Ketoacidosis Flashcards

1
Q

Rapid acting insulin

A

Lispro
Onset = 15-30 minutes
Peak = 30-90 minutes
Duration = 3-5 hrs

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2
Q

Long acting insulin

A

Glargine
Onset = 1-1.5 hrs
Duration = 24 hrs
NO PEAKS

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3
Q

Short acting

A

Regular
Onset = 30-60 min
Peak = 2-5 hrs
Duration = 5-8 hrs

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4
Q

Intermediate

A

NPH
Onset = 1-2 hrs
Peak = 4-12 hrs
Duration = 18-24 hrs

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5
Q

How does insulin effect menstrual cycle

A

Insulin stimulates gonadotropin hormone

- so, low insulin –> low gonadotropin hormone –> less FSH and LH –> dysregulation of menstrual period

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6
Q

Type 1 diabetes genetics

A

HLA-DR3 and DR4 –> 90% of Caucasians with diabetes have those haplotypes
Type IV hypersensitivity –> T cell destruction of pancreatic beta cells –> low insulin –> hyperglycemia

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7
Q

Mechanism of Insulin

A

Insulin binds to its receptor (tyrosine kinase) → tyrosine phosphorylation of receptor → glycogen, lipid, and protein synthesis as well as increased expression of GLUT-4 receptor for glucose uptake into cells (adipose tissue and skeletal muscle)

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8
Q

K+ Homeostasis

A

High K+ –> increased ROMK and BK channels in Principal Cells, increased Na/K ATPase activity in all cells
Low K+ –> decreased ROMK and BK channels in Principal Cells, increased K/H ATPase in alpha-intercalated cells

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9
Q

Causes of moving K into cells

A

Hyperinsulinemia
Increased catecholamines
Metabolic alkalosis

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10
Q

Causes of moving K out of cells

A

Insulin deficiency

Metabolic acidosis

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11
Q

Tm of glucose

A

Tm is the maximum amount of glucose the kidney can reabsorb. Once the kidney reaches its maximum, glucose can’t be reabsorbed any further because the channels are saturated –> glucosuria

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12
Q

Respiratory compensation of metabolic acidosis

A

Kussmaul respirations

rapid shallow breathing –> blow off CO2 –> shift equation toward CO2 and away from H+

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13
Q

Respiratory compensation of metabolic alkalosis

A

Hypoventilation

- decrease in breathing –> increase CO2 –> shift equation toward H+ and away from CO2

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14
Q

Most common precipitating factor of DKA

A

Not taking insulin

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15
Q

Stressors effects on precipitating DKA

A

Stressors cause release of Epi –> blocks insulin action and stimulates glucagon –> decrease utilization of glucose in periphery and increased gluconeogenesis –> severe hyperglycemia –> osmotic diuresis and dehydration

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16
Q

Clinical presentation of DKA

A

fatigue, N/V, abdominal pain, fruity odor breath, Kussmaul breathing –> all can lead to decrease cerebral perfusion and coma

17
Q

2nd major effect of insulin deficiency

A

increased ketogenic machinery
- stimulate lipoprotein lipase –> increased fatty acid beta oxidation –> lots of ketone bodies –> too many for kidney (ketonemia, ketonuria) –> metabolic ketoacidosis