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Endocrinology > Thyroid > Flashcards

Thyroid Flashcards

1
Q

Extra-thyroidal factors impacting thyroid hormone homeostasis

A
  • Most peripheral thyroid metabolism occurs in the liver and the kidneys, thus severe liver disease and CKD can significantly alter T3:T4 ratio.
  • Alcohol dependence results in hypothalamicpituitary-thyroid axis dysfunction demonstated by decreased TSH, T4 and T3 levels.
  • Smoking is associated with lower TSH levels in a dose-dependent manner: with heavy smoking (812 cigarettes/day) having more TSH suppression than light smokers (<4 cigarettes/day).
  • Heavy metal exposure including lead, mercury and cadamium has been shown to alter thyroid hormone function and peripheral metabolism.
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2
Q

Synthesis of T4 thyroxine and T3 triiodothyronine by the thyroid gland involves what

A

trapping and oxidation of iodide,

iodination of thyroglobulin,

digestion of thyroglobulin,

and release of T3 and T4

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3
Q

What is the difference between free and bound T3 and T4

A

free T4 (0.03%) and free T3 (0.3%) represent the hormonally active fraction of thyroid hormones

■ the remaining fraction is bound to thyroxine binding globulin (TBG) and albumin and is biologically inactive

T3 is more biologically active (3-8x more potent), but T4 has a longer half-life

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4
Q

Conversion between T3 and T4

A

85% of T4 is converted to T3 or reverse T3 (RT3) in the periphery by deiodinases

most of the plasma T3 pool is derived from the peripheral conversion of T4

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5
Q

What is RT3

A

RT3 is metabolically inactive but produced in times of stress to decrease metabolic activity

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6
Q

What produces calcitonin and what is its function

A

calcitonin, a peptide hormone, is also produced in the thyroid, by the parafollicular cells or C cells

■ Calcitonin functions by inhibiting osteoclast activity and increasing renal calcium excretion

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7
Q

Role of thyroid hormones

A
  • thyroid hormones act primarily through modifying gene transcription by binding to nuclear receptors
  • action of these hormones is diffuse, effecting nearly every organ system
  • thyroid hormones have different tissue-specific actions determined by the expression of the types of thyroid receptor isoform and the local production of T3
  • they increase the basal metabolic rate including: increased Na+/K+ATPase activity, increased O2 consumption increased respiration, heat generation, and increased cardiovascular activity
  • thyroid hormones also play crucial role during fetal life in both neurological and somatic development
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8
Q

Patterns of hormone levels in 1o and 2o hyper and hypothyroidism

A

1o hyper
TSH dec
T3, T4 inc

2o hyper
TSH inc
T3, T4 inc

1o hypo
TSH inc
T3, T4 dec

2o hypo
TSH dec or normal
T3, T4 dec

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9
Q

Regulation of thyroid function

A

• extrathyroid
■ stimulation of thyroid by TSH, epinephrine, prostaglandins (cAMP stimulators)
■ T3 negatively feeds back on anterior pituitary to inhibt TSH and on hypothalamus to inhibit TRH

• intrathyroid (autoregulation)
■ synthesis (Wolff-Chaikoff effect, Jod-Basedow effect)
■ there is varying thyroid sensitivity to TSH in response to iodide availability
■ increased ratio of T3 to T4 in iodide deficiency
■ increased activity of peripheral 5’ deiodinase in hypothyroidism increases T3 production despite low T4 levels

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10
Q

What is Wolff Chaikoff effect

A

Large doses of stable iodine acutely inhibit thyroid hormone synthesis (Wolff–Chaikoff effect) and thyroid hormone release. The former effect is mediated through inhibition of the enzyme thyroid peroxidase.

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11
Q

What is Jod-Basedow effect

A

hyperthyroidism following administration of iodine or iodide, either as a dietary supplement or as iodinated contrast for medical imaging.

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12
Q

When should free T3 be measured

A

Free T3 should only be measured in the small subset of patients with hyperthyroidism and suspected T3 toxicosis

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13
Q

Types of thyroid autoantibodies

A
  • thyroglobulin antibodies (TgAb), anti-thyroid peroxidase antibodies (TPOAb), and TSH receptor antibodies (TRAb) of the blocking variety are increased in Hashimoto’s disease; normal variant in 1020% of individuals
  • TRAb of the stimulating variety are also referred to as thyroid stimulatng immunoglobulins (TSI) and cause Graves’ disease. However, both TRAb receptor blocking and stimulating antibodies are seen in patients with Graves’ disease
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14
Q

What is plasma thyroglobulin used to monitor

A
  • used to monitor for residual thyroid tissue post-thyroidectomy, e.g. tumour marker for thyroid cancer recurrence
  • normal or elevated levels may suggest persistent, recurrent, or metastatic disease
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15
Q

When in serum calcitonin ordered in the context of thyroid pathology

A
  • not routinely done to investigate thyroid nodules
  • ordered if suspicion of medullary thyroid carcinoma or family history of MEN IIa or IIb syndromes ■ used to monitor for residual or recurrent medullary thyroid cancer
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16
Q

Thyroid imaging/scans

A

• thyroid U/S
■ to measure size of gland, solid vs. cystic nodule, facilitate fine needle aspirate biopsy (FNAB)

• radioisotope thyroid scan (Technetium-99)

• test of structure: order if there is a thyroid nodule and patient is hyperthyroid with low TSH
■ differentiates between hot (functioning → excess thyroid hormone production) and cold (nonfunctioning) nodules
◆ hot nodule → very low chance malignancy; treat hyperthyroidism
◆ cold nodule → ~5% chance malignancy; further workup required (U/S and FNAB)

• radioactive iodine uptake (RAIU)
■ test of function: order if patient is thyrotoxic
■ RAIU measures the turnover of iodine by thyroid gland in vivo
■ if inc uptake (i.e. incorporated), gland is overactive (hyperthyroid)
■ if dec uptake (i.e. not incorporated), gland is leaking thyroid hormone (e.g. thyroiditis), exogenous thyroid hormone use, or excess iodine intake (e.g. amiodarone or contrast dye which has high iodine content)

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17
Q

Thyroid biopsy purpose and what affects accuracy

A

• fine needle aspiration (FNA) for cytology
■ differentiates between benign and malignant disease
■ best done under U/S guidance
■ accuracy decreased if nodule is greater than 50% cystic, or if nodule located posteriorly in the gland

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18
Q

Drugs affecting thyroid function

A
  • Lithium plays an inhibitory role in thyroid hormone release, resulting in clinical hypothyroidism and goitre.
  • Amiodarone-Induced Hypothyroidism (AIH): Amiodarone, a class III anti-arrhythmic drug contains 2 atoms of iodine per molecule and is structurally similar to thyroid hormones, and may exert antagonistic effects on TSH receptors. It is also shown to inhibit type I deiodinases resulting in low T3 and high T4 levels. Amiodarone-induced hypothyroidism occurs in 5-15% of patients on amiodarone. AIH can also occur in people without pre-existng thyroid dysfunction.
  • Amiodarone-Induced thyrotoxicosis (AIT): occurs in 2-12% of patients on amiodarone. This may be due to either an increased iodine load in patients with previously autonomous thyroid (Graves’ disease, toxic multinodular goitre), or amiodarone-induced destructive thyroiditis.
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19
Q

What condition do you see thyroid stimulating Ig (TSI) in

A

Graves’

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20
Q

What condition do you see antithyroid peroxidase (TPOAb, TgAb) in

A

Hashimoto’s

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21
Q

Conditions with increased RAIU uptake

A

Graves’

Toxic multinodular goitre

Toxic adenoma

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22
Q

Conditions with decreased RAIU uptake

A

Subacute thyroiditis

Recent iodine load

Exogenous thyroid hormone

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23
Q

Graves’ Radioisotope Thyroid Scan

A

Homogeneous diffuse uptake

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24
Q

Multinodular goitre Radioisotope Thyroid Scan

A

Heterogeneous uptake

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25
Q

Toxic adenoma Radioisotope Thyroid Scan

A

single intense area of uptake with suppression elsewhere

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26
Q

Thyrotoxicosis definition

A

clinical, physiological, and biochemical findings in response to elevated thyroid hormone

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27
Q

Signs and symptoms of hyperthyroidism

A 
Tremor 
Heart rate up/afib/palpitations 
Yawning (fatigued) 
Restlessness 
Oligomenorrhea/amenorrhea/decreased fertility 
Intolerance to heat 
Diarrhea 
Irritability 
Sweating/warm skin
Muscle wasting (proximal)/weight loss with increased appetite and thirst 
Other: 
Hypokalemic periodic paralysis (more common in Asians) 
Fine hair 
Vitiligo 
Soft nails with onycholysis (Plummer's nails) 
Palmar erythema 
Pruritis 
Decreased bone mass

Graves’ disease - clubbing (acropachy) and pretibial myxedema (rare)
Leeukopenia, lymphocytosis, splenomegaly, lymphadenopathy
Lid lag, retraction, proptosis, diplopia, decreased acuity, uffiness, conjunctival injection

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28
Q

Thyroiditis presentation

A

TSH dec

Free T3/T4 inc

Thyroid antibodies up to 50% of cases

RAIU decreased (increases once entering hypothyroid phase, when TSH rises)

In classical subacute painful thyroiditis, ESR increased

Can be subacute, silent or postpartum

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29
Q

Common etiologies of thyrotoxicosis

A

Graves’ Disease

Toxic Nodular Goitre

Toxic Nodule

Thyroiditis

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30
Q

Common etiologies of hypothyroidism

A

Hashimoto’s

Congenital

Iatrogenic (thionamides, radioactive iodine or surgery)

Hypothyroid phase of thyroiditis

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31
Q

Causes of excessive thyroid stimulation

A

Pituitary thyrotrophoma

Pituitary thyroid hormone receptor resistance

Increased hCG (ex. pregnancy)

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32
Q

When should RAIU not be completed

A

pregnancy

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33
Q

Thyrotoxicosis treatment

A
  • thionamides: propylthiouracil (PTU) or methimazole (MMI); MMI recommended (except in first trimester pregnancy)
  • β-blockers for symptom control
  • radioactive iodine thyroid ablation for Graves’ disease
  • surgery in the form of hemi, subtotal, or complete thyroidectomy
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34
Q

Graves’ Disease definition

A

an autoimmune disorder characterized by autoantibodies to the TSH receptor that leads to hyperthyroidism

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35
Q

Graves’ Disease epidemiology

A
  • occurs at any age with peak in 3rd and 4th decade
  • F:M = 7:1, 1.5-2% of U.S. women
  • familial predisposition: 15% of patients have a close family member with Graves’ disease and 50% have family members with positive circulating antibodies
  • association with HLA B8 and DR3
  • may be associated with other inherited autoimmune disorders (e.g. pernicious anemia, Hashimoto’s disease)
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36
Q

Most common cause of thyrotoxicosis

A

Graves’ Disease

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37
Q

Graves’ Disease etiology and pathophys

A
  • autoimmune disorder due to a defect in T-suppressor cells
  • B lymphocytes produce TSI that binds and stimulates the TSH receptor and stimulates the thyroid gland
  • immune response can be triggered by postpartum state, iodine excess, lithium therapy, viral or bacterial infections, glucocorticoid withdrawal
  • ophthalmopathy (thyroid associated orbitopathy) is a result of increased tissue volume due to inflammation and accumulation of glycosaminoglycans, stimulated by TSI, that increase osmotic pressure within the orbit; this leads to fluid accumulation and displacement of the eyeball forward
  • dermopathy may be related to cutaneous glycosaminoglycan deposition
38
Q

Graves’ Disease clinical features

A
  • signs and symptoms of thyrotoxicosis
  • diffuse thyroid goitre ± thyroid bruit secondary to increased blood flow through the gland

• ophthalmopathy: NO SPECS (in order of changes usually)
No signs
Only signs: lid lag, lid retraction
Soft tissue: periorbital puffiness, conjuctival injection, chemosis
Proptosis/exophthalmos Extraocular (diplopia)
Corneal abrasions (since unable to close eyes)
Sight loss
(plus signs of hyperthyroidism: lid retraction, characteristic stare)

  • dermopathy (rare): pretibial myxedema (thickening of dermis that manifests as non-pitting edema
  • acropachy: clubbing and thickening of distal phalanges
39
Q

Graves’ Disease investigations

A
  • low TSH
  • increased free T4 (and/or increased T3)
  • positive for TSI (specific but not sensitive for Graves’ disease)
  • increased radioactive iodine (I 131) uptake
  • homogeneous uptake on thyroid scan (only do this test in the presence of nodule)
40
Q

Graves’ Disease treatment

A

• thionamides: propylthiouracil (PTU) or methimazole (MMI)
■ iodinated contrast agents: sodium ipodate and iopanoic acid can inhibit conversion of T4 to T3 and are especially effective in combination with MMI
■ MMI preferred vs. PTU due to longer duration of action (once daily for most), more rapid efficacy, and lower incidence of side effects
■ in pregnancy: use PTU during first trimester and MMI during second and third trimester. MMI is contraindicated in the first trimester due to risk of aplasia cutis; MMI is preferred in the second and third trimester due to the potential risk of hepatotoxicity with PTU in the second and third trimesters

• symptomatic treatment with β-blockers

• thyroid ablation with radioactive 131I if PTU or MMI trial does not produce disease remission
■ high incidence of hypothyroidism after 131I requiring lifelong thyroid hormone replacement
■ conraindicated in pregnancy
■ may worsen ophthalmopathy

• subtotal or total thyroidectomy (indicated for large goitres, suspicious nodule for Ca, if patient is intolerant to thionamides and refusing RAI ablation)
■ risks include hypoparathyroidism and vocal cord palsy

• ophthalmopathy/orbitopathy  
■ smoking cessation is important  
■ prevent drying of eyes 
■ high dose prednisone in severe cases  
■ orbital radiation, surgical decompression

Glucocorticoids have been useful in the treatment of severe Graves’ hyperthyroidism and thy oid storm, by inhibiting the conversion of peripheral T4 to T3

Lithium is also used to treat Graves’ hyperthyroidism. It acts by blocking thyroid hormone release, but its toxicity has limited its use in practice

41
Q

Graves’ Disease prognosis

A
  • course involves remission and exacerbation unless gland is destroyed by radioactive iodine or surgery
  • lifetime follow-up needed
  • risk of relapse is 37%, 21%, 6% in thionamides, radioiodine ablation, and surgery groups, respectively
42
Q

MMI and PTU MOA, duration of treatment, indicators for long-term remission and side effects

A

■ PTU and MMI inhibit thyroid hormone synthesis by inhibiting peroxidase-catalyzed reactions, thereby inhibiting organification of iodide, blocking the coupling of iodotyrosines
■ PTU also inhibits peripheral deiodination of T4 to T3
■ continue treatment until remission occurs (20-40% of patients achieve spontaneous remission at 6-18 mo of treatment)
■ small goitre and recent onset are good indicators for long-term remission with medical therapy
■ major side effects: hepatitis, agranulocytosis, and fever/arthralgias
■ minor side effects: rash

43
Q

Subacute thyroidits (thyrotoxic phase) definition and types

A

acute inflammatory disorder of the thyroid gland characterized by an initial thyrotoxic state followed by hypothyroidism eventually followed by euthyroidism in most cases

• two subtypes: painful (“De Quervain’s”) and painless (“Silent”)

44
Q

Subacute thyroidits (thyrotoxic phase) etiology and pathophysiology

A
  • acute inflammation of the thyroid gland characterized by giant cells and lymphocytes
  • disruption of thyroid follicles by inflammatory process results in the release of stored hormone rather than excessive production of new thyroid hormone
  • painful = viral (usually preceded by URTI), De Quervain’s (granulomatous thyroiditis)

• painless = postpartum, auto-immune, lymphocytic
■ occurs in 5-10% of postpartum mothers and is symptomatic in 1/3 of patients

45
Q

Subacute thyroidits (thyrotoxic phase) clinical features

A
  • painful (thyroid, ears, jaw, and occiput) or painless
  • fever and malaise may be present, especially in De Quervain’s
  • postparum: thyrotoxicosis 2-3 mo postpartum with a subsequent hypothyroid phase at 4-8 mo pospartum
  • may be mistakenly diagnosed as postpartum depression
46
Q

Subacute thyroidits (thyrotoxic phase) lab investigations

A
  • initial elevated free T4, T3, low TSH, RAIU markedly reduced
  • marked elevation of ESR in painful variety only
  • as disease progresses values consistent with hypothyroidism may appear
47
Q

Subacute thyroidits (thyrotoxic phase) treatment

A
  • painful – high dose NSAIDs prednisone may be required for severe pain, fever, or malaise
  • iodinated contrast agents (eg. iopanoic acid, ipodate) to inhibit peripheral conversion of T4 to T3
  • β-adrenergic blockade is usually effective in reversing most of the hypermetabolic and cardiac symptoms in both subtypes
  • if symptomatically hypothyroid, may treat short-term with thyroxine
48
Q

Subacute thyroidits (thyrotoxic phase) prognosis

A
  • full recovery in most cases, but permanent hypothyroidism in 10% of painless thyroiditis
  • postpartum: most resolve spontaneously without need for supplementation, however may recur with subsequent pregnancies
49
Q

Radioiodine Therapy for Graves’ Disease and the Effect on Ophthalmopathy: A Systematic Revie

A

RAI therapy for GD is associated with a small but definite increased risk of development or worsening of Graves’ ophthalmopathy (GO) compared with antithyroid drugs. Steroid prophylaxis is beneficial for patients with preexisting GO.

50
Q

Toxic adenoma/Toxic multinodular goitre etiology and pathophys

A
  • autonomous thyroid hormone production from a functioning adenoma that is hypersecreting T3 and T4
  • may be singular (toxic adenoma) or multiple (toxic multinodular goitre [Plummer’s disease])
51
Q

Toxic adenoma/Toxic multinodular goitre clinical features

A
  • goitre with adenomatous changes
  • tachycardia, heart failure, arrhythmia, weight loss, nervousness, weakness, tremor, and sweats
  • seen most frequently in elderly people, often with presentation of atrial fibrillation
52
Q

Toxic adenoma/Toxic multinodular goitre investtigations

A
  • low TSH, high T3 and T4

* thyroid scan with increased RAIU in nodule(s) and suppression of the remainder of the gland

53
Q

Toxic adenoma/Toxic multinodular goitre treatment

A
  • initiate therapy with PTU or MMI to attain euthyroid state
  • use high dose radioactive iodine (I-131) to ablate hyperfunctioning nodules
  • β-blockers often necessary for symptomatic treatment prior to definitive therapy
  • surgical excision may also be used as 1st line treatment
54
Q

Thyrotoxic crisis/Thyroid storm definition

A
  • acute exacerbation of all of the symptoms of thyrotoxicosis presenting in a life-threatening state secondary to uncontrolled hyperthyroidism – medical emergency!
  • rare, but serious with mortality rate between 10-30%
55
Q

Thyrotoxic crisis/Thyroid storm etiology and pathophys

A

• often precipitated by infection, trauma, or surgery in a hyperthyroid patient

56
Q

Thyrotoxic crisis/Thyroid storm ddx

A

• sepsis, pheochromocytoma, malignant hyperthermia, drug overdose, neuroleptic malignant syndrome

57
Q

Thyrotoxic crisis/Thyroid storm clinical features

A
  • hyperthy oidism
  • extreme hyperthermia (≥40°C), tachycardia, vomiting diarrhea, vascular collapse, hepatic failure with jaundice, and confusion
  • tachyarrhythmia, CHF, shock
  • mental status changes ranging from delirium to coma
58
Q

Thyrotoxic crisis/Thyroid storm investigations

A
  • increased free T3 and T4, undetectable TSH

* ± anemia, leukocytosis, hyperglycemia, hypercalcemia, elevated LFTs

59
Q

Thyrotoxic crisis/Thyroid storm management

A
  • fluids, electrolytes, and vasopressor agents should be used as indicated
  • a cooling blanket and acetaminophen can be used to treat the pyrexia
  • propranolol or other β blockers that additionally decrease peripheral conversion of T3 → T4 can be used, but should be used with caution in CHF patients as it may worsen condition
  • PTU is the anti-thyroid drug of choice and is used in high doses

• give iodide, which acutely inhibits the release of thyroid hormone, one hour after the first dose of PTU is given
■ Sodium iodide 1 g IV drip over 12h q12h OR
■ Lugol’s solution 2-3 drops q8h OR
■ Potassium iodide (SSKI) 5 drops q8h

• dexamethasone 2-4 mg IV q6h for the first 24-48 hours lowers body temperature and inhibits peripheral conversion of T3 → T4

60
Q

Thyrotoxic crisis/Thyroid storm prognosis

A

• probably <20% mortality rate if rapidly recognized and treated

61
Q

Hypothyroidism definition

A

• clinical syndrome caused by cellular responses to insufficient thyroid hormone production

62
Q

Hypothyroidism epidemiology

A
  • 2-3% of general population
  • F:M = 10:1
  • 10-20% of women over age 50 have subclinical hypothyroidism (normal T4, TSH mildly elevated)
  • iodine deficiency most common cause worldwide, but not in North America
63
Q

Hypothyroidism etiology and pathophys

A

• primary hypothyroidism (90%)
■ inadequate thyroid hormone production secondary to intrinsic thyroid defect
■ iatrogenic: post-ablative (I-131 or surgical thyroidectomy)
■ autoimmune: Hashimoto’s thyroiditis, chronic thyroiditis, idiopathic, burnt out Graves’
■ hypothyroid phase of subacute thyroiditis
■ drugs: goitrogens (iodine), PTU, MMI, lithium
■ infiltrative disease (progressive systemic sclerosis, amyloid)
■ iodine deficiency
■ congenital (1/4,000 births)
■ neoplasia

secondary hypothyroidism: pituitary hypothyroidism
■ insufficiency of pituitary TSH

• tertiary hypothyroidism: hypothalamic hypothyroidism
■ decreased TRH from hypothalamus (rare)

• peripheral tissue resistance to thyroid hormone (Refetoff syndrome)

64
Q

Thyroid hormone replacement for subclinical hypothyroidism

A

In current RCTs, levothyroxine replacement therapy for subclinical hypothyroidism did not result in improved survival or decreased cardiovascular morbidity. Data on health-related quality of life and symptoms did not demonstrate significant differences between intervention groups. Some evidence indicates that levothyroxine replacement improves some parameters of lipid profiles and left ventricular function.

65
Q

Serum TSH and Free T4 in overt primary hypothyroidism, subclinical primary hypothyroidism and secondary hypothyroidism

A

overt primary hypothyroidism
Serum TSH - inc
Free T4 - dec

subclinical primary hypothyroidism
Serum TSH - inc
Free T4 - normal

secondary hypothyroidism
Serum TSH - dec or not appropriately elevated
Free T4 - dec

66
Q

Clinical features of hypothyroidism

A

General - Fatigue, cold intolerance, slowing of mental and physical performance, hoarseness, macroglossia

CVS - Pericardial effusion, bradycardia, hypotension, worsening CHF + angina, hypercholesterolemia, hyperhomocysteinemia, myxedema heart

Respiratory - Decreased exercise capacity, hypoventilation secondary to weak muscles, decreased pulmonary responses to hypoxia, sleep apnea due to macroglossia

GI - Weight gain despite poor appetite, constipation

Neurology - Paresthesia, slow speech, muscle cramps, delay in relaxation phase of deep tendon reflexes (“hung reflexes”), carpal tunnel syndrome, asymptomatic increase in CK, seizures

GU - Menorrhagia, amenorrhea, impotence

Dermatology - Puffiness of face, periorbital edema, cool and pale, dry and rough skin, hair dry and coarse, eyebrows thinned (lateral 1/3), discolouration (carotenemia)

Hematology - Anemia: 10% pernicious due to presence of anti-parietal cell antibodies with Hashimoto’s thyroiditis

HIS FIRM CAP 
Hypoventilation 
Intolerance to cold 
Slow HR 
Fatigue 
Impotence 
Renal impairment 
Menorrhagia/amenorrhea 
Constipation 
Anemia 
Paresthesia
67
Q

Hypothyroidism treatment

A
  • L-thyroxine (dose range: 0.05-0.2 mg PO OD ~1.6 µg/kg/d)
  • elderly patients and those with CAD: start at 0.025 mg daily and increase gradually every 6 wk (start low, go slow)
  • after initiating L-thyroxine, TSH needs to be evaluated in 6 wk; dose is adjusted until TSH returns to normal reference range
  • once maintenance dose achieved, follow-up TSH with patient annually

• secondary/tertiary hypothyroidism
■ monitor via measurement of free T4 (TSH is unreliable in this setting)

68
Q

Most common form of primary hypothyroidism in North America

A

Hashimoto’s Thyroiditis

69
Q

Hashimoto’s Thyroiditis definition and types

A

• chronic autoimmune thyroiditis characterized by both cellular and humoral factors in the destruction of thyroid tissue

• two major forms: goitrous and atrophic; both forms share same pathophysiology but differ in the extent of lymphocytic infiltration, fibrosis, and thyroid follicular cell hyperplasia goitrous variant usually presents with a rubbery goitre and euthyroidism, then hypothyroidism becomes evident
■ associated with fibrosis

• atrophic variant patients are hypothyroid from the start
■ associated with thyroid lymphoma

70
Q

Hashimoto’s Thyroiditis etiology and pathophysiology

A
  • defect in clone of T-suppressors leads to cell-mediated destruction of thyroid follicles
  • B lymphocytes produce antibodies against thyroid components including thyroglobulin, thyroid peroxidase, TSH receptor, Na+/I– symporter
71
Q

Hashimoto’s Thyroiditis risk factors

A
  • female gender (F:M = 7:1)
  • genetic susceptibility: increased frequency in patients with Down’s syndrome, Turner’s syndrome, certain HLA alleles, cytotoxic T-lymphocyte-associated protein 4 (CTLA-4)
  • family Hx or personal Hx of other autoimmune diseases
  • cigarette smoking
  • high iodine intake
  • stress and infection
72
Q

Hashimoto’s Thyroiditis investigations

A
  • high TSH, low T4 (not necessary to measure T3 as it will be low as well)
  • presence of anti-thyroid peroxidase (TPOAb) and thyroglobulin antibodies (TgAb) in serum
73
Q

Hashimoto’s Thyroiditis treatment

A

• if hypothyroid, replace with L-thyroxine (analog of T4)

74
Q

Hashimoto’s Thyroiditis treatment

A

• if hypothyroid, replace with L-thyroxine (analog of T4)

75
Q

Myxedema coma definition

A
  • severe hypothyroidism complicated by trauma, sepsis, cold exposure, MI, inadvertent administration of hypnotics or narcotics, and other stressful events – medical emergency!
  • rare high level of mortality when it occurs (up to 40%, despite therapy)
76
Q

Myxedema coma clinical features

A

• hallmark symptoms of decreased mental status and hypothermia; hyponatremia, hypotension, hypoglycemia, bradycardia, hypoventilation, and generalized edema often present

77
Q

Myxedema coma investigations

A
  • decreased T4, increased TSH, decreased glucose

* check ACTH and cortisol for evidence of adrenal insufficiency

78
Q

Myxedema coma treatment

A
  • aggressive treatment required
  • ABCs: ICU admission
  • corticosteroids (for risk of concomitant adrenal insufficiency): hydrocortisone 100 mg q8h
  • L-thyroxine 02-0.5 mg IV loading dose, then 0.1 mg IV OD until oral therapy tolerated; also consider T3 therapy
  • supportive measures: mechanical ventilation, vasopressor drugs, passive rewarming, IV dextrose, fluids if necessary (risk of overload)
  • monitor for arrhythmia
79
Q

Sick Euthyroid Syndrome definition

A
  • changes in circulating thyroid hormones amongst patients with serious illness, trauma, or stress
  • not due to intrinsic thyroid or pituitary disease
  • initially low free T3 may be followed by low TSH and if severe illness low free T4
  • with recovery of illness, TSH may overshoot and become transiently high
80
Q

Sick Euthyroid Syndrome pathophysiology

A

• abnormalities include alterations in
■ peripheral transport and metabolism of thyroid hormone
■ regulation of TSH secretion
■ thyroid function itself

• may be protective during illness by reducing tissue catabolism

81
Q

Sick Euthyroid Syndrome investigations

A

• initially decreased free T3 followed by decreased TSH and finally decreased free T4

82
Q

Sick Euthyroid Syndrome treatment

A
  • treat the underlying disease; thyroid hormone replacement worsens outcomes
  • thyroid function tests normalize once patient is well (initially with a transient increase in TSH)
83
Q

Non-Toxic Goitre definition

A

• generalized enlargement of the thyroid gland in a euthyroid individual that does not result from inflammatory or neoplastic processes

84
Q

Non-Toxic Goitre pathophysiology

A

• the appearance of a goitre is more likely during adolescence, pregnancy, and lactation because of increased thyroid hormone requirements
■ early stages goitre is usually diffuse
■ later stages: multinodular non-toxic goitre with nodule, cyst formation and areas of ischemia, hemorrhage, and fibrosis

85
Q

Non-Toxic Goitre etiology

A
  • iodine deficiency or excess
  • goitrogens: brassica vegetables (e.g. turnip, cassava)
  • drugs: iodine, lithium, para-aminosalicylic acid
  • any disorder of hormone synthesis with compensatory growth
  • peripheral resistance to thyroid hormone
86
Q

Non-Toxic Goitre treatment

A
  • remove goitrogens
  • radioiodine therapy (need very high doses given low iodine uptake, used as last resort)
  • suppression with L-thyroxine (rarely done)
  • surgery may be necessary for severe compressive symptoms
87
Q

Non-Toxic Goitre complications

A
  • compression of neck structures causing stridor, dysphagia, pain, and hoarseness
  • multinodular goitre may become autonomous leading to toxic multinodular goitre and hyperthyroidism
88
Q

Thyroid Nodules definition

A
  • clearly defined discrete mass, separated from the thyroid parenchyma
  • palpable nodules are found in approximately 5% of women and 1% of men
89
Q

Thyroid Nodules etiology

A
  • benign tumours (e.g. colloid nodule, follicular adenoma)
  • thyroid malignancy
  • hyperplastic area in a multinodular goitre
  • cyst: true thyroid cyst, area of cystic degeneration in a multinodular goitre
90
Q

Thyroid Nodules investigations

A

sTSH

  1. If low TSH - thyroid scan
    a) It hot nodule - no biopsy, treat hyperthyroidism
    b) If cold nodule - thyroid ultrasound and biopsy, treat hyperthyroidism
  2. Normal/elevated TSH - Thyroid ultrasound and biopsy

Endocrinology (9 decks)

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