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Flashcards in Unit 4 Study Guide Deck (77):
1

v. What are the different types of grafts?

1. Autograft
2. Isograft (Identical twin or clone)
3. Allograft (Same species)
4. Xenograft (Different species)

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13. There are 3 types of cells that perform “nonphagocytic killing.” What are they?

a. Eosinophils
b. NK cells
c. Neutrophils

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31. What are pyrogens?

a. Trigger the hypothalamus to reset to a higher temperature

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iii. What cells become sensitized in hypersensitivity

1. Mast cells, basophils, eosinophils

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30. What is clonal deletion?

a. Deletion of self-reactive cells

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20. Endogenous antigens are presented on which type of MHC molecules?

a. Endogenous = Class I (cell-mediated)

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i. What causes a type III hypersensitivity response?

1. Antigens bound to antibodies (called immune complexes) avoid phagocytosis and stay in circulation until they ultimately get lodged in an organ or joint

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11. What are the 4 things that antimicrobial peptides do to fight pathogens?

a. Punch holes in cytoplasmic membranes
b. Interrupt internal signaling or enzymatic action
c. Chemotactic factors (recruit leukocytes to a site)
d. Form “nets” to ensnare invading bacteria

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32. When your internal thermostat gets reset at a higher temperature, what things does your body do to increase the temperature?

a. Nerve impulses trigger shivering
b. Higher metabolic rate
c. Inhibition of sweating
d. Vasoconstriction (keeps blood at the core)

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23. What is the end result of complement cascade activation?

a. Destruction of foreign cells
b. Note: Complement system is a set of serum proteins

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25. What are the different ways (2) in which the complement cascade can be activated? How do they differ?

a. Classical pathway – Occurs in conjunction with antibodies
b. Alternative pathway – Occurs independently of antibodies
c. C3 cleaved into two fragments (C3a and C3b)

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i. What is an allergen?

1. An antigen that stimulates an allergy

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10. What are the 3 ways in which normal flora act as part of the first line of defense?

a. Normal microbiota consumes all available nutrients
b. Changes the pH of regions of the body
c. Can generate antimicrobial compounds

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17. What is the main the surface glycoprotein on a Tc cell?

a. MHC class I

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21. What are interferons?

a. Inhibit viral infections nonspecifically
b. Cause malaise, muscle aches, chills, headache, and fever

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3. What is Graves’ disease?

a. Overstimulation of thyroid gland (excessive thyroid hormone)

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iv. What does it mean if someone gets a positive TB result?

1. They have been exposed to TB and have created antibodies

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7. What is the difference between a primary and an acquired immunodeficiency disease?

a. Primary is genetic

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11. What mechanisms do antibodies employ in order to destroy (or contribute to the destruction of) pathogens (6) and what is meant by each one?

a. Activation of complement
b. Inflammation
c. Neutralization – Antibodies bind to a critical portion of the pathogen so it can no longer cause harm
d. Opsonization – Antibodies act as opsonins, molecules that stimulate phagocytosis
e. Agglutination – Antibodies can bind to two epitopes at once, and bind many antigens together
f. Antibody-dependent cell-mediated cytotoxicity (ADCC) – Similar to opsonization, except NK cells are recruited to cause apoptosis

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27. What are the steps (3) during an inflammatory response?

a. Increased permeability and dilation
b. Migration (increase of phagocytes migrating via chemotaxis)
c. Tissue repair

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22. What is the mechanism of the interferon pathway?

a. Type I: Alpha and Beta
i. Nonspecific
ii. Macrophages, etc.
b. Type II: Gamma
i. Specific, works with adaptive immune system
ii. Produced much later

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12. What are the steps (6) of phagocytosis?

a. Chemotaxis – Phagocytes move towards or away from a chemical signal
b. Adherence – Coating of antimicrobial proteins = opsonization
c. Ingestion – The ingested microbe is now called a phagosome
d. Maturation – Fusion of lysosomes with phagosome = phagolysosome
e. Killing – Results in residual body
f. Elimination – Exocytosis – The phagolysosome becomes a residual body

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14. What pathogens do eosinophils usually attack?

a. Parasitic worms – attach and secrete toxins

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v. How do the chemicals released during an allergic reaction affect physiology?

1. Respiratory distress, rhinitis (runny nose), water eyes, inflammation, reddening of the skin

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24. What is a membrane attack complex (MAC)?

a. Forms circular holes in a pathogen’s membrane

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8. What is the lacrimal apparatus?

a. Lacrimal glands, ducts, canal, and duct to nasal passage

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6. What are goblet cells?

a. Produce a very sticky and thick mucous

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22. How does a cell-mediated immune response happen? What are the steps?

a. Antigen presentation
b. Th differentiation
c. Clonal expansion of Tc
d. Self-stimulation

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ix. What are some treatments for mild hypersensitivities and for anaphylactic shock?

1. Antihistamines
2. Epinephrine

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iv. What are some of the parts of the body that are affected in a Lupus patient?

1. Butterfly rash on the face

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1. What 5 attributes does adaptive immunity have and what is meant by each one?

a. Specificity
b. Inducibility
c. Clonality – Once induced, cells form many clones
d. Unresponsiveness to self – Doesn’t act against normal body cells (normally)
e. Memory – Subsequent invasions of the same pathogen will be acted upon more quickly

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16. What do helper T cells do?

a. Th cells = CD4 Tc
b. Regulate activity of B cells and Tc cells by providing signals and growth factors

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2. What is type I diabetes?

a. Autoimmune disease (attack on islets of Langerhans)
b. Unable to produce insulin

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18. What is the end result of TLR activation?

a. Inflammation, interferons, activation of adaptive immune responses, or apoptosis

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5. What cells are being attacked in multiple sclerosis?

a. Nervous tissue (myelin sheaths)

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3. What is an epitope?

a. The part of an antigen to which an antibody attaches

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27. How does a humoral (antibody-mediated) immune response happen?

a. Antigen presentation
b. Differentiation of Th Th2
c. Activation of B cells
d. Proliferation and differentiation of B cells

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2. What is an antigen?

a. A molecular shape which produces an immune response

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1. What are the 2 layers of the skin?

a. Epidermis
b. Dermis

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20. What is the end result of NOD protein activation?

a. Inflammation, apoptosis, innate immune responses

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iv. What happens when you encounter an allergen the 2nd time?

1. The allergen binds to the IgE molecules of sensitized cells
2. Degranulation occurs with release of inflammatory chemicals

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3. What is lysozyme?

a. Antibiotic
b. Destroys cell walls of bacteria

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vii. How do you figure out that you have an allergy (2 ways)?

1. CAP blood test (test for IgE directed at each allergen)
2. Skin testing

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iii. What is Lupus?

1. Antibodies attack self-antigens

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19. What are NOD proteins?

a. Receptors found in the cytoplasm

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16. What is neutrophil extracellular trap (NET) formation?

a. Released after cell lysis – traps bacteria

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29. What organ sets your internal temperature?

a. Hypothalamus

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2. What is a dendritic cell?

a. Phagocytic cells in the epidermis
b. Devours pathogens nonspecifically

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1. What are the 4 different types of hypersensitivities?

Type I - Immediate
Type II - Cytotoxic
Type III - Immune-Complex Mediated
Type IV - Delayed/Cell-Mediated

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6. What are the consequences of MS?

a. Deficits in vision, speech, and neuromuscular function

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15. What do natural killer cells target?

a. Virally infected cells and tumors (neoplasms)

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ii. What is sensitization? (related to hypersensitivity)

1. IgE antibodies are produced instead of IgG
2. IgE binds very strongly to defense cells

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15. What do cytotoxic T cells do?

a. Tc cells = CD8 Tc
b. Directly kill infected/abnormal cells

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viii. How can you avoid a type I hypersensitivity (2 ways)?

1. Avoidance of allergen
2. Immunotherapy

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12. Which type of immune response are the T cells “in charge” of?

a. Cell-mediated

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29. When B cells proliferate, what are the 2 kinds of cells that they could become?

a. Memory B cells
b. Antibody-secreting Plasma Cells

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5. Which type of immune response are the B cells “in charge” of?

a. Antibody-mediated response

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31. What are the types of acquired immunity? (List an example of each)

a. Naturally acquired active immunity
i. E.g., getting the flu
b. Naturally acquired passive immunity
i. E.g., acquiring antibodies via breastfeeding
c. Artificially acquired active immunity
i. E.g., vaccination
d. Artificially acquired passive immunotherapy
i. E.g., being given antibodies to combat rabies

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ii. Where are some common areas of the body that immune complexes settle and what effects do they have (4)?

1. Hypersensitivity pneumonitis (form of pneumonia)
2. Glomerulonephritis (kidney disease)
3. Rheumatoid arthritis
4. Systemic lupus erythematosus

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5. What are mucous membranes and where are they found?

a. Mucous-secreting membranes
b. Found all body cavities open to the environment

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i. What is different about type IV reactions (compared to the other 3)?

1. Delayed response (12-24 hours) while APCs and T cells arrive and divide

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19. What are the two different types of Th cells?

a. Th1 assist Tc
b. Th2 assist B cells

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32. What are the 3 types of vaccines?

a. Attenuated – Modified/weakened live virus
b. Inactivated – Killed virus
c. Toxoid – Contains the toxic portion of a virus only

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17. What are toll-like receptors (TLRs)?

a. A integral recognition protein
b. Found in cytoplasmic membrane of phagocytic cells

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21. Exogenous antigens are presented on which type of MHC molecules?

a. Exogenous = Class II (antibody-mediated)

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4. What are some of the signs and symptoms of Graves’ disease?

a. Goiter, protruding eyes, rapid heartbeat, fatigue, weight loss

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26. What is inflammation?

a. Nonspecific response to tissue damage

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7. What are ciliated cells?

a. Propel the mucous up and away from the lungs

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v. What it done to prevent hemolytic disease

1. Administration of Anti-Rh IgG – Destroys any Rh cells that may have entered the mother, thus preventing any immune response (no antibodies are created and future pregnancies are safer)

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18. What is the main surface glycoprotein on a Th cell?

a. MHC class II

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8. What are the types of primary diseases we talked about?

a. Chronic granulomatousus disease – ineffective phagocytosis
b. SCID – lack of T and B cells
c. Briton-type agammaglobulinemia – lack of B cells/immunoglobulins
d. DiGeorge syndrome – Lack of T-cells

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9. What is microbial antagonism?

a. Competitive inhibition

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4. Sebum?

a. Oil from sebaceous glands
b. Lowers pH of skin surface to around 5

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9. What is the structure of an antibody?

a. Y-shaped like a BCR, but without the two anchoring proteins (they are free immunoglobulins)

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7. What is the overall structure of a BCR?

a. Two long chains and two short chains + two more that anchor it into the membrane

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28. What is diapedesis?

a. Leukocytes arrive at site of dilation and squeeze between the cells of the vessel’s wall

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iii. What is hemolytic disease of the newborn? Who is at risk?

1. Rh- mother develops antibodies, passes them to 2nd+ fetus (who is Rh+).

(The fetus is at risk)