DKA, HHS Flashcards

1
Q

What are two of the most serious acute complications of DM

A

DKA and HHS

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2
Q

DKA involves

A

Ketoacidosis and hyperglycemia

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3
Q

HHS involves

A

more severe hyperglycemia without ketoacidosis

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4
Q

DKA is more common in people

A

under 65

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5
Q

DKA is associated with which type of DM

A

1

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6
Q

can DKA occur with type 2?

A

under extreme conditions

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7
Q

HHS is mostly associated with which type of DM

A

2

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8
Q

HHS is more common in people aged

A

over 65

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9
Q

extracellular concentration of glucose is regulated by

A

insulin and glucagon

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10
Q

when serum glucose rises glucose enters

A

the pancreas initiating insulin release

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11
Q

insulin restores normal glycemic levels by

A

diminishing hepatic glucose production
decreasing glycogenolysis and gluconeogenesis
increasing uptake by skeletal muscle and adipose tissue

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12
Q

insulin deficiency and/or resistance is more severe in

A

DKA than HHS

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13
Q

hyperglycemia

A
  • serum glucose can exceed 1000
  • glucose typically below 800 often 350-450 (these patients often present earlier with symptoms of ketoacidosis rather than HHS, tend to be younger and have higher GFR)
  • glucosuria
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14
Q

insulin deficiency and resistance cant get glucose into cells so the body uses

A

fat for energy (enhanced lipolysis in DK)

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15
Q

lipolysis of peripheral fat stores releases

A

free fatty acids and glycerol

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16
Q

fatty acids are transported to

A

liver and become acitvated

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17
Q

activated fatty acids are converted to ____, and enter ketogenic metabolic pathway forming ____.

A

acetyl-CoA, ketone bodies

18
Q

accumulation of ketone bodies causes a drop in

A

pH

19
Q

DKA typically presents with

A

an elevated anion gap metabolic acidosis

20
Q

elevated anion gap metabolic acidosis is caused by

A

production and accumulation of ketones

21
Q

severity of acidosis and increase of anion gap factors is caused by

A

rate and duration of ketoacid production
rate and metabolism of ketoacids
rate and loss of ketoacid anions in urine

22
Q

plasma osmolality is always elevated in

A

DKA, HHS

23
Q

hyperglycemia pulls water out of cells, expanding ECF thus reducing

A

plasma sodium (dilutional hyponatremia)

24
Q

glucosuria causes osmotic diuresis leading to

A

excretion of sodium, potassium and water

25
Q

Both DKA and HHS present with total decreased

A

potassium levels, r/t increased urinary loss and GI loss

26
Q

serum potassium is usually high related to

A

hyperosmolality and insulin deficiency
increased plasma osmolality causes water to move out of cells and potassium into ECF, insulin normally promotes potassium uptake by cells. Lack of insulin contributes to increased levels.

27
Q

increase in hydrogen concentration is seen with

A

acidosis
(hydrogen moves into cell, K+ moves out, electrical neutrality is restored inside cells, and temporary correction of pH)
process reverses as the pH returns to normal
if kidneys are working, they excrete K+, can cause depletion of K+

28
Q

precipitating factors of DKA and HHS

A
  • Infection (pneumonia or UTI) w/ w/o insulin correction
  • acute major illness or inflammation (MI, CVA, Sepsis, Pancreatitis)
  • new onset DM 1, (DKA common presentation)
  • drugs that affect carb metabolism (glucocorticoids, thiazide, dialectics)
  • SLG-2 inhibitors (DM 2 tx, DKA)
  • cocaine ( DKA)
  • poor insulin regimen
29
Q

DKA clinical presentation

A
  • rapid onset (24 hours)
  • polyuria, polydipsia
  • N/V, abdominal pain
  • volume depletion (poor skin turgor, dry oral mucosa, -tachy, hypotension)
  • fruity odor to breath
  • kussmaul respirations
30
Q

HHS clinical presentation

A

insidious (several days)
polyuria, polydipsia, WT loss
as glucose increases lethargy, obtunded, coma
signs of volume depletion similar to DKA

31
Q

treatment of DKA and HHS

A

fluid replacement
correction of electrolyte imbalances
insulin by infusion
sodium bicarb (DKA with metabolic acidosis, pH <7.2)

32
Q

dextrose can be added to a saline solution when serum glucose falls below

A

200 mg/dl (DKA) if the patient still has an anion gap)

while pt on continuous insulin infusion

33
Q

the DKA hyperglycemic crisis is resolved when

A
ketoacidosis resolves (anion gap is closed)
and patient is able to eat and can transition back to SQ insulin
34
Q

the HHS hyperglycemic crisis is resolved when

A

patient is mentally alert and plasma osmolality has dropped to 315
and patient is able to eat and can transition back to SQ insulin

35
Q

DKA is a condition of ketones in

A

the blood and metabolic acidosis leading to anion gap, and hyperglycemia associated with insulin deficency.

36
Q

what are common causes of DKA?

A

lack of adherence to insulin and/or physiologic stress

37
Q

how do you treat DKA

A

treat volume depletion rapidly with 0.9% NS, supplements K+ as needed, IV infusion of insulin

38
Q

what do you monitor in DKA?

A

glucose, electrolyte levels, anion gap

39
Q

HHS is defined by

A

marked hyperglycemia, dehydration, electrolyte imbalance, and hyperosmolality

40
Q

which has a higher mortality rate HHS or DKA?

A

HHS

41
Q

What can cause HHS

A
pneumonia
UTI
insulin deficiency
inflammatory conditions
MI
Stroke
Severe dehydration
drugs
42
Q

how do you treat HHS

A

treat volume depletion with rapid NS
IV insulin
Correct electrolyte imbalance