Medicine - Gastrointestinal System Flashcards
What is Leukonychia and what is it a sign of?
White spots on nails - low Albumin, CLD
What is Koilonychia and what is it a sign of?
Bent-up nails, sign of iron deficiency anaemia
What is finger clubbing a sign of?
IBD, Cirrhosis, Coeliac disease
What is Dupuytren’s contracture a sign of?
CLD
What is the top right hand corner of the abdomen referred to as?
Right Hyopchondrium
Nutrition
What scoring system is used to evaluate malnutrition?
What are the indications for an NGT?
What are the contraindications for an NGT?
What pH must be reached for the correct placement of an NGT?
What are the indications for PEG insertion?
What are the contraindications for PEG insertion?
TPN indications
Scoring: MUST
NGT Indications: Functioning gut, inability to meet nutritional requirement via food, unintentionally lost >10% body weight, anorexic
NGT Contraindications: Basal skull fracture, pharyngeal pouch, hiatus hernia, oesophageal varices
pH: 5.5
PEG Indications: Enteral feed >3 weeks, SALT assessment, long-term care required, capacity
PEG Contraindications: Pregnancy, cardiac or respiratory disorders, gastric surgery, hiatus hernia
TPN indications: Non-functioning gut, unsafe intake
What ions are affected in re-feeding syndrome?
Magnesium, Phosphate, Potassium
Will need IV Thiamine prior to feeding
Upper GI Bleeds
List 5 causes of upper GI bleeds:
What investigations would you do in query upper GI bleed?
What scoring systems are used and what do they assess?
What management would you give to someone with an acute upper GI bleed?
Causes: Peptic ulcer disease, varices, Mallory-weiss tear/Boerhaave’s, Upper GI Malignancy, Gastritis perforation, Epistaxis
Investigations: OGD, CT angio (if needed), FBC + U&Es, Urea, Liver Ultrasound
Scoring: ROCKALL - chance of adverse outcome
Glasgow-Blatchford - identify if needs intervention
Management: Drip and suck, Oxygen, PPIs IV, Endoscopic therapy
If Varices: Terlipressin IV, Minnesota-Sengstaken tube
Varices
Where are the 3 locations of variceal bleeding?
Pathophsyiology:
What prophylactic drug is given to prevent bursting of varices?
What are the treatments for active oesophageal varices bleeding?
How is the liver linked to the umbilicus?
Locations: Oesophageal, Umbilical, Anorectal
Pathophysiology: Liver cirrhosis leads to portal hypertension, leading to venous congestion - this then causes it to exit via systemic anastomoses
Prophylactic drug: Beta-blocker
Treatment: Transjugular intrahepatic portosystemic shunt (TIPS), Terlipressin
Liver is linked to the umbilicus via the ligamentum teres
Lower GI bleeds
Causes:
Causes: Diverticulitis, Colitis, Colorectal Cancer, Haemorrhoids, Anal fissure, Colorectal cancer, UC, Angiodysplasia, Shigella/Campylobacter
Crohn's Disease Name 5 unique features to Crohn's: Name 5 extra-intestinal features: Investigations: Gross Pathological changes seen: Management: Complications:
Unique: Skip lesions, distal ileum affected, transmural, perianal disease/fistulas
Extra-intestinal: Erythema nodosum, pyoderma gangrenosum, uveitis, nail clubbing, enteropathic arthritis
Investigations: Faecal calprotectin, Colonoscopy with biopsy, abdo X-ray to rule out toxic megacolon
Gross Pathological changes: Skip lesions, cobblestone appearance, fistulae, strictures, mucosal oedema, transmural inflammation
Management: Oral Prednisolone, Azathioprine to maintain remission and induce
TPMT levels low, then given Methotrexate instead of Azathioprine
Complications: Fistula formation, Strictures, Perianal abscess, Malignancy risk, Malabsorption
Ulcerative Colitis
Name 7 unique features to Ulcerative Colitis:
Name 4 extra-intestinal manifestations of UC:
Investigations:
Management:
Complications:
Unique: Starts in rectum, crypt abscesses, continuous pattern of inflammation, mucosal inflammation only (superficial), can cause toxic megacolon and perforations (acute exacerbations are fatal), tenesmus, painful red eye
Extra-intestinal: Enterohepatic arthritis, erythema nodosum, pyoderma gangrenosum, uveitis
Investigations: Faecal calprotectin, Colonoscopy or Sigmoidoscopy, CXR to check for lead pipe colon or mural thickening, CT for toxi megacolon
Management: Heparinisation (thromboembolic state), Mesalazine rectally, with added oral pred if not working, then Mesalazine as remission + infliximab
Total proctocolectomy is curative
Complications: Toxic megacolon, colorectal carcinoma, osteoporosis
Toxic Megacolon
Pathophysiology:
Symptoms:
Complication of C. Diff + UC
Symptoms:
- Severe abdominal pain
- Abdominal distension
- Pyrexia
- Systemic toxicity
Acute Liver Failure
Causes:
Symptoms:
Grades of hepatic encephalopathy:
Causes: Paracetamol toxicity, Hep A/B, Severe alcohol toxicity
Symptoms: Jaundice, Hepatic Encephalopathy, Haemorrhage (variceal) due to loss of clotting factor production, AKI (hepatorenal)
Grades: 1-4: 1 = Poor memory, reversed sleep pattern, slow thought
2 = Lethargy, disorientation, agitation
3 = Drowsy
4 = Coma
Jaundice causes - how can you tell easily if pre/hepatic/post?
Pre = no urine or faecal changes Renal = urine colour change, no faeces change Post = urine and faeces colour change (white)
Chronic Liver Disease
Causes:
Signs:
Cirrhosis investigations:
Causes: Alcoholic liver disease, Hepatitis B/C, NASH, PBC, PSC, Autoimmune hepatitis, Haemochromatosis, Wilson’s disease
Signs: Ascites, Jaundice, Hepatosplenomegaly. Spider naevi, Hepatic flap, Clubbing, Dupuytren’s, Leukonychia
Investigations: USS scan (fibroscan) of the liver, Liver screen
Jaundice
Pre-Hepatic:
Hepatic:
Post-Hepatic:
Pre-Hepatic: Sickle cell, malaria
Hepatic: Cirrhosis, alcoholic/viral hepatitis, pancreatic cancer, PBC, PBS, Haemochromatosis, Wilson’s, Paracetamol OD
Post-Hepatic: Cholecystitis/ Ascending Cholangitis/Malignancy
Wilson’s disease
Pathophysiology:
Symptoms:
Pathophysiology: Increased copper uptake and reduced secretion -> deposition
Symptoms: Keyser-Fleischer rings, Parkinsonian symptoms and memory loss, abnormal LFTs/jaundice
Hereditary Haemochromatosis
Pathophysiology:
Management:
Pathophysiology: Increased iron absorption from the small intestine, leading to iron deposition in tissues - “bronze diabetes”
Management: Venesection
Primary Biliary Cirrhosis
Pathophysiology:
Pathophysiology: Destruction of the intra-hepatic bile ducts, mainly affects women, ANA/Smooth muscle antibodies
Primary Sclerosing Cholangitis
Pathophysiology:
Associated conditions:
Pathophysiology: Fibrosis of the intra and extra hepatic bile ducts, common in men, ANCA antibodies
Associated with: UC, Cholangiocarcinoma, HCC
Gilbert’s Syndrome
Pathophysiology:
Pathophysiology: Reduced ability of the liver to process bilirubin, leading to short episodes of jaundice, usually incited by playing sports - self-resolving
Alcohol Intake
How many units of alcohol are recommended per week?
How can you calculate the number of units in a drink?
What conditions is alcohol intake associated with?
What condition is alcohol withdrawal associated with?
How is alcohol withdrawal managed?
Units: 14 units/ week
Calculated by: Quantity * ABV /1000
Conditions associated: Cirrhosis, Folate/B12 deficiency (Macrocytic anaemia), Mallory-Weiss tear, Delirium Tremens, Hepatic Encephalopathy, Alcoholic fatty liver disease
Withdrawal: Delirium Tremens
Management of alcohol withdrawal: B12, Folate, Thiamine, Benzodiazepine, Do a Clinical Institute Withdrawal Assessment for alcohol (CIWA), give Disulfiram and refer to CBT groups
Hepatorenal syndrome
Define the pathophysiology of hepatorenal syndrome
Cirrhosis -> Portal Hypertension -> Arterial vasodilation (splanchnic) -> RAAS activation -> Renal artery vasoconstriction (AKI)
Hepatitis
How are each of the Hepatitises primary caught?
Which of the hepatitises are chronic, which are mainly acute?
A = Faecal oral, usually abroad, immunisation available
B = Blood or sex, immunisation available
C = Blood or IVDU, no immunisation
E = Faecal-oral, unsafe drinking water
Chronicity:
A = Not chronic
B = Mostly acute, rare chance of developing into chronic (1/10) - no treatment
C = Chronic always, Interferon and Ribavirin treatment
E = Not chronic
Hepatitis B
Which antigen/antibody implies acute disease?
Which antibody implies immunity?
Which antibody implies a previous or current infection?
Acute disease: HBs Antigen
Immunity: Anti-HBs
Previous or Chronic infection: Anti-HBc (IgM acute, IgG late)
GORD Pathophysiology: Symptoms: Risk factors: Investigations: Management: Complications:
Pathophysiology: Acid exits the stomach and laps at the oesophagus. Usually limited from doing this due to LOS + Diaphragm + Acute Angle of Entry
Symptoms: Central crushing chest pain, retro-sternal, can radiate to back, worse after meals or bending over/lying down, acid taste in mouth, cough, flatus
Risk factors: Obesity, Male, Pregnancy, Hiatus Hernia, Smoking, Coffee, Alcohol, NSAIDs
Investigations: Clinical diagnosis, check for red flags (dysphagia/weight loss > 55 years old), OGD if PPIs not working, 24-hour pH monitoring
Management: Lifestyle modification, PPIs, Ranitidine, Antacids, fundoplication if hiatus hernia
Complications: Aspiration pneumonia, Barret’s Oesophagus, Oesophagitis
Barrett's Oesophagus Pathophysiology: Red Flags: Risk factors: Investigations: Management:
Pathophysiology: Stratified squamous undergo metaplasia to simple columnar epithelium -> Adenocarcinoma. Less common than SCC in the UK.
Red flags: Weight loss, Dysphagia, Early Satiety, Loss of appetite, Worsening dyspepsia despite PPI treatment, Anaemia of chronic disease
Risk factors: GORD, Male, Smoking, > 55, Hiatus Hernia, FH
Investigations: OGD with biopsy
Management: High-dose PPIs, stop NSAIDs, regular endoscopy, endoscopic mucosal resection
Gastritis (H Pylori-related) Pathophysiology: Causes: Symptoms: H Pylori pathogenesis: H Pylori invasion locations: Investigations: Management:
Pathophysiology: Inflammation of the mucosal lining of the stomach
Causes: H Pylori, Autoimmune (can lead to pernicious anaemia), Alcohol abuse, NSAIDs
Symptoms: Pain, nausea, vomiting, bleeding, can be asymptomatic (in the case of H Pylori)
H Pylori pathogenesis: Produces urease (urea -> ammonia, increasing pH), releases cytotoxins causing epithelial injury, degrades mucous layer
Invasion locations: Antrum - affects G cells, causing increased gastrin secretion
Investigations: Urease breath test (urea labelled with isotope of carbon taken in, measure if isotope labelled CO2 breathed out, showing urea breakdown), Stool antigen test
Management: Proton pump inhibitor + Amoxicillin + Clarithromycin
Paracetamol Overdose Symptoms: Investigations: Management: When is it safe to discharge?
Symptoms: Nausea, vomiting, sweating, RUQ pain
Investigations: Serum paracetamol level, ALT, ABG, INR for elevated prothrombin time
Management: TOXBASE, N-acetylcysteine - replenishes depleted glutathione reserves in the liver, to protect against NAPQI
Safe discharge: Mental health assessment, LFTs for permanent damage, blood paracetamol levels
Ulcers Pathophysiology: Causes: Symptoms: Investigations: Management: (If bleeding:) Complications:
Pathophysiology: Breach in the gastric or duodenal mucosa that extends through the muscularis mucosa, most commonly in the first quarter of the duodenum
Causes: H pylori, particularly duodenal ulcers, NSAIDs, Alcohol, Smoking (relapses), Acute Gastritis
Symptoms: Epigastric pain, relieved immediately by eating if duodenal, or worse on eating in gastric, anaemia, weight loss, early satiety
Investigations: OGD, Urease Breath Test
Management: Lifestyle modification, H Pylori testing and management (PPI + Amoxicillin + Clarithromycin)
If bleeding: IV Fluids, IV PPI, Stop antiplatelets, OGD
Complications: Pyloric stenosis, Perforation (splenic or gastroduodenal), Haemorrhage, Malignancy
Ascitic Tap
What is measured in an ascitic tap?
Appearance eg. turbidity
SAAG (serum-ascites albumin gradient)
Neutrophil count for SBP
LFTs What does a liver screen contain? What does a raised ALT imply? What does a raised Gamma-GT imply? What does an ALP + Gamma-GT being raised imply?
Liver screen: LFTs, Bilirubin, Albumin, Hepatitis tests, Iron studies, Autoantibodies, Alpha-antitrypsin, Coeliac serology (TTG)
ALT = Viral induced hepatitis, Paracetamol OD, autoimmune
Gamma-GT = Alcoholic liver disease
ALP + Gamma-GT = Cholestatic picture eg. gallstones, pancreatic cancer, PBC, PSC
Diarrhoea Definition: Salmonella: Campylobacter: Shigella: ETEC: Rotavirus: Norovirus: Cryptosporidium: Giardia Lamblia: Entamoeba Histiolytica:
Definition: 3 or more loose stools per day
Salmonella: Gram negative rod, Non-bloody diarrhoea, ingested water/food, lasts 2-3 days
Campylobacter: Faecal oral, Bloody Diarrhoea, Weeks - can lead to Haemolytic uremic syndrome, thrombotic thrombocytopenic purpura, reactive arthritis
Shigella: Infected stools, but also flies due to low infectious dose. Bloody diarrhoea with mucous and cramping, clears within 1 week.
ETEC: Not bloody, traveller’s diarrhoea, days
Rotavirus: Children - non-bloody diarrhoea
Norovirus: Most common gastroenteritis, any age, watery diarrhoea, vomiting
Cryptosporidium: Faecal oral route, swimming pools in particular
Giardia lamblia: From developing countries, can lead to lactose intolerance
Entamoeba histolytica: From developing countries, most cases are asymptomatic - can lead to toxic megacolon, requires anti-protozoals and metronidazole
Constipation Definition: Causes: Risk factors: Management: Types of laxative:
Definition: Straining/lumpy stools/incomplete evacuation >25% of defecations, or fewer than 3 unassisted bowel movements/week
Causes: Stress, Toxic Megacolon, Hypothyroidism, Diabetes, Parkinson’s, MS, Coffee
Risk factors: Female, Surgery, Increasing age, Low level of physical activity, low fibre diet
Management: Fybogel, Increased fluid intake, Increased fibre, Increased exercise, Laxatives
Laxative types:
Osmotic: Movicol (Macrogols) retain water they went in with), Lactulose (draws water into bowel)
Stimulatory: Sodium docusate/Senna
Bulk forming: Fybogel
Clostridium Difficile Pathophysiology: Symptoms: Management: Complications:
Pathophysiology: Gram positive rod, caused by cephalosporins and broad-spectrum antibiotics - toxins A and B
Symptoms: Watery diarrhoea, abdominal pain, distension, fever, NO vomiting
Management: Stop antibiotics, give fluid, Metronidazole IV, Faecal matter transplant
Complications: Psuedomembranous colitis and Toxic Megacolon
Spontaneous Bacterial Peritonitis
Pathophysiology:
Pathophysiology: Most commonly seen in patients with end stage liver disease - infection of the ascitic fluid
Vitamin B12 deficiency
Pathophysiology:
Causes:
Pathophysiology: B12 deficiency leads to megaloblastic (macrocytic) anaemia and neurological symptoms. Absorbed in the terminal ileum once bound by intrinsic factor.
Causes: Pernicious anaemia (lack of intrinsic factor), Crohn’s disease, Vegetarianism
Lactose Intolerance
Pathophysiology:
Pathophysiology: Lactase enzyme deficiency - acts as an osmotic diarrhoea causer
Coeliac Disease Pathophysiology: Symptoms: Investigations: Management:
Pathophysiology: Immunological response to gliadin, causing: Villous atrophy, lymphocyte infiltrate epithelium, impaired digestion/malabsorption
Symptoms: Diarrhoea, weight loss, flatulence, abdominal pain, anaemia, neurological symptoms
Investigations: tTG antibody testing (cannot diagnose though), Endoscopy + Biopsy looking for villous atrophy/ epithelial lymphocytosis
Management: Diet - gluten free diet
Acute Mesenteric Ischaemia Pathophysiology: Symptoms: Risk factors: Investigations: Management:
Pathophysiology: Symptomatic occlusion of the blood supply to the GI tract. Acute occlusion, usually in the SMA.
Symptoms: Disproportionate abdominal pain, usually 30 mins after eating
Risk factors: Cardiovascular disease, elderly, female
Investigations: CT angiography, erect CXR to check for perforation
Management: Resection of ischaemic bowel, thrombolysis
