1
Q
How to prevent recurrent diverticulitis
A
Eat healthy balanced diet and adequate fluid and fibre intake. Bulk forming laxative (isphagula husk) if high fibre diet insufficient or unacceptable, or if symptoms of constipation or diarrhoea persist.
2
Q
What is the commonest haematological abnormality found in advanced liver disease
A
Thrombocytopenia. Due to decreased production, splenic sequestration and increased destruction.
3
Q
test for coeliac disease
A
IgA transglutaminase antibody is the test of choice with specificity and sensitivity at least as good as endomysial antibody. EMA can be used if IgA tTGA is weakly positive.
4
Q
what surveillance for chronic pancreatitis
A
HbA1c every 6 months and DEXA scan 2 yearly
5
Q
causes of acute pancreatitis
A
IGETSMASHED
idiopathic
gallstones 50%
ethanol 25%
trauma
steroid use
mumps
autoimmune
scorpian stings
hyperglycaemia and hypertriglyceridaemia
ERCP
Drugs
6
Q
mortality rate of acute pancreatitis
A
5%
7
Q
Presentation of acute pancreatitis
A
Sudden onset abdo pain which may radiate to back.
Epigastric tenderness.
N&V
Fever
Tachycardia
Presence of risk factors
8
Q
Management of acute pancreatitis
A
If suspected, refer to hospital. Acute pancreatitis should never be managed in community. Encourage fluids on route if they can tolerate this.
9
Q
complications of acute pancreatitis
A
infected necrosis, pseudocysts, pancreatic ascites and pleural effusion, type 3c diabetes, recurrent attacks of pancreatitis.
organ failure
intensive care admissions
prolonged hospital stay
death
very long recovery
10
Q
Lifestyle advice following acute pancreatitis
A
Abstain from alcohol if this was the cause. Even if not the cause, alcohol may exacerbate pancreatitis.
11
Q
What is the meaning of endocrine and exocrine dysfunction following acute pancreatitis
A
exocrine insufficiency in up to 30% patients (lack of digestive enzymes). diabetes in 23%.
12
Q
What is chronic pancreatitis
A
This is prolonged inflammation of the pancreas. Results in fibrosis, cyst formation and strictures of pancreatic duct. most people will have had one or more attack of acute pancreatitis but in some people is insidious onset.
Most common presentation of chronic pancreatitis is chronic abdominal pain.
Also malabsorption, malnutrition, diabetes.
Increased risk of pancreatic cancer.
13
Q
What percentage of chronic pancreatitis is caused by alcohol
A
70%. more common in men than women.
Other causes of chronic pancreatitis are acute pancreatitis, idiopathic, structural/anatomical (trauma/cancer), genetic (eg CF), and hypercalcaemia, hyperlipidaemia and autoimmune.
So really, similar to acute.
14
Q
What symptoms should trigger us to think about chronic pancreatitis
A
Intermittent upper abdo pain or chronic/recurrent abdo pain. Weight loss or low BMI, diarrhoea, diabetes. Especially if known risk factors for pancreatitis.
(NB there is overlap here with suspected cancer pathway. Refer for suspected upper GI cancer if >55Yo with weight loss and upper abdo pain, or >55YO, N&V and weight loss or upper abdo pain.
15
Q
Invx of chronic pancreatitis
A
refer to secondary care if suspected
helpful to do abdo USS in primary care at the same time.
faecal elastase <200 is abnormal, but need level <50 to get steatorrhoea - NICE does not mention checking faecal elastase.
16
Q
Management of chronic pancreatitis
A
Incurable condition. Focus on reducing risk, lifestyle mod and symptom control
1. Abstain from alcohol.
2. Smoking cessation
3. Dietician assessment for all - due to risk of malabsoprtion - ideally specialist for pancreatitis
4. Long term pancreatic enzyme replacement therapy.
5. If type 3 diabetes - may or may not need insulin. if needs insulin manage like type 1, if doesnt management like T2.
6. If diabetic not on insulin, review every 6 months for potential benefits of insulin therapy.
really big problem seems to be nutritional state in these people.
17
Q
Complications of chronic pancreatitis
A
- Pancreatic cancer increased x13 (lifetime risk of 40% if hereditary pancreatitis)
- Chronic pain - paracet and NSAID first line. Not opioids. SSRIs, TCA or gabapentinoids are often used as adjuncts.
- Pancreatic duct obstruction - need surgery or lithotripsy.
- Pseudocysts - need endoscopic drainage.
- Pancreatic ascites and pleural effusion.
18
Q
monitoring in chronic pancreatitis
A
Exocrine
1. monitor exocrine function for insuff/malnut 12 monthly. treat vitamin def if required.
2. DEXA 2 yearly
Endocrine
1. HbA1c every 6 months if no known diabetes.
Lifetime risk of diabetes 80%
Pancreatic cancer - annual monitoring for pancreatic cancer if hereditary pancreatitis - secondary care will do this.
19
Q
How soon after chronic pancreatitis does pancreatic enzyme insufficiency causing malabsorption occur
A
around 10-15 years.
malabsorption of carbohydrates, proteins and fat.
including fat soluble vitamins A DEK
steatorrhoea when 90% function gone.
Osteoporosis/osteopenia in 60% those with pancreatic enzyme insufficiency.
Diagnose clincially, and with faecal elastase or serum trypsin.
20
Q
How to manage pancreatic enzyme insufficiency
A
PERT - pancreatic enzyme replacement therapy. Pancreatin eg Creon taken with meals and smaller dose with snacks.
Monitor response by level of steatorrhoea or weight gain. and measure fat soluble vitamin levels.
Take just before meal or with the first mouthful. Swallow capsule with a cold drink. If long meal, take half at the start and half at the middle.
21
Q
Indications for urgent admission or referral to GI/liver team
A
suspected cancer, ascites, jaundice, encephalopathy, sepsis, abnormal clotting, haematemesis, low albumin/platelets, ALP or ALT more than 5 times the upper limit of normal.
22
Q
What does a raised ALP mean
A
Measure of cholestasis.
So check GGT.
Also raised in bone pathology, vitamin D deficiency, metastatic cancer, and pregnancy.
Consider non liver causes especially if GGT is normal.
23
Q
Causes of raised ALT
A
Alcohol
Drugs see other card
viral hepatitis
Haemochromatosis
Wilsons disease
24
Q
Common hepatotoxic drugs
A
tetracyclines, amiodarone, tamoxifen, oestrogens, valproate, carbamazepine, macrolides, nitrofurantoin, statins, terbinafine, methyldopa, methotrexate.
25
common causes of cirrhosis
alcoholic liver disease
NAFLD (now called metabolic dysfunction associated steatotic liver disease), Hep B, Hep C.
rarer causes include autoimmune liver disease (including autoimmune hepatitis, PBC and PSC), metabolic or genetic causes eg haemochromatosis, Wilsons disease, a1 antitrypsin deficiency, CF. Drug causes include methotrexate, amiodarone, methyldopa, vit A.
Biliary causes eg biliary atresia. Vascular causes such as Budd chiari.
26
what is the spectrum of liver disease
normal - fibrosis - compensated cirrhosis - decompensated cirrhosis.
poor correlation between blood results, US findings and degree of fibrosis/cirrhosis.
27
what is the difference between compensated and decompensated cirrhosis
compensated: normal liver tissue being replaced with fibrotic tissue and nodules, but no symptoms
decompensated cirrhosis - cirrhosis with symptoms such as ascites, hepatic encephalopathy, varices, GI bleeding or jaundice.
28
what percentage of those with chronic liver disease progress to cirrhosis.
up to 20% over 10-20 years. Often present acutely with ascites or variceal bleed.
29
Limitations of standard tests in liver disease/fibrosis
Often LFTs and abdo USS are normal (especially if milder fatty liver changes).
30
What does the blood marker ALT and AST tell us
Raised if hepatocellular damage or death.
ALT more specific to liver. AST can rise with other things, however, AST is a more specific indicator of alcohol related liver disease and some autoimmune hepatitis.
AST:ALT ratio of >1 indicates advanced fibrosis/cirrhosis.
31
Bilirubin
Marker of liver function (byproduct of haem breakdown). Check if conjugated or unconjugated if raised.
Unconjugated - Gilberts or haemolysis.
Conjugated hyperbilirubinemia can be parenchymal liver disease or biliary obstruction.
32
What raises GGT
alcohol
obesity
some drugs eg antiepileptics.
If raised due to liver disease, it best predictor of mortality.
33
Which causes of abdominal pain typically radiate to back?
AAA rupture
pancreatitis
duodenal ulcer
34
Red flags/pathways for oesophageal/gastric cancers
Urgent suspected cancer pathway if dyspepsia with any of:
- upper abdo mass consistent with stomach cancer OR
- dysphagia OR
- more than 55YO with weight loss plus any of upper abdo pain/reflux/dyspepsia.
Urgent direct access OGD if dyspepsia and
- more than 40 with FHx gastro-oesophageal cancer OR
- from area at increased risk of gastric cancer (SE asia).
35
Criteria for urgent direct-access CT abdomen (or Urgent suspected cancer pathway for pancreatic cancer)
Age more than 40YO with jaundice - urgent suspected cancer pathway
direct access CT abdomen if over 60YO with weight loss plus any of diarrhoea, back pain, abdominal pain, nausea, vomiting, constipation, new onset diabetes.
-
36
When to do a FIT test? (to look for colorectal cancer? )
Anyone with abdominal mass OR change in bowel habit, OR iron deficiency anaemia OR >40YO with unexplained weight loss and abdo pain OR <50YO with rectal bleeding and abdo pain/weight loss OR >50YO with any of rectal bleeding/abdo pain/weight loss OR >60YO with anaemia even if not IDA.
Then refer USC if FIT >10.
NB if rectal mass, anal mass or unexplained anal ulceration, do not need a FIT, just refer.
37
Who should be referred for routine OGD (not red flags for suspected cancer)
More than 55YO plus
- treatment resistant dyspepsia OR
- upper abdo pain and anaemia, but not weight loss.
- raised platelets and any of dyspepsia/reflux/upper abdo pain, N&V, weight loss.
38
What is functional dyspepsia
Will cause pure epigastric symptoms (not retrosternal symptoms as this suggests reflux of acid).
Further invx are needed before a diagnosis of functional dyspepsia can be made.
- H pylori - test for this and eradicate if positive
- abdo USS - consider if abdo pain <1y and possibility of biliary colic (gallstones blocking bile duct).
- coeliac serology - if dyspepsia and overlapping IBS symptoms.
Diagnose functional dyspepsia if more than 8 weeks epigastric pain or burning, early satiety, or fullness after eating in the absence of alarm symptoms/signs. Vomiting is not typical, if present consider alternatives.
More common in younger people, females, other disorders of gut brain axis such as IBS, otehr somatoform type disorders, history of anxiety or depression, recent acute enteric infection, ?history of abuse.
Treat as you would uninvestigated dyspepsia or uninvestigated reflux like symptoms.
39
How to explain functional dyspepsia to patients
Disorder of brain gut axis - direct bidirectional link between two).
Symptoms can be caused by diet, stress, post infective, and can be affected by how you respond to symptoms - biopsychosocial.
Good communication skills and empathy important.
Brain gut axis includes immune function, microbiome, stress impact, and genetics.
40
If no red flags in dyspepsia history, and not meeting criteria for any urgent or routine investigation, what do you do?
TREAT OR TEST
Either treat with full dose PPI for 1 month OR test for H pylori
Full dose PPI is 30mg lansoprazole OD or omeprazole 20mg OD.
If treating with PPI - if still symptomatic after 1 month, test for H pylori.
If test for H pylori - if positive, eradicate, if negative, give 1 month PPI.
41
Management of uninvestigated dyspepsia (called uninvestigated because not met criteria for scope so not had a scope - this is most of the people in primary care).
NB - if red flags develop during treatment need to reassess.
1. Lifestyle - see next slide.
2. Check no medications causing symptoms
3. Test and treat or treat then test.
42
Lifestyle advice for dyspepsia
healthy eating, weight reduction, smoking cessation.
Avoid triggers (often fatty foods, red meat, chocolate, vegetables, spicy foods, carbs, coffee, fizzy drinks, citrus, alcohol.
Allow time between evening meal and bedtime.
?raise the head of the bed.
If functional dyspepsia - regular aerobic exercise
NO EVIDENCE for specific dietary modifications such as FODMAP.
In GORD - sleep hygiene and elevate head of bed. Keep meals small such as 4-5 small meals per day and avoid lying down after food. Avoid tight fitting clothes and bending down. Chewing gum may help as it promotes salivation which neutralises acid.
43
Ongoing management for dyspepsia after Test and treat or treat and test?
If resolved - stepwise progression to self care (stopping PPI unless indication for long term acid suppression). Annual review if on long term treatment.
If relapse - low dose acid suppression as needed.
If no response - trial H2RA for 1 month (famotidine). Can continue this long term as needed too.
If no response to PPI and H2RA and have tested/treated H pylori - then refer to gastro.
44
Who to do H pylori testing for dyspepsia
Everyone with low risk dyspepsia can be Test and treat or treat and test.
Better to test first if:
1. older people.
2. North african origin
3. Living in known high risk area.
4. Unexplained IDA (after OGD and other causes excluded).
5. Previous gastric or duodenal ulcer or bleed and not previously treated.
6. Previous gastric or duodenal ulcer or bleed before taking NSAIDs.
45
What are the practicalities of H pylori testing for dyspepsia
Use stool antigen testing or breath test.
(serology not recommended as lower specificity).
Stop PPI for 2 weeks before testing.
Need to have no antibiotics or bismuth for 4 weeks before
If significant flare of symptoms, can cover with H2RA.
46
When to retest after H pylori eradication
Retest if severe recurrent or persistent symptoms!!
If persistent symptoms and test was done within 2 weeks of PPI or 4 weeks of antibx.
SHOULD DO TEST OF CURE (regardless of symptoms)
If poor compliance or high local resistance rates.
If duodenal ulcer, gastric unler, MALToma, or after resection of early gastric cancer.
If increased risk of gastric cancer (fhx or origin high risk).
If taking aspirin without co-prescribed PPI (guideline doesnt explain why?).
Retest after 4-8 weeks - can use H2RA cover if symptomatic.
47
What is the regimen for H pylori eradication?
Twice daily PPI + amoxicillin + clarithromycin/metronidazole (choose either one - if used one before choose other one).
If pen allergy:
Twice daily PPI + Clarithromycin + metronidazole.
If pen allergy and had clarithromycin before:
Twice daily PPI + metronidazole + tetracycline + bismuth.
Further antibx regimens including quinolones too.
There are concerns about resistance and some people will have been treated multiple times which is why it is important to ask about previous antibiotics use.
All dose regimens will be 7 days total!!
48
When it is right to take PPI for longer than 8 weeks
If taken PPI for more than 8 weeks, consider if longer term use is needed.
Continue if any of:
- severe oesophageal disease (-itis, ulcer, stricture)
- Zollinger ellison syndrome
- High risk of GI bleeding due to NSAIDs, other drugs that cause bleeding, prev ulcer. older poeple on aspirin even!
- Patient not ameanable to stopping PPI.
- history of gastric or duodenal ulcer - can go down to low dose maintenence or PRN PPI.
49
Are long term PPIs needed for barretts?
Yes for symptom control.
Doesn't prevent progression to cancer.
50
Where might deprescribing of PPI be appropriate
Patient ameanable.
- mild mod oesophagitis and symptoms now controlled.
- GORD, 4-8w PPI and symptoms now controlled
- functional dyspepsia or uninvestigated dyspepsia, 2-12w PPI and symptoms now controlled
- H pylori eradication and now asymptomatic.
Risk benefit of deprescribing
- risk is return of symptoms
- benefit is less pills, decreased side effects/risks
PPIs are associated with - CVD CKD cancers fractures, dementia, hyponatraemia, hypoMg, B12 def, death.
- these are all associations not causations.
51
How to stop PPIs
Taper dose - 1 in 10 get symptoms back.
Use on demand/as required - 1 in 10 get symptoms back.
Change to H2RA - 1 in 5 get symptoms back
Stop abruptly - 1 in 2 get symptoms back.
OTC antacids and lifestyle can help this. Symptoms usually mild managable and will settle in days/weeks. Symptoms do not necessarily mean return of underlying cause. Make a plan for if symptoms become severe, frequent or persistent such as reconsult or restart PPI.
52
What in uninvestigated dyspepsia
Persistent recurrent epigastric pain/heartburn/acid reflux with or without nausea, vomiting, bloating that has not been investigated by endoscopy (most likely because not meeting criteria for it).
If had endoscopy - can be given one of several diagnoses - functional dyspepsia, GORD, PUD, or other findings such as oesophageal cancer, or gastric cancers.
53
Medications assocaited with dyspepsia
NSAIDs, calcium antagonists, opiates (due to effect on gut motility), bisphosphonates, corticosteroids, theophyllines, nitrates.
Some other medicines may worsen GORD by relaxing the GOJ - benzos, anticholinergics, progestogen, sildenafil, TCA.
54
What is H pylori associated with? High risk conditions wise
Peptic ulcers, MALT lymphoma, gastric cancer.
55
What options for further management of dyspepsia if acid suppression not worked.
If functional dyspepsia
- can trial TCA amitriptyline 10mg nocte and titrate up slowly based on symptom response.
In secondary care may also used antipsychotics, pregabalin or mirtazipine, not primary care! No evidence for SSRIs. If functional dyspepsia, avoid surgery or opioids.
CBT and psychological therapy option for functional dyspepsia!
surgical options if GORD - laparoscopic fundoplication or silicone implant
56
Any role for domperidone or metoclopramide in dyspepsia
No - there is MHRA drug safety alerts for both of these.
Metaclopramide due to extrapyramidal side effects.
Domperidone due to risk of cardiac arrhythmias.
57
What non GI symptoms can GORD cause
Respiratory - cough, wheeze, idiopathic pulmonary fibrosis.
ENT - globus and posterior laryngitis
Oral - dental erosions.
58
Management of severe oesopahgitis (endoscopy diagnosis)
Full dose PPI 8 weeks - lansoprazole 30mg OD is full dose.
If symptoms ongoing - double dose for 8w (eg to BD) or switch to alternative PPI full/high dose.
Refer if symptoms persist.
Long term will need continuous full dose PPI. if relapse later, switch to alternative full dose or double dos e PPI.
PPI effective in oesophagitis for healing, symptoms relief, prevention of relapse and complications.
59
Managemnt of non severe oesophagitis
Full dose PPI 8 w
if no response double dose PPI for 1m.
If still no response, can swap to H2RA for 1m.
If still no response - refer.
For non-severe oesophagitis, do low dose PPI maintenence or H2RA.
60
Management of endoscopy negative reflux disease
eg symptoms of reflux but normal scope
PPI full dose for 4 weeks, if no response, H2RA 4 weeks.
Low dose maintenece or as required treatment.
61
Management of benign oesopageal stricture
Continuous full dose PPI needed long term.
62
Management of gastric or duodenal ulcer with H pylori positive
Test for H pylori and eradication if positive.
- NB if NSAID associated ulcer need PPI for 8 weeks before eradication.
If gastric ulcer - need repeat endoscopy to check ulcer healed with H pylori testing 8 wks later.
If still H pylori positive - give second line eradication therapy and then repeat endoscopy.
Once H pylori negative, need low dose PPI as maintenence or as required.
Can be H2RA if poor PPI response.
If duodenal ulcer - dont need to do repeat endoscopy - just recheck H pylori status with breath test.
63
Management of gastric or duodenal ulcer if H pylori negative
Gastric ulcer - Full dose PPI for 4-8w then repeat endoscopy to check ulcer healed
Duodenal ulcer - Full dose PPI for 4-8w (don't need repeat endoscopy).
Maintenence low dose or as required PPI.
If NSAID associated ulcer - aim for no NSAID. if NSAID needed, use COX2 selective NSAID and always co prescribe a PPI.
64
What to do if duodenal ulcer doesnt respond to PPI treatment.
Causes
- non compliance
- malignancy
- failure to detect h pylori
- aspirin NSAID use
- ulceration due to ingestion of other drugs such as SSRI and bisphosphonates
- Zollinger Ellison syndrome
- Crohns disease.
65
How to take a PPI
30-60minutes before food
use regularly for maximum symptom control
if symptom control not achieved, before stepping up the dose, try splitting the dose across the day (off licence).
66
When is fatty liver reversible?
In non MASLD, there is element of reversibility (steatosis)
Metabilic associated steatohepatitis is steoatosis and inflammation (this is also reversible).
Then fibrosis
Then cirrhosis.
Even at fibrosis stage there can be some fibrosis regression.
No symptoms until decompensated cirrhosis.
67
Prevalence of MASLD and MASH
MASLD in 20-30%
MASH in 2-3% population.
<10% people with MASLD will go on to develop liver related complications such as cirrhosis or hepatocellular carcinoma in the 10-20Y after diagnosis.
Once compensated cirrhosis, 3-4% progress to decompensated cirrhosis each year.
68
Risk factors of MASLD and MASH progression
Comorbidities
Environmental factors
Certain genetic factors
Drugs causing fatty liver.
69
How to diagnose MASLD
Steatosis in hepatocytes + metabolic risk factors + absence of another cause (alcohol or chronic disease).
Diagnosis of exclusion.
- LFTs often normal initially.
- US - fatty liver is common US finding but is not sensitive or specific for NSALD.
Mild fatty changes can be missed.
Advanced fibrosis or mild steatosis can be missed on US.
Those most likely to have MASLD are those with T2DM or metabolic syndrome.
But how do we find them when MASLD is asymptomatic?
- start looking for it if abnormal ALT or AST, or if a scan suggests fatty liver.
70
Red flags in liver disease
ascites, jaundice, encephalopathy, sepsis, abnormal clotting, haematemesis, low albumin/low platelets, rapid deterioration in ALT/AST 5xULN
For these things - consider admission or urgent referal.
71
Investigation of abnormal LFT - raised ALT
Invx even if mildly raised as degree of abnormality does not correlate with degree of liver pathology
Ask about
- alcohol
- metabolic syndrome
- drugs such as tetrocyclines, amiodarone, tamoxifen, oestrogens, valproate, statins, carbamazipine, macrolides, nitrofurantoin, statins, terbinafine, methyldopa and methotrexate.
- Risk factors for viral hepatitis?
- personal history, comorbs, fhx eg haemochromatosis or wilsons disease.
Invx with liver function screen and liveer autoimmune screen, hepatitis screen, and abdominal US scan.
Also do HbA1c
May be alcoholic liver disease, MASLD, or hepatitis.
72
What does the AST:ALT ratio mean?
AST:ALT ratio of more than 1 suggests advanced fibrosis/cirrhosis.
In alcohol related hepatitis often more than 1.5
Ratio rises in cirrhosis as reduced hepatocyte production of ALT and impaired clearance of AST.
73
Interpreting liver autoimmune screen results
Autoimmune hepatitis
- AST ALT and/or IgG raised.
- ANA and SMA positive
Primary biliary cholangitis
- ALP GGT and IgM raised
- ANA and SMA usually positive
Primary sclerosing cholangitis
- Raised ALP and GGT
- ANA or SMA may be positive
74
Abnormal liver function tests - raised ALP
Marker of cholestasis so check GGT.
Also raised by bone pathology, vit D, metastatic cancer and pregnancy.
Consider non liver causes if GGT normal.
Questions to ask in the history - may be non specific fatigue, nausea, anorexia. May have other autoimmune conditions.
Primary sclerosing cholangitis is associated with inflammatory bowel disease, cholangiocarcinoma, and colorectal cancer.
Depending on what you think the cause is ?
- autoimmune liver disease -refer
- if liver screen normal but ALD or ALP remain raised, refer.
75
What is Gilberts syndrome
Unconjugated hyperbilirubinaemia due to a defect in the liver enzyme with conjugates bilirubin in the liver.
Conjugated biluribin is <20% of the total bili.
Therefore investigate with split bilis.
Do blood film, Hb, retibulocyte count - which should all be normal. Clotting should be normal.
Urine dip should not show bilirubin because unconjugated bilirubin is not water soluble.
If bloods suggest GIlberts syndrome - no need for USS. Make diagnosis, code and manage.
Usually autosomal recessive but less commonly can be autosomal dominant.
No effect on life expectancy. No effect on liver.
These patients should have painless non pruritic jaundice with no stigmata of liver disease. ULN for bili is 20, in Gilberts, will be no more than 85.
Jaundice likely to occur due to stressors such as exertion, fasting, sleep deprivation, alcohol, dehydration, surgery, concurrent illness.
Safety net if prolonged or severe jaundice or jaundice with dark urine/pale stools as this would not be due to gilberts so does need further invx at a later date if occuring.
The other big cause of unconjugated hyperbilirubinaemia is haemolysis.
Conjugated hyperbilirubinaemia can be due to hepatic or post hepatic causes eg hepatitis, ALD, MASH, malignancy, sarcoidosis and others.
76
Management of MASLD
Lifestyle
Offer testing for advanced liver fibrosis with ELF blood test.
If more than 10.5 - fibroscan, repeat every 2yrs. refer if cirrhosis.
If ELF <10.5, advanced liver fibrosis unlikely, reassess in 3 years.
77
What is the leading cause of death in people with MASLD
Cardiovascular disease!
(think about the risk factors)
Second leading cause of death in those with MASLD is extrahepatic cancers
Mx acronym is cardioWASP
Cardio - mx of cardio rf such as htn lipids diabetes
Weight loss - needs to be sustained
Alcohol - within recommended limits
Sugar in the form of fructose - associated with progression from MASLD to MASH and fibrosis progression - mediteranean diet is good.
Physical activity.
Any drugs (new developments) would only be started by secondary care.
78
What is primary sclerosing cholangitis
rare autoimmune liver condition. More common in men.
S for serious - increased risk of hepatobiliary and colon cancer.
S for Sits with IBD (70% those with PSC have IBD).
Intrahepatic and extrahepatic strictures with inflammation and bile duct fibrosis.
Causes impaired bile formation, cholestasis and progressive liver dysfunction.
79
Diagnosis of primary sclerosing cholangitis
Often asymptomatic - LFTs done for another indication show abnormality.
Common blood abnormalities would be raised ALP, raised GGT, raised ALT/AST (may suggest PSC AH overlap). Bili may be raise if advanced disease.
ANA or SMA antibodies may be positive.
atypical perinuclear ACNA may be positive but not disease specific, no impact on prognosis.
Symptoms may include
- general fatigue, pruritis, autonomic dysfunction, sleep disturbacne, confusion (due to cholangitis)
- RUQ pain
- recurrent cholangitis
- prolonged cholestasis can cause fat soluble vitamin defiency (ADEK)
- variceal bleeding
- advanced disease can have portal hypertension, HE, ascites, cirrhosis, jaundice obstructive
Need to rule out other causes of liver disease, then refer if you think PSC. Request abdo USS to exclude biliary calculi and assess for portal hypertension and gallbladder enlargement.
Secondary care will do ERCP/MRCP, ?liver biopsy (to ensure no AH),
80
What is the ELF test
This is a non invasive blood test to assess the risk of liver fibrosis and progression to cirrhosis, especially in patients with MASLD.
81
What is the treatment for PSC
No single drug proven to improve transplant free survival
UDCA - used widely but off licence. Secondary care decision. Improves biochemistry. Doesn't decrease risk of cancer or disease progression.
Vancomycin slight benefit.
Immunosuppressive treatments - trials small but no evidence improves outcomes.
Can do endoscopic management of strictures.
Liver transplant for advanced disease but 25% recur in the graft.
At higher risk of osteoporosis so assess for this, may be deficient in fat soluble vitamins so may need vit D.
82
What is the license for UDCA
Licensed for dissolution of gallstones, and for PBC.
Is widely used in PSC but no licence for it.
83
What are the three autoimmune liver diseases
Autoimmune hepatitis
Primary sclerosing cholangitis
Primary biliary cholangitis
84
What symptoms do you get in all 3 of PBC PSC and AH
Pruritus, dry eyes/mouth, vaginal dryness, raynauds, fatigue.
85
what other conditions is PSC associated with?
Inflammatory bowel disease (70% those with PSC have IBD but only 5% those with IBD have PSC).
CHOLANGIOCARCINOMA - PSC is a premalignant disease - up to 20% go on to get cholangiocarcinoma, think of this if rapidly worsening symptoms.
Colorectal ca - most of the risk is due to IBD.
Also higher risk of pancreatic cancer, and bacterial cholangitis.
86
what screening/surveillance for PSC
Colonoscopy at diagnosis to look for IBD. Annually if polyps present, 5yrly if absent.
Scrrening for cholangiocarcinoma may be US/MRI 6-12monthly and Ca19-9 - ask secondary care.
Variceal screening if cirrhosis or portal hypertension.
87
What are poor prognostic factors in PSC
extensive strictures, dominant strictures, recurrent cholangitis, IBD, progressive liver dysfunction synthetic function, cirrhosis, portal hypertension.
88
What is the commonest autoimmune liver disease
Primary biliary cholangitis
89
What is primary biliary cholangitis
Autoimmune condition causing chronic autoimmune destruction of the small intrahepatic bile ducts (compared to PSC can be intrahepatic and extrahepatic).
Untreated will cause cirrhosis and liver failure.
More common in females
Risk factors smoking, cholestasis in pregnancy, recurernt UTIs.
Intestinal biome reduced in those with PBC.
Genetic factors and environmental factors.
90
What is the pathophysiology of PBC
Antimitochondrial antibodies cause progressive lymphocytic inflammation of intrahepatic bile ducts. Without treatment will cause cholestasis, fibrosis, cirrhosis.
Treatment aiming to modify cholestasis, reduce inflammation, reduce risk of fibrosis.
91
Presentation of PBC
Either symptoms compatible with condition or someone presents with abnormal LFTs.
Symptoms not correlate with disease severity. May have symptoms of abdo pain, itching, fatigue, poor concentration, bone pain or dry eyes/dry mouth.
Common blood findings - ALP raised. GGT raised.
IgM raised. ANA or AMA positive (90% of time for AMA).
ALT/AST may be mildly raised.
Cholesterol often raised.
92
How to diagnose PBC
Cant see on abdo US becauses changes are localised to small bile duct.
But US can be used to rule out other causes.
ELF or fibroscan might be used to look for fibrosis.
Liver biopsy rarely used.
Diagnosis made in secondary care based on meeting criteria of bloods/antibodies and liver biopsy findings (sometimes).
93
Treatment of PBC
Aiming to reudce cholestasis, reduce inflammation and risk of fibrosis.
Initially used UDCA - lifelong treatment.
Aim to reduce ALP to <1.5x ULN, with normal bilirubin.
Poor response to UDCA is poor prognostic factor.
Second line is fibrates.
Liver transplant now rarely required - if jaundice or decompensated cirrhosis or intractable pruritus.
Even if liver transplant, still need lifelong UDCA.
94
Surveillance of PBC
blood tests and imaging/fibroscan for progressiobn to fibrosis/cirrhosis.
If signs of cirrhosis, then start surveillance for HCC and varices (like in all cirrhosis).
95
Associated conditions with PBC
Osteoporosis increased risk - need calcium and vit D supplementation, # risk assessmnet, DXA.
Hyperlipidaemia - but not usually CV concern unless other CV risk factors. Xanthelasma sometimes present.
May be linked to other autoimmune conditions - but do not screen for these.
96
Prognosis for PBC
If complete response to UDCA and no cirrhosis, survival very good, up to same as normal population.
97
What is autoimmune hepatitis
Rare autoimmune condition.
Destruction of hepatocytes resulting in self perpetuating inflammation of liver, progressing to cirrhosis and end stage liver disease.
More common women.
Occurs in teenagers then middle aged.
Environmental precipitants and genetic risk factors (maybe certain viruses or certain drugs)
98
Presentation of autoimmune hepatitis
Often presents as acute onset jaundice and transaminases 5-10x ULN, may have prolonged INR.
Less commonly, insidious onset non specific fatigue, joint pains, malaise, amenorrhoea. Progress to jaundice, itch, upper abdo pain, decompensated cirrhosis.
May be incidental on bloods.
99
Bloods in autoimmune hepatitis
diagnosis of exclusion. no pathognomic test.
Consider if raised transaminases or cirrhosis of unknown origin. Need to rule out viral hepatitis, ALD and MASLD.
Raised ALT Ast, raised IgG or polyclonal hypergammaglobulinaemia. ANA or SMA antibodies. other antibodies. Prolonged INR.
100
Is there overlap between AH and PSC/PBC.
yes, these patients will also have cholestatic bloods
101
Diagnosis of autoimmune hepatitis
Refer to secondary care
Liver biopsy needed for diagnosis, and fibroscan.
102
Treatment for autoimmune hepatitis
Steroids in secondary care to induce remission (work in 1-2wks).
Usually azathioprine for maintenance. Needed lifelong.
Remission defined as normalisation of bloods. 20% don't get remission with standard treatments.
Better prognosis if get disease later in life.
Liver transplant considered if do not respond or cannot tolerate.
103
Link between autoimmune hepatitis and HCC/varices
Like all causes of liver disease, if progresses to cirrhosis at increaed risk of HCC and varices and needs surveillance for these.
Of not PBC also increased risk of non hepatocellular cancers - may be due to immunosuppressive medication.
104
What is the NICE guidance for investigation of dysphagia
Any dysphagia requires urgent upper GI endoscopy (2ww). There is no age limit for this.
Also do urgent GI endoscopy for anyone age 55YO or more with weight loss and (upper abdo pain OR reflux OR dyspepsia).
105
What imaging for gallstones
Abdominal USS
106
What is the first line antimotility agent for diarrhoea in people with IBS.
Loperamide
Adjust dose to clinical response
107
Antibodies in hep A
IgM antibody indicates acute hepatitis A infection
IgG antibodies indicate previous hepatitis A infection. These antibodies would be detectable lifelong.
108
What advice to give people with hep A infection
Transmission faeco oral through contacts or travel to endemic area.
Incubation period of 2-6 weeks.
Usually self limiting illness.
Risk of acute liver failure very low <0.1% though this risk increases with age and pre existing liver disease.
No chronic infection state. Recovery from acute infection induces lifelong immunity
Hep A is notifiable disease.
109
What common medicine is implicated in C diff infections
PPIs - increased risk of enteric infections - especially C diff
Also think antibiotics.
110
Second line treatments for abdo pain in IBS
If laxatives/loperamide and antispasmodics do not work.
Amitriptyline is recommended as second line treatment for IBS - unlicenced indication in the BNF.
111
Why is ferritin and transferin saturation included in a liver screen?
In liver damage, hepatocytes release ferritin into the blood leading to raised levels.
Also raised in haemochromatosis.
Also raised in inflammation which can occur in multiple liver diseases
Raised ferritin can also be caused by fatty liver
112
In what oral condition should you test for coeliac disease?
Recurrent mouth ulcers
113
What conditions put you at risk of toxic megacolon
Toxic megacolon is recognised serious complication of ulcerative colitis.
Treatment with opiates increase risk of occurrence.
Bacterial gastroenteritis can also cause a toxic megacolon, though in a young otherwise healthy person this is unlikely.
114
What is haemochromatosis
This is a genetic condition which is autosomal recessive inheritance (or de novo mutation).
Causes increased iron absorption and release of iron from macrophages resulting in iron overload and multiorgan damage.
May present with cirrhosis of the liver, diabetes secondary to pancreatic islet cell failure, cardiomyopathy, arthritis, testicular failure, and tanning of the skin.
114
If you need to confirm H pylori eradication, which is the best test for this?
Use C13 rea breath test at 4 weeks post eradication
115
What test is used for long term monitoring of those with NAFLD (MASLD)
ELF test.
Blood test which measures 3 marker of fibrosis.
Results in a score which indicates the likelihood of liver fibrosis.
Do two yearly testing for children with NAFLD and three yearly testing for adults with NAFLD.
116
Common electrolyte imbalances in high output stomas
Hyponatraemia
Hypomagnesaemia
Also dehydration.
116
Presentation of cholecystitis
RUQ pain radiating to chest or back. Often triggered by eating.
May be pain on palpation of RUQ, which may be worse on deep inspiration (murphys sign)
117
Most common risk factor for sigmoid volvulus
Old age
Chronic constipation
Neurological and psychological disorders.
Higher incidence in those who have been institutionalised.
In those with long standing constipation they develop a capacious elongated relatively atonic colon, especially in sigmoid.
Sigmoid volvulus results in closed loop obstruction. If no resolved, will cause venous infarction, perforation and faecal peritonitis.
118
What percentage of those with PBC have AMA antibodies
85%
If you are suspecting PBC it is usefulto do an US to rule out gallstones and assess liver architecture (but PBC is small bile ducts so cannot see on US).
Need to refer to gastro and do liver biopsy for diagnosis.
119
When is CA125 indicated
Women (especially if over 50) with persistent or frequent
- abdominal distension/bloating
- early satiety or loss of appetite
- pelvic or abdo pain
- increased urinary frequency/urgency.
120
What is the gold standard investigation for diagnosing gastric cancer
Gastroscopy
121
Management of painful anal fissure
Simple analgesia
Warm baths
If pain on defaecation - topical local anaesthetic cream can be used.
GTN ointment can be used second line if symptoms ongoing.
Px soft/bulking laxative if stools hard. Avoid opioids.
122
What is gold standard diagnostic test for peptic ulcer
OGD.
Indicated in those with dyspepsia over the age of 55YO or with warning signs.
Barium swalow can be used if OGD CI.
123
There is a difference between whether abdo pain radiates through to the back or round to the back . What conditions present like this?
Through to the back - AAA rupture, pancreatitis, duodenal ulcer.
Round to the back - renal colic, biliary colic, cholecystitis.
Not sure how useful this is....
124
What is the referral for suspected oesophageal or stomach cancer?
Urgent direct access OGD within 2 weeks if
1. Dysphagia OR
2. 55YO plus weight loss plus (upper abdo pain or reflux or dyspepsia).
Non urgent direct access OGD if
1. Haematemesis
2. 55YO with
- treatment resistant dyspepsia OR
- upper abdo pain with low Hb OR
- raised platelets and one of nausea/vomiting/weight loss/reflux/dyspepsiaupper abdo pain OR
- N&V with any of weight loss/reflux/dyspepsia/upper abdo pain.
125
Management of ulcerative colitis
If mild to mod first presentation or exacerbation of proctitis
First line topical aminosalicylate
If not achieving remission in 4 weeks - add oral aminosalicylate.
126
Monitoring of oral salicylate eg mesalazine
Pre treatment FBC U&E creat LFT
FBC and LFT at 1 month
FBC U&E LFT at 3 months
If stable, then yearly.
Repeat bloods one month after dose changes.
127
What is botulism
Extremely severe form of food poisoning. Due to ingestion of butulin from clostridium botullinum. May be found in any food. Canned foods incompletly sterilised commonly implicated, as is home bottled vegetables in the UK.
128
What is the link between PPIs and clopidogrel
Omeprazole and esomeprazole reduce the effectiveness of clopidogrel.
Lansoprazole or pantoprazole are ok.
129
What to think about if new weight loss and new onset diabetes in over 60s
Think pancreatic cancer.
urgent suspected cancer referal .
130
Which antibiotics are bad for c diff
Cephalosporins, quinolones (floxacins - rarely used now), clindamycin.
131
Who should we test for c diff
Anyone over 65 with diarrhoea without a clear cause.
Less than 65 if risk factors for c diff eg fraim, hospitalised, recent antibitoics, comorbidities.
132
Management for C diff
Hydration
Infection control measures to prevent spread
Antibitiotics for all - vancomycin first line. Fidaxomicin if fails to respond or early relapse.
Also think kidneys - stop DAMN drugs
NOT antidiarrhoeal drugs.
Stop antibiotics if you can!
If symptoms recur, recheck stool, as can get recurrence, but also post infectious irritable bowel is common.
No benefit for pre or probiotics for c diff prevention.
Faecal transplant sometimes used for recurrent C diff - maybe will become norm for first episode too. Very short term GI side effects only. Cant be used if immunosuppressed, or pregnant, or anaphylactic food allergy.
133
What is dermatitis herpetiformis
Cutaneous manifestation of coeliac disease. blisters which appear in clusters, most commonly on scalp, shoulders, buttocks, elbows and knees.
134
What conditions link with coeliac disease
T1DM (6% have CD)
Autoimmune thyroid disease (2.4% have CD)
Downs (3%)
Turners 45XO (5%)
135
Testing for CD
IgA tTG and total IgA.
If weakly positive, can do IgA endomysial antibodies
If raised, refer to GI for diagnosis confirmation by biopsy, only then start gluten free diet.
Yearly FU.
Needs to include FRAX assessment as CD is secondary case of OP. Also height weight, symptoms, bloods.
May get splenic dysfunction and require additional vaccines.
136
Levator ani syndrome
Chronic rectal pain without identifiable cause.
137
Rational approach to prescribing laxatives in adults
1. First line ischagula husk with adequate hydration.
2. If stool hard - switch to macrogol eg movicol
3. If stool soft but difficult to pass - stimulant.
Naloxegol has been approved for opioid induced constipation in those not responding to laxatives, but limited clinical role as expensive ++
NB most constipation idiopathic but think about drugs that might be causing, exclude cancer.
138
Viral gastroenteritis
Incupation period 1-3d. Usually self limiting, recovery in 2-5d.
Only need bloods if suspecting diverticulitis or IBD, or if on renotoxic drugs and wanting to check kidney function.
Rotavirus and norovirus most common.
139
When to send a stool culture in suspected gastroenteritis
Systemically unwell, blood pus or mucus in the stool, recent hospitalisation or antibitoics, foreign travel in past 3 weeks, immunocompromised, persistent diarrhoea or malabsorption.
Also for public health reasons (eg food handler), and to investigate outbreaks.
Give info ++ on form to guide what tests lab will do.
140
Managemnt of uncomplicated gastroenteritis
Rehydration advice
Stop nephrotoxic drugs
Maybe probiotics (not if immunocompromised!)
Some may get post infectious IBS.
May get reactive arthritis after salmonella, yersinia or shigella infection.
141
What to do if stool culture grows E coli 0157
Admit for IV fluids and renal monitoring
Do not prescribe antibiotics.
(can cause severe pain, bloody diarrhoea, kidney failure) - causes HUS.
142
Which diarrhoeal illness are notifiable to public health
Infectious bloody diarrhoea
Food poisoning
HUS (e coli 0157)
Chlorera
Enteric fever (typhoid/paratyphoid).
143
Rare sequelae of campylobacter infection
Guillain - Barre syndrome.
Occurs about 2 months after infection.
Very rare.
Acute progressive polyneuropathy and life threatening complications.
144
Symptoms of diverticular disease
Tenderness LLQ and/or
intermittent LLQ pain with constipation/diarrhoea/occasional large rectal bleeds (!).
May get pain in other locations, especially if asian origin.
Pain may be caused by eating and relieve by passing stool.
Need imaging with flexisig, colonoscopy or CT colon (most of these people will meet criteria for FIT so may be referred for high FIT).
145
MX diverticular disease
Lifestyle - including high fibre diet. and usual lifestyle things.
Px bulk forming laxative. analgesia, antispasmodics. Not antibiotics if no diverticulitis.
146
When to suspected acute diverticulitis
Constant severe abdo pain usually LLQ with any of fever, sudden change in bowel habit with significant bleeding or mucus, or LLQ pain/abdo mass or distension in someone with known diverticular disease.
Remember RLQ tenderness if asian population.
147
Management of diverticulitis
Admit to hospital if complicated for any reason.
If managing in the community, no antibiotics needed if systemically well, no comorbidities and normal immune system.
If unwell but not meeting criteria for admission (or immunosuppressed or comorbidities but well) - then give antibiotics - co-amox first line, trimethoprim and metronidazole second line.
148
new dysphagia
cancer pathway referal for oesophageal and gastric cancer if dysphagia any age.
Also if >55Yo with weight loss and any of upper abdo pain/reflux/dyspepsia.
149
Dysphagia to liquids or solids
If liquids easier - more likely structural lesion eg cancer.
If solids easier than liquids - more likely vocal cord palsy (can be secondary to cancer), Achalasia.
150
What is globus
Sensation of lump when swallowing saliva but usually settled when eating or drinking, will not cause difficulty swallowing.
151
What virus increases risk of oropharyngeal cancers?
HPV 16 18.
152
Neurological causes of dysphagia
very common with dementia, stroke, MND, parkinsons, MS - thickening fluids may help.
SALT team key for assessment.
Dieticians help with nutritional intake.
153
Commonest route of transmission of hep C globally
Injecting drug use
Unsterline healthcare practices.
Can also be sexual or vertical transmission.
Test everyone raised transaminases, and those who are at risk for other reasons (if risks continue, test yearly).
Hep C antibodies tell us if ever infected.
Hec C RNA tells us if active infection.
DAA given 8-12 weeks, effective for acute and chronic infection. Can get reinfection so ongoing screening may be required if remains at risk.
154
Diagnostic pathway for symptoms suggestive of IBD
First rule out cancer - FIT (if meeting criteria)
Next do other tests to rule out other conditions eg stool culture, FBC CRP, coeliac, U&E, bone profile, TFTs, CA125. Manage if abnormal.
Then do calprotectin - if more than 250 - IBD.
If less than 100, IBS. If 100-250, repeat in 2w (stop PPI NSAID aspirin if on any of them). Ideally all caprotectins should be repeated in 2 weeks but if significant symptoms refer just with 1.
Urgent gastro referral if more than 250. Routine if 100-250.
If calprotectin normal, and IBS diagnosis made in someone over 50, routine gastro referal. Or if calprotectin 50-100 still want routine gastro referal to ensure not missed.
NB: only do calprotectin if cancer is NOT suspected.
155
UC management
5-ASAs eg sulfasalazine, mesalazine - topically if proctitis, oral if more extensive. Oral steroids may be needed.
5-ASA topical or oral for maitenence. helps reduce risk of CRC.
DMARDS also option if repeat exacerbations, cannot wean steroids etc.
Oral ASA can cause renal complications so check U&E at baseline, 3 m and annually.
156
Crohns disease mx
Oral steroids for disease flares.
DMARDS and -mabs are used for unresponsive disease (all secondary care).
Maintenence
- smoking worsens crohns so advice to stop.
- CRC surveillance needed.
- maintenence treatment for some not all.
- surgery for strictures/fistulas/other complications.
156
What is microscopic colitis
Inflammatory bowel disease with normal macroscopic bowel but microscopic inflammation (therefore need biopsy for diagnosis!)
Causes watery diarrhoea
Associated with drugs such as aspirin, PPIs, NSAIDs, SSRIs and statins - much higher risk if on these drugs.
Smoking also risk factor.
157
Complications of IBD
Anaemia - IDA and non IDA.
Osteoporosis.
Vit D calcium - check in all and supplement if low.
Malnutrition - monitor BMI, refer to dietician if required. Do bloods for nutritional deficiencies.
CRC - see screening
158
What anaemia should be offered a FIT
IDA in any age
Any anaemia in someone over 60.
159
When to screen for CRC in IBD
Colonoscopic surveillance after 10 years if UC or crohns involving more than 1 segment of colon.
Start from diagnosis if PSC.
Secondary care decide how often to do colonoscopies.
160
Diagnosis of IBS
Rare to diagnose in over 50. Make sure to exclude CRC and ovarian cancer before doing so.
FIT first line for most.
All should have FBC coeliac, CRP, ESR, likely faecal calprotectin.
If CA125 more than 35, urgent USS abdomen/pelvis and 2WW referal if abnormal.
If all above normal, make positive diagnosis of IBS using diagnostic criteria.
need abdo pain discomfort relieved by defication or associated with change in stool frequency or form and at least 2 of altered stool passage, abdo bloating/tension/hardness, symptoms worsened by eating, passage of mucus.
Consider microscopic colitis if chronic watery diarrhoea, especially if female over 50 other autoimmune or nocturnal symptoms.
161
Mx of IBS
Lifestyle
low fodmap for 4-8 weeks BUT then introduce.
CBT
Medications
antispasmodics for pain
laxatives if constipation - bulk forming, then macrogol.
Loperamide if antimotility required.
Tricyclic antidepressants second line - amitriptyline has most evidence.
SSRIs third line.
162
When to do admission/urgent referral for suspected liver disease
Suspected cancer, ascites, jaundice, encephalopathy, sepsis, abnormal clotting, haematemesis, low albumin/platelets, rapid deterioration or ALT or ALP more than 5 times ULN.
NB degree of derangement of ALT does not correlate to degree of lvier pathology so consider investigation even if mildly raised.
163
Causes of raised ALT
Alcohol
metabolic syndrome
Drugs - tetracyclines, amiodarone, tamoxifen, oestrogens, valproate, carbamazipine, macrolides, nitrofurantoin, statins, terbinafine, methyldopa, methotrexate.
Viral hepatitis
genetics - haemochromatosis or liver disease
Autoimmune.
164
Causes of raised ALP
Marker of cholestasis, also check GGT and bilirubin
ALP also raised in bone pathology, vit D deficiency, metastatic cancer, and pregnancy.
If GGT normal consider non GI causes
165
Initial tests if deranged LFTs
Liver function - bili alb ALT AST GGT FBC ferritin transferrin.
Liver autoimmune screen
Abdo USS
If raised ALT - also hepatitis screen, HbA1c.
NB: AST:ALT ratio >1 suggests advanced fibrosis/cirrhosos, in alcoholic hepatitis often >1.5.
alcoholic liver disease and MASLD may be able to be managed in primary care, if hepatitis or autoimmune or unsure, refer.
166
Autoimmune liver screen results
Autoimmune hepatitis
AST ALT and/or IgG raised
ANA and SMA positive
PBC:
ALP GGT IgM raised
AMA or ANA usually positive
PSC
ALP and GGT raised
ANA or SMA may be positive.
167
Most common cause of unconjugated bilirubinaemia
Haemolysis or gilberts
168
What is Gilberts
Unconjugated hyperbilirubinaemia due to defect in liver enzyme needed for conjugation.
Blood film Hb and retic and clotting should be normal.
Urine dip no bili as unconjugated is not water soluble.
If Gilberts suspected, dont need USS abdomen, make diagnosis.
Jaudnice more liekly if stressors.
May present with painless non pruritic jaudnice, or raised bilirubin on LFT.
Benign condition (not disease).
No treatment required.
169
Causes of conjugated bilirubinaemia
Intra hepatic or extrahepatic
Drugs
Infections
Obstruction - gallstones, strictures, malignancy NB jaundice in over 40YO if USC for pancreatic cancer.
Malignancy - liver, cholangiocarcinoma, pancreatic, lymphoma, biliary tract.
Hepatocellular disease such as ALF MASLD autoimmune.
Sarcoidosis
Metabolic eg wilsons (Cu) haemochromatosis.
170
How to investigate liver damage with alcohol excess (>50U/w men or >35u/w women for several months)
Offer fibroscan - if raised, refer gastro.
If normal, repeat scan in 3-5yrs if continues to drink to excess.
NB: if not meeting criteria for fibroscan (not excessive enough but still high) - can do AUDIT to guide level of alcohol harm, higher scores get ALF test or fibroscan and refer if abnormal. Lower scores can get brief alcohol intervention, check GGT and review in 3 months. Refer to alcohol services if consent.
171
How to screen for alcohol use disorders
Can use AUDIT -C short initial questionnaire.
If score is more than 5, proceed to full AUDIT.
172
Should we screen for MASLD?
No
So look for it in those with deranged ALT AST or scan suggesting fatty liver.
173
What is dupytrens contracture
Contracture of longitudinal palmar fascia. Typically starts as painless nodules.
Can occur with alcohol excess but is not a marker for fibrosis.
Commoner in men over 60.
174
Management of alcoholic liver disease
Stop drinking alcohol
If cirrhosis - input from secondary care and screening for oesophageal varices and hepatocellular carcinoma.
Rarely liver transplant is an option.
175
Common causes of cirrhosis
ALD
MASLD
Hep B and C
These may co exist eg most people with alcoholic liver disease also have cardiometabolic risk factors.
Less common autoimmune, gentic, drugs, biliary atresia, vascular causes.
176
Symptoms of decompensated cirrhosis
No symptoms of compensated cirrhosis.
If decompensated, ascites, hepatic encephalopathy, varices, GI bleeding, jaundice (will be conjugated).
Decompensation may be gradual or sudden.
If one of the common causes of cirrhosis, up to 20% will develop cirrhosis over 20 years - mostly diagnosed late with complication such as ascites or variceal bleed.
Of all liver diseases, risk of decompensation highest with ALD.
Need same day admission or urgent referal to hepatology depending on presentation.
Mean survival from diagnosis of decompensation is 2 years.
177
What US findings would be suggestive of portal hypertension
Splenomegaly, portosystemic collaterals and ascites.
178
Cirrhosis management
Nutrition exercise and BMI monitoring
Immunizations - flu, pneumococcal, COVID, hep A and B.
HCC surveillance USS 6 monthly.
Primary prevention of decompensation
- ?beta blocker (secondayr care decision)
Upper GI endoscopy for varices surveillance 3 yrly (if on B blocker do not need this).
179
Manegment of oesophageal varices
B blocker, or endoscopic variceal band ligation.
180
Symptoms of hepatic encephalopathy
Early symptoms apathy, personality change, inapproprite behaviour, disorientation, flapping tremor. then bizarre behaviours, gross confusion, somnolence, coma.
2 in 3 die within yr.
Manage with lactulose.
AKT
flashcards
Decks in class (33)
# Cards
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GI - done183
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Neurology - done128
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Cardiology167
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Occupational Health5
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Diabetes63
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Urology7
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Rheum - done110
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MSK - done93
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Paeds215
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Pharmacology62
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Infectious Diseases37
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Opthalmology - done91
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Dermatology - done111
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Misc2
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Womens Health116
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Psych65
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Environment1
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Respiratory89
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DVLA - done31
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Renal46
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Endocrinology23
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Haematology132
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Management - done95
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Contraception6
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elderly13
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palliative care29
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urology98
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allergy27
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ENT86
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cancer34
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stats29
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Gum37
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Drugs and alcohol3
