Immune System Disorders Flashcards

1
Q

innate immunity

A

non-specific; if surface barriers breached –> inflammatory response

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2
Q

adaptive immunity

A

specific, develops after exposure to a specific antigen

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3
Q

humoral immunity

A

antibodies produced to protect body

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4
Q

cell-mediated immunity

A

lymphocytes programmed to attack non-self cells to protect body

B and T

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5
Q

antibodies

A

produced by B-lymphocytes

occur freely in circulation

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6
Q

immunoglobulins

A

function as Abs

found on plasma membranes of B-LCs (also found on other immune cells)

IgG (most common; fights bacteria, viruses, toxins)
IgE (allergic responses)

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7
Q

active, natural immunity

A

natural exposure to antigen –> body creates antibodies to prep for second exposure
(primary and secondary response)

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8
Q

active, artifical

A

antigen purposefully introduced into body (immunization) –> simulates what would happen to a virus by our own immune cells

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9
Q

passive, natural

A

IgG transferred from mother to fetus (crossing placenta)

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10
Q

passive, artificial

A

injection of antibodies (anti-venom); short-term protection

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11
Q

type I hypersensitivity disorders

A

excessive or inappropriate activation of immune response

effects –> local (atopic); systemic (anaphylactic)

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12
Q

exposure to allergen can occur by:

A

inhalation, ingestion, skin contact

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13
Q

Type I HS d/o mediated by

A

IgE

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14
Q

local effects of type I HS d/o

A

atopic:

early phase –> inflammation
late phase: mucosal edema, mucous secretion

contained to epithelium, not bloodstream

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15
Q

mechanism of hypersensitivity

A

exposure to antigen (pollen) –> immune response: B-lymphocytes recognize as non-self –> produce antibodies (IgE)

IgE attaches to mast cells

second exposure –> IgE recognizes antigen –> sensitized mast cells release histamine –> immediate inflammatory response

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16
Q

anaphylaxis

A

systemic response to inflammatory mediators released

life-threatening

17
Q

anaphylaxis: vasodilation

A
histamine
ACh
kinins
leukotrienes
PGs

consequence: drop in BP

18
Q

anaphylaxis: bronchoconstriction

A

Ach
leukotrienes
PGs
kinins

consequence: impaired O2 delivery to capillary beds

19
Q

signs and symptoms of anaphylaxis

A

generalized itching or tingling (oral cavity)

coughing

difficulty breathing

weakness

dizzy/fainting

sense of fear/panic

edema (around eyes, lips, tongue, hands feet)

hives

collapse with LOC

20
Q

effects of anaphylaxis

A

inflammatory mediators into general circulation:

vasodilation (decreased BP)

bronchoconstriction (impairs O2 delivery)

mucous release

skin: nerve ending irritated (itchy)

***reducing availability of oxygenated blood to brain

21
Q

treatment of anaphylaxis

A

first aid: epipen and 911

Epi: stabilizes BP (vasoconstriction)

Glucocorticoids: reduce AA (AA produces leukotrienes and PGs –> reduced vasodilation and cap permeability)

antihistamines: reduce histamine locally and systemically

O2: help with bronchoconstriction –> drive partial pressure of O2 up

22
Q

autoimmune disorders

A

immune system attacking our own healthy cells; development of antibodies against self-cells and tissues

23
Q

autoimmune process

A

immune system forms antibodies against self-antigens

autoantibodies attack self-antigens

inflammation and tissue damage occur (local to organ or systemically)

24
Q

mechanisms of autoimmune

A
  1. genetic susceptibility

2. environmental triggers (virus, chemical)

25
Q

immunodeficiency

A

partial or total loss of one or more immune system components

26
Q

primary immunodeficiency

A

inherited –> basic developmental failure somewhere in system

27
Q

secondary or acquired immunodeficiency

A

loss of immune response from specific causes

infections; splenectomy, malnutrition, liver disease, immunosuppressant drugs, radiation, chemo