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Anatomy and Physiology > immune i > Flashcards

immune i Flashcards

1
Q

Immunity definition

2 systems within immune system

A

-resistance to disease

Innate and adaptive defense systems

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2
Q

Innate defense first line of defense

A

External body membranes (skin and mucosae and their secretions)

  • ward off pathogens
  • physical barrier to most microbes
  • keratin resistant to weak acids and bases, bacterial enzymes, and toxins
  • mucosae provides similar barriers
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3
Q

protective chems that inhibit or destroy microbes as part of the innate immune system’s 1st line of defense

A
  1. acidity of skin and secretions (acid mantle) –> inhibits growth
  2. enzymes (lysozyme of saliva, respiratory mucus, and lacrimal fluid) –> kills microbes
  3. Defensins (antimicrobial peptides) –> inhibit growth
  4. other toxic chems (lipids in sebum, dermcidin in sweat)
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4
Q

innate immune system

  • respiratory part
  • how to breach
  • expulsion
A
  • respiratory system has mucus coated hairs in nose –> also, cilia of upper respiratory tract sweep dust and bacteria mucus towards mouth
  • nicks and cuts
  • vomiting, shedding epithelial cells, peeing, pooping
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5
Q

Innate immune 2nd line of defense

  • when is it necessary
  • what does it include
A

-necessary if microbes invade deeper tissues

Includes

  • cells (phagocytes and NK cells)
  • Antimicrobial substances (interferons, complement proteins, and antimicrobial proteins)
  • fever
  • inflammatory response (macrophages, mast cells, WBCs, inflammatory chems)
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6
Q

Innate immune: 2nd line of defense: Phagocyte examples

A

Neutrophils = most abundant but dies fighting –> become phagocytic on exposure to infection material

Macrophages = main, robust, phagocytic cells developed from monocytes –> free macrophages wander tissue spaces –> fixed macrophages live in organs

-alveolar macrophages = free
-stellate macrophages = fixed in liver
microglia = fixed in brain

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7
Q

Innate immune: 2nd line of defense: Phagocyte function

A

adheres to particle, but sometimes this is difficult –> opsonization marks pathogens by coating them with complement proteins or antibodies which makes them easy to eat

  • ctoplasmic extensions bind to and engulf particle in vesicle called phagosome
  • phagosome fuses with lysosome = phagolysosome
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8
Q

Innate immune: 2nd line of defense: Phagocyte mobilization

A

Neutrophils lead and macrophages follow
-as this continues, monocytes arrive –> 12 hrs after they leave blood/enter tissue, they become macrophages –> replace dying neutrophils and stick around for clean up and repair

If there’s inflammation due to pathogens, complement is activated and adaptive immunity elements arrive

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9
Q

Steps for phagocytic mobilization

A
  1. Leukocytosis: release of neutrophils from bone marrow in response to leukocytosis-inducing factors from injured cells
  2. Margination: neutrophils cling to walls of capillaries in inflamed area in response to CAMs
  3. Diapedesis or emigration of neutrophils
  4. Chemotaxis: inflammatory chems (chemotactic agent) promote positive chemotaxis of neutrophils
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10
Q

Natural killer cells

A
  • Nonphagocytic large granular lymphocytes
  • attack cells w/o “self” cell-surface receptors
  • induce apoptosis in cancer and virus-infected cells
  • secrete potent chems that enhance inflammatory response
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11
Q

chems released by NKs

A

Perforin: forms transmembrane pore

Granzymes enter pore and cause apoptosis

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12
Q

Antimicrobial substances (2nd line of defence)

  • examples
  • possible functions
A
  • interferons and complement proteins

- some attack microbes directly; others hinder microbes’ ability to reproduce

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13
Q

Interferons

A
  • family of immune modulating proteins each with slightly dif effects
  • viral-infected cells secrete IFNs to warn neighboring cells
  • IFs enter neighboring cells and produce prots that block viral reproduction and degrade viral RNA
  • Artificial IFNs used to treat hepatitis C, genital warts, multiple sclerosis, hairy cell leukemia
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14
Q

IFN alpha and beta special skill

A

-activate NK cells –> indirectly fight cancer

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15
Q

IFN gamma

A

“immune interferon”

  • secreted by lymphocytes
  • widespread immune mobilizing effects
  • activates macrophages
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16
Q

Summary: 3 main actions of IFNs

A
  1. warn neighboring cells (causing the production of antiviral proteins)
  2. activate macrophages
  3. activate NK cells
17
Q

Complement system

A
  • 20 blood proteins that circulate in inactive form
  • C1-C9; factors B, D, and P; and regulatory proteins
  • major mechanism for destroying foreign substances
  • our cells have complement activation inhibitors
18
Q

How to complements work?

A
  • unleash inflammatory chems that amplify all aspects of inflammatory response
  • kills bacteria and certain other cell types by lysis
  • enhances both innate and adaptive defenses
19
Q

Classical pathway of complement activation

A
  • antibodies bind to invading organisms and to complement components
  • called complement fixation
  • first step in activation
20
Q

lectin pathway of complement activation

A
  • lectins are produced by innate system to recognize foreign invadors
  • when bound to foreign invaders, can also bind and activate complement
21
Q

Alternative pathway of complement activation

A

-activated spontaneously , lack of inhibitors on microbes’ surface allows process to proceed

22
Q

Similarities between the three complement activation pathways

A
  • each involves activation of proteins in orderly sequence
  • each step catalyzes the next
  • each pathway converges on C3 which cleaves into C3a and C3b

-Common terminal pathway initiated that enhances inflamation, promotes phagocytosis via opsonizations, and causes cell lysis (MAC)

23
Q

Actions of C3b and C3a

A

Cell lysis begins when Cb binds to target cell –> insertion of complement proteins called membrane attack complex (MAC) into cell’s membrane –> MAC forms and stabilizes hole in membrane –> influx of water –> lysis of cell

-C3b also causes opsonization

C3a and other cleavage products amplify inflammation –> stimulate mast cells and basophils to release histamine –> attract neutrophils and other inflammatory cells

24
Q

Inflammatory response

A
  • triggered whenever body tissues injured
  • prevents spread of damaging agents
  • disposes of cell debris and pathogens
  • alerts adaptive immune system
  • sets the stage for repair
25
Q

cardinal sign of acute inflammation

A
  • redness
  • heat
  • swelling
  • pain
26
Q

what does the inflammatory response begin with?

A

-begins with chems released into ECF by injured tissues, immune cells, blood proteins

27
Q

Inflammatory mediators

A

kinins, prostalandins (PGs) and complement

  • Dilate local arterioles (hyperemia), causing redness and heat of inflamed region
  • make capillaries leaky (swelling)
  • attract leukocytes to area
  • some have inflammatory roles
28
Q

Inflammatory response: edema

A
  • increase in capillary permeability –> exudate to tissues
  • fluid with clotting factors and antibodies causes local swelling
  • swelling pushes on nerve endings –> pain (pain also from bacterial toxins, PGs and kinins)
  • moves foreign material into lymphatic vessels
  • delivers clotting proteins and comlement
29
Q

Inflammatory response: clotting factors

A
  • form a fibrin mesh
  • scaffold for repair
  • isolates injured area so invaders can’t spread
30
Q

Fever

A
  • abnormally high body temp
  • systemic response to invading microbes
  • leukocytes and macrophages exposed to foreign substances secrete pyrogens
  • pyrogens act on body’s thermostat in hypothalamus, raising body temp
31
Q

Benefits of moderate fever:

A

causes liver and spleen to sequester iron and zinc (needed by microbes)
-increases metabolic rate

Anatomy and Physiology (50 decks)

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