Lecture 15 Chapter 20 Flashcards
What organ is most affected by extravascular hemolysis
Spleen
What condition affects your platelet aggregation and clot formation inside your vessels
Microangiopathic hemolytic anemia
Cell travels down vessel at high speed and crashes into platelet/clot formation destroying the cell
Can be intrinsic and extrinsic
Describe acute vs. Chronic
Acute = the progress of the symptoms are going to happen very quickly. (ie. symptoms accelerate within 3 months)
Chronic = symptoms extend beyond 3 months
Describe intrinsic vs. Extrinsic
Intrinsic = the problem that results in the destruction of RBCs is within the RBCs
Extrinsic = the causes are outside of the RBCs
Describe inherited vs. Acquired
Inherited = you are born with the condition that results in the destruction of RBCs
Acquired = you were not born with it (mutations/problems occurred after birth)
Describe intravascular vs. Extravascular hemolysis
Extravascular = the RBCs are destroyed outside of the blood vessels, such as in the bone marrow, liver, and spleen
Intravascular = the damage to the cells is done within the blood vessels
Can often have both but look at which is predominant
Normally intravascular = 10% and extravascular = 90%
Diseases that cause excessive extravascular hemolysis
Hemoglobinopathies
Thalassemias
If you receive a fecal specimen in the lab, and the fecal color/material is more gray like chalk, what can cause that?
Color comes from stercobilin
Could be a problem where bile that contains bilirubin cannot empty bile in intestinal tract, which could be a gallstone trapped in the biliary ducts
Worst cases: pancreatic cancer or biliary cancer cause tumor to grow blocking the pathway → bile doesn’t get into intestinal tract → no bilirubin there → bilirubin cannot break down to urobilinogen → no stercobilin produced → no fecal color
What tests/abnormal results support the cause of excessive extravascular hemolysis
Increased retic count cause problem is not in bone marrow
Unconjugated bilirubin goes up
Urobilinogen in urine increased - it you have increased destruction of RBCs in the spleen, you will increase the production of unconjugated bilirubin → goes to liver → albumin is removed and bilirubin get conjugated → gets put in bile that empties into intestinal tract → get broken down into urobilinogen → more bilirubin = more urobilinogen
What happens when a RBC is destroyed intravascularly
The hemoglobin breaks into molecules and the tetromeres become alpha/beta dimers. Haptoglobin binds to dimers and carries dimers to liver → gives them to hepatocytes → breaks it down into bilirubin → recycles everything else → puts bilirubin in bile
What does haptoglobin prevent
The hemoglobin dimers to be filtered through the kidney because if they get filtered through the kidney, your venal tubular cells and proximal convulated tubules will absorb it. The dinners have iron in them so it will increase iron in storage which causes oxidative stressed renal tubular cells → kills venal tubular cells → problems with kidney
What happens when hemoglobin is released into the environment outside of the RBCs
It becomes oxidized → becomes methemoglobin → albumin binds to methemoglobin → hemopexin can take the albumin/methemoglobin complex to liver → liver breaks it down
What can bind to free hemoglobin and take it to the liver
Haptoglobin (binds to a/b dimers)
Albumin
Hemopexin
What happens to your haptoglobin when you have excessive intravascular hemolysis
There will be a rapid drop in haptoglobin because it will grab hgb and take it to liver but will be taken inside liver as well.
Liver can only produce a set amount of haptoglobin so cannot increase amount even when there is an increase in free hemoglobin
What happens when too many cells are destroyed an liver cannot control it?
The hemoglobin will spill over to other organs such as the kidneys, causing kidney failure
