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8 Cards in this Set

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glucose released into cidrculation comes from what?
1. Glycogenolysis-from liver
2. Gluconeogenesis-
*glucose syntehsis de novo from liver and kidney
glucose uptake in postabsorptive & postprandial states
Post-absorptive:
-glucose uptake in insulin-independent tissues (brain)

Post-prandial:
-glucose uptake in insulin-dependent tissues
(SkM & adipocytes)
-SkM: glucose used to synthesize glycogen or it enters anaerobic glycolytic path
-adipocytes: glucose converted to glycerol and used to syn. TG
direct & indirect pathways
Direct Pathway:
-hepatic glycogen made directly from ingested glucose from meal load

Indirect pathway:
-hepatic glycogen made from glucose derived from gluconeogenesis
what are the elecrolyte imbalances in DKA?

why does this occur?
-intracellular K+ depleted d/t transcellular shifts d/t:

1. acidosis
2. excessive dehydration
3. protein catabolism
4. secondary hyper-ALDO
abnl levels in DKA?
low intracellular K
(high/nl plasma K+)
ph<7.3
HCO3 < 15

incr BUM
***Tx DKA
A. First: normal saline (0.9% NaCl)

*goal=restore vital signs!

For first 1-2 hrs:
*Adults: 500-1000 ml/hr
*Adolescents: 500 ml/m2 per hr

B. After 1-2 liters of isotonic fluid, change to hypotonic fluid (0.45% NaCl)
[Goljan: b/c you peed out hypotonic fluid [glucose + WATER], so replace with hypotonic fluid)

C. When plasma glucose <200,
add 5% dextrose to prevent hypoglycemia
*insulin administration must continue to overcome insulin resistance of DKA

D. Total body K+ stores are depleted (although plasma K may be low, nl, or high)
==>EKG can show:
-low voltage T waves
-U waves (hypo-K)
-peaked T waves (hyper-K)

*Replacement of K is guided by plasma levels:
K<3 ==>40 mEq/h
3<K<6==>10
K>6 ==>discontinue

*only give sodium bicarb if:
-initial pH<7.1
-inadequate resp compensation

*Insulin--do not stop insulin while pt is acidotic!!
-initial dose of regular insulin=0.25 unit/kg
-continueous regular insulin IV at 0.1 u/kg/h
does DKA occur in DM 2?
rarely
pH and bicarb levels in "mild DKA"
pH>7.3
bicarb>15