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Nut 2 Semester 1 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Describe the hormones of the HPA axis

A

Hypothalamus releases Thyrotropin releasing hormone TRH to anterior pituitary which then releasese Thyroid Stimulating Hormone to the Thyroid gland this signals the secretion of thyroxine T4 the weaker thyroid hormone which converts to triiodothyronine T3 which is 4 x more potent then T4. Reverse T3 is an inactive form of T3 which protects tissues from excess thyroid hormone.

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2
Q

What are iodothyronine deiodinases?

A

“They are selenoproteins which help to regulate thyroid hormone homeostasis
D1 & D2 convert T4 - T3 and D3 converts T4 to inactive RT3 (can bind to T3 receptors blocking action of T3)”

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3
Q

What are the functions of T3?

A

Increases growth, bone & CNS development, increases BMR, heart rate and activates metabolism

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4
Q

What is the ratio of secreted T3 & T4, how protein bound are they and how are they metabolised?

A

T4: 90% secreted from Thyroid. T3: 10% secreted the other is formed via peripheral conversion in liver and kidney tissues. They are metabolised via deiodonation, sulphation and glucuronidation. T4 highly protein bound 99.98% T3 99.8%

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5
Q

What nutrients are essential for thyroid hormone synthesis?

A

“Tyrosine and Iodine - TPO catalyses iodination of tyrosine in thyroglobulin to form T4 & T3
Selenium & Zn: Enzyme cofactors and receptor function
Vit A, C, E, B2,6,12 - Synthesis & function
Vit D - immune mod - AI & VDR polymorphism predisposes AITD
Fe = TPO is haem dependent
Cu - Cofactor deiodinase enzymes”

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6
Q

Iodine sources and deficiency and excess impacts

A

“Sources: Sea vegetables, ocean and shellfish, eggs & dairy, little in soil - dependent on where
Deficiency causes - lack of intake esp vegans, preg, low/no dairy or fish
Excess; Wolff-Chaikoff effect helps reject excess iodine or hormone synthesis - is inhibited in some people causing subclin or clin hypo. High consumption iodinised salt, lots dairy, or dietart supps or meds”

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7
Q

When does T4 conversion to RT3 increase?

A

“Chronic or critical injury - a normal response to low metabolic states ‘ Low T3 syndrome
High stress, Zn, Se, Fe def, liver dysfunction, advancing age (liver/ kidney function) sig cal reduction, myocardial infarction. High RT3 can present as hypothyroidism”

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8
Q

What do HPT disruptors do?

A

Interfere with thyroid hormone synthesis and secretion, transport, metabolism and function

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9
Q

Name 5 HPT disruptors

A

“Pesticides, PCB’s, Phalates, Glyphosphate
Halogens - Iodine, Chlorine, Bromine”

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10
Q

How to avoid HPT disruptors

A

Eat organic vegetables and wild fish, Flouride free toothpaste, don’t stay in chlorinated pools too long, drink filtered water, avoid processed foods and drinks

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11
Q

What medication decreases TSH secretion

A

Dopamine

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12
Q

What medication alters T3&4 metabolism

A

Phenytoin

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13
Q

What medication reduces T4 - T3

A

Beta-blockers

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14
Q

What medication reduces T4 - T3 binding

A

Dieuretics

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15
Q

What medication increases thyroglobulin?

A

Oestrogen, Tamoxifen

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16
Q

What can hyperthyroid meds induce 10-20 years later

A

Hypothyroidism in Graves disease

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17
Q

What role do gut microbes play with the thyroid?

A

Regulate uptake of iodine and are also involved in degregation and enterohepatic cycling

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18
Q

What microbiome profile may you see with AITD

A

Low SCFA producers, increased zonulin and elevated serum LPS

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19
Q

“What are optimal ranges for:
TSH
Total T4
Free T4
Free T3
RT3”

A

“TSH 0.4 - 2.5
Total T4 70-150
Free T4 12.8 - 19.5
Free T3 3.2 - 4.5
RT3 11-18”

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20
Q

What would a hormone profile look like for clinical and subclinical hypothyroidism?

A

“Subclin - TSH High: T4 Normal: T3: Normal
Clinical - TSH High: T4 Low: T3 Low/ Normal”

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21
Q

What would a hormone profile look like for clinical and subclinical hyperthyroidism?

A

“Subclin - TSH Low: T4 Normal: T3: Normal (unless on T4 therapy)
Clinical - TSH Low: T4 High/ Normal: T3 High/ Normal”

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22
Q

What would a hormone profile look like for secondary hyperthyroidism?

A

Low: Low: Low

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23
Q

How do you measure iodine and what are the ranges?

A

Via a urine test first thing in the morning:
Children & Adults 100-199mcg/L
Pregnant women 150 - 249
<100 = insufficiency <20 = severe deficiency

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24
Q

What is the banes basal temp test

A

You put a thermometer under arm on waking - before moving and tract temperature. Below 36.5 = diagnostic for hypo. Impacted by mestrual cycle, illness, circadian changes, alcohol intake

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25
Q

What are physical thyroid signs

A

Dry skin, dry hair, thining hair and eyebrows, goitre, protuding eyevalls, nail beading, low BP, bradycardia

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26
Q

What SNPs could impact thyroid function?

A

“SLCO1B/C can inhibit transport of hormones to cells
DIO2 impact activation of T4-T3
T3 requires cofactors such as Vit D (VDR/ GC) and retinol BC01
Detox SULT, UGT”

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27
Q

What are the classifications of hypothyroidism?

A

“Primary - pathology in the thyroid gland - high TSH due to low T4&T3 secretion
Secondary - pathology in the pituitary - inadequate TSH to signal secretion of T3&4
Tertiary - inadequate secretion of TRH in hypothalamus
Peripheral - tissue insensitivity to thyroid hormones
Subclinical - TSH is slightly elevated & T4 is normal, T4 - T3 conversion issue, high RT3 or thyroid cell receptor issues”

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28
Q

Describe general signs & symptoms of hypothyroidism

A

Dry skin, elbow keratinosis, dry hair, thining hair and eyebrows, goitre, nail beading, low BP, bradycardia, cold extremeties, feels the cold, tiredness/ fatigue, odema, puffy face, swollen eyelids, weight gain/ inability to lose weight, heavy or irregular menstrual periods

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29
Q

Describe subclinical hypo

A

Slightly elevated TSH and normal free T4. Optimal TSH <2.5. Undetected in c.10% of population experiencing s/s of hypo such as tiredness, weight gain, cognitive impairement and mood.Linked to increased risk of coronary artery disease, heart failure, CV events and infertility and miscarriage. Serum levels >10mU/L TSH and thyroid autoantibodies = increase risk overt hypo.

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30
Q

Describe 10 causes and risk factors for developing hypothyroidism

A

“1. Iodine deficiency or excess
2. Cofactor nutrient deficiency _se, tyrosine, Zn, Fe, Vit C, D, B2,6,12, Cu
3. Drug induced thyroiditis - i.e lithium
4. Women x 10 more likely Hashmioto’s - risk increased post partum & during/ post menopausal. AI also higher in women
5. AGE - peaks in 40’s
6. Prolonged stress - inhibits TSH, suppresses D1, T3, RT3 and receptor sensitivity. Also immunological shife from Th1 - Th2 predisposing AI
7. Smoking - disrupts iodine conversion
8. Alcohol - directly suppresses function blunts TRH response and chronic use can reduced peripheral conversion
9. Hereditary - 23.6% of mothers with children with HT had history of thyroid dysfunction
10.Postpartum thyroiditis”

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31
Q

Describe Hashimotos thyroiditis

A

Hashimotos is a autoimmune condition where thyroid tissue is damaged. It effects women 10 X to that of men. H-pylori and EBV are often implicated. Usually high TSH, normal FT4 but with raised antithyroid peroxidase (TPO) antibodies and sometimes increased anti-thyroglobulin antibodies (anti-Tg) and TSH receptor blocking antibodies (TSII).anti-TG & TSII may not always show on a blood test due to the intermittent nature of the AI attack but the person may be experiencing s/s. HT is often diagnosed late.

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32
Q

Outline 5 causes/ risks of Hashimoto’s

A

“Iodine excess - highly iodinated thyroglobulin is more immunogenic
Genetic polymorphisms i.e. VDR, MTHFR
Coeliac disease & HT often coexist
Sleep apnoea and HT influence one another
Heavy metals - mercury, cadnium increase TGO antibodies
Proinflammatory cytokines - IL-6/10/12, TNF-a”

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33
Q

What is the allopathic treatment for hypothyroidism?

A

Levothyroxine (synthetic T4) 25-220mcg/ day. Due to interactions take on empty stomach in morning 1 hor before food, drinks other drugs. Med failure often due to conversion problems eg nutrient deficiency = nutrition is key! Absorption effected by coffee, PPI use, coeliac disease, atrophic gastritis

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34
Q

Describe the 4 key natural approaches to hypothyroidism

A

“1. Address triggers & mediators and identify the cause
2. Reduce inflammation & IR
3. Reduce goitrogenic compounds
4. Balance T-Cell function”

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35
Q

Describe how to address triggers and mediators

A

“Adress iodine and micronutrient status
Optimise digestion (herbs, enzymes)
Support methylation - folate, B2,6,12, choline, betaine, zn (gen testing?)
Remove HTP disruptors
Address possible disbiosis/ SIBO common in AITD
Address stress - support HPAA
Assess for heavy metals, pathogens and toxins
Support detox and elimination - B Vits, NAC, glutathione, chloryphll, caratenoids, fibre
Support SCFA producers (pro/prebiotics, fibre, polyphenols)”

36
Q

Describe how to reduce inflammation

A

“Optimise O3:O6 ratio, avoids trans fats, sugar, alcohol, high GI foods, smoking, limit Arachadonic Acid
Blood sugar balance & improve insulin sensitivity - cinnamon, chromium, Low GL foods
Increase AO sources to decrease oxidative stress”

37
Q

Describe how to reduce goitrogenic compounds

A

Soaking, steaming, boiling - cooking activates myrosinase which destroys goitrogens

38
Q

How do you balance T-cell functioning?

A

“Address intestinal permeability - critical for immune tolerance, T-reg cells. Increase glutamine, Aloe, Zn, Vit A, EPA & DHA, curcumin
Increase butyrate producers to support T reg cells - pro/prebiotic foods/ supps, fibre, polyphenols.
Support sIgA levels. probiotics with S.boulardii, An, Vit A, D, O3, colostrum”

39
Q

What are the key nutrients to support hypothyroidism

A

Se, Fe, Zn, Vit A, Vit D, Iodine, Tyrosine

40
Q

Describe how selenium supports hypothyroidism

A

Dosage: 150-200mcg/ day. Important not to go over 400mcg so check multi’s so that there is no interaction. NTR: Can worsen iodine def but correct supp can correct iodine excess. Selenoenzymes such as glutathione peroxidase, deiodinase amd selenoprotein P important for thyroid function. AO, AI and increases T3.

41
Q

Describe how Fe supports hypothyroidism

A

Does: 10mg maintenance, 30mg if def - check! TPO is haem dependent. Fe-def anaemia decreases T4 & T3. peripheral conversion of T4, also blunts efficacy of iodine supplementation

42
Q

Describe how Zn supports hypothyroidism

A

Dose 15-30mg/ day. Cofactor for D2 & role in TRH synthesis. Zn def increases D2 which increases inactivation of thyroid hormones

43
Q

Describe how Vit A supports hypothyroidism

A

Dose 2000IU: Def: increases TSH and reduces iodine take up in thyroid. Supp decreases TSH and increases T3. Via retinoic acid receptors mods thyroid hormone receptor function. Insufficiency from low intake or BC01 SNPs

44
Q

Describe how Vit D supports hypothyroidism

A

Supp 2000IU or more. Def more likely in AITD’s. Immune modulatory role (T-reg cells). Levels inversley correlated with thyroid antibodies. Supp beneficial even for those with normal levels. Aim: 100-150nmol/ L

45
Q

Describe how idoine supports hypothyroidism

A

DoseL 140-400mcg. DO NOT USE in AITD, hyperthyroidism or thyroxine use. Modulates thyroid response to TSH via -ve feedback. If unsure use iodine urine test. Huge variability in kelp/ seaweed/ foods & supps

46
Q

Describe how tyrosine supports hypothyroidism

A

200-500mcg Thyroglobulin precursor. Modulates stress response in short term. Avoid high doses long term and with thyroxine, AITD, hyper.

47
Q

What other natural approaches can you take for hypothyroidism?

A

“Thyroid glandulars -like for like, have T3, T4, AA’s & micronutrients
Ashwaganda - shown to significantly support TSH, T4 & T3 levels
Nigella sativa, reduces TSH, TPO anti & increases T3 in HT. AO, immunomodulatory”

48
Q

What is hyperthyroidism and what is it subdivided into

A

“Hyperthyroidism is increased levels of thyroid hormones. It is subdivided into:
Thyrotoxicosis - increased SYNTHESIS - Grave 80% (AI), Multinodular goitre, adenoma
Thyroiditis - increased RELEASE of stored hormones due to thyroid damage - viral infection, AI
Both increase metabolic rate. Women 10 x 1”

49
Q

What are signs & sym of hyperthyroidism?

A

Thinning or loss of hair, warm moist skin, sweating, heat intolerance, tachycardia, high BP, heart failure, AF, inability to keep weight despite appetite, thirst and diarrhoea, Grave’s orbitophathy, goitre, anxiety, irritability, insomnia, mestrual irregularities

50
Q

Describe graves disease

A

“AI hyperthyroidism. B&T-lymph-mediated AI.
TSH receptor antibodies(TRAbs) occupy TSH receptors causing hyperplasia and excess production and secretion of thyroid antibodies
TPO antibody found in most people with Graves.

51
Q

Describe Grave’s S/S

A

“Grave’s orbitopathy in 25% - antibody mediated inflammation of orbital contents - asymmetrical
Photophobia: Watering, red swollen eyes, visible sclera, eylid retraction
Exopthalmos: eyeball protrusion, lid lag, double vision
Graves dermopathy, painless thick red (orange peel) rash, lower legs & tops of feet”

52
Q

List 10 causes & risk factors for Graves disease

A

“1. Family history - especially maternal (TRABs cross the placenta)
2. Stress - emotional shock
3. Other AI conditions
4. Iodine excess
5. Dysbiosis - bacteriodes and prevotella higher in GD
6. Food allergies/ intollerances
7. Smoking 3x risk Graves orbitopathy
8. Heavy metals - mercury, cadnium
9. Infections - Limes disease, Hep C
10. Vit D, Se, CoQ10 def”

53
Q

What investigations can diagnose hyperthyroidism and Graves disease??

A

“Hyperthyroidism: Low TSH, high T3, normal/high T4
Graves: T3/T4 >20 or FT3/FT4>0.3 suggestive Graves. Prescence of TRAbs & TPO antibodies”

54
Q

What investigations can diagnose subclin hyperthyroidism and thyroiditis?

A

“Subclin - Low but detectable TSH 0.1-0.4mIU/L T3 & T4 usually normal
Thyroiditis - raised ESR & CRP”

55
Q

What is the six step natural approach to hyperthyroidism?

A

“1. Address micro nutrient insufficiency and decrease oxidative stress
2. Inhibit thyroid hormone synthesis
3. Reduce inflammation and insulin resistance
4. Support the nervous system and address stress
5. Assess and address gut health & pathogen load
6. Support thyroid hormone clearance”

56
Q

How do you address micro nutrient insufficiency and decrease oxidative stress in hyperthyroidism

A

”:- Increase antioxidants, Se, Zn, Vits A, C, D, E
: - Increase B vits (Krebs), Carnitine (FA oxidation) Mg, CoQ10
:- Glutathione support - NAC milk thistle, reservatrol, Se
:- Se supplementation”

57
Q

How do you inhibit thyroid hormone synthesis in hyperthyroidism?

A

Increase goitrogens (raw- smoothies, coleslaw) and avoid iodine

58
Q

How do you reduce inflammation and insulin resistance in hyperthyroidism?

A

O3:O6 balance (not fish due to iodine). Avoid trans fats, refined sugar, processed foods and drinks, smoking, coffee, red meat. Take Querceting daily - inhibits LoX, Cox, NF-kB

59
Q

How do you support the nervous system and address stress in hyperthyroidism?

A

“Support blood sugar balance and the HPA axis
Passionflower & Valerian - anxiolytics, calms NVS & overactive thyroid
Ashwaganda - avoid stimulating adaptogens
Mg, Theanine
Reduce caffeine & alcohol.
Incorportate stress reduction techniques, breathwork, meditation, exercise. “

60
Q

How do you assess and address gut health & pathogen load in hyperthyroidism?

A

Possible 5 R. Pre/probiotics. Id and manage allergens/ triggers. Digestive support

61
Q

What nutritional support can you provide in hyperthyroidism?

A

“Eye health - increase carotenoids such as lutein
Increased metabolism - B complex and B rich foods
Weight loss - focus on nutrient dense foods such as nuts seeds, legumes, coconut. Include bitters to support absorption
Carnitine 2000-4000mg. Peripherally antagonises thyroid hormone. Can prevent or reverse muscle weakness. Can prevent thyroid storm. High T3/T4 = increase carnitine loss = skeleteal muscle myopathy
Vit D: - Key in innate and adaptive immunity. May slow disease progression. Low status = low BMD =fracture risk. 2000IU
Iodine - AVOID! “

61
Q

How do you Support thyroid hormone clearance in hyperthyroidism?

A

Support sulphation: Glucosinolates (brassicas), suplhur rich foods (onions etc), Se induces SULT, Methionine/ Folate/ B12, NAC, taurine, Vit A & %
Support glucuronidation: Quercetin, luteolin and chrysin rich foods (honey, broccoli. Onions, rosemary), Mg, Geren tea, B-glucuronidase inhibitors: milk thistle, brassicas reshi, probiotics

62
Q

What herbs can support hyperthyroidism?

A

“Bugleweed: thyroxine antagonist - treats mild hyper - decreases T4
Lemon balm - blocks thyroid hormone activity”

63
Q

What do GLUT1, 2 & 4 do?

A

“GLUT1 - Glucose uptake without isulin
GLUT4 - Insulin mediated glucose uptake 20-30 fold
GLUT2 - Mediates glycolysis and gluconeogenesis”

64
Q

What is Activated Protein Kinase upregulated by?

A

Exercise, Cold exposure or PGC1a

65
Q

What is DM and what are the different types?

A

“A metabollic disease characterised by hyperglyceamia, impaired insulin secretion or resistance to the action of insulin or both
Type 1 - AI - absolute insulin deficiency
Type 2 - insulin resistance/ relative deficiency
Pre-diabetic - hyperglycaemia, increase risk T2D & metabolic syndrome
Gestational diabetes - usually clears after birth but increased T2D risk
Secondary - pancreatic disease - cushings, acromegaly, hyperthyroidism”

66
Q

What is the HbA1C levels for normal, pre & diabetes

A

Normal <42 Pre 42-47 Diabetes 48mmol/ l or over

67
Q

What is the fasting blood glucose levels for normal, pre & diabetes

A

Normal <5.5 Pre 5.5-6.9 Diabetes 7mmol/ L or more

68
Q

What are s/s of T2D

A

Polyuria, polydypsia, polyphagia, fatigue, acanthosis nigricans, blurry vision, recurrent infections

69
Q

What are complications of T2D

A

CVD, stroke, retinopathy, neuropathy, depression, Alzhiemers

70
Q

What are the causes and risk factors for T2D?

A

Family history, diet (high GI/Gl, trans fat, processed foods, fizzy drinks, alcohol, low fibre), Ethnicity (Asian, african), Age (>45 or<17), Nutrient def (Vit C, E, B3,5,6, Mg, O3: Zn, Chromium), chronic stress, obesity, sedentary lifestyle, poor methylation, prediabetes

71
Q

How is the microbiome implicated in T2D?

A

“Dysbiosis creates inflammation which is a key factor in development of T2D with insulin resistance. Bifidobacteria, roseburia, akkermansia protective. Bifido increases glycogen synthesis and insulin stimulated glucose uptake.
Low diversity common in T2D, ruminococcus, blautia & fusobacterium associated with higher risk. “

72
Q

What 4 naturopathic goals support T2D?

A

“1. Balance blood sugar levels (Low GL diet, high fibre, protein, good fats)
2. Reduce inflammation and boost AO (avoid inflammatory foods/ drinks). Increase flavonoid-rich food (blue, purple, black), AO’s - Glutathoine, Vits C, E, alpha lipoic acid, sleep hygeine, environ toxins, GI health
3. Correct macro/ micronutrients: Optimise EFA’s and protein, support immune system - Mg, Zn, chromium, Vit D,C,E
4. Optimise insulin sensitivity - nutrition, nutricuticals & lifestyle incl exercise - pantax ginseng, chromium, cinnamon, CoQ10”

73
Q

What nutritional support can you provide in T2D?

A

“Sensible calorie restriction increases muscle & liver insulin sens
Low carb diet - focus on nuts, seeds, protein, MUFA
Low GI - better controls HbA1C and reduces post-prandial glucose secretion”

74
Q

What foods to avoid & include in T2D

A

“Avoid: Fructose, sucrose, fruit juices, processed foods, refined carbs, sweetners, large meals
Include: nuts, seeds, olive oil, protein sources, 03, fibre, cinnamon, green tea”

75
Q

What are 5 key nutrients in T2D and why?

A

“Chromium - increases sensitivity of tyrosine kinase & reduces carb cravings
Cinnamon - enhances insulin sensitivity & release
Alpha Lipoic Acid - improves peripheral neuropathy
Biotin - increases activity of glucokinase and glucose transporter
Myoinositol - improves insulin signaling”

76
Q

Describe the action of Berberine in T2D

A

“1. Decreases gluconeogenesis and facilitates GLUT4 transportation
2.Reduces expression of proinflammatory genes
3. Modulates the microbiome - reduces circulating LPS
Similar to metformin but metformin can increase homocysteine”

77
Q

What other natural approaches can you take for T2D?

A

Support microbiome, Exercise, Reshi, milk thistle

78
Q

What is T1D

A

An autoimmune condition which attacks the beta cells of the pancreas resulting in absolute insulin deficiency. Peaks during early childhood (up to 5years) and again in puberty. More common F then M. Reduces life expectancy by 11-15 years

79
Q

What s/s T1D?

A

Like T2D but more pronounced and aggressive. Diabetic ketosis common at diagnosis - nausea, vomitting, SOB. Anxiety, depression, hypoglycaemia, increased risk of other AI’s.

80
Q

Describe the AI of T1D

A

“AI: c.90% of T1D have destruction of pancreatic beta cells - shown by circulating AB’s to islet cells. Altered Th1/Th2 balance is suggested.
Auto-antibody negative T1D - lack of autoantibody response”

81
Q

What are the causes and risk factors for T1D?

A

Genetics, Stress, Viral infection (EBV, mumps), obestiy, early nutirion (gluten<4 months, dairy<12), Vit D & O3 deficinecy

82
Q

What nutritional support can be provided for T1D?

A

“ALA- AO & improves insulin sensitivity
EPA/ DHA - reduces inflam & protects cell membranes
Vit D - immunoregulatory
Vit C - AO, usually low in T1D”

83
Q

What naturopathically can you do to support T1D?

A

“Similar to T2D
Balance blood sugar - low GL, no refined carbs, avoid fructose, sucrose, fruit juices, alcohol, high fibre, protein & good fats. Focus on O3, Vit D & C. Reduce stress and weight if needed. Optimise sleep and reduce inflammation. Support GI health. Remove allergenic triggers. “

84
Q

Why is it important to support in early stages ‘honeymoon period’

A

Early intervention can halt or reverse beta cell destruction. Exercise & strict Low GL diet. Epicatechins and niacinamide support immune modulation

Nut 2 Semester 1 (5 decks)

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