Fakultas Kedokteran dan

Ilmu Kesehatan
Universitas Muhammadiyah Makassar

Kuliah Blok Endokrin Metabolik

HIPOTIROIDISME
HIPOTIROIDISME – TIROIDITIS
ADDISON’S DISEASE
HIPOGONADISME
TIROIDITIS

Nurmila
DEPARTEMEN ILMU PENYAKIT DALAM
PROGRAM PENDIDIKAN S1 KEDOKTERAN
FAKULTAS KEDOKTERAN DAN ILMU KESEHATAN UNIVERSITAS MUHAMMADIYAH
MAKASSAR
 VISION AND MISSION OF MEDICAL FACULTY AND HEALTH SCIENCE

•Vision
To become a leading Faculty of Medicine and Health Sciences in 2025 that produces Islamic,
trusted and excellent graduates in the field of emergency medicine.

• MISSION
• Organizing Medical and Health Sciences Education with a student-centered learning approach based on
information technology to produce graduates who are Islamic, trusted and superior in the field of emergency.
• Carrying out research to develop science, technology, and innovation, especially in the field of emergency and Al-
Islam Kemuhammdiyahan.
• Carrying out community service through the application of various aspects of medical science and health science,
especially in the field of emergency and Al-Islam Kemuhammdiyahan in improving the degree of public health.
• Organizing Faculty governance and study programs based on “Internal Quality Assurance Standards”.
• Establishing cooperation with stakeholders at home and abroad to improve the quality of the catur dharma of the
Faculty of Medicine and Health Sciences, Universitas Muhammadiyah Makassar.
Learning Outcome
Mampu menjelaskan definisi dan etiopatogenenis
Addison’s disease
Mampu menjelaskan definisi dan etiopatogenesis
hipogonadisme male dan porfiria
Mampu menjelaskan diagnosis dan tatalaksana awal
pada hipotiroid
Mampu menjelaskan diagnosis dan tatalaksana awal
pada tiroiditis
Mampu menjelaskan diagnosis dan tatalaksana awal
cushing syndrome
ACTH Secreting Pituitary Adenoma
(Cushing Disease)

• Harvey Cushing à 1932

• ACTH hypersecretion à billateral adrenal hyperplasia
• Spontaneous hypercorticolism (Cushing syndrome).
• DD: Adrenocorticosteroid excess-Ectopic ACTH
syndrome, and adrenal tumors
• Onset insidious, usual 20 -40 y, F:M = 8:1, Ectopic
ACTH à M:F = 3:1
Clinical Features of Cushing disease
Central obesity violaceous striae
hypertension hirsutism
glucose intolerance acne
gonadal disfunction poor wound healing
moon facies fungal infection
Plethora osteopenia
 Diagnosis & Treatment of Cushing disease

• Diagnosis :
Basal plasma ACTH
• Treatment :
Surgical treatment: microsurgery
Radiotherapy: Conventional radiotherapy
Medical therapy: no drugs supresses pituitary ACTH secretion.
* Ketoconazole to inhibit adrenal steroid biosynthesis,
* Metyrapone, aminoglutethimide à reduce cortisol à hypersecretion
 CUSHING’S SYNDROME
Chronic glucocorticoid excess à symptoms & physical
features à Cushing’s Syndrome

Etiology :
o Iatrogenic CS : Chronic glucocorticoid therapy (most
commonly)
o Spontaneous CS :
ØPituitary (Cushing disease)
ØAdrenal adenoma
ØACTH secrt non pituitary tumor (ectopic ACTH Syndrome)
Etiology
ACTH-independent
- adrenal tumor
- exogenous
glucocorticoid

ACTH-dependent
- pituitary adenoma
- Ectopic tumor secrt
ACTH
 CUSHING’S SYNDROME
Classification
ACTH-dependent Pituitary
adenoma (Cushing disease) 70%
Nonpituitary neoplasma (ectopic ACTH)

ACTH-independent Iatrogenic
(glucocorticoid, megestrol acetat) Adrenal neoplasma
(adenoma, carcinoma) Hyperplasia adrenal
Factitious
Indicative of
Cushing
Syndrome
Cushing disease

Tumor producing
ACTH
small cell (oat cell)
bronchogenic carcinoma ,
carcinoid tumors of the
thymus, pancreas, or ovary;
thyroid medullary carcinoma
bronchial adenomas

Adrenal tumor
 ETIOLOGY DIAGNOSIS OF
CUSHING’S SYNDROME
Cushing’s syndrome established
ACTH IRMA

<5 pg/mL >10 ug/mL

CT adrenals MRI pituitary

Unilateral mass Bilateral enlargement IPSS Normal Abnormal

CRH test

Peak ACTH Peak ACTH IPS:P<1.8 IPS:P>2.0

<10pg/ml >20 ug/dL

Adrenal surgery Ectopic ACTH Pituitary Surgery

 CUSHING’S SYNDROME
CUSHING’S SYNDROME
Treatment :
Cushing’s disease
Microsurgery, Radiation therapy
Adrenal tumors
Unilateral adrenalectomy
Ectopic ACTH syndrome
Benign à surgical treatment
Malignant à Ketokonazole, metyrapone
Iatrogenic (Cushingoid)
Tapering off
Alternate day regimen
PSEUDO CUSHING’S SYNDROME

Obesity
Chronic alcoholism
Depression
Hirsutism Post adrenalectomy
Addison’s Disease
Secondary - Deficient pituitary ACTH
secretion
Patients receiving long-term steroid therapy, despite physical
findings of Cushing’s syndrome à Adrenal insufficiency
Prolonged pituitary - hypothalamic suppression + adrenal
atrophy secondary to the loss of endogenous ACTH
 Addison’s Disease
• Laboratorium :
Hiponatremia- hiperkalemia (classic)
Radiologis /CT Scan
• Diagnosis
Basal adrenokortical steroid àNormal
Rapid ACTH stimulation test
ACTH plasma
• Treatment:
Replacement therapy à cortisol + fluid replacement
HYPOTHYROIDISM
Hypothyroidism
• Epidemiology
• Most common endocrine disease
• Females >Males–8:1 • Disease Burden
•Often unsuspected and grossly under diagnosed
•90 % of the cases are Primary Hypothyroidism
•5% of the general population are Sub-clinically Hypothyroid
•15 % of all women > 65 yrs. are hypothyroid
•Detecting sub-clinical hypothyroidism in pregnancy is highly essential – order
for TSH and FT4 routinely in all pregnant women at the beginning of each
trimester
•All persons aged above 60 years – Order for TSH
•Easily treatable with oral Levo-thyroxine
 HYPOTHYROIDISM
Etiology
• Primary:Hashimoto thyroiditis, Radio active
iodine therapy for Graves’ disease, Subtotal
thyroidectomy, Excesive iodide intake, subacute
thyyroiditis, Iodide deficiency
• Secondary :
Hypopituitarism due to pituitary adenoma
• Tertiary : Hypothalamic disfunction (rare)
HYPOTIROIDISM
Clinical finding
• Incidence : Various causes depending geographic & enviromental
factors
• Hashimoto thyroiditis the most common cause of hyperthyroidism
• Newborn infants (Cretinism)
• Fatigue, coldness, weight gain, constipation, menstrual
irregularities, muscle cramps
HYPOTIROIDISM
• Physical findings:
Cool,rough, dry skin, puffy face and hands, ahoarse voice,
slow reflexes
Cardiovascular sign: bradycardia, diminished CO, low
voltage QRS, cardiac enlargement
Pulmonary function: Respiratory failure
Intestinal paralysis slowed , chronic constipation, ileus
Renal function. Decresed GFR, renal impairement
Anemia, Severe muscle cramp, parestesias, muscle
weaknes
CNS symptoms: fatigue, inability to concentrate
 Pituitary- thyroid relationships in primary
hypothyroidism
Hypothalamus
TRH
Dopamine Somatostatin

Pituitary

Tissues TSH

T3, T4

THYROID
Complication
1. Myxedema coma à end stage of untreated hypothyroidism,
Cause Radiotherapy in Graves’ Disease
2. Myxedema & Heart disease à CAD
3. Hypothyroidism Neuropsychiatric disease à depression, confuse,
paranoid, manic
 Treatment Hypothyroidism
• Levothyroxine (T4), not liothyronine (T3) because rapid absorption,
short half life, transient effect. Dosis T4, 1X in the morning to avoid
insomnia 0.05 mg-0.2 mg/d
• Mixedema comaà ICU, intubation & mechanical ventilation, Treat
infection, heart failure, IV drips with caution, levothyroxin IV
EXAMPLES OF THYROID DISEASES

1° Hypothyroidism Hyperthyroidism
www.hsc.missouri.edu/~daveg/thyroid/thy_dis.html
Complication
• Myxedema coma à end stage of
untreated hypothyroidism, Cause
Radiotherapy in Graves’ Disease
• Myxedema & Heart disease à CAD
• Hypothyroidism Neuropsychiatric
disease à depression, confuse,
paranoid, manic
1. Thyroiditis
• Inflammation of thyroid
• Three types:
• Acute: bacterial; pain, malaise, fever, dysphagia; treat with antibiotics
•Subacute: viral infection; fever, chills, dysphagia, pain, hard & enlarged gland;
treat symptoms; antivirals
•Chronic: (Hashimoto’s)- auto immune, invade thyroid with antibodies and
lymphocytes causing tissue destruction; treat with thyroid hormone
•• Administer thyroid hormones; surgery; promote comfort and teaching • Acut
Thyroiditis
•• Self-limited
• B-blockers for adrenergic Sign
Definition
• Thyroiditis à heterogenous group of inflamatory
disorders the thyroid gland
• Etiologies range from autoimmune to infectious
origins
• Clinical course à Acute, subacute, or chronic.
Can be euthyroid, transient phase thyrotoxicosis
and / or hypothyroidism. Painless or painfull
HASHIMOTO’S THYROIDITIS
- MCC of hypothyroidism in areas where iodine intake is adequate
Clinically:
•- seen predominately in middle-aged women
•- hypothyroidism with painless enlargement of the gland
•- may have transient thyrotoxicos is early on
•- familial predisposition,associated withHLA-DR3 or HLA-DR5 Pathogenesis:
- defective function of thyroid-specific suppressor T cells
•Þ emergence of helper T cells reactive with thyroid antigens
- helper T cells stimulate B cells to secrete antithyroid antibodies, directed
against:
thyroid peroxidase, TSH-receptors, iodine transporter, & thyroglobulin, etc.
- Thyroid injury is mediated by complement fixing cytotoxic antibodies, ADCC &
CD8+ cytotoxic cells
Sub-clinical
Hypothyroidism
• Chronic autoimmune thyroiditis
• Graves’ hyperthyroidism with
radioiodine, surgery
• Inadequate replacement therapy for
hypothyroidism • Lithium carbonate
therapy (for depressive illness)
Classification of thyroiditis
I. Autoimmune thyroiditis
Chronic autoimune thyroiditis
Hashimoto’s thyroiditis
Atrophic thyroiditis
Focal thyroiditis
Juvenile thyroiditis
Silent thyroiditis / Postpartum thyroiditis
II. Subacute thyroiditis
III. Acute suppurative thyroiditis
IV. Riedel’s thyroiditis
Terminology for Thyroiditis.

Type Synonim
Hashimoto’s thyroiditis Chronic lymphocytic thyroiditis
Chronic autoimmune thyroiditis
Lymphadenoid goiter
Painlesspostpartum thyroiditis Postpartum thyroiditis
Subacute lymphocytic thyroiditis
Painless sporadic thyroiditis Silent sporadic thyroiditis
Subacute lymphocytic thyroiditis
Painful subacute thyroiditis Subacute thyroiditis
de Quervain’s thyroiditis
Giant-cell thyroiditis
Subacute granulomatous
thyroiditis
Pseudogranulomatous thyroiditis
Hashimoto’s thyroiditis (Chronic thyroiditis)

Hakaru Hashimoto (1912) à 4

patients chronic disorder of the
thyroidà diffuse lymphocytic
infiltration, fibrosis,
parenchymal atrophy, and
eosinophilic change in some
acinar cells

Dr Hakaru Hashimoto
Hashimoto’s thyroiditis
Hashimoto thyroiditis
is the most common
cause of hypothyroidism
& goiter
in the United States
Statosky J et al. Am Acad of Family physicians 2000;61:1054
 Hashimoto’s thyroiditis
Etiology & pathogenesis
HT is immunologic disorder which lymphocytes become
sensitized to thyroidal antigens and autoantibodies are
performed.
Thyroid antibodies in HT are:
1. Thyroglobulin antibody (Tg Ab)
2. Thyroid peroxidase antibody
(TPO Ab) = Microsomal antibody) 3. TSH
Receptor blocking antibody
(TSH-R Ab block)
 Clinical Manifestation
Hashimoto’s Thyroiditis
Symptom & Signs
HT usually presents with
goiter , euthyroid or mild
hypothyroidism.
Sex distribution : F/M 4:1
Painless & patients may be
anware of the goiter
Laboratory findings
•T4 N/ low, TSH will be elevated.
RAIU may be high, normal or low
•Tg Ab & TPO Ab positif
•Fine needle aspiration biopsy à
large infiltration lymphocytes à
Hurttle cells
 Diagnostic procedures
• Test of thyroid autoimmunity:
TPOAb à 95% + in Hashimoto thyroiditis & 90%
Atrophic thyroiditis
TgAb à less frequently +
Diagnostic specificity of thyroid
\antibody tests is not absolute.
• Test for thyroid function TSH, fT4
• RAIU: normal, low or high.
• USG:diffusely reduced echogenecity.
• FNAB not necessary,excep. rapidly enlarging goiter
Diagnosis of Hashimoto’s thyroiditis
Diffuse goiter
Anti microsomal (or TPO) antibody
Anti-thyroglobulin antibody Positive

Sign symptom of
hypothyroidism
Hashimoto’s
Negative thyroiditis

US Biopsy Positive
*Simple goiter,
adenomatous goiter etc

Negative Other diseases*

Treatment Hashimotos
thyroiditis
Treatment
• Goiter small & asymptomatic not require
therapy
• Levo-thyroxine is given over
hypothyroidism to supress TSH &
decreased serum thyroid antibody. Levo-
thyroxine in euthyroid, still controversial
Treatment
• Corticosteroids : regression pain,
reduction in size of the goiter, thyroid
antibody, not recommended in benign
disease.
•Surgery indicated pain, cosmetic,
or pressure symptoms after
levothyroxine and corticosteroid
therapy.
 Riedel’s thyroiditis
• Rare 1,06/100.000, middle age or elderly women
• Etiology unknown (autoimmune process or primary
fibrotic disorder)
• Characterized à fibrosis replaces normal thyroid
parenchyma,1/3 casesà multifocal fibrosclerosis
Riedel’s thyroiditis
• Thyroidà fibrosis (stony hard,woody), painless,
progressive anterior neck mass,
• Generalized fibrosing (1/3 patients), pressure
symptoms à laryngeal nerve paralysis or
hypoparathyroidism (rare)
• Usually euthyroidism, hypothyroidism (30%)
• Laboratorium : non spesific
• USG/CT-Scanà inconclusive
• Difinitive diagnosis à open Biopsy
Riedel’s thyroiditis
• Treatment:
Corticosteroids à medical treatment of choice
Tamoxipen, methotrexate à inhibitor fibroblast
proliferation ( early stages)
Levothyroxine à hypothyroidism
Surgical care à diagnosis, relieving tracheal
compression
• Mortality à asphyxia (6-10%), extrathyroidal fibrotic
lesions may complicate the prognosis
Subacute thyroiditis
• Cause unknown ( viral infection (?)
preceded URT infection, coincidence
viral disease (mumps, measles, Echo
virus, adeno virus, epst. Barr virus,
influenza)
• Women : Men (3-5:1)
• Onset: 20-60 yr
• Summer
Subacute thyroiditis
• Palpation thyroid: enlarged, asymetrical, nodul,
firm, tender & painful.
• Thyrotoxicosis during inflamatory phase à
euthyroidismà hypothyroidismà euthyroidism
(4th phases)
• Laboratorium: ESR increase, leukocyt N/ increase,
fT4,,TSH, RAIU
• Recovery 4-6 months, spontaneous remitting
 Treatment Subacute thyroiditis
• Symptomatic: Acetaminophen 4X 0,5g, NSAID or
glucocorticoid (prednison 3 X 20 mg (7-10 days)
• Betablockers à symptoms of thyrotoxicosis
• L-thyroxine 0.1-0.15 mg /daily à hypothyroid phase.
Long-term L-thyroxine à permanent hypothyroidism
(10%)
• Antibioticsàno value
• Thyroidectomy à rarely
 Clinical Differentiating of the Subtype Thyroiditis

NECK PAIN

YES N0

RAIU PRESENTING SYMPTOMS

INCREASED DECREASED HYPERTHYROIDISM HYPOTHYROIDISM

CHRONIC
MICROBIAL SUBACUTE RAIU LYMPHOCYTIC
INFLAMMATORY GRANULOMATOUS THYROIDITIS
THYROIDITIS THYROIDITIS

GRAVES DISEASE SUBACUT

LYMPHOCYTIC
THYROIDITIS

Statosky J et al. Am Acad of Family physicians 2000;61:1054

 Acute suppurative thyroiditis

• Rare, serious, bacterial inflamatory

disease, children, 20-40 yr, sex ratio 1:1
• Etiologi: Infectious: Staph. aureus,
strep.pyogenes, strep. pneumonia,
esch.coli, pseudomonas aeruginosa
• Infection by hematogenous, direct trauma
 Symptoms & signs
• Neck pain, warm, tenderness, the neck
unable to extend
• Dysphagia, dysphonia, referred to ear,
mandibula, lymphadenopathy
• Systemic manifestation: fever, chills,
tachycardia, malaise
• Palpation: unilateral, erythematous
 Acute suppurative
thyroiditis
• Thyroid function : Euthyroidism
• Laboratorium :TPO antibodies absent, ESR
high, PMN leukocytosis
• 24-hour 123I uptake normal
• FNA Biopsy: purulent material
• Treatment: antibiotics or surgical
drainage
 MALE HIPOGONADISME
Ø Hypogonadism is often heralded by decreased sex drive, reduced frequency of sexual
intercourse or inability to maintain erections, reduced beard growth, loss of muscle mass,
decreased testicular size, and gynecomastia.
Ø Less than 10% of patients with erectile dysfunction alone have testosterone
deficiency.Thus, it is useful to look for a constellation of symptom and signs suggestive of
androgen deficiency. Except when extreme, these clinical features may be difficult to
distinguish from changes that occur with normal aging.
Ø Moreover, androgen deficiency may develop gradually. Population studies, such as the
Massachusetts Male Aging Study, suggest that about 4% of men between the ages of 40
and 70 have testosterone levels <150 ng/dL. Thus, androgen deficiency is not uncommon.
Ø When symptoms or clinical features suggest possible androgen deficiency, the laboratory evaluation is initiated
by the measurement of total testosterone, preferably in the morning A total testosterone level <200 ng/dL
measured by a reliable assay, in association with symptoms, is evidence of testosterone deficiency. An early-
morning testosterone level >350 ng/dL makes the diagnosis of androgen deficiency unlikely. In men with
testosterone levels between 200 and 350 ng/dL, the total testosterone level should be repeated and a free
testosterone level should be measured.

v MALE CAUSES Known causes of male infertility include primary

testicular disease, disorders of sperm transport, and hypothalamic-
pituitary disease resulting in secondary hypogonadism.
v However, the etiology is not ascertained in up to half of men with
suspected male factor infertility.
v The key initial diagnostic test is a semen analysis.
v Testosterone levels should be measured if the sperm count is low
on repeated examination or if there is clinical evidence of
hypogonadism.
Reference
• Buku ajar Ilmu Penyakit Dalam ed 6. bab Hipotiroid. Perhimpunan dokter ahli
penyakit dalam Indonesia. 2014
• Konsensus tatalaksana hipotiroid Perkeni 2011
• Power C E. Reproductive male dysfunction . Endocrinology Harrison. Chapter
8. 2003
• Video Pembelajaran Male hypogonadisme :

https://www.youtube.com/watch?v=Z9XJeibntZg&pp=ygUZbWFsZSBoeXBvZ29u
YWRpc20gb3Ntb3Npcw%3D%3D
JAZAKUMULLAH KHAIRAN