Gastroenterology/Colorectal/ Hepatology Flashcards
1
Q
What is coeliac disease?
A
- chronic immune-mediated systemic disorder in genetically predisposed people, triggered by exposure to dietary gluten (the major complex protein component of wheat, barley, and rye).
- Coeliac disease is caused by a heightened immunological response to ingested gluten. The exact cause is not yet known
2
Q
What is the prevalence of coeliac disease in the UK?
A
- 1%
- affects all age groups, including the elderly, with more than 70% of new cases diagnosed in people over 20 years of age.
- two peaks of onset; one shortly after weaning with gluten in the first 2 years of life, and the other in the second or third decades of life
3
Q
What are the complications of coeliacs?
A
- reduced QoL
- mental health
- faltering growth, delayed puberty - in children
- malabsorption causing nutritional deficiencies
- Anaemia - due to malabsorption of iron, folate, B12
- reduced bone mineral density - malabsorption Ca/VitD
- hyposplenism - increased risk of encapsulated bacterial infection e.g. pneumococcus, H.influenzae, meningococcus.
- malignancy - rare. Hodgkins and Non hodgkins lymphoma (2-4x increased risk), and small bowel adenocarcinoma (30x increased risk).
- refractory coeliac disease - rare.
4
Q
What is the prognosis for coeliacs?
A
The majority of people with confirmed coeliac disease report a rapid improvement in symptoms after starting a gluten-free diet, and have a normal life expectancy
5
Q
What symptoms and associated conditions should lead us to suspect coeliac disease?
A
- Persistent, unexplained GI symptoms: acid reflux, diarrhoea, steatorrhoea, weight loss, abdo pain, reduced appetite, bloating, and constipation. (may be overweight on presentation)
- IBS
- faltering growth, short stature, delayed puberty - in children
- TATT
- persistent/recurrent mouth ulcers
- unexplained iron/b12/folate deficiency - may cause anaemia. Anaemia not responding to treatment.
- T1DM
- autoimmune thyroid disease e.g. Hashimotos thyroiditis
- autoimmune liver disease e.g. Primary biliary cholangitis, autoimmune hepatitis, primary sclerosing cholangitis.
- IgA deficiency
- first degree relative with coeliac (10% chance). Assoc with HLA-DQ2 or DQ8.
- dermatitis herpetiformis
- osteomalacia/osteopenia/osteoporosis/fragility fractures
- unexplained peripheral neuropathy/ataxia
- unexplained recurrent miscarriage/subfertility
- unexplained raised ALT/AST
- dental enamel defects - in children
- Downs/turners/williams syndrome
6
Q
What skin condition does this image show?
A
- dermatitis herpetiformis (due to coeliac disease)
- more common in adults and older teenagers.
- symmetrical clusters of itchy blistering skin lesions followed by erosions, excoriations, and hyperpigmentation, most commonly involving the elbows, knees, shoulders, buttocks, sacral region, and face.
7
Q
How should a person be investigated for suspected coeliac disease?
A
- serology - should have eaten gluten foods for at least 6/52
- IgA anti-tissue transglutaminase antibody (TTG) and total IgA first line.
- IgA anti-endomysial antibody (EMA) second line (if TTG not available or weakly positive/equivocal)
- If there is IgA deficiency - IgA TTG and EMA may give false negative result. Check IgG EMA, IgG TTG or IgG deamidated gliadin peptide (DGP).
8
Q
When should patients with suspected coeliacs be referred to gastroenterologist? What should they be advised?
A
- Positive serology
- in children - if IgA TTG or EMA are equivocal - refer for further investigation
- If serology negative, and no IgA deficiency - coeliac is unlikely . Does not rule out developing it in the future. If still strong suspicion - refer gastro.
- unwilling to introduce gluten back into diet to allow serological testing.
- When referring, advise pts to eat 1 meal a day containing gluten until specialist tests completed.
- explain diagnosis only confirmed on biopsy of small bowel.
- refer derm if DH suspected.
9
Q
How should a person with confirmed coeliacs be managed in primary care?
A
- annual review
- long term adherence to gluten free diet - some gluten free products can be prescribed on NHS - must be ACBS endorsed (only flour and bread mixes in england)
- assess for persistent symptoms (check inadvertent exposure)
- monitor annual bloods: coeliac serology (adherence), FBC, ferritin, B12/folate, TFT, LFT, calcium/vit D - check if supplements are needed
- assess risk of osteoporosis and need for DEXA
- monitor BMI, growth in children
- refer dietician if concerns re gluten exposure, recurrent symptoms, nutritional deficiencies, growth impairment
- influenza, meningococcal, pneumococcal vaccinations
10
Q
When should a person with confirmed coeliacs be referred back to specialist?
A
- non-responsive/refractory
- faltering growth in child
- suspected serious complication - 2ww if malignancy
11
Q
Which gluten-containing products should be avoided in coeliacs disease? (main groups and examples) Which other sources of starch can be eaten instead?
A
- Wheat
- Rye
- Barley
e.g. breakfast cereals, bread, flour, pasta, cakes, pastries, biscuits, beer.
Foods containing the above as fillers e.g. sausages, soups, sauces.
Foods contaminated with gluten in processing e.g. oats, use of same oil - chips cooked in batter oil.
Manufacturers by law must list GLUTEN as an ingredient on package.
Corn (maize), Rice, Potatoes may be eaten.
Coeliac UK website for more info.
12
Q
When should a FIT test be done to guide referral for suspected colorectal cancer in adults?
A
- abdominal mass
- change in bowel habit
- IDA
- age >=40 with unexplained weight loss and abdo pain
- age <50 with rectal bleeding and either abdo pain or weight loss.
- Age >=50 with any of: rectal bleeding/abdo pain/ weight loss.
- age >=60 with anaemia (even if no iron deficiency)
13
Q
When should adults be referred via 2ww for colorectal cancer?
A
- Rectal mass (PR exam)
- FIT result of >=10
- If not returned the FIT sample, or FIT is <10 : still refer if strong clinical concern due to ongoing unexplained symptoms.
14
Q
When should a person be referred via 2ww for anal cancer?
A
- unexplained anal mass
- unexplained anal ulceration
15
Q
What is the NHS bowel cancer screening programme?
A
- Age 60-74: screening for faecal blood every 2 years by FIT (faecal immunochemical test)- kit posted automatically
- people aged >75 can request screening kit every 2 years
- Abnormal FIT: colonoscopy or CT colonography
16
Q
Why was FIT recommended for screening over the faecal occult blood testing?
A
- easier to use for patients -increase uptake. Unscrew the cap of the test, dip the end of the stick into a single bowel motion, replace the stick in the tube, screw the lid shut and return the sample in the prepaid envelope provided. (Results are sent by letter to the person’s home address within 2 weeks of the lab receiving the completed kit.)
The person’s GP is informed of the result electronically. - More sensitive: can detect lower concentration of blood in faeces.
- more specific: FOBT was not specific for colonic bleeding - was positive with red meats, upper GI irritation. FIT detects blood using antibodies specific to human globin. Less likely to detect globin from UGIB- as this degrades as it passes through the gut.
17
Q
Which people are at high risk of bowel cancer and therefore should be screened with colonoscopy?
A
- familial adenomatous polyposis (FAP)- yearly colonoscopy
- Lynch syndrome (HNPCC) - colonoscopy aged 25 (or 5 years prior to age of diagnosis of youngest affected relative) - every 12-24 months.
- juvenile polyposis
- strong family history of bowel cancer: refer for colonoscopy aged 35-40. If no polyps - repat at age 55. 2x first degree relatives with Hx colorectal cancer, 1x first degree relative with Hx colorectal cancer aged <45yrs
- UC or Crohn’s: every 1-5yrs depending on risk.
- Previous bowel cancer
18
Q
What are the risk factors for bowel cancer?
A
- Obesity
- diet - too much red/processed meat, too little fibre
- smoking
- alcohol
- increasing age
- family Hx
- UC/Crohn’s
- T2DM
- gallstones
- acromegaly
19
Q
What are the colonoscopy outcomes after a positive FIT?
A
- normal 50%
- polyp 40%
- cancer 10%
20
Q
When should IBS be suspected?
A
if any of the following symptoms have been present for at least 6 months:
* Abdominal pain
* Bloating
* Change in bowel habit
21
Q
What red flag symptoms/signs would point to a diagnosis other than IBS?
A
- weight loss
- rectal bleeding
- positive FIT
- change in bowel habit >age 60
- raised FCP
- iron def. anaemia
- persistent/frequent bloating in females - ovarian Ca - esp if age >50
- abdo mass, rectal mass
- FHX of: bowel ca, ovarian ca, coeliacs, IBD.
22
Q
When should a diagnosis of IBS be made in primary care?
A
- abdominal pain/discomfort for 6 months: relieved by defecation OR assoc with altered bowel frequency OR assoc with altered stool form.
- PLUS at least 2 of:
- abdo bloating
- made worse by eating
- passage of mucus
- straining/urgency/incomplete evacuation
**Alternative conditions **have been excluded.
23
Q
Which investigations should be considered in possible IBS to exclude other diagnoses?
A
- food diary
- FBC - anaemia
- CRP - active inflammation/infection
- coeliac serology
- TFTs
- FCP - esp if age <=45
- Stool for MC&S
- STI screen if ?PID
- FIT if fulfil criteria
24
Q
How should IBS be managed in primary care?
A
- explain gut-brain axis, chronic condition - flares
- diet and lifestyle advice - regular meals, reduce caffeine, alcohol, fizzy drinks. if diarrhoea/bloating - reduce high fibre foods. Loperamide if ineffective.
- If constipation - increase soluble fibre or ispaghula. Laxatives if ineffective.
*If ineffective: Can refer dietician - trial Low FODMAP diet (FODMAPS e.g. apples, cherries, peaches, nectarines, sweetners, lactose, broccoli, sprouts, cabbage, peas. Needs dietician input. - if ongoing pain/spasm: mebeverine, or peppermint oil prn. If ineffective - low dose TCA (AMT)
- refer gastro - if no improvement / requests specialist & consider psychological therapies.
25
What are the 2ww criteria for **urgent direct access **UGI endoscopy (for oeseophageal or stomach cancer)?
*** dysphagia **OR
* aged >=55 with **weight loss AND **any of the following:
- upper abdo pain
- reflux
- dyspepsia
* send 2ww stomach cancer referral for people with **upper abdo mass **consistent with stomach cancer.
26
What are the criteria for** non-urgent direct access ** UGI endoscopy to assess for oesophageal and stomach cancer?
* haematemesis
* Aged >=55 with:
- treatment-resistant dyspepsia OR
- upper abdo pain with low Hb OR
- raised platelet count with any of the following:
* nausea
* vomiting
* weight loss
* reflux
* dyspepsia
* upper abdo pain
- nausea or vomiting with any of the following:
* weight loss
* reflux
* dyspepsia
* upper abdo pain
27
What are the 2ww criteria for pancreatic cancer - direct access CT scan (or USS if CT not available)?
* Age >=60 with with weight loss and any of the following:
* diarrhoea
* back pain
* abdominal pain
* nausea
* vomiting
* constipation
* new-onset diabetes.
Refer as 2ww pancreatic cancer if age >=40 with jaundice.
28
What are the 2ww criteria for gallbladder cancer- urgent direct access USS?
* Upper abdominal mass consistent with an enlarged gall bladder
29
What are the 2ww criteria for liver cancer - urgent direct access USS?
* upper abdominal mass consistent with an enlarged liver.
30
Which patients are most at risk of advanced NAFLD?
1. Age > 30 years
2. Increasing obesity
3. Type 2 diabetes
4. Aspartate aminotransferase:alanine aminotransferase (AST:ALT) ratio > 1.
31
What are the management steps for dyspepsia not meeting 2ww referral criteria (e.g. age <55)?
1. Review medications for causes of dyspepsia (NSAIDS, steroids, bisphosphonates, anticholinergics, benzos, Bblockers, CCBs, alpha-blockers, aspirin)
2. Lifestyle advice: address triggers (lose weight, avoid coffee, chocolate, tomatoes, spicy, fatty foods, smaller meals, eat 4 hours before bed, stop smoking, reduce alcohol)
3. Trial 4-8 weeks full dose PPI
4. If symptoms return after trial - test H.Pylori: either a carbon-13 urea breath test or stool antigen test can be used — ensure the person has not taken a PPI in the past 2 weeks, or antibiotics in the past 4 weeks. If positive: first line-eradication therapy.
5. If symptoms resolve - no need to do HPylori test for cure.
6. If severe persistent symptoms - arrange re-testing 4-8 weeks after eradication therapy. Use C13 urea Breath test.
7. May need long term PPI H2RA at lowest dose.
8. Refer Gastro - if refractory symptoms, 2nd Line H.Pylori eradication unsuccessful.
32
What is the first line treatment for H.Pylori eradication?
7 day triple therapy:
* PPI (lansoprazole 30mg, omeprazole 20-40mg) twice daily
* amoxicillin 1g BD
* clarithryomycin 500mg BD OR metronidazole 400mg BD.
If pen.all: use clarithrymycin and metronidazole.
33
What are the presenting symptoms of IBD in childhood?
* rare
* non-specific: weight loss, faltering growth, delayed puberty
* bloody diarrhoea, acute abdomen
* arthropathy, iritis
34
What are the presenting symptoms of UC?
* bloody diarrhoea (persisting >6 weeks)
* Faecal urgency/incontinence
* Tenesmus (persistent, painful urge to pass stool even when the rectum is empty)
* Lower abdo pain (esp LLQ)
* non specific: fatigue, fever, anorexia
35
What are the presenting symptoms of Crohn's?
* unexplained persistent diarrhoea (+/- blood & mucus) (can be nocturnal)
* Abdo pain (crampy)
* Mouth ulcers
* Peri-anal fistulas/abscesses
* bowel obstruction - due to fistulas
* weight loss more prominent
* non specific: fatigue, fever, anorexia
36
What are the extra-intestinal features of Crohn's and UC?
* Crohn's: gallstones more common
* UC: primary sclerosing cholangitis (jaundice) more common, autoimmune hepatitis
* Both: arthritis, ank.spond, anterior uveitis, episcleritis, erythema nodosum, pyoderma gangrenosum (UC>Crohn's), osteoporosis.
37
What does this image show? What disease is it associated with? What is the management?
* pyoderma gangrenosum
* painful
* refer urgently to derm
* super-potent topical steroids e.g. clobetasol (dermovate)
* Assoc IBD - especially UC , RA, myeloid leukaemias, MDS.
38
What does the below image show? Which disease is it associated with? How is it managed?
* Erythema nodosum
* painful, erythematous, and sometimes bruised-looking, nodules on the anterior surface of the legs
* IBD - UC or Crohn's, post-streptococcal (URTI), TB, sarcoid
39
What is the peak incidence of UC?
* most common type of IBD
* can develop at any age
* Peak incidece age 15-25, second smaller peak 55-65
* smoking is protective
40
What is the peak incidence of Crohn's disease?
* first and largest peak is age 15-30 , second smaller peak from 50-70
* smoking is a causative factor
41
What investigations should be done in primary care if IBD is suspected?
* FBC - anaemia
* CRP
* U&E - dehydration
* LFTs- low albumin
* B12, folate, ferritin, transferrin sats - malabsorption
* TTG, TFTs, stool MC&S - exclude other causes
* Faceal calprotectin (protein biomarker released into bowel when inflammation present). If over 50 mcg/g - possible IBD rather than IBS - refer for specialist Ax within 4 weeks. If negative - IBD unlikely.
42
When is emergency hospital admission indicated for suspected UC or Crohn's disease?
* systemically unwell - fever, tachycardia, hypotension
* severe abdominal pain (esp if tenderness)
* Severe diarrhoea (>8/day)
* bowel obstruction
* sudden dramatic weight loss
43
If Crohn's or UC is suspected but not requiring emergency admission - how should they be managed?
* urgent referral to secondary care (paeds/adult gastro) for confirmation of diagnosis and initiation of drug treatments.
* specialist investigations: colonoscopy, biopsy, MRI
* Refer rheum/derm/opth if extra-intestinal manifestations.
44
What are the first line treatments for Crohn's disease to induce remission?
| Started in secondary care
* 1. **Corticosteroids: **prednisolone / IV hydrocortisone -Gradually tapered.
* Aminosalicylates (sulfasalazine or mesalazine) - if steroids are contraindicated or declined. Less effective but may have fewer side effects
* 2. **Immunosuppresive drugs**: If two or more inflammatory episodes in a year or difficult to wean steroids, azathioprine/mercaptopurine may be added to the steroid to induce remission. Then used to maintain.
* Thiopurine methyltransferase (TPMT) activity- assessed before azathioprine. Should not be prescribed if TPMT activity is low/absent
* Methotrexate 2nd line if azathioprine or mercaptopurine cannot be prescribed
* Specialist enteral nutrition may be an alternative to conventional corticosteroids if there is concern about growth or side effects
* 3. **Biologics** - anti-TNF alpha: infliximab/adalimumab (IV). For severe active disease/perianal disease - not responding to conventional Rx. Then to maintain.
45
What are the side effects of anti-TNF biologics?
* Serious infections
* Reactivation of TB and hepatitis B
* lethal hepatosplenic T-cell lymphoma and demyelinating CNS disorders
* Pancytopenia, leukopenia and neutropenia
* Liver damage
46
How should remission be maintained in Crohn's disease after a complete macroscopic resection?
* 3 months of post-operative azapthioprine and metronidazole.
47
What are the first line treatments for UC to induce remission then maintain?
* 1. **Aminosalicylates** - mesalazine and sulfasalazine. Also maintain remission. Often topical (enema/supps). Or orally if remission not achieved within 4 weeks. If extensive- may need both first line. Then maintain remission.
* 2. **Corticosteroids** - if aminosalicylates not effective-then taper - short term (topical/oral/IV)
* 3. **Calcineurin inhibitors** - tacrolimus/ciclosporin - added to steroids to induce remission if not responding (IV)
* 4.** Immunosuppresives** - azathioprine/mercaptopurine (1st), MTX (2nd line) - to maintain remission if salycylates not working.
* 5. **Biologics**: anti-TNF alphas: IV infliximab and SC adalimumab - induce remission if severe unresponsive. Also to maintain remission.
* Specialist enteral nutritional supplementation may be used as an alternative to conventional therapy in some children for induction of remission
48
How should a flare of UC or Crohn's be managed?
* consider if needs emergency admission
* if not admitting - urgent referral back to gastro
* consider c.diff
* check adherence to regimen
* check shared care agreement - short course PO steroids may be advised. / discuss with gastro whilst awaiting appt if not in shared care agreement.
* Do not Px NSAIDS
* Dietician referral if weight loss/malnutrition
* If recurrent flares- d/w secondary care if maintenance regimen needs changing/surgery needed.
49
What blood monitoring is required for aminosalicylates?
* U&E - before starting oral treatment, at 3 months, then annually.
* FBC - baseline, then monthly for first 3 months
* LFT - monthly for first 3 months.
50
What blood monitoring is required for azathioprine?
| shared care protocol
* FBC - weekly for first 4 weeks, then every 3 months (myelosuppression)
51
What blood monitoring is required for mercaptopurine?
* measure TPMT activity before starting
* Monitor LFTs
52
How should fatigue be managed in IBD?
* check for alternative cause
* anxiety/depression, sleep, pain
* Check FBC, ferritin, B12, folate - may have anaemia of chronic disease, or IDA due to blood loss/decreased absorption
53
How should mouth ulcers be managed in IBD?
* persistent - refer oral medicine specialist
* Upper GI symptoms in Crohn's - refer back to gastro to assess if they have Crohn's of duodenum/stomach. Urgent if red flags.
54
How should perianal fistulae or sepsis in IBD be managed?
Urgent seconday care assessment
55
How should constipation in IBD be managed?
* exclude bowel obstruction
* increased fluids and soluble fibre
* Bulk forming laxative if lifestyle not worked - ispaghula husk or methylcellulose.
56
How should abdo pain be managed in IBD?
* could be sign of obstruction or flare up - assess
* mild analgesia only
* opiates can increase risk of toxic megacolon in UC
* Do not give NSAIDs - can reactivate disease, GI bleeding.
57
What should patients with IBD be advised on oral contraceptives?
* less reliable if Hx malabsorption, small bowel resection, diarrhoea.
* colectomy and ileostomy do not affect it
* male and females must use effective contraception when taking MTX, mercaptopurine and for 3 months after. And for 6 months after taking infliximab.
58
How often should height and weight be managed in children with IBD?
Every 3-6 months
* If they have an inflammatory exacerbation and are approaching or undergoing puberty or
* If there is chronic active disease
* If they are being treated with systemic corticosteroids
Every 12 months if none of the above.
Refer to secondary care if slow or absent pubertal growth for age.
59
Which extra vaccines should those with IBD receive?
* flu
* pneumococcal
* NO LIVE vaccines if on immunosuppresive/biologics.
60
What often causes a raised AST in isolation?
* fatty liver disease
61
What often causes a raised ALT in isolation?
* viral and autoimmune hepatitis
62
What ofte causes a raised GGT in isolation?
alcohol excess
63
What can cause a transient rise in liver enzymes (ALT/AST/GGT)?
* viral infection
* drugs
* alcohol
64
What should be done if raised liver enzymes (ALT/AST/GGT) are noticed?
* check medication, incl herbal
* stop/reduce alcohol
* repeat LFTs in 1 month (if AST/ALT <3x ULN)
* Repeat LFTs in 1 week (IF AST/ALT are >3x ULN)
* If still raised - request hepatitis screen and USS/refer hepatology
65
What could cause a raised bilirubin?
* hepatitis, or biliary obstruction - if ALT/AST raised - refer for liver USS and do hepatitis screen (refer if jaundiced)
* haemolysis - check FBC/reticulocyte count - refer haem if abnormal
* Gilbert's syndrome - likely if bilirubin <40, ALT/AST normal, FBC/reticulocytes normal
* Isolated raised bilirubin - likely still Gilberts - but refer.
| Normal is <21
66
What can cause a raised ALP?
* marked in biliary obstruction, primary biliary cholangitis
* any liver disease
* bone - more likely if raised Ca/phos and GGT normal.
67
Which meds can cause raised ALT/AST?
* penicillins (esp co-amoxiclav)
* antifungals
* statins
* antiepileptics
* NSAIDs
* herbal medicines
* recreational drugs
68
What is included in a hepatitis/NILS?
* Hep A, B , C serology
* EBV serology
* liver autoantibodies
* iron studes, transferrin sats (HH)
* alpha-1 anti-trypsin
* serum copper and caeruloplasmin
* AFP
* lipids
* HbA1c
69
What are the 3 types of jaundice and how are they distinguished?
* pre-hepatic - haemolytic anaemia, Gilberts. normal LFTs, low Hb, raised reticulocytes. Urine not darkened.
* hepatic - hepatitis, cirrhosis. LFTs raised.Dark urine, tender enlarged liver.
* obstructive - gallstones, pancreatic ca, PBC, PSC, cholangiocarcinoma. Raised ALP.Enlarged liver, itchy, pale stools.
Refer all patients with jaundice. If >=40 =2ww referral.
70
What is 'proven GORD'?
* GORD diagnosed by endoscopy.
- oesophagitis
- symptoms of GORD but no erosive change - endoscopy normal.
71
How should proven GORD be managed?
* lifestyle advice
* sleep with head of bed raised
* review meds - reduce/stop drugs which reduce LOS pressure
* full dose PPI for 4 weeks - to aid healing
* if severe oesophagitis - full dose PPI for 8 weeks, long term maintenance
* use PPI at lowest effective dose to control symptoms (if severe oesophagitis, may need to be full-dose)
72
What is the management for proven gastric or duodenal ulceration?
* lifestyle measures
* review meds
* test for H.pylori - breath test/stool test
* if positive H.Pylori but assoc NSAID use -give full dose PPI for 2 months first - then first line eradication therapy. If not assoc NSAID use -treat with first line eradication.
* if negative H.pylori - full dose PPI for 4-8 weeks.
* Follow up after - arrange repeat endoscopy and H.pylori testing to ensure ulcer healed.
* Use PPI or H2RA at lowest dose to control symptoms once healed.
* Refer gastro - if ulcer not healed on repeat endoscopy, refractory symptoms, second line Hpylori eradication unsuccessful.
73
What are full-dose and low-dose PPIs?
What H2RAs are available?
* full-dose: Omeprazole 20mg OD, lansoprazole 30mg OD
* low dose: lansoprazole 15mg OD, pantoprazole 20mg OD, omeprazole 10mg OD
* famotidine 40mg at night.
74
What is the difference between hepatic steatosis, and non-alcoholic steatohepatitis (NASH)?
75
In patients with NAFLD, how often should they be screened for fibrosis with ELF score? (bloods needed for scoring)
every 3 years
76
What are the secondary care interventions for NAFLD in adults?
* pioglitazone, vitamin E
77
In children/under 18s with T2DM/metabolic syndrome, who do not misuse alcohol - how often should they be screened for possible NAFLD? What secondary care interventions are available for children?
* every 3 years with USS
* refer to paeds hepatologist if suspected
* vitamin E
78
What is metabolic syndrome?
At least 3 of:
* Low HDL
* High triglyceride
* HTN
* Insulin resistance
* Central obesity (BMI >30)
79
How is NAFLD diagnosed?
Usually incidentally when LFTs abnormal or USS done for another reason (shows increased hepatic echogenicity).
* But LFTs and USS can be normal - not used to diagnose/rule out.
* Use a first line non-invasive tool to assess level of fibrosis : FIB-4 of NAFLD Fibrosis Score (NFS)
80
How should confirmed NAFLD be managed in primary care?
* lifestyle advice - exercise, diet
* reduce alcohol to national limits
* ensure any HTN, lipidaemia, T2DM, CKD managed
* reassess CVS risk annually
* reassess risk of liver fibrosis every 3 years (ELF/FIB-4) - refer if high risk.
* continue statins, unless liver enzymes double <3mths of starting them.
81
What are other causes of fatty liver disease?
* alcohol
* hepatitis C
* medication: amiodarone, steroids and tamoxifen.
82
What are the presenting symptoms of gallstone disease?
* biliary colic - most common. Severe pain in epigastrium/RUQ, lasts >30mins, assoc N&V. No fever or abdo tenderness.
* acute cholecystitis - second most common. Same as biliary colic, PLUS fever and tender RUQ.
* Cholangitis: fever (rigors), jaundice, RUQ pain (Charcot's triad)
* Gallstone pancreatitis: constant epigastric pain, radiates to back, vomiting.
* asymptomatic - incidental finding.
83
What are the risk factors for developing gallstones.
* FFF: Female, Fat, Forty
* Increasing age
* Meds: octreotide, GLP-1 agonists, ceftriaxone
* Rapid weight loss
* Assoc: Crohn's, DM
84
How should suspected gallstone disease be investigated in primary care?
* abdo USS (if normal-cannot exclude stones)
* LFTs - gallstones in CBD ->abnormal LFTs
* If results normal but suspicion high- refer for further Ix: MRCP - if CBD dilated and/or LFTs abnormal. EUS.
85
How should a person with asymptomatic gallstones be managed in primary care?
* If gallbladder and biliary tree normal - reassure - do not need Rx unless develop symptoms. Asymptomatic gallstones very common.
* If stones in CBD - refer for bile duct clerance and lap chole (high risk of cholangitis/pancreatitis)
86
How should patients with symptomatic gallstones be managed in primary care?
* emergency admission if unwell with complication.
* Urgent referral to HPB surgery if jaundice or significantly abnormal LFTs
* All others - refer to HPB surgery for consideration of lap chole
* analgesia whilst a/w appt: if **severe **pain - diclofenac 75mg IM. IM pethidine/morphine if diclofenac not suitable/sufficient.
* if intermittent **mild-moderate ** pain - paracetamol or NSAID - diclofenac PO/PR if nausea. Low fat diet.
* If pain cannot be managed in 1ry care- refer hospital as emergency
87
What are the causes of acute pancreatitis?
* Gallstones or alcohol - 80% of cases
* Mnemonic: GET SMASHED
* Gallstones
* Ethanol
* Trauma
* Steroids
* Mumps
* Autoimmune
* Scorpion venom
* Hypertrigluceridaemia, hypercalcaemia
* Hypothermia
* ERCP
* Drugs: azathioprine, mesalazine, thiazides, ACEI, statins, fenofibrate, DPP4 inhibitors (gliptins), valproate, furosemide, tetracyclines.
88
When should acute pancreatitis be suspected?
* acute sudden onset severe upper or generalised abdo pain
* typically radiates to back, worsens with movement, improves leaning forwards
* may be assoc with nausea and vomiting
* Hx of features of gallstones, alcohol misuse
89
How should someone with suspected acute pancreatitis be managed in primary care?
* Emergency hospital admission
* Specialist - IV fluids, oxygen, IV analgesia, IV ABX if needed, early nutritional support. Bloods: lipase, LFT, U&E, CRP. Imaging: CT/MRI.
90
What is chronic pancreatitis?
* chronic, irreversible inflammation and fibrosis of the pancreas. Usually due to recurrent acute pancreatitis causing fibrosis and loss of function.
* leads to endocrine and exocrine insufficiency - leads to malabsorption and DM
91
What are the causes of chronic pancreatitis?
* alcohol - 80% cases
* genetic: CF, haemochromatosis
* obstruction - stones, pancreatic cancer
* hyperparathyroidism - hypercalcaemia
* recurrent acute pancreatitis
* smoking - risk factor
92
What are the presenting symptoms of chronic pancreatitis?
* recurrent/persistent upper abdominal pain
* vomiting
* weakness
* jaundice
* steatorrhoea
* weight loss
* DM
93
How should suspected chronic pancreatitis be managed in primary care?
* investigate: LFTs, HbA1c, faecal elastase (if low - insufficiency), Abdo USS.
* emergency admission if suspected acute pancreatitis
* urgent referral if suspected complication of chronic pancreatitis
* routine referral - gastro - with suspected chronic pancreatitis
94
How should confirmed chronic pancreatitis be managed in primary care?
* lifestyle: alcohol, smoking, high lipids
* paracetamol/NSAID first line for mild-mod pain
* add codeine for severe pain. Add AMT/gabapentin for neuropathic pain
* pancreatic enzyme replacement with meals
* monitor BMI - may need supplements/dietician]
* screen for DM - HbA1c every 6 months
* screen for OP - DEXA scan every 2 years
95
What are haemorrhoids and how are they classified?
* abnormally swollen vascular mucosal cushions - help maintain anal continence. At 3, 7 and 11 oclock.
* Classified as internal or external (split by dentate line).
* Dentate line 2cm from anal verge (transition between upper and lower anal canal)
* external haemorrhoids originate below the dentate line - modified squamous epithelium - innervated with pain fibres. Therefore itchy and painful.
* Internal haemorrhoids originate above the dentate line - columnar epithelium - no pain fibres. Only painful if prolapse and strangulate
96
How are internal haemorrhoids classified?
* they are graded by the degree of prolapse
* first degree: remain within anal canal
* Second degree: prolapse beyond anal canal on straining, but spontaneously reduce.
* third degree: prolapse beyond anal canal and reduce fully on digital reduction
* fourth degree: proalpse beyond anal canal - cannot be reduced.
* Can have both internal and external haemorhoids at the same time.
97
Risk factors/contributory factors for haemorrhoids:
* constipation, straining
* Ageing
* pregnancy, ascites, pelvic mass
* chronic cough
* heavy lifting
* FH
* low fibre diet
98
What are the presenting symptoms for haemorrhoids?
* bright red, painless rectal bleeding (most common) - occurs with defecation , steraks on toilet paper, in toilet bowl, outside the stool (not mixed in)
* anal itching or irritation
* feeling of rectal fullness and incomplete emptying
* Pain if internal haemorrhoid strangulated, or external haemorrhoids if thrombosis
99
How should haemorrhoids be managed in primary care?
* admit - extremely painful, thrombosed external haemorrhoids within 72hrs onset (reduction/excision). Internal haemorrhoids prolapsed and swollen/incarcerated and thrombosed (haemorrhoidectomy). Perianal sepsis.
* refer if unable to visualise haemorrhoids/doubt about diagnosis.
* 2ww referral if anal or colorectal Ca suspected.
* refer for non-urgent management if: large 3rd or 4th degree haemorrhoids, perianal haematoma, combined internal and external with severe symptoms, thrombosed harmorrhoids - chronic irritation/leakage/bleeding, large skin tags.
* manage constipation. Increase dietary fibre and fluid intake. Correct anal hygeine - cleanse and pat dry.
* paracetamol. (avoid codeine and nsaids). Topical symptomatic relief - should not be prescribed routinely (get OTC).
100
What are the symptoms of acute viral hepatitis?
* prodromal phase lasts 3-10 days: flu like symptoms (fatigue, malaise, joint and muscle pain, low grade fever <39). GI symptoms: nausea, vomiting, RUQ pain. Non specific: headache, cough, sore throat, diarrhoea, itching.
* icteric phase lasts 1-3 weeks: jaundice, pale stools, dark urine, pruritis, fatigue, nausea and vomiting. Hepatomegaly, splenomegaly, hepatic tenderness.
* convalescent phase 6 months later: malaise, anorexia, muscle weakness, hepatic tenderness.
101
How is Hep A spread? Which groups of people are at high risk of Hep A infection?
* faecal oral route
* travellers to high prevalence areas
* MSM, oral-anal, digital rectal contact. Multiple sexual partners.
* IVDU - possible faecal contamination of drug equipment
* occupational risk - lab workers, large residental institutions, sewage workers, primates
* haemophilia- receiving clotting factors
102
What is the prognosis for HepA?
* 85% complete recovery <3 months. Almost all within 6 months
* does not cause chronic liver disease, no chronic carrier state, leads to lifelong immunity
* complications - rare: liver failure, relapsing course.
103
Who is HepA vaccination indicated for?
* travellers to high prevalence areas (2 weeks prior)
* CLD
* clotting factors for haemophilia
* IVDU
* MSM - with multiple partners
* Occupational risk
104
How should a person with probable Hep A be managed in primary care?
* admit if severely unwell
* Refer if AST or ALT >2000, bili >300, PT >3 secs. Or if LFTs worsening.
* otherwise - supportive care: if analgesia needed - paracetamol - reduce dose if bilirubin >300, PT >3secs. Ibuprofen. Avoid codeine in severe impairment.
* nausea- metoclopramide (5/7) or cyclizine - normal doses if mild liver imp. If severe - specialist advice.
* Itch - environmental, chlorphenamine at night (avoid in severe imp).
* Notify public health
* avoid alcohol, exclusion until 7 days after onset of jaundice
* handwashing, avoid food handling, avoid sex incl oral sex until 7 days after onset jaundice.
* refer GUM if needed
* F/U every 2 weeks- repeating lfts until normal.
105
How is HepB transmitted?
* blood-blood contact: IVDU equipment, needlestick, bites, eyes, breaks in skin, tattoos, piercings, toothbrushes and razors.
* sexual transmission (vaginal, anal and oral)
* mother-to-baby- during childbirth.
106
Which groups are at high risk of HepB ?
* IVDU
* multiple sexual partners, MSM, sex workers
* travellers to high prevalence area - sexual, procedures
* From country with high prevalence - perinatal
* chronic renal or liver disease
* occupational risk - healthcare, lab staff
* LAC, care homes, prison
107
What are the prognosis/complications of HepB infection?
* 95% adults can clear the HBsAg antigen - then lifelong immunity
* fulminant hepatitis - liver failure (<1%)
* Chronic HBV infection - HBsAg persists. Infants to HepB + mothers, if not immunised from birth. Children infected later in childhood. Immunocompromised adults, HIV, chronic renal failure.
* glomerulonephritis, vasculitis, polyarteritis nodosa
* Chronic infection - can lead to chronic hepatitis, cirrhosis and hepatocellular carcinoma.
108
Who should be immunised against Hep B?
* UK - routine childhood immunisation - at 2,3 and 4 months
* at risk groups: HCWs, sex workers, IVDU, family contacts of Hep B patient, regular blood transfusions, prisoners, CLD, end stage CKD.
* check anti-HBs for response after 3 doses -for those at risk of occupational exposure, and CKD.
* Babies born to HBV + mothers: immunised <24hrs.
109
When should people be tested for HepB?
* opportunistic - high risk groups - immigrants from high prevalence area, IVDU, sex workers. Sexual assault. Needlestick injury. HIV positive.
* those with clinical features: of acute infection (asymptomatic in most children and up to 50% adults), CLD, abnormal LFTs (can be normal in chronic HepB)
110
How is HepB tested for?
* serological:
* HBsAg (hepatitis B surface antigen) - suggests person is infectious, Chronic HBV if persists >6mo.
* HBeAg (HBeAg) (hepatitis B e antigen) - indicates high infectivity.
* Anti-HBe - present once HBeAg cleared.
* Anti-HBc (antibody to hepatitis core antigen) - indicates current or previous HBV infection. Persists for life.
* IgM to hepatitis core antigen - indicates recent HBV infection. Gradually replaced by IgG - persists for life.
* Anti-HBs (antibody to HBsAg) - indicates recovery from and immunity to HBV. Anti-HBs without anti-HBc is a marker of immunisation. It is checked to measure vaccination response.
* HBV viral load
111
How is confirmed Hep B infection managed in primary care?
* Refer anyone who is HBsAg positive to hepatology
* supportive care (as per HepA infection slide) - analgesia, antiemetic, antihistamine.
* request all serology, FBC, LFTs, serum AFP (for HCC), Liver USS.
* notify public health
* lifestyle advice: avoid alcohol, avoid sharing toothbrushes, razors, unprotected sex. Do not donate blood,semen, organs.
* pregnant women - inflant must be immunised at birth, increased risk preterm and low birth weight, breastfeeding safe if infant immunised.
* Refer GUM if needed.
* if chronic HBV - immuse against HepA
* ensure contacts immunised and offered immunoglobulin.
* repeat all serology at 6 mo.
* chronic HBV regular review by liver specialist - will Px antivirals, screen for HCC.
112
What is the transmission of HepC?
* contact with infected blood
* sexual transmission, less common. Increased if multiple partners or HIV positive, MSM.
* vertical - mother to baby - low rate. Can breastfeed.
* No vaccine for HepC.
113
What are the symptoms of HepC infection?
* Acute infection usually asymptomatic (>60%)
* Nausea and vomiting
* RUQ pain
* Jaundice, dark urine, pale stools
* non specific - fatigue, depression, poor memory, myalgia (chronic infection).
* Up to 45% will spontaneously clear the infection.
* 50-85% develop chronic infection. (HCV RNA in the blood for 6 months) Without treatment - leads to cirrhosis and liver cancer.
114
How is HepC tested for?
* anti-HCV antibody test - indicates if they have ever been infected with HepC. Can take 3 months for antibodies to become detectable.
* if antibody test positive, or if person is immunocompromised - send HCV RNA test. This shows current infection.
115
How should suspected HepC infection be managed in primary care?
* if acute infection suspected - clinical features and antibody positive/likely recent source - same day assessment/immediate specialist advice.
* If chronic HCV infection suspected - urgent referral.
* Notify public health.
* whilst a/w specialist - bloods: FBC, U&E, LFTs, clotting, HbA1c, TFTs, ferritin, HepB testing, Hep A testing, HIV, STI screen.
116
What is the specialist management of HepC?
* some spontaneously clear
* anti-viral treatment (direct acting anti-viral agents) can cure - lead to undetectable HCV RNA after 6 months post -therapy.
117
How should patients with HepC be followed up in primary care?
* immunise against Hep B and Hep A
* financial compensation available if hepC attributable to NHS treatment with blood products before 1991
* monitor adverse effects of Rx - hypoglycaemia, fluctuations in INR
* lifestyle advice- reduce obesity, stop smoking, stop alcohol
* no vaccine of Ig available - not immune from having had the infection. Reduce risk of further exposures.
118
Which medications may cause or worsen dyspepsia?
* NSAIDs
* Calcium blockers
* Nitrates
* Thophyllines
* Bisphosphonates
* steroids.
* tetracyclines (doxycyline)
