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Microbiology > CH 18 - Immunological Disorders > Flashcards

CH 18 - Immunological Disorders Flashcards

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Biology 101 flashcards
1
Q

Allergy
(definition)

A

A damaging immune response to a typically harmless environmental antigen (allergen)

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2
Q

Autoimmune Disease
(definition)

A

Damaging reaction of the immune system against “self” antigens

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3
Q

Delayed-type hypersensitivity
(definition)

A

Exaggerated immune response of antigen-specific T cells

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4
Q

Desensitization
(definition)

A

Allergy treatment that induces IgG production by gradual exposure to small amounts of allergen

IgG competes with IgE

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5
Q

Hypersensitivity
(definition)

A

Exaggerated immune response that damages tissue

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6
Q

Immune complex
(definition)

A

Combination of antibody & soluble antigen capable of triggering the classical pathway of complement system activation

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7
Q

Immunodeficiency
(definition)

A

Condition in which the immune system does not provide an adequate response, leaving a person vulnerable to infection

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8
Q

Systemic anaphylaxis
(definition)

A

Potentially life-threatening immediate hypersensitivity reaction caused by IgE attached to circulating basophils

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9
Q

Hypersensitivities:
Categorization

A

Categorized according to which parts of the immune system are involved & how quickly response occurs

Type I - Imediate IgE-mediated
Type II - Cytotoxic
Type III - Immune complex-mediated
Type IV - Delayed cell-mediated

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10
Q

Type I Hyper Sensitivities

A

Immediate IgE-mediated
- Allergic reactions

Driven by B cells
- IgE Abs bind to mast cells & basophils
- Ag binds to cells fixed with IgE Ab
(cross-linking of IgE)
- Degranulation (initiates immune reaction)

Immediate reaction
- Within mins of exposure

Hives, hay fever, anaphylaxis

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11
Q

Type II Hypersensitivities

A

Cytotoxic
- Tissue incompatibility

Driven by B cells

Complement-fixing Abs react with cell surface Ags
- Cause cell injury/death

Cells destroyed through complement fixation & Ab-dependent cellular cytotoxicity (ADCC)

Transfusion rxns (complement fixation)
Hemolytic disease of newborn (ADCC)

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12
Q

Transfusion Reactions

A

Transfused antigenically different blood can be lysed by recipient immune cells
- IgM Abs

Type A = alpha-B Abs
Type B = alpha-A Abs
Type O = alpha-B & alpha-A Abs
Type AB = neither

Symptoms:
- Low BP
- Pain
- Nausea
- Vom

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13
Q

Hemolytic Disease of Newborn

A

Incompatibility of Rh factor between mother & child
- Rh = RBC surface antigen (present if +)

Anti-Rh Abs form in Rh- mother upon delivery of Rh+ infant (mixing blood)
- 1st Rh+ fetus unharmed
- 2nd Rh+ fetus provokes strong secondary immune response

IgG Abs cross placenta & cause extensive damage to fetal RBCs

Prevention = administration of anti-Rh Abs to mother within 72 hrs of birth
- Blocks sensitization phase
- Rhogam

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14
Q

Type III Hypersensitivities

A

Immune complex-mediated
- Immune complexes = Ag & Ab bound

Form when excess of Ag & Ab in tissue (series of vaccines, horse serum)
- Usually adhere to Fc receptors on cells (removed & destroyed)

Persist in circulation or in sites of formation
- Initiate blood clotting mechanism
- Activate complement (inflammation)

Complexes often deposited in:
- Skin
- Joints
- kidney

Disseminated intravascular coagulation (DIC)
- Clots in small vessels (leaky blood vessels)
- Leads to system failure (dramatic BP drop)

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15
Q

Serum Sickness

A

Type III hypersensitivity

Immune complex disease caused by passive immunization
- Ab-containing serum from animal injected in humans (treat/prevent disease)

Symptoms manifest within days/weeks following exposure to foreign serum Ags
- Fever
- Weakness
- Generalized vasculitis (redness) with edema
- Inflammation of blood vessels
- Arthritis
- Glomerulonephritis (sometimes)

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16
Q

Type IV Hypersensitivities

A

Delayed cell-mediated
- Slowly developing response to Ag
- Reaction peaks 2-3 days (after Ag exposure)

Driven by T cells
- Caused by cell-mediated immunity
- Extensive host cell destruction & progressive loss of tissue function (in chronic infections)

Reactions can occur anywhere in body
- Contact dermititis
- Tissue damage
- Rejection of tissue grafts
- Some autoimmune diseases

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17
Q

Tuberculin Skin Test

A

Type IV hypersensitivity

Introduction of small quantities of protein Ags from tubercle bacillus into skin

+ test = site reddens & gradually thickens (peaks 2-3 days, return after 72 hrs)

T cells release cytokines
- Initiate inflammation that attracts macrophages
- Macrophages release mediators to add to inflammation

Granuloma (tubercle) containing live bacteria forms when macrophage fails to kill
- Result of prolonged DTH response

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18
Q

Contact dermatitis

A

Type IV hypersensitivity

Small molecules complex with skin proteins
- Internalized by APCs in skin (Langerhans cells), processed, & presented with MHC II
- Causes activation of sensitized Th1 cells

Rash takes few days to develop (T cells must migrate to site)

Ex: poison oak, poison ivy, nickel, cosmetics, hair dyes

19
Q

Autoimmune Diseases

A

Body usually recognizes self Ags
- Destroys cells that would destroy self
- Malfunction of immune recognition leads to autoimmunity

May result from reactions to Ags similar to MHC self Ags

May occur after tissue injury
- Self Ags released from injured organ
- AutoAbs form & interact with injured tissue

20
Q

Spectrum of Autoimmune Diseases

A

Organ-specific
- Thyroid disease (only affects thyroid)

Widespread response
- Lupus
- Rheumatoid arthritis
- Myasthenia gravis

21
Q

Lupus

A

AutoAbs made against nuclear constituents of all body cells

22
Q

Rheumatoid arthritis

A

Immune response made against collagen (in joints) & CT

Usually occurs in older people (immune system doesn’t function as well)

23
Q

Myasthenia gravis

A

AutoAb-mediated disease

AutoAb to ACh receptor proteins
- Act at NMJ
- Can lead to paralysis

24
Q

Immunodeficiency Disorders

A

Body’s inability to make & sustain adequate immune response

2 basic types:
1. Primary/congenital
2. Secondary/acquired

25
Q

Primary Immunodeficiencies

A

Inborn
- Genetic defect or developmental abnormality
- Generally rare

  1. Agammaglobulinemia
  2. Severe combined immunodeficiency disorder (SCID)
  3. Selective IgA deficiency
26
Q

Agammaglobulinemia

A

Few/no Abs produced

Occurs in 1 in 50,000 people

27
Q

Severe combined immunodeficiency disorder (SCID)

A

Neither B nor T cells functional
- Adaptive immune system

Occurs in 1 in 500,000 live births

28
Q

Selective IgA deficiency

A

Little/no IgA produced

Most common disorder
- 1 in 333-700 people

People with this condition notice that they get sick more often
(GI & lung illnesses - where IgA normally protects)

29
Q

Secondary Immunodeficiencies

A

Result of infection or other stressor
- Environment rather than genetics
- Malignancies, advanced age, infections, immunosuppressive drugs, malnutrition

Depletion of certain cells of immune system
- Syphilis, leprosy, & malaria
- Malignancies of lymphoid system
- AIDS

30
Q

Syphilis, Leprosy, & Malaria
(Secondary Immunodeficiency)

A

Affect T cell population & macrophage function

31
Q

Malignancies of Lymphoid System
(Secondary Immunodeficiency)

A

Decrease Ab-mediated immunity

32
Q

AIDS
(Secondary Immunodeficiency)

A

Destroys helper T cells

Inhibits initiation of cellular & Ab-mediated immunity

33
Q

Naturally Acquired Immunity

A

Acquisition of adaptive immunity through natural events

Passive or active

34
Q

Artificially Acquired Immunity

A

Mimicking natural events through immunization

Passive or active

35
Q

Active Immunity

A

Results from immune response upon exposure to Ag

Develops naturally following illness
Develops artificially after immunization

36
Q

Passive Immunity

A

Artificial passive immunity
- Transfer of Abs produced by another person/animal
- Prevents disease before/after likely exposure

Natural passive immunity
- During pregnancy mother’s IgG crosses placenta to infer protection to baby
- During breastfeeding mother’s IgA given to child

37
Q

Attenuated Vaccines

A

Weakened form of pathogen
- Generally unable to cause disease

Strain replicates in recipient
- Causes infection with mild/undetectable symptoms
- Results in long-lasting immunity

Most common form of flu vaccine

38
Q

Attenuated Vaccines:
Advantages

A
  1. Single dose usually sufficient to induce long-lasting immunity
    - Microbe multiplies in body
    - T cell activation
    - Continued stimulation of immune system
  2. Vaccine has potential for being spread
    - “Disease” could be spread to un-immunized inadvertently
39
Q

Attenuated Vaccines:
Disadvantages

A
  1. Potential to cause disease in immunocompromised
  2. Pregnant women should avoid
40
Q

Attenuated Vaccines Currently in Use

A
  1. Sabin polio vaccine
  2. MMR
  3. Yellow fever
41
Q

Inactivated Vaccines

A

Unable to replicate in vaccinated individual (not alive)

Retains immunogenicity of infectious agent
- Immunogenic NOT pathogenic

2 categories:
1. Whole agents
2. Fragments

42
Q

Inactivated Vaccines:
Whole Agents

A

Contain killed organisms of inactivated microbe

Does NOT change epitopes

Ex: Influenza & Salk polio

43
Q

Inactivated Vaccines:
Fragments

A

Portions of organisms or agents
- Toxins
- Proteins
- Cell wall components

Ex: toxoids, protein subunit vaccines, polysaccharide (capsule) vaccines, diphtheria vaccine

(kind of COVID vaccine)

Microbiology (15 decks)

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