HYPOTHYROID

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Hypothyroid

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SGD 01
Atomi Of The Thyroid Gland
ORGAN GLANDULA PARATHYROIDEA :
It is an endocrine gland located on the posteromedial
aspect of the thyroid gland. This gland produces
parathyroid hormone (parathormone / PTH) which works
to control calcium levels in the blood.
Locations :
The parathyroid glands are attached posterior to the thyroid gland,withim the pretracheal fascia. The
parathyroid gland is located at the level of the lower edge of the cricoid cartilage or 1cm above the
entrance of the inferior thyroid artery to the thyroid gland, whereas the inferior parathyroid gland is
usually close to the inferior pole of the thyroid gland. The superior paeathyroid gland is more stable
than the inferior.

MORPHOLOGY:
The parathyroid glands are 4 in number, oval in shape, yellowish brown in color, about 6mm in size.

Part : Lobus superior dextra, lobus superior sinistra, lobus inferior dextra, and lobus inferior sinistra.
Structure : Fascia pretrachealis.
ORGAN : GLANDULA THYROIDEA

BAGIAN ORGAN:
• Lobus dextra glandula thyroidea
• Lobus sinistra glandula thyroidea
• Lobus pyramidalis glandula thyroidea (variasi
anatomi)

STRUKTUR:
• Isthmus glandula thyroidea (connects lobus
dextra dan sinistra).
• Fascia pretrachealis (wrap glandula thyroidea
with trachea, oesophagus, and pharynx).
Thyroid Gland
Regulation
● Proses hormon endokrin dari kelenjar tiroid dikendalikan oleh mekanisme umpan balik
negatif yang melibatkan hipotalamus dan kelenjar hipofisis anterior otak. Jika tubuh
mengalami penurunan kadar triiodothyronine dan tiroksin dalam plasma darah. Maka
hipotalamus akan menerima sinyal untuk mengeluarkan hormon pelepas tirotropin atau
TRH. Hormon tersebut kemudian akan mengaktifkan kelenjar hipofisis anterior untuk
melepaskan hormon perangsang tiroid (TSH) yang dikirim dan masuk ke kelenjar tiroid.
Hormon TSH akan merangsang kelenjar tiroid untuk memproduksi
hormon triiodothyronine dan tiroksin.
Etiologi
Hypothyroid
ETIOLOGI
Hypothyroidsm can be classified as hypothyroidism primary,
secondary and tertiary. Primary hypothyroidism is caused bt
thyroid fails to produce thyroid hormone, whereas hypothyroidism
secondary to a deficiency of the hormone TSH produced by the
pituitary. Tertiary hypothyroidism is caused by TRH. Deficiency
produced by the hypothalamus. Most cpmmon cause of
hypothyroidism is a result of failure of thyroid hormone
production by the thyroid (hypothyroidism primary).
How to Make a Diagnosis ?
Anammesis
1. Age < 20 years or > 50 years.
2. History of exposure to neck radiation as a child.
3. Rapid enlargement of the thyroid gland.
4. Patients with goiter accompanied by a hoarse voice.
5. Accompanied by dysphagia and pain.
6. There is a family history of cancer.
7. Patients with goiter suspected of hyperplasia, treated with
the hormone thyroxine, remain enlarged.
8. Goiter with shortness of breath. Benign thyroid nodules are
most common at the age of 30-50 years.
If nodules are found at age < 20 years, 20-70% are malignant, as well as if
age > 50 years. The presence of local symptoms of hoarseness and
dysphagia can usually be an indication of the invasive nature of a thyroid
malignancy. A thyroid nodule that has remained large for many years is
usually benign, but if it changes to become enlarged in a short time
(months/weeks), it is necessary to watch out for it turning malignant. In the
anamnesis to find out if there are functional disturbances in goiter sufferers, it
is also necessary to ask the things that support the signs of hyperthyroidism,
including tremors, warm and wet akral, tachycardia, difficulty concentrating,
eating a lot but the body remains thin/weight loss, frequent diarrhea.
Physical examination.

Perform a systematic examination (from top to


bottom), symmetrically (compare right and left),
simultaneous (right and left together), carefully and
don't forget to look at the back of the head. Routinely
should be evaluated also the condition of the cervical
lymph nodes, is there any enlargement, do the
evaluation systematically as well. Enlargement of the
thyroid gland varies widely from not visible to very
large and puts pressure on the trachea, causing
dilation of the venous system and formation of
collateral veins.
We examine goiter patients from behind, the patient's head is slightly flexed so
that the sternocleidomastoid muscle relaxes, thus thyroid tumors are easier to
evaluate by palpation. Use both hands together with the thumb at the patient's
neck while the other 4 fingers from the lateral evaluate the thyroid and look for
the lower pole of the thyroid gland when the patient is asked to swallow. In a
large goiter that enters retrosternally, we cannot feel the trachea and the lower
pole of the thyroid. The normal thyroid gland is palpable as a soft formation and
moves during swallowing. Usually the goiter can still be moved laterally, and is
difficult to move in a vertical direction. Goiter becomes fixed if it is very large,
malignancy that has penetrated the capsule, thyroiditis, there is fibrotic tissue
after surgery.
On physical examination, if a nodule is found, it should be
described:
1. Location: right lobe, left lobe, isthmus.
2. Size: in centimeters, diameter length.
3. The number of nodules: one (uninodusa) or more than one
(multinodusa).
4. Consistency: cystic, soft, chewy, hard.
5. Pain: there is pain or not at the time of palpation
6. Mobility: presence / absence of attachment to the trachea,
m.sternocleidomastoid.
7. Enlarged lymph nodes around the thyroid: present or absent.
LABORATORY TEST

• Thyroid Function Test

blood test to measure levels of TSH, FT4 and T3 circulating in the


blood

• Thyroid Ultrasound

to evaluate anatomy of the thyroid. It can show nodules in the tyroid


gland, a change in a blood flow to your thyroid and the density of
the gland
• Thyroid Antibody Test

these are blood test to measure thyroid antibody that include


antithyroid (microsomal) antibodies or Thyroid Receptor Stimulating
Antibodies (TRAb). This test for thyroiditis caused by autoimmune
disease

• Erythrocyte Sedimentation Rate (ESR)

blood test that help detect inflammation

• C-reactive Protein (CRP)

• Radioactive Iodine Uptake (RAIU) Test

• Biopsy
Farmacological Treatment
Management

The management of thyroiditis is determined according to its etiology. In acute thyroiditis


due to bacterial infection, management includes antibiotics, while in subacute thyroiditis
due to viral infections, management is generally only symptomatic because the disease is
self-limiting. In other types of thyroiditis, management can be in the form of observation,
medicamentous therapy, or surgery according to the course of the disease
Farmacologi

● ANALGESIK DAN ANTI INFLAMASI


Cardio Aspirin 100 mg
● ANTI INFEKSI
Ampicillin 500 mg
● BETA BLOCKER
Propranolol 10 mg
● LEVOTIROKSIN
Euthyrox 100 mcg
Non Farmacological
Vitamin D

Helps Modulate the expression of immune cells, Reduce Autoimmune antibodies and decrease
the body’s inflammatory response
ZINC-RICH FOOD

 PEASE
 LEGUMES
 ASPARAGUS
 NUTS AND SEEDS
 MEAT
 WHOLE GRAINS
 SHELLFISH
 EGGS
 DAIRY
 KALE
FOOD THAT CAN
INCREASE SELENIUM

BRAZIL NUTS

RICE

BEANS

WHOLE-WHEAT BREAD
Pathophysiology

• The thyroid shows a characteristic patchy inflammatory


infiltrate with disruption of the thyroid follicles and
multinucleated giant cells within some follicles
• The follicular changes progress to granulomas accompanied
by fibrosis
• Finally, the thyroid returns to normal, usually several months
after onset
COMPLICATION OF THYROIDITIS
MYXEDEMA COMA

Myxedema coma is a extreme manifestation of


hypothyroidism.

Is a medical emergency with clinical features of


hypothermia, hyponatremia, and bradycardia
THYROID STORM

Is a life threatning endocrine emergency because of long-standing condition of


hyperthyroidism like Graves Disease.

Hyperpyrexia, tachycardia, agitation, and psychosis.


• Infectious thyroiditis can lead to an abscess and
septicemia if not treated promptly

• Patients with Hashimoto disease are at risk of


developing thyroid lymphoma and carcinona
Prognosis

Thyroiditis with or without thyroid dysfunction has a good


prognosis if treated well. But if it’s not treated well it can cause
long-standing hypothyroidism can lead to myxedema coma.

And it can cause long-standing hyperthyroidism can lead to


thyroid storm
Reference………….
 Fitzgerald MJT. Clinical neuroanatomy and neuroscience. 6th ed. New York,
PA: Saunders/Elsevier; 2012.
 Crossman AR, Neary D. Neuroanatomy. An Ilustrated Colour Text. 5th ed.
Manchester, PA: Churchill Livingstone/Elsevier; 2015.
 Netter FH. Atlas of Human Anatomy. 5th ed. Philadelphia, PA:
Saunders/Elsevier; 2011.
 Putz R. Sobotta Atlas of Human Anatomy. 14th ed. Stuttgart, PA: Urban &
Fischer/Elsevier; 2006.
 Mazzaferri EL. NCCN thyroid carcinoma practice guidelines. Oncology
1999;13
 Shaha AR, Jaffe M. Completion thyroidectomy: A critical appraisal. Surgery
1992; 112: 1148

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