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Basic Physician Training Written Prep > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

1st Line Treatment of Mild-Moderate Ulcerative Colitis

A

5ASA - Mesalazine or Sulfasalazine
(No role for methotrexate)

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2
Q

Treatment of Severe UC

A

IV Steroid Induction + VTEp

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3
Q

1st Line treatment Chrons Disease

A

no role for 5ASA
Steroid Induction
Maintain with methotrexate or azathioprine

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4
Q

1st Line for Crohns disease with perianal fistula

A

Infliximab

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5
Q

4 extra-intestinal manifestations that don’t correlate with disease activity in CD?

A

Uveitis, Pyoderma gangrenosum, PSC and small joint and axial arthritis

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6
Q

EPCLUSA

A

Sofosbuvir (NS5B inhibitor)
Velpatasvir (NS5A inhibitor)
- 1 pill daily for 12 weeks
- Preferred in those with cirrhosis
- Unable to use in renal failure

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7
Q

MAVYRET

A

Glecaprevir (NS3/4A)
Pibrentasvir (NS5A Inhibitor)
- 3 tabs daily for 8 weeks
- Ok for use in renal failure

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8
Q

VOSEVI

A

Voxilaprevir (NS3/4A inhibitor)
Sofosbuvir (NS5B inhibitor)
Velpatasvir (NS5A inhibitor)
- For treatment failure.

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9
Q

Ustekinumab

A

IL-12, IL23 inhibitor
Targets Th 17 T cell activity
Indicated for induction and maintenance crohns disease.

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10
Q

Serology In Crohns Disease

A

Positive pANCA - UC
Positive ASCA - Crohns

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11
Q

Sorafenib

A

Oral Multikinase inhibitor….
Prolongs disease free survival for 3 months in those with advanced HCC

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12
Q

First Line H Pylori Eradication therapy

A

14 days - Clarithromycin + Amoxicillin + Esomeprazole
(if penicillin allergy, substitute with metronidazole)

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13
Q

2nd Line H h pylori eradication therapy after failure

A

Quinolone based triple therapy - 10 days of Levofloxicin, amoxicillin + esomeprazole

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14
Q

3rd and 4th line Line H h pylori eradication therapy after failure

A

Bismuth based quadruple therapy - 14 days Bismuth, teracycline, metronidazole, PPI

Rifabutin based triple therapy - Rifabutin + amoxicillin + PPI

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15
Q

Hep C treatment in Cirrhosis

A

Compensated cirrhosis (Childs A) - as for no cirrhosis, Epclusa preferred.

Decompensated Cirrhosis (Childs B and C)
- Avoid use of NS3/4A inhibitors Glecaprevir, Voxilaprevir
- Epclusa + Ribavirin is recommended.

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16
Q

Follow-up after Hep C Treatment:

A

12 weeks post completion of treatment perform HepC RNA PCR - negative PCR at 12 weeks = SVR and is highly predictive of successful treatment.

No followup needed unless:
- Cirrhosis - 6 monthly US for HCC surveillance, monitoring for varicies and osteoporosis.
- Ongoing exposure risk - annual RNA testing, harm reduction strategies.

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17
Q

Vedolizumab

A

Alpha integrin (Gut selective) inhibitor used for induction and maintenance treatment of CD
(NATALIZUMAB = ALPHA INTEGRIN INHIBITOR, NOT GUT SELECTIVE)

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18
Q

Cutaneous manifestations of IBD

A

Pyoderma gangrenosum - papule that elvoles into an ulcer with a violaceous boader.

Erythema nodosum - tender eyrthematous nodules on extensor surfaces of lower limbs

Both correspond to disease activity.

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19
Q

Occular manifestations of IBD

A

Episcleritis - injection of the sclera and conjunctive. Corresponds to disease activity.

Uvetitis - headache, blurred vision, photophobia. Occular emergency requiring prompt referral. Does not correspond to disease activity.

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20
Q

5-ASA’s (5 aminosalicylates)

A

Sulfaslazine, Mesalazine.

Sulfasalazine - rash, nausea, vomiting, headache.

First line for induction and maintenance in mild-moderate UC.

NO role in CD.

Combination of PO and Topical administration is more effective.

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21
Q

Thiopurines (Azathioprine and 6-mercaptopurine)

A

Slow onset of action (2-3m) and need tapering steroid to bridge.

Measure thiopurine methyltransferase enzymes genotype or phenotype (preferred) to identify slow metabolises)

A/E:
- Myelosupression
- Hepatitis
- Pancreatitis
- Nausea/vomiting

Rare A/E: Hepatoslpenic T cell lymphoma
Non-melanoma skin cancer

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22
Q

Role of methotrexate in IBD

A

Effective for induction and maintenance in CD but not UC.

A/E: hepatotoxicity, bone marrow suppression, interstitial pneumonitis.

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23
Q

TNF inhibitors:

A

Intravenous:
- Infliximab

Subcutaneous:
- Adalimumab
- Certolizumab

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24
Q

Definition of acute severe UC

A

6 or more bloody stools per day + one or more:
- Temp > 37.8
- HR >90
- Hb < 105
- ESR > 30

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25
Q

Initial Mx of acute severe UC

A

High dose steroids for 3-5 days and then PO
- 100mg IV Hydrocortisone 6 hourly
OR
- Methylprednisolone 60mg IV daily

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26
Q

Oxford Criteria

A

Used to assess the need for salvage therapy in acute severe UC.
Assessed on Day 3:
- 8 or more stools per day
- OR 3 or more stools per day with CRP > 45

Assessed on day 7:
- 3 or more stools per day with visible blood

If meets criteria, for salvage therapy

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27
Q

Salvage therapy for acute severe UC

A

1 -Intravenous Infliximab 5mg/kg
OR
2- Ciclosporin 2mg/kg IV

If perforation or megacolon –> surgery

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28
Q

Induction therapy for proctitis or distal colitis

A

Note enemas are useful until the splenic flexure.

Combination therapy most effective:
Rectal Mesalazine daily
AND Oral Mesalazine or Sulfasalazine.

If isolated proctitis – use supposetry
If extending >20cm from anal verge - enema

Next step - add rectal corticosteroid (budesonide)

next step - 40mg prednisolone daily, until response, taper over 8 weeks. (consider budesonide if high risk of steroid induced adverse effects)

Next step - Tacrolimus

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29
Q

Maintenance therapy for UC

A

1 - PO and Rectal 5-ASA - Mesalazine

2 - If severe initial disease or frquent relapses, add Thiopurine to 5-ASA (Azathiopurine 2-2.5mg/kg daily)

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30
Q

Explain thiopurine shunting

A

Shunting occurs when thiopurines are preferentially metabolised to 6-methyl-mercaptopurine in preference to 6-thioguanine nucleotides.
High 6MMP can lead to nausea and hepatotoxicity,
6TGN is responsible for the theraputic effect, however high levels cause bone marrow supression.
Shunting can be reversed by co-administration of allopurinol 100mg daily.

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31
Q

Main differences in therapy for UC and Crohns

A

No role for 5-ASA or any rectal therapy in Crohns.
No role for methotrexate in UC.

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32
Q

Induction therapy in mild-mod Crohns

A

40mg Pred daily until response, taper for 8 weeks.

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33
Q

Induction therapy for Severe Crohns

A

High dose IV steroids for 3-7 days and then PO

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34
Q

Maintenance therapy for Crohns

A
  • Thiopurines
  • Methotrexate 10-25mg/week
  • Biologics:
  • TNF inhibitors (inflixmab)
  • Ustekinumab (IL12/23)
  • Vedolizumab (alpha integrin)
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35
Q

Perianal Fistula management

A

Long term antibiotic therapy (weeks to months)
Metronidazole 400mg 12 hourly (peripheral neuropathy) or Ciprofloxacin 500mg 12 hourly

TNF alpha inhibitor

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36
Q

Preventing recurrence of postoperative Crohns

A

After surgery CD will predictably recur at or proximal to the anastomosis.
Prevention:
- Metronidazole
AND
- Thiopurine, TNF inhibitor, or a combination of both.

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37
Q

Microscopic Colitis

A

Normal macroscopic appearance, however inflammation on biopsy - categorised into:
- Lymphocytic colitis
- collagenous colitis
Typically in older women with other autoimmune conditions.
Associated with medications - NSAIDS, SSRI, PPI
Mx: Stop offending medication. Supportive management with loperamide. Second line is PO budesonide.

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38
Q

Colorectal Ca screening in IBD

A

UC - Start 8 years after diagnosis and screen 3 yearly.
- If has PSC, risk is significantly increase. Screen from diagnosis and annually.
- Factors that increase risk a lead to annual screening:
- Active disease, PSC, FMHx <50 years, stricture, dysplasia.

CD - if >1/3 of bowel involved then screen for CRC as per UC. Some increase in small bowel Ca risk but very rare so not screened.

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39
Q

Adverse Effects of Anti-TNF

A

Infection
Melanoma risk if doubles
Drug induced lupus

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40
Q

High risk features in CD

A

Age <40
Perianal disease
High titre ASCA
NOD 2 mutation - associated with fibrostenotic complications.
Smoking, deep ulcers, strictures

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41
Q

High risk features in UC

A

< 40 years
Extensive disease
PSC
Deep ulcers
High titre pANCA

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42
Q

Anti-TNF

A

Infliximab, Adalinumab, Golimumab
- Work better in CD than UC

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43
Q

Adhesion molecule inhibitor for IBD

A

Vedolizumab
Works better for UC than CD
Gut specific and very little systemic immunosuppression, therefore good for people with issues with infection.

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44
Q

Anti-IL 12/23

A

Ustekinumab
ONLY for CD

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45
Q

Vaccination and immunosuppression

A

Don’t give live vaccines 3 weeks prior to, or for 3 months after immunosuppression.
Live vaccines: VZV, MMRV, Japanese E, Yellow Fever.

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45
Q

Vaccination and immunosuppression

A

Don’t give live vaccines 3 weeks prior to, or for 3 months after immunosuppression.
Live vaccines: VZV, MMRV, Japanese E, Yellow Fever.

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46
Q

Most common gene mutation in Lynch Syndrome (HNPCC)

A

Autosomal dominant Inherited mutation of DNA mismatch repair genes.
Most common mutation MSH2 60%, MLH1 (30%).

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47
Q

Testing for HNPCC?

A

Gene testing is expensive.

Test for micro-satellite instability which is a surrogate marker for DNA mismatch repair gene dysfunction.

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48
Q

Risk of Cancer in HNPCC?

A

80% lifetime risk for colon cancer (2/3 in proximal colon)
In women, 80% risk of endometrial ca.
Also increased risk of:
- ovarian
- Stomach
- small intestine
- hepatobiliary tract
- upper urinary tract
- brain
- skin

49
Q

Cetuximab

A

Cetuximab is a EGFR inhibitor that inhibits activation of wild type K ras.
Primary used for treatment of colorectal ca.

50
Q

Gastrin:
- Where is it released from? What is its role?

A

Released from G cells in the ANTRUM of the stomach.
Released in response to stomach distension and extrinsic nerves. Inhibited by low pH and somatostatin.
Effects:
- Secretion of HCL, pepsinogen and intrinsic factor
- increased gastric motility
- stimulated growth of gastric mucosa

51
Q

CCK
- Where is it from? What does it do?

A

From I cells in the upper small intestine
Released due to presence of protein and fat
Effects:
- Stimulates pancreas to release pancreatic enzymes
- Contraction of gallbladder and relaxation of sphincter of oddi
- Decreases gastric emptying

52
Q

Somatostatin
- where is it from ? what does it do?

A

Released from D cells in the pancreas and stomach
Released due to presence of fat, bile salts and glucose in the intestinal lumen.
Effects:
- DECREASES acid and pepsin production, gastrin
secretion, insulin and glucagon secretion

53
Q

Lynch Syndrome

A

Accounts for 2-3% of CRC
Autosomal dominant, high penetrance
Defect in DNA MMR genes - most common are MSH2, MLH1.
Germline mutation in one allele causes microsatelite instability. Somatic inactivation in second allele in CRC (second hit)
Mostly right sided/proximal

54
Q

Amsterdam Criteria for HNPCC

A

Used to detect patients for testing
3-2-1 rule:
- 3 relatives with lynch associated ca (CRC, endometrial, SB, upper tract TCC)
- 2 generations
- 1 diagnosis before age 50

55
Q

Explain Microsatellite Instability

A

Microsatellites are specific sequences of DNA bases made up of mono, di, tri or tetra tandem repeats.
DNA MMR is essential for maintaining genomic integrity by correcting small errors during DNA replication.
Characteristic feature of loss of MMR is expansion of contraction of micro-satellite regions in tumour compared with normal tissue.
Epigenetic silcencing of MLH-1 gene is associated with BRAF V6000E mutation - this generally rules of Lynch syndrome.

56
Q

How to test for microsatellite Instability

A

PCR to amplify sequences - expensive.

IHC to detect loss of staining of MSH2, MLH1, MSH6, PMS 2 - cheaper and easier. This is done.

57
Q

How to test for microsatellite Instability

A

PCR to amplify sequences - expensive.

IHC to detect loss of staining of MSH2, MLH1, MSH6, PMS 2 - cheaper and easier. This is done.

58
Q

FAP screening

A

Screen with sigmoidoscopy from 10-15 years olds
AFAP (attenuated FAP, <100 polyps) - screen with colonoscopy from 45 years.

59
Q

FAP Colectomy Indications

A

Suspected CRC
High grade dysplasia
Significant symptoms - bleeding
Marked increase in polyp numbers
Inability to survey colon

60
Q

NBCSP Screening Criteria

A

Overall population - 2 yearly FOBT from age 50-74
Patients at increased risk:
Category 1 = 1 relative diagnosed with CRC aged 55 or older. Lifetime risk approx 2 x general population. Start screening program at age 45.

Category 2 = risk is 3-6 times. 1 1st degree relative <55. 2 1st degree relatives of any age. 1 1st deg relative and 2 second degree relatives.
- FOBT 2 yearly from age 40-50, and colonoscopy every 5 years from 50-74.

Category 3 = risk is 7-10x. 3 first or second degree relatives with CRC, at least 1 diagnosed <55. or 3 1st deg relatives at any age.
- FOBT 2 yearly from 35 to 45, 5 yearly colonoscopy from 45-74

7% positivity rate for FOBT
1/30 will have cancer

61
Q

Lynch Syndrome screening

A

1-2 yearly colonoscopy from age 25 or 5 years younger than youngest effected case.

62
Q

FAP screening

A

Screening sigmoidoscopy from age 10-15 years,
Once adenoma detected then annual colonoscopy until colectomy and ileorectal anastomosis (then annual rectal/ileal pouch scope)

63
Q

A/E of EGFR MoAbs in CRC

A

Cetuximab and Panitumumab
- Acneform rash

ONLY used in RAS wild type tumours

64
Q

BRAF inhibitor in CRC

A

Encorafenib

65
Q

VEGF inhibitor in CRC

A

Bevacizumab
A/E: hypertension, delayed wound healing

66
Q

A/E Entecavir

A

Lactic acidosis (decompensated cirrhosis)
High risk of resistance if patient previously used lamivudine (therefore use tenofovir)

67
Q

A/E Tenofovir

A

Neuropathy
Fanconi Syndrome
Reduced BMD
Lactic acidosis

68
Q

Choosing between entecavir and tenofovir

A

Entecavir is first line. But dont use if:
- Prior exposure to nucleoside analogues (lamivudine) as high risk of resistance.
- Pregnancy
- Ok in cirrhosis, but risk of lactic acidosis

Tenofovir mainly used if previous exposure to lamivudine, pregnancy, or co-infection with HIV.
Dont use tenofovir if:
- Renal impairment (eGFR < 60)
- Risk of osteoporosis

69
Q

When to treat Hep B ?

A

HepB eAg positive:
- ALT >2x ULN (ULN = 19 in females, 30 in males)
- DNA >20 000
- evidence of fibrosis

HepB eAg negative:
- ALT >2 x ULN
- DNA > 2000
- Evidence of fibrosis

All patients with cirrhosis and any detectable HBV DNA should be treated.

70
Q

Monitoring of HBV treatment:

A

Measure HBV DNA every 12 weeks after starting treatment.
<60 IU/ml = complete response
60-2000 = Adequate response
>2000 IU/ml = sub-optimal response, consider add on therapy.

71
Q

When to treat HBsAg but cAb positive patients during immunosuppression?

A

Only with very high risk treatment:
- Stem cell transplant
- B cell depleting therapy
- Acute leukaemia and high grade lymphoma treatment

Otherwise don’t need to treat these patients as risk of reactivation is very low. (“cleared hep B”)

72
Q

Treatment of Hep B in Pregnancy:

A

If high viral load > 200 000 IU/ml -!!! treat with TENOFOVIR from 28 weeks. If Viral Load <200 000, then dont need to give antiviral.

No need to change method of delivery.

All infants should receive HBV Ig and Vaccination within 4 hours of birth.

No risk of transmission to vaccinated infant. Breastfeeding is encouraged.

Tenofovir ok for breast feeding.

73
Q

Hep D virus treatment:

A

Hep D is small defective RNA virus that requires HBsAg for transmission and packaging.
Co-infection confers high risk of advanced disease.
Hep B DNA often low as is suppressed by Hep D
Treatment: PegInterferon alpha for 48 weeks. New treatment is Bulevirtide.

74
Q

Hep E Virus facts

A

HEV virus is RNA virus
4 different genotypes:
- Genotype 1 and 2 - fecal oral route, in low income countries. Pregnant women have high mortality.
- Genotype 3 and 4 - zoonotic infections (pigs) found in higher income countries. Usually older males. Chronic infection only reported in types 3 and 4 and can occur in immunosuppressed patients.
Acquired through fecal oral route
Causes an acute viral hepatitis
Diagnosis is with HEV IgM or RNA
Recovery usually within 4-6 weeks
Treatment is supportive.

75
Q

Hep A virus Facts

A

Hep A is an RNA virus
Fecal oral transmission
Incubation 15-50 days
Causes an acute hepatitis
Treatment is supportive with 90% recovery in 3-6 MONTHS.

76
Q

Other viruses that may cause hepatitis:

A

EBV
CMV
HSV
VZV
Parvovirus

77
Q

Autoimmune hepatitis diagnosis

A

Positive ANA
Positive Anti-Smooth Muscle Ab
Anti-Liver Kidney Microsome (LKM) Ab
Elevated IgG Levels
Anti-Soluble Liver Ag/Liver Pancreas Ab
Liver Histology:
- Interface hepatitis, lymphocytic/lypmhoplasmacytic infiltrate in the portal tracts extending into the lobule.

78
Q

Drugs associated with autoimmune hepatitis

A

Minocycline
Nitrofurantoin
Isoniazid
Propylthiouracil
Methyldopa

79
Q

Definition of Primary Biliary Cholangitis

A

Autoimmune disease effecting the small and medium bile ducts, presenting with fatigue and pruritis.
Female to male 9:1

80
Q

Diagnosis of PBC

A

If ALP is >1.5 ULN and Positive Anti-Mitochondrial Ab - no biopsy needed.

If negative mitochondrial Ab, requires liver biopsy. May be positive for Anti GP120 or Anti SP 100

Look for other autoimmune disease.

81
Q

Treatment of PBC

A

Ursodeoxycholic acid
Manage pruritis: Cholestyramine, Antihistamines, rifampicin
Transplantation

81
Q

Treatment of PBC

A

Ursodeoxycholic acid - this leads to histologic improvement, better survival, and less need for liver transplant.
Manage pruritis: Cholestyramine, Antihistamines, rifampicin
Transplantation

82
Q

PSC Definition

A

Autoimmune fibro-inflammatory disease of the LARGE bile ducts (but can also affect the small ducts in small duct PSC).

More common in men than women.

83
Q

PSC-IBD Phenotype

A

85% of PSC cases have UC.
- rectal sparing, mild pancolitis with backwash ileitis
- high risk of CRC, more intensive screening from diagnosis

84
Q

Diagnosis of PSC

A

Diagnosis can be made non-invasively with MRCP:
- multifocal intra- and extra-hepatic bile duct stricturing with upstream bile duct dilation.

ERCP should be considered in patients with jaundice, worsening pruritis, bacterial cholangitis or a dominant stricture of bile duct mass on MRCP.

Biopsy is not needed (except for small duct PSC)

85
Q

Treatment of PSC

A

Liver transplantation. Median transplant free survival is 12 years.
- indications are decompensated cirrhosis, recurrent bacterial cholangitis, hilar cholangiocarcinoma.

No current medical therapy.

ERCP to dilate strictures.

15% lifetime risk of cholangiocarcinoma.
- Screen with yearly MRCP and Ca 19-9 level

85
Q

Treatment of PSC

A

ERCP should be considered in patients with jaundice, worsening pruritis, bacterial cholangitis or a dominant stricture of bile duct mass on MRCP.

Biopsy is not needed (except for small duct PSC)

86
Q

HCC surveillance guidelines:

A

6 monthly liver USS and serum AFP:
- Any patient with cirrhosis
- Non-cirrhotic patients with Hep B AND increased background risk (asian men >40, asian women >50, Subsaharan africans >20, ATSI >50)

If new lesion <1cm - repeat in 3 months

If new lesion >1cm proceed to further evaluation with quad phase CT or MRI

87
Q

Diagnosis of HCC

A

Can be diagnosed based on classical imaging with quad phase CT:
- non-rim arterial phase hyper-enhancement
- port venous delayed washout

88
Q

Staging of HCC

A

Staging is via Barcelona Clinic Liver Cancer staging system (BCLC)
- Stage 0 - single lesion less than 2cm - curative intent resection or ablation
- Stage A - Single lesion >2cm or 3 less than 3cm - curative intent resection or if unable than transplant.
….. From stage B onwards, non-curative therapy
- Stage B - >3 lesions or any lesions >3cm. Transarterial chemo-embolisation.
- Stage C - Vascular invasion or metastatic - treat with systemic therapy
- Stage D - Childs-Pugh C, ECOG >2, for supportive management.

89
Q

Transplant Criteria for HCC

A

Milan Criteria:
- 1 less than 5cm
- 3 less than 3 cm

No macrovascular invasion, no nodal disease, no mets.

90
Q

Systemic therapy for Stage C (advanced stage) HCC

A

Atezolizumab and bevacizumab shown to be suprior in recent RCT

Previous first line was -
- Sorafenib
- Lenvatinib

Atezolizumab and bevacizumab

91
Q

Acute management of paracetamol overdose

A

<2 hours - give charcoal
2-8 hours - measure paracetamol level and ALT at 4-8 hours and be guided by nomogram.
>8 hours - start NAC (acetylcysteine infusion)

If MR paracetamol >10g or 200mg/kg should be given charcoal up to 4 hours.

92
Q

Paracetamol toxic dose

A

> 10g or 200mg/kg

93
Q

Acetylcysteine regimen:

A

Standard 2 bag regimen:
- 200mg/kg in 500ml over 4hours
- 100mg/kg in 1000ml over 16 hours

Double the second bag to 200mg/kg if:
- massive overdose, double the nomogram line

94
Q

Criteria for ceasing NAC infusion:

A

Give for 20 hours.
2 hours before completion check the ALT and Paracetamol level.
Cease if:
- ALT decreasing
- INR <2
- patient clinically well.
and
For MR paracetamol and patients with initial paracetamol conc greater than double the nomogram line, paracetamol <10mg/L

95
Q

Kings College Criteria for Transplant in Paracetamol Toxicity

A

pH <7.3

Or all of the following criteria:
- INR >6.5
- Creatinine >300
Encephalopathy grade 3/4

96
Q

Criteria for consulting liver transplant unit:

A

Any of the following:

INR > 3.0 at 48 hours or greater than 4.5 at any time
Oliguria or Cr > 200
Persistent acidosis or lactate >3
Systolic hypotension <80
Hypoglycaemia
Severe thrombocytopenia
Encephalopathy of any degree
Any alteration in consciousness.

97
Q

Management of immune checkpoint hepatitis

A

Grade 1 = AST/ALT 1-3 x ULN or Bili 1-1.5 x ULN. Continue treatment and monitor weekly.

Grade 2 = AST/ALT 3–5 x ULN or Bilirubin 1.5-3 x ULN. Withold ICI (do not restart until grade 1), start steroids at 0.5 - 1 mg/kg/day. Monitor.

Grade 3 = AST/ALT >5 x ULN or Bilirubin >3 x ULN. Institute corticosteroids 1-2mg/kg and permanently discontinue ICI.

98
Q

Management of varices

A

No varicies - repeat endoscopy in 2-3 years.

Small <5mm

99
Q

4 H’s of acute liver failure

A

Treatment goals in acute liver failure:
Hypothermia
Hypernatraemia 145-150
Hypocapnia 30-45
Haemofiltration - renal replacement therapy.

100
Q

Pregnancy related liver disease:

A

Pre-eclampsia: late in pregnancy, other features of HELP

Acute fatty liver of pregnancy:
- 3rd trimester
- jaundice, AST/ALT 300-1000, high bilirubin, Synthetic liver dysfunction with hypoalbuminaemia, hyperammonaemia, coagulopathy
- Clinical: Polyurin and polydipsia

101
Q

Haemochromatosis pathogenesis

A

Autosomal recessive, mutation in HFE Gene (C828Y/C828Y most common)
Leads to deficiency of hepcidin
Ferroportin constantly active and absorbing iron.
Iron deposits in liver, pancreas, heart, pituitary

102
Q

Diagnosis

A

Iron studies - high transferrin sats, high ferritin

If confounding factors for high ferritin
MRI-T2 showing “black liver and white spleen”

Genetic testing for HFE C282Y mutation. If not homozygous, refer for further genetic testing of less common mutations.

103
Q

Haemochromotosis Management

A

Phebotomy:
- Aiming for serum ferritin 50ng/ml and transferrin sats of 50% (50/50)

Iron chelation with deferoxamine is rarely used.

Family genetic counselling.

104
Q

Wilsons Disease pathogenesis

A

Autosomal recessive, mutations in ATP7B gene.
ATP7B is a copper transporting transmembrane protein, which mediates excretion of copper into the bile and incorporates copper into ceruloplasmin (copper transport protein).
Defecting ATP7B stops ceruloplasmin formation and excretion of copper. Excess copper accumulates in the liver and the brain.

105
Q

Natural history of Wilsons Disease

A

18 years - Symptomatic liver disease

24 years - neuropsychiatric disease (tremor, rigidity, dystonia, psychiatric)

Classic patient is young patient <40 years, moderately elevated ALT and a high bili:ALP ration.
Look for haemolytic anaemia and encephalopathy with KF rings.

106
Q

Diagnosis of Wilsons Disease

A

Can present as any form of liver disease from acute liver failure to decompensated cirrhosis.

Low Ceruloplasmin
Copper content in biopsy elevated
Elevated 24 hour urine copper
Kayser-Fleischer rings - golden/brown rings in the membrane of the cornea .
MRI-B - Panda Sign, T2 shows Cu deposit in basal ganglia.

107
Q

Treatment of Wilsons Disease

A

Cu Chelators - D-penicillamine

Zinc supplementation inhibits the intestinal uptake of copper

Liver transplant is advanced disease.

108
Q

Alpha1 anti trypsin deficiency pathogenesis

A

Mutation in the SERPINA1 gene which encodes AAT.
Mis-folding and accumulation in liver (inclusion bodies) leads to toxicity and eventually cirrhosis.
Loss of function leads to lack of inhibition of proteases and proteolytic destruction causing pan-lobular emphysema.

Z allele (Glu342Lys)
S allele (Glu264Val)
M allele = wildtype

PiZZ (homozygosity for Z allelle) causes neonatal hepatitis, cirrhosis in adult, and lung disease.
PiSZ
PiMZ is a “contributor” which increased risk of COAD and liver disease in the presence of other risk factors.

109
Q

Type of renal stones in Crohns Disease?

A

Calcilum oxalate stone. Common complication of Crohns disease after bowel resection.

Decrease in bile acid absoprtion leads to fat malabsorption which binds to calcium. This leads to increased oxalate absorption, which is deposited in kidney.

110
Q

Indication for TIPs in Cirrhosis:

A

Refractory ascites defined as >4 LVP within 6 months.

111
Q

Most common indication for liver transplantin Aus?

A

Hepatitis C Cirrhosis with or without HCC (28%)

Others:
HCC 14%
Alcoholic Liver disease 13%
NASH 6%
Hepatitis B 3%

112
Q

Classic presentation of Chronic mesenteric ischaemia

A

Post-prandial abdominal pain, fear of eating, weight loss.

Older adult with cardiovascular risk factors.

113
Q

Definition of liver steatosis

A

> 5% hepatocytes loaded with fatty vacuoles or >5% of liver weight.

114
Q

Paracetamol metabolism

A

90% metabolised via glucuronosyltransferase and sulfotransferase into glucorinide and sulfate conjugates which are excreted in urine.

5% excreted unchanged in urine.

5% metabolised via CYP 2E1 into NAPQI, which binds glutathione and is excreted in urine.

Therefore increased risk of toxicity if:
- Fasting
- Alcohol intake - induces CYP2E1 expression
- CYP2EI inducing drugs

NAPQI is highly hepatotoxic

115
Q

Tacrolimus Side Effects

A

Diabetes
Nephrotoxicity - renal afferent artery constriction.
Electrolyte: hyperkalaemia, hypophosphataemia, hypomagnesiaemia, metabolic acidosis.
Hypertension
Hyperlipidaemia
Increased risk of infection
Neurotoxicity: tremor, insomnia, paresthesia. Rare serious neurotoxicity includes seizures, cortical blindness, encaphalopathy and central pontine myelinolysis.

116
Q

Mechanism of Terlipressin

A

Binds to V1a receptors on splanchnic vascular smooth muscle causing vasoconstriction –> reduced portal pressures, increased renal blood flow.

However also binds to V2 receptors in renal collecting duct - therefore can cause hyponatraemia.

117
Q

Contraindications to terlipressin

A

Unstable coronary artery disease, pregnancy. Caution in asthma and COPD.

118
Q

Portal Vein thrombosis

A

Thrombosis of the PORTAL VEINS (ie Inflow). Usually NOT due to hypercoaguable state.
Common in patients with cirrhosis.
Chronic thrombosis is usually asymptomatic and does not need anticoagulation.
Acute thrombosis can be symptomatic with development of ascites and or variceal haemorrhage. Anticoagulation can be considered if there is concern that thrombosis has extended into the superior mesenteric vessels.

119
Q

Budd-Chiari Syndrome

A

Thrombosis is u

Basic Physician Training Written Prep (20 decks)

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