Dyosisitah Notes Stress Response

8/14/2019 Dyosisitah Notes Stress Response

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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)(Neurohypophysis-

posterior/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


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c. Environmental

1. Physical Agents (Chemicals, Radiation)

2. Temperature (Cold, heat)

3. Pollution

4. Microbes (Influenza A H1N1 2009)

Stimulus Receptor (neural) BRAIN

a. Thermoreceptors

b. Mechanoreceptos

c. Nociceptors (Pain)

d. Afferent Nerves (sensory)

e. 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

genesb. 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


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Nearest part or organ that connected spinal nerves.

Epinephrine: Adrenal Medulla

Norepinephrine: Nerves in the presynaptic cleft

1. Epinephrine

Alpha receptors, Beta receptorsBronchi 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

cellss 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 inalveoli 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


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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 PathwayLeukotrines (LTD1 LTD4),Histamine Release

(Mast cells, Macrophages, Platelets)

Effects of Histamine:

a. Broncho-constriction: Binds to H1 Receptorb. 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)


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Dyosisitah Notes Stress Response