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D2 - FALL - Par 2 > Pathology - L1 - Immunologic Diseases > Flashcards

Pathology - L1 - Immunologic Diseases Flashcards

1
Q

antigen

A

any substance able to induce a specific immune response

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2
Q

B-lymphocyte functions?

A

neutralizes microbes, phagocytosis, complement activation

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3
Q

where are B-cells found?

A

in lymphoid follicles of lymph nodes, bone marrow, and extranodal lymphatic tissue (i.e. tonsils, appendix, Peyer’s patch)

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4
Q

types of T lymphocytes?

A

helper, cytotoxic, regulatory

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5
Q

helper T-cells functions?

A

activation of mac’s, in inflamm, activation (proliferation & differentiation) of T & B lymphocytes

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6
Q

Cytotoxic T lymphocyte function?

A

killing of infected cell or cells harboring microbes

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7
Q

regulatory T lymphocyte function?

A

suppression of immune response

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8
Q

where are 60-70% of circulating lymphocytes found?

A

in thymus and paracortical areas of lymph nodes.

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9
Q

60% of lymphocytes have what ?

A

CD4+ marker; so they are T-helper cells

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10
Q

T-helper cells regulate T and B cell rxns by secretion of _____.

A

cytokines

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11
Q

30% of circulating lymphocytes have ____. What cells are these?

A

CD8+ marker; = cytotoxic T-cells (kill cells harboring microbes).

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12
Q

To respond, T cells must have what?

A

the antigen presented by antigen-presenting cells (APC).

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13
Q

APCs express what molecules?

A

major histocompatibility molecules (MHC)

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14
Q

T-helper lymphocytes recognized antigens expressed on ____ molecules, whereas cytotoxic lymphocytes recognized antigens expressed on ____ molecules.

A

class II MHC; class I MHC

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15
Q

antibody-dependent cell-mediated cytotoxicity (ADCC)

A
  • mechanism of cell-mediated immune defense whereby an effector cell of the immune system actively lyses a target cell, whose membrane-surface antigens have been bound by specific antibodies.
  • one of the mechanisms through which antibodies, as part of the humoral immune response, can act to limit and contain infection.
  • Classical ADCC is mediated by natural killer (NK) cells; macrophages, neutrophils and eosinophils can also mediate ADCC.
  • ADCC is part of the adaptive immune response due to its dependence on a prior antibody response.
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16
Q

natural killer cells make what % of blood lymphocytes?

A

10-15%

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17
Q

Natural killer cells ?

A
  • have no T-cell markers or Ab production
  • lyse tumor cells or infected cells w/o previous sensitization
  • 1st line of defense against some tumors & viruses
  • also can lead to AB-dependent cell-mediated cytotoxicity (ADCC)
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18
Q

function of macrophages?

A

1) required to process and “present” antigens to lymphocytes;
2) effectors of cell-mediated immunity; produce cytokines influencing growth and function of lymphocytes, inflammation, fibroblast proliferation, and collagen deposition;
3) Phagocytic in response to T-cell activation or opsonization.

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19
Q

members of the macrophage family, although weakly phagocytic?

A

dendritic cells (in lymphoid tissue); Langerhans cell (in epidermis, oral mucosa)

  • important for presenting antigens
  • also produce anti-viral cytokines
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20
Q

Ag-Ab activates what…?

A

9 sequential components aka complement

21
Q

Complement activates ?

A
  • anaphylaxis (i.e. c3a, c5a)
  • chemotaxis (c5a)
  • opsoninization (c3b)
  • lysis of cells (MAC)
22
Q

what are cytokines of innate immunity?

A

intercellular mediators produced in response to microbes and other stimuli and mediate inflammation and anti-viral defense (TNF, IL-1, type 1 IFNs)

23
Q

functions of cytokines of adaptive immunity?

A

promote lymphocyte proliferation and differentiation and to activate effector cells (IL-2, IFN-y)

24
Q

____ stimulates hematopoiesis (colony stimulating factors).

A

cytokines

25
Q

innate immunity?

A

defense mechanisms that are present before infection (i.e. epidermis, phagocytic cells, dendritic cells, NK cells)

26
Q

adaptive immunity?

A
  • lymphocytes and their products

- humoral vs cell-mediated

27
Q

humoral immunity?

A
  • associated w/ AB production\
  • B lymphocytes and ABs play predominant role
  • AB (IgA, IgE, IgG, IgM) act on Ags, resulting in neutralization, lysis, phagocytosis.
28
Q

cell-mediated immunity?

A
  • cellular neutralization of Ags
  • predominant role is played by T-lymphocytes
  • Ags are destroyed by lymphocytes, macrophages, etc directly or via cytokines
29
Q

X-Linked Agammaglobulinemia?

A

aka Bruton Disease

  • failure of pre-B cells to differentiate into B cells
  • Ig molecules are not assembled due to failure of light chain production
30
Q

Clinical features of X-liked Agammaglobulinemia?

A
  • absent or decreased #’s of B cells
  • depressed serum levels of all Ig classes
  • normal T cell-mediated
  • germinal centers (composed mostly of B cells) reduced in size
  • recurrent bacterial (pharyngitis, sinusitis, pneumonia) and certain viral infections (enteroviruses)
31
Q

tx of X-linked Agammaglobulinemia?

A

replacement therapy w/ human Ig

32
Q

DiGeorge Syndrome?

A
  • failure of development of 3rd and 4th phraryngeal arches
  • absence of thymus, as well as parathyroids
  • facial structures will also be underdeveloped
33
Q

Severe combined immunodeficiency?

A
  • X-linked, associated w/ failure in lymphocyte (esp T-lymphocyte) development
  • autosomal recessive form associated w/ deficiency of adenosine deaminase
34
Q

Isolated IgA deficiency?

A

typically asymptomatic; compromised mucosal defenses; respiratory, GI, urogenital infections

35
Q

Complement deficiency?

A
  • angioedema–repaid swelling under dermis
  • causes:
    1. allergy
    2. complement deficency
36
Q

HIV primarily targets what?

A

the immune system and CNS

37
Q

how is HIV transmitted?

A

sexual contact, parenteral exposure to blood, maternal/fetal

38
Q

what is the target cell of HIV?

A

cells w/ CD4 receptors (primarily T-helper lymphocyte)

39
Q

Viral RNA is permanently integrated into host DNA via… ?

A

reverse transcription

40
Q

What is the half-life of HIV?

A

half-life of 2 days; rapid turnover of HIV

41
Q

what are the 3 things HIV virus can do?

A
  1. remain silent
  2. cause cell death
  3. disrupt normal cell function
42
Q

what is the clinical course of HIV infection?

A
  • acute, self-limited response (similar to infectious mononucleosis)
  • 8-10 year asymptomatic stage
  • symptomatic stage (AIDS-related complex)
43
Q

AIDS?

A
  • endpoint of HIV deficiency
  • 5 yrs after infection- 18% have AIDS
  • 13 yrs after infection - 65% have AIDS, 20% have symptoms, & 15% have no symptoms
44
Q

AIDS-related complex (ARC) clinical features?

A
  • fever, wt loss, diarrhea, candidiasis, herpes zoster, hairy, leukoplakia
  • increased infections: cytomegalovirus, herpes simplex, toxoplasmosis
  • pulmonary - pneumocystis carinii oneumonia (presenting sign in 50%)
  • AIDS-dementia complex
45
Q

Type 1 hypersensitivity

A

allergy/anaphylaxis; IgE mediated

- IgE binds to mast cells, releasing HISTAMINE and other vasoactive amines

46
Q

Type II hypersensitivity

A

antibody dependent

  • complement dependent (transfusion rxns, erythroblastosis fetalis)
  • Ab-dependent cell-mediated cytotoxicity (ADCC)
  • Ab-mediated cellular dysfunction (myasthenia gravis, Grave’s disease)
47
Q

Type III hypersensitivity

A
  • immune complex-mediated (SERUM SICKNESS, glomerulonephritis)
  • Ag + Ab + Complement - Recruitment of neutrophils, resulting in tissue destruction
48
Q

Type IV Hypersensitivty

A

cell-mediated

  • delayed type - TUBERCULIN RXN, poison ivy, contact rxns) T- cells & mac’s; chronic rxns may result in granulomatous inflamm
  • T- cell mediated cytotoxicity - type I diabetes - tissue is destroyed by cytotoxic (CD8+) T cells

D2 - FALL - Par 2 (7 decks)

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