the thyroglossal tract arises form a median bud in the pharynx, it passes from foramen caecum at...
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The thyroglossal tract arises form a median bud in the pharynx, it passes from foramen caecum at junction of anterior 2/3 and posterior 1/3 of the tongue and descend toward the root of the neck forming two lobes linked by isthmus. The fourth or fifth pharyngeal pouch gives rise to parafollicular cells ( C cell) which amalgamate with the lobes of the gland.
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It is composed of 2 lobes linked by isthmus lying over the second, third and fourth tracheal rings. WT is about 20 to 25 gm. its heavier in female, its just visible in normal person.
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The functioning unit is the lobule, which composed of follicles lined by cubical epithelium.
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The T.G secretes 3 hormones: Thyroxin T4 Tri-iodothyronine T3 Calcitonin (regulates Ca and ph. Levels) An adequate supply of iodine is required
for the synthesis of these hormones (100 microgram). The most common source is table salt and fish.
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Functions of thyroid Hormones1- Growth and development2- Carbohydrate, protein and fat metabolism3- Vitamin metabolism4- Basal metabolic rate5- Effect on the cardiovascular system6- Increase oxygen consumption by the tissue7- Increase oxygen release from Hb8- Effect on muscle function9- Increase oxidative phosphorylation10- Induce hyperglycemia.11- Augmentation of adrenalin and
noradrenalin function
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HYPOTHALAMUS
Thyrotropin releasing hormone (TRH)
PITUITARY
Thyroid stimulating hormone (TSH)
THYROID GLAND
Secretes T4 (main hormone) and T3.
•Metabolic demands •Drugs• Infection• Surgery•Trauma •Low temperature•Pit. disorders•Age•stress •Sleep
-VE FEEDBACK MECHANISM
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As blood concentrations of thyroid hormones increase, they inhibit both TSH and TRH, leading to "shutdown" of thyroid epithelial cells. Later, when blood levels of thyroid hormone have decayed, the negative feedback signal fades, and the system wakes up again.
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T3 is four times more powerful than T4 T3 less adherent to the binding protein.(98%
in comparison with 99.9% for T4) Half life of T3 is 3 days (8 to14 days for T4). All T4 change to T3 at the cellular level. The normal thyroid gland produces about 80%
T4 and about 20% T3.Every cell in the body depends upon thyroid
hormones for regulation of their metabolism.
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A- Hormone measurement1- Total T3 1.2 to 2.8 nmol\L2- Total T4 150 nmol\L3- TSH 0.5 to 5 mU\LB- Measurement of thyroid-pituitary-hypothalamic axis
(TSH stimulation test, TRH stimulation test).
C-Thyroid scanning: use of RAI131 then the gland is scanned to see its uptake.
D- Biopsy (FNA ,Core biopsy, Incisional biopsy, excisional biopsy.
E-Imaging study1-Ultrasound2-MRI3- CT scan.
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Due to either hypo- or hyper function of gland
They are the second most common endocrine disorder – mostly in woman
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Congenital (Agenesis / Ectopic as lingual, supra or infrahyoid , mediastinal ) / persistent thyroglossal duct result in cyst or fistula
Hypofunction (hypothyroidism)
Hyperfunction (thyrotoxicosis)
Thyroiditis.
Thyroid gland neoplasm.
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The enlargement may be diffuse, nodular, singular, functional or non-functional.
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Hyperthyroidism
Hypothyroidism
Euthyroid (normal levels)
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Failure of thyroid gland to produce adequate level of H. It is either1- Congenital
2-Acquired ( primary or secondary)
In adults called myxedemaIn children called cretinism
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A- Idiopathic (spontaneous)B- Autoimmune C- ThyroiditisC- Surgery (partial, sub-total or total )D- Radioactive iodineE- Drugs (thiocyanate, propyl-thiouracil -PTU, lithium,
phenylbutazone.F- Post- thyroiditis (Hashimotos)G- Iodine deficiency H- Secondary to pituitary gland failure.
Treatment is replacement therapy (Levothyroxine)
Hypothyroidism
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The commonest causes are Primary hyperthyroidism –toxic diffuse goiter - (Graves disease) Toxic nodular goiter Toxic solitary nodule Hashimotos thyroiditis Jud-basedow syndrome (excessive iodine intake) Factitious Thyrotoxicosis (excessive thyroxin intake) Ectopic thyroid H secretion (teratoma) Thyroid carcinoma Malignancies with thyroid stimulators Pitutary adenoma stimulating TSH (Thyroid - stimulating
hormone)
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THYROTOXICOSIS
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IMPORTANT NOTE
1- Thyrotoxicosis may be confused with acute anxiety
2 -In thyrotoxicosis, hands are sweaty and warm
3- In acute anxiety, palms are cold and clammy
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1-Anti-thyroid drugs Inhibit synthesis of thyroxin by
interference with trapping, oxidation and coupling of iodide.
Most commonly used drugs are carbimazole and propylthiouracil (PTU)
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2- Radioactive iodine: I131 is commonest isotope used and the aim is to destroy the thyroid tissue. 3- Surgery : The aim is to remove the thyroid tissue by Subtotal thyroidectomy (Preserves about 4g (10%) of thyroid tissue). Patients must be euthyroid prior to operation
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Detection of undiagnosed disease Symptoms Signs Referral Patient with diagnosed disease Determine original disease Past therapy Current medication Assessment of clinical status Referral if necessary
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Prevent the occurrence of life threatening situations ( Myxedema coma or thyroid storm)
Prevent the exacerbation of complications associated with them as cardiovascular diseases
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Avoidance of the following in untreated or poorly treated patients:
Surgical procedures Acute infection Epinephrine in local anesthetic solutions
and gingival retraction cords
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Patient under good medical treatment: Supine position Patient on PTU should be given stress management
medications as diazepam, lorazepam
For local anesthesia, use mepivicaine only If patient is off the anti-thyroid drug, THEN you can use
lidocaine,prilocaine , bupivicaine (max= 2 carpules) Epinephrine concentration as low as possible (1:200.000) over (1:100.000) over (1:50.000) In block injections, aspiration before injection Implement normal procedures and management Avoid atropine since it may lead to increase in heart
rate and precipitate a thyroid storm
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Patient under good medical treatment
Avoid acute infection
Treat all chronic infections
Patient on PTU causes agranulocytosis, thrombocytopenia and has an anti-vitamin k activity
Always check the complete blood picture (CBC), platelet count , prothrombin time and NR (normalized ratio)
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Thyroid storm Life-threatening exacerbation of
thyrotoxicosis. Has a mortality of 50%. Precipitating factors
Thyroid surgery, Radioiodine ,Withdrawal of antithyroid drugs, Acute illness (e.g. stroke, infection, trauma)
Clinical featuresSevere thyrotoxicosis, fever,
delirium ,seizure or coma, tachycardia, congestive heart disease, profuse sweating, .
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Treatment
ABC (BASIC LIFE SUPPORT)
Patency of airway (Head tilt-chin lift)
Assessment of breathing
Administration of O2 ( 100% - FLOW RATE 10L/ MIN)
Assessment of adequacy of circulation
If available , establish an IV LINE for 5% dextrose and water or
normal saline
Wet or ice packs
Medical assistance at once
High antithyroid drugs, beta- blockers, 200-300mg
hydrocortisone to prevent adrenal insufficiency
Sedation, hydration and electrolyte balance
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Detection of undiagnosed disease Symptoms Signs Referral Patient with diagnosed disease Determine original diagnosis Past therapy Current medication Assessment of clinical status Referral if necessary
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Avoidance of the following in untreated or poorly treated patients
Surgical procedures Acute infection CNS depressants (opioid analgesics, sedative
hypnotics as barbiturates and other anianxiety drugs
Administration of such drugs may become an overdose---- respiratory / or cardiovascular depression
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Patient under good medical treatment:
Avoid acute infection Implement normal procedures and
management
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An exacerbation of hypothyroid signs and symptoms
Usually in old people Seek medical aid Basic life support measures (BLPM) Oxygen – 100%- flow rate 10L/Min) I.V or i.m Hydrocortisone (100-300mg)
Myxedematous crisis:
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ThyrotoxicosisOsteoporosis of alveolar bone
Dental caries and PDD
Teeth and jaw develop rapidly
Premature loss of deciduous teeth
Early eruption of permanent teeth
Lingual thyroid
Hypothyroidism
Infants with hypothyroidism
may demonstrate thick lips,
enlarged tongue, delayed
eruption of teeth,
malocclusion
In adults there is
macroglossia
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