This document discusses hyperthyroidism and thyrotoxicosis. It begins by defining the terms and describing the thyroid gland's normal function. It then discusses the various causes of hyperthyroidism including Graves' disease, toxic multinodular goiter, subacute thyroiditis, and toxic adenoma. The document outlines the anatomy and physiology of the thyroid gland. It describes the clinical manifestations, diagnostic tests including thyroid function tests, ultrasound, and thyroid scintigraphy. It provides algorithms for diagnosis and outlines treatment options for hyperthyroidism including anti-thyroid medications, radioactive iodine treatment, and thyroidectomy.

2. DR.ADEEL RIAZ
PGR SURGERY DEPTT.
CPTH, LAHORE.
HYPERTHYROIDISM

3. INTRODUCTION:
Hyperthyroidism and Thyrotoxicosis are the terms
often used interchangeably, however each refers to
slightly different conditions.Hyperthyroidism refers to
over activity of the thyroid gland, with resultant
excessive secretion of thyroid hormones and
accelerated metabolism. Thyrotoxicosis refers to the
clinical effects of an unbound thyroid hormone,
regardless of whether or not the thyroid is the
primary source.
There are
number of pathological causes of hyperthyroidism in
children and adults.These include Grave’s disease,
Toxic Adenoma, Toxic Multinodular Goitre and
Thyroiditis.Of these, Grave’s disease accounts for
approx. 60% of cases of hyperthyroidism.To
understand the pathophysiology of hyperthyroidism,

4. THYROID GLAND:
The thyroid
gland is a butterfly-shaped endocrine
gland that is normally located in the lower
front of the neck. The thyroid gland’s job
is to make thyroid hormones, which are
secreted into the blood and then carried
to every tissue in the body. Thyroid
hormone helps the body use energy, stay
warm and keep the brain, heart, muscles,
and other organs working as they should.

5. DEFINITION:
Hyperthyroidism is due to increased levels of thyroid
hormone i.e. Diffuse Toxic Goitre (Grave’s disease),
Toxic Multinodular Goitre (Plummer’s disease) and
Toxic Adenoma.
According to SANJAY AZAD:
Hyperthyroidism is the hyperactivity of thyroid gland
with sustain increase in sythesis and release of
thyroid hormones.
According to WATSON:
Hyperthyroidism implies an excessive secretion of
thyroid hormones and may called as thyrotoxicosis,
but toxic goitre, exophthalmic goitre or Grave’s
disease. The term exophthalmic goitre or Grave’s
disease are reversal for hyperthyroidism that is

6. ANATOMY OF THE THYROID
GLAND
 It is butterfly-shaped located just inferior to larynx in
the lower front of the neck.
 It is composed of right and left lateral lobes, one on
either side of trachea, that are connected by
isthmus anterior to the trachea.
 Microscopic spherical sac called thyroid follicles
make up most of the thyroid gland.
 The walls of each follicles consist primarily of cells
called follicular cells.
 The thyroid gland is a highly vascularized organ
located in the neck, deep to the platysma,
sternothyroid and sternohyoid muscles, and
extending from the 5th cervical (C5) to the Ist
Thoracic (T1) vertebrae.

7. ANATOMY OF THE THYROID
GLAND
 The gland consists of two lobes (left and right)
connected by a thin, median isthmus overlying the 2nd
to 4th tracheal rings, typically forming an “H” or “U”
shape.
 Beneath the visceral layer of the pretracheal, deep
cervical fascia, the thyroid gland is surrounded by a
true inner capsule, which is thin and adheres closely to
the gland.
 The capsule sends projections into the thyroid forming
septae and dividing it into lobes and lobules.
 Dense connective tissue attachments secure the
capsule of the thyroid to both the cricoid cartilage and
the superior tracheal rings.
 Arterial supply is by superior thyroid, inferior thyroid and
thyroid ima artery,
 Venous drainage by superior , middle and inferior
thyroid veins.
 Nerves in relation are superior laryngeal and recurrent
laryngeal nerve.

8. PHYSIOLOGY OF THYROID
GLAND
 Thyroid gland secretes Tri-iodothyronine(T3) &
Thyroxine(T4).
 Steps involved in synthesis of these hormones are
 Iodine trapping from blood into the thyrocytes
(Thiocyanates and perchlorates block this step)
 Oxidation of iodide to inorganic iodine catalyzed by
peroxidase enzyme
(Carbimazole,Propylthiouracil and PASA block this
step)
 Formation of iodotyrosines: iodine + tyrosine= MIT
(monoiodotyrosine) + DIT (diiodotyrosine)
(carbimazole inhibits this step)
 Coupling reactions: coupling of 2 molecules of DIT
results in T4 and 1 molecule of DIT + MIT results in T3
(this stage is blocked by carbimazole)
 Hydrolysis: Hormones combine with globulin to form
thyroglobulin stored in thyroid gland and are released as
required by the process of hydrolysis.

9. PATHOPHYSIOLOGY
Hyperthyroidism characterized by loss of normal regulatory control of thyroid
hormone secretions
↓
Stimulatory action of thyroid in the body,
hyermetabolism results
↓
Increase in sympathetic nervous system results
↓
Alteration of secretion & metabolism of hypothalamic pituitary and gonadal
hormones
↓
Excessive thyroid hormone stimulates cardiac system and increase of adrenergic
receptors activity
↓
Tachycardia, increased cardiac output, stroke volume, adrenegic responsiveness
and peripheral blood flow
↓
Resultant state of nutrinional deficiency & -ve Nitrogen balance
↓
Hyperthyroidism

10. HYPERTHYROIDISM
 A hyper metabolic biochemical state
 It is a multi system disease with
 Elevated levels of FT4 or FT3 or both
 What is thyrotoxicosis ?
 What is hyperthyroidism ?
 What are the various causes ?
 How to differentiate the causes ?
 What is the appropriate treatment ?

11. CAUSES OF
HYPERTHYROIDISM
1. Graves Disease – Diffuse Toxic Goiter
2. Plummer’s Disease – Toxic MNG
3. Toxic phase of Sub Acute Thyroiditis - SAT
4. Toxic Single Adenoma – STA
5. Pituitary Tumours – excess TSH
6. Molar pregnancy & Choriocarcinoma (↑↑ βHCG)
7. Metastatic thyroid cancers (functioning)
8. Struma Ovarii (Dermoid and Ovarian tumours)
9. Thyrotoxicosis Factitia ; INF, Amiodarone, SSRIs

12. GRAVE’S DISEASE
 The most common cause of thyrotoxicosis
(50-60%).
 Organ specific auto-immune disease
 The most important autoantibody is
 Thyroid Stimulating Immunoglobulin (TSI) or TSA
 TSI acts as proxy to TSH and stimulates T4 and T3
 Anti thyro peroxidase (anti-TPO) antibodies
 Anti thyro globulin (anti-TG) Anti Microsomal
and other
 Autoimmune diseases - Pernicious Anemia,
T1DM
 RA, Myasthenia Gravis, Vitiligo, Adrenal
insufficiency.

13. GRAVE’S DISEASE
I 123 or TC 99m Normal v/s Graves

14. TOXIC MULTINODULAR
GOITRE
 TMG is the next most common hyperthyroidism - 20%
 More common in elderly individuals – long standing
goiter
 Lumpy bumpy thyroid gland
 Milder manifestations (apathetic hyperthyroidism)
 Mild elevation of FT4 and FT3
 Progresses slowly over time
 Clinically multiple firm nodules (called Plummer’s
disease)
 Scintigraphy shows - hot and normal areas

15. TOXIC MULTINODULAR
GOITRE
NUCLEOTIDE
SCINTIGRAPHY

16. SUBACUTE THYROIDITIS
 SAT is the next most common
hyperthyroidism – 15%
 T4 and T3 are extremely elevated in this
condition
 Immune destruction of thyroid due to viral
infection
 Destructive release of preformed thyroid
hormone
 Thyroid gland is painful and tender on
palpation
 Nuclear Scintigraphy scan - no RIU in the gland

17. TOXIC ADENOMA
 TSA is a single hyper functioning follicular thyroid
adenoma.
 Benign monoclonal tumor that usually is larger than
2.5 cm
 It is the cause in 5% of patients who are thyrotoxic
 Nuclear Scintigraphy scan shows only a single hot
nodule
 TSH is suppressed by excess of thyroxines
 So the rest of the thyroid gland is suppressed

18. TOXIC ADENOMA
NUCLEOTIDE
SCINTIGRAPHY

19. NUCLEOTIDE SCINTIGRAPHY

20. CLINICAL MANIFESTATIONS
OF HYPERTHYROIDISM
1. Those that occur with any type of
thyrotoxicosis
2. Those that are specific to Graves disease
3. Non specific changes of hyper metabolism

21. COMMON SYMPTOMS
 SKIN: warm, may br erythmatous (due to increased
blood flow), smooth (due to decrease in
keratin), sweaty and heat intolerance, oncholysis
(softening of nails and loosening of nail beds),
hyperpigmentation (due to increase ACTH
secretion)
 CVS: increased cardiac output (due to increased O2
demand), tachycardia, widened pulse pressure,high
output HF.
 RESPIRATORY: dyspnea on rest or exertion,
increased O2 consumption & CO2 production,
hypoxemia and hypercarbia,tracheal
obstruction,increased pulmonary arterial pressure,
resp. muscles weakness, decreased exercise

22. COMMON SYMPTOMS
 NEUROMUSCULAR: tremors and hyperactive
tendon reflexes
 REPRODUCTIVE: in females;
oligomenorrhea,amenorrhea
in males; gynecomastia, decreased libido, erectile
dysfunction, decreased or abnormal sperms.
 PSYCHIATRIC: hyperactivity, emotional liability,
anxiety, insomnia, decreased concentration.
 GENITOURINNARY: urinnary frequency and
nocturia.

23. COMMON SIGNS
1. Hyperactivity, Hyper kinesis
2. Sinus tachycardia or atrial arrhythmia, AF, CHF
3. Systolic hypertension, wide pulse pressure
4. Warm, moist, soft and smooth skin- warm handshake
5. Excessive perspiration, palmar erythema, Onycholysis
6. Lid lag and stare (sympathetic over activity)
7. Fine tremor of out stretched hands – format's sign
8. Muscle weakness, Diarrhea, Gynecomastia

24. Specific to Graves Disease
1. Diffuse painless and firm enlargement of thyroid
gland
2. Thyroid bruit is audible with the bell of stethoscope
3. Ophthalmopathy – Eye manifestations – 50% of
cases
 Sand in eyes, periorbital edema, conjunctival
edema (chemosis), poor lid closure, extraocular
muscle dysfunction, diplopia, pain on eye
movements and proptosis.
4. Dermoacropathy – Skin/limb manifestations – 20%
of cases
 Deposition of glycosamino glycans in the dermis
of the lower leg – non pitting edema, associated

25. MNG and Graves
Huge Toxic MNG Diffuse Graves Thyroid

26. Higher grades of Goiter
Toxic MNG (Diffuse) Graves

27. Grade IV Toxic MNG
Huge Toxic MNG Huge Toxic MNG

28. Proptosis
Lid lag
Thyroid Ophthalmopathy

29. Ophthalmopathy in Graves
Periorbital edema and chemosis

30. Severe Exophthalmia

31. Thyroid Dermopathy
Pink and skin coloured papules, plaques on the shin

32. Clubbing and
Osteoarthropathy
Thyroid Acropathy

33. Onycholysis

34. NON SPECIFIC CHANGES
1. Hyperglycemia, Glycosuria
2. Osteoporosis and hypercalcemia
3. ↓ LDL and Total Cholesterols
4. Atrial fibrillation, LVH, ↑ LV EF
5. Hyper dynamic circulatory state
6. High output heart failure
7. H/o excess Iodine, amiodarone, contrast
dyes

35. DIAGNOSTIC TESTS
 Thyroid Function Tests (TFTs)
 Thyroid antibodies – by ELISA
 Ultrasound
 Fine needle aspiration cytology
(FNAC)
 Thyroid Nucleotide Scintigraphy

36. THYROID FUNCTION TESTS
 Serum TSH is supressed in hyperthyroidism
(<0.05 mU/L)
 T3 & T4 are raised almost always from their
normal levels i.e. T3=1.5-3.5 nmol/L & T4=55-150
nmol/L but T3 is more sensitive.
 TSH receptor antibodies are not measured
routinely,but are commonly present.
 In developing hyperthyroidism, the free T3
concentration is more sensitive indicator of
developing disease than T4,and the former is
therefore preferred for confirming hyperthyroidism
that has already been suggested by a supressed
TSH result.

37. ULTRASOUND
 Ultrasound can be used to assess a thyroid
nodule.
 Its advantage over physical examination lies
alone in its ability to distinguish solid from cytic
nodules, whether more than one nodule
exists,and the exact size and extent of nodules.
 Infact, ultrasound can be used to access the size
and shape of the thyroid itself.
 Because of recent advances in this form of
imaging, ultrasound has become a sensitive
modality, particularly when assessing size and
numbers of nodules.

38. FINE NEEDLE ASIRATION
 Provided adequate sample is removed
on biopsy, FNAC of the thyroid nodule
can be used to categories tissue into
benign, malignant, thyroiditis, follicular
neoplasm.
 This technique has reduced
unnecessary operative procedure in
patients with benign disease and
increased the probability that surgery
will be performed on those with
malignant disease.

39. THYROID NUCLOTIDE
SCINTIGRAPHY
 The throid gland tissue can take up iodine
and certain other molecules.
 When radioactive isotopes of these
substances are swallowed or injected into
blood stream, they are taken up by thyroid
gland.
 As they decay, a special camera can detect
the energy that is released, creating a
picture of the thyroid gland.
 Most commonly used isotopes are Iodine-
123,
99m- Technetium, 131- iodine.

40. Measure TSH and FT4
 TSH,  FT4
Measure FT3
Primary (T4)
Thyrotoxicosis
High
Pituitary Adenoma FNAC, N Scan
Normal
 TSH, FT4 N  TSH,  FT4
T3 Toxicosis
Features of Grave’s
Yes
Rx. Grave’s
No
Single Adenoma, MNG
Low RAIU RAIU
Sub Acute Thyroiditis, I2, ↑ Thyroxine
F/u in 6-12 wks
Algorithm for Hyperthyroidism

41. Treatment Options
1. Symptom relief medications
2. Anti Thyroid Drugs – ATD
 Methimazole, Carbimazole
 Propylthiouracil (PTU)
3. Radio Active Iodine treatment – RAI Rx.
4. Thyroidectomy – Subtotal or Total
5. NSAIDs and Corticosteroids – for SAT

42. Symptom Relief
1. Rehydration is the first step
2. β – blockers to decrease the sympathetic
excess
 Propranalol, Atenelol, Metoprolol
3. Rate limiting CCBs if β – blockers
contraindicated
4. Treatment of CHF, Arrhythmias
5. Calcium supplementation
6. Lugol Iodine solution for ↓ vascularity of
the gland

43. Anti Thyroid Drugs (ATD)
Imp. considerations Methimazole Propylthiouracil
Efficacy Very potent Potent
Duration of action Long acting BID/OD Short acting QID/TID
In pregnancy Contraindicated Safely can be given
Mechanism of action Iodination, Coupling Iodination, Coupling
Conversion of T4 to T3 No action Inhibits conversion
Adverse reactions Rashes, Neutropenia Rashes, ↑Neutropenia
Dosage 20 to 40 mg/ OD PO 100 to 150mg qid PO

44. How long to give ATD ?
 Reduction of thyroid hormones takes 2-8
weeks
 Check TSH and FT4 every 4 to 6 weeks
 In Graves, many go into remission after 12-18
months
 In such pts ATD may be discontinued and
followed up
 40% experience recurrence in 1 yr. Re treat
for 3 yrs.
 Treatment is not life long. Graves seldom
needs surgery

45. Radio Active Iodine (RAI Rx.)
 In women who are not pregnant
 In cases of Toxic MNG and TSA
 Graves disease not remitting with ATD
 RAI Rx is the best treatment of
hyperthyroidism in adults
 The effect is less rapid than ATD or
Thyroidectomy
 It is effective, safe, and does not require
hospitalization.
 Given orally as a single dose in a capsule or

46. Radio Active Iodine (RAI Rx.)
 I123 is used for Nuclear Scintigraphy (Dx.)
 I131 is given for RAI Rx. (6 to 8 milliCuries)
 Goal is to make the patient hypothyroid
 No effects such as Thyroid Ca or other
malignancies
 Never given for children and pregnant/
lactating women
 Not recommended with patients of severe
Ophthalmopathy
 Not advisable in chronic smokers

47. Surgical Treatment
 Subtotal, Near Total & Total
Thyroidectomy
 Hemi Thyroidectomy with contra-lateral
subtotal
 ATD and RAI Rx are very efficacious and
easy – so
 Surgical treatment is reserved for MNG
with
1. Severe hyperthyroidism in children
2. Pregnant women who can’t tolerate ATD
3. Large goiters with severe Ophthalmopathy

48. Preoperative Preparation
 ATD to reduce hyper function before
surgery
 βeta blockers to titrate pulse rate to 80/min
 LUGOL’s solution 1 to 2 drops bd for 14
days
 This will reduce thyroid blood flow
 And there by reduce per operative bleeding
 Recurrent laryngeal nerve damage
 Hypo parathyroidism are complications

49. Dietary Advice
 Avoid Iodized salt, Sea foods
 Excess amounts of iodide in some
 Expectorants, x-ray contrast dyes,
 Seaweed tablets, and health food
supplements
 These should be avoided because
 The iodide interferes with or complicates
the management of both ATD and RAI
Rx.

50. Thyrotoxicosis Factitia
 Excessive intake of Thyroxine causing
thyrotoxicosis
 Patients usually deny – it is willful ingestion
 This primarily psychiatric disorder
 May lead to wrong diagnosis and wrong
treatment
 They are clinically thyrotoxic without eye signs
of Graves
 High doses of Thyroxine lead to TSH
suppression

51. Algorithm for Thyroid Nodule
Thyroid Nodule
Low TSH Normal TSH
TC 99 Nuclear Scan
FNAC or US
guided biopsyHot Nodule Cold Nodule
RAI Ablation,
Surgery or
ATD
Non diagnostic –
repeat FNAC
Surgery or
Cytology
CystBenign
T4
suppression
Suspicious or
follicular Ca
Malignant
Surgery
4% 10% 69% 17%

52. Summary of Hyperthyroidism
Hyperthyroidism Age %
Enlarge
d
Pain RAIU Treatment
Graves (TSI Ab
eye, dermo, bruit)
20 - 40 60% Diffuse None ↑↑ ATD – 18 m
Toxic MNG > 50 20% Lumpy
Pressur
e
↑ RAI, Surgery
Single Adenoma 35 - 50 5% Single None ± RAI, ATD
S Acute Thyroiditis
Any
age
15% None Yes ↓↓ NSAID, Ster.
TSH is markedly low, FT4 is elevated