Hyperthyroidism

1. HYPERTHYROIDIS
M

2. INTRODUCTION
• Result of excessive Thyroid hormone function
• Subclinical hyperthyroidism: little or no clinical
hyperthyroidism only having biochemical
abnormality of lo serum TSH

3. CAUSES OF HYPERTYHROIDISM
• HYPERTHYROIDISM WITH NORMAL OR HIGH RADIOIODINE UPTAKE
 Autoimmune Thyroid Disease
I. Graves’ disease
II. Hashitoxicosis
 Autonomus thyroid tissue
I. Toxic adenoma
II. Toxic mutinodular goiter
 TSH mediated hyperthyroidism
I. TSH producing pituitary adenoma
II. Non neoplastic TSH mediated hyperthyroidism

4. CAUSES OF HYPERTHYROIDISM
HCG mediated hyperthyroidism
I. Hyperemesis gravidarum
II. Trophoblastic disease
• HYPERTHYROIDISM WITH A NEAR ABSENT RADIOIODINE UPTAKE
Thyroiditis
I. Subacute granulomatous/de quervain’s thyroiditis
II. Painless/silent/lymphocytic thyroiditis
III. Postpartum thyroiditis
IV. Palpation thyroiditis
V. Amiodarone induced
VI. Checkpoint inhibitor induced thyroiditis

5. CAUSES OF HYPERTHYROIDISM
Exogenous thyroid hormone intake
I. Excessive replacement therapy
II. Intentional suppressive therapy
III. Factitious hyperthyroidism
Ectopic hyperthyroidism
I. Struma ovarii
II. Metastatic follicular thyroid cancer

6. CLINICAL FEATURES
• ANXIETY, HYPERACTIVITY, IRRITABILITY, DYSPHORIA
• EMOTIONAL LABILITY
• WEAKNESS
• TREMOR
• PALPITATION
• HEAT INTOLERANCE
• INCREASED PERSPIRATION
• WEIGHT LOSS DESPITE INCREASED OR NORMAL APPETITE –
CHARACTERISTIC
• OLIGOMENORRHEA OR AMENORRHEA
• ERECTILE DYSFUNCTION AND GYNECOMASTIA IN MALES
• HYPERDEFECATION

7. OTHERCONDITIONSTHATSUGGESTPOSSIBILITYOF
HYPERTHYROIDISM
• Osteoporosis
• Hypercalcemia
• Heart failure
• Premature atrial contraction
• Shortness of breath
• Deterioration of glycemic control in previously diagnosed
DM

8. SPECIFIC ORGAN SYSTEMS RELATED
SYMPTOMS
 SKIN
• Warm and smooth
• Sweating increases
• Onycholysis
• Hyperpigmentation
• Pruritus and hives
• Vitiligo and alopecia areata
• Thinning of the hair
 EYES
• Stare and lid lag
• Inflammation of extraocular
muscles and orbital fat and
connective tissue results in
proptosis
• Impairment of eye muscle function
and periorbital and conjunctival
edema
• Corneal ulceration ,optic
neuropathy and even blindness

9.  CARDIOVASCULAR
• Increase in CO
• Increase in heart rate and pulse
pressure is widened, PVR decreased
• Systolic hypertension is common
• High or normal output CHF in severe
hyperthyroidism and even worsens in
pts already have it
• True cardiomyopathy
• Atrial fibrillation
 METABOLIC/ ENDOCRINE
• Stimulates bone resorption
• Osteoporosis and increased fracture risk
• Thyroid acropachy
• Low serum total and HDL
• Increased insulin secretion and
antagonism to peripheral action of
insulin leads to glucose intolerance

10.  ADRENAL FUNCTION
• CBG levels decrese results in lower total
serum cortisol concentration
 RESPIRATORY
• Hypoxemia,hypercapnia stimulates
ventilation
• Dyspnea,redused exercise
capacity,decreased lung volume
• Tracheal obstruction due to large goitre
• Exarbates underlying asthma
• Pulmonary artery systolic hypertension
increased

11.  GASTROINTESTINAL
• Wt loss due to increased metabolic
rate
• Vomiting ,abd pain
• Dysphagia due to goiter
• Abnormality in LFT ,particularly
high serum alkaline phosphatase,
ALT and AST also raised
 TYHMIC ENLARGEMENT
• Seen in Graves’ disease
 HEMATOLOGIC
• RBC mass increased, plasma
volume increased more results in
normochromic,normocytic anemia
• Graves’ disease – ITP, pernicious
anemia, antineutrophil antibodies

12.  GENITOURINARY
• Urinary frequency and nocturia possible
cause primary polydipsia and
hypercalciuria
• SHBG high results in high serum
estradiol, high LH, reduced mid cycle
surgein LH
secretion,oligomenorrhea,anovulatory
infertility, amenorrhea.
• In men, gynecomastia,reduced libido,
erectile dysfunction, spermatogenesis
decreased or abnormal
 NEUROPSYCHIATRIC
• Behavioral and personality changes
such as psychosis, agitation, depression,
anxiety, restlessness, irritability,
emotional lability, insomnia, impaired
concentration, concentration, confusion,
poor orientation, immediate recall,
amnesia, constructional difficulties

13. IODINE IN TREATMENT OF
HYPERTHYROIDISM
• Acutely inhibits hormonal secretion within hours of the start of treatment
• WOLFF CHAIKOFF EFFECT – second effect inhibition of iodine organification in
thyroid gland, thereby diminishing thyroid hormone biosynthesis
• Used in short term for the following
 Preoperative preparation for thyroidectomy in graves’ disease
 Adjunctive therapy in graves’ disease
 Treatment of thyroid storm
• Long term therapy in mild disease,in those with thionamide intolerance and
contraindication to definitive treatment with initial or repeat radioiodine therapy or
surgery

14. IODINE PREPARATION
 Potassium iodide – 50 mg/drop orally
• 0.05 to 0.1ml TDS for 10 days in preop preparation of thyroidectomy in graves’ disease
• 0.25 four times daily for thyroid storm
• 0.15 twice daily BD mild hyperthyroidism that persists months after a dose of
radioiodine
 Potassium iodide- iodine solution
• 0.25 to 0.35 TDS for 10 days in pre op preparation for thyroidectomy in graves’ disease
• 0.5 ml TDS daily for thyroid storm

15. BETA BLOCKER IN TREATMENT OF
HYPERTHYROIDISM
• Ameliorate symptoms of hyperthyroidism caused by increased beta
adrenergic tone like palpitation, tachycardia, tremulousness, anxiety, heat
intolerance
• Started as soon as diagnosis is made and continue until resolution
• Propranolol in high dose
• Atenolol has advantage of single daily dosing start with 25 to 50 mg daily
and increase dose as needed

16. IODINATED RADIOCONTRAST IN
TREATMENT OF HYPERTHYROIDISM
• Ipodate and iopanoic acid marketed as oral cholecystographic agents
• Most potent inhibitor of 5’ – monodeiodinase impairing extrathyroidal
conversion of T4 to T3
• Used in conjuction with methimazole for treatment of severe
hyperthyroidism or thyroid storm
• Used as monotherapy in graves’, toxic adenoma, toxic mutinodular goiter

17. RADIOIODINE IN TREATMENT OF
HYPERTHYROIDISM
• Effective in Graves’ disease
• Administered orally as sodium iodide131-I in solution or capsule
• Rapidly incorporated in thyroid and its beta emissions result in extensive local
tissue damage
• Net effect is abalation of thyroid function over a period of 6 to 18 weeks
 INDICATION
I. Graves’ disease
II. Toxic adenoma or mutinodular goiter

18. CONTRAINDICATION
I. Pregnancy and breast feeding
II. moderate to severe thyroid eye disease

19. SURGICAL MANAGEMENT OF
HYPERTHYROIDISM
• Definitive therapy for hyperthyroidism varies with cause of disease and characteristics
of pt
 INDICATION
I. Graves’ disease with
 Pts with very large goiters [>80 grams]
 Goiter causing upper airway obstruction
 Non functional thyroid nodule with suspicious, indeterminate and positive cytology on
FNA
 Coexisting hyperparathyroidism who are surgical candidates for parathyroidectomy
 Moderate to severe graves’ ophthalmopathy in whom surgery is preferred over
radioiodine may exarbate graves’ ophthalmopathy

20. Pregnant women allergic to antithyroid drug and not tolerating hyperthyroidism
poorly have no alternative to surgery
Persistent hyperthyroidism despite treatment with antithyroid medication and
radioiodine
Toxic adenoma and toxic multinodular goiter
 CONTRAINDICATION
• Presence of substantial comorbidity, including cardiopulmonary disease or other
debilitating disease
• Surgery during pregnancy is associated with increased risk of spontaneous abortion
or premature delivery
• Pregnant women who require surgery because of inability to tolerate thionamides,
risk reduses during second trimester

21.  COMPLICATION
I. Wound infection, keloid formation
II. Transient or permenant hypothyroidism
III. Recurrent or superior laryngeal nerve palsy
IV. Transient vocal cord paralysis
V. Prolonged postoperative hypocalcemia
VI. Permenant hypoparathyroidism
VII. Recurrent hyperthyroidism

22. HYPERTHYROIDISM DURING PREGNANCY
• To meet increased metabolic needs during normal pregnancy, changes in
thyroid physiology reflected in altered TFT
TBG excess results in high serum total T4 and T3 but not free T4 and T3
Stimulation of TSHR by HCG during early pregnancy and even higher
concentration in hyperemesis gravidarum and multiple pregnancies results
in subclinical or overt hyperthyroidism

23. COMPLICATION
• Spontaneous abortion
• Premature labor
• LBW
• Stillbirth
• Preeclampsia
• Heart failure

24. TREATMENT
• Goal of treatment to maintain persistent but mild hyperthyroidism in mother in an
attempt to prevent fetal hypothyroidism since fetal thyroid is more sensitive to action of
antithyroid drugs
• Transient central hypothyroidism may be seen in infants whose mothers had poorly
controlled hyperthyroidism during pregnancy, presumably due to suppression of fetal
pituitary thyroid axis
• To attain goal of mild hyperthyroidism mother’s serum free thyroxine should be
maintained at or just above the trimester specific normal range for pregnancy or the
total T4 and T3 should be maintained at 1.5 times above the nonpregnant reference
range
• For attaining these goals requires assessment of thyroid function frequently at 4 week
intervals with appropriate adjustment of medication

25. • Most women are treated with thionamides
• Thyroidectomy in second trimester is an option for women who are unable to take
thionamides
• THIONAMIDES – primary treatment of hyperthyroidism due to graves’ disease, toxic
adenoma, toxic multinodular goiter
• BETA BLOCKER –Metoprolol or propranolol can be used to treat tachycardia and
tremor. Primary treatment for hydatidiform mole and gestational trophoblastic
neoplasia . long term treatment with this should be avoided because of chances of
hypoglycemia, fetal growth retardation especially with atenolol
• Plasmapheresis also used to rapidly control hyperthyroidism in trophoblastic disease
and severe hyperthyroidism

26. GRAVES’ DISEASE
• Accounts for 60- 80% of hyperthyroidism
• Occurs between 20 to 50 years of age
• Occurs in 2% of women but is one-tenth as frequent in men
• A combination of genetic and environmental factors , including polymorphism in HLA-
DR, immunoregulatory genes CTLA-4, CD25, PTPN22, FCRL3 and CD226 as well as
gene encoding TSH-R contributes to Graves’ disease
• Threefold increase in occurence of Graves’ disease in postpartum period, it may occur
during immune reconstitution phase after HAART or alemtuzumab, immune check
point inhibitor
• Caused by TSIs synthesized by lymphocytes in thyroid gland, bone marrow, lymph nodes
• TPO and Tg occurs in upto 80 % of case

27. • In old age fe,atures of thyrotoxicosis may be subtle or masked and patients
may present mainly with fatigue and weight loss condition known as
apathetic thyrotoxicosis
• Thyrotoxicosis is sometimes associated with a form of hypokalemic periodic
paralysis
• Graves’ opthalmopathy is characteristic, earliest manifestation is sensation
of grritiness, eye discomfort, excessive tearing

28. TREATMENT
CHOICE OF THERAPY - start with thionamide to achieve euthyroidism
quickly
Followed by abalative therapy with radioiodine or surgery,by continuation of
thionamide for one to two year or longer with hope of attaining remission