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MD1 endocrinologie > La thyroïde > Flashcards

La thyroïde Flashcards

1
Q

D’où est-ce que le thyroïde provient?

A

Provient de l’entoblaste:

  • Bourgeon qui se forme à partir du plancher du pharynx (foramen cecum) et descend antérieurement à la trachée puis bifurque de chaque côté formant les lobes thyroïdes
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2
Q

D’où est-ce que les parathyroïdes provient?

A

3e et 4e poches brachiales

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3
Q

What is a lingual thyroid?

A

abnormal mass of ectopic thyroid tissue seen in base of tongue caused due to embryological aberrancy in development of thyroid gland

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4
Q

What is a thyroglossal cyst?

A

A fibrous cyst that forms from a persistent thyroglossal duct

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5
Q

What are some examples of “dysgenèse thyroïdienne”? (5)

A
  1. Agénésie thyroïdienne (pas de thyroïde)
  2. Hypogénésie thyroïdienne (not enough hormone production)
  3. Thyroïde ectopique (wrong place)
  4. Thyroïde linguale
  5. Kyste thryéoglosse
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6
Q

Anatomy of the thyroid:

A
  • Usually 2 lobes but in 30% of patients there is a pyramidal lobe in between the two
  • Usually between 15-20g
  • Dimensions: 4x2x1 cm
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7
Q

Which veins and arteries supply the thyroid?

A

Three veins: superior, medial, inferior

Two arteries: superior, inferior

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8
Q

How/why would you observe and palpate the thyroid?

A
  • For signs of a: goiter, nodule, or signs of inflammation
  • Stand in front or behind the patient to palpate but usually it’s done from the back
  • You must also palpate the neck to look for adenopathies
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9
Q

How to auscultate the thyroid?

A

Place stethoscope on each lobe of the thyroid to listen for a murmur (souffle)

A murmur = increased vascularization/tubulant circulation

  • hyperT4 –> inc. vascularization –> inc. murmur +++
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10
Q

What are the two cell types in the thyroid?

A
  1. Follicular cells (epithelial): form unicellular thyroid follicles
    • Secrete:
      1. Thyroid hormones (T3 and T4)
      2. Thyroglubin: protein that stocks iodine
      3. Colloïde: amalgam of thyroglobulin
  2. Parafollicular cells/c-cells: found between the follicles
    • Secrete
      • Calcitonin: regulates levels of calcium and phosphate
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11
Q

What are the two thyroid hormones and their precursors?

A

Hormones:

  1. Thyroxine (T4)
  2. Triiodothyronine (T3)

Precursors:

  1. Diiodotyrosine (DIT)
  2. Monoiodotyrosine (MIT)
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12
Q

Thyroid histology:

A
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13
Q

What is the difference between T4 and T3?

A

T4:

  • Weaker hormone than T3
  • 100% comes from thyroid

T3:

  • Much stronger than T4
  • 85% comes from transformation of T4 –> T3 in the body
  • 15% comes from the thyroid
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14
Q

What are the 6 steps of thyroid hormone synthesis?

A
  1. Captation de l’iode
  2. Organification de l’iode
  3. Iodination des thyrosines
  4. Couplage des tyrosines iododées
  5. Libération du T3 et T4
  6. Récupération de l’iode (when hormones are used, iodine is recaptured and taken back to the thyroid)
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15
Q

What happens if there’s a problem with one of the steps of thyroid hormone synthesis?

A

It will cause hypothyroidism due to dyshormonogenesis thyroidienne

Usually congenital diseases that are dx during childhood

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16
Q

What happens to thyroid hormones in periphery?

A

T4 transformed into T3

T4 and T3 are degraded and iodine is put back into circulation either by:

  • Repris par less cellules folliculaires de la thyroïde (most)
  • Excrété par le rein
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17
Q

What is the half-life of T4 and T3?

A

T4 (thyroxine) –> around 7 days

T3 (triiodotyronine) –> 24 hours

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18
Q

Where does iodine come from?

A

Not very abundant in nature

  1. Iodine has been added to salt in most developed countries (in Asia/countries surrounded by water.. iodine can come from ocean)
  2. Contract products used in radiology
  3. Certain medications contain iodine (amiodarone)
  4. PSN: algae (found in a lot of PSNs), kelp, etc.
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19
Q

What does a normal thyroid do when there is a deficit/surplus/or sudden surplus in iodine?

A
  1. Deficit: increased captation
  2. Surplus: decreased captation
  3. Sudden surplus: Wolff-Chaikoff effect
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20
Q

Wolff-Chaikoff in normal thyroid:

A

Effect that allows your body to avoid forming excess thyroid hormone

Decrease capitation and organification of iodine

Transitory effect (2-4 weeks) and then once things are back to normal, T4 and T3 synthesis starts again

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21
Q

What does an abnormal thyroid do when there’s a deficit/surplus/or sudden surplus in iodine?

A
  1. Deficit: hypoT4
  2. Surplus: hyperT4
  3. Sudden surplus: hyperT4/hypoT4 depending on condition
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22
Q

How can iodine cause hypoT4?

A

Surplus in iodine –> Wolff-Chaikoff but it’s not transitory (you get stuck) which causes hypoT4

(Thyroïdite d’Hashimoto)

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23
Q

How can iodine cause hyperT4?

A

Thyroïde est avide d’iode d’où thryotoxicose

Examples:

  • Graves
  • Multinodular goiter
  • Nodule chaud
  • Goiter due to deficit in iodine
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24
Q

How are T4 and T3 transported in the body?

A

T4 and T3 are relatively insoluble in water –> bound to transport proteins

  • T4: 0.01% libre
  • T3: 0.1% libre
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25
Q

Which proteins transport thyroid hormones in the body?

A

Thyroxine-binding globulin (TBG): 70%

Transthyrétine (thyroxine-binding prealbumin): 20%

Albumine: 10%

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26
Q

Axe hypothalamo-hypophyso-throïdien = axe thyréotrope

A
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27
Q

How is the axe thyroïdien regulated?

A

Very tight regulation

T3 –> prodominant role in retroaction

TRH –> stimulates TRH

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28
Q

What is the difference between primary and central thyroid illnesses?

A

Primary: thyroid disease comes from thyroid itself

Central: thyroid disease comes from pituitary and hypothalamus

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29
Q

When looking for a primary thyroid illness what do different TSH levels indicate?

A

Normal –> no dysthyroidia

High –> primary hypoT4

Elevated –> hyperT4

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30
Q

How are thyroid hormones measured?

A

Total measurements don’t necessarily reflet the metabolic state of someone

T4 libre (FT4) –> not influenced by transport proteins

T4 totale –> influenced by transport proteins

T3 totale (TT3) –> influenced by transport proteins

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31
Q

What can modify TBG levels?

A

Increased by:

  • Genetics
  • Estrogen
  • Hepatitis

Decreased by:

  • Genetics
  • Androgens
  • Cirrhosis
  • Nephrotic syndrome
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32
Q

When is the TSH measurement not reliable?

A

in central hypoT4

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33
Q

When looking for a central thyroid illness what do different TSH levels indicate?

A

Normal –> doesn’t exclude anything

  • TSH normal + increased T4 = central hyperT4
  • TSH normal + decreased T4 = central hypoT4

TSH ABNORMALLY NORMAL

Increased –> TSH increased with T4 slightly increased = central hyperT4

Decreased –> TSH decreased with T4 decreased = central hypoT4

ALWAYS LOOK AT TSH FIRST AND THEN LOOK AT T4 AND WHAT IT SHOULD BE

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34
Q

What can a low T4 indicate?

A

If TSH increased –> primary hypoT4

If TSH not increased (normal or low) –> central hypoT4

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35
Q

What are the three common antibodies found in hypo/hyperT4?

A

Anticorps anti-TPO (Hashimoto)

Anticorps anti-Thyroglobuline (cancer)

Anticorps anti-récepteur de la TSH (TSI, TRab –> Graves, LATS)

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36
Q

In which percent of the population are the three kinds of antibodies found?

A

Anti-TPO:

  • Normal popuation: 10%
  • Hashimotos: 90%

Anti-thyroglobuline:

  • Normal population: 3%
  • Important in cancer follow ups

TRab:

  • Normal population: 1%
  • Graves: 90%
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37
Q

What is thyroglobulin hormone measurement useful for?

A

Cancer différentiés de la thyroïde (si élévée –> signe de récidive)

Hyperthyroïdie d’origine factice:

  • TBG should be increased in all causes of thyrotoxicosis except for factice
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38
Q

How does scintigraphie thyroïdienne work?

A

Usually done over 2 days

  1. Day 1: take radioactive tracer
  2. Day 2: measurement of capitation and take images of thyroid
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39
Q

What is the purpose of a scintigraphie thyroïdienne?

A

Evaluate function and anatomy of the thyroid

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40
Q

Why is scintigraphie thyroïdienne so important? (3)

A
  1. Permet de préciser la cause d’hyperT4
  2. Permet de différentier un nodule chaud d’un nodule froid
  3. Permet de localiser la thyroïde particulièrement chez l’enfant
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41
Q

Important things to know before doing a scintigraphie thyroïdienne?

A

Counter indicated in pregnant/breastfeeding women and in children (unless trying to locate thyroid)

Antithyroidiens and Synthroid must be stopped before doing a scintigraphie

Beta blockers don’t impact scintigraphie

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42
Q

What would cause increased iodine capture on a scinti?

A

Graves

Goitre multinodulaire toxique

Nodule chaud

Tumeur d’hypophyse produisant TSH (hyperT4 centrale)

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43
Q

What would cause decreased iodine capture on a scinti?

A

Thyroidite (silencieuse, post-partum, sub-aigue –> hypoT4 phase)

Ingestion of thyroid hormone

Antithyroid rx (methimazole, PTU)

Iodine contamination

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44
Q

What is a thyroid echo useful for?

A

Evaluating nodules and cancer followups

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45
Q

Why would you do a thyroid echo?

A

DO NOT DO IT BECAUSE OF BLOOD TEST RESULTS

Do if during examen physique you find a node, masse, or abnormal ganglion

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46
Q

What is a thyroid TACO useful for?

A

Determine if there’s an obstruction (trachea/oesophagus) by a goiter

Evaluate a sub-sternal goiter (médiastin)

Evaluate recurrence/externsion of néo

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47
Q

What do thyroid hormones do in the body?

A

Regulate metabolism

Surplus –> thyrotoxicosis (hypermetabolism)

Deficit –> hypoT4 (hypometabolism)

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48
Q

What do thyroid hormones do in children?

A

All the others +

Development/maturation of the brain

Growth and skeletal maturation

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49
Q

What are the signs of hyperT4 in children?

A

Irritability, emotional instability

Hyperactivity

Decreased academic performance

Accelerated growth (rare)

Accelerated bone maturation (rare)

CAN BE CONFUSED WITH ADHD IN SOME CHILDREN

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50
Q

What are the signs of hypoT4 in children?

A

All the normal ones +

Mental delay (cretinism) if before 3 years old

Delayed growth

Delayed bone maturation

Decreased academic performance

Delayed puberty or early puberty

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51
Q

What is the global action of thyroid hormones?

A

Increase O2 consommation

Increase basal metabolism

Increase heat production

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52
Q

What are the normal sx of hyperT4?

A

Fatigue

Heat intolerance

Hot/sweaty skin

Weight loss even if appetite is increased

Increased Rx metabolism

Hyperthermia (si tempête thyroidienne)

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53
Q

What are the normal sx of hypoT4?

A

Fatigue

Shivers

Cold skin

Weight gain and decreased appetite

Decreased Rx metabolism

Hypothermia (coma myxedémenteux)

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54
Q

What is the action of thyroid hormones on proteins, lipids, and glucose?

A

Proteins:

  • increased synthesis and degradation

Lipids:

  • Increased cholesterol synthesis and degradation

Glucose:

  • Increased hepatic neoglugenisis
  • Increased intestinal absorption
  • Increased glycogen degradation
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55
Q

Hypo and hyperT4 and lipids, protein, and glucose:

A

Hyper:

  • loss of muscle mass/force (proximal myopathy)
  • glucose intolerance (can cause db)
  • decreased cholesterol levels

Hypo:

  • muscular hypertrophy (rare)
  • hypoglycemia (coma myxodémateux)
  • hypercholesterol
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56
Q

What are the effects of hyperT4 on the CV system?

A

Tachycardia

Increased contraction –> SYSTOLIC hypertension

Palpitations

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57
Q

What are the effects of hypoT4 on the CV system?

A

Bradycardia

DIASTOLIC hypertension

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58
Q

What are the effects of hyperT4 on the SNS?

A

Shakes

Sweating

Palpitations

Réflexes ostéotendineux vifs

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59
Q

What are the effects of hypoT4 on the SNS?

A

Delayed relaxation phase in osteotendinous reflexes

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60
Q

What are the effects of hyperT4 on the respiratory system?

A

Tachypnée

Weakness of respiratory muscles

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61
Q

What are the effects of hypoT4 on the respiratory system?

A

Hypoventilation –> hypoxemia/hypercapnia

Weakness of respiratory muscles

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62
Q

What are the effects of hyperT4 on the digestive system?

A

Hyperdefecation –> diarrhea

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63
Q

What are the effects of hypoT4 on the digestive system?

A

Constipation

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64
Q

What are the effects of hyperT4 on the bones?

A

Osteoporosis

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65
Q

What are the effects of hypoT4 on the bones?

A

Delayed growth and bone maturation in children

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66
Q

What are the effects of hyperT4 on the SNC?

A

Hyperkinesis (muscle spasms)

Emotional liability

Decreased concentration

Depression

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67
Q

What are the effects of hypoT4 on the SNC?

A

Hypokinesis (movements have a “decreased amplitude”)

Decreased/slowed cognitive function

Depression

68
Q

What are the effects of hypoT4 on the muscles?

A

Muscular hypertrophy (rare)

Hypoventillation

Myalgia

69
Q

What are the effects of hyperT4 on the muscles?

A

Loss of muscle mass/force of skeletal muscles (proximal myopathy)

Dyspnea

70
Q

What are the effects of hypoT4 on the endocrine system?

A

Decreased GH

Increased PRL

Menometrorrhagia (prolonged or excessive uterine bleeding occurs irregularly and more frequently than normal)

Anovulation and infertility

Decreased/early puberty

Decreased cortisol clearance

71
Q

What are the effects of hyperT4 on the endocrine system?

A

Diabetes exacerbation

Oligomenorrhea, amenorrhea (loss/infrequent periods)

Anovulation, infertility, miscarriage

Gynecomastia (increased conversion of testosterone into estrogen)

Increased cortisol clearance

72
Q

What is euthyroidism?

A

Normal thyroid function that occurs with normal serum levels of TSH and T4

73
Q

What is the difference between hyperthyroidism and thyrotoxicosis?

A

Hyperthyroidism refers to increased thyroid hormone synthesis and secretion from the thyroid gland,

whereas thyrotoxicosis is characterized by the clinical manifestations of inappropriately high thyroid hormone action in tissues (increased thyroid hormone presence)

74
Q

What is a goitre?

A

Thyroid is bigger than usual

Usually provoked by increased thyroid stimulation: TSH, TRabs, other antibodies

75
Q

What is a simple goitre?

A

No nodes, uniform increased thyroid size

76
Q

What is a multinodular goitre?

A

Multiples nodes, heterogenous gland

(Zones with hyperplasia, fibrosis, and necrosis)

77
Q

What are the three main kinds of goitres?

A
  1. Toxic: hyperT4
  2. Euthyroid (normal T4 and T3)
  3. Associated with hypoT4
78
Q

What sx are associated with thyrotoxicosis?

A

Fatigue
Hyperactivity
Anxiety, nervousness, emotional liability
Heat intolerance/increased sweating
Palpitations
Shaking
Hyperdefication
Oligomenorrhea and amenorrhea

79
Q

What signs are associated with thyrotoxicosis?

A

Tachycardia, FA
Weight loss
Hyperkesisis
Lid lag (rétard palpébrale)
Hot, sweaty skin
Slight shaking
Proximal muscle weakness, loss of muscle mass
Réflexes ostéotendineux vifs

80
Q

Causes of thyrotoxicosis if scinti capture is high:

A

Graves

GMN toxique

Adénome toxique (nodule chaud)

Adénome hypophysaire secrétant de la TSH (VERY RARE!)

81
Q

Causes of thyrotoxicosis if scinti capture is low:

A

Hormones released cause thyroid was damaged:

  1. Thyroiditis (subacute, postpartum, silent, radiation)

Induced by iodine

Factice

82
Q

What are the possible treatment methods available for thyrotoxicosis?

A

Depending on cause and sx:

  1. Antithyroid synthesis (thionamides)
  2. Radioactive iodine (I-131)
  3. Thyroidectomy
  4. Beta-blockers (tx sx not cause)
83
Q

What are the two available thionamines?

A

PTU and methimazole (tapazole)

84
Q

PTU vs Tapazole:

A

PTU:

  • Half-life: 75 mins
  • Preferred in:
    • First trimester
    • Tempête thyroïdienne

Tapazole:

  • Half-life: 4-6 hours
85
Q

How does PTU work?

A

Inhibits organification of iodine

Inhibits iodinated tyrosine coupling

Decreases conversion of T4 into T3

86
Q

How does tapazole work?

A

Inhibits organification of iodine

Inhibits iodinated tyrosine coupling

87
Q

What are some side effects of PTU and tapazole?

A

Éruption cutanée

Liver: PTU –> hépatite toxique, tapazole –> cholestase hépatique

Agranulocytosis (acute condition involving a severe and dangerous lowered white blood cell count)

88
Q

How does radioactive iodine work?

A

Iodine is mainly captured by the thyroid and when radioactive iodine is captured it’ll cause destruction of thyroid cells

Side effects:

  • Transitory increase in thyroid hormone (due to tissue destruction)
  • Worsening of Graves orbitopathy (GRAVES IS A 100% COUNTER INDICATION)
  • Permanent hypoT4 in most patients
89
Q

Specifics on radioactive iodine:

A

Antithyroid rx must be stopped 5-7 days before to allow thyroid to regain function/start capturing iodine again

Beta-blockers can be continued/given at the same time

Can only be used in children if in later stages of puberty or if growth is basically done

90
Q

What are the counter-indications for taking radioactive iodine?

A

Severe thyrotoxicosis

Ophthamopathie

Pregnancy/breast feeding

Low iodine capture shown on scinti

91
Q

What are the two kinds of thyroidectomies and what the advantage of having one?

A

Total: graves, GMN

Partial: toxic adenoma in thyroid

Advantages: very quick resolution of thyrotoxicosis

92
Q

What are the risks involved with a thyroidectomy?

A

Damage to “nerfs récurrents laryngés”

  • vocal cord paralysis
  • if on both sides: risk of insuff. respiratoire (will need tracheostoma)

Damage to PTHs (can cause permanant/transitory hypoPTH)

HypoT4 if total thyroidectomy

93
Q

Why are beta-blockers used for thyrotoxicosis?

A

Decrease adrenergic sx

94
Q

What is Graves?

A

Most common cause of thyrotoxicosis

Autoimmune disorder:

  • TRabs stimulate TSH receptors causing overproduction of T4 and T3

More common in W > M

Genetic predisposition

Can be exacerbated by a sudden surcharge of iodine

95
Q

How does Graves present during investigations?

A

T4L and T3 increased

TSH decreased

Scinti:

  • Increased homogenous iodine capture
96
Q

What are some signs and sx of Graves?

A

Thyrotoxicosis signs and sx

AND specific to Graves:

  • Orbitopathy
  • Dermopathy
  • Neonatal hyperT4 (antibodies pass from mom to fetus)
97
Q

How to treat Graves? (5 ways)

A
  1. Antithyroid rx alone
  2. Radioactive iodine (must lower T4 levels first and cannot be done if orbitopathy)
  3. Antithyroid + radioactive iodine (get near hypo so iodine can enter)
  4. Surgery (rare but most remove whole thyroid.. done when rxn to antithyroid rx and iodine is counterindicated)
  5. Beta-blockers to tx sx
98
Q

What is orbitopathie de Graves?

A

TRab onto receptors in eyes that are very similar to TSH receptors in thyroid

Causes swelling of orbital muscles (lymphoid infiltration) which leads to proptosis, conjunctival congestion, periorbital edema, muscular fibrosis (diplopia), compression of optic nerve (can cause vision loss)

99
Q

What is dermopathie de Graves?

A

Rare: 2-3% of pts

a skin condition characterized by red, swollen skin, usually on the shins and tops of the feet

100
Q

What is a GMN toxique?

A

Maladie de Plummer

Usually in people > 50

History of GMN non toxique

Nodules become autonomous and no longer listen to TSH

HyperT4 can be provoked by a sudden charge in iodine (ex: contrast products and amiodarone)

101
Q

How does GMN toxique present during investigations?

A

T4L and T3 increased

TSH decreased

Scinti:

  • Heterogenous increased iodine capture (some cells are still normal and listen to TSH)
102
Q

What are some signs and symptoms of GMN toxique?

A

Normal signs/sx of thyrotoxicosis

BUT

usually takes more time to show sx compared to Graves and the gland is usually heterogenous, asymmetric, and a large volume

103
Q

How to treat GMN toxique?

A

Same as Graves except no counter-indication for iodine since there’s no orbitopathy

Surgery is more common

104
Q

What is a toxic adenoma?

A

Mutation of TSH receptor (makes it constantly activated) which causes excessive T4/T3 secretion and clonal expansion of cells which will cause a node (nodule chaud/toxique)

Same signs/sx as other forms of thyrotoxicosis but with a palpable nodule (sometimes)

105
Q

How does a toxic adenoma present during a scinti?

A

T4L and T3 increased

TSH decreased

Scinti:

  • Localized excessive +++ iodine capture –> nodule chaud autonome
  • Rest of thyroid doesn’t capture since TSH is decreased
106
Q

How to tx toxic adenoma?

A

Antithyroid alone

Radioactive iodine alone (MOST COMMON)

Antithyroid + radioactive iodine

Surgery (quite common)

Beta-blockers (for sx management)

107
Q

Radioactive iodine and toxic adenomas:

A

Will only destroy the cells in the adenoma (only ones capturing iodine)

Normal cells will later resume once adenoma is destroyed

Slight risk of post-iodine hypoT4 but much lower than in other pathologies

108
Q

What is thyroiditis?

A

Inflammation of the thyroid

109
Q

What are the 5 most common kinds of thyroiditis?

A
  1. Hashimotos: different than all the other ones (will just cause hypoT4)
  2. Subacute
  3. Silent
  4. Post-partum
  5. Radiation
110
Q

What are the three phases of thyroiditis?

A

ALL FORMS EXCEPT HASHIMOTOS:

  1. HyperT4 (thyroid cells destroyed and release T4/T3)
  2. HypoT4 (thyroid is damaged… TSH increased but can’t do anything)
  3. Euthyroid: thyroid heals and returns to normal
111
Q

What is the pathophysiology of thyroiditis?

A

Destruction (acute) of thyroid by aggressor –> sudden release of thyroid hormones –> temporary thyrotoxicosis

Thyroid stops producing and hormones released run out but takes a couple weeks/months for the thyroid to heal –> hypoT4

112
Q

Investigation during different phases of thyroiditis:

A

HyperT4:

  • TSH low
  • FT4 and T3 high
  • Scinti: VERY low capture (cells too damaged)

HypoT4:

  • TSH high
  • FT4 high and T3 high/normal

Euthyroid:

  • TSH, FT4, and T3 normal
113
Q

How to treat hyperT4 phase of thyroiditis?

A

Antithyroid Rx are useless because iodine isn’t being captured.. the thyroid is just releasing its stock

Beta-blockers to manage symptoms

114
Q

How to treat hypoT4 phase and euthyroid phase of thyroiditis?

A

Euthyroid: NO TREATMENT

HypoT4: no tx if asx but if sx –> Synthroid

Recuperation period:

  • Stop Synthroid after 4-6 months
  • Follow TSH levels for the following weeks/months
115
Q

What is subacute thyroiditis?

A

Also called De Quervain or Granulomatous

Usually preceded by IVRS

Most likely caused by viral infection

Unique aspects (during hyperT4 phase)

  • Fever, myalgia, general malaise
  • Painful thyroid
  • Increased “vitesse de sédimentation”
    • Permet de détecter une inflammation ou une infection​
  • Tx with AINS/anti-inflammatory or prednisone if pain +++
116
Q

What is silent thyroiditis?

A

Painless thyroiditis

Likely an autoimmune cause (lymphocyte infiltration of thyroid)

HyperT4 and hypoT4 usually quite mild

Normal thyroid size and tx usually unnecessary

117
Q

What is postpartum thyroiditis?

A

Usually in the 6 months after giving birth

Probably an autoimmune cause (maybe variant of Hashimotos)

  • Immune system drops when pregnant –> after giving birth it spikes back up which can exacerbate autoimmune disorders

HyperT4 and hypoT4 usually quite mild

Normal thyroid size and tx usually unnecessary

118
Q

What is radiation thyroiditis?

A

Caused by tx with radioactive iodine

Usually in 4-7 days after taking I-131

119
Q

What is factitious thyroiditis?

A

Due to excessive T4/T3 consumption

Can be done on purpose OR from PSNs that may contain thyroid extracts

Same symptoms of thyrotoxicosis but NO GOITRE

Investigation: TSH low, FT4 and T3 high

Scinti: low capture

IF SUSPECTED TEST TGB BECAUSE WILL BE INCREASED WITH ALL OTHER CAUSES OF THYROIDITIS

120
Q

What is a thyroid storm?

A

VERY SEVERE thyrotoxicosis

mortality –> 20-30%

Usually due to adjacent undiagnosed thyroid disease exacerbated by infection, chx, or iodine

121
Q

What are the cardinal sx of a thyroid storm? (4)

A

Fever > 38.5

Tachy > 140 (can even cause pulmonary edema)

N/V, diarrhea

Confusion all the way to coma

122
Q

What are the different causes of hypoT4?

A

Primary (95%)

Central (5%)

123
Q

Neonatal period of hypoT4:

A

Thyroid hormones are crucial for the development and growth of the brain especially before the age of 3

If hypoT4 is not treated, it can cause significant mental delays (cretinism)

Usually asx at birth and detected through heel prick test after birth

124
Q

What are the symptoms of hypoT4 in babies/toddlers?

A

Hypotonia

Difficulty latching and suckling

Lethargia

125
Q

What are the symptoms of prepubescent hypoT4?

A

Delayed growth (after 2)

Delayed/early period

126
Q

What are the classic sx of hypoT4?

A

Fatigue

Slowed cognitive function, and movement

Chills

Weight gain (< 10% pre hypoT4 weight)

Constipation

Myalgia

Menometrorragia

Dry skin and hair loss

127
Q

What are the classic signs of hypoT4?

A

Bradycardia, pericardial effusion, DIASTOLIC hypertension

Slowed reflexes (slowed relaxation phase)

Cold/dry skin

Oedème (sans godet)

Periorbital edema

Goitre often present

128
Q

What are the neonatal signs of hypoT4?

A

Jaundice +++

Macroglossia (unusually large tongue)

Abnormally large anterior fontanel

Umbilical hernia

129
Q

What are some other consequences of hypoT4?

A

Dlpd

Anemia

AST/ALT increase

Increased CK

130
Q

How does hypoT4 present during investigation?

A

TSH high

T4 low

T3 normal –> low

  • Normal at the start but will drop as hypoT4 progresses

Anti-TPO often + (most often in Hashimoto)

Imagery useless unless you’re trying to find a dysgenesis in a baby/child –> in this case use scinti

131
Q

What can cause a primary hypoT4?

A

Thyroiditis:

  • Hashimoto –> most frequent
  • Other ones –> hypoT4 phase

Destruction of thyroid:

  • Thyroidectomy
  • Iodine-131
  • External radiation

Medication:

  • Antithyroid
  • Lithium –> decrease synthesis and release of already formed
  • Amiodarone
  • Cancer medication: check point inhibitors and tyrosine kinase inhibitors

Diet:

  • Diète goitrogène ou déficit en iode
132
Q

Which congenital abnormalities can cause primary hypoT4?

A

Dysgènese: lungual, ectopic, anégésie

Dyshormogénèse: enzymatic deficit (usually goitre)

133
Q

What can cause a central hypoT4? and what will investigations show?

A

Pituitary or hypothalamic disorders

Investigations:

  • TSH normal or low –> useless
  • FT4 low
  • TT3 normal to low
134
Q

What are the signs and sx of a central hypoT4?

A

Sx: classic symptoms along with other potential hormonal deficits

Signs: NO GOITRE

135
Q

How to treat central hypoT4?

A

Treat cause not just sx

IF CORTISOL DEFICIT AS WELL

  • Always treat hypocortisolism first before hypoT4
  • Giving thyroid hormones first will increase metabolism nd further decrease cortisol levels and can send pt in to Addisonian choc
136
Q

What will happen to your thyroid tests if you take biotin?

A

Excess biotin will perturb TSH and T4 measurement which will make it look like hypoT4 with a very high TSH and very low T4

BUT THE PATIENT IS NORMAL AND THE TEST IS WRONG

If this is the case… stop taking biotin, redo the tests and they should be normal

137
Q

How to treat hypoT4?

A

Synthetic thyroid hormones:

SYNTHROID (L-Thyroxine) –> T4

Triiodotyronine (Cytomel ) –> T3

138
Q

L-Thyroxine:

A

Half-life: 7 days

DIE

4-6 weeks for it to stabilize in the blood

Dose varies depending on age and condition of patient

139
Q

How to treat older patient or patient with coronary disease for hypoT4?

A

Start with a small dose and increase very slowly otherwise risk of exacerbating angina or causing an infarctus

140
Q

Which medications can you not take with synthroid?

A

Calcium and iron

141
Q

L-Thyroxine in pregnant women:

A

Primary hypoT4: TSH in normal for first trimester

Central hypoT4: TSH (non fiable), FT4 between normal and the high limits of normal, absence of sx

Check labs 4 weeks after dose adjustment

142
Q

Information about triiodothyronine

A

Half-life: short

Must be taken multiple times a day

Taking with L-Thyroxine is very controversial right now

143
Q

What is Hashimotos?

A

Type of thyroiditis

Immune disorder (anti-TPO)

Infiltration of the thyroid by lymphocytes

144
Q

What are the signs and sx of Hashimotos?

A

Classic hypoT4 sx

Goitre is frequent but possible for the thyroid to have atrophied and become non-palpable

145
Q

How does Hashimotos present during investigations?

A

TSH high

FT4 low

TT3 normal to low

Anti-TPO +++

146
Q

How to treat Hashimotos?

A

Synthroid

147
Q

What is a myxedema coma?

A

Very severe hypoT4

Other factor usually present that makes things worse:

  • Infection such as pneumonia
  • Exposition to cold
  • Acute CV disease: infarctus, ACV

Used to be 50% mortality rate but getting better

148
Q

What can cause a myxedema coma?

A

Untreated hypoT4 or stopping treatment

Presents as normal sx and signs of hypoT4 + altered cognitive function (lethargia, +++ slowed, coma, convulsions)

  • hypothermia, hypotension, hypoxemia/hypercapnea, hypoglycemia, hynonatremia
149
Q

What are the most common kinds of benign thyroid nodules?

A

Cysts

Chronic focalized thyroiditis (Hashimotos, granulomateuse)

Focalized hyperplasia

Follicular adenoma

150
Q

What are the most common kinds of malignant thyroid nodules?

A

Papillary cancer (80%) –> MOST COMMON

Follicular cancer (10%)

Medullairy cancer (5%)

Anaplasic cancer (3%) –> MOST DANGEROUS

Lymphoma and metastasis of other cancers (1-2%)

151
Q

How to distinguish malignant vs benign thyroid nodules?

A

History:

  • Dysphonia, dysphagia, obstruction –> more likely malignant
  • Fast-growing –> more likely malignant
152
Q

What are some risk factors for thyroid cancer?

A

Radiation during childhood

Family history

Homme > femme (if you find nodule in man its more likely to be cancer but incidence of cancer is the same)

Examen physique:

  • Hard and immobile
  • Adjacent adenopathy
  • Large nodule (> 4cm)
153
Q

Labs and scinti for thyroid nodules:

A

Labs:

  • TSH high –> hypoT4
  • TSH normal
  • TSH low –> nodule chaud/autonome (rarely cancerous)

Scinti:

  • Nodule froid –> 5% chance of cancer
  • Nodule tiède/chaud –> cancer rare
154
Q

What signs on an echo suggest thyroid cancer?

A

NOT CONFIRMATION, SUGGESTION

Hypoechogenicity (darker than usual)

Microcalcifications

Irregular borders

Nodule higher than bigger

If spongiform –> 100% benign

155
Q

What is a thyroid fine-needle aspiration biopsy?

A

Distinguish benign, malignant, and follicular (20% malignant)

156
Q

Follow-up for thyroid nodules after thyroid fine-needle aspiration biopsy:

A

Benign: follow-up with palpation, TSH, and echo

Malignant: hemithyroidectomy vs full thyroidectomy

Indeterminate: depending on the patient, dx surgery vs. tight follow-up and aspirations

157
Q

What are differentiated thyroid cancers?

A

Come from follicular cells

Conserve their capacity to secrete TGB –> becomes cancer marker

Conserve their ability to capture iodine but less efficiently than normal so you can still tx with I-131

Prognostic: excellent (papillary 98% and follicular 92%)

158
Q

What are the two “forms” of differentiated thyroid cancers?

A

Papillaire: cellules arrangées sous forme de papilles

Folliculaires: cellules arrangées sous forme de follicules

159
Q

Why would someone with differentiated thyroid cancer die from cancer if the prognostic is so good?

A

Local invasion/compression of the trachea

Pulmonary metastasis –> insuffisance respiratoire

160
Q

How to treat differentiated thyroid cancer?

A
  1. Total/hemithyroidectomy
  2. Radioactive iodine
  3. Thyroid hormones

Chemo isnt really used

161
Q

What is medullary thyroid cancer?

A

Cellules C –> parafollicular cancer

Secrete calcitonin

162
Q

What is anaplastic thyroid cancer?

A

aggressive form of thyroid cancer characterized by uncontrolled growth of cells in the thyroid gland

very poor prognosis due to its aggressive behaviour and resistance to cancer treatments

163
Q

Signs during patient history that’ll point you towards anaplastic thyroid cancer:

A

F > H

Age around 65

History of goitre +++

Fast growth thyroid (changes visible day by day)

Dysphagia, dysphonia, and local pressure

164
Q

How to treat anaplastic thyroid cancer?

A

VERY AGRESSIVE TREATMENT OR PALLIATIVE CARE:

Aggressive treatment:

  • Total thyroidectomy
  • External radiotherapy
  • Chemotherapy

Palliative treatment: goal of avoiding unnecessary treatments but try to maintain the patients quality of life

165
Q

What is the ddx for thyroid pain?

A

Subacute thyroiditis

Hemorrhage of thyroid nodule

Trauma (or I-133 treatment)

Abscess

Cancer (quite rare to be painful)

MD1 endocrinologie (6 decks)

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