Gastroenterology

Omar K
MRCP Ireland
Gastroenterology fellow UMMC
 Dysphagia
1_Diffuse oesophageal spasm causes
intermittent dysphagia ―
chest pain.
Barium swallow:
abnormal contractions,
eg corkscrew oesophagus.
 Achalasia cardia
: The lower oesophageal sphincter fails to relax (due to degeneration
of the myenteric plexus), causing dysphagia (for fluids and solids),
regurgitation,
CXR: fluid level in dilated oesophagus (eg above heart); barium
swallow: dilated tapering oesophagus.
Treatment:
1_endoscopic balloon dilatation, or Heller’s cardiomyotomy—2_then
proton pump inhibitors (PPIS.
3_Botulinum toxin injection if a non-invasive procedure is needed
(repeat every few months).
4_Calcium channel blockers and nitrates also relax the sphincter.
Longstanding achalasia may cause oesophageal cancer.
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 dysphagia
3_Benign oesophageal stricture: Caused by
gastrooesophageal reflux (GORD, corrosives,
surgery, or radiotherapy.
Treatment: endoscopic balloon dilatation
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 Diarrhoea …Constibation
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 Jaundice
• Pre hepatic
• Overproduction: Haemolysis
• Impaired hepatic uptake: Drugs (contrast
agents, rifampicin), right heart failure.
• Impaired conjugation: Gilbert’s,; Crigler–
Najjar,
 Jaundice
• Hepatic
• Viruses: hepatitis (A, B, C), CMV, EBV; drugs; alcohol; cirrhosis;
• liver metastases/abscess; septicaemia; leptospirosis; syphilis; 
• Metabolic 1-anti trypsin deficiency, haemo chromatosis; Wilson’s
disease
• Budd–Chiari (p710); (p269);
• autoimmune hepatitis (AIH)
• failure to excrete conjugated bilirubin (Dubin–Johnson & Rotor
syndromes,
• right heart failure;
• toxins, eg carbon tetrachloride; fungi
 jaundice
• Post hepatic , Impaired hepatic excretion (cholestasis)
• Stones (common bile duct gallstones)
• Primary biliary cirrhosis; primary sclerosing cholangitis;
• drugs (BOX);; pancreatic cancer; compression of the bile duct,
eg lymph nodes at the porta hepatis; cholangiocarcinoma;
• As conjugated bilirubin is water soluble, it is excreted in urine,
making it dark. Less conjugated bilirubin enters
• the gut and the faeces become pale. When severe, it can be
associated with an intractable pruritus which is best treated
by relief of the obstruction.
 Invx
• Depends on the type
 UGIB
• Causes
• Peptic ulcers
• • Mallory–Weiss tear
• • Oesophageal varices
• • Gastritis/gastric erosions
• • Drugs (NSAIDS, aspirin, steroids, thrombolytics, anticoagulants)
• • Oesophagitis
• • Duodenitis
• • Malignancy
• • No obvious cause
MX
• 1_ ABC
• 2_identify the source

• Bleeding varix
Hyperdynamic circulation/increased portal flow,
Formation of collaterals between the portal and systemic
systems, eg in the lower oesophagus and gastric
cardiaGastro-oesophageal varices develop once portal
pressure
• varices may also be found in the stomach, around the
umbilicus (caput medusae
• is rare), and in the rectum.
 Bleeding varix mx
Acute variceal bleeding Get help at the bedside from your senior.
1_ (ABC) Resuscitate until haemodynamically stable
2_ If very anaemic, transfuse to Hb of 80g/L.
3_ Correct clotting abnormalities with vitamin K (p258), FFP and
platelet transfusions.
4_ Start IVI of terlipressin, eg 1–2mg/6h for ≤3d; relative risk of
death  by 34%.
Somatostatin analogues are alternatives
5_ Endoscopic banding (fi g 2) or sclerotherapy should be tried
(banding may be impossible because of limited visualization).
6_ If bleeding uncontrolled, a Minnesota tube or Sengstaken–
Blakemore tube
 Scopes
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 Liver failure
• acute-on-chronic hepatic failure.
• Fulminant hepatic failure is a clinical syndrome
resulting from massive necrosis of liver cells
leading to severe impairment of liver function:
• hyperacute = encephalopathy within 7d of
onset of jaundice;
• acute = within 8–28d;
• subacute = within 5–26wks.
 causes
• Causes Infections: Viral hepatitis (esp B, C, CMV), yellow fever,
leptospirosis.
• Drugs: Paracetamol overdose, halothane, isoniazid.
• Toxins: Amanita phalloides mushroom, carbon tetrachloride.
• Vascular: Budd–Chiari synd., veno-occlusive disease.
• Others: Alcohol, primary biliary cirrhosis, haemochromatosis,
• autoimmune hepatitis, 1-antitrypsin deficiency, Wilson’s
disease,
• fatty liver of pregnancy, malignancy, HELLP syndrome
(Haemolysis, Elevated Liver enzymes and Low Platelets; it is
usually associated with pre-eclampsia) (OHCS p26
 Mx of liver failure
1_treat sepsis,, GI bleeds/varices & encephalopathy:
2_ Nurse with a 20° head-up tilt in ITU. Protect the airway with intubation and insert an NG tube to avoid
aspiration and remove any blood from stomach. • Insert urinary and central venous catheters to help assess fl
uid status.• Monitor T°, respirations, pulse, BP, pupils, urine output hourly. Daily weights.

3_ 10% glucose IV, 1L/12h to avoid hypoglycaemia. Do blood glucose every 1–4h.
4_ Treat the cause, if known (eg GI bleeds, sepsis, paracetamol poisoning, p856). Nacetylcysteine
• probably does not help in non-paracetamol liver failure.
5_• If malnourished, get dietary help: good nutrition can decrease mortality (eg carbohydrate-
• rich foods).
6_ Give thiamine and folate supplements (p728).
7_• Treat seizures with lorazepam (p836).1 14
8_• Haemofiltration or haemodialysis, if renal failure develops
9_ Consider PPI as prophylaxis against stress ulceration, eg omeprazole 40mg/d IV/PO.
10_ Liaise early with nearest transplant centre regarding appropriateness—BOX 4.
11_Treat complications Cerebral oedema: On ITU: 20% mannitol IV; hyperventilate.
12_Ascites: Restrict fl uid, low-salt diet, weigh daily, diuretics (p260).
13_Bleeding: Vitamin K 10mg/d IV for 3d, platelets, FFP + blood as needed ―
 Cirrhosis
• causes
 sbp
• ascitic fluid neutrophil count of more than 250 cells/µL is
the single best predictor of spontaneous bacterial
peritonitis
• Tx
• cefotaxime 2g/6h or tazocin® 4.5g/8h for 5d or until
sensitivities known (+ metronidazole 500mg/8h IV if recent
instrumentation to ascites).
• Give prophylaxis for high-risk patients (albumin, PT/INR,
low ascitic albumin) or those who have had a previous
episode: eg norfloxacin 400mg PO daily continued until
death, transplant, or ascites resolves.
 Hereditary haemochromatosis (HH)
• Sx
• The patient Early on: Nil—or tiredness; arthralgia (2nd+3rd
MCP joints + knee pseudogout);
• Later: Slate-grey skin pigmentation; signs of chronic liver
disease; hepatomegaly; cirrhosis; dilated cardiomyopathy;
osteoporosis.
• Endocrinopathies:
• DM (‘bronze diabetes’ from iron deposition in pancreas);
hypogonadism from pituitary dysfunction (not from
testicular iron deposition, but may be
via cirrhosis,
 Hh mx
• Venesect ~1 unit/1–3wks, until ferritin 50μg/L
(may take 2yrs).
• Iron will continue to accumulate, so
maintenance venesection is needed for life (1U
every 2–3 months to maintain haematocrit
<0.5, ferritin <100μg/L, and transferrin
saturation <40%).
• Consider desferrioxamine (p336) if intolerant of
this. Monitor: LFT and glucose/diabetes
 tx
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 1-antitrypsin (A1AT) deficiency
• lung (emphysema) and liver (cirrhosis and
hepatocellular cancer, HCC)
• A1AT is a glycoprotein and one of a family of serine
protease inhibitors made in the liver that control
inflamatory cascades. Defi ciency is called a
serpinopathy
• The normal genotype is PiMM, the homozygote is
PiZZ;
• heterozygotes are PiMZ and PiSZ (at low risk of
developing liver disease).
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• Serum 1-antitrypsin (usually (eg <11μmol/L or
<75% of lower limit of normal, which is
~0.9g/L; labs vary).
 Immune liver dis
• PBS Mi2 , ADEK , osteoporosis
• PSC
• AIH ASM,ALKLM, ALP
 Wilson d
• Liver cirrhosis + Parkinson`s feature
• Lifelong penicillamine
SE: nausea, rash, WCC low, Hb, platelets,
haematuria, Say “report sore throat, T°, or
bruising at once” in
Trientine dihydrochloride 600mg/6–12h PO (SE:
rash; sideroblastic anaemia).
Liver transplantation
 IBD
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 UC crohn
inflammatory disorder of the transmural granulomatous infl
colonic mucosa affecting any part of the gut from
mouth to anus

cx 1_Perforation and bleeding 1_Small bowel

also: obstruction;
2_Toxic dilatation of colon 2_toxic dilatation (colonic
colonic diameter >6cm).
3_Venous thrombosis: give diameter >6cm,
prophylaxis to all inpatients 3_abscess formation (
4_ Colonic cancer: 4_fistulae eg colovesical
risk ≈ 15% with pancolitis for (bladder), colovaginal,
20yrs. perianal,
enterocutaneous;
perforation;
5_rectal haemorrhage;
6_colon cancer;
7_fatty liver, PSC
8_cholangio carcinoma,
9_renal stones,
10_osteomalacia,
11_malnutrition,
12_amyloidosis
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indicator Bowel motion
mild 5- Oral steroids
ASA3 :sulfasalazine
or mesalazine
Moderate Steroids (oral) Oral steroids

Severe IV steroids IV steroids+ metronid

rescue therapy infliximab infliximab
and adalimumab
 Coeliac disease
• Antibodies: anti-gliadin, transglutaminase
• and anti-endomysial—an IgA anti body,
 Chronic pancreatitis
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 tx
• Drugs: Give analgesia (coeliac-plexus block may give
brief relief);
• 2_lipase, eg CreonR; fat-soluble vitamins (eg MultiviteR).
• 3_Insulin
• 4_. Diet: No alcohol; low fat may help.
• 5_ Surgery: For unremitting pain; narcotic abuse
(beware of this);
• eg pancreatectomy or pancreaticojejunostomy (a duct
drainage procedure