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Year 1: Patho/Pharm > Diabetes PHARM Insulin > Flashcards

Diabetes PHARM Insulin Flashcards

1
Q

Insulin
Synthesis

A

Insulin is synthesized by the beta cells of the pancreas

Cleavage of the C peptide (connecting peptide) converts pro insulin into insulin

Peptide hormone

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2
Q

Insulin therapy
Examples

A
  1. Rapid acting, short duration
  2. Short acting, short duration
  3. Slow acting, intermediate duration
  4. Slowest acting, Longest duration
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3
Q

Rapid acting, Short Duration
Insulin
Examples
Pharmakokinetics

A

Glulisine > aspart > lispro

Onset: 15 minutes
Peak: 1.5hours
Duration: 5 hours

*take 15 minutes before meal onset

*change in 2 a.a decreases ability to cluster
increases absorption

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4
Q

Short acting, Short Duration
Insulin
Examples, peak, onset, duration

A

Humulin R
Novolin R

Onset: 30-60 minutes
Peak: 3 hours
Duration: 6.5 hours

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5
Q

Insulin
MOA

A

Anabolic hormone

Increase uptake of a.a, FFA, nucleic acids, and glucose by liver, muscle, adipose tissue

Synthesis of proteins, glycogen, and adipose

Decrease catabolism
- gluconeogenesis
- glycogenolysis
- FFA oxidation

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6
Q

Insulin
SE

A

Hypoglycemia
- too much insulin
- not enough carbohydrates

Lipohypertrophy at injection site
- anabolic
- fat deposites with subcutaneous injections
- rotate sites

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7
Q

Insulin
Dose adjustments

A

Preprandial BG

Alcohol
- Delayed hypoglycemia 24 hours post alcohol consumption
- prevents liver counter-regulatory response

Excessive exercise
- exercise induced hypoglycemia
- reduce basal and/or bolus dosage, eat carbohdyrate

Illness, stress, trauma
- counter-regulatory hormones -> hyperglycemia

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8
Q

Bolus Insulin therapy
Examples and indications

A

Pre-prandial or meal time

  1. Rapid acting, short duration
    - insulin aspart
    - insulin glulisine
    - insulin lispro
  2. short acting, short duration
    - humulin R
    - novolin R
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9
Q

Basal insulin
Examples and Indication

A
  1. Slower acting, intermediate duration
    - Humulin N
    - Novolin N
  2. slowest acting, longest duration
    - Degludec > glargine > detemir

Indication:
basal control
prevent glucose fluctuations between meals and overnight

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10
Q

Slower acting, Intermediate duration insulin
Examples, onset, peak, duration

A

NPH insulin
- neutral protamine hagedorn insulin
- conjugation with protamine slow absorption
- higher risk allergic reaction

Humulin N
Novolin N

Onset: 1-2 hours
Peak: 5-8 hours
Duration: up to 18 hours

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11
Q

Slowest acting, longest duration insulins
Indications and examples

A

Indication: basal insulin control
- less hypoglycemia than intermediate insulins
- U refers to concentration

Examples
- Degludec > glargine > detemir
- longest acting
- less hypoglycemic risk

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12
Q

Slowest acting, longest duration insulins
Pharmakokinetics

A

onset: 1.5 hours
Peak: no peak
Duration: 24,30,42 hours
Dosing: once a day

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13
Q

Pre-mixed insulin
Examples

A

Pre-mixed insulin
Indication: BID injection schedule, morning meal, night time meal

Dosage: Reported as ratio N:R

Examples:
Humulin N: Humulin R
Novolin N: Novolin R

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14
Q

Pre-mixed insulin
Pharmakokinetics and disadvantage

A

Onset: 30-60 minutes (short acting insulin)
Peak: variable, dependent on ratio
Duration: up to 18 hours (intermediate insulin)

CON
- not tight control
- no insulin dosed with lunch time meal

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15
Q

Therapy Regimes
T1DM

A
  1. Twice daily pre-mixed regime
  2. Intensive Basal-bolus regime

Advantages Basal-bolus regime
- better A1C control
- better macrovascular and microvascular outcomes

  • rapid acting insulin benefits > short acting insulin benefits (glulisine > aspart > lispro > humulin R)
  • Self management: pre-prandial BG, match insulin with BG and meal
  • Long acting insulin (degludec > glargine > detemir) used for basal control
  • prevents hypoglycemia

Glycemic targets
- Adults < 7%
- Children / adolescents < 7.5%
- elderly, pailiative, frail, functional dependence < 7.1-8.5%
- pregnancy <6.5%

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16
Q

Suboptimal control
T1DM
Strategies

A
  1. Intensive basal-bolus insulin regime
    - subcutaneous injections
    - BG monitoring at minimum TID
    - sliding scale based on carbohydrate intake
  2. continuous glucose monitoring with continuous subcutaneous insulin infusion
    - improves QOL, FOH, A1C control
  3. Patient education
    - diet, exercise, sick day/stress management
17
Q

Initiation Therapy
T2DM
Pre-assessment

A

Assess A1C
macrovascular and microvascular complications (heart, kidney, eyes, feet)
Determine target
healthy behaviour counselling (diet, exercise, weight loss, smoking cessation)

18
Q

Initiation Therapy
T2DM
Pathways

A
  1. Pre-diabetes A1C betwen 6.1%-6.4%
    - diet , exercise
    - re-assess 3 months
  2. Diabetes A1C < 1.5% over
    - metformin + exercise + diet
    - diet + exercise
    - re-assess 3 months
  3. Diabetes A1C > 1.5% above (7.5%)
    - Metformin + secondary medication
    - Second line: sulfonylureas, meglitinides, thionazolidinediones, GLP1 agonists, DPP4i, SGLT2i
  4. Symptomatic hyperglycemi, metabolic decompensation, elevated A1C > 6.5%
    - Metformin + insulin therapy (basal first)
19
Q

Re-assessment A1C in 3 months
T2DM
Treatment pathways

A
  1. Diabetic A1C not controlled, asymptomatic hyperglycemia
  • Addition SGLT2i (MACE, HF, nephroprotective)
  • Addition GLP1 agonist (MACE, CVE)
  • Avoid thiazolidinediones (weight gain, cardiotoxic)
  • Avoid sulfonylureas, meglitinides (weight gain, hypoglycemia with insulin)
  1. Symptomatic hyperglycemia, A1C still not controlled (on basal insulin therapy)
  • addition of Secondary medication (SGLT2i, GLP1 agonist, DPP4i)
  • addition of bolus insulin (intensive basal-bolus regime)

*advance therapy if no control in 3-6 months

20
Q

Do not combine these diabetic drugs

A

GLP1 agonist with DPP4i
Thiazolidinediones with insulin
Sulfonylureas with meglitinides

*same mechanism of action
hypoglycemia

21
Q

Somogyi Effect
Pathophysiology and management

A

BG high in the morning

Pathophysiology:
Hypoglycemia at night time
activation counter-regulatory hormones (cortisol)
increase glucose via glycogenolysis and gluconeogenesis (liver)

Treatment
- decrease basal insulin
- carbohydrate snack before bed

Diagnosis
- check insulin regular time points
- no hypoglycemia detected, likely dawn phenomenon

21
Q

Dawn Phenomenon
Pathophysiology and management

A

BG is high in the morning

Pathophysiology
- counter-regulatory hormones (cortisol, GH) released at night time 4am which result glucagon release and breakdown of glycogen to glucose and liver gluconeogenesis

Treatment
- increase basal insulin at night

Diagnosis
- take insulin mutiple times overnight
- if no hypoglycemia detected then dawn phenomenon

Year 1: Patho/Pharm (39 decks)

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