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Disease Mechanisms > Ch 6: Diseases of the Immune System > Flashcards

Ch 6: Diseases of the Immune System Flashcards

1
Q

what are the three main things that make up the immune system

A

epithelial barriers, leukocytes, and proteins

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2
Q

what is innate, natural, or native immunity

A

portion of the immune system that is present at birth
responds to all pathogens in the same way
dominant response for the first 12 hours of exposure
include first and second line of defense

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3
Q

what is adaptive, specific, or acquired immunity

A

respond individually to unique glycoprotein markers (antigens Ag)
takes 3-5 days for the response to kick in then it becomes that dominant response
include third line of defense

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4
Q

explain the first line of defense

A

surface barriers block entry of pathogens into the body
includes epithelial cells and secretory molecules
epithelial cells: skin and mucous membranes that line all open passageways into the body
secretory molecules: peptides like lysozymes, defensins, collectins, and lactoferrin
defense is constant, broadly specific, and has no memory

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5
Q

explain the second line of defense

A

inflammatory response against tissue injury and infection
defense is immediate, nonspecific, and has no memory
cells and proteins involved are always in the bloodstream
cells: mast cells, granulocytes, NK cells, platelets, and endothelial cells
proteins: complement system, clotting factors, kinins, and cytokines

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6
Q

explain the third line of defense

A

initiated when the immune system signals cells of adaptive immunity
cells: T and B lymphocytes, macrophages, and dendritic cells
proteins: antibodies, complement, and cytokines
delayed first response but immediate second response
specific response with memory by B and T lymphocytes and antibodies

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7
Q

what is the cell-mediated immunity (cellular) portion of the adaptive immune system

A

defense against intracellular microbes, foreign cells from transplanted organs, and cancer cells
brought about by: helpter T lymphocytes (CD4), cytotoxic killer T lymphocytes (CTL or CD8), and regulatory T lymphocytes (Treg)

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8
Q

what do the helper T lymphocytes of the adaptive immune system do

A

stimulate B lymphocytes to destroy microbes
and make antibodies (immunoglobulins)

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9
Q

what do cytotoxic killer T lymphocytes do in the adaptive immune system

A

kill infected cells

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10
Q

what do regulatory T lymphocytes in the adaptive immune system do

A

limit immune responses
prevent reactions again self antigens

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11
Q

what is the antibody-mediated immunity (humoral) portion of the adaptive immune systen

A

carried out by B cells from bone marrow and their antibody proteins
protect against extracellular microbes and their toxins

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12
Q

explain how T cells are made and differentiated

A

lymphoid stem cells divide in the bone marrow
immature T cells leave the bone marrow then go to the thymus to mature and make clones
mature naive cells go to lymphoid organs

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13
Q

what does the thymus screen for

A

immunocompetent cells: destroys clones that cannot recognize antigens
self tolerance: destroys clones that recognize your own cells as foreign

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14
Q

what is immunocompetent

A

ability to mount a normal response to a foreign antigen

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15
Q

how does activating a tell cell work

A

each T cell has a T cell receptor complex embedded in its plasma membrane thats made of signal 1 and 2
signal 1 binds to MHC complexes on antigen presenting cell
singal 2 binds to an additional signal on antigen presenting cell
T cell is now activated once both signals are bound

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16
Q

what are MHC complexes made of

A

MHC 1 or 2 molecule with a peptide antigen

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17
Q

what is a major histocompatibility complex molecule

A

cell surface glycoprotein
found on all nucleated cells except erythrocytes
serve as docking sites for specific components of antigens
class 1 and 2 MHC molecules

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18
Q

what are class 1 MHC molecules

A

found on surface of plasma membrane on nearly all nucleated cells
present endogenous antigens such as bacteria, cancer cells, or viruses

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19
Q

which MHC class do cytotoxic T cells interact with

A

class 1 MHC molecules
kills diseased cell

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20
Q

what are class 2 MHC molecules

A

found only on surfaces of antigen-presenting cells (APC)
present exogenous antigens

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21
Q

which cells are antigen presenting cells

A

macrophages, dendritic, and B cells

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22
Q

which class of MHC molecule do helper T cells interact with and what do they do

A

class 2 MHC molecules
stimulate other parts of the innate and adaptive defenses to combat threat

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23
Q

what are the three things that a naive CD4 T cell can differentiate into

A

Th1, Th2, and Th17

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24
Q

what does a Th1 T cell do

A

activate macrophages

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25
Q

what does a Th2 T cell do

A

stimulate IgE production
activate mast cells and eosinophils

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26
Q

what do Th17 T cells do

A

recruit neutrophils and monocytes

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27
Q

how are B cells formed

A

lymphoid stem cells divide in the bone marrow
B cells mature in the bone marrow
mature naive B cells exit bone marrow and live in lymphoid organs
B cells not exposed to their specific antigen within a few days or weeks die

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28
Q

why do only 10% of B cells finish their maturation process

A

prevents development of autoimmunity (body attacking itself)

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29
Q

explain how naive B cells are activated

A

antigen binds to receptor on B cell and becomes activated
now sensitized B cell processes antigen and presents it on its class 2 MHC molecules
B cell binds to a Th cell which secretes cytokines to activate B cell
B cell divides repeatedly into cells that can differentiate into plasma or memory B cells
plasma cells secrete antibodies

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30
Q

what is a clone

A

a group of B cells that binds to a specific antigen

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31
Q

what are proteins secreted by B cells called

A

antibodies

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32
Q

explain the structure of an antibody

A

Y-shaped molecule formed from four peptide chains (2 heavy (H) and two light (L) chains)
each heavy and light chain has a constant (C) and variable (V) region
antigen-binding site on V region

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33
Q

what does the constant (C) region on an antibody do

A

responsible for many of antibody’s affects

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34
Q

what does the variable (V) region of an antibody do

A

responsible for antigen recognition and binding

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35
Q

what are the three shape types of antibodies

A

monomer (1 antibody)
dimer (2 antibodies)
pentamer (5 antibodies)

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36
Q

what are the 5 classes of antibodies

A

IgG, IgA, IgM, IgE, and IgD

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37
Q

which type of shape of antibody is IgM

A

pentamer

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38
Q

which type of shape of antibody is IgA

A

dimer

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39
Q

which classes of antibodies are monomers

A

IgG, IgE, and IgD

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40
Q

what is the agglutination/precipitation action of antibodies

A

antibodies clump together to enhance phagocytosis

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41
Q

what is the opsonization action of antibodies

A

IgG coats antigens and binds phagocytes, enhancing phagocytosis

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42
Q

what is the neutralization action of antibodies

A

antibodies bind pathogenic components of toxins and block toxin effects

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43
Q

what is the complement activation action of antibodies

A

antibodies activate complement proteins, leading to cell lysis

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44
Q

what is the stimulation of inflammation action of antibodies

A

IgE binds mast cells and basophils and triggers release of inflammatory mediators

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45
Q

what do B cell receptor (BCR) complexes do

A

found on the surface of every naive B cell
must first bind to antigen then another signal

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46
Q

what is the first signal of B cell receptor complex

A

antigen binds to transmembrane protein and IgD or IgM

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47
Q

what is the second signal of the B cell receptor complex

A

complement protein and antigen bind to transmembrane protein

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48
Q

what do B lymphocytes do

A

neutralize microbes, phagocytosis, and complement activation

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49
Q

what do regulatory T lymphocytes do

A

limit immune response to prevent the reactions against self antigens

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50
Q

what is hypersensitivity

A

excessive or harmful reaction to an antigen that results in disease or damage to the host
results from failure of normal regulation

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51
Q

what are the four types of hypersensitivity

A

type 1: immediate (IgE-mediated)
type 2: antibody-mediated (tissue-specific)
type 3: immune complex-mediated
type 4: cell-mediated (delayed-type)

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52
Q

what is type 2 hypersensitivity

A

IgG and IgM antibody production
antigen binds and causes lysis of cell and leukocyte recruitment
ex. autoimmune anemia

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53
Q

what is type 3 hypersensitivity

A

antigen-antibody complexes are deposited
recruitment of leukocytes
release of enzymes
ex. lupus

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54
Q

what is type 4 hypersensitivity

A

activated T lymphocytes cause macrophage activation
ex. MS and tuberculosis

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55
Q

what is immediate type 1 hypersensitivity

A

rapid reaction to a previously exposed antigen binding to IgE on mast cell surface
immediate reaction: vasodilation and smooth muscle spasm
late phase: eosinophils, neutrophils, basophils, monocytes, and T cell - tissue damage
ex. allergies

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56
Q

what are three examples of preformed mediators in granules

A

vasoactive amines (histamine)
enzymes (proteases and hydrolases)
proteoglycans (heparin)

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57
Q

what are three examples of lipid mediators

A

leukotrienes
prostaglandin D2
platelet-activating factor (PAF)

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58
Q

what are three examples of cytokines

A

TNF, IL-1, and chemokines

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59
Q

what are 5 examples of a local allergic reaction

A

bronchial asthma
allergic rhinitis (nasal congestion)
urticaria (hives)
food allergies
atopic dermatisis (eczema)

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60
Q

what is an example of a systemic reaction

A

anaphylaxis from drugs, bee stings, or food

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61
Q

what are the common allergens and response of systemic anaphylaxis

A

allergens: drugs, serum, venoms, peanuts
response: edema, increased vascular permability, tracheal occlusion, circulatory collapse, death

62
Q

what are the common allergens and response of acute urticaria

A

allergens: insect bites and allergy testing
response: local increase in blood flow and vascular permability

63
Q

what are the common allergens and response of allergic rhinitis

A

allergens: pollen and dust-mite feces
response: edema and irritation of nasal mucosa

64
Q

what are the common allergens and response of asthma

A

allergers: cat dander, pollen, dust-mite feces
response: bronchial constriction, increased mucous production, airway inflammation

65
Q

what are the common allergens and response of food allergies

A

allergens: tree nuts, peanuts, shellfish, milk, eggs, and fish
response: vomiting, diarrhea, pruritis (itching), urticaria, and anaphylaxis

66
Q

explain anaphylactic shock

A

hypersensitivity reaction involving 2 or more body systems
systemic release of histamine that cause spasm of respiratory tract, vasodilation causing vascular shock, and increased capillary permeability causing edema
causes: heterologous proteins, hormones, enzymes, polysaccharides, drugs, food allergens, and insect toxins

67
Q

what are 6 treatments for type 1 hypersensitivity reactions

A

epinephrine (anaphylaxis shock)
bronchodilators (beta agonists and albuterol)
steroids (methylprednisolone)
antihistamines (H1 antagonists
avoidance
immunotherapy (desensitization)

68
Q

what is antibody-mediated (type 2) hypersensitivity

A

IgG or IgM antibodies react with antigens and cause disease
three types: opsonization and phagocytosis, inflammation, and cellular dysfunction

69
Q

explain how opsonization and phagocytosis of antibody-mediated (type 2) injury works

A

opsonized cells binds to a phagocyte
phagocyte engulfs cell
ex. transfusion reactions, hemolytic disease of fetus, AIHA, and certain drug reactions

70
Q

explain how complement and Fc receptor-mediated inflammation of antibody-mediated (type 2) injury works

A

deposited antibodies cause activation of leukocytes with Fc receptors
activation of leukocytes causes release of its substances like lysosomal enzymes which causes inflammation
ex. Goodpasture syndrome

71
Q

explain how antibody-mediated (type 2) cellular disfunction works

A

antibodies impair normal function of cell surface receptors but don’t cause cell damage
ex. Myasthenia gravis and Grave’s disease

72
Q

what is hemolytic disease of the fetus and newborn (erythroblastosis fetalis)

A

when a Rh-negative mother has a Rh-positive fetus
during childbirth, Rh-positive fetus cells can enter material bloodstream, making the female form antibodies again Rh-positive cells (sensitization)
if she has another Rh-positive baby, these antibodies will attack the fetus’s red blood cells

73
Q

what is Goodpasture syndrome

A

a type of type 2 hypersensitivity
complement and Fc receptor mediated inflammation
autoantibody attacks noncollagenous protein in basement membranes of kidney glomeruli and lung alveoli
presents with: glomerulonephritis and necrotizing hemorrhagic interstitial pneumonitis

74
Q

what is myasthenia gravis

A

type of type 2 hypersensitivity
antibodies block acetylcholine receptors at neuromuscular synapse which prevents muscle activation through antibody mediated cellular dysfunction
presents with: muscle weakness, especially ocular muscles, thymus hyperplasia, and thymoma
treated with: immunosuppressive drugs and plasmapheresis

75
Q

what is Graves’ Disease (hyperthyroidism)

A

type of type 2 hypersensitivity
antibodies stimulate TSH receptors leading to over expression and production of thyroxine (T4) and triiodothyronine (T3) through antibody-mediated cellular dysfunction
most common in women 20-40 yrs
presents with: goiter, ophthalmopathy, and weight loss

76
Q

what is autoimmune hemolytic anemia (AIHA)

A

a type of type 2 hypersensitivity
antibodies attack red cell membrane proteins by opsonization and phagocytosis of red blood cells
presents with: hemolysis and anemia

77
Q

what is immune complex-mediated (type 3) hypersensitivity

A

antigen-antibody complexes (IgG) or immune complexes not cleared by phagocytes produce tissue damage mainly by eliciting inflammation at sites of deposition
typically deposit in capillary beds in kidneys (glomerulonephritis), small blood vessels (vasculitis), and synovial membranes of joints (arthritis)
deposition triggers activation of compliment system, inflammation, then tissue damage
antigens can be exogenous or endogenous

78
Q

what type of hypersensitivity reaction is post streptococcal glomerulonephritis and what does it present with

A

local type 3 (immune complex-mediated)
presents with nephritis

78
Q

what type of hypersensitivity reaction is systemic lupus and what does it present with

A

type 3 (immune complex-mediated)
presents with: nephritis, skin lesions, and arthritis

79
Q

what type of hypersensitivity reaction is polyarteritis nodosa and what does it present with

A

systemic type 3 (immune complex-mediated)
presents with systemic vasculitis

80
Q

what type of hypersensitivity reaction is reactive arthritis and what does it present with

A

systemic type 3 (immune complex-mediated)
presents with acute arthritis

81
Q

what type of hypersensitivity reaction is serum sickness and what does it present with

A

systemic type 3 (immune complex-mediated)
presents with arthritis, vasculitis, and nephritis

82
Q

what type of hypersensitivity reaction is Arthus reaction (experimental) and what does it present with

A

local type 3 (immune complex-mediated)
presents with cutaneous vasculitis

83
Q

what is serum sickness

A

a type of systemic immune complex disease (type 3)
reaction due to foreign proteins
serum is injected and immune complex forms
once formed, it deposits in vessels, kidneys, and synovial joints leading to inflammation, fever, joint pain (arthralgia), lymph node enlargement, proteinuria, and urticaria
reaction occurs one week after injection

84
Q

what is Arthus Reaction

A

a type of local immune complex disease (type 3)
injected antigens and preformed antibodies react and lead to fibrinoid necrosis of vessel
leads to a localized area of skin tissue necrosis

85
Q

what is cell mediated (type 4) hypersensitivity

A

aka delayed-type hypersensitivity (DTH)
inflammation resulting from cytokines produced by antigen activated CD4+ helper T cells
two types: delayed hypersensitivity and T-cell mediated cytotoxicity

86
Q

what is the delayed-type (type 4) hypersensitivity

A

antigen is administered to someone who has already encountered antigen (immune)
cutaneous reactions takes 1-2 days
helper T cells recognize antigens and bind to MHC molecules as foreign
cells are destroyed by macrophages and neutrophils
ex. TB reaction, contact dermatitis, IBD

87
Q

what is the T-cell mediated cytotoxicity (type 4) hypersensitivity

A

antigen is presented by antigen presenting cells
cytotoxic T cell kills the APC and therefore antigen by releasing mediators which induce apoptosis
cytokines are produced as a result which causes an inflammatory reaction
ex. type 1 diabetes and viral hepatitis

88
Q

what is contact dermatitis

A

delayed-type hypersensitivity reaction
allergen such as poison ivy, metals, or other chemicals form complexes with skin proteins
APC displays allergen which activates helper T cells
macrophages and neutrophils destroy cells which causes inflammation and a itchy rash
reaction only happens on any contacts after the first

89
Q

what is type 1 diabetes mellitus

A

a type of type 4 hypersensitivity
destruction of pancreatic beta cells by cytotoxic T cells
leads to insufficient insulin production
usually develops before 15 yrs
treated with insulin injections

90
Q

autoimmune diseases affect what percentage of the U.S. population

A

5-10%

91
Q

what is an autoimmune disease

A

immune reaction against self antigens caused by adaptive immunity
immune system recognizes self antigens as foreign and attacks them

92
Q

what are the two main types of autoimmune disorders

A

organ specific vs systemic

93
Q

what is central tolerance

A

immature B and T lymphocyte clones recognize self antigens and either kill them or render them harmless

94
Q

what is peripheral tolerance

A

silencing of potentially auto reactive T and B cells in peripheral tissues

95
Q

what are the two factors that lead to failure of self-tolerance and development of autoimmunity

A

inheritance of susceptibility genes which leads to a failure of self-tolerance
environmental triggers like infections promote activation of self-reactive lymphocytes

96
Q

what is molecular mimicry

A

a mechanism of autoimmune reactions
microbes express antigens that share amino acid sequences with self antigens
immune response against these microbes can activate self-reactive lymphocytes

97
Q

explain what happens when an infection upregulates the expression of costimulators on APCs

A

a mechanism of autoimmune reactions
APC presents self antigen which activates APC
activated APC expresses costimulatory molecules which leads to activation of self-reactive T cells

98
Q

what is exposure of sequestered antigens

A

a mechanism of autoimmune reactions
sustentacular cells (nurse cells or Sertoli cells) surround spermatogenic cells to provide support
form blood-testis barrier which prevents immune system cells in bloodstream from detecting newly formed antigens on sperm cells

99
Q

what is systemic lupus erythematous (SLE)

A

multi systemic disease of autoimmune origin, typically due to type 3 hypersensitivity
causes injury to skin, joints, kidney, and serosal membrane
produces antinuclear antibodies (ANA)
diagnosed by looking for antibodies agains DNA and Smith antigen
presents with: arthritis, molar and discoid rash, vasculitis, renal disorders, photosensitivity, etc.

100
Q

what is Sjogren Syndrome

A

chronic autoimmune disease causes destruction of the lacrimal and parotid glands
least to keratoconjunctivitis (dry eyes) and xerostomia (dry mouth)
two most important antinuclear antibodies are SS-A (Ro) and SS-B (La)

101
Q

what is systemic sclerosis (scleroderma)

A

chronic inflammation resulting from autoimmunity
leads to widespread damage of small blood vessels and progressive interstitial and perivascular fibrosis in skin and multiple organs
usually leads to death from renal failure, cardiac failure, pulmonary in sufficiency, or intestinal malabsorption
presents with: skin fibrosis, Raynauds, dysphagia, trouble breathing, proteinuria, etc.

102
Q

what are the 5 main treatments of autoimmune diseases

A

1.) NSAIDS
2.) immunosuppressive drugs
3.) Thymectomy
4.) plasmapheresis
5.) surgery

103
Q

what are the three immunosuppressive drugs used to treat autoimmune diseases

A

corticosteroids, disease modifying anti-rheumatic drugs (DMARD), and cyclosporin A

104
Q

what are corticosteroids

A

drugs used to treat autoimmune disorders by inducing a transient lymphoctopenia
ex. methylprednisolone, prednisone, and cyclophosphamide

105
Q

what are disease modifying anti-rheumatic drugs (DMARD)

A

drugs used to treat autoimmune disorders by interfering with pathways of inflammatory cascade
ex. rituximab and methotrexate
used mainly to treat RA and SLE

106
Q

what is Cyclosporin A

A

drug used to treat autoimmune disorders by inhibiting the synthesis of interleukins like IL-2

107
Q

how does a thymectomy treat autoimmune disorders

A

decreases T-cell activation

108
Q

how does plasmapheresis help to treat autoimmune disorders

A

helps filter blood

109
Q

what is an example of how surgery can help to treat an autoimmune disorder

A

joint replacement to combat arthritis

110
Q

what is a host

A

someone who is receiving a transplant

111
Q

what is a graft

A

the donor tissue/organ

112
Q

what is a graft rejection

A

immunological response directed against the donor tissue

113
Q

what is an isograft

A

donation from an identical twin
no response from cytotoxic T cells because antigens bound to class 1 MHC molecules are no recognized as foreign
ex. bone marrow from one twin is transplanted to another with leukemia

114
Q

what is an autograft

A

donation from self
no response from cytotoxic T cells because antigens bound to class 1 MHC molecules are not recognized as foreign
ex. skin graft from one part of the body going to another

115
Q

what is an allograft

A

donation from same species
can lead to a rejection reaction
ex. kidney transplant from a relative or closely matched donor

116
Q

what is a xenograft

A

donation from a different species
can lead to a rejection reaction
ex. heart valves from pig or cow

117
Q

explain how allografts are rejected

A

T cells recognize donor HLA antigens (alloantigens) from graft
lymphocytes and antibodies are produced against these antigens and destroy tissue grafts
direct pathway: graft APC presents alloantigen to T cell directly
indirect pathway: alloantigens picked up and presented by host APC

118
Q

what is a hyperacute rejection

A

rejection is within minutes to hours after transplant
caused by antibodies specific for antigens on graft endothelial cells
direct pathway more involved

119
Q

what is an acute rejection

A

rejection within days or weeks after transplant
usually T-cell mediated, less often it’s B-cell/complement mediated
T-cells and antibodies are activated by alloantigens
acute cellular rejection: T-cells destroy graft cells or release cytokines
acute antibody-mediated rejection: antibodies bind to vascular endothelium and activate compliment

120
Q

what is a chronic rejection

A

rejection occurs over months or years leading to loss of graft function
fibrosis leads to narrowing of graft blood vessels
mediated by T cells and antibodies
indirect pathway is more involved

121
Q

what is graft versus host rejection (GvH)

A

immunologically competent cells are transplanted in an immunologically compromised host
transplanted cells recognize alloantigens as host
seen in bone marrow transplants

122
Q

what is a primary (congenital) immunodeficiency

A

genetically determined, usually result of a single gene defect
can have recurrent infections later in life more rare than secondary
present with: sinusitis, bronchitis, pneumonia, ear infections, and diarrhea

123
Q

what is a secondary (acquired) immunodeficiency

A

arise as a complication of other diseases
more common than primary

124
Q

what is the main hallmark of an immunodeficiency disease

A

recurrent infections with opportunistic organisms

125
Q

viral, fungal, yeast, and atypical microorganism infections lead to what deficiency

A

T cell deficiencies

126
Q

bacterial infections lead to what two types of deficiencies

A

antibody and complement deficiencies

127
Q

microorganisms requiring opsonization or catalase positive lead to what type of deficiency

A

phagocyte deficiencies

128
Q

what are the 5 groups of primary immune deficiencies

A

B lymphocyte
T lymphocyte
combined B and T lymphocyte
complement
phagocyte

129
Q

what are some of the most common symptoms of primary immune deficiencies

A

sinusitis
bronchitis
pneumonia
ear infections
diarrhea

130
Q

what is severe combined immunodeficiency (SCID)

A

defect in humoral and cell-mediated immune responses
less T cells, more B cells, and less serum immunoglobulins

131
Q

what is adenosine deaminase deficiency (ADA)

A

a recessive type of severe combined immunodeficiency (SCID)
deficiency of adenosine leads to a buildup of toxic metabolites which causes damage to immature lymphocytes
treated with: hematopoietic stem cell transplantation, enzyme administration, or gene therapy

132
Q

what are primary B-cell immune deficiencies

A

B-cell deficiencies
ex. X-linked agammaglobulinemia and isolated IgA deficiency

133
Q

what is X-linked agammaglobulinemia (Bruton agammaglobulinemia)

A

a type of primary B-cell immune deficiency
mutated Bruton tyrosine kinase (a intracellular signaling enzyme) prevents maturation of B-cells and plasma cells
treated with: immunoglobulin replacement (intravenous immunoglobulin)

134
Q

what is isolated IgA deficiency

A

a type of primary B-cell immunodeficiency
defect at terminal differentiation of IgA which leads to low serum and secretory IgA
most are asymptomatic but can lead to recurrent infections and diarrhea
increases frequency of autoimmune and allergies

135
Q

what is DiGeorge Syndrome

A

a type of primary T-cell immunodeficiency
thymus, parathyroids, and thyroid C cells don’t develop properly
leads to tetany (because of parathyroid glands), heart defects, facial anomalies, and poor infectious defense
treated with: thymus transplantation

136
Q

what is X-linked hyper-IgM syndrome

A

defects in helper T-cell-dependent B-cell and macrophage activation caused by mutation in CD40L gene
causes elevated levels of IgM, absence of IgG, IgE, IgA, and poor defense against infections

137
Q

what is chronic granulomatous disease (CGD)

A

X-linked phagocyte deficiency
defect in genes encoding oxidase enzyme which leads to defective production of ROS (bacteria killing)
macrophage walls off microbes leading to a granuloma
causes susceptibility to recurrent bacterial infections

138
Q

what is Chediak-Higashi Syndrome

A

a recessive phagocytic deficiency
defect in CHS1(LYST) gene leads to defective phagosome and lysosome function and therefore susceptibility to infections and giant granular aggregates
presents with: defective melanocytes (albinism), nervous system, and platelet function

139
Q

what is C3 deficiency

A

recessive complement cascade activation deficiency
leads to more infection by bacteria

140
Q

what is C9 deficiency

A

recessive complement deficiency
membrane attack complex (MAC) can no longer assemble
leads to an increased susceptibility in Neisseria specie bacterias

141
Q

what is Wiskott-Aldrich syndrome

A

X-linked mutation in WASP gene which leads to T-cell and B-cell defect
T-cell defect leads to progressive loss in peripheral blood and lymph nodes
B-cell defect leads to low IgM
often development of thrombocytopenia, eczema, infections, and B-cell lymphoma
treated with: hemopoietic stem cell transplantations

142
Q

what are some conditions associated with secondary immunodeficiencies

A

metabolic diseases (diabetes)
malnutrition (vitamin or zinc deficiencies)
malignancies (leukemia)
medial treatments (chemo and radiation)
chronic infections (AIDS)

143
Q

what is acquired immunodeficiency syndrome (AIDS)

A

disease caused by the untreated RNA retrovirus human immunodeficiency virus (HIV)
depletes the body’s CD4+ helper T cells
transmitted through sexual contact, blood to blood, and perinatal

144
Q

explain the mechanisms of HIV infection

A

gp120 protein binds to receptor on helper T-cell
now new recognition site on gp120 for coreceptors CCR5 and CXCR4
gp120 binds to CCR5 and CXCR4
binding causes fusion of viral and host cell membranes
virus enters cell to hijack replication machinery

145
Q

explain the acute phase of HIV

A

2-4 weeks
symptoms: headaches, fever, and flu-like
lots of virus in blood

146
Q

explain the chronic phase of HIV

A

months to years
no symptoms really
lots of antibodies in blood
helper T-cell destruction in blood

147
Q

explain the progression of HIV to AIDS

A

extreme decline of helper T-cells
lots of infections like pneumocystis jiroveci
increased opportunity for B-cell lymphoma and Kaposi sarcoma
eventually fatal

148
Q

what is the treatment for AIDS

A

antiretroviral therapy: drugs that stop HIV from entering cells or replicating once inside the cell
expensive and bad side effects
only slows progression

149
Q

what is an autoantibody

A

an antibody made by the body that will attack the body’s own proteins

150
Q

what is a neoantigen

A

new epitopes that are not normally expressed normally
created when there is an infection, tissue is injured, self antigens are modified
can activate T cells

151
Q

what is an antinuclear antibody

A

antibody elevated in autoimmune disorders

Disease Mechanisms (19 decks)

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