بسم الله الرحمن الرحيم

THYROID GLAND

DR.SULEIMAN JASTANIAH

FRCS(Ed),FACS

ANATOMY:

BLOOD SUPPLY : Sup.Thyroid a---ext. carotid artery Inferior thyroid a---thyrocervical trunk Thyrodea ima a----arch of aorta

*Sup.thyroid vein----Int. jugular v.*Middle. Thyroid vein----Int. jugular v.*Inf. Thyrod vein------brachiocephalic v

*The recurrent Laryngeal nerve*Ext.branch of sup. Laryngeal nerveHistory : .Evidence of Hypo or Hperfunction .Symptoms related to pressure on the neighboring structure: dysphagia,dyspnia,chocking sensation. .Change in voice .Presence of mass—duration -rate of growth -pain

H/O:>Exposure to radiation.>Diet .>Drugs e.g para amino salycilic acid Thiouracil,Carbimazole

Physical Examination : .Inspection .Palpation .Percussion .Auscultation

Thyroid Function Tests:

TSH (0.5 TO 4.0 U/ml ) increase in hypothyroidismdecrease in hyperthyroidism

T3 AND T4Radioactive iodine uptakeAntithyroglobulin &antimicrosomal

Hypothyroidism:Causes:1)Spontaneoushypothyroidism(Myexedema)2)Replacement of the gland by nonfunctional goiter ,adenoma, or thyroiditis3)Post thyroidectomy4)Post radioactive iodine therapy5)Hashimoto’s thyroiditis

Clinical Features:.Increasing fatigue and apathy.Physical and mental procedures are slowed.Headaches and dementia.Weight gain.The skin becomes dry, thickened, and puffy.The hair becomes dry and brittle.The tongue is enlarged and the voice is hoarse.Pulse is slow.Congestive heart failure.

.Constipation and changes in bowel habits.Menorrhagia.LibidoTreatment : L-thyroxine

Thyrotoxicosis :Causes :1)Grave’s Disease (toxic diffuse goiter)2)Toxic multinodular Goiter.3)Toxic Adenoma.4)De Quervains Thyroiditis.5)Thyroid Cancer.

Clinical Manifestations :-Goiter.-Symptoms and Signs related to excess amount of thyroxin.-Eye signs: *Lid Lag and Lid Retraction. *Ophthalmoplagia *Exophthalmos. *Supra orbital and ifra orbital swelling *Congestion and edema.

Treatment :>Ant thyroid drugs e.g. Propylthiouracil and carbimasole>Radioactive iodine.>Surgery.

Thyroiditis :Acute Chronic1.Suppurative 1.Hashimoto’s disease2.Non Suppurative 2.Giant cell thyroiditis (De Quervain’s ) 3.Riedel’s thyroiditis

Goiter :Enlargement of the thyroid gland.Causes :1)Familial :inherited enzyme defects.2)Endemic:iodine deficiency &ingestion of goitergenic.3)Benign and Malignant neoplasm.4)Thyroiditis.

Malignant Tumors:1)Papillary2)Follicular3)Medullary4)Anaplastic5)Lymphoma

Papillary:Common 20-30 years old.-F to M 3:1-Painless lump in the thyroid gland with enlarged lymph glands-Multicentric-Good prognosis

Follicular Ca :-30 to 40 years old.-Capsular and vascular invasion are prominent feature.-Blood metastesis

Modulary Ca :C-cell calcitonin producing tumor.-Familial.-Is part of endocrine neoplasm.-Elevated serum calcitonin.

Ana plastic :-Undifferentiated CA.-Locally invasive.-Poor prognosis.

SURGERY OF THYROID.COMPLICATIONS:

PARATHYROID GLAND:

Anatomy:

*4 glands

*Yellowish brown in co lour

*Variable in position

PTH :*It stimulates osteoclastic activity------increasing bone resorption*Increases the reabsorption of Ca by the renal tubules*Increases absorption of Ca from the gut*Reduces the renal tubular reabsorption of phosphate

Calcitonin :secreted by the parafollicular cells of thyroid gland .It has opposite action of PTH

Hypoparathyrodism :>Commonly after total thyrodectomy>Spontaneous hypoparathyroidism.

CLINICAL FEATURES :-Tingling and numbness in the face and toes-Carp pedal spasm-Strider ----------suffocation-Chevostek’s sign-Trousseau’s sign

Trousseau’s sign

Carpal spasm in response to inflation of BP cuff to 20 mm Hg above SBP for 3 min

Chvostek’s sign

Elicited by tapping over facial nerve causing twitching of ipsilateral facial muscles

Treatment :I.V Ca glucanate 10% 10 ml*Long term Vit. D &oral Ca.

HYPERPARATHYROIDISM :Primary : -Increase PTH -Increase CaDue to : >Adenoma >Hyperplasia >Rarely CarcinomaSecondary : >Ch .renal failure >Malabsorption

Tertiary :Further stage in the development of reactive hyperplasia where autonomy occurs as parathyroid s no longer respond to physiological stimuli

Clinical Features :*Asymptomatic Hypercalcemia*Non specific Symptoms : muscle weakness, thirst, polyurea, anorexia, weight loss.

*Bone Disease : -Generalized decalcification -single or multiple bone cysts -Loss of density and subperiosteal erosions (skull & phalanges )_

*Renal stones :Hyperparathyrodism must be considered in patients with renal stone or nephrocalcinosis *Dyspeptic cases :Nusea, vomiting, &anorexiaPeptic ulcersA.pancreatitis

*Psychiatric cases :Women complaining of tiredness or personality changes

DIAGNOSIS :>Increase serum Ca >2.6 mmol /l>Decrease serum phosphorus<0.8>Increase execration of Ca in urine >Increase alkaline phosphates>Increase PAT

Pre-operative Localization:

Ultra soundCT scanThallium-Tec subtraction scan (Tec—

Thy,Thal—thy&para ) enlarged Para thyroid as hot spot

MRISelective angiographyVenous samplingTreatment : Surgery