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MBBS VI - SpC - Family Medicine > Endocrine - Hyperthyroidism and Hypothyroidism > Flashcards

Endocrine - Hyperthyroidism and Hypothyroidism Flashcards

1
Q

Describe the physiological process of thyroid hormone synthesis

A

(1) Thyroglobulin biosynthesis
• Thyroglobulin is synthesized in ribosomes of follicle cells
• Stimulated by thyroid-stimulating hormone (TSH) and cAMP
• Thyroglobulin in follicular cells is incorporated into exocytotic vesicles and extruded into colloid in lumen of follicle

(2) Thyroid hormone biosynthesis
• Iodide trapping: Dietary iodide is taken up actively by Na-I symporter
• Oxidation: Iodide is oxidize to iodine by thyroidal peroxidase
• Iodination / Organification: Tyrosine residue in thyroglobulin is iodinated and form monoiodotyrosine (MIT) and diiodotyrosine (DIT)
• Coupling: MIT and DIT are coupled together to form T3 and T4

(3) Secretion of thyroid hormones
• Stimulation of thyroid gland leads to endocytosis of colloid
• Endocytic vesicles fuse with lysosomes inside the follicular cells
• T3 and T4 are cleaved from the thyroglobulin and released into circulation

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2
Q

Forms of thyroid hormone transport in blood

A

o Thyroxine-binding globulin (TBG) (70%)
o Pre-albumin (15%)
o Albumin (15%)
o Free in circulation (< 1%)

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3
Q

Describe activation and deactivation of thyroid hormone

A

Deiodination reactions in the peripheral tissues activate and inactivate TH
• Deiodinase Type 1 / 2 /3 to catalyse the reaction
• Deiodination of T4 into T3 (active) or reverse T3 (inactive)

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4
Q

Effect of thyroid hormone on target cells

A

Thyroid hormones receptors (TRs)
• Located in the nuclei of target cells
• Bound to thyroid hormone response elements in DNA

Mechanism of action
• Cells receive free thyroid hormones (TH) from blood
• T4 is deiodinated to T3 once inside cell
• T3 then enters nucleus and binds to thyroid hormone receptors (TRs)
• T3 triggers the dissociation of co-repressor from TRs and binding of co-activator
• TRs and T3 forms a complex with nuclear receptor- retinoid X receptor (RxR) to initiate gene transcription
• Results in mRNA and protein production

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5
Q

Compare T3 and T4

  • Mode of transport in blood
  • Pool size
  • Source
  • Location
  • Activity
  • Onset of action
  • Half-life
A
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6
Q

Compare T3 and T4

  • Mode of transport in blood
  • Pool size
  • Source
  • Location
  • Activity
  • Onset of action
  • Half-life
A
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7
Q

Effect of thyroid hormone on target end-organs

A
  1. Increase Basal metabolic rate: Increase O2 consumption and ATP production
  2. Growth: permissive effect on growth hormone, protein synthesis, bone remodeling, coordinate PTH and Calcitonin
  3. Biphasic control of carbohydrate and lipid synthesis/ breakdown: Increase glucose and lipid metabolism, remove LDL and cholesterol
  4. CVS: increase contractility, permissive effect on catecholamines, vasodilation
  5. CNS: development and behavior
  6. Temperature: heat production
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8
Q

Differentiate hyperthyroidism and thyrotoxicosis

A

Thyrotoxicosis is defined as the state of thyroid hormone excess

Hyperthyroidism is the result of excess thyroid function

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9
Q

Causes of primary hyperthyroidism

A

 Grave’s diseases
 Toxic multinodular goitre
 Toxic adenoma
 Metastatic thyroid cancer
 Mutation of TSH receptor
 Mutation of Gsa (McCune-Albright syndrome)

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10
Q

Causes of secondary hyperthyroidism

A

 TSH-secreting pituitary adenoma

 Chorionic gonadotropin-secreting tumour

 Gestational thyrotoxicosis

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11
Q

Causes of thyrotoxicosis without hyperthyroidism

A

(Very similar to transient hypothyroidism)

Subacute (De Quervain’s) thyroiditis

Silent thyroiditis

Destructive thyroiditis
• Amiodarone/ Irradiation
• Release of TH into blood

Levothyroxine (T4) overdose

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12
Q

Causes of primary hypothyroidism

A

 Iodine deficiency

 Autoimmune hypothyroidism
• Hashimoto’s thyroiditis
• Atrophic thyroiditis

 Congenital hypothyroidism
• Congenital absence or ectopic thyroid gland
• Thyroid gland dysgenesis (80 – 85%)
• Dyshormonogenesis (10 – 15%)
• TSH-R antibody-mediated (5%)

 Infiltrative hypothyroidism
• Sarcoidosis
• Amyloidosis
• Scleroderma
• Riedel’s thyroiditis

 Drug-induced hypothyroidism
• Amiodarone
• Lithium

 Iatrogenic hypothyroidism
• 131I treatment
• Subtotal or total thyroidectomy
• External irradiation of neck

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13
Q

Causes of secondary hypothyroidism

A

 Hypothalamic disease
• Hypothalamic tumours
• Trauma/ Infiltrative disorders

 Hypopituitarism
• Pituitary tumour
• Pituitary surgery or irradiation
• Sheehan’s syndrome
• Trauma/ Infiltrative disorders

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14
Q

Causes of transient hypothyroidism

A

 Subacute (De Quervain’s) thyroiditis
 Silent thyroiditis (including post-partum thyroiditis)
 Withdrawal of supraphysiologic T4 treatment
 Post-131I treatment
 Post-subtotal or total thyroidectomy

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15
Q

Tests for thyroid function

Which marker screens for thyroid dysfunction?

A
  1. Serum free thyroid hormone fT3, fT4: unbound thyroid hormone
  2. Serum TSH
  3. Serum total T4: T4 bound to plasma-binding proteins

Serum TSH screens for thyroid dysfunction

MOST sensitive indicator of thyroid function due to short t1/2

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16
Q

Symptoms of hyperthyroidism

A

 Hyperactivity/ Irritability/ Dysphoria
 Heat intolerance and increased sweating
 Palpitations
 Fatigue and weakness
 Weight loss with increased appetite

 Hair loss
 Diarrhea
 Polyuria
 Oligomenorrhea and amenorrhea
 Loss of libido

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17
Q

Signs of hyperthyroidism

A

 Tachycardia and AF
 Tremor
 Goitre
 Warm and moist skin
 Muscle weakness and proximal myopathy

 Lid lag and lid retraction
• Permissive effect on catecholamine leading to sympathetic overactivity
• Sustained contraction of superior tarsal muscles

 Thyroid eye signs

 Pretibial Myxoedema
 Gynecomastia

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18
Q

List all thyroid eye signs

A

Periorbital edema

Lid lag and lid retraction

Exophthalmos (proptosis)

Ophthalmoplegia (extra-ocular muscle involvement)

Corneal involvement (exposure keratitis)

Vision loss

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19
Q

Symptoms of hypothyroidism

A

General:
 Fatigue and weakness
 Cold intolerance
 Weight gain with decreased appetite
 Hair loss, Dry skin

Neuro:
 Difficulty concentrating and poor memory
 Impaired hearing
 Paraesthesia

GI:
 Constipation
Respi:
 Dyspnea
 Hoarseness
Gyn:
 Menorrhagia (later oligomenorrhea or amenorrhea)

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20
Q

Signs of hypothyroidism

A

Skin:
 Dry and cold skin
 Alopecia
 Puffiness of face, hands and feet/ Myxedema

Cardiovascular:
 Bradycardia
 Peripheral non-pitting edema

Neuro:
 Hyporeflexia
 Delayed tendon reflex relaxation
 Carpal tunnel syndrome

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21
Q

Grading of Grave’s ophthalmopathy

A
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22
Q

Pathophysiology of periorbital edema and proptosis

A

 T-cells and autoantibodies are reactive to extraocular muscles and retro-orbital tissues
 Inflammation leads to deposition of collagen and glycosaminoglycan in muscles
 Swelling of extraocular muscle and periorbital edema

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23
Q

Pathophysiology of Proptosis due to thyrotoxicosis

A

 ONLY occurs in Grave’s disease
 Protrusion of eyeball from orbit
 Sclera is not covered by the lower eyelid
 Eyes are anterior to the superior orbital margin when viewed from the back

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24
Q

How to examine for proptosis

A

 ONLY occurs in Grave’s disease
 Protrusion of eyeball from orbit
 Sclera is not covered by the lower eyelid
 Eyes are anterior to the superior orbital margin when viewed from the back

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25
Q

Complications of proptosis due to thyrotoxicosis

A

Opthalmoplegia/ Diplopia

Corneal ulceration

Chemosis

Conjunctivitis

Optic atrophy

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26
Q

Thyrotoxicosis hand signs

A

Fine tremor* - Due to sympathetic overactivity

Sweating, warm and moist skin* - Due to sympathetic overactivity

Onycholysis - Separation of nail from bed

Palmar erythema - Signs of Grave’s disease

Finger clubbing

Thyroid acropachy - Soft-tissue swelling of hands and finger clubbing

Abnormal pulse
 Sinus tachycardia (Sympathetic overactivity)
 Atrial fibrillation (Shortened refractory period of atrial cells related to sympathetic drive)
 Bounding pulse and wide pulse pressure (High cardiac output associated with AS murmur)

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27
Q

Signs of thyrotoxicosis on arms and legs

A

Arms

  • *- Proximal myopathy**
  • *- Hyperreflexia**

Legs
- Proximal myopathy: Ask patient to stand up from squatting position
- Pretibial myxedema
 Occurs in Grave’s disease and rarely Hashimoto’s thyroiditis
 Localized non-pitting edema of skin
 Bilateral firm, elevated dermal nodules and plaques
 Can be pink, brown or skin-colored
 Hyaluronic acid accumulates in dermis and subcutis

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28
Q

Hypothyroidism hand signs

A

Peripheral cyanosis - Reduced cardiac output

Palmar crease pallor

Anemia due to
• Anemia of chronic disease
• Iron deficiency (menorrhagia)
• Folate deficiency (bacterial overgrowth)

Dry and cool skin

Yellow discoloration
 Due to hypercarotenemia
 Slowing down of hepatic metabolism of carotene

Abnormal pulse

Carpal tunnel syndrome
 Sensory loss as carpal tunnel is thickened in myxoedema

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29
Q

Hypothyroidism signs on arms and legs

A

Arms

  • Proximal myopathy
  • “Hung-up” biceps reflex

Legs
- Non-pitting edema/ Myxoedema
- “Hung-up” Achilles reflex
 Rapid dorsiflexion followed by slow plantar flexion after the tendon is tapped

30
Q

Signs of hypothyroidism in children/ newborn

A

Newborn: Cretinism/ Short stature/ Mental retardation/ Puffy face/ Deaf mutism/ Protuberant abdomen/ Umbilical hernia

Children: Retardation of growth, mental retardation

31
Q

Advantage and limitations of serum TSH test

A

Advantage:

  • MOST sensitive indicator of thyroid function due to short t1/2
  • Normal TSH excludes a primary hyperthyroidism
  • Does NOT exclude secondary abnormalities (hypothalamic or pituitary)

Limitations:

  • Cannot indicate pituitary disease
  • High TSH can mean hypothyroidism or secondary hyperthyroidism
  • Low TSH can mean hyperthyroidism or secondary hypothyroidism
  • Low TSH in 1st trimester pregnancy, high dose corticosteroid or dopamine use
32
Q

Indication for fT3 and fT4 test

Why is total T4 less useful?

A

Hypothyroidism: only need fT4 (fT3 normal in 25% patients due to adaptive deiodinase response)

Hyperthyroidism: need both fT3 and fT4 (2-5% have only fT3 elevation in T3 toxicosis)

Total T4 is related to thyroxine-binding globulin with confounding factors:

  • High in pregnancy, oral contraceptive, hormonal therapy
  • Low in androgen use, hypoalbuminaemia
33
Q

List 3 thyroid autoantibodies and indications

A

Thyroid antibodies
• Thyrotropin receptor antibodies (TRA) (Anti-TSH antibodies)
• Anti-thyroid peroxidase (TPO) antibodies
• Anti-thyroglobulin (TG) antibodies

Anti-TSH: Grave’s disease

Anti- TPO: Hashimoto thyroiditis

Anti-TG: Multinodular goiter

34
Q

Pathophysiology of Grave’s disease

A

Autoimmune disease: Lymphocytes produce autoantibodies against self-antigen TSH receptor

Thyrotropin-receptor antibody (TRAb) stimulates TSH receptor on thyroid gland:

Stimulate thyroid cell hyperplasia and TH release

35
Q

Clinical diagnosis of Grave’s disease

A
  1. Diffusely enlarged thyroid gland
  2. High fT3 and fT4, Suppressed TSH
  3. Diffuse radioactive iodine uptake in scintigraphy scan
  4. Positive TSH receptor autoantibody in serum
36
Q

Function of radioisotope thyroid scan

A

Functional assessment of thyroid

Increased uptake:

  • Grave’s disease: diffuse uptake
  • TSH-secreting pituitary adenoma: diffuse uptake
  • Toxic adenoma: focal area of uptake only
  • Multinodular goiter: heterogenous uptake

Decreased uptake:

  • Thyroiditis
  • T4 overdose
  • Iatrogenic: e.g. hemithyroidectomy

Guide FNAC decision

o Hot nodules do NOT require FNAC
o Cold nodules require FNAC

37
Q

S/S of Grave’s disease

A

Goiter

S/S hyperthyroidism

Exophthalmos/ Proptosis

Pretibial Myxoedema

S/S of related autoimmune diseases: MG, DM

38
Q

Complications of hyperthyroidism

A

Thyroid storm

Thyrotoxic period paralysis (HypoK)

Atrial fibrillation and heart failure

39
Q

Clinical use of Thyrotropin-receptor antibody (TRAb)

A
  1. Prognostic indicator of Antithyroid drug against Grave’s disease: negative TRAb after Tx means better prognosis
  2. Forecast neonatal Grave’s disease (TRAb passes through placenta)
  3. Diagnosis of Grave’s disease and monitor response to antithyroid drugs
40
Q

Outline all treatment options for Grave’s disease

A
  1. Antithyroid drugs:
  • Thiouracil derivatives: Methimazole, carbimazole, propylthiouracil
  • Lithium
  1. Surgery: thyroidectomy
  2. RAI therapy
  3. Ancillary drugs:

Sedatives, B-blocker, Iodine

41
Q

Compare surgery, Anti-thyroid and RAI therapy

  • Relapse risk
  • Hypothyroidism risk
  • Long-term complication risk
  • Onset of therapeutic effect
A
42
Q

Beta-blocker for hyperthyroidism

  • Indication
  • Example
  • MoA
  • S/E
A
  • Indication: Thyrotoxic crisis, before surgery to prevent thyroid storm
  • Example: Propanolol
  • MoA

 Block β1-adrenoreceptors in heart
• Relive palpitations
 Block β1-adrenoreceptors in brain
• Relieve anxiety
 Block β2-adrenoreceptors in skeletal muscle
• Relieve tremor

  • S/E:

 Bronchospasm
 Hypoglycemia
 Heart failure (↓ CO)
 Coronary artery spasm

43
Q

Lugol’s solution

  • Indication
  • Contraindication
  • MoA
  • S/E
A
  • Indication: rapid onset, short-term use before thyroidectomy/ thyroid storm
  • Contraindication: pregnancy and breast-feeding
  • MoA:

High iodine concentration inhibits H2O2 and peroxidase > inhibit iodination of thyroglobulin and production of T3, T4

Decrease size and vascularity of hyperplastic thyroid gland

Decrease bleeding risk during surgery

  • S/E: Hypersensitivity (fever, rash, angioedema, conjunctivitis..etc)
44
Q

Thionamides

  • Indication
  • Tx course
  • Examples
  • MoA
  • S/E
A
  • Indication: Children/ Pregnancy/ Mild- moderate disease
  • Tx course: 12 - 18 months, onset of effects takes 4 weeks
  • Examples: Carbimazole/ Methimazole/ Propylthiouracil (PTU)
  • MoA:

Carbimazole/ Methimazole: Inhibit the action of peroxidase
• Inhibit iodination (organification) of tyrosine residues of thyroglobulin
• Inhibits coupling of iodotyrosine and production of T3 and T4
• Suppress intra-thyroidal antigen-presenting cells

PTU: Inhibits peripheral conversion of T4 into T3

  • S/E:

Skin rash, urticaria and pruritis

Agranulocytosis (first 2 months, fever, sore throat)

Rare: Hepatotoxicity, Acute arthralgia, Cholestatic jaundice, ANCA vasculitis

45
Q

Describe absorption of thionamide derivatives

Recommendation during pregnancy

A

Rapid absorption into thyroid in minutes

All transferable into milk

Metimazole/ Carbimazole more teratogenic than PTU

>> Give PTU until second trimester then change to methimazole/ Carbimazole

46
Q

Predictive patient features associated with higher recurrence of thyroid disease after anti-thyroid drugs

A
  1. Larger goiter
  2. Positive family history
  3. High initial T3 or T3/T4 ratio
  4. Shorter course of Tx
  5. Failure to normalize TSH
  6. High TSH receptor antibody levels
47
Q

Surgical treatment options for diffuse toxic goiter

Pre-op preparation

A

Bilateral subtotal thyroidectomy

Unilateral total and contralateral subtotal lobectomy

Near total thyroidectomy

Pre-op preparation:

  • Antithyroid until euthyroid
  • Beta-blocker for 2 weeks
  • Lugol’s solution 2-3 days before
48
Q

Indications for surgical treatment of diffuse toxic goiter

A
  1. Young age
  2. Failed medical treatment
  3. Refuse/ Refractory to anti-thyroid drugs
  4. Thyroid eye signs
  5. Pregnancy/ breast-feeding
  6. Refuse/ Refractory to RAI therapy
  7. Excessively large goiter +/- compressive symptoms
49
Q

Complications of thyroid surgery

A

 Hypoparathyroidism

 Thyroid storm

 Tracheomalacia - trachea cartilage collapse

 Vocal cord paralysis: RLN or SLN damage

 Wound complications: seroma, hypertrophic scar

 Hemorrhage
• Compression and edematous effect compresses on trachea

50
Q

RAI therapy

  • Indication
  • Contraindication
  • MoA
  • S/E
A

Indications:

  • Thyrotoxic heart disease; Refractory to antithyroid drugs; ablation of residual tumor after thyroidectomy; Relapse post-op; C/O surgery

Contraindication:

  • Pregnancy/ breast-feeding (transplacental, fetal risks)

MoA:

  • Taken up by Na-I symporter and incorporated into thyroglobulin
  • Emit B-radiation to cause necrosis of follicular cells, fibrosis and destroy colloid
  • Destroy intra-thyroid T-suppression cells, Inhibit release of TSH-receptor antibodies

S/E:

  • Hypothyroidism
  • Risk of thyroid eye disease after Tx
  • Thyroid storm due to radiation thyroiditis
51
Q

Advantage of RAI therapy

A

Low relapse rate

Simple procedure

Economical

No immediate complications

52
Q

Pathogenesis of Grave’s opthalmopathy

A
  1. TSH-receptor antibody stimulate orbital fibroblasts to differentiate into adipocytes/ adipogenesis
  2. Increase TSH receptor expression on orbital fibroblast after differentiation into adipocytes
  3. Orbital adipocytes hypertrophy and exerts pressure on eyeball
53
Q

Histological features of Grave’s ophthalmopathy

  • At extra-ocular muscles, retrobulbar fat and optic nerve
A

Extra-ocular muscles: edema, mononuclear cell infiltration, Mucopolysaccharide deposits, Fibrosis

Retrobulbar fat: Lymphocyte infiltration, fat replaced by fibrous tissue, collagen tissue replaced by hyaluronic acid

Optic nerve: atrophy, replaced by fibrous and fatty connective tissue

54
Q

Ophthalmopathy must be related to hyperthyroidism

True or False?

A

False

Can be hyper-, hypo- or euthyroid

80% opthalmopathy first develop eye signs within 18 months of thyrotoxicosis

55
Q

Treatment of Grave’s opthalmopathy

A
  1. Anti-thyroid treatment to achieve euthyroid
  2. Immunosuppressants against infiltrative ophthalmopathy:
  • Steroid - IV or oral methylprednisolone
  • Cyclosporin A
  • Plasmapharesis for autoantibody
  • Immunoglobulin
  • TNF-a inhibitor
  • IGF-1 receptor inhibitor
  1. Orbital irradiation
  2. Orbital decompression/ extra-ocular muscle operation
56
Q

Thyrotoxic period paralysis

  • Pathophysiology
A

Pathophysiology: hyperthyroidism results in
□ ↑Na+/K+/ATPase activity + ↑insulin release (esp after carbohydrate load) → intracellular shift of K+
□ Consequences: paralysis and hypokalemia

57
Q

Thyrotoxic Periodic Paralysis (TPP)

Clinical presentation: signs, course, S/S, precipitating events

A

Always preceded by thyrotoxic S/S (thyrotoxic state essential for pathogenesis)

Attacks of motor paralysis: proximal > distal, LL > UL, seldom respiratory/bulbar muscles
→ Signs: typically hypotonia with hypo/areflexia
→ Course: weekly/monthly attacks lasting mins-days

Precipitants:

  • Events a/w ↑adrenaline release: rest after strenuous activity, stress, SABA use
  • Events a/w ↑insulin release: namely ↑carbohydrate load

Cardiac arrhythmia due to severe hypoK

58
Q

Management of Thyrotoxic Periodic Paralysis (TPP)

A

Mx: usually spontaneous recovery
□ Cardiac monitoring

□ K supplement: use IV K 10-20mmol/h over 2h to accelerate recovery
→ Watch out for rebound hyperkalemia (40-59%) when transcellular shift reverses
→ IV propranolol may be useful to reverse excessive ↑Na+/K+/ATPase activity in refractory cases

□ Manage hyperthyroidism

□ Other prophylactic Tx: low salt diet, moderate carbohydrate intake ± propranolol

59
Q

4 clinical patterns of hypothyroidism

A

Cretinism

Juvenile myxedema

Adult myxedema

Myxedema coma

60
Q

Ddx painless thyroiditis

A

Autoimmune: Lymphocytic thyroiditis, Atrophic thyroiditis, Hashimoto’s thyroiditis

Silent thyroiditis e.g. Post-partum thyroiditis

61
Q

Hashimoto’s thyroiditis

  • Risk factors
  • Pathology
  • Histological features
A

RFs: older female, family history, HLA-DR3, High iodine intake, smoking

Pathology: T-cell mediated autoimmune disease against thyroid tissue

Anti-thyroid antibody after T-cell mediated thyroid injury: Anti-thyroglobulin, Anti-TPO

Histology: profuse lymphocytic infiltration, lymphoid germinal centres and destruction of thyroid follicles ± fibrosis

62
Q

Clinical presentation of Hashimoto’s thyroiditis

A

Clinical presentation:
□ Goitre: usually small or moderately sized, diffuse, painless
→ Characteristically firm, rubbery
→ Atrophic variant: predominantly TSHr-blocking Ab → no goiter

□ Hypothyroidism (25%)

Natural Hx: gradual loss in thyroid function over years

63
Q

Hashimoto’s thyroiditis

Investigations

Management

A

Ix:
□ TFT: may have ↑TSH + ↓fT4
□ Thyroid Ab: anti-TPO Ab (90-100%), anti-Tg Ab (80-90%), anti-TSHr (10-20%)

Mx:

T4 replacement: treats hypothyroidism + shrinks goiter

64
Q

List 4 types of subacute thyroiditis

A

□ Subacute granulomatous (de Quervain’s, giant cell) thyroiditis
□ Subacute lymphocytic thyroiditis
□ Postpartum thyroiditis
□ Palpation thyroiditis

65
Q

Subacute thyroiditis

Clinical course

S/S

Management

A

S/S:

□ Pain at thyroid, exacerbate by swallowing or neck movement, only in Quervain’s, not others

□ Goitre: palpable ± tenderness
□ Fluctuating thyroid status > transient hypothyroidism or thyrotoxicosis without hyperthryroidism
□ Systemic symptoms: fever, ↑WBC, ↑ESR

Clinical course:
□ Thyrotoxic phase (4-6w)
→ Due to damage to follicles release of stored T4 until depletion
→ ↓iodine uptake (↓TSH, follicular damage)
□ Hypothyroid phase (4-6mo) due to damage to follicular cells
→ ↓synthesis of thyroid hormones
□ Resolution

Mx: self-limiting → do NOT give antithyroid medications
□ No Mx: spontaneous resolution!
□ NSAIDs/corticosteroids for severe cases → manage systemic upset + pain
□ Temporary β-blocker for hyperthyroid phase (usually mild) → for symptomatic control only
□ Temporary T4 replacement for hypothyroid phase if pronounced or symptomatic

66
Q

Causes of simple goiter

A 
□ Causes: during ↑requirement (eg. pregnancy, pubertal) or
from food (goitrogen, iodine excess/deficiency)
67
Q

multinodular goiter

Pathology

TFT results

S/S

A

Pathology: recurrent episodes of hyperplasia and involution
(due to unknown stimulus)
→ hyperplastic nodules growing at varying rates
→ some may secrete thyroid hormone autonomously (toxic MNG, Plummer disease)

TFT findings:
→ 25% with complete suppression of TSH
→ T4/3 can be within reference range (subclinical thyrotoxicosis) or elevated (toxic MNG)

S/S: classically AF + multinodular goitre in elderly
→ Large goiter ± compressive S/S or retrosternal extension
→ Haemorrhage into nodule/cyst → sudden painful swelling
→ Thyrotoxic symptoms/complications, eg. AF

68
Q

Management of multinodular goiter

A

Mx:
→ No treatment + annual TFT to screen for toxic MNG in small, non-toxic MNG
- Consider T4 suppression therapy in selected patients → aim low-normal TSH

→ Early definitive treatment for large or toxic MNG (as relapse is invariable after cessation of ATD)49

  • Total thyroidectomy for large goitres with compression or cosmetic concerns
  • RAI for small toxic goitres
69
Q

Congenital hypothyroidism

Screening method

Causes

A

Neonatal cord blood TSH screening: fT4 <12pmol/L, TSH >7mlU/L

Causes:

  1. Athyroesis
  2. Dyshormonogenesis
  3. Ectopic thyroid gland
  4. Hypothalamic - Pituitary hypothyroidism
  5. Maternal factors: Anti-thyroid drugs, Iodine deficiency, TSH-autoantibodies, Premature birth
  6. Associated conditions: Down’s syndrome, Trisomy 18…etc
70
Q

Cardiac precaution with thyroid disease

A
  1. Hypothyroidism - lead to hyperlipidaemia due to decrease lipolysis, increase risk of Coronary atherosclerosis
  2. Must treat coronary atherosclerosis prior to T4 supplementation: Initiation of thyroxine raises CO and worsens IHD
  3. Give 4-6 weeks to equilibrate thyroxine
71
Q

Myxedema coma

  • S/S
  • Complication
  • Tx
A

 General features
• Severe hypothyroidism with hypothermia, respiratory failure with hypoxia and coma, convulsions, confusion

 General management
• Treatment of precipitating causes
• Maintenance of body temperature
• Correction of hypoglycemia with D10
• Correction of fluid and electrolytes with NS ± vasopressors

 Medical treatment
• Liothyronine (T3)
• Levothyroxine (T4)

MBBS VI - SpC - Family Medicine (42 decks)

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