gastroenterology Flashcards

(77 cards)

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
5ASA/ sulphonamides SE:
rashes headache Heinz body anaemia megaloblastic anaemia lung fibrosis oligospermia
26
mesalazine what is it?
delayed release form of 5-ASA (therefore avoids sulphonamide SE)
27
mesalazine SE:
headache GI upset pancreatitis interstitial nephritis agranulocytosis
28
azathioprine i. test to do prior to starting ii. is it pregnancy safe?
i. TPMT levels ii. yes
29
azathioprine SE:
bone marrow suppression N&V pancreatitis non-melanoma skin cancer
30
mercaptopurine SE
myelosuppression
31
methotrexate SE:
myelosuppression mucositis lung fibrosis liver fibrosis
32
ciclosporin SE
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
ascites classification:
based on SAAG >/< 11g/L
34
SAAG >11g/L causes
[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
SAAG <11g/L causes
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
acute liver F bloods:
increased PT low albumin
37
how to calculate alcohol units:
volume x %alcohol / 1000
38
Budd Chiari what is it?
hepatic vein thrombosis (usually seen in the context of underlying haematological disease or another procoagulant condition)
39
Budd Chiari causes (4)
polycythaemia rubra vera thrombophilia pregnancy COCP
40
Budd Chiari features:
TRIAD abdominal pain: sudden onset, severe ascites → abdominal distension tender hepatomegaly
41
Budd Chiari ix:
doppler USS
42
carcinoid tumours what is it/ what happens?
when liver mets release serotonin into systemic circulation
43
carcionoid tumours presentation:
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
carcinoid tumours ix
urinary 5-HIAA plasma chromogranin A y
45
carcinoid tumours mgt
somatostatin analogues e.g. octreotide diarrhoea: cyproheptadine may help
46
haemachromatosis inheritance and mutation
autosomal recessive HFE gene chromosome 6
47
haemachromatosis presentation
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
haemochromatosis reversible cx:
cardiomyopathy skin pigmentation
49
haemochromatosis irreversible cx:
liver cirrhosis diabetes Hypogonadotrophic hypogonadism Arthropathy
50
what is melanosis coli associated with
laxative abuse, especially senna
51
hepatocellular carcinoma- most common cause: i. in Europe ii. worldwide
i. hep C ii. Hep B
52
haemochromatosis monitoring:
FBC transferrin ferritin
53
typical iron study profile in haemochromatosis:
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
indications for upper GI endoscopy in pts with GORD: (4)
age >55 sx >4 weeks or persistent despite rx relapsing sx weight loss
55
h. pylori eradication rx :
a proton pump inhibitor + amoxicillin + (clarithromycin OR metronidazole) if penicillin-allergic: a proton pump inhibitor + metronidazole + clarithromycin
56
hepatic encephalopathy mgt
lactulose rifaximin
57
vitamin B3 deficiency sx
Pellagra 3Ds diarrhoea dermatitis dementia
58
HBSAg
implies acute disease if +ve for > 6months = chronic disease produces anti-HBS
59
anti- HBS
implies immunity or exposure only +ve one in previous immunisation -ve in chronic disease
60
what is HBeAg?
= breakdown product of core antigen of infected liver cells
61
anti-HBc
implies previous or current infection IgM anti-HBc acute/ previous infection (present for 6 months) IgG anti-HBC persists
62
Peutz-Jeghers syndrome inheritence
AD
63
Peutz-Jeghers syndrome features
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
adverse effects of PPIs:
osteoporosis increased c diff risk hyponatraemia hypomagnasaemia microscopic colitis
65
Wilson's disease inheritance
autosomal recessive ATP7B gene on chromosome 13
66
Wilson's disease features:
liver: hepatitis, cirrhosis neurological: basal ganglia degeneration: asterixis, chorea, dementia, parkinsonism Kayser-Fleischer rings renal tubular acidosis (esp. Fanconi syndrome) haemolysis blue nails
67
Wilson's disease bloods:
reduced caeruloplasmin reduced serum copper (as copper is carried by caeruloplasmin raised urinary copper
68
Wilson's mgt
penicillamine (chelated copper) trientine hydrochloride (2nd line)
69
PBC associations (4)
Sjogren's RA systemic sclerosis thyroid disease
70
PBC features:
initially asx but raised ALP cholestatic jaundice hyperpigmentation (especially on pressure points) RUQ pain xanthelasma/ xanthoma clubbing hepatoslpenomegaly --> eventually cirrhosis
71
PBC ix
AMA raised IgM MRCP
72
PBC mgt
ursodeoxycholic acid cholestyramine for itch
73
PBC cx
osteomalacia/ osteoporosis hepatocellular carcinoma cirrhosis --> portal HTN --> ascites + variceal haemorrhage
74
PSC associations
UC Crohn's (less so than UC) HIV
75
PSC features
cholestasis - jaundice - rasied bilirubin, raised ALP RUQ pain fatigue
76
PSC ix:
ERCP/ MRCP --> multiple strictures showing beaded appearance pANCA
77
PSC cx:
cholangiocarcinoma colorectal cancer