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Imunology > Lecture 28 - 29 (Type I & II Hypersensitivity) > Flashcards

Lecture 28 - 29 (Type I & II Hypersensitivity) Flashcards

1
Q

what is hypersensitivity?

A

a state of altered reactivity in which the body reacts with an exaggerated immune response to what is perceived as a foreign substance

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2
Q

hypersensitivity is a reflection of ____________ or ___________ immune responses

A

excessive or aberrant

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3
Q

*Immune Reactant: IgE
*Important Cells Involved: Mast cells (& eosinophils)
*Mechanism of Damage: TH2 response, degranulation of mast cells & eosinophils; inflammation
which hypersensitivity?

A

type I hypersensitivity

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4
Q

*Immune Reactant: IgG (& IgM)
*Important Cells Involved: Neutrophils, Macrophages
*Mechanism of Damage: Antibodies made against cell surface antigens or extracellular matrix antigens; opsonization, phagocytosis, etc.
which hypersensitivity?

A

type II hypersensitivity

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5
Q

*Immune Reactant: IgG (&IgM)
*Important Cells Involved: Neutrophils & Mast Cells
*Mechanism of Damage: Immune complexes of antigen and antibody aren’t removed by phagocytosis; deposited in vascular basement membranes, etc.
which hypersensitivity?

A

type III hypersensitivity

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6
Q

*Immune Reactant: TH1 & CTLs
*Important Cells Involved: T Cells, APCs, Macrophages
*Mechanism of Damage: CD4+ activating macrophages and producing cytokine-mediated inflammation or CD8+ causing direct target cell lysis
which hypersensitivity?

A

type IV hypersensitivity

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7
Q

which hypersensitivity is exemplified by all of the following:

-allergic rhinitis
-food allergies
-bronchial asthma
-systemic anaphylaxis
-vaccine reactions

A

type I hypersensitivity

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8
Q

which hypersensitivity is exemplified by all of the following:

-Immune Mediated Hemolytic Anemia (IMHA)
-Immune Thrombocytopenia (ITP)
-Hemolytic Disease of the Newborn (HDN)
-Myasthenia Gravis
-pemphigus vulgaris
-drug reactions
-Acute Rheumatic Fever

A

type II hypersensitivity

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9
Q

which hypersensitivity is exemplified by all of the following:

-Systemic Lupus Erythematosus (SLE)
-Purpura (Little bruises on the skin)
-Recurrent Airway Obstruction (RAO)
-Blue Eye
-Farmer’s Lung (Hypersensitivity Pneumonitis)
-serum sickness
-Rheumatoid arthritis (Non-Erosive)
-Glomerulonephritis associated with Rheumatic Fever

A

type III hypersensitivity

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10
Q

what cells are responsible for the acute inflammatory response in the early phase of type 1 hypersensitivity?

a. pre-formed Mast Cells
b. T cells (Like TH17)
c. neutrophils & macrophages

A

a. pre-formed Mast Cells

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11
Q

which hypersensitivity is exemplified by all of the following:

-allergic contact dermatitis
-Tuberculin reaction (used for Tb test)
-type 1 diabetes
-erosive arthritis
-Multiple sclerosis

A

type IV hypersensitivity

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12
Q

exaggerated TH2 response & exaggerated IgE production are characteristic of which hypersensitivity?

A

type I hypersensitivity

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13
Q

what cells are responsible for the second wave late phase reaction in a type 1 hypersensitivity 6-12 hours post exposure? (characterized by redness, edema, pruritus)

a. pre-formed Mast Cells
b. T cells (Like TH17)
c. neutrophils & macrophages

A

b. T cells (Like TH17)
c. neutrophils & macrophages

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14
Q

type I hypersensitivity:
binding of antigens with mast cell-bound IgE leads to…

A

mast cell degranulation

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15
Q

the exaggerated TH2 response & exaggerated IgE production seen in Type 1 Hypersensitivity is called:

A

atopy

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16
Q

what is type I hypersensitivity?

A

a form of acute inflammation that results from the interaction of antigens with mast cell-bound IgE

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17
Q

t/f: granule content causes acute inflammation

A

true

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18
Q

immediate hypersensitivity

a) type I hypersensitivity
b) type II hypersensitivity
c) type III hypersensitivity
d) type IV hypersensitivity

A

a) type I hypersensitivity

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18
Q

immune complex-mediated hypersensitivity

a) type I hypersensitivity
b) type II hypersensitivity
c) type III hypersensitivity
d) type IV hypersensitivity

A

c) type III hypersensitivity

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19
Q

antibody-mediated hypersensitivity

a) type I hypersensitivity
b) type II hypersensitivity
c) type III hypersensitivity
d) type IV hypersensitivity

A

b) type II hypersensitivity

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20
Q

T-cell mediated hypersensitivity

a) type I hypersensitivity
b) type II hypersensitivity
c) type III hypersensitivity
d) type IV hypersensitivity

A

d) type IV hypersensitivity

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21
Q

development of atopy and type I hypersensitivity depends upon the interaction of…

A

genes and environmental factors

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21
Q

excessive production of IgE is called __________ and affected individuals are said to be ____________

A

atopy; atopic

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22
Q

what are the two important features of type I hypersensitivity?

A

-exaggerated TH2 response
-excessive IgE production

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23
Q

what is the role of IL-4 in an IgE response such as in type 1 hypersensitivity reactions?

a) produced by TH1; promotes more TH1; promotes IgE
b) produced by TH2; promotes more TH2; promotes IgE
c) produced by TH1; promotes more TH1; inhibits IgE
d) produced by TH2: promotes more TH2; inhibits IgE

A

b) produced by TH2; promotes more TH2; promotes IgE

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24
Q

which of the following inhibit IL-44?

  1. IFNα/β or IFNγ?
  2. IL-2 or IL-12?
A
  1. IFNγ
  2. IL-12
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25
Q

what is Il-4 produced by?

A

TH2 cells

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26
Q

type I hypersensitivity:
once IL-4 is produced by TH2 cells, it promotes the development of more TH2 cells and promotes ______ responses

A

IgE

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27
Q

the response to IL-4 is inhibited by _________ and __________

A

IFNγ and IL-12

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28
Q

what causes degranulation upon a second exposure to allergen?

a) co-stimulation by B7 to stimulate mast cells
b) cross binding of allergen by IgE bound to mast cells

A

b) cross binding of allergen by IgE bound to mast cells

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28
Q

IgE binds to what on mast cells?

a) CD152
b) Fas
c) FcεRI receptor
d) TLR

A

c) FcεRI receptor

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29
Q

the allergy loop:
dendritic cells express trimeric ____________ and as a result can bind antigen-IgE complexes
*this antigen, once processed, stimulates TH2 responses and promotes the IgE response

A

FcεRI receptor

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30
Q

what is stimulated to cause the switch to IgE in the first exposure to an allergen?

a) TH1 cells
b) TH2 cells
c) TH17 cells
d) Treg cells

A

b) TH2 cells

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31
Q

IgE is associated with rapid degranulation. Which immunoglobulin is associated with normal gradual degranulation?

A

IgG

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32
Q

stimulation of α adrenergic receptors causes:
-[enhanced/suppressed] degranulation of mast cells
-[contraction/relaxation] of smooth muscle
-[constriction/dilation] of blood vessels

A

-enhanced degranulations of mast cells
-contraction of smooth muscles
-constriction of blood vessels

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33
Q

stimulation of β adrenergic receptors causes:
-[enhanced/suppressed] degranulation of mast cells
-[contraction/relaxation] of smooth muscle
-[constriction/dilation] of blood vessels

A

-suppressed degranulation of mast cells
-relaxation of smooth muscles
-dilation of blood vessels

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34
Q

to treat allergic reactions by reducing edema and raising blood pressure we use:

a) α agonist
b) β agonists

A

a) α agonist

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35
Q
A
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36
Q
A
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37
Q

epinephrine (or adrenaline) has both _____ and _____ adrenergic activity

A

α and β

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38
Q

Epinephrine has…

a) α adrenergic activity
b) β adrenergic activity
c) both α & β adrenergic activity
d) neither α or β adrenergic activity

A

c) both α & β adrenergic activity

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38
Q

what is the interleukin for eosinophils?

A

IL-5

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39
Q

______________ exacerbate the inflammation triggered first by mast cells via a complex array of molecules that contribute to the acute inflammatory response

A

eosinophils

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40
Q

clinical signs of type I hypersensitivity result from abrupt and excessive release of inflammatory mediators from…

A

mast cells, basophils, and eosinophils

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40
Q

type I hypersensitivity:
if the rate of release of vasoactive molecules exceeds its ability to adjust changes in the vascular system, an animal will undergo ________ ___________ and may die

A

allergic anaphylaxis

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40
Q

severe urticaria

a) type I hypersensitivity
b) type II hypersensitivity
c) type III hypersensitivity
d) type IV hypersensitivity

A

a) type I hypersensitivity

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41
Q

what is the shock organ in dogs?

A

hepatic veins (the liver)

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42
Q

treatments of type I hypersensitivity (4)

A

-prevent exposure to the offending allergens
-epinephrine for allergic anaphylaxis
-corticosteroids for local inflammation
-desensitizing injections of allergens

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43
Q

for local inflammation we use:

a) corticosteroids
b) epinephrine

A

a) corticosteroids

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44
Q

for anaphylaxis/systemic type 1 we use:
a) corticosteroids
b) epinephrine

A

b) epinephrine

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45
Q

what is the shock organ of most animals other than the dog?

A

respiratory tract

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46
Q

what 3 animals have the intestines as an additional shock organ?

A

horse, pig, and cat

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46
Q

type I hypersensitivities, also called immediate hypersensitivity, are mediated by __________ attached to mast cells

A

immunoglobulin E (IgE)

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46
Q

t/f: the clinical signs of allergic disease depend in large part on the route by which antigens (allergens) enter the body

A

true

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47
Q

“IgG or IgM Mediated Cytotoxic Hypersensitivity” is another name for which type of hypersensitivity?

A

type II hypersensitivity

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48
Q

type II hypersensitivity occurs when antibodies and complement attach to normal cells and cause ___________ and ___________ of cells

A

opsonization and phagocytosis

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49
Q

what are the 3 effects of type II hypersensitivity reactions?

A
  1. Complement/FcR mediated inflammation
  2. opsonization & phagocytosis
  3. abnormal physiologic responses without tissue injury (Ex: Myasthenia gravis)
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49
Q

blood antigens are controlled by _________ and __________

A

genes and inherited

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50
Q

RBCs express cell surface molecules, usually glycoproteins or glycolipids, that act as antigens and are called…

A

blood group antigens or erythrocyte antigens (EA)

51
Q

t/f: animals may possess antibodies against foreign blood group antigens even when never previously exposed to foreign red cells

A

true

52
Q

what are the 2 results of IgM binding donor RBC antigens?

A

agglutination & hemolysis

53
Q

the action of an antibody when it cross-links multiple antigens producing clumps of antigens

a) agglutination
b) hemolysis

A

a) agglutination

53
Q

antibody + complement - creates MAC and puts holes in RBC membrane causing hemoglobin to leak out

a) agglutination
b) hemolysis

A

b) hemolysis

54
Q

severity of blood transfusion reactions ranges from mild febrile response to rapid death - depends mainly on the amount of…

A

incompatible blood transfused

54
Q

a large number of lysed RBCs trigger ______________ and __________

A

blood clotting and DIC

55
Q

if a reaction is suspected while giving a blood transfusion what should you do?

A

-transfusion must be stopped immediately
-maintain urine flow with fluids and a diuretic

56
Q

how do you prevent a blood transfusion reaction?

A

cross-matching

57
Q

what is hemolytic disease of the newborn (HDN)?

A

-fetal RBCs leak into the bloodstream of their dams through the placenta
-if they have incompatible blood antigens the dam makes antibodies to the fetal RBCs
-in sensitized females, these anti-fetal RBC antibodies are concentrated into their colostrum
-when a newborn suckles, colostrum antibodies are absorbed through the intestinal wall and cause rapid destruction of fetal RBCs

58
Q

what four conditions must be met for HDN to occur?

A

-fetus must inherit a red cell antigen from its sire that’s not present in its mother

-the mother must be sensitized to this antigen

-the mother’s response must be boosted by transplacental hemorrhage/repeated pregnancies

-a newborn animal must ingest colostrum containing high-tiered antibodies to its red cells

59
Q

what are horses blood groups? (7)

A

EAA
EAC
EAD
EAK
EAP
EAQ
EAU

60
Q

in mules, hemolytic disease of the newborn (HDN) in foals is seen in about _____%

A

8-10%

60
Q

in thoroughbreds and Standardbreds, hemolytic disease of the newborn (HDN) is ___%

A

2%

61
Q

hemolytic disease is a problem in mares that have had…

A

several foals

61
Q

the most severe form of HDN results from the production of antibodies against the ___ antigen of the EAA system

A

Aa

62
Q

anti-Aa and anti-Qa accounts for a total of ____% of HDN in foals

A

90%

63
Q

t/f: antibodies produced by mares cross the placenta

A

false - do not cross the placenta

63
Q

how do antibodies produced by mares reach the foal?

A

through colostrum

64
Q

HDN in foals:
earliest signs are ____________ and _____________

A

weakness and depression

65
Q

HDN in foals:
mucus membrane of affected foals may be pale and may eventually show ___________

A

jaundice

66
Q

how does HDN in calves differ from HDN in foals?

A

-HDN is rare

-usually see similar issue from vaccination containing RBCs from infected calves sensitizing the mother

66
Q

how does HDN in pigs differ from HDN in foals?

A

-used to be associated with Hog Cholera vaccine
-true HDN is also rare

67
Q

HDN in calves is rare but has resulted from vaccination against ____________ or __________

A

anaplasmosis or babesiosis

68
Q

what is Bovine Neonatal Pancytopenia?

A

-hemorrhagic disease of newborn beef calves
-sudden onset of bleeding
-anemia and leukopenia
-bone marrow completely aplastic
-traced back to the use of BVD vaccine

69
Q

Bovine Neonatal Pancytopenia:
studies showed that the colostrum of dams of these calves contained antibodies against the ____________ antigens of neonatal leukocytes and bone marrow stem cells

A

MHC I

70
Q

HDN in pigs formerly occurred as a result of the use of ______ ________ vaccine containing pig blood

A

hog cholera

71
Q

talk about type II hypersensitivity reactions to drugs

A

-drugs and antibodies may combine directly and activate Complement and RBCs will be destroyed

-some drugs (Penicillin) may bind to RBCs and cause hemolytic anemia

71
Q

type II hypersensitivity, also called ___________ hypersensitivity, occurs when antibodies (and complement) destroy normal cells

A

cytotoxic

72
Q

the destruction of transfused red blood cells when administered to a mismatched recipient is an example of type ____ hypersensitivity

A

II

73
Q

some drugs may bind to blood cells and make them targets of antibodies in a type ____ hypersensitivity reaction

A

II

74
Q

type III hypersensitivity develops when antigens and antibodies combine to form __________ _________, which if deposited in large amounts in tissues, trigger severe inflammation

A

immune complexes

75
Q

type III hypersensitivity:
the prerequisite for the development of immune complex disease is the persistent presence of….

A

soluble antigen and antibody

75
Q

type III hypersensitivity:
timing of the clinical manifestation is usually ____-____ after exposure

A

6-8 hours

76
Q

type III hypersensitivity:
the most frequently affected sites include the…

A

lungs, kidneys, joints, and brain (i.e., where large capillary beds exist)

77
Q

what cells and mediators are responsible for type III hypersensitivity?

A

-neutrophils: granule contents
-macrophages: phagocyte
-mast cells: granule contents
-complement: Anaphylatoxins (C3a, C5a)

78
Q

_____ and ______ are also called anaphylatoxins since, when injected in sufficient amounts, they can kill an animal in a manner similar to anaphylaxis by causing mast cells to release histamine granules = pro-inflammatory

A

C3a and C5a

78
Q

______________ release oxidants and enzymes that lead to acute inflammation and tissue destruction in a type III hypersensitivity reaction

A

neutrophils

79
Q

what are the two major classifications of a type III hypersensitivity?

A

localized and generalized

79
Q

what is a localized type III hypersensitivity?

A

-immune complexes are deposited in tissues & the reaction is seen at the site of the antigen entry
-the antigen is introduced into the tissue and preformed antibody in circulation binds to its antigen

80
Q

what is a generalized or systemic type III hypersensitivity?

A

-there is excess antigen in the circulation

-antibody in the circulation (IgG) binds to circulating antigen and forms immune complexes

-immune complexes circulate and get deposited in blood filtration points

81
Q

-local reaction seen in the skin after subcutaneous or intradermal injection of an antigenic substance (post-vaccination)
-type III hypersensitivity
-starts as red edematous swelling and eventually there is local hemorrhage and thrombosis; even necrosis possibly
what is this reaction called?

A

Arthus Reaction

82
Q

what are the common sites of immune complex deposition?

A

Large Capillary Beds:
-skin
-lungs
-kidneys
-joints
-brain

82
Q

how is mast cell activation in type III hypersensitivity different from a type I hypersensitivity?

A

-instead of IgE, receptors are stimulated by complement intermediates (C3a/C5a) or IgG

-not fully activated, only some granules are released

82
Q

example of type III hypersensitivity:
-cause: Canine Adenovirus type 1 or vaccination with live modified virus
-effect seen: diffuse clouding of the cornea & opacity with anterior uveitis
-develops: 1-3 days post infection & usually resolves spontaneously

A

Blue Eye

83
Q

example of type III hypersensitivity:
-cause: inhaled antigens like mold from S. rectivirgula
-effect seen: pneumonia, severe cough, and difficulty breathing
-develops: 5-10 hours post exposure to moldy hay

A

Hypersensitivity Pneumonitis (“Farmer’s Lung”)

83
Q

generalized type III hypersensitivity:
immune complexes are deposited at sites of _________ __________

A

plasma filtration

84
Q

example of type III hypersensitivity:
-cause: immune complexes in the blood stream (after anti-toxin treatment for example)
-effect seen: systemic inflammation, edema, lymph node enlargement, joint swelling, & generalized vasculitis

A

Serum Sickness

85
Q

t/f: Penicillin can cause all four types of hypersensitivity

A

true

86
Q

talk about Methimazole drug reaciton

A

-Methimazole inhibits thyroid hormone synthesis by interfering with iodine incorporation

-sensitized patients develop antibodies to drug/hapten

87
Q

immune complexes contain: IgG, IgM, IgA, and C3
associated with: infectious diseases
deposits are in: Mesangial & Subendothelial regions
a) type 1 Membrano-proliferative Glomerulonephritis (MPGN)
b) type 2 Membrano-proliferative Glomerulonephritis (MPGN)
c) type 3 Membrano-proliferative Glomerulonephritis (MPGN)

A

a) type 1 Membrano-proliferative Glomerulonephritis (MPGN)

87
Q

immune complexes contain: C3 only (no antibodies)
associated with: dense deposits
deposits are in: glomerular basement membrane
a) type 1 Membrano-proliferative Glomerulonephritis (MPGN)
b) type 2 Membrano-proliferative Glomerulonephritis (MPGN)
c) type 3 Membrano-proliferative Glomerulonephritis (MPGN)

A

b) type 2 Membrano-proliferative Glomerulonephritis (MPGN)

88
Q

immune complexes contain: IgG, IgM, IgA, and C3
associated with: very small immune complexes
deposits are in: in subepithelial region
a) type 1 Membrano-proliferative Glomerulonephritis (MPGN)
b) type 2 Membrano-proliferative Glomerulonephritis (MPGN)
c) type 3 Membrano-proliferative Glomerulonephritis (MPGN)

A

c) type 3 Membrano-proliferative Glomerulonephritis (MPGN)

89
Q

what is Glomerulonephritis?

A

-immune complexes deposit in the glomeruli

-cause basement membrane thickening & stimulate glomerular cells to proliferate

90
Q

local deposition of immune complexes in the lungs following inhalation of antigenic dusts causes ___________ _________

A

hypersensitivity pneumonitis

90
Q

immune complexes formed in the bloodstream are deposited in the glomeruli of the kidney and cause…

A

membrane-proliferative glomerulonephritis

91
Q

type _____ hypersensitivity is a feature of many viral disease, especially if the virus is not neutralized by antibodies and large amount of immune complexes are generated as a result

A

type III

92
Q

what cell types are responsible for type IV hypersensitivity reaction?

A

T cells & macrophages are the main mediators

93
Q

which hypersensitivity is also known as the delayed hypersensitivity?

A

type IV hypersensitivity (T-cell mediated/antibody independent hypersensitivity)

94
Q

what are the 2 routes of a type IV hypersensitivity reaction to cell damage?

A
  1. soluble antigen causes cytokine mediated inflammation from CD4 cells that injures nearby tissue
  2. cell-associated antigen causes T-cell mediated killing (CTLs)
95
Q

clinical presentation of a type IV hypersensitivity reaction

A

-induration: hard, raised lesions
-erythema and vesicles: reddened skin and fluid filled vesicles

96
Q

reactive chemical on skin triggers reaction by binding to PRRs such as TLR4

a) atopic dermatitis
b) allergic contact dermatitis

A

b) allergic contact dermatitis

97
Q

pathogenesis: type I hypersensitivity
a) atopic dermatitis
b) allergic contact dermatitis

A

a) atopic dermatitis

98
Q

pathogenesis: type IV hypersensitivity
a) atopic dermatitis
b) allergic contact dermatitis

A

b) allergic contact dermatitis

99
Q

clinical signs: hyperemia, urticaria (hives), and pruritus (itch)
a) atopic dermatitis
b) allergic contact dermatitis

A

a) atopic dermatitis

100
Q

clinical signs: hyperemia, vesiculation, alopecia, and erythema
a) atopic dermatitis
b) allergic contact dermatitis

A

b) allergic contact dermatitis

101
Q

distribution: face, nose, eyes, feet, perineum
a) atopic dermatitis
b) allergic contact dermatitis

A

a) atopic dermatitis

102
Q

distribution: hairless areas, usually ventral abdomen and feet
a) atopic dermatitis
b) allergic contact dermatitis

A

b) allergic contact dermatitis

103
Q

major allergens: foods and pollens, fleas, inhaled allergens
a) atopic dermatitis
b) allergic contact dermatitis

A

a) atopic dermatitis

104
Q

major allergens: reactive chemicals, dyes in contact with skin
a) atopic dermatitis
b) allergic contact dermatitis

A

b) allergic contact dermatitis

105
Q

diagnosis: intradermal testing, immediate response
a) atopic dermatitis
b) allergic contact dermatitis

A

a) atopic dermatitis

106
Q

diagnosis: delayed response on patch testing
a) atopic dermatitis
b) allergic contact dermatitis

A

b) allergic contact dermatitis

107
Q

pathology: mast cell and eosinophil infiltration, edema
a) atopic dermatitis
b) allergic contact dermatitis

A

a) atopic dermatitis

108
Q

pathology: mononuclear cell infiltration, vesiculation
a) atopic dermatitis
b) allergic contact dermatitis

A

b) allergic contact dermatitis

109
Q

treatment: steroids, antihistamines, hyposensitization
a) atopic dermatitis
b) allergic contact dermatitis

A

a) atopic dermatitis

110
Q

treatment: steroids
a) atopic dermatitis
b) allergic contact dermatitis

A

b) allergic contact dermatitis

111
Q

sources of contact allergens in animals

A

-insecticides in flea collars, sprays, and dips
-wood preservatives
-floor waxes
-carpet dyes
-some pollens
-cream/ointments
-leather products
-paints
-house plants
-metals (nickel, etc.)

111
Q

talk about Stevens-Johnson Syndrome

A

-T cell mediated hypersensitivity to drugs: antibiotics/NSAIDS

-develop rash that blisters into vesicles/shed large areas of epidermis and develop skin ulcers

-sloughing of the skin

-type IV hypersensitivity

112
Q

what are the 3 drugs that are commonly associated with Stevens-Johnson Syndrome

A
  1. Antibiotics
  2. Sulfadrugs
  3. NSAIDs
113
Q

patients affected with this syndrome develop a rash that blisters into vesicles, then they shed large areas of epidermis and develop skin ulcers on the mouth, lips, eyes, and or genitals

A

Stevens-Johnson Syndrome

114
Q

tests if the patient’s lymphocytes react to a given antigen

a) T-Cell proliferation Assay
b) measuring T-Cell mediated cytotoxicity
c) measuring cytokine release
d) ELISA

A

a) T-Cell proliferation Assay

115
Q

tests if patients CTLs capable of killing affected cells

a) T-Cell proliferation Assay
b) measuring T-Cell mediated cytotoxicity
c) measuring cytokine release
d) ELISA

A

b) measuring T-Cell mediated cytotoxicity

116
Q

used as an alternative TB test

a) T-Cell proliferation Assay
b) measuring T-Cell mediated cytotoxicity
c) measuring cytokine release
d) ELISA

A

c) measuring cytokine release

117
Q

measures the frequency of cytokine producing cells; used to quantify active T cells (anti-cytokine bound to membrane in this case)

a) T-Cell proliferation Assay
b) measuring T-Cell mediated cytotoxicity
c) measuring cytokine release
d) ELISA

A

d) ELISA

118
Q

some antigens, when injected into the skin, induce a slowly developing inflammatory response called delayed, or type ____ hypersensitivity

A

type IV

119
Q

delayed hypersensitivity reactions are mainly mediated by _________ and ____________

A

T cells and macrophages

120
Q

a good example of delayed hypersensitivity is the reaction of ______________ cattle to intradermal injection of tuberculin

A

tuberculosis

121
Q

different form of type IV hypersensitivity occurs in allergic contact dermatitis. This is a slowly developing inflammatory response that occurs when reactive chemicals bind to skin cells and trigger ___________ responses

A

T cell

122
Q

____ _______ assays for cell-mediated immunity generally focus on detecting secreted cytokines or measuring cell division induced by exposure to antigens

A

in vitro

Imunology (10 decks)

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