Pathology Flashcards
1
Q
what is an oral ulcer?
A
a discontinuity in the oral mucosa
2
Q
what types of solitary mouth ulcers are there?
A
- trauma : chemical/physical
- malignancy
- infective: TB, syphilis
3
Q
what are the three types of multiple ulcers?
A
- minor
- major
- herpetiform
4
Q
what are oral signs of anaemia?
A
- mucosal pallor
- oral ulcers
- glossitis
- angular chelitis
- predisposition to candida
- disturbed taste
5
Q
what mucocutaneous disorders cause oral ulcers?
A
- lichen Planus
- vesiculobulous disease
- lupus erythematosus
6
Q
How does lichen planus present in the mouth?
A
- bilateral ulcer
- asymptomatic
- can affect the skin
- potentially malignant
7
Q
how does lupus erythematosus present in the mouth?
A
- ulcerations
- white patches
- red and white patches
- similar in appearance to lichen planus
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
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
10
Q
what GI disease may have mouth manifestations?
A
- Crohn’s
- ulcerative colitis
- Peutz Jeghers
- gardeners syndrome
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
12
Q
what are the oral manifestations of ulcerative colitis?
A
- oral ulcers
- pyostomatitis vegetans
- angular stomatitis
- reflects severity of intestinal disease
13
Q
what would white patches in the mouth that wipe off suggest?
A
usually pseudomembranous candidiasis/thrush
14
Q
what would white patches that don’t wipe off suggest?
A
- trauma
- epithelial dysplasia
- neoplasia
- chronic mucocutaneous candidiasis
15
Q
what are the causes of oral pigmentation?
A
- racial pigmentation
- melanotic macules
- malignancy
- smoking
- addison’s disease
16
Q
what are causes of xerostomia (dry mouth)?
A
- drugs
- sjogren’s
- radiation therapy
17
Q
what are oral manifestations of sjogren syndrome?
A
- enlarged salivary glands
- as a result of dry mouth - increased caries, decapilalated tongue
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
19
Q
what are the two types of inflammatory disorders of the oesophagus?
A
acute oesophagitis - rare
chronic oesophagitis - common
20
Q
what is reflux oesophagitis?
A
inflammation of oesophagus due to refluxed low pH gastric content
21
Q
what are the complications of reflux?
A
- ulceration (bleeding)
- stricture
- barrett’s oesophagus
22
Q
what is barrett’s oesophagus?
A
replacement of stratified squamous epithelium by columnar epithelial
23
Q
what does barrett’s oesophagus increase the risk of?
A
developing dysplasia and carcinoma of the oesophagus
24
Q
what benign oesophageal tumours exist?
A
- squamous papilloma - most common
- leiomyomas
- lipomas
- fibrovascular polyps
- granular cell tumours
25
what malignant oesophageal tumours exist?
squamous cell carcinoma
| adenocarcinoma
26
what is the aetiology of squamous cell carcinoma?
- vitamin A, zinc deficiency
- tannic acid/ strong tea
- smoking / alcohol
- HPV
- oesophagitis
- genetic
27
what is the pathogenesis of adenocarcinoma?
1. genetic factors, reflux disease, others
2. chronic reflux oesophagitis
3. barretts oesophagus
4. low grade dysplasia
5. high grade dysplasia
6. adenocarcinoma
28
what is the mechanisms of metastases of carcinoma of oesophagus?
- direct invasion
- lymphatic permeation
- vascular invasion
29
what are the presenting features of carcinoma of oesophagus?
- dysphagia (due to cancer obstruction)
| - general symptoms of malignancy (anaemia, weight loss, loss of energy) - due to effects of metastases
30
how does oral squamous cell carcinoma present?
white, red, speckled, ulcer, lump
31
what are high risk areas for oral squamous cell carcinoma?
floor of mouth, lateral border of and ventral tongue, soft palate, retromolar pad/tonsillar pillars
32
what types of chronic gastritis are there?
autoimmune
bacterial
chemical
33
what is the cause of bacterial chronic gastritis?
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
34
what does bacterial (H.pylori) gastritis increase the risk of?
duodenal ulcer, gastric ulcer, gastric carcinoma, gastric lymphoma
35
what is chemical gastritis due to?
NSAIDs, alcohol, bile reflux
| direct injury to mucus layer by fat solvents
36
where do chronic duodenal ulcers come from?
increased attack and failure of defence - too much acid and failure of mucosal defence
37
what are the complications of peptic ulcers?
```
perforation
penetration
haemorrhage
stenosis
intractable pain
```
38
what gastric benign tumours are there?
- hyperplastic polyps
| - cystic fundic gland polyps
39
what gastric malignant tumours are there?
- carcinomas
- lymphomas
- gastrointestinal stromal tumours (GISTs)
40
what is the pathogenesis of gastric adenocarcinoma?
1. H. pylori infection
2. chronic gastritis
3. intestinal metaplasia/atrophy
4. dysplasia
5. carcinoma
41
what other premalignant conditions increase the risk of gastric adenocarcinoma?
- pernicious aneamia
- partial gastrectomy
- HNPCC/ lynch syndrome
- menetrier's disease
42
what are the subtypes of gastric adenocarcinoma?
intestinal type -exophytic/polypoid mass
| diffuse type - expands/infiltrates stomach wall
43
what appearance differences are there between benign peptic ulcers and cancer?
mimics cancer but is more punched out and lacks a raised rolled edge
44
which subtype of gastric adenocarcinoma has a better prognosis?
intestinal type
45
what does haematogenous spread mean?
cancer spread to liver and beyond
46
what does transcoelomic spread mean?
cancer spread into peritoneal cavity and overies
47
what is gastric lymphoma also called?
maltoma
48
what happens during GORD?
incompetent LOS
poor oesophageal clearance
barrier function/visceral sensitivity
49
what are the symptoms of GORD?
```
heartburn
acid reflux
waterbrash
dysphagia
odynophagia
weight loss
chest pain
hoarseness
coughing
```
50
what investigations are used to diagnosis GORD?
endoscopy
Ba swallow
oesophageal manometry and pH studies
nuclear studies
51
how do you manage GORD?
- symptom relief
- healing oesophagitis
- prevent complications
52
what lifestyle modification may help with GORD?
stop smoking
lose weight if obese
prop up the bed head
avoid provoking factors
53
what is gastroparesis?
delayed gastric emptying, no physical obstruction
54
what are the symptoms of gastroparesis?
```
feeling of fullness
nausea
vomiting
weight loss
upper abdominal pain
```
55
what are the causes of gastroparesis?
```
idiopathic
diabetes mellitus
cannabis
medication e.g.opiates, anticholinergics
systemic disease e.g. systemic sclerosis
```
56
what investigations are used for gastroparesis?
gastric emptying studies
57
how is gastroparesis managed?
- removal of precipitating factors
- liquid/sloppy diet
- eat little and often
- promotility agents
- gastric pacemaker
58
what is dyspepsia?
epigastric pain or burning
postprandial fullness
early satiety
59
what are the causes of dyspepsia?
peptic ulcer disease
drugs (NSAIDs, COX2 inhibitors)
gastric cancer
idiopathic
60
what would be found during examination if patient had dyspepsia?
if uncomplicated: epigastric tenderness only
if complicated: cachexia, mass, evidence gastric outflow obstruction, peritonism
61
what are the causes of peptic ulcer disease?
H.pylori
| NSAIDs
62
when is H.pylori acquired?
in infancy
63
how is H. pylori spread?
oral-oral/ faecal oral spread
64
what is the pathophysiology of duodenal ulcer?
increase in duodenal acid load, increase in acid secretion due to increase in parietal cell mass, increase gastrin release due to decrease in somatostatin
65
how is H.pylori infection diagnosed?
gastric biopsy - urease test. histology, culture/sensitivity
urease breath test
FAT (faecal antigen test)
serology
66
what are the complications of peptic ulcer disease?
aneamia
bleeding
perforation
gastric outlet/duodenal obstruction - fibrotic scar
67
how are bleeding gastric ulcers treated?
1. endoscopic treatment
2. acid suppression
3. surgery
4. H. pylori eradication
68
what is the process of endoscopic treatment of peptic ulcers?
1. injection
2. heater probe coagulation
3. combinations
4. clips
5. haemospray
69
how does hemospray work?
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
which part of the bowel is most sensitive to hypoxia?
the mucosa
71
in non occlusive ischaemia of the small bowel what happens after reperfusion?
tissue damage
72
what are the complications of ischaemia of the small bowel?
resolution
fibrosis, stricture, chronic ischaemia and obstruction
gengrene, perforation, peritonitis, sepsis and death
73
what is meckel's diverticulum a result of?
incomplete regression of vitello-intestinal duct
74
what may meckel's diverticulum cause?
bleeding, perforation or diverticulitis that mimicks appendicitis
can be asymptomatic
75
what do primary tumours of the small bowel include?
lymphomas
carcinoid tumours
carcinomas
76
how are lymphomas of the small bowel treated?
by surgery and chemotherapy
77
what are the commonest site of carcinoid tumours of the small bowel?
appendix
78
how may carcinoid tumours of small bowel present?
cause inussusception and obstruction and flushing and diarrhoea
79
what is carcinoma of the small bowel associated with?
Crohn's disease and coeliac disease
80
how does appendicitis present?
vomiting
abdominal pain
RIF tenderness
increased WCC
81
what causes acute appendicitis?
```
unknown
faecoliths (dehydration)
lymphoid hyperplasia
parasites
tumours
```
82
what is the pathology of acute appendicitis?
acute inflammation (neutrophils)
mucosal ulceration
serosal congestion, exudate
pus in lumen
acute inflammation must involve the muscle coat
83
what are the complications of appendicitis?
```
peritonitis
rupture
abscess
fistula
sepsis and liver abscess
```
84
what is the cause of coeliac disease?
abnormal reaction to a constituent of wheat flour, gluten, which damages enterocytes and reduces absorptive capacity
85
what is the aetiology of coeliac disease?
gliadin is the suspected toxic agent
tissue injury may be a bystander effect of abnormal immune reaction to gliadin
mediated by intraepithelial lymphocytes
86
what is the normal lifespan of an enterocyte?
72 hours
87
what happens to enterocytes during coeliac disease?
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
which antibodies would be present in coeliac disease?
anti-TTG
anti-endomesial
anti-gliadin
89
what are the metabolic effects of coeliac disease?
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
what are the effects of malabsorption?
```
loss of weight
aneamia (Fe, vit B12, folate)
abdominal bloating
failure to thrive
vitamin deficiencies
```
91
what are the other complications of coeliac disease?
T-cell lymphomas of GI tract
increased risk of small bowel carcinoma
Gall stones
ulcerative-jejenoilleitis
92
what is the aetiology of malabsorption?
defective luminal digestion
mucosal disease
structural disorders
93
what are common causes of malabsorption?
```
coeliac disease
crohn's disease
post infectious
biliary obstruction
cirrhosis
```
94
what are the uncommon causes of malabsorption?
```
pancreatic cancer
parasites
bacterial overgrowth
drugs
short boewl
```
95
what are the clinical features of tropical sprue?
```
diarrhoea
steatorrhea
weight loss
nausea
anorexia
```
96
what is tropical sprue?
colonisation of the intestine by an infectious agent or alterations in the intestinal bacterial flora by the exposure to another environmental agent
97
how is tropical sprue treated?
tetracycline and folic acid
98
what are the clinical features of lactose intolerance?
induction of diarrhoea, abdominal discomfort, and flatulence following the ingestion of dairy products
99
how is diagnosis of lactose intolerance confirmed?
lactose breath hydrogen test
| oral lactose intolerance test
100
how is lactose intolerance managed?
lactose free diet
101
what is whipple's disease?
caused by tropheryma whipplei. multi system involvement increase in the frequency of HLA-B27
102
what are the clinical features of whipple's disease?
```
weight loss
diarrhoea
steatorrhea
abdominal distention
arthritis
fever
nutritional def symptoms
```
103
how is whipple's disease diagnosed?
demonstration of T.whipplei in involved tissue by microscopy
104
what are the clinical features of crohn's disease?
abdominal pain and diarrhoea, fever and weight loss, abdominal tenderness most classically in the right lower quadrant
105
how do you diagnose crohn's disease?
endoscopy
barium imaging of small bowel mucosal disease
CT
MRI
106
how is Crohn's disease treated?
steroids
immunosuppresants
azathioprine-6-MP
biological therapy (anti TNF)
107
what are risk factors for Giardia Lamblia infection?
travellling to area where the water supply may be contaminated, swimming in pond
108
what are the clinical features of Giardia Lamblia infection?
```
diarrhoea
flatulence
abdominal cramps
epigastric pain
nausea
vomiting
malabsorption
steatorrhea
weight loss
```
109
how is giardia lamlia infection treated?
metronidazole 1 week
110
what other parasitic infections can cause malabsorption?
coccidial
| stronglyoides
111
what are the clinical features of small bowel bacterial overgrowth?
diarrhoea
steatorrhea
macrocytic aneamia
112
what lab results would small bowel bacterial overgrowth show?
low cobalamin and high folate levels
113
how is small bowel bacterial overgrowth treated?
surgical correction of an anatomical blind loop, tetracyclines - 2-3 weeks
114
what is intestinal failure a result of?
inability to maintain adequate nutrition or fluid status via the intestines
115
what can intestinal failure occur due to?
obstruction, dysmotility, surgical resection, congenital defect, disease associated loss of absorption
116
what is intestinal failure characterised by?
inability to maintain protein-energy, fluid, electrolyte or micronutrient balance
117
what is intestinal failure?
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
what are the 3 types of intestinal failure?
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
what is malnutrition?
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
what are the disease related caused of malnutrition?
decreased intake
impaired digestion and/or absorption
increased nutritional requirements
increased nutrient losses
121
what are the adverse effects of malnutrition?
```
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
what are the two major forms of inflammatory bowel disease (IBD)?
Crohn's disease - can affect any part of GI tract
| ulcerative colitis - affects colon
123
what does colitis mean?
inflammation of the inner lining of colon
124
what are the risk factors for crohn's disease?
```
genetics - most common.
smoking
NSAIDs
Good hygiene
nutritional factors
psychological factors
appendicectomy
```
125
what are the risk factors for ulcerative colitis?
genetics
NSAIDs
nutritional factors
psychological factors
smoking - lowers risk
appendicectomy - lowers risk
126
what are the anal and perianal complications of crohn's disease?
```
fissure in ano
haemorrhoids
skin tags
perianal abscess
ischiorectal abscess
fistula in ano
anorectal fistulae
```
127
what are the inflammatory histological features of crohn's disease compared to ulcerative colitis?
deep (transmural) patchy in CD
| mucosal continuous in UC
128
which IBD are granulomas present in?
Crohn's disease
129
which IBD are goblet cells present in?
Crohn's disease, depleted in ulcerative colitis
130
what are the major symptoms of Crohn's disease?
diarrhoea
abdominal pain
weight loss
131
what are some minor symptoms sometimes present in Crohn's disease?
```
malaise
lethargy
anorexia
nausea
vomiting
low grade fever
```
132
what may be the main presenting feature of crohn's disease in children?
reduced growth velocity and delayed puberty
133
what will 50% of patients with crohn's disease require within 5 years of diagnosis?
intestinal resection
134
what are physical signs of crohn's disease?
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
which main pathogens cause gastroenteritis?
1. campylobacter - commonest
2. salmonella - outbreaks
3. E.coli 0157 - rare but morbidity/ outbreaks
other - C.diff, listeria, shigella, norovirus, rotavirus
136
what are the GI infection risk factors?
- 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
What are the bacterial factors of GI infection?
- 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
what is diarrhoea?
>3 unformed stool/day, stool holds the shape of container, departure from normal bowel habit
139
what does dysentry mean?
inflammation of the intestine, particularly the colon, causing diarrhoea associated with blood and mucus
140
what is dysentry normally associated with?
fever, abdominal pain and rectal tenesmus
141
what is the bacillus cereus incubation period?
1-6 hours
142
what type of bacteria is bacillus cereus?
gram positive bacillus
143
what type of food is likely to cause bacillus cereus infection?
starchy foods - especially reheated rice
144
what is the staphlococcus aureus incubation period?
1-6 hours
145
what type of bacteria is staphlococcus aureus?
gram positive coccus
146
what type of food is staphlococcus aureus found in?
foods left at room temperature - milk/meat/fish
147
how does staphlococcus aureus cause infection?
preformed toxin in food - rapid absorption, acts on vomiting centre in brain
148
what dies shiga toxin do?
binds to receptors found on renal cells, RBC and others, inhibits protein synthesis and causes cell death
149
what would happen if antibiotics were prescribed for E.coli 0157?
produces more shiga-toxin which has a high mortality - can cause haemolytic ureamic syndrome (HUS)
150
why are antibiotics not normally prescribed for gastroenteritis?
in case it causes haemolytic ureamic syndrome (HUS)
151
How does HUS present?
```
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
what is the incubation period of campylobacter?
16-48 hours
153
what causes campylobacter infection?
poultry, raw milk
154
what is a polyp?
a protrusion above an epithelial surface, a tumour (a swelling)
155
what is the differential diagnosis of a colonic polyp?
1. adenoma
2. serrated polyp
3. polypoid carcinoma
4. other
156
what is the adenoma-carcinoma sequence?
normal mucosa > adenoma (dysplastic) > adenocarcinoma (invasive)
157
what must be done to all adenomas?
must be removed as they are premalignant, either done endoscopically or surgically
158
what does dukes staging predict?
prognosis
159
what do the different dukes staging types indicate in colorectal carcinoma?
dukes A - confined by muscularis propria
dukes B - through muscularis propria
dukes C - metastatic to lymph nodes
160
what is the clinical presentation of left sided colorectal carcinoma?
blood PR
altred bowel habit
obstruction
161
what is the clinical presentation of right sided colorectal carcinoma?
anaemia
| weight loss
162
where does local invasion of colorectal carcinoma occur to?
mesorectum, peritoneum, other organs
163
where does lymphatic spread of colorectal carcinoma occur to?
mesenteric nodes
164
where does haematogenous spread of colorectal carcinoma occur to?
liver, distant sites
165
what are inherited cancer syndromes?
- hereditary non polyposis coli (HNPCC)(<100 polyps)
| - familial adenomatous polyposis (FAP) (>100 polyps)
166
What is the difference in HNPCC and FAP?
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
