CHPT 13 Flashcards

(50 cards)

1
Q

humoral immune deficieny mean

A

there is some deficiency or defect in the functioning of B.
So either in the production of antibodies by the B cell or the stimulation of the B cells itself.
In either case, the adaptive immune response take a hit.
And if it is only limited to the B cell deficiency, that is known as humoral okay.

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2
Q

cellular immune deficiency represents

A
  1. a defect in T cell either in the activation of T cell,
  2. proliferation of T cell,
  3. T cell helping the B cell activation.
  4. Even any defect in thymus itself, bc the T cell maturation happens in thymus

any kind of deficiency that limits the activation of the T cell component.

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3
Q

Innate immunodeficiencies

A
  1. any defect in the phagocytic function, any defect in the neutrophil function, macrophage function,
  2. any defect in the chemotaxis where the cells are not able to reach to the site of injury or to the site of infection, or they are not able to degregulate, they are not able to pick up the bacteria.
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4
Q

which cytokine is important for mediating tH1 response to mount an appropiate immune response towards an antigen

A

IL1

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5
Q

which immunodeficiecny is acquired and not genetic (they start with a normal immune response but then eventually their immune system become defective)

A

secondary immunodeficiencies

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6
Q

what is the #1 source of secondary immunodeficiencies

A

malnutrition

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7
Q

which drugs lead to suppression in immune system

A

coticosteroids, anticonvulsant, immunosuppressants

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8
Q

Usually drug-induced immunosuppression is__________ when the patient stops taking
the drug

A

reversed

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9
Q

people with HIV or aids have a reduction of what and why

A

CD4+ T cells (helper T cells), because this virus specifically infect those T cells, grows in it, lyse it and have more of its kind being released from those cells

These T helper cells help B cells produce antibodies so now you see decline in this

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10
Q

HIV affects

A

both cellular and humoral immunity

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11
Q

hypersensitivity examples

A

allergy and autoimmunity

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12
Q

there are 4 kinds of hypersensitivity reactions

A

type 1- dependent ON antibodies IgE
type 2- dependent ON antibodies IgG or IgM
type 3- dependent ON antibodies igG or IgM
type 4- dependent on T cells. no antibody mediated hypersenisitivity

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13
Q

first stage of type one hypersensitivity

A

sensitization stage

  1. The pollen is engulfed by antigen presenting cell. It should not be. It is not an antigen. The body should not have treated it as an antigen.
  2. B-cells. They get activated. Since this was a mucosal IgE is produceed

3.IgE is produced to a particular antigen or allergen. This is is released in the circulation or it reaches the tissue. It binds to the surface of muscles.

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14
Q

Second stage of type one hypersensitivity

A

is when the same individual is again exposed to the same antigen or pollen or allergen.

Now the antibodies are already bound on the surface of the cells, mast cells, and basophils

binding of these antigens on already bound antibody leads to or triggers the degranulation of mast cell and basophils

these granules are highly anaphylactic and induce hyperanaphylatic because these are vasoactive substance that are being released

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15
Q

inhaled allergens will cause

A

cause localized allergic response to that organ system

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16
Q

ingested allergens will cause

A

systemic reaction

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17
Q

severity of reaction is dependent on

A

the level of IgE produced

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18
Q

In type two hypersensitivity the antibodies involved are

A

IgG or IgM

NO IgE

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19
Q

does type two hypersensitivites compose autoimmune immunity

A

yes

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20
Q

what is the antigen in type one hypersensitivites

A

foreign antigen

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21
Q

what is the antigen in type two hypersensitivites

22
Q

what happens when antibody binds to a target

A

complements gets activated. once this happens we see either the formation of membrane attack complex or recruitment of phagoycytic cells

23
Q

what happens in type 2 hypersensitivies when the antibodies produces come in contract with our cells

A

complement is activated

24
Q

what cells have receptors for IgE

A

MAST CELLS AND BASOPHILS

25
what cells have receptors for IgG
Neutrophils, Natural Killer cells, Macrophages
26
in type 2 hypersensitivies, after the cell is bound to their respective antibody , what happens?
different immune cells come (depending on the antibody) and perform cell lysis and eat our normal cell
27
what type of antigen is present in the type two hypersensitivies
insoluable
28
what is an insoluable antigen
one that is present on a cell surface
29
exmaple of type two hypersensitivity
blood incompability
30
blood antigens (for example A + or A-) is dependent on
Rh antigen, + means we have additional protein antigen RH
31
Bood type (ABO) is dependent on what
what carb is present
32
if you are positive and you're recieving blood from negative. what will happen
nothing
33
if you are negative and you are recieving blood from positive what will happen
immune response triggered the antibodies will destroy the blood that is entering inside the body because they will recognize this as a foreign antigen.
34
universal recipient
AB +
35
universal donor
O- negative
36
ncompatible blood it causes
hemolytic transfusion reaction lysis
37
what is one way to prevent Rh factor incompatibility in pregancy effects
Rh(D) immunoglobulin (RhoGAM) therapy the antibodies will neutralize th Rh factor from the baby and the mom won't produce any immune response
38
39
example of soluable antigen
toxin, secreted protein, anything in circulation that is not bound to the cell
40
what happens when there is antibody +antigen complex present
complement gets activated
41
what happens when complement gets activated in type III hypersensitivites
different immune cells (neutrophils and macrophages) gets activated and release cytokine to clear this immune complex
42
In type three hypersensitivity the antibodies involved are
IgG or IgM
43
In type three hypersensitivity the antibodies bind to what
soluable targets
44
In type two hypersensitivity the antibodies bind to what
insoluable target
45
type 4 hypersensitivity is mediated by what
T cells against self antigen or harmless antigen
46
which type of hypersensitivity is slow
type 4, mediated by T cells
47
multiple sclerosis is what type of hypersensitivity
type 4, t cells are attacking the mylein sheath
48
which type of hypersensitivity has T-cells that were fine so there was no genetic predisposition for this individual to mount any type for hypersensitivity reaction. but when foregin particles bind to host skin it activates T cells to produce cytokines to remove it from the body
Non autoimmune Type 4 hypersensitivities
49
Like the type one hypersensitivity, there is a phase one of sensitization where T cells are sensitized during the first exposure. But the Re exposure is the time where T cells they get activated.
non-autoimmune type iv hypersensitivites
50
example of Non autoimmune type four hypersensitivity
1. transplant rejection If the donor has MHC that is very different from the recipient MHC, the T cell will identify it as a foreign and will mount an immune response. There will be transplant rejection. That's why we give immune therapy. graft versus host disease You can imagine you removed the bone marrow from the individual. The recipient gave a different bone marrow. It started producing immune cells. Now those immune cells, if they are coming from an individual that is very different, having a very different MHC from the recipient, whatever immune cells that are being produced in the bone marrow will come out in the circulation and will start attacking all the cells in the body. If you remember, MHC is a molecule that is present on all the cell surface. So in that case, even if you try to fix the individual, it ended up damaging the whole host.