Chapter 15 videos Flashcards

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1
Q

What is immunity ?

A

Immunity is the ability to defend against infectious agents, foreign cells/molecules and abnormal cells eg. cancerous cells

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2
Q

What is inate immunity?

A

innate (Non-specific) immunity
–Inborn, ancient protection existing in one form or another in all eukaryotic organisms

–Generalized responses  not targeted to
particular antigens

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3
Q

Innate Immunity Tools vs Adaptive Immunity Tools (Response time)

A

Innate Immunity Tools
Immediate
Adaptive Immunity Tools
4–7 days

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4
Q

Innate Immunity Tools vs Adaptive Immunity Tools (Organisms that have it )

A

Innate Immunity Tools
All eukaryotes (multicellular and unicellular eukaryotic organisms)
Adaptive Immunity Tools
Only vertebrates

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5
Q

Innate Immunity Tools vs Adaptive Immunity Tools (Distinguishes self from foreign)

A

Innate Immunity Tools
Yes
Adaptive Immunity Tools
Yes

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6
Q

Innate Immunity Tools vs Adaptive Immunity Tools (Kills invaders)

A

Innate Immunity Tools
Yes
Adaptive Immunity Tools
Yes

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7
Q

Innate Immunity Tools vs Adaptive Immunity Tools (Effective against diverse threats)

A

Innate Immunity Tools
Yes
Adaptive Immunity Tools
Yes

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8
Q

Innate Immunity Tools vs Adaptive Immunity Tools (Tailors response to specific antigen)

A

Innate Immunity Tools
No
Adaptive Immunity Tools
Yes

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9
Q

Innate Immunity Tools vs Adaptive Immunity Tools (Remembers antigen and amplifies response upon later exposure)

A

Innate Immunity Tools
No
Adaptive Immunity Tools
Yes

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10
Q

What is an An immune response?

A

An immune response is a physiological process coordinated by the immune system to eliminate antigens

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11
Q

Two key branches of immune system?

A

innate and adaptive immunity

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12
Q

The common features of both are that innate and adaptive immunity have

A
  • (1) recognize diverse pathogens
  • (2) eliminate identified invaders
  • (3) discriminate between self and foreign antigens
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13
Q

What is First line of defense?

A

A surface protection composed of anatomical and physiological barriers that keep microbes from penetrating sterile body compartments.

  1. Physical barriers
  2. Chemical barriers
  3. Normal micro biota
  4. Genetic components
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14
Q

What is Second line of defense

A

A cellular and chemical system that comes immediately into play if infectious agents make it past the surface defenses.

  1. Phagocytosis
  2. Inflammation
  3. Fever
  4. Antimicrobial proteins
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15
Q

What are Physical Barriers?

A
  • Structures that physically block pathogen entry
  • Examples: skin and mucus membranes
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16
Q

What are two major layers of skin?

A

Epidermis
– Multiple layers of tightly packed cells
* Few pathogens can penetrate these layers
* Shedding of dead skin cells removes
microorganisms
– Epidermal dendritic cells phagocytize pathogens

Dermis
– Collagen fibers help skin resist abrasions that could introduce microorganisms

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17
Q

What are skin chemical defenses?

A

Perspiration secreted by sweat glands
– Salt inhibits growth of pathogens
– Antimicrobial peptides act against microorganisms
– Lysozyme destroys cell wall of bacteria
Sebum secreted by sebaceous (oil) glands
– Helps keep skin pliable and less likely to break or tear
– Lowers skin pH to a level inhibitory to many bacteria

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18
Q

Where is Mucous Membranes found?

A

Mucous membranes line all body cavities open to environment

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19
Q

Two layers of Mucous membranes and function?

A

Epithelium
– Thin outer covering of the mucous membranes
– Epithelial cells are living
– Tightly packed to prevent entry of many pathogens
– Continual shedding of cells carries away microorganisms
– Dendritic cells below epithelium phagocytize pathogens
– Goblet and ciliated columnar cells help remove invaders
Deeper connective layer that supports the epithelium
– Produce chemicals that defend against pathogens

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20
Q

What are chemical Barriers?

A

Chemical barriers may directly attack invaders or establish environments that limit pathogen survival in or on a particular tissue

Examples:
* Lysozyme - found in secretions (e.g., tears, breast milk) and
breaks down bacterial cell walls
* Urine flushing microbes out of the body
* Hydrochloric acid in the stomach
* Skin is relatively dry, salty, and slightly acidic
* Fatty acids in sweat and earwax

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21
Q

What are Antimicrobial peptides (AMPs)

A
  • Also known as defensins
  • Proteins that destroy a wide spectrum of viruses, parasites, bacteria, and fungi
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22
Q

What are Genetic components?

A
  • Humans are incompatible (resistance) to most plant and animal pathogens
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23
Q

What are Species resistance

A
  • Correct chemical receptors are not present on human cells
  • Conditions may be incompatible with those needed for pathogen’s
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24
Q

What is Normal Microbiota

A

Microbial antagonism
* They kill and attack pathogens
* Activities of normal microbiota make it hard for pathogens to compete
* 1. Consume nutrients
* 2. Create an environment unfavorable
Physical barriers
Chemical barriers
Genetic components
* 3. Help stimulate the second line of defense
Normal microbiota
* 4. Promote overall health
* 5. Block pathogens from attaching
* 6. Produce antimicrobial compounds

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25
Q

For each of the barriers below, state whether it is a physical, chemical, or genetic barrier.
A. hydrochloric acid of the stomach
B. Skin
C. lysozyme in saliva and tears
D. mutation in the gene for complement proteins
E. ciliary escalator
F. Mucus membrane l

A

A. hydrochloric acid of the stomach -Chemical
B. Skin - Physical
C. lysozyme in saliva and tears - Chemical
D. mutation in the gene for complement proteins- Genetic
E. ciliary escalator - Physical
F. Mucus membrane - Physical

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26
Q

How does lysozyme on the skin and in tears protect against bacterial pathogens?
A. Lysozyme increases the amount of salt on the skin and therefore inhibits bacteria that are unable to withstand high salt concentrations.
B. Lysozyme lowers the pH of the skin’s surface, inhibiting the growth of many bacteria.
C. Lysozyme is a broad-spectrum antimicrobial that is active against Gram-positive bacteria, Gram-negative bacteria, and fungi.
D. Lysozyme breaks bonds in peptidoglycan in bacterial cell walls.

A

D. Lysozyme breaks bonds in peptidoglycan in bacterial cell walls.

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27
Q

How do mucous membranes protect the body?
A. Mucous membranes consist of many layers of tightly packed cells that microbes cannot easily penetrate.
B. Mucous membranes form a tough outer layer of dead cells that cannot be infected by pathogens.
C. Sebaceous glands in the mucous membranes produce sebum that lowers the pH, inhibiting bacterial growth.
D. Mucous membranes continuously shed cells with attached microbes.

A

D. Mucous membranes continuously shed cells with attached microbes.

28
Q

What is the role of normal microbiota in preventing disease?
A. Normal microbiota bind to pathogenic organisms, preventing them from attaching to host cells.
B. Normal microbiota cause continuous inflammation that destroys pathogens.
C. Normal microbiota consume essential vitamins such as biotin, pantothenic acid, and vitamin K, so pathogenic microbes cannot grow.
D. Normal microbiota compete with pathogens for resources, limiting their growth.

A

D. Normal microbiota compete with pathogens for resources, limiting their growth.

29
Q

What are the two important defense compentes of blood (Second defense)

A

Plasma and Leukocytes

30
Q

What is plasma and how does is it involed in defense?

A
  • Plasma is made of Water Electrolytes,Dissolved gases,Nutrients
  • It use Antimicrobial proteins as defense: Interferon
    Complement proteins
    Iron-binding proteins
    Antibodies or immunoglobulins
    Receptors
31
Q

What are Leukocytes and why are they important in second line of defense?

A

White blood cells
Defensive blood cells:
Granulocytes
Agranulocytes

32
Q

Know what Leukocytes look like and notes

A

Granulocytes
Neutrophils: Highly phagocytic; fight many invaders, especially bacteria and viruses

Eosinophils: Moderatley Phagocytic atacks allergens and parasites

Basophils: Attack allergens and parasites

Mast cells: Moderately phagocytic; attack bacteria, allergens, and parasites; reside in tissues

Agranulocytes
Monocytes: Highly phagocytic once they mature into marcophages (which can be fixed or wandering) aciviate adaptive immune resose

Dendritic cells: Highly phagocytic activate adaptive immune response

Lymphocytes: NK cells: innate immunity to viruses, bacteria, parasites, and tumor cells
B and I cells: adaptive immunity

33
Q

How can Differential white blood cell count can signal disease?

A
  • Increased eosinophils: Eosinophilia
  • _indicate allergies or parasitic worm infection
  • Increase in leukocytes and neutrophils:
  • indicate bacterial infection
  • Increase in lymphocytes:
  • indicate viral infection
34
Q

What is white blood cells task?

A

*must distinguish self from nonself cells

35
Q

How can white blood cells distinguish self from nonself cells?

A

*by examining markers on cell surfaces
*Glycoproteins: cell-cell recognition
* The most common method of
destruction: phagocytosis

36
Q

How do white blood cells cause Autoimmune disorder?

A
  • immune system mistakenly attacking the body’s own cells
37
Q

What is Phagocytosis?

A
  • Cells capable of phagocytosis are called phagocytes
  • Macrophages, Eosinophils, Neutrophils
38
Q

What are six stages of Phagocytosis?

A
  1. Chemotaxis (movement toward or away a chemical)
  2. Adherence (attachment)
  3. Ingestion (engulfment)
  4. Maturation (phagolysosome formation)
  5. Killing of microbes (by enzymes and chemicals)
  6. Elimination (by exocytosis)
39
Q

How do Phagocytes do the killing

A

Enzymatic killing
* Lysozyme, Dnase, Rnase,
Proteases and Peroxidases
Oxidative killing
* Superoxide, Hydrogen peroxide, Singlet oxygen, Hydroxyl ion, Hypochlorite
Acidic environment

40
Q

How phagocytosis can be enhance or improve?

A

Opsonization
* When antimicrobial proteins like, complement proteins and antibodies, covered or coat pathogens
* Tags the invader
* These opsonins help by increasing the number of binding sites on microbe’s surface stimulating phagocytosis

41
Q

How do phagocytes digest foreign agents such as pathogens?
A. By enclosing them in vesicles that are devoid of nutrients so that the microbes starve
B. By attaching to microbes, so that they cannot invade other cells
C. By secreting chemicals that kills the pathogenic microbes
D. By exposing them to the degradative enzymes in lysosomes

A

D. By exposing them to the degradative enzymes in lysosomes

42
Q

How does Killing by eosinophils work? (Nonphagocytic Killing/ dont ingulf)

A
  • Attack parasitic helminths by attaching to their surface
  • Secrete toxins that weaken or kill the helminth
  • Eosinophilia is often indicative of a helminth infestation or allergies
  • Eosinophil mitochondrial DNA and proteins form structure that kills some bacteria
43
Q

How does Killing by natural killer lymphocytes work?
(Nonphagocytic Killing/ dont ingulf)

A
  • Secrete toxins onto surface of virally infected cells and tumors
  • Differentiate normal body cells because they have membrane proteins similar to the NK cells
44
Q

How does Killing by neutrophils work?
(Nonphagocytic Killing/ dont ingulf)

A
  • Can destroy microbes without phagocytosis
  • Produce chemicals that kill nearby invaders
  • Generate extracellular fibers called neutrophil extracellular traps (NETs) that bind to and kill bacteria
45
Q

Which white blood cells secrete antimicrobial chemicals onto large parasites such as helminths?
A. Eosinophils
B. Natural killer cells
C. Basophils
D. Neutrophils

A

A. Eosinophils

46
Q

Describe Toll-like receptors

A

Surface (cytoplasmic) receptors found on phagocytes
* Bind pathogen-associated molecular patterns (PAMPs)
* Molecules shared by many organisms, but not present in humans* See table
TLR: defensive responses
* Apoptosis (cell suicide)
* Secretion of inflammatory mediators
* Interferon
* Stimulate adaptive immune response
* Secretion of cytokines and interleukins

47
Q

What are Toll-like receptors (TLRs)?
A. TLRs are proteins on the surface of pathogens that are recognized by phagocytic cells that will then ingest them.
B. TLRs are cytoplasmic receptors for pathogen-associated molecular patterns (PAMPs).
C. TLRs are membrane-bound proteins that recognize structures on the surface of pathogens.
D. TLRs are proteins that bind to and neutralize viruses.

A

C. TLRs are membrane-bound proteins that recognize structures on the surface of pathogens

48
Q

Describe NOD-like receptors

A

Cytosolic proteins that bind
PAMPS

* Found inside the cell of phagocytes
NOD-like receptor: defensive responses
* trigger inflammation
* apoptosis
* other innate responses
Mutations in NOD genes associated with some inflammatory bowel diseases

49
Q

What are ironbinding protiens?

A
  • Iron is a vital nutrient for most cells
  • Amount of freely available iron in circulation and within our tissues is well below the
    necessary amount microbes require for survival
  • IBP: Limit availability of free iron to reduce bacterial growth

Iron-binding proteins
* Hemoglobin
* Ferritin
* Lactoferrin
* Transferrin

50
Q

What pathogens can steal iron from us?

A
  • Siderophores - organic molecules that pull iron from our iron-binding proteins
  • Hemolytic bacteria - break down red blood cells to get to the iron-rich hemoglobin inside
51
Q

What are intereron?

A
  • Protein molecules released by host cells to nonspecifically inhibit the spread of viral infections
  • Cause many symptoms associated with viral infections
  • Two types
  • Type I (alpha and beta)
  • Type II (gamma)
52
Q

How do virus infected cells affect interferon?

A

Virus-infected cells make interferon as alarms that stimulate nearby uninfected cells to mount antiviral defenses

53
Q

What is one function of interferons?
A. Interferons trigger phagocytosis of viruses.
B. Interferons prevent viruses from replicating inside cells.
C. Interferons attract natural killer cells, which destroy virus-infected cells.
D. Interferons bind to viruses so they cannot attach to host cells.

A

B. Interferons prevent viruses from replicating inside cells.

54
Q

What are Roles of interferon?

A
  1. Signals uninfected neighboring cells to decrease protein synthesis, preventing viral replication
  2. Triggers apoptosis of infected neighboring cells
  3. Activates leukocytes
55
Q

A patient’s serum is found to have elevated interferon levels. What is most the probable cause?
A. A fungal infection
B. A bacterial infection
C. A viral infection
D. No infection, patient is normal

A

C. A viral infection

56
Q

What is complement system?

A
  • Consists of >30 different proteins that work together in a cascade fashion
  • Complement activation results:
  • in lysis of the foreign cell
  • Cytolysis/membrane attack complex:
  • trigger inflammation and fever
  • Opsonization
  • Enhancement of phagocytosis
57
Q

Which of these is not an important function of the complement cascade?
A. Chemotaxis of phagocytes
B. Killing by pore formation
C. Opsonization of pathogens
D. Expression of antiviral proteins

A

D. Expression of antiviral proteins

58
Q

What is the end result of the formation of the membrane attack complex by complement proteins?
A. Increased vascular permeability
B. Opsonization
C. Inflammation
D. Cytolysis

A

D. Cytolysis

59
Q

What is Acute inflammation?

A
  • Develops quickly and is short lived
  • Is typically beneficial
  • Three general phases
    1. Vascular Changes
  • Dilation and increased permeability of the blood vessels
    1. Migration of phagocytes
  • Leukocyte recruitment
    1. Tissue repair
  • Resolution
60
Q

Steps of inflammation

A
  1. A cut penetrates the epidermis barrier, and bacteria invade.
  2. Damaged cells release
    prostaglandins, leukotrienes, and histamine (shown in green here.)
    3.Prostaglandins and leukotrienes make vessels more permeable. Histamine causes vasodilation, increasing blood flow to the site.
    4.Macrophages and neutrophils
    squeeze trougn walls or blood vessels (diapedesis).
  3. Increased permeability allows antimicrobial chemicals and clotting proteins to seep into damaged tissue but also results in swelling, pressure on nerve endings, and pain.
  4. Blood clot forms.
  5. More phagocytes migrate to the site and devour bacteria.
  6. Accumulation of damaged tissue and leukocytes forms pus.
  7. Undifferentiated stem cells repair the damaged tissue. Blood clot is absorbed or falls off as a scab.
61
Q

What are three main goals of inflamation?

A

The three main goals of inflammation are:
1. Recruit immune defenses to the injured tissue
2. Limit the spread of infectious agents
3. Deliver oxygen, nutrients, and chemical factors essential for tissue recovery

62
Q

What is a fever ?

A
  • Abnormally high systemic body temperature
  • Results when pyrogens trigger the hypothalamus to increase the body’s core temperature
  • Various types of pyrogens
  • Bacterial toxins
  • Cytoplasmic contents of bacteria released by lysis
  • Antibody-antigen complexes
  • Pyrogens released by phagocytes that have phagocytized bacteria
63
Q

Steps of fever

A
  1. Chemicals secreted by phagocytes travel in blood to hypothalamus.
  2. Hypothalamus secretes prostaglandin, which resets hypothalamic thermostat.
  3. Nerve impulses cause shivering, higher metabolic rate, inhibition of sweating, and vasoconstriction.
  4. These processes increase body temperature to the point set by the hypothalamic thermostat.
64
Q

What are goals of a fever

A
  • Enhances effects of interferons
  • Inhibits growth of some microbes (temp. sensitive)
  • Enhance the activities of phagocytes
  • Promotes the process of tissue repair
  • Enhance leukocyte production
  • Speed up hematopoiesis
65
Q

What are side effects of fever?

A
  • Side effects of fever
  • Body aches, malaise, tiredness
  • If it rises too high:
  • Proteins are denatured
  • Nerve impulses are inhibited
  • hallucinations
  • coma
  • death
66
Q
A