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NUTR 441 > CHD labs and nutrigenomics > Flashcards

CHD labs and nutrigenomics Flashcards

1
Q

what is the intimal layer?

A

endothelium + internal elastic lamina

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2
Q

what is atherosclerosis?

A

occlusion/blocking of arteries that takes decades to develop (unless have predisposition like hypercholesterolemia), asymptomatic and a slow gradual accumulation of cholesterol -rich plaque beneath the monolayer

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3
Q

what is thrombosis?

A

break in monolayer around shoulders cuz of fibrosis (protein buildup), takes minutes, decisive event where damage to endothelial layer leads to platelet aggregation and sticking to site and each other (adhesion), brings on thrombus (blood clot) and heart attack

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4
Q

what are involved in non-specific immune response?

A

platelets, phagocytes (clean up after infection–macrophage)

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5
Q

what are involved in specific immune response?

A

T (thymus) and B (bone marrow) cells

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6
Q

what is immune response?

A

body’s natural defence system against foreign materials that have penetrated primary defences (skin, mucous membranes)

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7
Q

what is peyer’s patch?

A

clumps of lymph in GI tract

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8
Q

types of WBC:

A

T and B cells (lymphocytes) and phagocytes (eg. macrophages)

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9
Q

B cells engage in ___ immunity, through this process:

A

humoral; when encounter foreign protein (antigen) produce antibodies specific to protein–> epitope is part of protein that produces antibody by B cell and ONLY that part of protein–>antibodies attach to antigen and attract phagocytes

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10
Q

how are monocytes activated in macrophages?

A

encountering foreign protein covered in antibodies

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11
Q

how does phagocyte destroy foreign protein?

A

engulf and break down , releasing free radicals and chemoattractants to destroy antigen and call other immune cells

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12
Q

what are chemoattractants?

A

enhance overall inflammatory response (vasodilation), encourage proliferation of nearby cells, attract more immune cells to site

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13
Q

these cells are involved in children’s allergies and cancer, highly specific to whatever antigen activate them and respond by killing it

A

T cells

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14
Q

T cells are involved in ___ immunity

A

cell-mediated

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15
Q

cell mediated immunity causes ^ in ____

A

blood pressure bifurcations/breaches–>shear force–>direction changes in blood flow

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16
Q

what is inflammation?

A

recruitment and ensuing activity of immunological cells (macrophages, T cells) and repair cells (platelets) at site of injury

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17
Q

theories of CHD?

A

response to injury theory (base), modified lipoprotein theory (oxLDL), LDL retention theory (collect ox LDL in intimal), immunological importance of inflammation

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18
Q

first signs of endothelial dysfunction (stage 2) caused by

A

form of stress response to sheer force, turbulence, velocity occurring at arterial branches (bifurcations), sharp twisting turns –>expression of adhesion molecules (stress proteins) on endothelial surfaces (velcro for T cells and macrophages), ^ permeability of endothelial monolayer

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19
Q

key events in developing fatty streaks (stage 3)?

A
  • leukocytes migrate into arterial intimal –>pulled in by chemokine generated by endothelium
  • modified lipoproteins migrate into intima from circulation (smoking and ^LDL)
  • in intima, monocytes activated to macrophages that engulf oxLDL to become foam cells that release chemotactic compounds
  • smooth muscle cells migrate into intimal (^ collagen and muscle fibres) and collagen activates platelet binding
  • platelets adhere to dysfunctional endothelium and aggregate
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20
Q

platelets aggregate via ____ which does this:

A

thromboxane A2; vasoconstriction, potent platelet aggregators substance

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21
Q

thrombosis is stage ___ and is caused by:

A

5; chemotactic substances drawing in immune cells/platelets at shoulders, macrophages migrate back out of intimal to lumen (disrupt integrity), chemical injury to endothelium (Carbon monoxide), physical injury (stress, unaccustomed exercise), ongoing lipid per oxidation (fat break down to free radicals, foam cells)

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22
Q

fatty streak progresses to ____ and then ____

A

intermediate lesion; advanced atherosclerotic lesion

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23
Q

formation of advanced, complicated lesion of atherosclerosis is characterized by:

A

macrophage accumulation, formation of necrotic core, fibrous cap formation

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24
Q

ischemic vs hemorrhagic stroke?

A

lack of oxygen, same mech as CHD except in carotid artery; break/rupture/exploding of artery

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25
Q

4 types of lipoproteins?

A

chylomicron, VLDL, LDL, HDL

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26
Q

4 components of lipoproteins?

A

protein, cholesterol, TG, phospholipids

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27
Q

unconventional risk factors:

A

blood homocysteine, lipoprotein A (10x more atherosclerotic than LDL), fibrinogen, inflammation markers like CRP

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28
Q

antioxidants are a subcategory of ___

A

phytochemical

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29
Q

fxn of lipoproteins?

A

transport lipid and cholesterol around blood/lymph (aqueous enviro)

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30
Q

biggest effects on blood cholesterol are from these nutrients:

A

sat/trans fats, fibre, diet cholesterol

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31
Q

women have higher HDL cuz of ____

A

estrogen

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32
Q

overview of LP metabolism?

A

GIT–>chylomicron (mostly TG), has apoE and apoC2 proteins –>adipose (lipoprotein lipase turns on cuz of apoC2, allows clipping of fa and storage), drops off TG to become chylomicron remnant–>liver has docking stations to receive chylomicron remnant (B100/E receptor)–>break down components in liver, if excess cho and protein, converted to fat, needs to be packaged as VLDL rich in TG–>drop off fatty acids at adipose tissue, becomes smaller and smaller, becomes LDL which is rich in cholesterol,–> go
to various body tissues (ie. coronary artery)–>go back to liver to be broken down (B100/E receptor) –> liver will stop making these receptors if there is too much LDL, so it accumulates and gets oxidized

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33
Q

what is fxn of HDL?

A

liver makes it and it goes in tissues to pick up excess cholesterol to take back to liver (reverse cholesterol transport)

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34
Q

what is function of apoB-100?

A

ligand for LDL receptor (synth in liver)

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35
Q

what is function of apoC2?

A

activator of extra hepatic lipoprotein lipase

36
Q

what is function of apoE

A

ligand for chylomicron remnant receptor, present in excess in the b-VLDL

37
Q

purpose of chylomicron:

A

drop off fat from diet

38
Q

apoA-1 associates with HDL to activate other enzyme called:

A

LCAT (lecithin cholesterol acyl transferase)

39
Q

what is function of LCAT?

A

LCAT pulls cholesterol from tissues, links cholesterols with fatty acids in centre of HDL, esterized

40
Q

two pathways for HDL after picking up cholesterol?

A

to liver, or stored in VLDL/LDL through cholesterol ester transfer protein (CETP)

41
Q

major control points p.t. managing/regulating blood cholesterol levela

A

liver ldl receptors, ^ fecal bile acid losses, HMG CoA reductase, CETP (shut it down)

42
Q

why plant sterols?

A

complete fo absorption with cholesterol, so pick up more sterols which lower blood cholesterol (more cholesterol passed out in faeces)

43
Q

why soluble fibre?

A

forms gel which acts like cholestyramine , also readily fermented in colon to produce SCFAs (esp propionate which shuts down de novo cholesterol synth)

44
Q

examples of sol fibre?

A

xanthin gum, apples, citrus, pectins, oats, chia seeds

45
Q

cholestyramine by itself lowers LDL by __% , and with lovastatin it reduces LDL by __%

A

15; 50

46
Q

how to ^ serum HDL?

A

if overweight, lose weight; limit refined CHO and sugar; avoid/quit smoking; aerobic exercise (also shuts down CETP); maybe moderate alcohol intake (BUT ^ TG as well); fibre drugs shut down CETP (niacin and new CETP inhibitors not clinically helpful)

47
Q

what is metabolic syndrome?

A

^ WC, v HDL, ^ BP, ^ blood TG, ^ IR

48
Q

most hypercholesterolemic saturated fats:

A

12:0, 14:0, 16:0

49
Q

recommendations for PUFA:

A

< or = to 10% of kcal intake (so as not to have risk of oxidation and oxLDL)

50
Q

majority of fat should come from:

A

MUFAs

51
Q

these fats induce endothelial dysfunction

A

trans fat

52
Q

why high chylo and VLDL?

A

always in post-prandial state (ie. always eating), lot of fat in diet that takes longer to clear, eating too much in general

53
Q

ways to decrease TG ?

A

reduce total fat intake, reduce total kcal, ^ aerobic exercise (decreases postprandial [ ] of TG), wt reduction for overweight, ^ fish consumption

54
Q

why careful with fish oils?

A

could have been packaged in way that is already a bit oxidized, are caloric (not helpful for wt loss), diabetics maybe shouldn’t take

55
Q

what causes oxidation?

A

oxygen, heat, light

56
Q

why EPA?

A

BIGGEST: v TG and v platelet reactivity; also v fibrinogen lvls, v platelet counts, v BP, decrease cell proliferation

57
Q

omega 6s and platelets?

A

TxA2–>aggregation and adhesion, vasoconstrictor

58
Q

omega 3s and platelets?

A

TxA3–>not a vasoconstrictor or platelet activator

59
Q

____ inhibits all cyclooxygenase activity

A

aspirin

60
Q

omega 6s found in:

A

grain fed, grains

61
Q

which one less inflamm–leukotriene 4 or 5?

A

5

62
Q

is PGI2 good or bad?

A

good (reverse TxA2), comes from endothelial cells

63
Q

if have hx of heart attack, should you use fish oils?

A

under med supervision

64
Q

if no history of heart attack, should you use fish oils?

A

no, just get omega 3 from diet

65
Q

what is SNP?

A

single nucleotide polymorphisms

66
Q

what is genome?

A

your set of DNA

67
Q

DNA is wrapped around proteins called:

A

histones

68
Q

central dogma?

A

DNA transcription to RNA, translation to protein

69
Q

protein needs to bind to ____ to start coding

A

promoter region

70
Q

part of gene that will become protein

A

coding region

71
Q

___ factor binds with ___ to be activated and do something in the regulatory region

A

transcription ; ligand

72
Q

retinoic acid is a ___

A

ligand

73
Q

examples of monogenetic disorders

A

PKU, FAP

74
Q

what are examples of polygenetic diseases?

A

chronic diseases

75
Q

what is a mutation?

A

extremely rare base pair change

76
Q

different forms of the same gene

A

variants

77
Q

when common within a population (1%) the variant is called:

A

SNP

78
Q

GA and AA (more rare), HDL will be elevated with ^ PUFA intake in males or females?

A

females only

79
Q

heritable changes in gene expression that do not involve changes in DNA sequence

A

epigenetics

80
Q

types of epigenetic changes?

A

DNA methylation, histone modification

81
Q

DNA methylation (addition of methyl groups) is associated with ___

A

silencing

82
Q

histone acetylation is associated with ___

A

activation of genes (keep DNA unwound, less packed)

83
Q

__% of GC dinucleotides are methylated in human genome

A

70

84
Q

methylation is catalyzed by:

A

DNA MethylTransferases (DNMTs)

85
Q

type of mouse used for studying obesity and chronic disease

A

Agouti

86
Q

what is DOHaD?

A

developmental origins of health and disease

NUTR 441 (14 decks)

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