Pathophysiology

• 1) Alarm stage
• 2) Resistance/adaptation stage
• 3) Exhaustion stage

When the CNS senses a stressor which then triggers reactions from the hypothalamus and the SNS. The body's defenses are then mobilized. (fight or flight)

The body attempts to resist or adapt to the effects of the stressor by releasing and reacting to corticoid hormones (cortisol, Epi, NE) by attempting to re-balance itself or recover.

This is the 3rd stage in which the body is unable to recover from the stressors thereby leading to progressive breakdown of compensoatory mechanisms and homeostasis. This is the onset of the "diseases of adaptation". You see impairment of the immune response, heart failure, kidney failure, and/or death.

• 1) exogenous or endogenous stressor responsible for the disturbance
• 2) the chemical or physical disturbance produced by the stressor
• 3) the body's counteracting (adaptational) response to the disturbance

A physiologic response derived from the psychologic stressor.

When the body mounts a physiological stress response in anticipation of disruption of homeostasis.

When the body responds to a stimuli that is associated with danger or a previously produced stress response.

In the CNS and endocrine systems

Corticotropin-releasing hormone (CRH) is released from the hypothalamus, the SNS, the pituitary gland and the adrenal gland. It is also released peripherally at inflammatory sites.

Release Epi and NE

Release ACTH which then stimulates the Adrenal cortex to release cortisol.

Increase ADH/Vasopressin which causes water retention. (septic pts retain water, but can't use it intravascularly - only intracellularly leading to edema)

both alpha and beta adrenergic receptors.

Primarily alpha adrenergic receptors.

• regulates BP by:
• 1) smooth muscle vasoconstriction
• 2) peripheral vasoconstriction
• 3) dilates pupils
• 4) causes piloerection (goose bumps)
• 5) causes increased sweating

• Increases CO and BP by:
• 1) enhances myocardial contractility (+ inotrope)
• 2) increases HR (+chronotrope)
• 3) increases venous return to heart
• 4) skeletal muscle vasodilation leading to increase oxygenation
• 5) increases BG levels by stimulating gluconeogenesis and glycogenolysis
• 6) decreases insulin release from pancreas
• 7) stimulates lypolysis (aids cortisol)

• 1) stimulates gluconeogenesis
• 2) enhances elevation of BG levels
• 3) inhibits uptake and oxidation of glucose by many body cells.
• 4) suppresses Th1 cells thereby decreasing cellular immunity and proinflammatory response.
• 5) stimulates Th2 cells which increases adaptive humoral immunity and anti-inflammatory response.

Endogenous opiates with pain relieving capabilities that are released into the blood in response to stress.

Pituitary gland

Adrenal medulla

Pain transmission is modulated by a balance of impulses transmitted to the spinal cord by large A-delta and small C fibers. Stimulation of the A-delta fibers by touch, vibration, or thermal stimuli cause the cells to "close the pain gate" to decrease pain perception. Stim of small C fibers "opens the pain gate", enhancing pain perception.

Nociceptors that respond to chemical, mechanical, and thermal stimuli.

fingertips

A-delta fibers

C fibers

dorsal root ganglia

Dorsal horn

• 1) projection cells: relay info to higher brain areas (cephalad)
• 2) excitatory interneurons: relay nociceptive transmissions to projection cells, other interneurons, or motor cells responsible for reflexes like pain withdrawal.
• 3) inhibitory interneurons: modulate nociceptive transmission

Thalamus

To project to the somatosensory cortex so that the mind can discriminate types of pain. The cortex then is involved in what we "think" about pain.

We would not seem to care about pain. (frontal lobectomy)

Limbic and Reticular activating systems

Inflammatory, Pain excitatory, Pain inhibitory

Prostaglandins, TNF, nitric oxide, bradykinins, histamines

Glutamate and aspartate

GABA, Endogenous opiods (enkephalins), Endomorphins, endorphins, dynorphins.

• Connective tissure, muscle or bone, skin
• sharp and well localized, or dull, aching and pooly localized

• internal organs and abdomen
• transmitted by sympathetic afferents, poorly localized d/t lesser number of nociceptors in viscera

present in and area removed or distant from its point of origin.

Nociceptive pain, prolonged (>3months).

• Results from trauma or disease of nerves.
• Can be from peripheral causes: trauma, diabetic neuropathy, carcinoma, HIV.
• Can be from central causes: brain/spinal cord trauma, tumors, vascular lesions, MS, phantom limb pain.

• Permanent loss of sensory input from a part of the body.
• Trauma, chemical injury to PNS, tumor infiltration of nerve tissue, damage from radiation, chemo.
• Constant dull, viselike ache, paroxysms of burning or electric shock sensation

Hypothalamus

TSH-RH stimulates Ant-pit gland to release TSH which acts on the thyroid gland to stim the release of T₄ (thyroxine). T₄ then stimulates the adrenal medulla to release Epi into the bloodstream. Epi then causes vasoconstriction, stimulates glycolysis, and increases metabolic rates thereby increasing heat production.

Radiation

conduction

convection (wind-chill factor)

Vasodilation (peripheral)

Evaporation (sweating)

• *Kills or stunts growth and replication of micro-organisms.
• 1) High temps decrease serum levels of iron, zinc, and copper which are needed for bacterial replication.
• 2) body switches to lipolysis and proteolysis to deprive bacterial of glucose food sources.
• 3) lysosomal breakdown and autodestruction of infected cells to prevent viral replication.
• 4) increases lymphocytic transformation and motility of neutrophils, thus facilitating immune response.
• 5) enhances phagocytosis

severe spasmodic cramps in the abdomen and extremities that follow prolonged sweating and Na+ loss.

fever, tachycardia, increased BP

treat with rehydration of gatorade or dilute salts.

prolonged high core or environmental temps causing the hypothalamic response of vasodilation and profuse sweating. Leads to dehydration, decreased plasma volum, hypotension, decreased CO, tachycardia.

Sxs: weak, dizzy, nauseated, faint

Rx: drink warm fluids and lay down, rest.

• breakdown of thermoregulatory center
• sweating ceases and skin becomes dry and flushed
• Sxs: irritable, confused, stuporous, comatose
• Rx: remove from warm env., cooling blanket, cool water bath, ice packs

either increased Ca++ release or decreased Ca++ uptake with muscle contraction.

Allows intracellular Ca++ to rise, producing sustained, uncoordinated muscle contractions which increase muscle work, O2 consumption, and lacic acid production. Then acidosis develops and temps rise.

Rx: dantrolene sodium, procainamide, sodium bicarb