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Year 2 MIS > Overview and classification of immunological diseases > Flashcards

Overview and classification of immunological diseases Flashcards

1
Q

There are 4 types of hypersensitivity, which is an inn-appropriate response of the immune system, generally attack the host cells. Of the 4 types of hypersensitivity, which one is is not depending on an antibody?

1 - type I
2 - type II
3 - type III
4 - type IV

A

4 - type IV

- called immune cell mediate or delayed type hypersensitivity

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2
Q

What term is used to describe the bodies inappropriate response to host tissue?

1 - reactive oxygen deficiency
2 - pathogen associated
3 - host attack complexes
4 - immunodeficiency

A

4 - immunodeficiency

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3
Q

What is central tolerance?

1 - receiving vaccinations
2 - removing self-selective B and T cells
3 - removing innate immune cells
4 - injecting with B cells

A

2 - removing self-selective B and T cells

- B and T cells that bind self-antigens are re-processed or undergo apoptosis

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4
Q

What is the purpose of Gell an d Coombes classification?

A
  • identify the type of hypersensitivity

- type I, II, III and IV

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5
Q

What is a type I hypersensitivity?

1 - reaction to external antigen mediated IgE antibodies
2 - cytotoxic reaction mediated by IgG or IgM antibodies
3 - reaction mediated by immune complexes.
4 - delayed reaction mediated by cellular response

A

1 - reaction to external antigen mediated IgE antibodies

  • patient has low self tolerance as it should not respond to these antigens
  • hayfever for example, essentially allergies
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6
Q

What are the 2 stages of type I hypersensitivity?

1 - early phase and sensitisation
2 - early phase and late phase
3 - late phase and sensitisation
4 - early phase and chronic phase

A

2 - early phase and late phase

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7
Q

Type I hypersensitivity is a reactions to antigens from outside the body. These are generally allergens, where patient has low self tolerance and it mounts an immune response when it should not respond to these antigens. Which antibody is specifically associated with a type I hypersensitivity?

1 - IgG
2 - IgA
3 - IgM
4 - IgE

A

4 - IgE

- also called IgE mediated immune response

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8
Q

What cells bind and sample antigens that enter the body, even if we do not have an immune response to them?

1 - basophils
2 - eosinophils
3 - antigen presenting cells (dendritic, macrophages, B cells)
4 - neutrophils

A

3 - antigen presenting cells (dendritic, macrophages, B cells)

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9
Q

Generally antigen presenting cells bind antigens and then travel to the secondary lymphoid tissue and present the antigen on an MHC-II molecule to what cells?

1 - naive T helper cell
2 - primed CD4 helper cells
3 - CD4 T helper cell
4 - primed cytotoxic CD8 cell

A

1 - naive T helper cell

- then differentiates into a primed T2 T helper cell

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10
Q

Generally antigen presenting cells bind antigens and and then travel to the secondary lymphoid tissue and present the antigen on an MHC-II molecule to naive T helper cell. To turn into a T2 helper cell the naive T helper cell needs to be stimulated. What cytokines are involved in this stimulation?

1 - IL-1, IL-4 and IL-5
2 - IL-4, IL-5 and IL-10
3 - IL-4, IL-5, IL-13
4 - IL-6, IL-4 and IL-5

A

3 - IL-4, IL-5, IL-13

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11
Q

Generally antigen presenting cells bind antigens and and then travel to the secondary lymphoid tissue and present the antigen on an MHC-II molecule to naive T helper cell. To turn into a T2 helper cell the naive T helper cell needs to be stimulated IL-4, IL-5, IL-13 cytokines. This primed T2 helper T cell then releases cytokines to stimulate B cells in order to initiate class switching. These B cells then switch from producing IgM to which antibody?

1 - IgG
2 - IgA
3 - IgM
4 - IgE

A

4 - IgE

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12
Q

Generally antigen presenting cells bind antigens and and then travel to the secondary lymphoid tissue and present the antigen on an MHC-II molecule to naive T helper cell. To turn into a T2 helper cell the naive T helper cell needs to be stimulated IL-4, IL-5, IL-13 cytokines. This primed T2 helper T cell then releases cytokines to stimulate B cells in order to initiate class switching from IgM to IgE. Which cytokine do the type 2 CD8 helper cells secrete to stimulate the CD4 V cells?

1 - IL-1
2 - IL-8
3 - IL-10
4 - IL-4

A

4 - IL-4

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13
Q

In addition to stimulating B cells, the primed T2 helper cells are able to stimulate another innate immune cell through the release of IL-5. What type of innate immune cell is stimulated in this process?

1 - eosinophils and neutrophils
2 - basophils and mast cells
3 - neutrophils and mast cells
4 - macrophages and basophils

A

2 - basophils and mast cells

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14
Q

In addition to stimulating B cells, the primed T2 helper cells are able to stimulate basophils and mast cells through the release of IL-5. What do basophils release that initiates the first phase of a type 1 hypersensitivity?

1 - histamines
2 - IL-6
3 - IL-1
4 - toll like receptors

A

1 - histamines

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15
Q

In addition to stimulating B cells, the primed T2 helper cells are able to stimulate basophils through the release of IL-5. Basophils then release histamines that initiates the sensitisation stage of type 1 hypersensitivity. At the end of the sensitisation stage the IgE secreted by the B cells then binds with the Fc receptors on another type of innate immune cell that prime this immune cell in preparation for a 2nd exposure to the same antigen. What innate immune cell is this?

1 - natural killer cell
2 - mast cell
3 - neutrophil
4 - macrophage

A

2 - mast cell

- histamine is released from these cells to initiate an allergic reaction

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16
Q

During a 2nd exposure to an antigen the primed mast cell with IgE antibodies bound to its structure are able to bind with the antigen. The mast cell is then able to release a number of pro inflammatory mediators, with the main one being histamines. What receptor does histamines bind with?

1 - H1 receptors
2 - MHC-II molecules
3 - Fc receptors
4 - GPCR

A

1 - H1 receptors

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17
Q

During a 2nd exposure to an antigen the primed mast cell with IgE antibodies bound to its structure are able to bind with the antigen. The mast cell is then able to release a number of pro inflammatory mediators, with the main one being histamines, which then binds with H1 receptors. What affect does this have on the lungs?

A
  • binds H1 receptors on smooth muscle surrounding the bronchi
  • causes the smooth muscle to contract and cause breathing difficulty
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18
Q

During a 2nd exposure to an antigen the primed mast cell with IgE antibodies bound to its structure are able to bind with the antigen. The mast cell is then able to release a number of pro inflammatory mediators, with the main one being histamines, which then binds with H1 receptors. What affect does this have on blood vessels?

A
  • H1 receptors cause a release of nitric oxide from endothelium
  • causes vasodilation and increased permeability of blood vessels
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19
Q

During a late phase of an exposure to an antigen the primed mast cell with IgE antibodies bound to its structure are able to bind with the antigen. The mast cell is then able to release a number of pro inflammatory mediators, with the main one being histamines. What else are mast cells able to release that trigger a type I hypersensitivity?

1 - leukotrienes, prostaglandins, platelet activating factor
2 - leukotrienes, IL-6, platelet activating factor
3 - prostaglandins, TLRs, platelet activating factor
4 - prostaglandins, lymphocytes, platelet activating factor

A

1 - leukotrienes, prostaglandins, platelet activating factor

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20
Q

What is a type II hypersensitivity?

1 - reaction to external antigen mediated IgE antibodies
2 - cytotoxic reaction mediated by IgG or IgM antibodies
3 - reaction mediated by immune complexes.
4 - delayed reaction mediated by cellular response

A

2 - cytotoxic reaction mediated by IgG or IgM antibodies

- antibody specific

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21
Q

A type II hypersensitivity is when the cytotoxic T cells attack self tissue. In order to do this B cells that have escaped central tolerance begin producing antibodies that are self reactive. Which antibodies does this occur in?

1 - IgM and IgD
2 - IgM and IgE
3 - IgG and IgE
4 - IgG and IgM

A

4 - IgG and IgM

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22
Q

In a type II hypersensitivity there are 2 types of antigens, intrinsic and extrinsic. What are these?

A
  • intrinsic - self antigens

- extrinsic - antigens external to the body (food, medicine)

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23
Q

If a patient is allergic to penicillin, what happens when the patient is given penicillin?

1 - penicillin binds RBCs and IgD/IgE bind penicillin forming antibody-antigen complex
2 - penicillin binds RBCs and IgM bind penicillin forming antibody-antigen complex
3 - penicillin binds RBCs and IgM/IgG bind penicillin forming antibody-antigen complex
4 - penicillin binds RBCs and IgD/IgA bind penicillin forming antibody-antigen complex

A

3 - penicillin binds RBCs and IgM/IgG bind penicillin forming antibody-antigen complex

  • antibodies are specific to the penicillin, which is an extrinsic antigen
  • the above results in agglutination (clumping together of blood)
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24
Q

In a type II hypersensitivity once an antigen-antibody complex has been formed there are a number of mechanisms that will follow. How is the complement system activated?

1 - C1 binds with Fab region of antigen-antibody complex
2 - C1 binds with Fc region of antigen-antibody complex
3 - C3 binds with Fab region of antigen-antibody complex
4 - C4 binds with Fc region of antigen-antibody complex

A

2 - C1 binds with Fc region of antigen-antibody complex

25
Q

In a type II hypersensitivity once an antigen-antibody complex has been formed there are a number of mechanisms that will follow. The complement system is activated through the binding of C1 binds with the Fc region of antigen-antibody complex. In the complement system some fragments are cleaved. What 3 complement molecules are cleaved and then act as chemokines?

1 - C3b, C4b, C5b
2 - C3a, C4b, C5a
3 - C3a, C4a, C5a
4 - C3b, C4b, C5a

A

3 - C3a, C4a, C5a

- think all have an A and Attracts immune cells

26
Q

In a type II hypersensitivity once an antigen-antibody complex has been formed there are a number of mechanisms that will follow. The complement system is activated through the binding of C1 binds with the Fc region of antigen-antibody complex. In the complement system some fragments are cleaved. What 5 complement molecules create the membrane attack complex?

1 - C5b, C4, C6, C7, C9
2 - C5b, C6, C7, C9
3 - C5b, C6, C7, C8, C9
4 - C5a, C6, C7, C8, C9

A

3 - C5b, C6, C7, C8, C9

- the membrane attack complex is then able to lyse the cell

27
Q

What autoimmune condition results in death of RBCs quicker than they can be made?

1 - thrombocytopenia
2 - sepsis
3 - neutropenia
4 - haemolytic anaemia

A

4 - haemolytic anaemia

- thrombocytopenia, neutropenia, haemolytic anaemia can all be affected

28
Q

Goodpasture’s syndrome is a type II hypersensitivity. What is this syndrome?

1 - antibodies bind extrinsic antigens specifically in kidneys and lungs
2 - antibodies bind intrinsic antigens specifically in liver and spleen
3 - antibodies bind extrinsic antigens specifically in liver and kidneys
4 - antibodies bind intrinsic antigens specifically in kidneys and lungs

A

4 - antibodies bind intrinsic antigens specifically in kidneys and lungs

  • antigens are intrinsic and located on collagen basement membrane in kidney and lungs
  • activates complement system causing damage to membrane
29
Q

If you suspect a patient has haemolytic anaemia what tests can be done to diagnose the patient?

1 - lateral flow test
2 - coombs test
3 - cytology
4 - antibody testing

A

2 - coombs test

30
Q

If you suspect a patient has haemolytic anaemia (low RBCs) the Coombs test can be performed to diagnose the patient. What does the direct test show?

1 - anti-human antibodies in coombs reagent react with antibody-antigen complex on RBCs from patient
2 - anti-human antibodies in coombs reagent react with antibody-antigen complex on WBCs from patient
3 - anti-human antibodies in coombs reagent react with antibody-antigen complex on lymphocytes from patient
4 - anti-human antibodies in coombs reagent react with antibodies in plasma from patient

A

1 - anti-human antibodies in coombs reagent react with antibody-antigen complex on RBCs from patient

  • step 1 = patients RBCs are separated from plasma and should remove all antibodies
  • step 2 = Coombs reagent contaning anti-human antibodies (reacts with human antibodies) is added to RBCs
  • step 3 = if antigen-antibody complex is present on patients RBCs anti-human antibodies bind and cause the blood to agglutinate (clumping together)
  • provides info that the patient has pathology causing low RBCs
  • used to assess for blood transfusion
31
Q

If you suspect a patient has haemolytic anaemia the Coombs test can be performed to diagnose the patient. What does the indirect test show?

1 - anti-human antibodies in coombs reagent react with RBCs from patient
2 - anti-human antibodies in coombs reagent react with WBCs from patient
3 - anti-human antibodies in coombs reagent react with lymphocytes from patient
4 - anti-human antibodies in coombs reagent react with antibodies in plasma from patient

A

4 - anti-human antibodies in coombs reagent react with antibodies in plasma from patient

  • step 1 = lab based RBCs with known antigens are prepared
  • step 2 = patients serum (which will contain antibodies) is mixed with lab based RBCs
  • step 3 = Coombs reagent containing anti-human antibodies is then added
  • step 4 = if agglutination occurs then identifies antibodies are present in the blood prior to exposure to an antigen
32
Q

If i wanted to assess a patients blood type or if a patient had antibodies present in their blood prior to exposure to an antigen, would I use the direct or indirect Coombs test?

A
  • indirect
  • antibodies in Coombs reagent react with anti bodies in patients plasma
  • eg: patient is blood group A will have anti-B antibodies, so if given blood type B, there blood would agglutinate
33
Q

If i wanted to assess if a patient is allergic to a medication, would I use the direct or indirect Coombs test?

A
  • direct
  • antibodies in Coombs reagent react with antigen (penicillin for example) antibody complexes on RBCs
  • patients blood sample would then agglutinate
34
Q

In a type II hypersensitivity once an antigen-antibody complex has been formed there are a number of mechanisms that will follow. There is a component of the complement system that binds with the Fc portion of the IgG or IgM antibody. What aspect of the complement system bind with the Fc portion and what is this called?

1 - C3a and opsonisation
2 - C3b and opsonisation
3 - C5b and opsonisation
4 - C6b and opsonisation

A

2 - C3b and opsonisation

- can allow phagocytes to bind with pathogens or self antigens in type II hypersensitivity

35
Q

What type of hypersensitivity are haemolytic anaemia(sometimes calledautoimmune haemolytic anaemia), thrombocytopenia (platelet deficiency) andneutropenia (low numbers of neutrophils)?

1 - type I hypersensitivity
2 - type II hypersensitivity
3 - type III hypersensitivity
4 - type IV hypersensitivity

A

2 - type II hypersensitivity

- antibodies identify antigens on RBCs, platelets or neutrophils as foreign and flag them for phagocytosis

36
Q

What type of hypersensitivity is resus disease?

1 - type I hypersensitivity
2 - type II hypersensitivity
3 - type III hypersensitivity
4 - type IV hypersensitivity

A

2 - type II hypersensitivity

- mums antibodies target the rhesus antigen on babies RBCs

37
Q

What is type III hypersensitivity?

1 - reaction to external antigen mediated IgE antibodies
2 - cytotoxic reaction mediated by IgG or IgM antibodies
3 - reaction mediated by immune complexes
4 - delayed reaction mediated by cellular response

A

3 - reaction mediated by immune complexes

  • self antigen-antibody form called immune complexes
  • immune complexes group together and deposit in blood vessel walls
  • immune complexes cause tissue damage and inflammation
38
Q

What are the 2 co-stimulatory mechanisms that lead to class switching in a B cell?

1 - MHC-II, CD4, CD40 and CD40L
2 - MHC-I, CD8, CD40 and CD40L
3 - MHC-II, CD4, CD28 and CB7
4 - MHC-I, CD8, CD40 and CD40L

A

1 - MHC-II, CD4, CD40 and CD40L

  • MHC-II from B cell binds with CD4 on T cell
  • CD40L on T cell and CD40 on B cell
  • also requires cytokines from T cell binding to cytokine receptors on B cells
39
Q

The 2 co-stimulatory mechanisms that lead to class switching in a B cells are MHC-II, CD4, CD40 and CD40L:

  • MHC-II from B cell binds with CD4 on T cell
  • CD40L on T cell and CD40 on B cell

What do the T cells secrete following the above co-stimulation to lead to class switching?

1 - CD7
2 - cytokines
3 - chemokines
4 - antibodies

A

2 - cytokines

40
Q

CD4 T helper cells are able to secrete cytokines that cause B cells to class switch the type of antibodies they produce from IgM to which antibody typically in type II or III hypersensitivity?

1 - IgD
2 - IgE
3 - IgG
4 - IgA

A

3 - IgG

41
Q

What is the main distinguishing factor between type II and type III hypersensitivity?

1 - type II = cell bound tissue specific antigen, type III = soluble antigen not tissue specific
2 - type II = soluble bound tissue specific antigen, type III = soluble antigen not tissue specific
3 - type II = soluble bound tissue specific antigen, type III = cell bound antigen not tissue specific
4 - type II = cell bound tissue specific antigen, type III = cell bound antigen not tissue specific

A

1 - type II = cell bound tissue specific antigen, type III = soluble antigen not tissue specific

  • type II = antibody bound to antigen, where antigen is bound to a cell and tissue specific
  • type III = antibody bound to soluble antigen that are not tissue specific
42
Q

In a type II hypersensitivity reaction, once opsonisation has occurred. Which cells contains Fc receptors that are able to bind and initiate apoptosis, via C3b (part of the complement system) and antibodies that have opsonised the foreign bodies?

1 - natural killer cells
2 - macrophages
3 - neutrophils
4 - dendritic cells

A

1 - natural killer (NK) cells

  • NK are cross over between innate and adaptive immunity
  • remember if antibodies are present then likely to be NK over macrophages
43
Q

What 2 type of hypersensitivity is transplant rejection?

1 - type I hypersensitivity
2 - type II hypersensitivity
3 - type III hypersensitivity
4 - type IV hypersensitivity

A

2 - type II hypersensitivity = generally acute phase

4 - type IV hypersensitivity = generally chronic phase

44
Q

What type of hypersensitivity is myasthenia gravis?

1 - type I hypersensitivity
2 - type II hypersensitivity
3 - type III hypersensitivity
4 - type IV hypersensitivity

A

2 - type II hypersensitivity

- antibodies bind directly to ACh receptors at post synapse

45
Q

In type III hypersensitivity the immune complexes (antigen-antibody) clump together and get deposited in blood vessels, damaging tissue and causing inflammation. Which organ is able to break down this clumping in a normal healthy person?

1 - liver
2 - kidney
3 - spleen
4 - gall bladder

A

3 - spleen

- only able to achieve this when clumps are small

46
Q

In type II hypersensitivity neutrophils are able to phagocytose antigen-antibody complexes. However, why are neutrophils unable to do this in a type III hypersensitivity?

A
  • immune complex (antigen-antibody) are too large for neutrophils
47
Q

Glomerulonephritis is damage to the tiny filters inside the kidneys (the glomeruli). It’s often caused by the immune system attacking healthy body tissue. Which type of hypersensitivity is glomerulonephritis?

1 - type I hypersensitivity
2 - type II hypersensitivity
3 - type III hypersensitivity
4 - type IV hypersensitivity

A

3 - type III hypersensitivity

- immune complexes build up here causing tissue damage and inflammation

48
Q

Systemic lupus erythematosus (SLE) is an autoimmune disease that can cause damage and inflammation to any tissue in the body, but generally connective tissue (blood vessels, cartilage, skin, heart, kidney, lungs). Which type of hypersensitivity is SLE?

1 - type I hypersensitivity
2 - type II hypersensitivity
3 - type III hypersensitivity
4 - type IV hypersensitivity

A

3 - type III hypersensitivity

  • immune complexes build up here causing tissue damage and inflammation
  • systemic in the name tells us its not tissue specific
49
Q

Serum sickness is a reaction that is similar to an allergy. The immune system reacts to medicines or blood that contain proteins used to treat immune conditions. What type of hypersensitivity is serum sickness?

1 - type I hypersensitivity
2 - type II hypersensitivity
3 - type III hypersensitivity
4 - type IV hypersensitivity

A

3 - type III hypersensitivity

  • antigens are antibodies in serum or antigens in medication
  • antibodies in your own blood bind to the antigens and form immune complexes that then clump together
50
Q

What is a type IV hypersensitivity, also referred to as T cell hypersensitivity or delayed type hypersensitivity?

1 - reaction to external antigen mediated IgE antibodies
2 - cytotoxic reaction mediated by IgG or IgM antibodies
3 - reaction mediated by immune complexes
4 - delayed reaction mediated by cellular response

A

4 - delayed reaction mediated by cellular response

  • naive CD4 T helper cell binds with an antigen presented on MHC-II molecule on APC
  • T cells mature and initiates an immune response inappropriately
51
Q

A type IV hypersensitivity, also referred to as T cell hypersensitivity or delayed type hypersensitivity is when naive CD4 T helper cell binds with the antigen on an antigen presenting cells and the T cell matures initiating an inappropriate immune response. When the antigen presenting cell binds with CD4 T helper cell through its MHC-II molecule, the T cell receptor and CD4 also bind. What other co-stimulatory molecules are required to activate the CD4 T helper cell and trigger the antigen presenting cell to begin secreting IL-12?

1 - CD28 and CD40L
2 - CD28 and B7
3 - CD40 and B7
4 - CD40 and CD40L

A

2 - CD28 and B7

52
Q

What is the IL-12, that has been secreted by antigen presenting cells once the CD4 T helper cell has bound with the MHV-II complex able to initiate in the CD4 T helper cell?

1 - matures into a type II CD4 T helper cell
2 - matures into type I CD4 T helper cell
3 - matures into type CD8 T cell
4 - matures into type I CD8 T helper cell

A

2 - matures into type I CD4 T cell

53
Q

Once a type I CD4 T helper cell has matured it is able to secrete a specific cytokine. Which cytokine is this?

1 - TNF-a
2 - IL-6
3 - IL-2
4 - IL-1

A

3 - IL-2

- important for T cell clonal expansion

54
Q

Once a type I CD4 T helper cell has matured it is able to secrete a IL-2. What is the function of secreting IL-2?

1 - triggers CD4 cells to proliferate and secrete IFNy
2 - triggers CD4 cells to proliferate and secrete antibodies
3 - triggers CD8 cells to proliferate and secrete IFNy
4 - triggers CD4 cells to proliferate and secrete antibodies

A

1 - triggers CD4 cells to proliferate and secrete IFNy

55
Q

Once a type I CD4 T helper cell has matured it is able to secrete a IL-2, which then triggers CD4 cells to proliferate and secrete IFNy. What cell does the IFNy then stimulate?

1 - neutrophils
2 - dendritic cells
3 - T cells
4 - macrophages

A

4 - macrophages

56
Q

Once a type I CD4 T helper cell has matured it is able to secrete a IIL-2, which then triggers CD4 cells to proliferate and secrete IFNy, which stimulates macrophages to secrete pro-inflammatory cytokines. What 3 cytokines are secreted by the macrophages?

1 - IL2, IL-6, IL-10
2 - IL1, IL-6, TNF-a
3 - IL-1, IL-6, IL-10
4 - IL-6, IL-10, TNF-a

A

2 - IL1, IL-6, TNF-a

57
Q

How long does a type IV hypersensitivity generally take to initiate?

1 - seconds
2 - minutes
3 - days
4 - weeks

A

3 - days

- why its also called delayed type hypersensitivity

58
Q

What type of hypersensitivity is contact dermatitis?

1 - type I hypersensitivity
2 - type II hypersensitivity
3 - type III hypersensitivity
4 - type IV hypersensitivity

A

4 - type IV hypersensitivity

59
Q

What type of hypersensitivity is the tuberculin skin test, which is where a small part of mycobacterium tuberculosis, which causes TB, is inserted into the patients skin. This initiates a type IV hypersensitivity. How long does a response take?

1 - 1-2 hours
2 - 24-72 hours
3 - 1 week
4 - 1 month

A

2 - 24-72 hours

- causes local inflammatory response if exposed to TB previously

Year 2 MIS (48 decks)

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