quiz 5 Flashcards

1
Q

Location of lymphoid organs and tissues

A
  • primary lymphoid organs: T-cell maturation (thymus) , B-cell maturation (bond marrow)
  • secondary lymphoid organs: lymph nodes, spleen, tonsils, peyers patches in the intestine, appednix
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2
Q

Types of immune cells in lymph nodes

A
  • lymphocytes: b-cel and t-cell
  • macrophages: engulf and digest pathogens and present antigens
  • dendritic cells: antigen presenting cells that activate t-cells
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3
Q

Thymus Vs Bone marrow function

A

Thymus: site of T-cell maturation and differentiation

Bone marrow: site of B-cell maturation , and production of all blood cells, including lymphocytes

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4
Q

Nonspecific (innate) VS adaptive immunity

A

innate: first line of defense, non specific, includes physical barriers, phagocytes, inflammation

adaptive immunity: specific response, involves lymphocytes (B-cells and T-cells) and memory cells for long lasting protection

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5
Q

lines of immune defense

A

1st. physical and chemical barriers

2nd. innate immune response

3rd. adaptive immune response (b-cells producing antibodies, T-cells targetting infected cells)

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6
Q

PAMPS and PRRs in Non-specific immunity

A

PAMPS: molecuels found on pathogens

PRRS: receptors on immune cells that recognize PAMPS.

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7
Q

Leukocyte Abundance

A

Neutrophils: 50-70%
Lymphocytes: 20-40
Monocytes: 2-8
Eosinophils: 1-4
Basophils 0.5-1

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8
Q

Steps in inflammation

A
  1. Injury/infection: pathogens enter the body
  2. chemical signals: release of histamines, prostaglandins, and cytokines
  3. vasodilation: bood vessels expand, increasing blood flow to the area
  4. increased permeability: fluid proteins and immune cells leave the blood stream and enter the affected tissues
  5. phagocytosis: macrophages and neutrophils engulf pathogens
  6. Repair: tissue healing and regeneration.
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9
Q

General Steps in Phagocytosis

A
  1. chemotaxis: movement of phagocytes toward the site of infection
  2. recognition and attachment: phagocytes recognize PAMPS on the pathogen
  3. Engulfment: Pathogen is engulfed into a phagosome
  4. Phagosome fusion: phagosomes fuse with a lysosome, forming a phagolysosome
  5. digestion: enzymes in the lysosom
    e digest the pathogen
  6. exocytosis: waste material is expelled from the phagocyte.
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10
Q

Diapedesis

A
  • Diapedesis is the process by which leuocytes move out of the capillaries and into the tissues
  • This occurs in response to signals from pathogens and damaged tissues

steps:
1. rolling: leukocytes slow down and roll along the endothelial surface
2. Adhesion: leukocytes adhere to the endothelial cells through interactions between adhesion molecules
3. transmigration: leukocytes squeeze between endothelial cells and migrate into the tissue.

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11
Q

Chemotaxis

A
  • Chemotaxis is the movement of leukocytes towards the site of infection or inflammation in response to chemical signals
  • Leukocytes follow a gradient of chemotactic factors, which are molecules that attract them to the site of infection.
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12
Q

Chemotactic Factors

A
  • Exogenous: derived from microbial sources
  • Endogenous: produced by host cells.
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13
Q

Exogenous Vs. Endogenous pyrogens

A

Exogenous:
- external substances that induce fever
- usually microbial products such as LPS from the outer membrane of Gram negative bacteria
- these trigger an immune response that leads to the production of endogenous pyrogens .

Endogenous:
- Produced by the body in response to infection or inflammation
- include cytoines such as interleukin (IL-6) (IL-6) and tumor facotrs
- these cytokines act on the hypothalamus to increase the bodys set point for temperature, leading to fever.

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14
Q

Interferon (IFN)

A

A group of signalling proteins released by host cells in response to the presence of pathogens such as viruses, bacteria, and parasites.

  1. Detection : cells detect the presence of viral RNA/DNA
  2. Production: Infected cells produce and secrete interferons.
  3. Signal transduction: Interferons bind to receptors on neighboring cells, triggering a signaling cascade
  4. antiviral state: induced the expression of antivrial proteins:
    - inhibit viral replicaiton
    - enhance the degradation of viral RNA.
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15
Q

Four cardinal Features of inflammation and reasons for their formation

A
  1. Redness (rubor):
    - caused by the increased blood flow due to vasodilation of the blood vessels
    - mediated by histamines, prostaglandins, and other vasodilators released by injured tissues and immune cells
  2. Heat (calor)
    - also due to increased by blood flow
    - blood carries heat from the core of teh body to the affected area, contributing to the warmth observed during inflammation
  3. Swelling (tumor)
    - result of increased permeability of blood vessels
    - allows fluids, protiens, and leukocytes
  4. Pain (dolor):
    - caused by the release of chemicals such as bardykinin and histamine
    - these chemicals sensitize nerve endings, making the affected area more sensitive to pain.
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16
Q

Complement Protein Pathways

A

A part of the immune system that enhances the ability of antibodies and phagocytic cells to clear pathogens.

  1. Classical pathway
    - part of the specific adaptive immunity
    - activated by antigen antibody complexes
  2. MB-lectin pathway
    - part of innate immunity
    - activated by mannose binding lectin (MBL) binding to mannose residues on the surface of pathogens
  3. Alternative pathway:
    - also part of the nonspecific immunity
    - activated directly by pathogen surfaces without the need for antibodies.

C proteins:
- complement proteins are synthesized in the liver
- they circulate in the blood in an inactive form
- upon activation, they trigger a cascasde leading to the formation of a membrane attack cmplex that can lyse pathogen.

17
Q

Lineages of white blood cells

A

Hematopoiesis:
- the process of forming blood cellular components
- occurs in the bone marrow

Lineages:
1. myeloid lineage
2. lymphoid lineage

Differnetiation
- all blood cells originate from the hematopoietic stem cells in the bone marrow
- HSCs differentiate into their myeloid or lympohid progenitor cells, which then further differentiate into various types of blood cells .

18
Q

Types of Anthrax and their causes

A

Anthrax: caused by bacterium bacillus anthracis

Types:
1. cutaneous anthrax
- infectino through cuts or abrasions on the skin
- most common form

  1. inhalation anthrax
    - infection through inhalation of spores
    - most severe form
  2. Gastorinestirnal Anthrax:
    - infection through ingestion of contaminate dfood or water
    -rare but serious
  3. injection anthrax
    - infection through injecting drugs contaiminated with anthrax spores
    - rare and primairly seen in intravenous drug users
19
Q

Gangrene
- symptoms and causes

A

Gangrene: The death of body tissue due to a lack of blood flow or a serious bacterial infection

symptoms:
- discoloration of skin, red then black /brown
- severe pain follwe dby numbness
- severe pain followed by numbness
- swelling and formation of blisters filled with fluid
- fould smelling discharge

Gas gangrene
- cuaesd by cllostridium perfringens
- bacteria produce gas within tissue, leading to tissue death and systemic infection.

20
Q

Virulence factor of bacteria

A

Moleucles produced by pathogens that contribute to the pathogenicity and enable them to acheive
- colonization of the host
-evasion of the hosts immune response
-entry into and exit out of cells

21
Q

MRSA, Cellulitis, Folliculitis

A

MRSA
- stands for staph
- named for its resistance to methicillin and other beta lactam antibitoics

Cause: staph that have aquared resistance genes

Cellulitis:
- a bacterial infection of the skin and underlying tissues
- symtomps: redness, swelling, warmth, pain

Follicultis:
- inflammation of hair follicles, often cuased by a bacterial infection
- symptoms include red, swollen bumps that may be filled with pus

22
Q

Antigen (ag), Antibody (Ab), Epitope

A

Antigen:
- a substance that is recognized by the immune system as forgein
- can be proteins, polysaccharides, lipids, nucleic acids
- tiriggers an immune response

Antibody :
- proteins produced by B cells (plasma) in response to antigens
- specifically binds to anitvens to neutralize them for destruction
- 5 main classes of antibodies: IgM, IgA, I
gG, IgE

Epitope:
- specific part of the antigen that is recognized and bound by an antibody

23
Q

Hematopoiesis

A
  • The process of forming blood cellular components
  • occurs in the bone marrow
  • all blood cells originate from multipotent hematopoietic stem cells.
24
Q

Plasma Cells

A
  • differentiated B cells that produce large quantities of antibodies
  • short lived but highly active in secreting antibodies to fight current infection
25
Q

Memory B Cells

A
  • Long lived cells that remain in the body after an infection has been cleared.
  • provide rapid and robust antibody production upon re-exposure to the same antigen
26
Q

Effector T cells

A
  • activated T cells that actively engage in elimnating infected cells or pathogens
27
Q

igM , igA, igD, igG, igE

A

M - first antibody produced in response to an infection

A- found in mucosal area and in secretions. provides localized protection on mucosal surfaces

D- found on the surface of B cells as a receptor. Involved in initiating B cell activation

G: Most abundant antibody in blood and extracellular fluid. provides the majority of antibody based immunity against pathogens.

E: involved in allergic reactions and defense against parasitic infections. binds to mast cells and basophils, causing them to release histamine.

27
Q

Memory T cells

A
  • long lived T cells that persist after an infection has been cleared
  • provide a quicker and more effective response upon re-exposure to the same antigen.
28
Q

Number of antigen binding site per immunoglobin (Ig)

A
  • each immunoglobin molecule has two antigen binding sites
  • these sites are located at the tips of the Y shaped structure of the antibody and are formed by the variable regions of the heavy and light chains.