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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
What dietary antioxidants modulate Nrf2-Keap1 signalling?
Flavonoids(EGCG, Green Tea) Non-flavonoid polyphenols(Tumeric, Resveratrol) Phenolic acids(rosemary) Organosulfur compounds(isothiocyanate, sulforophane, thiosulfonate allicin)
26
What inhibits multiple inflammasomes that are Nrf2 independant?
Sulforaphane
27
What are ligands for PPARs
Free fatty acids, eicosanoids, PGE, LTE, 5 HETE and other AA metabolites
28
What are PPARs?
Group of nuclear receptor proteins that act as transcription factors after binding with retinoid X receptor.
29
What is PPARs role in inflammation?
They ameliorate inflammation and AI conditons
30
Limiting foods high in what compound helps symptoms of RA?
AA
31
What nutrient decreases symptoms of UC, fecal calprotectin and CRP?
Omega 3
32
What is a good ratio of Omega 6:3?
4-5:1
33
What are effects of transfats and inflammation?
It increases markers of inflammation. Increases TNFalpha in all women and increases IL6 and CRP in obese women.
34
How does EPA block metabolism of AA?
It inhibits Delta 5 desaturase
35
What are sources of AA and what are they a precursor to?
Meat, dairy, poultry, shellfish | Precursor to PGE2, L1B4, 5-HETE
36
How does lower ratio of Omega 6:3 affect the fatty acid pathway?
lowers enzyme competition(delta 6 desaturase) and reduces shunting towards AA
37
What are coenzymes for desaturases for metabolism of omega 3 PUFAs?
Zinc, Mg, Ascorbate, Niacin(aka Nicotinic acid, B3), Pyridoxine(B6)
38
What are some anti-inflammatory mechanisms of fiber?
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)
39
How does salt increase inflammation?
It promotes cellular shift toward Th1 and Th17. Th17 plays a role in AI dz. So salt can be a driver in AI dz.
40
What are some features of Mediterranean Diet?
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
41
How does Med diet lower inflammation?
Decreases CRP and IL6
42
How does vegetarian diet lower inflammation?
Higher levels of Vitamin C, decrease CRP | Lowers TGL, Uric acid and alpha tocopherol
43
What are triggers to AI dz?
Stress, Toxins, Trauma, Infections, Nutrient Insufficiencies, Food
44
How does elemental diet help Crohns?
Drops IP. Uses amino acids as sole nitrogen source so provides nutrients in a highly digestible form. Equally effective as steroids.
45
How do elemental and polymeric diets help IP?
Direct antiinflam effects on enterocytes(lining) | Modulates intestinal bacterial species(affects microbiome), Lowers Bacteroides Prevotella
46
What AI dz do elemental diets help?
Crohns and RA
47
What are some dietary interventions to lower inflammation in general?
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
How do phytonutrients/antiox in diet help inflammation?
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
What is insulin effects on fatty acid pathway?
Upregulates D5desaturase. Shifts DGLA toward PGE2 synthesis
50
What are some triggers to acute phase proteins(mild to moderate)?
``` Strenuous exercise Heatstroke Childbirth Emotional Stress Psychological illnesses ```
51
What are some triggers to acute phase proteins(major)?
``` Infection Trauma/Surgery Inflammatory Dz Tissue Infarction Advanced Cancer ```
52
What causes a low ESR?
Polycythemia Leukocytosis SC anemia Low plasma protein
53
What causes a high ESR?
``` Infection Inflammation AI Dz Malignancy PMR ```
54
What are some facts about CRP compared to ESR?
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
What are some facts of ESR?
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
What is the 1/2 life of Fibrinogen?
3-4 days
57
What is 1/2 life of ESR?
Days to weeks
58
What is 1/2 life of IgG?
7-21 days
59
What is 1/2 life of CRP?
4-19 hoursF
60
What acute phase reactants rise rapidly?
CRP Serum Amyloid A Plasma Glutathione
61
What are slower acute phase reactants?
Fibrinogen, prothrombin, complement proteins, ferritin, haptoglobin, ceruloplasmin alpha 1 glycoprotein
62
What do you get a transient decrease in when there are acute phase reactants?
``` Albumin Transferrin Antithrombin AFP IGF-1 TBG Retinol B globulin Zn, Iron ```
63
What is a surrogate marker for CRP?
IL6
64
What is ESR a surrogate marker for?
IgG, Fibrinogen
65
What is the release of Acute phase reactants mediated by?
IL6(chief stimulator), IL1B, IL8 TNFa, IFNg
66
What can turn off acute phase reactants?
TGF B, serpins(alpha 1 antitrypsin) and other antiinflammatory cytokines
67
What can cause WBC to increase?
``` Infection Inflammation Allergies Malignancy Obesity Stress Demargination(lithium, steroids, beta agonists) ```
68
What does neutrophilia usually indicate?
Bacterial infection
69
What does lymphocytosis usually indicate?
Viral infection
70
What does monocytosis usually indicate?
Chronic inflammation, infection
71
What does eosinophilia usually indicate?
Allergies, parasites
72
What can mild increase in WBC predict?
CV risk
73
What habits increase hsCRP?
Obesity, smoking
74
Which acute phase reactant binds ldl and increases atherosclerosis?
CRP
75
What can blunt CRP?
Liver dz, protein deficiency
76
What are some limitations with CRP?
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
When is ferritin the best marker for iron storage?
When esr, crp and clinical assessment have r/o systemic inflammation
78
What are indications to check ferritin?
Iron disorders - deficiency or hemochromatosis | Elevated with inflamm conditions, liver dz, RA, hyper thyroid and some cancers
79
What are some facts of fibrinogen?
Increases blood viscosity High levels increase ESR Increases typically occur after several days after infection/injury Baseline levels predict stroke/MI risk
80
What conditions can you see elevated fibrinogen?
Atherosclerosis, smoking, inactivity, excessive etoh, supplemental estrogen
81
What cells make complement?
Hepatocytes, macrophages, monocytes, endothelial cells of GI and GU tract.
82
Do complements increase or decrease with acute phase response?
Increase
83
How are complements activated?
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
What are type 1 IFN?
IFN a, IFN B, IFN G - inflammatory
85
What are inflammatory and acute phase IL?
IL 1,6,8
86
Which TNF is inflammatory?
TNF alpha
87
What conditions is TNF alpha elevated?
Obesity, induces IR
88
What are NK cells?
Lymphocytes part of innate immunity; induce apoptosis in target cells
89
What is an important biomarker for tailoring therapy for MS?
IL 17
90
When are cytokines useful biomarkers?
When assessing for inflammatory or AI dz esp when obtained as panels instead of individual cytokines
91
When is checking NK Cytoxic activity useful?
When assess deficient immune activity and response to immunomodulatory agents
92
What can be a valid predictive marker of RA?
ACPA
93
What can be used to predict or determine presence of systemic inflammatory disease, particularly when other markers are negative(ESR, ANA)?
Serum cytokines(esp IL-6)
94
What is IFM definition of food allergy?
IgE mediated type 1 hypersensitivity
95
What is IFM definition of food sensitivity?
Immunologic reaction to food - IgG mediated delayed hypersensitivity or IgA
96
What is IFM definition of food intolerance?
Non immunologic reaction to food. Ex: Lactose intolerance, histamine intolerance
97
What type of reaction is Celiac Dz?
Non IgE food allergy
98
What type of reaction is EOE?
Mixed IgE/Non IgE FA
99
What are some class features of IgG?
``` Complement Activation Transplacental 1/2 life 23 days 4 subclasses Dose dependant 75% of all IG ```
100
What is the major activity of IgG?
Protects tissue
101
What are some class features of IgE?
``` Attaches to mast cell Contact with allergen Causes release of histamine 1/2 life 2.3 days Can have memory for years ```
102
What are major activity of IgE?
Extreme Sensitivity Gatekeeper for IgA Antiparasitic
103
What are class features of IgA?
2 forms Serum - Monomer Secretions - Dimer 1/2 life 5-6 days
104
What are major activity of IgA?
Protects mucosa Clears Absorbed food Antigens - Biliary system
105
What can increase food allergies 10 fold?
Hypochlorhydria
106
What are some ATMs of food allergies?
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
What is gold standard for IgE testing?
Food challenge but must be done in appropriate setting, time consuming and risky
108
Features of skin prick testing.
``` For IgE Good reproducibility Variability Higher sensitivity, lower specificity Not appropriate with steroids or antihistamines or sig dermatitis as risk of anaphylaxis ```
109
Features of blood testing for IgE.
``` 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
What is best way to test IgG?
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
What are adv and disadv to IgG testing?
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
What is the most common protein involved in cross reactions?
PR10
113
What is most common condition presented in pts with cross reactions?
EOE
114
What type of food intolerance often develops secondary to SIBO, dysbiosis or GI inflammation?
Histamine
115
What enzyme metabolizes exogenous histamine?
Diamine oxidase(DAO)
116
What enzyme metabolizes endogenous histamine?
histamine N methyltransferase
117
What is antecedant in lectin intolerance?
mucosal inflammation

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