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3rd BDS IHD > GI > Flashcards

GI Flashcards

1
Q

what does the upper GI tract involve

A

mouth, oesophagus, stomach and duodenum

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2
Q

what is the most common problem with the oesophagus

A

Barrett’s oesophagus (and oesophageal cancer )

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3
Q

what stops reflux into the oesophagus (2)

A

cardiac sphincter
diaphragm constricting around the lower oesophagus

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4
Q

why is it important that we prevent acid reaching the oesophagus

A

mucous is needed to protect epithelium from acid
only glandular epithelium has mucous (stomach)
if acid reaches non-mucous lined squamous epithelium of the oesophagus, it is destroyed and acid then can ulcerate the tissue

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5
Q

compare the epithelium of the oesophagus and the stomach

A

oesophagus = non-keratinised stratified squamous epithelium

stomach= non-keratinized simple columnar epithelium with mucous glands

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6
Q

how might we diagnose barrettes disease (4)

A

endoscopy
normal oesophageal tissue is white and reflective
if red tissue is found in the lower oesophagus, this is columnar epithelium from the stomach growing

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7
Q

what is barrettes oesophagus

A

where we get metaplasia from stratified squamous epithelium in the oesophagus to columnar epithelium from the stomach

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8
Q

what is another name for barretts oesophagus

A

columnar lined lower oesophagus - CELLO

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9
Q

explain the mechanism of barrettes oesophagus

A

IF the acid refluxes, acid goes into the oesophageal epithelium and these cells cannot cope with low pH so they die.
This leads to no epithelium, ulceration and pain.
Squamous epithelial CAN regrow but if the acid keeps refluxing, then we get metaplasia or growth from epithelium from the stomach into the oesophagus.

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10
Q

what might barrettes oesophagus predispose and why

A

barrettes oesophagus has columnar epithelium in the oesophagus
This is not meant to be and is genetically unstable so predisposes oesophageal cancer
constant acid attack will constantly damage tissue and also increase chances of cancer

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11
Q

why is adenocarcinoma of the oesophagus infinitely increased chances with people with barrettes oesophagus

A

people without barrettes oesophagus cannot get oesophageal adenocarcinomas as this is cancer of glandular tissue
normal oesophageal tissue is not glandular so cannot get adenocarcinoma

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12
Q

what are some risk factors for barrettes oesophagus (3)

A

increased wieght = abdominal pressure increase on stomach contents

male
late age >50

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13
Q

why might oesophageal cancers be eligibly on the rise (2)

A

ageing population and old onset so more diagnosis

no longer grouped with gastric cancers

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14
Q

in asia and africa there are very high levels of oesophageal cancers. compare this cancer to the type of oesophageal caner found in europe.

A

Asia and Africa are commonly squamous cell carcinomas due to alcohol and smoking

Europe are usually barrettes related = adenocarcinomas

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15
Q

compare oesophageal adenocarcinomas and squamous cell carcinomas

A

AC = barrettes oesophagus, reflux, weight, age, europe

SCC = asia, africa, smoking and alcohol

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16
Q

give 2 reasons why oesophageal cancer has low prognosis

A

often not diagnosed until late stage so low prog

very close to important structures e.g. trachea, aorta, vena cava so can have very bad consequences if metastatic

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17
Q

what is Helicobacter Gastritis caused by

A

Helicobacter Pylori H. Pylori

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18
Q

what is the strcutre of H.Pylori (3)

A

rod shaped bacilli
motile
flagellum

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19
Q

how is Helicobacter Gastritis caused (3)

A

hide in the mucous layer of stomach
This bacteria produces chemicals that attract in inflammatory cells eg. neutrophils into the stomach, causing acute inflammation.
This causes ulceration in the stomach allowing acid to reach under the epithelium.

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20
Q

where do H.Pylori live

A

mucous layer of the stomach

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21
Q

how do we treat Helicobacter Gastritis

A

1 week
Antibiotic e.g. metronidazole

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22
Q

why is the incidence of gastric cancer reducing with time (2)

A

oesophageal cancer no longer included in ‘gastric cancers’ and they made up a large proportion of this
less frying with cast rion pans that = nitrosamines = carcinogen

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23
Q

where do we find high gastric cancer incidence, why?

A

east asia and eastern europe
high amounts of smoked and pickled foods - acidic

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24
Q

how do we treat acid reflux (3)

A

anti-acids e.g. Gaviscon
proton pump inhibitors e.g. Omeprazole or Lansoprazole
surgery

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25
Q

what are some side effects of proton - pump inhibitors

A

prolonged use = kidney damage
alcoholics should not take
diarrhea

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26
Q

what carcinogen is produced by frying in cast iron

A

Nitrosamines

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27
Q

what 3 main things lead to intestinal metaplasia

A

smoked/pickled foods, helicobacter pylori (gastritis) pernicious anaemia

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28
Q

why is intestinal metaplasia of the stomach bad (3)

A

where intestinal epithelium grows into the distal stomach
genetically unstable epithelium that is not protected by mucous = high damage
predisposes dyplasia and cancer

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29
Q

what is another name for coeliac disease

A

Gluten sensitive enteropathy

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30
Q

what 3 changes to the intestines do we see with coeliac disease

A

villous atrophy
crypt hyperplasia
increased neutrophil count on surface epithelium

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31
Q

how does coeliac disease work (4)

A

autoimmunity to gliadin protein
Gliadin protein from gluten is absorbed
Gliadin is presented to APCs causing
Activation of toxic T cells
On second gluten exposure = toxins that kill epithelial cells and cause: crypt hyperplasia, villus atrophy and leukocytes in epithelium

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32
Q

what is the prevalence and treatment for coeliac

A

1% of population
avoidance of gluten

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33
Q

What are the 2 major chronic idiopathic inflammatory bowel diseases

A

Crohns disease
Ulcerative Colitis

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34
Q

what can inflammatory bowel disease be divided into (2)

A

chronic idiopathic (ulcerative colitis and crohns disease)
other

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35
Q

what is crohns disease (3)

A

chronic idiopathic IBD
patchy discontinuous inflammation of the bowel
affecting all parts of the GI tract from mouth to anus and all layers of the bowel (transmural)

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36
Q

where does Crohns disease effect

A

all segments of the bowel from mouth to anus and all layres of the bowel = transmureal

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37
Q

what histological markers are there of crohns disease

A

grnauloma inflammation
These are characterised by pinkish ‘epithelioid’ macrophages surrounded by lymphocytes, also found in TB.

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38
Q

a histological section shows granuloma tissue with pink epithelioid macrophages, what diseases might this be

A

TB - likely to be lungs
Crohns - GI

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39
Q

what clinical representations of the bowel might we see in Crohns disease (3)

A

patchy inflammation
Aphthous ulcers (can present in mouth)
cobblestoned effect on bowel due to fibrosis

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40
Q

what are some signs and symptoms of Crohns disease

A

abdominal pain
diarrhoea
fibrosis of bowel
aphthous ulcers in Gi tract and mouth

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41
Q

where does ulcerative colitis affect

A

This disease only affects the MUCOSA of the COLON.
It will start at the rectum and then extend further up the bowel. This, as opposed to crohn’s disease, is always continuous and can affect the whole colon.

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42
Q

what is a distincitve feature of ulcerative colitis inflammation

A

There will be a very distinct cut off between normal and inflamed mucosa. This disease only affects the mucosa of the large colon, it doesn’t spread into the submucosa, muscle or fat.

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43
Q

compare the location of inflammation between Crohns disease and Ulcerative Colitis

A

C: non-continuous, whole GI tract, all layers of tissue

UC: continuous, starts at anus, only affects colon, only affects mucosa

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44
Q

a patient has ulceration on their tongue and soft tissues and then an endoscopy shows ulceration in the oesophagus, what is the likely diagnosis and how could we confirm this

A

Crohn disease
biopsy showing granuloma formation ?

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45
Q

what is the treatment for ulcerative colitis

A

anti-inflammatories
immunosuppressants

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46
Q

what is Diverticular Disease

A

diverticular - outpouching of the mucosa - tending to occur in the sigmoid colon which is the part of the colon just before the rectum

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47
Q

where is diverticular disease likely to act

A

sigmoid colon - just next to the rectum

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48
Q

what is a diverticular

A

outpouching in the mucosa - affecting sigmoid colon within diverticular disease of the colon

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49
Q

how does diverticular disease occur

A

The bowel wall has small perforations for blood vessels to enter and supply the bowel.
A lack of fibre in the diet leads to a raised pressure in the bowel and this can cause diverticular disease. The less fibre in the bowel, the more pressure the muscles have to put on the contents to push it along and when the mucosa is pushed down into these perforations, they enter the muscular perforations forming outpouches.

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50
Q

what is a major risk factor for diverticular disease

A

lack of fibre in the diet
And age

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51
Q

why is diverticular disease dangerous

A

blind ended sacs which can get clogged up with faeces and get inflamed and possibly rupture which is very bad as faeces is released into the peritoneal cavity causing
Faecal peritonitis

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52
Q

what is a major risk factor for faecal peritonitis

A

diverticular disease
blind ended sacs which can get clogged up with faeces and get inflamed and possibly rupture which is very bad as faeces is released into the peritoneal cavity

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53
Q

what is faecal peritonitis

A

where faeces and contents of colon are released into the peritoneal space causing infection

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54
Q

how could we diagnose faecal peritonitis

A

found commonly on elderly patients complaining of abdominal pain. On gentle probing, there is a rigid structure in the abdomen = Faecal peritonitis

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55
Q

how do we treat faecal peritonitis

A

surgery to remove faeces
if too severe and urgent, colostomy bag above the rupture until surgery can be done

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56
Q

why might colorectal cancer be low in africa

A

life expectancy lower due to malnutrition and lack of vaccination and health control e.g. HIV
colorectal cancer only becomes prelevent over age of 60

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57
Q

why is colorectal prognosis increasing with increasing incidence

A

This is likely to do with fibre optic colonoscopes, along with CT scans, aiding early diagnosis greatly leading to increased prognosis

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58
Q

what are polyps

A

adenomas
benign growths that predispose adenocarcinomas

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59
Q

how many people over 60 have colorectal polyps

A

1/3

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60
Q

explain the TMN staging

A

for cancer
N = if it has spread to lower or higher nodes
T = invasion depth
M = presence of metastasis

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61
Q

what is a possibly prevention strategy against adenoma polyps

A

low dose aspirin

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62
Q

how can we remove polyps

A

if colorectal, endoscopic resection

63
Q

how do we treat colorectal adenocarcinomas

A

surgical resection

64
Q

how do we treat colorectal metastatic adenocarcinomas

A

palliative care and chemotherapy
often non-treatable

65
Q

what liver metastasis are surgically removable and not trstable

A

if within 1 half of the liver, surgical removal is often viable as the liver regenerates. after both halves have been infiltrated, prognosis is very low

66
Q

what genetic disease leads to huge increased risk of adenocarinoma of the colorectal or GI tract

A

Familial Adenomatous Polyposis
Autosomal dominant genetic condition that affects young adults where they have healthy GI but in early adulthood gain thousands of small adenomas.

67
Q

what is familiar adenomatous polyposis

A

Autosomal dominant genetic condition that affects young adults where they have healthy GI but in early adulthood gain thousands of small adenomas.

68
Q

where does colorectal cancer often involve

A

Mainly occurs in rectum and sigmoid
but 13% in the caecum near the small intestine which requires a very flexible endoscope.

69
Q

why is cancer in the caecum hard to diagnose

A

in the colon very close to the small intestine
need a very flexible endoscope to reach this point

70
Q

what is Gastroentrinitis

A

Syndrome characterised by GI-symptoms including nausea, vomiting, diarrhoea and abdominal pain

71
Q

what is dehydration

A

Abnormal faecal discharge characterised by frequent and/or fluid stool. Associated with increased fluid and electrolyte loss- often disease of small intestine - bacteria, dehydration

72
Q

what is dysentery

A

Abnormal inflammation of GI-tract: often blood and pus in faeces and pain, fever, abdominal cramps- often disease of large intestine

73
Q

what is enterocolitis

A

Inflammation of mucosa of small and large intestine

74
Q

explain how the GI tract defends against infection

A

normal bacterial flora
saliva in mouth
rapid shedding of epithelium in mouth, small intestine and colon
pH in stomach
slow of fluid and peristalsis
mucous

75
Q

what is food poisoning

A

This strictly refers to ingestion of toxins or poisons in food: e.g. bacterial toxins or heavy metals causing vomiting, diarrhea and other symptoms
Bacteria grow and multiply in food
Cooking kills bacteria but toxin still active – intoxication

76
Q

what foods have risk of staph aureus food poisnoning

A

mainly dairy and cooked meats
pre-packed snadwhiches
things prepared and kept e.g. salsas at KFC

77
Q

how does staph aureus food poisoning present

A

3-6h of severe vomiting- self-limiting- complete recovery

78
Q

does cooking thouroughly prevent staph aureus food poisoning

A

not always
50% of strains produce heat-stable enterotoxins – also resistant to stomach acid and digestive enzymes

79
Q

where might we find botulism toxin

A

tinned foods, cheese sauce,

80
Q

what happens with botulism toxin

A

blockage of acetyl choline neurotransmitter
flaccid paralysis
death

81
Q

who is most likely to get botulism

A

infant botulism

82
Q

what bacteria causes ‘fried rice syndomre’

A

Bacillus Cereus

83
Q

explain how Bacillus Cereus causes infection (4)

A

spores found on most grains e.g rice, wheat
when cooked bacteria die but spore survive
if left to cool, spores germinate and produce toxin
heat stable toxin survives reheating and is ingested

84
Q

what is bacillus cereus found in

A

most pulses
rice and wheat products
spores found in ground

85
Q

what type of bacteria is bacillus cereus (3)

A

gram positive, spore forming bacillus rod

86
Q

how do helicobacter pylori survive in the stomach and what do they cause

A

bacteria produce urease
convert urea to ammonia
ammonia neutralised the low pH acid
forming an alkaline environment for long enough to implement self into mucin layer
cause inflammation of mucosa and destroy epithelium
cause stomach ulceration

87
Q

how do we test for helicobacter pylori food poisoning (3)

A

give high urea food diet
bacteria produce urease urea–> ammonia
ammonia breath test

88
Q

which part of the stomach does H. Pylori infect

A

lower stomach mucous membrane

89
Q

how do we treat H. Pylori gastric ulcers

A

proton-pump inhibitor e.g. omeprazole
PLUS metronidazole/ amoxicillin and Clarithromycin

90
Q

what two classifications of H.Pylori are there and why is this relevent (3)

A

CagA positive and negative
cytotoxin-associated gene A present or not
CagA is related to gastric cancers

91
Q

how do we treat severe diarrhea and what do we NOT do

A

Fluid and electrolyte replacement is essential and time to recover

Antibiotic treatment often not successful and may worsen problem- as wipes out competing organisms…. or stimulates toxin production (C.diff)

92
Q

what is some relevent history to dysphagia

A

Duration - progressive = structural cause malignancy, intermittent = motility e.g. spasm
Solids or liquids or both
Pain (odynophagia) = oesophagitis
Weight loss = red flag for malignancy
Previous medical history
Medications
Cigarettes and alcohol

93
Q

what are the three causes of dysphagia

A

1) Oropharyngeal Problem

2) Oesophageal Problem

3) Gastric problem

94
Q

what is Sjogrens syndrome and relate this to GI problems

A

autoimmune disease affecting fluid outputs like tears and saliva
reduced salivary flow = oropharyngeal dysphagia

95
Q

describe some causes of oropharyngeal dysphagia

A

Sjorgrens syndrome or polypharmacy= reduced saliva
neurone disorders e.g. ALS/parkinsons = lack of tongue control
hypothyroidism = enlarged thyroid = obsturction

96
Q

describe some causes of oesophageal dysphagia

A

peptic stricture (long standing reflux = narrowing oesophagus)
oesophageal pouch
achalasia
oesophageal carcinomas
oesophageal spasms = motility disorders

97
Q

what is a peptic stricture

A

stricture is a narrowing of a lumen
peptic strictures are narrowing’s of the oesophagus due to constant irritation, reflux or other damage
can cause oesophageal dysphagia

98
Q

what is achalasia

A

In achalasia, the muscles in the oesophagus do not contract correctly and the ring of muscle can fail to open properly, or does not open at all. Food and drink cannot pass into the stomach and becomes stuck. It is often brought back up.

99
Q

what are some signs of pharyngeal pouch (3)

A

regurgitation
halitosis
dysphagia
but most asymptomatic

100
Q

how do we diagnose pharyngeal pouch

A

barium swallow with xray helps identify a pouch
can be done by endoscopy but this can perforate pouch

101
Q

what is a pharyngeal pouch

A

Defect between the constrictor and the transverse cricopharyngeal muscle
diverticulum formation lateral to the pharynx
Very rare, 1 in 100,000 people

102
Q

how would we diagnose achalasia

A

bird beaks sign of the oesophagus, xray
constriction of distal portion of oesophagus

103
Q

what is the bird beaks sign

A

constriction of the distal portion of the oesophagus
tell-tale sign of achalasia

104
Q

what gastric problems can cause dysphagia

A

Carcinoma
Outlet obstruction- peptic ulceration

105
Q

how do we manage dysphagia

A

manage underlying problems
If nutritionally deplete, may require supplementation – oral supplements, NG, PEG feeding

106
Q

what is GORD

A

gastro-oesophageal reflux disease

107
Q

what percent of people have GORD

A

30%

108
Q

what are some signs and symptoms of GORD

A

Heartburn, epigastric pain, acid reflux, waterbrash, nausea, vomiting, tooth decay, asthma

109
Q

give some risk factors of GORD

A

Excessive relaxation of lower oesophageal sphincter
raised intra-abdominal pressure - obesity
hiatus hernia
delayed oesophageal clearance
dietary = alcohol, tea, coffee, acidic foods

110
Q

how do we manage GORD

A

PPI (omeprazole, lansoprazole)
anti-acids e.g. Gaviscon
H2 antagonists
Lifestyle advice (weight loss, smoking cessation, reduce alcohol) - avoid acidic and late meals, raise head in bed e.g. 2 pillows

111
Q

what non-medication management of GORD is there

A

Lifestyle advice (weight loss, smoking cessation, reduce alcohol) - avoid acidic and late meals, raise head in bed e.g. 2 pillows

surgery = fundoplication

112
Q

what is a fundoplication

A

wrapping part of the fundus of the stomach around the base of the oesophagus, to reinforce the sphincter and relieve inflammation caused by reflux

113
Q

what is a hiatus hernia

A

A hiatus hernia is when part of your stomach moves up into your chest. It’s very common if you’re over 50.
It does not normally need treatment if it’s not causing you problems. Causes reflux due to pressure gradient being lost between abdominal and thoracic cavities

114
Q

what are the three types of hiatus hernia

A

pre-stage = oesophagus stomach angle is obtuse
sliding hiatus hernia = constriction is in upper stomach in thorax
paraoesophageal type = pouch of stomach in thorax

115
Q

what pH is indicative of acid reflux in the oesophagus

A

<4pH

116
Q

how do we differentiate a gastric and duodenal ulcer

A

gastric is worsened by eating
duodenal is made better by eating

117
Q

give sings/symptoms of peptic ulcer

A

taking NSAIDs
H. Pylori infection
epigastric pain possibly radiating to back
pain/better on eating
vomiting or haematemesis

118
Q

why might peptic ulcers cause haematemesis and vomiting

A

Vomiting/ Hematemesis (due to gastric ulcer (=hematemesis) or pyloric outlet obstruction due to duodenal ulceration(=vomiting)).

119
Q

how many people over 50 are infected with H.Pylori

A

50%

120
Q

how do we treat H.Pylori (4)

A

PPI e.g. omeprazole
2 antibiotics
IF BLEEDING = endoscopic treatment
if this fails, surgical tx

121
Q

what are the symptoms of gastric cancer and when is this investigated

A

Epigastric pain, weight loss, vomiting
Must be suspected in anyone over 50 years with new onset symptoms
Epigastric pain
Weight loss
Vomiting
Early cancer can be asymptomatic

122
Q

what investigations do we undergo for gastric cancer

A

Gastrectomy
If positive, CT scan or endoscopic ultrasound

123
Q

how would we differentiate pancreatic cancer to gastric cancer

A

both would cause epigastric pains
pancreatic will be related to chronic Hep or liver problems, jaundice

124
Q

severe pain and high blood amylase. what is this

A

pancreatitis

125
Q

what are the common causes of pancreatitis

A

commonest cause alcohol > gallstones > pancreatic trauma, drugs, hypercalcamia / lipidaemia, familial

126
Q

how do we differentiate acute and chronic abdominal pain

A

chronic will be localised due to inflammation reaching pericardium
acute will be generalised
unless puncture/trauma where this will be localised
chronic is > 6 weeks

127
Q

what are these drugs for: cyclizine, metaclopramide

A

anti-emetics

128
Q

what causes acute diarrhoea

A

Infection (gastroenteritis: bacterial or viral)
Campylobacter, Salmonella, Shigella, E. Coli
Drugs
Antibiotics, PPIs, food intolerances, alcohol
Food allergy / intolerance

129
Q

what classes as chronic diarrhoea

A

> 6 weeks

130
Q

name the three main types of cause for chronic diarrhoea

A

Small bowel disease
lactase deficiency
Coeliac disease
Crohn‘s disease
Pancreatic disease
pancreatic insufficiency
pancreatic carcinoma
cystic fibrosis
Colonic disease
ulcerative colitis
Crohn’s disease
carcinoma

131
Q

what are the three histological features of coeliac disease

A

when on a gluten containing diet:
-Intraepithelial leukocytes increased in intestine
-crypt hyperplasia
-villous atrophy

132
Q

how common is coaeliac disease

A

1 in 100

133
Q

what are some signs and symptoms of coeliac disease

A

GI problems e.g. abdominal pain, diarrhoea
iron deficency
b12 anaemia
fatigue

134
Q

how do we investigate Coaelic disease

A

when on gluten diet blood test for high IgA
if high, endoscopy to look for scalloping

135
Q

what is Dermatitis Herpetiformis closely linked with and what is it

A

Itchy blisters on knees, backs and buttocks
closely related to coaeliac disease
treated by gf diet

136
Q

compare diarrhoea related to small bowel/pancreatic and from the colon (4)

A

Small bowel:
-floating, hard to flush stool
-throughout day
-pain is variable
-not relived by defication

colon:
-blood or mucous in stool
-usually in morning
-pain is during defication
-pain releived by defication

137
Q

what are some signs of ulcerative colitis

A

abdominal pain
diarrhoea and bleeding on defecation
Weight loss, fever, and anaemia

138
Q

what are some associated diseases with IBD

A

Vascular - thrombosis common so when admitted to hospital, prophylactic LMWH given
Liver - cirrhosis, CAH, pericholangitis. U.C: primary sclerosing cholangitis
Skin - erythema nodosum, pyoderma gangrenosum
Mouth - ulcers. Crohn’s: lips, buccal mucosa
Joints - arthritis, ankylosing spondylitis
Eyes - episcleritis, uveitis

139
Q

what is erythema nodosum

A

red markings on the skin e.g. legs
commonly associated with IBD

140
Q

if pt has gangrenosum on the legs, what might we suspect

A

IBD

141
Q

what are some risks for colon cancer

A

Polyps – Cancer
Over 50 more risk
Red meats, saturated fats, lack of fibre and fruit n veg
Polyps are a risk factor and removed if found endoscopically
Long standing IBD or acromegaly
Obesity and smoking

142
Q

compare rectal hameroiids anal bleeding to colorectal cancer

A

haemorrhoids cause bright red bleeding
cancer will be darker red/black

143
Q

what are some symptoms of colon cancer

A

None!! (Bowel Cancer Screening – FIT stool testing and if positive, colonoscopy )
Rectal Bleeding (may be hemorrhoids if bright red bleeding, with history of constipation and tx with creams or surgical intervention)
Altered Bowel Habit
Lethargy/ Weight Loss

144
Q

what is cholangitis

A

inflammation of the bile duct

145
Q

what might cause post hepatic jaundice

A

gallstones (with pain, fever)
cholangitis
bile duct stricture
pancreatic carcinomas (constant pain radiating to back, weight loss)

146
Q

what pain is specific to pancreatic carcinomas

A

constant abdominal pain radiating to the back

147
Q

what two antibiotic often cause hepatic jaundice

A

augmentin, flucloxacillin

148
Q

what are some signs of hepatic jaundice

A

Malaise
lethargy
anorexia
distaste for cigarettes
jaundice
pale stools (no conjugation)
dark urine (more renal excretion)
right upper quadrant discomfort

149
Q

compare stool and urine and bilirubin blood levles in pre- hepatic and post jaundice

A

pre:
-high unconjugated
-

hepatic:
-high unconjugated
-low conjugated
-pale stool
-dark urine (more renal excretion)

150
Q

give some causes of hepatic jaundice

A

liver infection e.g. Hep C and hep B or EBV
drugs e.g. Augmentin or flucloxacillin
alcohol hepatitis = high alcohol
chronic hepatitis or cirrhosis = Wilsons syndrome

151
Q

what is Wilsons syndrome and what might be a sign of this

A

increased copper deposits in the brain and liver
may present as jaundice causing hepatic jaundice

152
Q

what causes pre-hepatic jaundice

A

haemolytic anaemia, splenomegaly, sickle cell

153
Q

What can frying in cast iron cause (2)

A

Gastric cancer
Production of nitrosamines

3rd BDS IHD (14 decks)

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