if you're looking for a quick and brief ppt about thyroiditis, this one is for you- with main points and take home messages. source: Robbins pathology

1. THYROIDITIS

2. Background
◦ Inflammation of the thyroid gland
◦ Occurs in number of different settings
◦ Thyroiditis entities can be distinguished by:
1- the rapidity of onset and duration of disease
2- the predominant inflammatory response (polymorphonuclear, lymphocytic,
granulomatous)

3. Chronic lymphocytic thyroiditis (Hashimoto)
◦ The most common cause of hypothyroidism
◦ Autoimmune inflammatory disorder
◦ The frequency of other immune disorders like SLE and RA is
increased
◦ 45-65 YO, F>M (10-20:1)
◦ Painless enlargement of thyroid (usually symmetrical) + some
degree of hypothyroidism (gradually but may preceded by transient
thyrotoxicosis due to disruption of follicles and release of thyroid
hormones)
◦ T3+4 progressively decline, compensatory raise in TSH
◦ Increased risk for B call non Hodgkin lymphoma in thyroid

4. Subacute granulomatous thyroiditis (de quervain)
◦ 30-50 YO, F>M
◦ Unknown cause
◦ Preceded by URTI, suggesting a possibility of viral origin
◦ Acute onset, pain in the neck (when swallowing), fever, malaise, variable enlargement of the gland
◦ Transient hyperthyroidism – disruption of follicles and release of hormones
◦ Increased WBC and ESR
◦ Progression of disease- transient hypothyroid phase
◦ Self limited, lasts 6-8 W

5. Subacute lymphocytic thyroiditis
◦ Silent/painless thyroiditis
◦ May follow pregnancy, if so than may return in future pregnancies
◦ Autoimmune
◦ Painless neck mass/ features of thyroid hormone excess
◦ Middle aged women
◦ Initial phase of thyrotoxicosis followed by return to normal in a few months
◦ Rarely progresses to hypothyroidism

6. Others
◦ Riddle thyroiditis
unknown etiology, extensive fibrosis of the gland and neck structures
hard and fixed thyroid mass
associated with idiopathic fibrosis in other sites (ie retroperitoneum)
◦ Palpation thyroiditis
caused by vigorous clinical palpation of the gland
multifocal follicular disruption, chronic inflammatory cells, occasional giant cell formation
no abnormalities of gland function

7. Pathophysiology of any kind
1. Enlargement of thyroid gland due to lymphocyte infiltration
2. Destruction of thyroid parenchyma
3. Hypothyroidism if untreated

8. Clinical features
◦ Fatigue
◦ Drowsiness
◦ Dry skin, Hair and nails
◦ Constipation
◦ Difficulty learning
◦ Malaise
◦ Chills
◦ Thyroid tenderness
◦ Dysphagia
o Rapid heart rate
o tremors
o Dysphonia
o Fever
o Irritability
o Swelling
o Nervousness

9. diagnosis
◦ Blood test :
is there increased TSH levels?
Are there abnormal antibodies ? (anti-microsomal and antithyroglobulin)
◦ fine needle aspiration:
diffuse plasma cells and lymphocytes infiltration
Damage to follicular basement membrane
Atrophy of thyroid parenchyma

10. treatment
◦ During hyperthyroid phase treatment is not recommended, this phase usually lasts for 2-4 month, yet if
symptoms are extreme then beta blockers may be used to decrease heart rate and drowsiness.
◦ Treatments are usually according to the specific type which may include :
1. Antimicrobial medication
2. Fluid replacement
3. anti-inflammatory agents
4. Analgetics
5. Beta blockers

11. ◦ Thyrotoxicosis : beta blockers to treat symptoms carbimazole acts as an antithyroid drug iodine can
destruct the overly active gland if non are able to control the pathology then surgery can be considered
◦ Hypothyroidism: hormone replacement therapy, the medication should be given for six month then stopped
in order to asses thyroid gland function.
If function is back to normal then no need to continue medication, if not then there is permanent damage to
the thyroid gland in which hormonal therapy should be continued.
◦ Thyroidal pain : anti-inflammatory drugs like aspirin, or in more severe cases steroidal therapy with
prednisone for example can be given.