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98 Cards in this Set

  • Front
  • Back
what's leukoplakia
mucous membrane disorder characterised by white patches
mucous membrane disorder characterised by white patches
which cancer makes up 95% of oral cancers

what sex, & age likely

risk factors
squamous cell carcinoma

male 50+

smoking, UV, alcohol, immunosuppression
squamous cell carcinoma (SCC)

male 50+

smoking, UV, alcohol, immunosuppression, poor nutrition
presentation of oral cancer (signs)- SCC
appearance: leukoplakia, red/velvety, speckled
granular irregular
exophytic (protrudes)
non-healing ulcer 3wks+
swollen
mobile teeth
lymphadenopathy
when would urgent referral for oral cancer suspicion be approriate (1)
HOARSEness 3wks+

particularly in 50+ smokers/ heavy drinkers
oral manifestations of systemic diseases
ULCERS: chron's, coeliac, infections
ANGULAR STOMATITIS: iron def
GINGIVITIS: vit C def
GLOSSITIS: iron/ folate/ B12 def
THRUSH: DM, HIV.....loads
apart from systemic diseases, why else might someone have oral manifestations
- e.g.
side effects of drugs:
- NICORANDIL (K-channel openr) for angina
screen for colorrectal ca
FOBT
FOBT
what physiological mechanisms cause nausea
LOS & stomach RELAX
upper s.int & pyloric sphincer contract
move into body of stomach
wheres the vomiting centre
medulla oblongata
medulla oblongata
what symptoms precede vomiting
nausea
sweating
pale
profuse salivation
tachycardia
what's the major consequence of severe vomiting
DEHYDRATION (lose gastric protons H+) & Cl-
→ METABOLIC ALKALOSIS
- H+ accompanied by K+ excretion = hypokalaemia
which 4 areas can vomiting triggers signal to in the brain
VC, Vestibular nucleus, NTS or CTZ
VC, Vestibular nucleus, NTS or CTZ
vomiting triggers: sight, pain & smells signal to where in the brain
direct to VC
direct to VC
vomiting triggers: motion and vestibular disorders signal to where in the brain
Vestibular nucleus
Vestibular nucleus
vomiting triggers: pharyngeal/ gastric/ duodenal stimulation signal to where in the brain
NTS (nucleus tractus solitarus) or CTZ (chemoreceptor trigger zone)
NTS (nucleus tractus solitarus) or CTZ (chemoreceptor trigger zone)
how do drug & radiation chemotherapy induce emesis
release 5-HT from ENTEROCHROMAFFIN cells lining gut → 5-HT receptors in gut → vagal afferent → signal to CTZ
release 5-HT from ENTEROCHROMAFFIN cells lining gut → 5-HT receptors in gut → vagal afferent → signal to CTZ
how does dopamine cause emesis (vomiting)
D2 receptors prevalent in CTZ
which receptors are prevalent in the CTZ for vomiting
5-HT3 & D2 (receives dopamine)
5 major classes of anti-emetic drugs (anti-vomiting)
5-HT3 antagonists
muscarinic antagonists
H1-antagonists
Dopamine-receptor antagonists (D2)
Cannabinoids
eg of 5-HT3 antagonists used in vomiting
uses
SE's
ONDANSTERON
chemo & radio-induced
✔ well tolerated
x. constipation
x. headaches
eg muscarinic antagonists use in vomiting
uses
SE's
HYOSINE/ SCOPOLAMINE
prophylaxis motion sickness
x. burry vision
x. urinary retention
x. dry mouth
x. sedation
eg H1-antagonists use in vomiting
uses
SE's
CYCLIZINE (also blocks M receptors)
motion sickness
x. drowsy
eg dopamine antagonists use in vomiting
uses
SE's
DOMPERIDONE & metoproclamide
drug-induced vomiting, Gi disorders (e.g. GORD)
x. reduced GI transit

PENZOTHIAZINE used in severe vomiting
eg of a cannabinoid used last resort in chemo-induced vomiting unresponsive to other agents

SE's
NABILONE--> opiate receptors
x. dry mouth
x. drowsy
x. dizzy
x. mood changes
2 eg's acute inflam oesophagus
infection (in immunocompromised)
corrosive after chemical indigestion
common cause of chronic oesophagus inflam
GORD/ reflux oesophagitis
3 causes of GORD
defective sphincter mechanisms

abnormal oesophageal motility (achalasia, spasm, HTN peristalsis)

increased intra-abdominal pressure
3 complications of GORD
ulceration
stricture (fibosis & scarring = narrowing)
Barret's oesophagus
what's the cell change (metaplasia) in Barret's oesophagus
stratified squamous --> COLUMNAR epithelium
BENIGN...but...

(increase risk developing dysplasia & carcinoma)
what's allergic oesophagitis characterised by and what does the oesophagus look like on endoscopy
EOSINOPHILIA
corrugated, ridges
assoc with asthma, young, M
EOSINOPHILIA
corrugated, ridges
assoc with asthma, young, M
3 drugs for treatment of allergic oesophagitis
steroids, cromoglycate, ,montelukast
steroids, cromoglycate, ,montelukast
what is the main type of benign oesophageal tumour
what virus is it related with
squamous PAPILLOMA (wart-like growth)---HPV
squamous PAPILLOMA (wart-like growth)---HPV
2 main types MALIGNANT oesophageal tumours
SCC (epithelial layers)
ADENOCARDINOMA (glandular)
aetiology (causes) of SCC in oesophagus
vit A/ zinc def
tannic acid/ strong tea
smoking, alcohol
HPV
oesophagitis (GORD)
genetic
vit A/ zinc def
tannic acid/ strong tea
smoking, alcohol
HPV
oesophagitis (GORD)
genetic
epidemiology of oesophageal adenocarcinoma
aetiology - main BIG risk/ predisposition
pathogenesis
caucasians, M, obese
lower 1/3 oesophagus 
BARRET's --> dysplasia --> adenocarcinoma
caucasians, M, obese
lower 1/3 oesophagus
BARRET's --> dysplasia --> adenocarcinoma
3 mechanisms of cancer metastises
local - direct invasion
lymphatic
systemic - vascular- blood
symptoms of oesophgeal tumour/ cancer
DYSPHAGIA, retrosternal chest pain
regurgitation
anaemia, weight loss, fatigue, lymphadenopathy
what's the treatment of choice for oral cancers
surgery +/- adjuvant therapy
symptoms of oesophagitis GORD
heart burn/ acid reflux/ chest pain
belching
water brash (excessive salivation)
odynophagia (painful swallow)
weight loss
hoarseness/ cough (upper 1/3)
risk factors for oesophagitis (GORD)
ageing, obese, FH, smoking, alcohol, hiatus hernia, preg, big meals
when does GORD/ oesophagitis require Ix
ALARM symp's:
- gastroscopy OGD & biopsy
- Ba swallow (hiatus hernia?)
management of oesophagitis (GORD)
LIFESTYLE (weight loss, reg meals, raise bed, stop smoking, avoid fatty, hot drinks, alochol, eating late...)

DRUGS: antacids, PPIs
Gastropariesis can cause GORD or be a complication of it, what is it
causes
symps
DELAYED gastric EMPTYING (no physical obstruction:

DM, cannabis, meds, systemic disease

- early satiety, nausea, vomiting, epigastric pain
Ix & management of gastropariesis
IX: endoscopy & Ba swallow (exclude other causes)
gastric emptying studies

Rx: remove precipitating factors, soft diet, low fat
4 ALARM features of oesophageal and gastric cancer
ALARM age to suspect it
weight loss/ anorexia
HAEMATEMESIS
DYSPHAGIA
MASS
>55yrs
aetiology / important cause of gastric cancer
H.pylori infection
Ix's for oesophageal cancers
endoscopy + biopsy
bronchoscopy ?invasion

imaging: Ba swallow, CT

FITTNESS study--> potential surgery
4 types treatment for oesophageal cancer

prognosis
SURGERY
RADIOtherapy
INTUBATE/ stent
RECANALISATION

majority die <1yr
symptoms specific to gastric cancer
dyspepsia
early satiety
upper GI bleed
abdo mas- ALARM

general: weight loss, anaemia, >55yrs, fatigue
Ix's gastric ca
gastroscopy + biopsy

imaging: Ba meal, CT
3 options for gastric cancer treatment

5 yr survival
SURGERY
CHEMO
INTUBATION

15% 5-yr survival
6 main causes upper GI bleed "haematemesis"
peptic ulcer
GASTRIC EROSIONS
duodenal ulcer
varices
Mallory-Weiss tear
Oesophagitis
presentation upper GI bleed
haematemesis (bright or coffee-ground)
malena (dark, dig upper GI blood)
↑HR , ↓BP
collapse
haematemesis (bright or coffee-ground)
malena (dark, dig upper GI blood)
↑HR , ↓BP
dyspnoea
collapse
what does the rockall score measure/ predict
what factors does it consider
predict REBLEED & DEATH , triage- who to discharge...
- age
- shock
- cormobidity
- Dx
- sings of haemorrhage
which score to use to assess need for endoscopy / intervention
BLATCHFORD score or Rockall
initial management of upper GI bleed
ABCDE & RESUSCITATION
O2
IV fluids!
?blood transfusion >30% loss

asap endoscopy necessary?
management (after initial resuscitation) of non-variceal upper GI bleeding
- endoscopic
- pharmacological
1) ENDOSCOPIC therapy to ACTIVELY bleeding lesions/ visible vessels/ ulcers with adherent clot
- adrenaline, thermal , mechanical

2) DRUGS:
- H.pylori eradication (if applicable- e.g. omeprazole+amox+met )
- IV PPI
clinical clues (S&Ss) to suspect VARICEAL upper GI bleed (as oppose to non-variceal bleed)
portal HTN: ascites, caput medusa
CHRONIC LIVER DISEASE: palmar erythema, spider naevi, jaundice
confused
portal HTN: ascites, caput medusa
CHRONIC LIVER DISEASE: palmar erythema, spider naevi, jaundice
confused
management (after initial resuscitation) of VARICEAL bleed
- endoscopic
- pharmacological
- specifically for Chronic liver disease pt's
TERLIPRESSIN (vasoactive) 
BAND LIGATION 

CLD= Abx's
TERLIPRESSIN (vasoactive)
BAND LIGATION

CLD= Abx's
management of variceal re-bleed (2)
TIPS (transjugular intrahepatic portosystemic shunt)- treats portal HTN 

BALLOON TAMPONADE/ Sengstaken-Blakemore tube (temp)
TIPS (transjugular intrahepatic portosystemic shunt)- treats portal HTN

BALLOON TAMPONADE/ Sengstaken-Blakemore tube (temp)
causes of peptic ulcers (4)
bacterial/ viral infections
H.pylori!
IBS
GB/ liver disease
functional
6 causes of dyspepsia
peptic ULCER
oesophagitis/ duodenitis/ gastritis
gastric MALIGNANCY
GORD
S&Ss peptic ulcer
DYSPEPSIA
epigastric pain (assoc with food, nocturnal)
bloating/ early satiety
heartburn
weight loss
FH
structures which can cause epigastric pain
heart (eg MI)
oesophagus, stomach, duodenum
pancreas, liver, GB, CBD
heart (eg MI)
oesophagus, stomach, duodenum
pancreas, liver, GB, CBD
pharmacological therapy for peptic ulcers (2)

H.pyroli specific eradication
PPIs: omeprazole
H2-antagonists: ranitidine

H.pylori= abxs: omeprazole+amox+met/ claryth

STOP NSAIDs
what's produced by H.pylori to aid its survival
UREASE 
ammonium bicarb NEUTRALISES stomach pH
UREASE
ammonium bicarb NEUTRALISES stomach pH
tests/ Ix's for dx of H pylori
★UREA BREATH TEST★
or
culture biopsy
serology
how does H.pylori cause increased acidd (HCl) production
H.pylori reduces somatostatin release from D cells 
G cells → gastrin → parietal cells → HCl
H.pylori reduces somatostatin release from D cells
G cells → gastrin → parietal cells → HCl
when H.pylori colonises stomach, what disease ensues
chronic gastritis
how does chronic gastritis predispose to gastric cancer
ATROPHY of mucosa
↓parietal = ↓acid
H.pylori grows
dysplasia --> gastric cancer
treatment for H.pylori (triple therapy)
omeprazole + amox + metramidazole or clarythromycin
if dyspepsia is H.pylori -ve, how to manage?
PPI: omeprazole
or
H2-antagonist: ranitidine
4 causes of ACUTE gastritis
head injury
severe injury
shock
severe burns
4 causes of CHRONIC gastritis (ABCR)
AUTOIMMUNE (atrophic)

BACTERIAL: H.PYLORI

CHEMICAL: reflux, NSAIDs, alcohol

RARE: lymphocytic, eosinophilic, granulomatous
3 chemical causes of chronic gastritis
reflux bile
NSAIDs
alcohol
what do lamina propria cells produce in response to infection with H.pylori
anti-H.pylori IgA antibodies
which type of peptic ulcer most common- pathogenesis
DUODENAL
50% ↑acid secretion = gastric metaplasia, inflammation, epithlial damage
morphology of peptic ulcers
clear edges "punched out"
2-10cm diam or microscopic layered 
floor of nectrotic fibropurulent debris
base granulation tissue
deep fibrotic scar
neutrophils & exudate
clear edges "punched out"
2-10cm diam or microscopic layered
floor of nectrotic fibropurulent debris
base granulation tissue
deep fibrotic scar
neutrophils & exudate
3 complications of peptic ulcers
perforation 
haemorrhage
stenosis
perforation
haemorrhage
stenosis
2 types of benign gastric tumours
HYPERPLASTIC polyps
CYSTIC GLAND polyps
HYPERPLASTIC polyps
CYSTIC GLAND polyps
3 types MALIGNANT gastric tumours
ADENOCARCINOMA (epithlial cells)- most common!

lymphoma

GI Stromas Tumours (GISTs)
aetiology & asoociation of gastric adenocarcinomas
H.pylori- chronic gastritis
atrophic gastritis (autoimmune)
deprived
SMOKING
adenomatous POLYPS (e.g. genetic- FAP)
HNPCC/ Lynch syndrome
2 subtypes of gastric adenocarcinomas

what's the difference:
- loc
- formation
- prognosis
1) INTESTINAL- exterior, gland formation, better prognosis

2) DIFFUSE (pic) - stomach wall, thickening & fibrosis, worse prognosis
- linitis plastica, sclerosis, SIGNENT RING type
1) INTESTINAL- exterior, gland formation, better prognosis

2) DIFFUSE (pic) - stomach wall, thickening & fibrosis, worse prognosis
- linitis plastica, sclerosis, SIGNENT RING type
which type of malignant gastric tumour is derived from mucosal lymphoid tissue, shows clonal B-cell proliferation & lymphoid cells fill the stroma of stomach wall
gastric lymphoma (MALToma)
gastric lymphoma (MALToma)
dysphagia (difficulty swallowing) can be due to what 2 broad categories of problems
MECHANICAL BLOCK
MOTILITY disorder

other: inflam
important Q-s to ask about dysphagia- why
ONSET- gradual (mechanical- stricture), sudden (motility d.)
CONSTANT/ EPISODIC - stricture/ spasm
DURATION- ca over long period
PAIN- ca, inflam, spasm
ASSOC SYMPs
DYSPEPSIA
6 Common Ix's for dysphagia
FBC (anaemia)
U&Es (hydration)
CXR (mediatinum fluid, gastric bubble, aspiration)

★OGD +/- biopsy ★
Ba swallow ---normal?---> manometry
MECHANICAL causes of dysphagia
food bolus
Schatzki ring (benign fibrous narrowing lower oesophagus)
diverticulum
extrinsic pressure (lung ca, LA enlargement, mediastinal nodes, AAA)
MOTILITY causes of dysphagia
achalasia (LOS fails to relax)
diffuse spasm
Bulber palsy
Motor neurone disease
Cerebrovascular disease
4 pathogens causing oesophageal infection
candida
Herpes
CMV
EBV
what's the ROME III criteria for IBS
1) RECURRENT abdo pain for 3+ days/ month, for 3months
2) + 2 of:
- better with defaecation
- change stool freq
- change stool consistency
age and sex presentation for IBS
20-40yrs F>M
S&Ss IBS
abdo pain (central/lower)- better with defaecation
abdo bloating
altered bowel habit & freq
tenesmus
mucus PR
CHRONIC- exacerbated with stress, menstruation, fibre, drugs
pathophysiological feature of IBS
VISCERAL hypersensitivity
IBS ALARM features!
>50 - ?colorectal ca
short duration
woken at night- ?IBD
BLOOD PR- ?IBD/ ca
↓weight- ?IBD/Ca
anaemia
FH colorectal ca-----> scope!
recent abxs
Dx of IBS by Ix
Dx of EXCLUSION
FBC, U&Es, LFTs, ESR, CRP, coeliac serology
urinalysis
Stool if ?infection
Colonoscopy- if FH colorectal ca/ >50yrs
treatment/ management of IBS
Diet (reg, ↓fibre, ↓caffiene, hydrated)
Lifestyle (exercise, ↓stress)

DRUGS:
- laxatives- constipation
- antimotility (loperamide)- diarrhoea
- anti-spasmodics (mebeverine)- colic/bloating
- anti-depressants (amitryptiline)

PSYCHOLOGICAL therapies
main Ddx's for IBS (5)
IBD
colorectal ca
coeliac disease
malabsorption
gastroenteritis