Pathophysiology

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Author:
amypuls
ID:
38711
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Pathophysiology
Updated:
2010-09-30 13:56:21
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Pathophys test
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Description:
Stress/pain/temerature reg.
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  1. Name the 3 stages of General Adaption Syndrome.
    • 1) Alarm stage
    • 2) Resistance/adaptation stage
    • 3) Exhaustion stage
  2. Describe the Alarm stage of the GAS.
    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)
  3. Describe the Resistance/adaptation stage of the GAS.
    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.
  4. Describe the Exhaustion stage of the GAS.
    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.
  5. Name 3 components of physiological stress.
    • 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
  6. What is a reactive response?
    A physiologic response derived from the psychologic stressor.
  7. What is anticipatory response?
    When the body mounts a physiological stress response in anticipation of disruption of homeostasis.
  8. What is conditional response?
    When the body responds to a stimuli that is associated with danger or a previously produced stress response.
  9. Where is the stress response initiated?
    In the CNS and endocrine systems
  10. What is the hormone responsible for the start of a stress response?
    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.
  11. CRH stimulates the SNS to do what?
    Release Epi and NE
  12. CRH stimulates the anterior pituitary to do what?
    Release ACTH which then stimulates the Adrenal cortex to release cortisol.
  13. CRH stimulates the Posterior Pituitary to do what?
    Increase ADH/Vasopressin which causes water retention. (septic pts retain water, but can't use it intravascularly - only intracellularly leading to edema)
  14. Epinepherine binds to and activates what receptors?
    both alpha and beta adrenergic receptors.
  15. Norepinepherine binds to and activates to what receptors?
    Primarily alpha adrenergic receptors.
  16. What are some effects of NE?
    • regulates BP by:
    • 1) smooth muscle vasoconstriction
    • 2) peripheral vasoconstriction
    • 3) dilates pupils
    • 4) causes piloerection (goose bumps)
    • 5) causes increased sweating
  17. What are some effects of Epinepherine?
    • 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)
  18. What are some effects of 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.
  19. What are endorphins and enkephalins?
    Endogenous opiates with pain relieving capabilities that are released into the blood in response to stress.
  20. Where are endorphins released from?
    Pituitary gland
  21. Where are enkephalins released from?
    Adrenal medulla
  22. Describe the gate control theory.
    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.
  23. The efferent system contains sensory nerve endings called what?
    Nociceptors that respond to chemical, mechanical, and thermal stimuli.
  24. What part of the body would contain more nociceptors, the skin on the fingers or the back?
    fingertips
  25. Fast, localized, myelinated pain fibers that are the _____.
    A-delta fibers
  26. Slow, poorly localized, unmyelinated pain fibers are the ________.
    C fibers
  27. Primary-order neurons or pain-transmitting neurons reside where?
    dorsal root ganglia
  28. Second-order neurons are located where?
    Dorsal horn
  29. Name the 3 classes of the second-order neurons and what they are responsible for.
    • 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
  30. Third-order neurons are where?
    Thalamus
  31. What is the function of the third-order neurons?
    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.
  32. What would happen with bilateral thalamic lesions?
    We would not seem to care about pain. (frontal lobectomy)
  33. What subcortical systems of the CNS are involved in alerting the body to danger, initiating arousal, and emotionally processing perceived afferent signals as actual pain?
    Limbic and Reticular activating systems
  34. Name the 3 classifications of pain neurotransmitters.
    Inflammatory, Pain excitatory, Pain inhibitory
  35. Name the inflammatory mediators released after tissue injury.
    Prostaglandins, TNF, nitric oxide, bradykinins, histamines
  36. name the most common excitatory neurtransmitters in the brain.
    Glutamate and aspartate
  37. What are the most common inhibitory neurotransmitters?
    GABA, Endogenous opiods (enkephalins), Endomorphins, endorphins, dynorphins.
  38. Somatic tissure arises from where?
    • Connective tissure, muscle or bone, skin
    • sharp and well localized, or dull, aching and pooly localized
  39. Visceral pain arises from where?
    • internal organs and abdomen
    • transmitted by sympathetic afferents, poorly localized d/t lesser number of nociceptors in viscera
  40. What is referred pain?
    present in and area removed or distant from its point of origin.
  41. Describe chronic pain.
    Nociceptive pain, prolonged (>3months).
  42. What is neuropathic pain?
    • 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.
  43. What is deafferentation 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
  44. What part of the brain is responsible for temperature regulation?
    Hypothalamus
  45. Describe the process of heat production regulated by the 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.
  46. What is it called whe heat is lost thru electromagnetic waves?
    Radiation
  47. What is heat loss by direct molecule-to-molecule tranfer from one surfact to another.
    conduction
  48. What is the transfer of heat thru currents of gases and liquids?
    convection (wind-chill factor)
  49. When heat is lost by diverting core-warmed blood to the surface of the body.
    Vasodilation (peripheral)
  50. Loss of body water from the surface of the skiin and linings of the mucous membranes for the purpose of heat reduction.
    Evaporation (sweating)
  51. What are some benefits of fever?
    • *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
  52. Describe heat cramps
    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.
  53. Describe heat exhaustion
    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.
  54. Describe heat stroke
    • 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
  55. What causes malignant hyperthermia
    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

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