gastro - conditions overview Flashcards
what classically presents with dyspnoea, cirrhosis and cholestatic jaundice
which feature is more common in children and which is more common in adults?
what tests would you do to confirm the suspected diagnosis?
a1-antitrypsin deficiency
liver in children - commonest form of genetic liver disease in paeds
THE ELASTIC HAS ALL BEEN DESTROYED… THINK ACCELERATED COPD…
emphysema in adults
- serum a1AT levels decreased (nb - remember that a1at is part of the acute phase response - thus may be falsely high..)
- lung function testing - obstructive pattern, decreased fev1 (think the elastic has all been destroyed)
- liver biopsy - Periodic acid schiff stain positive
what is the function of lung a1-antitrypsin?
protect the lungs from neutrophil elastase - it is a serine protease inhibitor (made in the liver) that controls inflamm cascades
how do you manage a1at def?
what is the prognosis
smoking cessation (neut elastase inhibition usually aleviates damage caused by this - but no neutrophil elastase…)
prompt tx of lung infections
proph vacc for lung infections
liver transplant if decompensated cirrhosis
lung transplant
similar prog to copd if lung transplant
what might present early with tiredness / arthragia of 2nd/3rd MCP joints / knee pseudogout / decreased libido
and what would be the later stage presentation?
what organs may be involved?
Hereditrary haemochromatosis
later: slate-grey skin pigmentation / chronic liver disease / hepatomegaly / cirrhosis / cardiomyopathy
liver - cirrhosis
cardiac - c/megaly
kidneys - bronze dm - iron deposited
joints - iron deposited especially in working joints
hypogonadism - pituitary dysfunction because of iron deposition - less production of ACTH
what tests would you do to confirm a Dx of HH?
how would you manage it?
how do you monitor it?
what lifestyle recommendations?
anything else you need to do?
what prognosis?
LFTs raised ferritin raised (but obvs also raised in acute phase stuff) transferrin saturation raised CONFIRM Dx - HFE genotyping (gene most responsible for HH)
management:
venesect! between 0.5 and 2 units per 1/2 wks
once have venesected down to a nice low ferritin (iron stores lowered) - can just maintain with venesection about once a month
Desferrioxamine if intolerant of venesection
Monitoring:
- lfts
- FPglucose - monitoring for DM - as vnesection will throw the HBa1c off..
- if cirrhotic - screen for HCC with USS + AFP 6monthly
lifestyle:
- normal balanced diet - no raw seafood as may cont bacteria that thrive on the iron stores eg. listeria
- avoid alcohol
- ensure vitamins if they take any don’t contain Fe
SCREEN 1ST DEGREE RELATIVES BY GENETIC TESTING FOR HFE GENE - even if Asx and normal LFTs - until age of 30, when Fe deposition would have occured if it was going to….
prog:
normal LE if venesected and non-DM / non-cirrhotic
if cirrhosis - 1/4 get HCC
what does hepcidin do?
what is ferritin?
what is transferrin?
hepcidin reduces gut absorption of Fe and reduces haem iron recycling by Macs
ferritin - iron stores intracellular
transferrin - protein that transports Fe around the blood
where do liver tumours commonly originate?
90% are mets - breast / bronchus / GI tract
what Liver Ca presents early with jaundice…
cholangiocarcinoma. all other liver Cas only have jaundice later…
what Liver Ca presents early with jaundice…
cholangiocarcinoma. all other liver Cas only have jaundice later…
what condition do you suspect in someone presenting with fatigue, wt loss, ruq pain, ascites…
how would you screen for it in people with RFs?
HCC
AFP + ultrasound
what condiiton do you suspect in someone with fever, abdo pain, bili increased, and alp very raised + malaise
what are some causes of this condition?
cholangiocarcinoma
PSC (can screen with Ca19-9)
biliary cysts
HBV / HCV
what should you always exclude in diarrhoea + wt loss / anaemia?
coeliac
what is the management of an acute GI bleed?
- 2 large bore IV cannulae - take blood for LFTs, PT/APTT, group and save to enable crossmatching of blood
2.
what is the management of an acute GI bleed?
ABCDE approach - start by protecting the airway and giving high flow O2
Bedside:
1. 2 large bore IV cannulae - take blood for LFTs, PT/APTT, group and save to enable crossmatching of blood
2. give IV fluids (not saline if cirrhotic / varices…) to restore IV volume while waiting for crossmatched blood… - if still haemodynically deteriorating - give group O Rh-ve blood
3. urinary catheter - hourly UO
Tests:
4. CXR + ECG
5. ?call ICU for a CVP - monitor and guide fluid replacement…
6. transfuse if Hb<70g/L
7. correct clotting abnormalities - Vit K / FFP / platelets
8. ?Varices - GIVE TERLIPRESSIN + broad spectrum IV ABx cover…
9. pulse / BP / CVP monitoring
10. ARRANGE URGENT ENDOSCOPY - WHAT’S GOING ON….?
11. if endoscopic control fails - someone with experience could place a sengstaken-blakemore tube… to compress varices
what ant-emetics carry a dystonic and oculogyric crsis risk - and especially in who..?
anti-dopaminergics younger patients (especially early 20s..)
epigastric pain / heartburn is a common presenting symptom of peptic ulcer disease. What symptoms (red flag… nice acronym..) would make you suspect a more sinister cause
what would you do about it…
ALARMS 55 symptoms anaemia (iron def) loss of weight anorexia recent onset / prog Sx melaena / haemetemesis swallowing difficuluties age >55
all of the above - refer for urgent upper GI endoscopy
(likewise if treatment-refractory)
epigastric pain is a common presenting symptom of peptic ulcer disease. What symptoms (red flag… nice acronym..) would make you suspect a more sinister cause
what would you do about it…
ALARMS 55 symptoms anaemia (iron def) loss of weight anorexia recent onset / prog Sx melaena / haemetemesis swallowing difficuluties age >55
all of the above - refer for urgent upper GI endoscopy
(likewise if treatment-refractory)
are gastric ulcers or duodenal more common?
and what are some common / distinguishing features..
what is the management
common risk factors - H pylori / NSAIDs
both relieved by antacids
DUs - relieved by eating (worse after eating when emptying increases…) - nb often around the gastroduodenal artery - erosion / perforation can cause SERIOUS upper gi bleed
GU - exacerbated by eating
DUs 4x more common
management of dyspepsia: (see nice guidance..)
if <55 and no alarm features
- stop drugs causing dyspepsia eg. nsaids
- lifestyle changes (decreasing etoh and tobacco)
- otc antacids
- review after 4/52
IF IMPROVES - NO FURTHER ACTION - IF NOT:
1. Test for H pylori
IF PRESENT - TREAT WITH TRIPLE THERAPY
(PPI - lansoprazole + 2ABx - clarithromicin + amoxicillin)
check eradicated with Urea breath test 1wk-2wk
IF NOT PRESENT:
1.PPI (eg. omeprazole) or H2 blockers eg ranitidine for 4 weeks - if improves no further action
IF DOESN’T IMPROVE:
consider upper GI endoscopy
what would epigastric pain through to the back (worst 15/20mins post meal..) make you think of?
and what other Sx might you get….
what are the causes…?
chronic pancreatitis
other sx - LATE : steatorrhea (failure of exocrine pancreas - responsible for producing digestive enzymes…) - diabetes (failure of endocrine pancreas) - nb - both years after the onset of pain (failure of endocrine often later… 98% of pancreas is endocrine - so has more reserve capacity)
ETOH
CF / HH/ ductal obstruction (gall stones etc..)
how would you investigate suspected acute / chronic pancreatitis
USS / AXR / CT with contrast enhancement - pancreatic calcifications confirm the Dx
MR cholangiopancreatography (MRCP) - good for looking at the ducts…
ERCP - RISKS PRECIPITATING ACUTE PANCREATITIS - tends to be restricted to treatment - eg. removing bile duct stones..
Raised random plasma glucose
Faecal elastase - probably decreased…
Serum amylase - raised in acute
Urinary amylase - raised in acute
Serum lipase - usually raised in acute (for longer..)
CRP - severity and prognosis
what raises serum amylase other than acute pancreatitis - and what MUST you do to exclude it..?
gastroduodenal perforation
ERECT CXR
usually you would resuscitate properly before rushing an acute abdomen to theatre. In what suspected conditions would you go striaght to theatre?
if you can;t replace the blood faster than they're losing it ie: ectopic ruptured / leaking aneurysm trauma
what condiiton looks like peritonitis but doesn’t require a laparotomy
and how would you pick it up (simple blood test…)
acute pancreatitis
ALWAYS check serum amylase
patient is pacing around the room - abdo pain - what do you think of?
colic
gas under diaphragm
peritonitis
causes of acute pancreatitis
GET SMASHED
gallstones and alcohol in the western world
what antibiotics should you give to cover in peritonitis?
metronidazole IV (anaerobes) cefuroxime IV
(likewise cover with these in appendicectomy etc..)
who does sigmoid volvulus classically occur in?
what do you need to do
elderly
constipated
what is the commonest cause of HUS?
what are the s&s
what are the tests..
Mx?
E coli 0157 (makes a toxin that attacks the endothelial cells - young children, after eating undercooked meat…)
signs: TRIAD Abdo pain Bloody Diarrhoea AKI P.A.D
tests:haematuria / proteinuria / schstocytes on blood film / decreased platelts, decreased Hb
plasma exchange
coeliac disease
tests
diagnosis
what condition should you think of in someone with regular nosebleeds and red spots on the tongue / face/ chest / fingers / buccal mucosa
what is the pathophysiology of the disease? (ie. why do they get these particular symptoms…?)
how is it inherited?
Osler-Weber-Rendu syndrome
Hereditary haemorrhagic telengectasia
Blood vessels do not develop properly, and AVMs can result - causing bleeding
Can also present more insidiously with Fe-def anaemia and fatigue etc..
Autosomal dominant (ie. only one copy of the faulty gene needed..)
