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Type One Diabetes
- Due to no or very litle insulin
- Seen more in children
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Type Two diabetes
- Tissue is resistant to insulin
- Seen in adults and the obese
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Type 4 diabetes
Gestational Diabetes
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Where are insulin recepters found?
- Liver
- Adipose tissue and skeletal muscle
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What are the regulators of Insuline secretion?
Chemical--- Glucose Concentration and AAs
Hormonal--- GH, Corticosteroids, adrenaline and glucagon
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What are the Effects of Insulin?
-on K
-Liver
- Promotes Potassium Uptake
- Enhances Glucose uptake and Storage (glycogen)
- Increases triglycerides and VLDL production
- Decreases breakdown of Proteins
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insulin actions on:
Muscle
Adipose
- enhances Glucose uptake
- decreases the breakdown of proteins for energy and enhances their synthesis
Enhaces lipogenesis and glucose uptake
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What is added to Insulins to increase the stability, duration of action and shelf life?
Where is insulin metabolized?
Zinc and Protamine
In the Liver and Kindney
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What is the Function of Long or intermediate acting Insulins?
What is the function of Short Acting insulins
- To maintain the background or basal level of insulin
- to control postprandial hyperglycemia
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Ultra-rapid onset of action and very short
acting Insulins are? They dont LAG
- Insulin lispro,
- Insulin aspart,
- Insulin glulisine
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What are the Therapeutic uses of insulin?
- -All Type 1 DM patients
- -Only the type II patients that fail to maintain blood glucose
- Gestational DM
- Postpancreatectomy
- Diabetic Ketoacidosis ( regular insulin)
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Rapid onset - Short acting Insulin
- Crystalline Zinc insulin (Regular type)
- -Only insulin given in ketoacidosis !!!
- -Leads to early postprandial hyperglycemia and late postprandial hypoglycemia
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Intermediate Onset ?
NPH insulin
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Slow Onset & Long Acting insulins (takes to GD long)
Insulin Glargine and Insulin Detemir
Prevents hyperglycemia between the doses.
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Ultra-rapid onset and regular insulin types control?
- postprandial hyperglycemia &
- administered just before meal
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Intermediate onset and Slow onset control what?
maintain basal insulin levels and control blood glucose between meals
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When will you see Hyperosmolar, hyperglycemic syndrome (nonketotic coma)?
occurs in elderly patients with type II DM
Have hyperglycemia and dehydration
Treat: Faster fluid replacement and low dose insulin
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What are the Main Clinical Symptoms of Diabetic ketoacidosis?
- Dehydration (due to deep slow respirations)
- and Tachycardia
- See elevated Ketones in the urine
- Low blood pH
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What do you do to treat diabetic Ketoacidosis?
- -Insulin (Regular) by IV
- -IV fluids (normal saline or with glucose)
- - Monitor Potassium levels (because it would be peeed out when trying to concentrat the urine)
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What is Hyperosmotic Hyperglycemic syndrome?
Treatment?
- Seen in elderly patients with Type II
- See Hyperglycemia and dehydration
- decline in mental status and convulsions (see NO acidosis)
- - Faster replacement of fluids
- - prophylatic heparin
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What are the signs and symptoms of Hypoglycemia?
Treatment?
Sweating, anxiety, palpation, tremor, diziness and weakness.
Sever--> Seizures and Coma
- Mild- Sugar tablet
- Sever-- 50% Glucose IV, Glucagon
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What is the Effect of Betablockers on Insulin?
Prolongs Hypoglycemia by:
- Decreasing warning signs
- Inhibit Glycogneolysis
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What are the Effect of Thiazides, Furosemie and Vifedipine on insulin?
Corticosteroids act by?
They inhibit insulin secretion.
increaseing the Blood sugar and decreasing the effectivness of insulin
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ORAL HYPOGLYCEMIC AGENTS
(OHA), what are they?
- 1. Insulin secretagogues-- increase insulin production
- 2. Biguanides-- decreaseglucose production by the liver
- 3. Thiozolidinediones-- Increase uptake of sugar my muscle
- 4. Alpha- glucosidase inhibitors-- slow suger absorption in the gut
- 5. Incretin based therapy
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1. Insulin secretagogues, what are they?
Name the different ones
how do they work?
what are the newer ones?
What are they used for?
-Sulfonylureas
- 1st Generation – Tolbutamide, Chlorpropamide, Tolazamide
- 2nd generation – Glyburide, Glipizide, Glimepiride
-close the ATP sensitive K+ channels-->insulin released
- - Newer drugs - Repaglinide & Nateglinide
- - post prandial hyperglycemia in type II patients
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2. Biguanides
Name one
What is its mechanism?
Adverse reactions?
Metformin
-Inhibiting gluconeogenesis and Enhance tissue glucose uptake & utilization
- Lactic acidosis
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3. Thiazolidinediones / glitazones
name them.
Mechanism?
Adverse effect?
Pioglitazone & Rosiglitazone
binding to Peroxisome proliferator activated receptor –gamma (PPAR-γ)-->Increase tissue glucose uptake
Fluid retention
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4. Alpha-glucosidase inhibitors
Name them.
Mech?
AE?
- Acarbose & Miglitol
- -Decrease digestion & absorption of
- carbohydrates
Adverse effects: Flatulence
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Newer drugs used to control postprandial glucose?
- 1. Pramlintide
- by inhibiting glucagon release
- 2. Exenatide
- Increase insulin release
- 3. Sitaglipin
- Prolongs effect of GLP-1
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What are the Glucocorticoid drugs?
which are short acting and which are long acting?
- -Short acting - Hydrocortisone
- (cortisol), cortisone
-Intermediate acting - Prednisone , Prednisolone, Methylprednisolone, Triamcinolone,
-Long acting - Betamethasone, Dexamethasone
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What are the mineral corticoid drugs?
Fludrocortisone
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Glucocorticoids – pharmacological actions?
1. Anti-inflammatory & immunosuppressive effects
- -Predominantly act on peripheral leukocytes (IL-2), decreasing their production by Inhibiting activation of phospholipase A2 (PLA2)
- -Inhibits macrophages and APC
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Glucocorticoids – pharmacological actions 2?
Effects on metabolism of carbohydrates,
proteins & fats.
Prolonged use leads to?
- Stimulate gluconeogenesis, Increase serum glucose
- Breaks muscle proteins, Induce lipolysis & redistribution of fat.
adrenal atrophy
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When is glucocorticoids used for replacement theropy?
1. Acute adrenal insufficiency (Addison’s crisis):
2. Chronic adrenal insufficiency / Addison’s disease
3. Congenital adrenal hyperplasia
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What are some Non-endocrine uses of Glucocorticoids?
Should you use it for HSV?
- (a) Allergic diseases
- (b) Bronchial asthma
- (c) Collagen vascular disorders
- (d) Autoimmune diseases
- (e) Ocular diseases
- f) Skin diseases
- (h) Gastrointestinal diseases
- (i)To reduce cerebral edema
- (j) Malignancies
- (k) To prevent organ transplant rejection
- (l) In preterm labor
NO!!! it is Contraindicated
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Adverse effects of Glucocorticoids
- -Sudden withdrawal
- leads to Acute adrenal insufficiency
- -Iatrogenic Cushing’s
- syndrome: redistribution of fat -moon
- face, thin extremities, buffalo hump
- -Thin skin (fragile)
- with purple striae and easy bruising
- -Hypertension &
- edema
- -Hyperglycemia
- -Myopathy & muscle wasting
- -Susceptible for
- infection: TB, candidiasis etc
- -Peptic ulcer
- -Osteoporosis
- -Hypomania, acute psychosis & depression
- -Posterior subcapsular Cataract
- & glaucoma
- -Delays wound healing
- -Growth retardation in children
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Contraindications / cautiously used
- -Osteoporosis
- -Psychosis
- -Epilepsy
- -Peptic ulcer
- -Glaucoma
- -Diabetes Mellitus
- -Hypertension & congestive heart failure
- -Varicella & tuberculosis infections
- -Pregnancy (esp 2nd trimester)
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Mineralocorticoids: Aldosterone
What is the Drug?used in? what is a AE?
Fludrocortisone
replacement therapy in hypoadrenalism
Edema due to Na retention
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What are some Adrenalcorticoal Antagonists?
- Inhibitors of glucocorticoids synthesis
- Metyrapone
- Mifepristone
- Mitotane
- Aldosterone receptor blockers
- Spironolactone & eplerenone
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