GI Flashcards
Indications of splenomegaly
Splenomegaly ∆∆
Massive spleen (>8cm):
CML (most common).
Myelofibrosis.
Infections: painful nodes Infectious mononucleosis. Viral hepatitis (large liver). Malaria (recent travel). Haemolytic anaemia (↓Hb). Portal hypertension: Cirrhosis (alcohol; ↑liver initially). Schistosomiasis (travel). Sarcoidosis. Amyloidosis. Rheumatoid arthritis. Renal or colonic mass? Mild spleen (2-4cm): Lymphoma: NHL (extra-nodal disease). HL (20s & old, alcohol pain). Leukaemia: CML (most common; ↑WCC). CLL (chronic, older). ALL (acute, children). AML (acute, gum hypertrophy). Myeloproliferative: Myelofibrosis (large liver). Polycythaemia rubra vera (↑Hb). Essential thrombocythaemia (↑platelets).
Indications of lymphadenopathy
Lymphadenopathy ∆∆ Leukaemia Lymphoma Metastasis (firm, painless). Infectious mononucleosis. Mumps (parotids). Reactive lymphadenitis (soft, mobile, tender. TB, inf. mono., local inf’n). SLE (generalised lymphadenopathy). Sarcoidosis.
Gut nervous system
Enteric Nervous System
“The brain of the gut”: 100 million neurons stretching from oesophagus to the anus. Can function independently.
Myenteric plexus: mainly controls GI tract motility (frequency and strength of contraction) of muscularis.
Submucosal plexus: controls secretory cells of mucosal epithelium; chemoreceptors (chemicals within foods) and stretch receptors (food dispending wall).
Autonomic Nervous System
Vagus (X): supply parasympathetic fibers to most part of the GI tract, except last half of large intestine.
Pelvic Splanchnic: supply parasympathetic fibers to last half of large intestine.
Parasympathetic: parasympathetic nerves form neural connections with ENS. Parasympathetic stimulation cause increase in GI secretion and motility (by increasing activity of ENS neurons).
Sympathetic: form neural connections with ENS. Stimulation decrease GI secretion and motility.
Gastrointestinal Reflex Pathways
Regulate GI secretions and motility in response to GI tract stimuli. Sensory receptors (chemo and stretch) synapse with ENS, CNS and ANS neurons causing response.
Types
Colic, endoderm, vague pain.
Foregut: pharynx – ampulla of Vater. Referred to epigastric region.
Midgut: ampulla of Vater – 2/3 across transverse colon. Referred to umbilical region.
Hindgut: 2/3 across transverse colon – upper part of anus. Referred to hypogastric (pubic) region.
Constant, ectoderm, localized – includes parietal peritoneum.
Signs of gut ischaemia
Arterial, sudden, acidosis, bacteraemia, distention, colicky pain, septic pain out of proportion to physical signs (e.g., ischaemia bowel).
Oesophageal dysmobility
Achalasia: malfunction of myenteric plexus; lower oesophageal sphincter fails to relax as food approaches (dysphagia, regurgitation). Oesophageal distension causes chest pain (often confused with heart origin). Managed by endoscopic dilatation (weakening the sphincter). Bulbar palsy (e.g., motor neurone disease), diabetes mellitus. Oesophageal Diverticula: epithelial pouch causing dysphagia and regurgitation. Usually asymptomatic. Surgically repaired if severe symptoms. Benign Oesophageal Stricture: Peptic stricture (with smooth epithelial wall) secondary to reflux, corrosive ingestion, radiotherapy, varices sclerosis, prolonged NG intubation. Managed by dilatation (occasionally surgery).
Oesophageal carcinoma
Oesophageal Carcinoma
Aetiology: Adenocarcinoma (more common, related to Barrett’s oesophagus), squamous cell carcinoma (becoming more rare). Peaks in 60s. Usually ulcerative lesion, extending around oesophagus, causing stricture.
Clinical features: dysphagia (progressive, unrelenting), pain, weight loss, anorexia, aspiration (late).
Investigations: endoscopy, barium swallow, CT (staging).
Management: surgery (if within oesophagus wall), radio and chemo therapy (adenocarcinoma is radio-insensitive), stenting, brachytherapy.
History and interpretation
Difficult swallowing solids and liquids from the start? Yes: motility disorder (achalasia, neurological) or pharyngeal causes. No: solids then fluids: suspect stricture.
Difficulty initiating swallowing: bulbar palsy (especially if coughs on swallowing).
Painful swallowing (odynophagia): cancer, oesophagitis, achalasia, oesophageal spasm.
Intermittent dysphagia: oesophageal spasm. Worsening: malignant stricture.
Burge or gurgle on drinking: pharyngeal pouch.
Mallory-weiss tear
Linear mucosal tear at oesophagogastric junction due to intra-abdominal pressure (after coughing, retching, or alcohol binge). Presents with haemorrhage, which usually spontaneously stops (occasionally requires surgery).
Pyloric stenosis
Failure of the pyloric sphincter to relax produces hypertrophy of the adjacent pyloric muscle. Associations with Turner’s syndrome, oesophageal atresia and phenylketonuria. Occurs in 1 in 400, 4 males to 1 female, genetic component (polygenic, 5% risk of passing on).
Clinical features
Develops in first 3 to 6 weeks of life. Projectile vomiting, no bile, child hungry and will re-feed. Failure to gain weight (failure to thrive). Constipation (due to dehydration). 95% have a palpable RUQ pyloric mass (shape and size of an olive). Occasionally haematemesis.
Investigations
Barium meal (delayed gastric emptying, a dilated stomach and a narrowed and attenuated pyloric canal - the ‘string sign’), U&E (hypokalaemia, hypochloraemic), ABG (metabolic alkalosis).
Management
Stabilize electrolytes, Ramstedt’s operation (longitudinal incision is made through the hypertrophied muscle as far as the mucosa; the mucosa is left intact and is seen bulging into the incision the cut edges are separated), restart feeding after 3 hours (initially glucose, then milk).
Causes of Jaundice
Pre-hepatic
Excess production of bilirubin: high serum bilirubin with normal LFTs suggests non-liver cause (Gilbert’s syndrome, haemolysis, ineffective erythropoiesis, rifampicin).
Hepatocellular
High serum bilirubin, abnormal LFTs (congenital liver disease, cirrhosis or hepatitis, inflammatory cholestasis, paracetamol, methyldopa Pre-hepatic
Excess production of bilirubin: high serum bilirubin with normal LFTs suggests, barbiturates).
Obstructive (cholestatic)
Blockage of bile drainage, very high serum bilirubin, abnormal LFTs (gallstones / cholangitis, pancreatitis, duodenum or pancreatic Ca, isoniazid, chlorpromazine).
Neonatal jaundice
<24hr of birth: always abnormal. Sepsis, Rhesus haemolytic disease, ABO incompatibility, glucose-6-phosphate dehydrogenase deficiency.
>24hr after birth: common and usually physiological.
Prolonged jaundice (more than 14 days): breast-feeding, sepsis, hypothyroidism, CF, biliary atresia if conjugated and pale stools.
Managed by phototherapy; exchange transfusion.
Gilberts syndrome
Common (3-5% of population) prehepatic jaundice: jaundice, bilirubin (mainly unconjugated), normal urine, no risk factors, normal LFTs, no signs of haemolysis.
Caused by defect in glucuronyl transferase which conjugates bilirubin with glucuronic acid in liver.
Signs of hepatic cirrhosis
Jaundice (above), fever, spider naevi (in superior vena cava distribution, secondary to hyperoestrogenism, pressure on center blanches legs, >2 abnormal), palmar erythema, xanthomas (cholesterol deposits, palmar creases, above eyes; hypercholesterolaemia in chronic biliary obstruction), hepatomegaly (although ends up being small with chronic cirrhosis), splenomegaly (portal hypertension), gynaecomastia and testicular atrophy (oestrogen not being converted to testosterone), caput medusa (see portal hypertension), haematemesis (oesophageal varices: see portal hypertension), ascites (distended abdomen) and peripheral oedema (low albumin in blood), bleeding / bruising (reduced clotting factors), confusion (encephalopathy), liver flap, leukonychia, clubbing, sepsis (bacteria peritonitis), melaena (black tarry faeces, of partially digested blood, from 500mL+ upper GI bleed / haematemesis), dark urine (conjugated hyperbilirubinaemia), pale stools (lack of bile in stools), steatorrhoea (malabsorption of fat due to bile obstruction), pruritus (itching due to biliary obstruction resulting in bile salt accumulation).
Managing portal hypertension
Portal hypertension
Aetiology: portal vascular resistance due to chronic liver disease.
Prehepatic: portal vein thrombosis (esp children).
Intrahepatic: cirrhosis, schistosomiasis, fibrosis.
Posthepatic: heart failure, constrictive pericarditis.
Clinical features: haematemesis, melaena, oesophageal varices, ascites, encephalopathy.
Collateral circulation at portal-systemic anastomoses: oesophageal varices, haemorrhoids (rectum), caput medusa (systemic superficial epigastric veins communicate with paraumbilical veins), colon anastomoses (systemic retroperitoneal veins communicate with colic vein twigs).
Management: TIPS (transjugular portosystemic shunt (portal vein to hepatic vein)).
Managing liver failure
10% dextrose IV (avoiding hypoglycaemia), vitamin K and clotting agents, treat infections (not gentamicin - risk of renal failure), manage any ascites ( Na+ and water intake), haemofiltration and albumin IV (if renal failure develops), avoid drugs with hepatic metabolism, consult with transplant center for assessment
Coeliacs
Coeliac disease
Aetiology
Digestive disease that damages small intestine. Caused by protein called Gliadin (constituent of gluten) found in wheat, rye and barley. If eaten causes damaging immune response. Loss of villi occurs. Associated with lymphoma.
Clinical features
Chronic diarrhoea, steatorrhoea, abdominal distension, failure to thrive. Skin vesicles: Dermatitis herpetiformis.
Investigations
Gold standard blood test is endomysial antibodies, duodenal biopsy (flat mucosa), then gluten free diet, finally 9 months later another biopsy (normal mucosa).
Management
Gluten free diet.
Types of hernias
Reducible (hernia can be completely replaced into peritoneal cavity). May disappear on lying down, usually painless, reducible with cough impulse (a palpable impulse when the patient coughs).
Irreducible (cannot be reduced due to adhesion or contents being larger than sac neck). Does not reduce, usually painless, cough impulse.
Strangulated (contents of hernia constrict sac neck cutting off circulation). Severe hernia pain and colicky abdominal pain, obstruction signs (vomiting, distension, constipation). Cannot be reduced, no cough impulse.
Umbilical hernia: congenital failure of complete closure of umbilical cicatrix. Common in black children. Vast majority close spontaneously. Surgical repair only if hernia persists after 2 years old.
Para-umbilical hernia: acquired hernia occurring just above or below umbilicus. Common in obese, multiparous, middle-aged ♀. Narrow neck makes irreducibility and strangulation likely. Mayo’s operation overlaps rectus sheath above and below hernia.
Ventral hernia: upper midline ventral hernia. Gap between recti. Most require no treatment.
Epigastric hernia: form of ventral hernia, protruding through linea alba. Painful, requiring suturing of defect.
Incisional hernia: through defect in scar. Usually wide neck, so strangulation if rare. Surgically dissect out and re-suture; or mesh if large.
Congenital diaphragmatic hernia: through foramen of Morgagni: small and unimportant. Foramen of Bochdalek or central tendon are large, presenting as respiratory distress shortly after birth; urgent surgical repair is required. Congenital hiatus hernia presents with regurgitation, vomiting, dysphagia, progressive weight loss in small children; usually respond to feeding in sitting position, otherwise surgery.
Traumatic diaphragmatic hernia: rare. L>R sided. Herniation of stomach or spleen into thoracic cavity (gas filled stomach can be mistaken for pneumothorax). Urgent surgical repair.
Hiatus hernia: Sliding (90%): stomach slides though hiatus, producing effects of space-occupying lesion in chest and disturbance of cardio-oesophageal sphincter. Rolling (10%): produces partial volvulus (twisting of GIT). Most hiatus hernias are asymptomatic, others fall into 3 groups: mechanical (cough, dyspnoea, palpitations, hiccough), reflux (burning retrosternal or epigastric pain, aggravated by lying down or stooping), oesophagitis (dysphagia, bleeding). Sliding treated symptomatically. Rolling are often asymptomatic, but are more serious with risk of complete gastric volvulus – surgical repair indicated.
Intussusception
spasms occurring every 10-15 minutes, lasting 2-3 minutes, passage of blood and/or slime per rectum (late; red current jelly on examining finger), sausage-shaped mass usually palpable (often RUQ).
In <24 hours child can become intensely toxic, have a distended abdomen, and exhibit faeculent vomiting. Chronic intussusception is rare, presenting with milder features. It may cause failure to thrive.
Investigations
Assess hydration status, AXR (obstruction), US (Swiss-roll appearance), barium enema (stack of coins sign).
Management
Rehydrate if necessary.
Reduction by barium enema under radiological control (increase air pressure in bowel; contraindicated if features of perforation or peritonitis).
Surgical indications include: child under 3 months or over 2 years, clinical signs of peritonitis, gross dehydration, failure of medical treatment, or recurrence after medical treatment.
