Diabetes ppts

Regulates carbohydrate metabolism

Metabolism of fats and protein

• Lowers blood glucose levels by stimulating peripheral glucose uptake especially in the skeletal
• muscles

Type I--Absolute Insulin Deficiency

Type II--Relative Insulin Deficiency

Gestational

Prediabetes

• Diabetes Mellitus and Diabetes Insipidus (insufficient amount of Antidiuretic Hormone) are two different, distinct endocrine disorders!
• Commonality: both disorders produce large volume of urine.

Often manifests in childhood or puberty

Abrupt failure of the pancreas

Pathogenesis is unclear

5-10% of all diabetics

• Leading theory is born with predisposition and exposed to virus which pulls it out.
• Type 1-used to be referred to as IDDM (insulin dependent DM).

Correlated with obesity

• Usually seen in adults over the age of 30 but also
• identified in young

Insulin resistance

Type 2 was referred to as NIDDM(non insulin dependednt DM).

-insulin is still produced but cells arent as sensitive to it. Meds increase cell sensitivity

Hypoglycemia

Hyperglycemia

Diabetic Ketoacidosis (DKA)/Hyperosmolar Glycemic State (HHS)

50. brain damage can ensue if if it is below 40

140

Type 1 diabetes

• Type 2
• whats happening is the osmolality of the blood is
• completely off bc sugar is so highly concentrated in blood. Lot of urine.

–Hyperglycemia

–Dehydration

–Vomiting

–Electrolyte imbalance: Na+ and K+

–Hemoconcentration

–Ketoacidosis

–Shock

body starts to break apart fat and muscle to get glucose bc body doesn’t see all of the glucose that you have in your blood.

• This is why a manifestation of type
• 1 is weight loss. Your body thinks its starving itself of glucose when it really has an abundance.

• Fat will yield fatty acids and protein/muscle yeilds ketones=ketoacidosis. Throws the body
• into an acidic state. These people hyperventilate to blow off the acid. All of these things contribute to shock

–Arteriosclerosis

–Myocardial Infarctions

–Cerebral Vascular Accidents

–Hypertension

–Erectile dysfunction

–Blindness secondary to retinopathy

–Amputation secondary to Infections such as gangrene

–Renal damage

–Neuropathy

• Short-rapid Lispro (Humalog, Novolog),
• short-slow (Humulin–R, Novolon–R)
• intermediate NPH (Humulin–N, Novolin–N),
• long acting glargine (Lantus)
• combination
• (70/30)

Diabetic Agents

Glycemic control of diabetes mellitus type I to prevent complications

Necessary for carbohydrate, fat and protein metabolism

Increases glucose transport across muscle and fat-cell membranes to reduce serum glucose levels.

Promotes the conversion of glucose to its storage form: glycogen

Triggers amino acid uptake and conversion of protein in muscle calls and inhibits protein degradation

Stimulates triglyceride formation and inhibits release of free fatty acids from adipose tissue

Converts lipoproteins to fatty acids

Metabolic: hypoglycemia, hyperglycemia, or Somogyi, or dawn phenomenon

Local: lipoatropy, itching, swelling and redness

Decrease hyperglycemic effect

Increase hypoglycemic effect

Beta adrenergic blocking agents

Blood sugar, HgA1c, Cholesterol

• they take insulin and in morning sugars may be high. Rebound hypoglycemia.
• Body sees sugars go low so they start to use glycogen storage in the liver.

tried to get control of sugars but are unable to do this

per milliliter in concentrations of 100 or 500U/mL

parenterally because it is destroyed in the GI tract

provides slow steady absorption. Absorption is dependent on the site.

regular, aspart, lispro and glulisine can be given IV.

NPH, Detemir and glargine insulin cannot be given IV

• Stomach is most rapid absorption,
• followed by arm or thigh.
• Most people stick with one site and then rotate places in the site.
• You can give rapid and regular acting IV.
• You cannot give slow acting IV.

-Regular Insulin (Humulin R, Novolin R)

Onset: 0.5-1hr

Peak: 1-5 hr

Duration: 6-10 hr

(Humulin N, Novolin N)

Onset: 1-2 hr

Peak: 6-14 hr

Duration:16-24 hr

(Levemir)

Onset: 6-8 hr

Peak: 12-24 hr

Insulin Glargine (Lantus)

Onset: 70 minutes

Peak: none

Duration: 24 hr


Shouldn’t be mixed with other insulins. One drawback is basal control. Need to give something else before meals.

Isophane Insulin Suspension (NPH) and regular insulin (Novolin 70/30, Novolin 50/50)

Onset: 30 min

• Peak 70/30: 2-12 hr
• Peak 50/50: 2-5.5 hr

Duration: 24 hr

Exubera inhalation system withdrawn from the market in 2007 due to poor sales.

Side effects: cough, bitter taste, hypoglycemia

Higher cost than injectables

Concern about allergic reactions, pulmonary irritation and lung cancer

Biguanides

Sulfonylureas

Glinides (Meglitinides)

Thiazolidinediones

Alpha-glucosidase Inhibitors

Gliptins

Metformin (Glucophage)

Initial choice of treatment for most Type II DM patients Glycemic control of diabetes mellitus type II to prevent complications

Prevention of Type II DM

Used in treatment of polycystic ovary disease

Gestational diabetes

Produces its antidiabetic effects only in the presence of insulin

Decreases glucose production in liver

Facilitates insulin’s action on the peripheral receptor sites

Lowers triglycerides to promote weight loss

Peak: 2 hours

• Most Common: GI: nausea, vomiting, diarrhea,
• metallic taste, abdominal discomfort, flatulence, decreased appetite

Metabolic: lactic acidosis

Hematologic: symptomatic B12 deficiency or megoblastic anemia

Alcohol, Cimetidine, contrast dye for radiographic studies

Blood sugar, HgA1c, cholesterol

glipizide (Glucotrol)

1st generation: tolbutamide ( Orinase), chlorpropamide (Diabinase)

2nd generation: glyburide (Diabeta, Micronase), glimepiride (Amaryl)

beats pancreas into shape

Glycemic control of diabetes mellitus type II to prevent complications

• Lowers blood glucose level by stimulating insulinrelease from functioning beta cells in the pancreas
• Inhibits hepatic glyconeogenesis
• Increase number of insulin receptors in peripheral tissue increasing insulin sensitivity

Hypoglycemia, pallor, muscle weakness, blurred vision, agitation, irritability, mental confusion, tachycardia, alterations in consciousness

GI: nausea, anorexia, heartburn, metallic taste

Dermatologic: maculopapular rash, uticaria, pruritus and erythema


CV: ? Sudden cardiac death?

Alcohol-disulfiram reaction

Low BS: Alcohol, NSAIDS, sulfonamide antibiotics, cimetidine

Beta Blockers

Blood glucose, HgA1c, cholesterol

Onset: 2 hr

Peak: 2- 4 hr

Duration: 24 hr

Pregnancy Cat C

Renal or hepatic alterations will increase drug levels

Repaglinide (Prandin)

nateglinide (Starlix)

Glycemic control of diabetes mellitus type II to prevent complications

similar to sulfonylurea

Increase the release of insulin from the pancreas

Hypoglycemia

Gemfibrozil (Lopid)

Blood sugar, HgA1c, Cholesterol

drug that increases triglycerides. Affect the metabolism.

Pregnancy Cat C

Onset: rapid

Peak: within 1 hour

Duration: unknown

Rosiglitazone (Avandia)

Glycemic control of diabetes mellitus type II to prevent complications

Enhance the activity of endogenous insulin by improving target cell response

Decrease insulin resistance

Recent FDA warning regarding increased risk cardiovascular events!

pioglitazone (Actos)

Most common: respiratory tract infections,

Sinusitis, headache, myalgias, sore throat, fluid retention, edema, fatigue, diarrhea, increased LDLs

Most serious: ? hepatotoxicity

Weight, LFTs, Cholesterol, Blood sugars, HgA1c

Gemfibrozil (Lopid), Insulin

Acarbose (Precose)

miglitol (Glyset)

Glycemic control of diabetes mellitus type II to prevent complications

Inhibit alpha-glucosidase inhibitors in the small intestine which delays absorption of dietary carbohydrates; this reduces the rise in BS after a meal.

Does not depend on the presence of insulin

Mostly GI: flatulence, diarrhea, abdominal distention, borborygimus

Liver: elevated serum aminotransferases, especially ALT, AST

Hypoglycemia, anemia

Sulfonylureas, Insulin, Metformin

CBC, iron, blood sugars, HgA1c, LFT

Onset: less than 30 minutes

Duration: 4-6 hours

Metabolized mainly in the GI tract

Contraindicated in patients with GI disorders

Pregnancy Cat B

Cant give orange juice or table sugar

Sitagliptin (Januvia)

none

• Glycemic control of diabetes mellitus type II
• to prevent complications, used alone or in combination

Enhances the action of incretin hormones, endogenous compounds that stimulate insulin release and suppress postprandial release of glucagon

None known

Most common: upper respiratory infection, headache, nasal passage inflammation

blood sugars, HgA1c

pregnancy

• Injectable drug
• –Amylin mimetic

–Peak: 20 minutes Duration: 2 hr

–Adverse Effect: hypoglycemia, nausea

Injectable drug

–Incretin mimetic

–Peak: 2 hr Duration 5 hr

–Adverse Effect: hypoglycemia, GI effects, development of anti-exenatide antibodies

decreases gastric emptying and decreases glucagon secretion.

Insulin release

More insulin production. Worry about pancreatitis. Sign is abdominal and back pain.

Glucagon

-A hyperglycemic polypeptide

-Used in the unconscious diabetic patient to reverse hypoglycemia

-Usually given IV and onset is within 1 minute

Cannot give orange juice to someone who is fading in and out of consciousness. They could aspirate and they could have a lot of other problems. Cant give it orally.