DISORDERS OF

THYROID
FUNCTIONS
 NORMAL THYROID GLAND
 Actions of the thyroid
 Controls body temperature
 How body burns calories

 Controls how fast food

moves through digestive
tract
 Muscle strength

 Thyroid hormones:
 T3

 T4
 DIAGNOSTICS
 How do we diagnosis these disorders??
 Thyroid stimulation hormone (TSH) test
Normal levels of TSH are 0.4-
4.5milliunits/L. ( 0,3-5 ulU/ml )
 Thyroid hormone test
In adults, a normal total T3 level is 80-
230 ng/dL ( 75-200 ng/dl ). Total T4
levels should be at 5-14 mcg/dL.
( 4,5-11,5 mcg/dl )
 DISEASES OF THE
THYROID GLAND
Congenital diseases
Inflammation
Functional abnormality
Diffuse and Multinodular
goiters
NEOPLASIA
THYROID DISORDERS
 Hypothyroidism
 Underactive thyroid

 Hyperthyroidism
 Overactive thyroid

 Goiter
 Thyroid enlargement
CAUSES OF HYPERTHYROIDISM
1. Graves Disease – Diffuse Toxic Goiter
2. Plummer’s Disease – Toxic Mono Nodular Goiter
3. Toxic phase of Sub Acute Thyroiditis - SAT
4. Toxic Single Adenoma – STA
5. Pituitary Tumours – excess TSH
6. Molar pregnancy & Choriocarcinoma
7. Metastatic thyroid cancers (functioning)
8. Struma Ovarii ( Ovarian teratoma )
9. Iodine/thyroid hormone excess
 SIGNS AND SYMPTOMS OF HYPERTHYROIDISM

Hoarseness/
Nervousness/Tremor Deepening of Voice

Persistent Dry or Sore Throat

Mental Disturbances/ Irritability
Difficulty Swallowing
Difficulty Sleeping
Palpitations/
Bulging Eyes/Unblinking Stare/ Tachycardia
Vision Changes
Enlarged Thyroid (Goiter) Impaired Fertility
Weight Loss
Menstrual Irregularities
Heat Intolerance
Increased Sweating
Frequent Bowel Movements
Sudden Paralysis
Warm, Moist Palms

First-Trimester Miscarriage/ Family History of

Excessive Vomiting in Pregnancy Thyroid Disease
or Diabetes
 SYMPTOMS OF HYPERTHYROIDISM
 Diarrhea and weight loss
 Eye problems
 Enlarged thyroid gland
 Hair and skin changes
 Heat intolerance
 Heart palpitations
 Clubbing
 Menstrual cycle changes
 Muscle weakness
 Easily bruised
EMOTIONAL SYMPTOMS OF HYPERTHYROIDISM

 Nervousness/Tremor
 Restlessness

 Anxiety

 Irritability

 Sleeplessness or insomnia

 Exhaustion
 EpidEmiology of gravEs’ disEasE
- Cause of 50 – 80% of cases of hyperthyroidism
- Prevalence: 0.6% of population
- Incidence: 0.5/1000/year
- Female/male ratio: 5/1 – 10/1
- Incidence: 20 – 40 years of age
- Concordance rate: monozygotic twins 35%;
dizygotic twins 3%
- Predisposition: 79% genetic; 21% nongenetic
- Female siblings and female children have 5 – 8%
TRIGGER OF GRAVE , S DISEASE
1.Viral/bacterial infections
2.Stress
3.Smoke
4.Radiation
5.Exposure to iodide
6.Drug
Grave's Disease , toxic diffuse goiter,
Basedow , disease , struma difusa
It is hyperfunction of thyroid gland
due to autoimmune disease in which
autoantibodies called thyroid
stimulating immunoglobulins,
activate TSH receptors producing
excessive secretion of thyroid
hormones although TSH hormone
itself is low.
 MANIFESTATIONS
 Exophthalmos , diplopia, deterioration in hand
 writing , heat intolerance
 Increased BMR and heat intolerance.
 Cardiovascular symptoms ; tachycardia, arrhythmias
like .Atrial fibrillation, cardiac ischemia and high
cardiac output failure.
 Insomnia, irritability and hyperreflexia, nervousness
 Mentally and physically hyperactive
 Loss of weight and increase food intake., osteophorosis
 Malabsorbtion and diarrhea, sweating, muscle weaknes
 Dermopathy ( pretibial myxedema ) in a minority of
patients
 Dr. Mohamed Z Gad 1 February 2018

TRAb bind to TSH receptors in retro-orbital tissues, causing

infiltration of lymphocytes. This inflammatory response leads
to cytokine production that causes fibroblasts to
produce glycosaminoglycans, leading to ophthalmopathy.

Lid retraction and exophthalmos 15

• Fat
accumulation
behind eyes
• High TSH
• Patient
previously had a
thyroidectomy
PRETIBIAL MYXEDEMA
 Graves’ disease and thyroid stimulating hormone
receptor antibodies,TSHR antibodies .
Normal

In Graves’ disease,
the antibodies do
not destroy the
thyroid but act as if
they are TSH (i.e.,
they bind and
activate the TSH
receptor) (agonist)
(Anti) TSHR antibodies ( TSI, LATS )
- secreted by lymphocytes
in all patients with Grave’s
disease.
- It has the same action of TSH
on the thyroid gland.
- Can cross the placenta and
stimulate the fetal thyroid
gland.
Autoantibodies (IgG) can cross the placenta and affect the
fetus

Graves’ disease is an autoimmune form of

hyperthyroidism
Plasmapheresisis : the removal, treatment, and return
of (components of) blood plasma from blood circulation
 In severe case 
thyroid crisis ( fever ,
consciousness ↓ ,arrythmia
 death )
 LABORATORY
LABORATORY INVESTIGNATION
INVESTIGATION
Hyperthyroidism
Serum concentrations of:  Graves’ disease
TSH: undetectable or 
TSHRAb 


 FT4 : 
 FT3 :   Anti TPO antibodies
 TG antibodies 

T3-thyro toxicosis:
TSH: undetectable or 
FT3: 
FT4: ↔
 UNDER SECRETION OF THYROID HORMONES
(HYPOTHYROIDISM)
Defined as low free T4 level with a normal or high TSH.
Types of hypothyroidism
1- Primary : Thyroid gland dysfunction
Most common :
1- Congenital hypothyroidism (in neonates)
2- Chronic lymphocytic thyroiditis (Hashimoto`s thyroiditis)
Autoimmune disease of thyroid
Thyroid gland is enlarged
3- Iodine deficiency
4- Thyroid surgery
5- Radioactive iodine treatment

2- Secondary : Pituitary dysfunction (hypopituitarism due to

radiation therapy or destruction of the
pituitary)

3. Tertiary : Hypothalamic dysfunction

 ETIOLOGY
 1. CONGENITAL
 Hypoplasia
 Familial enzyme defects
 Iodine deficiency (endemic
cretinism)
 Intake of goitrogens during
pregnancy
 Pituitary defects
 Idiopathic
 2. ACQUIRED
 Iodine deficiency
 Auto-immune thyroiditis

 Thyroidectomy or RAI therapy

 TSH or TRH deficiency

 Medications (iodide & Cobalt)

 Idiopathic
 TIROIDITIS HASHIMOTO
 Hipotiroid karena proses imunologik
 Prognosis kurang baik krn proses
autoimun
 Lab :  T3 ↓ / T4 ↓

 TSH ↑
 anti peroksidase tiroid ( TPO )
antibodies positif
 Anti-TPO antibodies ( TPO ) are the most common anti-
thyroid autoantibody, present in approximately 90 % of
Hashimoto's thyroiditis, 75% of Graves' disease
TRAbs are present in 70 – 100 % of Graves' disease
so TRAbs are most commonly associated with
Grave ‘ disease
Thyroglobulin antibodies are specific for thyroglobulin, a
660kDa matrix protein involved in the process of thyroid
hormone production. They are found in 70% of Hashimoto's
thyroiditis, 60% of idiopathic hypothyroidism, 30% of
Graves' disease .TgAb (thyroglobulin antibody) is important
to test for in those who have thyroid cancer.
 CLINICAL FEATURES OF HYPOTHYROIDISM

Tiredness Puffy Eyes , puffy face

Forgetfulness/Slower Thinking Enlarged Thyroid (Goiter)

Moodiness/ Irritability
Depression
Inability to Concentrate
Thinning Hair/Hair Loss
Loss of Body Hair
Hoarseness/
Deepening of Voice
Persistent Dry or Sore Throat
Difficulty Swallowing
Slower Heartbeat

Dry, Patchy Skin Menstrual Irregularities

Weight Gain Infertility

Cold
Elevated Cholesterol Constipation
Muscle Weakness/
Family History of Thyroid Disease Cramps
or Diabetes
II. HYPOFUNCTION OF THE THYROID
GLAND
A.Myxedema (= hypothyroidism in
adults): It is caused by atrophy of the
thyroid gland as a result of disease
e.g. cancer and this type is called
primary hypothyroidism or caused by
lack of TSH secretion and this is
called secondary hypothyroidism.
 MANIFESTATIONS OF MYXEDEMA
 Dry yellow swollen skin.
 Decreased BMR.
 Decreased cardiac properties like decrease HR
and COP.
 Decreased mental functions with apathetic
look.
 Husky and slow voice.
 Increased blood cholesterol level.
 Depressed sexual functions
PATIENT WITH MYXEDEMA
 B- CRETINISM (HYPOTHYROIDISM IN CHILDREN)

 Itis commonly due to either maternal

iodine deficiency or congenital abnormality
in the thyroid functions.
 Manifestations:
 Delayed physical growth:
 Mental retardation: complete idiot.
 Sexual retardation
 General features: Swollen eye, depressed
nose and wide nostrils together with
protruded tongue and bulging abdomen.
Congenital Hypothyroidism
Cretinism
Stunted growth
Neurological /
cognitive
defects / mental
retardation
Infantile
appearance-
puffy face ,
protuberant
abdomen
 39

C. HASHIMOTO’S THYROIDITIS (HT)

 An autoimmune disease and associated with other
autoimmune disorders ( lupus, rheumatoid arthritis )
 Diffuse, non-painful thyroid enlargement
Most prevalent between 45 and 65 years of age
 More common in women than in men, with a female
predominance of 10:1 - 20:1.
 May occur in children and is a major cause of
nonendemic goiter in children
Diagnosis is made by detecting elevated
levels of anti-thyroid peroxidase antibodies
in the serum.
CYTOTOXIC T LYMPHOCYTE ( CTL )
CD = cluster of differentiation
 D. MULTINODULAR GOITER
ENDEMIC , SPORADIC , SIMPLE GOITER
 It reflects impaired synthesis of thyroid hormons
due to dietary iodine deficiency  TSH
hypertrophy & hyperplasia of thyroid follicular
cells  thyroid enlargement ( diffuse nontoxic
goiter), if I supplied or the demand decreased 
involution of follicular epithelial cells.
 Recurrant episodes of stimulation & involution
multinodular goiter, asymmetrically enlarged
gland, large size with focal cystic changes
fibrosis, haemorrhage & calcification
 SIMPLE GOITRE , ENDEMIC GOITRE ( GAKI =
GANGGUAN AKIBAT KEKURANGAN YODIUM )

 Hipotiroidi : paling sering di Indonesia

 Etiologi : tersering defisiensi yodium

(penduduk pegunungan)

 Klinis :  mudah lelah

 irama jantung ↓
 otot jantung lemah
 anemia, rambut rontok
 berat badan ↑
 menorrhagia
 impotensia
 Laboratory diagnosiS
44

IN HYPOTHYROIDISM
 Measurement of the serum TSH level is the
most sensitive screening test for this
disorder.
 The TSH level is increased in primary
hypothyroidism
 The TSH level is not increased in patients
with hypothyroidism due to primary
hypothalamic or pituitary disease.
 T4 levels are decreased
Clinical Picture of Simple Nodular Goitre
Three women of the himalayas with typical endemic
goiters.
 INVESTIGATIONS OF
GOITER

 ThyroidFunction
TSH ( 0.4 –5.0 mU/L)
Free T4 9.1 – 23.8 pM
Free T3 2.23-5.3 pM
 THYROID FUNCTION TESTS
1- Tests to establish whether there is
thyroid dysfunction
Thyroid hormone ( FT3 and FT4 )
in the serum / plasma , TSH , TRH , BMR
2- Tests to elucidate the cause of the
thyroid dysfunction,as for examples :
1. Thyroid autoantibodies : Anti
thyroglobulin, Anti thyroid peroxidase,
TSH receptor antibodies
2. Serum thyroglobulin
 THYROID FUNCTION TESTS
3. Thyroid enzyme activity
4. Biopsy of the thyroid
5. RAIU , Thyroid scanning , Perchlorate test
6. ECG, Serum cholesterol, Tendon reflexes
7. Thyroid ( T3 ) suppression test, TRH/TSH
stimulation test
5. Imaging : UG, CT scan, MRI
 EVALUATION TEST OF HYPOTHALAMUS ,
PITUITARY AND THYROID GLAND .
1. TRH/F TEST
1. HYPERTHYROID : RESPOND TRH TO TSH :
DECREASE OR NEGATIVE
2.TO DIFFER SECONDARY HYPOTHYROID AND
TERTIARY HYPOTHYROID .
3. PRIMARY HYPOTHYROID : IS NO VALUE
2. TSH STIMULATION TEST with R I U /
R A I U : TO DETERMINE THE ABNORMALITY
OF THYROID OR PITUITARY LEVEL
3. THYROID SUPPRESSION TEST
TO DETERMINE THYROID GLAND FUNCTION
4. TSH , FT3 and FT4 SERUM
51
 THERAPY
1. SURGERY
2. ISOTOP AMINISTRATION ( I 131 )
3. ANTI THYROID DRUG
A. TIOURASIL (TU), PROPYLTHIOURACIL(PTU),
KARBIMAZOL, THIOUREA , METHIMAZOLE :
INHIBIT PHASE : IODINATION, COUPLING
AND OXIDATION .
PTU DAN PROPANOLOL ALSO INHIBIT
A CHANGE T4 TO T3 IN PERIPHER.
B. KJ : INHIBIT HYDROLYSIS THYROGLOBULIN
STIMULATED BY TSH
C. THIOCYANATE DAN PERCHLORAT E ARE ABLE TO
COMPETE WITH IODIDE AT CONCENTRATION PHASE .
D. THIOCARBAMIDE INHIBIT PEROXIDASE ENZYME
QUESTION 1

• A woman, 43, presents with:

• weight loss over the last few weeks associated with an increase in

appetite

• sweating, exophthalmus and goitre

• What type of thyroid disease might you be expecting (hyper or

hypo)?

• Hyperthyroidism
QUESTION 1B

 What would you want to measure to

diagnose the hyperthyroidism?

 TSH, T3 and T4 levels in the

circulating blood ,called : a Thyroid
Function Test (TFT).
 This patient has:
Hypotha-
lamus TRH • Low TSH, high T3
and T4
• A history of
autoimmune
diseases
Anterior
• What is your
pituitary
primary differential?
TSH
Grave’s –
autoimmune
hyperthyroi -
Thyroid
dism
T3 T4
 LABORATORIUM FINDING
Laboratory findings in Graves disease
include :

1. Elevated free T4 and T3 levels

2. Depressed TSH levels

3.Thyroid-stimulating immunoglobulins

4. Radioactive iodine uptake is increased

diffusely
QUESTION 2

• A 37 year old man presents with:

• Weight gain (with poor appetite)

• Slow and lethargic

• Feeling cold

• What type of thyroid disease would you expect from these

symptoms?

• Hypothyroidism
 RADIOACTIVE IODIDE
The beta radiations of 131I destroy thyroid
parenchyma, so decreasing hormonal
release.

Advantages:
Easy administration (orally).
Effective.
It is not expensive.
Suitable for old ages and cardiac patients
with moderate to severe hyperthyroidism
and unfit to surgery.
 Adverse effects:
 As with iodine therapy, overdoses may cause
iodism (metallic taste, excessive salivation, with painful
salivary gland, diarrhea, productive cough, running
eyes & nose, sore throat and rashes mimic chicken-
pox).
Overdose is treated by large dose of sodium or
potassium iodide to compete with the radioiodine
uptake by the gland, and then hasten excretion by
fluids and diuretics.
Local pain & congestion at the site of the gland
Hypothyroidism
Malignant changes in the thyroid after many years

Contraindications: pregnancy, children and nursing

mother ( through placenta and milk )
 CONTRAINDICATIONS
1.Advanced thyroid carcinoma /
inoperable
2. Anaplastic thyroid carcinoma.
Cancer cells abnormal and difficult to
recognize . This type cancer is usually
very difficult to control because the
cancer cells tend to grow and spread
very quickly.
 Indications for 1 131

treatment
1. Severe thyrocardiac disease

2. Toxic nodular goiter

3. Adverse reaction to antithyroid drug

4. Relapse after 12 to 18 months of

antithyroid drug treatment
Indications for Thyroidectomy
1.Large goiter with compressive manifesta -
tions
2.Pregnant patient with adverse reaction to
antithyroid drug
3.Severe infiltrative eye disease
4. Recurrence after adequate therapy
5. Hyperthyroidism are difficult to control
with anti thyroid drugs
6. When T4 level > 70 p mol/L