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Mechanism of Disease > Immunopathology and Hypersensitivity > Flashcards

Immunopathology and Hypersensitivity Flashcards

1
Q

What are the general principles of the immune response?

A
  • Multilayer defense
  • Pathogen recognition
  • Effective inter-cellular communication
  • Self-regulation
  • Limitation of host damage
  • Adaptive responses to changing pathogen
  • Multiple mechanisms of pathogen clearance
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2
Q

What are the innate and adaptive branches of the immune system?

A 
Innate= Cellular (phagocytes & natural killer), PRR, barrier and chemical mechanisms
Adaptive= Cellular, humoral
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3
Q

What are pattern recognition receptors?

A
  • Antigen recognition receptors of innate system
  • Common recognition of PAMPs & DAMPs
  • 2 groups: cell surface & intracellular receptors
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4
Q

Name the major components of the innate immune system

A
  • Pattern recognition receptors
  • Antimicrobial peptides
  • Cells
  • Complement components
  • Cytokines
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5
Q

Describe fluid-phase recognition molecules

A
  • C type Lectin family= Collectins (surfactant protein A&D)
  • Recognition of microbial complex carbohydrates
  • Bind via CRDs
  • Neutralisation of pathogens
  • recruitment of adaptive response
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6
Q

What is the source and target of TNF?

A

Source: macrophages & T-lymphocytes

Target: Hepatocytes, neutrophils, inc inflammation & activation

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7
Q

What is the source and target of IL6?

A

Source: macrophages, T-lymphocytes, endothelia

Target: inc B-lymphocyte proliferation

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8
Q

What cell types of the innate immune system are there?

A
  • Macrophages
  • Natural killer
  • Eosinophil & neutrophil
  • Plasmacytoid & myeloid dendritic
  • Mast cells & basophils
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9
Q

What is the mechanism for antigen presentation?

A
  • Antigens internalised
  • Broken down to peptides
  • Associated with newly synthesised class 2 molecule and brought to surface
  • Foreign peptides recognised by T-helper which are activated
  • Produce cytokines needed by B&T cells
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10
Q

What does HLA stand for? What is its other name? What is ir?

A
  • Human leucocyte antigens
  • Histocompatability antigens
  • glycoproteins on cell surface making them unique
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11
Q

What are functions of Class 1&2 MHC proteins?

A

Class1: present peptides to cytotoxic T cells
Class2: present peptides to helper T cells

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12
Q

What is the function of

B-lymphocytes?

A

Potential to secrete antibodies: humoral immunity

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13
Q

What is the function of killer/cytotoxic T cells?

A

Kill- cellular immunity

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14
Q

What is the function of helper T cells?

A
  • Secrete growth factors (cytokines) which control immune response
  • Help B&T lymphocytes
  • Target of HIV
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15
Q

What is the function of suppressor T lymphocytes?

A

Dampen down immune response

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16
Q

How can binding of antibodies to antigens inactivate the antigens?

A

-Neutralisation (blocks viral binding sites& coats bacteria)
-Agglutination of microbes (clumping together)
-Precipitation of dissolved antigens
ALL ENHANCE PHAGOCYTOSIS
Activation of complement system (leads to cell lysis)

17
Q

How does cell lysis occur?

A

1) Cytotoxic T cell binds to infected cell
2) Perforin makes holes in infected cell’s membrane, enzymes enter
3) Infected cell destroyed

18
Q

Define immunosuppression and immunodeficiency

A

IS= Natural/artificial process which turns off the immune response
ID: A result of IS and the lack of an efficient immune system, susceptibility to infections

19
Q

When is immunosuppression seen?

A
  • Inhibit transplant rejection
  • Autoimmune diseases
  • Lymphoproliferative diseases
20
Q

Define hypersensitivity

A

Undesirable/damaging and sometimes fatal reactions produced by immune system in a pre-sensitized host.

21
Q

What types of hypersensitivity are there?

A

I) IgE Mediated
II) Cytotoxic reaction
III) Immune complex reaction
IV) Cell mediated reaction (DTH)

22
Q

Describe a form of type I hypersensitivity

A
  • Anaphylactic (severe reaction)
  • Mast cell & basophil degranulation
  • Release of preformed & de novo inflammatory mediators (histamine) & lipid mediators (leukotrienes)
  • Pollen, bee venom, animal dander, hayfever, allergic asthma
23
Q

What are the clinical features of anaphylaxis?

A
  • Fast onset
  • Weal & flare
  • Sometimes late 2nd phase
  • contraction of s.muscle
  • Dilatation of blood vessels
  • Mucous glands
24
Q

Describe immunoglobulin E

A
  • Produced by plasma cells from class-switched B cells
  • Under control of IL-4 & CD40L
  • Extremely low serum levels
  • High affinity receptor for IgE on mast cells & basophils
  • Stable binding over long periods
25
Q

What happens in the early phase response of a reaction?

A
  • Mast cell FCER1 presents at high density
  • cross-linking by allergen leads to activation of mast cells
  • degranulation & release of preformed mediators
  • synthesis of lipid mediators
26
Q

Name some preformed mediators

A
  • Histamine= s.muscle contraction, inc vascular permeability, stimulation of irritant nerve response
  • Kallikrein= activates bradykinin
  • Tryptase
27
Q

What are lipid mediators?

A
  • Arachidonic acid derivatives
  • Phospholipase A2 broken down to arachidonic acid
  • Finally forms leukotrienes
  • And Prostaglandins
28
Q

What happens in the late phase response of a reaction?

A
  • Basophils= similar properties to mast cells but over longer time scale
  • Eosinophils= Granules contain cytotoxic proteins, attracted to site of inflammation by chemokines, release contents of granules in tissue - major source of tissue damage in allergic response
  • T cell= in both early&late response, cytokine production by activated T cells needed for ongoing response
  • Cytokine-driven activity major source of pathogenesis in allergic reaction
29
Q

Name some examples of allergic diseases

A
  • Asthma
  • Rhinitis
  • Dermatitis
  • Food allergy
30
Q

Describe type II hypersensitivity

A
  • Antibody mediated cytotoxic
  • Binding of antibody to antigen causes activation of complement cascade=cell lysis
  • Aggregation of Fc portions of immunoglobulin binding to FcRs = opsonisation/phagocytosis/destruction
31
Q

What is type II hypersensitivity initiated by?

A
  • initiated by IgM (sometimes IgG)
  • IgM most efficient since pentavalent
  • IgG requires multiple binding
32
Q

What is effected in type II hypersensitivity?

A
  • Haematopoietic cells
  • Neutrophils
  • Platelets
  • Blood group incompatbility
  • Autoimmune haemolytic anaemias
33
Q

Describe type III hypersensitivity

A
  • IgG + Ag= AgAb complex
  • Complement activation leads to generation of activated complement fragments
  • C5a= attractant for neutrophils
  • C3b= opsonin
  • Attempted phagocytosis of complexes leads to release of enzymes& O2 radicals
  • Results in tissue damage
34
Q

Name some diseases from type III hypersensitivity, their route into the body and the site of immune complex deposition

A

-Vasculitis-Blood vessel walls
Nephritis- Renal glomeruli
Arthritis-joint space
ALL INTRAVENOUS ROUTE

Subcutaneous route- arthus reaction- perivascular area

Inhaled route- Farmer’s lung- alveolar/capillary interface

35
Q

Give some examples of other antibody-mediated immunopathology

A
  • Inactivation= DIRECT: Intrinsic factor in B12 deficiency
  • Inactivation= INDIRECT: binding to hormone results in clearance of AgAb complex
  • Receptor blockade= Myasthenia Gravis
36
Q

Describe type IV hypersensitivity

A
  • T cell mediated (CD4+/MHC class II)
  • Delayed (tuberculin skin reaction)
  • Age-specific T cell release cytokines- recruitment of macrophages
  • Activated macrophages cause tissue damage
  • Requires previous exposure to antigen
  • Hapten(allergen) presented to skin causes reaction in langerhan cells
37
Q

Give examples of other cell-mediated immunopathology

A
  • Tcell mediated cytotoxicity
  • CD8+/MHC class I
  • Contact dermatitis (combination of DTH& cytotoxic reaction)
  • Nickel/poison ivy can act as hapten with epidermal proteins
38
Q

What are granulomatous reactions?

A
  • Focal collections of inflammatory cells in tissue (macrophages, epithelioid cells, giant cells & lymphocytes)
  • Th1- type T cells secrete IL2& IFNy
  • _IL-12 release by macrophages critical in initial response
39
Q

Name some granulomatous diseases

A
  • Infections: mycobacterial= TB, atypical mycobacteria, Leprosy
  • unknown = Sarcoidosis, Wegener’s Granulomatosis, Crohn’s

Mechanism of Disease (18 decks)

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