Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GI > Pathology > Flashcards

Pathology Flashcards

1
Q

what is an oral ulcer?

A

a discontinuity in the oral mucosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what types of solitary mouth ulcers are there?

A
  • trauma : chemical/physical
  • malignancy
  • infective: TB, syphilis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are the three types of multiple ulcers?

A
  • minor
  • major
  • herpetiform
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what are oral signs of anaemia?

A
  • mucosal pallor
  • oral ulcers
  • glossitis
  • angular chelitis
  • predisposition to candida
  • disturbed taste
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what mucocutaneous disorders cause oral ulcers?

A
  • lichen Planus
  • vesiculobulous disease
  • lupus erythematosus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How does lichen planus present in the mouth?

A
  • bilateral ulcer
  • asymptomatic
  • can affect the skin
  • potentially malignant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

how does lupus erythematosus present in the mouth?

A
  • ulcerations
  • white patches
  • red and white patches
  • similar in appearance to lichen planus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

how does VB disease present in the mouth?

A
  • oral lesions are the first manifestation
  • oral lesions precede skin lesions by 1 year or more
  • painful extensive oral ulcerations
  • preceded by blisters -rupture easily
  • nikolsky sign
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is the difference between pemphigoid and pemphigus?

A

the level at which the bullae forms - sub epithelial in pemphigoid and intraepithelial in pemphigus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what GI disease may have mouth manifestations?

A
  • Crohn’s
  • ulcerative colitis
  • Peutz Jeghers
  • gardeners syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what are the oral manifestations of Crohn’s disease?

A
  • cobble-stoning of mucosa
  • localised mucogingivitis
  • linear ulcerations
  • tissue tags/ polyps
  • diffuse swelling - commonly of the lips
  • pyostomatitis vegetans
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what are the oral manifestations of ulcerative colitis?

A
  • oral ulcers
  • pyostomatitis vegetans
  • angular stomatitis
  • reflects severity of intestinal disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what would white patches in the mouth that wipe off suggest?

A

usually pseudomembranous candidiasis/thrush

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what would white patches that don’t wipe off suggest?

A
  • trauma
  • epithelial dysplasia
  • neoplasia
  • chronic mucocutaneous candidiasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what are the causes of oral pigmentation?

A
  • racial pigmentation
  • melanotic macules
  • malignancy
  • smoking
  • addison’s disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are causes of xerostomia (dry mouth)?

A
  • drugs
  • sjogren’s
  • radiation therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are oral manifestations of sjogren syndrome?

A
  • enlarged salivary glands

- as a result of dry mouth - increased caries, decapilalated tongue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what are the oral manifestations of leukaemia?

A
  • gingival enlargement
  • petechiae
  • mucosal bleeding
  • ulceration
  • infiltration of malignant cells - boggy gingiva
  • candida
  • herpes infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are the two types of inflammatory disorders of the oesophagus?

A

acute oesophagitis - rare

chronic oesophagitis - common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is reflux oesophagitis?

A

inflammation of oesophagus due to refluxed low pH gastric content

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what are the complications of reflux?

A
  • ulceration (bleeding)
  • stricture
  • barrett’s oesophagus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is barrett’s oesophagus?

A

replacement of stratified squamous epithelium by columnar epithelial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what does barrett’s oesophagus increase the risk of?

A

developing dysplasia and carcinoma of the oesophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what benign oesophageal tumours exist?

A
  • squamous papilloma - most common
  • leiomyomas
  • lipomas
  • fibrovascular polyps
  • granular cell tumours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what malignant oesophageal tumours exist?

A

squamous cell carcinoma

adenocarcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what is the aetiology of squamous cell carcinoma?

A
  • vitamin A, zinc deficiency
  • tannic acid/ strong tea
  • smoking / alcohol
  • HPV
  • oesophagitis
  • genetic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what is the pathogenesis of adenocarcinoma?

A
  1. genetic factors, reflux disease, others
  2. chronic reflux oesophagitis
  3. barretts oesophagus
  4. low grade dysplasia
  5. high grade dysplasia
  6. adenocarcinoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what is the mechanisms of metastases of carcinoma of oesophagus?

A
  • direct invasion
  • lymphatic permeation
  • vascular invasion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what are the presenting features of carcinoma of oesophagus?

A
  • dysphagia (due to cancer obstruction)

- general symptoms of malignancy (anaemia, weight loss, loss of energy) - due to effects of metastases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

how does oral squamous cell carcinoma present?

A

white, red, speckled, ulcer, lump

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what are high risk areas for oral squamous cell carcinoma?

A

floor of mouth, lateral border of and ventral tongue, soft palate, retromolar pad/tonsillar pillars

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what types of chronic gastritis are there?

A

autoimmune
bacterial
chemical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what is the cause of bacterial chronic gastritis?

A

bacteria inhibits a niche between the epithelial cell surface and mucous barrier, excites early acute inflammatory response, if not cleared then chronic active inflammation ensues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what does bacterial (H.pylori) gastritis increase the risk of?

A

duodenal ulcer, gastric ulcer, gastric carcinoma, gastric lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what is chemical gastritis due to?

A

NSAIDs, alcohol, bile reflux

direct injury to mucus layer by fat solvents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

where do chronic duodenal ulcers come from?

A

increased attack and failure of defence - too much acid and failure of mucosal defence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what are the complications of peptic ulcers?

A 
perforation
penetration
haemorrhage
stenosis
intractable pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what gastric benign tumours are there?

A
  • hyperplastic polyps

- cystic fundic gland polyps

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what gastric malignant tumours are there?

A
  • carcinomas
  • lymphomas
  • gastrointestinal stromal tumours (GISTs)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what is the pathogenesis of gastric adenocarcinoma?

A
  1. H. pylori infection
  2. chronic gastritis
  3. intestinal metaplasia/atrophy
  4. dysplasia
  5. carcinoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what other premalignant conditions increase the risk of gastric adenocarcinoma?

A
  • pernicious aneamia
  • partial gastrectomy
  • HNPCC/ lynch syndrome
  • menetrier’s disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what are the subtypes of gastric adenocarcinoma?

A

intestinal type -exophytic/polypoid mass

diffuse type - expands/infiltrates stomach wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what appearance differences are there between benign peptic ulcers and cancer?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

which subtype of gastric adenocarcinoma has a better prognosis?

A

intestinal type

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what does haematogenous spread mean?

A

cancer spread to liver and beyond

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

what does transcoelomic spread mean?

A

cancer spread into peritoneal cavity and overies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what is gastric lymphoma also called?

A

maltoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what happens during GORD?

A

incompetent LOS
poor oesophageal clearance
barrier function/visceral sensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

what are the symptoms of GORD?

A 
heartburn
acid reflux
waterbrash
dysphagia
odynophagia
weight loss
chest pain
hoarseness
coughing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

what investigations are used to diagnosis GORD?

A

endoscopy
Ba swallow
oesophageal manometry and pH studies
nuclear studies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

how do you manage GORD?

A
  • symptom relief
  • healing oesophagitis
  • prevent complications
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

what lifestyle modification may help with GORD?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

what is gastroparesis?

A

delayed gastric emptying, no physical obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

what are the symptoms of gastroparesis?

A 
feeling of fullness
nausea
vomiting
weight loss
upper abdominal pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

what are the causes of gastroparesis?

A 
idiopathic
diabetes mellitus
cannabis
medication e.g.opiates, anticholinergics
systemic disease e.g. systemic sclerosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

what investigations are used for gastroparesis?

A

gastric emptying studies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

how is gastroparesis managed?

A
  • removal of precipitating factors
  • liquid/sloppy diet
  • eat little and often
  • promotility agents
  • gastric pacemaker
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

what is dyspepsia?

A

epigastric pain or burning
postprandial fullness
early satiety

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

what are the causes of dyspepsia?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

what would be found during examination if patient had dyspepsia?

A

if uncomplicated: epigastric tenderness only

if complicated: cachexia, mass, evidence gastric outflow obstruction, peritonism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

what are the causes of peptic ulcer disease?

A

H.pylori

NSAIDs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

when is H.pylori acquired?

A

in infancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

how is H. pylori spread?

A

oral-oral/ faecal oral spread

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

what is the pathophysiology of duodenal ulcer?

A

increase in duodenal acid load, increase in acid secretion due to increase in parietal cell mass, increase gastrin release due to decrease in somatostatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

how is H.pylori infection diagnosed?

A

gastric biopsy - urease test. histology, culture/sensitivity
urease breath test
FAT (faecal antigen test)
serology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

what are the complications of peptic ulcer disease?

A

aneamia
bleeding
perforation
gastric outlet/duodenal obstruction - fibrotic scar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

how are bleeding gastric ulcers treated?

A
  1. endoscopic treatment
  2. acid suppression
  3. surgery
  4. H. pylori eradication
68
Q

what is the process of endoscopic treatment of peptic ulcers?

A
  1. injection
  2. heater probe coagulation
  3. combinations
  4. clips
  5. haemospray
69
Q

how does hemospray work?

A

when hemospray comes in contact with blood, the power absorb water, then acts both cohesively and adhesively, forming a mechanical barrier over the bleeding site

70
Q

which part of the bowel is most sensitive to hypoxia?

A

the mucosa

71
Q

in non occlusive ischaemia of the small bowel what happens after reperfusion?

A

tissue damage

72
Q

what are the complications of ischaemia of the small bowel?

A

resolution
fibrosis, stricture, chronic ischaemia and obstruction
gengrene, perforation, peritonitis, sepsis and death

73
Q

what is meckel’s diverticulum a result of?

A

incomplete regression of vitello-intestinal duct

74
Q

what may meckel’s diverticulum cause?

A

bleeding, perforation or diverticulitis that mimicks appendicitis
can be asymptomatic

75
Q

what do primary tumours of the small bowel include?

A

lymphomas
carcinoid tumours
carcinomas

76
Q

how are lymphomas of the small bowel treated?

A

by surgery and chemotherapy

77
Q

what are the commonest site of carcinoid tumours of the small bowel?

A

appendix

78
Q

how may carcinoid tumours of small bowel present?

A

cause inussusception and obstruction and flushing and diarrhoea

79
Q

what is carcinoma of the small bowel associated with?

A

Crohn’s disease and coeliac disease

80
Q

how does appendicitis present?

A

vomiting
abdominal pain
RIF tenderness
increased WCC

81
Q

what causes acute appendicitis?

A 
unknown
faecoliths (dehydration)
lymphoid hyperplasia
parasites 
tumours
82
Q

what is the pathology of acute appendicitis?

A

acute inflammation (neutrophils)
mucosal ulceration
serosal congestion, exudate
pus in lumen

acute inflammation must involve the muscle coat

83
Q

what are the complications of appendicitis?

A 
peritonitis
rupture
abscess 
fistula 
sepsis and liver abscess
84
Q

what is the cause of coeliac disease?

A

abnormal reaction to a constituent of wheat flour, gluten, which damages enterocytes and reduces absorptive capacity

85
Q

what is the aetiology of coeliac disease?

A

gliadin is the suspected toxic agent
tissue injury may be a bystander effect of abnormal immune reaction to gliadin
mediated by intraepithelial lymphocytes

86
Q

what is the normal lifespan of an enterocyte?

A

72 hours

87
Q

what happens to enterocytes during coeliac disease?

A

increasing loss due to IEL mediated damage, this leads to loss and villous structure, loss and surface area, a reduction in absorption and a flat duodenal mucosa

88
Q

which antibodies would be present in coeliac disease?

A

anti-TTG
anti-endomesial
anti-gliadin

89
Q

what are the metabolic effects of coeliac disease?

A

malabsorption of sugars, fats, amino acids, water and electrolytes
malabsorption of fats lead to steatorrhea
reduced intestinal hormone production leads to reduced pancreatic secretion and bile flow (CCK) leading to gallstones

90
Q

what are the effects of malabsorption?

A 
loss of weight
aneamia (Fe, vit B12, folate)
abdominal bloating 
failure to thrive 
vitamin deficiencies
91
Q

what are the other complications of coeliac disease?

A

T-cell lymphomas of GI tract
increased risk of small bowel carcinoma
Gall stones
ulcerative-jejenoilleitis

92
Q

what is the aetiology of malabsorption?

A

defective luminal digestion
mucosal disease
structural disorders

93
Q

what are common causes of malabsorption?

A 
coeliac disease
crohn's disease
post infectious
biliary obstruction
cirrhosis
94
Q

what are the uncommon causes of malabsorption?

A 
pancreatic cancer
parasites
bacterial overgrowth
drugs 
short boewl
95
Q

what are the clinical features of tropical sprue?

A 
diarrhoea
steatorrhea
weight loss
nausea
anorexia
96
Q

what is tropical sprue?

A

colonisation of the intestine by an infectious agent or alterations in the intestinal bacterial flora by the exposure to another environmental agent

97
Q

how is tropical sprue treated?

A

tetracycline and folic acid

98
Q

what are the clinical features of lactose intolerance?

A

induction of diarrhoea, abdominal discomfort, and flatulence following the ingestion of dairy products

99
Q

how is diagnosis of lactose intolerance confirmed?

A

lactose breath hydrogen test

oral lactose intolerance test

100
Q

how is lactose intolerance managed?

A

lactose free diet

101
Q

what is whipple’s disease?

A

caused by tropheryma whipplei. multi system involvement increase in the frequency of HLA-B27

102
Q

what are the clinical features of whipple’s disease?

A 
weight loss
diarrhoea
steatorrhea
abdominal distention 
arthritis
fever
nutritional def symptoms
103
Q

how is whipple’s disease diagnosed?

A

demonstration of T.whipplei in involved tissue by microscopy

104
Q

what are the clinical features of crohn’s disease?

A

abdominal pain and diarrhoea, fever and weight loss, abdominal tenderness most classically in the right lower quadrant

105
Q

how do you diagnose crohn’s disease?

A

endoscopy
barium imaging of small bowel mucosal disease
CT
MRI

106
Q

how is Crohn’s disease treated?

A

steroids
immunosuppresants
azathioprine-6-MP
biological therapy (anti TNF)

107
Q

what are risk factors for Giardia Lamblia infection?

A

travellling to area where the water supply may be contaminated, swimming in pond

108
Q

what are the clinical features of Giardia Lamblia infection?

A 
diarrhoea
flatulence
abdominal cramps
epigastric pain 
nausea
vomiting 
malabsorption 
steatorrhea
weight loss
109
Q

how is giardia lamlia infection treated?

A

metronidazole 1 week

110
Q

what other parasitic infections can cause malabsorption?

A

coccidial

stronglyoides

111
Q

what are the clinical features of small bowel bacterial overgrowth?

A

diarrhoea
steatorrhea
macrocytic aneamia

112
Q

what lab results would small bowel bacterial overgrowth show?

A

low cobalamin and high folate levels

113
Q

how is small bowel bacterial overgrowth treated?

A

surgical correction of an anatomical blind loop, tetracyclines - 2-3 weeks

114
Q

what is intestinal failure a result of?

A

inability to maintain adequate nutrition or fluid status via the intestines

115
Q

what can intestinal failure occur due to?

A

obstruction, dysmotility, surgical resection, congenital defect, disease associated loss of absorption

116
Q

what is intestinal failure characterised by?

A

inability to maintain protein-energy, fluid, electrolyte or micronutrient balance

117
Q

what is intestinal failure?

A

the reduction in function below the minimum necessary for the absorption of macronutrient and/or water and electrolytes such that IV supplementation is required to maintain health and/ or growth.

118
Q

what are the 3 types of intestinal failure?

A

type 1 - short term, self limiting
type 2 - medium term, significant and prolonged PN support (>28 days)
type 3 - long term, chronic IF (long term PN support)

119
Q

what is malnutrition?

A

a state of nutrition in which a deficiency. excess or imbalance of energy, protein and other nutrients causes measurable adverse effects on tissue, body form, function and clinical outcome.

120
Q

what are the disease related caused of malnutrition?

A

decreased intake
impaired digestion and/or absorption
increased nutritional requirements
increased nutrient losses

121
Q

what are the adverse effects of malnutrition?

A 
impaired immune responses
impaired wound healing 
reduced muscle strength and fatigue
reduced respiratory muscle strength
inactivity
water and electrolyte disturbances
impaired thermoregulation
menstrual irregularities
impaired psycho-social function
122
Q

what are the two major forms of inflammatory bowel disease (IBD)?

A

Crohn’s disease - can affect any part of GI tract

ulcerative colitis - affects colon

123
Q

what does colitis mean?

A

inflammation of the inner lining of colon

124
Q

what are the risk factors for crohn’s disease?

A 
genetics - most common.
smoking 
NSAIDs
Good hygiene
nutritional factors
psychological factors
appendicectomy
125
Q

what are the risk factors for ulcerative colitis?

A

genetics
NSAIDs
nutritional factors
psychological factors

smoking - lowers risk
appendicectomy - lowers risk

126
Q

what are the anal and perianal complications of crohn’s disease?

A 
fissure in ano
haemorrhoids
skin tags
perianal abscess
ischiorectal abscess
fistula in ano
anorectal fistulae
127
Q

what are the inflammatory histological features of crohn’s disease compared to ulcerative colitis?

A

deep (transmural) patchy in CD

mucosal continuous in UC

128
Q

which IBD are granulomas present in?

A

Crohn’s disease

129
Q

which IBD are goblet cells present in?

A

Crohn’s disease, depleted in ulcerative colitis

130
Q

what are the major symptoms of Crohn’s disease?

A

diarrhoea
abdominal pain
weight loss

131
Q

what are some minor symptoms sometimes present in Crohn’s disease?

A 
malaise
lethargy
anorexia
nausea
vomiting 
low grade fever
132
Q

what may be the main presenting feature of crohn’s disease in children?

A

reduced growth velocity and delayed puberty

133
Q

what will 50% of patients with crohn’s disease require within 5 years of diagnosis?

A

intestinal resection

134
Q

what are physical signs of crohn’s disease?

A

loss of weight
malnutrition
aphthous ulceration of the mouth
abdominal exam may be normal, although tenderness and/or right iliac fossa mass are occasionally found.
anus should be examined for oedematous anal tags, fissures or perianal abscesses

135
Q

which main pathogens cause gastroenteritis?

A
  1. campylobacter - commonest
  2. salmonella - outbreaks
  3. E.coli 0157 - rare but morbidity/ outbreaks

other - C.diff, listeria, shigella, norovirus, rotavirus

136
Q

what are the GI infection risk factors?

A
  • malnutrition (micronutrient) deficiency
  • closed/semi-closed communities
  • exposure to contaminated food/water/travel
  • winter congregating/ summer floods
  • age <5, not breastfeeding
  • older age
  • acid suppression - C.diff more common.
  • immunosuppression
  • microbiome
  • genetics
137
Q

What are the bacterial factors of GI infection?

A
  • adherence / attachment to the GI mucosa
  • cellular invasion
  • production of exotoxins
  • changes in epithelial cell physiology
  • loss of brush border digestive enzyme and/or cell death
  • increased intestinal motility, net fluid secretion, influx of inflammatory cells, and/or intestinal haemorrhage
138
Q

what is diarrhoea?

A

> 3 unformed stool/day, stool holds the shape of container, departure from normal bowel habit

139
Q

what does dysentry mean?

A

inflammation of the intestine, particularly the colon, causing diarrhoea associated with blood and mucus

140
Q

what is dysentry normally associated with?

A

fever, abdominal pain and rectal tenesmus

141
Q

what is the bacillus cereus incubation period?

A

1-6 hours

142
Q

what type of bacteria is bacillus cereus?

A

gram positive bacillus

143
Q

what type of food is likely to cause bacillus cereus infection?

A

starchy foods - especially reheated rice

144
Q

what is the staphlococcus aureus incubation period?

A

1-6 hours

145
Q

what type of bacteria is staphlococcus aureus?

A

gram positive coccus

146
Q

what type of food is staphlococcus aureus found in?

A

foods left at room temperature - milk/meat/fish

147
Q

how does staphlococcus aureus cause infection?

A

preformed toxin in food - rapid absorption, acts on vomiting centre in brain

148
Q

what dies shiga toxin do?

A

binds to receptors found on renal cells, RBC and others, inhibits protein synthesis and causes cell death

149
Q

what would happen if antibiotics were prescribed for E.coli 0157?

A

produces more shiga-toxin which has a high mortality - can cause haemolytic ureamic syndrome (HUS)

150
Q

why are antibiotics not normally prescribed for gastroenteritis?

A

in case it causes haemolytic ureamic syndrome (HUS)

151
Q

How does HUS present?

A 
abdominal pain
fever
pallor
petechiae
oliguria
bloody diarrhoea - 90% cases
high white cells
low platelets
low HB
red cell fragments
LDH >1.5 x normal
may develop after diarrhoea stopped
152
Q

what is the incubation period of campylobacter?

A

16-48 hours

153
Q

what causes campylobacter infection?

A

poultry, raw milk

154
Q

what is a polyp?

A

a protrusion above an epithelial surface, a tumour (a swelling)

155
Q

what is the differential diagnosis of a colonic polyp?

A
  1. adenoma
  2. serrated polyp
  3. polypoid carcinoma
  4. other
156
Q

what is the adenoma-carcinoma sequence?

A

normal mucosa > adenoma (dysplastic) > adenocarcinoma (invasive)

157
Q

what must be done to all adenomas?

A

must be removed as they are premalignant, either done endoscopically or surgically

158
Q

what does dukes staging predict?

A

prognosis

159
Q

what do the different dukes staging types indicate in colorectal carcinoma?

A

dukes A - confined by muscularis propria
dukes B - through muscularis propria
dukes C - metastatic to lymph nodes

160
Q

what is the clinical presentation of left sided colorectal carcinoma?

A

blood PR
altred bowel habit
obstruction

161
Q

what is the clinical presentation of right sided colorectal carcinoma?

A

anaemia

weight loss

162
Q

where does local invasion of colorectal carcinoma occur to?

A

mesorectum, peritoneum, other organs

163
Q

where does lymphatic spread of colorectal carcinoma occur to?

A

mesenteric nodes

164
Q

where does haematogenous spread of colorectal carcinoma occur to?

A

liver, distant sites

165
Q

what are inherited cancer syndromes?

A
  • hereditary non polyposis coli (HNPCC)(<100 polyps)

- familial adenomatous polyposis (FAP) (>100 polyps)

166
Q

What is the difference in HNPCC and FAP?

A

HNPCC - late onset, autosomal dominant, defect in DNA mismatch repair, inherited mutation in MLH-1,MSH-2,PMS-1 or MSH-6 genes, right sided, mucinous tumours, crohn’s like inflammatory response, associated with gastric and endometrial carcinoma

FAP- early onset, autosomal dominant, defect in tumour suppression, inherited mutation in FAP gene, throughout colon, adenocarcinoma NOS, associated with desmoid tumours and thyroid carcinoma

GI (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions