Gastrointestinal Examination Flashcards
What is xerostomia?
Dry mouth
What is halitosis?
Bad breath due to gingivitis, dental or pharyngeal infection
What is dysgeusia?
Altered taste sensation
What is cacageusia?
Foul taste sensation eg. rotting food
What is haematochezia?
Rectal bleeding
Causes of a painful mouth
Idiopathic- recurrent aphthous ulcers
Infections- candidiasis, dental sepsis, herpes simplex virus
Trauma
Systemic disorder
Skin disorder- pemphigoid, lichen planus, pemphigus vulgaris, erythema multiforme
Dyspepsia that is worse on an empty stomach and relieved by eating is likely to be
Peptic/ duodenal ulceration
Likely causes of odynophagia
Oesophagitis or candidiasis
Severe abdominal pain sudden onset that rapidly becomes progressively generalised and constant is likely…
Hollow viscus perforation, ruptured AAA or mesenteric infarction
Clues may be in the previous history- constipation from colorectal cancer or diverticular disease, dyspepsia
Severe abdominal pain sudden onset radiating to the back
Ruptured or dissecting abdominal aortic aneurysm
Angor animi
The feeling of impending death
Achalasia
Lower oesophageal sphincter fails to relax normally- dysphagia with both solids and liquids
Neuromuscular causes of dysphagia
Achalasia, pharyngeal pouch, myasthenia gravis, oesophageal dysmotility
Oral causes of dysphagia
Tonsillitis, glandular fever, peritonsillar abscess, painful mouth ulcers, pharyngitis
Symptom checklist in dysphagia
Painful or painless? Intermittent or progressive? Length of history and onset? Solid or liquid or both? Previous Hx of dysphagia or heartburn? Where does food stick? Complete obstruction with regurgitation?
Gastric outlet obstruction causes what type of vomiting?
Projectile non-bilious vomiting
Neurological causes of vomiting
Raised ICP- SOL, meningitis Labyrinthitis Meniere's disease Migraine Vasovagal syncope, shock, fear and severe pain
Causes of ascites
Common- hepatic cirrhosis with portal hypertension, intra-abdominal malignancy with peritoneal spread
Uncommon- hepatic vein occlusion (Budd-Chiari syndrome), constrictive pericarditis and other right sided heart failure, hypoproteinaemia (nephrotic syndrome), tuberculosis peritonitis, pancreatitis
Causes of bloody diarrhoea
IBD, colonic ischaemia or infective gastroenteritis
What is Mallory- Weiss syndrome?
Forceful retching and vomiting ruptures oesophageal mucosa causing the vomiting of fresh blood
Coffee ground vomit
Blood that has been degraded by gastric pepsin is vomited
Causes of melaena
Upper GI bleeding that is then passed through the system- excessive alcohol ingestion causing erosive gastritis, Mallory-Weiss tear, bleeding oesophageal varices, peptic ulceration
Causes of rectal bleeding
Haemorrhoids Anal fissure Colorectal polyps/ cancer IBD Ischaemic colitis Complicated diverticulitis disease Vascular malformation
Causes of angular stomatitis
Denture problems, candidiasis, iron deficiency or B12 deficiency
ALARMS symptoms
Anaemia Loss of weight Anorexia Recent progression or onset of symptoms Melaena/ haematemesis Swallowing difficulty
Differentials for dyspepsia
Non-ulcer dyspepsia Duodenal/ gastric ulcer Duodenitis Oesophagitis/ GORD Gastric malignancy Gastritis
When should upper GI endoscopy be done in dyspepsia cases?
Dysphagia
>55
ALARMS symptoms
Treatment for H. pylori
PPI
2 antibiotics eg. Clarithromycin and amoxicillin
Treatment of GORD
Conservative- lifestyle, smoking cessation, weight loss, small regular meals, avoidance of causative food and drink, raise the bed head, avoid eating 3 hours before bed
Medical- antacids, PPI, H2 receptor antagonist, avoid drugs that can affect oesophageal motility or that damage mucosa
Surgical- laparoscopic Nissen fundoplication to increase resting LOS pressure
Symptoms of GORD
Retrosternal burning
Discomfort after eating, straining, lying
Belching
Acid regurgitation
Odynophagia from oesophagitis or ulceration
Extra-oesophageal such as nocturnal cough
Acute management of an upper GI bleed
A-E assessment
Senior involvement
High flow oxygen and protection of the airway
Insert 2 large bore cannulae
Bloods- FBC, U&Es, LFT, clotting and crossmatch
IV fluids whilst waiting for crossmatched blood
Catheter insertion and monitor hourly fluids
CXR, ECG, ABG
Transfuse if significant Hb drop (<70)
Correct clotting abnormality
If suspicion of varices then give terlipressin
Broad spectrum abx cover
Monitor obs hourly until stable
URGENT ENDOSCOPY (clips, cautery, adrenaline)
If endoscopic control fails then surgery or emergency mesenteric embolisation may be needed
If uncontrollable oesophageal variceal bleeding then Sengstaken-Blakemore tube may compress varicies
Risk score used for upper GI bleeds
Rockall score
Predicts risk of rebleeding and death
Causes of portal hypertension (leading to gastro-oesophageal varices)
Pre-hepatic- thrombosis
Intra-hepatic- cirrhosis (80% in UK), schistosomiasis (commonest worldwide), sarcoid, myeloproliferative diseases
Post-hepatic- budd-chiari syndrome, right heart failure, constrictive pericarditis
Management of gastro-oesophageal varices
Endoscopic banding or sclerotherapy
Non-selective beta blockade
TIPS for resistant varices
Causes of bloody diarrhoea
Campylobacter, Shigella, Salmonella, E. coli, amoebiasis
UC, Crohn’s, colorectal cancer, colonic polyps
Colitis (ischaemic)
Treatment of C. difficile in mild and severe cases
Mild- metronidazole
Severe- vancomycin
Proctalgia fugax
Temporary pain around the anal area of unknown origin
Usually intense muscle spasm- similar to levator ani syndrome
Endocrine causes of constipation
Hypercalcaemia
Hypothyroidism
Description of UC pathology
Continuous inflammation limited to the mucosa and distal to the ileocaecal valve
Haemorrhagic colonic mucosa +/- pseudopolyps formed by inflammation
What kind of UC flare?
5 motions/per day, some rectal bleeding
70-90BPM
Moderate
Complications of UC
Acute- toxic megacolon with risk of perforation
VTE, hypokalaemia
Chronic- colonic cancer, risk related to disease activity and extent- surveillance colonoscopy important
Treatment of UC
Mild
Moderate
Severe
Mild- 5-ASA PR eg mesalazine for distal disease or PO if more extensive. Steroids may be used in addition
Moderate- 4-6 motions per day but otherwise well(ish)
oral prednisolone to induce remission, maintain on 5-ASA
Severe- admission, IV hydration, eletrolyte replacement, IV steroids- hydrocortisone 100mg, VTE prophylaxis, stool MC&S to exclude infection
Description of Crohn’s disease pathology
Chronic inflammatory condition characterised by transmural granulomatous inflammation affecting any part of the gut.
Skip lesions
Rose thorn ulceration
Clinical features of Crohn’s disease
20-40 years old classically Diarrhoea Generally unwell- fever, malaise, fatigue, anorexia Failure to thrive Weight loss Abdominal pain
Signs: adbo tenderness/ mass, perianal abscess, fistulae, skin tags, anal strictures, clubbing, skin and joint involvement, anterior uveitis/ iritis/
Crohn’s disease treatment
SMOKING CESSATION
mild-moderate- Prednisolone 40mg and then taper off, dietary advice
Severe- Admission for IV hydration/ electrolyte replacement, IV steroids- hydrocortisone or methylpred, VTE prophylaxis, MC&S to exclude infection
Daily FBC, ESR, CRP, U&E and AXR, blood transfusions and nutritional support if necessary
If improving switch to oral pred, consider biologic use
Peri-anal disease:
TNF-alpha, other immunosuppressants, oral antibiotics, local surgery and seton insertion
Biologic therapies that can be used in Crohn’s disease
Azathioprine
Methotrexate
TNF-alpha- infliximab, adalimumab
Other monoclonal antibodies
Genetic associations with coeliac disease
HLA DQ2 is 95%
HLA DQ8 are the rest
Autoimmune disease
Dermatitis herpetiformis
Presentation of coeliac disease
Any age but peaks in childhood and 50-60
Steatorrhoea, diarrhoea, abdo pain, bloating, nausea and vomiting, aphthous ulcers, angular stomatitis, weight loss, fatigue, osteomalacia, failure to thrive
Antibody in coeliac disease and further test to confirm
Anti-tissue transglutaminase and total IgA check to exclude subclass deficiency Duodenal biopsy to confirm (whilst on a gluten containing diet)
Mucosal changes in coeliac disease
Villus atrophy
Crypt hyperplasia
Intra-epithelial WBC’s
Complications of coeliac disease
Anaemia Dermatitis herpetiformis Osteopenia/osteoporosis Hyposplenism- flu and pneumococcal vaccine Increased risk of malignancy
Things to rule out when diagnosing IBS
Chronic >6 months Query if age >60 No weight loss, anorexia, waking at night with pain/ diarrhoea, mouth ulcers Abnormal CRP, ESR FH of ovarian or bowel cancer (CA-125) Endometriosis- cyclical pain Stool culture FBC, LFTs, U&Es, coeliac serology
Clinical features of scurvy
Poor, pregnant or odd diet
Anorexia, cachexia, gingivitis, loose teeth, halitosis, bleeding from gums or into joints, bladder, gut, muscle pain, weakness, oedema
Beriberi
Thiamine deficiency
Wet beriberi- heart failure with general oedema
Dry beriberi- neuropathy
Classical triad of pellagra
Lack of nicotinic acid- B3- niacin
Diarrhoea, dementia and dermatitis
Causes of acute pancreatitis
Gallstones Ethanol Trauma Steroids Mumps and other infections Autoimmune Scorpion bites Hypercalcaemia, hypertriglyceridaemia, hypothermia ERCP Drugs
Tests for pancreatic cancer query
CA19-9
Bloods show cholestatic jaundice
Imaging- US or CT- pancreatic mass, biliary tree dilatation or hepatic mets
What is a Whipple’s resection?
Pancreatoduodenectomy
Gilbert’s syndrome
Decreased UGT-1 activity resulting in unconjugated hyperbilirubinaemia
Often presents with intermittent jaundice in young adulthood during infections
Crigler-Najjar syndrome
Inherited unconjugated hyperbilirubinaemia presenting in the first days of life
Mutation in the UGT enzyme causing absent (1) or impaired (2) bilirubin excretion
Causes of unconjugated hyperbilirubinaemia
Haemolysis, ineffective erythropoiesis
Impaired hepatic uptake- drugs- paracetamol, rifampicin, ischaemic hepatitis
Impaired conjugation
Physiological neonatal
Causes of conjugated hyperbilirubinaemia
Hepatocellular dysfunction- viruses- hepatitis, CMV, EBV, drugs, alcohol, cirrhosis etc
Impaired hepatic excretion- PBC, PSC, gallstones, pancreatic CA, compression, cholangiocarcinoma,
Questions to ask the patient in jaundice
Blood transfusions IV drug use Piercings Tattoos Sexual activity Travel Jaundiced contacts FH Alcohol Medications
Investigations for jaundice
Haematology- FBC, clotting, blood film, Coomb’s test, haptoglobins
Biochemistry- U&Es, LFTs, GGT, total protein, albumin, paracetamol levels
Microbiology- blood cultures, hepatitis serology
USS- bile duct dilatation, masses, gallstones
‘Coagulopathy’ in terms of INR
> 1.5
Causes of liver failure
Infections- viral hepatitis- B,C, CMV, yellow fever, leptospirosis Drugs- paracetamol, isoniazid Toxins- deathcap Vascular- Budd Chiari syndrome- occlusion of the hepatic veins Alcoholic Liver Disease Non Alcoholic Fatty Liver Disease PBC PSC Haemochromatosis Autoimmune hepatitis Alpha-1 antitrypsin deficiency Wilson's disease Malignancy Fatty liver of pregnancy
Hepatic encephalopathy pathogenesis
Nitrogenous waste builds up from liver failure
Astrocytes mop up by conversion of glutamate to glutamine and this excess causes osmotic imbalance and cerebral oedema
Signs of liver failure
Jaundice
Hepatic encephalopathy- incoherent, restless, confusion, asterixis, stupor
Asterixis
Signs of acute or chronic liver failure
What is hepatorenal syndrome?
Cirrhosis+ ascites + renal failure
Abnormal haemodynamics result in renal vasoconstriction and hypoperfusion
Treating ascites
Restrict fluid, low salt diet, weight daily, diuretics
Signs of liver cirrhosis
Leukonychia Telangiectasia Clubbing Palmar erythema Dupuytren's contracture Spider naevi Xanthelasma Gynaecomastia Loss of body hair Parotid enlargement- alcohol Hepatomegaly (small in late disease) Ascites Splenomegaly
Complications of liver cirrhosis
Hepatic failure: coagulopathy, hypoalbuminaemia, encephalopathy, sepsis, spontaneous bacterial peritonitis, hypoglycaemia
Portal hypertension- ascites, caput medusae, splenomegaly, oesophageal varices
When should spontaneous bacterial peritonitis be considered?
Any patient with ascites that deteriorates very quickly
Only definitive treatment for cirrhosis
Liver transplant
Investigations once recovery from a HepB virus infection
Normal LFTs
Anti-HBs
Anti-HBc IgG
Vaccinated against HepB virus
Anti-HBs
Normal LFTs
What does HBeAg mean
Implies high infectivity, present 6-12 weeks after acute illness
Hep C percentage of chronic silent infections
85%
Managing alcoholic hepatitis
Hospital admission Stop alcohol consumption + alcohol withdrawal- long acting benzodiazepine- CIWA-Ar IV vit K and pabrinex- B1 Optimise nutrition Daily weight, INR, LFT and U&Es Steroids
Antibody in primary biliary cholangitis
Anti-mitochondrial antibodies
Signs of primary biliary cholangitis
Jaundice Skin pigmentation Xanthelasma Xanthomata Hepatosplenomegaly
Tests for primary biliary cholangitis
Raised ALP
Raised GGT
AMA
USS- exclude extrahepatic cholestasis
Treatment for primary biliary cholangitis
Symptomatic- pruritus, diarrhoea, osteoporosis prevention, fat soluble vitamin ADEK prophylaxis
Ursodeoxycholic acid/ cholestyramine
Monitoring
Liver transplant for end-stage disease
Primary sclerosing cholangitis who gets it, increased risk of…
Over 80% have IBD- usually UC
Men 30-40
Increased risk of cancers- yearly colonoscopy and ultrasound
Antibodies in primary sclerosing cholangitis
ANA
SMA
pANCA
Who does autoimmune hepatitis tend to affect?
Young or middle aged women in a bimodal distribution
Antibodies likely to be positive in autoimmune hepatitis
ASMA
Type 1 autoimmune hepatitis
80% of cases
Typically women <40
ASMA positive, IgG in 97%
25% have cirrhosis at presentation
Type 2 autoimmune hepatitis
Children
Less treatable and more commonly progresses to cirrhosis
LKM1 antibodies
ASMA negative
Management of autoimmune hepatitis
Immunosuppressant therapy- prednisolone
Azathioprine as steroid sparing agent to maintain remission
Liver transplant indicated for decompensated cirrhosis
Associations of autoimmune hepatitis
Pernicious anaemia UC Glomerulonephritis Autoimmune thyroiditis Autoimmune haemolysis DM PSC
Pathology of non-alcoholic fatty liver disease
Increased fat in the hepatocytes- steatosis
Wilson’s disease pathology
Rare inherited disorder of copper excretion with excess deposition in the liver and CNS
Autosomal recessive
Signs of Wilson’s disease
Children- liver disease- hepatitis, cirrhosis, fulminant liver failure
Young adults- CNS signs- tremor, dysarthria, dysphagia, dyskinesias, dystonias, dementia, parkinsonism, ataxia
Mood- depression, mania, labile emotions, personlity change
Cognitive deprivation
Kayser-Fleischer rings- copper deposition in iris
Management of Wilson’s disease
Diet- avoidance of copper rich food
Lifelong penicillamine
Liver transplantation
How can you tell if ALP is from bone or liver?
Other deranged LFTs, particularly GGT
Alcoholic liver disease LFT classic
AST/ALT ratio is 2:1
Suspected liver tumour investigations
Bloods- FBC, LFT, clotting, hepatitis serology, alpha-fetoprotein
US or CT to identify lesions and guide biopsy
ERCP and biopsy if cholangiocarcinoma suspected
Two most common mutations for hereditary haemochromatosis
C282Y and H63D
Signs of haemochromatosis
Tiredness early on Arthralgia Decreased libido Slate grey skin Signs of liver disease, cirrhosis Bronze diabetes from iron deposition in the pancreas
Management of haemochromatosis
Venesection
Well balanced diet
Avoid alcohol and uncooked seafood
Monitor LFTs and glucose
Tests if suspecting A1AT deficiency
Serum A1AT levels low (but can be disguised by inflammation as it is an acute phase protein)
Lung function tests- obstructive picture (emphysema)
Liver biopsy
Best imaging modality for acute diverticulitis
CT abdomen
Symptoms of diverticulitis
Altered bowel habit Left-sided colic relieved by defecating Pyrexia Increased CRP/ESR and WCC Tender colon +/- localised or general peritonism
Complications of diverticulitis
Perforation Haemorrhage Fistulae Abscesses Post-infective strictures
Fissure-in-ano often if chronic found with a…
‘Sentinel pile’ or mucosal tag at the external aspect
Treatment for fissure-in-ano
conservative- dietary fibre, fluids, stool softener and hygiene advice
5% lidocaine ointment and GTN ointment or topical diltiazem
Treatment for fistula-in-ano
Fistulotomy and excision
High require a seton suture
Low need to be laid open to allow healing by secondary intention
Symptoms of haemorrhoids
Bright red rectal bleeding (on wiping or coating stools)
Mucous discharge and pruritus ani
Anaemia may be severe
