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Physiology Unit 3 > The Immune System > Flashcards

The Immune System Flashcards

1
Q

The immune system

A

Not a distinct anatomical system has functional overlap with lymphatic and cardiovascular system

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2
Q

Immunity

A

Collective process of protecting the body from
•pathogens bacteria/viruses allergens •abnormal cells cells cancer cells and •removal of dying expiring cells (red blood cells)

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3
Q

What type of cells respond in the immune system what do they rely on

A

Immune response is carried out by leukocytes which rely on contact dependent signals to communicate and cytokines

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4
Q

What are the four steps in the basic flow of immune response

A
  1. Detection/identification of pathogens
  2. Communication between immune cells
  3. Recruitment/coordination of the attack/response
  4. Destruction/suppression of pathogen 🦠
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5
Q

What are the three layers to immunity

A
  1. External barriers “first line of defense”
    - physical (skin, mucosal, secretions )
    - mechanical (tears, swallowing, cilia)
    - chemical (low ph, enzymes in tears and saliva)
  2. Innate immunity: rapid non-specific actions such as (fever information and phagocytosis) 
  3. Adaptive immunity: acquired immunity slower very specific
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6
Q

Innate immunity

A

Born with
Rapid non-specific actions.
Actions of leukocytes and chemicals complement and interferon.
General attack such as fever inflammation phagocytosis

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7
Q

Adaptive immunity/acquired immunity

A

Slower very specific cell mediated immunity.

Memory cells and antibody mediated immunity. B lymphocytes T cells (antibodies they produce)

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8
Q

Leukocyte Development early stages bone marrow

A

Pluripotent hematopoietic stem cells >
• lymphocyte stem cells
• committed progenitors cells

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9
Q

Leukocyte development circulation and tissue

A

From lymphocyte stem cells>

  1. Natural killer (NK)
  2. T lymphocytes (thymus)
  3. B lymphocytes> plasma cells (in tissue)

From committed progenitors cells>

  1. Eosinophils *
  2. Basophils * >mast cells (in tissue)
  3. Neutrophils *
  4. Monocytes* > macrophages (in tissue

Tissue only :
Dendritic cells

*leukocytes (WBC)

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10
Q

Where are leukocytes the most abundant

A

Leukocytes are circulating in the blood, some can leave blood vessels and reside in tissue temporary for days, weeks, months. Some are rarely in the blood at all.

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11
Q

Abundance of leukocytes in blood

A

Never let monkeys eat bananas

Neutrophils, lymphocytes, monocytes, eosinophils, basophils

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12
Q

Leukocytes anatomically

A

Granulocytes versus agranulocytes. Granulocytes are grainy due to vesicles of cytokines inside that are able to release the cytokines granulation via exocytosis

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13
Q

Functionality of leukocytes

A

•Phagocytes : neutrophils eosinophils monocytes >(macrophages) cell eaters

• antigen presenting cells (APC):
Eat and display the pathogens that help identify for others cells 
(Monocytes and dendritic cells)

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14
Q

Basophils

A

Rare in blood, circulatory involved with inflammation and innate immunity when fixed in tissue called mast cell

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15
Q

Eosinophils

A

Rare in blood hang out in the digestive track lungs urinary tract genitalia. Phagocytic on parasites. And responsible for part of allergic reactions inflammation and tissue damage

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16
Q

Neutrophils

A

Most abundant in blood 50 to 70% of white blood cells. Can also leave blood and go into the tissue. Short-lived 1 to 2 days phagocytes can eat up to 20 bacteria. It release cytokines for mediating the inflammatory response

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17
Q

Monocytes

A

Fairly uncommon 1 to 6% of white blood cells. Most exist in the tissue as macrophage. Can eat up to 100 bacteria and red blood cells and neutrophils. Other forms are microglia and CNS, osteoclast, Kupffers cells in the liver (mononuclear phagocyte system)

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18
Q

Dendritic cells

A

Not in blood, rarely found in blood. Found in skin and part of antigen presenting cells. Act as a functional link between innate and acquired immune systems (Langerhan cells)

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19
Q

Lymphocytes

A

Somewhat common in the blood 20 to 35% of white blood cells. But this portion only represents 5% of total abundance most hang out in the lymphoid tissue. Main function/role is an adaptive immune responses. Special forms are: T and B lymphocytes plasma and natural killer cells

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20
Q

Innate immunity

A

Born with general nonspecific attacks. Includes variety of chemicals/molecules for:
-Communication
- identification
- recruitment
- coordination
- attack
Most players are in circulation already and respond to signals (cytokines) or pathogens themselves

Responses include: Phagocytosis, inflammation response, complement system, natural killer cells if pathogen is a virus.

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21
Q

Major histocompatibility complex class 2

A

Phagocytes ( neutrophils macrophages(monocytes) eosinophils) eat the pathogen and display the antigens on its membrane to help other cells identify the pathogen (APC)

  • this process of recognition is mostly an acquired immunity response (mostly)
22
Q

Inflammation

A

Includes swelling, heat, redness of affected tissue due to increase in blood flow. Caused by histamine released by basophils and mast cells (degranulation)
Also by signaling of cytokines and interleukins (chemical signals)

23
Q

Effects of vasodilation

A

Increase blood flow,

increases white blood cells in area,

increases redness and heat,

increases blood vessel Permeability which allows proteins, neutrophils to leave blood and enter the tissue,

increases swelling

24
Q

Other cytokines

A

•Chemotaxins: chemicals that attract/draw away other cells to an area ( positive or negative )
•pyrogens: increase the regulation setpoint and hypothalamus which causes a fever
• compliment: 25+ proteins in a cascade with varying responses


25
Q

Complement system effects

A

-Opsonization: coating of pathogen with opsonins that increase Recognition by white blood cell Phagocytes to be eaten or attacked.
- production of chemotaxins
- degranulation of mast cells (inflammatory response)
-induces fever through pyrogens -formation of membrane attack complex MAC)


26
Q

Membrane attack complex

A

Complement proteins insert themselves into the membrane of pathogens creating pours water and ions to enter pathogen cells. Salas Wells then lysis.

  • cytolytic compounds cause pathogens to Lyse
27
Q

Natural killer cells

A

Act on viruses that are (inside the cell)
(Lymphocytes) and initiate apotosis (cell suicide) via cytotoxic compounds.
They initiate apotosis to MHC 1

28
Q

Major histocompatibility complex 1

A

Located on all cells as an ID badge natural killer cells can initiate apotosis if virus is inside cell

29
Q

Acquired immunity

A
  • Specific to type of pathogen it’s attacking. Body learns how to fight specific pathogens (specific lymphocytes)
  • Pathogen and lymphocytes need to match each other to start the process. -There are Millions of variations of antigen receptors on different lymphocytes
30
Q

When the antigen receptors match the lymphocytes Receptor

A

-Antigen is recognized, it activates the lymphocyte and the lymphocytes clones itself (through colonial expansion)
- forms an army of lymphocytes and launches an attack on pathogens
(T lymphocytes) effector cells do attacking

31
Q

Self tolerance

A
  • The process of immune cells recognizing self cells/tissues so they know what not to attack.
  • Via identification inventory of self antigens early in life.
  • If recognize lymphocyte is destroyed if not lymphocyte is kept
  • when it does not work you get an auto immune disease example diabetes mellitus, arthritis, lupus
  • watch again
32
Q

Acquired immunity types

A
  1. Antibodies: mediated immune response a.k.a. fluid humoral immunity. Antibodies attack pathogens made by B cells
    
  2. Cell mediated immunity: a.k.a. cellular immunity, T cells/lymphocytes directly attack pathogens
33
Q

Antibody mediated immunity

A
  • B cells are activated when they are anti-body like receptors match the antigen of pathogens. (On MHC 2 APC or on free pathogen)
  • colonial expansion starts: B cells differentiate into affect are cells a.k.a. plasma cells that produce/secrete antibodies and
  • form memory cells to launch a faster attack on the a second exposure
34
Q

Antibody mediated immunity first attack versus second attack

A

First attack: primary immune response slower and lower magnitude, some plasma cells remain after suppression of pathogen most staff and release low levels of antibodies just in case

Second attack immune response: faster huge magnitude and relies on memory cells from the primary response clones self fast

35
Q

Antibodies (gamma globulin Proteins) a.k.a. immunoglobulins (Ig) anatomical structure

A

About 20% of circulating Proteins in Blood.
Consist of: two heavy chains, two light chains, hinge region that allows for movement, FAB region, FC region ( defines what class of IG) and two antigen binding sites (top of Y)
* polypeptide chain / string of amino acids.
* has 4 to 5 sub units (snowflake)

36
Q

Five antibodies classes

A
  • IgG: Dominant form about 75%
  • IgA: found in secretions tears, breast milk, saliva
  • IgE: Allergies and allergic reaction associated
  • IgM: associated with Early immune response (high levels = new infection)
  • IgD: act as receptors and help activate B lymphocytes 
37
Q

6 actions depending on the class of Ig

A
  1. Agglutination (clumping)
    - antibodies attach to the antigens on pathogens and causes clumping (makes them easier targets)
  2. Inactivation of bacteria (diphtheria toxins)
  3. Opsonization (seasoning)
  4. Degranulation of immune cells (boost overall immune response of NK and Mast cells)
  5. Activation of complement cascade
  6. Activates B cells
38
Q

Types of immunity based on antibodies development

A
  1. Active immunity:
    - naturally acquired active immunity >from exposure to pathogens
    - artificially acquired active immunity (vaccine) short effectiveness need booster
  2. Passive immunity:
    - natural acquired passive immunity: antibodies come from another organism (mothers placenta& milk> baby)
    - artificially acquired passive immunity: injection of antibodies from someone who’s been sick or has natural resistance (monoclonal antibodies) short lived injections
39
Q

Cell mediated immunity

A
  • T lymphocytes are activated when receptors match antigen displayed on APC (MHC 2).
  • once activated clinal expansion begins and differentiate into effector cells
    1. Cytotoxic T cells: attack cells infected by virus/pathogen once inside cell.
  • makes infected cell commit suicide by releasing *perforins (pores that destroy cell) and other enzymes that cause apotosis.
    2. Helper T cells (TH): help attack by attaching to antigens and releasing cytokines to immune cells. *HIV attacks helper T cells (opportunistic diseases)
    3. Regulatory T cells (T reg): moderate and suppress immune responses from overreacting.
40
Q

Types of pathogens

A

Bacteria, viruses, parasites (protozoan, worms), fungi.

  • also non pathogenic substances and tissue exchanges through blood and organ transfusion
41
Q

Most susceptible tissue

A

Soft tissue in lungs, GI tract,
Found in soft tissue (MALT) : protects against / identifies pathogens
“immune surveillance“ system

42
Q

Bacterial infection response

A
  • via break in skin/mucosa, once inside ECF/lymph nodes actions include:
    1. Initiation of innate responses :
  • compliment,
  • opsonization,
  • degranulation of mast cells: release chemotaxins & histamine (increases permeability of blood cells, draws in more WBC = more leukocytes on scene)
    2. Phagocytosis
    3. Implementation of adaptive response:
  • antibodies (if 2nd + exposure)
  • activation of naive B cells by APC & T helper etc.
43
Q

Viral infection 2 phases

EC and IC (viral replication)

A 
EC phase: innate responses 
IC phase: 
-antibodies don’t affect viruses. 
-antigens are displayed on MHC 2 to activate acquired immune responses.
1. Production of interferon-alpha 
- stimulates production of antiviral proteins ( doesn’t allow virus to infect other cells)
2. Activation of T helper (Th) 
- release cytokines to activate Bcells
3. Activation of memory Bcells 
(If previously exposed, they produce more antibodies) 
4. Activation of cytotoxic T cells
-cause apotosis by releasing perforins
44
Q

Allergic reactions

A

Immune response to nonpathogenic antigens (allergies)

  • can be almost any exogenous molecule (strong genetic link
  • exposure: injection, inhalation, ingestion, skin contact.

2 types:

  1. Immediate hypersensitivity
  2. Delayed hypersensitivity
45
Q

Immediate hypersensitivity allergic reactions (type 1,2,3)

A

-mediated through antibodies (occurs within minutes of exposure)
Ex: allergens : pollen, pet dander, bug bites, food, medication
Reaction responses:
-APC displays antigen,
-activates Th cells,
-forms memory B cells and release of antibodies —- over production of IgE.
- includes release of histamine > anaphylaxis (circulatory collapse, vasodilation, bronchi construction)
*can kill you in about 20 mins

Treatment : Epi pen

46
Q

Delayed hypersensitivity allergic reactions (Type 4)

A

Mediated by Th cells and macrophages
— slower response (about 3 days)
Allergens: metals, perfumes, latex, poison ivy, topical antiseptics.

Response: skin rash, edema, formation of bullae (blisters that can rupture and for crusty scaly skin.)

47
Q

Tissue and blood transfusion allergic immune response

A

Foreign tissue (skin graft, organ transplant, *blood transfusion)
- recognition: MHC proteins (Human Leukocyte antigen HLA)
And MHC1
*matching HLA lowers chance of rejection (related people better chance)

If not matched agglutination/clumping by antibodies occurs.
Prevented by:
- typing blood (A+, B- etc.)
- cross matching in dish before

48
Q

2 blood groups

A

ABO antigens / types

Rh antigen / types

49
Q

ABO blood groups

A

-due to antigens
(Co dominant genes control production/ expression)

Blood type:

  • A blood type> antibody B
  • B blood type> antibody A
  • O blood type > both A & B antibody (universal donor [can give but not recieve])
  • AB blood type> neither A or B antibodies (universal recipient[can only recieve])
50
Q

Rh blood groups ( 49+ antigens )

A

-D antigen is most important in transfusion.

Blood type:
Rh- > no antibodies until exposed
Rh+ > no antibodies

Example: 
Mother Rh-(D-) 
Baby Rh+
If mom is exposed to Rh+ blood she will develop antibodies that can attack baby (especially 2nd) 
-called : Hemolytic disease of newborn
HDN
51
Q

3 ways the immune system won’t work

A
  1. Incorrect response: autoimmune disease.
    - body doesn’t recognize self antigens
    Ex: diabetes mellitus (beta cells destroyed in pancreas) graves, arthritis, lupus, celiac.
  2. Overactive responses: allergens/ hypersensitivity.
    - anaphylaxis/ anaphylactic shock
    Ex: multi system inflammatory syndrome in children (MIS-C) adults (Misc-A) *eg with Covid
  3. Lack of response: immunodeficiency diseases.
    -genetic: primary immunodeficiency
    -acquired : eg HiV > AIDS (virus attacks CD4 Th cells) open to more opportunistic infections such as pneumonia, TB, herpes.

Physiology Unit 3 (4 decks)

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