3 - Ward Immunopathology Part 1

Front 1

Exogenous things such as environmental (dust, drugs) or homologous things (blood) cause what type of reaction?
If antigens are endogenous and cause a reaction, what is it called?

Back 1

Hypersensitivity

Autoimmune

Front 2

Which type of hypersensitivity is this?
In individuals previously sensitized to an antigen, an immunologic reaction immediately follows upon rechallenge i.e. combination of that antigen with antibody bound to mast cells.

Back 2

Type I Hypersensitivity

Exposure and Re-challenge

Front 3

Type I Hypersensitivity Rxn:
1) ________ substances (____ dilate, edema)
2) _________ substances (smooth m spasm)
3) __________ cytokines (from ____ cells, recruit things)

Back 3

Vasoactive
bvs
Spasmogenic
Proinflammatory
mast

Front 4

After previous sensitization in Type I Hypersensitivty, ______ occurs 5-30/60 min later. THis includes vaso_____, edema, smooth muscle spasm, increased ______ (important in bronchi), shock/death if rechallenge is ________

Back 4

rechallenge
dilation
glandular secretions
intravenous

Front 5

What type of Hypersensitivity can have a late-phase reaction 2-24 hours after antigen exposure, and lasts several days?

Back 5

Type I

Front 6

What caues bronchial spasm, vascular permeability, and increased secretions in the acute Type I reaction?
What causes the first two x 1000, but no secretions?

Back 6

Histamine

LTC4, LTD4 (leukotrienes)

Front 7

During the intermission of Type I Hypersensitivty Rxn LTB4, PAF, and TNF-alpha all do what?

Back 7

Recruit inflammatory cells
Chemotaxis!

Front 8

In the late phase of type I Hypersensitivity reaction, the _______ cells arrive and release ________-damaging mediators/cytokines

Back 8

inflammatory
epithelium

Front 9

Primary mediators of Type I Hypersensitivty reactions come from ____ cell granules
The products include biogenic amines: _______ (triple action), enzymes (proteases, acid hydrolases... ____, C3a), and proteoglycans (____ which mediates packging in granules)

Back 9

mast
histamine
kinins
heparin

Front 10

There are other secretagogues (cause mast cells to release granules) other than IgE:
C_a and C_a (anaphylatoxins), IL-_ from mos, _______ derivatives, mellitin, cold

Back 10

C3a
C5a
IL-8

Front 11

______ cells take epitope from antigen and present it to naive _______ which become ___ cells. These begin to secrete a bunch of things:
IL-_, _, _, and 13

Back 11

lymphocytes
Th2
IL-3,4,5

Front 12

IL-_ causes B-cells nearby to differentiate into ___ producing cells. These arm the mast cells. Happens during silent period

Back 12

IL-4
IgE

Front 13

IL-3 and IL-5 do what?
What is the cytokine called that epithelial cells form to recruit eosinophils?

Back 13

Take care of eosinophils - provides pleasant place, activation, grnaules/mediator formed that can damage epithelium.
Eotaxin

Front 14

What does IL-13 do? Where does it come from?

Back 14

Comes from Th2 cell
causes increased mucous secretion on a long term basis

Front 15

3 things happen after cross-linking of IgE:
Signal for degranulation (histamine, proteases, chemotactic ECF/NCF)
Signals for nucleus to activate and secrete ______ (IL-1, _,_,_,_)
Signal for activation of ________A2 which leads to activation of membrane phospholipids which branch into AA and ___. AA further differentiates.

Back 15

cytokines IL-1,3,4,5,6
phospholipase

Front 16

Secondary mediators from _____ cells:
PhospholipaseA2 activity -> PAF
Also AA which makes:
LTC4, D4 (_____-like effects) E4
ProstaglandinD2 (does what?)
Cytokines: TNF, IL-_,_,_,_,_, GM-CSF(does what)

Back 16

mast
histamine
bronchospasm, secretion
factor that stimulates differentiation into granulocytes and monocytes from stem cells

Front 17

Secondary mediators for Type I Hypersensitivity:
Neutrophils and monocytes makes what?
Macrophages make inflammatory proteins (___-1alpha and beta)
Epithelial cells make IL-_ and -_, GM-CSF

Back 17

LTB4 - chemotaxis
MIP
IL-6 and IL-8

Front 18

What function do these have in the late phase reactin?
Leukotrienes, PAF, TNF-alpha, cytokines

Back 18

Recruitement of cells:
neutrophils, eosinophils, basophils, monocytes, CD4 T cells

Front 19

What do the recruited cells release in the late phase reaction of type I hypersensitivity:
LT__, LT__, PAF
eos - MBP/ECP which damage ______
all amplify and sustain response without more _____
_____ blunt cell response

Back 19

LTB4, LTC4
epithelia
antigen
steroids

Front 20

People who get local anaphylaxis have ____ - genetically determined state. 10% pop, 50% have _____ hx. Higher serum ___ levels.

Back 20

atopy
family
IgE

Front 21

Atopics have higher numbers of IL-_ producing Th2 cells in the blood

Back 21

IL-4

Front 22

What are the little bits of inflammatory cell membrane called that form spirals in the sputum of asthmatics?

Back 22

Kurschman's spirals

Front 23

______ ______ is very thick in polyps, respiratory bronchi, anwhere in asthmatics

Back 23

basement membrane

Front 24

What skin condition is common due to chronic allergies?

Back 24

Atopic dermatitis

Front 25

Antisera, hormones, enzymes, drugs (esp penicillin) all cause what reaction in certain people?

Back 25

Systemic Anaphylaxis
More severe - itching, hives, erythema, constriction of bronchioles, laryngeal edema, hoarseness, vomiting, cramps,diarrhea, laryngeal obstruction, shock, death

Front 26

Histamine, PAF, Leukotrienes C4, D4, E4, proteases that activate comlpement and kinins, Prostaglandin D2 all cause what

Back 26

Vasodilation - increased vascular permeability

Front 27

Leukotrienes C4, D4, E4, histamine, PAF, Prostaglandins all cause what?

Back 27

Smooth Muscle Spasm

Front 28

Cytokines (TNF), LTB4, ECF/NCF, PAF all cause what?

Back 28

Cellular Infiltration

Front 29

What type of hypersensitivity is this?
Mediated by antibodies directed against antigens already present on cell surfaces or in extracellular matrix

Back 29

Type II

Front 30

Type II Hypersensitivty is a ______ response. Antibodies are directed against:
intrinsic Ag on ____ surface
absorbed antigens (drugs) on _____ surface
cell surface receptors
Basement membranes in ________ syndrome

Back 30

humoral
RBC
RBC
Goodpasture (glomerular and alveolar BM)

Front 31

Antibodies in Type II reactions:
phagocytosis - like opsonins (___ and C_b)
Lysis of cells
Dysfunction of ______
Destruction of _______ _______

Back 31

IgG
C3b
receptors
basement membranes

Front 32

___ activates complement C1-4-2-3/3b
___ promotes formation of C5b-6-7-8-9 killer complex which drills holes in ___ bilayer causing lysis

Back 32

IgG
IgM
RBC

Front 33

IgG happens ____vascular, in ____ autimmune hemolytic anemia
IgM is ____vascular in _____ autoimmune hemolytic anemia

Back 33

extra
warm
intra
cold

Front 34

Victims of antibodies in Hypersensitivty Type __ reaction:
RBC:
Autoimmune _____ anemia
Transfustion reactions
Erythroblastosis fatalis (maternal __ crosses placenta)
___: agranulocytosis
______: thrombocytopenia

Back 34

II
hemolytic
IgG
WBC
Platelets

Front 35

C3a and C5a have a role in both type I and type II hypersensitivities
type I - activate ____ cells
type II - chemotaxis, call in _____

Back 35

mast
neutrophils

Front 36

In type II reactions, antibodies are attached to what?
Activated by ________
The Rc receptor on ______ binds to antibody causing the release of free radicals, poisonous enzymes

Back 36

antigen on basement membrane
complement
neutrophils

Front 37

What syndrome has a characteristic radiologic appearance known as the pepper pot lung?

Back 37

Goodpasture syndrome
Glomerular and Alveolar basement membranes

Front 38

Pemphigus vulgaris is caused by type II antibody attack on ________, causing loose epithelial cells and suprabasal ____ formation

Back 38

desmosomes
bulla (suprabasal)

Front 39

Which condition results in the "fishnet stocking" appearance of epithelium?

Back 39

Pemphigus vulgaris

Front 40

Type II reactions can create antibodies against receptors such as the ___ hormone receptor causing them to make ___ hormone which results in _____ disease. What is this?

Back 40

TSH
more - stimulates them
Graves disease - hyperthyroidism (big lumps on neck, eyes stick out, hyper)

Front 41

Antibodies against which receptor in Type II reactions causes Myasthenia gravis due to impairment of neuromuscular transmission?

Back 41

Acetylcholine receptor (motor end-plate)
Exhaust what little Ach you had immediately, can't do more than a couple flexions

Front 42

Which type of Hypersensitivty is this:
Circulating antigen-antibody complexes produce tissue damage by eliciting inflammation at sites of deposition.

Back 42

Type III Hypersensitivity

Front 43

Which complexes are more dangerous - large or small? And why?

Back 43

Large removed by RES
Intermediate/smaller are more dangerous because there are more formed and they overload the RES
"Gum up the spleen" and canuse functional hyposplenism

Front 44

Complex deposition in Type II can happen in two ways:
1) complexes formed in ______ deposit in tissues. Distributes bodywide
2) complexing occurs __ ____ after initial implantation of antigen (overtones of Type __). Distributes locally (kidney, joints, skin, serosa)

Back 44

circulation
in situ
II

Front 45

How many days after antigen introduction do antibodies form?

Back 45

7 days
enter blood, form complexes with circulating Ag, deposit in tissues

Front 46

At day __ after antigen presentation, drama begins:
Fever, Urticaria, lymphoadenopathy, proteinuria

Back 46

10

proteinuria occurs before hemoturia - complexes damage glomerular BM and they are leaky. Proteins smaller than RBC

Front 47

Ag:ab complexes cause tissue damage by activating ______ ______, attracted cells activated by attachment to C_b and __ receptors, aggregation of _____, activation of ______ factor

Back 47

coagulation cascade
C3b and Fc receptors
platelets
Hageman

Front 48

Activation of the complement cascade in Type III reactions causes formation of _____ factors (esp C_a for pmns, mos) and release of anaphylatoxins (C_a, C_a) which increase permeability

Back 48

chemotactic
C5a
C3a, C5a

Front 49

Which hypersensitivty reaction has a net effect of glomerulonephritis, vasculitis, arthritis, serositis, etc.

Back 49

Type III - complexes lodge here

Front 50

In Type III hypersensitivity what 3 elements come out of the blood vessel wall, leading to fibrinoid necrosis?
Doesn't occur in what?

Back 50

Fibrin, Ig, complement

veins

Front 51

If you see a round thing with fibrin, bvs with destroyed lumen - indicates what condition?

Back 51

fibrinoid necrosis
Some kind of vasculitis

Front 52

What is the Arthus reaction? What is it testing for?

Back 52

Arthus reaction – type III experimental thing… just need to know that if you have a pt with known circulating antibodies to something and you inject that antigen into his skin all hell breaks loose. This the Arthus reaction.

Front 53

What do each of the complement fractions do?
C3b:
C3a, C5a (anaphylatoxins):
C5a:
C5-9:

Back 53

promotes phagocytosis of complexes
increase permeability
chemotactic for pmns and monocytes
membrane damage or cytolysis

Front 54

Duration of Type III diseases:
Acute post-streptococcal glomerulonephritis - ___-term
Systemic lupus erythematosus - ____-term

Back 54

short - self-limited (immune complexes catabolized)

long - chronic IC disease, ICs formed in agn excess most likely to be deposited