APPROACH TO HYPERTHYROIDISM

Dr. Wishama Abdul Razzag

NAMS, Bir Hospital.
Graves disease

• Graves’ disease accounts for 60–80% of

thyrotoxicosis
• Prevalence 2 % in female and 1/1o th in male
• Age group common is 20-50 years and elderely
• The term ‘‘hyperthyroidism,’’ is a form of
thyrotoxicosis due to inappropriately high synthesis
and secretion of thyroid hormone(s) by the thyroid.
(ATA defination)
Thyrotoxicosis
• Thyrotoxicosis is a state of thyroid hormone excess
American thyroid association
defination
• Thyrotoxicosis is a condition having multiple eti-
ologies, manifestations, and potential therapies. The
term ‘‘thyrotoxicosis’’ refers to a clinical state that
results from inappropriately high thyroid hormone
action in tissues generally due to inappropriately
high tissue thyroid hormone levels.
 Signs and Symptoms of
Thyrotoxicosis
• Hyperactivity, irritability, dysphoria
• Heat intolerance and sweating
• Palpitations
• Fatigue and weakness
• Weight loss with increased appetite
• Diarrhea, mild steatorrhea
• Polyuria
• Oligomenorrhea, loss of libido
• Tachycardia; atrial fibrillation in the elderly
• Tremor, muscle wasting, proximal myopathy, hyperreflexia
• Goiter ,( osteopenia in long bone) fractures
• Warm, moist skin, pruritus, urticaria, diffuse hyperpigmentation, fine hair texture, Alopecia
• Muscle weakness, proximal myopathy
• Lid retraction or lag
• Gynecomastia
Inspection
• Alopecia
• Proptosis
• Goiter
• Lean and thin body build
• Sweating hand
• Palmar erythema
• Hyperpigmentation of skin
• Gynecomastia
• Anxious and anxiety
• Swelling of leg
Graves opthalmopathy
Pathogenesis
• TSI and TBII assays. The presence of TBII in a patient with thyrotoxicosis
implies the existence of TSI, and these assays are useful in monitoring
pregnant Graves’ patients in whom high levels of TSI can cross the
placenta and cause neonatal thyrotoxicosis. Other
• TPO antibodies occur in up to 80% of cases and serve as a readily
measurable marker of autoimmunity.
• Cytokines appear to play a major role in thyroid-associated
ophthalmopathy
• TSH-R
 Assessment of thyroid function
Serum TSH Serum free T4 Serum T3 Assessment
Normal hypothalamic-pituitary function
Normal Normal Normal Euthyroid
Euthyroid
Normal Normal or high Normal or high hyperthyroxinemia

Normal Normal or low Normal or low Euthyroid hypothyroxinema

Normal Low Normal or high Euthyroid: T3 therapy

Euthyroid: thyroid extract
Normal Low-normal or low Normal or high
therapy
High Low Normal or low Primary hypothyroidism
High Normal Normal Subclinical hypothyroidism
Low High or normal High Hyperthyroidism

Low Normal Normal Subclinical hyperthyroidism

Abnormal hypothalamic-pituitary function

TSH-mediated
Normal or high High High hyperthyroidism
Normal or low* Low or low-normal Low or normal Central hypothyroidism
• Subclinical hyperthyroidism is defined as a normal
serum free T4 and normal total T3 or free T3, with
subnormal serum TSH con- centration.
• overt hyperthyroidism, serum free T4, T3, or both
are elevated, and serum TSH is subnormal (usually
<0.01 mU/L in a third-generation assay).
• mild hyperthyroidism, serum T4 and free T4 can be
normal, only serum T3 may be elevated, and serum
TSH will be low or undetectable.
• Subacute thyroiditis is thought to be caused by viral
infection and is characterized by fever and thyroid
pain
• Painless thyroiditis:- due to lithium, Amiodarone,
postpartum
Note
• Serum TSH levels are considerably more sensitive
than direct thyroid hormone measurements for
assessing thyroid hormone excess
• Before doing TFT we should know error or abnormal
TFT report due to biotin, heterophilic antibody
• Stop biotin 2 days before
 Investigation
• Drugs history intake history
• Thyroid function test, LFT, gamma gt, ALP, serum calcium, Blood sugar, bilirubin
• Anti TPO
• TBII assay, transthyretin, measurement of TRAb
• Ultrasound neck, thyroidal blood flow on ultrasonography
• Ultrasound pelvis
• B hcg level in urine and blood
• spot urine iodine adjusted for urine creatinine concentration or a 24-hour urine
iodine concentration)
• Radioiodine uptake scan (99mTc, 123I, or 131I)
• ECG
• Echocardiography
• Holter monitor
• Eye examination
• magnetic resonance imaging
• The ratio of total T3 to total T4 can also be useful in assessing the
etiology of thyrotoxicosis when scintigraphy is contraindicated.
Because a hyperactive gland produces more T3 than T4, T3 will be
elevated above the upper limit of normal more than T4 in
thyrotoxicosis caused by hyperthyroidism
• T4 is elevated more than T3 in thyrotoxicosis caused by thyroiditis
• A high T4 to T3 ratio may be seen in thyrotoxicosis factitia (from
exogenous levothyroxine).
• Patients with painless thyroiditis presenting within the first year
after childbirth (postpartum thyroiditis) often have a personal or
family history of auto-immune thyroid disease and typically have
measurable serum concentrations of anti–thyroid peroxidase
antibodies
How do thyroid function tests change
during pregnancy?
• Normal pregnancy is associated with an increase in
renal iodine excretion, an increase in thyroxine
binding proteins, an increase in thyroid hormone
production, and thyroid stimulatory effects of hCG.
What is the normal reference range
for serum TSH concentrations in each trimester
of pregnancy?
• A downward shift of the TSH reference range occurs during
pregnancy, with a reduction in both the lower (de-creased by
about 0.1–0.2 mU/L) and the upper limit of ma- ternal TSH
(decreased by about 0.5–1.0 mU/L), relative to the typical
nonpregnant TSH reference range.
• The largest decrease in serum TSH is observed during the first
trimester because of elevated levels of serum hCG directly
stimulating the TSH receptor and thereby increasing thyroid
hormone production
• recommendations for a TSH upper reference limit of 2.5 mU/L
in the first trimester and 3.0 mU/ L in the second and third
trimesters
Evaluation
How to establish differentials??
Treatment modality of Graves disease
• Antithyroid drugs:
• Propylthiouracil 100-200 mg every 6 to 8 hourly
• Carbimazole 10-20 mg every 8 10 12 hourly
• Methimazole 10-20 mg every 8 10 12 hourly

• Beta blokers:- Propanolol 20-40 mg every 6 hourly

• Radioiodine
• Anticoagulant therapy
• Subtotal or near total thyroidectomy
Subacute thyroiditis

• large doses of aspirin (e.g., 600 mg every 4–6 h) or

NSAIDs
• 40–60 mg of prednisone (Steroid)
• Levothyroxine replacement (50–100 μg daily)
 Treatment of opthalmopathy
• Explain natural history of ophthalmopathy
• Avoid smoking.
• Discomfort can be relieved with Artificial tears (e.g., 1%
methylcellulose), eye ointment
• Dark glasses with side frames.
• Periorbital edema may respond to a more upright
sleeping position or a diuretic.
• Corneal exposure during sleep can be avoided by using
patches or taping the eyelids, Minor degrees of diplopia
improve with prisms fitted to spectacles. is preferable to
oral glucocorticoids,
Severe opthalmopathy
• Severe ophthalmopathy, with optic nerve
involvement or chemosis resulting in corneal
damage, is an emergency treatment
• Pulse therapy with IV methylprednisolone (e.g., 500
mg of methylprednisolone once weekly for 6 weeks,
then 250 mg once weekly for 6 weeks)
• Orbital decompression can be achieved by removing
bone from any wall of the orbit, thereby allowing
displacement of fat and swollen extraocular
muscles.
Thyroid dermopathy
• Thyroid dermopathy does not usually require
treatment, but it can cause cosmetic problems or
interfere with the fit of shoes.
• Surgery not required
• potency glucocorticoid ointment under an occlusive
dressing.
• Octreotide may be beneficial in some cases.
Indications for treatment of endogenous subclinical
hyperthyroidism in nonpregnant adults*
THANK YOU