DKA PBL Flashcards

1
Q

K+ status in DKA

A

[K+]serum is elevated but total body K+ is depleted due to osmotic diuresis and sometimes emesis

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2
Q

What causes elevated [K+]serum in DKA?

A
  1. H+/K+ buffering: cells try to buffer acidosis by taking up H+, but have to eject K+ in order to maintain charge balance
  2. Decreased Na+/K+ ATPase activity: insulin activates Na+/K+ ATPase, without it K+ cannot be pumped into cells → leaked back into interstitium → peritubular capillaries
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3
Q

Tx of K+ status in DKA

A

monitor carefully

[K+]serum will drop when Tx is initiated

supplement as needed

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4
Q

Why does [K+]serum decrease when DKA Tx is initiated?

A
  1. Insulin pushes K+ into cells by upregulating activity of Na+/K+ ATPase
  2. H+/K+ buffer is reversed, H+ is put back into plasma and K+ is put back into cells
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5
Q

Carrier for Acyl-CoA into mitochondrial matrix

A

carnitine shuttle

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6
Q

ABG findings in DKA

A

decreased HCO3-

decreased pCO2

elevated H+

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7
Q

Why is HCO3 low in DKA

A

Le Chatelier’s principle:

H2O + CO2 ⇔ H2CO3 ⇔ H+ + HCO3-

you push this equation left by adding protons

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8
Q

Why is pCO2 low in DKA?

A

elevated H+ leads to increased respirations

→ blow off more CO2 than you would normally

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9
Q

Anion gap equation

A

[Na+] - ([Cl- + HCO3-])

normally 8-10

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10
Q

Osmotic diuresis

A

high amounts of solute in tubule lead to increased water retention in tubule

→ pee it out

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11
Q

Tm glucose

A

transport maximum for glucose

normally Glc completely reabsorbed in proximal tubule, but when Tm is reached then you lose Glc in the urine

⇒ osmotic diuresis

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12
Q

2 HLA genes associated w/ T1D

A

HLA-DR3

HLA-DR4

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13
Q

Insulin _____

lispro

aspart

glulisine

A

rapid acting insulins

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14
Q

Insulin _____

glargine

detemir

A

long-acting insulins

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15
Q

What type of receptor is insulin receptor?

A

tyrosine kinase

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16
Q

1˚ gain

vs

2˚ gain

A

1˚: positive reasons to use Tx → not sick

2˚: reasons patient would not take insulin, ie attention from boyfriend and others