Intercellular Communication: Endocrine & Nervous Systems

Intercellular Communication

• Communication coordinates body functions and maintains homeostasis
• It also helps cells respond to internal and external changes
• Key components include hormones (endocrine) and neurotransmitters (nervous)
• Target cells possess specific receptors for messengers
• Signal transduction involves second messengers (e.g. cAMP) or direct gene effects

Endocrine vs. Nervous System

Hormone Types, Glands, and Mechanisms

• Endocrine glands are ductless, secreting hormones into the blood (e.g. thyroid)
• Exocrine glands use ducts, secreting onto surfaces (e.g. sweat glands)

Hormone Classes

Mechanisms of Action

• Second Messenger (cAMP): Peptides/proteins bind outside, activating internal signals
• Direct Gene Activation: Steroids/TH enter cell, bind DNA, changing transcription

Pituitary Gland

• Location: Sella turcica (skull), below hypothalamus

Divisions

• Anterior (Adenohypophysis): TSH, ACTH, FSH, LH, PRL, GH, MSH
• Posterior (Neurohypophysis): ADH (water retention), OXT (uterine contraction, milk ejection)

Disorders

• GH increase in kids results in Gigantism
• GH increase in adults results in Acromegaly
• GH decrease results in Dwarfism
• ADH decrease results in Diabetes insipidus (polyuria)
• ADH increase results in Fluid retention

Thyroid Gland

• Location: Below larynx

Hormones

• T3 & T4 increase metabolism, oxygen use, ATP
• Calcitonin decreases blood calcium (inhibits osteoclasts)

Disorders

• Hyperthyroidism (Grave’s): Increased metabolism, weight loss, exophthalmos
• Hypothyroidism in infants leads to Cretinism
• Hypothyroidism in adults results in Myxedema, goiter

Parathyroid Glands

• Located behind the thyroid

Hormone

• PTH increases blood calcium, stimulating osteoclasts

Disorders

• PTH increase results in Weak bones, kidney stones
• PTH decrease results in Muscle cramps/spasms, excitable nerves

Adrenal Glands

• Located on kidneys

Parts & Hormones

• Cortex: Aldosterone (sodium/water retention), Cortisol (stress, increases glucose metabolism)
• Medulla: Epinephrine (EPE), Norepinephrine (NE) for fight-or-flight

Disorders

• Cushing’s (increased cortisol): Fat face, high sugar, hump back
• Addison’s (decreased hormones): Low BP, dehydration, bronzed skin

Pineal Gland

• Location: Epithalamus

Hormone

• Melatonin controls sleep-wake cycle (circadian rhythm)

Pancreas

• Located behind stomach

Hormones

• Alpha cells: Glucagon increases blood glucose
• Beta cells: Insulin decreases blood glucose

Disorders

• Type I Diabetes: No insulin
• Type II Diabetes: Cells don’t respond to insulin

Hormones from Other Organs

Hormone Interactions & Aging

• Synergism: Hormones enhance each other (e.g. EPE + glucagon)
• Antagonism: Hormones oppose each other (e.g. insulin vs glucagon)

General Adaptation Syndrome (GAS)

• Alarm: Immediate stress, EPE/NE
• Resistance: Long-term stress, Cortisol
• Exhaustion: Body’s resources depleted, fatigue, breakdown

Aging Effects

• Decreased hormone levels (e.g. estrogen, GH, testosterone)
• Increased risk of diabetes, osteoporosis, thyroid issues

Endocrine Interactions with Other Systems

• Nervous: Hypothalamus–pituitary control
• Circulatory: Hormones travel in blood
• Skeletal: PTH and calcitonin regulate calcium
• Digestive: Insulin and glucagon manage nutrients

Components and Functions of Blood

• Cardiovascular System Components: Heart (pumps), Blood Vessels (transport), Blood (connective tissue)

Physical Characteristics of Blood

• Color: Opaque, red
• Viscosity: Thicker than water
• pH: Slightly alkaline (7.35–7.45)
• Volume: ~5L (~8% of body weight)
• Hematocrit (HCT): ~45% (percentage of RBCs)
• Plasma Volume: ~55% of total blood volume

Functions of Blood

• Distribution: Carries O₂, nutrients, hormones, and waste
• Regulation: Maintains pH, temperature, and fluid balance
• Protection: Blood clotting and immune defense (WBCs)

Red Blood Cells (RBCs) and Gas Transport

• Quantity: ~5 million per mm³ of blood
• Function: Transport O₂ and CO₂
• Structure: Biconcave, anucleate, contains hemoglobin (Hb)
• O₂ binds to the iron in heme
• CO₂ binds to the globin part of hemoglobin
• Lifespan: ~120 days
• Recycling: Iron and amino acids are reused

Hemopoiesis (Blood Cell Formation)

• Fetus: Yolk sac, liver, spleen
• Child: All bones active in production
• Adult: Vertebrae, pelvis, sternum, ribs, cranial bones
• Erythropoietin (EPO): Stimulates RBC production (released by kidneys and liver)
• Nutrients needed for RBC formation: Iron, B12, folic acid

Blood Typing and ABO/Rh Incompatibilities

• Type A: Antigen A, Anti-B antibodies, can receive A and O, donate to A and AB
• Type B: Antigen B, Anti-A antibodies, can receive B and O, donate to B and AB
• Type AB (Universal Recipient): Antigens A and B, no antibodies, can receive A, B, AB, O, donate to AB
• Type O (Universal Donor): No antigens, Anti-A and Anti-B antibodies, can donate to A, B, AB, O, receive from O

Rh Factor

• Rh⁺: Has Rh antigen, no anti-Rh antibodies, can receive Rh⁺ or Rh⁻
• Rh⁻: No Rh antigen, develops anti-Rh antibodies after exposure
• Erythroblastosis Fetalis: Rh⁻ mother, Rh⁺ baby; treated with RhoGAM shot to prevent antibody production

White Blood Cells (WBCs)

• Quantity: ~7,000 per mm³
• Function: Defense and immunity, including phagocytosis of pathogens
• Diapedesis: WBCs exit the bloodstream and enter tissues

Types of WBCs

• Granulocytes (Lobed Nuclei): Neutrophils (60%, phagocytize bacteria), Eosinophils (fight allergies and parasitic infections), Basophils (release histamine)
• Agranulocytes (Round Nuclei): Lymphocytes (25%, B cells produce antibodies, T cells attack viruses and tumors), Monocytes (largest, become macrophages)

WBC Disorders

• Leukemia: Cancer of WBCs (overproduction)
• Mononucleosis: Viral infection (Epstein-Barr)
• Low WBC Count: Caused by drugs or bone marrow issues

Platelets (Thrombocytes)

• Function: Blood clotting
• Produced: In red bone marrow from megakaryocytes
• Lifespan: 9–12 days
• No nucleus, cell fragments
• Thrombocytopenia: Low platelet count, impairs clotting

Hemostasis and Clotting

• Vascular Spasm: Blood vessels constrict (via thromboxane)
• Platelet Plug Formation: Platelets stick to the injury site, release serotonin (vasoconstriction), and ADP (recruit more platelets)

Coagulation (Clotting Cascade)

• Extrinsic: Tissue factor
• Intrinsic: Platelet factor
• Both activate prothrombinase, converts prothrombin to thrombin
• Thrombin converts fibrinogen to fibrin (clot forms)
• Platelets contract to seal the wound
• TPA converts plasminogen to plasmin, dissolving the clot

Clotting Disorders

• Thrombus: Clot in unbroken vessel
• Embolus: Traveling clot
• Hemophilia: Missing clotting factors
• Liver Disease: Impaired protein production (affects clotting)

Plasma (55%)

• Composition: 90% water, 10% solutes

Solutes

• 7% Proteins: Albumin, globulins, fibrinogen
• 3% Solutes: Nutrients, hormones, electrolytes, wastes

Plasma Proteins

• Albumins (60%): Regulate osmotic pressure, water balance
• Globulins (35%): Alpha (HDL), Beta (LDL), Gamma (Antibodies IgG, IgE)
• Fibrinogen: Precursor for clotting

Plasma Solutes

• Organic: Glucose, amino acids, fatty acids, hormones
• Waste: Urea, uric acid, bilirubin, creatinine
• Electrolytes: Sodium (Na⁺), potassium (K⁺), calcium (Ca²⁺), bicarbonate (HCO₃⁻) maintains pH balance

Clinical and Emergency Notes

• IV Therapy: Colloid solutions or isotonic saline used when blood is unavailable
• Plasma Expanders: Restore volume, do not restore formed elements like RBCs

Anatomy of the Heart

• Function of the Heart: Pumps blood throughout the circulatory system
• Location: Mediastinum (center of chest), apex pointing left, base toward the right shoulder
• Size/Weight: About the size of a fist, weighing less than 1 pound

Pericardium

• Fibrous Pericardium: Dense CT, protects and anchors the heart, prevents overfilling
• Serous Pericardium with Parietal and Visceral layers

Heart Wall Layers

• Epicardium: outer layer
• Myocardium: cardiac muscle for contraction
• Endocardium: inner layer, smooth

Heart Chambers

• Atria receive blood
• Ventricles pump blood: Right to lungs, Left to the body

Heart Valves

• Atrioventricular (AV) Valves: Tricuspid (right), Bicuspid/Mitral (left)
• Semilunar (SL) Valves: Pulmonary, Aortic

Blood Flow

• Right Side (Pulmonary Circuit): SVC/IVC → RA → Tricuspid → RV → Pulmonary valve → Pulmonary trunk → Lungs
• Left Side (Systemic Circuit): Pulmonary veins → LA → Bicuspid → LV → Aortic valve → Aorta → Body

Cardiac Action Potential

• Cardiac Muscle: Striated, branched cells connected via intercalated discs (desmosomes and gap junctions)

Cardiac Action Potential Phases

• Depolarization: Na⁺ channels open, rapid influx
• Plateau: Ca²⁺ influx balances K⁺ efflux
• Repolarization: K⁺ efflux dominates

Calcium Role

• Influx of Ca²⁺ triggers action potential in autorhythmic cells

Conduction System

• SA Node: Pacemaker, generates heartbeat (~75–100 bpm)
• AV Node: Delays impulse
• Bundle of His & Purkinje Fibers: Carry impulse through ventricles for coordinated contraction

Electrocardiogram (ECG)

• P Wave: Atrial depolarization
• QRS Complex: Ventricular depolarization
• T Wave: Ventricular repolarization

Cardiac Cycle

• Atrial Systole: Atria contract
• EDV (End-Diastolic Volume): Maximum blood volume in ventricles
• Ventricular Systole: Ventricles contract
• ESV (End-Systolic Volume): Blood remaining after contraction
• Ventricular Diastole: Ventricles relax, blood passively fills

Heart Sounds

• 1st Sound ("Lub"): AV valves close
• 2nd Sound ("Dup"): SL valves close
• Wigger’s Diagram: ECG, heart sounds, and pressure/volume changes

Cardiac Output Regulation

• EDV: Blood in ventricles before contraction
• ESV: Blood left in ventricles after contraction
• SV: Stroke volume = EDV - ESV
• CO: Cardiac output = HR × SV

Stroke Volume Factors

• Preload: Ventricular stretching
• Contractility: Strength of contraction for given preload
• Afterload: Resistance to pump blood

Heart Rate Factors

• Autonomic Nervous System: Sympathetic (increases HR), Parasympathetic (decreases HR)
• Hormones: Epinephrine and Thyroxine (increase HR)

Exercise

• Venous return increases preload
• Sympathetic activity increases HR and contractility