STRESS, ADAPTATION, HOMEOSTASIS PHYSIOLOGIC RESPONSES TO STRESS & ILLNESS

STRESS MODERN STRESS THEORY (HANS SELYE) Stress is the non-specific response of the body to any demand made upon it ADAPTATION The adjustments that a person make in different situations TYPES OF ADAPTATION A. GENERAL ADAPTATION SYNDROME (GAS) Man, whenever he respond to stress, the entire body is involve There are similar manifestations that characterize different disease conditions; & there are very few specific manifestations that characterize a particular disease. Fever weakness fatigue, headache, anorexia, pain are examples of manifestations that characterize various disease conditions STAGES OF GAS

1)

Stage Of Alarm (SA) Person becomes aware of the presence of threat or danger Levels of resistance are decreased Adaptive mechanisms are mobilized ( fight or flight reactions) If the stress is intense enough, even at the stage of alarm death may ensure. Stage Of Resistance Characterize by adaptation Levels of resistance are increased The person moves back to homeostasis Stage Of Exhaustion Results from prolonged exposure to stress & adaptive mechanism can no longer persist Unless other adaptive mechanisms will be mobilized, death may ensure.

2)

3)

B. LOCAL ADAPTATION SYNDROME (LAS) Man may respond to stress through a particular body part or body organ Eg. Inflammation, backache, headache, diarrhea CHARACTERISTIC OF ADAPTIVE RESPONSES 1. attempts to maintain homeostasis 2. whole body/total organism responses 3. have limits 4. require time 5. vary from time to time 6. inadequate or excessive 7. egocenteric, tiring. Requires body energy & tax physical & psychological resources

CONCEPTS OF HOMEOSTASIS (HEMODYNAMICS) SYSTEMIC PHYSIOLOGIC RESPONSE TO STRESS

A. Sympatho-Adreno-Medullary Response (Walter Canon) SAMR or fight or flight response STRESSORS Physical injury, increase body temp, dehydration

hypothalamus

STRESSORS Physical injury, increase body temp,dehydration

STRESSORS Physical injury, increase body temp,dehydration

Brain: Eyes: Mouth: Heart: Lungs: Blood vessels: Skin: Liver: Muscles: G.I. tract: Spleen: Pancreas: Urinary bladder:

increased alertness; restlessness dilated pupils; increased visual perception decreased salivary secretion; thirst & dryness of mouth tachycardia; coronary vasodilatation; increased force of cardiac contractility; increased cardiac output hyperventilation; bronchodilation peripheral vasoconstriction; increased BP pallor; diaphoresis; cold, clammy skin increased glycogenolysis & gluconeogenesis; increased blood glucose level increased glycogegenolysis; increased muscle tension decreased gastric motility; decreased HCL secretion; decreased peristalsis, constipation; flatulence contraction; decreased hemolysis decreased secretion of insulin & pancreatic enzymes relaxation of the detrusor muscles; contraction of the sphincter; Urinary retention

B. ADRENO-CORTICAL RESPONSE

STRESSOR Hypoglycemia (blood glucose level=60mg/dl & below

Hypothalamus

activates Anterior pituitary releases ACTH triggers Adrenal cortex

secretes Glucocorticoid Mineralocorticoid gluconeogenesis blood glucose levels retention of sodium & water ECF volume BP (sex hormones)

Androgen/estrogen

999

c. NEUROHYPOPHYSEAL RESPONSE

STRESSORS Blood loss(hemorrhage, excess of body fluids

hypothalamus

Activates Posterior pituitary

releases ADH

Acts on Kidneys (renal tubules)

Retention of water in the renal tubules

oliguria

Conservation of circulating volume

Prevention of hypovolemic shock

LOCAL PHYSIOLOGIC RESPONSES TO STRESS

 Mobilization of specific & non-specific defense mechanism in response to tissue injury or infection. Purposes Of Inflammation To localize tissue injury To protect tissue from injury To prepare tissue for repair

INFLAMMATORY RESPONSE Physical (thermal, radiation) Mechanical Chemical Microbial Electrical

inflammmants

Tissue injury

1. VASCULAR RESPONSE transitory vasoconstriction followed immediately by vasodilation (due to the release of histamine, bradykinin, prostaglandin E)

Increased capillary permeability

Hyperemia Redness (rubor) Heat (calor)

Fluid/cellular exudation

Edema (tumor)

Pain (dolor) Compression of nerve endings by edema fluids Injury to nerve ending Release of bradykinin

Exudates Serous Serosanguinous Sanguinous Purulent Mucoid/catarrhal

Impaired function

2. CELLULAR RESPONSE Neutrophils first to be launched at the site of tissue Monocytes perform phagocytosisn in chronic tissue injury Lymphocytes responsible for immune response Process involved: Marginal/pavementation. Phagocytes line up at the peripheral walls of the blood vessels Emigration/diapedesis. Phagocytes shift out of the blood vessels Chemotaxis. Injured tissue release substances which exert magnet- like force to the phagocytes to bring them to the area of injury Phagocytosis. Phagocytes ingest or engulf the antigens 3. HEALING PROCESS (REPARATIVE PHASE) Regeneration involves replacement of damaged tissue cells by new cells which are identical in structure or function Scar formation involves replacement of damaged tissue cells by fibrous tissue formation. In the early stage, granulation tissue (pink or red, fragile gelatinous tissue) forms; later in the process, a cicatrix or scar forms because the tissue shrinks & the collagen fibers contract.

Healing may also be classified as follows: First intention: occurs in clean-cut wound (surgical wound). The wound edges are approximated, there is minimal or no scar tissue formation ( primary intention healing or primary union) Second intention: occurs when the wound is extensive & there is great amount of tissue loss (decubitus ulcer). The repair time is longer; the scarring is greater (secondary intention healing) Third intention: occurs when there is delayed surgical closure of infected wound (tertiary intention healing)

THE SYSTEMIC MANIFESTATIONS OF INFLAMMATION a. FEVER Endogenous pyrogens (prostaglandins, leukotrienes, bacterial endotoxins, interleukin 1) Act on hypothalamus Resetting of the body temperature set-point at a higher level Increasing heat production/ decreasing heat loss (shivering; sweating is inhibited; vasoconstriction) Increased production of interferon (protects the cell from viral invasion) Increasd phagocytic activity

b. c. d. e. f. g. h.

LEUKOCYTOSIS (elevated wbc) ELEVATED ESR (erythrocytes sedimentation rate) LYNPHADENOPATHY ANOREXIA HEADACHE BODY WEAKNESS/FATIGUE BODY MALAISE