HYPERTHYROIDISM

Muhammad Kautsar
10711181
Kepaniteraan Klinik Ilmu Penyakit
Dalam
RSUD dr. Soediran M.S.

Normal Thyroid State

Synthesis

and release of thyroid

hormone is controlled by TSH
relaesed form the anterior
pituitary
TSH is controlled by the release
of thyroid releasing hormone
(TRH) from the hypothalmus and
a negative feedback loop to the
pituitary
Thyroid hormone production s
dependent on adequate

Normal Thyroid State

Thyroid

hormone is reversible bound

to various proteins including
thyronine-binding globulin (TBG)
Free unbound portions are
biologically active
T4 is the predominant circulating
hormone
T4 is deiodinated to t3
T3 is biologically more active than T4
but has a shorter half-life

H-P
Thyroid
Axis

Thyrotoxicosis
Defined

as the
clinical,physiologic,and
biochemical findings that result
when the tissues are exposed
to,and respond to,excess thyroid
hormone.
Rather than being a specific
disease,thyrotoxicosis can
originate in a variety of ways.
RAIU is subnormal

Hyperthyroidism
Denotes

only those conditions in

which sustained hyperfunction of
the thyroid gland leads to
thyrotoxicosis.
Increased RAIU is the hallmark.

Varieties of Thyrotoxicosis
Associated

with

thyroid
hyperfunction:
Excess production of
TSH(rare)
Abnormal thyroid
stimulatorEg:Graves disease
Intrinsic thyroid
autonomyEg:Hyperfunctioning
adenoma, Toxic
multinodular goitre

Not

associated with
thyroid
hyperfunction:
Disorders of hormone
storage-Eg:Subacute
thyroiditis, chronic
thyroiditis
Extrathyroid source
of hormoneThyrotoxicosis
factitia,ectopic
thyroid tissue- struma
ovarii, functioning
follicular Ca.

Waynes Index

Hyperthyroidism
Graves disease
Also

known as Parrys or Basedows

disease.
Graves disease is a disorder with
three major manifestations:
1)Hyperthyroidism with diffuse goitre
2)Ophthalmopathy and
3)Dermopathy.
These three manifestations may not
appear together.

Incidence and prevalence

Relatively

common disease that can

occur at any age
More common in the 3rd and 4th
decade
Disease is more frequent in
women(7:1)
Genetic factors play a important role
An overlap exsists with other
autoimmune diseases suggesting
Graves is also a autoimmune thyroid
disease

Etiology and Pathogenesis

Cause

of Graves is unknown
No single factor is responsible for the entire
syndrome
With respect to hyperthyroidism,the central
disorder is a disruption of homeostatic
mechanisms that normally control hormone
secretion.This disruption results from the
presence in the plasma of thyroid
stimulating immunoglobulins(TSIs) of IgG
class and inhibition of the binding of TSH to
its receptors(TBIIs).These factors represent
TRAbs.

Pathology
Thyroid

gland is diffusely enlarged,soft

and vascular.
There is parenchymatous hyperplasia and
hypertrophy with lymphocytic infilteration.
The ophthalmopathy is characterized by
an inflammatory infilterate of the orbital
contents,with lymphocytes,mast cells and
plasma cells
The dermopathy of Graves disease is
characterized by thickening of the
dermis,which is infilterated by
lymphocytes and mucopolysaccharides

Clinical features
The

clinical manifestations include

those that reflect the associated
thyrotoxicosis and those specifically
related to Graves disease

Clinical features of thyrotoxicosis

Neuromuscular:
Nervousness,irritability,emotional

liability,psychosis
Tremor
Hyperreflexia,ill sustained clonus
Muscle weakness,proximal
myopathy,bulbar myopathy
Reproductive:Amenorrhoea,Oligome
norrhoea
Infertility,impotence

Thryotoxicosis..
Gastrointestinal:
Weight

loss despite increased appetite

Hyperdefecation
Diarrhoea and steatorrhoea
Vomiting
Cardiorespiratory:
Palpitations,Sinus tachycardia,Atrial
fibrillation
Increased pulse pressure
Dyspnea on exertion
Angina,cardiomyopathy and heart
failure

Thyrotoxicosis..
Others:
Heat

intolerance
Increased sweating
Fatigue
Gynaecomastia
Palmar erythema, Onycholysis

Manifestations of Graves
disease
The

distinctive manifestationsdiffuse hyperfunctioning

goiter,ophthalmopathy,and
dermopathy-appear in varying
combinations,and in varying
frequencies,goiter being the most
common.
Premature greying of hair and
patchy vitiligo are non specific
features of Gravess

Goiter
Is

diffuse and toxic and maybe

asymetric and lobular.
There may be presence of bruit
over the goiter

Ophthalmopathy
Signs

of Gravess ophthalmopathy are

divided into two components:
1) Spastic: Stare, lid lag and lid
retraction which account for the
frightened facies.
2) Mechanical: Proptosis of varying
degrees,ophthalmoplegia,and
congestive occulopathy characterized
by chemosis,conjunctivitis,periorbital
swelling and the potential
complications of corneal
ulceration,optic neiritis and optic
atrophy.

Dermopathy
Usually

occurs over the dorsum of the legs or

feet and is termed localized or pretibial
myxedema.
It is usually a late phenomenon
The affected area is usually demarcated from
the normal skin by being raised andthickened
and having a peau d orange appearance;it
may be pruritic and hyperpigmented.
The most common presentation is non pitting
oedema,but lesions maybe plaque
like,nodular or polypoid.
Clubbing of the fingers and toes accompanies
and is termed thyroid acropachy

Investigations
Thyroid

function test:
TSH- Undetectable
T4 - Raised
T3 - Raised
RAIU- Raised
TSH-receptor antibodies(TRAb)elevated in Gravess disease
Isotope scanning- Increased uptake

Other non specific

findings
Hepatic

dysfunction- Raised

AST,ALT
Mild hypercalcemia
Glycosuria- Associated diabetes
mellitus

Treatment of
Hyperthyroidism
H Y P E R T H Y R O ID IS M
T y p e t it le h e r e
M E D IC A L

S U R G IC A L

IO D IN E

A n ti t h y r o id d r u g s
B e ta b lo c k e r s

S u b t o t a l t h y r o id e c t o m y

R a d io a c t iv e io d in e
L u g o l's s o lu tio n

Anti thyroid drugs

Chemically

block hormone synthesis

Enhance evolution to remission
Best indicated for
children,adolescents,young adults and
pregnant women.
Propylthiouracil-100-150mg every 6or
8 hrs

Duration of treatment
18-24

months
Side effects- Rash
Leukopenia
Agranulocytosis

Control of adrenergic
symptoms
Adrenergic

antagonists:
Propranolol-40-120mg/day

Complications of
thyrotoxicosis
1)Cardiac- Heart failure
Atrial fibrillation
2)Thyrotoxic

crises: or storm:
Fulminating increase in signs and
symptoms of thyrotoxicosis.
Occurs in medically untreated or
inadequately treated patients.May be
precipitated by surgery or sepsis
The syndrome is characterized by extreme
irritability,delirium or coma,fever 41C or
more,tachycardia,restlessness,hypotensio
n,vomiting and diarrhea.

Treatment of thyroid crisis

Provide

supportive care;
Treat dehydration
Administer glucose and saline
Vitamin B complex and glucocorticoids
Digitalization is required in those with
atrial fibrillation
Immediate and large doses of anti
thyroid agents(Eg-propylthiouracil
100mg every 2h)
Iodine intravenously or by mouth
Propranolol 40-80mg every 6h
Dexamethasone(2mg every 6h) and to
be tapered later.