- Lesser curve of gastric antrum (medial curve that is smaller)
- Beware ulcers elsewhere (could be malignant)
Risk factors for GASTRIC ulcers?
- Lifestyle: Smoking, DECREASED gastric emptying
- Infection: H.pylori
- Drugs: NSAIDS, Steroids, SSRI, bisphosphonates
- Stress:
Cushing’s Ulcer due to intracranial disease? Increased vagal stimulation, Increased stomach acid
Curling’s ulcer: Burns, Sepsis, Trauma (reduced plasma volume)
What is the presentation of GASTRIC ulcers?
Worse ON eating
Relieved by antacids
Weight Loss
What are the complications of peptic ulcer disease?
Start from ulcer:
Bleeding –> Haemorrhage:
- Haematemesis or melaena
- Fe deficiency anaemia
Duodenal ulcer bleeds from gastroduodenal artery.
Even more? –> Perforation
- Peritonitis
Growing and blocking? –> Gastric Outflow obstruction
- Vomiting, colic, distension
Long term? Malignancy
- Increased risk with H.pylori
Investigations for peptic ulcer disease?
- Obs: RR, HR, O2, BP
- Bloods: FBC (anaemia/maleana), urea (increased in haemorrhage)
- C13 breath test.
- OGD (Stop PPIs >2 weeks before). Initially order if patient >60. Urease test for H.Pylori. Take biopsies to check for malignancy.
- Gastrin (Hypergastrinaemia) levels if Zollinger-Ellison suspected.
Forrest Score: on endoscopy
- GBS - (Rockall is old) - Glasgow Blatchford.
Management of a bleeding ulcer?
- 1st line Endoscopy ± blood transfusion. PPI reduces rebleeding (omeprazole 80). Discontinue NSAIDs.
Surgery is indicated in patients with ongoing acute bleeding despite repeated endoscopic therapy.
- 2nd line: Surgery or embolisation
Management of non-bleeding H.pylori negative ulcer?
Conservative (Treat underlying cause) : Lose weight/Stop smoking + decrease ETOH. Avoid hot drinks + spicy food. Stop drugs such as NSAIDS, Steroids.
+ Medical:
1st line: Give PPI for 4 weeks (lansoprazole 15-30mg OD)
2nd line: H2 Antagonist (Ranitidine 150mg)
For patients who need NSAIDS: Misoprostol 100-200microgram 4x OD.
Management of non-bleeding H.pyloti positive ulcer
- Eradication therapy
(triple = PPI, Clari, Amox or Metro)
(Quad = PPI, Tetracycline, Metronidaole, bismuth)
Surgical treatment of PUD - Vagotomy?
Rarely used today.
- Vagotomy:
Truncal (must be included with a pyloroplasty (open opening to duodenum) or gastroenterostomy)
- Selective: Vagus nerve only denervates where it supplies lower oesophagus. (Nerves of Laterjet)
Surgical treatment of PUD - Antrectomy with vagotomy
Removal of the distal half of stomach + anastomosis:
- Directly added to duodenum: Biliroth 1
- To small bowel loop with duodenal stump oversewn: Biliroth 2 or Polya.
Surgical treatment of PUD - Subtotal gastrectomy with Roux-en-Y
Sometimes performed for Zollinger-Ellison
Physical complications of Surgical treatment of PUD
Physical complications
- Duodenal stump leakage
- Abdominal fullness
- Reflux or bilious vomiting (improves with time)
- Stricture formation
Metabolic complications of surgical treatment of PUD
Dumping syndrome
- Abdominal pain, flushing + N/V
- Early pain (10-30 mins) = Osmotic hypovolaemia
- Late: (2-3 hrs) Reactive hypoglycaemia due to rapid increase in insulin due to excess sugar in intestine.
Also during gastric surgery.
Blind loop syndrome –> Malabsorption, Diarrhoea
- Overgrowth of bacteria in duodenal stump
- Anaemia: FB + B12
- Osteoporosis
Weight loss: Malabsorption of decreased calories intake
What is blind loop syndrome?
Blind loop syndrome –> Malabsorption, Diarrhoea
- Overgrowth of bacteria in duodenal stump
- Anaemia: FB + B12
- Osteoporosis
What is the pathophysiology of GORD?
Dysfunction of the lower oesophageal sphincter –> leading to stomach acid reflux up the oesophagus –> oesophagitis.
What are the risk factors of GORD?
Lifestyle: Smoking, ETOH, Obesity Physiological: Pregnancy Anatomical: Hiatus Hernia Iatrogenic: drugs (nitrates, CCB, TCA, anti-ACHm. Surgical: Heller's Myotomy
What are the oesophageal symptoms of GORD?
- Heart burn that is related to meals, lying down, and gets better with antacids.
- Belching
- Acid Brash (salivation due to excess acid)
- Odynophagia
What are the extra-oesophageal symptoms of GORD?
- Chronic cough
- Laryngitis, sinusitis
- Nocturnal asthma (chest tightness, SOB, Wheeze)
Complications of GORD?
- From excess acid = Oesophagitis
- Oesophagitis can cause ulceration
- Chronic oesophagitis can cause strictures + dysphagia
- Furthermore, Barrett’s oesophagus and oesophageal adenocarcinoma.
GORD is single strongest risk factor for development of Barrett’s oesophagus.
What are the differential diagnosis for GORD?
- Other causes of oesophagitis: Infection, IBD, burns.
- PUD
- Oesophageal cancer
Investigations for GORD?
- If isolated no need for further investigations –> trial of PPI
- Bloods: FBC
- CXR: Hiatus Hernia may be seen.
- OGD if: >55 yrs old, symptoms >4 weeks, Dysphagia, persistent symptoms, Weight Loss.
- Barium Swallow (rule out other causes): Hiatus hernia or dysmotility
- 24 pH testing ± manometry (pH <4 for > 4hrs). Pre-operative workup for patients. Measures pressures within the lower oesophageal sphincter and helps with diagnosis.
What is the Los Angeles classification for GORD?
Grade A = One or more mucosal breaks < 5mm in maximal length.
Grade B = Breaks >5 mm but without continuity across mucosal folds.
Grade C = Mucosal breaks between >2 mucosal folds = less than 75% of oesophageal circumference.
Grade D = Involving more than 75% of oesophageal circumference.
What is the conservative management of GORD?
- Lose weight
- Raise head of bed
- Small regular meals at least 3hrs before bed
- Stop smoking + decreased alcohol intake
- Avoid hot/spicy food
- Stop drugs: NSAIDs, Steroids, CCBs, Nitrates.
What is the medical management of GORD?
- OTC: Gaviscon, Mg Trisilicate
- First line: Full dose PPI for 1-2 months (omeprazole 20mg/lansoprazole 30mg OD)
- Second line: If no response double dose of PPI BD.
- Third line: If no response: add H2RA such as ranitidine 300mg ON.
What is the surgical management of GORD?
Nissen Fundoplication
- Indications: Need all 3 of
- Severe symptoms
- Refractory to medical therapy
- Confirmed reflux (pH monitoring)
Explain the procedure of the Nissen fundoplication
Aim: prevent reflux, repair diaphragm.
- Normally laparoscopic
- Mobilise gastric fundus + wrap around lower oesophagus.
- Close any diaphragmatic hiatus
- Complications: Gas-bloat syndrome: inability to belch/vomit.
- Dysphagia if wrap too tight.
What are the 3 classifications of a hiatus hernia?
1) Sliding (80%) - Gasto-oesophageal junction SLIDES up into chest. Associated with GORD.
2) Rolling (15%) - Gasto-oesophageal junction remains in abdomen, but a bulge of stomach rolls into chest alongside the oesophagus. LOS remains in abdomen therefore little GORD. Can become strangulated.
3) Mixed
What are the investigations for a hiatus hernia?
Bloods: FBC, U+E
CXR: Gas bubble + fluid level within the chest cavity.
Ba Swallow: Diagnosis
OGD: Can help visualise the mucosa but is not diagnostic.
24hr pH + manometry: exclude dysmotility or achalasia
Management of a hiatus hernia?
Conservative: Lose weight
Medical: Management of reflux?
Surgical: Only if medical treatment is unmanageable. - NB should repair a rolling hernia as it can strangulate.
What are the differentials for haematemesis?
- VINTAGE
- Varices
- Inflammation: (Oesophagus, stomach or duodenum).
- PUD (DU is most common)
- Neoplasia (Oesphageal or gastric Ca)
- Trauma: Mallory-Weiss because of vomiting.
- Boerhaave’s Syndrome - Full thickness tear 2cm proximal to LOS.
- Angiodysplasia + other vascular anomalies
Angiodysplasia (vascular malformation), HHT or Osler-Weber-Rendu (hereditary haemorrhagic telangiectasia, Dieulafoy lesion: rupture of large arteriole in stomach or other bowel. - Generalised bleeding diathesis
Warfarin, thrombolytics
CRF (chronic renal failure) - Epistaxis
What are the differentials for rectal bleeding?
DHIPING ARSE - Diverticulae - Haemorrhoid - Infection: Campy Shigella E.coli C.diff Amoebic dysentery - Polyps - Inflammation (Crohn's, UC) - Neoplasia - Gastric-Upper Bowel Bleeding - Angio (Ischaemic colitis, HHT, Angiodysplasia)
What is the history for an upper GI bleeding?
- May have had previous bleeds
- Known ulcers or dyspepsia
- Dysphagia/Weight loss
- Liver disease or known varices
- Drugs and EtOH
- Co-morbidities
If there is an iron deficiency anaemia
- Check FBC
- Then if low Hb and low MCV in non-pregnnacy person check the ferritin. Ferritin can be elevated in disease malignancy etc.
- If this is the case consider iron, TIBC, transferrin.
Once confirmed as iron deficiency anaemia = serum ferritin less than 15mcg/L.
What would you see on examination of an Upper GI bleed?
- CLD (jaundice, ascites, encephalopathy, clubbing, spider naevi, Dupuytren’s)
- PR: Melaena
- Signs of Shock
Clammy, cool, CRT >2s
Decreased BP (<100) or postural hypotension (>20 drop)
Decreased urine output (<30ml/h)
Tachycardia
Decreased GCS.
What are the common causes of an Upper GI bleed?
1) PUD: 40% (mostly DU)
2) Gastritis/Erosions: 20%
3) Mallory-Weiss tear: 10%
4) Varices: 5%
5) Oesophagitis: 5%
6) Ca Stomach/oesophagus
7) Boerhaave’s
What is the Rockall Score?
- Prediction of re-bleeding and mortality
- 40% of rebleeders die
- Initial score pre-endosocopy
–>
Age (60-79 = +1) (>=80 = +2)
Shock: BP (SBP <100=1) , Pulse (tachy = 1) ,
Comorbidities (any = +2, if it is renal, liver or malignancy = +3)
Diagnosis: Malignancy = +2, All other diagnoses = +1)
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.
What does the presence of N+V in the setting of melaena suggest?
Upper GI bleeding source distal to pylorus.
What does coffee ground vomiting suggest?
More for PUD and makes variceal bleed less likely.
What does a spontaneous tear of oesophagus from retching suggest? - Vomiting, thoracic pain, subcutaneous emphysema.
Boerhaave’s syndrome.
What is Haematochezia?
Fresh blood through the anus, in or with stools.
Different to melaena which is black. More associated with LGIB than UGIB.
Outline the primary management of an Upper GI Bleed
- Resuscitate
- (consider blood/terlipressin)
- Maintenance
- Urgent Endoscopy
- Management after endoscopy
Outline the resuscitation of a patient with an Upper GI bleed?
- Head down
- 100% O2, protect airway
2 x 14G cannulae + IV crystalloid infusion up to 1L (orange/Grey)
If patient remains shocked after initial resuscitation in UGIB?
Blood Group specific or O- until Xmatched.
Initial management after resus of patient with variceal bleed?
- Terlipressin IV (splanchnic vasoperssor
- Prophylactic Abx: e.g ciprofloxacin 1g/24hr
What maintenance would you give to a patient after resus with a UGIB?
- Crystalloid IV, with transfusion if necessary
- Catheter + consider CVP (aim for >5cm H20) (central venous pressure)
- Correct coagulopathy: vit K, FFP, platelets
- Pabrinex if EtOH
- Notify surgeons
Once resuscitation and maintenance have occured, what is the next part of treatment for an UGIB?
Urgent Endoscopy: All patients with suspected Upper GI bleed require an endoscopy within 24hrs of admission.
- Haemostasis of vessel or ulcer: Adrenaline injection Thermal/laser coagulation Fibrin glue Endoclips
- Variceal bleeding
: 2 of:
1st line banding, 2nd line sclerotherapy,
adrenaline, coagulation
Balloon tamponade with
Sengstaken-Blakemore tube
- Only used if exsanguinating haemorrhage endoscopic therapy failure.
- TIPPS if bleeding can’t be stopped endoscopically.
Transjugular intrahepatic portosystemic shunt - TIPS procedure connects the hepatic vein and the portal vein.
What happens after an urgent endoscopy for an Upper GI bleed?
- Omeprazole IV + continuation PO (decreased re-bleeding). Do not do it before as it may mask the bleeding.
- Offer Vit K
- Antibiotic
- Keep NBM for 24hr –> Clear fluid –> light diet @ 48hr
- Daily bloods: FBC, U+E, LFTs, Clotting
- H.pylori testing and eradication
- Stop NSAIDs, Steroids etc.
What are the indications for surgery after an UGIB?
- Rebleeding
- Bleeding despite transfusing 6U
- Uncontrollable bleeding at endoscopy
- Initial Rockall score >3 or final >6.
When to avoid 0.9% NS?
Uncompensated liver disease (makes ascites worse).
- Use blood or albumin for resus and 5% dextrose for maintenance.
What are oesophageal varices?
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%: increased severity of liver disease.
What are the causes of portal HTN?
Pre-hepatic: Portal vein thrombosis
Hepatic: cirrhosis (80% in UK), schisto (worldwide), sarcoidosis
Post-hepatic: Budd-Chiari (occlusion of hepatic vein), RHF, constrict pericarditis
Prevention (not stopping once) of a primary UGIB?
Betablockers (propranolol), repeat endoscopic banding
Prevention of secondary UGIB?
Betablockers (propranolol), repeat banding, TIPSS.
What does TIPSS stand for?
Transjugular Intrahepatic Porto-Systemic Shunt
Interaction with clarithromycin and warfarin
Can increase effect of warfarin
What is the glasgow-blatchford bleeding score?
First assessment score (candidates for outpatient management)
- Haemoglobin <100 = 6 points.
- Blood urea (think about protein meal)
- Systolic blood pressure = <90 = 3 points.
- Pulse >100/min = 1 point.
- Presentation with melaena = 1 point.
- Presentation with syncope = 2 points.
- Hepatic disease = 2 points
- Cardiac failure = 2 points.
- Sex
What is a TIPSS procedure?
- IR creates an artificial channel between hepatic vein and portal vein –> Decreased portal pressure
- Colapinto needle creates tract through liver parenchyma, expand using a balloon and maintained by placement of a stent.
- Used prophylactically or acutely if endoscopic therapy fails to control variceal bleeding.
What is the normal range for normal bilirubin?
- Normal bilirubin = 3-17
At what level is jaundice visible?
50uM (3x upper limit of normal)
What cells convert Hb to unconjugated BR?
Splenic macrophages
Unconjugated bilirubin converted to conjugated by what enzyme?
BR-UDP-glucuronyl transferase in the liver.
Where is conjugated bilirubin secreted?
Into the bile, where it becomes urobilinogen (colourless)
What is the 3 fates of urobilinogen in the bile?
- Reabsorbed, returned to the liver, and back into the bile
- Excreted in the urine
- into the GIT, converted to sterobilin (brown).
What are the 3 overarching causing of jaundice?
- Pre-hepatic
- Hepatic
- Post-hepatic
What are the causes of pre-hepatic jaundice?
- Excess bilirubin production
- -> Haemolytic anaemia
- > Ineffective erythropoiesis (thalassaemia, sickle cell, G6PD)
What are the causes of unconjugated hepatic jaundice?
Unconjugated?
- Decreased BR uptake due to using up liver’s ability to take it up.
1) Drugs: contrast, Rifampycin
2) Congestive cardiac failure - Decreased bilirubin conjugation
1) Hypothyroidism (decreased movement + conjugation)
2) Gilbert’s (AD)
3) Crigler-Najjar (AR)
Neonatal jaundice is both increased production and reduced conjugation.
What are the causes fo conjugated hepatic jaundice?
Problems with the liver/Hepatocellular dysfunction?
- Congenital
- Infection
- Autoimmune
- Neoplastia
- Vascular
What are the congenital causes of conjugated hepatic jaundice?
- Hereditary Haemochromatosis
- Wilson’s
- a1ATD
What are the infectious causes of conjugated hepatic jaundice?
- CMV
- Hep A/B/C
- EBV
What are the toxin causes of conjugated hepatic jaundice?
- EtOH
- Drugs
What are the autoimmune, neoplastic and vascular causes of conjugated hepatic jaundice?
AI: AIH
Neoplasia: HCC, Mets
Vascular: Budd-Chiari
What are the causes of decreased hepatic bilirubin excretion leading to a conjugated hepatic jaundice?
- Dubin-Johnson (black liver due to melanin deposits)
- Rotors
What are the post-hepatic causes of jaundice?
- Obstruction Stones Ca Pancreas Drugs PBC PSC Biliary Atresia Choledochal Cyst Cholangio carcinoma
What are the causes of drug-induced haemolytic jaundice?
Antimalarials - Dapsone
What are the causes of drug-induced hepatitis and jaundice?
- Paracetamol OD
- RMP, INH, PZA
- Valproate
- Statins
- Halothane
- MAOIs –> Monoamine oxidase
What are the causes of drug induced cholestasis and subsequent jaundice?
- Flucloxacillin (weeks after Rx)
- Co-amoxiclav
- OCP
- Sulphonylureas
- Chlopromazine, prochlorperazine (antipsychotic)
What is Gilbert’s syndrome?
- Autosomal dominant UDP-GT deficiency
- 2% of the population
- Jaundice occurs during intercurrent illness
- Dx: increase in uBR on fasting, normal LFTs.
What is Crigler-Najjar syndrome?
Rare auto rec total UDP-GT deficiency
- Severe neonatal jaundice and kernicterus
Rx: liver Tx
What are the investigations for pre-hepatic jaundice?
Urine: No Bilirubin, increased urobilinogen, increased Hb if intravascular haemolysis
LFTs: increased uBR, increased AST, increased LDH
Others: FBC and film, Coombs Test, Hb Electrophoresis
What are the investigations for hepatic jaundice?
Do a PR for melaena
Urine: Increased bilirubin, increased urobilinogen
LFTs: Increased conjugated bilirubin, increased AST:ALT
- If >2 = ETOH
if < 1 = Viral
- Increased GGT (EtoH, Obstruction)
- Increased ALP
- Function: decreased albumin, increased PT.
- Others: FBC = Anaemia
Anti-SMA (AIH), LKM (AIH), SLA (Chronic Hep C), ANA
a1AT, ferritin, caeruloplasmin, Liver biopsy.
What are the investigation for post hepatic jaundice?
- Urine: Increased BR ++, no urobilinogen
- LFTs: Increased CBR, Increased AST, increased ALT, Increased ALP, Increased GGT.
- Other: Abdo US - Ducts >6mm, ERCP, MRCP, Anti-AMA, ANCA (PSC), ANA.
What are the causes of liver failure?
1) Cirrhosis
2) Acute failure due to:
- Infection: Hep A/B, CMV, EBV, Leptospirosis
- Toxin: EtOH, Paracetamol, Isoniazid, halothane
- Vascular: Budd-Chiari
- Other: Wilson’s, AIH
- Obs: Eclampsia, Acute Fatty Liver of pregnancy.
What are the signs of liver failure?
Jaundice
Oedema + ascites
Bruising
Encephalopathy - normally in acute liver failure.
- Aterixis, Constructional apraxia
Fetor hepaticus (sweet breath/thiols pass into lungs)
Signs of cirrhosis/chronic liver disease
What are the investigations of liver failure?
Bloods:
- FBC: infection, GI bleed, decreased MCV (ETOH)
- U+E: Decreased urea, increased creatinine: Hepatorenal syndrome
(urea synthesised in liver so poor test of renal function).
- LFT:
AST:ALT >2 = ETOH
AST:ALT <1 = Viral
Albumin: decreased in chronic liver failure
PT: Increased in acute liver failure. - Clotting: Increased INR - Glucose - ABG: Metabolic acidosis Causes: Ferritin, a1AT, caeruloplasmin, Abs, paracetamol lvls.
Difference in a cholestatic picture and a hepatocellular picture?
Cholestatic: Bili, ALP, GGT
Hepatocellular: Bili, AST, ALT.
Microbiological investigations of liver failure?
- Hep, CMV, EBV serology
- Blood and urine culture
- Ascites MCS + SAAG
Radiological investigations of liver failure?
- CXR
- Abdo US + portal vein duplex. (US is preffered).
- For patients with suspected cholangitis, cholecystitis, pancreatitis = CT study.
What is hepatorenal syndrome?
- Renal failure in patients with advanced CLF.
- Diagnosis of exclusion
What is the pathophysiology of hepatorenal syndrome?
- Cirrhosis –> Splanchnic arterial vasodilation –> effective hypovolaemia circulatory volume –> RAS activation –> Renal arterial vasoconstriction.
- This persistent underfilling of renal circulation –> failure.
Systemic trop in PVR causes activation of sympathetic system and vasocontrictiors.
What are the two types of hepatorenal failure?
Type 1: Rapidly deteriorating (survival <2 weeks)
Type 2: Steady deteriorating (survival ~6 months)
Management of hepatorenal failure?
- IV albumin + splanchnic vasoconstrictors (terlipressin)
- Haemodialysis as supportive management
- Liver Transplant is management of choice
Management of liver failure?
- Manage in ITU
- Rx of underlying cause: NAC in paracetamol OD
- Good nutrition: e.g. via NGT with high carbs.
- Thiamine supplements
- prophylactic PPI vs stress ulcers
Monitoring in liver failure?
Fluids: urinary and central venous catheters.
Bloods: Daily FBC, U+E, LFTs, INR
Glucose: 1-4hrly + 10% dextrose IV 1L/12hrs.
Complications of liver failure?
- Bleeding: Vit K, platelets, FFP, Blood.
- Sepsis: Tazocin (avoid gen: nephrotoxicity)
- Ascites: fluid + salt restriction, spironolactone (K+ sparing), furosemide, tap, daily weight.
Hypoglycaemia: Regular BMs, IV glucose if <2mM - Encephalopathy: avoid sedatives, lactulose ± enemas, rifaximin.
Seizures: lorazempam
Cerebral oedema: mannitol
Drugs to avoid in Liver failure?
- Avoid: Opiates, oral hypoglycaemics, Na-containing IVI. Effect of warfarin effects increased.
- Hepatotoxic drugs: paracetamol, methotrexate, isoniazid, salicylate, tetracycline.
Poor prognostic factors for liver failure?
- Grade 3/4 hepatic encephalopathy
- > 40 yrs old
- Albumin <30g/L
- Increased INR
- Drug-induced liver failure
Types of liver transplants?
- Cadaveric: heart-beating or non-heart beating
- Live: right lobe
What is the Kings College Hospital Criteria in Acute Failure?
Paracetamol-induced - pH <7.3 24hr 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 - >1 week from jaundice to encephalopathy - PT >50s - BR >300uM
Common causes of cirrhosis?
Chronic ETOH
Chronic HCV
NAFLD/NASH
Less common causes of cirrhosis?
Genetic: Wilson’s, a1ATD, HH, CF
AI: AH, PBC, PSC
Drugs: Methotrexate, amiodarone, Methylodopa, INH
Neoplasm: HCC, Mets
Vasc: Budd-Chiari, RHF, constrictive pericarditis
What are the signs of cirrhosis in the hands?
- Clubbing (± periostitis)
- Leuconychia (decreased albumin)
- Terry’s nails (white proximally, red distally)
- Palmar erythema
- Dupuytron’s contracture
What are the signs of cirrhosis in the face?
Pallor: ACD
Xanthelasma: PBC
Parotid enlargement: espc with ETOH
What are the signs of cirrhosis in the trunk?
- Spider naevi (>5 fill from centre)
- Gynaecomastia (low albumin - altered sex hormone metabolism
- Loss of 2ndry sexual hair
What are the signs of cirrhosis in the abdomen?
- Striae
- Hepatomegaly (may be small in late disease)
- Splenomegaly
- Dilated superficial veins (caput medusa)
- Testicular atrophy
What are the complications of cirrhosis?
- Decompensation –> Hepatic Failure
- Jaundice (conjugated)
- Encephalopathy
- Hypoalbuminaemia –> oedema + ascites
- Coagulopathy –> bruising
- Hypoglycaemia - Spontaneous Bacterial Peritonitis
- Portal Hypertension
- Increasing risk HCC
What is the mnemonic for portal hypertension?
SAVE
- Splenomegaly
- Ascites
- Varices (Oesophageal varices, caput medusa, worsens existing piles)
- Encephalopathy
What are the blood investigations for cirrhosis?
Bloods:
- FBC:
decreased WCC,
decreased platelets indicate hypersplenism. Thrombocytopenia is the most sensitive and specific lab finding for diagnosis of liver cirrhosis in those with liver disease.
- Increased LFTs (2.5 increase ratio of AST to ALT). Urea should go down.
- Increased INR
- Decreased Albumin
What investigations may demonstrate an alcoholic cause of cirrhosis?
EToH: increased MCV, increased GGT
What investigations may demonstrate a NASH cause of cirrhosis?
Hyperlipidaemia, increased glucose.
What investigations may demonstrate an infective cause of cirrhosis?
Hep C, Hep B, CMV, EBV serology
What investigations may demonstrate a genetic cause of cirrhosis?
Ferritin (Haemachromatosis), a1AT, caeruloplasmin (decreased in Wilson’s)
What are the antibodies for AIH?
AIH: SMA, SLA, LKM, ANA
Antibodies for PBC
AMA
Antibodies for PSC
ANCA, ANA
Immunoglobulins in AIH?
Increased IgG = AIH
Increased IgM = PBC
What imaging is used for cirrhosis?
Transient elastography and acoustic radiation force (for patients with NAFLD, enhanced liver fibrosis). This is fibroscan. Measures the stiffness of the liver.
Abdo US + Portal Vein Duplex
- Small liver, nodularity, splenomegaly, increased diameter of the portal vein.
- Reversed portal vein flow
- Ascites
- Also liver biopsy
Ascitic tap that indicates SBP?
PMN > 250mm indicates SBP, whether or not culture has grown.
Most common organism = E.coli
Symptoms of SBP?
- Frequently encountered bacterial infection in patients with cirrhosis, most commonly seen in patients with end-stage liver disease.
- Key symptoms = abdo pain, fever, vomiting, altered mental status and GI bleeding. However can also present asymptomatically.
What is the management of cirrhosis?
- General - Good nutrition,
- ETOH abstinence: baclofen helps decreasing cravings
- Colestyramine for pruritus
- Screening: HCC -US and AFP every 6 months.
- Oesophageal varices: endoscopy.
Specific management for HCV?
- Interferon-a/Oral antiviral = Sofosbuvir, Elbasvir
Specific management for SBP?
- IV Cefotaxime 2g every 8-12 hrs + Vancomycin 500-1000mg
- Prophylaxis given to patient who have had an episode of SBP
- Patients with fluid protein <15 and either a Child-Pugh score of at least 9 or hepatorenal syndrome.
- Offer oral cipro or norfoxacin prophylaxis for people with cirrhosis + ascites.
What is PBC?
Primary Biliary Cholangitis
- Disease of small intrahepatic bile ducts (and eventual loss) occuring in the context of chronic portal tract inflammation. Develops fibrosis, then bile acids remain in the liver, resulting in cirrhosis.
How is PBC managed?
- Bile acid analogues - ursodeoxycholic acid.
- Prednisolone: 20-30mg
- Antipruritic: colestyramine
What is Wilson’s?
AR disease - copper accumulation due to enzyme defect in biliary excretion of copper.
Hx: Hepatitis, cirrhosis, hepatic decompensation, psychiatric disorder.
Ix:
- Reduced serum caeruloplasmin
- Reduced serum copper (95% of plasma copper is carried by ceruloplasmin
- Increased 24hr urinary copper excretion
- slit lamp examination, liver biopsy.
What is the Nazer score for Wilson’s?
The Nazer score is a triage tool on deciding who should receive a liver transplant and those who should receive anti-copper medical therapy. It is based on the severity of abnormality for each of:
- Serum AST
- Bilirubin
- Prothrombin time
0 = Bili <100, AST <100, PT <4
10-12 should be transplanted.
1 - 6 = Medical treatement
7-9 = Evaluated by clinical judgement
What is the medical treatment for Wilson’s?
penicillamine (chelates copper) has been the traditional first-line treatment
Trientine and Zinc 4-6 months.
What is the management of decompensation in cirrhosis?
Ascites: fluid and salt restrict, 1st line: spiro
2nd line: fruse, tap, daily weights.
Coagulopathy: vit K, platelets, FFP, blood.
Encephalopathy: avoid sedatives, lactulose ± enemas, rifaximin (used to reduce the recurrence of episodes of overt hepatic encephalopathy - use if refractory to lactulose). Neomycin is another medication licensed for use in hepatic encephalopathy.
Sepsis/SBP: Tazocin? Cefotaxime + Vanc
Hepatorenal syndrome: IV albumin + terlipressin
What is the Child-Pugh Grading of Cirrhosis?
Predicts risk of bleeding, mortality and need for Tx
- Graded A-C using severity of 5 factors.
- Albumin - 1,2 or 3 points for each.
- Bilirubin -
- Clotting -
- Distension: Ascites
- Encephalopathy .
Class A = 5-6 points (1yr survival 100%)
Class B = 7-9 points
Class C = 10-15 points (45%)
Causes of portal hypertension?
Pre-hepatic - portal vein thrombosis (pancreatitis)
Hepatic - cirrhosis or schisto (worldwide)
Post-hepatic - Budd-Chiari, RHF, constrictive pericarditis, TR
What are the three portosystemic anastomoses?
Oesophageal varices =
Portal - Left and short gastric veins.
Systemic = Inf. oesophageal veins.
Caput medusae = Peri-umbilical vein. Superficial abdo wall veins.
Haemorrhoid = Super rectal veins. Inferior and middle rectal veins.
What are prominent Abdominal Veins
- A lot more common than caput medusa.
- Blood flow down below towards legs: portal HTN.
- Blood flow towards the head: IVC obstruction.
What is the pathophysiology of encephalopathy?
- Decreased 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
- Increased glutamine –> osmotic imbalance –> cerebral oedema.
What is the classification of encephalopathy (NICE)?
1: Confused - irritable, mild confusion, sleep inversion
2: Drowsy - Increased disorientated, slurred speech, asterixis
3: Stupor - rousable, incoherence
4: Coma - unrousable, ± extensor plantars
What are the possible precipitants of encephalopathy?
Constipation (commonest cause - due to excessive nitrogen load and can lead to Liver decompensation.
HEPATICS - Hepatic encephalopathy
- Haemorrhage: e.g varices
- Electrolytes: decreased K, decreased Na
- Poisons: diuretics, sedatives, anaesthetics
- Alcohol
- Tumour: HCC
- Infection: SBP, pneumonia, UTI, HDV
- Constipation (commonest cause - due to excessive nitrogen load
- Sugar (glucose) decrease: e.g low calorie diet.
What is the underlying mechanism for hepatic encephalopathy?
- Excessive nitrogen loading
- Electrolyte or metabolic disturbances
- Drugs and medication
- Infection (pneumonia)
What key investigations is needed for encephalopathy?
increased plasma NH4
Management of encephalopathy?
- Nurse 20 degrees head up
- Correct any precipitants
- Avoid sedatives
- Lactulose ± PO4 enemas to decreased nitrogen-forming bowel bacteria –> 2-4 soft stools/d
- Consider rifaximin PO to kill intestinal microflora.
What is the pathophysiology of ascites?
- back-pressure –> Fluid exudation
- decreased effective circulating volume –> RAS activation
- (in cirrhosis): decreased albumin –> Decreased plasma oncotic pressure and aldosterone metabolism impaired.
What are the symptoms of ascites?
- Distension –> abdo discomfort and anorexia
- Dyspnoea
- decreased venous return
What are the differentials for ascites?
Serum Ascites Albumin Gradient (SAAG) = Serum albumin - ascitic albumin
- SAAG >=1.1g/L = Portal HTN. (pre, hepatic, post), Cirrhosis in 80%.
- SAAG <1.1g/dL = other causes.
= Neoplasia: peritoneal or visceral
= Inflammation: e.g pancreatitis
= Nephrotic syndrome
= Infection: TB peritonitis
What are the investigations for ascites?
- 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
Management of ascites
- Daily weight aiming for <0.5kg/d reduction
- Fluid restrict <1.5L/d and low Na diet (
- Spironolactone + frusemide
- Therapeutic paracentesis with albumin infusion) 100ml 20%/L drained. - Respiratory compromise, pain/discomfort, renal impairment.
Need to give albumin
- To avoid PICD - Paracentesis-Induced Circulatory Dysfunction
- Refractory ascites?: TIPSS.
What is SBP?
- Patient with ascites and peritonitic abdomen
- Caused by E.co.i, Klebsiella, Streps
- Complicated by hepatorenal syndrome in 30%
- Ix: Ascites PMN > 250mm + MCS
- Rx: Tazocin or cefotaxime/vancomycin until sensitivities known
As part of portal hypertension - you can get splenomegaly
Splenic congestion
- Hypersplenism: decreased WCC, decreased platelets.
Massive splenomegaly - CML, Myelofibrosis, Visceral leishmaniasis, Malaria.
Mild: Infections: IE, EBV, CMV, amyloidosis, sarcoidosis, SLE, RA(Felty’s).
Hepatic effects of alcoholism?
Hepatic: Fatty liver –> hepatitis–> cirrhosis
AST: ALT >2, increased GGT.
GIT effects of alcoholism?
- Gastritis, erosions
- PUD
- Varices
- Pancreatitis
- Carcinoma
CNS effects of Alcoholism?
- Poor memory/cognition
- Peripheral polyneuropathy (mainly sensory)
- Wernicke’s encephalopathy: confusion, ophthalmoplegia (nystagmus, LR (6th nerve palsy - eye cannot turn outwards, looking in slightly), ataxia. –> Mamillary bodies.
- Korsakoff’s: amnesia –> Confabulation
- Fits, Falls
Cardiac effects of alcoholism?
Arrhythmias: e.g AF
Dilated cardiomyopathy (completely reversible)
Increased BP
Blood effects of alcoholism?
Increased MCV
Folate deficiency –> anaemia
What questions can you ask in an alcoholism history?
CAGE
- Cut Down?
- Annoyed by people’s criticisms?
- Guilty about drinking?
- Eye opener?
What are the signs of alcohol withdrawal?
10-72hrs after last drink
- Consider in new ward pt (<3 days) with acute confusion
- Signs
= increased HR, decreased BP, tremor
= Confusion, fits, hallucinations: esp formication (DTs).
What is the management of alcohol withdrawal?
- Tapering regime of chlordiazepoxide PO 50-100mg /lorazepam IM
- Thiamine
Investigations to order in alcohol withdrawal?
- Serum urea (in case it is renal)
- Serum Creatinine
- Liver function (hepatic dysfunction)
- Electrolytes (Na/K)
What is the management of alcoholism?
Group therapy or self-help AA
- Naltrexone (50-100mg) OD: patients still drinking + Decreased pleasure.
- Acamprosate: 666mg TDS. Decreases cravings
- Disulfiram (500mg orally for 1 week then 250mg) : aversion therapy
- Baclofen: decreased cravings
What is the presentation of alcoholic hepatitis?
- Anorexia
- Diarrhoea, vomiting,
- Tender hepatomegaly,
- Ascites
- If severe = Jaundice, varices, encephalopathy
What is the investigations for alcoholic hepatitis?
- Bloods: increased MCV, Increased GGT, AST: ALT >2, elevated bilirubin, decreased albumin, INR prolonged
- Ascitic tap
- Abdo US + PV duplex - fatty liver, hepatomegaly, cirrhosis
Management of alcoholic hepatitis?
- Stop ETOH
- Management of withdrawal
- High Dose B vitamins: Pabrinex
- Optimise nutrition (BCAA)
- Immunisation - Pneumo, influenza, Hep A/B.
- Daily weights, LFTs, U+E, INR
- Mx complications of liver failure
- Corticosteroids for severe alcoholic hepatitis. HDF valve >32.
Score for prognosis of alcoholic hepatitis?
Maddrey score - Looks at Prothrombin, thrombin and bilirubin.
- Mild: 0-5% 30 day mortality
- Severe: 50% 30d mortality
- 1yr after admission: 40% mortality
Name the types of Viral hepatitis, their spread and cause?
Type A = Faeco-Or, by seafood (especialyl abroad).
Type B = IV, from blood, body fluids, babies (vertical)
Type C = IV, mainly blood, less vertical.
Type D, IV = Dependent on prior Hep B infection
Type E = FO - Developing world.
What is the presentation of the prodromal phase of viral hepatitis? Which virus has a prodromal phase?
Seen in Hep A and B
- Flu-like, malaise, arthralgia, nausea.
- Distaste for cigarettes in Hep A.
- Ranged between 5-7 days.
What is the presentation of the icteric phase in hepatitis?
- Acute jaundice in A>B>C (99, 75, 25%)
- Hepatitis (abdo pain, hepatomegaly, cholestasis: Dark urine, pale stools.
What are the signs of the prodromal phase of hepatitis A and B.
- Splenomegaly
- Right upper quadrant pain
- Posterior cervical adenopathy
- Bradycardia
During the icteric phase what distinguishes Hep A from Hep B?
Hep B has extrahepatic features (serum sickness syndrome):
- Urticaria or vasculitis rash
- Cryoglobulinaemia
- PAN (polyarteritis nodosa)
- GN (glomerulonephritis)
- Arthritis
Which hepatitis notably has a chronic phase?
Hepatitis C and Childhood Hep B
- Can lead to cirrhosis and increased risk of HCC.
Chronic phase in Hep B facts?
Carriers = 10%. HBsAg +ve > 6 months.
- Chronic hepatitis: 10%
Cirrhosis: 5%
Chronic phase in Hep C facts?
Carrier: 80% - HCV RNA+ve > 6 months.
Chronic hepatitis: 80%
Cirrhosis: 20%
Investigations in hepatitis B?
- FBC,
- LFTs (Raised ALT/AST), Alk phos,
- HBsAg for more than >6 months = chronic HBV infection. Implies ongoing infection - either acute or chronic if present >6 months.
- Serum anti-HBs = Provides life-long immunity, suggests resolved infection and is also detectable in those immunised with HBV vaccine.
Therefore positive HBs and negative anti-HBs means no immunity and hence means that patient is chronically infected.
- Serum anti-HBc = IgM anti-HBc may be only way of diagnosing acute HBV infection. Anti IgM is acute.
- Serum anti-HBc (IgM + IgG) = IgM anti-HBc appears during acute or recent hep B and present for 6 months. Positive in acute infection, chronic infection. Single best test for screening household contacts of HBV infection.
- Serum HBeAg = indicates high likelihood of developing chronic HBV infection with HIGH viral replication.
- clotting
Ground glass appearance of the cytoplasm of hepatocytes.
Investigations for Hepatitis C?
- Enzyme immunoassay or Hep C antibodies (Exposure to Hep C)
- NAATs (active infection)
- Viral genotyping (predicts response to antiviral therapy)
Management of Hep B?
Acute HBV infection?
- Supportive care
- Some patient suitable for antiviral (Lamivudine, entecavir)
Chronic HBV infection:
- Entecavir, tenofovir, peginterferon alpha.
Management of Hep C?
Acute HCV
- Monitor or decide to start treatment
Chronic infection
- Ribavirin, NS3 protease inhibitor, sofosbuvir.
What does NAFLD stand for?
Non-alcoholic Fatty Liver Disease
What is NAFLD?
- Cryptogenic cause of hepatitis and cirrhosis associated with insulin resistance and the metabolic syndrome.
- Non-alcoholic steatohepatitis is most extreme form and –> cirrhosis in 10%.
NAFLD presentation?
- Typically asymptomatic
- Obesity, insulin, diabetes, hyperlipidaemia, HTN, metabolic syndrome.
- Absence of alcohol use
- Fatigue and malaise
- Hepatosplenomegaly
- truncal obesity
- Right upper quadrant abdo discomfort
A 42-year-old man is referred to the liver clinic with mild elevation in aminotransferases for several years. He has a medical history significant for obesity, hypertension, and hypercholesterolaemia. He does not smoke or drink alcohol and there is no high-risk behaviour. He has a family history of premature cardiac disease. He is taking a diuretic and, because of his elevated liver tests, was recommended to discontinue his statin medication several months ago. Other than complaints of mild fatigue, the patient feels well. Examination is notable for a BMI of 37 kg/m², truncal obesity, and mild hepatomegaly.
Likely cause?
NAFLD
A 40-year-old asymptomatic man presents for a routine visit with elevated alanine aminotransferase (ALT) level (55 international units [IU]/mL). His mother died of hepatocellular carcinoma and he has a middle-aged sister with “hepatitis B infection”. He has a normal physical examination and has no stigmata of chronic liver disease.
Likely cause?
Hepatitis B presentation
Hepatitis C presentation
A 60-year-old man presents with several months of gradually worsening abdominal swelling, intermittent haematemesis, and dark stool. He denies chest pain or difficulty breathing. Past medical and family history are not contributory. Past surgical history is significant for back surgery requiring blood transfusion in 1990. Social history is significant for occasional alcohol use. BP is 110/80 mmHg. Physical examination is significant for spider angiomata on the upper chest, gynaecomastia, caput medusae, and a fluid wave of the abdomen. The rest of the examination is normal.
A 62-year-old man presents for a routine initial visit in New York. He has occasional arthralgia or myalgia, and takes an ACE inhibitor and a thiazide diuretic for hypertension. A retired accountant and non-smoker, he drinks 1 or 2 beers per week and denies current drug use. Physical examination is normal except for being overweight. Routine blood chemistries are normal, but a screening hepatitis C virus (HCV) antibody test is positive. At follow-up, the patient is concerned about whether he will develop liver problems. He had heard on television that new oral medications are easier to take than older regimens that used injections and asks about the next diagnostic and treatment steps.
What are the components for metabolic syndrome associated with NAFLD?
- Central obesity (increased waist circumference) and two of:
- Increased triglycerides
- Decreased HDL
- HTN
- Hyperglycaemia: DM, IGT, IFG
What are the investigations for NAFLD?
BMI Liver profile: increased (AST: ALT <1) Glucose Fasting lipids Liver biopsy
In patients with incidental finding of NAFLD - typically asymptomatic fatty changes on liver US. Liver Fibrosis blood test should be performed to assess for more severe liver disease.
- Hyaluronic acid + procollagen III + tissue inhibitor of metaloproteinase 1.
Associated with obesity, T2DM, hyperlipidaemia, jejunoileal bypass.
Sudden weight loss/starvation.
Management of NAFLD?
- Diet + Exercise
- Control HTN, DM, Lipids
- Consider surgery (Roux en Y)
What is Budd-Chiari Syndrome?
Hepatic vein obstruction (from level of small hepatic veins to inferior vena cava) –> ischaemia and hepatocyte damage –> Liver failure or insidious cirrhosis
What are the causes of Budd-Chiari Syndrome?
- Hypercoagulable state -
- Myeloproliferative disorders (PV most common), PNH, anti-phospholipid, OCP.
Local Tumour: HCC
Congenital: membranous obstruction of IVC
What is the presentation of Budd-Chiari?
Triad
- RUQ pain: stretching of Glisson’s capsule
- Hepatomegaly
- Ascites: SAAG >1.1g/dL
Jaundice (and other features)
What are the investigations for Budd-Chiari?
Bloods: FBC, clotting (prolonged prothrombin), LFTs
US + hepatic vein Doppler. Very sensitive and is radiological investigation.
Ascitic Tap: increased protein (>2.5g/dL), with increased SAAG (>1.1g/dL)
Other: JAK2 mutation analysis, RBC, CD55 and CD59 (PND)
What are the treatments for Budd-Chiari?
- Treat underlying disease
- Anticoagulate: unless varices present
- Ascites: fluid and salt restrict, spiro, frusemide, tap, daily weights
- Other options: Thrombolysis, angioplasty, TIPSS
- Transplant if fulminant hepatic failure or cirrhosis
What is the epidemiology of Hereditary Haemochromaosis?
- Prevalence: 1/3,000; 10% are carriers
- Age of onset - 40-60 years (women later due to menses)
What are the genetic associations of Hereditary Haemochromaosis?
Autosomal recessive: HFE gene (High FE) on chromosome 6 (C282Y)
What is the pathophysiology of Hereditary Haemochromaosis?
Inherited, mutisystem disorder resulting from abnormal iron metabolism
Increased intestinal Fe absoprtion (increased enterocyte DMT + decreased hepatocyte hepcidin) -> deposition in multiple organs
Clinical features of Hereditary Haemochromaosis?
Early signs: Fatigue, erectile dysfunction and arthralgia.
iron MEALS
-Myocardial:restricted then dilated cardiomyopathy, arrhythmia
- Endocrine:
- Pancreas (DM),
- pituitary (hypogonadism -> amenorrohea, infertility), - parathyroid (hypocalcaemia, osteoporosis)
The menses delay presentation due to reducing iron.
- Arthritis: 2nd and 3rd MCP joints, knees and shoulders
- Liver: Chronic liver disease -> cirrhosis -> HCC and hepatomegaly
- Skin: slate grey discolouration
- tan + cirrhosis + pseudogout + RCM/DCM + hypogonadism + DM.
Investigations for Hereditary Haemochromaosis?
- Bloods: increased LFT, ferritin (>55) , iron, LOW TIBC, glucose, genotype
Transferrin = protein that iron binds to for transport. INcreased iron so more available to bind to transferrin so saturation goes up. Ferritin is the intracellular storage form of iron therefore going up.
TIBC - binding sites on transferrin - less capacity so low.
- XR - chondrocalcinosis (cartilage calcification)
- ECG, ECHO (heart failure)
- Liver biopsy - Pearl’s stain to quantify Fe and severity
- MRI liver- can estimate iron loading
Screening - General population: transferrin saturation > ferritin
Family members: HFE genetic testing
Treatment of Hereditary Haemochromaosis?
- Iron removal : venesection - aim for Hct <0.5, (transferrin <50) Desferrioxamine is 2nd line
- General: Monitor DM, low Fe diet
- Joint x-ray = Chondrocalcinosis
- Screening: Se ferritin and genotype, screen 1st degree relatives
- Transplant in cirrhosis
Prognosis of Hereditary Haemochromaosis?
- Venesection returns life expectancy to normal if non-cirrhotic and non-diabetic
- Cirrhotic patients have >10% chance of HCC
Epidemiology of alpha1-Antitrypsin Deficiency?
- Prevalence: 1/4,000; 10% are carriers
Genetic relations of alpha1-Antitrypsin Deficiency?
Autosomal recessive, Chromosome 14
Homozygotes have PiZZ phenotype
Pathophysiology of alpha1-Antitrypsin Deficiency?
alpha1-Antitrypsin (a1AT) is a serpin involved in control of inflammatory cascade inhibiting neutrophil elastase
a1AT is synthesised in liver and comprises 90% of sea10globulin on electrophoresis
Presentation of alpha1-Antitrypsin Deficiency?
Variable
- Neonatal and childhood hepatitis
- 15% adults develop cirrhosis by 50 Y
- 75% adults have emphysema (especially smokers)
Investigations for alpha1-Antitrypsin Deficiency?
- Blood - reduced serum a1AT levels
- Liver biopsy: PAS+ve, diastase-resistant globules
- CXR: emphysematous changes
- Spirometry: obstructive defect
- Prenatal Dx: possibly by CVS
Management of alpha1-Antitrypsin Deficiency?
Mostly supportive for pulmonary and hepatic complications
- Quit smoking
- Can consider a1AT therapy from pooled donors
Wilson’s Disease epidemiology?
Prevalence: 3/100,000
Age: presents between childhood and 30 (never >56)
Genetics: AR, ATP7B gene on Chr 13
What is the pathophysiology of Wilson’s disease?
- Mutations of the Cu transporting ATPase
- Impaired hepatocyte incorporation of Cu into caeruoloplasmin and excretion into bile
- Cu accumulation in the liver and in other organs
What are the clinical features of Wilson’s Disease
- Cornea - Kayser Fleischer rings (70% may need slit-lamp)
- Liver disease - Children present with acute hepatitis with necrosis/ cirrhosis
- Arthritis Chondrocalcinosis/Osteoporosis
- Neurology - Parkinsonism = Bradykinesia, tremor, chorea, tics. Ataxia + depression, dementia, psychosis.
- Kidney - Fanconi’s syndrome (T2 RTA) type 2 renal tubular acidosis loss of bicarbonate) Osteomalacia
- Abortions
- Haemolytic Anaemia
Mnemonic of Wilson’s clinical symptoms
CLANKAH
- Cornea
- Liver
- Arthritis
- Neurology
- Kidney - Fanconi’s syndtome
- Abortions
- Haemolytic anaemia - Coombs negative
Investigations of Wilson’s Disease?
- Bloods: decreased copper, decreased caeruloplasmin.
Caeruloplasmin is an acute-phase protein + may be high during infection. May be low protein states: nephrotic syndrome or malabsorption
- Increased 24hr urinary copper
- Liver Biopsy: increased hepatic copper
- MRI: basal-ganglia degeneration
Management of Wilsons
- Conservative: Diet = Avoid high Cu foods: liver, chocolate, nuts.
- Medical: Penicillamine lifelong (Cu Chelator). SE: Nausea, rash, decreased WCC, decreased Hb, decreased plats, lupus haematuria. Monitor FBC and urinary Cu excretion.
- Liver Tx if severe liver disease
- Screen siblings
Autoimmune Hepatitis pathophysiology
- Inflammatory disease of unknown cause characterised by Abs directed vs hepatocyte surface antigens
- Predominately young and middle-aged women
- Classified according to Abs
T1 = Adult, SMA+ (80%), ANA+ (10%), Increased IgG
T2 = Young, LKM+
T3 = Adult, SLA+
AIH Presentation?
Teens and early 20s (25%)
- Constitutional: fatigue, fever, malaise
- Cushingoid: hirsute, acne, striae
- Hepatitis
- HSM (hepatosplenomegaly)
- Fever
- Amenorrhoea
- Polyarthritis
- Pulmonary infiltration
- Pleurisy
Post/peri-menopausal
- Present insidiously with chronic liver disease
Associated diseases with AIH?
- Autoimmune thyroiditis
- DM
- Pernicious anaemia
- PSC
- UC
- GN
- AIHA (Coombs +ve)
Investigations for AIH?
- Increased LFTs
- Increased IgG
- Auto Abs: SMA, LKM, SLA, ANA
- Decreased WCC + decreased platelets due to hypersplenism
- Liver Biopsy
Management of AIH?
Immunosuppression
- Prednisolone
- Azathioprine as steroid-sparer
Liver Transplant (disease may recur)
Prognosis of AIH?
- Remission in 80% of patients
- 10yr survival 80%
What is primary biliary cholangitis?
Intrahepatic bile duct destruction by chronic granulomatous inflammation –> cirrhosis
Epidemiology of PBC?
Prev: <4/100,000
Sex: F»M = 9.1 (90% womeN)
Age: 50
Middle age woman with liver failure - signs of rheum/autoimmune conditions.
Presentation of PBC
THe M rule of Primary Biliary Cholangitis - Anti-Mitochondrial antibodies, middle aged females, IgM.
- Often asymptomatic and Dx incidentally (Increased ALP)
- Jaundice occurs LATE
- Pruritis and fatigue - occurs first.
- Pigmentation of face
- Bones: osteoporosis, osteomalacia (decreased VIt D)
- Big organism: hepatosplenomegaly
- Cirrhosis and coagulopathy (decreased Vit K)
- Cholesterol increased: xanthalasma, xanthomata
- Steatorrhoea
Associated disease of PBC?
- Thyroid
- RA, Sjogrens, scleroderma
- Coeliac
- Renal tubular acidosis
- Membranous GN
Investigations for PBC?
LFTs: very high ALP, very high GGT, moderately high AST/ALT.
Abs: AMA + (98%) Increased IgM Increased Cholesterol ± Increased TSH US to exclude extra-hepatic cholestasis Liver biopsy: non-caseating granulomatous inflammation
Management of PBC?
Symptomatic:
- pruritis: cholestyramine, naltrexone
- Diarrhoea: Codeine phosphate
- Osteoporosis: bisphosphonates
Specific
- ADEK vitamins
- Ursodeoxycholic acid: decreased LFTs but no effect on mortality or need for transplant
- Immunomodulatory therapy: Prednisolone 20-30mg orally once daily intially. Can consider azathioprine or mycophenolate mofetil.
Liver transplant
- End stage disease or intractable pruritis
- Recurrence occurs in 20% but doesn’t usually lead to graft failure.
Primary sclerosing cholangitis - what is it?
Inflammation, fibrosis of strictures and intra- and extra-hepatic ducts. Chronic biliary obstruction –> 2ndry biliary cirrhosis –> liver failure
Epidemiology of PSC?
Epidemiology
- Age: 30-50yr
- Sex: M>F = 2: 1
Presentation of PSC?
May be asyptomatic and diagnosis incidentally (increased ALP).
Symptoms of PSC?
- Jaundice
- Pruritus
- Fatigue
- Abdo pain
Signs of PSC?
- Jaundice: dark urine, pale stools
- Hepatosplenomegaly
Complications of PSC
- Bacterial cholangitis
- Increased cholangiocarcinoma
- Increased risk of colorectal carcinoma
Associated diseases with PSC?
- 3% of those with UC have PSC
- 80-100% of those with PSC have UC/Crohns
- Crohns much raiser
- AIH
- HIV
Investigations for PSC?
- LFTs: increased ALP initially, then increased BR
- Abs: pANCA, ANA and SMA may be +ve
- MRCP: beaded appearance of ducts (beads on string) is standard to diagnose primary sclerosing cholangitis.
- Can use ERCP if MRCP is contra-indicated.
They are the investigation of choice for diagnosing PSC.
Biopsy: fibrous, obliterative cholangitis
Management of PSC?
- No curative medical therapy: transplant needed
- Symptomatic:
Pruritus: colestyramine, naltrexone
Diarrhoea: codeine phosphate - Specific
ADEK vitamins
Ursodeoxycholic acid improves cholestasis only
Abs - Screening
Cholangiocarcinoma: US + Ca19-9
CRC: colonoscopy
Transplant
- Recurrence occurs in 30%
High risk
Liver Tumours pathology?
90% are 2ndry mets
-primary in men: stomach, lung colon.
- primary in women: breast, colon, stomach, uterus
- Less common: pancreas, leukaemia, lymphoma
90% of primary tumours are HCC
- Benign tumours: haemangiomas = reddish purple hypervascular lesion. Hyperechoic on US.
- Liver adenomas = Linked to OCP. Solitary lesion sharply demarcated. Mixed echoity, hypodense.
cyst.
Symptoms of liver tumours?
- Benign tumours usually asymptomatic
- Systemic: fever, malaise, weight loss, anorexia
- RUQ pain: stretching of Glisson’s capsule
- Jaundice is often late except in cholangiocarcinoma
- May rupture –> intraperitoneal haemorrhage
Signs of liver tumorus
- Hepatomgealy: smooth, hard or irregular
- Signs of chronic liver disease
- Abdominal mass
- hepatic bruit (HCC)
Investigations for liver tumours
Bloods: LFTs, Hepatitis serology, AFP (HCC)
Imaging: US or CT/MRI ± guided diagnostic biopsy
ERCP + biopsy in suspected cholangiocarcinoma
- Biopsy (seeding may occur along tract)
- Find primary e.g colonoscopy, mammography
What are liver mets?
- Rx and prognosis vary with type and extent of primary
- Small solitary CRC mets may be resectable
- Advanced disease therefore prognosis < 6months.
Hepatocellular carcinoma epidemiology?
- Rare in west, common in china and sub-saharan africa
Causes of HCC?
- Viral hepatitis
Hepatitis B most common cause in world
Hepatitis C most common cause in Europe - Screening with ultrasound (+/- alpha-fetoprotein) for high risk groups.
- Patients liver cirrhosis secondary to hepatitis B and C or haemochromatosis.
- Men with liver cirrhosis secondary to alcohol
- Cirrhosis: EtOH, HH, PBC
- Aflatoxins (produced bu aspergillus
Management of HCC?
- Resection of solitary tumours improves prognosis (13–> 59%), but 50% have recurrence
- Also: Chemo, percutaneous ablation and embolisation (transarterial chemoembolisation).
Sorafenib: mutlikinase inhibitor.
Staging of HCC?
Staging = Liver MRI, chest abdo and pelvic CT. Check testes.
BCLC - 0A, B, C,D.
A = Liver transplantation alongside TACE (transarterial chemo-embolisation and/or radiofrequency ablation bridging therapy.
B = TACE + percutaneous ablation
C = sorafenib or lenvatinib - oral multikinase inhibitors.
D = Hospice care (± liver transplant)
Cholangiocarcinoma is a malignancy of what?
- Biliary tree malignancy
Causes of cholangiocarcinoma?
- Flukes (clonorchis)
- PSC
- Congenital biliary cysts
- UC
(intrahepatic from cirrhosis + Hep B + C.
Presentation of cholangiocarcinoma?
Fever, malaise
Abdo pain, ascites, jaundice
Increased bilirubin, increased ALP
Diagnosis
- Obstructive picture with liver function tests-
- Ca 19-9^^, CEa, CA125
- CT/MRI and MRCP
Management of cholangiocarcinoma?
30% resectable
- Consider neoadjuvant chemo or chemoradiotherapy.
- Palliative stenting: percutaneous or ERCP
Types of Liver transplant in CLD?
- Cadaveric: heart-beating or non-heart beating
- Live - right lobe
Indications of liver transplant?
- Advanced cirrhosis
- HCC
- Cholangiocarcinoma
- Alpha-1 antitrypsin deficiency.
Contraindications of liver transplant?
- Extra-hepatic malignancy
- Severe cardiorespiratory disease
- Systemic sepsis
- HIV infection
- Non-compliance with drug therapy
Management of post-op Liver transplant?
- 12-24hr on ITU
- Immunosuppression
: Ciclosporin/Tacrolimus +
Azathioprine/Mycophenolate Mofetil +
Prednisolone
Complications of post-op liver transplant?
- Acute rejection (T-cell mediated) 50% @ 5-10 days Pyrexia, tender hepatomegaly increased or change immunosuppressants - Sepsis - Hepatic artery thrombosis - CMV infection - Chronic rejection (6-9 months): shrinking bile ducts - Disease recurrence (e.g HBV)
Prognosis of liver transplant in CLD?
Depends on disease aetiology
60-90% 5 yrs.
Inflammatory bowel disease - which is more common?
UC = 100-200/100,000 Crohns = 50-100/100,000.
Are Crohns or UC patients younger?
Crohns = 20s UC = 30s
Smoking with IBD?
UC is protective
Crohns increased risk
Immune response in UC/Crohns?
UC = TH2 mediated Crohns = Th1/Th17 mediated
Macroscopic location of UC?
Rectum + colon + backwash ileitus
Macroscopic location of Crohn’s?
Mouth to anus esp terminal ileum
Distribution of UC
Contiguous
Distribution of Crohns
Skip lesions
Which IBD do you get strictures?
Crohns
Microscopic inflammation of UC?
Mucosal
Crypt Abscesses
Microscopic inflammation of Crohns?
transmural
- Granulomas
- Increased goblet cells
Ulceration in UC?
Shallow and broad
Ulceration in Crohns?
Deep, thin, serpiginous –> Cobblestone mucosa
Fibrosis in which IBD?
Crohns
Granulomas in which IBD?
Crohns
Pseudopolyps in which IBD?
Ulcerative Colitis
Fistulae in which IBD?
Crohns
Systemic symptoms presentation of IBD
Fever
Malaise
Anorexia
Weight Loss
Abdominal symptoms presentation in UC?
- Diarrhoea
- Blood ± mucus PR
- Abdominal discomfort
- Tenesmus, faecal urgency (more rectally)
Nocturnal diarrhoea and incontinence are typical features of IBD.
Abdominal symptoms presentation in Crohns?
- Diarrhoea (not bloody mostly)
- Abdominal pain
- Weight loss more prominent
- Extra-intestinal signs
Abdominal signs for UC?
- Fever
- Tender, distended abdomen
Abdominal signs for Crohns?
- Aphthous ulcers
- glossitis
- Abdominal tenderness
- RIF mass
- Perianal abscesses, fistulae, tags
- Anal/rectal stricture
Extra-abdominal manifestations in IBD? Skin?
Skin
- Clubbing
- Erythema nodosum
- Pyoderma gangrenosum (not related to disease activity)
Perianal skin tags in Crohns
Extra-abdominal manifestations in IBD? Eyes
Eyes
- Iritis
- Episcleritis
- Conjunctivitis
Extra-abdominal manifestations in IBD? Joints?
- Arthritis (non-deforming, asymm) (related to disease activity - if asymmetrical)
- Sacroiliitis
- Ank Spondylitis
- Osteoporosis (related to disease activity)
HPB
- PSC + cholangiocarcinoma (mainly UC). UC has PSC - (not related to disease activity) Primary sclerosing cholangitis
- Gallstones (esp. Crohn’s)
- Fatty liver
Other
- Amyloidosis
- Oxalate renal stones (esp. Crohns)- due to reduced bile acid reabsorption
Complications for UC
- Toxic megacolon = Diameter >6cm - Risk of perforation
- Bleeding
- Malignancy
: CRC in 15% with pancolitis for 20yrs
: cholangiocarcinoma - Strictures –> obstruction
- Venous thrombosis
Complications of Crohn’s?
Fistulae
- Entero-enteric/colonic –> diarrhoea
- Enterocutaneous = intestine to skin (high or low) output. Can be duodenal/jejunal fistulae which excoriates skin. Colo-cutaneous fistulae leak faeculent material.
- Enterovesical –> frequency as it goes to bladder.
Investigate with Pelvic MRI to categorise course of fistula.
Management
- Heal provided no underlying IBD.
- When skin involvement = protect underlying skin with stoma bag.
- Nutritional complications may require need for TPN.
- Crohns perianal fistula requires drainage through use of setons.
UTI - Enterovaginal - Perianal --> Pepperpot anus. Abscesses - Abdominal, anorectal Malaborption - Fat --> Steatorrhoea, gallstones - B12 --> megaloblastic anaemia - Vit D --> osteomalacia - Protein --> Oedema
Toxic megacolon and Ca may occur (< cf UC)
What are the blood investigations for ulcerative colitis?
Ix - Bloods: FBC: decreased Hb, Increased WCC LFTs: decreased albumin Increased CRP/ESR (>30 suggestive of a severe flare up)
Faecal calprotectin.- NICE advise the use of faecal calprotectin to differentiate IBS from IBD.
Blood cultures
What are the stool investigations for UC?
MCS: exclude campy, shigella, salmonella
CDT: C.diff may complicate or mimic
Imaging for UC?
AXR: megacolon (>6cm) wall thickening (also caused by C.diff, ameobosis)
CXR: Perforation
CT
Ba/gastrograffin enema
- Lead-pipe: no haustra
- Thumbprinting: mucosal thickening
- Pseudopolyp: regenerating mucosal island
- Ileocolonoscopy + regional biopsy: Baron Score
= Minimum of two biopsies from at least 5 sites along the colon, including the rectum and terminal ileum.
During acute flares endoscopic examination should be limited to flexible sigmoidoscopy without bowel prep, due to increased risk of perforation.
Severity of UC assessment?
Truelove and Witts Criteria
- Motions (<4), (4-6), <6
- PR bleed (small, moderate, large)
- Temp (aprexic) or (>37.8)
- HR (>70), >90
- Hb (>11) (<10.5)
- ESR <30 >30
Management of Acute Severe ulcerative colitis?
- Resus: Admit, IV hydration, NBM
- Hydrocortisone: IV 100mg QDS + PR. (IV ciclosporin can be used if steroids are contraindicated). If after 72hrs no improvement, consider ciclosporin IV + steroids or surgery.
- Transfuse if required
- Thromboprophylaxis: LMWH
- Monitoring
Bloods: FBC, ESR, CRP, U+E
Vitals + stool chart
Twice daily examination
± AXR
Acute complications of acute severe ulcerative colitis
- Perforation
- Bleeding
- Toxic Megacolon (>6cm)
- VTE
Later on - DALM lesion can lead to metasitic disease.
How to manage an improving acute flare up UC patient?
- Switch to oral pred + a 5-ASA
- Taper pred after full remission
How to manage a severe UC patient that is not improving
Rescue therapy?
- On day 3: Stool frequency >8, or CRP >45: Predicts 85% chance of needing a colectomy during the admission.
- Discussion between patient, physician and surgeon.
Medical: cyclosporin, infliximab, visiliuzumab (anti-T)
Surgical
Inducing a remission in mild/moderate disease in an OPD-basis?
Oral -
1st line: 5-ASAs (mesalazine) - 1000mg once daily at bedtime for 3-6 weeks.
2nd line: prednisolone (30-40mg)
Which topical therapies are availabe for mild/moderate UC?
- Mainly for left sided disease
For Mild-to-moderate
- Proctitis: suppositories. Topical, rectal aminosalicylates. For distal colitis rectal masalazine is better. If not improving add oral aminosalicylates. If still not improving give oral steroids.
- More proximal disease: (proctosigmoiditis + left-sided ulcerative colitis)
Rectal 5-ASA ± steroids (prednisolone or budesonide)
If not working switch to high dose oral aminosalicylate or aminosalicylate + steroid.
Extensive (left, transverse and right)
- rectal Aminosalicylate + high-dose oral aminosalicylate.
Maintaining Remission in UC?
1st line: 5-ASA PO- sulfasalazine or mesalazine.
Can lead to Mesalazine > Sulfasalazine in terms of pancreatitis.
(Topical Rx may be used in proctitis)
2nd line - beclometasone dipropionate.
Management of refractory UC?
1st line = Mercaptopurine (2-2.5mg/kg) / Azathioprine
2nd line - TNF-alpha inhibitor = infliximab, adalimumab
3rd line
- vedolizumab or tofacitinib
(Janus Kinase inhibitor)
4th line - Ciclosporin
5th line - Colectomy
Indications for emergency surgery in UC?
- 20% need surgery
- Toxic megacolon
- Perforation
- Extensive haemorrhage
- Failure to respond to medicine
Procedure for UC in emergency?
Emergency presentation - Subtotal colectomy.
This is because removal of the rectum is not always conducted in an emergency setting. End ileostomy is created and rectum is stapled off or left in situ.
Elective = Curative
- proctocolectomy with permanent ileostomy
- proctocolectomy with continent ileostomy
restorative option
- ileal-pouch anal anastomosis (IPAA) ( J pouch) = restorative option. Only when rectum is in situ and cannot usually be underaken
- Panproctocolectomy + permanent end ileostomy (removal of entire colon, rectum and anal canal)
Elective Surgery in UC Indications?
- Chronic symptoms despite medical therapy
- Carcinoma or high-grade dysplasia
Procedures in elective surgery in UC Indications?
- Panproctocolectomy with end ileostomy or IPAA (J pouch)
- Total colectomy with IRA
Surgical complications of UC?
Abdominal
- Small bowel obstruction
- Anastomotic stricture
- Pelvic Abscess
Stoma complications: Retraction, stenosis, prolapse, dermatitis Pouch - Pouchitis (50%): - metronidazole + ciprofloxacin - Decreased female fertility - faecal leakage
Investigations for Crohn’s Disease?
Bloods (top 3 are severity markers)
- FBC: decreased Hb, increased WCC
- LFTs: decreased albumin
- increased CRP/ESR
- Haematinics: Fe, B12, Folate
- Blood cultures
Stools
- MCS: exclude Campy, Shigella, Salmonella
- CDT: C.diff may complicate or mimic
Imaging
- AXR: obstruction, sacroileitis
- CXR: perforation
- MRI: assess pelvic disease and fistula. Assess disease severity
- Small bowel follow-through or enteroclysis (liquid passing through)
Shows: Skip lesions, rose thorn ulcers, cobblestoning: ulceration + mural oedema
- String sign of kantor
Endoscopy
- Ileocolonoscopy + regional biopsy: Ix of choice
- Wireless capsule endoscopy
- Small bowel enteroscopy
Assessment of a severe attack of Crohns?
- Increased temp, increased HR, increased ESR, increased CRP, increased WCC, decreased albumin
Management of an acute flare of Crohns
- Resus: Admit, NBM, IV hydration
- Hydrocortisone: IV + PR if rectal disease. Budesonide is an alternative if cannot be tolerated. 5ASA - Mesalazine is second line. - Azathioprine + mercaptopurine is add-on.
If 5 days without improvement - add:
- Infliximab as refractory disease.
- Abx: metronidazole PO or IV
Thromboprophylaxis: LMWH
- Dietician Review Elemental diet: liquid prep of amino acids, glucose and fatty acids. Consider parenteral nutrition. - Monitoring Vitals + stool chart Daily examination
Management once patient improves from an acute flare in Crohns?
- Switch to oral pred (40mg/d)
Management if patient doesn’t improve after rescue therapy in Crohns?
- Discuss with patient physician and surgeon
- Medical: methotrexate ± infliximab
- Surgical
How to induce remission in mild/moderate disease in Crohns?
OPD treatment
- Supportive = High fibre diet, vitamin supplements.
Oral therapy to induce remission in Crohns?
- 1st line ileocaecal = budesonide
- 1st line colitis = sulfasalazine
- 2nd line: prednisolone (tapering) (or with methotrexate)
- 3rd line: methotrexate
- 4th line: infliximab or adalimumab
Perianal disease in Crohn’s, inducing remission?
Occurs in ~50% Ix: MRI + EUA Rx - Oral antibiotics: metronidazole - Immunosuppression ± infliximab - Local Surgery ± seton insertion
Maintaining remission in Crohn’s Disease?
1st line: azathioprine or mercaptopurine. Ensure you check the thiopurine methyltransferase activity. Leads to greater risk fo severe side effects.
2nd line: methotrexate
3rd line: infliximab/adalimumab
Surgery in Crohn’s?
50-80% need >1 operation in their life
Never curative
Should be as conservative as possible
Indications for Crohn’s?
Disease pattern in Crohns ends in terminal ileal disease - ileocaecal resection.
Emergency
- Failure to respond to medical management
- intestinal obstruction or perforation
- Massive haemorrhage
Elective
- Abscess or fistula
- Perianal disease
- Chronic ill health
- Carcinoma
Procedures in Crohn’s?
Primary remove most of the bowel as Crohns can recur if just segmental. Surgery is NOT a cure.
Severe perianal or rectal = proctectomy (pouch not recommended)
- Limited resection: e.g ileocaecal.
Extensive small bowel resections may result in short bowel syndrome and localised stricturoplasty may allow preservation of intestinal length.
Complications of Crohn’s surgery?
Stoma complications
Enterocutaneous fistulae
Anastomotic leak or stricture
Short gut syndrome?
<1-2m small bowel - Features: Steatorrhoea, ADEK and B12 malabsorption Bile acid depletion --> gallstones -Hyperoxaluria --> renal stones
Rx
- Dieticians
- Supplements or TPN
- Loperamide
Coeliac disease epidemiology
Prev: 0.5-1%
Age: any, bimodal: infancy and 50-60yr
Sex: F>M
Geo: Increased in Ireland and N.Africa
Coeliac Pathophysiology
HLA-DQ2 and DQ8
CD8+ mediated response to gliadin in gluten
What is the presentation of coeliac’s GI malabsorption?
GI malabsorption: fatigue, weakness
- Carbs: N/V/D. Abdo distention + colic, Flatus, weight loss.
- Fat: Steatorrhoea, hyperoxaluria –> Renal stones
- Protein: protein-losing enteropathy
- Haematinic: decreased folate and fe –> Anaemia
- Vitamins: Vit D and ca –> bone pain, osteoporosis
Vit K –> Petechiae and increased INR
B2 (riboflavin)–> angular stomatitis
B1 and B6 –> Polyneuropathy
Other presentations of Coeliacs?
Lymphoma and carcinoma
- Enteropathy - associated T cell lymphoma
- Adenocarcinoma of small bowel
Other Ca: breast, bladder
Immune Associated
- IgA deficiency
- T1DM
- PBC
Anaemia
- Increased or decreased MCV
- Hyposplenism: Howell-Jolly bodies, target cells
Dermatological - Dermatitis herpetiformis: Everyone: Symmetrical vesicles, extensor surfaces - Esp elbows V.itchy responds to gluten-free diet or dapsone Biopsy: granular deposition of IgA Aphthous ulcers
Investigations of Coeliac’s Disease?
- Bloods: FBC, LFTs (decreased albumin), INR, VitD and bone, red cell folate, serum B12.
Iron in proximal, Then folate in jejunum, and then B12 in the terminal ileum.
Likely to be deficient in iron, folate, V12.
- Ab: Anti-endomysial IgA (95% specificity)
1st line: Anti-TTG IgA - Both above decreased with exclusion diet
Anti-Gliadin IgG persists with exclusion diet.
Patient must eat gluten for at least 6 weeks before they are tested.
IgA increased in most but may have IgA deficiency. Need to look for selective IgA deficiency, which would give a false negative coeliac result. Cannot interpret TTG without looking for IgA total.
Stools
- Stool cysts and antibody: exclude Giardia
OGD and duodenal biopsy
- Subtotal villous atrophy
- Crypt hyperplasia
- Intra-epithelial lymphocytes
Management of Coeliac Disease?
Lifelong gluten free diet, - Avoid barley, rye, oats, wheat - OK: Maize, soya, rice - Verify diet by endomysial Ab test Pneumovax for HYPOSPLENISM Dermatitis herpetiformis: dapsone
Annual blood test - FBC, Ferritin, TFTs, LFTs, B12, Folate.
Malabsorption
- Diarrhoea/Steatorrhoea
- Weight loss
- Lethargy
Causes of malabsorption?
- Common in UK: Coeliac, Chronic pancreatitis, Crohn’s (3 Cs)
- Rarer:
decreased bile: PBC, ileal resection, colestyramine
Pancreatic insufficiency: ca, CF, chronic pancreatitis - Small bowel: resection, tropical sprue, metformin
- Bacterial overgrowth: spontaneous, post-op, blind loops, DM, PPIs
Infection: Giardia, Strongyloides, Cryptoparvum, Whipples (Fever, arthritis + steatorrhoea.
PAS Positive macrophages. T.whipplei
Hurry: post-gastrectomy dumping
Investigations for Malabsorption?
Coeliac Tests Stool Microscopy Faecal elastase Hydrogen breath test MRI/CT ERCP (chronic pancreatitis ) Small bowel endoscopy
ELEVATED FOLATE - bacterial overgrowth.
Pancreatic cancer risk factors?
SINED
- Smoking
- Inflammation: chronic pancreatitis
- Nutrition (high fat diet)
- EtOH
- DM
- HNPCC
- MEN
- BRCA2
Pathology of pancreatic cancer?
- Mostly ductal adenocarcinoma
- Metastasis early, present late
- 60% head
- 25% body
- 15% tail
- Endocrine tumours are rare
Presentation of pancreatic cancer?
Typically male >60 Head: painless obstructive jaundice - with dark urine + pale stools Body/Tail: epigastric pain - Radiates to back, relieved sitting forward Anorexia and weight loss Acute pancreatitis Sudden onset DM in the elderly
Signs of pancreatic cancer?
- Epigastric mass
- Jaundice
- Palpable gallbladder
- Thrombophlebitis migrans (Trousseau Sign) - episodes of vessel inflammation due to blood clot
- Splenomegaly: PV thrombosis –> Portal HTN
- Ascites
Investigations of pancreatic cancer?
- Bloods: cholestatic LFTs, increased Ca19-9, increased Ca.
- Imaging: US: pancreatic mass, dilated ducts, hepatic mets allow biopsy
- Can consider CT - HRCT for diagnosis
EUS: better than CT/MRI for staging
ERCP
- Shows anatomy. Allows Stenting.
Management of pancreatic cancer?
Surgery:
- Fit, no mets, tumour <3cm (<10% of patients)
- Whipple’s pancreatoduodenectomy
- Post-op chemo delays progression
- 5yrs = 5-14%
Palliation
- Endoscopic/percutaneous stenting of CBD
- Palliative bypass surgery
- Pain relief: may need coeliac plexus block
Prognosis of pancreatic cancer?
Mean survival <6 months
5yrs = <2 %.
Chronic Pancreatitis Cause?
AGITS
- Alcohol
- Genetic (CF, HH, Hereditary pancreatitis)
- Immune (Lymphoplasmacytic sclerosing pancreatitis (increased IgG4)
- Triglycerides increased
- Structural (Obstruction by tumour or Pancreas divisum)
Presentation of chronic pancreatitis?
- Epigastric pain (bores through to back, relieved by sitting back or hot water bottle –> Erythema ab igne)
- exacerbated by fatty food ot EToH.
- Steatorrhoea
- Weight loss
- DM
- Epigastric mass: pseudocyst
Investigations of chronic pancreatitis?
increased glucose decreased faecal elastase US: pseudocyst AXR: speckled pancreatic calcification CT: pancreatic calcification
Management of chronic pancreatitis?
Drugs
- Analgesia: may need coeliac plexus block
- Creon (Enxymes) /Pancreatin
- ADEK vitamins
- DM management
Diet
- no ETOH
- decreased fat, increased carb
Surgery
- Ind: Unremitting pain, weight loss
- Pancreatectomy
Complications of chronic pancreatitis?
- Pseudocyst
- DM
- Pancreatic cancer
- Biliary obstruction
- Splenic vein thrombosis - splenomegaly
Carcinoid tumours pathology?
Neuroendocrine tumours of enterochromaffin cell origin capable of producing 5HT.
- May secrete 5-HT, VIP, gastrin, glucagon, insulin, ACTH.
- Carcinoid syndrome suggest bypass of first-pass metabolism and strongly assoc with metastatic disease.
- 10% part of MEN1
- Sites
:Appendix: 45%, Ileum 30%, Colorectum 20%, Stomach 10%, Elsewhere in GIT and bronchus.
Consider all as malignant.
Presentation of carcinoid tumours locally?
- Appendicitis
- Intussusception or obstruction
- Abdo pain
Presentation of carcinoid syndrome? 5HT?
- Flushing: Paroxysmal, upper body ± wheals
- Intestinal: diarrhoea
- Valve fibrosis: tricuspid regurg and pulmonary stenosis –> affected the right side of the heart.
- Wheeze: Bronchoconstriction
- Hepatic involvement: bypassed 1st pass metabolism
therefore only when liver mets have occured will you get serotinin syndrome. - Tryptophan deficiency –> Pellagra (3Ds)
May also present with some classic Cushingoid features - moon-face, central fat accumulation and bruising. Cortisol causes hypokalaemia and hypernatraemia.
Investigations of carcinoid tumours?
- Increased urine 5- hydroxindoleacetic acid
- Increased chromogranin A
- CT/MRI: find primary
Management of carcinoid tumours?
Symptoms: octreotide or loperamide
Curative: Resection (tumours are v.yellow, give octreotide to avoid carcinoid crisis)
What is a carcinoid crisis?
Tumour outgrows blood supply or is handled too much –> massive mediator release
- Vasodilator, hypotension, bronchoconstriction, hyperglycaemia
- Management: High-dose octreotide
Prognosis of carcinoid tumours?
- Median survival is 5-8yrs (~3 yrs if mets present)
Nutritional deficiences Vitamin A?
- Xerophthalmia
- Dry conjunctivae, develop spots (Bitots spots)
- Corneas become cloudy then ulcerated
- Night blindness –> total blindness
Taken in excess can be teratogenic
Thiamine deficiency (B1)
Beri Beri
- Wet: heart failure + oedema
- Dry: Polyneuropathy
- Wernicke’s: ophthalmoplegia, ataxia, confusion
Niacin deficiency (B3)
Pellagra - Think about Vegans
- Diarrhoea, Dermatitis, Dementia. Leads to sunburn-like dermatitis rash.
- Also, neuropathy, depression, ataxia
- Causes: dietary, isoniazid, carcinoid syndrome
Pyridoxine B6
Peripheral sensory neuropathy
- Causes: PZA
Cyanocobalamin B12
Glossitis –> Sore tongue
Peripheral neuropathy
- Paraesthesia
- Early loss of vibration and proprioception –> ataxia
SCDC (subacute cord degeneration)
- Dorsal and corticospinal tracts
- Sensory loss and UMN weakness
OVerall mixed UMN and LMN signs with sensory disturbance
- Extensor plantars + absent knee and ankle jerks.
Vitamin C deficiency
Scurvy
- Gingivitis
- Bleeding: gums, nose, hair follicles (petechial)
- Muscle pain/weakness
- Oedema
- Corkscrew hairs
Vitamin D –> osteomalacia
Bone pain + fractures
Vitamin K
Decreased factors 2,7,9, 10 C and S
- Bruising: petechiae
- Bleeding: e.g epistaxis, menorrhagia
Patient with T1DM should also be screened for what?
Coeliac’s
- Villous atrophy = malabsorption
- Associated with dermatitis herpetiformis (vesicular, pruritic skin eruption and AI disorders T1DM and Hepatitis). Associated with HLA-DQ2
Complications of Coeliac’s
- Anaemia = Iron, folate, Vit B12.
- Hyposplenism
- Osteoporosis
- EATL
- Subfertility
Patient with no abdo pain, jaundice but has palpable gallbladder.
Courvoisier’s law states that painless, enlarged gallbladder unlikely to be gallstones.
Pancreatic Cancer
- RF = Age, Smoking, Diabetes, Chronic Pancreatitis, HNPCC, BRCA2
- Classically painless jaundice, loss of exocrine function (steatorrhoea), loss of endocrine function, Trousseau’s sign = migratory thrombophlebitis
- Investigations = US, High resolution CT
Management
- Whipple’s resection (pancreaticoduodenectomy)
- Adjuvant chemo
- ERCP with stenting
Child’s Pugh Classification
A - Albumin B - Bilirubin C - Clotting - Prothrombin D - Ascites E - Encephalopahty
MELD
- Combination of patient’s bilirubin, creatinine, and INR gives mortality 3 month score.
- Model end stage liver disease
- Takes into account aetiology
Ischaemia to the lower GI tract, which part most likely to be affected?
- Acute mesenteric ischaemia (sudden, sharp pain from mostly likely superior mesenteric artery, with a history of AF)
- Chronic mesenteric ischaemia
- ischaemic colitis
- Mesenteric ischaemia
(small bowel, embolism, sudden onset, urgent surgery, high mortality). - Ischaemic colitis
(Large bowel, multifactorial, less severe symptoms, bloody diarrhoea, thumbprinting, conservative management.
Will see high lactate and metabolic acidosis with low bicarb.
- Ischaemic colitis = acute but transcient compromise in blood flow to large bowel. More likely to occur in watershed areas, such as splenic flexure. Located at the borders of the territory supplied by superior and inferior mesenteric arteries.
See Thumbprinting on AXR.
Surgery in a minority of cases if conservative measures fail.
Ischaemic hepatitis?
Diffuse hepatic injury resulting in acute hypoperfusion (shock liver). Usually has a inciting event + marked increased ALT levels 50x normal. Associated with AKI
Rooftop scar?
Liver transplant
Whipples
Rutherford Morrison
Hockeystick scar
- Kidney Surgery
Frequency of liver flap
1Hz. Need 30 second to check for liver flap.
Presentation of Liver
Mr J has evidence of fingernail clubbing conjunctival jaundice, palmar erythema and evidence of digital clubbing.
The jugular venous pressure was elevated and there were mutliple spider naevi in the distribution of the SVC. The abdomen is distended with dilated veins which fills away from the umbilicus suggestive of caput medusae.
I noted 8 finger breadth of smooth-non tender heptaomgealy extending below the right costal margin, There is no associated splenomegaly.
He has a distended abdomen with shifting dullness in keeping with ascites which is non-tense. There is peripheral oedema likely from hypoalbuminaemia.
These finding would be most consistent with a diagnosis of cirrhosis liver disease with some evidence of decompensation.
To complete my examination
- Examine the CVS system to look for underlying valvular heart disease.
- Perform a urine dip to look for glucosuria, as diabetes is a risk factor for NASH
- examine external genitalia looking for loss of secondary sexual characteristics
Perform a DRE to look for melaena as a sign of decompensation
Request a URine dip
Neuro exam for cerebellar ataxia and peripheral neuropathy.
Causes of gynaecomastia
Verapamil Cimetidine Spironolactone Digoxin Cannabis Conns
Clues to CLD
Tatoos/IVDU - viral Xanthelasma - PBC - Tan - haemachromatosis Parotid swelling, neuropathy, gout, cerebellar - alcohol - BM Stix - NASH - Afro-caribbean = Sarcoidosis - Dysarthria, tremor - Wilson's Female, vitilgo - autoimmune - Barrel chest, urse lip breathing
Signs of severity
Cachexia
Organ failure
- Bruising from coagulopathy
- Peripheral oedema (hypoalbuminuria)
- Fetor hepaticus (portosystemic shunting - varices)
- Portal HTN - splenomegaly, ascites, caput medusa + varices.
Causes of decompensation
AScites, jaundice, encephalopathy
Alcohol
Sedatives: Benzos and opiates
NSAIDS - worsen renal failure
- Excess diuretics
- Hypokalaemia - results in decreased renal ammonia.
Excess diuretics
- Hypokalaemia - results in decreased renal ammmonia
Constipation
- Any source of increased protein/nitrogen: GI bleed, renal failure.
Infections: SBP (E.coli is commonest)
Hepatic encephalopathy
Diural sleeping pattern disturbance
Asterixis
Bradykinesia
Decerebrate then coma
Hep +ve doesnt know which one. Rash on his hand which look vasculitis and he has clinically got signs of CLD>
Hepatitis C
What are the Diabetic GI complications
Achalasia Neurological plexus damage Gastroparesis Constipation Diarrhoea Gallstones NASH
Oesophageal malignancy
Until recent times oesophageal cancer was most commonly due to a squamous cell carcinoma but the incidence of adenocarcinoma is rising rapidly. Adenocarcinoma is now the most common type of oesophageal cancer and is more likely to develop in patients with a history of gastro-oesophageal reflux disease (GORD) or Barrett’s.
Diagnosis
- Upper GI endoscopy is the first line test. Gold standard to take biopsy.
- Contrast swallow may be of benefit in classifying benign motility disorders but has no place in the assessment of tumours
- Staging is initially undertaken with CT scanning of the chest, abdomen and pelvis. If overt metastatic disease is identified using this modality then further complex imaging is unnecessary
- If CT does not show metastatic disease, then local stage may be more accurately assessed by use of endoscopic ultrasound
- Staging laparoscopy is performed to detect occult peritoneal disease. PET CT is performed in those with negative laparoscopy. Thoracoscopy is not routinely performed.
Management
- Operable disease is best managed by surgical resection.
The most standard procedure is an Ivor- Lewis type oesophagectomy. This procedure involves the mobilisation of the stomach and division of the oesophageal hiatus. The abdomen is closed and a right sided thoracotomy performed. The stomach is brought into the chest and the oesophagus mobilised further. An intrathoracic oesophagogastric anastomosis is constructed. - Alternative surgical strategies include a transhiatal resection (for distal lesions), a left thoraco-abdominal resection (difficult access due to thoracic aorta) and a total oesophagectomy (McKeown) with a cervical oesophagogastric anastomosis.
- The biggest surgical challenge is that of anastomotic leak, with an intrathoracic anastomosis this will result in mediastinitis. With high mortality. The McKeown technique has an intrinsically lower systemic insult in the event of anastomotic leakage.
In addition to surgical resection many patients will be treated with adjuvant chemotherapy.
Globus Hystericus
- History of anxiety
- Intermittent and relieved by swallowing
- Persistent sensation of having a ‘lump in the throat’ when there is none.
- Usually painless - presence of pain should warrant further investigation.
Triad of chronic mesenteric ischaemia?
- Colicky post-prandial abdominal pain
- Weight loss
- Abdominal bruit
What is a Dieulafoy Lesion?
Tortuous arteriole - located in the upper stomach, which causes an upper GI bleed.
Approximately 6 cm from OG junction.
Gastric cancer
Associated with H.pylori, blood group A: gAstric cancer
Pernicious anaemia (lemon tinge and parasthesia)
Gastric adenomatous polyps
Smoking
Path: Signet ring cells
Features -
- Dyspepsia
- Nausea
- Anorexia
- Dysphagia
Malnutrition definition?
BMI <18.5
Weight loss >10% within last 3-6 months unintentially
BMI <20 and unintentional weight loss >5% within 3-6 months.
Screening with the MUST (Malnutrition Universal Screen Tool).
- Done on admission or if there is concern - pressure sores.
- Takes into account BMI
- Categorises patients into low, medium and high risk.
What is malignant ascites?
Patients with malignancies in the peritoneum which lead to ascites, via increased production of peritoneal fluid + concurrent decreased resorption.
What is the MOA of Metoclopramide
Dopamine antagonist which may worsen symptoms in patients with Parkinson’s.
Metoclopramide is a D2 receptor antagonist* mainly used in the management of nausea. Other uses include:
gastro-oesophageal reflux disease
prokinetic action is useful in gastroparesis secondary to diabetic neuropathy
often combined with analgesics for the treatment of migraine (migraine attacks result in gastroparesis, slowing the absorption of analgesics)
Adverse effects extrapyramidal effects: oculogyric crisis. This is particularly a problem in children and young adults hyperprolactinaemia tardive dyskinesia parkinsonism
Metoclopramide should be avoided in bowel obstruction, but may be helpful in paralytic ileus.
How to calculate units in alcohol?
Alcohol units = volume x ABV/1,000.
Hydatid cyst management?
Hydatid cysts are endemic in Mediterranean and Middle Eastern countries. They are caused by the tapeworm parasite Echinococcus granulosus. An outer fibrous capsule is formed containing multiple small daughter cysts. These cysts are allergens which precipitate a type 1 hypersensitivity reaction.
Clinical features are as follows:
Up to 90% cysts occur in the liver and lungs
Can be asymtomatic, or symptomatic if cysts > 5cm in diameter
Morbidity caused by cyst bursting, infection and organ dysfunction (biliary, bronchial, renal and cerebrospinal fluid outflow obstruction)
In biliary ruputure there may be the classical triad of; biliary colic, jaundice, and urticaria
CT is the best investigation to differentiate hydatid cysts from amoebic and pyogenic cysts.
Surgery is the mainstay of treatment (the cyst walls must not be ruptured during removal and the contents sterilised first).
Drug-induced liver disease - hepatocellular picture?
- paracetamol
- sodium valproate, phenytoin
- MAOIs
- halothane
- anti-tuberculosis: isoniazid, rifampicin, pyrazinamide
- statins
- alcohol
- amiodarone
- methyldopa
- nitrofurantoin
Drug-induced cholestasis picture (+/- hepatitis)
- combined oral contraceptive pill
- antibiotics: flucloxacillin, co– amoxiclav, erythromycin*
- anabolic steroids,
- testosterones
- phenothiazines:
- chlorpromazine,
- prochlorperazine
- sulphonylureas
fibrates
rare reported causes: nifedipine
Liver cirrhosis drugs?
Methotrexate
Methyldopa
Amiodarone
Giardia diarrhoea?
Giardia causes fat malabsorption, therefore greasy stool can occur.
Resistant to chlorination, hence risk of transfer in swimming pool.
Floats in water therefore steatorrhea.
Common causes of hepatomegaly?
- Cirrhosis: if early disease, later liver decreases in size.
Associated with a non-tender, firm liver - Malignancy: metastatic spread or primary hepatoma. Associated with a hard, irregular. liver edge
- Right heart failure: firm, smooth, tender liver edge. May be pulsatile
- viral hepatitis
- glandular fever
- malaria
- abscess: pyogenic, amoebic
- hydatid disease
- haematological malignancies
- haemochromatosis
- primary biliary cirrhosis
- sarcoidosis, amyloidosis
Barrett’s oesophagus
Metaplasia of the lower oesophagus mucosa - squamous being replaced with columnar epithelium.
- Increased risk of adenocarcinoma.
Barrett’s can be subdivided into short (<3cm) and long (>3cm).
Management
- Endoscopic surveillance with biopsies
- High dose PPI: whilst this is commonly used in patients with Barrett’s the evidence .
Endoscopic surveillance
- Metaplasia endoscopy is recommended every 3-5 years
If dysplasia of any grade is identified endoscopic intervention is offered
- Endoscopic mucosal resection
- Radiofrequency ablation
Kochers’ scar
Incision under right subcostal margin e.g. Cholecystectomy (open)
Rooftop
Upper abdomen access for Whipple’s
McEvedy’s
Groin incision e.g. Emergency repair strangulated femoral hernia - NOW OBSOLETE
Rutherford Morrison
Extraperitoneal approach to left or right lower quadrants. Gives excellent access to iliac vessels and is the approach of choice for first time renal transplantation.
Gridiron
Oblique incision centered over McBurneys point- usually appendicectomy (less cosmetically acceptable than Lanz
Refeeding syndrome
- Refeeding syndrome describes the metabolic abnormalities which occur on feeding a person following a period of starvation. It occurs when an extended period of catabolism ends abruptly with switching to carbohydrate metabolism. The metabolic consequences include:
- hypophosphataemia
- hypokalaemia
- hypomagnesaemia: may predispose to torsades de pointes
- abnormal fluid balance
Patients are considered high-risk if one or more of the following:
BMI < 16 kg/m2
unintentional weight loss >15% over 3-6 months
little nutritional intake > 10 days
hypokalaemia, hypophosphataemia or hypomagnesaemia prior to feeding (unless high)
Levels are already depleted due to malnutrition. Carbohydrate ingestion causes insulin release which causes rapid intracellular shift of potassium, magnesium and phosphate
MOA Dimenhydrinate
Histamine H1 receptor antagonist
MOA Ondansetron
5HT-3 serotonin receptor
MOA Chlorpromazine and promethazine
Dopaminergic receptors, used as antipsychotic agents.
Sulphasalazine
Sulphapyridine and 5-ASA
Many side-effect are due to the sulphapyridine moiety: rashs, oligospermia, headache, Heinz body anaemia, megaloblastic anaemia, lung fibrosis.
Other side-effects are common to 5-ASA drugs.
Mesalazine
A delayed released forms of 5-ASA
mesalazine is still however associated with side-effects such as GI upset, headache, agranulocytosis, pancreatitis*, interstitial nephritis
Small Bowel Bacterial overgrowth syndrome
Risk factors for SBBOS
- Neonates with congenital gastrointestinal abnormalities
- Scleroderma
- Diabetes Mellitus
Presents with chronic diarrhoea, bloating, flatulence, abdominal pain
Diagnosis
- Hydrogen breath test
- Small bowel aspiration and culture: this is used less often as invasive and results are often difficult to reproduce
- Clinicians may sometimes give a course of antibiotics as a diagnostic trial. Rifaximin is now treatment of choice.
What is Melanosis Coli?
MElanosis Coli is a disorder of pigmentation of the bowel wall. Histology demonstrates pigment-laden macrophages.
Associated with laxative abuse, especially senna.
Faecal occult blood?
Concerns about bowel malignancy
Calprotectin?
Gut inflammation as part of workup for inflammatory bowel disease.
Hepatitis D?
Think about Hep B patient with IVDU.
Superinfecetion: A hep B surface antigen positive patient subsequently develops Hep D. LEads to fulminant hepatitis, chronic hep status and cirrhosis.
Alcoholic ketoacidosis?
Alcoholic ketoacidosis is a non-diabetic euglycaemic form of ketoacidosis. It occurs in people who regularly drink large amounts of alcohol. Often alcoholics will not eat regularly and may vomit food that they do eat, leading to episodes of starvation. Once the person becomes malnourished, after an alcohol binge the body can start to break down body fat, producing ketones. Hence the patient develops a ketoacidosis.
It typically presents with a pattern of: Metabolic acidosis Elevated anion gap Elevated serum ketone levels Normal or low glucose concentration
The most appropriate treatment is an infusion of saline & thiamine. Thiamine is required to avoid Wernicke encephalopathy or Korsakoff psychosis.
Liver Abscess?
Biliary sepsis is a major predisposing factor
Structures drained by the portal venous system form the second largest source
Common symptoms include fever, right upper quadrant pain. Jaundice may be seen in 50%
Ultrasound will usually show a fluid filled cavity, hyperechoic walls may be seen in chronic abscesses
Amoebic abscess?
Entamoeba Histolytica
Liver abscess is the most common extra-intestinal manifestation of amoebiasis
Between 75 and 90% lesions occur in the right lobe
Presenting complaints typically include fever and right upper quadrant pain.
- profuse, bloody diarrhoea
there may be a long incubation period
stool microscopy may show trophozoites if examined within 15 minutes or kept warm (known as a ‘hot stool’)
treatment is with metronidazole
Ultrasonography will usually show a fluid filled structure with poorly defined boundaries
Aspiration yield sterile odourless fluid which has an anchovy paste consistency
Treatment is with metronidazole
Hydatid cyst
Seen in cases of Echinococcus infection - A parasitic Tapeworm.
Typically an intense fibrotic reaction occurs around sites of infection
The cyst has no epithelial lining
Cysts are commonly unilocular and may grow to 20cm in size. The cyst wall is thick and has an external laminated hilar membrane and an internal enucleated germinal layer
Typically presents with malaise and right upper quadrant pain. Secondary bacterial infection occurs in 10%.
Liver function tests are usually abnormal and eosinophilia is present in 33% cases
Ultrasound may show septa and hyatid sand or daughter cysts.
CT is best to investigate hydatid cyst.
Percutaneous aspiration is contra indicated = this is due to risk of anaphylaxis and seeding of daughter cysts through abdomen.
Treatment is by sterilisation of the cyst with mebendazole and may be followed by surgical resection. Hypertonic swabs are packed around the cysts during surgery
Acute pancreatitis?
Hypocalcaemia = saponification of fats. As lipase leaks out of damaged pancreas = breaks down fat into triglyceride + fatty acid. These combine with calcium to make soap.
Amylase does not correlate with disease severity.
Serum lipase is more sensitive and specific.
Assessment of severity
- Glasgow, Ranson scoring systems and APACHE II
Predicts severe attack with 48hrs = Clinical impression of severity - Body mass index >30 - Pleural effusion - APACHE score >8
24hrs = Clinical impression of severity APACHE II >8 Glasgow score of 3 or more Persisting multiple organ failure CRP>150
48hr
= Glasgow Score of >3
CRP >150
Persisting or progressive organ failure
- Patients with acute pancreatitis due to gallstones should undergo early cholecystectomy.
- Patients with obstructed biliary system due to stones should undergo early ERCP.
- Patients who fail to settle with necrosis and have worsening organ dysfunction may require debridement, fine needle aspiration is still used by some.
- Patients with infected necrosis should undergo either radiological drainage or surgical necrosectomy. The choice of procedure depends upon local expertise.
