Gastro Flashcards
Common causes of GI bleed?
Chronic/acute peptic ulcer Drugs Mallory-Weiss Varices Gastric erosions Erosive oesophagitis
Bloods in GI bleed?
FBC, U+E, LFT, amylase, glucose, clotting
Urea raised due to increased protein load
G+S if low risk, X-match if high risk
Investigations besides bloods in upper GI bleed?
Erect CXR/ECG
OGD - identification of cause and permits treatment
What does Glasgow Blatchford Score assess?
Assesses likelihood that patient will need transfusion or endoscopic intervention.
Results and management from GBS?
0/1 and stable - LOW RISK - discharge with O/P OGD or discuss with gastro reg
> 2 and stable - INTERMEDIATE RISK - discuss with reg and routine OGD (24 hours)
> 2 and unstable or varices suspetred - HIGH RISK - urgent review by gastro reg and emergency OGD
What does Rockall Score assess?
Identifies patients at risk of adverse outcome following GI bleed
Contains diagnosis (MW, malignancy etc) so can assess outcome
Results of Rockall score?
<3 = good prognosis, low risk of mortality/rebleeding
> 8 = high risk of mortality, high risk of mortality/rebleeding
What can you give in variceal bleed?
Terlipressin
Constipation + rectal bleeding = ?
Constipation + distenstion + active BS = ?
Constipation + menorrhagia = ?
- cancer
- stricture/GI obstruction
- hypothyroidism
Mnemonic for causes of constipation?
OPENED IT
Obstruction, pain, endocrine, neuro, elderly, diet/dehydration, IBS, toxins
Cause of chronic constipation in kids?
Hirschsprung’s
Investigations for constipation in elderly?
Bloods - exclude metabolic causes (hypothyroid, hypercalcaemia)
Review drug history
Sigmoidoscopy/barium enema to exclude cancer or diverticulitis
Name a bulk forming laxative and how they work?
Bran powder, fybogel (ispaghula husk), methylcellulose, sterculia granules
↑Faecal mass –> stimulate peristalsis – must be taken with plenty of fluid and take a few days to act.
Name a softener laxative and when you use them?
Liquid paraffin, arachis oil, sodium docusate (also has a simulant action)
Useful when managing painful anal conditions (fissure)
Name an osomotic laxative and how they work and side effects?
Lactulose, macrogol (movicol)
Retain fluid in the bowel
SE = bloating
Name stimulant laxatives and how they work and side effects?
Bisacodyl, senna (pure stimulant)
Docusate sodium, danthron (stimulant and softening)
Increase intestinal motility, so don’t use in obstruction or acute colitis. Avoid prolonged use as may cause colonic atony and hypokalaemia.
SEs = abdominal cramps
What can you do for rapid bowel evacuation prior to procedures?
Phosphate enema
Bloods in diarrhoea?
FBC - ↓MCV/Fe deficiency (coeliac/colon ca), ↑MCV if alcohol abuse or ↓B12 absorption (coeliac/Crohn’s)
ESR/CRP - Raised in infection, Crohn’s/UC, cancer
U+E - ↓K+ = severe D+V
TFTs - ?hyper
Coeliac serology
Investigations in diarrhoea?
Bloods
Stool MC+S
Rigig sigmoidoscopy + biopsy (Crohn’s)
Colonoscopy/barium enema - ?malignancy ?colitis
General management of diarrhoea?
Treat Causes
Food handlers – no work until stool samples are -ve. If hospital outbreak, isolation/ward closure may be necessary.
Avoid abx unless infective diarrhoea causing systemic upset.
Rehydration in diarrhoea?
Oral rehydration better than IV, but if impossible –> 0.9% saline + 20mmol K+/L IV.
ORS in children
Anitmotility agents in diarrhoea?
Codeine phosphate 30mg TDS PO or loperamide 2mg PO after each loose stool (max 16mg/day) –> ↓stool frequency
Avoid in colitis (may precipitate toxic megacolon)
Little evidence to suggest their use in acute diarrhoea increases risk of colonic dilatation
Should not be given to children
Risk factors and treatment of C.diff?
> 70 yrs, past C.diff infection, use of antiperistaltic drugs
Stop abx. Treatment not usually needed. Metronidazole or vanc 10 days if severe.
Complication –> toxic megacolon
Screening tool for malnutrition?
MUST (Malnutrition universal screening tool)
BMI score
Weight loss score
Acute disease effect score
0 = low risk 1 = medium risk 2 = high risk
Biochemical features of refeeding syndrome?
Fluid-balance abnormalities
Abnormal glucose metabolism (low insulin requirement –> high insulin requirement)
Hypophosphataemia
Hypomagnesaemia
Hypokalaemia
Thiamine deficiency
Prevention of refeeding syndrome?
Start refeeding at no more than 50% of energy requirements in “patients who have eaten little or nothing for more than five days”
Oral, enteral or intravenous (IV) supplements of potassium, phosphate, calcium and magnesium should be given unless blood levels are high before refeeding
What is Marasmus and Kwashiorkor?
M = Inadequate energy intake in all forms
K = Protein deficiency with adequate energy intake
What are anthropometric measures?
Body weight
Triceps skin-fold thickness
Mid-arm muscle circumference
Plasma albumin with or without transferrin and pre-albumin
3 general causes of GORD?
Raised intra-abdominal pressure
Faulty oesophageal sphincter
Drugs
What are the ALARMS symptoms
Anaemia (iron deficiency) Loss of weight Anorexia Recent onset/progression Melena/haematemesis Swallowing difficulty
Complications of GORD?
Oesophagitis
Ulcers
Benign stricture
Iron deficiency
Barrett’s (squamous –> columnar)
Investigations in GORD?
Endoscopy - usually normal
Barium studies
24 hour oesophageal pH monitoring (GORD = acid in oesophagus >4% of day)
Where does oesophageal cancer tend to arise?
SCC = upper 2/3 Adeno = lower 1/3
Tumours tend to arise in areas of partial narrowing
• Pharyngo-oesophageal junction (40%)
• Junction of upper and middle 1/3 (40%)
• Where oesophagus passes through diaphragm (20%)
Spread of oesophageal Ca?
Can be locally invasive too
liver, lungs, brain, bones
Curative treatments for oesophageal Ca?
Surgical treatment – open oesophagectomy/minimally invasive oesophagectomy
Neo-adjuvant chemo-radiotherapy
Definitive chemo-radiotherapy
Palliation in oesophageal ca?
Endoscopic stenting
Brachytherapy
Chemotherapy/external radiotherapy
Feeding through gastrostomy, jejunostomy or IV
Pain relief
Types of hiatus hernia?
Sliding/Axial - direct herniation through oesophageal hiatus
Paraoesophageal/rolling - organ pushing up beside oesophagus
Causes of hiatus hernia?
Increased intraabdominal pressure –> Large ovarian cysts, pregnancy, obesity
Oesophageal shortening –> Oesophageal spasm and fibrosis from reflux – accentuated by excessive swallowing
Widening of diaphragmatic hiatus –> Muscular degeneration – around lower end of oesophagus and fundus of stomach
Diagnosis of hiatus hernia on endoscopy?
Diagnosed when the distance between diaphragmatic indentation and the squamocolumnar junction is greater than 2cm
Aetiology of duodenal ulcers?
4x more common in men – 30-50 years
Strong genetic influence – 3x more common if 1st degree relative
H.pylori infection in 95% of patients
Smoking is a risk factor
Aetiology of gastric ulcers?
2x more common in men – common in late middle age
NSAIDs – 3/4 fold increase in risk
Less related to H.pylori than duodenal – 70% of patients
Pain of duodenal ulcers?
Epigastric – onset 2-3 hours after eating
Relieved by eating and drinking milk
Radiates to back, often worse at night
Precipitating factors = missing a meal, anxiety or stress
Lasts for 1 to 2 months and occurs in 4 to 6 month cycles
Pain of gastric ulcers?
Epigastric pain – 15-30 mins after eating
Relieved by vomiting and worsened by eating
Pain often worse during the day
Lasts for a period of 2 weeks and occurs in cycles of 1-2 months
Presentation of perforated PU?
Severe, constant, sudden onset epigastric pain – may be hematemesis.
Patient looks ill, usually still, in pain, tachycardia, shallow respiration
Abdomen is flat, very tender (intense guarding) – if air has escaped into peritoneal cavity then liver dullness may be absent.
Peptic ulcer perforation results in a chemical peritonitis rather than a bacterial peritonitis in the initial stages (unlike bowel perforation)
Testing for H/Pylori?
Carbon-13 urea breath test
OR
Stool antigen test
Production of radiolabelled CO2 from swallowed urea – most accurate test. If urease (enzyme that uses H.pylori to metabolise urea) is present, H.pylori is present.
Need to have not taken PPI or abx in past 4 weeks
Imaging for peptic ulcer?
Endoscopy
Gastric ulcer should be biopsied (?malignancy) – further endoscopy after treatment to ensure healing.
Duodenal ulcer - not necessary to biopsy – follow up endoscopy is not required if patient has become asymptomatic
3 steps for treating H pylori?
Step A = lifestyle changes
Step B = H.pylori testing
Step C = Eradication therapy
Step B (H.pylori testing) of peptic ulcer treatment?
If +ve and associated with NSAID use –> full dose PPI for 2 months then step C
If +ve and not associated with NSAID use –> step C
If –ve –> full dose PPI for 1-2 months
Eradication therapy for H.Pylori?
7 day, twice-daily course of
o A PPI
o Amoxicillin 1g
o Clarithromycin 500mg or Metronidazole 400mg
Metabolic abnormaliites in coeliac disease?
Iron/folate deficiency, vitamin K deficiency, vitamin D deficiency and hypocalcaemia
Skin sign in coeliac?
Dermatitis herpetiformis
60-80% - intensely itchy blisterning rash on trunk and extensor surfaces of limbs
Bloods in coeliac?
Anti-TTG
FBC (anaemia)
LFTs (elevated transminases)
B12, folate, ferritin, calcium
Definitive diagnosis of coelic?
Jejunal biopsy (endoscopic)
Must be on gluten diet until biopsy (villi return to normal on gluten-free)
Will show subtotal villous atrophy
Signs in acute pancreatitis?
Fever, hypotension, tachycardia, tachypnea, or diaphoresis
Epigastric tenderness, with guarding on abdominal examination
Decreased bowel sounds
Jaundice - suggests choledochal obstruction from gallstone pancreatitis
Grey-Turner’s sign - ecchymosis of the flank and Cullen sign - ecchymoses in the periumbilical region
Local complications of acute pancreatitis?
Acute pancreatic fluid collection (first 4 weeks)
Pancreatic pseudocyst (after 4 weeks)
Acute necrotic collection (first 4 weeks)
Walled off necrosis (after 4 weeks)
Systemic complications of acute pancreatitis
Circulatory shock (kinin activation, haemorhage)
DIC
Respiratory insufficiency (hypoxaemia, atelectasis, pleurak effusion, ARDS)
Acute renal failure
Metabolic (hypocalcaemia, hyperglycaemia/DM, hypertriglyceridaemia)
Pancreatic encephalopathy (confusion, delusions, coma)
Retinal arteriolar obstruction (sudden blindness)
Metastatic fat necrosis
Diagnostic criteria for acute pancreatitis
ATLANTA CLASSIFICATION
- Abdominal pain - acute onset of a persistent, severe, epigastric pain often radiating to the back)
- Serum lipase activity (or amylase activity – lipase more sensitive) at least three times greater than the upper limit of normal
- CECT - Characteristic findings of acute pancreatitis on contrast-enhanced CT
(CT not usually required)
Bloods in acute pancreatitis?
FBC - leucocytosis/raised Hb due to haemoconcentration
U+E. LFTs – elevated liver enzymes –> gallstones probably cause
Triglyceride, calcium, LDH, CRP levels
ABG
Urinalysis
Imaging in acute pancreatitis?
Abdo USS - look for gallstones
Erect CXR - rule out perf DU
AXR - may show ground glass appearance due to presence of peritoneal exudate. Bowel gas usually absent apart from central dilated section of duodenum/jejunum (‘sentinel’ loop) - indicates localised ileus
What is the Glasgow criteria?
Valid for gallstone and alcohol induced pancreatitis –> 3 or more needs ICU
P - PaO2 <8kPa A - Age >55-years-old N - Neutrophilia: WCC >15x10(9)/L C - Calcium <2 mmol/L R - Renal function: Urea >16 mmol/L E - Enzymes: LDH >600iu/L; AST >200iu/L A - Albumin <32g/L (serum) S - Sugar: blood glucose >10 mmol/L
Management of acute pancreatitis
Fluid resuscitation and oxygen supplementation
Analgesia (opioids - improves respiratory function)
Nutritional support (if no N+V and no pain, can start eating. If severe enteral feeding recommended)
Surgical management in acute pancreatitis?
ERCP
If existing cholangitis or biliary obstruction
Cholecystectomy
For gallstones – after initial symptoms have resolved.
Percutaneous aspiration or Surgical debridement
For patients with severe pancreatitis and infected necrosis or persistent fluid collections
Subsequent things in acute pancreatitis?
May affect pancreatic endocrine function –> hyperglycaemia (needs monitoring)
May need pancreatic enzyme supplements
Contents of the spermatic cord?
External/internal spermatic and creamasteric fascia
Spermatic cord
o Vas, obliterated processus vaginalis, vasculature, pampiniform plexus, genital branch of genitofemoral nerve + sympathetic nerves
Ilioinguinal nerve
What is an indirect inguinal hernia?
Originate lateral to inferior epigastric artery.
Pass through internal inguinal ring along inguinal canal and, if large, out through the external ring
What is a direct inguinal hernia?
Originate medial to inferior epigastric artery.
Push their way directly through a weakness the posterior wall of the inguinal canal (Hesselbach’s triangle)
What is a congenital inguinal hernia?
Results from a patent processus vaginalis. Can be large enough to allow abdominal or pelvic organs to descend.
What happens in a strangulated inguinal hernia?
Most commonly occurs at external inguinal ring. Most commonly in elderly and in first 6 months of life.
- Constriction of the hernial neck, or twisting of the hernia, initially obstructs venous return
- Oedema eventually obstructs arterial supply
- Eventually the bowel necroses and perforates into the hernial sac
Symptoms of an inguinal hernia?
Discomfort/pain in groin
Lump/mass in scrotum (can be reducible)
Abdo pain (if colicky –> obstruction)
Vomiting, abdominal distension, absolute constipation (obstruction)
What would irreducibility of an inguinal hernia indicate? What would local tenderness and warmth over a reducible mass indicate?
Incarceration
Strangulation
How do you assess for an inguinal hernia?
Occlude deep ring and ask patient to cough (midway between ASIS and pubic symphysis)
Indirect - hernia not restrained (protrudes obliquely behind the scrotum when patient stands)
Direct - hernia restrained (protrudes directly forwards when patient stands)
Differentials for a groin lump?
Femoral hernia, hydrodcele, spermatocele, varicocele, undescended testes, lipoma
Repair or an inguinal hernia?
Should always be repaired unless specific contraindications
Herniorrhaphy - open (mesh) is preferred
Avoid heavy lifting/straining for a week after
Femoral vs inguinal hernia location?
Inguinal = above and medial Femoral = below and lateral
TO PUBIC TUBERCLE
What does lateral compartment of femoral canal contain?
Medial to lateral
Femoral vein + artery (femoral sheath)
Genitofemoral nerve
Femoral nerve
Medial compartment is the femoral ring, where hernias occur
Who are femoral hernias more common in? What is the aetiology?
More common in women - but less common overall than inguinal hernias
Increased intra-abdo pressure - pregnancy, chronic cough, GI obstruction, straining
Laxity or weakness of tissue - pregnancy, rapid weight loss, previous hernia repair
Is incarceration and strangulation more common in femoral or inguinal hernias?
Femoral - because it is a smaller hole
How does congenital umbilical hernia occur? Who does it occur in?
Occurs through weak umbilical scar
Black children - males 2x more than females
How do acquired para-umbilical hernias occur? Who do they occur in?
Just above the umbilicus, weakness of linea alba
5x more common in women than men (age 35-50)
RFs = multiple pregnancy, ascites, obesity, large abdominal tumours
Symptoms and signs of acquired para-umbilical hernia?
Sharp pain on coughing/straining
GI symptoms due to traction on stomach/transverse colon
Transient colic due to subacute obstruction
Soon becomes irreducible due to adhesions within the sac
Management of congenital and acquired umbilical hernia?
CONGENITAL
Non-intervention successful in 93% of cases. No surgery before age 2.
ACQUIRED
Should be repaired to avoid complications
Who gets gallstones
Fat, female, forties, flatulent
90% remain asymptomatic
RFs for becoming symptomatic = smoking/parity
In what situations do gallstones become symptomatic?
Acute cholecystitis Chronic cholecystitis Biliary colic Pancreatitis Cholangitis Obstructive jaundice Gallstone ileus
Management of symptomatic gallstones?
NON-SURGICAL
Analgesia (opioids + NSAIDs), adequate hydration, abx
SURGICAL
Cholecystectomy (within 1 week if acute)
What is cholecystitis precipitated by?
Risk factors?
Fatty food
Gallstones, female gender, age, obesity, rapid weight loss, pregnancy, Crohn’s disease, hyperlipidaemia
What is Murphy’s sign?
pain and cessation of deep inspiration during palpation in RUQ, not present in LUQ
What is Charcot’s triad?
fever, RUQ pain, jaundice
Bloods in cholecystitis? Imaging?
Other differentials?
↑WCC, ↑CRP, abnormal LFTs
USS – gallstones and thickened, shrunken gallbladder; pericholecystic fluid
Biliary colic – RUQ pain, but no fever/WCC and no jaundice
Cholangitis – RUQ pain and fever/WCC and jaundice
Management of acute cholecystitis?
NBM
IV access and bloods o FBC (WBC), U&E, glucose, amylase, LFTs
IV analgesia and antiemetic
IV Abx (co-amoxiclav)
Surgery
o Urgent laparoscopic cholecystectomy vs interval procedure. ERCP if distal CBD stone.
o Open procedure required if perforation
How is the portal vein formed?
Union of the splenic and the superior mesenteric veins at the level of L2 behind the head of the pancreas
What happens in portal hypertension?
blood is diverted into collaterals between the portal and the systemic venous systems
Causes of portal hypertension? (increased resistance)
Most common is cirrhosis (worldwide is schistosomiasis)
PRE-HEPATIC
Portal vein thrombosis, splenic vein thrombosis, congenital atresia/stenosis, extrinsic compression
HEPATIC
Pre-sinusoidal = Hepatitis, congenital hepatic fibrosis, idiopathic non-cirrhotic portal hypertension, schistosomiasis
Sinusoidal = cirrhosis
POST-SINUSOIDAL
Budd-Chiari syndrome (hepatic vein thrombosis), veno-occlusive disease, constrictive pericarditis, RHF
Symptoms of portal hypertension?
Often asymptomatic with splenomegaly the only sign
Haematemesis of melena – rupture of varices
Hepatic encephalopathy
Signs of portal hypertension?
Ascites – with low albumin
Porto-systemic shunts – caput medusa
Venous hum
Haemorrhoids
Peripheral oedema
Management of portal hypertension (prophylaxis against bleeding)?
Conservative = salt restricted diet
Medical = Beta blockers /spiro/furosemide - decreases portal pressure
Surgical = porto-systemic shunt (TIPS procedure) portal vein to hepatic vein
What is a TIPS procedure? What is a risk?
Transjugular intrahepatic portosystemic shunt
Can cause encephalopathy
How are hepatitis A B and C transmitted?
A = faecal oral
B = parenteral (blood, body fluids)
C = parenteral (IV drugs, sexual, needlesticks, perinatal)
Symptoms of viral hepatitis?
N+V, myalgia, fatigue/malaise, RUQ pain, change in sense of smell/taste, coryza, photophobia, headache.
Signs of viral hepatitis?
Often no signs unless jaundice develops.
Hepatomegaly, splenomegaly and lymphadenopathy may then be present.
Complications of viral hepatitis?
CHRONIC INFECTION
Consequence of hep B, C or D infection. Presentation varied and may be asymptomatic.
Subclinical infection –> vague symptoms (fatigue/dyspepsia).
Chronic infection –> chronic hepatitis, cirrhosis and hepatocellular carcinoma.
Investigations in viral hepatitis?
Bloods – FBC, U+E, LFTs, clotting
Hepatitis serology
Imaging – USS/CT/MRI to assess for presence of cirrhosis or other causes of symptoms
What is HBsAg?
Hep B Surface Antigen
Protein on surface of HBV (patient has infection –> used to make vaccine)
sAgGy face because currently infected
What is anti-HBc?
Total Hep B Core antibody
Appears at onset of symptoms and persists for life (previous or ongoing infection)
c = CAUGHT IT
What is anti-HBs?
Hep B surface antibody
Indicates recovery/immunity from hep B
S = SAFE
What is IgM anti-HBc?
IgM Antibody to Hep B Core Antigen
Acute (<6 months) infection
IgM = OMG acutely infected
Management of hep A and B?
Avoid unprotected sex.
Treatment mainly supportive (fluids, antiemetics, rest).
Avoid alcohol until liver enzymes normal. Review medications, stop non-essentials.
Treatment with antiviral agents not usually indicated
Management of hepatiits C?
Aim = prevent cirrhosis, liver failure and cancer developing –> refer to specialist
Early treatment with interferon alpha can reduce chronic infection
Abstinence from alcohol
Barrier contraception
Should not donate blood, organs, tissues or semen
What is cirrhosis?
Fibrosis and conversion of liver into structurally abnormal nodules –> abnormal vascular relationships
- entire liver affected (not focal scarring)
- parenchymal injury and fibrosis precedes nodule formation
- is irreversible
Micronodular and macronodular cirrhosis?
Micronodular = <3mm in diameter - alcoholism, wilson’s disease, A-1-antitrypsin deficiency
Macronodular = >3mm in diameter - viral or autoimmune forms of chronic active hepatitis
Causes of cirrhosis?
Alcoholic liver disease Viral hepatitis Biliary cirrhosis Haemochromatosis Wilson's disease A-1-antitrypsin deficiency Hepatic venous outflow obstruction (Budd-Chiari syndrome)
Signs of cirrhosis?
Skin = Jaundice, bruising, spider naevi, skin telangectasias, dupuytren’s contracture
Hands = finger clubbing, leuconychia, palmar erythema
Sexual = gynaecomastia/reduced body hair, erratic menstruation/breast atrophy
Organomegaly = small liver, splenomegaly
Symptoms of cirrhosis?
Lethargy, itching, fever, weight gain, swelling of abdomen and ankles
Complications of cirrhosis?
Anaemia (folate deficiency, haemolysis)
Thrombocytopenia (hypersplenism)
Coagulopathy (synthetic function of liver affected, and cholestasis –> reduced vit K absorption)
Varices
Ascites (transudate)
SBP (E.coli)
Hepatocellular carcinoma (Hep C)
How does cirrhosis cause ascites?
Portal hypertension –> increased capillary pressure –> lymph formation –> ascites
Portal HTN –> splanchnic vasodilation –> RAAS activation and ADH release –> increased retention –> ascites
Bloods in cirrhosis?
LFTs - AST/ALT raised, gamma-GT raised in active alcoholics
FBC - anaemia, thrombocytopenia, macrocytosis (if alcohol)
U+E - hyponotraemia, renal dysunfction
Albumin - hypoalbuminaemia
Coagulation - PT and INR raised
Classification for liver disease?
Child Pugh Score
Score >7 –> transplant list
Management of cirrhosis?
ALCOHOL/NUTRITION
Abstinence, ensure adequate intake, zinc supplementation
PRURITIS
Antihistamines/topical ammonium lactate
Colestyramine is mainstay
PREVENTING COMPLICATIONS
Osteoporosis prevention, regular exercise to prevent wasting
Prophylactic Abx
Vaccination - hep A, influenza, pneumococcal
Avoid hepatic metabolised drugs
Surveillance of varices/cancer
TRANSPLANTATION
What can you give in hepatic encephalopathy?
High dose lactulose
Avoid CNS depressants, use haloperidol instead
Definition of transudate and exudate?
Trans = protein <3g per 100ml of fluid
Caused by increased hydrostatic pressure or reduced oncotic pressure
Ex = protein >3g per 100ml of fluid
Caused by inflammation
Specific causes of ascites?
TRANSUDATE
Cirrhosis, HF, nephrotic syndrome, constrictive pericarditis, ovarian tumours
EXUDATE
Malignant disease, pyogenic infection, TB, pancreatitis, lymphoedema/myxoedema
Investigation of choice in ascites?
USS + Diagnostic paracentesis
30-50ml of fluid withdrawn to allow identification of…
Protein count (albumin and total protein) Malignant cells Bacteria WBCs (if >250 then SBP) Glucose
Management of ascites?
Therapeutic paracentesis of 4-6 litres
Plasma volume expansion with albumin
Bed rest, reduced salt intake, spironolactone
Areas affected in UC and Crohn’s?
Crohn’s = all GI tube, mainly terminal ileum and ascending colon, rectum in 50% of cases
UC
Rectum always involved
Colon, appendix and terminal ileum may be involved
Pancolitis = involvement beyond splenic flexure
Macroscopic appearance in Crohn’s?
Small bowel thickened Deep ulcers and fissures Cobblestone appearance Fistula and abscesses in colon Apthoid ulceration is early feature Granulomas present (50-60%) Non caesating epitheloid cell aggregates with Langhan’s giant cells
Macroscopic appearance in UC?
Mucosa is reddened Inflamed and bleeds easily Ulcers may be present if severe Pseudopolyps formed by inflammation Mainly mucosal Inflammatory cells in lamina propria No granulomas
Which IBD has strictures?
Crohn’s
Which IBD has crypt abscesses?
UC
Which IBD has goblet cell depletion?
UC
Extra-intestinal features of IBD?
Clubbing Uveitis Arthritis Erythema nodosum Pyoderma gangenosum (HLA-B27)
Complications of Crohn’s
SBO
Toxic dilatation
Abscess formation
Fistulae (infalmmation –> stricture –> obstruction –> fistulae) - colovesical, colovaginal ,perianal, enterocutaneous
Perforation
Malnutrition
Rectal haemorrhage
CANCER
Complications of UC?
Perforation/bleeding
Toxic dilatation of the colon
VTE – prophylaxis for all inpatients
Colonic cancer
Bloods in IBD?
FBC, ESR, CRP, U+E, LFT, blood culture, (INR, ferritin, B12, folate in Crohn’s due to TI involvement)
Stool stuff in IBD?
MC+S
Exclude campylobacter, C.dff, Salmonella, Shigella, E.coli, amoebae
Faecal Calprotectin
Recommended to distinguish between IBS/IBD
AXR signs in IBD?
Thumbprinting = wall oedema = active disease
Lead pipe colon = chronic disease (featureless)
Fluoroscopy in IBD?
BARIUM ENEMA
Not during acute attack
Crohn’s - cobblestoning and strictures (string sign), ‘rose thorn ulcers’
UC - lead piping
SMALL BOWEL ENEMA
Detects ileal disease in Crohn’s
Staging of IBD?
Trulove and Wit’s criteria
Inducing remission in IBD?
CROHN'S • Steroids (oral or IV) • Enteral nutrition - in younger people • Azathioprine, mecaptapurine, methotrexate • Smoking cessation can induce remission
UC
• Oral mesalazine/ sulfasalazine
• Steroids (Oral or IV)
Maintenance in IBD?
CROHN’S
• Azathioprine, mecaptapurine, methotrexate
• Infliximab, adalimumab – in patients that don’t respond to treatment (mabs = TNF-a inhibitors)
UC
• Oral mesalazine/ sulfasalazine
• Rectal treatments often given – salazine enema
• Immunosuppressants (Azozthiprine, mecaptopurine) can be used
• Cyclopsorin for refractory colitis – large side-effect profile
Surgery in IBD?
CROHN’S
Indicated in limited disease, refractory disease, life-threatening flares
UC
Can be curative – indicated in disease refractory to medical treatment, life-threatening acute flares, or treatment of complications (carcinoma)
Surveillance of IBD patients?
Regular scoping for cancer
What causes diverticulae?
Lack of dietary fibre –> hypertrophy of longitudinal and circular muscle
Increased intraluminal pressure –> outpouching
Where are diverticulae most often found?
Sigmoid colon
Symptoms of diverticulosis?
Pain/indigestion - not worsened by food; distension, flatulence, belching
Constipation - infrequent motions and hard stool
Appetite and weight normal
Symptoms of acute diverticulitis?
Severe LIF pain exacerbated by movement
Abdo distension
Nausea and anorexia
Constipation and diarrhoea
Symptoms of chronic diverticulitis?
MIMICS COLON CANCER
Diarrhoea alternating w/constipation
Vomiting, distension, colicky abdo pain
Passage of mucus, bright red blood or melena
Complications of diverticular disease?
Obstruction due to stricture Abscess Perforation Fistula Haemorrhage
Investigations in diverticular disease?
DIAGNOSIS OF EXCLUSION
Barium meal/enema - shows outpouchings of diverticula and narrowed sigmoid colon
Sigmoidoscopy - shows inflammation but poor at showing diverticula
CXR - rule out perforation
Management of acute diverticulitis?
Bed rest
IV ceph and met/fluids
Analgesia
Indications for surgery in diverticulitis?
Peritonitis Fistula formation Persistent haemorrhage Pericolic abscess formation Intestinal obstruction Recurrent diverticulitis resistant to medical therapy
Management of chronic diverticular disease?
High fibre diet
Antispasmodics
Laxatives (lactulose)
Where is McBurney’s point?
1/3 distance from ASIS to umbilicus
What is Psoas sign?
Pain on extending hip if retrocaecal appendix
PR in appendicitis?
Tender on the right (sign of low-lying appendix)
Investigations in appendicitis?
BLOODS FBC, U+E, LFT, CRP, G+S (WCC raised, neutrophilia, raised CRP) Blood cultures (if pyrexial)
Urine PT and urinalysis
USS and CECT (if appropriate)
Immediate management of appendicitis?
NBM
IV fluids
Analgesia
IV abx pre-op (ceph and met or co-amoxiclav)
Appendicectomy
Causes of bowel obstruction?
SMALL = adhesions and hernias LARGE = tumours and volvulus
Others = intussception, IBD, gallstone ileus, foreign bodies
AXR signs in bowel obstruction?
Excess gas in abnormall dilated bowel loops
Bowel proximal to obstruction dilates
Bowel distal to obstruction shrinks and collapses
Management of bowel obstruction?
DRIP AND SUCK
NBM and IV fluids
NGT in SBO or if vomiting - minimises risk of aspiration
Pain relief
IV abx
Conservative treatment for 2-3 days (unless causes by an incarcerated hernia)
If no resolution, or deterioration –> surgery
Causes of ileus?
ABDOMINAL - post-op, peritonitis, vascular occlusion
SYSTEMIC - hypokalaemia, DKA, uraemia, hypoT, hypomagnasaemia
DRUGS - anticholinergics, TCAs, parkinsonian drugs
REFLEX CAUSES - postpartum, renal colic, retroperitoneal haemorrhage
Most common sites of gallstone ileus?
Ileum (60%)
Jejunum (15%)
Stomach (15%)
Colon (5%)
Most common places for colorectal cancer?
Rectum (27%)
Caecum and ascending (22%)
Sigmoid (20%)
Features of right-sided colon cancer?
Weight loss, anaemia, painful palpable RIF mass, rectal bleeding
More likely to be advanced at presentation
Features of left-sided colon cancer?
Early change in bowel habit, colicky pain, rectal bleeding, bowel obstruction, tenesmus, mass in LIF
Less advanced at presentation
Features of rectal colon cancer?
Change in bowel habit commonest feature, bleeding, rarely associated with pain
Investigations in colon cancer?
BLOODS - FBC, LFT
Colonoscopy = gold standard
Barium enema/flexible sigmoidoscopy = patient with major co-morbidity. APPLE CORE SIGN
CT colonograpy = substantially less invasive and does not require sedation
Who is offered colon cancer screening?
Age 60-69 (being extended to 74)
Every 2 years
FOB test - if abnormal –> colonoscopy
And high risk individuals - age >40, fhx of colon ca, personal hx of colon ca, FAP, UC
Rome criteria for IBS?
Abdo pain (or discomfort) - relieved by defecation or associated with altered stool form or frequency
More than 2 of... Urgency Incomplete evacuation Abdominal bloating/distension Mucous PR Worsening of symptoms after food
Investigations in IBS-type picture?
Bloods - FBC, U+E, CRP, LFT, coeliac serology
Colonoscopy - if features of systemic disease
Serum CA-125 - exclude ovarian cancer
Symptomatic treatment in IBS?
Constipation –> laxatives
Diarrhoea –> loperamide after each loose stool
Colic/bloating –> buscopan
Causes of rectal prolaspe?
Pelvic floor muscle weakness, prior pelvic surgery
Neurologic disorders = CVA, dementia, pudendal neuropathy
Other = multiparity
Symptoms of rectal prolapse?
Something coming down - during defecation, mucous and bleeding
Dull anal pain - indicates strangulation (constitutional symptoms - fever, chills, sweating, N+V)
Faecal incontinence - passive (leakage they are unaware of) urge (unable to get to toilet in time)
Majority also have urinary incontinence
Rectal prolapse on examination?
Protruding mass with concentric rings of mucosa
Differentiate mucosal prolapse (thin, segmental) from full thickness (circumfrential, plum coloured, with mucosal folds)
Management of rectal prolapse?
Conservative - manual reduction, circumanal ring
Surgical - abdominal procedures preferred if patient fit as perineal procedures have higher rate of recurrence
What are haemorrhoids? Where do they arise?
Abnormally enlarged vascular muscosal cushions in the anal canal
Above the dentate line = internal
Below the dentate line = external
Dentate line = 2cm above the anal verge (anatomical delineation between upper and lower canal)
Grading of haemorrhoids?
Grade 1 = do not prolapse out of canal
Grade 2 = prolapse of defecation but reduce spontaneously
Grade 3 = require manual reduction
Grade 4 = cannot be reduced
Who do haemorrhoids affect more?
Men, and affects them for longer
Women affected at certain periods - pregnancy and perperium
Causes of hamorrhoids?
Constipation and prolonged straining and stool (low fibre diet)
Increased anal sphincter tone
Obstruction of venous flow (pregnancy, portal hypertension)
Symptoms of haemorrhoids?
Bright red painless bleeding after defecation
Faecal soiling
Mucus discharge
Pruritis ani
Rectal fullness, discomfort or incomplete evacuation
Prolapsed –> lump at anal verge
Examination of haemorrhoids?
EXTERNAL
- Not visible if not prolapsed
- Local perineal irritation
- Straining may make them visible at anal verge
- Thrombosed haemorrhoids are purple, swollen and acutely tender perianal lumps
RECTAL
- internal haemorrhoids not palpable (they empty with finger pressure)
- Excludes other pathology (cancer)
Complications of haemorrhoids?
Strangulation
Investigations for haemorrhoids?
Proctoscopy – to diagnose first or second degree piles (seen bulging into lumen as proctoscope is withdrawn)
Sigmoidoscopy – indicated if history of bleeding or symptoms suspicious of malignancy
Conservative management of hamorrhoids?
Ensuring perineum is dried and washed after defaecation (prevents pruritis ani) – application of talcum powder
Digital replacement of prolapsed haemorrhoids
Local anaesthetic creams and ointments
Treatment aimed at reducing spasm of internal anal sphincter (Nitroglycerine ointments, Botulinum toxin injection)
Surgical management of harmorrhoids?
Sclerotherapy, rubber band ligation, cryotherapy (small piles)
Anal dilatation under GA, haemorrhoidectomy (big piles)
Prevention of haemorrhoids?
Eat more fibre and bulk up stools
Minimise time spent defecating
How does perianal abscess arise?
Infection in perianal gland (lies between internal and external sphincters)
Glands are V small and become obstructed by faeces –> infection
Conditions that pre-dispose to perianal abscess?
TB, actinomycosis, mucinous carcinoma, IBD (esp Crohn’s)
Men affected more than women
Symptoms of perianal asbcess?
Gradual onset pain around the anus
Becomes more severe and throbs. Defaecation and sitting are painful.
Sitting with one buttock raised is pathognomonic
Signs of perianal asbcess?
Abscess may be seen deep in the skin next to the anus.
Localised tenderness and swelling.
Proctoscopic examination –> may see damaged opening to affected gland, with pus discharging from it.
Investigations for perianal abscess?
None usually necessary – rectal exam usually sufficient for diagnosis.
Screen for STDs/investigate for IBD, diverticular disease or lower GI malignancy.
Culture pus for routine gut and skin organisms
Management of perianal abscess?
Surgical drainage if established
Medication for pain relief
Abx not usually necessary unless diabetes or immunocompromised (if found early, abx may abort the infection).
Complications of I+D for perianal abscess?
31% of I+D patients develop fistula
Where do anal fissures usually arise?
Directly posteriorly and in the midline
Longitudinal tears
Who do anal fissures affect?
Men and women equal
20-30 years peak
Secondary to IBD (Crohn’s)
What is a sentinel pile?
Torn, bunched up strip of mucosa at the base of a fissure
Consevative/medical management of anal fissures?
Warm baths, stool softeners, bulk laxatives, add bran to diet, analgesia, reassurance
Topical GTN/diltiazem
Botulinum toxin (if topical GTN fails)
Surgical management of anal fissure?
Internal sphincterotomy
Manual diltation (reduces sphincter pressure - rarely indicated as can cause incontinence)
Cause of sigmoid volvulus?
Chronic constipation –> baggy, atonic bowel
May become twisted on mesenteric axis and produce a closed loop obstruction
Venous infarction –> perforation and faecal peritonitis
Who gets sigmoid volvulus?
Elderly constipated patients
M:F 4:1
More common than caecal (younger)
Feature of history in sigmoid volvulus other than obstruction things?
Previous episodes - colonic twists may spontaneously untwist
Feature of rectal exam in sigmoid volvulus?
Capacious, empty rectum
Features of AXR in sigmoid volvulus?
Enormously dilated oval gas shadow in upper abdomen (gas-filled hepatic flexure)
May be looped on itself to give inverted U “coffee bean sign”
Management of sigmoid volvulus?
Decompression with flatus tube
Laparoscopic derotation or laparotomy +/- bowel resection
Prevention of recurrence of sigmoid volvulus?
Sigmoidplexy
What is achalasia?
Neuromuscular failure of relaxation at the distal oesophagus
Progressive dilatation, tortuosity, incoordination of peristalsis and often hypertrophy of the oesophagus above.
A functional obstruction
When and how does achalasia present?
Any age (peak 30-40, both sexes equal)
Dysphagia (progressive, less rapid than cancer, more for solids than liquids)
Regurgitation –> vomiting or aspiration
Chronic malnourishment
Management of achaliasa?
Surgical management
Botulinum toxin
Nitrates/CCBs (least effective)
Causes of chronic pancreatitis?
Alcohol (by far biggest cause) Familial CF Haemochromatosis Pancreatic duct obstruction ↑PTH Congenital (pancreas divisum
Features of chronic pancreatitis?
epigastric pain Anorexia and weight loss Exocrine insufficiency Endocrine insufficiency Obstructive jaundice Portal hypertension Pancreatic duct strictures
Exocrine and endocrine insufficiency in chronic pancreatitis?
EXOCRINE
o Steatorrhoea
o Hypocalcaemia (unabsorbed fat chelates calcium)
o Malabsorption of fat (but no bleeding tendency)
o Protein catabolism (exacerbates weight loss)
ENDOCRINE
Impaired glucose tolerance
Biochemical profile of chronic hepatitis?
Raised aminotransferases out of proportion of alk phos
Conjugated hyperbilirubinaemia
Prolongation of PT which is resistant to correction with parenteral vitamin K
What is a subphrenic abscess?
Localised collection of pus underneath right/left hemidiaphragm.
Usually the result of a breach in integrity of the peritoneum.
Occur as result of generalised peritonitis (appendicitis, perforated ulcer, perforated gallbladder, faecal contamination).
Clinical picture of a subphrenic abscess?
Patient who develops features of toxicity 2-21 days after making initial recovery from an episode of peritonitis or an operation
Swinging fever
Malaise, nausea, weight loss
Upper abdo pain radiating to shoulder tip
Breathlessness (lower lung collapse or development of pleural effusion)
How is subphrenic abscess diagnosed?
Diagnosed using USS or abdominal CT
CXR: high diaphragm on affected side, gas and fluid below diaphragm, may be pleural effusion
Features of liver abscess?
Fever, RUQ pain, tender hepatomegaly.
Rarely jaundice and referred shoulder tip pain. •
Raised alk phos/gamma GT
Normal/moderately increased serum bilirubin
Due to enzyme induction in parts of liver where there is impaired bile excretion
Causes of liver abscess?
Bacterial - usually polymicrobial (strep milleri)
Amoebic - entamoeba hystolitica
Fungal - candida
Risk factors for hepatocellular carcinoma?
Liver cirrhosis (80% cases – any cause)
Chronic HBV/HCV carriage
Drugs (anabolic steroids, COCP)
Toxins (aflatoxin)
Parasites (schistosomiasis, echinococcus, clonorchis sinensis)
Features of hepatocellular carcinoma?
General = malaise, fever
GI = anorexia, jaundice, constipation, ill-defined upper abdominal pain, abdominal fullness, bleeding oesophageal varices
Hepatomegaly = liver is often irregular or nodular, may be tender
Ascites
Dyspnoea
Spread of hepatocellular ca?
lung, bone, brain, lymph nodes (right supraclavicular)
Classification of acute hepatic failure?
Severe hepatic dysfunction within 6 months of onset of symptoms –> encephalopathy or coagulopathy
Hyperacute = within 7 days Acute = within 8-28 days Subacute = within 5-12 weeks
What is chronic (decompensated) liver disease?
Deterioration in liver function superimposed on chronic liver disease
Presentation of hepatic failure?
CNS - encephalopathy
Renal failure
Sepsis - bacterial infection w/o fever and leucocytosis
Coagulpathy
CVS - HF and hypotension if heart disease
Metabolic - hypoglycaemia
Hypoxia
Why is there coagulopathy in liver failure?
Synthesis of coagulation factors (I, II, V, VII, IX, X) affected.
Inhibition of fibrinolysis (liver produces protein C, protein S and antithrombin III)
Clearance of activated coagulation factors affected (liver removes fibrin and tPA from circulation)
Absorption of vitamin K affected (malabsorption)
Why is there encephalopathy in liver failure?
Accumulation of toxins from gut –> cerebral oedema and changes in level of consciousness –> coma.
What causes an epigastric hernia? Who gets them?
Protrusion of extra-peritoneal fat where linea alba is pierced by a blood vessel
Drags a pouch of peritoneum with it
Age 20-50 and more women than men
Symptoms of epigastric hernia?
Pain - aggravated by eating
Abdominal mass
Vomiting/nausea
Relieved by reclining
3 polyposis coli syndromes?
FAP
Gardner’s syndrome
Turcot’s syndrome
All autosomal dominant and require endoscopic surveillance from teenage years
What are Gardner’s and Turcot’s also associated with?
Gardner’s - soft tissue and bone tumours
Turcot’s - malignant CNS tumours
Anal carcinoma types?
Most = squamous
Other = bcc/melanoma of overlying skin
Presentation of anal carcinoma?
Mainly occurs in elderly
Anal pain and discomfort
Discharge and bleeding (similar to haemorrhoids)
Enlarged groin LNs indicate metastasis
O/E – may feel hard and woody due to invasion of perianal tissues
Presentation of perianal haematoma?
Caused by rupture of a blood vessel beneath the anal skin – acutely painful and onset after straining at stool.
O/E - blue-black bulge in the skin near the margin of the anus
What is fistula-in-ano? Causes?
Abnormal communication between the perianal skin and the anal or rectal lumen (both epithelial surfaces)
Chronic version of peianal abscess
Causes = Crohn’s, TB, HIV, previous surgery, radiotherapy, trauma, foreign bodies, anorectal cancer
Presentation of fistula-in-ano?
- Intermittent discharge in perianal region
- Pain and discomfort in perianal area
- Chronic irritation
External opening of fissure generally seen lateral to anus – may be seen as a small papilla of granulation tissue.
Internal opening may be felt on rectal examination.
