Intestinal Failure and Liver Disease Flashcards
How long is GI tract?
3-6m
vitamin D acronym
V-Vascular; I-Infectious/Inflammatory; T-Traumatic/Toxic; A-Autoimmune; M-Metabolic; I-Idiopathic; N-Neoplastic/Nutritional; D-Degenerative
bedside tests to assess nutritional status?
full history and examine inc temperature, rectal exam. ecg - mesenteric ischemia, blood glucose test, urinalysis
blood tests to assess nutritional status
hba1c -diabetes,
U+E - electrolyte imbalance,
CRP - inflammation,
FBC - microcytic anaemia from iron def, macrocytic anaemia from b12, folate deficiency, celiac screen,
LFT
microbiology to assess nutritional status
stool tests for celiac, h pylori
radiology to assess nutritional status
abdominal x-ray for dilatation
special/other tests to assess nutritional status
ct, endoscopy
management of ischemic bowel
laparotomy
excision of ischemic tissue
ostomy
nutritional implications pre surgery
not eating pre surgery - water soluble vitamin supply low
MUST score steps
- BMI
- weight loss
- acute sickness
How to improve nutrition?
artificial nutrition
nutritional implications of large amount of small bowel removed
more water = passed more easily
less absorption of macronutrients - parenteral nutrition and fluids
normal stoma output
600-1200ml per day
high output stoma
> 1500ml +dehydration
sodium is kept as high as possible using:
rehydration solution - hypertonic
nutritional approach
rehydration
encourage a hypercaloric diet - high salt high fat high protein
increase gastric pH
slow GI transit - loperamide, codeine
bile salt sequestrants
micronutrient replacement
management of short bowel syndrome
- determine length of bowel resected
- replace fluid loss and manage diarrhoea
- appropriate oral nutrition
- replace mineral and vitamin deficiencies
will a stoma patient open bowels?
no, some mucous discharge
causes of acute liver disease
viruses - hepatitis A,B,C,E,CMV,EBV
drugs - paracetamol, ecstasy, herbal remedies
autoimmune
cause of jaundice
increase in serum bilirubin
presentation of acute liver disease
jaundice
pale stools, dark urine
increased serum bilirubin
nausea
unwell
occassionally fever
features of cirrhosis
spider naevi, low platelets
high alkaline phosphatase and high gamma GT suggests?
bile duct disease - primary biliary cholangitis
acute - likely to be obstruction
liver function tests
Bilirubin
Albumin
Alanine transaminase
Aspartate transaminase
Alkaline Phosphatase
Gamma glutamyl transpeptidase
INR – measures factors II, VII, IX and X – all synthesized in liver
commonest causes of abnormal liver function tests?
fatty liver disease and alcohol
higher ast/alt ratio suggests
alcohol or significant fibrosis
treatable causes of liver disease
alcohol
viral hepatitis B, C, D,
autoimmune liver disease
celiac disease (causes abnormal LFT)
wilsons disease - caused by copper accumulation
iron toxicity
primary biliary cholangitis
alanine transaminase and aspartate transaminase catalyse ______
aspartane and alanine
unconjugated fraction of bilirubin binds to
serum albumin
low serum albumin
infection, renal loss - nephrotic syndrome , impaired synthesis - severe liver disease, severe malnutrition
very high transaminases signify
liver cell injury with release of enzymes into circulation e.g., acute viral hepatitis
very very high transaminases
paracetamol overdose, ischemic hepatitis
moderately elevated ALT and AST
fatty liver, cholangitis
alkaline phosphatase is found in
liver, bone, biliary, placenta, intestine
marked increase in alkaline phosphatase suggests
biliary obstruction, primary sclerosing cholangitis, primary biliary cholangitis
what should you always check with inc alk phos
corresponding increase in gamma GT
if not measure alk phos isoenzymes
very high gamma GT indicates
biliary obstruction, cholestasis, alcohol
what is the fib4 score
indirect biomarker of liver fibrosis
calculated from alt, ast, platelet count and age
causes of chronic liver disease
alcohol
chronic viral hepatitis B,C
fatty liver disease
autoimmune liver disease
other - iron overload, biliary disease, inherited disease
chronic inflammation leads to ______
cell death, regeneration, fibrosis (scar tissue)
alcohol is metabolised to
acetaldehyde and fat
to develop alcohol related cirrhosis need to drink
> 50-100 units per week >10 years
how is fatty liver disease diagnosed?
ultrasound scan or other imaging since only 50% have abnormal liver function disease
critical determinate of fatty liver disease?
Non-alcoholic steatohepatitis or simple steatosis
significant fibrosis can only be determined by
liver biopsy or fibroscan
do abnormal liver tests tell if a patient has NASH or simple steatosis?
no
what is a fibroscan?
determines liver stiffness and CAP score
measures how wobbly the liver is
CAP score measures fat content
what hepatitis types cause chronic viral hepatitis?
B and C
what do hepatitis b and c cause?
chronic inflammation of the liver and cirrhosis
treatment for primary biliary cholangitis
usrodeoxcholic acid
severe - obetocholic acid
primary sclerosing cholangitis
causes stricturing of small and large bile ducts
complications of cirrhosis
portal hypertension - ascites, varices, hepatorenal syndrome, hepatic encephalopathy
immune paresis
hepatitis D only affects ____
people with hepatitis B
hepatorenal syndrome
renal failure that occurs in patients with severe liver disease in the absence of any pathological cause for kidney failure
what reverses hepatorenal syndrome?
liver transplant
acute kidney injury
acute significant reduction in the glomerular filtration rate
most practical biomarker of renal function
serum creatinine
influenced by bodyweight, race, age, gender
use of serum creatinine in patients with cirrhosis is affected by
less formation of creatinine in muscles
increased renal tubular secretion of creatinine
interference with assays for sCr by elevated bilirubin
measurement overestimates gfr
diagnostic criteria for Acute kidney injury
> 50% inc in sCR from known baseline
increase in sCr >2 micromol within 48 hrs
main features of hepatorenal syndrome
functional renal failure caused by intra renal vasoconstriction
circulatory dysfunction caused by vasodilatation leading to effective hypovolemia
factors involved in the pathogenesis of HRS
hemodynamic factors
impaired cardiac ouput
activation of sympathetic nervous system
POSSIBLY inc formation of vasoactive mediators
does a low CO increase risk of HRS?
yes
how does activation of sympathetic nervous system affect renal blood flow in HRS
a small decrease in blood pressure reduces blood flow by a lot more
renal vasculature more sensitised to changes in BP and CO
what do vasoactive mediators do?
cause mesangial cell contraction
reduced SA of glomerulus
low GFR
management of HRS
treat underlying cause
support renal function - hemofiltration or dialysis
vasoconstrictors to optimise BP
liver transplant
paracentesis for tense ascites
drug example for HRS
terlipressin
