Hypoglycemia Flashcards

1
Q

reduced metformin clearance is worsened by

A

lactic acidosis, metabolic acidosis, renal impairment (AKI), poor perfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is the relationship between metformin clearance and creatinine clearance?

A

proportionally decrease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

metformin toxicity symptoms

A

non-specific
ab pain, N/V, malaise, myalgia
blindness, hypothermia, hypotension, respiratory insufficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

mechanisms of metformin metabolic acidosis

A
  1. interfere with cellular aerobic metabolism by inhibiting ETC, thus shifting to anaerobic metabolism –> lactic acidosis
  2. suppresses hepatic gluconeogenesis from pyruvate, decreases hepatic pH and lactate uptake –> lactic acidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

metformin toxicity treatment

A

ABCDs, vasopressors, fluids
Extracorporeal treatment (intermittent hemodialysis preferred)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

When is extracorporeal treatment recommended for metformin toxicity?

A
  1. lactate concentration > 20 mmol/L
  2. pH =< 7
  3. failure of standard supportive measures
  4. comorbid conditions - shock, liver/kidney failure, decreased consciousness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How long should ECTR be done?

A

until lactate conc < 3 mmol/L
AND
pH > 7.35

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

insulin toxicity management

A

initial bolus (D10W at 75 mL/hr and titrate)
maintenance infusion (D5W or D10W)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

how to proceed transitioning off dextrose in insulin toxicity management?

A

consider measuring C-peptide (bc insulin will not be accurate)
or trial octreotide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

target BG range for maintaining euglycemia

A

100-150 mg/dL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

when to consider central venous access

A
  1. dextrose conc greater than or equal to D10W
  2. large volume administrations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what to monitor for peripheral

A

glucose every 30 min to 1 hr initially, then less frequently
serum phosphate levels
serum potassium levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

maximum peripheral dextrose concentrations (IV bolus)

A

adult = D50W
children = D25W
infants = D10W

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

which hypoglycemia causing agents are highly protein bound and cannot be removed via dialysis?

A

sulfonylurea (glimepiride, glipizide, glyburide)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

sulfonylurea MoA

A
  1. inhibit K+/ATP channels on beta cells –> prevents efflux of K
  2. cellular depolarization
  3. calcium influx via opening of Ca channels
  4. insulin release
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

how does sulfonylurea toxicity cause prolonged hypoglycemia?

A

long duration of action causes prolonged cell depolarization, thus prolonged insulin release

17
Q

in sulfonylurea toxicity, how long is the delayed onset of hypoglycemia

A

1st gen = up to 48 hrs
2nd gen = up to 24 hrs

18
Q

sulfonylurea toxicity: further insulin release after dextrose infusion can cause

A

rebound hypoglycemia

19
Q

sulfonylurea toxicity causes failure of counterregulatory mechanisms such as

A

adrenalin, cortisol, growth hormone, glucagon

20
Q

sulfonylurea toxicity management

A

ABCDs, activated charcoal, dextrose (only for correction), octreotide (for maintenance)

21
Q

octreotide MoA

A

mimics somatostatin, inhibits release of insulin, glucagon, secretin, motilin by decreasing cytoplasmic calcium

22
Q

octreotide dosing

A

50 mcg as single dose SUBQ/IV
repeatable every 6 hours

23
Q

octreotide dosing for refractory hypoglycemia

A

continuous infusion up to 125 mcg/hr

24
Q

when to use octreotide

A

when euglycemic and high risk for prolonged, delayed, or rebound hypoglycemia

25
Q

octreotide AE

A

N/V/D, ab pain, injection site pain, sinus bradycardia, hypertension, cholelithiasis, necrotizing enterocolitis, glucose dysregulation

26
Q

octreotide monitoring

A

observe patient up to 24 hrs after last dose
if asymptomatic, observe in hospital 12-24 hrs
do not discharge pt at night

27
Q

conditions that cause hypoglycemia

A

hepatic cirrhosis, chronic kidney disease, alcoholism, sepsis, burns, AIDS, Addison’s Disease, sarcomas/carcinomas

28
Q

xenobiotics that cause hypoglycemia

A

beta blockers, ethanol, fluoroquinolones, GABA agonists, haloperidol, MAOis, salicylates, sulfonamides

29
Q

glucagon dosing

A

1 mg IM/IV/SUBQ

30
Q

glucagon AE

A

N/V (IV more than IM)
adrenergic surge - tachycardia, hypertension

31
Q

dextrose bolus dosing

A

0.5-1 g/kg IV bolus

32
Q

maximum peripheral dextrose bolus concentration (adults and pediatrics)

A

D10W

33
Q

rule of 15

A

15 g of glucose intake, wait 15 min, recheck blood glucose
improvement seen in 15 minutes, if not, repeat

34
Q

risk factors of hypoglycemia

A

age over 65
polypharmacy (for diabetes, coingestions)
frequent hospitalizations
long-acting agents
impaired drug clearance

35
Q

in hypoglycemia, BG level is

A

< 60 mg/dL

36
Q

symptoms of hypoglycemia

A

decreased alertness, fizziness, confusion, seizures, tachycardia, pallor, bizarre behavior

37
Q

ABCDs

A

airway, breathing, circulation, disability, exposure