3. RESULTADOS
3.2. Desarrollo del turismo y transformaciones socioculturales
3.3.3. Valoración de la comunidad respecto el proyecto de turismo del Parque Arví
Dubin Johnson; Rotor syndromes: Genetic dz’s involving prob getting rid of CONJ bilirubin in the bile ducts. So, this is predominantly a conj hyperbilirubinemia. In Dublin Johnson, have a black colored pigment that builds in the liver and
get black liver.
III. Liver Function Test (LFTs)
What are transaminases used for? They are indices of liver cell necrosis (hepatitis). AST (SGOT) and ALT (SGPT); ALT is more specific b/c it is only found in the liver; AST is in muscle, RBC’s and liver.
Therefore, if you have a viral hepatitis, with massive liver cell necrosis, which would be the predominant transaminases elevated? ALT. Ex: 2500 ALT and 2200 AST. So ALT will be the main liver cell enzyme elevated in diffuse liver cell
In alcoholic hepatitis, this is not what happens. There is a reason: AST is present in the mito of hepatocytes. ALT is not – it’s in the cytosol. Alcohol is a mito poison (remember that it uncouples). AST is predominantly in mito, and when pt has alcoholic hep, AST is higher than ALT (forget the 2:1 relationship). Therefore, if you see AST higher than ALT, this is due to alcoholic liver dz. Could be fatty change, alcoholic cirrhosis, and alcoholic hepatitis. If it’s VIRAL hepatitis, ALT is bigger than AST. So, what are the enzymes of OBSTRUCTION (obstruction of bile ducts)? Alkaline phosphatase and Gamma glutamyl
transferase. Transaminases will also be up, but not to the same degree. Gamma glutamyl transferase is located in the SER.
When the SER is rev’d up, it undergoes hyperplasia (ie due to drugs: alcohol, barbs, rifampin, and phenytoin); you not only increase the metabolism of the drug, but also increase the synthesis of gamma glutamyl transferase. So, what would the classic thing you would see in any alcoholic liver dz? AST>ALT, along with INCREASED gamma glutamyl transferase. There is a problem: alk phos is in other things other than the liver – in bone (osteoplastic activity), placenta. So, how will you know where the alk phos comes from (ie if it’s from bile duct obstruction vs. other things)? Look at gamma glutamyl transferase
b/c its specific for the liver (so, if alk phos up, look at gamma glutamyl transferase!). If the gamma glutamyl transferase IS elevated along with alk phos, this is BILE DUCT OBSTRUCTION.
Albumin protime = marker of severity of liver damage. It is made in the liver, therefore if you have severe liver dz (ie
cirrhosis), it will be decreased. Even better than that is prothrombin time b/c coagulation factors are made there (most are made there – vWF is not, however). So, if you have liver damage, the production of coagulation factors will be decreased, and PT will be prolonged (increased). So, albumin levels and PT are the 2 best tests for liver severity (PT is a little better
than albumin).
There is only one autoAb that is important: anti –mito Abs in primary biliary cirrhosis.
Tumor markers: alpha feto protein is a marker for hepatocellular carcinoma. Can also use alpha-1 antitrypsin b/c it
is made in the liver (it is increased in hepatocellular carcinoma).
If you have fractionation of bilirubin (less than 20%, 20-50%, and 50+ %), can start d/d; then give transaminase levels – see how it correlates with liver dz: transaminases correlate with viral hep and conj bilirubin of 20-50, or obstructive liver dz (alk phos, gamma glut) and conj bilirubin over 50%.
IV. Viral Hepatitis A. MC on hepatitis:
MC hep = A (followed by B, C, D, E – in that order)
A and E = fecal oral; all the others are transmitted parentally Hep A = No chronic carrier state
Hep E = produces a chronic carrier state only if you are pregnant, leading to chronic liver dz Hep D = Requires Hep B to infection
Hep A = Daycare centers (therefore should get vaccine to prevent; outbreaks can occur in daycare centers) Hep A = Jail
Hep B = IVDA
Hep C = Post transfusion Hepatitis
Hep B = MC infection by accidental needle stick
B. Serology:
HAV: anti A IgM= have hep A; anti A IgG = had it and won’t get it again
HCV: anti C IgG Ab’s are NOT protective and mean that you have the dz; there are no known protective Ab’s
HDV: (same as HCV) – anti D IgG = have the dz, and no known Ab’s will help cure; if you are anti-D IgG positive it means
you have the active dz now
So, only protective Ab’s are HAV, HBV (surface Ab), and HEV.
Hep B (HBV)
First marker that comes up issurface Ag (HBsAg). It comes up about 1 month after you have the infection. You don’t know you have it and are asymptomatic. The enzyme studies are normal. The next thing that comes up is the bad guys: E Ag (HBeAg) and HBV DNA, b/c these are only ones that are infective. Then the first Ab comes up a lil after the DNA and E Ag, which is core Ab IgM (Anti-HBc) (this is expected b/c the first Ab against acute inflammation is IgM). The majority of people with Hep B recover (about 90%); those with HIV+ never recover and will have chronic cases b/c they have no immune response to knock it off. If you do recover the first things to go away are E Ag (HBeAg) and HBV DNA. The last of the Ag’s that goes away is surface Ag (HBsAg). So, surface Ag is the first to come and the last to leave (like a “house within a house” – look at the chart and will see that S Ag is the big house and E Ag and HBV DNA are the lil houses under big house). In other words, it is IMPOSSIBLE to be E Ag positive and S Ag negative (E Ag and DNAcome up after S Ag and leave before).
Surface Ab doesn’t come up until about 1 month after S Ag is gone, so there is this gap, which is a ‘window’ with nothing elevated (only has one Ab there; S Ag, E Ag, HBV DNA are all gone, and S Ab not there yet). So, how do you know the pt HAD Hep B? Core IgM doesn’t leave – it stays there and becomes IgG over time. So, the marker for that window period when all the bad guys are gone and surface Ab hasn’t arrived yet, is core Ab IgM (which tells you that you HAD Hep B and are in the process of recovery). There is no way you are infected during this period – why? B/c E Ag and HBV DNA are not there. Therefore, you are not infective – it just means that you HAD Hep B and are in the process of recovering. YOU ARE NOT INFECTIVE – this is between the 5th and 6th month.
So, if you had Hep B, there should be 2 Ab’s that you have: core Ab IgG and surface Ab IgG.
If you have been vaccinated, cannot have anything b/c you had yeast make surface Ag, which is what the vaccine consists of. The only bad Ab you can get from injecting surface Ag is Ab’s against it. So, only Ab you will have if you were vaccinated is Surface Ab. NOT core Ab IgG b/c were not injected with that. Core Ab is not a protective Ab.