HYPO-HYPERGLYCEMIA

ENDOCRINE GLAND

Produces hormones in the islets of Langerhans

ALPHA CELLS

produce glucagon, in response to ↓ blood sugar

BETA CELLS

produce insulin, in response to ↑ blood sugar

DELTA CELLS

produce somatostatin, blocks the secretion of insulin & glucagon

EXOCRINE GLANDS

• Releases sodium bicarbonate and pancreatic enzymes directly into the common bile duct to be released into the small intestine

• Neutralizes the acid chyme from the stomach and aids digestion

INSULIN

Hormone produced by the beta cells of the islets of Langerhans

ACTIONS OF INSULIN

• Released into circulation when the levels of glucose around these cells rise

• Stimulates the synthesis of glycogen, the conversion of lipids into fat stored in the form of adipose tissue, and the synthesis of needed proteins from amino acids

HYPERGLYCEMIA

Increased blood sugar

GLYCOSURIA

• Sugar is spilled into the urine

• glucose concentration in blood too ↑ for complete reabsorption

POLYPHAGIA

• Increased hunger

• hypothalamic centers can’t take in glucose & sense they are starving

POLYDIPSIA

• Increased thirst

• tonicity of the blood is ↑ owing to the ↑ glucose & waste products in the blood & the loss of fluid with glucose in the urine

LIPOLYSIS

• Fat breakdown

• body breaks down stored for energy because glucose is not usable

KETOSIS

Ketones cannot be removed effectively

ACIDOSIS

• Liver cannot remove all of the waste products

• Acid = primary waste product

DIABETES MELLITUS

• Complex disturbances in metabolism

• Affects carbohydrate, protein, and fat metabolism

DM CLINICAL SIGNS

• Hyperglycemia (fasting blood sugar level greater than 126 mg/dL)

• Glycosuria (the presence of sugar in the urine)

ATHEROSCLEROSIS

• Disorder Associated with Diabetes

• Heart attacks and strokes related to the development of atherosclerotic plaques in the vessel lining

RETINOPATHY

• Disorders Associated with Diabetes

• With resultant loss of vision as tiny vessels in the eye are narrowed and closed

NEUROPATHIES

• Disorders Associated with Diabetes

• With motor and sensory changes in the feet and legs and progressive changes in other nerves as the oxygen is cut off

NEPROPATHY

• Disorders Associated with Diabetes

• With renal dysfunction related to changes in the basement membrane of the

TYPE 1: INSULIN DEPENDENT DM

• Usually a rapid onset; seen in younger people

• Connected in many cases to viral destruction of the beta cells of the pancreas

• Taken for life

• Treated with insulin subcutaneous injections

TYPE 2: NON INSULIN DEPENDENT DM

• Usually occurs in mature adults

• Has a slow and progressive onset

• Treated with oral hypoglycemic agents

S/S OF HYPERGLYCEMIA

•     Fatigue

•     Lethargy

•     Irritation

•     Glycosuria

•     Polyphagia

•     Polydipsia

•     Itchy skin

SIGNS OF DANGEROUS HYPERGLYCEMIA

•     Fruity breath as the ketones build up in the system and are excreted through the lungs

•     Dehydration as fluid and important electrolytes are lost through the kidneys

•     Slow, deep respirations (Kussmaul’s respirations) as the body tries to rid itself of high acid levels

•     Loss of orientation and coma

HYPOGLYCEMIA

–     Blood sugar concentration lower than 40 mg/dL

Occurrence:

• Starvation

• Lowering the blood sugar too far with treatment of hyperglycemia

PAST INSULIN DELIVERY

• Subcutaneous injection

PRESENT INSULIN DELIVERY

• Subcutaneous injection, insulin jet injector, insulin pen, extended insulin pump, long-acting insulin

FUTURE INSULIN DELIVERY

• Implantable insulin pump, insulin patch, inhaled insulin

ORAL ANTIDIABETIC AGENTS

• Sulfonylureas

• Non Sulfonylureas

• Biguanides

• Meglitinides

• Alpha-glucosidases

• Thiazolidinediones

SULFONYLUREA

• First oral agents introduced

• Stimulate the pancreas to release insulin

NON-SULFONYLUREA

• Introduced more recently

• Act to decrease insulin resistance or alter glucose absorption and uptake

ADVANTAGES OF SECOND-GENERATION SULFONYLUREAS

•     Excreted in urine and bile, making them safer for patients with renal dysfunction

•     Do not interact with as many protein-bound drugs as the first-generation drugs do

•     Have a longer duration of action; can take them only once or twice a day, increasing compliance

DIAZOXIDE AND GLUCAGON

Types of Glucose-Elevating Agents

GLYBURIDE

Sulfonylurea Prototype

PROGLYCEM

Diazoxide Prototype

GLUCAGEN

Glucagon Prototype

DIAZOXIDE

• Can be taken orally

GLUCAGON

• The hormone produced by the alpha cells of the pancreas to elevate glucose levels

• Can be given only parenterally; preferred for emergency situations 

• IV , onset in 1 min.

BIGUANIDES

• Action: inhibit hepatic glucose production and increase the sensitivity of peripheral tissue to insulin

• May be given with sulfonylureas

• Side Effects: Abdomen bloating, nausea, cramping, and diarrhea

MEGLITINIDE

• Action: Stimulate the beta cells of the pancreas to secrete insulin

• Minimal risk of hypoglycemia

ALPHA-GLUCOSIDASE INHIBITORS

• Action: inhibit an enzyme called alpha-glucosidase (enzyme responsible for the hydrolysis of saccharides to be converted to glucose)

• Must be taken with meals

• May be given with sulfonylureas

• Side Effects: Flatulence, diarrhea, and abdominal pain

THIAZOLIDINEDIONES

• Action: Decrease insulin resistance by decreasing gluconeogenesis, glucose output, and triglyceride synthesis in the liver

• Monitor for hepatic toxicity.

• May be given with sulfonylureas

• Side Effects: Hepatic toxicity, weight gain, edema, and mild anemia

SIDE EFFECTS OF SULFA

• Hematology

• Hemolytic anemia, thrombocytopenia, and jaundice

• Gastrointestinal

• Nausea, epigastric fullness, and heartburn

EFFECTS OF INSULIN

• Allergic reactions

• Lipodystrophy

• Insulin resistance