Gastroenterology Flashcards
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
