CLINICAL SCIENCE SESSION

THYROID
Rd. Sophia M
Helena Eka Putri
Asthia Ratna M
Merissa Auditanya

CRISIS

Control of thyroid function

(1) The classic hypothalamic- pituitary-thyroid axis,
(2) The pituitary and peripheral deiodinases,
modify the effects of T4 and T3;
(3) Autoregulation of hormone synthesis by the thyroid

land
(4) Stimulation or inhibition by TSH receptor

utoantibodies.

Effects of TSH on the Thyroid cell

Changes in thyroid cell morphology
Cell growth
Iodine metabolism
TSH stimulates all phases of iodide
metabolism,
Other effect of TSH
increased secretion of T4 and T3 from the
gland.
increased activity of type 1 5-deiodinase,
conserving intrathyroidal iodine.
Stimulation of glucose uptake, oxygen
consumption,

The serum level of TSH is about 0.5-5 mU/L;

it is increased in hypothyroidism and
decreased in hyperthyroidism

The Action of thyroid hormones

. The thyroid hormone receptor

Free thyroid hormones bind to a specific receptor in the cell nucleus.
Within the cell , T4 - T3 biological effect

. Physiologic Effects of Thyroid Hormones

-- on tissue growth, brain maturation,

-- increased heat production and oxygen consumption,
-- increased beta adrenergic receptors.

Effects on Oxygen Consumption,

Heat Production,
* increased basal metabolic rate
Cardiovascular Effects
improving cardiac muscle contractility.
Increase inotrophic and chronotrophic
Increase CO and HR
Increase sensitivity -adrenergic

Sympathetic Effects
number of beta adrenergic receptors
in heart muscle,
skeletal muscle,
adipose tissue
myocardial alpha adrenergic receptors.

Amplify catecholamine action at a posttreceptor

ite

Pulmonary Effects
The increased cellular demand for O2 in
hyperthyroidism
Increase oxygen consumption
increase erytropoetic= increase amount of red blood cell

Gastrointestinal Effects
Thyroid hormones stimulate gut motility
increased motility and diarrhea in hyperthyroidism.
Slowed bowel transit and constipation in
hypothyroidism.

Skeletal Effects

Thyroid hormones increase bone turnover

increasing bone resorption

Neuromuscular Effects
increase synthesis of many structural
proteins,
Hyperthyroidism protein turnover
and loss of muscle tissue myopathy.
speed of muscle contraction and
relaxation
hyperreflexia

Metabolism

Hyperthyroidism hepatic gluconeogenesis

and glycogenolysis
intestinal glucose
absorption
hyperthyroidism
will
exacerbating
underlying
diabetes mellitus.
Cholesterol synthesis and
degradation

Patients with thyroid disease will usually

complain of
1.thyroid enlargement, diffuse or nodular;
2.symptoms of thyroid deficiency
( hypothyroidism)
3.symptoms of thyroid hormone excess
( hyperthyroidism) or
4.complications of a specific form of
hyperthyroidism e.g Graves disease
* prominence of the eyes (exophthalmos)
and,
* thyroid dermopathy

Hyperthyroidism & thyrotoxicosis

Thyrotoxicosis = clinical syndrome that results when
tissues are exposed to high levels of
circulating thyroid hormone

due to hyperactivity of the thyroid gland,

hyperthyroidism

Conditions associated with thyrotoxicosis

1. Diffuse toxic goiter (Graves disease)
2. Toxic adenoma (Plummers disease)
3. Toxic multinodular goiter
4. Subacuta; thyroiditis
5. Hyperthyroid phase of Hashimotos thyroiditis
6. Thyrotoxicosis factitia

Diffuse Toxic Goiter (Graves Disease)

emales > males (5) : (1)

etween 20-40 years of age.

onsists of one or more of the following features :

(1) thyrotoxicosis,
(2) diffuse goiter,
(3) ophthalmopathy (exophthalmos), and
(4) dermopathy (pretibial myxedema).

Etiology
an autoimmune disease of unknown cause.
strong familial predisposition.

Pathogenesis
T lymphocytes sensitized to antigens within the
thyroid gland
stimulate B lymphocytes to synthesize antibodies to
these
antigents.
against the TSH receptor cell membrane
stimulate the thyroid cell
increased growth and function
(TSH-R Ab [stim]).

involve cytotoxic lymphocytes (killer

cells)
and cytotoxic antibodies
sensitized to a common antigen
found in
orbital fibroblasts,
orbital
muscle,

Clinical Features
A. Symptoms
* palpitations,
* nervousness,
* easy fatigability,
* hyperkinesia,
* diarrhea,
* excessive sweating,
* intolerance to heat,
* preference for cold.
* marked weight loss without loss
of appetite

thyroid enlargement,
B.*Signs
* thyrotoxic eye signs
tachycardia
skin : smooth, moist and warm
fine tremor of the fingers
* muscle weakness and
* loss of muscle mass (
myopathy)
* atrial fibrillation insensitive to

Gejala yang baru

terjadi
Dan bertambah
berat
Sesak pada kerja
Berdebar-debar
Lekas lelah
Lebih suka hawa
panas
Lebih suka dingin
Berkeringat banyak
Gugup
Nafsu makan
bertambah
Nafsu makan
berkurang
Berat badan
bertambah

INDEKS WAYNE
+

Tandatanda

Tiroid teraba
Bising pembuluh
Eksopthalmus
Retraksi palpebra
Kelambatan
palpebra
Hiperkinesis
Tremor jari
Tangan panas
Tangan lembab
Denyut nadi
sewaktu
< 80 / menit
80-90 / menit
> 90 / menit
Jumlah
Fibrilasi atrium
Nilai : 19 : toksik, 11 19 : Equivocal, < 11 : non
+1
+2
+3
-5
+5
+3
+2
+3
-3
-3

+3
+2
+2
+2
+1
+4
+1
+2
+1

-3
-2
-2
-1
-1

-3
+3
+4

toksik

Laboratory Findings
High FT4 + suppressed TSH (< 0,1 uU/L)

yperthyroidism.
+eye signs

sts.

diagnosis of Graves
disease can be made without further

Differential Diagnosis

Muscle atrophy / myopathy

DD/ primary neurologic disorder

Thyrotoxic periodic paralysis DD/ periodic paralysis

Patients with thyrocardiac

DD/ primary heart disease

Treatment of Graves
Disease
Management has been largely directed toward
controlling
the hyperthyroidism.
1. Blocking of hormone synthesis by antithyroid drug
therapy,
2. Partial ablation of the thyroid gland by surgery,
and
3. Destruction of thyroid cells by radioactive iodine
therapy.

A. Antithyroid Drug Therapy

The drugs (propylthiouracil or methimazole)

Started with large divided doses;

when the patient becomes clinically euthyroid,

maintenance therapy with a lower dose.

Propylthiouracil (PTU) also inhibits the conversion of T 4 to T3

Me thimazole longer duration of action

Could be given as a single daily dose

Duration of therapy
Can range from 6 months to 20 years or more.
Remission may be predicted in the following
circumstances;
1.if the thyroid gland returns to normal size;
2.if the disease can be controlled with
3.a relatively small dose of antithyroid drugs;
4.if TSH-R Ab [stim] is no longer detectable in
the serum; and
5.if the thyroid gland becomes normally
suppressible following the administration of
iodothyronine.

Reaction to antithyroid drugs

Allergic reactions
Agranulocytosis cessation of all
antithyroid
drug therapy.
shifting to an
alternative
therapy radioactive
iodine.

B.Surgical Treatment
Subtotal thyroidectomy treatment of choice for very
large
glands or multinodular
goiters.
The patient should be euthyroid
Starting 2 weeks before the day or operation,
saturated solution KJ is given to I hypervascularity

Complication to surgical
therapy
Hypothyroidism
Hypoparathyroidism
Recurrent laryngeal nerve injury

in about 1% of cases.

. Radioactive Iodine Therapy

Following the administration of radioactive
iodine,
the gland will shrink and
the patient will become euthyroid
over a period of 6-12 weeks.
The major compication of radioactive iodine
therapy
hypothyroidism

D. Other Medical Measures

Beta-adrenergic blocking agents are extremely
helpful.
Propranolol to control tachycardia,
hypertension, and
atrial fibrillation.

Adequate nutrition + including multivitamin

supplements

needed

Choice of Therapy
Choice of therapy will vary with
* the nature and severity of the
illness
* prevailing customs.
In the opinion of many authors :
1. Treatment with antithyroid drugs
2. Surgery
3. RAI

Complications
Thyrotoxic crisis (thyroid storm) is
- the acute exacerbation of all of the
symptoms of
thyrotoxicosis,
- often presenting as a syndrome that
may be of
life- threatening severity,
- has the mortality rate of 50%.

It may occur :

] After surgery,
] After radioactive odine therapy
] On parturition in a patient with
]
]
]
]
]
]

inadequately controlled
thyrotoxicosis
During a severe, stressful illness
Sever uncontrolled diabetes,
trauma,
acute infection,
severe drug reaction
myocardial infarction.

ical manifestations of thyroid crisis

arked hypermetabolism
xcessive adrenergic response
ver ranges from 38 to 41OC
sweating.
arked tachycardia,
atrial fibrillation
high pulse pressure
casionally with heart failure.

CNS symptoms : marked agitation,

restlessness,
delirium, and coma.
Gastrointestinal symptoms:
nausea,
vomiting
diarrhea, and jaundice.
A fatal outcome will be associated with heart
failure and shock.

Pathogenesis
binding sites for catecholamines
increases,
in heart and nerve tissues
sensitivity to circulating
catecholamines.

Treatment of Thyrotoxic Crisis

Thyrotoxic crisis requires vigorous management.
Propranolol, 40-80 mg every 6 hour orally,
Prophylthiouracil, 250 mg every 6 hours block
hormone synthesis (or methimazole in a dose of
60 mg
every 24 hours.)
After administration of an antithyroid drug
saturated
solution KJ 10 drops
twice
daily