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Acute Care I - Spring 2017 > Module 5: DKA & HHS > Flashcards

Module 5: DKA & HHS Flashcards

1
Q

anabolic effects of insulin on liver

A
  1. promotes glycogen synthesis 2. promotes fatty acid synthesis
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2
Q

anabolic effects of insulin on adipose

A
  1. promote fatty acid uptake 2. promote triglyceride formation & storage
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3
Q

anabolic effects of insulin on muscle

A
  1. promote protein synthesis 2. promote glycogen synthesis
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4
Q

anticatabolic effects of insulin on liver

A

inhibits 1. glycogenolysis 2. gluconeogenesis 3. ketogenesis

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5
Q

anticatabolic effects of insulin on adipose

A

inhibits lipolysis

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6
Q

anticatabolic effects of insulin on muscle

A

inhibit proteolysis

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7
Q

criteria for DKA

A

glucose > 250; arterial pH < 7.35; positive serum ketones; increased anion gap (Anion gap = Na+ - (HCO3- + Cl-)

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8
Q

criteria for HHS (DM2)

A

glucose >600; arterial pH > 7.3; serum bicarb > 15; >320 mOsm/L

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9
Q

effective osmolarity?

A

Eosm = 2(Na + K) + Blood glucose/18 don’t use BUN b/c isn’t considered effective OSM b/c doesn’t create an osmotic gradient b/c can flow into /out of cell

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10
Q

mixed DKA & HHS?

A

pH 7.3 or serum bicarb < 15; positive serum ketones; Esom >320

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11
Q

different types of ketosis?

A

diabetic ketoacidosis; starvation ketosis; alcoholic ketoacidosis; ketogenic (high fat) diets

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12
Q

symptoms of hyperglycemia?

A

polyuria; polydipsia; nocturia; polyphasic; weight loss; vomiting; abdominal pain; fatigue; confusion –> coma; blurred vision; vulvovaginitis; poor wound healing; asymptomatic

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13
Q

causes of polyuria

A

hyperglycemia; hypokalemia; hypercalcemia; renal disorders; psychogenic polydipsia; neurogenic/nephrogenic diabetes insipidus; drugs (diuretics, lithium, demeclocycline)

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14
Q

precipitating factors for DKA

A
  1. new onset DM1 2. omission of insulin therapy 3. acute illness (UTI, PNA, medication, MI, CVA, trauma, hyperthyroidism, intra-abdominal catastrophe)
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15
Q

risk factors for DKA at onset

A

age < 12; no first degree relative with diabetes; lower SES; high dose glucocorticoids/atypical antipsychotics; poor access to medical care; uninsured

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16
Q

why insulin omission

A

weight control, fear of hypoglycemia, teenage rebellion

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17
Q

cocaine use and DKA

A

14% of all DKA admissions more frequent admissions for DKA, more likely to miss taking insulin prior to admission, higher admission glucose

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18
Q

risk factors for DKA leading to ER visit/hospitalization

A

A1C; african american; female; psychiatric disorder; under insured; limited self care skills; illness; substance abuse

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19
Q

physical exam for DKA

A

temperature; tachycardia; orthostatic BP/hypotension; dry mucosa; fruity odor of breath; abdominal pain; drowsiness–>coma; heme positive stool?

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20
Q

why heme positive stool?

A

gastric bleeding from retching, from vomiting, Hct is concentrated d/t increased urination, will start to dilute once return fluids so don’t necessarily thing with drop in Hct and heme positive stool that its a GI bleed

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21
Q

what mOsm do you have decreased LOC

A

if decreased level of consciousness with eosm < 320 look for other source of change in mental status

generally see decreased LOC with mOsm > 320

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22
Q

what does corrected sodium tell you?

A

helps evaluate severity of dehydration use measured Na for anion gap, not the calculated corrected Na.

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23
Q

anion gap acidosis

A

ketoacidosis, lactic acidosis, chronic renal failure, salicylate, methanol, ethylene glycol, paraldehyde

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24
Q

what is winter’s formula?

A

if the equation doesn’t equal the resulted PCO2 then you have to think of something besides just a standard acid base imbalance

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25
Q

causes for mixed acid base issues

A

respiratory alkalosis - PNA; metabolic alkalosis - vomiting, diuretics

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26
Q

treatment goals for DKA

A

rehydrate; correct hyperglycemia; reverse ketosis; replace electrolytes;

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27
Q

how fast should you change serum osmolality in DKA?

A

3 mOsm/kg H2O/hour goal replace ~50% deficit in 8 hours

28
Q

fluid choice for DKA replacement?

A

NS then NS or 1/2 NS based on clinical assessment/volume status/urine output/labs

29
Q

which takes longer to clear, ketones or hyperglycemia

A

ketones

30
Q

when do you start giving D5W in DKA?

A

when plasma glucose reaches 200 mg/dL; administer D5W at 100-200 mL/hour; giving D5W allows us to keep the insulin drip at a higher rate and to get rid of ketones faster.

31
Q

concerns for insulin and K+?

A

K+ should be > 3.3 before giving insulin. bolus is optional: 0.1 units/kg regular insulin 0.1 units/kg/hr regular insulin as continuous infusion or 0.14 units/kg/hr if NO bolus decrease rate of insulin infusion when glucose is 200. goal is to decrease glucose ~50-75 mg/dL/hr (if it goes to fast worry about osmotic shifts especially in the brain)

32
Q

do you give bicarbonate for DKA?

A

not routinely recommended. no improvement in outcome pH>6.9 but no studies evaluating outcome with pH<69

33
Q

what happens to phosphate with DKA

A

normal to increased at presentation. decreases with treatment

34
Q

how do you treat low phosphate?

A

with potassium phosphate only if low

35
Q

complications of treating for low phosphate

A

hypocalcemia, metastatic calcification, hypomagnesemia

36
Q

do you replace low calcium in DKA?

A

only if symptomatic w/ calcium gluconate

37
Q

what lab studies you order in DKA?

A

CBC, CMP, ABG, serum/urine ketones (for initial diagnosis, likely will go up when getting better), Q1H glucose, Q1-2H K+, Q2-4 hr electrolytes, calcium, phosphate, magnesium culture of blood, urine, sputum as indicated (to figure out infection as the precipitating factor to DKA)

38
Q

what do you trend to know when to stop iv insulin?

A

bicarbonate, stop when bicarb is > 18 & patient tolerating PO

39
Q

complications of treatment?

A

hypoglycemia, hyponatremia/hypernatremia, hypokalemia, hyperchloremia, hypotension (you want to correct this first before giving IV insulin), cerebral edema

40
Q

what happens during recovery of DKA?

A

hyperchloremic metabolic acidosis. loss of ketones in urine & loss of buffering capacity Cl- is reabsorbed leading to hyperchloremic acidosis will likely resolve on its own over a couple of days

41
Q

most feared complication of DKA

A

cerebral edema. most common < 5 year old; rare in patients > 20; occurs only 1% of the time & more common in newly diagnosed diabetics

42
Q

why do you do hourly neuro checks?

A

cerebral edema - can have headache; impaired LOC; bradycardia; elevated blood pressure; urinary incontinence; vomiting; unequal/fixed dilated pupils

43
Q

risk factors for cerebral edema with DKA

A
  1. treatment with HCO3 2. bad initial pCO2 3. bad initial BUN (r/t dehydration) not r/t rate of sodium or glucose correction
44
Q

when should you start long active sub Q insulin?

A

start subQ2-3 hours prior to stopping IV insulin IV insulin only lasts 20 minutes in blood stream

45
Q

what does basal insulin do?

A

controls glucose and ketone production between meals and overnight; withholding basal insulin in insulin deficient patients results in rapid rise in glucose and DKA should be about 50% of daily insulin requirements

46
Q

what does prandial insulin do?

A

insulin required to cover meals; limits post prandial hyperglycemia; 10-20% of total daily insulin requirement at each meal

47
Q

what does correction/supplemental insulin do?

A

used to correct hyperglycemia; used in combination w/ long acting insulin; should be adjusted based on recent glucose levels, previous insulin requirements & changes in patient’s medical condition

48
Q

how do you calculate starting dose of basal insulin?

A

weight based, 50/50 basal/nutritional. ranges from 0.3 with malnourished, no h/o DM, cognitive impairment to 0.6 units/kg/day to DM2, obese & on glucocorticoids

49
Q

what is the goal blood glucose?

A

140-180

50
Q

how do you figure out basal insulin based on IV insulin infusion?

A

project 24 hour requirement based on most recent 4 hour period, do 80% of TDD; if not eating when receiving the IV insulin multiply that by 2

51
Q

equation for correction/supplemental rapid acting insulin?

A

=1800/TDD

52
Q

do studies show benefit w/ SSI?

A

nope! increase risk of hypoglycemia and hyperglycemia when used alone; it’s not proactive - it’s responding to hyperglycemia; generally not adjusted based on glucose levels & clinical status

53
Q

flow diagram for hyperglycemic hyperosmolar state

A
54
Q

when does hyperglycemic hyperosmolar state tend to happen

A

new/unrecognized diabetes; neglected diabetes; medications; concurrent illness; volume depetion; limited access to fluids; impaired thirst perception

55
Q

what are some drugs causing hyperglycemia

A

glucocorticoids; cyclosporine/tacrolimus; sirolimus; everolimus; protease inhibitors, clozapine, TKI, bevacizumab, diuretics

56
Q

predisposing factors for HHS

A

female; acute infection, NH resident; dementia

57
Q

HHS clinical manifestations

A

polyuria, polydipsia, dehydration, neurological abnormalities; heme positive stool; normal temperature; lethargy & disorders of sensorium

58
Q

HHS treatment

A

fluids, insulin (not as critical since not producing ketones like DKA)

59
Q

reasons for early mortality in HHS

A

sepsis, shock, underlying illness,

60
Q

causes of late mortality in HHS

A

thrombosis d/t dehydration, hypercoagulable state

61
Q

HHS management

A

depends on reason for HHS

safest to start on sub Q when stopping IV insulin

depending on other medical conditions and if total insulin dose is <30 might be able to switch to oral diabetic medicaion

62
Q

considerations for non-insulin therapies

A

sulfonylureas can prolong hypoglycemia

metformin contraindicated w/ decreased renal function, use of iodinated contrast dye, and any state of poor tissue perfusion

thiazolidinediones are associated w/ edema and CHF

GLP1 can cause N/V & act by lowering post prandial glucose so less effective is patient is NPO

SGLT2 may cause hyperkalemia and hypovolemia b/c it increases glucose in the urine

63
Q

sick day management for diabetics

A

take diabetes medication even if eating less

check glucose at least 4 times a day, more often for severe illness

check ketones if glucose >250

push fluids (sugar free if able to eat, w/ sugar if can’t eat)

call health care provider: presistent vomiting/diarrhea; BS > 250 x 2 checks of BS does not decrease w/ extra insulin; moderate/large ketones

64
Q
A
65
Q

what is stress hyperglycemia?

A

no prior history of diabetes; inpatient hyperglycemia (check A1C to see where they’ve been); follow up testing for DM w/in 1 month of hospital discharge

66
Q

adrenergic symptoms of hypoglycemia

A

palitations; diaphoresis; anxiety; agitation; hunger; tremor; pallor

67
Q

neuroglycopenic symptoms of hypoglycemia

A

fatigue/listlessness; inappropriate behavior; cognitive impairment; focal neurologic deficits; seizure; loss of consciousness; death

Acute Care I - Spring 2017 (10 decks)

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