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Pathophysiology > Immunity and Defects in Mechanisms of Defense > Flashcards

Immunity and Defects in Mechanisms of Defense Flashcards

1
Q

Define host

A

organism being “infected”
ex: human

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2
Q

Define agent

A

a factor whose presence (excessive or absent) is essential for the occurrence of a disease or other adverse health outcome

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3
Q

Define pathogen

A

organism that causes disease or other adverse health outcome

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4
Q

Define colonization

A

act of establishing a presence without damage
ex: commensal (normal) flora

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5
Q

Define infection

A

invasion of the body tissues of a host by an infectious agent causing disease or other adverse health outcome

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6
Q

Define communicability

A

ability to spread an agent from one individual to others
- communicability differs between agents
- depends on port of entry (ex: direct contact, inhalation, ingestion)

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7
Q

Define infectivity

A
  • the ability of an agent to cause infection (to invade and multiply in the host)
  • measured as proportion of persons exposed to an infectious agent vs those who become infected
  • lessened by memory/vaccination
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8
Q

Define virulence

A
  • ability of an infectious agent to cause severe disease
  • measured as proportion of person with the disease who become severely ill or die
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9
Q

Define pathogenicity

A
  • ability of an agent to cause disease or other adverse health outcome
  • success depends on communicability. infectivity, and virulence
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10
Q

Define immunogenicity

A
  • ability to induce an immune response
  • depends on number of exposures
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11
Q

Define antigen

A
  • substances that react with molecules of the immune system (ex: antibodies, receptors on B and T cells)
  • recognized as foreign by the human body
  • on infectious agents, noninfectious substances from the environment, drugs, vaccines, transfusions, and transplanted tissues
  • stimulate the production of antibodies
  • epitopes = part of antigen that antibody attaches to
  • immunogen = bind to receptors and induce immune response → all immunogens are antigens but not all antigens are immunogens
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12
Q

Define antibody

A
  • any of a variety of proteins in the blood that are produced in response to an antigen as an immune response
  • Y shaped
  • produced by B cells
  • circulate in blood and bind to antigens on infectious agents
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13
Q

List the order of pathogenicity

A

(1) communicability
(2) infectivity
(3) virulence

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14
Q

Potential local/specific signs and symptoms of infection

A
  • diarrhea
  • rash
  • convulsions
  • hemorrhage
  • pneumonia
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15
Q

Potential systemic/nonspecific signs and symptoms of infection

A
  • fever
  • myalgia (muscle pain)
  • headache
  • lethargy (inflammation + sickness behavior)
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16
Q

Define culture

A

propagation of microorganisms outside of the host

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17
Q

Define serology

A

measures serum antibodies in the host
- after exposure to an infectious agent the body produces antibodies
- antibody titer concentration rises
- IgM = rises and falls during acute phase
- IgG = remains elevated after the acute phase

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18
Q

Steps of disease course

A

(1) infection
(2) incubation (latent) period → clinical threshold
(3) prodromal stage
(4) invasion or acute illness period
(5) convalescence (recovery) → or disease is fatal; critical threshold
(6) resolution

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19
Q

Incubation (latent) period

A
  • from initial exposure to onset of first symptoms
  • pathogens undergoing initial colonization
  • can reach clinical threshold
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20
Q

Prodromal stage

A
  • occurrence of initial symptoms (often mild) → before full development
  • pathogens continue to multiple
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21
Q

Invasion or acute illness period

A
  • immune and inflammatory responses triggered
  • pathogens multiply rapidly and invade further
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22
Q

Convalescence (recovery)

A
  • recovering from illness
  • usually immune and inflammation systems remove pathogens and symptoms decline OR disease becomes fatal
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23
Q

Define clinical threshold

A
  • signs and symptoms develop
  • cells damaged
  • pathogen has evaded innate immune system
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24
Q

Define subclinical disease

A
  • symptoms don’t develop
  • immune system handles pathogen
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25
Q

List infection control measures

A

environmental measures
- waste disposal
- water treatment and contamination prevention
- food safety
- insect (vector) control → safe insecticides

hygiene
- hand washing
- face masks
- social distancing
- quarantine
- isolation

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26
Q

List possible interventions during acute phase

A

antibiotics
- disrupt cell wall synthesis, protein synthesis, nucleic acid synthesis, metabolism

antivirals
- disrupt RNA or DNA synthesis, viral enzymes, virus binding to cells, production of the protein coats of new viruses

antifungals
- disrupt cell membrane

surgical interventions
- remove infected tissue/organ, draining of abscesses, debridement (cleaning)

27
Q

True or False? S&S show up in the subclinical phase

A

false

28
Q

Difference between innate and adaptive immunity

A

Innate
- rapid response
- activated by receptors for microbial signature molecules
- cytokine production
- antigen presentation
- present at birth
- non specific → PAMPs and PRRs
- induces inflammation

Adaptive
- slow response
- activated by T or B cell receptors
- antigen specific
- memory
- develops after exposure
- specific

29
Q

Pathway of innate to adaptive response

A

Antigen/pathogen → innate immune response (inflammation = severe response) → antigen presenting cells (APCs) (present to adaptive immune cells) → cell-mediated response (T cells) OR humoral response (B cells/antibody)

30
Q

Define humoral immunity

A
  • secrete antibodies from B cells
  • B cell receptors = alpha chain + beta chain
  • initiates immune response by APC and T helper cells
  • APC + naive B cell → activated B cells + activated T helper cells → plasma cells + antibodies
31
Q

Define cell-mediated immunity

A
  • T cells → coordinate attacks of effector cells
  • IgM and IgD
  • can attack and kill targets or stimulate activity of other leukocytes through secretion of cytokines
  • initiates immune response by APCs
  • APC + naive T helper cell → activated T helper cell
  • APC + naive cytotoxic T cell → activated cytotoxic T cells ← activated T helper cells
32
Q

Components of antibody

A

(1) antigen-binding fragment (Fab) (variable region)

(2) crystalline fragment (Fc) (biologic function

(3) 4 polypeptide chains (2 light and 2 heavy)

33
Q

Describe lymphocyte development

A

(1) produced in bone marrow (immature) → B cells mature in bone marrow; T cells in thymus → positive or negative selection → move to lymph nodes waiting for activation

(2) dendritic cell phagocytizes microbe → carries antigens to closest lymph node and because an antigen presenting cell (APC) → APC activates T cells with receptors that “fit” the MHC/antigen being displayed → clonal proliferation → released from lymph node into bloodstream to fight infection (some become memory T cells or B cells)

34
Q

Role of T cells

A

T-helper cells → stimulate B cells to secrete antibodies or become memory cells, stimulates inflammatory response, or stimulates anti-inflammatory response

Cytotoxic T cells → kill and destroy pathogen

35
Q

Role of B cells

A

become plasma cells that pump out antibodies to eliminate pathogen or memory cells that stay in the body for quicker subsequent reactions

36
Q

Antibody functions

A

(1) direct: through action of antibody
- neutralization
- agglutination (between cells)
- precipitation (between antigens)

(2) indirect: requiring activation of other components
- inflammation
- phagocytosis
- complement

37
Q

Steps of adaptive immunity

A

(1) Develop a population of T and B cells that are specific for “ONE” antigen and have them in lymph tissue

(2) Infection

(3) Innate system kicks in fight infection (could be final step)

(4) If infection is bad, with a lot of inflammation, it might get APCs to present antigen on MHC II

(5) APCs travel to closest lymph tissue

(6) If the right T cells are there, it will bind with the APCs MHC II/antigen

(7) Clonal proliferation of T cells and activation of the same B cells

(8) T cells leave lymph tissue; B cells turn into plasma cells churning out antibodies

(9) T cells find site of infection (cytokines/chemokines/inflammation at site)

(10) T cells recruit macrophages/cytotoxic T cells/other effector cells to kill off infection

(11) Formation of memory T/B cells and continued antibody production

38
Q

Which immune cell creates antibodies in response to antigens?
A - Cytotoxic T lymphocytes
B - Helper T lymphocytes
C - Cytokines
D - B lymphocytes

A

D - B lymphocytes

39
Q

Define MHC

A
  • major histocompatability complex (MHC)
  • glycoproteins found on the surface of all human cells (except RBCs)
  • also human leukocyte antigen (HLA) → genes encoding MHC proteins
40
Q

Difference between MHC-I and MHC-II

A

MHC-I
- present antigens that are endogenous (within the cell) on an infected cell
- on all nucleated cells, platelets

MHC-II
- present exogenous antigens (from outside body)
- on dendritic cells, macrophages, B cells

41
Q

Define dendritic cell

A

antigen-presenting leukocyte that is found in the mucosa, skin, and lymphoid tissues that initiate a primary immune response

42
Q

Describe clonal proliferation

A
  • second phase
  • once T cell is activated
  • cells proliferate → some released into bloodstream to fight infection, others become memory T/B cells in blood/tissues
43
Q

Describe primary immune response

A
  • antigen presented on MHC-II
  • T helper cells activated → B cell proliferation and differentiation → plasma cells produce antibodies; memory B cells for secondary response
  • plasma antibody levels rise
  • can take 2-3 weeks/10-14 days because APCs need to find the right T cell and have time for clonal proliferation

vaccination produces primary immune response

44
Q

Describe secondary immune response

A
  • Second or subsequent exposure to antigens: more rapid
  • Memory B cells respond to the antigen immediately
  • Plasma antibody levels rise within days
  • Booster shots cause a secondary immune response, so antibody levels will be high before the disease is encountered
45
Q

Steps of adaptive immunity response

A
  • innate and memory B and T cells
  • second/subsequent exposure to antigens → quicker response
  • memory B cells respond to antigen immediately
  • plasma antibody levels rise within days

booster shots cause a secondary immune response so antibody levels are high before disease is encountered

46
Q

Define hypersensitivity

A

altered immunologic response to an antigen that results in disease or damage to the host
- allergy
- autoimmunity
- alloimmunity

47
Q

Define allergy hypersensitivity

A

hypersensitivity to environmental allergens (exogenous)
ex: anaphylaxis

48
Q

Define autoimmunity hypersensitivity

A

disturbance in immunologic tolerance of self-antigens (endogenous)
ex: autoimmune disorders

  • circulating immune complexes form = type III
  • genetic predisposition with mutations in MHC-II
  • more common with pregnancies
  • tolerance: recognition of self by immune system → breakdown of tolerance causes T cells to recognize self antigens as foreign

ex: molecular mimicry

ex: systemic lupus erythematosus (SLE) → most common, complex, and serious of autoimmune disorders
- chronic multisystem inflammatory disease → remissions and exacerbations

49
Q

Define alloimmunity hypersensitivity

A

reactions to tissues of another individual

type II
- improper blood type matching for transfusions
- Rh incompatibility during pregnancy
- transplant rejection (MHC incompatibility; need to do cross matching)

type IV
- graft vs host disease (GVHD): bone marrow transplant
- T cells in donor bone marrow attack hot cells

50
Q

Four classes of hypersensitivity

A

Type I: IgE on mast cells (immediate)
Type II: IgG/IgM → tissue-specific
Type III: Immune complex-mediated reactions (antibody blobs)
Type IV: Cell-mediated reactions

type I-III = immediate
type IV = delayed (cells need to develop)

51
Q

Describe type I hypersensitivity

A

“allergic reactions”

  • IgE on mast cells release histamine
  • first exposure = no reaction → second reaction = mast cell degranulates histamine → signs and symptoms
  • genetic predisposition

local/atopic reactions:
- diarrhea, vomiting
- hives (urticaria), itching (pruritus)
- conjunctivitis, rhinitis
- bronchial constriction (spasm) and hypersecretion of mucous, edema
- angioedema (skin swelling), hypotension

tests
- food challenges
- skin tests
- lab tests

52
Q

Describe anaphylaxis

A
  • systemic or anaphylactic reactions
  • can be life-threatening
  • systemic response to type I hypersensitivity
  • bronchoconstriction (can’t breathe) → hypoxia
  • vasodilation → sudden BP drop → shock/organs and brain not perfused
53
Q

Describe type II hypersensitivity

A

IgG and IgM

  • complement and antibody mediated cell destruction/inflammation OR cell/tissue dysfunction (specific)

(1) cell is destroyed by antibodies and complement

(2) cell destruction through phagocytosis

(3) tissues destroyed by complement and neutrophil granules

(4) antibody-dependent cell-mediated cytotoxicity (binding tells cell to die)

(5) target cell malfunction
ex: myasthenia gravis (autoimmune disease) → receptors for contraction blocked by antibodies

54
Q

Describe type III hypersensitivity

A
  • free floating antigen and antibody → circulating immune complex
  • immune complexes (globs) deposit on vessel walls or extravascular tissues → activate complement → lysosomal enzymes released → damaged tissue (vascular damage)
  • not organ specific

ex: serum sickness: immune complexes of foreign serum protein (medication) in blood deposited in tissues → blood vessels, joints, kidneys (anti-venom)

  • systemic or local
55
Q

Describe type IV hypersensitivity

A
  • T/Tc cells (not antibodies)
  • sensitized T cells attack antigen (cytotoxic T cells)
  • 24-72 hours

ex: TB test; allergic reactions from poison ivy or metals; graft rejection; MS

56
Q

True or false? Administration of certain antibiotics may result in type III sensitivity reaction

A

true - ex: penicillin

57
Q

Type I, II, III, or IV → Involves tissue specific antigens bound to IgG

A

Type II

58
Q

Type I, II, III, or IV → Involves environmental specific antigens bound to IgE

A

Type I

59
Q

Type I, II, III, or IV → Involves blocking of receptors by antibodies

A

Type II

60
Q

Type I, II, III, or IV → Involves T cells

A

Type IV

61
Q

Type I, II, III, or IV → Involves endogenous/exogenous immune complexes

A

Type III

62
Q

Types of solid organ graft rejection

A

(1) hyperacute (crossmatching)
- immediate and rare
- preexisting antibody to the antigens of the graft

(2) acute (type IV)
- days to months
- cell-mediated immune response against unmatched HLA antigens
- take immunosuppressants to avoid

(3) chronic (type IV)
- months of years
- weak cell-mediated reaction against minor HLA antigens (HLAs match but not perfectly)
- take immunosuppressants to avoid

63
Q

Primary immunity deficiency

A

principal component of immune system is defective

(1) B (antibody) or T cell deficiencies
ex: hypogammaglobulinemia: don’t make enough IgGs

(2) Combined (no B or T cells)
- can’t mount an adaptive response

(3) Complement (C3 deficiency)
- most severe because of role in compliment cascade
- recurrent life-threatening infections

(4) Phagocyte
- ex: chronic granulomatous disease (CGD) → deficient production of products needed for phagocytic kiling
- recurrent pneumonia, tumorlike granulomata in lungs, skin, bones, and other infections

(5) Innate
- ex: chronic mucocutaneous candidiasis
- defective immune response to C. albicans → severe recurrent candida infections

64
Q

Acquired (secondary) immunity deficiency

A
  • more common
  • caused by other illness
  • pregnancy, infancy, aging, emotional trauma, eating disorders, dietary insufficiencies (malnutrition), malignancies, burns, medical treatments, diabetes, alcoholic cirrhosis, immunosuppressant drugs, AIDS

Pathophysiology (6 decks)

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