Insulin Preps MT2 Flashcards by Jessyka Yard

this is a group of metabolic diseases characterized by high blood sugar (glucose) levels, which result from defects in insulin secretion, action or both

diabetes

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how are glucose utilization, glucose production and insulin secretion affected in DM

glucose utilization: decreased
glucose production: increased
insulin secretion: decreased

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normally, blood glucose levels are tightly controlled by _______ which is a hormone produced by the pancreas

insulin

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what are the three main symptoms of diabetes

polydipsia - excessive thirst
polyphagia - increased appetite
polyuria - excessive passing of urine

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type I or type II DM?
onset occurs usually < 20 y/o

type I

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type I or type II DM?
obesity is usually present

type II

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type I or type II DM?
onset occurs usually > 30 y/o

type II

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type I or type II DM?
normal or increased blood insulin

type II

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type I or type II DM?
decreased blood insulin

type I

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type I or type II DM?
anti-islet cell antibodies are present

type I

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type I or type II DM?
ketoacidosis is common

type I

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type I or type II DM?
50% concordance in twins

type I

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type I or type II DM?
60-80% concordance in twins

type II

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type I or type II DM?
no HLA association

type II

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type I or type II DM?
HLA-D linked

type I

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type I or type II DM?
severe insulin deficiency

type I

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type I or type II DM?
insulin resistance is present

type II

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type I or type II DM?
autoimmune, immunopathologic mechanisms present

type I

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type I or type II DM?
no insulitis present

type II

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type I or type II DM?
marked atrophy and fibrosis

type I

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type I or type II DM?
focal atrophy and amyloid deposits (amyloid gets secreted alongside insulin and if have this type of DM the amyloid gets deposited)

type II

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type I or type II DM?
severe beta-cell depletion

type I

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type I or type II DM?
mild beta-cell depletion

type II

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what are some of the organs/systems that complications may occur in DM

cardiovascular
eyes
kidneys
nervous systems
pancreas

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what is used to diagnose diabetes

- fasting plasma glucose (above 7 mol/L) - plasma glucose (above 11.1 mol/L) - hemoglobin A1c (above 6.5%) - symptoms of DM

true or false: type 1 DM is reversible

false

true or false: type 2 DM is reversible

true

true or false: gestational DM is reversible

true

blood glucose levels tend to be higher in untreated ____1____ than untreated ___2____ because _____3____ subjects retain some insulin action

1 - type 1 2 - type 2 3 - type 2

this is stored in the liver in the form of glycogen

glucose

its effect is to lower blood glucose levels. it is activated during the fed state, where blood glucose levels are high. low levels release adipocytes from inhibition

insulin

this peptide increases glucose levels. hepatocytes have receptors for this peptide which convert the glycogen polymer to individual glucose molecules to be released into the blood. when glucose stores are depleted, this peptide induces glycogenolysis by the liver and kidney

glucagon

this is stored within granules in the beta-cells of the pancreas. the half life is 3-5 mins

endogenous insulin

two organs are responsible for removing insulin from circulation. these organs are

- liver - kidney

free insulin binds to insulin receptors primarily on what organs

liver, muscle and adipose tissue

what type of receptors are insulin receptors?

tyrosine kinase - alpha subunit is the binding domain - beta subunit is the ATP-binding and tyrosine kinase domains

only ___% of insulin receptors need to be occupied to produce the maximum effect

when the activated insulin receptor phosphorylates, it becomes an insulin receptor substrate. rapid effects are mediated by this pathway

PI3K

when the activated insulin receptor phosphorylates, it becomes an insulin receptor substrate. long term effects are mediated by this pathway

MAP kinase

this GLUT transporter is found in all tissues, especially red cells and the brain. function: basal glucose uptake & transport across the BBB

GLUT1

this GLUT transporter is found in the beta-cells of the pancreas; liver, kidney and gut. function: regulation of insulin release & glucose homeostasis

GLUT2

this GLUT transporter is found in the brain, kidney, placenta and other tissues function: uptake into neurone and other tissues

GLUT3

this GLUT transporter is found in the muscle and adipose tissue. function: insulin-mediated uptake of glucose

GLUT4

this GLUT transporter is found in the gut and kidney function: absorption of fructose

GLUT5

what are the different ways insulin preparations differ by?

- source (human or animal species from which they are derived) - purity - concentration - solubility - time of onset and duration of action

these insulin preparations are dispensed as clear solutions at a neutral pH. they also have small amounts of zinc to increase shelf-life.

ultra short acting and short acting insulins

these insulin preparations are cloudy and have been modified in some way to permit slower onset and longer duration.

intermediate and long acting insulins

what are some adverse effects of insulin

- hypoglycaemia - loss of fatty tissue at site of injections (rotate!) - insulin allergy (rare) - insulin resistance (very rare)

examples include Insulin Lispro, Insulin Aspart and Insulin Glulisine

rapid acting human insulin analogs

examples include regular insulin

short acting insulin

examples include NPH insulin

intermediate acting insulin

examples include insulin glargine and insulin detemir

long acting human insulin analogs

what is the onset of action, peak and effective duration of very rapid acting insulin (e.g. Aspart, Glulisine and Lispro)

onset: <0.25, peak is 0.5-1.5 hr and may last for 3-4 hrs

what is the onset of action, peak and effective duration of short acting (regular) insulin

onset 0.5-1 hr, peak is 2-3 hrs and may last for 4-6 hrs

what is the onset of action, peak and effective duration of long acting insulin (e.g. detemir, glargine, degludec and NPH - intermediate)

onset: 1-4 hrs, peak = relatively constant and may last for 10-42 hrs, depending on specific insulin

what is the onset of action, peak and effective duration of combination insulins (long acting and short acting)

onset: 0.25-1hr, peak is 1.5 hr and may last for 10-16 hrs

what is the FIRST LINE treatment of type II DM

lifestyle changes such as diet, weigh loss, exercise, education.

what pharmaceutical agents may be used to treat type II DM

oral hypoglycemics such as sulphonylureas, biguanides, thiazolidinediones, meglitinides and alpha-glucosidase inhibitors (sometimes insulin)

this type of oral hypoglycemic are derived from sulfonic acid and urea. examples include gliclizide, tolbutamide, glyburide, etc.

sulphonylureas and secretagogues

what are some side effects of sulphonylureas and secretagogues

hypoglycaemia weight gain or anorexia nausea, heartburn weakness or numbness of the extremities

what is the MOA of sulphonylureas and secretagogues

act similar to glucose as they inhibit the ATP sensitive K+ channel, but they bind to the SUR portion. this depolarizes the channel and allows influx of Ca++ which stimulates the release of insulin

these oral hypoglycemic enhances secretion of insulin similar to that as sulfonylureas. it has a rapid onset of action and short duration. is generally taken before a meal because if a meal is skipped or delayed it can cause hypoglycemia

meglitinides (nateglinide and repaglinide)

this oral hypoglycemic agent decreases hepatic glucose production

biguanides (metformin)

what is the MOA of biguanides (metformin)

blocks gluconeogenesis in the liver. increases insulin sensitivity in the muscle and fat by sensitizing the insulin receptors. promotes glucose uptake by skeletal muscle.

these drugs are good agents for restoring glucose into normal or non-diabetic range without causing hypoglycemia

thizolidinediones (e.g. pioglitazone)

what is the MOA of thiazolidinediones

agonists of PPAR-gamma. increases the sensitivity of tissues (muscle and adipose) to insulin. reduces insulin resistance

what are some side effects of thiazolidinediones

weight gain, edema, GI, h/a, increased respiratory infections

what is the MOA of alpha-glucosidase inhibitors (acarbose)

competitive inhibitor of intestinal alpha-glucosidase (enzyme that breaks down disaccharides). delays absorption of carbohydrates from the gut. reduces postprandial glucose rise

what are some side effects of alpha-glucosidase inhibitors

GI!!! may wanna stay away from this drug

Insulin Preps MT2 Flashcards

(69 cards)