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IFM Study > Immune APM > Flashcards

Immune APM Flashcards

1
Q

How do nutrients/phytonutrients found in foods help to mediate inflammation?

A

Thru their effects on:

1) Microorganisms in the gut and translocation of LPS
2) Composition of cell membranes and building blocks of inflammatory mediators
3) Specific pathways(IC, EC, transcriptional) - dampening the inflammatory pathway and activating the counterregulatory pathway

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2
Q

What are eicosanoids?

A

Signaling molecules made from AA or PUFAs

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3
Q

What are agents that inhibit/modulate NFKB?

A 
Glucocorticoids
Calorie restriction
DHA, EPA
Alpha Lipoic Acid
NAC
Vitamin B12, C and E
Botanicals/Phytochemicals/Spices/Flavonoids
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4
Q

What botanicals/phytochemicals modulate NFKB?

A 
Brassica
Bosweillia
Cats claw
Chinese Skullcap
Citrus flavonoids(Quercetin, grape seed, soy)
Devils claw
Echinacea
Feverfew
Garlic
Gingko Biloba
Japanese knotweed(Transresveratrol)
Milk Thistle
Pomegrante(Ellagitannins) -convert to Urolipin A
Tumeric
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5
Q

Does Vitamin A inhibit NFKB?

A

No

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6
Q

What inflammasome gets activated with poor diet or stress?

A

NLRP3

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7
Q

What happens when you eat a moderate mixed meal?

A

It stimulates NFKB and CRP within 1 hour and lasts > 3 hours.

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8
Q

What are dietary mechanisms that affect inflammation?

A 
Glycemic load
Oxidative stress
Modulation of signal transduction pathways
Types and balance of fatty acids
Fiber
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9
Q

What happens with high glycemic load?

A

Increases CRP; Decreasing load,makes a difference in overweight/obese women with or without weightloss but not in normal BMI patients by decreasing CRP and increasing adiponectin. Those with higher BMI who ate same glycemic load as normal BMI had a higher rise in CRP.

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10
Q

How can you explain the protective effects of low glycemic load on systemic inflammation?

A

Reduction in hyperglycemia induced overproduction of oxidative stress and amelioration in insulin resistance, adiposity, HLD, HTN.

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11
Q

What can lower risk of inflammatory polyarthritis?

A

Zeaxanthin and Bcryptoxanthin, but not lutein or lycopene

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12
Q

What is effect of Vitamin C on PAD?

A

It is inversely related to CRP and tPA, marker of endothelial dysfunction; Lower in smokers with PAD and correlated with more severe disease. Vitamin C from fruit seems to be more effective on CRP as vegetable intake only affected tPA

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13
Q

What is low alkaline phosphatase as surrogate marker for?

A

Vitamin C and zinc

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14
Q

What is correlation of F&V on Met syn?

A

Lowers risk(inverse relationship) and lowers CRP

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15
Q

What is nutrigenomics?

A

How food affects expression of our genes

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16
Q

What is nutrigenetics?

A

The way our genes affect the foods we eat(ex:how we absorb vitamin C)

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17
Q

What can modulate inflammasome activation?

A 
EGCG
Cucurmin
Propolis
Quercetin
Resveratrol
Sulphoraphane
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18
Q

Where are the majority of our antioxidants made?

A

By our body

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19
Q

What plays a crucial role in regulating antioxidant gene induction?

A

Nrf2?

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20
Q

What protein is bound to Nrf2 and what part of cell does this complex reside?

A

Keap1 is bound to Nrf2 in cytosol

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21
Q

What does Nrf2 bind to and where to turn on antioxidant genes?

A

ARE(antioxidant response element) in the nucleus

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22
Q

What pharmaceutical drugs turn on Nrf2?

A

Statins and Metformin

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23
Q

What happened to mice when Nrf2 was deleted?

A

They developed autoimmune disease

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24
Q

What food preservative activates Nrf2 and what is the effect?

A

Thbq activates Nrf2 to skew CD4+ cells towards Th2 differentation. Activation of Nrf2 suppresses IFN gamma production while inducing production of Th2 cytokines - IL4, IL5 and IL13. This can promote food allergies.

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25
Q

What dietary antioxidants modulate Nrf2-Keap1 signalling?

A

Flavonoids(EGCG, Green Tea)
Non-flavonoid polyphenols(Tumeric, Resveratrol)
Phenolic acids(rosemary)
Organosulfur compounds(isothiocyanate, sulforophane, thiosulfonate allicin)

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26
Q

What inhibits multiple inflammasomes that are Nrf2 independant?

A

Sulforaphane

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27
Q

What are ligands for PPARs

A

Free fatty acids, eicosanoids, PGE, LTE, 5 HETE and other AA metabolites

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28
Q

What are PPARs?

A

Group of nuclear receptor proteins that act as transcription factors after binding with retinoid X receptor.

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29
Q

What is PPARs role in inflammation?

A

They ameliorate inflammation and AI conditons

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30
Q

Limiting foods high in what compound helps symptoms of RA?

A

AA

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31
Q

What nutrient decreases symptoms of UC, fecal calprotectin and CRP?

A

Omega 3

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32
Q

What is a good ratio of Omega 6:3?

A

4-5:1

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33
Q

What are effects of transfats and inflammation?

A

It increases markers of inflammation. Increases TNFalpha in all women and increases IL6 and CRP in obese women.

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34
Q

How does EPA block metabolism of AA?

A

It inhibits Delta 5 desaturase

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35
Q

What are sources of AA and what are they a precursor to?

A

Meat, dairy, poultry, shellfish

Precursor to PGE2, L1B4, 5-HETE

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36
Q

How does lower ratio of Omega 6:3 affect the fatty acid pathway?

A

lowers enzyme competition(delta 6 desaturase) and reduces shunting towards AA

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37
Q

What are coenzymes for desaturases for metabolism of omega 3 PUFAs?

A

Zinc, Mg, Ascorbate, Niacin(aka Nicotinic acid, B3), Pyridoxine(B6)

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38
Q

What are some anti-inflammatory mechanisms of fiber?

A

1) Decreased energy density of diet, slowing absorption and lowering glycemic index, obesity
2) Chemical structures of fiber may have inherent anti inflammatory properties
3) Changes in commensal bacteria which increases resistance to pathogens, immune system modulation/regulation, Anti inflam bacteria metabolites(SCFA- butyrate)

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39
Q

How does salt increase inflammation?

A

It promotes cellular shift toward Th1 and Th17. Th17 plays a role in AI dz. So salt can be a driver in AI dz.

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40
Q

What are some features of Mediterranean Diet?

A

Higher ratio of MUFA to saturated so lower levels of AA
Higher ratio of Omega 3 to 6
Abundance of F, V, legumes, whole grains - increased Antiox

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41
Q

How does Med diet lower inflammation?

A

Decreases CRP and IL6

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42
Q

How does vegetarian diet lower inflammation?

A

Higher levels of Vitamin C, decrease CRP

Lowers TGL, Uric acid and alpha tocopherol

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43
Q

What are triggers to AI dz?

A

Stress, Toxins, Trauma, Infections, Nutrient Insufficiencies, Food

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44
Q

How does elemental diet help Crohns?

A

Drops IP. Uses amino acids as sole nitrogen source so provides nutrients in a highly digestible form. Equally effective as steroids.

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45
Q

How do elemental and polymeric diets help IP?

A

Direct antiinflam effects on enterocytes(lining)

Modulates intestinal bacterial species(affects microbiome), Lowers Bacteroides Prevotella

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46
Q

What AI dz do elemental diets help?

A

Crohns and RA

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47
Q

What are some dietary interventions to lower inflammation in general?

A

Moderate AA intake
Increase EPA/DHA from cold water fish
Lower Omega 6:3 ratio
Ensure adequate intake of zinc, mg, vitamin c, niacin and B6
Increase dietary antioxidants/phytonutrients
Eliminate hydrogenated/partially hydrogenated, TFA, Sugars, Alcohol, refined carbs
Optimize BG and lower insulin
Eliminate Antigenic foods
Increase fiber

48
Q

How do phytonutrients/antiox in diet help inflammation?

A

1) Reduce oxidative biosynthesis of inflamm eicosonaids and isoprostanes
2) Decreased inflamm signal transduction pathways and increase anti inflamm ones
3) Quench ROS and reduce ox stress
4) Decrease glycemic load

49
Q

What is insulin effects on fatty acid pathway?

A

Upregulates D5desaturase. Shifts DGLA toward PGE2 synthesis

50
Q

What are some triggers to acute phase proteins(mild to moderate)?

A 
Strenuous exercise
Heatstroke
Childbirth
Emotional Stress
Psychological illnesses
51
Q

What are some triggers to acute phase proteins(major)?

A 
Infection
Trauma/Surgery
Inflammatory Dz
Tissue Infarction
Advanced Cancer
52
Q

What causes a low ESR?

A

Polycythemia
Leukocytosis
SC anemia
Low plasma protein

53
Q

What causes a high ESR?

A 
Infection
Inflammation
AI Dz
Malignancy
PMR
54
Q

What are some facts about CRP compared to ESR?

A

CRP is more precise marker for systemic inflammation
No increase with age in CRP. ESR can increase with age.
Rises within 24-48 hours as opposed to ESR which is slow to rise and fall
Longterm serial measurements have prognostic value in RA and AS
Broader meaningful range of abnormal values(if over 100, indicates infection)
Elevations of CRP in febrile children more predictive of sepsis than wbc or neutrophil

55
Q

What are some facts of ESR?

A

Increases with age
Can differentiate inflammation from allergies(doesn’t go up with allergies)
Increases with local and systemic inflammation
Indirect functional marker for increases in acute phase proteins(fibrinogen, immunoglobulins)
Can be elevated in noninflammatory states(anemia)
Can have false positives
Higher in women

56
Q

What is the 1/2 life of Fibrinogen?

A

3-4 days

57
Q

What is 1/2 life of ESR?

A

Days to weeks

58
Q

What is 1/2 life of IgG?

A

7-21 days

59
Q

What is 1/2 life of CRP?

A

4-19 hoursF

60
Q

What acute phase reactants rise rapidly?

A

CRP
Serum Amyloid A
Plasma Glutathione

61
Q

What are slower acute phase reactants?

A

Fibrinogen, prothrombin, complement proteins, ferritin, haptoglobin, ceruloplasmin
alpha 1 glycoprotein

62
Q

What do you get a transient decrease in when there are acute phase reactants?

A 
Albumin
Transferrin
Antithrombin
AFP
IGF-1
TBG
Retinol B globulin
Zn, Iron
63
Q

What is a surrogate marker for CRP?

A

IL6

64
Q

What is ESR a surrogate marker for?

A

IgG, Fibrinogen

65
Q

What is the release of Acute phase reactants mediated by?

A

IL6(chief stimulator), IL1B, IL8 TNFa, IFNg

66
Q

What can turn off acute phase reactants?

A

TGF B, serpins(alpha 1 antitrypsin) and other antiinflammatory cytokines

67
Q

What can cause WBC to increase?

A 
Infection
Inflammation
Allergies
Malignancy
Obesity
Stress
Demargination(lithium, steroids, beta agonists)
68
Q

What does neutrophilia usually indicate?

A

Bacterial infection

69
Q

What does lymphocytosis usually indicate?

A

Viral infection

70
Q

What does monocytosis usually indicate?

A

Chronic inflammation, infection

71
Q

What does eosinophilia usually indicate?

A

Allergies, parasites

72
Q

What can mild increase in WBC predict?

A

CV risk

73
Q

What habits increase hsCRP?

A

Obesity, smoking

74
Q

Which acute phase reactant binds ldl and increases atherosclerosis?

A

CRP

75
Q

What can blunt CRP?

A

Liver dz, protein deficiency

76
Q

What are some limitations with CRP?

A

Doesn’t go up with all inflammatory conditions
Can be normal in SLE, cancer and active inflam dz
May be blunted with liver dz, protein deficiency

77
Q

When is ferritin the best marker for iron storage?

A

When esr, crp and clinical assessment have r/o systemic inflammation

78
Q

What are indications to check ferritin?

A

Iron disorders - deficiency or hemochromatosis

Elevated with inflamm conditions, liver dz, RA, hyper thyroid and some cancers

79
Q

What are some facts of fibrinogen?

A

Increases blood viscosity
High levels increase ESR
Increases typically occur after several days after infection/injury
Baseline levels predict stroke/MI risk

80
Q

What conditions can you see elevated fibrinogen?

A

Atherosclerosis, smoking, inactivity, excessive etoh, supplemental estrogen

81
Q

What cells make complement?

A

Hepatocytes, macrophages, monocytes, endothelial cells of GI and GU tract.

82
Q

Do complements increase or decrease with acute phase response?

A

Increase

83
Q

How are complements activated?

A

By PAMP and DAMP pathways:

1) Classical IgM and IgG antigen
2) Alternative - low level activation from spont breakdown of C3
3) Lectin(MBL activated by mannose)

84
Q

What are type 1 IFN?

A

IFN a, IFN B, IFN G - inflammatory

85
Q

What are inflammatory and acute phase IL?

A

IL 1,6,8

86
Q

Which TNF is inflammatory?

A

TNF alpha

87
Q

What conditions is TNF alpha elevated?

A

Obesity, induces IR

88
Q

What are NK cells?

A

Lymphocytes part of innate immunity; induce apoptosis in target cells

89
Q

What is an important biomarker for tailoring therapy for MS?

A

IL 17

90
Q

When are cytokines useful biomarkers?

A

When assessing for inflammatory or AI dz esp when obtained as panels instead of individual cytokines

91
Q

When is checking NK Cytoxic activity useful?

A

When assess deficient immune activity and response to immunomodulatory agents

92
Q

What can be a valid predictive marker of RA?

A

ACPA

93
Q

What can be used to predict or determine presence of systemic inflammatory disease, particularly when other markers are negative(ESR, ANA)?

A

Serum cytokines(esp IL-6)

94
Q

What is IFM definition of food allergy?

A

IgE mediated type 1 hypersensitivity

95
Q

What is IFM definition of food sensitivity?

A

Immunologic reaction to food - IgG mediated delayed hypersensitivity or IgA

96
Q

What is IFM definition of food intolerance?

A

Non immunologic reaction to food. Ex: Lactose intolerance, histamine intolerance

97
Q

What type of reaction is Celiac Dz?

A

Non IgE food allergy

98
Q

What type of reaction is EOE?

A

Mixed IgE/Non IgE FA

99
Q

What are some class features of IgG?

A 
Complement Activation
Transplacental
1/2 life 23 days
4 subclasses
Dose dependant
75% of all IG
100
Q

What is the major activity of IgG?

A

Protects tissue

101
Q

What are some class features of IgE?

A 
Attaches to mast cell
Contact with allergen
Causes release of histamine
1/2 life 2.3 days
Can have memory for years
102
Q

What are major activity of IgE?

A

Extreme Sensitivity
Gatekeeper for IgA
Antiparasitic

103
Q

What are class features of IgA?

A

2 forms
Serum - Monomer
Secretions - Dimer
1/2 life 5-6 days

104
Q

What are major activity of IgA?

A

Protects mucosa
Clears Absorbed food
Antigens - Biliary system

105
Q

What can increase food allergies 10 fold?

A

Hypochlorhydria

106
Q

What are some ATMs of food allergies?

A

Barrier permeability - permeability is required for IgE sensitization
Iatrogenic - abx, nsaids, ppis, vaccines
Toxins - POP, GMO, pollution
Nutrient deficiencies - Vit D, Omega 3, Antiox
Hypochlorhydria
Genetics/epigenetics
Microbiota(increased hygeine, antibiotics)
Stress
Obesity
Delayed exposure to allergens

107
Q

What is gold standard for IgE testing?

A

Food challenge but must be done in appropriate setting, time consuming and risky

108
Q

Features of skin prick testing.

A 
For IgE
Good reproducibility
Variability
Higher sensitivity, lower specificity
Not appropriate with steroids or antihistamines
or sig dermatitis as risk of anaphylaxis
109
Q

Features of blood testing for IgE.

A 
Useful
positive suggest IP
low grade findings may be significant
use same lab for baseline and f/u
more sensitive ref ranges
May miss anaphylaxis - can't base dx on titer levels as they can fade with time
110
Q

What is best way to test IgG?

A

Eliminate for at least 4 weeks to assess improvement
If shows reaction to many foods, consider IP
Response may show an exacerbation before improvement

111
Q

What are adv and disadv to IgG testing?

A

Has demonstrated clinical utility - motivating for pts
May improve adherence
Elevation of IgG may be evidence of underlying inflammation symptoms or not
Use consistent and trusted lab
If odd results in patients with seasonal allergy - check cross reaction
If odd results otherwise, call lab

112
Q

What is the most common protein involved in cross reactions?

A

PR10

113
Q

What is most common condition presented in pts with cross reactions?

A

EOE

114
Q

What type of food intolerance often develops secondary to SIBO, dysbiosis or GI inflammation?

A

Histamine

115
Q

What enzyme metabolizes exogenous histamine?

A

Diamine oxidase(DAO)

116
Q

What enzyme metabolizes endogenous histamine?

A

histamine N methyltransferase

117
Q

What is antecedant in lectin intolerance?

A

mucosal inflammation

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