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MSRA > gastroenterology > Flashcards

gastroenterology Flashcards

1
Q

duodenal biopsy findings in coeliac: (4)

A

villous atrophy
crypt hyperplasia
increase in intraepithelial lymphocytes
lamina propria infiltration with lymphocytes

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2
Q

when to give SBP (spontaneous bacterial peritonitis) prophylaxis?

abx of choice?

A

previous SBP
protein concenration </=15g/L
+ 1 of:
ascites
Child-Pugh score of at least 9
hepatorenal syndrome

give ciprofloxacin/ norfloxacin

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3
Q

most commonly affected site for Crohn’s

A

terminal ileum and colon

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4
Q

what makes extra-intestinal features more common in Crohn’s

A

peri-anal disease

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5
Q

IBD extra-intestinal features that ARE associated with disease activity (4)

A

asymmetrical pauciarticular arthritis
erythema nodosum
episcleritis (more common in CROHN’s)
osteoporosis

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6
Q

IBD extra-intestinal features NOT associated with disease activity (5)

A

symmetrical periarticular arthritis
uveitis (more common in UC)
pyoderma gangrenosum
clubbing
PSC (more common in UC)

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7
Q

occular manifestation of IBD more common in:
i. Crohn’s
ii. UC

A

i. episcleritis

ii. uveitis

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8
Q

most common site for UC

A

rectum

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9
Q

Crohn’s mgt - INDUCING remission

A
  1. PO steroids / budesonide (less common)
  2. 5-ASA (e.g. mesalazine)
  3. +ons sulphasalazine/ methotrexate
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10
Q

Crohn’s mgt MAINTAINING remission

A

stop smoking

  1. azathioprine/ mercaptopurine (require measurement of TPMT 1st)
  2. methotrexate
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11
Q

UC: classification of severity

A
  1. mild
    <4 stools/ day
    minimal blood
  2. moderate
    4-6 stools/ day
    varying blood
  3. severe
    6+ stools /day
    systemic upset
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12
Q

INDUCING remission UC
mild - moderate proctitis mgt

A
  1. topical aminosalicylate
  2. add PO aminosalicylate if no improvement after 4 weeks
  3. add PO steroids if still no improvement
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13
Q

INDUCING remission UC
mild-mod proctosigmoisitis + L-sided UC

A
  1. topical aminosalicylate
  2. add PO aminosalicylate/ topical steroid
  3. add PO aminosalicylate + PO steroid
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14
Q

INDUCING remission UC
mild-mod extensive UC

A
  1. topical aminosalicylate +PO aminosalicylate
  2. PO aminosalicylate + PO steroid
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15
Q

INDUCING remission
severe UC

A

hospital admission + iv steroids
if no improvement after 72 hours consider addition of ciclosporin or surgery

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16
Q

MAINTAINING remission UC
proctitis and proctosigmoiditis:

A

topical (rectal) aminosalicylate alone (daily or intermittent)
or
an oral aminosalicylate plus a topical (rectal) aminosalicylate (daily or intermittent)
or
an oral aminosalicylate by itself: this may not be effective as the other two options

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17
Q

MAINTAINING remission UC
left-sided and extensive ulcerative colitis:

A

low maintenance dose of an oral aminosalicylate

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18
Q

MAINTAINING remission UC
following severe relapse or >=2 exacerbations in the past year

A

oral azathioprine or oral mercaptopurine

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19
Q

Crohn’s histology

A

inflammation of all layers
^^ goblet cells
granulomas

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20
Q

UC histology

A

submucosal inflammation only
decreased goblet cells
rarely granulomas
crypt abscesses

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21
Q

Crohn’s on endoscopy

A

skip lesions “cobblestone appearance”

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22
Q

UC on endoscopy

A

psuedopolyps

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23
Q

Crohn’s radiology
i. ix
ii. findings

A

i. small bowel enema

ii. strictures
proximal bowel dilatation
“rose thorn” ulcers
fistulae

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24
Q

UC radiology
i. ix
ii. findings

A

i. barium enema

ii. loss of haustrations
pseudopolyps
drainpipe colon in extensive disease

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25
Q

5ASA/ sulphonamides SE:

A

rashes
headache
Heinz body anaemia
megaloblastic anaemia
lung fibrosis
oligospermia

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26
Q

mesalazine
what is it?

A

delayed release form of 5-ASA
(therefore avoids sulphonamide SE)

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27
Q

mesalazine SE:

A

headache
GI upset
pancreatitis
interstitial nephritis
agranulocytosis

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28
Q

azathioprine
i. test to do prior to starting
ii. is it pregnancy safe?

A

i. TPMT levels
ii. yes

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29
Q

azathioprine SE:

A

bone marrow suppression
N&V
pancreatitis
non-melanoma skin cancer

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30
Q

mercaptopurine SE

A

myelosuppression

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31
Q

methotrexate SE:

A

myelosuppression
mucositis
lung fibrosis
liver fibrosis

32
Q

ciclosporin SE

A

note how everything is increased - fluid, BP, K+, hair, gums, glucose

nephrotoxicity
hepatotoxicity
fluid retention
hypertension
hyperkalaemia
hypertrichosis
gingival hyperplasia
tremor
impaired glucose tolerance
hyperlipidaemia
increased susceptibility to severe infection

33
Q

ascites classification:

A

based on SAAG >/< 11g/L

34
Q

SAAG >11g/L causes

A

[indicates portal HTN]

  1. liver disorders
    –> cirrhosis, alcoholic liver disease, acute liver F, liver mets
  2. cardiac
    - R heart F
    - constrictive pericarditis

Budd-Chiari syndrome
portal vein thrombosis
veno-occlusive disease
myxoedema

35
Q

SAAG <11g/L causes

A

Hypoalbuminaemia
- nephrotic syndrome
- severe malnutrition (e.g. Kwashiorkor)

Malignancy
- peritoneal carcinomatosis

Infections
- tuberculous peritonitis

pancreatitis
bowel obstruction
biliary ascites
postoperative lymphatic leak
serositis in connective tissue diseases

36
Q

acute liver F bloods:

A

increased PT
low albumin

37
Q

how to calculate alcohol units:

A

volume x %alcohol / 1000

38
Q

Budd Chiari

what is it?

A

hepatic vein thrombosis
(usually seen in the context of underlying haematological disease or another procoagulant condition)

39
Q

Budd Chiari
causes (4)

A

polycythaemia rubra vera
thrombophilia
pregnancy
COCP

40
Q

Budd Chiari
features:

A

TRIAD
abdominal pain: sudden onset, severe
ascites → abdominal distension
tender hepatomegaly

41
Q

Budd Chiari ix:

A

doppler USS

42
Q

carcinoid tumours

what is it/ what happens?

A

when liver mets release serotonin into systemic circulation

43
Q

carcionoid tumours presentation:

A

flushing (earliest symptom)
diarrhoea
bronchospasm
hypotension
right heart valvular stenosis (left heart can be affected in bronchial carcinoid)

Cushing’s (if other molecules
such as ACTH and GHRH are secreted)
pellagra (rarely)

44
Q

carcinoid tumours ix

A

urinary 5-HIAA
plasma chromogranin A y

45
Q

carcinoid tumours mgt

A

somatostatin analogues e.g. octreotide
diarrhoea: cyproheptadine may help

46
Q

haemachromatosis inheritance and mutation

A

autosomal recessive

HFE gene chromosome 6

47
Q

haemachromatosis presentation

A

early symptoms: fatigue, erectile dysfunction and arthralgia (often of the hands)
‘bronze’ skin pigmentation
diabetes mellitus
liver: stigmata of chronic liver disease
cardiac failure (2nd to dilated cardiomyopathy)
hypogonadism (2nd to cirrhosis and pituitary dysfunction - hypogonadotrophic hypogonadism)
arthritis (especially of the hands)

48
Q

haemochromatosis reversible cx:

A

cardiomyopathy
skin pigmentation

49
Q

haemochromatosis irreversible cx:

A

liver cirrhosis
diabetes
Hypogonadotrophic hypogonadism
Arthropathy

50
Q

what is melanosis coli associated with

A

laxative abuse, especially senna

51
Q

hepatocellular carcinoma- most common cause:
i. in Europe
ii. worldwide

A

i. hep C
ii. Hep B

52
Q

haemochromatosis monitoring:

A

FBC
transferrin
ferritin

53
Q

typical iron study profile in haemochromatosis:

A

HIGH transferrin saturation > 55% in men or > 50% in women (this is the first bit of bloods to go “off”)
raised ferritin (e.g. > 500 ug/l) and iron
low TIBC

54
Q

indications for upper GI endoscopy in pts with GORD: (4)

A

age >55
sx >4 weeks or persistent despite rx
relapsing sx
weight loss

55
Q

h. pylori eradication rx :

A

a proton pump inhibitor + amoxicillin + (clarithromycin OR metronidazole)

if penicillin-allergic: a proton pump inhibitor + metronidazole + clarithromycin

56
Q

hepatic encephalopathy mgt

A

lactulose
rifaximin

57
Q

vitamin B3 deficiency sx

A

Pellagra

3Ds
diarrhoea
dermatitis
dementia

58
Q

HBSAg

A

implies acute disease
if +ve for > 6months = chronic disease

produces anti-HBS

59
Q

anti- HBS

A

implies immunity or exposure

only +ve one in previous immunisation

-ve in chronic disease

60
Q

what is HBeAg?

A

= breakdown product of core antigen of infected liver cells

61
Q

anti-HBc

A

implies previous or current infection

IgM anti-HBc acute/ previous infection (present for 6 months)

IgG anti-HBC persists

62
Q

Peutz-Jeghers syndrome inheritence

63
Q

Peutz-Jeghers syndrome
features

A

hamartomatous polyps in the gastronintestinal tract (mainly small bowel)

small bowel obstruction, often due to intussusception
gastrointestinal bleeding

pigmented lesions on lips, oral mucosa, face, palms and soles

mgt = conservative unless cx develop

64
Q

adverse effects of PPIs:

A

osteoporosis
increased c diff risk
hyponatraemia
hypomagnasaemia
microscopic colitis

65
Q

Wilson’s disease inheritance

A

autosomal recessive

ATP7B gene on chromosome 13

66
Q

Wilson’s disease features:

A

liver: hepatitis, cirrhosis
neurological:
basal ganglia degeneration: asterixis, chorea, dementia, parkinsonism
Kayser-Fleischer rings
renal tubular acidosis (esp. Fanconi syndrome)
haemolysis
blue nails

67
Q

Wilson’s disease bloods:

A

reduced caeruloplasmin
reduced serum copper (as copper is carried by caeruloplasmin

raised urinary copper

68
Q

Wilson’s mgt

A

penicillamine (chelated copper)

trientine hydrochloride (2nd line)

69
Q

PBC
associations (4)

A

Sjogren’s
RA
systemic sclerosis
thyroid disease

70
Q

PBC features:

A

initially asx but raised ALP
cholestatic jaundice
hyperpigmentation (especially on pressure points)
RUQ pain
xanthelasma/ xanthoma
clubbing
hepatoslpenomegaly

–> eventually cirrhosis

71
Q

PBC ix

A

AMA
raised IgM
MRCP

72
Q

PBC mgt

A

ursodeoxycholic acid
cholestyramine for itch

73
Q

PBC cx

A

osteomalacia/ osteoporosis
hepatocellular carcinoma

cirrhosis –> portal HTN –> ascites + variceal haemorrhage

74
Q

PSC associations

A

UC
Crohn’s (less so than UC)
HIV

75
Q

PSC features

A

cholestasis
- jaundice
- rasied bilirubin, raised ALP

RUQ pain
fatigue

76
Q

PSC ix:

A

ERCP/ MRCP
–> multiple strictures showing beaded appearance

pANCA

77
Q

PSC cx:

A

cholangiocarcinoma
colorectal cancer

MSRA (16 decks)

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