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N290 Seminar > DKA & HHS > Flashcards

DKA & HHS Flashcards

1
Q

what is DKA caused by?

A

caused by absence or a markedly inadequate amount of insulin that results in disorders in the metabolism of carbs, proteins, and fats

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2
Q

what are 3 main clinical features of DKA

A
  1. hyperglycemia
  2. dehydration & electrolyte loss
  3. acidosis
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3
Q

describe short patho of DKA

A
  • no insulin so the amount of glucose that goes into cells is reduced
  • because there’s a decrease in glucose, the liver will increase glucose production
  • then in order to rid body of excess glucose, kidneys will excrete it (with water and electrolytes)
  • osmotic diuresis (polyuria) leads to dehydration and electrolyte loss
  • lipolysis converts into free fatty acids and glycerol
  • free fatty acids are converted into ketone bodies by the liver
  • insulin would normally prevent ketones from occurring but because people with DKA have no insulin
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4
Q

are ketones acids or bases?

A

ketones are acids! with accumulation of acids it leads to metabolic acidosis

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5
Q

what are 3 main causes of DKA

A
  1. decreased or missed dose of insulin
  2. Illness or infection
  3. undiagonosed/untreated DM
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6
Q

which hormones promote glucose production?

A

glucagon, epinephrine, norepinephrine, cortisol and growth hormone

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7
Q

how do the hormones interfere with glucose utilization?

A

normally hormones enhance break down of triglycerides into free fatty acids and gluconeogenesis (leading to increased glucose and ketones)

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8
Q

list mnfts of DKA

A
  • hyperglycemia –> polyuria/polydipsia
  • orthostatic hypotension from intravascular volume depletion
  • ketosis and acidosis (GI symptoms will present)
  • kussmaul respirations
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9
Q

what BG level range could you find with someone with DKA?

A

16.6-44.4mmol/L

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10
Q

what lab value shows evidence of ketoacidosis?

A

low serum bicarbonate (0-15mmol/L) and low pH (6.8-7.3)

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11
Q

would you have low or high PCO2 and why?

A

you would have low PCO2 (respiratory compensation) which are kussmaul respirations to compensate for metabolic acidosis (short, deeper breathing), blowing off more CO2

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12
Q

in addition to treating hyperglycemia, what is management aimed at?

A

correcting dehydration, electrolyte loss, and acidosis

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13
Q

why is rehydration important?

A
  • maintains tissue perfusion
  • fluid enhancement increases glucose secretion by kidneys
  • monitor for FVE in elderly and those with renal/HF
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14
Q

what is the main electrolyte of concern with DKA?

A

potassium

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15
Q

what are factors of DKA that reduce serum K+ concentration?

A
  • rehydration (leads to increased plasma volume with subsequent decreases in K and increased excretion)
  • insulin admin which enhances movement of K from the ECF into cells
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16
Q

why must potassium be infused even if levels are normal?

A

because extracellular potassium drops during DKA

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17
Q

when would replacement of K be held?

A

only if hyperkalemia is present or if pt is not urinating

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18
Q

ketones accumulate in body as a result of what?

A

result of fat breakdown

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19
Q

how does insulin help with acidosis?

A

acidosis is reversed with insulin which inhibits fat breakdown, which stops acid buildup

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20
Q

when is the cue to stop IV insulin?

A

when the ketosis is resolved (you know this by having a normal anion gap)

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21
Q

at what BG level should IV dextrose be administered and why?

A

once its at 14mmol/L to avoid hypoglycemia

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22
Q

why is it crucial to flush the insulin solution through the entire IV infusion set and discard first 50ml?

A

because insulin molecules adhere to inner surface of IV infusion sets and can cause the initial fluid to cause a decreased concentration of insulin

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23
Q

what is monitored before potassium is administered?

A

urine output is monitored to prevent hyperkalemia

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24
Q

as DKA resolves and K+ replacement is decreased, what does the nurse ensure?

A
  • that there are no signs of hyperkalemia in ECG
  • lab values of K are normal or low
  • patient is urinating
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25
Q

what is HHS?

A

a serious condition in which hyperosmolarity and hyperglycemia predominate with alterations of the sensorium (sense of awareness)

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26
Q

does ketosis occur in both DKA and HHS?

A

usually only in DKA

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27
Q

what occurs with HHS? (quick patho)

A

lack of effective insulin (insulin resistance) leads to patient persistent hyperglycemia that causes osmotic diuresis (resulting in losses of water and electrolytes)

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28
Q

what is the typical onset of people with HHS

A

50-70 years old with no known Hx of DM or with mild T2DM

29
Q

what precipitating events can lead to HHS?

A

pneumonia, stroke, meds that exacerbate hyperglycemia or dialysis

30
Q

what is the Hx of someone with HHS ?

A

days to weeks of polyuria with adequate fluid intake

31
Q

what is the difference between DKA and HHS?

A 
DKA= ketosis and acidosis
HHS= NO ketosis and acidosis d/t difference in insulin levels
32
Q

is there insulin present in DKA

A

insulin is NOT present. Because of this, it promotes breakdown of fats which lead to production of ketones

33
Q

is there insulin present with HHS

A

insulin is present in small amounts and is too low to prevent hyperglycemia but high enough to prevent fat breakdown

34
Q

Mnfts of HHS

A
  • hypotension
  • profound dehydration (dry mm, poor skin turgor)
  • tachy
  • variable neurologic signs
  • bicarb level normal, BUN/creatinine elevated
35
Q

is onset slower or faster in HHS?

A

onset is SLOWER

36
Q

what are secondary signs of cerebral dysfunction for people with HHS

A

mental status changes, focal neurologic deficits, and hallucinations

37
Q

what mnft accompanies dehydration with HHS

A

postural hypotension

38
Q

what is the medical mgmt of HHS

A
  • fluid replacement (0.9% or 0.45%)
  • correction of electrolyte imbalances
  • insulin admin (not as much needed as for DKA b/c not reversing acidosis)
  • close monitoring of volume and electrolyte status
39
Q

what is nursing mgmt of HHS

A
  • close monitoring of vitals, fluid status and lab values
  • strategies to prevent injury r/t changes in pt sensorium secondary to HHNS
  • fluid status and urine output closely monitored
40
Q

what are the hallmarks of HHS

A
  • profound dehydration
  • marked hyperglycemia-variable degrees of neurological impairment
  • mild or no ketosis
41
Q

what are mortality predictors of HHS

A
  • age
  • degree of dehydration
  • hemodynamic instability (hypotension, absence of reflect tachy)
  • degree of consciousness
  • infection and Hx of cancer
42
Q

describe the patho of HHS

A
  • elevated levels of counterregulatory hormones initiate HHS by stimulating hepatic glucose production through glycogenolysis and gluconeogenesis
  • this leads to hyperglycemia, intracellular water depletion and subsequent osmotic diuresis
  • glycosuria causes greater loss of water leading to hyperosmolarity and dehydration
43
Q

why are elderly with T2DM at increased risk for HHS

A

because they often take dehydrating meds (diuretics)

44
Q

risk factors for HHS in children

A
  • morbid obesity
  • long term steroid use
  • gastroenteritis
  • black rate
  • acanthosis nigricans
  • fam HX of DM
45
Q

what levels are almost always elevated in HHS

A

creatinine, BUN and hct

46
Q

what is the four piece Tx approach to HHS

A
  • vigorous IV rehydration
  • electrolyte management
  • IV insulin
  • diagnosis and management of precipitating and coexisting problems
47
Q

what is the first and most important step in treating HHS?

A

aggressively replacing fluids

48
Q

why can total body potassium depletion be unrecognized in someone with HHS?

A

because initial K levels may be normal or high

49
Q

what causes GI symptoms in DKA? (anorexia, N+V, pain)

A

ketosis and acidosis

50
Q

what is the fruity breath of DKA r/t?

A

due to the elevated ketone bodies and acidosis

51
Q

how do you prevent DKA

A

OT more often (q1-4hrs), diet teaching, rehydration

52
Q

what’s important about rehydration in DKA

A
  • maintain tissue perfusion
  • increase low BP
  • enhances kidney excretion (excrete glucose and K/Na)
53
Q

what is the onset of DKA

A

rapid (<24hrs)

54
Q

what is the onset of HHS?

A

slower (over several days)

55
Q

what are the BG levels of someone with DKA

A

usually >13.9

56
Q

what are the BG levels of someone with HHS

A

usually >33.3

57
Q

are serum and urine ketones present or absent in both?

A

present in DKA and absent in HHS

58
Q

are serum bicarb levels present in DKA and HHS

A

decreased in DKA and normal in HHS

59
Q

are BUN and creatinine present in DKA and HHS

A

elevated in both

60
Q

is the mortality rate higher in DKA and HHS

A

much higher in HHS (10-40% rate in HHS)

61
Q

what is gluconeogenesis

A

makings glucose from proteins and fats

62
Q

what is the precipitating event of HHS

A

physiologic stress (infection, surgery, CVA, MI)

63
Q

what is the precipitating event of DKA?

A

omission of insulin; physiologic stress (infection, surgery, CVA, MI)

64
Q

what is the onset of HHS?

A

50-70 years old

65
Q

what is the arterial ph for DKA and HHS?

A

DKA is <7.3 and HHS is normal

66
Q

what is the clinical presentation of HHS?

A
  • hypotension
  • dry mucous membranes, poor skin turgor)
  • variable LOC, altered sensorium which can lead to seizures
67
Q

what system is the most affected by blood sugar levels

A

the neuro system

68
Q

how long do neurological systems take to resolve?

A

about 3-5 days

N290 Seminar (1 decks)

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