Summary of Waterhouse-Friderichsen syndrome
Transcript for Waterhouse-Friderichsen syndrome
Waterhouse-Friderichsen syndrome occurs when the blood vessels in the adrenal gland rupture during a severe bacterial infection, turning the adrenal glands into sacks of blood.
This results in adrenal crisis, or acute adrenal insufficiency, which is when the adrenal gland suddenly stops producing hormones.
The syndrome is named after two physicians - Waterhouse and Friderichsen who separately described the syndrome back in the early 1900’s.
Now, there are two adrenal glands, one above each kidney, and each one has an inner layer called the medulla and an outer layer called the cortex.
The adrenal cortex is subdivided into three more layers, the zona glomerulosa, zona fasciculata, and the zona reticularis.
The adrenal cortex secretes hormones under the control of adrenocorticotropic hormone, released by pituitary gland.
The outermost layer is the zona glomerulosa, which makes the hormone aldosterone.
Aldosterone acts on the nephrons of the kidney, and decrease potassium levels, increase sodium levels, and increase blood volume and blood pressure.
The main job of glucocorticoid is to increase blood glucose levels, especially when there’s emotional and physical stress.
Finally, the innermost layer is the zona reticularis, which makes a group of sex hormones called androgens.
In men, androgen stimulates development of male reproductive tissues and secondary sex characteristics like facial hair and a large Adam’s apple.
In women, androgen causes a growth spurt, and growth of underarm and pubic hair during puberty.
The adrenal gland gets blood through three main arteries- the superior, middle, and inferior suprarenal arteries.
All three divide into branches that supply the adrenal cortex and the adrenal medulla.
After delivering oxygen to those tissues, the blood starts to collect again in the medullary vein and eventually into the suprarenal vein.
The root cause of Waterhouse-Friderichsen syndrome is severe bacterial infection, or sepsis.
The outer membrane of these bacteria contains endotoxins, which are large clunky lipopolysaccharide molecules, or LPS.
These LPS molecules directly damage endothelial cells of the blood vessels, and cause them to release procoagulant-like tissue factor, which promotes blood clot formation within blood vessels.
When that happens during an infection, bacteria can start growing in these clots, forming septic emboli, which can drift away and get lodged within other blood vessels.