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Pharmacology -- Test #5 > Insulin and Diabetes Part 1 > Flashcards

Insulin and Diabetes Part 1 Flashcards

1
Q

Criteria for diagnosing diabetes?

A
  1. A1C over 6.5%
  2. Fasting Plasma Glucose over 126 mg/dL
  3. 2h plasma glucose over 200 mg/dL during OGTT
  4. Random plasma glucose over 200 mg/dL
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2
Q

Who gets Type 1?

A

Early age (mean=12) usually, but can show up in adults
family history often negative
Maybe triggered by viruses, chemicals, etc. in predisposed

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3
Q

Two types of non insulin dependent DM? Who gets them?

A

Non-obese – Under 25, MODY

Obese – Over age 35 (AODM)

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4
Q

Three effects of hyperglycemia caused by a lack of insulin

A
  1. Low glucose uptake
  2. low glycogen synthesis
  3. More conversion of AA to Glu
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5
Q

Goals of diabetes treatment

A

HbA1c below 7 (ideally 6)
Keep blood glucose below 150 mg/dL
Prevent/Delay complications

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6
Q

Main studied (first slide…) method that hyperglycemia may cause damage

A
  • Oxidation products with glu react irreversibly with proteins to form Advanced Glycation End-products. These may lack normal protein function and accelerate the aging process. Example - Crystalin + Glu –> Cataracts
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7
Q

Pathway proposed for why hyperglycemia damages nerves

A

POLYOL PATHWAY

Aldose reductase pathway depletes nerves of NADPH, increasing vulnerability to Oxygen radicals

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8
Q

Other than the polyol pathway, what other pathways are upregulared with hyperglycemia and may lead to increased protein modification

A

Hexosamine pathway
OKC Pathway
AGE Pathway

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9
Q

What are the parts of the Insulin receptor? What do they do?

A

alpha – suppresses beta till insulin binds

beta – tyrosine kinase (autophos)

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10
Q

How does insulin receptor upregulate Glut4

A
  1. IRS –> P13K –> PKB –> GLUT4

2. IRS –> P13K –> PDK1 –> aPKC –> GLUT4

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11
Q

Insulin effects on the liver

A

Inhibits – glycogenolysis, ketogenesis, gluconeogenesis

Stimulates – Glycogen and triglyceride synth

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12
Q

Insulin effects on the skeletal muscle

A

Stimulates glucose+AA transport

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13
Q

Insulin effects on adipose tissue

A

Stimulates triglyceride storage + glucose transport

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14
Q

Where does glucose go when fasting

A

75% non-dependent – Liver, GI, brain

25% dependent – Skeletal Musc

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15
Q

Where does glucose go when fed

A

80-85% dependent – skeletal muscle

4-5% – dependent – adipose (inhibits FFA release, low FFA enhances action on skeletal muscle)

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16
Q

Important details on the 4 GluTs

A

1 – widely expressed
2 – beta cells, liver. High Km
3 – Neurons
4 – Insulin Induced, Skeletal muscle+Adipocytes

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17
Q

Action of Amylin

A

Co-secreted with insulin
Slows gastric emptying, decreases food intake
Inhibits glucagon secretion

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18
Q

In secretory granules, Insulin is cleaves by…

A

Proconvertases

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19
Q

Human insulin cDNA is expressed in…

A

E. Coli – Humulin

Yeast – Novolin

20
Q

Three main Ultra Rapid Onset/Very short action insulins

A

Lispro
Aspart
Glulisine

21
Q

Insulin preparation with Intermediate onset and action?

A

NPH

22
Q

Insulin preparation with slow onset and long action (basal insulins)

A

Glargine, Detemir, Degludec

23
Q

How does NPH (Neutral Protamine Hagedorn) insulin work?

A

Bunch of insulin is bound to a protamine.
Over time tissue proteases chew up the protamine to release the insulin.
Only (non-regular) insulin product that is unmodified

24
Q

What is Lispro?

A

Insulin with a reversal of P28 and K29 that decreases self association. This will decrease complex formation and make it faster acting.

25
Q

What is Aspart?

A

Human insulin with P28 switched to Aspartate. Same reason as Lispro

26
Q

What is Glulisine?

A

Human insulin with Asn 3 and Lys 29 switched to Lys and Glu

27
Q

What is Glargine?

A

Asn21–> Gly + two bonus Args at the end (30+31)

Inject in a pH 4.0 solution. Precipitates as neutralized, so slow release over 24 hours.

28
Q

What is Detemir?

A

Thr 30 deleted and Lys 29 is MYRISTYLATED (has a long fatty acid added on to it). This allows it to bind albumin extensively for a slow release (12 hr)

29
Q

What is degludec?

A

Thr 30 of b chain replaced by fatty acid to bind albumin

30
Q

Describe a common multi-dose insulin regimen

A

Fast onset, short acting taken before meals

Long/Intermediate taken at bedtime (and sometimes after breakfast)

31
Q

What is Humalin? Humalog?

A 
Humalin = NPH + Regular
Humalog = NPL + Lispro
32
Q

Which insulin is given via inhaler?

A

Afrezza

33
Q

Important details about Afrezza?

A

Inhaler, Rapid onset, shorter duration than injection

Pre-prandial insulin

34
Q

Who can’t use Afrezza?

A

Asthma, COPD (decreased FEV)

35
Q

Three main adverse reactions to insulin?

A

Lipodystrophy
Lipoatrophy
Insulin Resistance

36
Q

What is lipodystrophy?

A

Lump of fat that develops at the overused injection site

37
Q

What is lipoatrophy?

A

Concavities in subcutaneous tissue where you normally inject

38
Q

Things that increase the likelihood of insulin hypoglycemia

A

Ethanol, Anabolic Steroids, Unaccoustombed Exercise
ACE Inhibitors, Beta-Blockers
Fluoxetine, MAO Inhib, Somatostatin

39
Q

Some common agents that increase blood glucose

A

Catecholamines, Glucocorticoids.
Contraceptives, Thyroid Hormone
Morphine, Isoniazid

40
Q

How do Sulfonylurea drugs work?

A
  1. Bind Sulfonylurea receptor, inactivating K/ATP channel. This makes K stuck in the cell.
  2. Cell depolarization, more voltage gated Ca chan. open
  3. Increased Ca –> Increased Exocytosis of insulin granules
41
Q

How to K/ATP channels usually work

A

Glu thru GLUT2 receptor
Glucose metabolism to increase ATP conc
ATP closes K/ATP channel.
In absence of glucose, channel opens, preventing insulin release

42
Q

Name the three main first gen sulfonylureas

A

TOLBUTAMIDE (less potent, 6-12 hr duration)
Tolazamide
Chlorpropamide

43
Q

Name the three main 2nd gen sulfonylureas

A

Glipizide
Glyburide
Gilmepiride

44
Q

Difference between first and second generation sulfonylureas

A

2nd gen are much lower dose, higher potency. All once daily

45
Q

What is Repaglinide (Prandin)?

A

Mechanism like sulfonylureas with quick onset (preprandial)

Binds directly to the K-ATP channel

46
Q

What is Starlix?

A

A non-SU K/ATP Channel blocker
Very specific for pancreas + CV
Shorter half time, less hypoglycemic risk
Metformin synergy

Pharmacology -- Test #5 (12 decks)

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