Mechanism of Defense (week4-5) Flashcards
Sjogren’s syndrome
autoimmune disease that dries up all lubricating fluids in the body.
Not enough inflammation
- defect in phagocytic functions
a. quantitative defect (example– from chemotherapy)
1) leukopenia –deficiency in WBCs
2) specific deficiency in neutrophils-neutropenia
b. qualitative defects
1) chemotactic defects—won’t respond appropriately when “summoned.”
2) impaired function; ex—phagocytes damaged by diabetes mellitus have decreased ability to fight microbes.
- complement deficiencies
a. these are a group of disorders that stem from a genetic defect in synthesis of complement proteins
b. patients who have defects in these have problems that are very similar to those seen in patients with antibody deficiencies— they will be extra susceptible to infections.
Too Much Inflammation
SIRS
sepsis
septic shock
chronic inflammation
SIRS
SIRS – systemic inflammatory response syndrome
a. occurs when a normal systemic inflammatory response goes into overdrive – the normal “braking” system of the inflammatory process does not occur. Instead, wide spread
systemic inflammation occurs in the entire body, not just in the original injured or inflamed area.
b. this excessive systemic inflammation contributes to widespread impaired tissue function and organ damage.
1) a localized injury with infection of the big toe → local inflammation is initiated →local inflammatory mediators activate a systemic response → instead of healing, systemic inflammation goes into overdrive → SIRS →
widespread tissue/organ damage
c. SIRS is present when 2 (usually more) of the following S & S are present;
1) unexplained change in mental status (confusion, not as
awake and alert as normal).
2) fever of more than 100.4° F
3) increased heart rate
4) increased respiratory rate
5) abnormal white blood cell count (WBC)
sepsis
occurs when there is a known or suspected INFECTION AND the person has SIRS.
1) a localized injury with infection of the big toe → local inflammation is initiated →local inflammatory mediators activate a systemic response → inflammation overdrive
→ S&S of SIRS → sepsis
septic shock
a. occurs when sepsis (infection + SIRS)
is complicated by LOW BLOOD PRESSURE.
b. high levels of systemic inflammatory mediators trigger widespread, extreme vasodilation = no arterial vessel “tone” as arteries become too relaxed, “floppy” -> blood pools in periphery instead of being part of circulation -> eventually low blood volume reduces amount of O2 being brought to tissues as well as decreasing BP
c. S&S of septic shock:
1) SIRS S&S – change in mental status, fever, increased heart rate, increased resp rate, abnormal white blood cells (WBCs) +
2) low BP. Low BP causes ischemia to organs so patient can have renal failure, respiratory failure, heart failure or death.
chronic inflammation
chronic inflammation
a. difference between acute & chronic inflammation is duration—chronic lasts weeks or longer, regardless of cause
b. inflammation can be prolonged to become chronic, due to persistent bacterial contamination, foreign objects (splinters, etc)
hypersensitivities– “too much” immunocyte response
a. a hypersensitivity is when the immunocyte response that is supposed to help us goes “too far” and harms us.
b. one way to create subcategories of hypersensitivity responses is to base them on the target antigen (the antigen that is attacked by antibodies or T- cells):
1) allergic response (“allergic reaction”): hypersensitivity to a target antigen (environmental, medical, or pharmaceutical),
called an allergen.
2) autoimmune response: hypersensitivity to self-antigens (the target antigen) – a reaction of our body to our own antigens.
3) alloimmune response: hypersensitivity to another person’s antigens (the target antigen), such as when an organ is transplanted.
local allergic hypersensitivity S&S
1) once a person is sensitized, the S&S appear immediately upon 2nd or more exposures
2) localized reaction: dermatitis (skin rash that can cause itching and swelling), nasal allergic rhinitis, conjunctivitis as a result of histamine, leukotriene, and prostaglandin release from the mast cell.
4) treatment—meds that work against
a) histamine—antihistamines
b) inflammatory properties of PGs: steroids
c) against bronchoconstrictive properties of leukotrienes: leukotriene blockers (FYI–Singulair).
systemic allergic hypersensitivity S&S
systemic reaction– anaphylaxis:
a) occurs when someone is more severely allergic to the antigen (determined by previous exposures and person’s genetic makeup)
b) histamine, leukotrienes, PGs, and acute phase reactants such as complement system are overactivated throughout body—all the S&S noted for localized reactions become systemic.
(1) itching all over; hives (urticaria)
(2) angioedema —-abnormal vasodilation and edema of small blood vessels; usually occurs in lips tongue & hands
(3) N, V, D, cramps
(4) wheezing (from bronchial edema, but also from leukotriene-induced bronchoconstriction),
dyspnea; possibly laryngeal edema
(5) hypotension & shock if bad enough—what causes the hypotension in this context?systemic vasodilation.
autoimmune hypersensitivity
a. overview / general mechanisms:
1) reasons why our bodies’ antibodies (or T-cells) sometimes attack our own antigens:
a) sometimes after we “fight off” an infection, our immunocyte system stays “primed.”
(1) instead of “standing down”—ie, sending post-attack immunocytes back to lymph tissue
appropriately—our immunocyte system begins
attacking antigens on our own cells.
(2) example—the etiology of rheumatic heart disease,
multiple sclerosis
a) T-lymphocytes destroy random patches of the myelin sheath that insulates the fibers of neurons in the brain
b) results in asymmetric weakness and/or malfunction of various areas of the body.
Graves disease
a) disease that causes most cases of hyperthyroidism
b) autoantibody stimulates thyroid gland cells to oversecrete thyroid hormone (TH), causing S&Ss of hyperthyroidism
Goodpasture’s syndrome
a) autoantibody attacks connective tissue in pulmonary & glomerular basement membrane.
b) results in pulmonary hemorrhage & glomerulonephritis
myasthenia gravis
a) autoantibody attacks acetylcholine receptors on cells of muscles
b) this means that acetylcholine would not have enough effective post-synaptic gap receptor; what kinds of S&S? muscle weakness
