Hyperthyroidsm: Epidemiology

HYPERTHYROIDSM:
EPIDEMIOLOGY:
• Graves’ disease is the most common form of hyperthyroidism.

• Approximately 60-80% of cases of thyrotoxicosis.
• 0.5 cases per 1000 population during a 20-year period.
• Peak occurrence in people aged 20-50 years or above.
PATHOPHYSIOLOGY:
• Synthesis of thyroid hormone requires iodine. Disturbances of the normal homeostatic

mechanism (pituitary gland, thyroid gland, or periphery.) the result in an increase in
transcription in cellular proteins, causes an increase in the basal metabolic rate.
Basal metabolic rate is the amount of energy per unit time that a person needs to keep the
body functioning at rest. The basal metabolic rate accounts for about 60 to 75% of the daily
calorie expenditure by individuals.
• Thyroid hormones control the rate of many activities in the body. These include how fast you
burn calories and how fast your heart beats.
• If the thyroid is too active, it makes more thyroid hormones than your body needs. Thus leads to
HYPERTHYROIDSM.
CLINICAL EVLUATION:
RISK FACTORS:
• GRAVES’DISEASE
• Women
• Presence of other thyroid problems
• Enlarged thyroid gland
• Aged above 50 years old
• Family history
• Hx of chronic illness; T1DM and Pernicious anaemia
CAUSES:
Primary causes:
 Grave’s Disease
-autoimmune disorder
-B cells produce antibodies
-most common cause of Hyperthyroidism
- Autoimmune disorder, in which the body produces antibodies to the receptor for thyroid-
stimulating hormone.
 Toxic Nodular Goiter

-Follicles start generating lots of thyroid hormone
-involves an enlarged thyroid gland. The gland contains areas that have increased in size and
formed nodules. One or more of these nodules produce too much thyroid hormone.
 Jod-Basedow Syndrome
- Iodine-induced thyrotoxicosis
- is hyperthyroidism following administration of iodine or iodide,[1] either as a dietary
supplement or as iodinated contrast for medical imaging.
- In some ways the Jod-Basedow phenomenon is the opposite of the Wolff–Chaikoff effect,
which refers to the short period of thyroid-hormone suppression which happens in normal
persons and in persons with thyroid disease, when comparatively large quantities of iodine
or iodide are ingested.
 Hyperfunctioning Thyroid Adenoma

-Benign tumor making excess thyroid hormone
-a functional tumor, producing excessive thyroid hormone ("hot" adenoma). In this case, it may
result in symptomatic hyperthyroidism, and may be referred to as a toxic thyroid adenoma.
 Thyroiditis
- is the inflammation of the thyroid gland. The thyroid gland is located on the front of the neck
below the laryngeal prominence, and makes hormones that control metabolism.
 Neonatal hyperthyroidism
-in most cases is transient and results from the transplacental passage of maternal stimulating
TSH receptor antibodies (TRAb) known as neonatal Graves’ disease (GD).
- Large release of pre-formed thyroid hormones.
Other causes:
• Thyroiditis
• Intake of too much iodine
• Drug-induced; (Amiodarone, Levothyroxine (T4))
SIGNS AND SYMPTOMS:
 Hair loss  Heat intolerance  Infertility
 Bulging eyes  Irritability  Muscle weakness
 Sweating  Tremors of fingers  Weight loss
 Enlarged thyroid  Sleeping difficulty  Frequent bowel movement
 Rapid heartbeat  Warm moist palm  Soft nails
 Nervousness  Scant menstrual period
HYPERTHYROIDSM WITH HYPERGLYCEMIA:

• Worsening blood glucose control.
• Increased insulin requirements.
• Increased glucose production in the liver.
• Rapid absorption of glucose through the intestines thus increasing insulin resistance.
PATHOPHYSIOLOGY:
 Elevated Thyroid hormones Affects: Protein, Carbohydrate and Lipid metabolism.
 Protein= Synthesis and Degradation
Negative nitrogen balance

(Increase excretion of Nitrogen)
 Increasing Glucose tolerance leading to Hyperglycemia.
 Increased Fat metabolism (Lypolysis)
Signs and Symptoms:

1. May experience tremor in the body because of undetected overreactive thyroid
2. May confuse it with low sugar level.
3. Increases sugar intake to counterbalance suspected low glucose level
4. Leads to high sugar level, which may increase risk of complication.
Implication:
I. Diagnosis of Glucose intolerance need to be considered cautiously.
II. Underlying Hyperthyroidism should be considered in DM patients.
III. Should monitor for deterioration in glycemic control and Adjusting dose treatment
(Glucocorticoids).
Diagnosis:
• HIGHLY SENSITIVE IMMUNOASSAY
-Test for Serum TSH detection.
-TSH levels typically fall between 0.4 and 4.0 mU/L

MANAGEMENT:
• Radioactive Iodine (RAI) therapy
-no contraindication to the use of antithyroid medications in diabetic patients
-But long-term remission rate of Graves' disease is <40%.
-Regular screening for thyroid abnormalities in all diabetic patients will allow early treatment of
subclinical thyroid dysfunction.
• In Type 1 diabetic patients, it is helpful to determine whether anti-TPO antibodies are present.
-annual TSH screening is warranted. done every 23 years.
• In Type 2 diabetic patients, a TSH assay should be done at diagnosis and then repeated at least
every 5 years.
TREATMENTS: (Over All)
NON-PHARMACOLOGICAL:
•
Subtotal thyroidectomy (Graves’ disease)
-Partial removal of the thyroid gland.
-When drug therapy fails or if RAI is
Undesirable of contraindicated
• Avoid too much intake Iodine containing foods
PHARMACOLOGICAL:
THIOAMIDES
• Porpylthiouracil
• Methimazole
-Carbimazole (Podrug)
MOA: Both agents inhibit iodide oxidation and iodothiouracil coupling.
PTU METHIMAZOLE
Onset Fast Slow
Duration Short Long
Mostly Tx: Throid storms Maintenance

use
Adv/Disad For Pregnant woman (1st trimester) Teratogenic: Choanal and esophageal atresia
vanteges of fetus. Maybe cont. on 2nd trimester
A/E Agranulocytosis; Reversible Hepatitis Agranulocytosis; Cholestatic Jaundice

ANION INHIBITORS
 Perchlorate
-Peak plasma concentration: 3 hours.
-DOA: 6-8 Hours
-DOC: for type-1 Amiodarone-Induced Thyrotoxicosis
MOA: inhibits iodide uptake in the thyroid gland by competitively binding with NIS.
S/E: Aplastic anaemia
LITHIUM CARBONATE (IR/SR)

-Peak plasma concentration: 1-2 hours and 4-5 hours after administration, respectively.
-DOA: 18–36 hours
- Adjuvant Therapy for type-1 Amiodarone-Induced Thyrotoxicosis
MOA: inhibition of thyroid hormone release by inhibiting the action of TSH on cAMP and inhibit thyroid
hormone synthesis
S/E: Lithium clearance is considered to decrease with aging and renal impairment.
GLUCOCORTECOIDS
 Hydrocortisone
 Dexamethasone
- are commonly used as an adjuvant drug in the treatment of hyperthyroidism.
MOA: inhibitory effect on peripheral T4 to T3 conversion.
S/E: might include increased blood glucose, increased blood pressure, and suppression of immunological
response
IODIDES
 Strong Iodine solution (Lugol’s solution)
 Saturated solution of Potassiu Iodide
MOA: Prevents Organification of Iodine and prevents thyroid hormone release.
-WOLFF-CHAIKOFF EFFECT - auto regulatory phenomenon that inhibits organification in the thyroid
gland, the formation of thyroid hormones inside the thyroid follicle, and the release of thyroid
hormones into the bloodstream.
S/E: Iodism
Contraindication: Pregnancy and Lactations
- Fetal Goiter
RADIOACTIVE IODINE (RAI)

 Iodine-131 (Therapeutic)
 Iodine-125 (Diagnostic)
MOA: Emits Beta-Particles that’s destroys thyroid cell (Oxidation)
S/E: Late onset Hypothyroidsm
Contraindication: Pregnancy and Lactations
BETA-BLOCKERS
 Propranolol
-Provides symptomatic relief (Tachycardia, sweating, severe tremor and nervousness)
-Primary Adjunct therapy for RAI.
MOA: inhibits peripheral conversion of T4 to T3.
(At high doses)
CHOLESTYRAMINE
-It decreases enterohepatic circulation of thyroid hormone and can be used to control hyperthyroidism.
-Adjuvant Therapy of Graves’ Disease.
-Alternative Therapy of Hyperthyroidism
MOA: Decreases absorption of levothyroxine from the intestine.
S/E: bloating, flatulence, and constipation.

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HYPERTHYROIDSM:

• Graves’ disease is the most common form of hyperthyroidism.

• Synthesis of thyroid hormone requires iodine. Disturbances of the normal homeostatic

 Toxic Nodular Goiter

 Hyperfunctioning Thyroid Adenoma

- Large release of pre-formed thyroid hormones.

HYPERTHYROIDSM WITH HYPERGLYCEMIA:

Negative nitrogen balance

Signs and Symptoms:

-TSH levels typically fall between 0.4 and 4.0 mU/L

• Radioactive Iodine (RAI) therapy

-no contraindication to the use of antithyroid medications in diabetic patients

-But long-term remission rate of Graves' disease is <40%.

-annual TSH screening is warranted. done every 23 years.

TREATMENTS: (Over All)

Onset Fast Slow

Duration Short Long

Mostly Tx: Throid storms Maintenance

A/E Agranulocytosis; Reversible Hepatitis Agranulocytosis; Cholestatic Jaundice

LITHIUM CARBONATE (IR/SR)

RADIOACTIVE IODINE (RAI)

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