MedEd Flashcards
what does dyspepsia indicate
an upper GI problem
what are symptoms of dyspepsia
epigastric pain or burning or discomfort early satiety and post-prandial fullness belching bloating nausea
A 47 year old man presents to clinic with a 3 month history of epigastric dull abdominal pain. He states that the pain is worse at night and is relieved on eating. On direct questioning, there is no history of weight loss. He is not anaemic. Duodenal ulcer Zollinger-Ellison Syndrome Gastric ulcer Gastro-oesophageal reflux disease Non-ulcer dyspepsia
Duodenal ulcer
2. A 59 year old man presents with severe retrosternal burning pain. Upper GI endoscopy shows ‘metaplastic changes within the epithelium’. Gastric ulcer Gastric carcinoma Oesophageal carcinoma Gastro-oesophageal reflux disease Barrett’s oesophagus
Barrett’s oesophagus
3. A 41 year old man is referred to gastroenterology outpatients out patients with a 3 month history of worsening epigastric pain and dyspepsia. Upper GI endoscopy confirms multiple ulcers in the stomach and duodenum. Serum gastrin is elevated. Duodenal ulcer Zollinger-Ellison Syndrome Gastric ulcer Gastric carcinoma Gastro-oesophageal reflux disease
Zollinger-Ellison Syndrome
4. A 40 year old woman presents with a 2 month history of burning upper abdominal pain which is worse on eating. On examination there is mild tenderness to palpation of the epigastric region. Duodenal ulcer Zollinger-Ellison Syndrome Gastric ulcer Gastric carcinoma Gastro-oesophageal reflux disease
Gastric ulcer
what is Zollinger-Ellison Syndrome
rare condition in which one or more tumours form in the pancreas or duodenum
these gastrinomas secrete large amounts of gastrin causing increased stomach acid production
5. A 37 year old overweight woman presents to the GP with burning upper abdominal pain. She says it is especially bad when she goes to bed. She also complains of a tickly cough and a funny taste in her mouth. Zollinger-Ellison Syndrome Gastric ulcer Oesophageal carcinoma Gastro-oesophageal reflux disease Non-ulcer dyspepsia
Gastro-oesophageal reflux disease
def of peptic ulcer disease
a break in the superficial epithelial lining of either the stomach or duodenum
what sort of peptic ulcer is more common, gastric or duodenal
duodenal
what is a common cause of PUD in developing countries
h. pylori
what is a common cause of PUD in developed countries
NSAID use
what are the two most important risk factors for PUD
h. pylori
NSAIDs
how do NSAIDs increase risk of PUD
NSAIDs inhibit COX which leads to decreased prostaglandins and this can lead to mucosal damage
what are rare associations with PUD
increased gastrin (zollinger-ellison)
what sort of organism is h.pylori
gram-negative flagellate
how common is h.pylori
very common in developing countries
what does h. pylori infection lead to
gastritis
peptic ulcers
gastric cancer
what sort of pain is PUD associated with
recurrent epigastric pain which is a burning and knawing pain
what does pain in PUD commonly occur
related to eating a meal (dyspepsia)
what symptoms are associated with PUD
N+V
getting full very quickly
weight loss or anorexia
what are the signs of PUD on examination
epigastric tenderness
‘pointing sign’
PR blood
when does pain from duodenal ulcers occur
hours after eating
can wake patients up in the night
when does pain from gastric ulcers occur
immediately after eating
what relieves the pain of duodenal ulcers
eating
antacids
what relieves the pain of gastric ulcers
minimal relief with antacids
what is pointing sign
in PUD
patient can point to site of pain with one finger (specific area of pain)
A 40 year old woman presents with a 2 month history of burning upper abdominal pain which is worse on eating.
You suspect she has a gastric ulcer. What is the most appropriate investigation?
Upper GI endoscopy
Full blood count
Abdominal X-Ray
H.Pylori Breath Test
Trial of Proton Pump inhibitor
H.Pylori Breath Test
what are the indications for a h.pylori breath test or antigen test
<55yrs and NO alarm symptoms
what are the indications for 2wk UGI endoscopy
> 55yrs or alarm (red flag) symptoms or no response to treatment
if an ulcer is present after a UGI endoscopy, what must be done
1 histology (neoplasia?) 2 h. pylori testing (biopsy urease testing?)
if a gastric ulcer is present after after a UGI endoscopy and is treated, what must be done as follow up?
repeat endoscopy after 6-8wks to rule out malignancy
what are red flag symptoms
weight loss bleeding anaemia vomiting dysphagia early fullness on eating
what is the treatment for h.pylori
triple therapy
1PPI
2xantibiotics
for example
1lansoprazole/omeprazole
2xamoxicillin + clarithromycin
what is the treatment for PUD if h.pylori negative
PPI or H2 antagonist
what complications are associated with PUD
haemorrhage
perforation
malignancy
what is GORD
reflux of stomach contents into the oesphagus
risk factors for GORD
obesity
smoking
pregnancy
haitus hernia
what foods are associated with GORD
large fatty meals
coffee or alcohol
what conditions are associated with GORD
achalasia
what symptoms are associated with GORD
burning retrosternal pain related to good
a sour taste in the mouth
what makes GORD better and worse
better - anatacids
worse - bending or lying flat
what are the extra-oesophageal features of GORD
nocturnal asthma
chronic cough
laryngitis (hoarseness)
A 37 year old overweight woman presents to the GP with burning upper abdominal pain. She says it is especially bad when she goes to bed. She also complains of a tickly cough and a funny taste in her mouth. She has no other significant symptoms and you suspect she has GORD. What is the most appropriate next step? UGI endoscopy Start her on a proton pump inhibitor Barium Swallow study Start her on a H2 antagonist Oesophageal manometry
Start her on a proton pump inhibitor
what investigations are completed for GORD
a clinical diagnosis generally
however a trial of PPI is often diagnostic and therapeutic
what is the conservative management for GORD
lose weight
avoid precipitants (large fatty meals and coffee and alcohol before bed)
elevate bed for sleeping
stop smoking
what is the medical management for GORD
PPIs
what is the MOA of PPIs
inhibits H+/K+ ATPase pump
what drugs affect oesophageal tone and could lead to GORD
nitrates and CCBs
how does GORD lead to oesophageal adenocarcinoma
GORD leads to oesophagitis which leads to barretts this leads to dysplasia and oesophageal adenocarcinoma
what changes occur for oesophagitis to turn into barretts oesophagus
squamous to columnar (metaplasia)
what history is associated with oesophageal stricture
intermittent progressive dysphagia
how should barretts oesophagus be treated
1 surveillance (regular endoscopy + biopsy)
2 treatment
-high grade dysplasia with radiofrequency ablation and PPI
-nodule with endoscopic mucosal resection and PPI or oesophagectomy
what is zollinger ellison syndrome
gastrin-secreting tumour of the pancreas
what endocrine condition is ZE syndrome associated with
MEN1
how does ZE syndrome cause gastric ulcers
increased gastrin from gastrinomas
hypertrophy of the gastric mucosa and stimulation of acid secreteing cells
this leads to damaged mucosa and ulceration
how does ZE syndrome cause malabsorption
damage of GI mucosa and inactivation of pancreatic enzymes
when should ZE syndrome considered
with multiple ulcers
what are symptoms of ZE syndrome
abdominal pain (similar to PUD)
diarrhoea
heartburn
what are symptoms of ZE syndrome when associated with MEN1
PPP
pituitary
parathyroid
pancreatic
what are the investigations for for ZE syndrome
fasting serum gastrin
serum calcium
what is the management for ZE syndrome
PPIs
surgical resection
what are common DDx for dyspepsia
GORD
PUD
cancer
non-ulcer dyspepsia
1) A 29 year old woman presents with 2 week history of passing bloody diarrhoea with mucus up to 12 times a day. This is associated with lower abdominal, cramp like pain and malaise. On examination she looks pale and generally unwell and there is some tenderness in the left iliac fossa. a gastroenteritis b crohns disease c IBS d hyperthyroidism e UC
e UC
2) A 55 year old woman with diabetes presents with weight loss, diarrhoea and angular stomatitis. Blood tests reveal presence of tTG antibodies. a hyperthyroidism b colorectal carcinoma c IBS d coeliacs e CD
d coeliacs
3) A 16 year old boy is brought to paediatric out patients by his mother with a 9 month history of weight loss, abdominal pain and diarrhoea. On examination, he is on the 10th centile for height and weight, having been on the 50th centile previously. tTG antibodies are negative. a gastroenteritis b coeliacs c UC d hyperthyroidism e CD
CD
4) A 28 year old medical student returns from his elective in Thailand with a short history of severe lower abdominal cramps and passage of blood diarrhoea. a gastroenteritis b pseudomembranous colitis c UC d hyperthyroidism e CD
gastroenteritis
5) A 24 year old woman gives a long history (several years) of intermittent diarrhoea and constipation. She also complains of abdominal bloating and left iliac fossa pain. The pain and bloating are made worse by eating and are relieved by defecation. a gastroenteritis b coeliacs c IBS d hyperthyroidism e CD
IBS
what is IBD
a group of chronic disorders which cause inflammation to the GI tract
def of UC
a relapsing and remitting inflammatory disorder of the colonic mucosa
how is UC classified
by location
by severity
who does US commonly affect
adolescents or young adults
def of CD
a chronic inflammatory condition which may affect any part of the GI tract from mouth to anus
who does CD commonly affect
bimodal peak of onset
1 adolescents and young adults
elderly
where does UC affect
starts distally and spreads proximally (no further than ileocaecal valve)
mucosa and submucosa
where does CD affect
any part of the GI tract from mouth to anus
transmural
what sort of inflammation is typical in UC and CD
UC - continuous
CD - discontinuous (skip lesions)
what does non-caseating granulomas indicate
CD
what are symptoms of UC
bloody diarrhoea
tenesmus
diffuse abdomen pain
what are symptoms of CD
diarrhoea
steatorhoea (when the ileum is affected)
weight loss and generally more ill than in UC
what is p anca associated with
IBD
- positive in UC
- negative in CD
what does UC increase risk of
PSC
cholangiocarcinoma
colorectal cancer
what are granulomas
collections of immune cells which leads to inflammation
what does non-caseating mean
no area of central necrosis
what is cobblestone mucosa associated with
CD
what is rose thorn appearance associated with
UC
what are extra GI features of IBD
mouth ulceration
erythema nodusum
pyoderma gangrenosum
what is episcleritis
uncomfortable red eye with no loss of vision
associated with IBD
what is scleritis
painful red eye with no loss of vision
what is uveitis
painful red eye with loss of vision
what is an acute severe UC attack
12x a day
how is IBD diagnosed?
stool sample
-faecal calprotectin
what is coeliacs disease
a chronic autoimmune disease of small intestine which leads to intolerance to dietary gluten
this leads to villous atrophy and malabsorption
who does coeliacs commonly affect
infants and middle aged
what are symptoms of coeliacs
N+V+D
weight loss
abdominal pain + distension
what are signs of coeliacs
aphthous ulcers
angular stomatitis
anaemia with pallor
dermatitis herpetiformis
what causes angular stomatitis
B12/iron deficient
what antibodies indicate coeliacs
tissue transglutaminase antibodies
anti-endomysial antibody
anti-gliadin
what is found on endoscopy and duodenal biopsy
villous atrophy
crypt hyperplasia
intraepithelial WBCs
what is the treament for coeliacs
gluten free diet
what is gastroenteritis
acute gastrointestinal infection
who is at risk of gastroenteritis
young and old
travellers
is bacterial or virla gastroenteritis more common
bacterial
what is dysentry
bloody diarrhoea
pathology of diarrhoea
toxins or bacteria sticking to gut mucosa
pathology of dysentry
pathogens penetrate the intestinal mucosa and epithelial cells are destroyed
this leads to bloody diarrhoea and abdominal pain
what pathogen causes diarrhoea and dysentry
campylobacter
c. difficile
salmonella
what pathogens cause diarrhoea
s aureus
vibrio cholera
e coli
bacillus cereus
what pathogens cause dysentry
haemorrhagic e.coli
entamoeba histolytica
shigella
name an antidiarrhoeal
codeine phosphate
how is gastroenteritis investigated
stool microscopy and culture
how is gastroenteritis treated
oral rehydration therapy
antibiotics (if systemically unwell, elderly, suppressed)
what is IBS
mixed group of abdominal symptoms with no obvious cause
who does IBS commonly affect
women>men
onset in <40yrs
which set of criteria is used to diagnose IBS
ROME II/III
what are features of ROME II/III
chronic (>6months) abdo pain: -relieved by defaecation -associated with altered stool form or bowel frequency and 2 of: -urgency -tenesmus -abdo bloating/distension -mucuous -symptoms worse after food
how is IBS diagnosed
diagnosis of exclusion
what are features of colorectal carcinoma history
elderly
‘red flags’
what are features of a pseudomembranous colitis history
c diff infection after recent antibiotic treatment
what are infective causes of diarrhoea
gastroenteritis
pseudomembranous colitis
what are inflammatory causes of diarrhoea
IBD
what are malignant causes of diarrhoea
colorectal carcinoma
what are autoimmune causes of diarrhoea
coeliacs disease
what is used to classify severity of UC
Truelove and Witts severity index
what are features of a mild UC
<4 bowel movements/day
no blood in stools
ESR <30mm/hr
what are features of moderate UC
4-6 bowel movements/day
minimal blood in stools
ESR <30mm/hr
what are features of severe UC
>6 bowel movements/day with at least one systemic feature: -obvious blood in stools -pyrexia -HR>90bpm -anaemia ESR >30mm/hr
how is mild and moderate UC flare ups treated with proctitis (inflammation of rectum and anus) or proctosigmoiditis (inflammation of from anus to sigmoid colon)
topical 5-ASA
+/- oral 5-ASA
(to induce remission)
give an example of a topical ASA
mesalazine
give an example of a oral ASA
sulfasalazine
how is mild and moderate UC flare ups treated with left sided and extensive colitis
high dose oral 5-ASA
+/- topical 5-ASA
or oral beclomethasone
(to induce remission)
what should be given to mild or moderate UC if no improvement
oral prednisolone
and if no response to this oral tacrolimus
how is severe UC flare ups treated
admit
1 IV corticosteroids + IV fluids
2 consider IV ciclosporin or surgery if no improvement or worsening in 72hrs
(to induce remission)
how is remission maintained in proctitis (inflammation of anus and rectum) or proctosigmoiditis (inflammation from anus to sigmoid colon)
topical or oral 5-ASA
or both
how is remission maintained in left sided or extensive colitis
oral 5-ASA
when should oral azathioprine or oral mercatopurine be considered
with exacerbations
1. A 20 year old man presents with diarrhoea. He is passing stool 3 times a day. He is generally well with no fever. After a number of investigations he is diagnosed with Ulcerative Colitis, confined to the rectum. What treatment should be given first? Oral prednisolone IV corticosteroid Oral tacrolimus Topical 5-ASA High dose oral 5-ASA IV ciclosporin
Topical 5-ASA
2. A 20 year old man presents with diarrhoea. He is passing bloody stool 7 times a day. He looks unwell and on examination he is tachycardic and has a fever. After a number of investigations he is diagnosed with Ulcerative Colitis. What treatment should be given first? Oral prednisolone IV corticosteroid Oral tacrolimus Topical 5-ASA High dose oral 5-ASA IV ciclosporin
IV corticosteroid
does smoking make UC or CD better
UC better
CD worse
what are the medical treaments for inducing remission in active CD
1 corticosteroids
2 5-ASA
3 immunosuppressants (azathioprine or mercaptopurine)
4 infliximab or adalimumab (anti-TNF)
what is the medical treatment for maintaining remission in CD
monotherapy with azathioprine or mercaptopurine
5-ASA, steroids, immunosuppressants are for which IBD
UC
steroids, immunosuppressants, anti-TNF are for which IBD
CD
what are the two main functions of the liver
synthetic function
metabolic function
what does the liver synthesise
clotting factors
albumin
what does the liver metabolise
bilirubin
oestrogens
ammonia
what happens to the synthetic function of the liver with disease
reduced synthesis of:
clotting factors
albumin
what is a sign of reduced clotting factor synthesis
bruising
what are signs of reduced albumin synthesis
ascites
leukonychia
what happens to the metabolic function of the liver with disease
reduced breakdown, so increased:
bilirubin
oesotrogen
ammonia
what is a sign of increased bilirubin levels
jaundice
what are signs of increased oestrogen levels
palmar erythrema
spider naevae
gynaecomastia
what are signs of increased ammonia
confusion
asterixis
what are true measures of liver function
bilirubin
albumin
INR (clotting factors or PTT)
what are markers of acute liver injury
ALT
AST
ALP
GGT
A 19-year-old male is admitted following an alcohol binge. His friends report he has vomited several times and fell over. You notice some bruises on his hands.
Which of the following is likely to be most elevated?
AST ALT GGT ALP All of the above
GGT
raised GGT in isolation is common after recent alcohol consumption
A 42-year-old female is admitted with severe RUQ pain that is worse on eating fatty foods. After obtaining her LFTs, you notice a remarkably high ALP.
What is the most likely diagnosis?
Viral hepatitis Alcoholic hepatitis Short-term alcohol abuse Biliary tract obstruction Gilbert’s syndrome
Biliary tract obstruction
A 45-year-old chronic alcoholic presents with jaundice, bruising and abdominal pain. His stools and urine are of normal colour. His bilirubin and AST are raised.
What other marker is likely to be abnormal?
ALT Albumin ALP Haemoglobin GGT
ALT
what does a AST:ALT ratio of >2.5:1 indicate
alcoholic liver disease
what does a AST:ALT ration of <1:1 indicate
viral hepatitis
what causes a rise in ALP
BLIP
Bone
Liver
Intestines
Placenta
what are the important markers of liver injury
AST
ALT
what are the important markers of biliary duct injury
ALP
GGT
what does an isolated GGT indicate
acute alcohol intake
A 38-year old woman presents with vague, colicky right-sided abdominal pain. She reports it is got worse 6 hours ago after eating an Indian take-out. On examination her sclera appear icteric, and her abdomen is soft and non-tender. Select the investigation needed to confirm her diagnosis:
Liver function tests Ultrasound of the biliary tree Split bilirubin ratio ERCP Liver biopsy
Ultrasound of the biliary tree
While waiting for her cholecystectomy, the same woman falls more unwell. She feels feverish, has vomited twice and reports that the pain initially felt colicky, but now is constant in her RUQ. She also feels dull pain in her right shoulder. On examination, she displays rebound tenderness in her RUQ and a positive Murphy’s sign. Select the likely diagnosis:
Biliary colic Primary Biliary Cholangitis Ascending Cholangitis Acute Cholecystitis Cholangiocarcinoma
Acute Cholecystitis
A 48-year old obese man presents to A&E in agony. He is shivering visibly, clutching his right upper quadrant. You notice his hands are yellow and there are excoriations on his arms. His bloods show a raised white cell count and CRP. Select the likely diagnosis:
Biliary colic Primary Sclerosing Cholangitis Primary Biliary Cholangitis Viral hepatitis Ascending Cholangitis
Ascending Cholangitis
2 hours later, the same man has deteriorated whilst waiting for a hospital bed. His BP is 87/45, HR is 128 and RR is 35. He is drowsy, responding only to pain. Select the likely cause of shock:
Septic shock Hypovolaemic shock due to low albumin Neurogenic shock Hypovolaemic shock due to blood loss Cardiogenic shock
Septic shock
what are risk factors for gallstones
4Fs Fat Female Fertile Forty
what is a classical presentation of gallstones
colicky RUQ pain
worse on eating fatty foods
what investigation is gold standard for gallstones
USS of biliary tree
what would you see on LFTs with a gallstone
a raised ALP (and GGT)
why are women more prone to gallstones
increased oestogen causes an increase in the cholesterol content of the bile, this makes cholesterol gallstone formation much more likely
what sort of gallstones show up on AXR
calcium bilirubinate
what is the management for a gallstone in the gallbladder
cholecystectomy
what is the management for a gallstone in the common bile duct
cholecystectomy
bile duct clearance
how is bile duct clearance completed
ERCP
US lithotripsy
what can a gallstone in the common bile duct progess into
a gallstone in the common bile duct leads to bile stasis
bacteria from the gut can move into the bile ducts
this is ascending cholangitis
what can a gallstone in the gallbladder or cystic duct progress into
a combination of bile stasis, inflammation and bacterial infection can lead to acute cholecystitis
how does acute cholecystitis present
constant RUQ pain which radiates to the R shoulder and scapula
associated with fever, N+V
what sign is indicative of acute cholecystitis
murphys sign
what would be found O/E of acute cholecystitis
jaundice (if CBD stone)
rebound tenderness
murphys sign
what investigations would be used to diagnose acute cholecystitis
FBC (raised WCCs)
LFTs (raised ALP + GGT)
imaging (USS, CT/MRI)
what is the management for acute cholecystitis
cholecystectomy <1wk
what is charcots triad associated with
ascending cholangitis
what is ascending cholangitis
bacterial infection of the biliary tract due to obstruction
what is charcots triad
RUQ pain
jaundice
fevers
how does a gallstone in the biliary tract lead to bacterial infection
bile stasis (reduced bile out of the common bile duct) therefore bacterial from the duodenum ascends the biliary tract and causes infection
what does reynolds pentad indicate
acute suppurative cholangitis (more severe ascending cholangitis)
which is pus in the biliary ducts
what is reynolds pentad
RUQ pain jaundice fevers hypotension confusion
how does ascending cholangitis become acute suppurative cholangitis
bacteria enters the bloodstream
what are the 2 main forms of autoimmune biliary disease
PBC
PSC
what antibody is classic of PBC
AMA
what antibody is classic of PSC
pANCA
why is primary biliary cholangitis also called primary biliary cirrhosis
autoimmune damage to small bile ducts leads to intrahepatic cholestasis
stasis of bile leads to liver damage
how is PBC diagnosed
biopsy
how is PSC diagnosed
ERCP
what is PBC associated with
RA
thyroid disease
sjogrens
what is PSC associated with
UC
what is the pathology of PBC
autoimmune damage to small bile ducts which leads to intrahepatic cholestasis
what is the pathology of PSC
autoimmune damage to intra and extrahepatic bile ducts which causes inflammation, scarring and narrowing
A 53-year old man staggers into A&E having vomited 6 times in 2 hours. He is intoxicated and jaundiced. His friend said his vomit was initially “normal”, but after the first couple of episodes has had fresh blood in it. What is the likely diagnosis?
Ruptured oesophageal varices Mallory-Weiss tear Ruptured peptic ulcer Boerhaave syndrome Oesophagitis
Mallory-Weiss tear
what is a mallory-weiss tear
tear in the mucosal layer of the oesphagus
what is associated with a mallory-weiss tear
common after many episodes of severe vomiting
vomiting always precedes bleeding
what does the blood look like in mallory-weiss tear
blood is streaked in vomit
where does the tear occur in MW
gastro-oesophageal junction
how quickly does a MW tear resolve
1-2days
what is boerhaaves syndromes
more severe MWT
complete rupture of oesphageal wall
how is boerhaaves syndrome diagnosed
CXR and CT scan
-pneumediastinum
what are the 2 main causes of oesophageal varices
liver cirrhosis
chronic alcohol use
how does liver cirrhosis cause oesophageal varices
1 decreased clotting factors which increases bleeding risk
2 increased extrahepatic blood shunting which leads to portal HTN
how does chronic alcohol use lead to oesophageal varices
oesophageal irritation
how does oesophageal varices present
PMH of liver cirrhosis +/ chronic alcohol use
large volume of fresh blood
what investigations can confirm oesophageal varices
FBC (macrocytic anaemia)
LFTs (raised GGT from alcohol, low albumin from cirrhosis)
UEs (raised urea)
how is oesophageal varices managed
ABCDEFG
IV fluids and reduce portal HTN
endoscopy (band ligation is first line)
what is used to reduced portal HTN
terlipressin
what is the first line management of oesophageal varices
band ligation
how does ruptured peptic ulcer present
PMH of PUD, NSAID use, H.pylori
a “coffee ground” vomit +/ meleana
what investigations confirm ruptured peptic ulcer
decreased BP
management of ruptured peptic ulcer
1 endoscopy
-IM adrenaline at site of ulcer
2 omeprazole
3 triple therapy (with H.pylori)
A 76-year old retired greengrocer visits her GP with difficulty swallowing solids. She says this has been getting progressively worse over 1 month. There is no coughing, choking or heartburn. She reports food getting “stuck” 2-3 seconds after swallowing. She attributes her weight loss to not eating properly, and also thinks this has caused loose, brown-black stools. Bloods show a microcytic anaemia. Select the likely diagnosis:
Stroke Oesophageal cancer Pharyngeal pouch Plummer-Vinson syndrome Benign stricture
Oesophageal cancer
what is plummer-vinson syndrome
rare disease characterized by difficulty in swallowing, iron deficiency anemia, glossitis, cheilosis and esophageal webs
A 27-year old lawyer presents with a 2-year history of mild dysphagia to both solids and liquids. She has no weight loss. She has symptoms of heartburn and nocturnal cough, but PPIs and bronchodilators haven’t helped. She is systemically well, and her examination is unremarkable. A “bird’s beak” appearance is noted on barium swallow. Select the diagnosis:
Achalasia Benign stricture Plummer-Vinson syndrome Oesophageal spasm Stroke
Achalasia
A 45-year old man presents with a 6-week history of dysphagia. This is associated with pain in his fingers, with him noting that he sees the colour vary from red, to white, to blue. He also has several red, vascular marks on his face. Select the diagnosis:
Plummer-Vinson syndrome Ortner’s syndrome Pharyngeal pouch Limited cutaneous scleroderma Oesophageal spasm
Limited cutaneous scleroderma
what are functional causes of high dysphagia
stroke
parkinsons
what are functional causes of low dysphagia
achalasia
oesophageal spasm
CREST
what are structural causes of high dysphagia
pharyngeal pouch
what are structural causes of low dysphagia
cancer
benign stricture
plummer vinson
ortners syndrome
when is a barium swallow indicated
high (functional or structural) or low dysphagia (achalasia)
when is endoscopy indicated
first line for low dysphagia
when is videofluoroscopy indicated
functional high dysphagia
when is manometry indicated
differentiate between motility disorders
what cancer commonly occurs in the middle third of the oesphagus
squamous cell carcinoma
what cancer commonly occurs in the lower third of the oesophagus
adenocarcinoma
GORD to oesophagitis to barretts (metaplasia) to adeoncarcinoma (dysplasia
how does achalasia lead to dysphagia
absence of ganglion cells in the myenteric plexus (auerbachs plexus)
this causes a failure of relaxation fo the LOS and aperistalsis
what sort of dysphagia is oesophageal cancer and achalasia
oesophageal cancer is structural dysphagia
achalasia is functional dysphagia
who does oesophageal cancer commonly affect
elderly
who does achalasia commonly affect
young people
what investigations are used for oesophageal cancer
OGD
what investigations are used for achalasia
barium swallow (birds beak) manometry
what causes neurological dysphagia
stroke
parkinsons
what symptoms are present with neurological dysphagia
coughing immediately on swallowing
choking which implies a problem with the swallowing process
what are features of pharyngeal pouch
coughing up food
halitosis (bad breath)
gurgling/dysphonia
what are features of plummer-vinson syndrome
iron deficiency anaemia (signs of severe IDA such as cheilosis, atrophic glossitiis, koilonychia)
oesophageal webs
dysphagia
what are features of limited cutaneous scleroderma
CREST 1 calcinosis 2 raynauds 3 esophageal dysmotility 4 sclerodactyly 5 telangiectasia
what antibodies are associated with limited cutaneous scleroderma
ANA and anti-centromere
what is calcinosis
calcium deposits on the skin
what is sclerodactyly
abnormal build up of fibrous tissue in the skin can cause the skin to tighten so severely that the fingers curl and lose their mobility
A 32 year old woman returns from a holiday in India. She started getting diarrhoea after eating at a seafood restaurant on the last night. She is feverish, nauseous and is sore all over. The whites of her eyes are yellow. Hepatitis A Hepatitis B Hepatitis C Hepatitis D Hepatitis E
Hepatitis A
A 29 y/o male comes to the GP with fever, fatigue, joint pain and urticaria-like skin rash. He had unprotected anal sex a month ago. He comes back a week later for a blood test, which shows raised ALT and AST. Now, he complains of feeling sick, RUQ pain and looks a bit yellow. Hepatitis A Hepatitis B Hepatitis C Hepatitis D Hepatitis E
Hepatitis B
A 67 year old man is investigated under the two-week wait for jaundice, tender hepatomegaly, ascites and anorexia. His blood tests show a raised aFP. He mentions that he was diagnosed with hepatitis years ago. What virus(es) are likely? Hepatitis A Hepatitis B Hepatitis C Hepatitis D Hepatitis E
Hepatitis B + C
Which hepatitis virus requires another virus to be present for it to successfully infect? Hepatitis A Hepatitis B Hepatitis C Hepatitis D Hepatitis E
Hepatitis D
what is the triad of symptoms which applies to all hepatitis
1 fever
2 jaundice
3 raised ALT and AST
what are faeco-oral hepatitis’
Hepatitis A + E
“the vowels which hit your bowels”
what are features of hepatitis A
Asymptomatic (usually)
Acute
what are features of hepatitis E
Enteric
Epidemics (water)
Expectant mothers
how is hepatitis A spread
when faecal matter containing viral hep A is ingested
what is a characteristic history of hepatitis B
prodromal symptoms -non-specific flu like symptoms -rash -lymphadenopathy followed by symptoms of acute infection -RUQ pain -N+loss of appetite -jaundice
what is the prognosis of hep B
majority recovery
few develop chronic infection
what is the management for acute hep B
supportive
what is the management for chronic hep B
peginterferon alpha or tonofovir
what is the most common risk factor for developing hepatocellular carcinoma
hepatitis
how does hep B increase risk of hepatocellular carcinoma
virus integrates into host chromosome
acts as an oncogene
how does hep C increase risk of hepatocellular carcinoma
causes chronic inflammation
mutations accumulate
what hepatitis must be present for hepatitis D to occur
hepatitis B
why does hepatitis D require hepatitis B
hepatitis D enters hepatocytes via hep B surface antigens
A 41 year old man is brought into A&E by police after being found wandering the streets seemingly confused. He is completely disorientated and is unable to give a history. As part of your neurological assessment, you examine his eyes and notice the following: Which of the following is characteristic of this patient’s condition: A) High serum caeruloplasmin B) Low serum copper C) High serum iron D) Low total iron binding capacity E) Low transferrin saturation
B) Low serum copper
A 56-year-old man, diagnosed with emphysema, presents with a one-month history of jaundice and ascites. Your registrar tells you that the man has had breathing problems for the majority of his life. What is the most likely diagnosis Sickle Cell Disease COPD Epstein-Barr Virus Idiopathic Pulmonary Fibrosis Alpha-1 Antitrypsin Deficiency
Alpha-1 Antitrypsin Deficiency
why is there a low serum copper in wilsons diseases
copper incorporation into caeruloplasmin in hepatocytes and its excretion in bile is impaired
therefore copper is deposited
where is copper deposited in wilsons disease
firstly liver
then basal ganglia
eyes
what sort of genetic disorder is wilsons disease
autosomal recessive
what does wilsons disease present with
1 ataxia
2 tremor
3 dysarthria
what is seen in the eyes of wilsons disease patients
kayser fleischer rings
what sort of genetic disorder is alpha-1 anti-trypsin deficiency
autosomal recessive
what is the pathology of A1AT deficiency
A1AT is genetically mutated leading to it being prevented from release from hepatocytes
this causes a loss of its protective function in the lungs against elastase, leading to emphysema occurs and a build up in the liver leading to destruction an liver disease
how does A1AT deficiency normally present
emphysema in a young non-smoker with late onset liver signs
what are the stages of liver failure
1 healthy
2 fatty liver
3 liver fibrosis
4 cirrhosis
A 63-year-old woman stumbles into A+E. She looks unwell with a flushed face. An F1 mentions that when she presented last week, examination of her upper limbs suggested a sensory polyneuropathy. Cytomegalovirus Primary Biliary Cirrhosis Paracetomal Overdose Alcoholic Liver Disease Primary Sclerosis Cholangitis
Alcoholic Liver Disease
A 65 year old presents with suspected liver failure. Which of the following tests would NOT be included in a liver screen for liver failure Alpha-1 Antitrypsin Caeruloplasmin HIV Screen Anti-GBM Antibody Aspartate Aminotransferase
Anti-GBM Antibody
A 56-year-old man with a long history of alcohol abuse presents to the emergency department with abdominal pain. On examination he has a distended abdomen with shifting dullness and has a temperature of 38.2°C.
What is the most likely diagnosis?
A Bowel obstruction
B Liver cirrhosis
C Mallory–Weiss syndrome
D Perforated peptic ulcer
E Spontaneous bacterial peritonitis (SBP)
E Spontaneous bacterial peritonitis (SBP)
A 66-year-old man presents to his GP with increasing weight loss, lethargy and fever over the last 3 months. He has also noticed pale stools and dark urine. Crigler-Najjar Syndrome Gilberts Syndrome Opiate Overdose Pancreatic Carcinoma Haemolysis
Pancreatic Carcinoma
A 50-year-old man comes to you because he is worried about his skin which occasionally turns yellow. On further questioning you notice that these episodes are particularly bad during periods of stress or illness. He is otherwise well. Gilbert’s Syndrome Hepatic Metastases Megaloblastic Anaemia Hepatitis A Dubin-Johnson Syndrome
Gilbert’s Syndrome
how is conjugated bilirubin formed
haem is converted to unconjugated bilirubin which is then converted to conjugated bilirubin in the liver by UDP glucuronyltransferase
how is bilirubin excreted
as urobilinogen in the urine
as stercobilin in the stools
how does bilirubin cause the yellow colour in our urine
bilirubin is converted to urobilinogen which is converted to urobilin giving the distinct yellow colour
how does bilirubin cause the brown colour in our stool
bilirubin is converted to stercobilin
what causes jaundice
excess bilirubin
what are the causes of jaundice split up into
pre-hepatic
hepatic
post-hepatic
aetiology of pre-hepatic jaundice
dysfunctional transport from spleen to liver
what sort of bilirubin is increased in pre-hepatic jaundice
unconjugated
what are causes of pre-hepatic jaundice
1 haemolysis (low Hb, malaria, haemolytic anaemias) 2 inherited disorders of bilirubin metabolism (gilberts)
aetiology of hepatic jaundice
dysfunctional hepatocytes
abnormal conjugation/excretion
what sort of bilirubin is increased in hepatic jaundice
conjugated or unconjugated
what are causes of hepatic jaundice
VADAM
Viruses - hep A/B/C/E, EBV, CMV Alcohol Drugs - paracetomal, isoniazid, rifampicin Autoimmune - PBC PSC Metabolic
aetiology of post-hepatic jaundice
obstructive jaundice
what sort of bilirubin is increased in post-hepatic jaundice
conjugated bilirubin
why is there dark urine and pale stools in obstructive jaundice
flow of bilirubin into GI tract is blocked
1 bilirubin is forced into renal system where it is converted to urobilinogen and from there to urobilin (yellow) which in excess causes dark urine
2 less bilirubin in the GI system means less stercobiln (brown) so pale stools
what are causes of obstructive jaundice
1 stones in common bile duct (biliary colic)
2 carcinoma at head of pancreas
3 stricture
