3200 online osu physio endocrine system

Endocrine Glands

Ductless glands that release hormones directly into the bloodstream to regulate functions like growth and metabolism

Exocrine Glands

Glands that utilize ducts to release non hormone secretions outside the blood system

Endocrine Signaling

Chemical communication where hormones travel through blood circulation to distant target cells

Paracrine Signaling

Chemical communication acting locally on nearby target cells

Autocrine Signaling

Chemical communication acting directly on the same cell that secreted it

Norepinephrine Dual Role

Serves as both a hormone and a neurotransmitter depending on release location

Epinephrine Dual Role

Serves as both a hormone and a neurotransmitter depending on release location

Dopamine Dual Role

Serves as both a hormone and a neurotransmitter depending on release location

Amine Hormones

Class of hormones derived from the amino acid tyrosine

Thyroid Hormones T3 and T4

Amine hormones produced by the thyroid gland containing iodine

Catecholamines

Class of tyrosine derived chemical messengers including epinephrine norepinephrine and dopamine

Peptide Hormones

Major class of water soluble hormones synthesized from DNA to mRNA to preprohormone to prohormone to active hormone

Steroid Hormones

Lipid soluble hormones synthesized from cholesterol

Adrenal Cortex Hormones

Produces aldosterone cortisol and sex androgens from cholesterol

Female Androgen Excess Mechanism

Blocked cortisol synthesis in females leads to overproduction of adrenal androgens causing masculinization

Gonadal Hormones

Testes produce testosterone while ovaries use aromatase to convert testosterone into estradiol

Aromatase

Enzyme in ovaries responsible for converting testosterone into estradiol

Vitamin D Precursors

Steroid derived compounds created in the skin from cholesterol to regulate calcium levels

Water Soluble Hormone Transport

Peptides and catecholamines that circulate freely in blood plasma

Non Water Soluble Hormone Transport

Steroids and thyroid hormones that circulate bound to carrier proteins where only the free fraction is active

Hormone Clearance

Excretion in urine or feces metabolic inactivation or tissue receptor uptake and recycling

Immunoassays

Diagnostic tests using highly specific antibodies to measure hormone levels

Hormone Control Inputs

Secretion is regulated by humoral neural or hormonal inputs

Receptor Specificity

Requirement that target cells possess exact receptors to respond to a specific hormone

Membrane Receptors

Binding sites located on the outer plasma membrane for water soluble hormones

Intracellular Receptors

Binding sites located inside target cells for non water soluble hormones

Up Regulation

Increase in total receptor count due to low hormone levels which increases target cell sensitivity

Down Regulation

Decrease in total receptor count due to high hormone levels which decreases target cell sensitivity

Permissive Action

Phenomenon where the presence of one hormone enhances the responsiveness or effectiveness of another

Tropic Hormones

Hormones that function primarily to stimulate other endocrine glands to release their hormones

Hypothalamo Pituitary Portal Vessels

Specialized blood vessels delivering hypophysiotropic hormones directly from the hypothalamus to the anterior pituitary

Three Hormone Sequence

Regulatory cascade running from hypothalamus to anterior pituitary to target gland to target cell

Anterior Pituitary

Adenohypophysis releasing FSH LH ACTH TSH prolactin and GH

TRH

Hypothalamic hormone that stimulates anterior pituitary release of TSH

CRH

Hypothalamic hormone that stimulates anterior pituitary release of ACTH

GnRH

Hypothalamic hormone that stimulates anterior pituitary release of FSH and LH

GHRH

Hypothalamic hormone that stimulates anterior pituitary release of GH

Dopamine or PIH

Hypothalamic hormone that inhibits anterior pituitary release of prolactin

Somatostatin

Hypothalamic hormone that inhibits anterior pituitary release of GH

HPA Axis Activation

Stress triggers CRH to ACTH to cortisol release alongside rapid sympathetic epinephrine and norepinephrine release

HPA Axis Feedback

Rising cortisol suppresses CRH and ACTH to prevent excessive hormone release and maintain homeostasis

ACTH Release Inputs

Secretion is stimulated by neural inputs vasopressin and cytokines

Neuroendocrine Immune Interplay

Cytokines activate the HPA axis during stress while cortisol down regulates immune activity as a physiological brake

Cortisol Vascular Function

Maintains normal blood pressure by exerting permissive effects on smooth muscle and enhancing responsiveness to catecholamines

Cortisol Metabolic Function

Increases liver metabolic enzyme expression and supports gluconeogenesis to keep plasma glucose stable between meals

Cortisol Anti Inflammatory Function

Inhibits leukotrienes and prostaglandins to suppress immune and inflammatory reactions

Cortisol Developmental Function

Required for tissue and gland differentiation as well as fetal lung maturation

Stress Induced Cortisol Effects

Raises blood glucose mobilizes protein and fat for energy enhances vascular reactivity and inhibits growth and reproduction

Pathological Catabolism

Severe stress or illness causes significant protein breakdown and can reduce growth rates in children

Hypotension in Low Cortisol

Insufficient cortisol reduces vascular reactivity leading to low blood pressure or circulatory failure under stress

Glucocorticoid Therapy

Exogenous cortisol analogues used clinically to treat arthritis allergies and prevent organ graft rejection

Addisons Disease

Primary adrenal insufficiency caused by destruction or dysfunction of the adrenal glands themselves

Secondary Adrenal Insufficiency

Deficient cortisol production resulting from reduced ACTH secretion by the pituitary gland

Primary Hypercortisolism

Overproduction of cortisol caused directly by adrenal adenomas or adrenal carcinomas

Secondary Hypercortisolism

Excessive cortisol secretion driven by an ACTH secreting pituitary tumor

Cushing Syndrome Symptoms

Excessive protein catabolism high blood glucose moon face fat redistribution obesity and hypertension

T4 Prohormone Function

Major circulating thyroid hormone that acts primarily as a precursor converted to active T3

Thyroglobulin

Protein synthesized by thyroid follicles to store iodine in colloids

Thyroid Hormone Synthesis Steps

Iodide trapping transport oxidation iodination coupling endocytosis and proteolysis

TSH Control Mechanism

Stimulates every major step of thyroid hormone synthesis and release

Nuclear Thyroid Hormone Receptors

Intracellular receptors bound by T3 and T4 to regulate gene expression and protein synthesis

Basal Metabolic Rate Regulation

Thyroid hormones increase metabolic enzymes and increase carbohydrate and fat consumption for energy

Calorigenic Effect

Increase in whole body heat production driven by thyroid hormone activation of Na K ATPase activity

Cretinism

Irreversible cognitive impairment resulting from uncorrected thyroid hormone deficiency in early development

Thyroid Beta Adrenergic Effect

Thyroid hormones upregulate beta adrenergic receptors increasing sympathetic sensitivity

Primary Hypothyroidism

Low plasma thyroid hormones due to intrinsic thyroid defect or iodine deficiency accompanied by elevated TSH

Secondary Hypothyroidism

Low plasma thyroid hormones caused by deficient pituitary TSH secretion

Tertiary Hypothyroidism

Low plasma thyroid hormones caused by deficient hypothalamic TRH secretion

Goiter Formation

Thyroid enlargement caused by persistently elevated TSH levels when hormone synthesis is impaired

Graves Disease

Autoimmune hyperthyroidism where TSH mimicking antibodies chronically stimulate thyroid receptors causing low TSH and high T4

Primary Hyperthyroidism Lab Profile

High T4 paired with low TSH due to intrinsic thyroid overactivity or Graves disease

Secondary Hyperthyroidism Lab Profile

High T4 paired with high TSH due to pituitary overstimulation

Thyroid Hormone Resistance

High T4 paired with high TSH because target tissues are completely unresponsive to hormone

Absorptive State

Metabolic period of nutrient use and storage driven by insulin where excess glucose is saved as glycogen or fat

Lipoprotein Lipase

Enzyme that breaks down ingested triglycerides into fatty acids for tissue storage or energy

Postabsorptive State

Metabolic period focused on maintaining plasma glucose through catabolism driven primarily by glucagon

Glycogenolysis

Metabolic pathway breaking down stored glycogen into free glucose

Gluconeogenesis

Metabolic synthesis of glucose from non carbohydrate precursor sources

Ketogenesis

Production of ketone bodies from fatty acids to provide alternative fuel during postabsorptive state

Insulin Counter Regulators

Glucagon epinephrine sympathetic nervous system cortisol and GH all work to elevate blood glucose

Cholesterol Structural Role

Essential component of cell membranes and precursor for steroid hormones bile acids and vitamin D

LDL Lipoprotein

Low density lipoprotein delivering cholesterol to tissues and contributing to plaque formation

HDL Lipoprotein

High density lipoprotein clearing cholesterol from cells and plaques back to the liver

Healthy Cholesterol Indicator

Characterized clinically by a low LDL to HDL ratio

Epiphysis

The expanded structural ends of an immature long bone

Diaphysis

The central tubular shaft of an immature long bone

Epiphyseal Plate

Cartilage zone situated between epiphysis and diaphysis where longitudinal bone growth occurs

Chondrocytes

Specialized cells within the growth plate that produce new cartilage

Osteoblasts

Specialized cells that ossify and convert cartilage into mature bone

Major Height Growth Periods

Characterized by rapid height increases during infancy and puberty

Compensatory Growth

Accelerated growth period following a temporary slowdown caused by illness or nutrient deprivation

Growth Hormone Primary Function

Drives postnatal cell division protein synthesis blood glucose elevation and liver IGF 1 production

GH Diurnal Rhythm

Fluctuates daily with high concentration during sleep and low concentration during wakefulness

IGF 1 Role

Insulin like growth factor 1 driven by GH that directly stimulates chondrocyte and osteoblast bone activity

Sex Hormone Growth Role

Drives pubertal growth spurt by enhancing GH and IGF 1 while ultimately triggering epiphyseal plate closure

Testosterone Anabolic Effect

Directly increases protein synthesis leading to greater muscle mass in males

Age Related Endocrine Changes

Declines in GH sex hormones and insulin lead to loss of bone and muscle mass and increased adipose tissue

Gigantism

Excess GH secretion occurring before epiphyseal growth plate closure usually caused by a pituitary tumor

Acromegaly

Excess GH secretion occurring after epiphyseal growth plate closure in adulthood

Dwarfism

Stunted growth resulting from deficient GH or IGF 1 or reduced target tissue responsiveness