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Thompson class fall 2015 > Exam 2: Week 7 > Flashcards

Exam 2: Week 7 Flashcards

1
Q

10 cells involved in immunity that were highlighted in lecture

A
  1. Pathogen
  2. Macrophage
  3. Antigen Presenting Cell
  4. T-Helper Cell
  5. Interleukin 1
  6. Interleukin 2
  7. Cytotoxic T-cell
  8. B-cells
  9. Memory B-cells
  10. Antibody Replacing Plasma Cells
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2
Q

What is immunology?

A

Study of the mechanisms that allow the body to recognize a material as foreign and neutralize it

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3
Q

Why is immunity important?

What happens if it doesn’t work?

A
  • Protects the body from infection and disease
  • Failure results in localized or systemic infection or disease
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4
Q

4 types of immunity

A
  1. Innate- natural or native
  2. Acquired- adaptive or specific
  3. Active acquired- antigen present in host, naturally or by vaccination
  4. Passive acquired- antibodies transferred from another ie. Mother to baby, immunoglobulin (IVIG)
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5
Q

Which type of immunity is the body’s first line of defense?

describe (2)

A

Innate

  • Bodies first line of defense against pathogen- inflammatory response
  • Phagocytic cell release, inflammatory mediators, NK cells- non-specific response with no memory created
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6
Q

What are 2 important qualities of acquired immunity?

A
  1. Specificity- recognize and destroy foreign objects while preventing proliferation
  2. Memory- same invader enters the body the response is ready with a more rapid and stronger reaction
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7
Q

How long does active acquired immunity last?

A

Most cases last a lifetime or booster may be required

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8
Q

How long does passive acquired immunty typically last?

A

temporary

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9
Q

What is an antigen?

A

Foreign substance that enters the body-
such as bacteria, virus, parasite, etc.

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10
Q

What is an epitope?

A

Subunit of an antigen
•create antigen response with antibody

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11
Q

Factors that can affect immunity (13)

A
  1. Aging
  2. Nutrition
  3. Environmental pollution
  4. Trauma or illness
  5. Medications
  6. Spleen function
  7. Stress
  8. Psychosocial factors
  9. Burns
  10. Surgery
  11. Socioeconomic status
  12. Spirituality
  13. Exercise
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12
Q

What is the first and most important thing that immune cells (such as T-cells) must be able to do?

A

Be able to recognize self

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13
Q

What is so special about cell markers? (3)

A
  1. Cell markers unique to individual antigen
  2. Cell markers determine which antigen to respond to and how strong
  3. Cell markers allow communication between immune cells
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14
Q

What is the purpose of phagocytes? What cells are primarily phagocytes?

A
  • Ingest and kill microorganisms
  • Neutrophils and monocytes are primary
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15
Q

What cells are considered granulocytes and why?

A

Leukocytes or WBC’s- because of appearance

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16
Q

5 types of whte blood cells important to immunity in the order of their population size

A
  1. Neutrophils
  2. Lymphocytes
  3. Monocytes
  4. Eosinophils
  5. Basophils

Never Let Monkeys Eat Bananas

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17
Q

What do neutrophils do?

A

kill antigen by ingesting then die and form pus

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18
Q

Why do I care about Lymphocytes?

A

They make up the T-cells and B-cells

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19
Q

What do Monocytes do? (2)

A
  • They turn to macrophages and engulf debris and injured bacteria
  • Present material (epitope) of pathogen to lymphocyte or helper cell
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20
Q

What do eosinophils do? (2)

Where are they produced?

A
  • Produced in bone marrow, they release contents of granules to kill organisms
  • Present for allergen and parasites specifically or for large organisms
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21
Q

What do basophils do? (2)

A
  • Found in stem cells, they work with Mast cells (contain histamine)
  • Vasodilation and increased blood flow delivering primary phagocytes
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22
Q

How are erythrocytes and platelets involved in innate immunity?

A

Play a role in clearance of byproducts

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23
Q

Pathogen

Where does it come from?

What is it’s purpose?

A
  • Microorganism that comes from outside the host. Can be a virus, bacteria, fungi, ect.
  • To search and destroy (basically)
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24
Q

Macrophage

Where does it come from?

What is it’s purpose?

A
  • Come from Monocytes which are produced in bone marrow
  • Macrophages are attracted to site of injury by chemotatic factors released by neutrophils. They eventually take over for neutrophils and kick some ass by cleaning up site through phagocytosis, promoting angiogenesis, and releasing cytokines, and growth factors which all eventually lead to renewal of the injured area
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25
Q

Antigen Presenting Cell (APC)

Where does it come from?

What is it’s purpose?

A
  • Well….they don’t really come from any one place and several different types of cells can take the role of APC such as dendritic cells and some types of B cell.
  • These cells take the antigens in via phagocytosis or by receptor-mediated endocytosis. Then the antigens are processed and displayed on the APCs like a hood ornament.
  • What may be more imprtant to know is where are they going? They travel in the lymph system and gather in the lymph nodes to talk to the T-cells to say “Hey, check out this antigen! Their crew is invading us and we need you to fight them!” If APC did not do this, the T-cells would have no clue.
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26
Q

T-Helper Cell

Where does it come from?

What is it’s purpose?

A
  • Born in bone marrow but raised in the thymus, thus it’s name T-cell. Most of them graduate and then move on to the lymph system (there is a much longer answer that is stupidly dense and complicated).
  • Get the covert messages from APCs and acts as the alarm system for the immune system kind of like Paul Revere. Release cytokines to spread message. Helper T-cells help the activity of other immune cells by releasing T cell cytokines
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27
Q

Interleukin 1

Where does it come from?

What is it’s purpose?

A
  • derived primarily from macrophages
  • Activate monocytes, other macrophages, and lymphocytes (innate AND acquired immune systems). Acts as a growth factor for some cells. Encourges neutrophils to proliferate. Acts on receptors in hypthalmus and is ultimately responsible for fevers.
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28
Q

Interleukin 2

Where does it come from?

What is it’s purpose?

A
  • a type of cytokine signaling molecule in the immune system secreted by T-cells
  • stimulates proliferation of T-lymphocytes. Promotes the differentiation of T cells into effector T cells and into memory T cells
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29
Q

Cytotoxic T Cell

Where does it come from?

What is it’s purpose?

A
  • Born and mature in the thymus, thus it’s name T-cell.
  • Attack and destroy cells that have been infultrated by the antigens (or abnormal cells such as cancer)
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30
Q

B Cells

Where does it come from?

What is it’s purpose?

A
  • a type of lymphocyte born and raised in bone marrow thus it is called a B cell. They graduate and hang in the lymph system.
  • Function in the humoral immunity component of the adaptive immune system by secreting antibodies.They can also act as antigen-presenting cells and secrete cytokines.
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31
Q

Memory B Cells

Where does it come from?

What is it’s purpose?

A
  • Memory B cells develop from B cells thus they have the same hometown- bone marrow
  • Their function is to circulate through the body and initiate a stronger, more rapid antibody response (known as the secondary antibody response)
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32
Q

Antibody Replacing Plasma Cell

Where does it come from?

What is it’s purpose?

A
  • AKA Plasma cells
  • Formed from normal B cells
  • Produces and secretes into body fluids a specific antibody to a corresponding specific antigen
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33
Q

List the functions of the complement system (5)

A
  1. Vasodilation to increase blood flow to the injured area
  2. Facilitates movement of leukocytes to the are via chemotaxis
  3. Coats surface of antigen to make it vulnerable to phagocytosis- opsonization
  4. Formation of a cyst or tubercle walling off infection from the body
  5. Formation of a membrane attack complex (MAC)- creates a pore in the cell of antigen to allow Na+ and fluid to enter the cell leading to cell lysis
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34
Q

What are cytokines?

A

Short answer- messengers

Long answer- Biologic Response Modifiers: involved in immune response and communication with other body systems

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35
Q

What are interferons and what do they do?

A
  • Type of cytokine (TNF, Interleukin, etc.)
  • Provide direct defense. When a virus infects cell, gene within cell produces interferons, coating of surrounding cells to prevent spreading of the virus, contain the tumor.
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36
Q

When the alarm is sounded for the body to start the inflammatory process, what do T-cells and B-cells do? (3 points)

A
  • T and B cells migrate in the blood and lymph throughout the entire body in 30 minutes
  • Specific antibodies for specific antigen; Like police officers looking for specific criminals
  • Antigen-specific T or B cells bind to an antigen and initiate immune response which get the immunoglobulins, antibodies, regulatory and suppressor T-cells, and cytokines moving into action
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37
Q

Two types of acquired immunity

A
  1. humeral immunity
  2. cell-mediated immunity
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38
Q

What is humeral immunity?

A

the aspect of immunity that is mediated by macromolecules (as opposed to cell-mediated immunity) found in extracellular fluids such as secreted antibodies, complement proteins and certain antimicrobial peptides.

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39
Q

What is cell mediated immunity?

A

an immune response that does not involve antibodies, but rather involves the activation of phagocytes, antigen-specific cytotoxic T-lymphocytes, and the release of various cytokines in response to an antigen.

40
Q

Purple Mountains (1925-1926)

by Marsden Hartley (painter from Maine)

A
41
Q

6 things to note about humeral immunity (B-cell immunity)

A
  1. B lymphocytes originating in bone marrow and produce 5 Lg molecules
  2. They are IgG, IgM, IgA, IgD, IgE
  3. Rapid immune response
  4. Mediated by antibodies in saliva, blood, vaginal secretions and other body fluids (macromolecules)
  5. B cells are coated with Ig and have specific receptor site for antigen
  6. Once antigen is identified they are converted into plasma or memory B cells and circulate looking for specific antigen to attac
42
Q

8 things to note about cell mediated immunity (T-cell immunity)

A
  1. T-cells learn to differentiate self from non-self
  2. Search out and destroy viruses and some bacteria
  3. Interact with specific antigen
  4. Produce sensitized T-cells: Helper T- cells- produce lymphokines like IL-1 and IL-2 and interferons
  5. Activate macrophages (from innate immunity) to destroy large bacteria
  6. Help cytotoxic T-cells destroy viruses
  7. Help NK cells (from innate immunity) kill infected cells
  8. Suppressor T cells help prevent autoimmune disease by SUPRESSING activation of immune response
43
Q

What are IgG, IgM, IgA, IgD, IgE?

A

5 antibodies produced for specific response

  1. IgM- primary immune response; located in vasculature
  2. IgG- antibacterial and antiviral; found in blood, only antibody to cross placenta
  3. IgA- protects body surfaces; found in mucus membranes and body secretions
  4. IgD- antigen receptor function controlling activation or suppression
  5. IgE- Parasitic reaction and allergic reaction; with allergic reaction activates mast cells and histamine
44
Q

Are pathogens easy to find once the alert for an immune response is made?

A

No

Usually the virus and bacteria are found hiding deep inside the cell where other mechanisms for destruction can not find them

45
Q

Positive (1) and negative (3) aspects of cell mediated immunity?

A

Positive

  • Reason TB skin test and allergy skin tests are effective

Negative

  • Responsible for transplant rejection,
  • contact dermatitis,
  • some autoimmune diseases
46
Q

Where is the immune response in the body?

A

Occurs in lymph nodes, spleen and mucosa tissue (tonsils, adenoids, and Peyer’s patches)

47
Q

The Spark Notes version of the immune response

in 6 easy steps

A
  1. Pathogen enters
  2. Innate immunity- Complement system recognizes and destroys
  3. If no innate immunity organism presented to body (acquired immunity)
  4. B lymphocyte recognizes it and produces antibodies (Ig-): Humoral response
  5. T lymphocyte recognizes it as bacteria and helps macrophages lyse and phagocytose it: Cell mediated response
  6. Virus- cytotoxic T lymphocytes recognize and destroy: also Cell mediated response
48
Q

Neuroimmunology; neuroimmunomodulation; psychoneuroimmunology; neuroimmunoendocrinology

What is it good for?

A

Endocrine system, CNS and immune system interaction

49
Q

Role of the spleen in immunity

A

It is the major clean up place for erythrocytes so that oxygen is maintained. If we lose spleen function then we are not able to cycle through the red blood cells, get rid of the old red blood cells, and make oxygen carrying capabilities is up to speed

50
Q

How do neural and endocrine system modify function of immune system? (2)

A
  • ANS and pituitary gland work together during chronic stress
  • Reduced lymphocyte sensitivity with chronic distress
51
Q

What is the role of neurocytokines: interleukins, interferons?

A

They function to communicate with other cells and mediate immune response to local CNS injury

52
Q

Types of Immunodeficiency diseases (3)

A
  1. Primary Immunodeficiency- children, especially newborns who have very weak immune systems
  2. Secondary Immunodeficiency- result of earlier disease or event
  3. Acquired Immune Deficiency Syndrome- such as AIDS. Infection of the immune system. Progressive destruction of T-cells
53
Q

Iatrogenic causes of Secondary Immunodeficiency (3)

A

Produced by drugs, radiation, or splenectomy

  1. Corticosteroids, anti-rejection medication, cytotoxic medication
  2. Radiation therapy can kill lymph nodes
  3. Spleen necessary to fight infection
54
Q

What is a hypersensitivity disorder?

A

Exaggerated or inappropriate immune response

55
Q

What happens with an allergic response

to antigen called allergen? (7)

Time line for reaction?

Always quick?

what immunoglobulin is involved and where?

What are the chemicals involved?

What are the effects on the tissue (and name for this)? (4)

A
  1. Tissue destruction from the immune response is greater than from allergen
  2. Immediate- occurs within minutes
  3. Late-phase- hours and days of inflammation and other symptoms
  4. Delayed hypersensitivity reaction- takes days to cause symptoms ie. antibiotics
  5. IgE on Mast cell
  6. Histamine release followed by other inflammatory mediators
  7. Vasodilation, bronchospasm, increased mucus secretion, edema- anaphylaxis
56
Q

Examples of other hypersensitivity (4)

A
  • Hemolytic disorders: anemia or self-antigen disorders- agglutination (clumping together) and phagocytosis of pathogen (self)
  • Rheumatic fever: immune system attacking mitral valve recognizing it as foreign while attacking the streptococci
  • Guillain-Barre: virus causing immune system to attack PNS while attacking virus
  • SLE: excessive circulating antigen-antibody complex depositing in tissues
57
Q

Examples of delayed hypersensitivities (4)

A
  • latex sensitivity
  • poison ivy
  • TB skin test sensitivity, etc.
  • usually dermatitis
58
Q

What is isoimmune response? (3)

A
  • transplant rejection
  • Incompatibility of cell surface antigens
  • Donor matching is key, but true compatibility is about 25% (family is not always a sufficient match)
59
Q

True or False: Exercise has no effect on white blood cell count

explain

A

False

  • increases neutrophils and macrophages – greatest is exercise has eccentric component
  • increases Natural Killer Cells when there is physiologic stress with exercise
  • may be an adverse cumulative effect in athletes who exercise intensely several times a week
  • may have a transient effect on WBC though and not a sustain increase for the immune system
60
Q

A method for measure exercise response in patients

A

Check vitals, document, and monitor changes over several days

61
Q

What is the neck check?

A
  • All should avoid strenuous exercise during an infectious episode
  • neck and above: stuffy nose, scratchy throat, ect.- then exercise
  • below the neck: lung congestion, joint aches, overall weakness- rest or exercise at 1/2 speed
62
Q

Why are mast cells important?

A

biggest and most important trigger for activating the inflammatory process

63
Q

What 2 ways are mast cells stimulated to release their inducers of inflammation?

A
  1. —Degranulation- —Release of contents of mast cell granules
  2. Synthesis- New production and release of mediators in response to stimuli
64
Q

Maturation phase- how long?

A

day 9 - up to 2 years (for tissue to complete the healing process)

65
Q

Where do we find Type 1 collagen? (4)

A
  1. —Bone
  2. skin
  3. tendon
  4. mature scars
66
Q

Where do we find Type 2 collagen? (2)

A
  1. —Fibrocartilage
  2. articular cartilage
67
Q

Where do we find Type 3 collagen? (3)

A
  1. —GI tract
  2. uterus
  3. blood vessels

* about 24 types of collagen

68
Q

What is a keloid scar?

treatment?

A
  • When collagen goes wild and scar tissue grows beyond boundaries of injury
  • Treatment- surgical but poor outcomes
69
Q

What are hypertropic scars?

treatment?

A
  • —collagen synthesis greater than lysis
  • Treatment- pressure garments
70
Q

True or False: Silicon covering for scar management is better than paper tape.

A

False

Paper tape can work just as well.

71
Q

What are joint contractures?

A

—arthrofibrosis if joints involved, joint capsule and capsular ligaments; can be muscle, tendon, skin, etc.

Ex: can occur after manipulation performed under anethesia.

72
Q

What does a pink scar mean?

A
  • vascular supply and moldable
  • if it is blanched, then it is mature and will not change
73
Q

Factor that can determine final collagen structure (9)

A
  1. —Muscle tension
  2. Joint movement
  3. —Soft tissue loading/unloading
  4. —Fascial gliding
  5. —Temperature changes
  6. Mobilization
  7. —Regeneration- regrowth, if basement membrane is intact. Proper environment- blood flow, if cells are able
  8. Repair-scar tissue
  9. Both Regeneration and Repair- most common
74
Q

Important technique to apply in rehab for scar mamanagement

A

soft tissue mobility

ex: cross friction massage

75
Q

Lung Tissue healing prognosis

A

Pretty good

  • —Regeneration can occur if basement membrane is intact
  • Repair if damage is extensive
76
Q

Cartilage (both types) healing prognosis

why?

A

Poor

  • —Poor blood supply
  • Poor healing
77
Q

Bone healing prognosis

(and phases)

A

Good prognosis, but must undergo phases below

  • —Inflammation
  • —Soft callus
  • Hard callus- —3 weeks to 4 months
  • —Regeneration and Remodeling- Months to years
78
Q

What occurs with skeletal muscle healing (very basic)?

A
  • —Regeneration can occur
  • Scarring is likely
79
Q

What is involved with tendon healing? (5)

A
  • —72 hour inflammation
  • —Collagen synthesis- 2 weeks
  • —Tendons no AROM X 3 weeks
  • —Tendons no max force for 8 weeks (depending on quality of tissue)
  • —PROM indicated for both tissues within limits
80
Q

A complication with bone healing

(and three things about it)

A

Heterotopic Ossification

  • higher risk with SCI patients
  • calcium deposits lay down after some type of injury
  • myoblasts turn into osteoblasts
81
Q

Myositis Ossificans (definition, four things about it)

A

healing gone wrong

  • typically occurs from a muscle bruise
  • calcium deposits form in the muscle
  • important to put ice on the muscle right after
  • create a lot of pain and limited ROM
82
Q

Local factors influencing healing (5)

A
  • —Type, size, and location of injury
  • —Infection
  • —Vascular supply
  • —External forces such as —modalities
  • —Movement
83
Q

Systemic factors influencing healing (4)

A
  • —Age
  • —Disease
  • Medications
  • —Nutrition
84
Q

5 points to note with regards to healing and pediatrics

A
  1. —Neonates have transiently depressed inflammatory and immune function
  2. —Neutrophils are not capable of efficient chemotaxis
  3. Neonates express complement deficiency
  4. —Deficient oxidative and bacterial responses
  5. Develop overwhelming sepsis
85
Q

5 point to note with regards to healing and the elderly

A
  1. —Impaired function of innate immune cells (phagocytes)
  2. —Impaired inflammation is likely a result of chronic illness: —Diabetes, cardiovascular disease, etc.
  3. Chronic medication intake decreases the inflammatory response
  4. —Healing response is diminished because of skin’s loss of regenerative ability
  5. Infections and chronic inflammation are more common in older adul
86
Q

What biologically active molecules do Mast cells release in the degranulation phase? (2)

A
  • histamine
  • chemotactic factors
87
Q

What do histamines do? (2)

A
  • —Cause temporary, rapid constriction of smooth muscle and dilation of the postcapillary venules = increased blood flow
  • —Increases vascular permeability and improves adherence of leukocytes to the endothelium
88
Q

What do chemotactic factors do?

Name 2 types of chemotactic factors

A

—Chemotactic factors (like TNF-a): form a gradient that causes directional movement (chemotaxis) of cells toward the inflammation

—Two types of chemotactic factors

  1. —Neutrophil chemotactic factor- attracts neutrophils
  2. Eosinophil chemotactic factor of anaphylaxis- attracts eosinophils
89
Q

What inflammatory mediators are released as a result of mast cell synthesis? (3)

A

—leukotrienes, prostaglandins,

platelet-activating factors, ect.

90
Q

What are Leukotrienes role in inflammatory response (3 things)

A
  • —Similar effects to histamine, except slower and longer response than histamines.
  • More important in later stages of inflammation
  • Sustain (not as quick acting as histamines)
91
Q

What are Prostaglandins role? (3)

A

cause increased vascular permeability, neutrophil chemotaxis, and pain

92
Q

What are Platelet-activating factors role? (3)

A
  • causes endothelial retraction to increase vascular permeability
  • leukocyte adhesion to endothelial cells
  • platelet activation (helps in clotting)
93
Q

What are neutrophils role in the inflammatory response? (4 points)

A
  • —Predominant phagocytes in the early inflammatory process.
  • Arrive 6-12 hrs after initial injury
  • Incapable of cell division thus short lived and becomes a component of the exudate/pus and removed from body
  • Primary role is to remove debris and dead cells from sterile lesions and phagocytosis of bacteria in nonsterile lesions
94
Q

What is the role of monocytes? (4 points)

A
  • —largest of the normal blood cells. Produced in bone marrow
  • immature cell that enters circulation to develop into macrophages upon entry into inflammatory site
  • Enter site 24 hrs later after injury and replace neutrophils
  • Better for long term defense
95
Q

What is the role of eosinophils? (3 points)

A
  • —Mildly phagocytic
  • —Serve as body’s primary defense against parasites
  • Help regulate vascular mediators released by mast cells- helps to limit inflammation
96
Q

What is the role of basophils?

A

—Mobile mast cells which release similar inflammatory agents

97
Q

What is the Complement system? (4)

A
  • —Consists of large number of proteins
  • —Once activated, these proteins can destroy pathogens directly and/or collaborate with other components of the inflammatory response
  • Most important part of complement system is activation of C3 and C5
  • —C3 and C5 result in subunits: —Opsonins, Chemotactic factors, and Anaphlatoxins

Thompson class fall 2015 (12 decks)

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