Hyperthyroidism
Thyrotoxicosis is defined as the state of
thyroid hormone excess
Hyperthyroidism is the result of excessive
thyroid function
Wolf Chaikoff Effect: Reduction in thyroid
hormone levels caused by ingestion of large
amount of iodine
It is an autoregulatory phenomenon that
inhibits organification in the thyroid gland,
the formation of thyroid hormones inside
the thyroid follicles, and their release into
the blood stream
Jod Basedow Effect is iodine induced
Hyperthyroidism typically presenting in a
patient with goitre
It occurs with comparatively small increases
in iodine intake, in people who have thyroid
abnormalities that causes the gland to
function without the control of pituitary
Causes
Primary
Graves' disease
Toxic multinodular goiter
Toxic adenoma
Functioning thyroid carcinoma metastases
Activating mutation of the TSH receptor
Struma ovarii
Drugs: iodine excess ( Jod-Basedow
phenomenon)
Secondary hyperthyroidism
TSH-secreting pituitary adenoma
Thyroid hormone resistance syndrome:
occasional patients may have features of
thyrotoxicosis
Gestational thyrotoxicosis
Thyrotoxicosis without hyperthyroidism
Subacute thyroiditis
Silent thyroiditis
Other causes of thyroid destruction:
amiodarone, radiation, infarction of
adenoma
Ingestion of excess thyroid hormone
(thyrotoxicosis factitia) or thyroid tissue
Clinical Features
Hyperactivity, irritability
Heat intolerance and sweating
Palpitations
Fatigue and weakness
Weight loss with increased appetite
Diarrhea
Polyuria
Oligomenorrhea, loss of libido
Tachycardia; atrial fibrillation in the elderly
Tremor
Goiter
Warm, moist skin
Muscle weakness, proximal myopathy
Lid retraction or lag
Gynecomastia
Thyroid-associated O
phthalmopathy
The onset occurs within the year before or
after the diagnosis of thyrotoxicosis in 75%
of patients but can sometimes precede or
follow by several years
The earliest manifestations are
sensation of grittiness
eye discomfort
excess tearing
proptosis
corneal exposure and damage
Periorbital edema
scleral injection
chemosis
diplopia
papilledema, peripheral field defects
permanent loss of vision
0 = No signs or symptoms
1=Only signs (lid retraction or lag), no
symptoms
2=Soft tissue involvement (periorbital
edema)
3=Proptosis (>22 mm)
4=Extraocular muscle involvement
(diplopia)
5=Corneal involvement
6=Sight loss
Thyroid Dermopathy
Occurs in <5% of patients with Graves'
disease
almost always in the presence of moderate
or severe ophthalmopathy
most frequent over the anterior and lateral
aspects of the lower leg (pretibial
myxedema)
skin changes can occur at other sites after
trauma
Typical lesion is a noninflamed, indurated
plaque with a deep pink or purple color and
an "orange-skin" appearance
Nodular involvement can occur
Rarely extend over the whole lower leg and
foot (elephantiasis)
Diagnosis
TSH
FT4
Thyroid Radionuclide Scan
Treatment
It is treated by
1) Reducing thyroid hormone synthesis
Antithyroid Drugs
2) Reducing the amount of thyroid tissue
radioiodine (131I) treatment
Thyroidectomy
No single approach is optimal and that
patients may require multiple treatments to
achieve remission
Antithyroid Drugs
Thionamides
1) propylthiouracil
2) Carbimazole
3) Methimazole
MOA:
Inhibit the function of TPO
Reduces oxidation
Reduces organification of iodide
Also reduce thyroid antibody levels
Doses:
Propylthiouracil: 100–200 mg TID/QID
Carbimazole / Methimazole: 10–20 mg
BID/ TID
Titrartion Regimen: The starting dose of
antithyroid drugs can be gradually reduced
as condition improves
Block-replace regimen: High doses may
be combined with levothyroxine
supplementation
Follow up
Thyroid function tests and clinical
manifestations are reviewed 3–4 weeks
dose is titrated based on F T4 levels
Side Effects
Rash
Urticaria
Fever
Arthralgia (1–5% of patients)
May resolve spontaneously or after
substituting an alternative antithyroid drug
Rare but major side effects
Hepatitis
SLE-like syndrome
Agranulocytosis (<1%)
Beta blocker
Propranolol / Atenolol
Dose: (20–40 mg every 6 h)
To control tachycardia
especially in the early stages before
antithyroid drugs take effect
Anticoagulation
Vitamin K antagonists should be considered
in all patients with atrial fibrillation
Digoxin
Radioiodine
Progressive destruction of thyroid cells
can be used as
Initial treatment
Relapses after a trial of antithyroid drugs
Small risk of thyrotoxic crisis
Minimized by pretreatment with antithyroid
drugs for at least a month before treatment
Antecedent treatment with antithyroid drugs
should be considered for all elderly patients /
cardiac problems,
To deplete thyroid hormone stores before
administration of radioiodine
Carbimazole or methimazole must be
stopped at least 3 days before radioiodine
administration to achieve optimum iodine
uptake
Propylthiouracil has a prolonged
radioprotective effect
Fixed dose based on clinical features such
severity of thyrotoxicosis
the size of the goiter (increases the dose
needed)
level of radioiodine uptake (decreases the
dose needed)
131I dosage generally ranges between 185
MBq (5 mCi) to 555 MBq (15 mCipatients
<40 years of age
Many authorities favor an approach aimed
at thyroid ablation (as opposed to
euthyroidism), given that levothyroxine
replacement is straightforward and most
patients ultimately progress to
hypothyroidism over 5–10 years
Side effects
Mild pain due to radiation thyroiditis 1–2
weeks after treatment.
Hyperthyroidism can persist for 2–3 months
before radioiodine takes full effect.
Adrenergic blockers or antithyroid drugs can
be used to control symptoms during this
interval.
Persistent hyperthyroidism can be treated
with a second dose of radioiodine, usually 6
months after the first dose
Absolute contraindications :
Pregnancy
Lactation
Presence of severe ophthalmopathy
requires caution, and some authorities
advocate the use of prednisone, 40 mg/d, at
the time of radioiodine treatment, tapered
over 2–3 months to prevent exacerbation of
ophthalmopathy
Surgery
Subtotal or near-total thyroidectomy
Indications:
Patients who relapse after antithyroid drugs
Who prefer this treatment to radioiodine
Some experts recommend surgery in young
individuals, particularly when the goiter is very
large.
Careful control of thyrotoxicosis with antithyroid
drugs, followed by potassium iodide (3 drops SSKI
orally tid), is needed prior to surgery to avoid
thyrotoxic crisis and to reduce the vascularity of
the gland
Major complications of surgery
bleeding,
laryngeal edema,
hypoparathyroidism, and
damage to the recurrent laryngeal nerve
Thyrotoxic crisis, or thyroid
storm
Rare, life-threatening exacerbation of
hyperthyroidism,
C/F : fever, delirium, seizures, coma,
vomiting, diarrhea, and jaundice
The mortality rate due to cardiac failure,
arrhythmia, or hyperthermia is as high as
30%, even with treatment.
It is usually precipitated by acute illness
stroke,
Infection,
trauma,
diabetic ketoacidosis
surgery (especially on the thyroid)
Radioiodine treatment of a patient with
partially treated or untreated
hyperthyroidism
Management
Intensive monitoring and supportive care,
identification and treatment of the
precipitating cause
measures that reduce thyroid hormone
synthesis
Large doses of propylthiouracil (600 mg
loading dose and 200–300 mg every 6 h)
should be given orally or by nasogastric
tube or per rectum
Stable iodide
Block thyroid hormone synthesis via the Wolff-Chaikoff
effect (the delay allows the antithyroid drug to prevent
the excess iodine from being incorporated into new
hormone)
Potassium iodide (5 drops SSKI every 6 h), or ipodate or
iopanoic acid (0.5 mg every 12 h), may be given orally
Propranolol
To reduce adrenergic manifestations
Dose: 40–60 mg orally every 4 h or
2 mg iv every 4 h
Additional therapeutic measures
Glucocorticoids (e.g., dexamethasone, 2 mg
every 6 h)
Antibiotics if infection is present
Cooling
Oxygen
Intravenous fluids
What is Thyrotoxicosis?
What is hyperthyroidism?
Most common cause of Hyper
What is wolf Chaikof Effect?
What is Jod Basedows Effect?
Name two features of Hyper
How will u investigate for Hyper
What are the treatment options?
Name 2 drugs for hyper?
What is Thyroid storm?