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YOU BETTER WERK > GIT/Hepatology > Flashcards

GIT/Hepatology Flashcards

1
Q

What HLA is associated with coeliac disease?

A

HLA DQ2 HLA DQ8

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2
Q

What are two rashes associated with IBD?

A

Pyoderma gangrenosum (painful ulceration) Erythema nodosum (painful lumps)

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3
Q

What single symptom with ongoing diarrhoea is a key indicator of inflammatory bowel disease?

A

Waking to pass stools overnight

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4
Q

Which form of IBD is smoking protective against?

A

Smoking is protective against ulcerative colitis Smoking is a risk factor for Crohn’s and associated with more severe disease

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5
Q

Faecal calprotectin

A
  • highly accurate at distinguishing between inflammatory bowel disease and irritable bowel syndrome - not medicare rebatable - FOBT is not useful in diagnosis of IBD - infectious diarrhoea can give a false positive calprotectin
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6
Q

What sinister diagnosis must be considered in patients with vomiting with bg of cancer?

A

Cerebral metastasis!

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7
Q

Which bowel disease is discolouration of teeth associated with?

A

Coeliac disease can cause loss of tooth enamel

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8
Q

Which bloods would you order in suspected Coeliac disease?

A
  • transglutaminase-IgA (tTg-IgA) - deamidated gliadin peptide-IgG (DPG-IgG)
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9
Q

Management of 1 out 3 positive FOBT?

A

Refer for colonoscopy

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10
Q

What is the most common adverse effect of azathioprine?

A

Leucopenia, anaemia and thrombocytopenia - hepatitis occurs infrequently

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11
Q

How common in non-specific abdominal pain in children?

A

5-10% of primary school aged children - present with severe episodes of abdominal pain, child is well between episodes, usually no impact on oral intake or bowel habit

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12
Q

Clinical manifestation of coeliac

A
  • malabsorption - abdominal symptoms - extra-intestinal symptoms: fatigue, rashes
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13
Q

What are some atypical presentations of coeliac disease?

A
  • iron deficiency - infertility - osteoporosis - headaches - lethargy - transaminase elevation - dermatitis herpetiformis - other autoimmune conditions
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14
Q

What are the eligibility for weight loss surgery?

A

BMI >40 or >35 with obesity related co-morbidity

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15
Q

Management for patients at “moderate risk of bowel cancer”

A
  • first degree relative diagnosed <55 or two first degree relatives - Q5yearly colonoscopy from 50-74 - Q2yearly FOBT from 40-49 - consider low dose aspirin 100-300mg daily for at least 2.5 years
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16
Q

How long should aspirin at minimum should aspirin be used to be prophylactic against bowel cancer?

A

For at least 2.5 years between 50-70

  • can consider even in patients without a family history of colorectal cancer
  • also may need to consider limiting processes meat consumption and limiting lean red meat to 455g per week
  • FOBT every 2 years ffrom 50-74
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17
Q

Clinical presentation of acute mesenteric ischemia?

A
  • acute onset abdominal pain
  • nausea and vomiting
  • associated with minimal abdominal signs
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18
Q

What vaccination is contraindicated in children with history of intussusception?

A

Rotavirus vaccination

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19
Q

What is the triad of ascending cholangitis?

A

Fever

RUQ tenderness

Jaundice

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20
Q

Spot diagnosis: painless jaundice + palpable gallbladder?

A

Malignant obstruction of common bile duct

“Courvoisier’s law”

50-70% of patients with periampullary cancer of the head of pancreas will have these findings

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21
Q

Causes of trismus?

A
  • acute and chronic TMJ disorders
  • oral infections
  • surgery
  • haematoma following dental injection
  • tetanus
  • acute dystonic reastion
  • oral firbosis
  • head and neck radiotherapy
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22
Q

Drugs use for inflammatory bowel disease

A
  • steroids
  • thiopurines (azathioprine, mercaptopurine)
  • methotrexate
  • ciclosporin
  • TNF inhibitors (adalimumab, infliximab)
  • anti-integrin antibodies (vedolizumab)
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23
Q

What pre screening must be done prior to starting immunomodulatory therapy for IBD?

A
  • screening for TB and hep B as these are the most common reactivations seen from immunomodulation
  • vaccination history + serology (live vaccines MMR, varicella, yellow fever, JE, BCH, rotavirus, typhoid, poilo) cannot be given to immunocompromised patients
  • need to ensure influenza and pneumoboccal vaccinations are UTD
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24
Q

TNF inhibitors

A
  • adalimumab, infliximab
  • need to be reviewed clinically every 3-6 months to check efficacy and adverse effects (especially infection)
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25
Q

Azathioprine and mercaptopurine

A
  • need baseline FBC, LFTs prior to starting
  • check FBC every week for first 4 weeks and then every 2 weeks and again at 12 weeks and every 3 months while on therapy
  • macrocytosis and lymphoenia are common side effects
  • assess LFTS every 3 months
  • need annual skin check
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26
Q

Methotrexate

A
  • commonly causes abnormal LFTs, especially if diabetic, obese, CKD, viral hepatitis or ETOH
  • hepatotoxicity correlates with total cumulative dose and manifests as fibrosis leading to cirrhosis
  • FBC, UEC, LFT monthly for 6 months and then every 1-2 months
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27
Q

Ciclosporin initiation and monitoring

A
  • FBC, EC, LFT, electrolytes, fasting lipis and BP at baseline
  • monitor as per specialist
  • annual skin check to detec early skin cancer is recommended
  • routine blood concentration monitoring is not generally required
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28
Q

Ulcerative colitis

A
  • chronic inflammatory condition confined to the mucosal layer of the colon
  • inflammatory changes are continuous and extend from rectus toward to the caecum
  • diagnosis is made by endoscopy and histology and in absence of infection
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29
Q

Initial therapy for active proctitis or distal colitis in UC?

A

Mesalazine rectal preparation

PLUS

5-aminosalicylate oral preparation

Note patients with isolated proctitis can be treated with suppositories alone if inflammation is limited to 20cm from anal verge

IF inaffective

  • add rectal steroids: budesonide/hydrocort/prednisolone
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30
Q

Name four 5-aminosalicylate preperations used in UC

A
  1. sulfasalazine
  2. mesalazine
  3. balsalazide
  4. olsalazine

2 different doses, first for induction and second for maintenance

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31
Q

Management for unresponsive active proctitis or distal colitis with UC?

A

Prednisolone 40-50mg (children 1-2mg/kg) daily until clinical response and then taper over 6-8 weeks

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32
Q

First line management for mild to moderate extensive ulcerative colitis

A

Oral 5-aminosalicylate +/- prednisolone if no response

(sulfasalazine: 2-4g daily initiation and 1-2g maintenance)
(mesalazine: 2-4.8g daily initiation and 1-3g maintenance)

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33
Q

Treatment of moderate to severe chronically active or frequently relapsing

A

Thioprine (azathioprine, mercaptopurine)

OR

TNF inhibitor (infliximab, vedolizumab)

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34
Q

What is the definition of acute ulcerative colitis?

A
  • in the presence of 6 or more blood stools/day plus at least one of the following
  • Temp > 37.8
  • HR >90
  • HB <105
  • ESR >30

** always need to exclude GIT infection i.e. Cdiff or CMV)

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35
Q

Rescue therapy in severe crohn’s flare

A

Hydrocortisone 100mg IV Q6H

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36
Q

Crohn’s disease

A
  • can effect any part of the GI tract
  • inflammation is often focal and trasmural
  • smoking is a risk factor and marker for severity
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37
Q

What is the first line induction treatment for mild to moderate Crohn disease?

A

40-50mg of prednisolone daily until clinical response and taper over 6-8 weeks

Note - induction therapy for severe crohn’s is IV hydrocortisone 100mg Q6H

If this isn’t working need to escalate to thiopurines or methotrexate and then consider TNF inhibitor (mab)

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38
Q

What are the first line agents for Crohn’s maintenance/

A
  • azathioprine
  • mercaptopurine
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39
Q

Crohn’s considerations

A
  • smoking: should cease smoking
  • malabsorption: blie salt malabsorption, may require long term B12 supplementation
  • dietary measures: malnutrition is common in Crohn’s, low fibre diet with flares may be useful, lactose intolerance can occur in patients with diffuse small intestine disease
  • micronutrients at risk” zinc, iron, B12, calcium, magnesium, folic acid and vitamin D
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40
Q

Fertility, pregnancy and IBD

A
  • recommended patients delay pregnancy until remission
  • active disease at time of conception increases risk of persistent disease during pregnancy
  • no evidence that drugs used in management if IBD affect fertility
  • potential harm of steroid use in pregnancy is much less that that of untreated IBD
  • 5-aminosalicylates are consider safe in pregnancy
  • silfasalaze can cause oligospermia and reduce sperm motility
  • methotrexate is contraindicated in pregnancy, need to wait 3 months before conception
  • thiopurines are cat D however not associated with risk of congenital abnormality
  • if immunomodulators are used shoudl not give the bub a live vaccine for the first 12 months of life
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41
Q

Does IBD predispose to oestopenia or osteoporisis?

A

YES!

Need to be screened and monitored for same

  • aim for 1000-1300mg calcium daily
  • advise general preventative measures: regular weight baring exercise, calcium, cease smoking and reduce excessive ETOH
  • if starting systemic steroids measure BMD and given vitamin D + calcium supplements
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42
Q

What is the most common systemic complication of IBD?

A

Iron deficiency anaemia

  • parenteral iron is preferred
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43
Q

Indications for gastroscopy in suspected GORD

A

Red flags:

  • anaemia, dysphagia, odynophagia, haematemesis, melaena, vomiting, weight loss
  • new symptoms in older person
  • changing symptoms
  • severe/frequent symptoms
  • indaquate response to treatment
  • diagnostic clarification
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44
Q

Non-pharmacological management of mild GORD

A
  • weight loss
  • eating smaller meals
  • drink fluids mostly between meals rather than with meals
  • avoid lying down after eating
  • avoid eating dinner for 2-3 hours before bed or exercise
  • elevate the head of the bed at night
  • stop smoking!
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45
Q

First line medical management of mild GORD

A
  1. Antacid
  2. H2 receptor OR PPI

Standar PPI doses

  • esomeprazole 20mg daily
  • omeprazole 20mg daily
  • pantoprazole 40mg dialy
  • rabeprazole 20mg daily
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46
Q

What is defined as “frequent” GORD symptoms?

A

2 or more episodes a week

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47
Q

How long should initial treatment course of PPI go for?

A

4-8 weeks and if symptom control is adequate can step down to maintenance therapy

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48
Q

What is GORD maintenance therapy?

A
  • aims to control symptoms and reduce complications from condition and treatment!
  • down titrate to PPI to lowest dose and frequency at which symptoms are controlled
  • stopping PPI can results in prolonged remission of symptoms in 30% of patients, however can possible cause rebound hypersecretion of acid

-

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49
Q

Potential risks of long and short term PPI use

A
  • interstitial nephritis (short term use)
  • hypomagnesaemia
  • increased risk of pneumonia
  • C diff and other GIT infections
  • impaired nutrient absorption
  • risk of fracture
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50
Q

Which anti-reflex rx is safe in pregnancy?

A

H2-receptor antagonists

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51
Q

GORD In children

A
  • may present with vomiting and regurg
  • common in infants and usually improves by 12 months
  • signs: FTT, oesophatitis, stricture, refusing to feed, recurrent pneumonia, anaemia, dental erosinons, apnoea, apparent life threatening events
  • GORD can be a symptom of allergy to cow milk protein, often irritable child with diarrhoea and can be difficult to feed
  • change of formula to non-dairy may help
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52
Q

Suggested formula for ? GORD In infants

A

Changing the type of formula (eg dairy to soy, or soy to protein hydrolysate) may be helpful if allergy is suspected. A 2- to 4-week trial of an extensively hydrolysed formula (eg Alfaré, Pepti-Junior Gold) or elemental formula (eg Neocate, EleCare) may be appropriate; these are only available on prescription

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53
Q

Barrett’s oesophagus

A
  • premalignant condition
  • metaplastic epitherlium replaced the stratified squamous epitherlium that normally lines the oesophagus
  • can be associated with strictures or oesophagitis
  • significantly increased risk of adenocarcinoma (75%)
  • should be under endoscopic surveillance
  • PPI therapy is effective for sx of oesophagitis
  • aspirin may be protective, studies are underway
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54
Q

Achalasia

A
  • degeneration of ganglia of nerves innervating the oesophagus
  • unclear cause
  • cardinal features: lack of relaxation of the LOS, aperistalsis of oesophageal body
  • causes dysphagia, regurgitation, chest discomfort/pain
  • management: laparoscopic myotomy, balloon dilation, botox injection
  • could trial nitrates and CCB in mild disease
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55
Q

Distal oesophageal spasm

A
  • can cause dysphagia and regurgitation
  • can also cause non cardiac chest pain
  • always exclude cardiac cause
  • may ebe precipitated or exacerbated by GORD
  • ingestion of warm water at onset of attack may help
  • rx: GTN may shorten attack
  • if frequent and disabling can consider nifedipine or diltiazem
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56
Q

Oesophageal food bolus

A
  • underlying causes: GORD, stricture, schatzki ring, esophagitis, spasm, cancer
  • 25-50ml carbonated drink
  • otherwise try a smooth muscle relaxant: GTN and or glucagon 1mg s/c or IV
  • if these measure fail patient may require endoscopic retrieval of bolus
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57
Q

Management of oesophageal candidiasis

A

Nystatin 100 000 units/ml

1ml Q6H for 10-14 days

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58
Q

In which group of patients is viral oesophagitis seen?1

A

Generally severely immunocompromised patients

  • present with dysphagia and odynophagia
  • causes: HSV and CMV
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59
Q

What percentage of aussies have H pylori?

A

30%

Migraines, low SES, institutionalised and elderly patients have a higher prevalence

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60
Q

H pylori risks

A
  • PUD 15-20%
  • gastric cancer up to 2%
  • associated risk with gastric MALT lymphoma (though uncommon)
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61
Q

H pylori and peptic ulcer disease

A
  • most duodenal ulcers are due to HP
  • 2/3 of gastric ulcers can be attributed to HP also
  • NSAIDs are the most common cause of other ulcers
  • rare causes = Zollinger-Ellison syndrome, Crohn disease and viruses
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62
Q

What is the most common presentation of PUD?

A
  • epigastric pain or discomfort
  • may be accompanied by associated nausea, vomiting and heart burn
  • ulcer is more likely if there is a remitting and relapsing course with noctural waking with epigastric pain
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63
Q

Management of PUD

A
  • If uncomplicated can be treated by HP eradiction alone
  • if complicated or NSAID related will need to have ongoing PPI therapy for 8 weeks
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64
Q

Why should H pylori be excluded prior to empircal PPI?

A

Gastritis/PUD/GORD have a lot of overlap, difficult to tell based on clinical picture without endoscopy.

If not ruling out HP unable to eliminate the ongoing risks of PUD and gastric cancer

Also long term use of PPI in patients with HP accelerates the progression of adverse gastric mucosal changes.

Hence should always test and treat H pylori before starting long term PPI!

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65
Q

What is the “test and treat” strategy for dyspepsia?

A
  • non invasive HP testing and eradication
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66
Q

What is the test of choice for H pylori diagnosis?

A

C13/14 urea breath test

  • C13 is not radioactive and preferred for women of childbearing age

Serology has lots of false positive and false negatives

Need to ensure that antiboitics therapy should not be taken for at least 4 weeks and PPI should be withheld for 1 week (preferrably 2 weeks) prior to breath test

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67
Q

How is H pylori eradication confirmed?

A

Repeat U13/14 urea breath test at least 4 weeks AFTER therapy (again need to w/h PPI for at least 1 week)

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68
Q

What are the indications for H pylori eradication?

A
  1. PUD past or present
  2. dyspepsia
  3. selected NSAID users
  4. atrophic gasrtitis
  5. patients requiring long term PPI
  6. high risk of gastric cancer
  7. low grade gastric MALT lymphoma
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69
Q

What are the benefits of H pylori eradication?

A
  • heals ulcer and reduces relapses
  • may reduce symptoms and long term risk of PUD and cancer
  • reducses risk of PUD and gastric bleeding
  • reduces long term risk of gastric cancer
  • reduces progression of intestinal metaplasia
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70
Q

What is first line management for H pylori eradication

A
  • esomeprazole 20mg BD for 7 days
  • amoxicillin 1g BD for 7 days
  • clarithromycin 500mg BD for 7 days

Success rate of above is 85-90%

Most common cause for failure is HP resistance to clarithromycin

Adverse effects: taste disturbance, nausea and loose stools

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71
Q

What is the recommended H pylori eradication regimen for patients with allergy to penicilin?

A
  • esomeprazole 20mg BD for 7 days
  • metronidazole 400mg BD for 7 days
  • clarithromycin 500mg BD for 7 days
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72
Q

Risk factors ofr NSAID GIT bleed or perforation

A
  • older age
  • history of upper GIT bleed
  • history of PUD
  • H pylori infection
  • concomitant drugs (anticoagulants, antiplatatlelts, SSRIs, SNRIs and corticosteroids)
  • significant comorbidity
  • smoking
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73
Q

How many patients on NSAIDs have ulcers on endoscopy?

A

15-30%

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74
Q

Which NSAIDs carry the highest ulcer risk?

A
  • NSAIDs with long hald lices r.e. piroxicam
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75
Q

Which NSAIDs are safest from an ulcer point of view?

A
  • COX2 selective NSAID (celecoxib) reduce thr risk of ulcer disease
  • however concomitant aspirin negates this effect!

-

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76
Q

Factors influencing management choices to minimise CVD and GIT risks of NSAID use

A

4 groups

  1. Low GIT risk, low CVD risk (non selective NSAID)
  2. high GIT risk, low CVD risk (COX2 or non selective + PPI)

TEST AND TREAT H PYLORI

  1. low GIT risk, high CVD risk on aspirin (non selective NSAID)
  2. high GIT risk, high CVD risk on aspirin (avoid OR non selective NSAID + PPI)
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77
Q

Management of bleeding peptic ulcer

A
  • prompt endoscopy
  • PPI infusion: pantoprazole 80mg IV over 15-30min, then 8mg/hour for up to 3 days (or 40mg pantop Q12H)
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78
Q

Which patients need prophylactic PPI to prevent stress ulcers?

A
  • patients with > 30% TBSA burns
  • severely ill patients with coagulopathy
  • mechanical ventilation > 48 hrs
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79
Q

Autoimmune gastritis

A
  • associated with autoantibodies to parietal cells and intrinsic factor
  • causes glandular mucosal atrophy reducing secretion of acid and intrinsic factor
  • reduction of acid leads to impaired iron absorption
  • reduction of intrinsic factor reduces B12 absorption
  • often asymptomatic, may develop pernicious anaemia as a result
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80
Q

Common anti-emetics and their actions/dosing

A

Multiple neural pathways targetted: dopaminergic, serotonergic, histaminergic, cholinergic, neurokinin and cannabinoid

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81
Q

First line management of hyperemesis gravidarim

A
  • usually begins around week 6 and resolves around 14 weeks
  • non pharm: small frequent meals, high carb, low fat, change to multivitamin without iron, hydration, high protein snacks, plain biscuits/crackers mane, avoid spicy and strong odours
  • pyidoxine 12.5mg mane, midday and 25mg nocte PLUS
  • doxylamine 2mg nocte, increase as tolerated to 12.5mg mane, midday and 25mg nocte
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82
Q

Second line management of hyperemesis in pregnancy

A
  • metoclopramide (cat A)
  • ondasetron (cat B)
  • prochlorperazine (cat C)
  • promethazine (cat C)
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83
Q

Management of chronic idiopathic nausea and vomiting

A
  • reflux is underdiagnosed cause of nausea
  • consider trialing acid suppression
  • may consider low dose TCA or anxiolytic drugs and CBT in refractory cases
  • alternatively consider mitrazapine for patients with poor appetite and weight loss
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84
Q

Functional dyspepsia

A
  • epigastric pain/burning, early satiety and or discomfort after meals
  • symptoms present for > 6 months
  • with appropriate investigation to rule out structural and metabolic causes
  • epigastric burning = PPI
  • bloating/discomfort = domperidone 10mg TDS before meals
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85
Q

Gastroparesis

A
  • bloating, epigastric fullness, early satiety, nausea and vomiting
  • common causes: diabetes, thyroid disease, chronic renal failure, oesophagitis, scleroderma, upper GIT surgery
  • may need to try prokinetic (domperidone 10mg TDS prior to meals)
86
Q

Irritable bowel syndrome

A
  • altered bowel motility, visceral hypersensitivity, psychological factors may all contribute to symptoms
  • abdominal pain associated with change in bowel habit over extended period of time
  • may experience faecal urgency, need to strain, incomplete evacuation, abdominal bloating, passage of mucus
  • increased prevalence of other disorders (dyspepsia, urinary frequency, headaches, dysmenorrhoea, dyspareunia, fibromyalgia, anxiety and depression)
87
Q

Diagnosis of irritable bowel syndrome

A
  • ROME III Criteria
  • abdominal pain or discomfort occurring at least 3 days pero month for last 3 months, associated with at least 2 of the following
    a) improvement after defecation
    b) onsent symptoms associated with change in bowel frequency
    c) onsent of symptoms associated with change in stool appearance

Subtype: diarrhoea type, constipation type, mixed type

88
Q

What investigations should be performed in suspected cases of IBS?

A
  • FBC, coeliac serology, CRP, faecal calprotectin
89
Q

Management of IBS

A
  • explore and avoid triggers (common triggers: caffeine, alcohol, carbonated drinks, fatty food, fibre, lactose, wheat)
  • adequate fibre intake ~25g females and ~30g males
  • ensure hydrated
  • low FODMAP diet (fermetable oligosaccharides, disaccharides, monosaccharides ad polyols)
90
Q

Acute pancreatitis

A
  • lipase x 3 ULN
  • central epigastric pain which radiates to back
  • generally triggered but excessive ETOH, gaslltones or idiopathic
  • can be induced by drugs: azathioprine, ?DPP4
91
Q

Management of acute pancreatitis

A
  • IVF, analgesia + NBM
  • antibiotics are generally not indicated
  • risk factors for severe pancreatitis: age > 55, obesity, comorbidities, altered mental status, persistent SIRS
  • may need ICU
  • NGT, early enteral nutrition or parenteral, treatment of hyperglycaemia, treatment of symptomatic hypocalcaemia
92
Q

Causes of pancreatic exocrine insufficence

A

Cystic fibrosis

Chronic pancreatitis

Pancreatectomy

  • need oral enzyme supplemet to digest and absort fat, protein and starch
93
Q

Most common cause of autoimmune pancreatitis

A
  • manifestation of systemi immunoglobulin (IgG4) related disease
  • abdominal pain, jaundice, weight loss
94
Q

What does SIBO stand for?

A

Small intestinal bacterial overgrowth

  • caused by strep, bacteroides, e coli, lactobacillus
  • causes bloating, diarrhoea, weight loss, anaemia du eto B12 deficiency
  • usually associated with intestinal stasis due to anatomical abnoormalities (chronic pancreatitis, cirrhosis, scleroderma, immunocompromise)
95
Q

Coeliac disease

A
  • small bowel autoimmune disorder
  • abnormal immune response to ingested wheatgliadins (related proteins in ry, oats, barley) causing inflammation and tissue damage
  • 30-40% carry HLA DQ2 or HLA DQ8
  • 1:100 have coeliac disease
  • associated with: dermatitis herpetiformis, thyroid disorders, IgA deficiency, PBC, T1DM
  • 1:10 risk of first degree relative developing coeliac
96
Q

Screening for coeliac disease

A
  • antibody testing can be done if patient is eating gluten
  • igA anti-tissue transglutaminase and anti-deamidated gliadin antibodies tests are high sensitive and specific for coeliac disease
  • should use HLA testing in patients who have already started gluten free diet (can exclude coeliac if HLA negative)
97
Q

Management of coeliac disease

A
  • gluten free diet for life
  • avoiding foods containing wheat, rye , barley and oats
  • need to svreen for thyrodi disease and diabetes
98
Q

Short bowel syndrome

A
  • malabsorption disorder from extensive small bowel resection
  • symptoms: diarrhoea, fluid and electrolyte disturbances and malabsorption of nutrients
99
Q

Transient lactor intolerance

A
  • stools commonly remain loss for 1-2 weeks after episode of acute gastro
  • lactose intolerance can occur but is usually transient in infants and young children
  • frothy, watery and explosive stools shortly after drinking mild may indicate lactose intolerance
100
Q

Management of anal fissure

A
  • GTN 0.2% ointment
  • avoid hard stools
  • if chronic fissure need to r.o cancer/underlying cause
101
Q

Patients are risk of refeeding syndrome

A
  • BMI < 16
  • loss of more than 15% of body weight in 3-6 months
  • little to no nutritional intake for > 10 days
  • low potassium, phosphate or magnesium prior to re-introducting nutrition
102
Q

Management of refeeding

A
  • slow feeding, 30-50% of estimated caloric requirement
  • and gradually increase over 5-7 days
  • measure daily electrolytes (K, phos, Mg)
  • give thiamine before starting and for first 7-10 days
  • multivitamin daily for 7 days
  • need to monitor vital signs and in high risk patients (cardiac rhyth, oedmea, CCF, deteriorating mental state)
103
Q

Fat soluble vitamins

A
  • vitamin A
  • vitamin D
  • vitamin E
  • vitamine K

DAKE, DEAK, KEAD

104
Q

Water soluble vitamins

A
  • thiamine (B1)
  • pyridoxine (B6)
  • vitamin B12
  • folate
  • vitamin C
105
Q

What is the best measure of total body iron stores?

A

Ferritin

106
Q

Oral iron supplementation

A
  • elemental iron 100-210mg daily
  • children: 3-6mg/kg/day

An overdose of iron can be fatal for a child

107
Q

Pathophysiology of coeliac disease

A
  • gluten enteropathy
  • T cell mediation reaction
  • gluten: rye, wheat, barley and oats
  • cause distruction of the villous epitherlium in the small intestine
  • causes weight loss, failure to thrive, abdominal cramping, bloating, flatus, nausea, vomiting, muscle wasting, diarrhoea, steatorrhoea
108
Q

What other autoimmune disorders are commonly seen in association with coeliac disease?

A
  • Type 1 diabetes
  • thyroid
  • HLA gene association
109
Q

Diagnosing Coeliac disease

A
  • adequate gluten intake is necessary for 6 weeks before investigation (2 slices of wheat or rye bread/day)
  • serology: anti-tTG antibodies, anti-gliadine antibiodies IgA and IgG
  • sereology must be followed up with small bowel biopsy
  • changes on serology and biopsy should remiss if gluten free diet is maintained
110
Q

Diagnostic pathway for coeliac disease

A
  • if eating gluten –> coeliac serology

> if positive tTG and or DGP antibodies –> gastroscopy

  • if not eating gluten and unwilling –> HLA DQ2/8 genotyping

> if HLA negative Coeliac is unlikely

111
Q

When to consider testing for coeliac disease

A
  • classical symptoms: diarrhoea, weight loss
  • non classical symptoms: lethargy, headaches, osteoporosis, iron deficiency, transmeinase elevation, infertility, other autoimmune disease, dermatitis herpetiformis
  • a positive family history of coliac disease carries the strongest predictive value for the disease
112
Q

Tips and pitfalls of coeliac diagnossi

A
  • median age of diagnosis si 40
  • modest female predominance but men are often overlooked
  • clinical heterogenity is substantial
  • 1/3 of patients are overweight or obese at presentation
113
Q

Coeliac serology

A

= transglutaminase (tTG) and deamidated gliadin peptide (DPG) antibody tests

  • both have > 85% sensitivity and >90% specificity
  • the DGP has replaced the whole-protein anti-gliadin antibodiy assay (AGA)
114
Q

Tips and pit falls of coeliac serology

A
  • positive serology is NOT diagnostic on its own
  • the higher the titre of serology the greater the positive predictive value for coeliac disease
  • false negative rate of 10-15%
  • if still have risk factors for coeliac disease but negative serology still require further investigation
  • patients may have latent disease (positive serology but negative biopsy)
115
Q

Human leukocyte antigen genotyping in coeliac disease

A
  • HLA DQ2 and HLA DQ8 are commonly linked
  • these HLAs are seen in 99% of coeliac cases but only 40-50% of the wider community
  • HLA genotyping has benefit in its ability to exclude coeliac disease diagnosis (if negative <1% likelihood of coeliac disease)
  • however positive HLA does not diagnose!

(like d-dimer)

  • expensive to order on medicare, only can be ordered once!
116
Q

When to test for coeliac disease

A
  • persistent unexplained abdominal symptoms
  • fattigue
  • unexpected weight loss
  • severe or persistent mouth ulcers
  • unexplained vitamine B12 or folate deficiency
  • type 1 diabetes (at diagnosis)
  • autoimmune thyroid disease (at diagnosis)
  • IBS
  • first degree relatives of peple with coeliac disease
117
Q

Gluten challenge in ?coeliac disease

A
  • need to consume 3-6g of gluten for 2 weeks to cause intestinal changes in 50-70% of coeliac patients
  • to optimise yield need to have 3-6g for ideally at least >6 weeks
  • 2 -4 slices of bread, 2-4 weetbix or 0.5-1 cup of cooked pasta
118
Q

“How to not miss IBD”

A
  • when diagnosing IBS think, could this be IBD?
  • beware of symptoms suggestive of gastro which continue or worsening after 4 days
  • think of IBD if abdominal symptoms and signs of inflammation
  • think of IBD for unexplained abdominal pain
  • rectal bleeding ALWAYS needs investigation
119
Q

Signs and symptoms of IBD

A
  • rectal bleeding
  • weight loss
  • abdominal pain
  • fever
  • nocturnal symptoms
  • pallor
  • tachycardia
  • elevated CRP, WCC, ESR
120
Q

Mesalazine

A
  • key drug for ulcerative colitis
  • 5 aminosalicylic acid (5-ASA)
  • oral and rectal preparations
  • reduce chance of relapse by 2/3
121
Q

Stepwise management of ulcerative colitis

A
  • 5-ASA
  • steroids
  • immunosuppression
  • surgery
122
Q

Management in crohn disease

A
  • cease smoking
  • 5-ASAs not useful
  • thiopurines first line
  • steroids
  • antibiotics for complications and to reduce inflammation
  • other immunosuppression forms (TNF inhibitors)
123
Q

IBD and colorectal cancer

A
  • increased risk
  • need to ensure some forms of surveillance
  • patients with UC involving at least the LEFT colon = second yearly conoscopy with multiple biopsies after 7-10 years of the disease
124
Q

UC vs CD

A
125
Q

Montreal classification of CD and UC

A
126
Q

Describe the required physical examination in IBD

A
  • general: vitals, BMI, pallor
  • abdominal examination
  • perianal examination
  • oral inspection
  • extra-intestinal manifestations: eyes, skin joints
127
Q

Investigation of IBD

A
  • Blood: FBC, biochem, iron studies, CRP/ESR, coeliac testing
  • Faecal: calprotectin (great for differentiating between IBD/IBS)
128
Q

What is faecal calprotectin used for?

A
  • assist in differentiation between IBD and IBS
  • can also be used to monitor level of inflammation in patients with established IBD
129
Q

Adverse effects of prolonged steroid use in IBD

A
  • weight gain
  • osteonecrosis
  • suspectibility to infection (usually if > 25mg for > 2 weeks)
  • acne, facial hair
  • HTN
  • glucose intolerance/diabetes
  • sleep and mood distrubance
  • dyspepsia
  • prolonged use: cataracts, oesteoporosis, myopathy
130
Q

What is the australian recommended intake for:

a) calcium
b) vitamin d

A

a) calcium: 1000mg/day for men and premenopausal women and 1300mg/day for men>70 and women > 51
b) vitamin D levels should remain above 50nmol/L

131
Q

Bone health with IBD

A
  • need to aim to prevent osteoporosis in IBD
  • avoid excess ETOH, stop smoking, regular weight baring exercise, good nutrition, avoid steroids as much as possible
  • if known reduced BMD or on steroids should also be on vitamin d and calcium supplementation
  • DCA: osteoporosis is T score of less than -2.5
132
Q

Vaccination in IBD

A
  • influenza and pneumococcal recommended
  • live vaccinations can be used in patients who are only on 5-ASA (not immunmodulators)
133
Q

What are the 6 live vaccines that should be avoided if patients are immunomodulated in IBD?

A
  • oral polio
  • MMR
  • typhoid
  • yellow fever
  • varicella
  • BCG
134
Q

Management of IBD in pregnancy

A
135
Q

Assessment of patients with abnormal LFTS

  • history, examination, investigation
A

History: medications, recreational drugs, OTC, ETOH, risk factors for nonalcoholic fatty liver disease, risk factors for syphilis and viral hepatitis

Examination: BMI, waist circumference, stigmatal of CLD

Investigation: FBC, LFT, INR

136
Q

Red flags associated with deranged LFTS

A
  • signs of synthetic dysfunction: jaundice, low albumin, elevated INR
  • hepatic encephalopathy
  • suspected malignanct (weight loss, marked cholestasis)
137
Q

Assessment of incidental liver lesions: red flags

A
  • systemic symptoms: weight loss, fatigue
  • risk factors for malignancy: advanced age, smoking
  • history of malignancy
  • features suggestive of primary malignancy at another site
  • history of cirrhosis
  • chronic hep B
  • FHx of hepatocellular carcinoma
  • enlarging liver lesions on scans
138
Q

Investigation of suspicious liver lesiosn

A
  • FBC, biochemistry, INR, hep B and C serology
  • CT liver
  • tumour markers: AFP, CA19.9 and CEA
139
Q
A
140
Q

When ordering hep B and C serology what should you request?

A

HEP B: HBsAG, anti-HBs, anti-HBc

HEP C: HCV antibody and if positive HCV RNA

141
Q

Overview on viral hepatitis

A
  • symptoms: fatigue, fever, anxorexia, nausea, vomiting, abdominal pain, jaundice, raised LFTs
  • causes: hepatitis a/b/c/d/e, EBV, yellow fever
  • other infections: lepto, syphilis
  • non infective causes: autoimmune, drugs, wilson’s
142
Q

Clinical features of hepatitis A –> E

A
  • acute: hepatitis A and E but B/C/D all can present acutely
  • contaminated food/water = hepatitis A and E
  • blood borne infection = B/C/D
  • antiviral theapy = B/C/D
  • curable: hep C, hep A is self limiting
143
Q

What are the diagnostic tests for each hepatitis?

A

HEP A: HAV antibodies

HEP B: HBsAG, anti-HBc, anti-HBs

HEP C: HCV antibodies

HEP D: HDV antibodies

HEP E: HEV

144
Q

Heptitis A

A
  • acute viral hepatitis
  • does not progress to chronic hepatitis
  • most cases come from contaminated food or water
  • faecal oral route of transmission
  • vaccination or prior hep A exposure causes life long immunity
  • hep A vaccination is advice for anyone at high risk (travel, occupation, lifestyle, and patients with pre-existing liver disease)
  • time from exposure to manifestation of symptoms = 30 days
  • diagnosed by identifying HAV IgM or HAV RNA in stool PCR
  • management is supportive
145
Q

Hep B vaccination

A
  • 4 dose schedule: at birth, 2, 4 and 6 months
  • effective response to vaccination = anti-HBx antibody titre >10
  • if has documented titre > 10 even if this wanes the person is considered to have memory immunity (booster vaccination is not needed for these people)
146
Q

What hep B serology results woudl you expect in someone who has been immunised against Hep B?

A

Hep B surface antigen: negative

Anti Hep B surface antigen antibody: positive!

Hep B core antibodiy: negative

147
Q

What do the following hep B serology results mean?

A) HBsAG

B) anti-HBsAG

C) anti-HBc

A

A) Hep B surface antigen: active infection (acute or chronic)

B) Hep B SA antibodies: immunity (vaccination or infection)

C) Hep B core antibody: infection (past or current)

148
Q

What serology would you expect to see in…

A) susceptible patient

B) resolved HBV

C) vaccinated

D) acute HBV infection

E) chronic HBV infection

A

A) HBsAG: negative, anti-HBs: negative, anti-HBc: negative

B) HBsAG: negative, anti-HBs: positive, anti-HBc: positive

C) HBsAG: negative, anti-HBs: positive, anti-HBc: negative

D) HBsAG: positive, anti-HBs: negative, anti-HBc: positive
(anti-HBc IgM high titre)

E) HBsAG: positive, anti-HBs: negative, anti-HBc: positive
(IgM negative for anti-HBc)

149
Q

How can you differentiate chronic vs acute HBV on serology?

A

Acute: high titre IgM anti-HBc

Chronic: negative IgM anti-HBc

150
Q

In what states will HBsAG be positive?

A
  • acute and chronic hepatitis B infections
  • will be negative if only exposure is through vaccination and negative in resolved cases
151
Q

What does positive anti-HBs infer?

A

Vaccination or resolved hepatitis B

152
Q

When is hepatitis D most commonly seen?

A

In conjunction with hepatitis B

  • all patients with hep B should be tested for hep D
153
Q

Aim of management of chronic hepatitis B

A
  • aim of treatment is to suppress viral replicated (indicated by undetectable HBV DNA)
  • this reduces necroinflammation and liver fibrosis with aim to reduce progress to liver failure and HCC
154
Q

What are the phases of chronic HBV?

A
  1. Immune tolerance: HBeAG positive
  2. Immune clearance: HBeAG positive
  3. Immune control: anti-HBe positive
  4. Immune escape: anti-HBe positive
155
Q

Management approach to each HBV phase

A
  1. Tolerance: monitor for progression to clearance
  2. Clearance: consider anti-viral rx, goal is HBeAG seroconversion which is usually associated with remission
  3. Control: monitor for progression to escape (monitor LFTs and HBV DNA)
  4. Escape: consider antiviral therapy if ALT and HBV DNA are high, usually treatment is lifelong at this stage

Cirrhotic patients with HBV DNA detectable should be started on anti-viral rx lifelong

156
Q

Characteristics of antiviral drugs for chronic hepatitis

A
  • entecavir
  • tenofovir
  • peginterferone alfa-2a
157
Q

Duration of antiviral therapy for chronic hepatitis B

A
  • entecavir or tenofovir - atleast 12 months after HBeAG seroconversion or long term (until HBsAG lost)
  • peginterferon alfa-2a: 48 weeks but not recommended with cirrhosis with detectable HBV DNA
158
Q

Surveillance for HCC in patients with chronic HBV

A

6 monthly liver US and AFP is recommended for patients at risk:

  • cirrhosis
  • first nations > 50 years of age
  • asian males > 40, asian females > 50
  • African patients > 20
  • patients with family history of HCC
159
Q

Hep B and HIV co infection

A
  • patients with HIV have higher prevalence of chronic HBV
  • co-infection is associated with more rapid progression of fibrosis and complications i.e. HCC + liver failure
  • should be treated with antiretroviral therapy
  • an acute flare of hep B can occur if antiretroviral drugs active againts hep B are stopped
  • co-infected patients who are not on antiretrovirals shouldn’t be treated with HBV antivirls as this can causes drug resistant HIV
160
Q

Hepatitis B and pregnancy

A
  • most antiviral drugs for chronic HBV are class B3 in pregnancy
  • tenofoir is recommended in pregnancy (nil increased risk for mothers or infants in pregnancy)
  • should continue antiviral treatment while pregnant due to risk of severe flare if rx if stopped
  • antiviral rx may be indicated to reduce risk of mother to child transmission
  • antibiral therapy is indicated in women with HBV DNA >200,000, shoudl be started at 28 weeks and continued until birth and maybe every 4-12 weeks after delivery
161
Q

Infants of hep b positive mothers

A
  • should be immunised for hep b at birth and given hep b immunoglobulin within 12 hours of birth
  • hep b is not an indication for LUSCS
  • all infants should be tests for HBsAg and anti-HBs after 9 months of age to ascertained whether transmission has occurred or immunity has been achieved
  • breastfeeding is not associated with higher chance of HBV in infants
162
Q

What are the aims of HCV treatment?

A
  • prevent cirrhosis, liver failure and HCC
  • prevent transmission of HCV
163
Q

Key steps in pretreatment assessment for HCV

A
  • confirm current HCV infection but checking HCV RNA
  • ascertain if treatment-naive or previously treated
  • assess for prescence of cirrhosis
  • consider if co-infection with hep b or HIV
  • review medications for potential interactions
  • consider pregnancy
  • consider if patient has decompensated liver disease
164
Q

What are the first line treatment options for treatment-naive adults with HCV?

A
  • glecaprevir + pibrentasvir for 8-12 weeks
  • sofosbuvir + velpatasvir for 12 weeks

Monitoring - nil need for routine assessment during treatment, test for HCV RNA at least 12 weeks after completion of therapy to confirm cure

165
Q

Risk factors for hepatitis C infection

A
  • IVDU, current or past
  • being in prison
  • sexual partner of person with HCV (increased in MSM)
  • HIV or HBV
  • child of mother with known HCV
  • evidence of liver disease
  • needlestick injury
  • birth in high prevalence region
  • blood transfusion or organ transplant before 1990
  • tattoos or body piercing
166
Q

How to test for hep C

A

HCV antibody = indicates infection (past or present)

HCV RNA = active infection

167
Q

What is the most common cause of acute hepatitis worldwide?

A

Hepatitis E!

  • acute and usually transmitted though dirty drinking water
  • faecal oral transmission
  • diagnosed by presence of HEV antibodies with clinical evidence of hepatitis
  • acute infection resolves spontaneously but in pregnancy may cause acute liver failure
168
Q

Alcoholic hepatitis: basics and LFTs

A
  • ETOH can cause acute and chronic liver disease
  • usually presents with rapid onset jaundice, associated with marked neutrophillia, fever, liver pain and occassionally encephalopathy and ascites
  • characteristic liver biochemistry: AST concentration 2-3 times higher than ALT (however ALT/AST generally <300), elevated bilirubin, elevated GGT
  • if very high aminotransferase levels consider other causes: paracetamol ovderose, acute viral hepatitis
169
Q

What is the characteristic LFT profile for patients with alcoholic hepatitis?

A
  • reversed AST to ALT ratio
  • AST generally 2-3 times higher than ALT
  • generally ALT and AST concentrations are <300
  • elevated bilirubin and GGT
170
Q

Management of alcoholic hepatitis

A
  • alcohol abstinence
  • role of prednisolone is contraversial
  • need to ensure adequate nutritional intake
171
Q

What ist the MELD score?

A

Model for end stage liver disease

  • gives a prediction for 90 day mortality
    1. Dialysis at least twice in past week
    2. Creatinine
    3. Bilirubin
    4. INR
    5. Sodium
172
Q

Child- Pugh scoring

A
  1. Bilirubin (total)
  2. Albumin
  3. INR
  4. Ascites
  5. Encephalopathy

Child pugh A: score 5-6, 100% 1 year survival

Child pugh B: 7-9, 80% 1 year survival

Child pugh C: 10-15, 45% 1 year survival

173
Q

Autoimmune hepatitis

A
  • more common in female
  • bimodal age range: 10-20 and 45-75
  • consider with abnormal LFTs after exclusion of common causes: ETOH, hepatitis and NAFLD
  • may be triggered by a virus or drug
  • diagnosis: positive autoantibodies (ANA, SMA and anti-LKM1), elevated IgG, abscence of viral hepatitis
  • liver biospy is required to confirm diagnosis
174
Q

Management of autoimmune hepatitis

A
  • should be managed by liver specialist
  • treatment is via immunosuppression with aim to normalise liver function results
  • prednisoloe is indicated for initial treatment with addition of azathiopurine as a steroid sparing measure
175
Q

Prior to starting a thiopurine (azathiopurine) which should be tested for to predict risk of adverse effects?

A
  • TPMT testing
  • thiopurine methyltransferase
176
Q

Management of cholestatic itch in patients with liver disease

A
  • general skin care management: loose fitting clothes, emollients, soap substitutes
  • colestyramine 4-16g daily (in up to 4 divided doses)

* all other drugs should eb taken at least 1 hour before colestyramine or 4-6 hours after *

  • can trial ursodeoxycholic acid if colestyramine doesn’t work but this can paradoxically worsen itch
177
Q

Drugs associated with hepatic injury

A
  • analgesics: NSAIDs, paracetamol
  • antiepileptics: carbamazepine, lamotrigine, phenytoin, valproate
  • antimicrobials: augmentin, cephalosporins, fluclox, antifungals, trimethoprim, rifampicin
  • antineoplastic drugs
  • antiretrovirals
  • cardiovasc drugs: amiodarone, hydralazine, methyldopa
  • immunomodulatory drugs: azathiopurine, methotrexate, TNF inhibitors
  • other: allopurinol, NOACs
178
Q

Herbal supplements associated with liver injury

A
  • black cohosh
  • body building supplements
  • chinese herbs
  • echinacea
  • green tea extract
  • kava
  • kombucha
  • weight loss supplements
179
Q

Hereditary haemochromatosis

A
  • inherited disorder causes excessive intestinal iron absorption leading to iron overload
  • autosomal recessive associated with mutations in HFE gene
  • if undiagnosed can cause multiorgan damage (liver fibrosis/cirrhosis, HCC, arrhythmias, cardiomyopathy, diabetes, arthropathy, hypogonadis, skin pigmentation)
180
Q

Which HFE gene mutations are associated with clinically significant iron overload?

A
  • C282Y homozygotes most common
  • can be combine heterozygote but not common
181
Q

What are the 3 most common HFE mutations?

A

C282Y

H63D

S65C

182
Q

Management of hereditary haemochromatosis

A
  • treated via venesection to normalise total body iron stores
  • usually done by taking 500ml of blood every 1-2 weeks until ferritin between 5-100
  • can take months to achieve
  • maintenance venesection usually required around 3 times a year to keep ferritin <100
  • should screen patients for development of cirrhosis and HCC with US and elastography
183
Q

Intrahepatic cholestasis of pregnancy

A
  • fetal complications: preterm delivery, mec stained liqor, SCU admission and stillbirth
  • fetal complications are associated with maternal bile acid concentration > 40 and increased risk of still birth if > 100
  • symptoms: itch, often starts in 3rd trimester staring with palms and soles but can progress
  • diagnosis = serum bile acid > 10
  • need to r.o HELLP, PET, AFLP which may all co-exist
184
Q

Management of intrahepatic cholestasis of pregnancy

A
  • skin measures: loose fitting clothes, emollients, soap substitutes
  • can consider antihistamines
  • if above not effective can consider ursodeoxycholic acid 500mg BD and can increase to 200mg daily
  • if not effective for itch should cease
  • need to monitor bile acid concentration, LFT, INR and AAPPT weekly in third trimester until delivery
  • usually resolved after delivery, but if LFTs are still deranged 6 weeks post need to refer to hepatology
185
Q

Definition of NAFLD

A
  • > 5% liver steatosis (fat) in abscence of excessive ETOH
  • divided into NAFL (simple fat deposition, nil fibrosis) and NASH (fat deposition with liver cell injury with inflammation, with or without fibrosis)
  • MAFLD: liver steatosis, overweight/obesity, T2DM, evidence of metabolic dysregulation (HTN, waist circumference, dyslipidaemia, pre diabetes)
186
Q

Stratification of NAFLD

A

Low risk = lifestyle modification, check CVD risk annually, reassess fibrosis score every 2 years

Moderate risk = refer

High risk = refer

187
Q

NAFLD fibrosis score

A
  • age
  • BMI
  • impaired GTT or diabetes
  • AST
  • ALT
  • platelet count
  • albumin
188
Q

Lifestyle modification of NAFLD

A
  • weight loss and diet: loss of 7-10% of body weight improved histological features of firbosis
  • minimise ETOH consumption
  • physical actrivity
  • monitoring and management of CVD risk factors (3-5 x more likely to have AMI or stroke)
189
Q

NAFLD and HCC

A
  • in patients with NAFLD and cirrhosis need to screen 6 monthly for development of HCC
190
Q

Primary biliary cholangitis

A
  • formerly primary biliary cirrhosis
  • uncommon cause of CLD
  • seen in females, between 30-65
  • present with itch, fatigue and cholestatic picture on LFTs
  • first line management: ursodeoxycholic acid
  • asymptomatic females with abnormal LFTs are increasingly being diagnoised du eto positive AMA-M2 antibodies
191
Q

Primary sclerosing cholangitis

A
  • stricturing of the intrahepatic or extrahepatic bile ducts causing chronic cholestasis
  • associated with IBD in up to 70-80% of patients
  • MRCP is preferred to ERCP for diagnosis as less invasive
  • important DDC is IgG4 related sclerosis cholangitis
  • ursodeoxycholic improved LFTS but doesnt improve survival
  • Abx are indicated with acute/ascending cholantitis and may need to be used prophylactically to prevent recurrent cholangitis
  • complications: dyslipidaemia, fat soluble vitamin deficiency, OP and itch
192
Q

Surveillance for primary sclerosising cholangitis

A
  • annual colonoscopy for PSC and inflammatory bowel disease
  • annual US of gallbladder
  • 6 monthly surveillance of HCC in patients with cirrhosis and PSC
193
Q

Wilson disease

A
  • copper overload
  • copper accumulates particularly in liver, brain, kidney and cornea
  • can cause progressive cirrhosis
  • may present with neuropsychiatric symptoms or LFT derangement
  • can be diagnosed by presence of Kayser FLeischer rings
  • treatment with chelating agents, zinc (to reduce absorption) or both
194
Q

Spot diagnosis

A

Kayser fleisher ring

Wilson’s disease

195
Q

Complications of liver cirrhosis

A
  • Ascites
  • Coagulopathy
  • Varices
  • Encephalopathy
  • HCC
  • Renal impairment
196
Q

Management of ascites

A
  • aim is symptomatic treatment
  • sodium restriction, ensure adequate protein intake
  • diuretics
  • large volume paracentesis + IV albumin in severe cases
  • TIPS (transjugular intrahepatic portosystemic shunt)
  • liver transplant
197
Q

Drug therapys for ascites

A
  • spironolactone: 50-100mg daily (max 400mg daily)
  • if unable to tolerate spironolactone: amiloride
  • can add frusemide as a third line agent
  • diuretics can cause hyponatraemia, changes in potassium and renal impairment, need to check serum electrolytes frequently
198
Q

What is the dose of albumin for a large volume ascitic tap?

A
  • albumin 20%, 40ml for every litre of ascitic fluid drained
  • can give during or immediately after paracentesis
199
Q

Portal vein thrombosis

A
  • occurs in up to 25% of patients with cirrhosis
  • can be asymptomatic or cause abdominal pain, worsening ascitis, bleeding varices
  • can occur in non cirrhotic patients
  • anticoagulation is on a case by case basis du eto risk of anticoag especially in setting of varices
200
Q

Anticoagulation for patients with cirrhosis

A
  • liver disease without cirrhosis and child pugh A cirrhosis = same anticoagulation as general population
  • in decompensated cirrhosis choice is limited: LMWH can be used
  • warfarin should not be used and NOACs shouldn’t be used in child pugh B cirrhosis
201
Q

Primary prevention of bleeding varices in cirrhosis

A
  • non selective beta blockers

Cervediolol or propranolol, aim is to reduce resting HR by 25% (but not less than 60 bpm) while maintaining SBP > 90mmHg

Refer for banding

202
Q

Management of acute variceal bleed

A
  • massive transfusion protocol
  • ICU for CVP monitoring
  • aim Hb 70-80
  • can use terlipressin or ocreotide
  • also need prophylactic antibiotics (ceftriaxone 1g IV daily)
203
Q

Features of hepatic encephalopathy

A
  • change in cognition, personality, sleep disturbance, disorientation
  • flapping tremor (asterixis) is strongy suggestive
204
Q

Management of hepatic encephalopathy

A
  • severe acute encephalopathy: lactulose 30ml Q1-2H to induce rapid laxative effect and then maintain TDS to QID
  • aim for 2-3 semi soft stools/day
205
Q

HCC surveillance

A
  • liver US and measure AFP every 6 months in high risk patients
  • if nodule <10mm on US repeat 3/12 to check for increase in size
  • if nodule >10mm further investigate with further imaging
206
Q

Causes of renal impairment in patients with cirrhosis

A
  • AKI can be cause by hypovolaemia (bleeding, diuretics, diarrhoea), acute tubular necrosis, sepsis, nephrotoxins, NSAIDs
  • heptorenal syndrome: type 1 (acute) and type 2 (chronic)
  • hepatorenal symptom (chronic) often seen in patients with severe ascites and hyponatraemia)
  • management: stop diurectics, use albumin to expand plasma volume for 2 days
207
Q

Describe dietary aims for patients with cirrhosis

A
  • protein requirement is almost double of a healthy adult

* 1.2-1.5g/kg of body weight *

  • need to restrict salt <2.5g/day
  • high protein, high energy diet
208
Q

When should DXA be considered in patients with cirrhosis?

A
  • every 2 years in all patients with cirrhosis
  • diagnosis of osteoporosis is T score under -2.5 (osteopenia -1.5 to -2.4)
209
Q

Describe a cholestatic pattern of LFT derangement

A
  • ALP >200
  • ALP more than 3 times ALT

Causes: biliary obstruction, pregnancy, drugs, infiltration (malignancy)

210
Q

Describe a hepatocellular pattern of LFT derangement

A
  • ALT >200
  • ALT more than three times ALP

Causes

  • infection: hepatitis, EBV, CMV
  • alcohol, AST often x 2 ALT
  • fatty liver
  • drugs: paracetamol
  • metal overload
  • hypoxia: LD usually > 1.5 x AST
  • autoimmune
211
Q
A

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