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85 Cards in this Set

  • Front
  • Back
Alpha cell
1. % islet cell
2. Hormone
3. Function
1. 20%

2. Glucagon

3. Mobilize glycogen
Delta cell
1. % islet cell
2. Hormone
3. Function
1. 3-5%

2. Somatostatin

3. Inhibit secretory cells
F cell
1. % islet cell
2. Hormone
3. Function
1. <2%

2. Pancreatic Polypeptide

3. Facilitate digestion
Beta cell
1. % islet cell
2. Hormone
3. Function
1. 75%

2. Insulin

3. Storage and Anabolic hormone
Aside from Insulin, what other 2 things do pancreatic Beta cells secrete?
1. C-peptide

2. Islet amyloid polypeptide = amylin
Insulin Structure:
-insulin comes from __1__ synthesized in pancreatic __2__ cells
-Proinsulin is __3__ to release: __4__ & __5__
1. Proinsulin
2. Beta
3. hydrolyzed
4. Insulin
5. C-peptide
Removal of __1__ forms Insulin, a small protein consisting of __2__(#) amino acids arranged in __3__(#) chains
1. C-peptide

2. 51

3. two
How many amino acids does the alpha chain of Insulin contain?

Beta chain?
Alpha = 21

Beta = 30
How is Insulin stored in Beta cells?
Insulin crystals are stored in secretory granules
How much Insulin does the human pancreas normally contain?
8 mg (200 U)
Explain the resting state Beta cells, when Insulin is not secreted
-At rest, Beta cells have low ATP

-Low ATP causes ATP-gated K+ channels to be open

-K+ diffuses out to keep Beta cell depolarized (negative)

-Insulin secretion is minimal
Explain the mechanism of Insulin secretion
1. Stimulation by Hyperglycemia or Insulin Secretagogues

2. intracellular ATP increases → closes K+ channels

3. Depolarization of Beta cell → Ca++ chennels open

4. Ca++ enters Beta cells and increases Intracellular Ca++ → Insulin is secreted
What is the principle stimulus of Insulin secretion?

What are some other minor stimuli?

Sugars, Amino acids, Secretagogues
What are the basal values of circulating insulin detected by RA in normal subjects?

Peak levels? When are peak levels found?
Basal = 5-15 mU/mL (30-90 pmol/L)

Peak = 60-90 mU/mL (360-540 pmol/L) = during meals

**multiply times 6 to convert from mU/mL to pmol/L
What are the 3 main sites of Insulin receptors?
1. Liver

2. Muscle

3. Adipose tissue
What is the half-life of circulating Insulin?

What is the reason for this half-life? (Be specific)
3-5 minutes

Removed by circulating Insulinase acting in:
--Liver = 60%
--Kidney = 35-40%
Explain the structure of the Insulin Receptor
Consists of 2 Covalently linked Heterodimers each containing:
-Alpha subunit = extracellular recognition site
-Beta subunit = spans cell membrane and contains Tyrosine Kinase
Explain what happens when Insulin binds to the Insulin Receptor
-Insulin binds to the Alpha subunit -> brings the catalytic loops of the Cytoplasmic Beta subunits closer together to facilitate Tyrosine Kinase activity

-Activated TK P's the docking proteins IRS to translate the insulin signal

-Phosphorylation network causes translocation of Glucose Transporters (GLUT4) to the cell membrane

-Increased glucose uptake, glycogen formation, & multiple effects of protein synthesis, lipolysis, & lipogenesis
List the 4 main sites of Action of Insulin
1. Glucose transporters

2. Liver

3. Muscle

4. Adipose tissue
Explain Insulin's effect on Glucose Transporters

Which is the most important transporter for Hypoglycemia?
Insulin facilitates glucoses movement across cell membranes

Explain Insulin's effects on the Liver
-increases storage of GLYCOGEN

-decreases postabsorptive catabolism (breakdown)
Explain Insulin's effects on Muscle
promotes Protein and Glycogen synthesis
What are Insulin's effects on Adipose Tissue?
reduces free fatty acids → promotes Triglyceride storage

** = fat deposition
What 2 Insulin effects cause Hypoglycemia?
1. inhibition of liver glucose production (decreases gluconeogenesis and glycogenolysis)

2. stimulates glucose uptake and metabolism in liver, adipose, skeletal muscle
How is insulin usually administered clinically and what are onset, peak, and duration of action related to?

Onset, peak, & duration are DOSE-related
Short-acting or Regular insulin mimic the __1__ rise in insulin and is given IV for __2__ or __3__
1. post-prandial (= the rise in insulin after meals)

2. Hyperglycemic emergencies

3. Diabetic Ketoacidosis
Insulin preparations that mimic the basal level of insulin
Describe the administration of Insulin preparations
Are given as mixtures to produce desired times of onset, peak, and duration of action

Varies from patient to patient
Ultra-long-lasting insulin that produces a sustained "peakless" absorption profile, and can provide once-daily effective 24-hour plasma levels
List the 2 Ultra-short-acting Insulin preps and their duration
Lispro & Aspart

3-4 hours
List the short acting Insulin prep and its duration

5-7 hours
List the Intermediate-acting Insulin prep and duration
Lente or NPH

18-24 hours
List the Long-lasting insulin prep and duration

18-28 hours
What is the Ultra-long-acting insulin prep and duration?

>24 hours
What is the name for the Inhalable Insulin preparation?

Describe its characteristics

rDNA origin used as a hand-held inhaler for use in combo with oral hypoglycemic drugs or longer-acting insulin
When is Inhalable Insulin used?
Before meals

**is a rapid-acting insulin powder inhaled through the mouth into the lungs
Inhalable Insulin is as effective as __1__ insulin injections, but exact __2__ is difficult
1. Short-acting

2. dosing
In what 2 situations should Exubera not be used?
1. Smokers = either still smoking or stopped smoking < 6 months ago

2. Patients with Chronic Lung Disease (asthma, COPD, emphysema)
In which type of diabetes is Insulin therapy the mainstay treatment?
Type I diabetics

**Insulin is deficient in these patients so give Insulin
When is Insulin treatment used in Type II Diabetics?
when the diabets is not adequately controlled by DIET &/or Oral Hypoglycemic drugs

**1 of 5 will need insulin therapy
In what 2 ways does Insulin injected SubQ differ from endogenously secreted insulin?
1. does not reproduce the rapid rise and fall occuring when insulin is secreted due to stimulation by ingested food

2. diffuses into the systemic circulation instead of being secreted into the portal circulation (SubQ eliminates the direct hepatic effects produced by normal secretion)

**these are 2 drawbacks
What is the ideal goal in Insulin therapy?
Normalize blood glucose and all aspects of glucose metabolism

**this is difficult to achieve
What is the most common complication of Insulin therapy? What things can trigger it?
Insulin Hypoglycemia (low blood sugar)

Delayed meals, unusual physical exertion, or insulin overdose
What plasma level do signs of Hypoglyecmia manifest at?
60-80 mg/dL
What are the signs of Hypoglycemia?
1. Neuroglycopenic = CNS impairment manifested as mental confusion, bizarre behavior, convulsions, or coma

2. Autonomic hyperactivity
-Sympathetic = tachycardia, palpitations,sweating, tremors
-Parasympathetic = nausea & hunger
What rapidly releives Insulin Hypoglycemia?

What should be given to unconscious patients?
Glucose = OJ or any sugary food or drink

IV 50% glucose, 20-50 mL over 2-3 min
Which type of Diabetes are Oral antidiabetic drugs usually used for?
Type II
List the 4 categories of Oral Hypoglycemics
1. Insulin Secretagogues

2. Biguanides

3. Thiazolidinediones

4. Alpha-glucosidase inhibitors
What is the general mechanism of the Insulin Secretagogues?
stimulate Insulin release by closing K+ channels in pancreatic Beta cells
What are the 2 groups of Insulin Secretagogues?
1. Sulfonylureas

2. Meglitinides
Describe the mechanism of Sulfonylureas?
1. bind to high affinity receptors for K+ channels in pancreatic beta cells

2. inhibit K+ efflux to cause depolarization

3. Open voltage-gated Ca++ channels

4. Ca++ influx

5. Insulin release
List 4 1st generation Sulfonylureas
1. Acetohexamide
2. Chlorpropamide
3. Tolazamide
4. Tolbutamide
List the 4 2nd generation Sulfonylureas
1. Gli-me-piride
2. Gli-cazide
3. Gli-pizide
4. Gly-buride

**all start with Gl-
Aside from stimulating Insulin secretion, what other effect do Sulfonylureas have?
reduce serum Glucagon levels
When are Sulfonylureas mainly used?
Treating Type 2 diabetes whose hyperglycemia cannot be controlled by diet alone
What are 2 important properties of 2nd generation of Sulfonylureas?
1. more effective BUT cause fewer adverse effects = good quality

2. may produce dangerous hypoglycemia in diabetics who are elderly or have Cardiovascular disease = bad effect
Which 2nd Generation Sulonylurea has the shortest half-life and is less likely to cause severe Hypoglyemia

**less likely to cause hypoglycemia b/c it has a short half-life and therefore has less time to cause tissue to uptake glucose
Would you use 1st or 2nd generation Sulfonylureas in Elderly & CV disease patients?
1st generation
What 2 Sulfonylureas are safest for the elderly? Why?
Tolazamide & Tolbutamide

-relative short duration of action
-severe hypoglycemic episodes are unlikely
What are the 2 available Meglitinides?

What is the main use for Meglitinides?
controlling postprandial Glucose levels
What are the sites of action of Meglitinides?
1. unique binding site

2. two other sites in common with Sulfonylureas
In what type of patient should you be cautious when giving Meglitinides?
someone with Hepatic dysfunction
What is the distinction between Sulfonylurea and Meglitinides?
Meglitinides (Repaglinide specifically) can be used in Type II diabetics who are allergic to Sulfonylureas b/c Repaglinide structure does not contain Sulfur
Oral Hypoglycemic under the category of Biguanides
Hypoglyemic drug that is referred to as "euglycemic" or antihyperglycemic b/c it does not cause hypoglycemia but reduces fasting or postprandial blood glucose levels
List the 4 proposed mechanisms of Metformin
1. direct stimulation of tissue glycolysis

2. reduced hepatic gluconeogenesis

3. reduced GI glucose absorption

4. reduced plasma glucagon
When is Metformin used? (2)
1. obese patients with "insulin resistance syndrome"

2. Type II diabetics who do not respond to Sulfonylureas alone
What is the most frequent side-effect of Metformin?
GI effects
-anorexia, NVD, abdominal discomfort
Under what 4 instances is Metformin contraindicated?
1. Renal disease

2. Hepatic disease

3. Alcoholism

4. Chronic Cardiopulmonary dysfunction
List the 2 Thiazolidinediones (TZD's)


What is the mechanism of the TZD's?
diminish insulin resistance by enhancing the tissue sensitivity to insulin
Diabetic drugs that are agonists of PPAR-gamma (peroxisome proliferator-activated receptor-gamma) nuclear receptors found in muscle, fat, and liver
= Rosi-glitazone
= Pio-glitazone
What does PPAR-gamma do?
activates insulin-responsive genes that regulate carbohydrate and lipid metabolism (increases glucose uptake and metabolism in muscle and adipose tissue)
What is the major site of action of the TZD's (-glitazones) in diabetics?

What beneficial efects may this have?
Adipose tissue

Redistribution of body fat causing reduced visceral fat mass and loss of central obesity
Rosiglitazone and Pioglitazone are clinically effective in __1__ diabetes without producing __2__
1. Type II

2. Hepatotoxicity
What are the adverse effects of TZD's? (4)
1. Edema
2. Anemia
3. Fluid retention
4. Weight gain
What are the 2 Alpha-Glucosidase Inhibitors?

What is the mechanism of Alpha-Glucosidase Inhibitors in treating Diabetes?
-inhibit intestinal alpha-glucosidases that normally facilitate digestion of starches and disaccharides into monosaccharide molecules absorbed in the duodenum and upper jejunum

-cause hypoglycemia by reducing upper intestinal digestion of starch and disaccharides to defer digestion to the distal small intestine
What are the Alpha-Glucosidase Inhibitors used for clinically?
Type II diabetics prior to ingestion of the first portion of each meal
What are the prominent side-effects of Alpha-Glucosidase Inhibitors?
Flatulence, diarrhea, and abdominal pain caused by gas released by short-chain fatty acids fermented from undigested carbohydrates in the colon
When are Alpha-Glucosidase Inhibitors contraindicated?
Chronic or inflammatory bowel disease

Any intestinal condition that may be worsened by gas and distention
Oral Antidiabetics associated with Disulfarim-effect
1st Generation Sulfonylurea's
Anti-diabetic drug that causes Lactic Acidosis
Pancreatic hormone product that is used as a stimulant in beta-adrenergic blocker overdose