DKA/HHS Flashcards

1
Q

what does DKA involve?

A

ketoacidosis and hyperglycemia

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2
Q

what does HHS involve?

A

hyperglycemia without ketoacidosis

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3
Q

specifics of DKA

A

–more common in people under 65
–associated with type 1 diabetes
–can occur in type 2

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4
Q

specifics of HHS

A

–mostly with T2DM
–more common in individuals over 65

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5
Q

normal response to hyperglycemia

A

–extracellular concentration of glucose regulated by insulin and glucagon
–when serum glucose rises, glucose enters pancreas initiating insulin release
–insulin restores normal glycemic levels by (1) diminishing hepatic glucose production and (2) increases glucose uptake by skeletal muscle and adipose tissue

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6
Q

causes of hyperglycemia

A

–insulin deficiency and/or resistance
–glucagon excess
–increased catecholamines
–increased cortisol

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7
Q

BG for HHS

A

can exceed 1000 mg/dL

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8
Q

BG for DKA

A

generally below 800 mg/dL, often 350-450

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9
Q

other symptoms of DKA

A

–often present earlier with symptoms of ketoacidosis rather than hyperosmolality
–tend to be younger and have higher GFR

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10
Q

ketone production

A

–can’t get glucose into cells so body uses fat for energy
–lipolysis of peripheral fat stores releases free fatty acids and glycerol
–fatty acids are transported to liver and become “activated”
–activated fatty acids are converted to acetyl-CoA and enter ketogenic metabolic pathway forming “ketone bodies”
–accumulation of ketone bodies causes a drop in pH

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11
Q

anion gap specifics with DKA/HHS

A

–DKA
–caused by production and accumulation of ketones

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12
Q

severity of acidosis and increase of anion gap factors include:

A

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

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13
Q

plasma osmolality with DKA/HHS

A

–hyperglycemia pulls water out of cells, expands ECF, reducing plasma sodium
–glucosuria causes osmotic diuresis leading to excretion of sodium, potassium, and water

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14
Q

potassium with DKA/HHS

A

–both have total decreased potassium levels: increased urinary loss and GI losses
–serum potassium is normal to high due to hyperosmolality and insulin deficiency

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15
Q

cause of increased serum potassium in DKA/HHS

A

–increased plasma osmolality causes water to move out of calls and potassium also moves into ECF
–insulin normally promotes potassium uptake by the cells so lack = increased levels

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16
Q

cellular compensation in DKA

A

INCREASE in H+ IN ACIDOSIS
–H+ move into cell
–more positively charged ions in cell
–K+ moves out of cell
–electrical neutrality is restored inside cell
–temporary correction of pH
process will reverse as pH returns to normal
–if kidneys are working, they will excrete excess K+ –> depletion

17
Q

precipitating factors for DKA/HHS

A

–infection without insulin adjustment
–acute major illness or inflammatory process
–new onset T1DM = DKA common
–drugs that affect carb metabolism (glucocorticoids, thiazide diuretics)
–use of SGLT2 inhibitors
–cocaine use or substance abuse
–poor compliance with insulin regimen or faulty SQ insulin infusion devices

18
Q

symptoms of DKA

A

–rapid onset (over 24 hours)
–polyuria, polydipsia
–GI effects
–may have neuro effects
–volume depletion (decreased skin turgor, dry oral mucosa, tachy, hypotension)
–fruity odor of breath
–Kussmaul’s respirations

19
Q

symptoms of HHS

A

–insidious
–polyuria
–polydipsia
–weight loss
–lethargy, obtunded, coma (as glucose increases)
–signs of volume depletion like DKA

20
Q

treatment of DKA/HHS

A

–fluid replacement
–correction of electrolyte imbalance
–admin of insulin by infusion
–sodium bicarb
–dextrose may be added to NS when glucose < 200 if patient still has anion gap while still on continuous insulin drip

21
Q

when is hyperglycemic crisis resolved?

A

–DKA = ketoacidosis has resolved
–HHS = patient is mentally alert and plasma osmolality has dropped to 315
–patient is able to eat and can transition back to SQ insulin

22
Q

what is DKA overall?

A

condition of ketones in the blood, metabolic acidosis leading to anion gap, and hyperglycemia associated with insulin deficiency