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Pathology 2 > 4.7 Hypersensitivities > Flashcards

4.7 Hypersensitivities Flashcards

1
Q

What types of hypersensitivities are there

A

I, II, III, IV

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2
Q

Type I hypersensitivity

A

rapidly developing reaction occuring with minutes of exposure, IgE and mas cell mediated, Complement (C3a, C5a) and cytokines (IL1 and TNF) later mediators

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3
Q

With allergen exposure

A

there is a rapid immediate response, don’t need a second exposure. There is also a late-phase reaction.

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4
Q

Mast cells are full of

A

mediators, like histamine

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5
Q

Local type I reactions

A

hay fever or allergic reactions depending on portal of entry

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6
Q

Systemic type I reactions

A

anaphylaxis and possible shock. When there is bronchoconstriction that is really bad.

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7
Q

A combination of you and the thing you react to leads to

A

ag presented by APC to CD4 T cell can mediate a Th1 response. Macs secrete IL1 and IL12. CD4 secretes IFN gamma and IL2. Cellular immune response. BUTTT when in contact with an alergen, CD4 cells instead secrete IL3, 4, 5, 13 and GMCSF mediating a TH2 response, leading to B-cell production of IgE

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8
Q

CD4 Th1 secretes

A

Il2 IFN gamma

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9
Q

CD4 Th2 secretes

A

IL3, 4, 5, 13, GMCSF

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10
Q

CD4 Th17 secretes

A

IL17, 22

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11
Q

Th2 can go in different directions

A

IL4 –> IgE, IL4 + IL10 –> IgG

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12
Q

IL4

A

induces IgE and sustains Th2 cells

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13
Q

IL3

A

eosinophil survival

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14
Q

IL5

A

activates eosinophils

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15
Q

IL 13

A

promotes IgE and stimulates epithelial cells to produce mucin

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16
Q

GMCSF

A

eosinophil support and survival

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17
Q

Th1 or Th2 depends on

A

both host and ag characteristics

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18
Q

allergens

A

certain substances (like pollens and bee venom) that elicit allergic responses more than others, hence are often called allergens. There is a strong familial link in allergic individuals (atopy). 50% + history. Atopic individuals have higher circulating IgE levels.

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19
Q

Mast cells

A

bone marrow derived cells containing metachromatic granules.

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20
Q

Where do mast cells live

A

in tissues especially around blood vessels, nerves, and epithelial surfaces

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21
Q

What do mast cells have on their surfaces

A

Fc receptors for IgE. When the bound IgE bind ag, the receptors dimerize and crosslink triggereing secretion.

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22
Q

other stimuli that cause mast cell degranulation

A

C3a, C4a, IL8, codeine, morphine, mellitin (bee venom), heat, cold, sunlight

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23
Q

What is released from mast cell granules

A

Histamine, LTC4, LTD4, PGD2, IL1, TNF

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24
Q

Primary mediators

A

very rapid and preformed in mast cell granules: include histamine, adenosine, chemotactic factors for neutrophils and eosinophils, and proteases (kinin and complement activation)

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25
Q

What are some primary lipid mediators

A

LTC4, LTB4, LTD4

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26
Q

Secondary mediators

A

includes a virtual soup of lipid and cytokine mediators secreted by both mast cells and infiltrating leukocytes

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27
Q

What are some secondary mediators leading to bronchospasm

A

leukotrienes C4, D4 and PGD2

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28
Q

what are does PAF do

A

secondary mediator – release of histamine, increased vascular permiablity and dialation, bronchospasm, leukocyte activation

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29
Q

What are some cytokines that are secondary mediators

A

TNF (proinflammatory) and GMCSF (enhances survival of eosinophils)

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30
Q

Systemic Anaphylaxis

A

life threatening reaction including shock, anasarca, and difficulty in breathing. Can be caused by sensitization to proteins, sugars, hormones, enzymes and DRUGS (penicillin), severity depeinds on level of sensitization, very small amounts of exposure can trigger response. Response only takes minutes – itching, hives and erythema, closely followed by bronchoconstriction. Laryngeal edema leads to hoarsness. Vomiting, diarrhea, cramps, laryngeal obstruction, vascular shock and death

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31
Q

Type II hypersensitivity

A

humoral autoimmunity to cells, membranes, and other solid body structurs (self or coated ag), activation of complement and cytolysis, ab dependent cell-mediated cytotoxicity (ADCC), Ab mediated cellular dysfunction. When these ab bind they activate complement and complement can kill, or fragments that are cehmotactic activated inflammatory cells to come in and cause damage, or we get ab to receptors on cells so they act as a ligand that can be an agonist or antagonist, so type 2 spans a wide range of sypmptoms and disease

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32
Q

Goodpasteur Syndrome

A

involves basement membrane of the capillary bed of glomeruli and alveoli – anti basment membrane antibodies – involves the non collagenous domain of alpha 3 chain of type 4 collagen – usually folded away from exposure

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33
Q

Good pasture affects

A

males in their 20somethings most commonly, in some studies 89% of pts are smokers

34
Q

what HLA is overrepresented in Good pasteur syndorme

A

HLA-DRB1*1501 and 1502

35
Q

Goodpasteur clinical presentation

A

respiratory symptoms first (hemoptysis), then rapidly progressive acute glomerulonephritis (with crescents) leading to rapide renal failure

36
Q

What does immuno fluorescence of good pasteur’s look like

A

smooth coating of basement membranes of lungs and kidneys with antibody mostly IgG and complement seen on immunofluorescence (“painted” for type 2)

37
Q

Myasthenia Gravis clinical presentations

A

ptosis and double vision usually presenting symptoms, then generalized flucturating muscle weakness

38
Q

Myasthenia gravis affects

A

3/100,000 ppl, onset begins before 40, females predominate

39
Q

Myasthenia gravis pts have a history of

A

thymic hyperplasia ro thymoma commonly associated

40
Q

Myasthenia gravis

A

decreased numbers of acetylcholine receptors bc of anti-AChR ab – antagonism/inhibition of the receptor

41
Q

Myasthenia gravis symptoms caused by

A
  1. fixation of complement and injury to synaptic membrane 2. increased internalization and degredation and competitive inhibition of binding of acetylcholine
42
Q

Anticholinesterase durgs improve myasthenia gravis

A

symptoms but death occurs eventually from respiratory failure

43
Q

survival rate of Myasthenia gravis

A

95% 5-year survival with steroids and plasmaphoresis, anticholinesterase drugs, thymectomy can also improve symptoms—-morning is better night is worse

44
Q

Myasthenia

A

agonism of the TSH receptor leading to hyperthyroidism.

45
Q

Hyperthyroidism

A

enlargement of gland, sympathetic over activity, cardiac hypertrophy and ischemic changes, Temp intolerance, emotional liability

46
Q

Graves disease affects

A

females 20-40 (ratio female:male = 7-10:1) –>10 % of your pts will be male

47
Q

Graves disease and MHC associations

A

HLA-B8 and DR3

48
Q

Graves disease symptoms

A

exphotalmia, orbital edema, fibrosis (ophthalmopathy) due to autoimmunity not thyrotoxicosis, Pre-timibal myxedema (non-pitting bc of glycoaminoglycans) in minority of pts, dec TSH, inc T3 and T4

49
Q

Graves disease genetics

A

30-40% concordance in monozygotic twins.

50
Q

What are features specific to graves

A

Ophthalopathy specific to graves_vacant stare due to hyperthyrodism (sympathetic overactivity), Autoimmunity, secretion of glycosaminoglycans, and stimulation of fibroblasts in the orbit and other places

51
Q

Type III hypersensitivity

A

Ag-Ab comlex mediated, complement activation, inflammatory cell induced tissue damage — deposition of complexes that percipitate out, they love to go deposit in capillary bets under endothelium and where they deposit is the site of disease.

52
Q

Proximate cause of type III hypersensitivity

A

Proximate cause, when they accumulate somewhere they activate complement and you ave accute inflammation in delicate capillaries – neutrophils come in and release O2-, H2O2, OHCl, proteases

53
Q

Is complex formation normal

A

yes, you make them all the time_.think of the achy joint feeling with the flue due to deposition and inflammation

54
Q

steps of Type III HSR

A

complex formation, complex deposition in vessels, complement activation and infalmmatory reaction

55
Q

Post-Streptococcal Acute Proliferative glomerulonephritis

A

immune complexes in glomeruli.

56
Q

Post strep is seen in

A

children 6-10 years old, 1-4 weeks following a strep throat or impetigo

57
Q

What types of Strep are involved in post-Strep

A

types 1, 4, and 12, beta hemolytic strep

58
Q

What do you see in post strep acute proliferative glmerulonephritis

A

onset of nephr-i-tic syndrome hematurea, proteinura (moderate), and hypertension(as opposed to nephrotic), low complement bc it is used up.

59
Q

Pathogenesis of Post strep

A

glomeruli are supposed to filter and retain a lot of large MW proteins by size and charge exclusion (charge is more important and due to BM, size exclusion is due to endothelium) and you have tubules to resorb smaller things. Now if you have neutorphils that are damaging, they begin to leak so bad that they can have red cells come out.

60
Q

Difference btw nephritic and nephrotic syndrom

A

nephrotic syndrom is worse bc you damaged the underlying structures and lost the charge barrier so you get wrose proteinuria than nephritic syndrome

61
Q

Urinalysis of post strep

A

blood, protein, RBC cast, protein cast (casts are from things that got lodged in tubules)

62
Q

how you tell the difference btw UTI and post strep

A

both will have bleeding and proteins but only post strep glomerulonephritis will show RBC casts —cylindrical casts of packed red cell proteins of tubules, so you know its not a UTI

63
Q

Post strep pt recovery

A

most pts recover with supportive care but a small percentage go on to rapidly progressive glomerulonephritis and renal failure. Mostly this is found in children bc the first time you see strep it can happen. There is an adult form that happens and it is not as benign so you have to treat aggressively.

64
Q

what will you see histologically in Post strep

A

splotches of red in tubules, big glmeruli bc they are hypercellular (you might see lots of glomeruli indicating that it is a child), crecent on glomeruli (also seein in goodpasteur – due to cytokine storm stimulating bowman’s epithelium to grow—crescents mean rapid progression to disease we think bc of higher inflammation), see lots of little blue cells (both acute and chronic cells), splotchy lumpy bumpy flourescence since type III

65
Q

Factors Affecting Complex Disease

A

Ag-Ab mix (slight ag excess), charge and structure of complexes, fn of mononuclear phagocyte system***most imp bc normally macs clear these complexes so in these pts there is something wrong, organ - high pressure filtration (kidney, joints)

66
Q

Immune complexes are present in

A

arthritis, vasculitis, glomerulonerphritis, serum sickness, arthus reaction

67
Q

Serum sickness

A

immunized towards proteins and then you get a massive formation of ab-ag complexes– think of snake bite story

68
Q

Arthus reaction

A

localized serum sickness–preformed ab to proteins, it localizes right there and you get a rxn.

69
Q

what is the difference btw a PPD for TB and an Arthus rxn

A

time. arthus rxn is immediate bc you have preforemd ab. PPD is delayed type 4 HSR so it will take longer.

70
Q

Type 4 hypersensitivity

A

cell mediated, sensitized T cells. CD4 (Th1) in delayed hypersensitivity; CD8 in direct cytotoxicity. Tubercilin reaction, contact dermatitis

71
Q

Contact dermatitis

A

type 4 hsr where an ag modifies you and you react to your protien–> nickle for example leehes out of jewlery and modifies your protein ex. Poison ivy, chemical sensitizers like nickle, post viral infection

72
Q

Delayed type HSR

A

tubercilin rxn, peak induration/swelling in 24-48hrs, mononuclear cells cuffing vessels, some rxns lead to granuloma formation

73
Q

T cell mediated cytotoxicity

A

direct killing of targets by CD8 killer cells, virally infected cells (hepatitis), foreign cells (graft rejection), muscle cells polymyocitis (cd8 killing of mus cells)

74
Q

CD14 is a marker for

A

macrophages

75
Q

Immuno peroxidase stain shows

A

CD4 T cells

76
Q

the arthus rxn can be differentated from type 4 hsr by

A

timing of the rxn

77
Q

hsr that accouns for most immune mediated disease

A

type I

78
Q

most direct form of autoimmunity

A

type II

79
Q

HSR caused by sensitization of T cells to cryptic self ag

A

Type IV

80
Q

HRS that have common mechanisms of the induction of tissue damage

A

Type II and III

Pathology 2 (15 decks)

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