Human Physiology: Endocrine Control of Growth, Metabolism, and Cardiovascular Physiology (Chapters 23 & 14 Study Guide)

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Cortisol is a glucocorticoid hormone produced by the adrenal cortex, playing a vital role in metabolism, immune response, and stress adaptation.

Secretion Control: Cortisol secretion is regulated by the hypothalamic-pituitary-adrenal (HPA) axis. The hypothalamus releases corticotropin-releasing hormone (CRH), stimulating the pituitary to secrete adrenocorticotropic hormone (ACTH), which then prompts the adrenal cortex to release cortisol.
Physiological Effects:
- Increases blood glucose via gluconeogenesis
- Suppresses immune system activity
- Promotes protein catabolism in muscle
- Stimulates lipolysis in adipose tissue
Health Implications of High Cortisol: Chronic elevation can lead to Cushing's syndrome, characterized by muscle wasting, hyperglycemia, hypertension, and immunosuppression.
Therapeutic Use: Cortisol and synthetic glucocorticoids are used to treat inflammation and autoimmune diseases.
Exogenous Administration Risks: Long-term use can cause adrenal suppression, osteoporosis, and increased infection risk.

Abnormal cortisol levels can result from primary (adrenal) or secondary (pituitary) dysfunction.

Primary Hypercortisolism: Caused by adrenal tumors or hyperplasia.
Secondary Hypercortisolism: Due to excess ACTH from pituitary adenomas.
Symptoms: Weight gain, muscle weakness, mood changes.
Additional info: Adrenocorticotropic hormone (ACTH) stimulation tests help differentiate causes.

Thyroxine (T4) and Triiodothyronine (T3) are hormones produced by the thyroid gland, essential for regulating metabolism and growth.

Functions:
- Increase basal metabolic rate
- Promote protein synthesis and growth
- Enhance nervous system development
Hyperthyroidism: Excess T3/T4 leads to weight loss, heat intolerance, tachycardia.
Hypothyroidism: Deficiency causes weight gain, cold intolerance, bradycardia, and developmental delays in children.

Growth hormone (GH) is secreted by the anterior pituitary and stimulates growth, cell reproduction, and regeneration.

Factors Affecting GH Secretion:
- Stimulated by sleep, exercise, stress, and low blood glucose
- Inhibited by high blood glucose and somatostatin
Chronic Stress: Can increase cortisol, which may suppress GH secretion and impair growth.
Reduced GH Impacts: Leads to stunted growth, increased fat mass, and decreased muscle mass.
Conditions for Bone Growth: Requires adequate GH, thyroid hormone, sex steroids, and nutrition.

Calcium is essential for bone structure, muscle contraction, nerve transmission, and blood clotting.

Calcium Compartments:
- Bone (99%)
- Extracellular fluid (1%)
- Intracellular fluid (0.1%)
Importance of Calcium Balance: Prevents tetany, osteoporosis, and cardiac arrhythmias.
Hormonal Control:
- Parathyroid hormone (PTH): Increases blood calcium by stimulating bone resorption and renal reabsorption.
- Calcitonin: Lowers blood calcium by inhibiting bone resorption.
- Vitamin D (Calcitriol): Enhances intestinal calcium absorption.

Bone remodeling is regulated by osteoblasts and osteoclasts.

Osteoblasts: Cells that build bone by synthesizing matrix and promoting mineralization.
Osteoclasts: Cells that resorb bone, releasing calcium into the bloodstream.
Osteoporosis: Disease characterized by decreased bone mass and increased fracture risk.
Risk Factors: Age, female sex, low calcium/vitamin D intake, sedentary lifestyle, smoking, glucocorticoid use.

The heart pumps blood through two circuits: pulmonary (to lungs) and systemic (to body).

Oxygenated Blood: Left side of the heart receives oxygenated blood from the lungs and pumps it to the body.
Deoxygenated Blood: Right side receives deoxygenated blood from the body and pumps it to the lungs.
Vessels:
- Pulmonary artery: Carries deoxygenated blood from right ventricle to lungs.
- Pulmonary vein: Carries oxygenated blood from lungs to left atrium.
- Aorta: Carries oxygenated blood from left ventricle to systemic circulation.

Cardiac tissue contains two main cell types: autorhythmic (pacemaker) and contractile cells.

Autorhythmic Cells: Generate spontaneous action potentials, setting heart rate.
Contractile Cells: Respond to action potentials by contracting and pumping blood.
Depolarization: Caused by Na+ influx in contractile cells; Ca2+ influx in pacemaker cells.
Plateau Phase: Maintained by Ca2+ influx, prolonging contraction and preventing tetany.
Repolarization: K+ efflux restores resting potential.

Action potentials in cardiac cells coordinate heartbeats.

Pacemaker Potential: Gradual depolarization in SA node cells due to Na+ and Ca2+ influx.
Heart Rate: Determined by rate of pacemaker cell depolarization (e.g., SA node ~70 bpm).
Pathway of Conduction: SA node → AV node → Bundle of His → Bundle branches → Purkinje fibers.

The refractory period is the time during which a cell cannot be re-excited.

Cardiac Muscle: Long refractory period prevents tetanus, ensuring rhythmic contractions.
Skeletal Muscle: Shorter refractory period allows for summation and tetanus.

An EKG records the electrical activity of the heart, with distinct waves representing different phases.

Wave	Represents
P wave	Atrial depolarization
QRS complex	Ventricular depolarization
T wave	Ventricular repolarization

Atrial Repolarization: Occurs during QRS complex, not separately visible.
Cardiac Arrhythmias: Abnormal rhythms may cause palpitations, dizziness, syncope.
Heart Block: Impaired conduction between atria and ventricles, seen as abnormal EKG intervals.
Ischemic Disease (e.g., Myocardial Infarction): Detected by ST segment changes on EKG.

The autonomic nervous system regulates heart rate via sympathetic and parasympathetic pathways.

Parasympathetic Control: Vagus nerve releases acetylcholine, increasing K+ permeability and decreasing heart rate.
Sympathetic Control: Norepinephrine increases Ca2+ and Na+ influx, raising heart rate.