01-03 D.K.A. Flashcards

1) Review the basic physiology of metabolism 2) Know the pathophysiology of DKA 3) Know the rationale behind treatment 4) Understand why DKA does not happen in DM 2 5) Be able to explain the difference between DKA and HONK

1
Q

Your body never has no insulin

A

control of insulin is more “reostat” than “on/off switch”

—DKA is at its most basic, the result of a complete lack of insulin

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2
Q

Pathophys of DKA

A

USUALLY IN TYPE 1 DM
1. pt stops insulin → glucose ↑s → osmotic diuresis → low ECV → stress hormones triggered (epi, cortisol, GH) which exacerbates insulin resistance
2. glucagon:
—TONES DOWN: glycogen synthase, phosphofructokinase
—REVS UP: liver G-6-Pase (↑ glucose), SKM proteolytics (↑ Ala) & adipocyte HSL (↑ FFAs)
**Ala → Liver → glucose released
**All this even though glucose is SKY HIGH; now glucose even higher!
3. Ketone formation
—insulin normally inhibs HSL; now that it is uninhib’d, trigs are made into FFAs in fat cells
—FFAs → liver
—Normally, insulin would block Carnitine shuttle via inhib of malonyl-CoA, however it is absent; so FFAs → liver’s mitos
—normally FFAs in liver mitos → acetyl-CoA → shuttled to citric acid cycle or lipid synth, however that’s overwhelmed b/c not enough NAD+
—acetyl-CoA → 3-hydroxybutyrate + acetoacetate(→ acetone and CO2)
4. Acidosis → neural decline; acetone → fruity breath

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3
Q

s/sx of DKA

A

—neural ∆s → coma (from acidosis/hyperosmolarity, too?)
—abdominal pain (reason unknown)
—fruity breath (from acetone)
—arrythmias and hyperkalemia (acidosis)
—s/sx of volume depletion (lacking both H2O & NaCl)

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4
Q

Potassium ∆s over the course of DKA

A

1) increasing acidosis causes HYPERKALEMIA b/c of shift of K+ to outside of cells
2) however, you are likely to become HYPOKALEMIC shortly after correction

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5
Q

What is the strategy for DKA Tx?
—What does tx do?
—What is time course?

A
  1. Replete Volume (meaning BOTH H2O & NaCl)
    —restores BP
    —lowers osmolarity
    —lower [Epi]
  2. High dose iv insulin to:
    **Much more than lower BG
    —control nutrient flux from muscle/fat*
    —control gluconeogenesis
    —promote glucose uptake
    —control ketoacid production

*inhibition of lipolysis takes the longest to “calm down”

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6
Q
HHS vs. DKA
—Age of occurance
—ketones?
—acidosis?
—[HCO3-]
—serum glucose pre-tx?
—degree of volume depletion
—rate of evolution?
A

(HHS = HONK)
—HHS usually in older pts, DKA usualy 1000 (vs. usually <800 in DKA)
—HHS has WORSE total water, Na+, K+ and Cl- deficits (down 10-15L! vs. 2-4L in DKA)
—HHS evolves over 3-5 days vs. 8-24 hrs in DKA

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