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Types of Hormonal and Metabolic Dysfunction (Anterior pituitary (Follicle…
Types of Hormonal and Metabolic Dysfunction
Anterior pituitary
Follicle-stimulating hormone (FSH)
Regulates the development, growth, pubertal maturation, and reproductive processes of the body.
Decreased levels
Females: cessation of reproductive cycles is commonly observed
Hypogonadism
Males: failure in production of normal numbers of sperm
Increased levels
Indication of subfertility and/or infertility.
Menopause
Adrenocorticotropic hormone (ACTH)
Hypercorticism
Cushing syndrome
Diagnostic criteria
24 hour urine college observing for elevation in cortisol excretion (false positives occur)
Imaging studies to locate tumors secreting excess ACTH or cortisol
Clinical manifestations
Glucose intolerance
Diabetes mellitus
Behavioral changes
Psychosis
Euphoria
Obesity of the trunk, face, and upper back.
"Buffalo hump"
"Moon face"
Suppression of the inflammatory and immune responses
Increased infections
Poor wound healing
Osteoporosis
Hirsutism
Development of excessive body and facial hair
Cause: prolonged exposure to glucocorticoids such as cortisol
Tumors of the adrenal gland that stimulate excess cortisol production
Tumors of the pituitary gland that stimulate excess ACTH production
Ectopic production of ACTH or CRH from a tumor at a distant site, such as small cell carcinoma of the lung
Long-term administration of corticosteroid medications
Prednisone
Treatment
Surgery or radiation to remove tumor
Corticosteroid medications to avert adrenal crisis during acute illness and gradually withdrawn
Component of the hypothalamic-pituitary-adrenal axis and is often produced in response to biological stress
Hypocorticism
Addison disease
One of the most serious endocrine disorders because it can lead to severe hypotension, shcok, and death
Diagnostic critera
Laboratory measurements demonstrating hyponatremia and hyperkalemia. Serum corticosteroid level that remains depressed after ACTH administration
Causes
Lack of CRH or ACTH
Destruction of the pituitary gland from tumors, hemorrhage, trauma, radiation, or surgical removal.
.
Lack of secretion of hormones from the adrenal cortex
Lack of hormones secreted from the adrenal cortex.
Autoimmune destruction of the layers of the adrenal cortex
Clinical manifestations
Hyperpigmentation of skin and mucous membranes from stimulated melanocytes
Hypoglycemia
Hyperkalemia
Treatment
Isotonic IV fluid replacement is infused along with hydrocortisone sodium succinate or phosphate.
eSalt intake may need to be increased in hot weather. The exception to this is for those patients with Addison disease caused by tuberculosis.
Growth hormone (GH)
a peptide hormone that stimulates growth, cell reproduction, and cell regeneration
Increased levels
somatotroph adenomas
Acromegaly
Decreased levels
Osteoporosis
Growth failure
Thyroid-stimulating hormone (TSH)
Decreased levels
Hypothyroidism
Diagnostic criteria
Laboratory measurements: sensitive TSH assay, free T4, total T4, and T3 uptake, thyroid autoantibodies, and antithyroglobulin tests
Patient history & physical examination
Clinical Manifestations
Constipation
Dry skin
Coarse hair
Lethargy
Weight gain
Myxedema
Protein–carbohydrate complexes accumulate in the extracellular matrix drawing water into the tissues
Treatment
Replacing deficient hormones to normalize TSH, T4, and T3
Levothyroxine (Synthetic T4)
Causes
Deficient thyroid hormone synthesis
Impaired TSH or TRH secretion
Destruction of the thyroid gland
Increased levels
Hyperthyroidism
Clinical manifestations
Agitation
Palpitations
Weigt loss
Irregular mentrual cycle
Fine hair
Goiter: enlargement of the thyroid gland due to follicular epithelial cell hyperplasia
Exophthalmos: a protrusion of the eyeballs
Causes
Excessive stimulation to the thyroid gland, diseases of the thyroid gland, or excess production of TSH by a pituitary adenoma
Certain medications containing large amouts of iodine
Health food supplements that contain seaweed
Cough expectorants,
Iodinated contrast dyes
Graves disease
Excessive stimulation of the thyroid gland, is the most common cause of hyperthyroidism and is the most common autoimmune condition in the United States.
Treatment
Medications to block thyroid hormone production
Methimazole
Gland destruction via radioactive iodine
Ablation of thyroid gland
Diagnostic criteria
Physical examination: enlarged and slightly firm thyroid gland as well as protrusion of the eyes
Patient history: family history of autoimmune disease, thyroid disease, or emigration from an iodine-deficient location
Laboratory measurements: Measurement of serum TSH level to test for the presence of hyperthyroidism.
Diagnosis of hyperthyroidism must be confirmed by the measurement of serum-free thyroxine.
Elevated serum levels of T3 and T4.
Lutinizing hormone (LH)
Decreased levels
Hypogonadism
Amenorrhea
Increased levels
Polycystic ovary syndrome
Works upon endocrine cells in the gonads to produce androgens.
Prolactin
The hormone that tell the body to make breast milk when pregnant.
Elevated levels
Women: Amenorrhoea & Anovulation
Men: Erectile dysfunction & loss of libido
Decreased levels
Women: Hypoprolactinemia (associated with ovarian dysfunction)
Men: Premature ejaculation, hypofunction of seminal vesicles, and hypoandrogenism
Posterior pituitary
Oxytocin
Released into the bloodstream as a hormone in response to stretching of the cervix and uterus during labor and with stimulation of the nipples from breastfeeding
Increased levels
Oxytocin levels during labor and delivery increase release of additional oxytocin until the birth of the baby.
Decreased levels
Occur after the birth of the baby, decreases stretching of cervix, and cycle is interrupted
Vasopressin (ADH)
Works at the level of the kidney to promote reabsoroption of water from the renal-collecting ducts into the vasculature, reducing fluid loss through decrease in urine output.
Inceased levels:
Syndrome of Inappropriate Antidiuretic Hormone secretion (SIADH)
A condition of excessive production and release of ADH despite changes in serum osmolality and blood volume.
Causes
Most common: tumor, somewhere in the body, which is secreting ectopic ADH.
Dysregulate ADH secretion in the central nervous system
Drugs that increase ADH secretion
Carbamazepine
Valproic acid
Chlorpropamide
Morphine
Amitriptyline
Clinical manifestations
Nausea
Anorexia
Hypotonic hyponatremia and include a decreased and concentrated urine output.
Tremor
Delirium
Psychosis
Gait disturbances
Treatment
Water restriction
Isotonic or hypertonic saline administered intravenously.
Drugs that can decrease ADH
Conivaptan: an antagonist of both V1A and V2 vasopressin receptors
Demeclocycline: most potent inhibitor of Vasopressin (ADH/AVP) action
Diagnostic criteria
Hypotonicity (plasma osmolality less than 280 mOsm/kg)
Hyponatremia
Highly concentrated urine with a high sodium content
Absence of renal, adrenal, or thyroid abnormalities
Decreased urine volume
Decreased levels:
Diabetes Insipidus
The inability of the body to concentrate or retain water
Causes
Ingestion of extremely large volumes of fluids and decreasing ADH levels; water intoxication can sometimes be attributed to a psychiatric disturbance
Inadequate kidney response to the presence of ADH, also called nephrogenic DI
Insufficient production of ADH by the hypothalamus or ineffective secretion by the posterior pituitary
Clinical manifestations
Polyuria: large volume urine output
Excessive thirst
Diagnostic criteria
Patient history: recent surgery to remove a tumor of the brain, or other cranial surgery, or head trauma.
Physical examination: may detect signs of dehydration and possibly an enlargement of the bladder due to constant over-filling.
Laboratory measurements: serum solute concentration, ADH levels, and urine-specific gravity
A urine-specific gravity of 1.005 or less and a urine osmolality less than 200 mOsm/kg are often found in DI.
Treatment
Hydration through oral water intake
IV hydration with a hypotonic solution
Desmopressin (DDAVP), a synthetic vasopressin analog, which acts as a potent antidiuretic.