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gastrointestinal_week_3_20190518174140 Flashcards

1
Q

what causes oral cancer

A

tobacco and alcohol, HPV, candida

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2
Q

what diet factors cause cancer

A

low in vitamin A, C and iron - causes atrophy of oral mucosa which makes it more susceptible to local carcinogens

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3
Q

how is oral sex tied to cancer

A

HPV 16 and 18associated with oropharyngeal cancer

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4
Q

what is high risk sites for oral cancer

A

soft sites eg ventral tongue/floor of mouth and lateral tongue

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5
Q

what are potentially malignant lesions which can occur in mouth

A

erythroplaskia, arythroleukoplakia, leukoplakia, erosive lichen planus, submucous fibrosis, dyskeratonsis congenita

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6
Q

what is the warning signs for oral cancer

A

red and white lesion, ulcer, numb feeling, unexplained pain in mouth or neck, change in voice, dysphagia

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7
Q

what are other orofacial manifestations of cancer

A

drooping eye lid or facial palsy, fracture of mandible, double vision, blocked or bleeding from nose, facial swelling

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8
Q

what is DMF index

A

sum of decayed, missing or filled teeth of surfaces

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9
Q

what is def

A

a count of all primary teeth that are decayed, extracted due to caries or filled

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10
Q

what is DMFS

A

a count of all decayed or missing or filled tooth surfaces

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11
Q

what diseases can be characterised by inflammation of peridontal tissues

A

gangivitis, peridonitis, necrotising ulcerative gingivitis, peridontal abscess, perio-endo lesion, gingival enlargement

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12
Q

what can endoscopes visually diagnose

A

oesophagitis, gastritis, ulceration, coeliac disease, crohns disease, ulcerative colitis, sclerosing cholangitis

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13
Q

which vascular abnormalities can it detect

A

varices, ectatic blood vessels (GAVE, dieulafoy) and angiopsyplasia (small vessels)

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14
Q

which miscellaneous conditions can it detect

A

mallory-weiss tears, diverticulae, foreign bodies, stones, worms

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15
Q

what is able to be treated down endoscope

A

GI bleeding, nerve blocks, resection of early cancer

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16
Q

how is variecal bleeding treated

A

ABCinjection sclerotherapy (ethanolamine)banding histocryl glue

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17
Q

what is component of ingested lipids

A

fats/oils, phospholipids, cholesterol and cholesterol esters and fatty acids

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18
Q

what is the solubility properties of lipids

A

either insoluble (cholesterol esters) or poorly soluble (causing special problems for digestion and absorption - triacylglycerols and cholesterol)

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19
Q

lipids must be converted from solid fat an oil masses into an emulsion of small oil droplets suspended in water. How does emulsification occur

A

mouth - chewing stomach - gastric churning and squirting through the narrow pylorus - content mixed with digestive enzymes from mouth to stomach SI - segmentation and peristalsis mix luminal content with pancreatic and biliary secretions

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20
Q

how are emulsion droplets stabilised

A

addition of coat of amphiphilic molecules that form surface layer on droplets that include:product of lipid digestion (fatty acids, monoacylglycerols)biliary phospholipids cholesterolbile salts (when droplets have progressively been reduced to unilamellar and mixed micelles)

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21
Q

how does lipid digestion of TAG by enzymes (triacylglycerols - fat)

A

mouth - lingual phasestomach - gastric phase - by gastric lipase - resistant to digestion by pepsin (and lingual lipase in salvia)duodenum - intestinal phase - by pancreatic TAG lipase (produces 2-monoacylgylcerol and free fatty acids

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22
Q

how are bile salts released into duodenum

A

released in bile from the gall bladder in response to CCKThey act as detergents to help emulsify large lipid droplets to small droplets

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23
Q

what does failure to secrete bile salts result in

A

lipid malabsorption - steatorrhoea (fat in faeces)secondary vitamin deficiency due to failure to absorb fat soluble vitamins (A, D, E and K)

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24
Q

what is the downside to bile salts

A

they increase SA for attack by pancreatic lipasethis problem solved by colipase

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25
Q

how are free fatty acids and monoglycerides absorbed

A

transfer between mixed micelles and the apical membrane of enterocyte entering the cell by passive diffusion

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26
Q

what happens to short and medium chain fatty acids once absorbed

A

diffuse through enterocyte, exit through basolateral membrane and enter the villus capillaries

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27
Q

what happens to long chain fatty acids and monoglycerides once absorbed

A

resynthesised to triglycerides in endoplasmic reticulum and are subsequently incorporated into chylomicrons

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28
Q

how is cholesterol absorbed

A

mainly due to transport by endocytosis in clatherin coated pits by Niemann-Pick C1-like 1 (NPC1L1) protein ezetimibe binds to NPC1L1 so prevents cholesterol absorpton

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29
Q

what is acute oesophagitis (rare)

A

corrosive following chemical ingestion infective in immunocompromised patients eg candidiasis, herpes, CMV

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30
Q

what is chronic oesophagitis (common)

A

reflux disease (reflux oesophagitis)rare causes include crohns disease

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31
Q

what is definition of reflux oesophagitis

A

inflammation of oesophagus due to refluxed low pH gastric content

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32
Q

what is potential causes of reflux oesophagitis

A

defective sphincter mechanism abnormal oesophageal motility increased intraabdominal pressure (pregnancy)

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33
Q

what does reflux oesophagitis look like under microscope

A

basal zone epithelial expansion intraepithelial neutrophils, lymphocytes and eosinophils

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34
Q

what are the complications of reflux

A

ulceration (bleeding)stricture barretts oesophagus - replacement of stratified squamous epithelium by columnar epithelium

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35
Q

what is barretts oesophagus look like macroscopically

A

red velvety mucosa in lower oesophagus

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36
Q

what does barretts oesophagus look like microscopically

A

columnar lined mucosa with intestinal metaplasiaincreased risk of developing dysplasia and carcinoma

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37
Q

what is allergic oesophagitis (eosinophilic oesophagitis)

A

not due to reflux - increased eosinophils in blood corrugated or spotty oesophagus asthma, young, males > females

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38
Q

what is treatment for allergic oesophagitis

A

steroids, chromoglycate, montelukast

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39
Q

what is most common benign oesophageal tumour

A

squamous papilloma

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40
Q

what are common malignant tumours of oesophagus

A

squamous cell carcinoma and adenocarcinoma (now most common)

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41
Q

what is the pathogenesis of adenocarcinoma

A

genetic factors, reflux or others - chronic reflux oesophagitis - barretts oesophagus, low grade dysplasia - high grade - adenocarcinoma

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42
Q

what is the different mechanisms of metastases

A

direct invasion, lymphatic permeation, vascular invasion

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43
Q

what is most common oral cancer

A

squamous cell carcinoma

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44
Q

what is the characteristics of GORD

A

incompetent LOS, poor oesophageal clearance, barrier function/visceral sensitivity

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45
Q

what are the symptoms of GORD

A

heartburn, acid reflux, waterbrash, dysphagia, odynophagia, weight loss, chest pain, hoarseness, coughing

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46
Q

what investigations are involved in GORD

A

endoscopy, barium swallow test, oesophageal manometry & pH studies, nuclear studies

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47
Q

what are the alarming symptoms of dyspepsia (indigestion)

A

dysphagia, weight loss, anaemia, vomiting, UGI cancer, barretts, pernicious anaemia, PUD surgery > 20 years

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48
Q

what is the management of GORD

A

symptom relief, healing oesophagitis, prevent complications

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49
Q

what are the lifestyle modifications which help GORD

A

stop smoking, lose weight if obese, prop up the bed head, avoid provoking factors

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50
Q

what is the role of antacids in GORD

A

symptomatic relief in the majority of reflux patients no benefit in healing or preventing complications

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51
Q

H2 antagonists can also be used for symptomatic relief. What are examples of these drugs

A

cimetidine (rapid symptom relief, less effective at healing than placebo)ranitidine (tolerance after 4/52 therapy, poor in preventing relapse and complications)

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52
Q

what is the role of surgery (nissen fundoplication) in GORD

A

controls symptoms, heals oesophagitis, young patients, severe/unresponsive disease

53
Q

what is barretts oesophagus

A

complication intestinal metaplasia irreversibleincreased risk of adenocarcinoma

54
Q

what is the treatment for dysplasia

A

more frequent surveillance, optimise PPI dose, endoscopic mucosal resection (EMR), radiofrequency albation (HALO), argon

55
Q

what is gastroparesis

A

delayed gastric emptying, no physical obstruction

56
Q

what is symptoms of gastroparesis

A

feeling of fullness, nausea, vomiting, weight loss, upper abdominal pain

57
Q

what is the causes of gastroparesis

A

idiopathic, diabetes mellitus, cannabis, mediation (opiates, anticholinergics), systemic diseases eg systemic sclerosis

58
Q

what is investigation in gastroparesis

A

gastric emptying studies

59
Q

what is the management of gastroparesis

A

removal of precipitating factors eg drugs liquid/sloppy diet eat little and often promotility agents gastric pacemaker

60
Q

characteristics of autoimmune chronic gastritis (rarest)

A

anti-parietal and anti-intrinsic factor antibodies atrophy and intestinal metaplasia in body of stomach

61
Q

what is consequence of autoimmune chronic gastritic

A

pernicious anaemia, macrocytic, due to B12 deficiency increased risk of malignancy SACDC

62
Q

what is H.pylori associated chronic gastritis (most common)

A

bacteria (gram -ve curvillinear rod) inhabits niche between epithelial cell surface and mucous barrier

63
Q

what is consequence of H.pylori gastritis

A

lamina propia plasma cells produce anti H.pylori antibodiesincreased risk of duodenal ulcer, gastric ulcer, gastric carcinoma, gastric lymphoma

64
Q

what is chemical gastritis

A

gue to NSAIDs, alcohol, bile refluc direct injury to mucus layer by fat solvents marked epithelial regeneration, hyperplasia, congestion and little inflammation

65
Q

what is consequence of chemical gastritis

A

erosions or ulcers

66
Q

what is peptic ulceration

A

breach in GI mucosa as result of acid and pepsin attack

67
Q

what is chronic peptic ulcers

A

ulcer longstanding and often deep

68
Q

what are sites predisposed to developing chronic peptic ulcers

A

1st part of duodenumstomach (junction of body and antrum)oseophago-gastric junctionstomal ulcers

69
Q

what causes chronic peptic ulcers

A

not just due to increased acid productionfailure of mucosal defence also important

70
Q

what is the microscopic view of peptic ulcers

A

layered appearance, floor of necrotic fibrinopurulent debris, base of inflamed granulation tissue, deepest layer is fibrotic scar tissue

71
Q

what is complication of peptic ulcers

A

perforation penetration haemorrhage stenosisintractable pain

72
Q

what are benign gastric tumours

A

hyperplastic polypscystic fundic gland polyps

73
Q

what are malignant gastric tumors

A

carcinomaslymphomas gastrointestinal stromal tumours

74
Q

pathogenesis of H.pylori causing gastric adenocarcinoma

A

H.pylori - chronic gastritis - intestinal metaplasia/atrophy - dysplasia - carcinoma

75
Q

what are other causes of gastric adenocarcinoma

A

pernicious anaemia, partial gastrectomy, HNPCC/lynch syndrome, menetriers disease

76
Q

what is a benign peptic ulcer

A

mimics cancer but is more punched out and lacks raised rolled edge

77
Q

where does gastric adenocarcinoma spread

A

local (other organs and into peritoneal cavity and ovaries - kruckenberg)lymph nodes haematogenous (to liver)

78
Q

what is a gastric lymphoma (maltoma)

A

derived from mucosa associated lymphoid tissue (MALT)associated with h.pylori infection continuous inflammation induces evolution into clonal B cell proliferation - if unchecked evolves into high grade B cell lymphoma

79
Q

what does nausea usually involve

A

pallor, sweating, excessive salivation and relaxation of stomach and lower oesophagusupper intestinal contractions, forcing intestinal contents by reverse peristalsis into stomach

80
Q

what is retching

A

rhythmic reverse peristalsis of stomach and oesophagus forceful contraction of abdominal muscle and diaphragm

81
Q

what is the events in vomiting

A

suspension of intestinal slow wave activity retrograde contractions from ileum to stomach suspension of breathing (prevents aspiration)relaxation of LOS - contraction of diaphragm and abdominal muscles compresses stomachejection of gastric contents through open UOS

82
Q

what cells in mucosa are stimulates by toxic material in gut lumen or systemic toxins

A

enterochromaffin cells (release mediators eg 5-HT)

83
Q

what does this stimulation of enterochromaffin cells cause

A

depolarisation of sensory afferent terminals in mucosa (eg via 5-HT3 receptors)

84
Q

what does this depolarisation result in

A

action potential discharge in vagal afferents to brainstem (CTZ - chemoreceptor trigger zone in area postrema - and NTS - nucleus tractus solitarius)

85
Q

what does this action potential discharge result in

A

co-ordination of vomiting by vomiting centre

86
Q

what are consequences of severe vomiting

A

dehydrationloss of gastric protons and chloride (causes alkalosis)hypokalaemia (mediated by kidney)rarely acidosis may also occur due to loss of duodenal bicarbonateoesophageal damage

87
Q

what classes of drugs predictably cause nausea and vomiting

A

cancer chemotherapy (cisplatin, doxorubicin) and radiotherapy general anaesthetic agents with dopamine agonist properties (levodopa in parkinsons)morphine and other opiate analgesicscardiac glycosides (digoxin)drugs enhancing 5HT (SSRIs in depression)

88
Q

when are 5-HT3 receptor antagonists (setrons eg ondanserton and palonosetron)

A

used to suppress chemo and radiation induced emesis and post up nausea corticosteroid and NK1 receptor antagonist used in later phase

89
Q

what kind of vomiting are these drugs not useful for

A

motion sickness or vomiting induced by agents increasing dopaminergic transmission

90
Q

what are side effects of 5-HT3 receptor antagonists

A

constipation and headaches

91
Q

what drugs can be used for motion sickness

A

muscarinic acetylcholine receptor antagonists (hyosine, scopolamine)direct inhibition of GI movements and relaxation of GI tract

92
Q

what is adverse effects of muscarinic acetylcholine receptor antagonists

A

blurred vision, urinary retention, dry mouth and sedation due to blockage of parasympathetic NS

93
Q

what is role of histamine H1 receptor antagonists eg cyclizine, cinnarizine and others

A

motion sickness and acute labyrinthitis and nausea/vomiting caused by irritants in stomach less effective against substances that act on CTZ

94
Q

what is adverse effects of H1 receptor antagonists

A

CNS depression and sedation - drowsiness may affect performance of skilled tasks

95
Q

what is role of dopamine receptor antagonists (domperidone and metoclopramide)

A

used for drug induced vomiting (chemo, treatment of parkinsons) and vomiting in GI disorders - no motion sicknessblock D2 and D3 receptor in CTZexert prokinetic action on oesophagus, stomach and intestine

96
Q

why is domperidone superior to metoclopramide

A

domperidone does not cross BBB and is less likely to result in the many unwanted effects (disorders of movement)

97
Q

when are NK1 receptor antagonists used

A

in combo with 5HT in acute phase of highly ementogenic chemo in combination with dexamethasone in delayed phae

98
Q

when are cannabinoid (CB1) receptor agonists used

A

in chemo, when not respond to anything else

99
Q

what is dyspepsia

A

epigastric pain or burning, postprandial fullness, early satiety

100
Q

what makes dyspepsia more common

A

if H.pylori infected or NSAID use overlap with IBS/GORD

101
Q

what are organic causes of dyspepsia (25%)

A

peptic ulcer disease, drugs (NSAIDs, COX2 inhibitors), gastric cancer

102
Q

what are functional causes of dyspepsia (75%)

A

idiopathic - no evidence of culprit structural disease associated with other functional gut disorders eg IBS

103
Q

symptoms of uncomplicated dyspepsia

A

epigastric tenderness

104
Q

symptoms of complicated dyspepsia

A

cachexia, mass, evidence gastric outfly obstruction, peritonism

105
Q

what are the alarm symptoms of dyspepsia

A

dysphagia, evidence of GI blood loss, persistent vomiting, unexplained weight loss, upper abdominal mass

106
Q

what is the management of dyspepsia

A

H.pylori status - eradicate if infected if HP -ve - treat with acid inhibition as required

107
Q

what kind of pain felt in peptic ulcer disease

A

epigastric pain - often radiates to backaggravated (duodenum) or relieved (gastric) by eating

108
Q

what are causes of peptic ulcer disease

A

H pylori NSAIDs (COX1, COX2, PGE)

109
Q

characteristics of H.pylori

A

acquired in infancy, gram -ve in microareophilic flagellated bacillus, oral-oral or faecal-oral spreadconsequences of infection do not arise until later in life

110
Q

what are consequences of peptic ulcer disease

A

peptic ulcer diseasegastric cancer (almost all non-cardia gastric adenocarcinoma, also low grade B cell gastric lymphomas)

111
Q

what is pathophysiology of duodenal ulcer

A

increased duodenal acid load (metaplasia and H.pylori colonisation), increased acid secretion and thus increased gastrin release (due to decreased somatostatin)

112
Q

how is H.pylori infection diagnosed

A

gastric biopsy - urease test, histology and culture/sensitivity urease breath test FAT (faecal antigen test)serology (IgA - not accurate with increased patient age)

113
Q

what is the treatment of peptic ulcer disease

A

all antisecretory therapy (PPI)all tested for H pylori (if +ve, eradicate and confirm, if -ve antisecretory therapy)withdraw NSAIDslifestyle

114
Q

what triple therapy is used alongside PPI for one week

A

PPI + amoxycillin + clarithromycin PPI + metrondiazole + clarithromycin

115
Q

what are complications of peptic ulcer disease

A

anaemia bleedingperforation gastric outlet / duodenal obstruction - fibrotic scar

116
Q

follow up of duodenal ulcer

A

uncomplicated DU requires no follow up, only if ongoing symptoms

117
Q

follow up of gastric ulcer

A

follow up endoscopy at 6-8 weeks to ensure healing and no malignancy

118
Q

how does GI bleeding present

A

haematemesis (vomiting blood)melaena (black bloody faeces)

119
Q

how to manage GI bleeding

A

Airway Breathing Circulation airway protection, O2, IV access and fluids

120
Q

how to assess severity of haemorrhage - rockall risk scoring

A

Rockall Risk scoring:systolic BP<100mmHgpuse >100Hb<100age>60 comorbid disease postural drop in BPBlatchford Scoring is newer

121
Q

treatment of bleeding peptic ulcers

A

endoscopic treatment (high risk ulcer)acid suppression surgery (H.pylori eradication is secondary prevention)

122
Q

describe the endoscopic treatment of bleeding peptic ulcers (achievement of homeostasis)

A

injection heater probe coagulationcombinationclipshaemospray (forms mechanical barrier over bleeding site)

123
Q

which complications cause acute variceal bleeding

A

sepsis and liver failure

124
Q

what is the risk factors for acute variceal bleeding

A

portal pressure >12 mmhgvarices > 25% oesophgageal lumen presence of red signsdegree of liver failure

125
Q

when would you expect varices in a bleeder

A

chronic alcohol excess chronic viral hepatitis infection metabolic or autoimmune liver disease intra-abdominal sepsis/surgery on examination - stigmata of chronic liver disease

126
Q

what is the aims of manageent of variceal bleeding

A

resuscitationhaemostasisisprevent complications of bleeding prevent deterioration of liver function prevent early re-bleeding

127
Q

what is the initial considerations in varicel bleeding

A

coagulopathy (FFP, platelets, vit K)CVP monitoring parenteral vitaminsantibioticshypoglycaemia replace K+, MG2+ and PO42-delirium tremens (perhaps later)

128
Q

how is haemostasis achieved

A

1) terlipressin (vasopressin analogue - splanchnic vasoconstrictor)2) endoscopic variceal ligation (banding)3) sclerotherapy 4) sengstaken-blakemore balloon 5) TIPS

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