Modifiers of Immune System Flashcards

1
Q

protein energy malnutrition types

A

kwashiorkor and marasmus energy deficiency

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2
Q

kwashiorkor insufficient protein symptoms

A

leads to edema and bloating

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3
Q

marasmus energy deficiency symptoms

A

acute wasting

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4
Q

dual burden of nutritional problems

A

classic issues of undernutrition versus the emerging issue of over nutrition

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5
Q

synergism of malnutrition and infection

A

low nutrients leads to higher susceptibility of infection and then infection causes you to use more nutrients when you are having a fever and dairrhea vomiting etc.

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6
Q

Protein Energy Malnutrition cell effects

A

reduces epithelial and physiological barriers as wel as function of macrophages and neutrophils and NK cells

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7
Q

What immune cells need Iron to function?

A

macrophages and neutrophils need for enzyme pathways

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8
Q

What cytokines need iron?

A

pr inflammatory cytokines like TNF and IL6

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9
Q

Effects of low iron on lymphocytes?

A

inhibits the proliferations of T cells, also B cells but not as much

Thymic function is diminished

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10
Q

Hepcidins role with Iron

A

Hepcidin helps iron enter into macrophages form the blood stream…makes them survive

decreases serum iron by pushing into macrophages and decreases dietary iron absorption during infection

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11
Q

Problems with iron in excess amount?

A

pathogens/microbes love iron and therefore if you have too much microbes may proliferate

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12
Q

vitamin A deficiency problem

A

skews immune system to a Th1 response and reduces Th2 responses

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13
Q

why is vitamin A supplementation beneficial?

A

it can reverse the issues with vitamin a deficiency

helps reduce morbidity and mortality from measles and diarrhea

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14
Q

role of obesity in immunity

A

often leads to chronic inflammation due to increases in TNF and pro inflamm cytokines

reduces T cell diversity because induces thymic aging

cytokines reduced so not as goof active immune response

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15
Q

obesity linkage to influenza?

A

is a risk factor for influenza and death due to cytokine reduction and less T cell diversity

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16
Q

stages of B cell production in fetus

A

9-10 weeks have precursors in liver
12-14 weeks have pre B cells
16-17 weeks have a lot in spleen blood and bone marrow
20-30 B cells start secreting antibodies

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17
Q

stages of T cell production in fetus

A

5-6 weeks have precursors in liver
9-10 weeks have precursors in thymus
12-14 weeks have cd4 and cd8 in liver and spleen
16-17 weeks have T cells in blood and lymphoid
20-30 weeks have increase in T lymphocyts secreting cytokines

18
Q

IgG stages in fetal development

A

start transfer at 12-14 weeks

gradual increase at 20-30 weeks

19
Q

How does maternal IgG inhibit fetal immunity?

A

sometimes it can bind pathogens too well, preventing humoral immunity from acting on the pathogen and developing memory

20
Q

Levels of IgG through pregnancy and first year

A

really ramps up 4 months prior to term, peaks before birth and at birth it is decreasing…then around 5-6 months the maternal IgG should be gone, at same time you start to make your own

21
Q

IL-12 levels in neonates and effects of levels

A

extremely low, so Th1 pathway not stimulated

22
Q

IL-6, IL-1, IL-10, IL-13 levels in neonates

A

these are all higher to induce active inflammation and also activates the Th2 and Th17 pathways

23
Q

Why is cell mediated immunit impaired in neonates?

A

co stimulatory molecules are sparse, so difficult to mount an attack

24
Q

When do IgG, IgM, IgA and lymphocytes reach adult levels?

A

IgG IgM and lymphocytes all around age 6

IgA is slower than these

25
Q

Primary hallmarks of aging

A

genomic instability, telomere attrition, epigenetic alterations and loss of proteostasis

these are the instigators of cellular damage

26
Q

antagonistic hallmarks of aging

A

deregulate nutrient sensing, mitochondrial dysfunction, cellular senescence

these are in charge of countering the cellular damage but if going on too much are hurtful

27
Q

integrative hallmarks of aging

A

stem cell exhaustion and altered cellular communication

when damage from primary and antagonistic cannot be overcome….this is the phenotype of aging

28
Q

B and T cell production in elderly

A

it becomes lower, and they have diminished function of mature secondary lymphocytes

29
Q

primary cause of low T cells in adults

A

involution of the thymus

30
Q

more effector/memory T cells or more naive T cells in elderly?

A

more memory T cells due to involuted thymus and not as much maturation

31
Q

issue with CD4 in elderly causes what?

A

CD4 cells are lower and cannot help stimulate important humoral responses with B cells anymore

32
Q

antibody changes with age?

A

quantity and quality is reduced

33
Q

B cell changes in elderly?

A

reduced function and blunted vaccine responses

34
Q

CD4 T cell changes in elderly?

A

reduced function and IL2 production

dampened costimulation

35
Q

CD8 cell changes in elderly?

A

narrowing of cell repertoire and more memory cells

36
Q

TLR changes in the elderly?

A

TLR 789 are all altered in the elderly

37
Q

aging affect on macrophages?

A

decreases their efficacy and function

reduced expression of MHC class II

38
Q

aging affect on neutrophils?

A

impairs function

39
Q

aging affect on dendritic cells?

A

impairs ability of costimulation

40
Q

aging affect on NK cells?

A

decreases cytotoxicity