Endocrine Dysfunction Adrenal Pituitary Endocrine System comprehensive source
- Slides: 60
Endocrine Dysfunction: Adrenal & Pituitary Endocrine System (comprehensive source) Endocrine Review (narrated online review) Medications-Endocrine (narrated PPTs) q q q Endocrine Drugs Overview Pituitary Drugs Adrenal Drugs Endocrine System
Pituitary Gland- “master gland” + Hypothalamus
Hypothalamus-functions Hypothalamus- integrative center for endocrine and autonomic nervous system *Hypothalamus and pituitary integrate communication between nervous and endocrine system Control of some endocrine glands by neural and hormonal pathways Two major groups of hormones secreted: inhibiting and releasing
Hypothalamus Two major groups of hormones secreted: inhibiting and releasing
ANTERIOR PITUITARY (Adenohypophysis) n SECRETES 6+ HORMONES: q ACTH (adrenocorticotropic hormone) controls release of cortisol in adrenal glands q *ACTH release; controlled by corticotropin-releasing hormone (CRH)
ANTERIOR PITUITARY(adenohypophysis) q q TSH (thyroid stimulating hormone) n Thyroid –releasing hormone; secreted by hypothalamic neuronscontrol release of TSH GH (growth hormone) (Somatotropin) stimulates growth of bone/tissue
q q q Prolactin- promotes mammary gland growth and milk secretion FSH (follicle stimulating hormone)- stimulates growth of ovarian follicles & spermatogenesis in males LH (lutenizing hormone)- regulates growth of gonads & reproductive activities
Posterior Pituitary (Neurohypophysis) What hormones are released by the posterior pituitary signaled by the hypothalamus? Antidiuretic hormone (ADH) ______ Oxytocin & ______.
ANTERIOR PITUITARY DISORDERS
ANTERIOR PITUITARY HYPERFUNCTION DISORDERS n ETIOLOGY Primary: defect in gland itself -releases a particular hormone that is too much or too little. q Secondary: defect is somewhere outside of gland i. e. GHRH from hypothalamus q TRH from hypothalamus
PITUITARY TUMORS n n 10% OF ALL BRAIN TUMORS What diagnostic tests diagnose a pituitary tumor? *Determined by symptoms presented; evaluate serum/urine hormone levels; stimulation/suppression tests for hormone levels; CT, MRI, etc n Tumors usually cause hyper release of hormones
ANTERIOR PITUITARY HYPERFUNCTION n What happens if: q TOO MUCH secretion of prolactin (prolactinoma)? Anovulation; menstrual irregularities; galactorrhea q TOO MUCH release of Lutenizing Hormone (LH)? “Polycystic ovary syndrome; , due to effect on corpus lutea q Too much growth hormone secretion? GIGANTISM IN CHILDREN; ACROMEGALY IN ADULTS n Which goolish character on the Addam’s Family had too much GH secretion
Effects of growth hormone. A, Comparison of (from left to right) gigantism, normal, and dwarfism. B and C, The patient’s hands and face show; Clinical signs of acromegaly. D, Acromegaly. Excessive secretion of growth hormone in the adult caused characteristic malocclusion of the teeth resulting from the overgrowth of the mandible.
n. Sing along
TOO MUCH GROWTH HORMONE n GIGANTISM IN CHILDREN q n skeletal growth; may grow up to 8 ft. tall; > 300 lbs ACROMEGALY IN ADULTS q q enlarged feet/hands, thickening of bones, prognathism (jaw projects forward), diabetes, HTN, wt. gain, H/A, Visual disturbances, diabetes mellitus
n ACROMEGALY IN ADULTS n progessive change in facial features n Hand in acromegaly; normal hand
What assessment findings would the nurse document? What priority health risks associated with acromegaly?
Video-You Tube Lecture “Effects of GH Deficiency in Adults” You Tube-Pituitary Giantism/Agromegaly “Egor” the Giant Video You Tube-Pituitary Giantism- Robert Wadlow “Worlds Tallest Man” died age 22
Cont. Hyperfunction of the Anterior Pituitary. An individual has a tumor of anterior pituitary gland which causes excess ACTH secretion • What “disease” is this? • What signs and symptoms are likely to be found? Cushing’s disease- condition in which pituitary gland releases too much adrenocorticotropic hormone (ATCH). Cushing's disease- a form of Cushing syndrome See next slide for Video. Remember this one-see adrenal disorders
Cushing’s Disease-
MEDICAL INTERVENTIONS PITUITARY TUMOR n *Medications (goal…. . . reduce GH levels) q Somatostatin analogs (octreotide) q GH receptor antagonists (Pegvisomant) q Dopamine agonists (cabergoline) Dostinex *inhibits prolactin (prolactinoma) n FYI- If inadequate GH prior to puberty- what “condition” will this individual have? what drug might be given to treat? Pituitary Dwafism (panhypopituitarism)- give GH (somatostatin)
MEDICAL INTERVENTIONS PITUITARY TUMOR/REPLACEMENT THERAPY n Radiation therapy q External radiation- bring down GH levels 80% of time q Steriotactic radiosurgeryn n Click to view You Tube video Risk post-procedure-increased risk for seizures
n Neurosurgery: q Transsphenoidal hypophysectomy n Most commonly used approach n Incision thru floor of nose into sella turcica.
Newer Method. Endoscopic. Transsphenoidal Hypophysectomy New Method Click to view! • No incisions ! • Less recovery time • Fewer complications
Posterior Pituitary-(Neurohypophysis) Name the hormones released by posterior pituitary when signaled by hypothalamus! ADH (vasopressin) and oxytocin
ADH (Vasopressin) n n secreted by cells in hypothalmus-stored in posterior pituitary acts on distal & collecting tubules of kidneys making more permeable to H 20 volume excreted ADH is released when? With decreases blood volume, increased concentration of Na+ or other substances (drugs as opiooids, thiazide diuretics) also, pain, stress n ADH has vasoconstrictive or vasodilation properties? vasocontrictive
Oxytocin n n Controls lactation & stimulates uterine contractions ‘Cuddle hormone’ Research links oxytocin and socio-sexual behaviors
Posterior Pituitary Disorders n n SIADH (TOO MUCH ADH!!) Numerous causes: q q *Small cell lung cancer , other types cancer CNS disorders *Medications as, thiazide diuretics, opioids, general anesthetics, tricyclic antidepressants, others Miscellaneous
SIADH (Syndrome of Inappropriate Antidiuretic Hormone Secretion)
If too much ADH, what clinical signs and symptoms are “typical”? n n Weight gain urine output serum Na levels (less than 120 m. Eq/L) n q q q weakness muscle cramps H/A
SIADH-if hyponatremia worsens-high risk neuro manifestations n n n lethargy decrease tendon reflexes *seizures-life threatening! (if serum Na less than 120 m. Eq/L)
Posterior Hypopituitary-ADH disorders Diabetes Insipidus-(DI) (too little ADH) Etiology: (50% idiopathic) • *Central- neurogenic- i. e. brain tumors • Nephrogenic - inability of tubules to respond to ADH • Psychogenic-
What Clinical Manifestations-DI? n n n Polydipsia Polyuria (10 L in 24 hours) Severe fluid volume deficit q wt loss q tachycardia q constipation q shock
FOCUS-DISORDERS OF ADRENAL GLANDS Adrenal Cortex n Adrenal Medulla n How Stuff Works
ADRENAL CORTEX n Think q q q Salt Sugar Sex SUGAR
SALT n Mineralocorticoids (F & E balance) q Aldosterone (renin from kidneys controls adrenal cortex production of aldosterone) n Na retention n Water retention n K excretion
Question: If Na level is low, does aldosterone promote renal reabsorption of sodium and excretion (loss) of potassium? YES or NO? ? YES
SUGAR (Cortisol)n GLUCOCORTICOIDS (regulate metabolism; critical in stress response) q CORTISOL responsible for control & metabolism of n CHO (carbohydrates) q amt. glucose formed q amt. glucose released n FATS-control of fat metabolism q Stimulates fatty acid mobilization from adipose tissue n PROTEINS-control of protein metabolism q stimulates protein synthesis in liver q protein breakdown in tissues n INFLAMMATORY and allergic response q immune system-more prone to infection
SEX n ANDROGENS q hormones which n q male characteristics release of testosterone Seen more in women than men
What is the RELEASE OF GLUCOCORTICOIDS CONTROLLED BY ______ ACTH (adrenocorticotropic hormone) Produced in anterior pituitary gland
ACTH n Circulating levels of cortisol q levels cause stimulation of ACTH q levels cause dec. release of ACTH What type of feedback mechanism is this? ? Negative
AFFECTED BY: n Individual biorhythms q q q n ACTH LEVELS -HIGHEST 2 HOURS BEFORE AND JUST AFTER AWAKENING. usually 5 AM - 7 AM Gradually decrease rest of day Stress- cortisol production and secretion
ADRENAL MEDULLA n n Fight or flight What is released by the adrenal medulla? CATECHOLAMINE RELEASE • Epinephrine • Norepinephrine
HYPER AND HYPOFUNCTION ADRENAL CORTEX HORMONES: Too much: Too little CUSHING’S Syndrome (TOO MUCH CORTISOL!) n n n secretion of cortisol from adrenal cortex 4 X more frequent in females Usually occurs at 35 -50 years of age *Cushing’s disease if due to inc ACTH secreting tumor from pituitary
ETIOLOGY: Cushing’s Syndrome n Due to q Excess of corticosteroids, particularly glucocorticoids: most common cause: n q q Iatrogenic administration of exogenous corticosteroids Prolonged adm. of coricosteroids 85% of endogenous cases due to ACTH-secreting pituitary tumor (Cushing’s disease) Other causes include n n Adrenal tumors (Cortisol secreting neoplasm within adrenal cortex) Ectopic ACTH production in tumors outside hypothalamic– pituitary– adrenal axis q : usually lung and pancreas tumors
SIGNS & SYMPTOMS: Cushing’s n n protein catabolism q muscle wasting q loss of collagen support n thin, fragile skin, bruises easily q poor wound healing s in CHO metabolism q hyperglycemia q Can get diabetesn q q q insufficient insulin production Polyuria s in fat metabolism truncal obesity buffalo hump “moon face” weight but strength (review video)
Cushigns-SIGNS & SYMPTOMS immune response More prone to infection q resistance to stress q Death usually from infection n Before Cushings After Cushings
What assessment findings indicate Cushings’ syndrome?
SIGNS & SYMPTOMS: Cushing’s Syndrome! n n Androgen secretion q excessive hair growth q acne q change in voice q receding hairline Mineralocorticoid activity water retention q ____ and _______ NA q Marked hypokalemia hypervolemia q b. p. from ____
SIGNS & SYMPTOMSz; Cushings MENTAL CHANGES n n n n Mood swings Euphoria Depression Anxiety Mild to severe depression Psychosis Poor concentraion and memory Sleep disorders n s in hematology n. WBCs n. Lymphocytes n. Eosinophils
Summary Signs and symptoms: Related to excess corticosteroids • Weight gain most common feature • Trunk (centripetal obesity) • Face (“moon face”) • Cervical area • Transient weight gain; from sodium and water retention • Protein wasting • Catabolic effects of cortisol • Leads to weakness especially in extremities • Protein loss in bones leads to osteoporosis, bone and back pain • Hyperglycemia Glucose intolerance associated with cortisol-induced insulin resistance • Increased gluconeogenesis by liver Loss of collagen • Wound healing delayed • Purplish red striae on abdomen, breast, or buttocks • Mood disturbances • Insomnia Irrationality • Psychosis Mineralocorticoid excess may cause hypertension secondary to fluid retention Adrenal androgen excess may cause • Pronounced acne • Virilization in women • Feminization in men • Seen more commonly in adrenal carcinomas • Women: Menstrual disorders and hirsutism • Men: Gynecomastia and impotence
ACTH and cortisol
Hypofunction Adrenal Cortex- ADDISON’S DISEASE n Remember-Adrenocortical insufficiency may be q Addison’s disease (hypofunction of adrenal cortex)*primary cause q From lack of pituitary ACTH *secondary cause n What hormones will BE LACKING/decreased in Addison’s disease q Glucocorticoids (corticosteroids as cortisol, hydrocortisone) q Mineralocorticoids (aldosterone) q Androgens (testosterone, androsterone) and estrogen ______
Trivia Question: Which President had Addison’s Disease?
Addison’s Disease
n n n Addison’s Disease: Etiology/Pathophysiology Common cause-autoimmune response to adrenal tissue (esp. white females) Susceptibility genes; other endocrine conditions often found Other causes of Addison’s disease q Tuberculosis (rare in North America) q Infarction q Fungal infections q AIDS q Metastatic cancer q *Iatrogenic Addison’s disease-due to adrenal hemorrhage Most often occurs in adults <60 years old Affects both genders equally Disease not evident until 90% of adrenal cortex destroyedadvanced before diagnosis
Addison’s Disease: Clinical Manifestations n Primary features q q q Progressive weakness Fatigue Weight loss Anorexia Skin hyperpigmentation primarily in n q Areas exposed to sun Pressure points Over joints In skin creases, especially palmar creases
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