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Nimna's Flash Cards > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

Fibrosis in the liver is caused by which inflammatory cell?

A

Stellate cell

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2
Q

3 ways of diagnosing liver cirrhosis

A

Liver biopsy
Fibroscan
MRI-E

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3
Q

5 parameters in the Child Pugh score

A
  1. Bilirubin
  2. Albumin
  3. Ascites
  4. Encephalopathy
  5. INR
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4
Q

Mortality risk score in cirrhosis

A

MELD score - Uses creatinine, Bilirubin and INR.

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5
Q

What is the SAAG score and its cut off

A

Serum albumin: Ascites albumin.

>11 = portal hypertension (transudative)

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6
Q

Medical management of ascites

A
  1. Spironolactone
  2. Frusemide
  3. Low salt diet
  4. Albumin
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7
Q

Role of Rifaximin

A

Reduced encephalopathy

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8
Q

Management of variceal bleeding

A
  1. Antibiotics - Ceftriaxone or Norfloxacin
  2. Octerotide or Teripressin (to vasocontrict Splanchnic circulation)
  3. Variceal banding/ Glue injection/ Balloon Tamponade
  4. TIPS
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9
Q

Blood pressure aim in variceal bleeding

A

SBP 90

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10
Q

Hb Aim in variceal bleeding

A

Hb 70

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11
Q

MOA of Octreotide

A

Somatostatin analogue

  • decreases glucagon to decrease splanchnic vasodilation
  • decreases gastric acid production
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12
Q

MOA of Terlipressin in UGI bleeds

A

Vasoconstricts splanchnic circulation

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13
Q

Management of stage 2 and 3 HCC

A

TACE + Sorafenib/Levatinib (multi-kinase inhibitors)

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14
Q

What percentage of adults exposed to Hep B develop chronic infection?

A

5%

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15
Q

Hep B e Antigen positive indicates:

A

Active viral replication

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16
Q

Fibroscan is only diagnostic for what stages?

A

Stage 1 - cirrhosis ruled out

Stage 4 - cirrhosis ruled in

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17
Q

When is Hep B treated?

A

During Clearance and Escape phase.

Rising ALT = development of fibrosis

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18
Q

Hep B treatment

A

Entecavir

Tenofovir

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19
Q

Hep B treatment in pregnancy + birth

A

Use tenofovir for treatment of mum

Immunoglobulin and Vaccination to baby

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20
Q

Endoscopic management of peptic ulcer disease

A

INJECT adrenaline + CLIP or CAUTERIZE

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21
Q

Ulcerative Colitis histological features:

A

Lymphocytes+ Goblet cell depletion + crypt distortion/ abscesses.

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22
Q

Crohn’s histological features

A

Granulomas

Transmural

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23
Q

IBD high risk genes

A

NOD2/CARD 15

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24
Q

Marker used for monitoring IBD disease activity

A

Faecal calprotectin

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25
Q

Initial therapy Crohn’s Disease

A

Corticosteroids + AZA/6MP/MTX

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26
Q

Initial therapy UC

A

Corticosteroids + AZA/6MP/MTX/5ASA

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27
Q

Management of refractory disease in IBD

A
  1. Infliximab/Adalimumab
  2. Vedolizumab/Ustekinumab

Rescue therapy in UC only - Cyclosporine

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28
Q

Drug which reduces risk of colorectal cancer in UC

A

Sulfasalazine/Mesalazine (5ASAs)

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29
Q

MOA of Thiopurines

A

Inhibit purine synthesis
Inhibit Tcell and Bcell proliferation
Induce T cell apoptosis

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30
Q

Why do we measure TMPT levels

A

High TPMT means increased shunting to inactive 6MMP metabolite.

Low TPMT means increased 6-TGN active metabolite which increases the risk of myelotoxicity.

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31
Q

Interaction of Thiopurines and Allopurinol

A

Allopurinol blocks Xanthine Oxidase pathway –> Increased shunting to active 6-TNG metabolite.

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32
Q

MOA of Cyclosporine

A

Calcineurin Inhibitor. Blocks synthesis of IL-2 in T-cells.

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33
Q

Steroid of choice in UC

A

Budesonide

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34
Q

Vedolizumab MOA

A

a4b7 integrin inhibitor. Gut specific.
Blocks T lymphocytes interacting with intestinal endothelium MAdCAM–1 cells.

Note: Works on T lymphocytes, not on intestinal cells.

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35
Q

MOA Ustekinumab

A

IL-12 and IL-23 inhibitor

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36
Q

Crohn’s 1 year risk of recurrence post bowel resection

A

80%

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37
Q

Drug which improves the histological features of NASH

A

Pioglitazone

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38
Q

Inheritance of Hereditary Hemochromatosis

A

Autosomal recessive

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39
Q

Complications of Hereditary Hemochromatosis

A
  • cirrhosis
  • HCC
  • Diabetes
  • Cardiomyopathy
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40
Q

Management of Hereditary Hemochromatosis

A
  1. Phlebotomy ONLY if ferritin >400 or iron deposition tissue injury. (Iron chelation NOT used)
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41
Q

Changes in starvation

A
  1. Ketosis
  2. Proteolysis
  3. Pancytopenia
  4. Electrolyte loss
  5. Reduced hypothalamic hormones
  6. Cardiac dysfunction/arrythmias
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42
Q

Mechanism of re-feeding.

A

Over-shoot of insulin to carbohydrate load.
Leads to K, Mg, PO4 moving intracellularly.
Increased salt retention = oedema

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43
Q

Increased risk of which type of gall stone in bowel resection

A

oxalate stone.

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44
Q

Management of short gut

A
  1. Electrolyte supplementation
  2. Vit B, C supplementation
  3. PPI/ octreotide to reduce GI secretions
  4. Imodium/Codeine to slow transit.
  5. Pancreatic enzymes
  6. Dry meals
  7. Teduglutide
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45
Q

MOA of Teduglutide

A

a GLP-2 analogue. Promotes mucosal growth

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46
Q

Antibodies for Coeliac disease - and which are most specific.

A
  1. Tissue transglutaminase (TTG) antibody
  2. IgA endomysial antibodies
  3. Deaminated gliadin peptide (DGP) antibody

EMA and TTG most specific

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47
Q

Histological findings in coeliac disease

A

Villous atrophy
Crypt hyperplasia
Increased lymphocytes

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48
Q

Rule out genetic tests for Coeliac disease

A

HLADQ2

HLADQ8

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49
Q

MOst common Hep C genotype in Australia

A

Type 3

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50
Q

Other Hepatitis C manifestations

A

Cryoglobulinemia
Membranoproliferative GN
Porphyria cutanea Tarda

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51
Q

Hepatitis cancer screening schedule

A

6 monthly liver US and AFP

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52
Q

Variceal bleed prophylaxis

A

Beta-blockers - propanolol/ carvidelol
OR
Banding

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53
Q

Pathophysiology of Hepatorenal syndrome.

A

Arterial vasodilatation in the splanchnic circulation, which is triggered by portal hypertension, causes progressive rise in cardiac output and fall in systemic vascular resistance. This leads to renal hypoperfusion and AKI. Bacterial translocation may play a role.

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54
Q

Hepatorenal Syndrome types

A

HRS-AKI Type 1 - Atleast 2x increase in serum creatinine in 2 weeks.

HRS-AKI Type 2 - Less than 2x increase in serum creatinine. < 90days.

HRS-CKD - eGFR <60 for >3 months with no other cause.

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55
Q

HCC transplant criteria - nodule size and number

A

<3 nodules <4.5cm (or 6.5 if only 1)

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56
Q

Assessment of oesophageal motility/ dysphagia

A

Manometry

Gastroscope

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57
Q

Management of oesophageal spasm

A

soft food, PPI, GTN, Ca Channel blockers, botox, dilatation

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58
Q

Endoscopic findings in eosinophilic oesophagitis

A

exudate rings

furrows

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59
Q

Management of eosinophilic oesophagitis

A 
PPI
fluticasone puffer 
budesonide slurry 
dilatation if stricturing 
Food elimination diet
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60
Q

Pathophys of Achalasia

A

Lower oesophageal sphincter unable to relax

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61
Q

Manometry and Barium swallow findings in achalasia

A

Pressure wave contractions
Aperistalsis
Steeple/birds beak appearance

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62
Q

Management of Achalasia

A 
Botox
Balloon dilatation
Ca channel blockers, GTN 
POEMS procedure 
surgical myotomy
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63
Q

Drugs causing transaminitis
Drugs causing mixed picture
Drugs causing cholestatic picture

A

Drugs causing transaminitis
- Paracetamol, statins, Isoniazid.
Drugs causing mixed picture
- Anti-epileptics - Carbamazepine, Phenytoin, Lamotrigine.
Drugs causing cholestatic picture
- Abx - flucloxacillin, Amoxycillin, Cephalosporins.

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64
Q

Causes of severe transaminitis

A

Ischaemic hepatitis, Viral hepatitis, Paracetamol, Thrombosis.

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65
Q

Pathophys of EtOH withdrawal.

A

EtOH is a CNS depressant. Therefore there is compensatory upregulation of GABA, glutamate and NMDA receptors with time. Cessation of EtOH unmasks CNS upregulation.

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66
Q

AST:ALT >2 = ?

A

Alcoholic hepatitis

Note: mortality benefit with prednisolone.

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67
Q

AST:ALT <2 = ?

A

NASH

68
Q

Drug which reduces EtOH cravings

A

Naltrexone

69
Q

Symptoms of a Carcinoid tumor

A
  • Secretory diarrhoea
  • Flushing
  • Telangiectasia
  • Valvular heart lesions
  • Asthma/ bronchocontriction
70
Q

Management of C.difficle

A
  1. Oral Vancomycin/Metronidazole
  2. Bezlotoxumab –> MAB for toxin B
  3. Faecal transplant
71
Q

Pathologic feature of alcoholic hepatitis

A

Neutrophil influx

72
Q

Precipitants of hepatic encephalopathy

A 
Drugs 
Dehydration 
Ammonia (GI bleed, constipation, protein)
Thrombus 
HCC 
Portosystemic shunts
73
Q

Which part of the bowel are bile acids re-absorbed

A

Terminal Ileum

74
Q

Drug of choice in managing agitation in hepatic encephalopathy

A

Haloperidol.

Avoid Benzo’s due to up-titration of Benzo receptors in encephalopathy.

75
Q

Management of hepatic encephalopathy

A
  1. Treat cause + correct hypokalemia
  2. Lactulose
  3. Rifaximin
  4. Neomycin
  5. L-ornithine-L-aspartate (LOLA
76
Q

Effect of hypokalemia in hepatic encephalopthy

A

Increases renal ammonia production

77
Q

IBS trigger foods

A

Foods that may trigger symptoms include high fiber foods, lactose, high-fat foods, gluten, partially absorbed sugar alcohols like sorbitol and mannitol, and FODMAP (Fermentable Oligo-Di-Monosaccharides and Polyols)

78
Q

Familial screening for colorectal cancer in first degree relatives.

A

5 yearly colonoscopies starting age 40 or at 10years younger than affected family members diagnosis, whichever is earliest.

79
Q

MOA of Lactulose in Hepatic encephalopathy

A
  1. Decreased intestinal pH - leads to increased uptake of ammonia by bacteria to produce non-toxic ammonium.
  2. Reduces Urease producing bacteria
  3. Reduces glutamate absorption.
80
Q

Initial nutrition for ICU patients with pancreatitis

A

Nasojejunal feeding

81
Q

Primary Biliary Cirrhosis pathology and histology

A

Pathology - ALP raised, AMA 1:40 or higher. Other PBC specific antibodies are sp200 and gp210.
Can have positive ANA.

Histology - liver histology in PBC is featured by chronic inflammation in the portal tracts
and the formation of noncaseating granulomas.

82
Q

Auto-immune Hepatitis pathology

A

AIH is associated with positive

  • anti-smooth muscle (65%)
  • anti-dsDNA
  • anti-ssDNA
  • ALKM-1
  • ALC-1 (anti liver cytosol)
  • p-ANCA
  • AMA
  • ANA
83
Q

In what trimester does Acute Fatty liver of pregnancy occur

A

3rd trimester. Week 30-38
If maternal-fetal fatty acid metabolism is defective, products of metabolism can accumulate in maternal blood and hepatocytes, medical emergency.

84
Q

Mechanism of A1AT disease in liver and lung

A

A1AT is a protease inhibitor.

Liver - non-functioning mutant A1AT proteins accumulate

Lung - AAT usually breaks down elastase. Loss of A1AT causes excess elastase therefore elastin deficiency.

85
Q

Pathophys of Gilbert’s disease

A

defect in bilirubin glucuronidation

86
Q

Side effect of high 6MMP levels

A

hepatotoxicity

87
Q

High risk features requiring yearly colonoscopies

A
  • Primary sclerosing cholangitis
  • active IBD
  • Colorectal dysplasia
  • Colonic strictures
  • Pseudo polyps
  • FHx of colorectal ca <50yrs age
88
Q

Antibody marker for Primary biliary cirrhosis

A

AMA

89
Q

Skin symptom asscoaited with coeliac disease

A

Dermatitis Herpetiformis

90
Q

Faecal transplantation has the most evidence in which disease ?

A

Pseudomembranous colitis

91
Q

Absolute contraindications to TNF inhibitors

A

Heart failure
Demyelinating disease
Solid organ tumors

92
Q

Histological findings in NASH

A

Hepatocyte ballooning

93
Q

What proportion of the livers blood supply comes from the portal vein

A

75% (most of the rest is from hepatic artery)

94
Q

Drug of choice for alcohol withdrawal in patients with liver disease

A

Oxazepam/ Lorazepam

95
Q

Two cell types involved in iron absorption

A

Duodenal enterocytes - Fe3+ is converted to Fe2+ via VitC reductase then brought into the enterocyte by the DMT transporter.
It is transported out of the enterocyte by ferroportin.
Reticuloendothelial macrophages - found in spleen. Eats old RBCs and releases iron back into circulation - inhibited by hepcidin.

96
Q

Which cell secretes Gastrin. What are its triggers and inhibitors.

A

Secreted by G-cells in the gastric antrum. Works on parietal cells to increase HCL release.

Stimulated by: Vague nerve, aromatic amino acids, Stomach distention, hypercalcaemia.

Inhibited by: Low pH, Somatostatin, glucagon.

97
Q

Why is the Faecal immunochemical test better than FOBT?

A

More sensitive and specific.

No dietary changes/restrictions required.

98
Q

Symptoms of Thiamine deficiency

A

Dry Beriberi - motor and sensory symmetrical peripheral neuropathy
Wet Beriberi- Heart failure, tachycardia, cardiomyopathy.
Wernike encephalopathy - nystagmus, ophthalmoplegia, ataxia, and confusion.
Korsakoff encephalopathy - selective anterograde and retrograde amnesia.

99
Q

Clinical signs of Budd-Chiari

A 
Ascites 
Hepatomegaly 
Loss of hepatojugular reflex 
Peripheral oedema 
Distension of abdominal veins
100
Q

H.pylori treatment

A

Esomeprazole + Clarithromycin + Amoxycillin (metronidazole if penicillin allergy) for 7 days.
Then cease. No requirement for ongoing PPI.

101
Q

In which disease is periodic acid Shiff positive macrophages seen?

A

Tropheryma Whipplei infection

102
Q

Most sensitive test for spontaneous bacterial peritonitis

A

High ascitic fluid neutrophil count

103
Q

Malnutrition deficiencies in bacterial overgrowth

A

Calcium
Vik K
Vit A
B12 (but high folate)

104
Q

Two Hep C treatment regimes

A
  1. Sofosbuvir (NS5B) + Velpatasvir (NS5A)

2. Glecaprevir (NS3/4A) + Pibrentasvir (NS5A)

105
Q

What is NOD 2 associated with?

A

ilieal Crohns disease

106
Q

B12 absorption

A
  1. Binds to transcobalamin 1
  2. Cleaved from transcobalamin in duodenum by Trypsin
  3. Binds to intrinsic factor
  4. Absorbed in ileum
  5. Binds to transcobalamin 2 for transport to organs
107
Q

What molecule does NOD2/CARD15 act on?

A

muramyl dipeptide

108
Q

Extra-intestinal manifestation in IBD which mirrors intestinal disease activity

A

large joint arthritis

109
Q

Benefit of pre-endoscopic PPI

A

reduced endoscopic intervention

110
Q

Criteria for liver transplant in paracetamol overdose

A
  • pH <7.3
    OR
  • Cr>300 + PT>100secs/ INR >6.5 + encephalopathy
111
Q

Criteria for liver transplant in non-paracetamol cause

A 
PT > 100secs / INR >6.5
OR
3 other minor criteria (Kings college criteria)
- age <11 or >40 
- bili >300 
- coma in >7 days (not acute) 
- INR >3.5 
- drug toxicity/ acute hepatitis
112
Q

Where is folate absorbed

A

proximal jejunum

113
Q

Pernicious anaemia best test

A

gastroscopy and biopsy

114
Q

Pernicious anaemia can be triggered by

A

H.pylori

Thyroid disorders

115
Q

What is destroyed when iron is high

A

ferroportin by Hepcidin

116
Q

Haemachromatosis complication unlikely to resolve after treatment

A

Diabetes

117
Q

Sulfasalazine effect on extra-intestinal arthritis in IBD

A

No effect on sacro-iliac disease

Has effect on peripheral joints

118
Q

Active disease for IBD peripheral signs

A

Erythema nodosum
Episcleritis
Arthritis

119
Q

Infliximab in pregnancy

A

Can use. Stop in 3rd trimester

120
Q

Post op Mx for Crohns

A
  • Metronidazole for 3 months
  • Smoking cessation
  • Azathioprine or infliximab
121
Q

T cell involved in Hep B

A

CD8

122
Q

T cell involved in Hep C

A

CD4

123
Q

Medications which induce CYP281 - causing worse liver failure

A

Phenytoin
Carbamazepine
TB drugs

Note higher risk in chronic alcoholism but not in acute ingestion

124
Q

A1AT genetics

A

PiMM - normal
PiZZ - liver disease
Nul - respiratory disease only

125
Q

NAFLD gene for progressive disease

A

PNPLA3

126
Q

Most important management for alcoholic hepatitis

A

Nutrition

127
Q

When to give steroids in Alcoholic hepatitis

A

MELD or MADDREY score > 21

128
Q

MOA of terlipression

A

Splanchnic vasoconstriction

129
Q

1st line for eosinophillic oesophagitis

A

PPI

130
Q

components of the MELD score

A

INR, bilirubin, creatinine

131
Q

HNPCC features

A

R sided
age <50
MSI high

132
Q

Drug most likely to achieve clinical remission in 1 year in ulcerative colitis

A

Vedolizumab

133
Q

Calcifications and recurrent pancreatitis

A

Hereditary Pancreatitis

134
Q

Variceal haemorrhage risk is best assessed by:

A

Variceal size

135
Q

Management of perianal Crohns

A

TNFa - Infliximab, Adalimumab

136
Q

Should steroids in acute severe UC be delayed until infective colitis is ruled out.

A

NO. Give steroids immediately

137
Q

Management of CMV colitis in IBD

A

Treatment of CMV colitis is intravenous ganciclovir 5mg/kg twice daily
for 3-5 days followed by oral valganciclovir 900mg PO twice daily for 2-3
weeks.

138
Q

Autoimmune hepatitis antibody screen

A

antinuclear antibodies (ANA)
anti-smooth muscle antibodies (ASMA)
anti-mitochondrial antibodies (AMA)
anti-liver/kidney microsomal-1 antibodies (anti-LKM-1)
immunoglobulin G (IgG) or gamma globulin level.

139
Q

Management of auto-immune hepatitis

A

Prednisolone monotherapy +/- Azathioprine if moderate-severe disease.

140
Q

Drug which is added to Hep C treatment (Sofosbuvir + Velpatasvir) in decompensated liver disease patients

A

Ribavirin - It is a guanosine (ribonucleic) analog used to stop viral RNA synthesis and viral mRNA capping, thus, it is a nucleoside inhibitor.

141
Q

Use of glecaprevir plus pibrentasvir is contraindicated with the use of which other drug

A

Oestradiol

142
Q

Use of sofosbuvir with a second DAA for the treatment of HCV is contraindicated with concomitant use of which other drug.

A

Amiodarone - high risk of bradycardia.

143
Q

APRI score

A

100xAST ratio / Plt count - estimates fibrosis of the liver for those with hepatitis C

144
Q

Highest risk immunosuppression for Hepatitis reactivation

A
  1. CD20 and Haematopoietic SCT

2. Prednisolone and Alemtuzumab

145
Q

Evaluation of ascites

A
  1. SAAG >11 (note this is a GRADIENT not a RATIO)
  2. Protein count >25 = infection/ malignancy/ cardiogenic
  3. WCC (neuts, PMN) >250 = treat for SBP.
146
Q

Ammonia metabolism in liver

A

converted to glutamine

147
Q

Holotranscobalamin (holoTC) transports vitamin B-12 into the cells by binding to which receptor

A

CD320

148
Q

Most common extra-intestinal manifestation in IBD

A

Joint - IBD is a.w. a non-destructive peripheral arthritis, primarily affecting the large joints and ankylosing spondylitis.

149
Q

surveillance intervals for polyps on colonoscopy

A 
No polyps - FOBT 
Low risk (<1cm, <2 polyps)- 5 years 
High risk (>1cm, <4 polyps) - 3 years 
Multiple (>4) - 1 year 
Incomplete colonoscopy/resection <6 months.
150
Q

What is absorbed at each part of the GIT

A

Stomach - water, alcohol, iodide, fluoride
Duodenum/proximal jejunum - iron, vitamins, minerals, folate
Ileum - B12, lipids, monosaccharides, amino acids
Large bowel - Vit K, water, short chain fatty acids

151
Q

Highest risk feature and lowest risk feature for varices from the following:

  • high number of variceal columns
  • large size
  • red wale markings
  • Child Pugh C
  • High portal vein pressure
A

Highest risk - variceal size

Lowest risk - number of variceal columns

152
Q

What type of mutation causes the C282Y mutation in hereditary hemochromatosis

A

cysteine to tyrosine substitution

153
Q

Complications of Hemochromatosis

A

• Liver disease with fibrosis or cirrhosis, with hepatocellular
carcinoma occurring in up to a third of cirrhotic patients
• Arthritis
• Gonadal failure
• Diabetes mellitus
• Cardiac failure and arrhythmias.

154
Q

Symptoms of hemochromatosis that do not improve post treatment (regular venesection)

A
  • arthropathy

- insulin dependant diabetes may partially improve

155
Q

HCC surveillance method and timing

A

6 monthly liver US and AFP

156
Q

Causes of high ferritin (5)

A
  • liver disease
  • HLH
  • chronic inflammation
  • HIV
  • malignancy
157
Q

Markers for macrocytic anaemia that differentiates if it is due to B12 or folate deficiency + interpretation.

A

B12 deficiency - homocystine high/ MMA high
Folate deficiency - homocystine high/ MMA normal.

MMA = methylmalonic acid

158
Q

Management for fistulising Crohns disease

A

TNF agents - work really well for fistulizing disease

159
Q

When should the follow up C-scope be after bowel resection for Crohns?

A

6 months - early scopes due to high risk of recurrence

should also give metronidazole to everyone post op

160
Q

Least effective TNFa agent for Ulcerative colitis

A

Adalimumab - more evidence in Crohns

161
Q

IBS diagnostic criteria (Rome IV criteria)

A
  1. Symptoms >3month and >once a week
  2. Pain on defecation
  3. Associated with change in frequency and form of stool
162
Q

Can Hep C patients be used as organ donors?

A

Yes - treatment with 4 weeks of antivirals prevents recipient infection,

163
Q

Which TNF agent has poor efficacy in IBD

A

Etanercept - as it only works on soluble TNF

164
Q

Why is Certolizumab preferred in pregnancy

A

It is PEGylated therefore dont cross the placenta

165
Q

Which gene controls hepcidin expression

A

HFE

166
Q

Liver zones and causes of injury

A

Zone I: The periportal zone
Is best oxygenated and, therefore, is most resistant to ischemia. Affected first in viral hepatitis and toxic substance ingestion, e.g., cocaine.

Zone II: intermediate zone (affected in yellow fever)

Zone III: pericentral vein/centrilobular zone
The least oxygenated zone, and thus most susceptible to ischemia. Most sensitive to metabolic toxins (e.g., ethanol, CCl4, halothane, rifampin, acetaminophen)
Has the highest amount of cytochrome P-450

Nimna's Flash Cards (15 decks)

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