Endocrine Review Notes PDF

1. Comparison of Endocrine and Nervous Systems Feature Endocrine System Nervous System Control Hormonal signaling via the Electrical signaling through Mechanism bloodstream...

1. Comparison of Endocrine and Nervous Systems Feature Endocrine System Nervous System Control Hormonal signaling via the Electrical signaling through Mechanism bloodstream neurons Speed of Response Slow (seconds to days) Fast (milliseconds) Duration of Effects Long-lasting (hours to weeks) Short-term Target Range Widespread (systemic) Speci c (localized) Example of Re ex actions (e.g., pain Regulating growth (e.g., GH, insulin) Function withdrawal) 2. Hormone Action Based on Chemical Structure Chemical Examples Mechanism of Action Target Type Peptide Bind to surface receptors, use second Plasma membrane Insulin, glucagon Hormones messengers (e.g., cAMP) receptors Direct gene Steroid Cortisol, Cross cell membranes, bind transcription in the Hormones estrogen intracellular receptors nucleus Amine Thyroxine (T4), Act like peptides or steroids depending Membrane or nuclear Hormones epinephrine on solubility receptors 3. Key Determinants of Hormone-Target Cell Interactions 1. Hormone Concentration: Availability in the bloodstream (e.g., controlled by secretion rate or degradation). 2. Receptor Availability: Speci city and density of receptors on the target cell. 3. Af nity: The strength of binding between hormone and receptor. 4. Hypocalcemia Effects Bodily Response Muscle spasms or tetany (e.g., Increased PTH secretion to elevate Ca²⁺ levels carpopedal spasm) Vitamin D activation enhances calcium absorption Tingling or numbness in extremities from the gut Cardiac arrhythmias Bone resorption releases calcium into circulation fi fl fi fi  5. Fluticasone for Asthma Reason to Continue Use: ◦ Fluticasone reduces in ammation over time, preventing asthma exacerbations. ◦ Stopping abruptly can lead to a rebound of symptoms or loss of control over the in ammatory process. ◦ It requires continuous use to maintain baseline anti-in ammatory effects. 6. Adipose Tissue Hormones Hormon Composi Trigger Target Effect e tion Suppresses appetite; increases Leptin Peptide Proportional to fat stores Brain energy expenditure Liver, fat, Resistin Peptide Proportional to fat stores Antagonizes insulin muscle Adipone Inversely proportional to Same as Peptide Enhances insulin sensitivity ctin fat stores resistin 7. Short-Term Stress Response (Adrenal Cortex) Hormones Source Function Maintain blood glucose levels, energy Glucocorticoids Zona fasciculata metabolism Mineralocorticoid Zona Regulate Na⁺, K⁺ balance, blood volume/pressure s glomerulosa Fight-or- ight response (e.g., epinephrine Catecholamines Adrenal medulla release) 8. Thyroid and Parathyroid Glands Hormone Gland Location Function s Anterior neck, below Metabolic rate, growth, and Thyroid T3, T4 larynx development Parathyroi Posterior thyroid PTH Regulates calcium and phosphate levels d fl fl fl fl 9. Renin-Angiotensin-Aldosterone System (RAAS) Step Mechanism Outcome From kidneys in response to low Converts angiotensinogen to angiotensin Renin Release BP/Na⁺ I ACE Conversion Lungs convert Ang I → Ang II Vasoconstriction; stimulates aldosterone Aldosterone Na⁺ reabsorption; water retention; Adrenal cortex Release increases BP 1. Overview of cAMP in Cellular Signaling Key Features of cAMP: 1. Ubiquity: Expressed in every tissue and cell. 2. Activation Effects: ◦ Brief but powerful. ◦ Depend on available downstream targets. 3. Degradation: Quickly inhibited and broken down by phosphodiesterase (PDE). Pathway of cAMP Activation: Step Details Hormone binds Activates the G-protein coupled receptor. GPCR G-protein activation GTP replaces GDP on the α-subunit, activating adenylate cyclase. cAMP synthesis Adenylate cyclase converts ATP to cAMP. cAMP activates protein kinase A (PKA), leading to target protein Cellular effects phosphorylation. Termination PDE degrades cAMP, ending the signal. 2. Hormone Classes and Their Mechanisms Hormon Solubil Mechanism Examples e Type ity Water- Hydrop Cannot cross the plasma membrane; bind to GPCR and use Insulin, Soluble hilic second messengers (e.g., cAMP, Ca²⁺). epinephrine Lipid- Hydrop Cross plasma membrane; bind intracellular receptors; Cortisol, Soluble hobic directly affect gene transcription. thyroid hormones 3. Water-Soluble Hormones: Second Messenger Mechanism Key Steps for Amino Acid-Based Hormones: 1. Hormone Binding: Hormone binds to the extracellular GPCR. 2. G-Protein Activation: ◦ G-Protein Subunits: α (active), β, and γ (inactive heterodimer). ◦ GDP is exchanged for GTP on the α-subunit. ◦ βγ subunit dissociates, leaving α-GTP free to activate enzymes. 3. Second Messenger Production: ◦ Adenylate Cyclase Activation: Converts ATP to cAMP. ◦ Phospholipase C Activation: Converts PIP2 to DAG and IP3. ▪ DAG: Activates protein kinase C (PKC). ▪ IP3: Releases Ca²⁺ from the endoplasmic reticulum (ER). 4. Signal Termination: ◦ cAMP is degraded by PDE. ◦ Ca²⁺ signaling is reduced via sequestration in the ER. 4. Lipid-Soluble Hormones: Intracellular Mechanism Process Details Plasma Membrane Hormones pass through the membrane due to hydrophobic nature (e.g., Diffusion steroids, thyroid hormones). Receptor Binding Hormones bind to intracellular receptors in the cytoplasm or nucleus. Gene Activation The receptor-hormone complex binds DNA, promoting transcription. Newly synthesized proteins mediate the hormone's effects (e.g., metabolic changes). Protein Synthesis 5. G-Protein Coupled Receptor (GPCR) Signaling G-Protein Action Type Gs Stimulates adenylate cyclase, increasing cAMP levels. Gi Inhibits adenylate cyclase, reducing cAMP levels. Activates phospholipase C (PLC), initiating PIP2 signaling (DAG & Gq IP3). PIP2-Calcium Signaling Pathway: 1. Hormone binds GPCR → activates Gq. 2. Gq activates PLC → splits PIP2 into DAG and IP3. 3. IP3 releases Ca²⁺ from ER → activates proteins (e.g., calmodulin). 4. DAG activates PKC → phosphorylates target proteins. 6. Comparison of cAMP and PIP2 Pathways Feature cAMP Pathway PIP2-Calcium Pathway Second cAMP DAG and IP3 Messenger Effector Enzyme Adenylate cyclase Phospholipase C (PLC) Downstream Activates PKA, phosphorylates DAG: Activates PKC, IP3: Releases Effects proteins Ca²⁺. 1. Overview of Endocrine Glands Primary Function: Produce and release hormones directly into the bloodstream. Key Characteristics: ◦ Lack ducts (unlike exocrine glands). ◦ Systemic effects due to hormone transport via blood. ◦ Can act on distant targets in the body. 2. Types of Endocrine Glands Dedicated Endocrine Organs Pituitary gland Thyroid gland Parathyroid glands Adrenal glands Pineal gland Dual-Function Organs (Endocrine + Exocrine) Organ Endocrine Function Exocrine Function Pancrea Insulin, glucagon secretion (blood sugar Digestive enzyme production s regulation) Gonads Sex hormones (testosterone, estrogen) Gamete production (sperm, ova) Nutrient/waste exchange for Placenta Hormones (hCG, estrogen, progesterone) fetus  Noncanonical Endocrine Organs Organ Hormones Function Adipose Appetite regulation; insulin sensitivity Leptin, resistin, adiponectin Tissue modulation Thymus Thymosin, thymopoietin T-cell development, immune function Small Gastrin, secretin, cholecystokinin Regulates digestion and enzyme secretion Intestine (CCK) Kidneys Erythropoietin (EPO), renin RBC production; blood pressure regulation Heart Atrial natriuretic peptide (ANP) Blood pressure and sodium regulation 3. Nervous vs. Endocrine System Comparison Feature Nervous System Endocrine System Response Speed Rapid (milliseconds) Slow (seconds to days) Duration of Short-lived Long-lasting Response Mechanism of Action potentials, neurotransmitters Hormones in blood Action Target Speci c (determined by axonal Broad (targets anywhere blood Speci city pathways) circulates) Primary Immediate control (e.g., re exes, Regulation of growth, metabolism, Function movement) reproduction 4. Examples of Hormone-Producing Glands and Their Hormones Gland/Organ Hormones Function Pituitary Growth hormone (GH), Growth, stress response, and other endocrine Gland ACTH control Thyroid T3, T4 Regulates metabolism, energy use Gland Adrenal Cortisol, aldosterone Stress response; uid and electrolyte balance Glands Pineal Gland Melatonin Regulates sleep-wake cycle Pancreas Insulin, glucagon Blood glucose regulation Gonads Testosterone, estrogen Secondary sex characteristics, reproduction fi fi fl fl  5. Hormones and Their Broad Mechanisms Category Examples Mechanism Water-Soluble Insulin, Bind to plasma membrane receptors; use second Hormones epinephrine messengers. Lipid-Soluble Cortisol, thyroid Cross plasma membranes; bind to intracellular receptors; Hormones hormones direct gene transcription. 6. Highlights from Table 16.1: Systems Comparison Nervous System Endocrine System Initiates responses rapidly Initiates responses slowly Short-duration responses Long-duration responses Acts via action potentials/ Acts via hormones in the blood neurotransmitters Acts diffusely (targets accessible via Acts at speci c locations (axon pathways) blood) fi