Goitre

1. GOITER

2. INTRODUCTION
The term GOITER is applied to any
enlargement of the thyroid gland regardless of
the cause.

3. GOITER
 The normal thyroid gland is impalpable. The term
goitre (from the Latin guttur = the throat) is used to
describe generalised enlargement of the thyroid
gland.
 A discrete swelling (nodule) in one lobe with no
palpable abnormality elsewhere is termed an
isolated (or solitary) swelling.

4. Causes of thyroid disease
inflammatory
Acute
Subacute
chronic
toxic
Primary
secondary
autoimmune
Hashimoto
Reidel thyroiditis
simple
Physiological
Colloidal
nodular
neoplastic
Benign
malignant

5. Classification of thyroid swellings
 Simple goitre (euthyroid)
 Toxic goiter
 Neoplastic
 Inflammatory
 Other (Amyloid)

6. Classification of thyroid swellings
 Simple goitre (euthyroid)
1. Physiological
Pubertal ,Pregnancy
2. Diffuse hyperplastic
Multinodular goitre
 Toxic goiter
1.Diffuse (Graves’ disease)
2.Multinodular
 Neoplastic
1.Benign 2.Malignant

7. Simple goiter
Aetiology
Simple goitre may develop as a result of stimulation of the
thyroid gland by TSH,
 Inappropriate secretion from the anterior pituitary a
microadenoma
 In response to a chronically low level of circulating thyroid
hormones.
1. The most important factor in endemic goitre is dietary
deficiency of iodine, Goitrogens in food.

8. Simple goiter
 There is chronic deficiency of Thyroxine (T4) and or
triiodotrynine (T3) in the body which in turn causes
compensatory elevation of TSH because of the lack
of necessary negative feedback.
 Prolonged stimulation of TSH in attempt to bring
normal thyroid hormones level leads to simple
goiter.

9. Classification of simple goiter
simple diffuse goiter
simple colloid goiter
simple nodular goiter

10. Pathophysiology
Chronic absence of T4/T3 causes elevated
level of TSH, which then leads to diffuse
hypertrophy and hyperplasia of follicular
cells and colloid (secretory follicles) in
efforts to produces more thyroid hormones.

11. Clinical presentation
Gradual onset of painless anterior neck
swelling, usually long standing in
endemically iodine deficient areas.
Recent onset of pain or increase in size may
indicate secondary changes.

12. Clinical presentation
• Obstruction of airways
• Laryngeal nerve compression
• Esophageal obstruction
• Neck veins obstruction

13. Investigation in simple goiter
Thyroid function test
– thyroxine (T4),
– tri iodothyronine (T3),
– thyroid stimulating hormones (TSH)
• This helps to know if the thyroid gland is
normal, hyper or hypo functioning.

14. Thyroid scan with radioactive iodine
(I123 or I131)
• In this investigation a traceable radioactive Iodine or
Technetium is injected into the blood stream, the thyroid
gland concentrates radioactive iodine.
• I123 has a shorter half life as compared to I131 and therefore
preferred because it has less exposure of the patient to
radiation.

15. Radiological investigations
Normal AP and lateral
chest X-rays may
demonstrate
retrosternal extension
of the goiter
(retrosternal shadow)

16. Thoracic inlet X-rays
may demonstrate
compression or
deviation of the
trachea, this
important to
anesthetist if surgery
is contemplated
(difficult intubation).

17. Computed tomography
may be indicated if
more details are
needed before surgery
or there is suspicion of
malignancy
transformation.

18. Fine needle aspiration cytology
To rule out malignancy

19. Treatment and prevention of simple
goiter
Dietary
• Iodine supplementation in iodine deficient
areas, food iodine fortification is one of the
best preventive measures of goiters.
Medical
Thyroxin supplementation
• In patients with diffuse hyperplastic goiter for
several months

20. Surgery indications
In patients with obstructive
symptoms,
When malignancy is suspected
clinically or after FNAC
For cosmetic reasons

21. Hypothyroidism is a condition
characterized by abnormally low
thyroid hormone production.
Because thyroid hormone affects
growth, development, and many
cellular processes, inadequate
thyroid hormone has widespread
consequences for the body.
HYPOTHYROIDSM

22.  Medications and food (GOITROGENS)
 Pituitary or hypothalamic disease
 Severe iodine deficiency
 Thyroid destruction (from radioactive iodine
or surgery)
 Hashimoto's thyroiditis
Aetiology

23. FOOD
Soybeans
Millet
Cassava
Cabbage
Excess iodine or lithium ingestion, which
decrease release of thyroid hormone
GOITROGENS

24. In this condition, the thyroid gland is usually
enlarged (goiter) and has a decreased ability
to make thyroid hormones.
Hashimoto's is an autoimmune disease in
which the body's immune system
inappropriately attacks the thyroid tissue.
Hashimoto's thyroiditis

25. Increased antibodies to the enzyme, thyroid
peroxidase (anti-TPO antibodies).
Hashimoto's can be identified by detecting
anti-TPO antibodies in the blood
Hashimoto's thyroiditis

26. If for some reason the pituitary gland or the
hypothalamus are unable to signal the thyroid
and instruct it to produce thyroid hormones, a
decreased level of circulating T4 and T3 may
result, even if the thyroid gland itself is normal.
If this defect is caused by pituitary disease, the
condition is called "secondary hypothyroidism."
If the defect is due to hypothalamic disease, it is
called "tertiary hypothyroidism."
Pituitary or Hypothalamic disease

27.  Fatigue
 Depression
 Modest weight gain
 Cold intolerance
 Excessive sleepiness
 Dry, coarse hair
 Constipation
 Dry skin
 Muscle cramps
 Increased cholesterol
levels
 Decreased
concentration
 Vague aches and pains
 Swelling of the legs
Common symptoms

28. • As the disease becomes more severe, there
may be puffiness around the eyes, a
slowing of the heart rate, a drop in body
temperature, and heart failure.
• In its most profound form, severe
hypothyroidism may lead to a life-
threatening coma (myxedema coma).

29. A diagnosis of hypothyroidism can be suspected
in patients with fatigue, cold intolerance,
constipation, and dry, flaky skin.
A blood test is needed to confirm the diagnosis.
When hypothyroidism is present, the blood levels
of thyroid hormones are usually decreased.
However, in early hypothyroidism, the level of
thyroid hormones (T3 and T4) may be normal.
Diagnosis of hypothyroidism

30. Treatment of hypothyroidism requires life-long
levothyroxine (T4) therapy.
Treatment of hypothyroidism

31. Cretinism
Clinical features:
 Impaired skeletal development
 Impaired CNS development
 Inadequate maternal thyroid hormone prior to
fetal thyroid gland formation
 SEVERE mental retardation
 Normal brain development if maternal thyroid
deficiency occurs after fetal thyroid gland
development

32. Toxic goiter, thyrotoxicosis or
hyperthyroidism
 Hyperthyroidism is a condition in which an overactive
thyroid gland is producing an excessive amount of
thyroid hormones that circulate in the blood.
 Thyrotoxicosis can be caused by an excessive intake of
thyroid hormone or by overproduction of thyroid
hormones by the thyroid gland.
 Hyperthyroidism can be primary or secondary
depending on the etiology.

33. Causes of hyperthyroidism
 Graves' Disease
 Functioning adenoma ("hot nodule") and
toxic multinodular goiter (TMNG)
 Excessive intake of thyroid hormones
 Abnormal secretion of TSH
Thyroiditis (inflammation of the thyroid
gland)

34. Primary hyperthyroidism
Grave’s disease
Graves’s disease is an autoimmune disease of
the thyroid gland, where there is an over-
production of the thyroid hormone which
causes enlargement of the thyroid and other
symptoms such as exophthalmos, heat
intolerance and anxiety.

35. In patients with secondary hyperthyroidism,
there is a pre existing thyroid pathology for
example multinodular goitre (occurs due to
hypertrophy and hyperplasia of gland
leading to excess production of thyroid
hormones).
Secondary hyperthyroidism

36. Inflammation of the thyroid gland may occur
after a viral illness (Subacute thyroiditis).
This condition is associated with a fever and a
sore throat that is often painful on swallowing.
The thyroid gland is also tender to touch.
There may be generalized neck aches and pains.
Inflammation of the gland with an accumulation
of white blood cells known as lymphocytes
(lymphocytic thyroiditis) may also occur.
Thyroiditis

37. Central nervous system
Central nervous system features are very
common in patients with primary
thyrotoxicosis.
tremors which can be observed on the tongue
and fingers,
nervousness,
emotional liability (patients become irritated
easily), they may also be lethargic or agitated
and usually they have warm and moist hands.
Clinical features of hyperthyroidism

38. Increased metabolic rate
weight loss,
 heat intolerance,
excessive sweating, and
tiredness cause by muscle weakness
as a result of proteolysis.

39. Gastro intestinal tract (GIT);
loss of body weight despite having good or
increased appetite, and
increase bowel motions (diarrhea).

40. Genital urinary tract (GUT)
irregular menstruation,
amenorrhea,
loss of libido and
erectile dysfunctions

41. Opthalmological features:
Exophthalmos
Ophthalmoplegia can be bilateral or
unilateral and can be associated with
diplopia (double vision).

43.  A rare presentation of thyrotoxicosis, there is extreme
signs of thyrotoxicosis associated with severe metabolic
disturbances.
 It occurs in patient with hyperthyroidism who has not
been well prepared (hyperthyroidism is not controlled)
before surgery.
 Clinical features includes;
 hyper-thermia,
 tachycardia,
 irritability,
 profuse sweating and
 diarrhea.
Thyroid storm (thyrotoxic crisis)

44. • This targets central nervous system and
cardiovascular symptoms.
• Beta adrenergic blockers are the mainstay of
symptomatic therapy for thyrotoxicosis.
• Propranolol has benefit of inhibition of
peripheral conversion of T4 to T3
Symptomatic treatment

45. These drugs either blocks iodine binding to
tyrosine and decrease antibody titers
(Carbimazole) or block iodine binding and
prevent conversion of T4 to T3
(propylthiouracil).
Antithyroid treatment

46. Antithyroid drugs
Inhibitors of hormone synthesis
1.Propylthiouracil (PTU)
2.Methimazole (Tapazole)

47. All patients must be euthyroid before
embarking in surgery, ECG, CXR, and
Echocardiogram must be done to rule out
arrhythmia and heart failure.
Thoracic inlet X-ray in huge goiters to rule
tracheal deviation and compression as
discussed above.
Surgical treatment

48. Subtotal thyroidectomy; leaves about 8-10 gram
of thyroid tissue, either 4-5gram on each side or
8-10 gram on one side.
Near total thyroidectomy removes nearly all
thyroid tissue leaving only about 4gm thyroid
tissue
Lobectomy removes the entire lobe one side with
isthmusectomy eg in solitary toxic nodule
Types of surgery