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Himawan Sanusi

THE THYROID GLAND

Thyroid
cartilago
Pyramidal
lobe
Left lobe

Isthmus
Right lobe

Internal
jugular vein
External
carored
arteri
THYROID GLAND HISTOLOGY

http://arbl.cvmbs.colostate.edu/hbooks/pathphys/endocrine/thyroid/anatomy.html
Thyroid hormone synthesis, storage and release

TRAPPING ORGANIFICATION
I I PEROXIDASE
OXIDIZED
H2O2 IODIDE MIT DIT T3
TGB TGB
COUPLING STORAGE
Tyrosine?
Tyr Tyr
DIT DIT T4
Iodinase
AA TGB TGB TGB
Tyrosine

MIT MIT DIT


DEIODINATION DIT

RELEASE TGB
PROTEOLYSIS
T3 T T3 --
Protease
3T TGB
T4
4 T4 --
TGB
CAPILLARY FOLLICULAR CELL
COLLOID Cryer PE. Diagnostic endocrinology 1976:35
HYPOTHALAMUS
Basic elements in regulation TRH
of thyroid function

T3

PORTAL SYSTEM
I

ANTERIOR
PITUITARY
T4
+
“FREE” T3 _ TSH
T4 T3

TISSUE

I +
THYROID
T4
Usually Complain thyroid
disease
• Thyroid enlargement which
may be diffuse or nodular
• Symptom of thyroid deficiency
or Hypothyroidism
• Symptoms of thyroid hormon
excess, or Hyperthyroidism
Usually Complain thyroid
disease
Complications of a Spesific form
hyperthyroidism : Graves’ disease
which may present which prominence
of the eyes or exophthalmos and
thickening of the skin over the lower
legs (rare) or thyroid dermopathy
THYROID DISEASES
HYPERTHYROIDISM
HYPOTHYROIDISM
THYROIDITIS
THYROID NODUL
THYROID DYSFUNCTION PREVALENCE

• Hypothyroidism 2%
• Sublinical hypothyroidism 5-7 %
• Hyperthyroidism 0,2 %
• Subclinical hyperthyroidism 0,1-6,0%
Hyperthyroidism & Thyrotoxicosis

• Thyrotoxicosis is the clinical syndrome


that results when tissues are exposed to
high levels of circulating thyroid hormone.

• Thyroxicosis is due to hyperactivity of the


thyroid gland or hyperthyroidism

• Occasionally, thyrotoxicosis may be due to


other causes such us excessive ingestion
of the thyroid hormone or excessive
thyroid hormon from ectopis site
Conditions associated with thyrotoxicosis

• Diffuse toxic goiter (Graves’ disease)


• Toxic adenoma (Plummer’s disease)
• Toxic multinodular goiter
• Subacute thyroiditis
• Hyperthyroid phase of Hashimoto’s
thyroiditis
• Thyrotoxicosis factitia
• Rare: Ovarian struma, metastatic thyroid
carcinoma, hydatiform mole
Graves’ disease
GRAVES’ DISEASE (DIFFUSE
TOXIC GOITER)
• GD is the most common form of
thyrotoxicosis, may occur at any age, more
commonly in females than in males (5X)
• The syndrome consist one or more of the
following features:
1. THYROTOXICOSIS
2. GOITER
3.OPHTHALMOPATHY(Exophthalmos)
4. DERMOPATHY (Pretibial myxedema)
ETIOLOGY & PATHOGENESIS

• GD is currently viewed as an
autoimmune disease of unknown cause
• There is a strong familial predisposition
in that about 15%.
• 50% GD have circulating thyroid
autoantibodies
• Peak incidence 20-40-year
• T-lymphocytes sensitized to antigen
within thyroid gland and stimulate B
lymphocyte  antibodies
Autoimmune thyroiditis
Agonist Antagonist
TSHR-Ab Antibody Antibody

TSHR

CELL CELL
STIMULATION BLOCKADE
Davies TR. Graves’ disease in Werner & Ingbar’s : The thyroid ; 2000 ;520
Clinical features Graves’ disease

• Symptoms: in younger patients: palpitation,


nervousness, easy fatigability, hyperkinesia,
diarhhea, excessive sweating, intolerance to
heat, weight loss, without loss appetite

• Signs: Thyroid enlargement, exophthalmos,


tachycardia, muscle weakness, tremor
Older patients cardiovascular & myopatic
predominate clinical manifestation 
palpitatation, dyspnea on exersice, tremor,
nervousness, weight loss
Ophtamopathy Graves disease
• Infitratif  sympathetic overstimulation
Lid retraction (Dalrymphe’s sign)
Van Graves sign late palpebra sup
Stellwat’s sign the wink eyes late
Jefroy’s sign  fold of forehead not see
Mobius’sign  convergention of the eyes late
• Infiltratif  autoimmune
Exophthalmus, oculopathy congestif: cheimosis,
conjunctivitis, periorbital edema
Ulcerasi Cornea , neuritis optica, atrophi n
opticus
LID RETRACTION
HERTEL EXOPHTHALMOMETER
EXOPHTHALMOS : >18 MM
Computerised Axial
Tomography
Thyroid Dermopathy
• Thickening of the skin,over the
lower tibia due to accumulation
glycosaminglicans , rare (2-3%)
• TSH-R Ab high titer
• Osteopathy in the metacarpal
bones
Non Pitting oedema
Suspected hyperthyroidism

TSH &FT4

Low TSH Low TSH & Normal / high


Normal
& Normal high FT4 TSH & high
FT4 &TSH FT4
FT4
Measure FT3
Hyperthyroidism TSH- secreting
excluded pituitary adenoma.
Normal FT3 High FT3 Hyperthyroidism Thyroid hormone-
resistance syndrome
Subclinical hyperthyroidism
Evolving Graves’ disease T3 Hyperthyroidism
Or toxic nodular goiter
Excess thyroxine replacement
Non thyroidal illness
Graves’disease
Toxic nodular goiter
Thyroiditis
Repeat tests in 2-3 months: annual Gestational Hyperthyroidism
follow-up if no progression Factitious or iatrogenic hyperthyroidism
Thyroid Carcinoma
Struma Ovarii
Tumor secreting Chorionic gonadotropin
Laboratoy tests useful in DD of hyperthyroidism
Familial nonautoimmun hyperthyroidism
Atypical fashion Graves’ Disease
• Thyrotoxic periodic paralysis:
• usually Asian males, sudden attack flacid
paralysis, hypokalemia, usualy subsides
spontaneously.
• Prevention: K+ supplement & Beta
blockers
• Thyrocardiac disease :
• Primarily with symptoms of heart
involvement : refrsctory AF insensitif
digoxin or high output heart failure, no
evidence underlying heart disease (50%).
Treatment of thyrotoxicosis  cure
Atypical fashion Graves’ Disease

• Apethetic hyperthyroidism :
Older patients: weight loss, small
goiter, slow AF, severe depression
with none clinical features
Treatment modalities
• Anti-thyroid
• Surgery
• I131 radioactive
Treatment of Graves’ Disease
1. Antithyroid drug therapy
Young pts, small glands, mild disease
Propylthiouracil, methimazole (6m-15 mo),
relaps 50-60%.
PTU inhibits the conversion T4T3, effect
more quickly compare to methimazole
Methimazole - longer duration, single dose
Therapy 3-6 months  tapering dose and
combination levothyroxin 0.1 mg/d 12-24
mo.
Side effects : Allergic reaction (rash),
agranulocytosis, jaundice, liver failure
Treatment of Graves’ diseae
• Surgical treatment
Subtotal thyroidectomy  treatment of
choice for very large glands, or
multinodular goiter, prepared wth anti
thyroid drug (about 6 months)
Complication : Hypothyroidism ,
recurent laryngeal nerve injury,
hypoparathyroidism
Treatment of Graves’ disease

• Radioactive
iodine therapy
USA  NaI 131I 
euthyroid over 6-
12 weeks
Complication:
hypothyroidism
Treatment of Graves’ disease
• Other medical measures:
Beta-adrenergic blocking agents
Propranolol 10-40 mg every 6
hours, multivitamin supplements,
phenobarbital as sedative + to
lower T4 levels
Cholestyramine, 4 gr orally 3X
daily lower T4
Complication of Graves’
Disease
Thyrotoxic crisis (thyroid storm)
Acute exacerbation symptoms thyrotoxicosis.
May be mild & febrile until life threatening.

Etiology : after thyroid surgery in patients


who has been inadequatlely prepared, RAI131,
parturition inadequately controlled
thyrotoxicosis or stressfull illnes.
• Thyrotoxic crisis (thyroid “storm”)

Clinical manifestation:
Fever, Sweating, flushing, tachycardia
/ AF, heart failure, agitation, delirium,
coma, jaundice, nausea, vomiting and
diarrhea.

75% death………….
Treatment of Thyrotoxic crisis
(“thyroid storm”)
• Prophylthiourasil (PTU): 4 x 300 mg atau
• Neomercazole 6 x 20 mg.
• Yodium : Sodium yodida IV 1 mg/12 jam,
atau lugol 5% 3x10 tts /hr
• Propranolol (Inderal): IV 1-5 mg/6 jam, atau
tab 4 x 60-80 mg/hr via sonde lambung
• Kortikosteroid: Dexamethason 2 mg/6 jam
• Antibiotik dianjurkan jika infeksi sebagai
pencetus.