Insulin used in diabetes Flashcards

1
Q

insulin sources

A

recombinant human insulin could be produced in large quantities using cDNA found in E. Coli, humulin (Lilly), and in transformed yeast, novolin (Novo Nordisk)

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1
Q

standard unit of insulin

A

100 units/mL

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2
Q

how many units/mg of insulin?

A

28 units/mg

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3
Q

unitage of humulin R

A

500 units/mL

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4
Q

onset/duration of lispro (humalog)

A

15 minutes / 6-8 hours

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5
Q

onset/duration of aspart (novolog)

A

15 minutes / 3-5 hours

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6
Q

onset/duration of glulisine

A

15 minutes / 3 to 5 hours

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7
Q

onset/duration of regular insulin (R)

A

30 minutes to 1 hour / 8 to 12 hours

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8
Q

onset/duration of NPH insulin (N)

A

1 to 1.5 hours / 24 hours

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9
Q

onset/duration of glargine (lantus)

A

1 to 1.5 hours / over 24 hours

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10
Q

onset/duration of detemir (levemir)

A

1 to 2 hours / over 24 hours

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11
Q

onset/duration of degludac (tresiba)

A

1 hour / over 24 hours

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12
Q

mimicking natural insulin secretion pattern

A

modifies insulin to alter the availability and absorption from subcutaneous injection sites
delayed absorption - prolong onset and duration
increase absorption - decrease time to onset and duration

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13
Q

purpose of modified insulins

A

provide flexibility/convenience in dosing
be able to mimic basal levels (2nd phase) and preprandial dose levels (1st phase)

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14
Q

NPH (Neutral Protamine Hagedorn) insulin (N)

A

The insulin is complexed with protamine, tissue proteases have to break down protamine to be able to release the insulin, slows absorption time

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15
Q

lispro insulin

A

reverse positions of P28 and K29 on insulin B chain. Interferes with the ability to form a dimer. Monomers are absorbed much more readily from the site of injection, fast absorption time.

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16
Q

ultra fast onset/very short action insulin place in therapy

A

injected immediately before meals

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17
Q

insulin aspart

A

proline 28 in B chain is switched to aspart
interferes with ability to dimerize
monomer is absorbed much quicker from site of injection, rapid onset

18
Q

insulin glulisine

A

Asn 3 and Lys 29 in B chain are switched to Lys and Glu
Interferes with ability to dimerize
Monomer is absorbed much quicker from site of injection, rapid onset

19
Q

insulin glargine

A

Ask 21 of a chain is changed to Gly and 2 Arg residues are added to the end of the B chain (30 and 31)
insulin solubility can change at different pH (Clear solution at pH=4, when introduced to physiological pH it precipitates). Slowly and steadily released from injection site over 24 hours

20
Q

basal insulins place in therapy

A

inject once daily

21
Q

insulin detemir

A

discontinued
the 30 of B chain is deleted and Lys 29 is myristylated
binds to serum albumin extensively

22
Q

insulin degludec

A

Thr 30 of B chain is replaced by y-Glu/C16 fatty acid. Binds to serum albumin extensively. insulin will hang out in blood stream for a long time, gradually little amounts will come off albumin and is absorbed very slowly

23
Q

multi-dose insulin regimens

A

fast onset, short acting is taken before meals and long, or intermediate acting is taken at bedtime or at bedtime and after breakfast

24
Q

Afrezza

A

regular human insulin in a dry powder that can be inhaled

25
Q

Afrezza onset/duration

A

rapid onset/shorter duration of action than SC injection

26
Q

Afrezza place in therapy

A

used as pre-prandial insulin

27
Q

Afrezza contraindications

A

patients with asthma and COPD, may reduce lung function (decreased FEV)

28
Q

Afrezza mechanism

A

molecules aggregate and for a large surface area for insulin to bind

29
Q

IV insulin place in therapy

A

regular human insulin for severe hypoglycemia or ketoacidosis

30
Q

mode of action of insulin

A

decreased liver glucose output
increase fat storage
increase glucose uptake

31
Q

adverse reaction to insulin

A

hypoglycemia
lipodystrophy
lipohypertrophy
lipoatrophy

32
Q

hypoglycemia

A

blood glucose <70 mg/dL; caused by too much insulin and/or not enough food (glucose)

33
Q

symptoms of hypoglycemia

A

weakness, sweating, hunger, tachycardia, increase irritability, tremor, blurred vision, seizures, coma, increased sympathetic output

34
Q

treatment of hypoglycemia

A

glucose if awake and alert
glucagon if unconscious or can’t swallow

35
Q

agents that increased blood glucose

A

catecholamines
thyroid hormone
isoniazid
glucocorticoids
calcitonin
phenothiazines
oral contraceptives
somatropin
morphine

36
Q

agents that may increase the risk of insulin hypoglycemia

A

ethanol
ACE inhibitors
Fluoxetine
somatostatin
anabolic steroids
MAO inhibitors
B-adrenergic blockers
Vigorous, unaccustomed exercise

37
Q

ethanol’s role in increase risk of hypoglycemia

A

inhibits gluconeogenesis so glucose is not brought back into the blood

38
Q

B blocker’s role in increase risk of hypoglycemia

A

counteract catecholamines and mask symptoms of hypoglycemia

39
Q

exercise’s role in increase risk of hypoglycemia

A

skeletal muscle muscle contraction stimulates glucose uptake

40
Q

lipodystrophy

A

changes in fat (i.e. on upper leg) at over used injection site

41
Q

lipohypertrophy

A

accumulation of fat in subcutaneous tissue

42
Q

lipoatrophy

A

loss of fat in subcutaneous tissue; less common with recombinant insulin

43
Q

treatment of T1DM

A

insulin + diet + exercise