2. Thyroid Disorders-learning objects
How it is formed
Where it is formed
What are & how it functions
Main disorders
How are these diagnosed
What are the treatment options
3. THYROID GLAND
• Two lobes
• Situated in the lower neck
• Synthesise, stores, release T3 & T4
(triiodothyronine & thyroxine)
BIOSYNTHESIS
• Dietary iodine Inorganic iodide
• Iodide + Tyrosine Monoiodotyrosine
• Monoiodotyrosine + Iodide Diiodotyrosine
• A coupling reaction binds MIT & DIT to T3(Tri) &
T4(Tetra)idothyronine(thyroxin).
6. HORMONE TRANSPORT
• TSH Stimulation T3 & T4 Cleaved from
thyroglobulin Released into
circulation
• In circulation ,Thyroxin binds to plasma proteins,
75% TBG, pre albumin, albumin, only 2.5% free
Advantages of binding
Protect from premature metabolism and excretion.
Prolongs half life in circulation.
Reach its site of action.
Hormone is metabolized by deiodination.T3 & rT3
7. HORMONE FUNCTIONS
Growth and development
Increasing rate of metabolism
Increase metabolic rate, in CVS
increases blood flow, cardiac output, heart
rate.
Regulating cerebral conduction in CNS
Sleep
Lipid metabolism
8. THYROID FUNCTIONS TESTS
Serum total thyroxine (TT4)/f T4
Serum total triiodothyronine (TT3) / fT3
Serum thyrotropin assays (TSH)
Resin triiodothyronine uptake (RT3U)
Free thyroxine index
TRH stimulation test
Serum thyroid Ab.antimicrosomal, antithyroglobulin
in Hashimoto’s thyroiditis & Grave’s D-TSI
Serum thyroglobulin, FNAC
9. Serum free / total thyroxine (f/tT4)
Test indicating hormone availability to tissues
Total (free & bound) T4 is determined by
radioimmunoassay.
fT4 is determined by two site immunoassay. More
sensitive.
Disease & condition interactions are possible in tT4.
Normal range : 5-12 mcg/dL(tT4) & 8-21 pmol/L
10. Serum total triiodothyronine (tT3)
Measures total (free & bound) T3
Useful for early detection or to rule out
hyperthyroidism
Not diagnostically significant for hypothyroidism
Normal range : 80 -180 ng/dL or 1.1-2.7 nmol/L
11. Resin triiodothyronine uptake (RT3U)
Test clarifies whether abnormal T4 levels are the result of
a thyroid disorder or abnormalities in the binding
proteins.
Evaluate binding capacity of thyroxine binding globulin
(TBG).
If abnormalities in binding proteins underlie the
abnormal levels of TH , TH level decreases with TBG
level increases.
12. Serum thyrotropin (TSH) assays
Most sensitive test for detecting the
hypothyroid state
Slight decrease in TH level release more
TSH
Done by radioimmunoassay(RIA) or two site
immunoassay(using monoclonal antibody)
method. Later is most sensitive test. Used for
diagnostic and monitoring purpose.
13. Free thyroxine index
Estimation of the free T4 level through a mathematical
interpretation of the relationship between resin
triiodothyronine uptake and T4 levels.
FTI = TT4×RT3U/mean serum RT3U.
Normal range – 5.5 to 10.5. these days this test is not
done due to availability of free T4 assay.
Elevated in hyperthyroidism.
14. • MOST IMPORTANT to remember
• best test for diagnosis &
monitoring of treatment for
hyperthyroidism is fT4.
• Best test for diagnosis & monitoring
of treatment for hypothyroidism is
TSH by two site immunoassay.
• The best single test is TSH by two
site immunoassay for both.
19. PRIMARY HYPOTHYROIDISM
gland destruction or dysfunction caused by disease or medical
therapies (e.g. Radiation or surgical procedure)
Or failure of the gland to develop or congenital incompetence
(cretinism) leading to decreased production.
So decreased levels of T3/T4 & increased TSH/TRH
SECONDARY HYPOTHYROIDISM
pituitary disorder that inhibits TSH secretion. So lack of
appropriate stimulation causing decreased secretion. So increased
TRH but decreased TSH & T3/T4 levels.
TERTIARY HYPTHYROIDISM
defect of hypothalamus to secrete TRH , to stimulate pituitary. So
decreased levels of TRH,TSH & T3/T4
20. SUBCLINICAL HYPOTHYROIDISM
Refers to patient without clinical
symptoms
Normal free thyroxine level and
slightly elevated TSH level.
Treatment not recommended.
21. CAUSES OF HYPOTHYROIDISM
1)Hashimoto’s thyroiditis
Autoimmune disorder
In which the thyroid gland is gradually destroyed by a
variety of cell- and antibody-mediated immune
processes. Anti microsomal & anti thyroglobulin
antibodies would be detected in the serum.
2) over usage of anti thyroid drugs/Surgery
22. 3) Goiter
ENDEMIC
• Due to
inadequate
dietary intake
of iodine
SPORADIC
• Due to
ingestion of
drugs and
foods
containing
progoitrin.
23. Progoitrin hydrolysis Goitrin (activated)
Goitrins inhibit oxidation of iodine to iodide.
So they decrease the TH production.
Food & drugs containing Progoitrin
• Cabbage, Spinach, Mustard,
Cauliflower, Peanuts etc.
Food
• Propylthiouracil, Phenylbutazone,
Cobalt, Lithium etc.
Drug
24. SIGNS AND SYMPTOMS
EARLY…………………….
Lethargy
Fatigue
Forget Ness
Unexplained weight gain
Sensitivity to cold
Constipation
PROGRESSIVE……………..
Dry, inelastic skin
Slowed speech and thought
Puffy face
If untreated – MYXEDEMA COMA
25. MYXEDEMA COMA
Life threatening complication with high mortality rate.
Most common in – preexisting or under diagnosed
hypothyroidism.
Predisposing factors includes…….
Alcohol, sedative, or narcotic use
Over use of antithyroid drug
Sudden discontinuation of TH therapy.
Infections
Exposure to cold
Radiation therapy etc.
26. TREATMENT
• Thyroxin - synthetic
preparations with careful
monitoring of thyroid
hormones.
27. HYPERTHYROIDISM
Thyrotoxicosis
Over activity of thyroid gland
3 main types:Diffuse toxic goiter (Grave’s Disease)
Toxic Nodular Goiter, Toxic Adenoma
1. GRAVE’S DISEASE (Diffuse toxic goiter)
Most common form
Autoimmune disorder – antibodies bind to and activate
TSH receptor(TSI) ------------ over production of TH
28. Signs and symptoms
Enlarged goiter
Anxiety, insomnia, irritability
Tremor and muscle weakness
Stare, Exophthalmos
Heat intolerance
Palpitations, tachycardia
Weight loss
Periorbital edema
Pretibial edema
29. 2. PLUMMER DISEASE (Toxic nodular goiter)
Less common
Incidence is highest in patients <50 years of age
Signs & symptoms
Same as for Graves disease with nodular masses
Cardiac abnormalities – Congestive cardiac failure,
tachyarrhythmias are more prominent, no
exophthalmos.
3. TOXIC ADENOMA- Autonomous tissue
producing T3/T4 not controlled by TSH.
30. Other causes of Hyperthyroidism
JODBASEDOW PHENOMENON
Over production of thyroid hormone following a sudden , large
increase in iodine ingestion
Or by introduction of iodide or iodine in contrast agents or
drugs (amioderone).
FACTITIOUS HYPERTHYROIDISM
Abusive ingestion of thyroid replacement agents to lose weight
Diagnosis is aided by ……………….
Absence of glandular swelling, exophthalmos
Lack of autoimmune activity (Graves disease)
31. TREATMENT
BETA BLOCKERS
Propranolol
Reduce peripheral manifestations like tachycardia, sweating,
tremor, nervousness etc.
Also inhibit peripheral conversion of T4 to T3
ANTITHYROID AGENTS
1) Propylthiouracil
2) Methimazole
Directly interfere with thyroid hormone synthesis.
Inhibit iodine oxidation and coupling
32. RADIO ACTIVE IODINE
Thyroid gland picks up iodine-131
takes advantage of the fact that thyroid cells are the only
cells in the body which have the ability to absorb iodine
By giving radioactive iodine, the thyroid cells which absorb
it will be damaged or killed.
ADVANTAGES
1. High cure rate
2. Avoid surgical risk
3. Less expensive
33. DISADVANTAGES
1. Risk of delayed hypothyroidism (excessive cell death).
2. Genetic damage, teratogenic ( So should not be given in
reproductive age or pregnancy). Best in old age.
DOSAGE
A dose of 80-100 mCi of iodine 131/estimated gram of
thyroid gland recommended.
PRECAUTIONS & MONITORING
Generally reserved for patients past the child bearing years.
Monitored for early recurrent of hyperthyroidism and later
for hypothyroidism.
34. SURGERY
Subtotal thyroidectomy
If drug therapy fails or radioactive iodine is
undesirable
Rapid cure
Success rate is high
Difficult procedure & complications like
damage to Parathyroid or recurrent laryngeal
nerve
35. THYROID STORM
Sudden exacerbation of hyperthyroidism
Rapid release of thyroid hormone
Fatal, if not treated
Leads to dehydration, shock and death
Precipitating factors includes
Thyroid trauma
Surgery
Radio active iodine
Infection and sudden stopping of antithyroid therapy
Fever, tachycardia, restlessness, tremor
37. Assignment on Thyroid Disorders
Q1. a. What is the difference between Primary,secondary &
tertiary Hypothyroidism ? 5
b. How would you investigate a case of hypothyroidism? 5
Q 2.a. What are different types of Hyperthyroidism? 5
b.How would you investigate a case of hyperthyroidism? 5
Note : please read the topic from book & my slides. If u have
any question/query, u can ring/sms me on 03335638699.
