This document provides tips and instructions for using a PowerPoint presentation on goiter: 1. The presentation can be freely downloaded, edited, and modified. Blank slides are included to engage students by asking what they know about each topic before presenting additional information. 2. The presentation follows an active learning approach, showing blank slides, soliciting student questions and responses, and then revealing more content. This cycle repeats for deeper learning. 3. Bibliographic references are included in the notes section for further study. The presentation covers classification, pathophysiology, causes, and treatment of goiter.

1. Tips on using my ppt.
1. You can freely download, edit, modify and put your
name etc.
2. Don’t be concerned about number of slides. Half the
slides are blanks except for the title.
3. First show the blank slides (eg. Aetiology ) > Ask
students what they already know about ethology of
today's topic. > Then show next slide which enumerates
aetiologies.
4. At the end rerun the show – show blank> ask questions >
show next slide.
5. This will be an ACTIVE LEARNING SESSION x
three revisions.
6. Good for self study also.
7. See notes for bibliography.

2. Introduction

3. Introduction
Goiter/Goitre
Non specific term to indicate
diffuse enlargement of
thyroid gland.

4. Classification

5. • Simple goiter
• Toxic goiter:
• Inflammatory goiter:
• Neoplastic goiter:
Classification

6. Simple goiter:
- No hormonal abnormalities
and therefore no systemic
effects.
- Either diffuse or nodular
Classification

7. Simple goiter:
1.Physiological
Pubertal ,Pregnancy
2.Diffuse hyperplastic
3. Multinodular goitre
diffuse goiter often evolves into a
nodular goiter
Classification

8. Toxic goiter:
- Increased production of thyroid
hormones.
- Diffuse (graves dis.)
- nodular
- single nodule toxic adenoma
Plummer disease
- on the top of multinodular goiter.
Classification

9. Classification
Inflammatory goiter:
1. Autoimmune Chronic lymphocytic thyroiditis
Hashimoto’s disease
2.Granulomatous : De Quervain’s thyroiditis
3. Fibrosing: Riedel’s thyroiditis
4. Infective
Acute (bacterial thyroiditis,viral thyroiditis,
‘subacute thyroiditis’
Chronic (tuberculous, syphilitic)
5.Other: Amyloid

10. Neoplastic goiter:
Either benign (adenoma) or
malignant
Classification

11. Pathophysiology:TRH-TSH thyroid
hormone axis

12. Pathophysiology:TRH-TSH thyroid
hormone axis
• The thyroid gland is controlled byTSH secreted
from the pituitary gland,
• Pituitary is stimulated by thyrotropin-releasing
hormone (TRH) from the hypothalamus.
• TSH acts on TSH receptors located on the
thyroid gland
 TSH permits growth, cellular differentiation,
and thyroid hormone production and secretion
by the thyroid gland.
 Serum thyroid hormones levothyroxine and
triiodothyronine feed back to the pituitary,
regulating TSH production

13. Pathophysiology:TRH-TSH thyroid
hormone axis
•

14. Pathophysiology:TRH-TSH thyroid
hormone axis
• Stimulation of the TSH receptors of the thyroid
by TSH, TSH-receptor antibodies, or TSH
receptor agonists, such as chorionic
gonadotropin, may result in a diffuse goiter.
• When a small group of thyroid cells,
inflammatory cells, or malignant cells metastatic
to the thyroid is involved, a thyroid nodule may
develop.

15. Pathophysiology

16. Pathophysiology
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. Dietary deficiency of iodine,
2 Goitrogens in food.
3. Defective hormone synthesis
(Dyshormonogenesis)
sporadic goitres.

17. Pathophysiology
Somewhat surprisingly TSH levels
are normal in simple goiter

18. GOITROGENS

19. DRUGS
Anti-thyroid
Cough medicines
Sulfonamides
Lithium
Phenylbutazone
PAS
iodine
Oral hypoglycemic agents
GOITROGENS

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

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