Immunopathology of Infectious Diseases Continued Flashcards

1
Q

What are some defects caused by pathogenic mechanisms?

A

Induction by physical means
Granulocyte and monocyte defects in movement, phagocytosis or killing or decreased number of cells (neutropenia)
Individual components of complement system
T cells (Di Georges Syndrome)
B cells (Brutons syndrome)
Combined Immunodeficiency (T and B cell ) pathogen

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2
Q

Immune Deficiency: Congenital and Acquired include what general categories?

A

Hereditary complement deficiencies
Defective phagocytes
Immune suppression

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3
Q

Consequences of hereditary complement deficiencies include deficiencies of what enzymes?

A

C1q, C1r, C1s, C4 and C2 are associated with defects in activation of the classic complement pathway
(defects lead to greater susceptibility to pyogenic staphylococcal and strep infections)

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4
Q

A deficiency in C3 in the complement pathway leads to what?

A

leads to defect in activation of both the classic and the alternative pathways, which also results in a higher incidence of pyogenic infections

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5
Q

A deficiency of the properdin factors of the complement pathway leads to what?

A

Impair activation of the alternative pathway predisposes to pyogenic infections

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6
Q

Deficiencies of C5 through C9 are associated with what?

A

with defective cell killing with increased susceptibility to disseminated neisserial infections

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7
Q

Consequences of deficiencies in the complement pathways. Factor B binds to C3b on cell surfaces and what happens?

A

Plasma serine protease D cleaves and activates B-C3b as part of the alternative pathway

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8
Q

What factors limit the inappropriate activation of complement?

A

Factors FI and FH
FH bins to C3b and prevents activation and is a cofactor for FI
FI is a serine protease that cleaves C3b and C4b.

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9
Q

What are some features of hereditary angioneurotic edema?

A

Genetic form of Angioedema, also called Qunike’s disease
Persons with it are born lacking C1 esterase inhibitor
Non-pitting edema

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10
Q

What is autoimmunity?

A

persons are tolerized to self antigens which prevents autoimmune disease

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11
Q

Deregulation of the immune response may be initiated by cross reactivity with what?

A

microbial antigens

ex: group A step or rheumatic factor

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12
Q

Polyclonal activation of lymphocytes induced by what?

A

tumors or infection

Ex: malaria, epstein barr virus infection

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13
Q

Autoimmune reactions result from the presence of what?

A

autoantibodies, activated T cells, and hypersensitivity reactions

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14
Q

Individuals with certain MHC antigens are at a higher risk for what?

A

autoimmune responses
ex: human leukocyte antigen, juvenile RA, ankylosing spondylitis
responses are associated with inflammatory TH1 type responses

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15
Q

Multiple sclerosis, an inflammatory response directed against myelin basic protein, may be triggers by what?

A

immune responses to one or more viruses, such as human herpesvirus 6 or measles

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16
Q

Systemic Lupus Erythematosus (SLE) is a chronic inflammatory autoimmune disorder may affect what?

A

organ systems
skin
joints and
internal organs

17
Q

SLE may be mild or severe and life threatening, for most only a mild disease. What two categories of people are affected more then others?

A

African Americans and Asians

18
Q

90% of individuals have discoid rash rather then ?

A

generalized SLE

19
Q

Pediatric autoimmune neuropsychiatric disorders (PANDA) is associated with streptococcal infections. What are some examples of these disorders?

A

Describes children who have obessive compulsive disorder and/or tic disordres such as Tourette’s Syndrome
symptoms worsen following strep or scarlet fever

20
Q

What is the mechanism for PANDA?

A

It is thought to be similar to that of rheumatic fevers know as syndenhams chorea or st.vitus dance

21
Q

Immunosuppression therapy is important for reducing excessive inflammatory or immune responses of macrophages and T cells or for preventing the rejection of tissue transplants by T cells. Each card will go through the different immunosuppression treatments. 1. Anti-inflammatory treatments

A

Primarily target the production and action of TNF, IL-12 and IL-1

22
Q

2nd immunosuppression therapy is Corticosteriods

A

Prevents their production by macrophages and may be toxic to T cells. Soluble forms of the TNF receptor and antibody to TNF can be used to block the binding of TNF and prevent its action

23
Q

3rd is immunosuppression therapy for transplantation

A

generally inhibits the action or causes the lysis of T cells.

24
Q

4th immunosuppression therapy is cyclosporin

A

tacrolimus and rapamycin prevent the activation of T cells. Anti-CD3 and antiCD25 prevent action of T cells to prevent a response

25
Q

5th immnuosuppression therapy is antibody administation

A

to costimulatory molecules such as B7 or CD40 ligand at the time of transplant can block proper T-cell activation and promote anergy rather then responsiveness

26
Q

Exotoxins are what?

A

Proteins that can produced by gram positive or gram negative bacteria and include cytolytic enzymes and receptor-binding proteins that alter a function or kill the cell

27
Q

What are superantigens?

A

A special group of toxins that activate t cells by binding simultaneously to a t cell receptor and a major histocompatibility complex class II (MHCII) molecule on another cell without requiring antigen

28
Q

Nonspecific means of activating T cells can trigger life threatening what?

A

Autoimmune like responses by stimulating the release of large amounts of interleukins, such as IL-1 and IL2

29
Q

Superantigen stimulation of T cells can also lead to death of what?

A

the activated T cells causing the loss of specific T cell clones and their immune responses

30
Q

Superantigens include what?

A
  • -toxic shock syndrome of S. aureus
  • -staphylococcal enterotoxins
  • -erythrogenic toxin A or C of S. pyogenes