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Endocrine Glands
Secrete hormones directly into bloodstream that stimulates action in target tissues
Negative Feedback
Hormone level communicated back to gland (ex: secretion of insulin) → most common type
Positive Feedback
Increasing level of hormone triggers further elevation of hormone (ex: menstrual cycle)
Biological Rhythms
Natural body cycles that control hormone levels → ex: cortisol is low at night and high in morning
What triggers release of hormones when activated?
SNS
Perimenopause
Transitional period, lasts 1-8 years
Menopause
12 months without a period (~50yo) d/t decreased ovarian function l/t low estrogen + progesterone and high FSH + LH (increases risk of breast cancer, osteoporosis, heart disease)
Osteoporosis
Low bone density d/t low intake of nutrients for growth or increase in resorption that occurs with aging
Estrogen (Females)
Inhibits PTH release, slowing osteoclast formation and bone resorption
Parathyroid Hormone (PTH)
Stimulates osteoclast formation/function
Most common disease that affects bone in adults
Osteoporosis
Osteoporosis Risk Factors
Affects 50% of women 50yo+ (post-menopause), asians + caucasians, elderly males, active young athletes, low body fat
T3
Triiodothyronine
T4
Thyroxine
Calcitonin
Thyroid → Osteoblastic
PTH
Parathyroid → Osteoclastic
Osteoblastic
Lowers serum calcium
Osteoclastic
Raises serum calcium
Primary Dysfunction
Occurs in Thyroid
Secondary Dysfunction
Occurs in Pituitary
What is the Thyroid Gland needed for?
Brain development, neurologic function, metabolism
Primary Hyperthyroidism
Graves Disease (most common cause) → autoimmune condition l/t autoantibodies against TSH receptor
Manifestations of Primary Hyperthyroidism
Goiter, forward displacement of eyes, thickening of skin on shins, dysrhythmias, anxiety, weight loss
What does Primary Hyperthyroidism lead to?
Increase in thyroid stimulation l/t increase in T3 + T4 secretion (pituitary attempts to stop with negative feedback by decreasing TSH)
Primary Hyperthyroidism Diagnosis
Decreased TSH + Increased T3 + T4
Secondary Hyperthyroidism Diagnosis
Normal/High TSH + Elevated T3 + T4
Thyroid Storm (Thyrotoxicosis)
D/t extreme levels of thyroid hormone / insufficient treatment of hyperthyroidism + excessive stress + manipulation of gland during thyroid surgery
Thyroid Storm Manifestations
Hyperthermia, tachycardia, HTN, heart failure, agitation, delirium, N, V, D, cardiac collapse, death
Hashimoto’s Thyroiditis (Primary Hypothyroidism)
Destruction of thyroid gland d/t autoimmune dysfunction → autoantibodies directed to thyroglobulin l/t fibrosis
Hashimoto’s Diagnosis
Decreased T3 + T4 + Increased TSH
Secondary Hypothyroidism
Tumors/trauma to pituitary → Increased TRH + Decreased TSH + T3 + T4
Tertiary Hypothyroidism
Tumors/trauma on hypothalamus → Decreased TRH + TSH + T3 + T4
Myxedema Coma
D/t lack of treatment of hypothyroidism, manifestations include HYPOthermia/ventilation/tension/glycemia (hypo-anything)
Catecholamines
Norepinephrine, Epinephrine, Dopamine
Pheochromocytoma
Formation of malignant tumor in adrenal medulla that increases secretion of catecholamines (high vitals)
Adrenal Medulla Releases
Catecholamines
Adrenal Cortex Releases
Aldosterone + Glucocorticoids
Aldosterone
Promotes Water and Na+ resorption and excretion of K+ (RAAS)
Glucocorticoids (aka Cortisol)
Increases blood sugar (gluconeogenesis), suppresses immune system, and promotes anti-inflammatory mechanisms
Primary Adrenocortical Insufficiency
Addison’s Disease → autoimmune disorder affecting adrenal cortex (deficiencies of cortisol + aldosterone)
Addison’s Disease Diagnosis
Increased ACTH + Low Cortisol
Secondary Adrenocortical Insufficiency
Dysfunction of anterior pituitary l/t loss of ACTH d/t chronic glucocorticoid use OR surgery/damage
Secondary Adrenocortical Insufficiency Disorder Diagnosis
Decreased ACTH + Cortisol (d/t insulin induced hypoglycemia)
Manifestations of Secondary Adrenocortical Insufficiency Disorder
Fatigue, weakness, N/V, hypoglycemia, hyponatremia, hyperkalemia
Hyponatremia
Low sodium levels in the bloodstream
Hyperkalemia
High potassium levels
Adrenal Crisis
Acute insufficiency that is life-threatening, precipitated by stressors l/t dehydration, fever, hyperkalemia
Cushing’s Syndrome
D/t excess of cortisol + glucocorticoids (over years): ACTH independent
Cushing’s Syndrome Diagnosis
ACTH Decreased + Cortisol Increased
Cushing Syndrome Causes
Chronic exposure to excess exogenous medications OR endogenous overproduction (too much cortisol)
Cushing’s Disease
D/t pituitary corticotropic adenoma: ACTH dependent (cortisol + ACTH increased)
Primary Hyperaldosteronism
Conn Syndrome → Aldosterone producing adenoma l/t elevated aldosterone and suppressed renin levels
Manifestations of Conn Syndrome
Hypertension, weakness, headaches, polydipsia, polyuria
Secondary Hyperaldosteronism
Renin Dependent → Aldosterone secreted d/t excess secretion of renin (as a response to hypovolemia)
Hypovolemia
Retention of fluid and increase in blood pressure
Renin Dependent Diagnosis
Elevated Aldosterone + Renin
ACTH
Stimulates production of glucocorticoids by Adrenal Cortex
Anterior Pituitary Releases
ACTH, GH, TSH, FSH, LH
Posterior Pituitary Releases
ADH + Oxytocin
Antidiuretic Hormone
L/t conservation of body water by promoting water reabsorption by renal tubules (increased collecting duct permeability)
SIADH Manifestations
Thirst, anorexia, fatigue, decreased NA+, confusion, lethargy
SIADH Diagnosis
Serum hyperosmolality + hyponatremia + urine hyperosmolarity
SIADH
Excess ADH (often from paraneoplastic cancer) or surgery l/t water retention + fluid and volume changes
Central Diabetes Insipidus
Insufficient secretion of ADH, rapid onset; ADH levels low
Nephrogenic Diabetes Insipidus
Inadequate response of renal tubules to ADH (d/t genetics or kidney injury), slow onset, normal or increased ADH
Diabetes Insipidus Diagnosis
Low urine osmolality (unable to concentrate urine), hypernatremia, continued diuresis (water deprivation testing)
Manifestations of Diabetes Insipidus
Polyurina, polydipsia (continuous thirst)