Gastro Flashcards
chronic liver disease + transplant, colon cancer, haemochromatosis, IBD, coeliac, chronic pancreatitis , peptic ulcer disease , GORD
Causes of chronic liver disease
Fatty Liver
- Alcoholic
- Non-alcohol liver disease (NASH)
o DM/metabolic syndrome
o Pregnancy
o Idiopathic
Infectious
- Hepatitis : A – acute, B, C - chronic
- EBV
- CMV
Genetic
- Hereditary Hemochromatosis (AR)
o Increased intestinal iron absorption
- Wilson’s Disease (AR)
o Toxic accumulation of copper
- Alpha-1-antitrypsin deficiency (AR)
o Protease inhibitor (makes up most of alpha-1 globulin on protein electrophoresis)
Congestion
- Budd-Chiari Syndrome
- RHF/CHF
Autoimmune
- Autoimmune Hepatitis
o Ab against hepatocyte surface antigen
- Primary Biliary Cirrhosis
- Primary Sclerosing Cholangitis
Toxins/drugs
- Alcohol
- Paracetamol overdose
- Isoniazid, methotrexate, methyldopa, nitrofurantoin
Complications of chronic liver disease
- Portal Hypertension
- Hepatic Encephalopathy/Cerebral oedema
- Synthetic dysfunction causing coagulopathy, hypoalbuminaemia and feminization
- Hepatocellular Carcinoma
- Spontaneous bacterial peritonitis
- Hepatorenal syndrome
- Ascites
- Hypoglycaemia
Investigations for chronic liver disease - bloods and imaging + others
Bedside
- Fluid balance, weight
Bloods
- FBC, CRP (infection, GI bleed, leucopenia and thrombocytopenia suggest hypersplenism)
- Chemistry (urea synthesized in liver, creatinine for hepatorenal syndrome, CRP, ammonia for encephalopathy)
- Glucose
- Coags (↑ PT, ↑APTT, ↑Thrombin time)
- LFT’s (AST/ALT – hepatocellular, GGT/ALP –cholestatic, AST:ALT ration of>2 suggests alcoholic liver disease)
- Liver screen
o Viral serology (Hep B surface and core antigen, Hep C antibody, Hep A IgM, EBV, CMV)
o Autoantibodies
Autoimmune hep: ASMA, ALKM1, AMA
- PBiliaryC: AMA
- PSscleroC: ANA
o Caeruloplasmin, serum copper
o Ferritin
o Alpha-1 Antitrypsin (protein
electrophoresis 1 band) α
o Alpha fetoprotein - HCC
Imaging
- Abdo USS +/- portal vein Doppler (BC syndrome)
- Fibro scanning to diagnose cirrhosis
- MRCP
Other
- Ascitic tap
o High protein exudate
o Blood malignancy
o High cell count SBP
o Lactate SBP
o Amylase pancreatitis
Management of chronic liver disease
- non pharm, underlying cause, nutritional, ascites, varices, encephalopathy, pruitis, sbp
Non-Pharmacological
- Low salt diet, fluid restriction
- Alcohol abstinence
- Optimize nutrition
Pharmacological
- Treat underlying cause
o Hep B – entecavir od, sub cut PEG interferon
o Hep C – maviret 3 tab daily for 8, 12, 16 weeks
o Haemochromatosis – regular
venesection
o AIH – steroids
o NASH – weight loss, exercise, statins, Vit E in absence of DM
- Nutritional
o NG feeding if decompensated
o Vitamin B supplementation
o Glucose infusion if hypo - Ascites
o Bed rest and fluid restrict, low salt diet
o Spironolactone 100mg + Frusemide if response is poor
o Therapeutic paracentesis with concomitant albumin infusion can be tried - Varices
o If present, prophylactic treatment with B-blockers or if contraindicated variceal band ligation - SBP (spontaneous bacterial peritonitis)
o Antibiotics e.g. cefotaxime + metronidazole or Tazocin until sensitivities known.
o Prophylaxis in high risk patients - Encephalopathy
o Remove precipitating factors
Enemas to rid gut of blood
Low protein diet
Attack urea splitting organisms with lactulose or
antibiotics like neomycin or metronidazole
o Lorazepam for seizures
o Mannitol in cerebral oedema - Pruritus – treat with cholestyramine
- Bleeding – vitamin K
- Avoid
o Gentamicin
o Naltrexone
o NSAIDS, opiates
o Sedatives
Different Hepatitis - ABCD as well as interpretation of serology
Hep A
Acute infection
Faecal oral transmission, more common from overseas travel, also body fluid-sex and drugs
- Anti-HAV IgM (recent infection)/ IgG (past infection/immunisation)
Has vaccine
Hep B
Most common, acute or chronic
Transmit by body fluid e.g. sex, IV drug use
- Hep B surface antigen: active infection
- Anti-hepB surface antigen - recovery from hep B or vaccination
- anti hep B core antigen - past or ongoing infection. - IgM core -acute
Vaccine routinely
More kids get chronic
Hep C
Chronic can lead to cirrhosis
Transmit through blood e.g. iv drug, blood transfusion pre 1992
- anti HCV core- exposure
- HCV RNA - active infection
Invasive treatment and hccancer screening for chronic liver disease and in those after liver transplant
Invasive
- TIPSS (trans jugular intrahepatic
portosystemic shunt)
- Liver transplant
Screening
- abdo USS +/-alpha -fetoprotein every 6 months to screen for HCC (esp if cirrhosis from Hep B or Hep C)
OR annual MRI for HCC in pt with recurrent viral hep or hx of hcc (in transplant)
Risk factors, examination, screening for colon cancer
Screening
- Faecal occult blood home testing kits - + result requires colonoscopy
- High risk pt require more routine colonoscopy eg. IBD, adematous polyps, colorectal ca, fam hx of colorectal ca
Lynch syndrome: HNPCC have increased risk of CRC but also increased risk of other cancers of stomach, small intestine, liver, gall bladder, upper
urinary tract, skin +/- ovaries & endometrium. May have benign polyps.
Risk factors
- Polyps
- Family hx: colon cancer, familial adenomatous polyposis (FAP), hereditary
non-polyposis colon cancer (HNPCC).
- Inflammatory bowel disease
- Previous cancer
- Smoking
- Diet – low fibre, high red meat
- Alcohol
EXAMINATION
- Anaemia or jaundice
- Abdo – masses, radio skin changes, scars
- Ask for PR exam results
- Lymph nodes
- Skin lesions and mucosal pigmentation
Investigations and management for colon cancer (surgical, rads, chemo)
INVESTIGATIONS
Bloods
- FBC (microcytic anaemia)
- LFT
- CEA to monitor disease and effectiveness of treatment
- Faecal occult blood (if screening)
Imaging
- Colonoscopy or CT colonography
- Liver USS
Other
- If polyposis or HNPCC in family, refer for genetic testing once > 15 years.
- aspirin can be used as prevention to inhibit polyp growth in those high risk
MANAGEMENT
Surgery
- R hemi –> caecal, ascending and proximal transverse colon tumours
- L hemi –> distal transverse or descending colon
- Sigmoid colectomy sigmoid tumours
- Anterior resection low sigmoid or high rectal tumours
- Abdomino-perineal (A-P) resection with permanent colostomy and removal or anus and rectum +/- reconstruction tumours low in rectum (< 8 cm from anus)
- Hartmann’s procedure emergency bowel obstruction
- If metastatic, not for resection unless isolated liver met only.
Endoscopic
- Transanal microsurgery local excision in those unfit for surgery
Stenting palliation in malignant
obstruction or bridging to acute surgery
Radiotherapy
- usually pre-op for rectal tumours or to
downstage irresectable tumours
Chemotherapy
- 5-fluorouracil +/- others for involvement of regional lymph nodes
Dukes classification for staging colon cancer
A: 90% 5yr tx survival -confined to beneath the muscularis mucosa
B: 65% - extension through the
muscularis mucosa
C: 30% Involvement of regional
lymph nodes
D: <10% Distant metastases
the post transplant complications of liver transplant and treatment/ monitoring (7)
Hypertension - due to CNI use
- Self monitoring for first 6 months every week and GP every month, w/out HTN then every 6mo
- Ca blocker (avoid first gen as interact with CNI
- Cardioselective BB (meto)
DM
- Fasting plasma glucose or HbA1c every 6 months and annual retinal screening in patients with dm
Renal disease
- eGFR every 2-3 months for first year , then eGFR + Cr every 3-6 months
- Urinalysis annually for microalbuminuria
Gout/Hyperuricaemia – both CNIs decrease uric acid excretion
- Acute attack treated with colchicine, then prednisone. NSAIDS avoided.
- Maintenance is allopurinol 1.5mg x eGFR (max 100)
Metabolic bone disease
- DEXA scan prior to transplantation and every second year after
Screening for skin and non-skin malignancy
- Annual physical exam – +oropharynx + full body
- PSA annual
-PAP + mammography annual
- Colon screening as per national schedule
- Liver screening
Smoking cessation + sunblock
Infection risk
- CMV screening
- live vaccines given pre LT + vaccines for Hep A B
What are differentials for dyspepsia (epigastric pain related to food, bloating,heartburn, early satiety, postprandial fullness). What are the red flags symptoms indicating need for gastroscopy, and points to get on exam
= GORD/Oesophagitis,
- peptic ulcer disease: gastric ulcers and duodenal
ulcer,
- gastritis,
- gastric malignancy, functional/non-ulcer dyspepsia
- chronic pancreatitis/ cancer
- biliary pain
- intestinal angina (chronic mesenteric ischaemia
- crohns disease
Red flags
Anaemia (iron deficiency), Losing weight, Anorexia,
Recent onset of progressive symptoms, Melaena, Swallowing difficulty)
others
-Duodenal ulcers are typically relieved by eating and gastric ulcers worsened
- NSAID use, smoking, fam hx
Exam
- Abdominal examination
- Usually tender in epigastrium
- Don’t forget to check (L supraclavicular node indicative of gastric Ca metastasis)
- Look for signs of anaemia
- Check for mass in abdomen (cancer)
What are the investigations ordered for dyspepsia ; how does it change if you have over 55/ have alarm symptoms
- FBC (check for anaemia from ulcer bleeding)
- Urease breath test (for H. Pylori) OR faecal antigen test (stop PPI for 2 weeks)
OGD - with biopsy and histology of these these samples
If alarm symptom or if onset >55yo, or if no improvement after medications then Gastroscopy with biopsy
If under 55 + no ALARM symptoms, then you can just treat with PPIs and H pylori
eradication without the need for a scope.
- CXR (look for free air under diaphragm = perforation)
- Barium swallow – hiatus hernia or poor LOS function
- 24h oesophageal pH monitoring if endoscopy is normal
what is the management of dyspesia due to peptic ulcer + complications
Lifestyle
- Avoid food that worsens symptoms,
- stop smoking (slows healing of ulcers).
Pharm
- H. Pylori triple eradication therapy : (omeprazole, clarithromycin, and
metronidazole/amoxicillin) for 7 days if present
- Acid reduction with PPIs (omeprazole 40mg od/bd) for 4 weeks (DU) or 8 weeks (GU).
Can also use H2 antagonists (ranitidine PRN) but not as effective.
- Stop NSAIDs and steroids or
- May require lifelong PPIs if require long term NSAIDs for
another condition.
SURGICAL
- Gastric surgery if severe bleeding or perforation.
- All patients should be followed up after treatment with another gastroscopy to confirm healing.
Complications
- perforation, bleeding,
malignancy
What are the discerning features of GORD on hx and exam, investigations
- Heartburn (retrosternal burning pain related to meals and lying down)
- Acid regurgitation
- Odynophagia, Hoarse voice
- Chronic cough
- Nocturnal asthma
- Risk factors = hiatus hernia, smoking, alcohol, obesity, LOS dysfunction, pregnancy, drugs (TCA’s and nitrates)
Examination
-Abdominal, also look at throat and look for signs of anaemia
Investigations
- Barium swallow (looking for hiatus hernia and assess LOS function)
- Scope to look for cobble stoning.
Specific management for GORD
- ppis better than h2 antagonists
Lifestyle
- Avoid foods that trigger symptoms, lose weight, decrease alcohol, stop smoking
Acid reduction = first try antacids (Mylanta and Gaviscon), then PPI’s (omeprazole), then H2 antagonists (ranitidine).
Compare the definition of ulcerative colitis with crohns including protective/ risk factors
- Ulcerative Colitis is a relapsing, remitting inflammatory disorder of the colonic mucosa which may involve just the rectum
(proctitis 50%), extend to the colon (left colitis 30%) or the entire colon (pancolitis 20%).
RISK : Possible genetic susceptibility. Smoking protective.
- Crohn’s Disease is a chronic, transmural inflammatory disorder which can affect any
part of the GI tract from mouth to anus, but favours the terminal ileum and proximal
colon.
RISK : Mutations of NOD2/CARD15 gene
increase risk. Smoking increases risk
what are the symptoms of presentation, and exam points for IBD
Symptoms
- Diarrhoea +/- blood +/- mucous
- Abdominal pain
- Urgency
- Tenesmus with rectal disease
- Systemic symptoms – weight loss, anorexia,
fever, malaise
- Extraintestinal – skin changes, eye problems, joint problems, renal stones, liver
problems
EXAMINATION
Hands – clubbing
Eyes – conjunctivitis, scleritis, iritis
Mouth – angular stomatitis, aphthous ulcers
Abdo – tenderness, distension in acute, enlarged fatty liver
Anus – Perianal abscesses/fistulae/skin tags, rectal strictures in Crohn’s and rectal lesions in UC
Joints – large joint arthritis, sacroiliitis, ank spond
What are the differential diagnoses for IBD
DIFFERENTIAL DIAGNOSIS
- Infective proctitis
- NSAID, OCP, retinoic acid use
- Infections – C. difficile, salmonella, shigella, campylobacter, E. coli.
- Ischaemic colitis
What are the complications of ulcerative colitis vs crohns local and extra colonic (5)
LOCAL
o anorectal disease - Strictures, fistula, abscess (C> UC)
o Toxic megacolon & perforation (UC»C)
o Haemorrhage
UC : carcinoma of colon, haemorrhage
C: carcinoma of small + large bowel, obstruction
EXTRACOLONIC
UC
o Liver – fatty, PSC, cirrhosis, cholangiocarcinoma, amyloidosis
o Blood – anaemia, thromboembolism
(antithrombin III deficiency)
o Arthropathy – large joints, ankylosing spondylitis
o Skin and Mucous membranes – erythema nodosum, pyoderma gangrenosum, ulcers
o Ocular – conjunctivitis, episcleritis,
uveitis
Crohns : similar to UC except (joint, skin and eye)
- Gallstones more common
PSC rare
- Renal stones, pyelonephritis and hydronephrosis
Malabsorption
Osteomalacia
What are the investigations for IBD including typical findings on scope UC vs C
Bloods
- FBC – anaemia (chronic disease, blood loss, macrocytic in ileal disease, haemolytic),
- B12, Vit D, folic acid
- WCC (leucopenia with azathioprine)
- ESR, CRP – active inflammation
- U&E – renal disease in Crohn’s.
- LFT – liver disease; albumin
- Antibody testing – pANCA negative and
ASCA positive more likely to have Crohn’s. (vs UC)
- Stool microscopy and culture to exclude
infection; Faecal calprotectin if differentiating ibs vs ibd
Imaging
- AXR – bowel wall thickening, gaseous
distension, evidence of toxic megacolon,
evidence of obstruction
- Erect CXR – evidence of perforation
- Barium Enema – contraindicated in active disease and megacolon due to risk of perforation.
colonoscope
o UC- rectum involved, contiguous
lesions, loss of haustra, ulceration,
spasm, pseudo polyps and bowel shortening, strictures, carcinoma
o CD - rectum not always involved, skip lesions, mucosal thickening and luminal narrowing, cobble stoning, fistulas and fissures (sinus tracts)
Rectal biopsy (however may not differentiate)
o UC – mucus depletion, prominent
crypt abscesses
o CD – granulomas
What is the management of ulcerative colitis depending on 4 motions/day, 4-6, or >6 + unwell.
Mild (<4 motions a day, well)
- 5-Aminosalicylates (e.g. mesalazine) are the mainstay of inducing remission
- Steroids also help induce remission
(prednisolone 20mg po bd). Give for two
weeks then taper
- Topical: hydrocortisone foam or retention prednisolone enema BD can help also
- If no improvement at 2 wks, rx as moderate
Moderate (4-6 motions a day, well)
- Oral prednisolone (initially 40mg po bd for 1 week then tapering) for 6 weeks + mesalazine
- Topical: BD steroid enema
- If no improvement at 2 wks, rx as severe
Severe (>6 motions a day, unwell)
- Admit for NBM and IV maintenance fluids
- IV: hydrocortisone AND rectal:
hydrocortisone
- Regular obs and stool chart, twice daily
examination, daily bloods
- If on day 3 CRP >45 or stool frequency >6
consider ciclosporin /infliximab/surgery
what are the topical therapies for proctitis . proctosigmoiditis, L) sided colitis
what is the treatment for perianal disease
Topical Therapies
- Proctitis: suppositories (5-ASA > steroids)
- Procto-sigmoiditis: foams
- L sided colitis retention enemas
Perianal disease
- MRI + examination under anaesthetic
- Oral antibiotics, immunosuppressant
therapy +/- infliximab, local surgery +/- seton insertion (tube to allow draining while healing
What is the treatment for mild (symptomatic but systemically well) vs severe attacks of Crohns.
what are the initial immunotherapies to induce remission from steroids and cautions with immunotherapy
Mild attacks (symptomatic but systemically well)
- prednisolone 30mg, tapering down
Severe attacks (symptomatic + systemically unwell)
- Admit for NBM and IV maintenance fluids
- IV: hydrocortisone
- Rectal: hydrocortisone
- PO/Oral metronidazole
- Regular obs and stool chart, twice daily
examination, daily bloods
- If no response, consider CT abdo and seek surgical advice
Initially
- Combined immunotherapy (azathioprine + infliximab + steroids)
- 5-ASA (sulfasalazine)
- Methotrexate monthly IM for
induction of remission and withdrawal from steroids.
- TNF α inhibitors e.g. infliximab and humira, can
reduce disease activity by countering
neutrophil accumulation, granuloma formation, activating complement and cause cytotoxicity to CD4+ cells.
- Avoid in those
with malignancy. Test for TB before starting.
- Elemental diets: food in a nutrient predigested form liquid/ powder
Compare surgery + indications for UC vs crohns
UC
Surgery
- indicated in perforation, massive
haemorrhage, toxic dilatation, failure to
respond to medical therapy
- proctocolectomy + terminal ileostomy +
later ilio-anal pouch
Crohns
Surgery
- indicated in perforation, intestinal
obstruction, fistulae, abscesses, failure to
respond to medical therapy
- aims are to 1) defunction distal disease with a temporary ileostomy or 2) limited resection of worse areas (beware of short
bowel syndrome). Pouch surgery not done in Crohn’s.
what is the screening for IBD patients to see if they need colectomy
Screening
- Patients who have had pancolitis for >
7years or left sided colitis for > 15 years
should have colonoscopic screening with
biopsy every 1 – 2 years.
- High-grade dysplasia in the absence of inflammation indicates colectomy
What is the presentation, risk factors, investigations for Haemochromatosis - disorder of increased iron metabolism
Risk factors homozygous HFE gene
Presentation
- Early: nil or tiredness; arthralgia (2nd + 3rd MCP, knee CPPD), Erectile dysfunction
- Later: slate-grey skin pigmentation,
hepatomegaly, signs of CLD, cirrhosis,
dilated cardiomyopathy, osteoporosis
- Endocrinopathies: bronze DM, hypogonadism (pituitary dysfunction),
Investigations
Bloods:
- Raised LFT, raised Ferritin (>1mg/L),
- Transferrin sat >45%
- Glucose
- HFE genotype
Imaging:
- Xray – chondrocalcinosis
- Liver MRI – Fe overload
Biopsy:
- Iron loading
ECG/Echo:
- If cardiomyopathy suspected
Management/ screening of haemochromatosis + prognosis
MANAGEMENT
Venesection:
- 1 unit/1-3weeks
- Until ferritin <50mcg/L
- Maintenance for life
- Monitor:
o LFTs, Glucose/DM
Other:
- Low-iron, well balanced diet
- Avoid alcohol.
- Check OTC vits don’t contain Fe
SCREENING
- Ferritin and genotype
- 1st degree relatives, even if asymptomatic
and LFT normal
PROGNOSIS
- Venesection returns life expectance to
normal, if no DM/cirrhosis
- Arthropathy may improve or worsen
- Gonadal failure is irreversible
- If cirrhosis; 22-30% get HCC (esp if >50y,
HBsAG+, alcohol abuse)
What are the differentials of malabsoprtion, expected presentation (which vit deficiencies) and questions to ask on hx
CAUSES
- Coeliac Disease: Gluten free diet treatment?
- Chronic Pancreatitis
History of liver or pancreatitic disease? - Drugs (alcohol, neomycin)?
- Previous radiotherapy
- History of DM
- Crohn’s Disease?
fam hx - Previous Gastric Surgery :
- Gastrectomy or other bowel surgery?
PRESENTATION
- Pale, bulky offensive stools (steatorrhoea)
- Weight loss
Weakness,Bruising (K+ def)
- Anaemia (megaloblastic, iron deficiency)
- Bone pain (osteomalacia from Vit D def)
- Glossitis and angular stomatitis, Peripheral neuropathy (Vit B Def)
- Oedema, amenorrhoea (protein deficiency)
- Skin rash (eczema, dermatitis herpetiformis)
What are the examination points for malabsorption and investigations
EXAMINATION
- Weight and nutritional status
- Skin – bruising, dermatitis herpetiformis,
pigmentation, erythema nodosum,
stomatitis, perianal lesions
- Signs of anaemia
- Signs of chronic liver disease
- Signs of peripheral neuropathy and
lymphadenopathy
GENERAL INVESTIGATIONS
Bloods
- FBC – iron deficiency or megaloblastic
anaemia
- Iron, B12, folate
- Serum albumin
- Serum calcidiol, calcium, phosphate, ALP
- Lipids and LFT’s
- Coagulation screen – prolonged PT/INR
- coeliac antibody
Stool sample
- Sudan stain for fat globules
- Faecal fat over 3 days
Other
- Glucose or lactulose breath hydrogen analysis (bacterial overgrowth)
- Endoscopy + small bowel biopsy
What is the criteria for diagnosis of Coeliac disease - what is the aetiology
DESCRIPTION
T-cell mediated autoimmune disease of the small bowel characterized in which prolamin (alcohol soluble protein in wheat, barley, rye) causes villous atrophy and malabsorption
DIAGNOSIS
1) Positive Serology
o Anti-α -gliadin antibody
o Anti-transglutaminase antibody
o Anti-endomysial antibody
2) Abnormal Duodenal Biopsy
o Subtotal villous atrophy
o Increased intraepithelial WBC
o Crypt hyperplasia
3) Clinical, biochemical and histological improvement on gluten-free diet
Management and complications of coeliac
MANAGEMENT
- Gluten free diet
- Verify by anti-endomysial antibody tests
- Pneumococcal vaccine
- Management of osteoporosis (impaired calcium absorption)
COMPLICATIONS
- Anaemia, lactose intolerance, osteoporosis
- GI T cell Lymphoma
- Increased risk of malignancies (gastric,
oesophageal, bladder, breast, brain)
- Myopathies and neuropathies
- Hyposplenism
What is the presentation, examination, causes and investigations for chronic pancreatitis
HISTORY
- epigastric pain, bores through to back
- brittle diabetes (hard to control
EXAMINATION
- Erythema abignes from hot water bottles
CAUSES
- Common – alcohol
- Rare – CF, haemochromatosis, pancreatic duct obstruction, high PTH
INVESTIGATIONS
- Faecal elastase and -1-antitryptase α
- increase glucose on breath test
- USS + CT, MRCP + ERCP
- AXR – speckled calcifications
Management and complications of chronic pancreatitis
MANAGEMENT
Drugs – analgesia, lipase, fat soluble vitamins, insulin
Diet – no alcohol, low fat, medium chain
triglycerides
Surgery – for unremitting pain, narcotic abuse,
weight loss
COMPLICATIONS
- Diabetes
- Biliary obstruction
- Pancreatic carcinoma
- Lymphoma
What is the maintenance treatment of remission of UC and the side effects
Maintenance
- Sulfasalazine 1st line, or Mesalazine/5-aSA/pentasa more expensive
SE: temp, rash, haemolysis, hepatitis, pancreatitis, worsening colitis, reversible oligospermia
- Azathioprine (immunomodulatory)
indicated in those with steroid SE or who
relapse quickly when steroids withdrawn
SE: leucopenia
