Understand Diabetic Ketoacidosis (DKA) with this clear explanation from Dr. Seheult of http://www.medcram.com.

This is video 1 of 2 on diabetic ketoacidosis (pathophysiology and signs of diabetic ketoacidosis / DKA):

0:08 DKA stats
0:47 DKA – cellular anatomy
1:00 mitochondria
1:48 beta-oxidation
2:30 insulin function
3:08 pyruvate
3:19 diabetes mellitus type 1
3:26 diabetes mellitus type 2
4:48 ketone bodies (acetone, acetoacetate, b-hydroxybutyrate)
6:09 carboxylic acid
6:23 conjugate base (anion gap acidosis)
7:38 beta-oxidation
8:17 DKA review
8:57 diabetic ketoacidosis – hyperkalemia
9:37 diabetic ketoacidosis – dehydration
9:50 osmotic diuresis
10:10 dehydration
10:27 diabetic ketoacidosis – potassium effects
11:04 diabetic ketoacidosis – Cr elevation / renal failure
11:30 anion gap metabolic acidosis
12:09 measuring ketone bodies (serum ketones, b-hydroxybutyrate)

Speaker: Roger Seheult, MD
Clinical and Exam Preparation Instructor
Board Certified in Internal Medicine, Pulmonary Disease, Critical Care, and Sleep Medicine.

MedCram: Medical topics explained clearly including: Asthma, COPD, Acute Renal Failure, Mechanical Ventilation, Oxygen Hemoglobin Dissociation Curve, Hypertension, Shock, Diabetic Ketoacidosis (DKA), Medical Acid Base, VQ Mismatch, Hyponatremia, Liver Function Tests, Pulmonary Function Tests (PFTs), Adrenal Gland, Pneumonia Treatment, internal medicine, usmle prep, dka, and many others. New topics are often added weekly- please subscribe to help support MedCram and become notified when new videos have been uploaded.

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Recommended Audience: Health care professionals and medical students: including physicians, nurse practitioners, physician assistants, nurses, respiratory therapists, EMT and paramedics, and many others. Review for USMLE, MCAT, PANCE, NCLEX, NAPLEX, NDBE, RN, RT, MD, DO, PA, NP school and board examinations.

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Produced by Kyle Allred PA-C

Please note: MedCram medical videos, medical lectures, medical illustrations, and medical animations are for medical education and exam preparation purposes, and not intended to replace recommendations by your health care provider.

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Marko Šestan and colleagues show that the hormone insulin can boost the antiviral immune system. Upon viral infection, the immune system therefore induces insulin resistance in order to increase insulin production by the pancreas, which stimulates the antiviral immune response. In lean people this is not a problem, because the pancreas easily compensates for temporary insulin resistance. But in obese people, who usually already have insulin resistance, infection may overload the ability of the pancreas to compensate, resulting in diabetes mellitus type 2.
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Developed and produced for http://www.MDPracticeGuide.com, a CME resource for physicians and healthcare providers.

Animation Description: Under normal circumstances, bacterial infection results in the release of chemokines that attract circulating neutrophils to the endothelium. This process is known as chemotaxis.

A variety of molecules are expressed on the endothelial cell surface that allow the neutrophil to be captured, then roll along the endothelium, then adhere.

Following adherence, the neutrophil migrates into the subendothelial tissue to reach the site of infection.

The neutrophil engulfs the bacteria and eliminates them via breakdown within the phagosomes — a process known as phagocytosis.

In states of hyperglycemia, chemotaxis is reduced. Adherence is also adversely affected.
Phagocytosis is also impaired by hyperglycemia.

Hyperglycemia also adversely affects the macrophage system. Under normal circumstances, circulating monocytes are attracted to sites of infection, roll, adhere, and then migrate into the subendothelial space. The monocyte then transforms into a macrophage.

which is then activated by cytokines released by the bacteria. The activated macrophage then engulfs the bacteria.

However, hyperglycemia results in decreased activation of macrophages, thereby arresting the process of macrophage phagocytosis of bacteria.

In addition to affecting neutrophil and macrophage function, hyperglycemia also affects the complement cascade. Under situations of normal glycemia, bacteria can activate the complement cascade.

Activation of the complement cascade results in the formation of transmembrane protein channels known as membrane attack complex (MAC) in bacterial membrane.

Membrane attack complexes make the bacterial membrane porous and the rapid influx of fluid results in the bacterial cell death.

Hyperglycemia inhibits the proper activation of the complement cascade, thereby reducing another pathway of the immune system.
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