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2a SB-CS > GI 3 - cancers, infections + drugs. > Flashcards

GI 3 - cancers, infections + drugs. Flashcards

1
Q

give 3 bacterial causes of infective diarrhoea

A

C difficile - e.g. hx of abx use (rest are travel).
shigella, salmonella, campylobacter, aeromonas, vibrio cholera.
E coli

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2
Q

what would you test the stool for, when investigating infective diarrhoea?

A

MC&S, ova cysts, parasites, C diff toxin.

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3
Q

give 2 viral causes of infective diarrhoea

A

norovirus - cruise ships etc.

rotavirus.

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4
Q

give 2 protozoal causes of infective diarrhoea

A

Giardia intestinalis
Entamoeba histolytica
Cryptosporidium parvum
Cyclospora cayetanensis

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5
Q

describe the pathogen that causes cholera

A

Vibrio cholera.
gram -ve curved flagellated motile vibrating/swarming rod.
faecal-oral spread.

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6
Q

describe the clinical features of cholera

A

profuse (1L/h) rice water stools, fever, vomiting, rapid dehydration.

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7
Q

how would you treat cholera?

A

tetracycline.

oral rehydration sachets.

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8
Q

how would you treat infective diarrhoea caused by salmonella, shigella or campylobacter?

A

ciprofloxacin oral/IV

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9
Q

describe the clinical features of bacillary dysentery.

A

abdo pain and bloody diarrhoea ± sudden fever and headache

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10
Q

what organism causes bacillary dysentery? how would you treat it?

A

shigella.

ciprofloxacin + avoid antidiarrhoeal drugs.

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11
Q

what type of tumours can arise from the oesophagus and where?

A

adenocarcinoma - lower third.

squamous carcinoma - upper 2 thirds.

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12
Q

name 2 risk factors for oesophageal carcinoma

A

smoking, alcohol, Barrett’s/GORD, obesity, achalasia, low vitamin A/C, nitrosamine exposure

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13
Q

give 3 symptoms of an oesophageal tumour

A

progressive dysphagia (initially for solids, then liquids too).

cough, weight loss, anorexia, retrosternal chest pain, dyspepsia

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14
Q

what would be your investigations of choice for diagnosis of oesophageal cancer, and then for staging?

A

endoscopic ultrasound with fine needle aspiration/biopsy of tumour.

CT for staging.

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15
Q

given most oesophageal cancers present late, what kind of treatment would you consider?

A

palliative - soft diet, oesophageal stent, analgesia - chemo/radiotherapy can be used palliatively.

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16
Q

what AIDS defining illness affects the oesophagus?

A

Kaposi’s sarcoma - found in mouth, oesophagus and hypopharynx

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17
Q

give 2 signs that indicate an oesophageal carcinoma is in the upper 1/3rd of the oesophagus

A

hoarseness and cough

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18
Q

give 2 differential diagnoses of oesophageal cancer

A

those of dysphagia

oesophagitis, diffuse oesophageal spasm, achalasia, benign oesophageal stricture

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19
Q

how are oesophageal cancers staged?

A 
TNM system.
T1 = invading lamina propria
T2 = muscularis propria 
T3 = adventitia
T4 = invasion of adjacent structures
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20
Q

what curative treatment might you attempt in a patient who has presented with early (local T1/T2) oesophageal carcinoma?

A

radical curative oesophagectomy + pre-op chemo with cisplatin

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21
Q

what is the main type of carcinoma affecting the stomach?

A

adenocarcinoma

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22
Q

give 3 things associated with gastric adenocarcinoma

A

pernicious anaemia, blood group A, H pylori, atrophic gastritis, adenomatous polyps, lower social class, smoking.
diet - high nitrates, salt, pickling, low vit C

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23
Q

what main lymph node is infiltrated in gastric tumours?

A

Virchow’s node (neck)

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24
Q

give 2 symptoms of gastric adenocarcinoma

A 
epigastric pain relieved by food and antacids
nausea
vomiting
anorexia
weight loss
dyspepsia
dysphagia
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25
Q

give 2 signs of gastric adenocarcinoma

A

anaemia, jaundice, palpable epigastric mass with tenderness, Virchow’s node infiltration, dermatomyositis, acanthosis nigricans

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26
Q

in which part of the stomach do adenocarcinomas most commonly occur?

A

antrum

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27
Q

what makes up the Borrmann classification of gastric adenocarcinomas?

A

i. polypoid
ii. excavating
iii. ulcerating and raised
iv. diffusely infiltrative

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28
Q

how might gastric adenocarcinomas spread?

A

locally, lymphatics, blood borne (haematogenous), transcoelomic

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29
Q

what investigations would you perform in gastric adenocarcinoma?

A

gastroscopy + multiple ulcer edge biopsies.
endoscopic ultrasound.
CT for staging.

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30
Q

describe the treatment options for gastric adenocarcinoma

A

partial/total gastrectomy.
chemo - epirubicin, cisplatin, 5-fluorouracil.
surgical palliation - for obstruction, pain or haemorrage.

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31
Q

give 2 cell types that gastrointestinal stromal tumours (GIST)s could be

A

leiomyomas, leiomyosarcomas, leiomyoblastomas, Schwannomas

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32
Q

what are the treatment options for gastrointestinal stromal tumours?

A

1st line - surgical resection

2nd line - imatinib.

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33
Q

what is gastric lymphoma?

A

arises from mucosal areas from mucosa-associated lymphoid tissue - MALToma.

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34
Q

how would you treat a gastric lymphoma?

A

most are associated with H pylori - eradication.

surgery or chemo ± radiotherapy

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35
Q

which type of gastric polyp is pre-malginant?

A

adenomatous polyps.

hyperplastic polyps aren’t malignant, but can be accompanied by pre-malignant atrophic gastritis.

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36
Q

which types of gastric polyps are benign?

A

cystic gland, inflammatory fibroid polyps, hyperplastic polyps

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37
Q

where are adenocarcinomas and lymphomas found in the small intestine?

A

adenocarcinoma - duodenum and jejunum.

lymphoma - ileum.

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38
Q

what are the different types of lymphoma that can arise in the intestine?

A

Non-Hodgkin’s.
B cell, arising from MALT - polypoid masses in distal/terminal ileum.
T cell - ulcerated/strictures in proximal ileum.

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39
Q

what AIDS defining lymphoma can occur in the small intestine and where?

A

Burkitt’s lymphoma - terminal ileum of children

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40
Q

how might malignant small intestinal tumours be treated?

A

surgical excision ± chemo/radiotherapy

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41
Q

what autosomal dominant condition can cause benign small bowel tumours?

A

Peutz-Jeghers syndrome - mucocutaneous pigmentation and hamartomatous GI polyps - can undergo malignant change.

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42
Q

what type of cells do carcinoid tumours arise from and where in the small intestine are they found?

A

enterochromaffin cells, in appendix, ileum and rectum

43
Q

what is carcinoid syndrome?

A

only occurs with liver mets, spontaneous red-blue flushing mainly on face and neck (kinins), pulmonary stenosis/tricuspid incompetence (5-HT), hepatomegaly.

tumours secrete serotonin, bradykinin, histamine, prostaglandins.

44
Q

how would you treat carcinoid tumours?

A

somatostatin analogues - ocreotide and lanreotide.

45
Q

what is a polyp? what type of lesion are most colonic polyps?

A

abnormal growth of tissue projecting into the intestinal lumen from the normally flat mucosal surface.
usually adenomas.

46
Q

what is the clinical significance of colonic polyps?

A

they’re the precursor lesions of most colorectal cancer

47
Q

list 3 features of an adenomatous polyp that increases the risk of malignant change

A 
size >1cm.
sessile polys (attached to colon wall directly) > pedunculated polyps (mucosal stalk between polyp and wall).
severe dysplasia (>mild)
villous histology > tubular.
multiple polyps > singular.
48
Q

what is HNPCC?

A

hereditary nonpolyposis colorectal cancer.

DNA mismatch repair genes are mutated.

49
Q

what is the pathway of developing a colorectal cancer from a polyp?

A

normal epithelium => adenoma (polyp) => colorectal adenocarcinoma

50
Q

how is colorectal cancer risk increased in patients HNPCC?

A

accelerated progression from polyps to CRC - doesn’t increase no. polyps, just speeds up their progression to malignancy.

51
Q

what gene is mutated in familial adenomatous polyposis?

A

APC gene

52
Q

how does FAP increase risk of colorectal cancer?

A

patient develops loads and loads of colorectal polyps in teenage years - increased risk of extracolonic malignancies.
100% lifetime risk of CRC, onset in young adults.

53
Q

how can colorectal cancer be prevented in people with FAP?

A

regular screening from age of 12, prophylactic total colectomy at 20.

54
Q

what other cancers, apart from CRC, are associated with FAP?

A

thyroid, pancreatic and hepatoblastomas.

55
Q

give 3 risk factors of colorectal carcinoma

A

increasing age, obesity, IBS, diabetes, obesity, alcohol, FHx, colorectal polyps, low fibre diet, genetic predisposition (FAP. HNPCC), smoking, UC and Crohn’s

56
Q

explain the different clinical features of right and left sided colorectal carcinomas

A

left - PR bleeding/mucus, obstruction, tenesmus, PR mass.
right - weight loss, anaemia, abdo pain, usually asymptomatic.

either - abdo mass, perforation, haemorrhage, fistula

57
Q

what is the gold standard investigation in colorectal carcinoma?

A

colonoscopy with biopsy

58
Q

describe the UK bowel cancer screening programme

A

all >60yrs has faecal occult blood testing every 2yrs - positive result = endoscopy.

59
Q

which parts of the colon/rectum are most commonly affected by colorectal cancer?

A

rectum - 27%.
sigmoid colon - 20%.
caecum - 14%

60
Q

what are the urgent referral criteria for bowel cancer?

A

1) over 40 with PR bleeding and change in bowel habit
2) any age with R lower abdo mass
3) palpable rectal mass
4) men/non-menstruating women with unexplained iron deficiency anaemia

61
Q

explain the Dukes’ criteria system for staging colorectal carcinoma

A

A - limited to muscularis mucosae
B - extension through muscularis mucosae
C - involvement of regional lymph nodes
D - distant metastases

62
Q

what is generally the treatment for colorectal carcinoma?

A

surgical resection followed by post-op chemo/radiotherapy.

63
Q

are most liver tumours primary or secondary?

A

90% are secondary.

64
Q

list some common origins of secondary liver tumours

A

men - stomach, lung, colon.

women - breast, colon, stomach, uterus.

65
Q

what are the 5 types of primary malignant liver tumours?

A 
hepatocellular carcinoma (HCC).
cholangiocarcinoma
angiosarcoma
hepatoblastoma
fibrosarcoma and hepatic GIST
66
Q

list the 5 types of primary benign liver tumours

A

cysts, haemangioma, focal nodular hyperplasia, fibroma, benign GIST

67
Q

list 3 symptoms of liver tumours

A

fever, malaise, anorexia, weight loss, RUQ pain.

jaundice - late, apart from in cholangiocarcinoma.

68
Q

list 3 signs of liver tumours

A 
hepatomegaly - smooth, or hard and irregular (mets, cirrhosis, HCC).
signs of chronic liver disease.
jaundice/ascites.
abdo mass. 
bruit over liver = HCC.
69
Q

how would you investigate liver cancer?

A

bloods.

US guided biopsy / MRI.

70
Q

what protein is raised in serum in HCC?

A

alpha fetoprotein

71
Q

how would you treat liver metastases? what is the prognosis?

A

mostly palliative treatment - prognosis is often less than 6/12

72
Q

list 3 causes of HCC

A

*HBV.

HCV, autoimmune hepatitis, cirrhosis, non-alcoholic fatty liver, aflatoxin, clonorchis sinesis, anabolic steroids.

73
Q

how would you diagnose HCC?

A

4 phase liver CT.
MRI.
biopsy.

74
Q

how might HCC be treated?

A

resect solitary tumours.
liver transplant.
percutaneous ablation, tumour embolisation and sorafenib.

75
Q

give 3 causes of cholangiocarcinoma

A

flukes, primary sclerosing cholangitis, HBV, HCV, diabetes mellitus.

76
Q

what breakdown product is raised in the serum of those with cholangiocarcinoma?

A

bilirubin

77
Q

how might cholangiocarcinoma be managed?

A

precutaneous (or via ERCP) stenting of obstruction.

surgery not an option.

78
Q

what is the usual prognosis of cholangiocarcinoma?

A

5 months

79
Q

what is the most common benign liver tumour? should it be biopsied?

A

haemangiomas.

incidental finding on US/CT - DON’T biopsy.

80
Q

what are hepatic adenomas associated with? when is surgical resection indicated?

A

oral contraceptives, anabolic steroids.

only if symptomatic.

81
Q

list some risk factors for pancreatic carcinoma

A 
male >60yo
smoking
alcohol
carcinogens
diabetes mellitus
chronic pancreatitis
central adiposity
diet high in fat + red/processed meat
82
Q

what is the genetic association seen in pancreatic carcinoma?

A

95% have mutations in KRA52

83
Q

what are the clinical features of carcinoma of the head of pancreas?

A

painless obstructive jaundice (pain late on, radiates to back).

pruritus, Courvoisier’s sign (enlarged, palpable gallbladder), central abdo mass, hepatomegaly

84
Q

what are the clinical features of carcinoma of the body/tail of pancreas?

A

abdo pain, weight loss, anorexia, dull ache radiating to back, relieved when sitting forward.
polyarthritis, skin nodules

85
Q

what investigations would you carry out in pancreatic carcinoma?

A

transabdominal ultrasound.
CT.
bloods - Ca19-9 antigen - not specific, but good marker for monitoring progress.

86
Q

how would you manage a patient with pancreatic carcinoma? what is their prognosis like?

A

surgical resection with post-op chemo or palliative endoscopic stents.
opiates/radiotherapy for pain.

mean survival less than 6/12.

87
Q

name 2 PPIs

A

lansoprazole, omeprazole, pantoprazole

88
Q

how do PPIs work?

A

reduce gastric acid secretion by irreversibly inhibiting H+/K+ ATPase in gastric parietal cells - this is the proton pump responsible for secreting H+.
suppresses gastric acid production almost completely.

89
Q

give an example of an H2 receptor antagonist

A

ranitidine

90
Q

why are H2 receptor antagonists not as good at suppressing gastric acid secretion as PPIs?

A

blocking the H2 receptor reduces the activation of the proton pump - but the pump can be activated by other pathways, so does not completely suppress secretion like PPIs do.

91
Q

how does loperamide work?

A

agnoist of the opioid mu-receptors in GI tract - increases non-propulsive contractions of the gut smooth muscle, but reduces peristaltic contractions.

transit of bowel content is thus slowed, and anal sphincter tone is increased - more water absorbed from faeces as there’s more time for this, so stools are hardened.

92
Q

give 2 examples of aminosalicylates - what are they used for?

A

mesalazine - UC.

sulfasalazine - UC + RA.

93
Q

how do aminosalicylates work to treat UC?

A

release 5-ASA, which has anti-inflammatory and immunosuppressive effects and acts topically on the gut.

94
Q

name an antimuscarinic with a GI use - what disease is used to treat and why?

A

hyoscine butylbromide - first line for IBS, used for their antispasmodic effects.

95
Q

how do antimuscarinics work in the gut?

A

bind to muscarinic ACh receptor and competitively inhibit ACh - increase in peristaltic contraction and reduction in smooth muscle tone, and reduced gut secretions - opposite to parasympathetic rest and digest effects.

96
Q

name an acetylcholinesterase inhibitor with a GI indication and what it is used for?

A

neostigmine - used for pseudoobstruction of the colon.

97
Q

how does neostigmine work?

A

it is a reversible acetylcholinesterase inhibitor - increases about of ACh available to stimulate both nicotinic and muscarinic receptors - produces muscle contraction to restore bowel motility.

98
Q

how does ursodeoxycholic acid work?

A

reduces cholesterol absorption and is used to dissolve cholesterol gallstones.
it’s a bile acid that is present in the body anyway.

99
Q

how does cholestyramine work?

A

binds bile in GI tract to prevent its reabsorption by forming insoluble complexes with bile acids, which are then excreted in the faeces.
useful for pruritus in primary biliary cirrhosis/liver failure.
also reduces plasma cholesterol levels.

100
Q

vasoconstrictors such as terlipressin are used to medically manage bleeding oesophageal varices, how do they stop the bleeding?

A

analogue of vaopressin, which itself causes vasoconstriction - reduced blood flow to the area.

101
Q

imatinib is used when surgery isn’t an option for treatment of gastric stromal tumours - how does it work? what haematological disorder is it the principal treatment for?

A

it’s a tyrosine kinase inhibitor, so blocks the transfer of a phosphate group from ATP to a protein in a cell.
cell cannot proliferate.
also used to treat CML.

102
Q

why are somatostatin analogues used to treat carcinoid syndrome?

A

carcinoid tumours release hormones including serotonin, bradykinin etc.
somatostatin analoges inhibit the release and action of these hormones.

103
Q

which types of oesophageal cancer occur in the upper 2/3rd and lower 2/3rd?

A

upper 2/3rd - squamous carcinoma

lower 1/3rd - adenocarcinoma

2a SB-CS (18 decks)

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