L8 Flashcards

(60 cards)

1
Q

which 2 responses is given from mast cells?

A

immediate response: degranulation
long-term response: synthesis

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2
Q

mast cells involved in which 2 reactions?

A

helminth infections and allergic reaction

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3
Q

what is optimal immunity?

A

sufficient to combact pathogens

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4
Q

what is innate immunity

A

distinguish self/ non-self microbes by the use of pattern recognition receptor system(e.g. PAMPs)

early and rapid protection

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5
Q

what is adaptive immunity

A

develop antibodies and memory

first, delayed; second: immediate

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6
Q

examples of active immunity

A

infection
vaccination

long lasting

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7
Q

examples of passive immunity

A

IgG are transferred from mother to baby via placenta
breast milk
immune globulin

immediate but lasts for few weeks

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8
Q

cardial symptoms of inflammation

A

redness, swelling, heat, pain,loss of function, malaise, increase in WBC, increaase heart rate

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9
Q

3 process in inflammation

A

the release of inflammatory mediators
vascular response
cellular response(recruit the WBC into the blood)

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10
Q

main inflammatory mediators

A

histamines, prostagladins, pro-inflammatory cytokines(e.g. IL-1,IL-6,TNF)

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11
Q

effects of histamines

A

dilate small blood vessels
increase the permeability of capillaries

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11
Q

what is the functions of cytokines

A

attracting/ producing neutrophils
stimulate phagocytosis
cause fever

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12
Q

effects of prostaglandins

A

cause pain and vasodilation

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13
Q

why inflammation will cause blood clot

A

fluid moves out from the vessels
increased the concentration of blood constitudent
increase in viscosity
stagnation of flow
blood clot

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14
Q

what is bradykinins

A

one of the inflammatory mediators
vasodilation and increased the permeability and
pain

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15
Q

what is the component of exudate

A

cell debris, bacteria and immune cells

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16
Q

which 3 WBCs will recruite to the site of inflammation

A

neutrophils, monocytes, macrophages

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17
Q

what is the function of leukotrients

A

attracts the leukocytes
increase the permeability of capillaries

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18
Q

3 classess of prostanoids

A

PGI2, prostaglandins, TXA2

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19
Q

what is the function of PGI2

A

vasodilation, inhibit the platelets aggregation

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20
Q

what is the function of TXA2

A

pletelets aggregation

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21
Q

where can find COX-1 and COX-2

A

COX-1: most tissues
COX-2: sites of inflammation(inducible)

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22
Q

what side effects can cause by NSAIDs?

A

nephrotoxic, bronchospasm,risk of bleeding, fluid retention(edema), risk of thrombotic events, anaphylactic shock (過敏性休克)

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23
Q

if aspirin is prescribed to children with aged smaller than 12 years old, what will it happen?

A

Reye’s syndrome

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24
4 types of hypersensitivity
Type I,II,III,IV (allergic anaphylaxis, antibody, immune complex, delayed)
25
what is alloimmunity?
antigens produced by members of same species 同一物種但其他人的抗原 | type II hypersensitivity
26
what is the mechanism of allergy?
B cells produced IgE IgE combines to the antigens on mast cells mast cells become sensitized mast cell occur degranulation when exposed to the allergens again release histamines
27
what is the treatment for allergy
epinephrine(adrenaline: increase B.P. antihistamine( adjunctive to epinephrine)
28
why allergy cause vasodilation
histamine is produced histamine binds with H1 receptor smooth muscles relax vasodilation
29
how to give the allergens gradually for desentization
subcutaneous
30
what is the mechanism of desentization
increase the production of IgG IgG combines to allergens, instead of IgE similar to 'neutralization' prevent the degranulation of mast cells
31
what is transfusion complication
acute haemolytic reaction (-->haemoglobiuria) febrile non-haemolytic reaction allergic reaction circulatory overload bacterial contamination disease acquisition疾病獲得
32
Can a person with Rh+ blood receive Rh- blood?
yes
33
anti-Rh antibodies same as IgG?
yes | Anti-Rh antibodies can pass through the placenta
34
what is the health problems to the fates with Rh- antibodies if the mother is Rh+?
haemolytic anaemia
35
4 classess of transplant rejection
hyperacute rejection, acute cellular rejection, acute vascular rejection, chronic allograft failure
36
examples of type III hypersensitivity
systemic lupus erythematosus (SLE) Rheumatoid arthritis lupus nephritis(kidney)
37
most susceptibility sites of occuring type III hypersensitivity
joints and kidney
38
two major cells cause the damage of type III hypersensitivity
platelets and neutrophils(lysosomal enzymes)
39
name of immune complex in SLE
anti-DNA-DNA immune complex
40
How the immune complex in SLE cause the damage to kidney?
the complex contains DNA high affinity to bind with the basement membrane of glomerulus deposit inflammation damage to kidney
41
why UV light will worsen the symptoms of SLE?
UV light will damage the skin cells necrosis of cells release more DNA generate more autoantibodies
42
what is haemoglobinuria
RBC ruptures haemoglobin release kidney cannot filtrate completely some of the haemoglobin present in urine
43
4 clinical manifestation of SLE
butterfly rash photosensitivity proteinuria hemolytic anemia
44
which two cells in response to the type IV hypersensitivity?
macrophages and T cells
45
examples of type IV hypersensitivity
allergic contact dermatitis | treatment: corticosteroid (reduce inflammation and activity of T cells)
46
two ways of attacking cells in type IV hypersensitivity
CD 8+ cells: directly kill the cells CD 4+ cells (+ macrophages): release cytokines -->inflammation
47
type I hypersensitivity can be classified as the autoimmune disease?
NO -->IgE give the immediate allergic response
48
examples of autoimmune disease
type 1 DM Rheumatoid arthritis multiple sclerosis(MS) myasthenia gravis(MG)
49
what is myasthenia gravis(MG)
fatigable muscle weakness | 肌肉好易攰、越用越冇力
50
what will HIV do to cells?
directly attack T cells
51
the function of immunoglobins respectively
IgG: cross the placenta IgM: appears when early infection IgA: on the mucosal surface IgE: allergic reaction IgD: found on the surface of B cells | IgG & IgM: circulate in body fluid (neutralize the toxins & opsonization
52
3 categories of immunodeficiency
B cell-mediated immunodeficiency disorders T cell-mediated immunodeficiency disorders combined
52
explain the T cell-mediated immunodeficiency disorders
defective expression of T cell receptor -->unable to recognize the antigens defective cytokines production -->inactivate the T cells
53
general presentation of primary immunodeficiency disorders
hard to treat infection opportunistic infections higher risks for development of malignancy frequent and reoccur the inflammation and infection delayed growth
54
medical management of PIDDs
prophylactic drug treatment treatment to boost the immune system bone marrow transplantation
55
3 treatment to boost the immune system
immunoglobulin therapy(IVIG/SCIG) interferon-gamma therapy growth factors
56
how does the interferon-gamma therapy works?
interferon-gamma: synthetic subs. promote phagocytosis treat for chronic granulomatous disease (weaken ability of killing microorganisms)
56
how does the growth factor works?
help proliferation and maturation of WBCs
57
how to show IVIG is an immuno-modulating agents
saturation of Fc receptor on macrophages suppression of inflammatory mediators suppression of idiotypic antibodies(=self attack cells)