Hyperthyroidism, Thyrotoxicosis, Grave's Disease with MCQs.pptx

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Learning Objectives
At the end of this session the learner will be able to
describe-
• Aetiology
• Clinical Features
• Management
Of Thyrotoxicosis and Hyperthyroidism

Learning Objectives
1. Introduction & History
2. Relevant Anatomy, Physiology
3. Aetiology
4. Pathophysiology
5. Pathology
6. Classification
7. Clinical Features
8. Investigations
9. Management
10. Controversies
11. Prevention
12. Guidelines
13. Take home messages

Hyperthyroidism
• It is a term reserved for disorder
that result in overproduction of
hormone by the thyroid gland.
• In hyperthyroidism the pathology
is in the thyroid gland itself.

Thyrotoxicosis
• Biochemical and physiological
manifestation of Excessive thyroid
hormone.
• Thyrotoxicosis need not be due to
hyperthyroidism
• But hyperthyroidism mostly
produce thyrotoxicosis.

Hyperthyroidism Vs thyrotoxicosis
No Hyperthyroidism Toxicosis without
hyperthyroidism
1, Grave’s disease Subacute thyroiditis
2, Toxic nodular goitre Ectopic functioning thyroid
3, Toxic adenoma Silent thyroiditis
4, Jod – Basedow’s
disease
Struma ovarii
5, Metastatic follicular
carcinoma
6, Trophoblastic tumours
7, Postpartum thyroiditis

• The Jod-Basedow effect (also Jod-Basedow
syndrome and Jod-Basedow phenomenon) is
hyperthyroidism following administration of
iodine or iodide, either as a dietary supplement
or as iodinated contrast for medical imaging.

Classification
• Primary hyperthyroidism,
• Graves’ disease is the most common cause
• Toxic multinodular goiter
• Toxic adenoma.
• Secondary hyperthyroidism.
• Pituitary adenoma, which secretes thyroid-
stimulating hormone (TSH)
• Thyrotoxicosis without hyperthyroidism
• Subacute thyroiditis
• Factitious hyperthyroidism (thyrotoxicosis factitia).

• Wolff-Chaikoff effect is an autoregulatory
phenomenon, whereby a large amount of
ingested iodine acutely inhibits thyroid
hormone synthesis within the follicular cells,
irrespective of the serum level of thyroid-
stimulating hormone

Thyroid Hormone Function
• Increased metabolism:
• Increased transcription of cell membrane Na+
/K+
-adenosine
triphosphatase (ATPase) → oxygen consumption
• Enhanced fatty acid oxidation and heat generation
• Gluconeogenesis ,, glycolysis, , lipolysis
• Growth and development:
• Protein synthesis
• Regulates cholesterol and triglyceride metabolism
• Affects brain , reproductive and bone development , and growth
• Interrelated actions with catecholamines
• :Thyroid hormones enhance responsiveness
to catecholamines (producing inotropic and chronotropic cardiac
effects).
• ↑ Expression of catecholamine receptors
• Regulates pituitary hormone synthesis (feedback loop)

Diffuse toxic goitre
(Grave’s disease)
• This disorder is known as Graves' disease after Robert
Graves, an Irish physician who described three
patients in 1835.
• It is an autoimmune disease with a strong familial
predisposition, female preponderance (5:1).
• Peak incidence between the ages of 40 to 60 years.
• Graves' disease is characterized by thyrotoxicosis,
diffuse goiter, and extrathyroidal conditions including
ophthalmopathy, dermopathy (pretibial myxedema),
thyroid acropachy, gynecomastia, and other
manifestations.

Aetiology
• Idiopathic
• Traumatic
• Infections /Infestation
• Neoplastic (Benign/Malignant)
• Congenital/ Genetic
• Nutritional Deficiency/excess
• Autoimmune
• Degenerative / lifestyle
• Iatrogenic
• Psychosomatic
• Poisoning/ Toxins/ Drug induced

Etiology, Pathogenesis, and Pathology
• The exact etiology of the initiation of the
autoimmune process in Graves' disease is
not known.
• Postpartum state, iodine excess, lithium
therapy, and bacterial and viral infections
have been suggested as possible triggers.
• Genetic factors also play a role-HLA-B8
and HLA-DR3 and HLADQA1*0501.

Etiology, Pathogenesis, and Pathology
• Some unknown factors Stimulate B lymphocytes,
which produce antibodies directed against the thyroid
hormone receptor.
• TSIs or antibodies that stimulate the TSH-R, as well as
TSH-binding inhibiting immunoglobulins or
antibodies have been described.
• The thyroid-stimulating antibodies stimulate the
thyrocytes to grow and synthesize excess thyroid
hormone, which is a hallmark of Graves' disease.
• Graves' disease also is associated with other
autoimmune conditions such as type I diabetes
mellitus, Addison's disease, pernicious anemia, and
myasthenia gravis.

Pathology
• Macroscopically, the thyroid gland in
patients with Graves' disease is diffusely
and smoothly enlarged, with a concomitant
increase in vascularity.
• Microscopically, the gland is hyperplastic,
and the epithelium is columnar with
minimal colloid present.
• The nuclei exhibit mitosis, and papillary
projections of hyperplastic epithelium are
common.

Demography
Incidence and Prevalence-

Demography
Incidence and Prevalence-
• Incidence of hyperthyroidism is estimated
between 0.05% and 1.3%

Demography
• Age-
• Graves disease predominantly affects those
aged 20-40 years
• Incidence increases with age.

Demography
• Sex- strong female preponderance, with
women being affected 5 to 10 times more
frequently than men.

Demography
• Race. White and Hispanic populations in
the United States have a slightly higher
prevalence .

Demography
• Temporal behaviour

Demography
• Temporal behaviour- Incidence is Rising.

Clinical manifestation
• Clinical features of thyrotoxicosis are
mostly due to
– An increase in the metabolic rate and
– Overactivity of the sympathetic nervous system
(i.e., an increase in the β-adrenergic “tone”).
• Thyroid hormone affects every tissue and
organ system; thus, hyperthyroidism will
have a constellation of symptoms.

Goiter
• Diffusely enlarged thyroid gland in Graves’
disease.
• Prominent nodule in TA
• Irregular with multiple nodules in TMG
• Usually smooth borders and nontender; t
• Tenderness suggestive of thyroiditis
• A bruit may be audible at the superior poles
of the gland due to increased blood flow
• .

Cardiovascular
• Tachyrrhythmias: atrial fibrillation
• Premature atrial contractions

Metabolism alterations
• Protein, carbohydrate, and lipid
metabolism:
– Increased basal metabolic rate
– Increased appetite
– Heat intolerance
– Severe cases have a decrease in tissue protein:
• Muscle wasting
• Weight loss
• Hypoalbuminemia
– Accelerated turnover of insulin and insulin
resistance.

Metabolism alterations
• Protein, carbohydrate, and lipid
metabolism:
– Increased lipolysis
• High levels of free fatty acids
• High glycerol levels
• Low cholesterol levels
• Calcium and phosphorus metabolism:
– Increased excretion of calcium and phosphorus
in urine and stool
– Demineralization of bone
– Increased total and ionized serum calcium
concentrations

Nervous system alterations
•

Nervous system alterations
• Sympathetic nervous system
and catecholamines
– Epinephrine and norepinephrine levels are not
increased.
– Thyroid hormones increase sensitivity
to catecholamines .
• Neuropsychiatric symptoms:
– Nervousness,Emotional lability
– Hyperkinesia, Insomnia
– Fatigue
– Mental disturbances in severe cases (manic
depressive, schizoid, and paranoid reactions)

Musculoskeletal alterations
• Weakness in proximal muscles of the limbs
• Muscle wasting (thyrotoxic myopathy)
• ↑ Bone resorption

Skin and hair symptoms
• Warm, moist skin (vasodilation)
• Easy blushing
• Palmar erythema
• Friable hair and nails, increased hair loss

Respiratory alterations
• Dyspnea
• Reduced vital capacity owing to muscle
weakness.

Gastrointestinal alterations
• Hyperdefecation
• Hypoproteinemia
• Increased ALT
• Hepatomegaly and jaundice in severe cases
• Liver failure in untreated Graves’ disease

Reproductive/hormonal alterations
• Delayed sexual maturation
• Low or absent menstrual flow
• Reduced fertility with a high risk
of miscarriage
• Decreased libido
• Gynecomastia.

Eye signs
• Lid retraction: Overactivity of sympathetic part of levator palpebrae superioris (Muller's
muscle)
• Exophthalmos
– Naffziger's test: Go behind the patient, extend the neck, see through the supraciliary ridge,
you can diagnose exophthalmos.
– Gifford's test: Test to differentiate exophthalmos from proptosis (where pathology is behind
the eyeball).Evert the upper eyelid. Impossible to do it in exophthalmos due to Muller's
muscle hyperactivity. This test is possible in proptosis
– Stallwag's sign - Staring look with infrequent blinking and wide palpebral fissures.
– Von Graefe's sign- Lid lag sign. Tested by asking the patient to look up and down many
times fixing the head, you can see the upper lid lags behind.
– Joffroy’s sign-Absence of wrinkling of forehead. The patient looks the roof of the room
without forehead wrinkling
– Dalrymple's Sign -Visible upper sclera due to lid retraction.
– Mebius sign-Inability to converge the eyeball.
– Jellinek's sign-Increased pigmentation of eyelids.
• Opthalmoplegia (malignant exophthalmos)-
• Weakness of ocular muscles due to edema and cellular infiltration of these muscles.
• Paralysis of superior rectus, inferior oblique and lateral rectus.On paralysis of these
muscles, patient is unable to look upwards and out-

Hyperthyroidism, Thyrotoxicosis, Grave's Disease with MCQs.pptx

Investigations
• Laboratory Studies
– Routine
– Special
• Imaging Studies
• Tissue diagnosis
– Cytology
• FNAC
– Histology
– Germ line Testing and Molecular Analysis
• Diagnostic Laparotomy.

Investigations
• Laboratory Studies
–

Diagnostic Studies
Imaging Studies
• X-Ray
• USG
• CT
• Angiography
• MRI
• Endoscopy
• Nuclear scan

Tests of Thyroid Function
Serum Thyroid-Stimulating Hormone (Normal 0.5–5
U/mL): Serum TSH levels reflect the ability of the anterior
pituitary to detect free T4 levels. Small changes in free T4
lead to a large shift in TSH levels (Inverse relation).
Total T4 (Reference Range 55–150 nmol/L) and T3
(Reference Range 1.5–3.5 nmol/L).
Free T4 (Reference Range 12–28 pmol/L) and Free T3
(3–9 pmol/L).
Thyroid Antibodies : Thyroid antibodies include anti-Tg,
antimicrosomal, or anti-TPO and thyroid-stimulating
immunoglobulin (TSI).

Diagnostic Tests
• Suppressed TSH with or without an elevated free T4 or T3
level.
• If eye signs are present, other tests are generally not needed.
• In the absence of eye findings, an 123
I uptake and scan should
be performed.
• An elevated uptake, with a diffusely enlarged gland, confirms
the diagnosis of Graves' disease
• It helps to differentiate it from other causes of
hyperthyroidism.
• Anti-Tg and anti-TPO antibodies are elevated in up to 75% of
patients.
• Elevated TSH-R or thyroid-stimulating antibodies (TSAb) are
diagnostic of Graves' disease and are increased in about 90%
of patients

Differential Diagnosis
• Diabetes, malabsorption
• Anxiety states:
• Menopause
• Phaeochromocytoma:
–

Management
• Graves' disease may be treated by any of
three treatment modalities—
- Antithyroid drugs
- Thyroid ablation with radioactive 131
I
- Thyroidectomy

Anti Thyroid Drugs
• Antithyroid medications generally are administered in
preparation for RAI ablation or surgery.
• The drugs commonly used are propylthiouracil (PTU,
100 to 300 mg three times daily) and methimazole (10
to 30 mg three times daily, then once daily).
• Both drugs reduce thyroid hormone production by
inhibiting the organic binding of iodine and the
coupling of iodotyrosines (mediated by TPO).
• PTU also inhibits the peripheral conversion of T4 to
T3, making it useful for the treatment of thyroid storm.
• PTU has a lower risk of transplacental transfer.

Anti Thyroid Drugs
• Side effects of treatment include reversible
granulocytopenia, skin rashes, fever, peripheral
neuritis, polyarteritis, vasculitis, and, rarely,
agranulocytosis and aplastic anemia.
• The catecholamine response of thyrotoxicosis
can be alleviated by administering beta-
blocking agents.
• Propranolol is the most commonly prescribed
medication in doses of about 20 to 40 mg four
times daily.

Radioactive Iodine Therapy (131
I)
• RAI forms the mainstay of Graves' disease treatment in
North America.
• The major advantages of this treatment are the avoidance
of a surgical procedure and its concomitant risks.
• The 131
I dose is calculated after a preliminary scan, and
usually consists of 8 to 12 mCi administered orally.
• After standard treatment with RAI, most patients
become euthyroid within 2 months.
• However, only about 50% of patients treated with RAI
are euthyroid 6 months after treatment, and the
remaining are still hyperthyroid or already hypothyroid

Radioactive Iodine Therapy (131
I)
• RAI therapy is therefore most often used in older
patients with small or moderate-sized goiters, those
who have relapsed after medical or surgical therapy.
• Contraindication :
Absolute : Women who are pregnant or
breastfeeding.
Relative : Young patients (i.e., especially children
and adolescents), those with thyroid
nodules, and those with
ophthalmopathy.

Surgical Treatment
• Surgery is recommended when RAI is contraindicated
(a) Have confirmed cancer or suspicious
thyroid nodules.
(b) Young.
(c) Pregnant or desire to conceive soon
after treatment.
(d) Severe reactions to antithyroid medications
(e) Large goiters causing compressive
symptoms.
(f) Reluctant to undergo RAI therapy.

Surgical Treatment
• What surgical Procedure ?
1) Near total thyroidectomy
2) Subtotal thyroidectomy
3) Total thyroidectomy
4) Hartley- Dunhill procedure
- Solely based on discretion of surgeon and
their experience.

Management of Ophthalmopathy
• Tight-fitting sunglasses.
• Saline eye drops
Exposure keratitis
 Saline gel or drops
 Taping eyelids closed with paper tape
before sleep.
 Goggles at night to keep the eyes moist

Management of Ophthalmopathy
• A medical emergency -Optic nerve
compression with early loss of color vision
and orbital pain>permanent vision loss.
• High-dose glucocorticoids
• Orbital decompression surgery
• Ocular radiation therapy.

Toxic MNG(Plummer's Disease)
• Toxic multinodular goiters usually occur in older
individuals, who often have a prior history of a
nontoxic multinodular goiter.
• Over several years, enough thyroid nodules become
autonomous to cause hyperthyroidism.
• Hyperthyroidism also can be precipitated by iodide-
containing drugs such as contrast media and the
antiarrhythmic agent amiodarone (Jodbasedow
hyperthyroidism).
• Symptoms and signs of hyperthyroidism are similar to
Graves' disease, but extrathyroidal manifestations are
absent.

Toxic MNG
• Blood tests are similar to Graves' disease
with a suppressed TSH level and elevated
free T4 or T3 levels.
• USG shows nodules.
• RAI uptake also is increased, showing
multiple nodules with increased uptake and
suppression of the remaining gland.
• Treatment – After adequately controlling
hyperthyroid state total thyroidectomy is
treatment of choice.

Toxic Adenoma
• Hyperthyroidism from a single hyperfunctioning nodule
typically occurs in younger patients who note recent growth
of a long-standing nodule along with the symptoms of
hyperthyroidism.
• Most hyperfunctioning or autonomous thyroid nodules have
attained a size of at least 3 cm before hyperthyroidism
occurs.
• Physical examination usually reveals a solitary thyroid
nodule without palpable thyroid tissue on the contralateral
side.
• RAI scanning shows a "hot" nodule with suppression the rest
of the thyroid gland. These nodules are rarely malignant.
• Surgery (lobectomy and isthmusectomy) is preferred to treat
young patients and those with larger nodules.

Thyroid Storm
• Thyroid storm is a condition of hyperthyroidism accompanied
by fever, central nervous system agitation or depression,
cardiovascular dysfunction that may be precipitated by
infection, surgery, or trauma.
• Beta blockers are given to reduce peripheral T4 to T3 conversion
and decrease the hyperthyroid symptoms.
• Oxygen supplementation and hemodynamic support should be
instituted.
• Non-aspirin compounds can be used to treat pyrexia and Lugol's
iodine or sodium ipodate (intravenously) should be administered
to decrease iodine uptake and thyroid hormone secretion.
• PTU therapy blocks the formation of new thyroid hormone and
reduces peripheral conversion of T4 to T3.
• Corticosteroids often are helpful to prevent adrenal exhaustion
and block hepatic thyroid hormone conversion.

Controversies
• Defining subclinical hyperthyroidism treatment thresholds,
especially in the elderly and postmenopausal women;
• Determining the optimal choice of anti-thyroid drugs (atds),
particularly methimazole vs. Propylthiouracil (PTU)
• Managing graves' disease during pregnancy
• Regarding thyroid-stimulating hormone receptor (TSHR)
antibody screening,
• Timing of treatments,
• Effects on the fetus and infant.
• Monitoring for adverse effects from atds, such as vasculitis
• Use of radioiodine treatment in children and adolescents.

Future
• Developing targeted immunotherapies to address the
autoimmune basis of graves' disease,
• Improving existing treatments like long-term antithyroid
drugs (atds),
• Exploring wearable devices
• Artificial intelligence for better diagnosis and
monitoring,
• Investigating the role of the gut microbiome and specific
environmental factors such as diet and infections to
prevent the disease's development.
• Emerging therapies also focus on
novel biologics targeting the tsh receptor and
combination treatments to achieve sustained remission.

MCQ
• Grave’s disease or Basedow’s disease is
due to-
(a) Hyperactivity of adrenal cortex
(b) Hypoactivity of the thyroid gland
(c) Hyperactivity of thyroid gland
(d) Hypoactivity of islets of Langerhans

MCQ
• Sometimes, the thyroid symptoms are
mistaken for which condition?
• (a) Menopause
• (b) Posttraumatic stress
• (c) Pregnancy
• (d) Crohn’s disease

MCQ
• Q3. Which of the following is/are the
symptoms of release of excess of T3 and T4
hormones?
• a) Anxiety
• b) Hair loss
• c) Nervousness
• d) All of the above

MCQ
• An autoimmune disease of thyroid tissue is
referred to as
• a) Graves’ Disease
• b) Thyroid cancer
• c) Thyroiditis
• d) None of these

MCQ
• Which of the following conditions marked
by the low TSH?
• a) Hypothyroidism
• b) Goitre
• c) Hyperthyroidism
• d) Thyroid Cancer

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