Dyosisitah Notes Stress Response

DYOSISITAH NOTES STRESS RESPONSE Dr. ROXAS 6/18/09

Homeostatsis  state of balance (Neuro-Endo-Immunological Response) a. Neural  Receives the stimulus via receptor. 1. Sensory (afferent nerves)  from receptor travels to the brain 2. Motor (efferent nerves)  from brain travels to your target source that elicits response b. Endocrine  release of hormones (hypothalamus, pituitary & target organs) 1. CRH (Hypothalamus) (releasing hormones) 2. ACTH (Pituitary Gland)(Neurohypophysisposterior/adenohypohysis- anterior) 3. Insulin, Epinephrine, thyroxine c. Immune  Release chemical mediators (defends & damages) a. TNF – alpha b. Histamine c. Leukotrines d. Interleukines Stress  it is stimulus that entails any form response coming from the environment (Internal/External) a. Unpleasant (Anxiety, Problems, Loss, Death, Diseases) b. Pleasant (General activities, oxygen energy (36 ATP), Oxygen  ATP ( 3 Pi – high energy phosphate/3,200kcal) Oxidative Stress  O2 + RBC (hgb  Fe) :O2 + Fe+2 ---> Fe+3 (ferric) (free radicals) that damages the cell membrane. Response of Stress: Stimuli: (Form of Stress) a. Physical 1. Chemical Mediators (TNF alpha, INTERLEUKINS) 2. Viruses/bacteria/fungi/parasites 3. Diseases 4. Aging b. Psychological 1. Feelings (Fear, happiness) 2. Thoughts 3. Spiritual

c. Environmental 1. Physical Agents (Chemicals, Radiation) 2. Temperature (Cold, heat) 3. Pollution 4. Microbes (Influenza A H1N1 2009) Stimulus  Receptor (neural) a. b. c. d. e.

 BRAIN

Thermoreceptors Mechanoreceptos Nociceptors (Pain) Afferent Nerves (sensory) Optic nerve/Olfaction/Vestibulo-cochlear

Receptors (Immunologic) a. Antigen Presenting Cells (Neutrophils, Basophils, Macropahges, NK cells)

BRAIN: a. Hypothalamus (Amygdala  feelings)  CRH b. Pituitary Gland  ACTH Target Organs: ACTH (organs that affected) a. Pancreas: Releases Glucagon (Alpha Cells) (Epinephrine Release)  BOOST OF ENERGY  Catabolic (stored glycogen will be released)  Fat ( release free fatty acids)  pyruvate  Kreb cycle Inhibition Insulin (Beta Cells)  Reabsorbs stores glucose (Glycogen)  Binding to the Insulin receptor in the cell membrane (translocates GLUT 4 receptor)  Mitogenesis that enhances cellular regeneration Prevents the activation of Pro-apoptotic genes b. Andrenal : (SEX (steroid)-SALT(ADH)-STESS (EPI) CORTEX a. Zona Glumerulosa (ADH) b. Zona Faciculata (endogenous steroid  CORTISOL) c. Zona Reticularis MEDULLARY  SITE release of Epinephrine

–

Nearest part or organ that connected spinal nerves.

Epinephrine: Adrenal Medulla Norepinephrine: Nerves in the presynaptic cleft 1. Epinephrine  Alpha receptors, Beta receptors Bronchi  bind into the alpha receptors (relaxation of the smooth muscle of the bronchial wall  increase diameter  BRONCHODILATION. Blood Vessel binds alpha receptors  contraction of the smooth muscle of the blood vessel wall  decrease diameter  VASOCONSTRICTION Effects Vasoconstriction: 1. Increase the peripheral resistance to flow 2. Increase blood pressure 3. Can damage Endothelial cell wall (pressure and flow changes  Phospholipase A2 release and Arachidonic acid activation  clot formation (some cases only, chronic) 4. Kidney (Afferent arteriole)  decrease renal blood flow  release of JG cells’s RENNIN Epinephrine also triggers the release of RENNIN Steps in conversion of ANGIOTENSIN 2 1. Release RENNIN in the JG cells  Converts ANGIOTENSINOGEN (inactive prohormone) 2. ANGIOTENSIN 1 (LIVER)  ANGIOTENSIN 2 (Endothelial cell in alveoli  Agiotensin Converting Enzyme) EFFECTS of ANGIOTENSIN 2: 1. AT 1 receptor (Angiotensin Receptor 1) : a. VASOCONSTRICTION b. Activation of the Vasopressin Release Pituitary (Thirst Activation) c. Activation of ADH in the Zona Glomerulosa (Adrenal Cortex) d. AT 2 receptor  VASODILATION Epinephrine  catabolism (release from glycogen  Glucose)  Activate Immune Activation (ACUTE)  Immunosuppressive Effects (increases cAMP  decrease in Lymphocytic Activity) (CHRONIC) a. Adhesion (ICAM or VCAM) b. Rolling

– –

–

c. Transmigration d. Chemotaxis e. Chemical Release (peroxides, sulfatases, nucleases) 2. Anti-diuretic Hormone (ADH)  ZONA GLOMERULOSA 1. Collecting Tubules (Site Concentrating urine) Cell membrane of Collecting tubule is impermeable to the Na + H2O ADH causes opening of the Aquaporins (Na channels )  Water + Na reabsorption & K+ secretion  increasing concentration gradient  Concentrated urine. Water Retention  Affects blood pressure increases ( blood volume  mass  pressure) STEROIDS: CORTISOL 1. Acute  Energy (catabolism) 2. Chronic  Immuno-suppression by decreasing lymphocytic activity HOW? CORTISOL  Inhibits Phospholipase A2 ( Arachidonic Acid Synthesis) Phospholipase A2 ( Phospholipases  (cell membrane damage)  Arachidonic Acid ARACHIDONIC ACID 1. Leukotrine Pathway Leukotrines (LTD1 – LTD4),Histamine Release (Mast cells, Macrophages, Platelets) Effects of Histamine: a. Broncho-constriction: Binds to H1 Receptor b. Vasodilation: Binds H1 Receptor c. Hypersecretion Goblet cells : Alveoli  mucus production (obstruction) d. Increases the production of HCl (parietal cell) H2 receptor binding (Risk Ulcer) 2. Cyclooxigenase Pathway (COX) a. COX 1 1.a. Thromboxane A2 (Platelet Aggregation/Potent Vasoconstrictor) 2.a. Prostaglandins (PGE1 & PGE 2) 3.a. Prostacycline (Vasodilator, Vasodilation)  smooth surface b. COX2 1.a. Bradykinin (Pain, & Inflammation)

Thyroid Gland: Thyroxine (Increases Protein synthesis)