Study Guide: Endocrine Control of Growth, Metabolism, and Cardiovascular Physiology

Chapter 23 – Endocrine Control of Growth and Metabolism

Cortisol: Secretion, Effects, and Clinical Relevance

• Cortisol is a glucocorticoid hormone produced by the adrenal cortex, primarily in response to stress and regulated by the hypothalamic-pituitary-adrenal (HPA) axis.

• Secretion Control: Cortisol release is stimulated by adrenocorticotropic hormone (ACTH) from the anterior pituitary, which is itself regulated by corticotropin-releasing hormone (CRH) from the hypothalamus.

• Physiological Effects:

  • Suppresses immune system activity

  • Increases blood glucose via gluconeogenesis

  • Promotes protein catabolism in muscle and lipolysis in adipose tissue

• Health Implications of High Cortisol: Chronic elevation can lead to Cushing's syndrome, characterized by muscle wasting, hyperglycemia, hypertension, and immune suppression.

• Therapeutic Use: Cortisol and synthetic glucocorticoids are used to treat inflammation and autoimmune diseases, but long-term use can cause adverse effects.

• Exogenous Administration Risks: Prolonged use may suppress endogenous cortisol production and cause symptoms similar to Cushing's syndrome.

Hyper- and Hypocortisolism

• Primary Hypercortisolism: Caused by adrenal tumors producing excess cortisol.

• Secondary Hypercortisolism: Due to excess ACTH from pituitary tumors.

• Hypocortisolism: Often results from Addison's disease (adrenal insufficiency), leading to fatigue, weight loss, and hypotension.

• Additional info: Iatrogenic hypercortisolism refers to excess cortisol due to medical treatment.

Thyroid Hormones: T4 and T3

• Thyroxine (T4) and Triiodothyronine (T3) are hormones produced by the thyroid gland that regulate metabolism, growth, and development.

• T3 is the more active form; T4 is converted to T3 in target tissues.

• Deficiency leads to hypothyroidism (fatigue, weight gain); excess causes hyperthyroidism (weight loss, increased heart rate).

Growth Hormone and Bone Growth

• Growth hormone (GH) stimulates growth, cell reproduction, and regeneration.

• Chronic stress can reduce GH secretion, impairing growth.

• Reduced GH leads to stunted growth and metabolic disturbances.

• Bone Growth: Occurs at epiphyseal plates during childhood and adolescence, requiring adequate GH, thyroid hormone, and sex steroids.

Calcium Homeostasis

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

• Body Compartments:

  • Bone: ~99% of total body calcium

  • Extracellular fluid: ~0.1%

  • Intracellular fluid: ~0.9%

• Hormonal Control:

  • Parathyroid hormone (PTH): Increases blood calcium by stimulating bone resorption, increasing renal reabsorption, and activating vitamin D.

  • Calcitonin: Lowers blood calcium by inhibiting bone resorption.

  • Vitamin D (calcitriol): Increases intestinal absorption of calcium.

Bone Cells and Osteoporosis

• Osteoblasts: Cells that build bone by depositing new matrix.

• Osteoclasts: Cells that break down bone, releasing calcium into the blood.

• Osteoporosis: A disease characterized by decreased bone mass and increased fracture risk.

• Risk Factors: Age, female sex, low calcium/vitamin D intake, sedentary lifestyle, smoking, and certain medications.

Compartment	Percentage of Total Body Calcium
Bone	~99%
Extracellular Fluid	~0.1%
Intracellular Fluid	~0.9%

Chapter 14 – Cardiovascular Physiology

Heart Anatomy and Blood Flow

• The right side of the heart receives deoxygenated blood from the body and pumps it to the lungs.

• The left side receives oxygenated blood from the lungs and pumps it to the systemic circulation.

• Pulmonary artery: Carries deoxygenated blood from the right ventricle to the lungs.

• Pulmonary vein: Carries oxygenated blood from the lungs to the left atrium.

Cardiac Muscle Cells: Autorhythmic vs. Contractile

• Autorhythmic cells (pacemaker cells): Generate spontaneous action potentials; set the heart rate.

• Contractile cells: Responsible for the forceful contraction of the heart muscle.

• Depolarization: Caused by Na+ influx in contractile cells; Ca2+ influx in pacemaker cells.

• Plateau phase: Maintained by Ca2+ influx, prolonging depolarization and preventing tetanus.

• Repolarization: Due to K+ efflux.

Refractory Periods

• Cardiac muscle: Long refractory period prevents summation and tetanus, ensuring rhythmic contractions.

• Skeletal muscle: Shorter refractory period allows for tetanus.

Pacemaker Potential and Heart Rate

• Pacemaker potential: The gradual depolarization of autorhythmic cells due to Na+ and Ca2+ influx.

• Heart rate: Determined by the rate of pacemaker cell depolarization (e.g., SA node: 70–80 bpm).

• Pathway of conduction: SA node → AV node → Bundle of His → Bundle branches → Purkinje fibers.

Electrocardiogram (EKG/ECG)

• P wave: Atrial depolarization

• QRS complex: Ventricular depolarization

• T wave: Ventricular repolarization

• Atrial repolarization is masked by the QRS complex.

Cardiac Arrhythmias and Heart Block

• Arrhythmias: Abnormal heart rhythms; may cause palpitations, dizziness, or syncope.

• Heart block: Impaired conduction between atria and ventricles; can be detected on EKG.

Ischemic Heart Disease

• Myocardial infarction (heart attack): Caused by blockage of coronary arteries; detected by EKG changes (e.g., ST elevation).

• Symptoms: Chest pain, shortness of breath, nausea.

Parasympathetic Control of Heart Rate

• Parasympathetic stimulation (via the vagus nerve) releases acetylcholine, which binds to muscarinic receptors on pacemaker cells.

• This increases K+ permeability and decreases Ca2+ permeability, slowing depolarization and reducing heart rate.

EKG Wave	Electrical Event
P wave	Atrial depolarization
QRS complex	Ventricular depolarization
T wave	Ventricular repolarization

Key Equations

• Cardiac Output: $CO = HR \times SV$

• Mean Arterial Pressure: $MAP = CO \times TPR$

Additional info: For a more comprehensive understanding, students should review the mechanisms of hormone action, feedback regulation, and the integration of endocrine and cardiovascular responses to stress and exercise.