endocrine system

Glands

secrete their products directly into the chemical substances secreted by the endocrine glands

Hormones

chemical substances secreted by the endocrine glands.

HYPOTHALAMUS

Produce and secrete pro- hormones (hormones that stimulate or inhibit production/ release of pituitary
hormones.)

PITUITARY GLAND

Commonly referred to as the master gland because of the influence it has on secretion of hormones by other endocrine glands

Somatostatin/ Growth hormone (GH)

o Inhibits growth hormone and thyroid- stimulating hormone.

o Stimulates growth of bone and muscle, promotes protein synthesis and fat metabolism, decreases carbohydrate metabolism.

Adrenocorticotropic hormone (ACTH)

Stimulates synthesis and secretion of adrenal cortical hormones

Thyroid-stimulating hormone (TSH)

Stimulates synthesis and secretion of thyroid hormones

Follicle- stimulating hormone (FSH)/ Sertoli cell-stimulating hormone (males)

o Female: stimulates growth of ovarian follicle, ovulation.

o Male: stimulates sperm production

Luteinizing hormone (LH) / Leydig cell-stimulating hormone (males)

o Female: stimulates development of corpus luteum, release of oocyte, production of estrogen and progesterone.

o Male: stimulates secretion of testosterone, development of interstitial tissue of testes

Prolactin

o Prepares female breast for breast- feeding

Antidiuretic Hormone (ADH)/ Vasopressin

Increases water reabsorption by kidney

Oxytocin

o Stimulates contraction of pregnant uterus, milk ejection from breasts after child birth

ADRENAL CORTEX

The outer portion of the adrenal gland; stimulated by ACTH to produce corticosteriods.

Mineralocorticoids (aldosterone)

o Increase sodium absorption, potassium loss by kidney.

Glucocorticoids (cortisol)

o Affect metabolism of all nutrients; regulates blood glucose levels, affects growth, has anti- inflammatory action, and decreases effects of stress

Adrenal androgens

Have minimal intrinsic androgenic activity; they are converted to testosterone and dihydrotestosterone in the periphery

ADRENAL MEDULLA

The center of the adrenal gland that reacts to autonomic nervous system signals to release catecholamines.

Epinephrine/Adrenaline

Prepares the body for the fight or flight response by converting glycogen, stored in the liver, to glucose and increasing cardiac output.

Norepinephrine/Noradrenaline

Produces effect similar to epinephrine and produces extensive vasoconstriction

THYROID GLAND

Butterfly- shaped organ located in the lower neck, anterior to the trachea

PARATHYROID GLANDS

Small glands, usually four, surround the posterior thyroid tissue; they are often difficult to locate and may be removed accidentally during thyroid or other neck surgeries.

PANCREATIC ISLET CELLS

A slender, elongated organ lying horizontally in the posterior abdomen behind the stomach which function as an exocrine and an endocrine gland.

Glucagon (alpha cells)

o Glycogenolysis- breakdown of stored glucose.

o Gluconeogenesis- production of new glucose from amino acids and other substances

Insulin (beta cells)

• Lower blood glucose by facilitating glucose transport across cell membranes of muscle, liver, and adipose tissue

Somatostatin (delta cells)

o Delays intestinal absorption of glucose.

KIDNEY

Paired organs located on either side of the vertebral column. They are between the 12th thoracic and 3rd lumbar vertebrae in the posterior abdomen behind the peritoneum.

1,25- Dihydroxy vitamin D

Stimulates calcium absorption from the intestine

Renin

Activates renin- angiotensin-aldosterone system.

Erythropoietin

Increases red blood cell production

Progesterone

o Regulates the endometrium of the uterus

o Maintains pregnancy

GIGANTISM

Oversecretion of GH results in gigantism in children; a person may be 7 or even 8 feet tall

Causes:
• Tumor of somatotrophs (signs of increased ICP)
Diagnostic Tests:
• CT and MRI.
• Serum levels of pituitary hormones.

Management:
• Pharmacological Management
o Bromocriptine (Parlodel)

- A dopamine antagonist
o Octreotide (Sandostatin)
- A synthetic analogue of GH
• Surgical Management
o Hypophysectomy.

ACROMEGALY

An excess of Growth hormone in adults, results in bone and soft tissue deformities and enlargement of the viscera without an increase in height.

Diagnostic Tests:
• CT and MRI.

• Serum levels of pituitary hormones

Management:
• Pharmacological Management
-Bromocriptine (Parlodel) - a dopamine antagonist.
-Ocreotide (Sandostatin) - a synthetic analogue of GH
• Surgical Management
-Hypophysectomy

DWARFISM

Generalized limited growth resulting from insufficient secretion of growth hormone during childhood.

Diagnostics Tests:
• X-ray
• Computed tomography and MRI
• Blood sample

Management:
• Pharmacological Management
-Somatrem (Protropin)
-Somatropin (Humatrope)
• Nursing Interventions
-Provide psychologic support and acceptance for alteration of body image.

HYPERPROLACTINEMIA

Female:

• Prolactin-secreting tumors
• Amenorrhea
• Galactorrhea

Male:
• Gynecomastia
• Decreased sex drive
• Impotence

SYNDROME OF INAPPROPRIATE ANTI-DIURETIC HORMONE (SIADH

Excessive ADH secretion from the pituitary gland even in the face of subnormal serum osmolality.
Patients cannot excrete dilute urine, retain fluids, and develop a sodium deficiency known as dilutional hyponatremia.

DIABETES INSIPIDUS (DI)

Disorder of the posterior lobe of the pituitary gland that is characterized by a deficiency of ADH (vasopressin )

GOITER

Thyroid tumors or enlargement sufficient to visible swelling in the neck.

HYPERTHYROIDISM

Other terms: Grave’s disease/ Basedow’s/ Parry’s disease.
-Description: Results from an excessive output of thyroid hormones caused by abnormal stimulation of the thyroid gland by circulating immunoglobulins.
-Diffuse toxic non-nodular goiter

HYPOTHYROIDISM

Description: State of insufficient serum thyroid hormone.

Cause: Autoimmune thyroiditis

Myxedema

• Refers to the accumulation of mucopolysaccharides in subcutaneous and other interstitial tissues
• Mucinous (mucus-filled) edema
• Extreme symptoms of severe hypothyroidism

Exophthalmos

-Bulging eyes, which produces a startled facial expression
-von Graefe’s sign: eyelid lag when looking downwards
-Dalyrimple’s sign: upper eyelid retraction

Thyrotoxicosis

ü Nervousness

ü Irritable and apprehensive

ü Palpitations
-Tachycardia
-Heat intolerance
-Diaphoresis
-Flush skin, warm, soft and moist
-Tremor

HYPERPARATHYROIDISM

Overproduction of parathormone by the parathyroid glands, is characterized by bone decalcification and the development of renal calculi (kidney stones) containing calcium.

HYPOPARATHYROIDISM

Inadequate secretion of parathormone after interruption of the blood supply or surgical removal of parathyroid gland tissue during thyroidectomy, or radical neck dissectio.

PHEOCHROMOCYTOMA

Tumor that is usually benign and originates from the chromaffin cells of the adrenal medulla.
-It is one form of hypertension that is usually cured by surgery; however, without detection and treatment, it is usually fatal

ADDISON’S DISEASE

Adrenocortical insufficiency, occurs when adrenal cortex function is inadequate to meet the patient’s need for cortical hormones.
-Autoimmune or idiopathic atrophy of the adrenal glands is responsible for the vast majority of cases.

CUSHINGS DISEASE

Excessive, rather than deficient, adrenocortical activity caused by use of corticosteroid medications.
-Is infrequently the result of excessive corticosteroid production secondary to hyperplasia of the adrenal cortex, tumor of the pituitary gland

DIABETES MELLITUS

Group of metabolic diseases characterized by increased levels of glucose in the blood (hyperglycemia) resulting from defects in insulin secretion, insulin action, or both

TYPE 1 DIABETES MELLITUS

• Characterized by destruction of the pancreatic beta cells.
• Abnormal response in which antibodies are directed against normal tissues of the body, responding to these tissues as if they were foreign.

TYPE 2 DIABETES MELLITUS

-Idiopathic

• This is called metabolic syndrome, which includes hypertension, hypercholesterolemia, and abdominal obesity

Short-acting insulins

are called regular insulin (marked R on the bottle). Regular insulin is a clear solution and is usually administered 20 to 30 minutes before a meal. Regular insulin is the only insulin approved for IV use

Human insulin

preparations have a shorter duration of action than insulin from animal sources because the presence of animal protein triggers an immune response that results an in the binding of animal insulin.

Intermediate-acting insulins

are called NPH insulin (neutral protamine Hagedorn) or lente insulin. Intermediate-acting insulins

“Peakless” basal or very long-acting insulins

that’s is, the insulin is absorbed very slowly over 24 hours and can be given once a day

Local Allergic Reactions.

Redness, swelling, tenderness, and induration or 2- to 4-cm wheal) may appear at the injection
site 1 to 2 hours after the insulin administration

Systematic Allergic Reactions.

When they do occur, there is an immediate local skin reaction that gradually spreads into generalized urticaria (hives).

Lipodystrophy

refers to a localized reaction, in the form of either lipoatrophy of lipohypertrophy, occurring at the site of insulin injections.

Lipoatrophy

is loss of subcutaneous fat; it appears as slight dimpling or more serious pitting of subcutaneous fat

Resistance to Injected Insulin

Most patients have some degree of insulin resistance at one time or another. The most common being obesity, which can be overcome by weight loss

Morning hyperglycemia

An elevated blood glucose level on arising in the morning is caused by an insufficient level of insulin, which may be caused by several factors: the dawn phenomenon, the Somogyi effect, or insulin waning

Sulfonylureas

Stimulate beta cell of the pancreas to secrete insulin; may improve binding between insulin and insulin receptors of increase the number of insulin receptors or increase the number of insulin receptors

Biguanide

Ø Inhibits production of glucose by the liver

Ø Increase body tissues sensitivity to insulin

Ø Decrease hepatic synthesis of cholesterol

Ø The only biguanide in the market: Metformin

Alpha-glucosidase inhibitors

Delay absorption of complex carbohydrates in the intestine and slow entry of glucose into systemic circulation

Non-sulfonylureas Secretagogues (Meglitinides and phenylalanine derivatives)

Stimulate pancreas to secrete insuli

Thiazolidinediones (Glitazone)

Sensitized body tissue to insulin; stimulate receptor sites to lower blood glucose and improve action of insulin

Dipeptide-pepidase-4 (DDP-4) Inhibitors

Increase and prolongs the action of incretin, a hormone that increases insulin release and decreases glucagon levels, with the result of improved glucose control

Insulin Waning

Progressive rise in blood glucose from bedtime to morning

Treatment
- Progressive rise in blood glucose from bedtime to morning Increase evening (predinner or bedtime) dose of intermediate acting or long-acting insulin, or institute a dose of insulin before the evening meal if one is not already part of the treatment regimen.

Dawn Phenomenon

Relatively normal blood glucose until about 3 am, when the level begins to rise

Treatment

-Change time of injection of evening intermediate-acting insulin from dinnertime to bedtime

Somogyi Effect

Normal or elevated blood glucose at bedtime, a decrease at 2-3 am to hypoglycemic levels, and a subsequent increase caused by the production of counterregulatory hormones

Treatment

-Decrease evening (predinner or bedtime) dose of intermediate acting insulin, or increase bedtime snack

HYPOGLYCEMIA

Occurs when the blood glucose falls to less than 50 to 60 mg/dL (2.7 to 3.3 mmol/L), because of too much insulin or oral hypoglycemic agents, too little food, or excessive physical activity.

Severe hypoglycemia

-Patient needs the assistance of another person for treatment of hypoglycemia.
-Disoriented behavior
-Seizures
-Difficulty arousing from sleep
-Loss of consciousness.

DIABETES KETOACIDOSIS

Caused by an absence or markedly inadequate amount of insulin. This deficit in available insulin results in disorders in the metabolism of carbohydrate, protein, and fat. The three main clinical features of DKA are:
• Hyperglycemia
• Dehydration and electrolyte loss
• Acidosis

HYPERGLYCEMIC HYPEROSMOLAR NONKETOTIC SYNDROME (HHNS)

-Serious condition in which hyperosmolarity and hyperglycemia predominate, with alterations of the sensorium (sense of awareness)
-Ketosis is usually minimal or absent
-Persistent hyperglycemia causes osmotic diuresis, which results in losses of water and electrolytes