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MNI (immuno path) > L24- Hypersensitivity Reactions > Flashcards

L24- Hypersensitivity Reactions Flashcards

1
Q

definitions:

  • Antigen
  • Immunogen
A

Ag- substance that evokes production of one or more Abs

Immunogen- substance that evokes adaptive immunity response if injected alone

**not all Ags are immunogens

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2
Q

definitions:

  • Antigenicity
  • Immunogenicity
A

Immunogenicity- ability to induce humoral and or cell-mediated immune response

Antigenicity- ability to combine specifically with the final products of the immune response

Note- not all Ags are immunogens

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3
Q

Innate / (1) immunity:

  • (non-/specific)
  • (slow/rapid) action
  • (4) main components
A

1- natural
2- non-specific (no Ag required)
3- rapid / immediate response
4:
-tissue barriers: skin, mucosa (respiratory, GI)
-cells: neutrophils, macrophages, NK cells
-plasma proteins: complement (no memory)

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4
Q

Adaptive / (1) immunity:

  • (non-/specific)
  • (slow/rapid) action
  • (4) main components
A 
1- acquired
2- specific: in response to Ag --> **memory
3- slow response
4:
-cells: B and T lymphcytes
-lymphocyte products: Abs, CKs
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5
Q

list the results of activating complement, include specific factors (hint- 3 results)

A

Inflammatory response; C3a, C5a

Opsonization, C3b –> phagocytosis

MAC formation (C5b-C9) –> lysis of microbe

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6
Q

briefly compare humoral vs cell-mediated immunity

A

Humoral:
-mediated by soluble Abs via plasma cells (B lymphocytes)

Cell-mediated:

  • mediated by T lymphocytes
  • mechanisms: direct cytotoxicity, CK production
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7
Q

At the introduction of a microbe to the body, (1) are the cells that initially respond and take action. (2) is required for the stimulation of adaptive immunity.

A

1- **neutrophils, macrophages, NK cells

2- capture and display of microbial Ags via APCs, mostly *dendritic cells

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8
Q

CD4+ lymphocytes:

  • (1) subset will stimulate macrophages via (2)
  • (3) subset will stimulate (4) cells

CD8+ lymphocytes = (5) and functions destroy and target (6)

A 
1- Th1
2- IFN-γ
3- Th2
4- plasma cells, eosinophils, mucus secreting epitheliam
Th cells --> phagocytosis

5- Tc cells (cytotoxic)
6- intracytoplasmic microbes via apoptosis

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9
Q

list the general categories for diseases of the immune system

A

Overactive:

  • hypersensitivity
  • transplant rejection
  • autoimmune diseases

Underactive:

  • primary immune deficiency diseases
  • acquired immune deficiency diseases
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10
Q

Hypersensitivity diseases:

  • (1) definition
  • (2) list the three basic characteristics of these reactions
  • (3) causes
A

1- reaction of Ag with Ab or sensitized lymphocyte that is harmful to the host

2:

  • prior Ag sensitization (sensitizing dose)
  • re-exposure to Ag (challenge dose)
  • additional exposures => inc reaction severity
3:
-microbial Ags
-environmental Ags: organic, inorganic
-self-Ags (= autoimmunity)
Note- Ags are difficult to eliminate and or avoid (common in environment / in host)
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11
Q

Type I hypersensitivty:

  • (immediate/delayed) type
  • (2) is the main mediator –> it is normally in (3) location and activation by (2) binding Ag => (4)
  • (5) are the effector cells that carry out this response
A 
1- immediate
2- IgE
3- surface of mast cell
4- mast cell degranulation
5- mast cells, eosinophils, basophils
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12
Q

In type I hypersensitivity, (1) is the first step which includes (1) presentation to (2) via (3). This process allows for the development of (4). The second step is (5) causing (6) progression.

A

1- sensitization — exposure to Ag
2- Th2 cells
3- APCs
4- IgE (via B-cell) –> binds to mast cell
5- re-exposure to Ag / allergen
6- Ag binds IgE –> mast cell degranulation

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13
Q

Type I hypersensitivity, first phase = (1):

  • (2) time-frame
  • (3) mediators
  • (4) physiological changes
A

1- immediate response
2- minutes

3- histamine (+ other vasoactive amines), proteases, PG-D2

4:

  • vasodilation (flushing)
  • inc vascular permeability (angioedema)
  • bronchoconstriction
  • inc mucus secretion
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14
Q

describe the mast cell contents released in type I hypersensitivity

A

Immediate Phase:

  • Histamine
  • Proteases
  • PG-D2

Late-Phase:

  • LT B4, C4, D4
  • CKs and chemokines
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15
Q

Type I hypersensitivity, second phase = (1):

  • (2) time-frame
  • (3) mediators
  • (4) physiological changes
A

1- late phase response
2- 2-8hrs

3- LT-B4/C4/D4, chemotactic cytokines

4:

  • inflammatory response –> neutrophils, eosinophils, lymphocytes (leukocyte infiltration + tissue destruction)
  • epithelial injury via inflammation (tissue destruction)
  • bronchospasm
  • hypoxic Sxs
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16
Q

Localized type I hypersensitivity:

  • (1) definition and common affected sites
  • (2) is the main predisposition with (3) and (4) as signs and symptoms
A

1- Ag confined to particular site —> lungs, GIT, skin

2- Atopy, familial predisposition
3- hay fever, urticaria, some form of asthma
4- inc IgE levels

Note- atopy allows for quicker and stronger type I hypersensivity responses

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17
Q

Systemic type I hypersensitivity:

  • (1) definition
  • usually in response to (2)
  • (3) is the main dangerous effect
  • (4) are the initial and other effects
A

1- involves 2 or more organ systems

2- IV administration of Antisera (foreign Abs), hormones, penicillin products

3- anaphylaxis –> hypotension

4- (w/in minutes) itching, hives, skin erythema —- angioedema, laryngeal edema

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18
Q

list some histological features of each Acute and Late phase type I hypersensivity

A

Acute:

  • masts cell currently degranulating
  • vascular congestion (dilated)
  • edema surrounding vessel

Late:

  • little mast cells – most fully degranulated
  • many eosinophils
19
Q

Type II hypersensitivity:

  • (1) binding occurs in (2) location
  • (3) are the possible progressions after (1) occurs
A

1- Ag-Ab interactions
2- cell surface (plasma membranes)

3:

  • complement / Fc mediated inflammation (+ tissue injury)
  • opsonization –> phagocytosis
  • altered cell function
20
Q

Autoimmune hemolytic anemia:

  • (1) target Ag
  • type (2) hypersensitvity
  • (3) mechanism
  • (4) clinical manifestations
A

1- RBC membrane protein
2- type II
3- opsonization, phagocytosis
4- hemolytic anemia

21
Q

Hemolytic transfusion reaction:

  • (1) target Ag
  • type (2) hypersensitvity
  • (3) mechanism
  • (4) clinical manifestations
A

1- RBC membrane protein
2- type II
3- opsonization, phagocytosis
4- hemolytic anemia, ARF

22
Q

Goodpasture syndrome:

  • (1) target Ag
  • type (2) hypersensitvity
  • (3) mechanism
  • (4) clinical manifestations
A

1- basement membrane protein (part of type IV collagen – kidneys, lungs)
2- type II
3- complement / Fc mediated inflammation
4- nephritis, lung hemorrhage

23
Q

Graves disease:

  • (1) target Ag
  • type (2) hypersensitvity
  • (3) mechanism
  • (4) clinical manifestations
A

1- TSH receptor
2- type II
3- Ab stimulation of TSH receptor
4- hyperthyroidism

24
Q

Myasthenia gravis:

  • (1) target Ag
  • type (2) hypersensitvity
  • (3) mechanism
  • (4) clinical manifestations
A

1- AChR
2- type II
3- Ab blockade of AChR – dec number of receptors
4- muscle weakness, paralysis

25
Q

Pemphigus vulgaris:

  • (1) target Ag
  • type (2) hypersensitvity
  • (3) mechanism
  • (4) clinical manifestations
A

1- intercellular proteins in keratinocytes – desmosomes
2- type II
3- disruptions of intercellar adhesions
4- skin vesicles – easily rupturing blisters

26
Q

Type III hypersensitivity:

  • (1) is the main mediator binding (endo/exo)-genous Ags
  • (3) is the common location of (1)/(2) binding followed by (4)
  • (5) is an additional location/mechanism of (1)/(2) binding
  • both (3)/(4) and (5) are mediated by (6) process
A 
1- IgM, IgG
2- both endogenous and exogenous Ags
3- plasma / serum
4- tissue deposition of Ab-Ag complex
5- tissue deposition of Ag followed by binding of Ab
6- complement activation
27
Q

list the favored sites of type III hypersensitivity reactions and the associated disease process (hint- 6)

A
  • renal glomeruli –> glomerulonephritis
  • joints –> arthritis
  • skin
  • heart –> carditis
  • serosal surfaces (serositis)
  • small BVs (vasculitis)
28
Q

In type III hypersensitivity, Ab-Ag complex within tissue will initiate (1). (2) will mediate (3) progression; (4) will mediate (5) progression where (3) and (5) both result in injury of the local tissue.

A

1- complement activation

2- C3a, C5a
3- anaphylactoid rxn + chemotactic rxn –> neutrophil infiltration (+ inc vascular permeability) –> CKs + other mediators –> tissue destruction

4- C3b
5- opsonization –> phagocytosis –> tissue destruction

29
Q

SLE:

  • (1) target Ag
  • type (2) hypersensitvity
  • (3) mechanism
  • (4) clinical manifestations
A

1- nuclear Ags
2- type III
3- immune complex deposition
4- nephritis, arthritis, skin and other lesions

30
Q

Post-Streptococcal Glomerulonephritis:

  • (1) target Ag
  • type (2) hypersensitvity
  • (3) mechanism
  • (4) clinical manifestations
A

1- streptococcal wall Ag
2- type III
3- immune complex deposition
4- nephritis

31
Q

Polyartheritis nodosa:

  • (1) target Ag
  • type (2) hypersensitvity
  • (3) mechanism
  • (4) clinical manifestations
A

1- HepBs Ags + others
2- type III
3- immune complex deposition
4- necrotizing vasculitis

32
Q

Reactive arthritis:

  • (1) target Ag
  • type (2) hypersensitvity
  • (3) mechanism
  • (4) clinical manifestations
A

1- bacterial Ags
2- type III
3- immune complex deposition
4- arthritis

33
Q

Serum sickness:

  • (1) target Ag
  • type (2) hypersensitvity
  • (3) mechanism
  • (4) clinical manifestations
A

1- foreign Ag like xenobiotic serum used in therapy
2- type III
3- immune complex deposition
4- necrotizing vasculitis, nephritis, arthritis

34
Q

discuss Dx of a type III hypersensitivity reaction

A

1) demonstration of immune complexes in target organ (microscopy) — immunofluorescence, SEM/TEM
2) immune complex blood assays

35
Q

Type IV hypersensitivity:

  • (1) mediated
  • (2) are the two mechanisms
  • (3) are the possible Ags
A

1- sensitized T cells (Th or Tc)

2- DTH (delayed type hypersensitivity), direct cytotoxicity (autoimmune diseases, viral infections)

3- broad range: mycobacterium/bacteria, fungi/protozoa/helminths/viruses, chemical agents, tissue grafts, self-Ags

36
Q

DTH, type IV hypersensitivity:

  • (1) mediated, reaction to Ag presented by (2)
  • (1) will secrete (3) and (4), include functions
A

1- Th1, Th17 (mostly fungi)
2- MHC-II, APCs (Ag presenting cells)

3- IFN-γ –> activated macrophages

4- TNF, IL-17 –> recruit neutrophils, macrophages

Note- possible granuloma formation

37
Q

Direct cytotoxicity, type IV hypersensitivity:

  • (1) mediated, reaction to Ag presented by (2)
  • (1) will secrete (3) and (4), include functions
A

1- Tc
2- MHC-I from targeted cells

3- Porforin –> promotes entry of granzymes
4- Granzymes (proteases) –> initiates apoptosis

38
Q

describe the development of a granuloma (indicate hypersensitivity type)

A

Type IV, DHC subtype:

  • Th1 cells release IFN-γ –> macrophage recruitment
  • macrophages surround indigestable microscopic aggregation
  • macrophages differentiate into epthelioid (–> possible giant cell formation via fusion)
  • architecture => granuloma
39
Q

Tuberculosis:

  • (1) target Ag
  • type (2) hypersensitvity
  • (3) mechanism
  • (4) clinical manifestations
A

1- mycobacterium components
2- type IV
3- delayed type hypersensitivity, Th1
4- caseating granuloma w/ inflammation + tissue destruction

40
Q

DM, type I:

  • (1) target Ag
  • type (2) hypersensitvity
  • (3) mechanism
  • (4) clinical manifestations
A

1- β-cell Ags, pancreatic islets
2- type IV
3- direct cytotoxic, Tc
4- β-cell destruction –> no insulin –> hyperglycemia

41
Q

MS:

  • (1) target Ag
  • type (2) hypersensitvity
  • (3) mechanism
  • (4) clinical manifestations
A

1- proteins in CNS myelin
2- type IV
3- direct cytotoxic, Tc
4- range of sensory and motor deficits

42
Q

RA:

  • (1) target Ag
  • type (2) hypersensitvity
  • (3) mechanism
  • (4) clinical manifestations
A

1- unknown Ag in synovium
2- type IV
3- direct cytotoxic, Tc
4- chronic arthritis –> destruction of articular cartilage and bone

43
Q

Contact Dermatitis:

  • (1) target Ag
  • type (2) hypersensitvity
  • (3) mechanism
  • (4) clinical manifestations
A

1- various environmental Ags
2- type IV
3- delayed type hypersensitivity, Th1
4- skin inflammation with blisters

MNI (immuno path) (14 decks)

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