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RACP 2024 > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

Is coeliac an autoimmune disease?

A

No, because driving antigen is exogenous

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2
Q

What HLA type is associated with coeliac disease?

A

HLA-DQ2/8

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3
Q

What is the pathophysiological basis of coeliac disease?

A
  • tranglutaminase modifies gluten to increase binding affinity
  • B-cells can acts as APCs
  • pro inflammatory gluten-specific CD4+ T-cells
  • transglutaminase antibodies
  • small intestine enteropathy
  • systemic effects
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4
Q

What is the treatment for coeliac disease?

A

Strict gluten free diet

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5
Q

What genetic syndromes are associated with coeliac disease?

A

Turners syndrome
Downs syndrome

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6
Q

What autoimmune diseases are strongly linked with coeliac disease?

A

Autoimmune thyroid disease
Type 1 diabetes

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7
Q

How is coeliac disease diagnosed?

A

Clinical history + serology + histology

Clinical History: improvement on gluten free diet

Serology:
tTG-IgA + total IgA OR tTG-IgA + DGP-IgG
(90% sensitivity and specificity)

Histology: villous atrophy, crypt hyperplasia, raised IELs in multiple biopsies in 1st and 2nd part of duodenum

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8
Q

What are other non-coeliac causes for villous atrophy?

A
  • infection: tropical Sprue, H. pylori, giardia lamblia, SIBO
  • immune: CVID, Crohn’s, cows milk protein intolerance, autoimmune enteropathy
  • drugs: olmesartan, NSAIDs, mycophenylate
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9
Q

What is refractory coeliac disease and how is it managed?

A

Malabsorption + villous atrophy despite 12 months of gluten free diet

First rule out other causes/misdiagnosis

Type 1 = normal IELs, managed with immunosuppression

Type 2 = monoclonal IELs (precursor T-cell lymphoma), managed with chemotherapy +/- ASCT

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10
Q

What is the difference between NAFLD, NAFL and NASH?

A

NAFLD = term that describes fatty liver disease without significant alcohol use from hepatitis to cirrhosis

NAFL = hepatosteatosis without evidence of hepatocellular injury. Minimal risk of progression.

NASH = Hepatosteatosis with inflammation, hepatocyte ballooning +/- fibrosis. Can progress to cirrhosis, liver failure and cancer

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11
Q

What is the pathological basis of NAFLD?

A

Lipid and carbohydrate deposition within the liver, develops pro-fibrotic inflammatory response (key driver is often insulin resistance) resulting inflammation

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12
Q

How is NAFL diagnosed?

A

Either liver biopsy
OR increased hepatic echogenecity on USS compared to right renal cortex
OR MRI

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13
Q

How is NASH diagnosed?

A

Only on liver biopsy

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14
Q

How is NAFLD managed?

A
  • weight loss (10%) and exercise
  • metformin for NASH
  • Bariatric surgery
  • Liver transplant
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15
Q

What is the pathological basis of herediatry haemachromatosis?

A

AR inheritance
Biallelic mutations in HFE gene (most common = C282Y and H63D)

Increased intestinal absorption of iron due to hepcidin deficiency leads to organ damage from ROS

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16
Q

How is hereditary haemachromatosis diagnosed?

A
  • screening with Tsat (>45%) and elevated serum ferritin
  • HFE genotyping
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17
Q

How is hereditary haemachromatosis managed?

A

If C282Y homozygote:
- phlebotomy
- liver biopsy if Serum ferritin > 1000 or abnormal liver enzymes

Others:
- phlebotomy if ferritin >1000, evidence of tissue injury or iron deposition on MRI/biopsy

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18
Q

What muscle wasting signifies malnutrition?

A

1st dorsal interosseus
Masseter
Temporalis

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19
Q

What happens to serum potassium and phosphate in refeeding syndrome?

A

Both drop (due to increase in insulin)

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20
Q

What happens to sodium and water in refeeding syndrome?

A

Increased fluid and salt retention
Increased ADH

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21
Q

When is home TPN indicated for short bowel syndrome?

A
  • <60-90 cm with colon
  • < 150 cm small bowel alone
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22
Q

What is the daily TPN requirement?

A

Energy 25-30 kcal/kg/day
protein 1-1.25 g/kg IBW

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23
Q

What are indications for exclusive enteral nutrition in IBD?

A
  • alternative to corticosteroids for remission induction in crohn’s disease
  • ileal disease
  • able to tolerate EEN
  • complicated crohn’s disease
  • downstage crohn’s severity pre-op
  • ERAS
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24
Q

What are advantages of EEN over corticosteroids for crohn’s?

A
  • avoid steroid side effects
  • improve nutrition
  • improve quality of life
  • improves bone mineral density
  • treats complications to avoid surgery
  • results in mucosal healing
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25
Q

What is the role of metallothionien in the enterocyte?

A

Competitive absorption of
- zinc
- copper
- phytates
- calcium

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26
Q

Where is GLP-2 produced and what does it do?

A

Enter-endocrine L-cells of distal small bowel and colon
Also released in CNS

Increase proximal bowel mucosal absoprtion

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27
Q

What changes happen with liver cirrhosis to cause portal hypertension?

A
  • increase vascular resistance due to change in architecture (fixed component)
  • altered metabolism leads to imbalance in vasoconstrictors and vasodilators ->localised hepatic sinusoidal vasoconstriction (alterable component)
  • systemic vasodilation
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28
Q

What mechanism leads to ascites and renal failure in cirrhotic liver disease?

A
  • RAAS overactivation (salt + water retention, afferent renal vasoconstriction)
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28
Q

What is the gold standard for diagnosing portal hypertension?

A

Measure hepatic venous gradient (HVPG)

HVPG = WHVP - FHVP
HVPG > 5 = portal hypertension
HVPG > 10 = clinically significant (pressure at which ascites and varices occur)

Note HVPG could be normal in non-cirrhotic portal hypertension

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29
Q

What are surrogate markers for diagnosing portal hypertension?

A
  • dilated portal vein
  • reversal of flow in portal vein
  • recanalised ligamentum teres
  • splenomegaly
  • thrombocytopenia
  • presence of varices and porto-systemic shunts
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30
Q

What is cALCD and the rule of 5s?

A

cACLD = compensated advanced chronic liver disease

Rule of 5s:
- liver stiffness < 5 kpa = normal
- liver stiffness < 10 kpa rules out cACLD
- liver stiffness > 15 kpa rules in cACLD
- liver stiffness < 20 kpa and PLT > 150 rules out clinically significant portal hypertension
- liver stiffness > 25 kpa = clinically significant portal hypertension

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31
Q

What is compensated liver disease?

A

Hepatic synthetic function is preserved without current or prior complication of cirrhosis
Child-Pugh A, normal bilirubin and INR
No symptomatic ascites or hepatic encephalopathy or prior variceal bleeding

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32
Q

What is decompensated liver disease?

A
  • ascites
  • variceal bleeding
  • hepatic encephalopathy
  • jaundice
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33
Q

What is the median survival of compensated and decompensated liver disease?

A

Compensated: 12 years
Decompensated: 2 years

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34
Q

What is the most decompensating event in advanced liver disease?

A

ascites

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35
Q

How is portal hypertension as a cause of ascites determined?

A

Serum-ascites albumin gradient > 11

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36
Q

What total protein level is considered high risk for SBP?

A

< 15 g/L

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37
Q

How is cirrhotic ascites managed?

A
  • sodium restriction to 4.6-6.9 g salt
  • diuresis: spirinolactone (max 400 mg), frusemide
  • paracentesis
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38
Q

How should albumin be replaced in large volume paracentesis to prevent circulatory dysfunction and AKI?

A

Replace 1 bottle 20% for every 2L drained

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39
Q

How is SBP diagnosed?

A

Neuts > 250 mm3 on diagnostic tap

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40
Q

How is SBP treated?

A
  • 3rd generation cephalosporin (ceftriaxone, ceftazidime) or tazocin for 5-7 days (note 60% culture resistant)
  • drained dry
  • 1-1.5g/kg/day albumin for 3 days
  • secondary prophylaxis with co-trim until resolution of ascites
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41
Q

Who should get primary prophylaxis for SBP?

A

Low protein < 10 g/L

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42
Q

What is the most common site of varices in chronic liver disease?

A

oesophageal

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43
Q

What is the major determinant of ongoing variceal bleeding?

A

Portal pressure

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44
Q

What are risks of variceal bleeding?

A
  • large varix size
  • High Child class
  • red wale mark on varix
  • excessive alcohol consumption
  • HVPG > 12
  • previous bleed
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45
Q

What prophylaxis is used for high risk varices?

A
  • primary: 1st line = non-selective beta blockade (carvedilol > propanolol), 2nd line = endoscopic banding and ligation
  • secondary = non-selective beta blockade + endoscopic banding and ligation
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46
Q

How should acute variceal bleeding be managed?

A
  • aim Hb > 70 (want to avoid exacerbating raised portal pressure)
  • ocrteotide or terlipressin for 5 days
  • antibiotics (ceftriaxone) for 5 days
  • PPI until ulcer excluded
  • endoscopy: danis stent or Sengstaken-Blakemore tube to tamponade
  • TIPS if bleeding continues despite banding or if high risk for re-bleed (Child-Pugh 8-13)
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47
Q

How do non-selective beta blockers prevent complications of chronic advanced liver disease? What complications do they prevent?

A
  • reduce portal pressure by reducing splanchnic in flow through splanchnic vasoconstriction AND reduce cardiac output through negative chronotropy
  • carvedilol preferred as alpha blockade leads to vasodilatation of liver sinusoids
  • variceal bleeds, decompendation with ascites, mortality
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48
Q

How is AKI managed in cirrhosis?

A
  • remove precipitants
  • volume expand with albumin (20-40g/day)
  • look for infection, low threshold for empiric antibiotics
  • with-hold non-selective B-blockers
  • terlipressin for hepatorenal syndrome
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49
Q

What is the diagnostic criteria of hepato-renal syndrome?

A

AKI in cirrhosis with ascites and no alternate explanation

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50
Q

What is the most effective treatment for hepatorenal syndrome?

A

Liver transplantation

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51
Q

What is the mechanism of action of terlipressin?

A

Long-acting vasopressin analogue
Acts of vasopressin1 receptor to mediate vasoconstriction, preferentially expressed on vascular spooch muscle beds within splanchnic bed

reverses splanchnic vasodilation to improve renal perfusion

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52
Q

What are the key parts to pathogenesis of hepatic encephalopathy?

A

Portosystemic shunting to brain
Hepatic insufficiency (unable to detoxify)
Sarcopenia leading to reduced muscle ammonia clearance

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53
Q

How is hepato-encephalopathy managed?

A
  • treat for precipitant
  • lactulose

Secondary prophylaxis: lactulose, can add in rifaximin

54
Q

What is the mechanism of action of lactulose for hepatic encephalopathy?

A

Acidifies colon, leading to conversion of NH3 (absorbale ) to NH4+ (non absorbable) and increases intestinal transit to increase faecal ammonia excretion

55
Q

What is the mechanism of action of rifaximin?

A

non-absorbable antimicrobial antibiotic that alters the microbiome to reduce ammonia-producing colonic bacteria to reduce ammonia production

56
Q

How is acute on chronic liver failure defined?

A

Acute decompensation with extra-hepatic organ failure

ACLF-1 = renal or cerebral failure only, or renal dysfunction with other organ failure

ACLF-2 = double organ failure

ACLF-3 = three or more orgnas failing

57
Q

When is liver transplantation considered in acute on chronic liver failure?

A

ACLF-3

58
Q

What is hepatopulmonary syndrome?

A

Intrapulmonary vascular dilatation resulting from systemic imbalance in vasoconstrictors and vasodilators from liver disease result in shunting and V/Q mismatch

Presents with SOB, hypoxia, clubbing, normal CXR

Diagnosed with ABG demonstrating elevated A-a gradient, TTE with agitated saline

Treated with supplemental O2, liver transplant

59
Q

What is portopulmonary hypertension?

A

Circulating mediators lead to remodelling of pulmonary vasculature

Presents with dyspnoea, hypoxia and right heart failure

Screened with TTE, diagnosed on right heart catheter

Managed with pulmonary vasodilators (PDE5i, endothelin receptor antagonists), liver transplant

60
Q

What is the King’s College Hospital criteria for liver transplantation in acute liver failure?

A
  1. Paracetamol induced AND pH < 7.3 on ABG AND all of:
    - INR > 6.5
    - Cr > 300
    - grade III or IV encephalopathy
  2. Non-paracetamol induced AND INR > 6.5 OR 3 of:
    - age < 11 or > 40
    - Bili > 300
    - jaundice to coma time > 7 days
    - INR > 3.5
    - drug toxicity
61
Q

What size cholangiocracinomas can be considered for liver transplant?

A

< 2cm intrahepatic
< 3 cm hilar

62
Q

What nerves supplies the oesophagus?

A

Vagus

63
Q

What is the muscle structure of the oesophagus?

A

Upper 1/3: striated muscle (vagal motor)
Lower 1/3: smooth (vagal pasympathetic)
Middle 1/3: mixed

64
Q

What are the phases of oesophageal motility?

A
  1. Upper sphincter relaxation
  2. Relaxation of oesophageal body and lower oesophageal sphincter (mediated by NO, VIP)
  3. Co-ordinated contraction of smooth muscle: meditated by acetylcholine, progressive circular smooth muscle contraction + longitudinal muscle shortening (peristalsis)
  4. Lower oesophageal sphincter closes and longitudinal muscles relax
65
Q

What is the pathophysiology of gastro-oesophageal reflux disease?

A

excess exposure of acid, pepsin and bile salts in gastric contents to oesophagus

66
Q

What are the 4 structures that contribute to the gastro-oesophageal junction?

A
  • instrinsic sphincter
  • diaphragmatic crura
  • intra-abdominal oesophagus
  • oblique angle of entry
67
Q

What mechanisms contribute to gastro-oesophageal reflux?

A
  • transient lower oesophageal sphincter relaxation (response to proximal gastric distension) = most common
  • weak LOS (low pressure, hiatus hernia)
  • increased intra abdominal pressure
68
Q

What is normal oesophageal acidification?

A
  • post prandial
  • < 4% time
  • occurs only in upright position
69
Q

What is Barrett’s oesophagus?

A

Squamous mucosa of oesophagus undergoes metaplasia to columnar mucosa (intestinal metaplasia has goblet cells)

70
Q

How should PPIs be prescribed to be effective for GORD?

A
  • 30-60 mins before food
  • BD dosing more effective than OD
71
Q

When is surgery indicated for GORD?

A
  • failed medical management
  • intolerant of medications
  • need endoscopy, manometry and pH studies to confirm diagnosis
72
Q

What feature of Barrett’s oesophagus carries the biggest cancer risk?

A

Intestinal metaplasia

73
Q

How is Barrett’s oesophagus managed?

A
  • BD PPI + aspirin (slows progression to malignancy)
  • endoscopic surveillance
    • 3-5 years if no dysplasia
    • 6 months if low grade
74
Q

What are mechanisms of oesophageal dysphagia?

A
  • narrowing or compression
  • mucosal inflammation
  • changes in NMJ function
75
Q

What are clinical features if eosinophillic oesophagitis?

A
  • Th2 driven inflammatory condition
  • presents with dysphagia and food impaction
  • common in young males (Atopy)
76
Q

How is eosinophilic oesophagitis diagnosed and managed?

A

Endoscopic diagnosis:
- patches of exudate
- rings and furrowing of mucosa
- biopsy: eosoniphilic infiltration seen throughout mucosa (cfGORD where less eosinophils and only distal)

Management:
- PPI
- budesonide PO
- dietician for diet
- dupilumab (IL4/IL13)

77
Q

What are clinical features of achalasia?

A
  • dysphagia (solids and liquids)
  • regurgitation (postural, non acid)
  • chest discomfort
78
Q

What is the pathophysiology of achalasia?

A

Loss of oesophageal neurons results in incomplete LOS relaxation, ineffective peristalsis

79
Q

How is achalasia diagnosed?

A
  • endoscopy: food in oesophagus, tight LOS, dilated oesophagus (can be normal)
  • barium swallow: rats tail/birds beak sign, dilated oesophagus, aperistalsis
  • oesophageal manometry demonstrating incomplete LOS relaxation, aperistalsis
80
Q

What is the most sensitive test for achalasia?

A

Oesophageal manometry

81
Q

How is achalasia managed?

A
  • laparoscopic cardiomyotomy
  • Per oral Endoscopic Myotomy (POEM), best for Type 3
  • balloon dilatation
  • botox to LOS (palliation)
  • PEG (palliation)
82
Q

What cancer is associated with achalasia?

A

Oesophageal SCC

83
Q

How is distal oesophageal spasm diagnosed?

A
  • barium swallow: uncoordianted contractions, poor bolus passage, diverticulae
  • endoscopy: retained food, uncoordinated contractions
  • manometry: premature pressure waves, LOS relaxation
84
Q

How can achalasia and distal oesophageal spasm be differentiated on manometry?

A

Oesophageal spasm will have LOS relaxation

85
Q

How is distal oesophageal spasm managed?

A

1st line = conservative
- diet modification: soft food, eat slow, water
- acid suppression
- Ca blocker
- GTN spray PRN

2nd line:
- BOTOX to oesophageal body
- oesophageal dilatation
- POEM

86
Q

What is the key cell that contributes to cirrhosis?

A

Hepatic stellate cells (liver macrophages)

87
Q

What is the most sensitive and specific imaging modality for cirrhosis?

A

MRI

88
Q

What is the Child-Pugh score for cirrhosis?

A

Predicts survival:
A (5-6pt) 100% 1 year, 85% 2 year
B (7-9pt) 81% 1 yr, 57% 2 yr
C(10-15) 45% 1 yr, 35% 2 yr

Encephalopathy
- 1 pt for non
- 2 pt for I-II
- 3 pt for III - IV
Ascites
- 1 pt for none
- 2 pt for mild
- 3 pt severe
INR
- 1 pt < 1.7
- 2 pt 1.7 - 2.2
- 3 pt > 2.2
Albumin
- 1 pt > 35
- 2 pt 28-35
- 3 pt < 28
Bilirubin
- 1 pt < 34
- 2 pt 35 -50
- 3 pt > 50

89
Q

How is HCC diagnosed?

A

Radiologically (arterial enhancement with portal vein washout)

90
Q

What are risk factors for HCC?

A
  • cirrhotic liver disease
  • HBV
  • aflatoxin (produced by aspergillus flavus and parasiticus found in corn)
91
Q

How can HCC be screened for?

A

With AFP monitoring in cirrhotic, HBV or HCV patients

92
Q

What is the biggest determinant of treatment for HCC?

A

Liver function

93
Q

How would a small, single HCC in patient with Child-Pugh A liver disease be treated (stage BCLC A)?

A

Resection or ablation (Ablation only if < 3 cm)
Curative intent

94
Q

How would a multi-nodular HCC with Child-Pugh A liver disease without portal hypertension be treated (stage BCLC B)?

A

TACE (palliative intent)

95
Q

How is HCC with portal invasion or extensive spread with preserved liver function treated (stage BCLC C or widespread B)?

A

1st line: immunotherapy
- atezolizumab-bevacizumab (aPDL1/aVEGF)
- if unavailable then TKIs sorafenib, lenvatinib or duravalumab

Palliative intent

96
Q

When should endoscopy be performed for UGIB? What about variceal bleeding

A

UGIB: within 24 hours
Variceal: within 12 hours

97
Q

What is the Forrest score with regard to UGIB?

A

Endoscopic appearance of ulcer and it’s corresponding risk of re-bleeding on medical management

1a = spurting bleed
1b = oozing bleed
2a = non-bleeding visible vessel
2b = adherent clot
2c = flat spot in ulcer crater
3 = clean base ulcer

Patients 2c and 3 can be discharged early

98
Q

How are bleeding ulcers treated endoscopically?

A

Dual therapy:
- inject 4 quadrants with adrenaline
- endoscopic clips OR cautersation

99
Q

In what IBD are non-caseating granuloma seen?

A

Crohn’s

100
Q

In what IBD is smoking protective?

A

Ulcerative colitis
(smoking makes crohn’s worse)

101
Q

In ulcerative colitis, what proprotion of the following patterns are seen?
Proctitis
Left sided
Extensive
Backwash ileitis

A

Proctitis 28%
Left sided 25%
Extensive 50%
Backwash ileitis 7%

102
Q

What is the best initial treatment of mild to moderate ulcerative colitis?

A

5ASA (mesalazine > sulfasalazine)
Supps for proctitis
Enema for lieft sided colitis
Oral for extensive colitis

If fails to respond to topical then add in oral 5ASA

103
Q

What is used for induction in mild relapsed UC?

A

Oral corticosteroids

104
Q

How is acute severe colitis treated?

A

IV steroids and DVT prophylaxis
AXR every 2nd day (risk of toxic megacolon)

104
Q

What are features of severe ulcerative colitis?

A

Truelove and Witt’s criteria
- > 6 episodes of diarrhoea
- very bloody stool
- T > 37.5
- HR > 90
- Hb < 100
- ESR > 30

105
Q

What is the Travis criteria with regard to a serious ulcerative colitis flare?

A

Assessment criteria used on day 3 to assess response to steroids

If has > 8 stools/day or 3-8 stools per day + CRP > 45 then needs salvage therapy (medical with infliximab or ciclosporin OR surgical)

106
Q

What are advsere effects of azathioprine?

A
  • pancreatitis (must stop, cannot use 6-MP)
  • serum sickness (must stop, cannot use 6-MP)
  • myelosuppression (dose dependent on 6TGN level)
  • hepatitis (idiosyncratic = acute, severe must stop, or 6MMP = dose dependent)
  • non melanoma skin cancer
  • lymphoma
107
Q

What are the two metabolites of azathioprine and what do they correlate with?

A
  • 6TGN = treatment response
  • 6MMP = liver injury
108
Q

What is the only monoclonal antibody used for UC salvage therapy?

A

Infliximab

109
Q

What is the mechanism of action of vedolizumab and what are its benefits?

A

a4B7 integrin receptor inhibitor = gut specific, prevents adhesion of lymphocytes and entry into GIT parenchyma

Safest esp. for traveller to TB endemic areas, elderly, have cancer

Does not work for extra-intestinal manifestations

110
Q

What monoclonal antibody for UC can be used in someone with a history of melanoma?

A

Vedolizumab

111
Q

When can you start someone with latent Tb on a TNF mAb?

A

1 month after starting treatment

112
Q

How is Crohn’s managed?

A
  1. induce with steroids
  2. Maintain with azathioprine or methotrexate
  3. If fails above the infliximab, adalimumab, vedolizumab or ustekinumab

If complex perianal fistula then start biologic at same time as azathioprine

(no role for 5ASA)

113
Q

What extra-intestinal mainfestations of crohn’s do not correlate with disease activity?

A
  • pyoderma gangrenosum
  • primary sclerosing cholangitis
  • small joint and axial arthritis
  • uveitis
  • renal stones
114
Q

What is the most common cutaneous extra-intestinal manifestation of IBD?

A

Erythema nodosum

115
Q

What is the agent of choice to induce remission of pyoderma gangrenosum in IBD?

A

Infliximab

116
Q

What is Sweet syndrome? How is it treated?

A

Raised tender nodules on face, arms and trunk associated with fever

Biopsy shows intense neutrophilic infiltrate without vasculitis.

Rx is with steroids

(erythema nodosum in non tender)

117
Q

What biologic agent should be used for the treatment of IBD with psoriasis?

A

Ustekinumab

118
Q

What are clinical features of the following IBD EIM:
Episcleritis
Scleritis
Anterior uveitis

A

Episcleritis: painful red eye, no visual change
Scleritis: painful red eye with vision impairment
Anterior uveitis: painful red eye with photophobia

119
Q

What are clinical features of primary sclerosing cholangitis as and EIM of IBD?

A
  • associated with UC or colonic crohn’s
  • elevated ALP
  • best evaluated with MRCP
  • doesn’t correlate with disease activity
  • manage symptoms
  • need annual colonscopies due to risk of CRC
120
Q

What patients with IBD need yearly surveillance colonscopies for cancer?

A

High risk = Extensive UC or >50% Crohns colitis AND
- PSC
- FHx CRC < 50y
- dysplastic polyp in colitic area in last 5 years
- colonic stricture

121
Q

What patients with IBD need 2-3 yearly surveillance colonscopies for cancer?

A

Intermediate risk = extensive UC or >50% Crohn’s colitis AND
- inflammatory polyps
- FHx CRC > 50y

122
Q

What patients with IBD need 5-yearly surveillance colonscopies for cancer?

A

Low risk = no high or intermediate risk features and more than one segment of colon with colitis

123
Q

When can sustained viral response for hepatitis C be checked?

A

At 4 weeks post completion of therapy (negative PCR result indicates cure)

124
Q

What is the virology of hepatitis C?

A
  • RNA virus
  • blood borne
  • copy errors lead to diversity
  • 7 genotypes (genotype 1 = most common)
125
Q

What proportion of people infected with hepatitis C become chronically infected?

A

75% (persistance beyond 6 months)

126
Q

What are the extra-hepatic manifestations of hepatitis C infection?

A
  • membrano proliferative GN (immune complex deposition)
  • porphyria cutanea tarda
  • cryglobulinaemia
127
Q

How should hepatitis C be tested for?

A
  • hepatitis C antibody (exposure)
  • if positive then test for HCV RNA
128
Q

What is the lifecycle of hepatitis C in the cell?

A

After viral entry translated into polyprotein
Polyprotein cleaved by NS3/4A proteases
Viral particle is assembled, key protein involved is NS5A
Viral RNA replication is mediated by NS5B RNA polymerase

129
Q

What are the mechanism of action of the following anti-virals for Hepatitis C?
- voxilaprevir
- paritraprevir
- grazoprevir
- glecaprevir

A

All are NS3/4A protease inhibitors, prevent cleavage of polyprotein

130
Q

What are the mechanism of action of the following anti-virals for Hepatitis C?
- ledipasvir
- ombitasvir
- elbasvir
- pibrentasivr
- Daclatasvir
- velpatasvir

A

All are NS5A inhibitors, prevent viral RNA replication

131
Q

What are the mechanism of action of the following anti-virals for Hepatitis C?
Sofosbuvir
Dasubuvir

A

Sofosbuvir = nucleoside polymerase inhibitor (terminates NS5A chain)
Dasubuvir = non-nucleoside polymerase inhibitor (inhibits NS5B)

132
Q

What drugs interact with anti-virals for hepatitis C?

A
  • PPIs (reduce treatment efficacy)
  • statins (can cause rhabdo)
  • amiodarone (can cause bradyarrhythmia)
  • anti-epileptics

RACP 2024 (15 decks)

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