Hypo hyper thyroid graves

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1. Thyroid disorder

2. Thyroid disorder
•Hyperthyroidism (increased levels of free T3
and T4)
•Hypothyoridism (decreased thyroid hormone)

3. Hyperthyroidism
Cause:
Primary:
•Diffuse toxic hyperplasia (Graves disease)
•Hyperfunctioning multinodular goiter
•Hyperfunctioning adenoma
Secondary:
•TSH secreting pituitary adenoma

4. Clinical features
Increased sympathetic activity:
Skin: soft, warm, flushed
Weight loss despite increase appetite
Cardiac:
Tachycardia,palpitation
Neuromuscular system: tremor,anxiety
Occular changes: staring gaze, lid lag
GIT: malabsorption,diarrhoea
Skeletal system: osteoporosis, increased risk fracture

5. Lab diagnosis
TSH (thyroid stimulating hormones): Decreased
T4 and T3: increased.

6. Hypothyroidism
Structural or functional derrangement that
interfer with production thyroid hormones
(decreased T3 and T4)

7. Cause:
Primary:
•Developmental: thyroid dysgenesis,thyroid
agenesis
•Defect in thyroid hormone receptor
•Autoimmune hypothyroidism: Hashimoto
thyroiditis
•Iodine deficiency
Secondary:
•Pituitary failure: pituitary adenoma

8. CRETINISM
•Cretinism refers to hypothyroidism that
develops in infancy or early childhood.
Clinical features
•impaired development of the skeletal system
and central nervous system: manifested by
•severe mental retardation
•short stature
•protruding tongue
•umbilical hernia

9. MYXEDEMA
• hypothyroidism developing in the older child
or adult.
•Also called Gull disease
•Clinical features of myxedema are
characterized by a slowing of physical and
mental activity.

10. Graves Disease

11. Graves disease
•Graves disease is characterized by a triad of
clinical findings
1. Hyperthyroidism: due to diffuse, hyperfunctional
enlargement of the thyroid
2. Infiltrative ophthalmopathy: with resultant
exophthalmos
3. Localized, infiltrative dermopathy, sometimes
called pretibial myxedema, (which is present in a
minority of patients)
Syn: Basedow’s disease/ diffuse toxic goiter

12. •Age: between 20 and 40 years of age
•Women are affected as much as 10 times
more frequently than men.

13. Pathogenesis
• breakdown in self-tolerance to thyroid auto-
antigens, most importantly the TSH receptor.
The result is the production of multiple
autoantibodies, including
1.Thyroid-stimulating immunoglobulin
This IgG
binds
TSH recptor

14. Mimic the action of TSH
Adenyl cyclase
Increase release of thyroid hormones

15. 2. Thyroid growth-stimulating immunoglobulins
•directed against the TSH receptor
•proliferation of thyroid follicular epithelium
3. TSH-binding inhibitor immunoglobulin
anti–TSH receptor antibodies prevent TSH from
binding normally to its receptor on thyroid
epithelial cells

16. •Autoimmunity also plays a role in the
development of the infiltrative
ophthalmopathy
•The volume of the retro-orbital connective
tissues and extraocular muscles is increased
for several reasons
1.marked infiltration of the retro-orbital space
by mononuclear cells, predominantly T cells
2.inflammatory edema and swelling of
extraocular muscles;

17. 3.accumulation of extracellular matrix
components
4.increased numbers of adipocytes (fatty
infiltration)
These changes displace the eyeball forward

18. Morphology
•Gross: symmetrically enlarged because of
diffuse hypertrophy and hyperplasia of thyroid
follicular epithelial cells
•On cut section- soft, meaty appearance (Red
fleshy) resembling normal muscle

19. •Microscopic:
•Papillae formation: The follicular cells are tall
and more crowded and thrown into papillae
with lack of fibrovascular core.
•The colloid is thin and pale with scalloped
margins

20. Changes in extra thyroid tissue
•lymphoid hyperplasia
•Heart: hypertrophied and ischemic changes
•Opthalmopathy:
•orbit are edematous
•Infiltration by lymphocytes and fibrosis
•Dermatopathy: thickening of the dermis due
to deposition of glycosaminoglycans and
lymphocyte infiltration.

21. FIGURE 24-13 Graves disease. A, There is diffuse symmetric
enlargement of the gland and a beefy deep red parenchyma.
The follicles are lined by tall, columnar epithelium. The crowded,
enlarged epithelial cells project into the lumens of the follicles. These
cells actively resorb the colloid in the centers of the follicles, resulting
in the scalloped appearance of the edges of the colloid

22. Clinical features
•Diffuse hyperplasia of the thyroid,
•Ophthalmopathy : abnormal protusion of eye
ball (exophthalmos)
•Dermopathy: most common in the skin
overlying the shiny scaly thickening and
induration

24. Lab findings…
•Free T4 and T3: Increased
•TSH levels: Decreased

25. Thyroiditis

26. Thyroiditis
•inflammation of the thyroid gland
Types
•Acute thyroiditis: Caused by bacteria/fungus
•Hashimoto thyroiditis
•Granulomatous (de Quervain) thyroiditis
•Subacute lymphocytic thyroiditis.
•Reidel (Fibrous) Thyroiditis

27. Hashimoto Thyroiditis
•Characterized by gradual thyroid failure
because of autoimmune destruction of the
thyroid gland
•Most common cause of hypothyroidism
• Age: 45 and 65 years of age
•Sex:
Female:Male -10 : 1 to 20 : 1

28. Pathogenesis
•Multiple immunologic mechanisms may contribute
to thyroid cell death:
•The main defect in Hashimotos thyroiditis is a T cell
defect
•The T cell recognises the thyroid antigen and causes
proliferation of T cells
•CD8+ cytotoxic T cell–mediated cell death: CD8+
cytotoxic T cells may cause thyrocyte destruction.
•.

29. • Cytokine-mediated cell death: Excessive T-cell
activation leads to the production of T
H
1
inflammatory cytokines such as interferon-γ in
the thyroid gland: recruitment and activation
of macrophages and damage to follicles
•Binding of anti-thyroid antibodies (anti-
thyroglobulin, and anti-thyroid peroxidase
antibodies

30. Pathogenesis
FIG:athogenesis of Hashimoto thyroiditis. Breakdown of peripheral tolerance to thyroid auto-antigens,
results in progressive autoimmune destruction of thyrocytes by infiltrating cytotoxic T cells, locally
released cytokines, or by antibody-dependent cytotoxicity.

31. Morphology
•Gross:
-The thyroid diffusely enlarged
-The capsule is intact, and the gland is well
demarcated from adjacent structures.

32. Microscopic:
•Extensive infiltration of parenchyma by a
mononuclear inflammatory infiltrate
containing small lymphocytes and plasma cells
•Lymphoid follicle formation with well
developed germinal centers
•Thyroid follicles are atrophic and are lined by
Hurthles cells
•Hurthle cells: epithelial cells with abundant
eosinophilic granulkar

33. Fig.Hashimoto thyroiditis showing lymphoid follicles with
prominent germinal centers and oncocytic follicular
epithelium
Fig.Hashimoto thyroiditis with extensive fibrosis,
atrophy of follicular epithelium

34. Clinical features
•painless enlargement of the thyroid
•Hypothyroidism…

35. THANK YOU