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Immunology -- Jones > Final- Immunopathology > Flashcards

Final- Immunopathology Flashcards

1
Q

What organism causes Tuberculosis and how does one get it? How does the microbe avoid death?

A

Mycobacterium tuberculosis

  1. Microbes are inhaled and macrophages ingest them
  2. Microbes evade death by preventing the interaction of the phagosome and lysosome
  3. Microbes hide in macrophages and multiply
  4. Burst out of cell and induce inflammatory reaction
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2
Q

What is a systemic immune response caused by an infection?

A

Sepsis

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3
Q

What does Sepsis mean? How does this occur?

A

pathogens or toxins throughout the body

  1. Cells respond and produce large quantities of cytokines (TNF)
  2. increases blood vessel permeability and causes organ damage
  3. drop BP and results in SEPTIC SHOCK
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4
Q

What are some defects in general in the immune regulation that may result in disease?

A
  1. Allergies (Type I Hyper.)
  2. Overproduction of IgE–> responses to “harmless” allergens
  3. Atopic inds tend to push Th2 response–> to more IgE
  4. Hygiene hypothesis and genetics??
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5
Q

What the memory response to normal tissue and involves loss of tolerance?

A

Autoimmunity

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6
Q

What is a response to innocuous antigens causing harm?

A

Hypersensitivity

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7
Q

T/F. Autoimmune conditions are hypersensitive reactions and all hypersensitive reactions are autoimmune conditions.

A

False– yes, all autoimmune conditions are hypersensitive reactions–BUT NOT all hypersensitive reactions are autoimmune conditions

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8
Q

What is Autoimmunity caused by? What percentage of Americans suffer from a form of autoimmunity?

A

caused by failure of tolerance processes

5%

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9
Q

What may autoimmunity involve?

A 
May be organ specific or systemic
Could Involve:
- antibodies
- T cells
- immune complexes
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10
Q

What three things are needed for autoimmunity?

A
  1. MHC present self peptide
  2. T and B cells recognize self Ag
  3. Breakdown of self tolerance
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11
Q

What are some ways autoimmunity is induced?

A
  • infections and molecular mimicry
  • inflammation
  • damage/stress events that expose sequestered Ag
  • altered gut microbiota
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12
Q

Does intrinsic or extrinisc factors favor susceptibility to autoimmune disease?

A

BOTH

  • env. –> diff an geographic areas
  • Certain MHC genes linked to specific autoimmune disorders (HLA-B27 expression = 90x more likely to develop ankylosing spondylitis– inflam. disease of vert. joints)
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13
Q

What does Hashimoto’s Thyroiditis attack? What are produced in this disease?

A

thyroid(organ specific); autoantibodies and sensitized T-Helper 1 cells–> specific for thyroid Ag

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14
Q

What does the Ab produced in Hashimoto’s Thyroiditis interfere with? What type of response is induces in the thyroid? What will inflammation result in?

A

iodine uptake

DTH response in thyroid

goiter–> visible enlargement of thyroid gland

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15
Q

What does Type 1 Diabetes Mellitus attack? Specifically what cells? What cells are invading and what are they causing?

A

autoimmune attack against insulin-producing beta cells in pancreas (organ specific)

CTLs infiltrate pancreas and activate macrophages–> cytokine release follows–> then production of autoantibodies and DTH responses

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16
Q

What does Myasthenia gravis attack? What is being blocked? What is the result?

A

autoantibodies bind to ACh receptors on motor end plates of muscles (organ specific)

block normal binding of ACh–> induces complement-mediated lysis of cells

Results in: progressive weakening of skeletal muscles

17
Q

What does Systemic Lupus Erythematosus (SLE) attack? What type of hypersensitivity is this?

A

Auto-Ab against DNA, histones, other self structures (systemic)

Deposition of immune complexes activates complement (TYPE III)

18
Q

What individuals is SLE (lupus) MC in? What are some symptoms that occur?

A

MC in women (9:1 ratio)

Symptoms:

  • fever
  • weakness
  • arthritis
  • skin rashes
  • kidney dysfunction
19
Q

What does Multiple Sclerosis attack? Who is it MC in? What are common symptoms?

A

Autoreactive T cells form inflammatory lesions along myelin sheaths around nerve fibers in brain and spinal cord (systemic)

women (2-3x MC)

MC cause of neurologic disability in Western countries

numbness to paralysis and loss of vision

20
Q

What does Rheumatoid Arthritis attack? What hypersensitivity type is it? Who is it MC in? What is the major symptom?

A

attacks joints (systemic)–> due to Ab-Ag complexes (IgM and IgG) –Type III hyper.

MC in women

chronic inflammation

21
Q

What are some mechanisms to treat autoimmune disease?

A
  1. Broad-spectrum therapies
  2. strategies that target specific cell types
  3. Therapies that block steps in inflammatory process
  4. Strategies that interfere with co-stimulation
  5. Target auto-reactive cells
22
Q

What are the two basic types of Immunodeficiency?

A
  1. Congenital (Primary)– some form of inherited deficiency

2. Acquired (Secondary)- inf., drug Tx, malnutrition, disease, age, etc

23
Q

What are six examples of Congenital (Primary) Immunodeficiency?

A
  1. SCID (Severe Combined Immunodeficiency)
  2. MHC deficiencies
  3. Hyper IgM Syndrome (X-linked)
  4. X-linked Agammaglobulinemia (Bruton’s)
  5. Leukocyte Adhesion Deficiency (LAD)
  6. Complement Deficiencies
24
Q

What is lacking in SCID? What causes SCID? What does it result in? How is it Tx?

A

lack of T cells (and B cells in some cases)

Caused by defective cytokine signlaing, VDJ segment rearrangement

severe infections w/ life-threatening consequences

Tx: bone marrow transplats and in some cases gene therapy

25
Q

What can occur in MHC deficiencies? What is one with this susceptible to?

A

MHC 1 expression
- missing TAP gene
- Lack of CD8 cells
(lose killer T cell system)

  • Susceptible to virus
26
Q

How is Hyper IgM Syndrome inherited? What to Th cells lack?

A

X-linked

Th cells lack CD40L

27
Q

What will Hyper IgM Syndrome result in? What is lacking and what is active?

A

Th cells lack CD40L

    • so T cells don’t activate APC’s and B cells
  • T-dependent Ag response LACKING
  • T-independent Ag response ACTIVE

OVER production of IgM, lack of other isotypes–> do NOT class switch

28
Q

What is occurring in X-Linked Agammaglobulinemia (Bruton’s)? What is one susceptible to getting?

A
  • Low levels of IgG, lack other isotypes
  • Lacking intracellular signaling molecule (Btk, tyrosine kinase)
  • B cells don’t mature and don’t produce BCRs

bacterial infections–> Tx w/ antibiotics and passive antibodies

29
Q

What is defective in Leukocyte Adhesion Deficiency (LAD)? What is therefore inhibited?
What type of infections are common?

A

defect in integrin adhesion molecules

therefore WBC recruitment is inhibited

bacterial and fungal infs are common

30
Q

What will a Complement Deficiency result in?

A

depends on which component is lacking on what pathway it effects (Classical, Lectin, or Alternative)

Ex: if miss C3 -> mess up all 3

31
Q

What are Acquired (secondary) immunodeficiencies caused by?

A
  • infection (our focus)
  • drug Tx
  • malnutrition
  • disease
  • age
32
Q

What is a classic example of an Acquired (secondary) immunodeficiency?

A

HIV/AIDS

33
Q

What are the three phases of an HIV infection?

A
  1. Acute phase
  2. Asymptomatic phase
  3. AIDS
34
Q

What is the criteria for one to be considered to have AIDS?

A
  • evidence of infection with HIV-1
  • less than 200 CD4+ T cells/ per micro-liter of blood
  • occurrence of opportunistic infections
35
Q

What are some Therapeutic agents to help Tx AIDS?

A
  • block recptors
  • block fusion
  • block RT
  • block inegrase
  • block protease
36
Q

What does HIV contain on and what type of receptors does it target in our body?

A

HIV has gp120 and gp41 on surface of it

goes through CD4 receptors–> therefore “helper T cells” are sensitive to HIV infections

Immunology -- Jones (14 decks)

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