general gastro - passmed Flashcards
(38 cards)
what would the triad of :
- abdo pain
- ascites
- tender hepatomegaly
make you suspect..?
what is it?
and how would you investigate it?
budd-chiari syndrome
thrombosis of hepatic vein
USS with doppler flow studies of hepatic vein
Budd chiari syndrome causes:
anything pro-coagulant…
PRV / thrombophilia / pregancy / COCP
- raised bili, ALP and ALT + abdo pain + ascites + tender hepatomegaly
- budd-chiari syndrome
liver pain, fevers, haematemesis (oesophageal /gastric varices)
Portal vein thrombosis - usually 2y to varices..
- raised ALT, raised AST (ALT raised more than AST usually), +/- raised bili
hepatitis
usually general malaise, non specific other symptoms etc…
- raised ALP (much more than others), raised GGT, raised bili
gallstones
both ALP and GGT are in the walls of the biliary system - released with damage..
- isolated raised bili
gilbert’s syndrome?
/ haemolytic disease eg. hereditary spherocytosis
where are
- alt
- ast
- alp
- bilirubin
- ggt
found and where are they
alt and ast are released in hepatocellular damage - ast by mitochondria - alt by cytosol
alp and ggt are increased in obstruction (usually biliary..)
isolated raised ALP , bony pain
? pagets
? sarcoma / bony mets
? ckd mbd - renal mineral bone disease
isolated raised ALT
barn door NAFLD
AST>ALT
may also see rise in GGT
Acute alcoholic hepatitis – AST>ALT (usually AST 3: ALT 1)
Sauce – AST
primary sclerosing cholangitis
https://www.youtube.com/watch?v=ZXs6FkjnBIs
give some common differentials of dysphagia?
and what are your key investigations?
- oesophageal Ca - + wt loss, anorexia / vimiting during eating. progressive symptoms (solids to fluids)
- oesophagitis - odynophagia but no weight loss and systemically well
- oesophageal candidiasis -will be HIV+ve / steroid inhaler use..
- achalasia - LOS fails to open during swallowing - dysphagia of both solids and fluids from the start - regurgitation of food - cough / aspiration pneumonia etc.
- pharyngeal pouch - midline lump in the neck that gurgles on palpation - symptoms are dysphagia, regurgitation, aspiration and chronic cough.
- systemic sclerosis - other features of CREST syndrome
- mysathenia gravis - fatigueable / extraocular muscle weakness / ptosis
upper GI endoscopy barium swallow (for motility disorders) FBC
are you more likely to see Gastric parietal cell antibodies in pernicious anaemia OR Intrinsic factor antibodies
gastric parietal cell autoantibodies
hepatorenal syndrome: what is it, and how do you treat it?
Complication of end-stage liver disease
vasoactive mediators cause splanchnic vasodilation which in turn reduces the systemic vascular resistance. This results in ‘underfilling’ of the kidneys. This is sensed by the juxtaglomerular apparatus which then activates the renin-angiotensin-aldosterone system, causing renal vasoconstriction which is not enough to counterbalance the effects of the splanchnic vasodilation.
Management options:
1. CONSTRICT THE SPLANCHNIC VEINS - vasopressin analogues, for example Terlipressin, have a growing evidence base supporting their use. They work by causing vasoconstriction of the splanchnic circulation
volume expansion
2. VOLUME EXPAND - 20% albumin
3. transjugular intrahepatic portosystemic shunt
4. liver transplant..
what antibodies might you see raised in coeliac disease?
anti-tissue transglutaminase (anti-TTG)
anti-endomysial Ab
(don’t do anti-gliadin anymore…)
which condition would you see AMA (antimitochondrial antibodies) in?
PBC
what is Wilson’s disease
how does it present
what are the investigations
what is the first line treatment for it?
what are some potential compications?
- autosomal recessive
- XS deposition of Cu in tissues - causes Liver and Neuro problems
presents with features resulting from excessive copper deposition in the tissues, especially the brain, liver and cornea:
liver: hepatitis, cirrhosis (children tend to start with liver disease)
neurological: basal ganglia degeneration, speech, behavioural and psychiatric problems are often the first manifestations. Also: asterixis, chorea, dementia, parkinsonism (adults tend to present with neruo disease)
Kayser-Fleischer rings
renal tubular acidosis (esp. Fanconi syndrome)
haemolysis
blue nails
Ix: 24hr Cu excretion high / nonspecifically deranged LFTs / serum copper decreased / serum caeruplasmin low (very low - pathognomic - think impaired excretion, because of low amounts of the protein that carries copper round in blood
Tx:
penicillamine (chelates copper) has been the traditional first-line treatment - chelates it - allows it to be excreted..
trientine
Fanconi’s syndrome - renal tubular acidosis caused by XS deposition of heavy metal (copper obvs..)
how should you manage oesophageal varices?
- acute variceal haemorrhage
- prophylaxis of acute haemorrhage
- ABCD
MAKE SURE THEY’RE CLOTTING - FFP / vitamin K
STIMULATE HAEMOSTASIS - Terlipressin - vasoactive agent to stimulate initial haemostasis
ABX: - eg. ciprofloxacin / levofloxacin
LIGATE THE VARICES - endoscopic variceal band ligation
IF STILL UNCONTROLLED BLEEDING - Sengstaken-Blakemore tube
Transjugular Intrahepatic Portosystemic Shunt (TIPSS) if above measures fail - prophylaxis of variceal haemorrhage
- propranolol (reduces rebleeding / mortality)
- PPI + Endoscopic variceal band ligation - 2wkly (PPI prevents
what are the severities of UC exacerbations?
mild:
Fewer than four stools daily, with or without blood
No systemic disturbance
Normal erythrocyte sedimentation rate and C-reactive protein values
moderate:
Four to six stools a day, with minimal systemic disturbance
severe: More than six stools a day, containing blood Evidence of systemic disturbance, e.g. fever tachycardia abdominal tenderness, distension or reduced bowel sounds anaemia hypoalbuminaemia ADMIT TO HOSPITAL
what are the risks of ERCP?
Bleeding 0.9% (rises to 1.5% if sphincterotomy performed)
Duodenal perforation 0.4%
Cholangitis 1.1%
Pancreatitis 1.5%
what is gallstone ileus?
small bowel obstruction secondary to an impacted gallstone
what does the serum albumin ascites gradient represent?
SAAG - if high - non peritoneal cause of ascites eg. budd-chiari / hepatic stuff. if low - intra peritoneal eg. ovarian Ca?
what is the treatment of ascirtes?
Management
reducing dietary sodium
fluid restriction is sometimes recommended if the sodium is < 125 mmol/L
aldosterone antagonists: e.g. spironolactone
drainage if tense ascites (therapeutic abdominal paracentesis)
large-volume paracentesis for the treatment of ascites requires albumin ‘cover’. Evidence suggests this reduces paracentesis-induced circulatory dysfunction and mortality
paracentesis induced circulatory dysfunction can occur due to large volume paracentesis (> 5 litres). It is associated with a high rate of ascites recurrence, development of hepatorenal syndrome, dilutional hyponatraemia, and high mortality rate
prophylactic antibiotics to reduce the risk of spontaneous bacterial peritonitis. NICE recommend: ‘Offer prophylactic oral ciprofloxacin or norfloxacin for people with cirrhosis and ascites with an ascitic protein of 15 g/litre or less, until the ascites has resolved’
a transjugular intrahepatic portosystemic shunt (TIPS) may be considered in some patients
