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A1. DKA Introduction

A. Ketone body

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์ˆ˜์šฉ์„ฑ, ์ง€๋ฐฉ์—์„œ ์œ ๋ž˜ํ•œ ์—๋„ˆ์ง€ ์—ฐ๋ฃŒ
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Glucose ์‚ฌ์šฉ์ด ์ œํ•œ๋œ ํ™˜๊ฒฝ์—์„œ ์—๋„ˆ์ง€์›์œผ๋กœ ์“ฐ์ด๋ฉฐ, ํŠนํžˆ brain์—์„œ ์‚ฌ์šฉ๋Ÿ‰์ด ๋งŽ์Œ.
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ATP ์‚ฌ์šฉ์˜ 60%๊นŒ์ง€ ๊ณต๊ธ‰ํ•  ์ˆ˜ ์žˆ์Œ.
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๊ฐ„์—์„œ ์ƒ์„ฑ ์ธ์Š๋ฆฐ level ๊ฐ์†Œ, glucagon level ์ฆ๊ฐ€ ์ € ์ธ์Š๋ฆฐ์€ ํ˜ธ๋ฅด๋ชฌ ๋ฏผ๊ฐ์„ฑ Lipase ํ™œ์„ฑํ™” โ‡’ triacylglycerols์„ glycerol+fatty acid๋กœ ๋ถ„ํ•ด Long-chain FA ๋Š” ๊ฐ„์„ธํฌ์˜ ๋ฏธํ† ์ฝ˜๋“œ๋ฆฌ์•„๋กœ ์šด๋ฐ˜
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3๊ฐ€์ง€ ํ˜•ํƒœ๋กœ ์กด์žฌํ•˜๋ฉฐ, ์•„์„ธํ†ค์€ ํœ˜๋ฐœ์„ฑ์ด ๊ฐ•ํ•˜์—ฌ ํ˜ธํก ์ค‘ ์•„์„ธํ†ค ๋ƒ„์ƒˆ๋ฅผ ์ผ์œผํ‚ด
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Ketoacidosis ๋ฅผ ๊ฐ€์ง„ ํ™˜์ž ์—์„œ ๊ฐ€์žฅ dominant form์€ B-hydroxybutric acid : ์ •์ƒ์ ์ธ ์ƒํƒœ์—์„œ๋Š” acetoacetic acid ์™€ ๋น„์œจ์ด 1:1 : DKA์—์„œ๋Š” 3:1, AKA์—์„œ๋Š” 10:1๊นŒ์ง€ BHBA ๊ฐ€ ์ฆ๊ฐ€ํ•  ์ˆ˜ ์žˆ์Œ. : Urine dipstick ๊ฒ€์‚ฌ๋Š” acetoacetic acid๋งŒ ํ™•์ธ โ‡’ DKA ๋“ฑ์—์„œ ketouria ๊ฐ€ underestimation ๋  ์ˆ˜ ์žˆ์Œ.

A. Insulin์˜ counterregulatory Hormon

(1) Glucagon / Catecholamine / Cortisone / Growth hormone

(2) Action

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Gluconeogenesis & glycogenolysis๋ฅผ ์ฆ๊ฐ€
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Fat์„ free fatty acids์™€ glycerol๋กœ ๋ถ„ํ•ด
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Proteolysis๋ฅผ ์ผ์œผ์ผœ amino acid level์ด ์ฆ๊ฐ€

A2 Free fatty acid๋Š” ๊ฐ„์œผ๋กœ ์ด๋™ํ•˜์—ฌ Ketone body๋กœ ์ „ํ™˜๋จ

(1) Ketone body : Acetoacetic acid (AcAc) & beta-hydroxybutyrate (ฮฒHB)
(2) AcAc + NADH โ‡Œ ฮฒHB + NAD ์˜ ํ‰ํ˜•์ƒํƒœ๋ฅผ ์ด๋ฃฌ๋‹ค.
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NAD : Nicotinamide Adenine Dinucleotide, ์„ธํฌํ˜ธํก์—์„œ ํ•ด๋‹น๊ณผ์ •๊ณผ TCA ํšŒ๋กœ์— ์“ฐ์ž„
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NADH : NAD์˜ ํ™˜์›ํ˜•ํƒœ, ์ „์ž์ „๋‹ฌ๊ณ„๋ฅผ ๊ฑฐ์น˜๋ฉด์„œ ATP๋กœ ์ „ํ™˜๋˜๊ฑฐ๋‚˜ ๋™ํ™” ๋ฐ˜์‘์— ์“ฐ์ž„
(3) AcAc๋Š” another major ketone body์ธ acetone์œผ๋กœ ๋Œ€์‚ฌ๋œ๋‹ค.

B. Ketosis

B1. ๋ฐœ์ƒ์›์ธ

(1) ์ง€๋ฐฉ๋ถ„ํ•ด๊ฐ€ ์—๋„ˆ์ง€ ์ƒ์„ฑ์˜ ์ฃผ ์—ฐ๋ฃŒ์ผ ๋•Œ

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1์ผ ์š”๊ตฌ ์—๋„ˆ์ง€์˜ 5-10% ๋ฏธ๋งŒ์˜ ์‹์ด๋งŒ ์œ ์ง€
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ketogenic diet (ํƒ„์ˆ˜ํ™”๋ฌผ ๋น„์œจ์ด ๋งค์šฐ ์ ์€ ์‹์‚ฌ)
โ‡’ ๋ถˆ์ถฉ๋ถ„ํ•œ ์—๋„ˆ์ง€ ๊ณต๊ธ‰์œผ๋กœ ์ธํ•ด ์ฒด์ง€๋ฐฉ ๋น„์ถ•์œผ๋กœ๋ถ€ํ„ฐ ์šฐ์„ ์ ์œผ๋กœ ์—๋„ˆ์ง€ ์ƒ์‚ฐ โ‡’ ์ธ์Š๋ฆฐ ์ˆ˜์น˜๊ฐ€ ๊ฐ์†Œํ•˜๋ฉด์„œ ์ง€๋ฐฉ ๋ถ„ํ•ด๊ฐ€ ํ–ฅ์ƒ
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์žฅ๊ธฐ๊ฐ„์˜ ์šด๋™ ์ค‘์—๋„ ๋ฐœ์ƒํ•  ์ˆ˜ ์žˆ์Œ
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์ •์ƒ์ ์ธ ํ˜ˆ๋‹น ์ˆ˜์น˜๋Š” ๊ฐ„์˜ ํฌ๋„๋‹น ์‹ ์ƒํ•ฉ์„ฑ์— ์˜ํ•ด ์œ ์ง€๋จ

(2) ์ธ์Š๋ฆฐ ์ˆ˜์น˜๊ฐ€ ๋‚ฎ๊ฑฐ๋‚˜, ์ €ํ•ญ์„ฑ์ด ๋†’์€ ์ƒํ™ฉ

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ํ˜ˆ๋‹น์„ ์—๋„ˆ์ง€์›์œผ๋กœ ์‚ฌ์šฉํ•  ์ˆ˜ ์žˆ๋Š” ๋Šฅ๋ ฅ์ด ๋–จ์–ด์ง
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์ฒด์ง€๋ฐฉ์—์„œ ์šฐ์„ ์œผ๋กœ ์—๋„ˆ์ง€๋ฅผ ์ƒ์„ฑํ•˜๊ฒŒ ๋จ.
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infection ๋˜ํ•œ ์ธ์Š๋ฆฐ ์ €ํ•ญ์„ฑ์„ ๋†’์ด๋Š” ์ƒํ™ฉ

B2. ๋ฐœ์ƒ๊ธฐ์ „

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๊ตถ๊ธฐ ์‹œ์ž‘ํ•œ ์ง€ 12-14์‹œ๊ฐ„ ์ดํ›„๋ถ€ํ„ฐ mild ketosis๊ฐ€ ์œ ๋ฐœ (1mmol/L, ๋ณธ์› ๊ฒ€์‚ฌ๋กœ๋Š” 1000)
20-30์‹œ๊ฐ„ ์ดํ›„ ํ”ผํฌ โ‡’ ์ผ์ • ์ˆ˜์ค€ ketone body level์ด ์˜ฌ๋ผ๊ฐ€๋ฉด ์ž๊ฐ€๋กœ stabilization ๊ธฐ์ „๋ฐœ์ƒ
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๋†’์€ ์ผ€ํ†ค์ฒด ๋†๋„
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๋‚ฎ์€ ํฌ๋„๋‹น ์ˆ˜์ค€์—๋„ ๋ถˆ๊ตฌํ•˜๊ณ  ์ธ์Š๋ฆฐ ๋ฐฉ์ถœ์„ ์ž๊ทน
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์ง€๋ฐฉ ์กฐ์ง์€ ์ธ์Š๋ฆฐ์ด ์ง€๋ฐฉ์‚ฐ ๋ฐฉ์ถœ์„ ์–ต์ œ์‹œํ‚ค๋Š” ํšจ๊ณผ๋ฅผ ์ฆ๊ฐ€
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์ผ€ํ†ค์ฒด ์ž์ฒด๊ฐ€ ์ง€๋ฐฉ๋ถ„ํ•ด๋ฅผ ์ง์ ‘์ ์œผ๋กœ ์–ต์ œ
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๋‡Œ๊ฐ€ ์—ฐ๋ฃŒ ๊ณต๊ธ‰์›์œผ๋กœ์„œ ํฌ๋„๋‹น์—์„œ ์ผ€ํ†ค์œผ๋กœ ์ „ํ™˜ํ•จ์— ๋”ฐ๋ผ ์ค‘์ถ”์‹ ๊ฒฝ๊ณ„ ์ผ€ํ†ค์‚ฐ ํก์ˆ˜์œจ์ด ์ฆ๊ฐ€ํ•˜๋ฉฐ, ๋ง์ดˆ ์กฐ์ง ์ผ€ํ†ค ์ด์šฉ๋ฅ ์ด ์ฆ๊ฐ€ํ•˜๊ฒŒ ๋จ.
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๋Œ€์‚ฌ์„ฑ ์‚ฐ์ฆ์˜ ์ •๋„๋Š” ์ผ๋ฐ˜์ ์œผ๋กœ ๋น„๊ต์  ๊ฒฝ๋ฏธํ•˜๊ธฐ ๋•Œ๋ฌธ์— ์ผ๋ฐ˜์ ์œผ๋กœ ๏ผ‚์ผ€ํ†ค์‚ฐ์ฆ๏ผ‚๋ณด๋‹ค๋Š” ๏ผ‚์ผ€ํ† ์‹œ์Šค๏ผ‚๋ผ๋Š” ์šฉ์–ด๊ฐ€ ์‚ฌ์šฉ
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๊ณต๋ณต ์ผ€ํ†ค์ฆ๊ณผ ๊ด€๋ จ๋œ ๋ถ€์ž‘์šฉ์— ๋Œ€ํ•œ ์ฆ๊ฑฐ๋Š” ์—†์Œ

C. Insulin

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Central action : ์ธ์ง€๊ธฐ๋Šฅ ์ƒ์Šน ๋ฐ ์‹์ด ์–ต์ œ
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Peripheral action : ๊ฐ„์˜ glucose ์ƒ์„ฑ์–ต์ œ, : ์ง€๋ฐฉ์ƒ์„ฑ์„ ์œ ๋„ํ•˜๋ฉฐ ์ง€๋ฐฉ๋ถ„ํ•ด๋ฅผ ์–ต์ œ : ์ €ํ˜ˆ๋‹น์˜ adrenal response๋ฅผ ๊ฐ•ํ™” : ์ƒ์‹๋Šฅ๋ ฅ์„ ๊ฐ•ํ™”

D. DKA ๋ณ‘ํƒœ์ƒ๋ฆฌ

DKA์—์„œ ์ฃผ๋œ ์—ญํ• ์„ ํ•˜๋Š” 3๊ฐ€์ง€ pathyphysiologic syndrome
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Metabolic acidosis
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Osmotic duuresis
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Electrolyte disturbance

Metabolic acidosis

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High anion gap Excessive blood concentration of ketone bodies (keto-anions) Anion gap Unmeasured anion โ€“ Unmeasured cation Na+ - (HCO3-+Cl-)
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Compensatory tachypnea Can lead to respiratory fatigue

Osmotic diuresis

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Glycosuria๋Š” osmotic diuresis ์œ ๋ฐœ
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์ „ํ•ด์งˆ์ด ์ƒ๋Œ€์ ์œผ๋กœ ์ ์€ ์†Œ๋ณ€๋ฐฐ์ถœ์ฆ๊ฐ€
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serum Na, osm ์ฆ๊ฐ€
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Plasma hyperosolality
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HHS์—์„œ DKA๋ณด๋‹ค ๋” ์ฆ๊ฐ€
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intracellular dehydration ๋ฐ hypertonicity๋Š” ํ™˜์ž์˜ ์˜์‹์ €ํ•˜์— ์˜ํ–ฅ
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์ฃผ๋กœ Sosm > 320 .. DKA๋ณด๋‹ค HHS์—์„œ ํ”ํ•จ
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ECF osmolality and tonicity ์ฆ๊ฐ€ โ‡’ Shift water ICF -> ECF
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Loss of free water by vomiting
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High plasma acetone contribute to elevated osmolality

Electrolyte disturbance

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Osmotic diuresis ๋ฐ ๊ตฌํ†  ๋“ฑ์— ์˜ํ•ด GI tract์œผ๋กœ electrolyte loss์ผ์–ด๋‚จ.
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๊ฐ€์žฅ ์ค‘์š”ํ•˜๊ฒŒ ์ƒ๊ฐ๋˜๋Š” ๊ฒƒ์€ potassium
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potassium ์ „์ฒด ์–‘์€ ๋ถ€์กฑํ•˜๋‚˜, srum potassium ๋†๋„๋Š” ๋Œ€๊ฐœ ์ •์ƒ์ด๊ฑฐ๋‚˜ ์ƒ์Šน
Cell dehydration state์—์„œ ICF contraction
Solvent์ด๋™ -> K+์„ ๋Œ๊ณ  ๋“ค์–ด๊ฐ.
Insulin deficeicy
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DKA์—์„œ acidosis ๊ฐ€ hyperkalemia ์— ๊ธฐ์—ฌํ•˜๋Š” ๋ถ€๋ถ„์€ ์ ์Œ.
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