DKA/HHS Flashcards

1
Q

DKA

A

ketones in blood
Metabolic acidosis – anion gap
Hyper glycemia with insulin deficiency

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2
Q

Who is DKA more common in?

A

under 65 years
Type one diabetes

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3
Q

HHS

A

Marked hyperglycemia
Dehydration, electrolyte imbalance
Hyper osmolality
No ketoacidosis

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4
Q

Who does HHS occur more in?

A

over 65
Type two diabetes

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5
Q

response to hyperglycemia

A

Extracellular concentration of glucose is regulated by insulin and glucagon

When serum insulin increases glucose goes to the pancreas to initiate insulin release

Insulin restores normal glucose by decreasing hepatic production, gluconeogenesis, glycogenolysis

Increased glucose uptake by skeletal muscles and Adipose tissue

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6
Q

Patho of hyperglycemia

A

Decreased insulin or resistance

Increased catecholamines and cortisol – increased hepatic production

Dehydration and electrolyte abnormalities

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7
Q

hyperglycemia with HHS

A

Serum glucose greater than 1000

Glucosuria results from osmotic diuresis

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8
Q

hyperglycemia with DKA

A

Serum glucose less than 800, 350 to 450

Presents earlier with symptoms of ketoacidosis

Tends to be with younger patients with increased GFR

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9
Q

ketone production

A

Insulin deficiency in resistance – cells. Use fat for energy

Lipolysis of peripheral fat stores, releases free fatty acids and glycerol

free fatty acids go to the liver to become activated

Activated free Fatty acids convert to acetyl coA– ketone bodies

Ketone bodies decrease pH – metabolic acidosis

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10
Q

why doesn’t ketone production occur with HHS?

A

Patient still can produce some insulin to minimize lipolysis

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11
Q

anion gap

A

Occurs with DKA

Caused by production and accumulation of ketones

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12
Q

what is the severity of acidosis within anion gap depend on?

A

Rate and duration of keto acid production

Rate of metabolism of keto acids

Rate of loss of ketoacid anions in urine

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13
Q

is plasma osmolality increased or decreased with elevated glucose?

A

Increased

Hyperglycemia pulls water out of cells results in decreased plasma, sodium-dilutional hyponatremia

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14
Q

how is plasma osmolality affected by glycosuria?

A

Decreased from osmotic diuresis

Excretion of sodium, potassium, water

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15
Q

potassium

A

Decreased with both DKA & HHS

Increased urinary loss, G.I. loss

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16
Q

Cellular compensation

A

H+ moves into the cell
K+ moves out of the cell

17
Q

precipitating factors

A

Infection – pneumonia, UTI
Acute major illness – MI, CVA, sepsis, pancreatitis
New onset type one diabetes, DKA
Drugs – glucocorticoids, thiazide, diuretics
SLG T2, inhibitors
Cocaine/substance use
Poor compliance with insulin regimen

18
Q

DKA s/sx

A

rapid, 24 hours
Polyuria, polydipsia
N/V/abdominal pain
Fruity odor breath **
Kussmaul respirations **
Neuro effects
Decrease volume – decrease skin turgor, drymucosa, tachycardia, hypotension

19
Q

HHS s/sx

A

insidious – several days
Polyuria, polydipsia
Decreased weight

As glucose increases, – lethargy, obtunded, coma**

s/sx fluid volume deficit

20
Q

treatment

A

Fluid replacement, rapid-isotonic saline
correct fluid and electrolyte imbalance
Administer insulin by infusion

Sodium bicarb – DKPH less than 7.2

Dextrose added to fluids, if glucose less than 200 with anion gap

21
Q

how to know if DKA is resolved

A

Keto acidosis is gone
Anion gap closed

Monitor fluid and electrolyte, glucose, anion gap

22
Q

how to know if HHS is resolved

A

Patient is mentally alert
Plasma osmolality greater than or equal to 315

Patient is able to eat in transition to sub Q insulin