Hormonal Regulation Endocrine

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Last updated 6:08 PM on 3/24/26
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67 Terms

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Endocrine Glands

Secrete hormones directly into bloodstream that stimulates action in target tissues

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Negative Feedback

Hormone level communicated back to gland (ex: secretion of insulin) → most common type

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Positive Feedback

Increasing level of hormone triggers further elevation of hormone (ex: menstrual cycle)

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Biological Rhythms

Natural body cycles that control hormone levels → ex: cortisol is low at night and high in morning

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What triggers release of hormones when activated?

SNS

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Perimenopause

Transitional period, lasts 1-8 years

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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)

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Osteoporosis

Low bone density d/t low intake of nutrients for growth or increase in resorption that occurs with aging

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Estrogen (Females)

Inhibits PTH release, slowing osteoclast formation and bone resorption

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Parathyroid Hormone (PTH)

Stimulates osteoclast formation/function

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Most common disease that affects bone in adults

Osteoporosis

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Osteoporosis Risk Factors

Affects 50% of women 50yo+ (post-menopause), asians + caucasians, elderly males, active young athletes, low body fat

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T3

Triiodothyronine

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T4

Thyroxine

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Calcitonin

Thyroid → Osteoblastic

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PTH

Parathyroid → Osteoclastic

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Osteoblastic

Lowers serum calcium

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Osteoclastic

Raises serum calcium

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Primary Dysfunction

Occurs in Thyroid

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Secondary Dysfunction

Occurs in Pituitary

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What is the Thyroid Gland needed for?

Brain development, neurologic function, metabolism

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Primary Hyperthyroidism

Graves Disease (most common cause) → autoimmune condition l/t autoantibodies against TSH receptor

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Manifestations of Primary Hyperthyroidism

Goiter, forward displacement of eyes, thickening of skin on shins, dysrhythmias, anxiety, weight loss

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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)

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Primary Hyperthyroidism Diagnosis

Decreased TSH + Increased T3 + T4

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Secondary Hyperthyroidism Diagnosis

Normal/High TSH + Elevated T3 + T4

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Thyroid Storm (Thyrotoxicosis)

D/t extreme levels of thyroid hormone / insufficient treatment of hyperthyroidism + excessive stress + manipulation of gland during thyroid surgery

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Thyroid Storm Manifestations

Hyperthermia, tachycardia, HTN, heart failure, agitation, delirium, N, V, D, cardiac collapse, death

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Hashimoto’s Thyroiditis (Primary Hypothyroidism)

Destruction of thyroid gland d/t autoimmune dysfunction → autoantibodies directed to thyroglobulin l/t fibrosis

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Hashimoto’s Diagnosis

Decreased T3 + T4 + Increased TSH

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Secondary Hypothyroidism

Tumors/trauma to pituitary → Increased TRH + Decreased TSH + T3 + T4

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Tertiary Hypothyroidism

Tumors/trauma on hypothalamus → Decreased TRH + TSH + T3 + T4

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Myxedema Coma

D/t lack of treatment of hypothyroidism, manifestations include HYPOthermia/ventilation/tension/glycemia (hypo-anything)

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Catecholamines

Norepinephrine, Epinephrine, Dopamine

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Pheochromocytoma

Formation of malignant tumor in adrenal medulla that increases secretion of catecholamines (high vitals)

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Adrenal Medulla Releases

Catecholamines

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Adrenal Cortex Releases

Aldosterone + Glucocorticoids

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Aldosterone

Promotes Water and Na+ resorption and excretion of K+ (RAAS)

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Glucocorticoids (aka Cortisol)

Increases blood sugar (gluconeogenesis), suppresses immune system, and promotes anti-inflammatory mechanisms

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Primary Adrenocortical Insufficiency

Addison’s Disease → autoimmune disorder affecting adrenal cortex (deficiencies of cortisol + aldosterone)

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Addison’s Disease Diagnosis

Increased ACTH + Low Cortisol

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Secondary Adrenocortical Insufficiency

Dysfunction of anterior pituitary l/t loss of ACTH d/t chronic glucocorticoid use OR surgery/damage

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Secondary Adrenocortical Insufficiency Disorder Diagnosis

Decreased ACTH + Cortisol (d/t insulin induced hypoglycemia)

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Manifestations of Secondary Adrenocortical Insufficiency Disorder

Fatigue, weakness, N/V, hypoglycemia, hyponatremia, hyperkalemia

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Hyponatremia

Low sodium levels in the bloodstream

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Hyperkalemia

High potassium levels

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Adrenal Crisis

Acute insufficiency that is life-threatening, precipitated by stressors l/t dehydration, fever, hyperkalemia

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Cushing’s Syndrome

D/t excess of cortisol + glucocorticoids (over years): ACTH independent

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Cushing’s Syndrome Diagnosis

ACTH Decreased + Cortisol Increased

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Cushing Syndrome Causes

Chronic exposure to excess exogenous medications OR endogenous overproduction (too much cortisol)

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Cushing’s Disease

D/t pituitary corticotropic adenoma: ACTH dependent (cortisol + ACTH increased)

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Primary Hyperaldosteronism

Conn Syndrome → Aldosterone producing adenoma l/t elevated aldosterone and suppressed renin levels

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Manifestations of Conn Syndrome

Hypertension, weakness, headaches, polydipsia, polyuria

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Secondary Hyperaldosteronism

Renin Dependent → Aldosterone secreted d/t excess secretion of renin (as a response to hypovolemia)

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Hypovolemia

Retention of fluid and increase in blood pressure

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Renin Dependent Diagnosis

Elevated Aldosterone + Renin

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ACTH

Stimulates production of glucocorticoids by Adrenal Cortex

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Anterior Pituitary Releases

ACTH, GH, TSH, FSH, LH

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Posterior Pituitary Releases

ADH + Oxytocin

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Antidiuretic Hormone

L/t conservation of body water by promoting water reabsorption by renal tubules (increased collecting duct permeability)

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SIADH Manifestations

Thirst, anorexia, fatigue, decreased NA+, confusion, lethargy

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SIADH Diagnosis

Serum hyperosmolality + hyponatremia + urine hyperosmolarity

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SIADH

Excess ADH (often from paraneoplastic cancer) or surgery l/t water retention + fluid and volume changes

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Central Diabetes Insipidus

Insufficient secretion of ADH, rapid onset; ADH levels low

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Nephrogenic Diabetes Insipidus

Inadequate response of renal tubules to ADH (d/t genetics or kidney injury), slow onset, normal or increased ADH

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Diabetes Insipidus Diagnosis

Low urine osmolality (unable to concentrate urine), hypernatremia, continued diuresis (water deprivation testing)

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Manifestations of Diabetes Insipidus

Polyurina, polydipsia (continuous thirst)

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