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Pharmacology (Winter) > Diabetes Drugs - Part 1 > Flashcards

Diabetes Drugs - Part 1 Flashcards

1
Q

Diabetes Mellitus:

A

insufficiency of insulin signaling relative to the req’s of the tissues for this hormone

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2
Q

Diabetes Mellitus sx’s?

A

polyuria, polydipsia, polyphagia

elevated fasting blood sugar, ketosis, weight loss etc.

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3
Q

Fasting plasma glucose DM level

A

> / 7.0

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4
Q

Plasma glucose 2 hours after 75-g glucose load

A

> / 11.1

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5
Q

T1D

A

10-20%, (Insulin – Dependent Diabetes Mellitus, IDDM; Juvenile onset diabetes). Autoimmune destruction of beta cells of pancreas.

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6
Q

T2D

A

10-20%, (Insulin – Dependent Diabetes Mellitus, IDDM; Juvenile onset diabetes). Autoimmune destruction of beta cells of pancreas.

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7
Q

Insulin secretion from the b cells of the pancreas

A

Resting state (low glucose prior to meal): GLUT2 is a equilibritor transporter b/c driven by [ ] of glucose
- if increased glc outside, glc will enter cell & it’ll equilibrate the [ ]
- ratio of ATP/ADP stays low & Katp channel opens due to hyperpolarization
- VG Ca channel closed & no insulin released

Glucose-stimulated state:
- Post meal (high glc)
- Picked up by metabolism machinery & metabolize glc to increase ATP/ADP ratio
- Katp channel closes & depolarization of mem. & therefore opens Ca channels
- Ca increases & stimulation insulin release

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8
Q

Increased glucose uptake (GLUT4) - insulin dependent glucose transporter - controls insulin dependent reuptake

A
  • skeletal muscle
  • cardiac muscle
  • smooth muscle
  • liver
  • adipose tissue
  • leucocytes
  • pituitary
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9
Q

No effect glucose (GLUT 1/2) 0 equilibrium forms if increased glc outside cell, you’ll see movement of glucose inside the cell (independent of insulin)

A
  • brain
  • kidney
  • intestinal mucosa
  • RBC
  • endothelium
  • pancreas
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10
Q

What are the insulin actions?

A
  • insulin increase glycogen production
    – glc is converted & stored as glycogen
  • this also inhibits gluconeogenesis (break down of glycogen) to free up glucose
  • increase TG storage (esp. in adipose tissue) & throughout tissues it increases protein syn.
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11
Q

Defects in glucose levels in diabetes:

A

Increase in EXTRACELLULAR glucose
- result of loss of insulin & insulin sensitivity

Decrease in INTRACELLULAR glucose (in tissues with insulin-sensitive glucose transporters)
- skeletal muscle is starved of glucose (why you get muscle wasting in diabetes)

Increase in INTRACELLULAR glucose (in tissues with non-insulin sensitive transporters)
- in tissue (brain, endothelial cells etc. b/c they primarily express GLUT2 or GLUT2, increase external glc –> increase intracellular glucose (toxic to the cell; what drives diabetic complications in multiple organ systems)

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12
Q

How insulin can control insulin dep. glucose uptake (GLUT4) in skeletal muscle for ex

A
  1. Insulin triggers association of IRS 1 & 2
  2. => activation of P13kinase which phosphorylates Akt/PKb
  3. Interacts directly w/ GLUT4 & moves it to the membrane where it can allow glucose entry
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13
Q

Insulin & glucagon are ______ after a meal

A

antagonistic

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14
Q

_____ is central for controlling the BG levels & this goes wrong in T2D pts

A

liver

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15
Q

In T2D the _____ is dysfunctional => increased glucose production contributing to hypoglycaemia => T2D

A

liver

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16
Q

Complications of diabetes:

A
  • Coma (serious situation)
  • BV’s (angiopathy)
  • Eyes (retinopathy)
  • Kidneys (nephropathy)
  • Nerves (neuropathy)
17
Q

What are the 3 forms in the insulin synthesis pathway?

A
  1. Pre-proinsulin
  2. Proinsulin
  3. Insulin

Chain C is the segment of peptide cleaved

18
Q

Insulin LISPRO & ASPART:

A

Onset: 10-30 min
Peak: 0.5-3
Duration: 3-5

RAPID-ACTING

19
Q

Regular NOVOLIN R:

A

Onset: 0.5-1
Peak: 2-5
Duration: 4-12

SHORT-ACTING

20
Q

NPH/Humulin N:

A

Onset: 1-2
Peak: 4-8
Duration: 10-20

INTERMEDIATE

21
Q

NPH/Regular:

A

Onset: 0.5-1
Peak: 2-12
Duration: 18-24

LONG-ACTING

22
Q

Insulin Glargine:

A

Onset: 1-4
Peak: no peak
Duration: 22-24

LONG-ACTING

23
Q

Insulin Detemir:

A

Onset: 1-4
Peak: flat
Duration: 12-20

LONG-ACTING

24
Q

Insulin Lispro Characteristics:

A
  • Analog of human insulin in which amino acids #28 and #29 (lysine and proline) in the beta chain are reversed.
  • Pharmacokinetics differ from normal insulin
  • Reduces anti-parallel dimer formation
  • Monomer > dimer
  • Rapid absorption & shorter duration of action (similar to endogenous insulin)
  • More closely resembles insulin response to a meal
  • Insulin Aspart
25
Q

Insulin Lispro Use:

A
  • Should be taken 15 mins prior to a meal
  • Both TID & T2D pts can use Humalog
  • Total daily dose 0.5-1 U/kg
26
Q

Insulin Lispro Benefits:

A
  • Tighter control of glucose, no AE on HbA1c
  • Decreased incidents & risk of hypoglycemia
27
Q

Regular Novolin R Characteristics:

A
  • Recombinant insulin
  • Dimers form hexamers in the vial – stable
  • Delays absorption into blood stream – acts as a depot
  • Over time hexamers breakdown to release bioactive insulin monomers
  • Taken 30-45 min before a meal
  • 0.5-1.0 U/kg/day (maintenance dose)
  • Regular Humulin R
28
Q

Insulin Glargine Characteristics:

A
  • Human long acting insulin
  • Differs in 3 AA’s in beta chain
  • Aspargine replaced by glycine, 2 arginine added at C-terminus
  • Soluble & clear in pH 4 solution
  • Precipitates at neutral pH in subcutaneous tissue
  • One injection per day (but 2 in some cases) – 15-30 U
  • Slowly absorbed, duration of action 24 hours
  • No peak
  • Insulin Determir

Less nocturnal hypoglycemia

29
Q

Insulin Glargine AE’s:

A
  • Pain at the site of injection
  • Other potential effects (tumor growth) – remains to be established

NB it cannot be diluted or mixed w/ any other insulins

30
Q

New preps & technology:

A
  1. Nasal sprays
  2. Insulin inhalers
  3. Insulin pumps
31
Q

Hypoglycemic actions of insulin decreased by:

A
  • Glucocorticoids
  • Glucagon
  • Epinephrine
  • Growth Hormone
  • Thyroid Hormone
32
Q

Hypoglycemic actions of insulin increased by:

A
  • ACE inhibitors
  • Alcohol
  • Salicylate
  • Beta blockers
  • MAO inhibitors

(dangerous)

33
Q

AE’s of Insulin:

A
  1. Hypoglycemia - hunger, sweating, blurred vision, headache, fatigue
    – coma & death
    – unawareness in the elderly
    due to insulin overdose, exercise, failure to eat, labile disease
    - treat w/ oral or IV glucose, sc glucagon
  2. Lipoatrophy
  3. Allergy

Pharmacology (Winter) (23 decks)

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