Abscesses

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High Yield Notes

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Abscesses

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Abscess p. 487

lung p. NaN

Alcoholism p. 589

lung abscesses and p. 704

Bacteremia

brain abscesses p. 177

Bacteroides spp.

lung abscesses p. 704

Bartholin cyst/abscess p. 661

Brain abscesses

HIV-positive adults p. 177

Toxoplasma gondii p. , 174

Chest X-rays

lung abscesses p. 704

Clindamycin

lung abscesses p. 704

Epilepsy

lung abscesses p. 704

Fusobacterium spp.

lung abscesses p. 704

Lung abscesses p. 704

Mastoiditis

brain abscesses p. 177

Otitis media

brain abscesses with p. 177

Perinephric abscesses p. 619

Sinusitis

brain abscesses p. 177

Staphylococcus aureus p. , 133

brain abscesses p. 177

Viridans streptococci p. 134

brain abscesses p. 177

Transcript

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Everyone who has ever had a pimple has had an abscess, even though they’re tiny, they’re still abscesses.

An abscess forms when normal tissue, like skin for example, is split apart and that new space is invaded by nearby pathogens like bacteria.

And there are roughly ten bacterial cells for every one human cell and they cover every surface of the human body.

So any cut or break in the skin or closed off area within the body is an invitation for bacteria to dive in and multiply.

When that happens the immune system typically responds and a battle ensues with the result being pus - a mixture of bacteria, immune cells, and dead tissue.

So, in response to an injury, the tissue releases small chemicals in the local area called cytokines, like tumor necrosis factor, interleukin-1, interleukin-6 and interleukin-17, and chemokines which attract nearby white blood cells which are part of the immune system. It’s kinda like yelling for help and being heard by the nearby police.

In addition to attracting immune cells, the cytokines also dilate nearby capillaries - which brings more blood to the site, and make the capillaries more leaky, so that the white blood cells that do show up, can slip out of the blood and get into the tissue more easily.

Often times, the first immune cells at the scene are neutrophils, which release chemicals and enzymes that kill bacteria and dissolve pieces of of dead cells, creating a pool of dead material.

This is a specific type of acute inflammatory response called suppurative inflammation, which simply means that pus is created in the process.

From a macroscopic view, this is sometimes referred to a liquefactive necrosis, because the area of dead tissue turns to liquid.

As those immune cells get to a point where they can’t withstand the environment, they die too, and become part of that pool.

Initially the debris might be intermixed with healthy tissue, but over time it can coalesce into a single area - a process that is often sped up when more immune cells get involved.

Around this pool of pus, a wall of fibrinogen - which is the same protein that holds together blood clots - starts to harden into a barrier.

Occasionally sheets of fibrin form septations, creating loculations or pockets of pus within the abscess itself...kinda like an abscess within an abscess.

Even though the pus is largely dead material, there are still plenty of live bacteria within the pus, which makes it highly infectious if it gets spread from one place to another.

Sources

  1. "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
  2. "CURRENT Medical Diagnosis and Treatment 2020" McGraw-Hill Education / Medical (2019)
  3. "Yen & Jaffe's Reproductive Endocrinology" Saunders W.B. (2018)
  4. "Bates' Guide to Physical Examination and History Taking" LWW (2016)
  5. "Robbins Basic Pathology" Elsevier (2017)
  6. "Etymologia:<i>Staphylococcus</i>" Emerging Infectious Diseases (2013)
  7. "Patterns of Contrast Enhancement in the Brain and Meninges" RadioGraphics (2007)
  8. "A play in four acts: Staphylococcus aureus abscess formation" Trends in Microbiology (2011)