Laz Gastro Flashcards
(25 cards)
What are the three main causes of chronic liver disease
alcoholic liver disease
NAFLD
viral hep
what are secondary causes of CLD
haemochromatosis (accumulation of iron)
Wilson’s disease (accumulation of copper)
CF
alpha-1 antitrypsin deficiency
link the functions of the liver to what occurs in liver failure
- albumin production > oedema, leuconychia
- bilirubin metabolism > jaundice
- clotting factors > coagulopathy (easy bruising)
- detox > encepalopathy
explain how blood arrives to the liver in a normal physiological state
blood from the GI system (so dirty, with lots of toxins) travels to liver via HEPATIC PORTAL VEIN
Explain what happens to blood arriving to liver in CLD and how this causes signs
there is increased resistance from the liver
due to nodules and fibrosis
This puts backpressure onto the portal system (portal hypertension)
this leads to formation of portosystemic anastamoses
what portosystemic anastamoses are formed by CLD backpressure onto the portal system?
- oesophageal varices
- hypersplenism
- caput medusae
- rectal varices
why does oedema occur in liverfailure
hypoalbumniaemia –> drop of oncotic pressure and increase in hydrostatic pressure intravascularly
What two indices are important in someone with ascites
SAAG
neutrophil count
What is SAAG
Serum Ascites Albumin Gradient
SAAG = serum albumin - ascites albumin
what is the boundary in SAAG
11.1g/L
what does a HIGH SAAG indicate
> 11.1g/L = TRANSUDATIVE -> the albumin in ascites > albumin in blood
* due to portal HTN (also CLD, HF, RF)
* Raised hydrostatic pressure in hepatic portal system forces water into peritoneum while albumin (which is too big to travel through membrane) stays intravascular
what does a LOW SAAG indicate
<11.1g/L =-EXUDATIVE
- albumin is being created in the peritoneum, and the fluid is due to a peritonitic problem e.g. infection, inflammation (pancreatitis, malignancy (pancreatic cancer) or nephrotic syndrome
what is jaundice caused by
accumulation of bilirubin in blood
explain the process of producing and moving bilirubin
RBC are broken down in bloodstream to produce bilirubin
bilirubin travells to the liver, where it is conjugated
then it is moved to gallbladder and stored
then via biliary tract it is ejected when necessary into the GI tract
in the GI tract it becomes urobilinogen
urobilinogen that is kept in GI tract becomes stercobilin > secreted in poo
some urobilinogen leaves circulation > travels to kidneys > excreted out
What are PREHEPATIC causes of jaundice
issues with increased RBC breakdown
- AIHA
- sickle cell disease
- G6PD deficiency
- Malaria
What are HEPATIC causes of jaundice
issues with liver conjugation of bili
- liver disease
- hepatitis
- Gilbert’s
- drugs
what are POST HEP causes of jaundice
Biliary disease
- gallstones
- PSC / PBC
- Cholangiocarcinoma
Pancreatic cancer
what will parameters be like in pre-hep jaundice
RAISED unconjugated bilirubin (as there is too much bili for the liver to conjugate and excrete, while the bili that the liver is able to conjugate is excreted normally) Urine normal (as unconjugate bilirubin is insoluble so does not reach the urine) Stool normal (same but for stool)
What are parameters like in hep jaundice
RAISED unconj and conj bilirubin (as liver cannot dispose of bilirubin well and cannot conj it well)
Urine dark (raised urobilinogen) Stool normal / silghtly pale
what are parameters like in post-hepatic / obstructive jaundice
RAISED conjugated bilirtubin as it leaks from the bililary tree (it cannot drain normally due to the obstruction)
urine is DARK (as all this conj bilii is drained by kidneys)
stool is very PALE (as due to obstruction the bilirubin can no longer reach the intestine)
what should you do in acute abdomen in a female of child bearing age
PREGNANCY TEST IS MANDATORY (EVEN IF THEY SAY THEYRE NOT ACTIVE)
what kind of drug is orlistat
p
inhibits pancreatic and gastric lipase –> prevent digestion of fat
causes of gastroentreitis and infctious colitis
- viral: rotavirus (children), norovirus (adults)
- bacteria: campylobacter jejuni, e.coli, salmonella
- protozoa: entamoeba histolytica
investigations for gastroenteritis and infectious colitis
- ASSESS HYDRATION STATUS (postural hypotension, dry tongu, tachycardia, weakness, , reduced urine output
- Bloods: FBC, blood culture, U&Es (dehydration), C diff = raised WCC
- Stool sample: faecal microscopy and analysis for toxins (C. difficile toxin causes pseudomembranous colitis)
- AXR or ultrasound: exclude other causes of abdominal pain (e.g. bowel perforation)