This document provides information on thyroid disorders including hypothyroidism and hyperthyroidism. It defines the conditions, identifies their causes, describes clinical presentations and goals of treatment. Hypothyroidism results from inadequate thyroid hormone secretion and is most commonly caused by Hashimoto's thyroiditis. Hyperthyroidism occurs when there is excessive thyroid hormone production, often due to Graves' disease. Treatment of hypothyroidism involves levothyroxine replacement while hyperthyroidism may be treated through antithyroid medications, radioiodine ablation, or surgery. The goals are to normalize thyroid function and minimize symptoms.

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Thyroid disorders

2. Objectives
 At the end of this session you will able to:
 Define hyperthyroidism and hypothyroidism
 Differentiate hyperthyroidism and hypothyroidism
 Identify causes of hyperthyroidism and
hypothyroidism
 Select appropriate regimen for hyperthyroidism and
hypothyroidism
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3. Introduction
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The thyroid gland is located at the base
of neck in front of the Trachea, just
above the breastbone.

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5. Cont’d
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• The thyroid gland synthesized, store
and secrete thyroid hormones which
are:
1. Thyroxine (T4)
2. Triiodothyronine (T3)

6. Regulation of thyroid hormone secretion by
negative feedback control
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Hypothalamus
Thyrotropin releasing hormone
Anterior pituitary gland
TSH
Inhibits
Thyroid gland
T3 and T4
Metabolic effects

7. Cont…
Thyroid hormone (T3, T4) actions
Have three principal actions:
1.Stimulation of energy use
 Increase in 02 consumption & Heat
production
2. Stimulation of the heart
 Heat rate
force of contraction &Co
3. Promotion of growth & development
•Brain & other components of the NS
•Maturation of skeletal muscle
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8. Synthesis of thyroid hormones
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• Uptake of plasma iodide by the follicle cells.
• Iodide from diet is taken by a symporter known
as sodium iodide symporter
• Oxidation of iodide (thyroid peroxidase) and
iodination of tyrosine residues in the thyroglobulin
• Monoiodotyrosine and diiodotyrosine are formed

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• Coupling of the iodinated tyrosines
• Monoiodotyrosine + Diiodotyrosine  T3
• Diiodotyrosine + Diiodotyrosine  T4
 T4 and T3 are transported in the
bloodstream by three proteins: thyroxine-
binding globulin, thyroid-binding prealbumin
(transthyretin), and albumin.

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 Free thyroid hormone elicit a biologic effect
 T4 is secreted solely from the thyroid gland, but
less than 20% of T3 is produced there
 T3 is formed from the breakdown of T4
catalyzed by the enzyme 5'-monodeiodinase
found in peripheral tissues.

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 T3 is about 10 to 15 times more active than T4.
 T4 may also be acted on by the enzyme 5'-
monodeiodinase to form reverse T3, which has no
significant biologic activity.

12. Actions of the thyroid hormones
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• Increased glycogenolysis results in rise in
blood sugar
• The thyroid hormones also enhance
metabolic circulatory and somatic
neuromuscular actions of catecholamines

13. Abnormalities of the thyroid gland
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• Hypothyroidism ( under activity)
• T3, T4 decreased while TSH is increased.
• Hyperthyroidism( over activity)
• T3, T4 increased while TSH is reduced.

14. Hypothyroidism
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• Is the most common clinical disorder of thyroid
function.
• It is the clinical syndrome that results from
inadequate secretion of thyroid hormones

15. Common Causes of
Hypothyroidism
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 Primary Hypothyroidism
 results from failure of the thyroid gland to
secrete sufficient thyroid hormone
 Autoimmune thyroiditis (Hashimoto’s
disease)
 Iatrogenic (irradiation, surgery)
 Drugs (amiodarone, radiocontrast media,
lithium, -interferon)
 Idoine deficiency
 Enzyme defect

16. Cont’d
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 Secondary Hypothyroidism
 Pituitary disease
 Hypothalamic disease

17. Clinical Presentation
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 Symptoms
 Fatigue
 Lethargy
 Sleepiness
 Mental impairment
 Depression
 Cold intolerance
 Hoarseness
 Dry skin
 Decreased
perspiration
 Weight gain
 Decreased appetite
 Constipation
 Menstrual
disturbances
 Arthralgia
 Paresthesia

18. Cont’d
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 Signs
 Slow movements
 Slow speech
 Hoarseness
 Bradycardia
 Dry skin
 Non-pitting edema (myxedema)
 Delayed relaxation of reflexes

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20. Diagnosis
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  in the TSH level is the first evidence of primary
hypothyroidism.
 Many patients have a free T4 level within the
normal range (compensated hypothyroidism)
 As the disease progresses, the free T4
concentration drops below the normal level.
 The T3 concentration is often maintained in the
normal range despite a low T4.

21. Cont’d
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 Pituitary failure (secondary hypothyroidism)
should be suspected in a patient with decreased
levels of T4 and inappropriately normal or low
TSH levels.

22. DESIRED OUTCOME
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 The treatment goals for hypothyroidism are to:
 normalize thyroid hormone concentrations in
tissue
 provide symptomatic relief
 prevent neurologic deficits in newborns and
children
 reverse the biochemical abnormalities of
hypothyroidism.

23. Treatment of hypothyroidism
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Levothyroxine (L-thyroxine, T4)
 Drug of choice
 chemically stable
 relatively inexpensive
 free of antigenicity, and has uniform potency
 drug of choice for pregnant women

24. Cont…
Dosing
 Initial
 In healthy adults, 1.6 mcg/kg per day.
 In patients 50–60 years of age, consider
50 mcg/day.
 In those with existing cardiovascular
disease, consider 12.5–25 mcg/day
 Dosage titration based on response
 Can increase or decrease in 12.5- to 25-
mcg/day increments
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25.  Adverse effects
(a) Hyperthyroidism
(b) Cardiac abnormalities (tachyarrhythmias,
angina, myocardial infarction)
 Efficacy
Considered drug of choice because of its
adverse effect profile, cost, lack of
antigenicity, and uniform potency
Management of Hypothyroidism

26. Special Populations and
Conditions
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Hypothyroidism and Pregnancy
 Hypothyroidism during pregnancy has a variety of
maternal and fetal adverse effects.
 During pregnancy, â-human chorionic gonadotropin
(â-hCG) acts as a TSH receptor agonist
 increasing the amount of thyroid hormone available for
fetal growth and development.

27. Cont’d
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 Maternal hypothyroidism results in an increased
rate of miscarriage and decreased intellectual
capacity of the child.
 Endocrinologists recommend a TSH
measurement as soon as the pregnancy is
confirmed.
 Most hypothyroid women who become pregnant
will quickly need an increased dose of LT4,
averaging 50% above the prepregnancy dose.

28. Children
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 As soon as the hypothyroid state is identified, the
newborn should receive the full LT4
replacement dose.
 The replacement dose of LT4 in children is age-
dependent.
 In newborns, the usual dose is 10 to 15 mcg/kg
per day.

29. Myxedema Coma
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 This is a life-threatening condition owing to
severe, longstanding hypothyroidism and has a
mortality rate of 60% to 70%.

30. TREATMENT OF MYXEDEMA
COMA
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 Immediate and aggressive therapy with IV bolus
levothyroxine, 300 to 500 mcg, has traditionally
been used.
 Initial treatment with IV liothyronine or a
combination of both hormones has also been
advocated because of impaired conversion of T4
to T3.
 Glucocorticoid therapy with IV hydrocortisone
100 mg every 8 hours should be given until
coexisting adrenal suppression is ruled out.

31. EVALUATION OF THERAPEUTIC
OUTCOMES
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 Serum TSH concentration is the most sensitive
and specific monitoring parameter for adjustment
of levothyroxine dose.
 Concentrations begin to fall within hours and are
usually normalized within 2 to 6 weeks.
 TSH and T4 concentrations should both be
checked even elevated TSH level indicates
insufficient replacement.

32. Cont’d
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 In patients with hypothyroidism caused by
hypothalamic or pituitary failure, alleviation of the
clinical syndrome and restoration of serum T4 to the
normal range are the only criteria available for
estimating the appropriate replacement dose of
levothyroxine.
 Excessive doses of thyroid hormone may lead to
heart failure, angina pectoris, and myocardial
infarction

33. HYPERTHYROIDISM
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34. HYPERTHYROIDISM
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 Hyperthyroidism is a condition caused by the
effects of too much thyroid hormone.
 Hyperthyroidism: usu. excess synthesis and
secretion of thyroid hormone by the thyroid gland,
also known as
  free thyroxine (T4), free triiodothyronine (T3), or
both.
 Thyrotoxicosis: state of thyroid hormone excess
and is not synonymous with hyperthyroidism,

35. Causes of Thyrotoxicosis
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 Primary hyperthyroidism
 Diffuse toxic goiter (graves disease, ~50-60%)
 Toxic multinodular goiter (plummer disease, 15-
20%)
 Toxic adenoma (3-5%).
 Iodine excess (including radiocontrast, amiodarone)

36. Cont’d
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 Thyrotoxicosis without hyperthyroidism
 Subacute thyroiditis
 Silent (painless) thyroiditis
 Excess thyroid hormone intake (thyrotoxicosis
factitia)
 Secondary hyperthyroidism
 TSH-secreting pituitary tumors

37. Cont’d
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 Amiodarone may induce thyrotoxicosis (2% to
3% of patients) or hypothyroidism.
 It reduced conversion of T4 to T3,
 Iodide release from the drug may contribute to
iodine excess.
 Causes a destructive thyroiditis with loss of
thyroglobulin and thyroid hormones.

38. Clinical Presentation of
Hyperthyroidism
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 Symptoms
• Nervousness
• Fatigue
• Weakness
• Increased perspiration
• Heat intolerance
• Tremor
• Hyperactivity,
irritability
• Palpitations
• Appetite change
(usually increased)
• Weight change
(usually weight loss)
• Menstrual
disturbances (often
oligomenorrhea)
• Diarrhea

39. Cont’d
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 Signs
• Hyperactivity
• Tachycardia
• Atrial fibrillation (especially in elderly)
• Hyperreflexia
• Warm, moist skin
• Ophthalmopathy, dermopathy (Graves’ disease)
• Goiter

40. DESIRED OUTCOME
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 Therapeutic objectives for hyperthyroidism are to
 normalize the production of thyroid hormone
 minimize symptoms and long-term consequence.
 provide individualized therapy based on
 the type and severity of disease,
 patient age and gender,
 existence of nonthyroidal conditions, and
 response to previous therapy.

41. Management of Hyperthyroidism
 Therapy goals
Minimize or eliminate symptoms, improve quality of life.
Minimize long-term damage to organs
 Heart disease
 Arrhythmias
 Sudden cardiac death
 Bone demineralization
 Fractures
Normalize free T4 and TSH concentrations

42. TREATMENT
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 Nonpharmacologic Therapy
 Surgical removal of the thyroid gland should be
considered in patients with
 a large gland (>80 g)
 severe ophthalmopathy
 lack of remission on antithyroid drug
treatment

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 If thyroidectomy is planned, PTU or methimazole
is usually given until the patient is biochemically
euthyroid (usually 6 to 8 weeks)
 It should be followed by the addition of iodides
(500 mg/day) for 10 to 14 days before surgery
 Levothyroxine may be added to maintain the
euthyroid state while the thionamides are
continued.

44. pharmacotheraphy,Thioureas
 Inhibit iodination and synthesis of thyroid hormones; PTU may
block T4/T3 conversion in the periphery as well
(a) PTU
(1) Preferred agent in pregnant women in the 1st trimester
(2) Dose:
 Initial: 100 mg by mouth three times daily
 Maximal: 400 mg three times daily
 Once euthyroid, may reduce to 50 mg 2-3 times daily
(b) Methimazole
(1) Preferred agent, except in pregnant women (1st trimester)
(2) Dose:
 Initial: 10–20 mg by mouth once daily
 Maximal: 40 mg three times daily
 Once euthyroid, may reduce to 5–10 mg/day

45. Thioureas
 Therapy duration: usually 12 – 18 months
 Adverse effects
Hepatotoxicity risk with PTU: Baseline LFT
Rash
Arthralgias,
Fever
Agranulocytosis: Baseline CBC

46. B-blockers
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 Propranolol has been used for several weeks
preoperatively and 7 to 10 days after surgery
to maintain a pulse rate less than 90
beats/min
 Dosing
Initial: 20–40 mg by mouth three or four
times daily
Maximal: 240–480 mg/day
Combined pretreatment with propranolol

47. Pharmacotherapy
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 Radioiodine 131 I
 By destruction of the gland by beta particles
emitted
 It is a first line treatment
 It has a half-life of eight days
 By two months its radioactivity has
effectively disappeared
 It is used in one single dose

48. Cont’d
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 Hypothyroidism will eventually develop, but
is easily managed by replacement therapy
with thyroxine.
 It is best avoided in children and also in
pregnant patients because of potential
damage to the fetus.

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50. Iodine and iodides
 Inhibits the release of stored thyroid hormone.
 Minimal effect on hormone synthesis.
 Helps decrease vascularity and size of gland before
surgery.
 Dosing: 120–400 mg split three times daily
(a) Lugol’s solution (6.3–8 mg iodide per drop)
(b) Saturated solution of potassium iodide (38–50 mg iodide
per drop)
(c) Potassium iodide tablets: (130-mg tablets contain 100 mg
of iodide)

51. Thyroid Storm
 Severe and life-threatening decompensated
thyrotoxicosis.
 Mortality rate may be as high as 20%.
 Precipitating causes:
Trauma
Infection
Antithyroid agent withdrawal
Severe thyroiditis
Postablative therapy (especially if inadequate pretreatment)
 Presentation:
Fever, tachycardia, vomiting, dehydration, coma, tachypnea,

52. Management of Thyroid Storm
1) PTU: 500-1000-mg loading dose, then 250 mg Q4
hours
Blocks new hormone synthesis
2) Alternative: methimazole 60–80 mg daily
3) Iodide therapy 1 hour after PTU initiation
4) β-Blocker therapy: Propranolol to control symptoms and
block conversion of T4 to T3
5) Paracetamol as antipyretic therapy, if needed (avoid
NSAIDs)
6) Corticosteroid therapy: Prednisone 300 mg IV loading
dose then 100 mg every 8 hours (Dexamethasone,

53. Case-1
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 HT, a 34-year-old woman, comes to the clinic
complaining of fatigue, lethargy, and having a
“fuzzy head” for the past 6 months. She
thought it was because she was working too
hard, but the symptoms have not improved
despite a better work schedule. She has
noticed a 2.3-kg weight gain, her menses
have become heavier, she feels cold all the
time, and her skin is drier. She takes no
medications other than occasional
paracetamol for headache and milk of
magnesia for constipation. Her vital signs and

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 Labs
Serum cholesterol: 220 mg/dL (5.7
mmol/L; normal less than 200 mg/dL,
or 5.2 mmol/L)
TSH: 9.7 milliunits/L (normal 0.5–2.5
milliunits/L)
Free T4: 0.6 ng/dL (7.7 pmol/L; normal
0.7–1.9 ng/dL, or 9–24.5 pmol/L)
She weighs 66 kg (145 lb), and she is
5 ft, 7 in (170 cm) tall.

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 One year later, HT comes to you and excitedly
states that she is pregnant. She just saw her
obstetrician, who started her on a prenatal
vitamin. She states that she has felt very well
since her LT4 was started and that she is amazed
at how much better she feels (“I didn’t know how
bad I felt until I started the thyroid medicine”). The
most recent TSH determination, obtained 6
months ago, was 1.5 milliunits/L (normal 0.5–2.5
milliunits/L).∗ Her current LT4 dose is 88 mcg/day.

56. Case-2
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 GD is a 24-year-old woman who comes to the
clinic stating, “I’m so nervous and hungry, and I’m
losing weight. What is wrong with me?” She first
noticed these symptoms 2 months ago, and they
have worsened steadily. She feels anxious for no
reason and has trouble sleeping. She has noticed
that her appetite has increased, although she has
lost about 2.3 kg.

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 Sometimes she can feel her heart beating in her
chest, but she denies chest pain or syncope. She
also has noticed that she is always sweaty and
that her menses have become very light. Her only
medications are a hormonal oral contraceptive
and occasional naproxen for dysmenorrhea. She
thinks that her mother had some kind of thyroid
problem when she was pregnant.

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 PE
 VS: Pulse 112 beats per minute, blood
pressure 108/72,
 RR 12, temperature 37.4°C (99.32°F)
 HEENT: Diffusely enlarged thyroid; mild
exophthalmos
 CV: Tachycardic
 Exts: Fine tremor
 Skin: Warm and moist
 ECG: Sinus tachycardia

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 Labs
 Electrolytes, complete blood count normal.
Urine hCG negative.
 TSH less than 0.5 milliunit/L (normal 0.5–2.5
milliunits/L);
 FT4 3.1 ng/dL (39.9 pmol/L; normal 0.7–1.9
ng/dL, or 9.0–24.5 pmol/L); +TSHR-SAbs

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 One month later, GD is back for a follow-up visit.
She notes that her thyrotoxic symptoms are gone,
and overall, she feels great. She is receiving
propylthiouracil 100 mg three times daily. Her
most recent TSH was 0.9 milliunit/L (normal 0.5–
2.5 milliunits/L)∗, and her free T4 was 1.6 ng/dL
(20.6 pmol/L; normal 0.7–1.9 ng/dL, or 9.0–24.5
pmol/L). However, over the past few days she
has developed a sore throat and feels achy.