Hello and welcome to the Zero to Finals podcast.

My name is Tom and in this episode I'm going to be talking to you about hemolytic anemia.

And you can find written notes on this topic at zero to finals.com slash hemolytic anemia

or in the hematology section of the second edition of the

Zero to Finals Medicine book. So let's get straight into it. Hemolytic anemia involves the

destruction of red blood cells, which is called hemolysis, and this results in a low hemoglobin

concentration, which is called anemia.

Several inherited conditions can cause the red blood cells to become more fragile

and break down faster than normal, leading to chronic hemolytic anemia.

And these inherited conditions include hereditary spheroscytosis, hereditary spheroocytosis,

hereditary elliptocytosis,

thalcemia, sickle cell anemia,

and G6PD deficiency.

Several acquired conditions,

which the patient develops during their lifetime, can lead to the

destruction of red blood cells, including autoimmune hemolytic anemia, aloeimmune hemolytic

anemia, for example, transfusion reactions and hemolytic disease of the newborn, paroxysmal nocturnal hemoglobinuria, micro-angiopathic

hemolytic amoe, and prosthetic valve-related hemolysis. These all sound very intimidating,

but we're going to go through each one in detail to explain it simply.

Let's start by talking about the features of hemolytic anemia.

The features are a result of the destruction of red blood cells, including anemia, or a low hemoglobin concentration, spleenomegaly, where the spleen becomes filled with the destroyed red blood cells,

and jaundice, where Billy Rubin is contained within red blood cells and released when they're destroyed.

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