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Peds Patho > Immunology > Flashcards

Immunology Flashcards

1
Q

types of white cells

A
  • -neutrophils
  • -bands
  • -eosinophils
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2
Q

role of mast cells

A

degranulate to release histamine

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3
Q

role of complement

A

like adding sugar, helps reaction along and needed for everything else to work

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4
Q

role of platelet activating factor

A

like vanilla; adds taste

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5
Q

role of neutrophils

A

1st line of defense!

–w/bacterial infection, early neutrophils will eat bacteria up

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6
Q

role of white cells

A

“gobble” up bacteria!

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7
Q

Bands

A

= premature neutrophils

–come in when neutrophils are done

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8
Q

role of eosinophils

A

come in after neutrophils; clean up a bit more

** predominantly seen in inflammatory, allergic reactions

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9
Q

role of interleukin/Interferon

A

helpers in reaction: help it come along

…but too much –> problem

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10
Q

most common type of immune deficiency

A

deficiencies in immunoglobulins

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11
Q

most common type of immunoglobulin/immune deficiency

A

IgA: 1 out of 600 ppl

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12
Q

5 types of Immunoglobulins

A

1) IgA
2) IgD
3) IgE: bound to mast cells
4) IgG
5) IgM

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13
Q

IgA

A
  • -provides antibodies for external body fluids

- -activates alternative complement pathway

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14
Q

IgD

A
  • -in membrane-bound form

- -function unknown

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15
Q

IgE

A
  • -bound to mast cell surfaces
  • -binding of antigen stimulates mast cell degranulation
  • -> causes immediate hypersensitivity responses (allergy)
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16
Q

IgG

A
  • -4 subclasses
  • -no tx for subclass deficiency, so a waste of time to check!
  • -prevalent in secondary responses
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17
Q

IgM

A
  • -prevalent in primary responses

- -activates classic complement pathway

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18
Q

when you get an infection, which antibody initially occurs?

A

IgM

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19
Q

which antibody denotes ACUTE infection?

A

IgM

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20
Q

when antigen and antibody unite, what happens?

A

a cascade of events that culminates in biochemical reactions

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21
Q

how does an allergy occur?

A

as part of a specific acquired alteration in the body that has an immunologic basis

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22
Q

all 4 types of allergic reactions are mediated by what?

A

circulating or cellular (esp. T-cell) antibodies

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23
Q

definition of antigen

A

a protein that is far into the body

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24
Q

what activates the classic complement pathway?

A

IgM

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25
Q

which immunoglobulin is prevalent in primary responses?

A

IgM

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26
Q

what activates the alternative complement pathway?

A

IgA

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27
Q

why do kids often get sick more in the first 2 years of life?

A

B Cells aren’t mature yet

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28
Q

when does a cell make IgE antibodies?

A

after it turns into a Plasma Cell

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29
Q

what does a Plasma Cell come from?

A

antigen presenting cell attaches to HLA Class II, IL-3, IL-4 –> then (goes to??) becomes a B cell –> then becomes a Plasma cell

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30
Q

what is a sensitized mast cell?

A

a mast cell attached to IgE antibodies

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31
Q

for you to be allergic to something, what must happen?

A
  • -antigen-presenting cells have gone through their processes
  • -you now have IgE antibodies & sensitized mast cells
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32
Q

what type of cell is an antigen-presenting cell?

A

a T-cell

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33
Q

after an antigen-presenting cell is presented to a naive t-cell, what happens?

A

it either goes towards:
1) infection –> TH1
OR
2) allergy –> TH2

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34
Q

if APC goes towards infection, what do you see?

A

increasing Neutrophils

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35
Q

inside Mast Cells, what is the most important cellular component in regards to allergy?

A

Histamine!

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36
Q

Initial phase of allergic reaction

A
  • -prostaglandins cause peripheral vasodilation

- -BP drops

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37
Q

functions of histamine released from mast cells

A
  • -bronchoconstriction
  • -mucus production
  • -vasodilatation
  • -pruritus
  • -arrythmias
  • -chemoattractant
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38
Q

functions of Prostaglandins D-2 (PGD2) released from mast cells

A
  • -bronchoconstrictor
  • -peripheral vasodilator
  • -coronary vasoconstrictor
  • -neutrophil chemoattractant
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39
Q

functions of Platelet Activating Factor (PAF) released from mast cells

A
  • -bronchoconstrictor
  • -vasodilator
  • -chemotaxis
  • -degranulation of neutrophils
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40
Q

functions of Leukotriene B4 (LTB4) released from mast cells

A

–neutrophil chemotaxis

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41
Q

functions of Leukotriene C4 & Leukotriene D4 (LTC4 & LTD4) released from mast cells

A
  • -bronchoconstrictor
  • -increase vascular permeability
  • -chemotaxis
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42
Q

chemotaxis

A

movement of an organism in response to a chemical stimulus

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43
Q

late phase of allergic reaction

A

–12-24 hrs. later
–prednisone takes care of this latephase reaction.
(steroids really slow this down)

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44
Q

Type I Allergic Reaction

A
    • IgE mediated **
  • -local & systemic manifestations from interaction b/t antigen & tissue cells
  • -allergen interacts w/IgE Antibody on surface of mast cells & basophils –>
    1) cross-link of IgE, FcERI receptor apposition
    2) mediator release from these cells
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45
Q

if you see hives alone, what type of reaction is it?

A

Type I Allergic reaction (but is not anaphylaxis)

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46
Q

what do you see anaphylaxis?

A

drop in BP, cardiac arrhythmia, vomiting & diarrhea (trying to get rid of antigen!), respiratory compromise
–> v. severe!!

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47
Q

how long will epi-pen last?

A
  • -lasts 20 min max

- -need to have pack of 2 just in case! –> must have 2nd epipen available

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48
Q

what is an ananphylactoid reaction?

A
    • non-IgE mediated ** reaction that causes anaphylaxis

ex: CT dye, strawberries

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49
Q

what are the 3 stages in IgE-mediated sensitivity?

A

1) Sensitization
2) Early Phase
3) Late phase

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50
Q

what is sensitization?

A
  • -1st stage in IgE-mediated sensitivity
  • -initial exposure leading to increase in allergen-specific IgE
  • -cell mediator sx increase
  • -occurs w/in minutes of subsequent exposure to antigen w/release of mediators such as histamine
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51
Q

what is stage 2 in IgE-mediated sensitivity?

A

Early Phase:

  • -lasts for minutes
  • -mast cells release histamine, leukotrienes, & cytokines
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52
Q

what is stage 3 in IgE-mediated sensitivity?

A

Late Phase:

–lasts for hours

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53
Q

what does the plasma cell release?

A

IgE antibodies

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54
Q

what does the mast cell release?

A

mediators! including HISTAMINE & leukotrienes

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55
Q

what happens before the Th2 cell becomes a B cell?

A

–it releases interleukins!

IL-4, 9, 13

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56
Q

clinical manifestations of immediate allergic reactions

A

sneezing, hives, wheezing, vomiting, anaphylaxis

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57
Q

clinical manifestations of Late-Phase response

A

release of toxic mediators by activated eosinophils & mononuclear cells recruited to the site of the acute allergic reaction

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58
Q

cause of late phase reactions?

A

–mast cells and T-cells
–mediators at post-capillary endothelial cells
–adhesion of circulating leukocytes
–infiltration of tissues by eosinophils, neutrophils, & basophils
–outflow of plasma –> local edema
–eosinophils produce mediators that promote tissue damage
–Th2 lymphocytes release cytokines that promote IgE production
–eosinophil chemoattraction
–increased #s of mucosal mast cells
??????????

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59
Q

what are some factors that can intensify anaphylaxis?

A

underlying asthma, cardiac disease, on certain drugs (tricyclics) or delay in administering epi

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60
Q

4 clues to presentation of allergic rhinitis:

A

1) nasal itching
2) repeated nose rubbing (“allergic salute”)
3) mouth breathing
4) allergic shiners

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61
Q

Type II Allergic Reaction

A
    • cytoxic reactions **
  • -IgG or IgM antibody is directed against antigens on the individual’s own tissue
  • -the binding of the antibody to the cell surface results in complement activation, signalling WBC influx & tissue injury
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62
Q

examples of Type II allergic reactions (4)

A
  • -lung & kidney damage in Goodpasture syndrome
  • -acute graft rejection
  • -hemolytic disease of the newborn (ABO incompatibility)
  • -certain bullous skin disease
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63
Q

“the rash that moves”

A

urticaria

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64
Q

clinically, urticaria always:

A

moves!
& doesn’t always itch
** IgE mediated! **

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65
Q

allergic shiners

A

puffy-like bags under eyes

–seen w/ allergic rhinitis (IgE-mediated!) Type I rx!

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66
Q

graft vs. host disease is what type of reaction?

A

Type II

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67
Q

Goodpasture is what type of reaction?

A

Type II

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68
Q

allergic rhinitis is what type of reaction?

A

Type I, IgE mediated

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69
Q

example of hemolytic disease of the newborn

A

ABO Incompatibility

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70
Q

what is a Type III reaction?

A

Immune Complex disease

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71
Q

what happens in a Type III reaction?

A

IgG & IgM antigen-antibody complexes of a critical size are not cleared from circulation

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72
Q

w/Type III reaction, what are the effects of IgG & IgM antibodies not being cleared from circulation?

A
  • -they fix in the small capillaries throughout the body

- -> leads to influx of inflammatory WBCs resulting in tissue damage

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73
Q

tissue damage in Type III reactions causes what diseases? (3)

A

1) Serum sickness
2) Lupus erythematosus
3) Glomerulonephritis after common infection

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74
Q

sx of serum sickness

A

fever, lymphadenopathy, joint swelling, rash (many diff. types)

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75
Q

what causes swelling with serum sickness?

A

IgG & IgM antibodies fix to small capillaries

–> swelling

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76
Q

what is special about rash seen with serum sickness?

A

does not look like a “nice, normal” rash

  • -“funny” rash
  • -can happen at any time: 1 day out, 2 days out, 5 days out, etc.
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77
Q

what are the culprits of serum sickness?

A
  • -Ceclor (Cefaclor)

- -Penicillin

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78
Q

if we have really sick kids (10 days..) on epileptic drugs, what should we consider?

A

serum sickness

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79
Q

EM

A

erythema multiforms

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80
Q

what can be a manifestation of serum sickness?

A

EM (erythema multiforme)

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81
Q

what is the hallmark of EM?

A

bullseye lesions

NOT hives, bc they’re FIXED

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82
Q

Type IV reaction

A

delayed-type hypersensitivity (T-CELL mediated)

** NOT IgE-mediated **

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83
Q

what happens w/Type IV reaction?

A
  • -T-cell antigen receptor of the Th1 lymphocytes bind to the tissue antigen
  • -> clonal expansion of lymphocyte population
  • -> T-cell activation w/release of inflammatory lymphokines
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84
Q

w/ Type IV reactions, what type of toxic lymphoid cell products are released?

A

???

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85
Q

examples of Type IV reactions? (3)

A

1) Tuberculin skin test reactions
2) contact dermatitis
3) Leprosy

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86
Q

what is leprosy?

A

a type 4 delayed hypersensitivity rx to the bacteria

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87
Q

what type of reaction is a latex allergy?

A

can be BOTH immediate and delayed hypersensitivity rx

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88
Q

mow lawn by poison ivy, oil blows and can make you itchy

A

is a type 4, T-cell mediated delayed hypersensitivity

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89
Q

Type IV A1 reaction

A
  • -mediated by CD4 TH1 cells causing classic hypersensitivity
      • allergic contact **
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90
Q

Type IV A2 reaction

A
  • -mediated by Th2 cells resulting in cell-mediated eosinophilic hypersensitivity
      • asthma **
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91
Q

Type IV b1 reaction

A

–Cytotoxic CD cells that mediate graft rejection & Stevens-Johnson syndrome

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92
Q

Type IV b2 reaction

A

–mediated by CD8+ lymphocytes that produce IL-5, resulting in cell-mediated eosinophilic hypersensitivity assoc. w/viral mucosal infection

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93
Q

causes of ananaphylactoid reaction

A
  • -Drugs: aspirin, NSAID, gammaglobulin, morphine, codeine, anesthesia meds
  • -Physical causes: exercise, cold, heat, sunlight
  • -exercise-dependent food induced
  • -radio-contrast material
  • -idiopathic
    • NON- IGE mediated **
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94
Q

most common cause of anaphylaxis outside of the hospital?

A

food allergy!

in hospital –> latex allergy

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95
Q

is atopy the same as allergic response?

A

NO! atopy does not equal allergic response!

** atopy involves genetic predisposition

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96
Q

atopic triad

A

1) Asthma
2) Allergic Rhinitis
3) Atopic Dermatitis

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97
Q

definition of atopy

A

the inherited risk to develop IgE-mediated responses following exposure to allergens
–puts a person at greater risk for development of the atopic triad

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98
Q

allergy definition

A

involves hypersensitivity that occurs upon re-exposure to sensitizing allergens

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99
Q

how does a person develop an atopic disorder?

A
  • -involves a susceptible individual who is both:
    1) exposed to an offending antigen
    2) has a predisposition to selective synthesis of IgE when in contact w/common environmental allergens
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100
Q

atopy is typically assoc. w/ …?

A

a genetically determined capacity to mount IgE responses to common allergens
–> esp. inhaled allergens & food allergens

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101
Q

IgE is produced by what?

A

plasma cells

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102
Q

first event in allergic reaction cascade

A

contact w/an offending antigen occurs

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103
Q

after contact w/offending antigen in allergic cascade, what happens next?

A

brisk proliferation of T helper type 2 (Th2) cells

–> secretions of cytokines: interleukin (IL-3, 4, 5, 9, 13)

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104
Q

what do cytokines (IL-3, 4, 5, 9, 13) do in allergic cascade?

A

are involved in IgE synthesis & activation of eosinophils

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105
Q

role of IgE in allergic cascade?

A
  • -is produced by plasma cells

- -> binds to receptors on mast cells, basophils, & Langerhans cells

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106
Q

when IgE binds to different cells, what happens?

A

chemical mediators that cause biochemical reactions & allergic-related injury to target organs (skin, resp. tract) are released:
–Histamine, prostaglandins, leukotrienes, eosinophil chemotactic factor of anaphylaxis, high-molecular-weight neutrophil chemotactic factor, platelet-activating factor, arachidonic acid–cyclo-oxygenase & lipoxygenase products

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107
Q

end result of allergic cascade

A

tissue injury of a target organ

–inflammation & hyperresponsiveness

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108
Q

symptoms of tissue injury from allergic cascade (3)

A

1) airway obstruction
2) increased mucus production
3) pruritus

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109
Q

most damage in allergic cascade comes from what?

A

most damage is from inflammatory reaction & local edema–NOT from bronchospasm

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110
Q

common cause of oral allergy syndrome

A

mango!

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111
Q

who often gets oral allergy syndrome?

A

teenagers!/young adults

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112
Q

oral allergy syndrome is assoc. w/ …?

A

allergic rhinitis

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113
Q

sx of oral allergy syndrome

A
  • -tingling, pruritus, erythema
  • -angioedema of lips, tongue
  • -throat itch, tightness
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114
Q

do you see anaphylaxis w/oral allergy syndrome?

A

NO! no anaphylaxis

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115
Q

how does severity vary with oral allergy syndrome?

A

severity varies with season

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116
Q

how quickly does oral allergy syndrome occur?

A

immediate on contact w/raw fruits & vegetable

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117
Q

who gets food induced anaphylaxis?

A

any age

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118
Q

when does food induced anaphylaxis occur?

A

in minutes to 2 hrs

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119
Q

sx of food induced anaphylaxis?

A
  • -cutaneous or respiratory manifestation

- -abdominal pain, vomiting, & diarrhea

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120
Q

dx of oral allergy syndrome?

A

positive skin prick test

–oral food challenge w/raw vegetable positive, & negative when cooked

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121
Q

dx of food induced anaphylaxis?

A
  • -positive skin test

- -IgE

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122
Q

end result/prognosis of food induced anaphylaxis?

A
  • -milk, soy, egg, wheat outgrown

- -peanut, tree nut, shellfish allergies persist

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123
Q

6 types of allergic disease

A

1) Rhinitis
2) Asthma
3) Atopic Dermatitis
4) Conjunctivitis
5) Anaphylaxis
6) Food

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124
Q

allergic disease: rhinitis

sx?

A

nasal:

sneezing, rhinorrhea, nasal itching, congestions

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125
Q

allergic disease: asthma

sx?

A

lungs:

coughing, wheezing, shortness of breath

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126
Q

allergic disease: atopic dermatitis

sx?

A

skin:

itching & rash

127
Q

allergic disease: conjunctivitis

sx?

A

eye:

redness, itching, & tearing

128
Q

allergic disease: anaphylaxis

sx?

A

systemic:

hypotension, shock, & death

129
Q

allergic disease: food

sx?

A

GI tract:

bloating, vomiting, diarrhea, cramping

130
Q

s&s in nose that indicate allergy?

A

boggy, blue, swollen, little papules

131
Q

prevention of atopy manifestation?

A

–elimination of the offending substance to prevent IgE development & antigen-antibody interaction
–breastfeeding! –> benefit of maternal IgA, IgG antibodies
(early breastmilk full of IgA!)

132
Q

goal of pharmacologic therapy w/allergy?

A

–reduces symptoms & checks the allergic process

133
Q

4 types of allergy meds

A

1) corticosteroids
2) antihistamines
3) Montelukast
4) cromolyn sodium

134
Q

purpose of using corticosteroids in allergy tx?

A

control inflammation

135
Q

purpose of using antihistamines in allergy tx?

A

compete w/histamine for receptor sites on target tissues

136
Q

purpose of using Montelukast in allergy tx?

A

act as a selective leukotriene receptor antagonist

137
Q

purpose of using cromolyn sodium in allergy tx?

A

prevent mast cell degranulation & mediator release

138
Q

history of atopic individuals who develop allergic disease?

A

genetic susceptibility, environmental factors w/allergen exposure, presence of other risk factors, small family, passive smoke exposure, Western lifestyle, early use of antibiotics, diet

139
Q

how does maternal transferred immune protection work?

A

the immune state of the infant is modified by maternal factors that are transferred by:

  • -Placenta
  • -Mammary Gland
    • provides protection against pathogens to which the mother was immune **
140
Q

what maternal factor is transferred to the infant through the placenta?

A

Maternal IgG

141
Q

what maternal factor is transferred to the infant through the mammary gland?

A

Maternal IgA

142
Q

why could an infant have decreased resistance to infection?

A
  • -if the degree or duration of placental transfer is decreased
  • -infant not breastfed
143
Q

what could cause a lesser degree or duration of placental transfer?

A
  • -prematurity

- -placental insufficiency

144
Q

in embryology, B cells give rise to:

A

humoral immunity

145
Q

in embryology, T cells give rise to:

A

cellular immunity

146
Q

humoral immunity arises from:

A

B cells

147
Q

cellular immunity arises from:

A

T cells

148
Q

why are cells of infants’ immune system naive at birth?

A

–bc exposure in utero is limited

even though fetal immune sys. does have the potential to respond to large #s of foreign antigens!

149
Q

in embryology, when are B & T cells present?

A

??

150
Q

function of immune system?

A

protects the host against a vast array of foreign pathogens

151
Q

immune system’s 3 lines of defense?

A

1) external barriers
2) inflammatory response:
- -innate immunity (1st line of immune defense)
3) adaptive immunity (antigen-specific response)

152
Q

what is the body’s first line of immune defense?

A

innate immunity

153
Q

what is adaptive immunity?

A

antigen-specific response

154
Q

are you likely to see a cold in a baby’s 1st month of life?

A

no! v. rare to see a cold in 1st month of life d/t maternal transfer of antibodies

155
Q

external barriers of immune defense:

physical & mechanical barriers

A

1) Skin: INTACT skin
2) Epithelial lining of:
- -GI (lined w/IgA–> less infection)
- -GU
- -Resp. tract (cough, cilia, mucus)

156
Q

external barriers of immune defense:

biochemical barriers found in what 3 places?

A

1) Perspiration, tears, saliva
2) Lungs
3) GI tract

157
Q

what biochemical barriers are found in perspiration/tears/saliva?

A

Lysozomes: attack cell wall of gram+ bacteria

158
Q

what biochemical barriers are found in the lungs?

A

Collectins (aka surfactant protein A & D)

–>promotes phagocytosis & interacts w/acquired immune system

159
Q

how can lungs act as a barrier to disease?

A

act as biochemical barrier, w/cells that have phagocytic qualities

160
Q

what biochemical barriers are found in the GI tract?

A

1) Gastric hydrochloride
2) Normal bacteria flora
- -probiotics! finally accepted

161
Q

how do normal bacterial flora function as a biochemical barrier?

A

produce chemicals that inhibit colonization by pathogenic microorganisms

162
Q

the immune system is made up of what 2 parts?

A

1) Innate (primitive form; exists w/out prior exposure)

2) Adaptive (from being exposed to disease)

163
Q

vaccines are based on what principle?

A

adaptive immunity

164
Q

what does innate immunity do?

A

uses specific cells’ pattern recognition & soluble factors to provide a first line of host defense

165
Q

how is innate immunity activated?

A

by direct contact w/specific microbial products

166
Q

what microbial products can activate an innate immune response? (3)

how do they respond?

A

1) Lipopolysaccharide
2) cell wall components
3) microbial nucelotides

–> activate monocytes, macrophages

167
Q

what is a lymphoid member?

A

natural killer cell

–>innately have v. strong function in responding to bacteria

168
Q

what do natural killer cells do?

A

secrete soluble mediators:

cytokines, chemokines

169
Q

4 types of phagocytes

A

1) PMNs (polymorphonuclear neutrophil)
2) monocytes
3) macrophages
4) eosinophils

170
Q

examples of soluble mediators?

A
  • -complements

- -cytokines in blood & body surfaces

171
Q

role of soluble mediators in innate immunity?

A

–enhance effectiveness of cells
–link innate & adaptive immunity
(direct activation of complement system by microbial products–> promotes opsonization)

172
Q

antibody opsonization

A

the process by which a pathogen is marked for ingestion and destruction by a phagocyte

173
Q

what become macrophages?

A

monocytes become macrophages

174
Q

definition of adaptive immunity

A

specific process of recognition & response in the host defense to a foreign substance
–>specificity directed @the inducing antigen (microorganism)

175
Q

central players in adaptive immunity?

A

T & B lymphocytes

176
Q

important cellular component of T lymphocytes?

A

cellular arm

177
Q

impt cellular component of B lymphocytes?

A

specific antibody or immunoglobulins
(each express antigen specific responses;
time lag following initial antigen interaction)

178
Q

in adaptive immunity, what do memory cells do?

A

magnify & hasten immune response

179
Q

what secreted mediators are released to cause many effects of the adaptive response?

A

cytokines & chemokines

180
Q

2 types of adaptive immune response:

A

1) Humoral immunity

2) Cellular immunity

181
Q

humoral immunity is mediated by:

A

antibodies (immunoglobulins) produced by B cells

182
Q

cellular immunity is mediated by:

A

the direct action of T cells & via secreted cytokines

183
Q

what produces antibodies?

A

B cell

184
Q

an initial innate response is often to linked to… ?

A

the development of an adaptive respose

185
Q

types of adaptive immune cells (4)

A

1) Regulatory T cells
2) Killer T cells
3) Cytokines
4) Helper T cells

186
Q

site of B & T cell differentiation?

A

lymphoid tissue

187
Q

3 types of lymphocytes:

A

1) natural killer cells
2) b cells
3) t cells
(are all agranulocytes)

188
Q

immature lymphocytes are differentiated where?

A

central (primary) lymphoid tissue

  • -Bone marrow: B lymphocytes
  • -Thymus: T lymphocytes
189
Q

where are B cells differentiated?

A

in the bone marrow

190
Q

where are T cells differentiated?

A

in the Thymus, from lymphocytes

191
Q

mature lymphocytes are differentiated where?

A

peripheral (secondary) lymphoid tissue:

lymph nodes, spleen, adenoid, tonsils, Peyer’s patches (ileum)

192
Q

what happens in primary exposure?

A

antigen is exposed to B cell

193
Q

B cell role in primary exposure

A
  • -antibodies in 3-7 days (IgM)

- -make memory cells to recognize antigen for future exposure

194
Q

what happens in secondary exposure?

A 
antigen re-exposure --> immunologic memory
antibody production w/in hours
   --> mainly IgG bc it has memory cells
more intense & rapid response
protects against illness (immunization)
195
Q

what type of immunity is antibody-based?

A

humoral immunity

196
Q

function of antibodies

A
  • -provide protection against bacteral infections: lungs, sinuses, middle ear, GI tract
  • -promote ingestion of bacteria, neutralization of toxins, inactivation of certain viruses
197
Q

3 classes of antibodies:

A

1) IgM & IgG: protect against systemic infections
2) IgA: protects at mucosa surfaces (GI, lung)
3) IgE: allergic disorders & protects against parasites

198
Q

antigen specificity depends on:

A

T-cell antigen receptors

B-cell surface immunoglobulin

199
Q

natural killer cells are part of which respones?

A

Innate response

200
Q

mesenteric adentitis

A

an inflammation of peyer’s patches (found in all areas of the ileum)

201
Q

what can be develop specificity for?

A

virtually any antigen!

202
Q

cytokines act where?

A

primarily locally

203
Q

examples of cytokines?

A

interleukins, interferons

204
Q

different functions of cytokines (3)

A

1) mediating innate immunity
2) mediating adaptive specific immunity
3) stimulating blood cell formation
(each has many activities that overlap w/each other!)

205
Q

you can have 2 types of responses to an inhaled allergen:

A

1) Atopic

2) Non-atopic

206
Q

w/atopic response to inhaled allergen, what happens?

A

Th2 response:

IgE –> local eosinophil inflammation

207
Q

w/ non-atopic response to inhaled allergen, what happens?

A

Th1 response:

No IgE –> little or no inflammation

208
Q

T cells: function in cellular immunity

A

1) recognize antigen
2) release cytokines
3) generate memory cells following the initial encounter w/the antigen (underlying foundation for successful immunizations!)

209
Q

what types of cytokines do T-cells release?

A

1) Immunoregulatory: IL-2

2) Pro-inflammatory: IL-10

210
Q

what happens after the T cell recognizes the antigen?

A

it binds to antigenic fragment displayed by HLA molecule

211
Q

what are cytokines?

A

hormones that affect the immune response

212
Q

another name for CD4 cells?

A

helper T cells

213
Q

2 types of CD4 cells:

A

1) TH1: cellular immunity

2) TH2: enhance antibody formation by B-cells

214
Q

function of TH1 cells:

A

–cytokines: IL-1, interferon-gamma
–enhance cytotoxic T-cells
–activate macrophages
–recognize antigens from intracellular infecting agents:
viruses, mycobacteria, fungi

215
Q

function of TH2 cells:

A
  • -cytokines: IL-4, 6, 10

- -increase IgG production & mediate eosinophil recruitment & activation

216
Q

function of CD8–cytotoxic/suppressor T cells

A
  • -recognize antigen from nucleated host cells
  • -mount cytotoxic response in response to viral infection involving any tissue
  • -secrete cytokines that can modulate immune reactions
  • -may have role in negatively regulating (suppressing) immune responses
    • “turn off” the reaction **
217
Q

difference b/t B and T cells?

A

B cells respond generally
T cells rather specific, interact w/HLA
??

218
Q

selectivity in immune response should cause:

A
      • response to foreign antigens

- -no response to self antigens

219
Q

selectivity in immune response depends on:

A

deletion of autoreactive lymphocytes during T cell development
–> you develop Immunologic Tolerance

220
Q

what happens w/autoimmunity?

A

Immunologic tolerance not effective

221
Q

examples of autoimmune diseases (4)

A

1) Type 1 diabetes
2) Hashimoto’s thyroiditis
3) Celiac disease
4) vitiligo

222
Q

w/what 2 diseases are you prone to autoimmune disease?

A

Down’s, Turner Syndrome

223
Q

CD4 T-cells interact w/… ?

A

Antigen-expressing antigen-presenting cells

typically in the lymph node

224
Q

CD8 T-cell function

A
  • -capable of destroying any cell that has undergone change (viral infection w/viral antigenic properties)
  • -source of cytotoxic effector T cells
225
Q

HDL class II molecules bind w/which cells?

A

CD4 T-cells

** is restricted to a specific cell type (APC cell) **

226
Q

HDL class I molecules bind w/which cells?

A

CD8 T-cells

** is expressed on virtually all cells **

227
Q

which are more specific: CD4 or CD8 T-cells?

A

CD4 is restricted to specific cell type!

228
Q

WBC role in inflammation?

A
  • -adhere to inner walls of vessels

- -migrate through vessel walls to site of injury

229
Q

effects of blood vessel dilation w/inflammation?

A
  • -increased b’flow & concentration of RBC at site of injury

- -warmth, redness

230
Q

inflammation occurs w/what type of immunity?

A

innate immunity –> non-specific response

231
Q

vascular response w/inflammation: 4 things

A

1) blood vessel dilation
2) increased vascular permeability & leakage of fluid out of the vessel
3) WBC action
4) vascular changes bring leukocytes, plasma proteins, & biochemical mediators to site of injury

232
Q

purpose of vascular response during inflammation

A

1) limit & control inflammatory process to prevent spread of inflammatory response to healthy tissue
2) prevent infection & further damage
3) interact w/components of adaptive immune system
4) prepare area of injury for healing

233
Q

structures involved in limiting spread of inflammatory response (3)

A

1) plasma protein systems
2) plasma enzymes
3) cells (eosinophils)
???????????

234
Q

deficiency in complements leads to…. ?

A

risk of infection

235
Q

w/inflammation, how does the vascular response interact w/components of the adaptive immune system?

A

by eliciting more specific response to contaminating pathogen by influx of macrophages & lymphocytes

236
Q

w/inflammation, how does the vascular response prepare the area of injury for healing?

A

through removal of bacterial products, dead cells, etc.

237
Q

complement system

A
  • -3 pathways
  • -amplifies immune response by providing critical factors to:
    1) enhance phagocytosis (opsonins)
    2) attract cells to site of inflammation (chemoattractants)
238
Q

role of platelets in inflammatory response

A

move out of the capillary to seal the wounded area

239
Q

neutrophil function w/inflammation

A

first: are there to be phagocytes
later: help remove debris from area & out of blood

240
Q

are neutrophils specific?

A

no! v. non-specific: just go in there & kill

241
Q

w/inflammation, what directs migration to the source of infection?

A

neutrophils

242
Q

what is a phagolysosome?

A

is generated by neutrophils:

internalizes organism into an intracellular compartment

243
Q

phagocytosis

A

process by which cell ingests & disposes of foreign material, including microorganisms

244
Q

what activates neutrophils to come to inflammatory site?

A

activated by inflammatory mediators:

  • -bacterial proteins
  • -Complement
  • -mast cell
  • -neutrophil chemotactic factor
245
Q

neutrophil: primary role in burns

A

removal of debris

246
Q

neutrophil: primary role in nonsterile lesions

A

phagocytosis of bacteria

247
Q

B cell differentiation requires:

A

intracellular single

248
Q

X-linked B-cell differentiation causes:

A

Bruton agammaglobulinemia = has defect intracellular protein, Bruton Tyrosine kinase

  • -> Blocks B cell differentiation
  • -> results in lack of circulating B-cells & absent antibody response
  • -> problem! kid will get sick a lot
249
Q

major function of B cells

A

production of immunoglobulins/antibodies:

host protection against encapsulated bacteria & other microbes

250
Q

immunologic memory: mom and baby

A

–antibody repertoire of mother influences susceptibility of child to infectious agents/future infections

251
Q

when will infants be protected by maternal antibodies?

A

3-12 mos after birth
(IgG –> fetal circulation, through placenta
IgA –> gut, through breastmilk)

252
Q

monocytes & macrophages

A

monocyte = precursor to macrophage

253
Q

when do macrophages appear at inflammatory site?

A

1-7 days after initial neutrophil infiltration

254
Q

role of eosinophil in inflammatory activity

A
  • -mild phagocytic activity
  • -body’s primary defense against parasites
    • help regulate vascular mediators released from mast cells
    • impt. role in hypersensitive allergic response
255
Q

what cell has an impt. role in hypersensitive allergic responses?

A

eosinophil

256
Q

what helps to regulate vascular mediators released from mast cells?

A

eosinophils

257
Q

what is the body’s primary defense against parasites?

A

eosinophils

258
Q

Interleukins

A

biochemical messengers

259
Q

interleukins are produced by:

A

macrophages & lymphocytes

260
Q

role of interleukins

A
  • -induce chemotaxis
  • -cause cells to proliferate in bone marrow
  • -both enhance & suppress inflammation
261
Q

Interferons

A

Protect against viral infections:

  • -don’t kill directly, but prevent further infection
  • -enhance efficiency of development of acquired immune response
    • no effect on cells already infected
262
Q

tumor necrosis factor alpha

A

a cytokine secreted by macrophages & mast cells

  • -> induces fever
  • -> causes increased synthesis of inflammatory serum proteins by liver
  • -> causes cachexia & intravascular thrombosis
263
Q

cachexia

A

muscle wasting

264
Q

what can cause cachexia & intravascular thrombosis?

A

tumor necrosis factor alpha

cytokine secreted by macrophages & mast cells

265
Q

function of chemokines

A

induce leukocyte chemotaxis

266
Q

cellular components of immune system

A
  • -primarily B & T cells
    • -> mediate adaptive immunity
  • -phagocytic lymphocytes and NK cells
    • -> mediate innate immunity along w/non-immune cells
267
Q

which cells mediate adaptive immunity?

A

B and T cells

268
Q

which cells mediate innate immunity?

A

phagocytic lymphocytes & NK cells

269
Q

soluble protein components of immune system

A

–antibodies IgA, IgM (humoral immunity)

??

270
Q

what makes up immune system

A
  • -cellular components (primary B & T cells) + other non-immune cells
  • -soluble protein components
271
Q

are defects of the Adaptive immune system cellular or humoral?

A

both!
T cells –> cellular
B cells –> humoral

272
Q

are defects of the Innate immune system cellular or humoral?

A

primarily cellular abnormalities

+ soluble protein defects

273
Q

what is the Jeffrey Modell Criteria?

A

10 Warning Signs of Primary Immunodeficiency (PI):

1) 4 or more ear infections w/in 1 year
2) 2 or more serious sinus infections w/in 1 year
3) 2 or more months on antibiotics w/little effect
4) 2 or more pneumonias w/in 1 year
5) Failure of an infant to gain weight or grow normally
6) Recurrent, deep skin abscesses
7) Persistent thrush in mouth or fungal infection on skin.
8) Need for IV antibiotics to clear infections
9) 2 or more deep-seated infections including septicemia
10) A family hx of PI

274
Q

what is the principle underlying pediatric immunizations?

A

Immunologic Response

275
Q

what heightened awareness of immunology & immune deficiency d/o?

A

HIV pandemic

276
Q

what might you see? HIV infected kid, e.g.

immunodeficiency

A
  • -pneumocystic infection: most ppl don’t get this!
  • -hepatosplenomegaly, lymphadenopathy
  • -opportunistic infections
277
Q

clinical presentation of cellular immune defect

A

recurrent opportunistic infection

278
Q

clinical presentation of humoral immune defect

A

recurrent sinopulmonary infection w/encapsulated bacteria

279
Q

clinical presentation of neutrophil defect

A

recurrent bacterial & fungal infections involving the skin & organs

280
Q

Autoimmunity

A

occurs when the immune system begins attacking “self” components of the body aberrantly

281
Q

examples of autoimmune disease (4)

A

1) MS
2) rheumatoid arthritis
3) lupus
4) type 1 diabetes

282
Q

Alloimmunity

A

immune system reacts against antigens on tissues of other members of the same species:
–neonatal diseases where maternal immune system becomes sensitized against antigens expressed by fetus
–transplant rejection & transfusion reactions
(immune sys. of organ transplant/blood transfusion recipient reacts against antigens on donor cells)

283
Q

what happens in organ transplant/blood transfusion alloimmunity reactions?

A

immune sys. of organ transplant/blood transfusion recipient reacts against antigens on donor cells

284
Q

alloimmunity, mom and baby:

2 forms

A

** Fetus affected by maternal antibodies:
1) Rh & ABO alloimmunization
can –> Erythroblastosis fatalis
2) Graves Disease
maternal antibody against TSH receptor–> neonatal hyperthyroidism

285
Q

Erythroblastosis fatalis

A

hemolytic disease of the newborn

286
Q

disorder of the immune system can be caused if the immune response is:

A

inappropriate, excessive, or lacking

e.g. HIV: excess of NK cells

287
Q

Complements are:

A

plasma proteins

10% of plasma proteins are complements

288
Q

ex. of B cell or humoral immunodeficiency (2)

A

1) selective IgA deficiency

2) x-linked Bruton agammaglobulinemia

289
Q

ex. of T cell or cellular immunodeficiency

A

DiGeorge Syndrome

290
Q

ex. of phagocytic system immunodeficiency

A

chronic granulomatous disease

cellular deficiency

291
Q

complement system immunodeficiency

A

protein defect:
early= recurrent sinopulmonary infection, increase in systemic autoimmune disease
terminal= recurrent neisseria infections & increased risk of meningitis

292
Q

Primary Immunodeficiency

A

caused by genetic or developmental defects in the immune system

293
Q

Secondary or acquired immunodeficiency

A

loss of immune function as a result of exposure to disease agents, environmental factors, immunosuppression, or aging

294
Q

ex of Primary immunodeficiency

A

SCID

severe combined immunodeficiency

295
Q

ex of Secondary immunodeficiency

A

congenital HIV

296
Q

SCID

A

severe combined immunodeficiency

297
Q

what can result from delayed dx of immunodeficiency?

A

chronic infection in lung

  • -> Bronchiectasis
  • -> pulmonary failure
298
Q

what therapies are used to improve outcomes w/immunodeficiency?

A

gamma globulins, HIV meds

299
Q

what types of infections will you see w/immunodeficiency?

A

more severe, atypical, persistent infections (recurrent abscesses)

300
Q

physical signs of immunodeficiency

A

may look normal! (SCID)
no tonsils or small tonsils
no lymph nodes –> think X linked agammaglobulinemia

301
Q

lab values w/immunodefiency

A

MUST do an ANC

302
Q

levels of neutropenia

A

<800 = severe

303
Q

cellular immune deficiency diseases (5)

A

1) DiGeorge Syndrome
2) SCID
3) x-linked hyper-IgM syndrome
4) Wiskott-Aldrich syndrome
5) Ataxia Telangiectasia

304
Q

dysmorphic features of DiGeorge Syndrome

A
  • -short philtrum
  • -micrognathia
  • -hypertelorism
  • -low set ears
305
Q

hypertelorism

A

wide-set eyes

306
Q

which is a disease of variable penetrance?

A

DiGeorge Syndrome

307
Q

defects w/DiGeorge Syndrome

A

–congenital thymic hypoplasia
(hypoplasia of thymus to varying degrees)
–dysmorphogenesis of 3rd & 4th pharyngeal pouches
–other issues: congenital heart disease, hypoparathyroidism

308
Q

hypoparathyroidism in DiGeorge syndrome causes what?

A

low Ca –> tetany

tetany = a medical sign consisting of the involuntary contraction of muscles

309
Q

what can happen w/thymic hypoplasia?

A

can –> cellualr immunodeficiency

bc thymus produces T cells!

310
Q

what chromosome is affected in DiGeorge?

A

deletion of several genes on Chromosome 22

311
Q

when does SCID present?

A

early in life

312
Q

major signs of SCID

A

Diarrhea

FTT

313
Q

characteristics of SCID

A
    • has no thymus
  • -absence of T cell function
  • -w/out bone marrow transplant, will die by age 2
314
Q

Wiskott-Aldrich Syndrome is what type of d/o?

A

X-linked disorder:

  • -eczema
  • -thrombocytopenia w/small platelets
  • -immunodeficiency

Peds Patho (8 decks)

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