Thyroid PPT 2024 PDF

THE THYROID GLAND ANATOMY ANATOMY  GROSS ANATOMY: 4 LOBES MADE UP OF 2 PEAR-SHAPED GLANDS inferior to the larynx - extends from 5th cervical to the 1st thoracic vertebrae. AN ISTHMUS at level of Trachea rings 2,3,4 PYRAMIDAL LOBE (from body...

THE THYROID GLAND ANATOMY ANATOMY  GROSS ANATOMY: 4 LOBES MADE UP OF 2 PEAR-SHAPED GLANDS inferior to the larynx - extends from 5th cervical to the 1st thoracic vertebrae. AN ISTHMUS at level of Trachea rings 2,3,4 PYRAMIDAL LOBE (from body of hyoid bone to the isthmus connnected by a fibro-musclar band called levator glandulae thyroideae) THE MOST POSTERIOR EXTENSION OF THE LATERAL THYROID LOBES IS CALLED THE TUBERCLE OF ZUCKERKANDL  INVESTITURE THE GLAND IS INVESTED BY: * A TRUE CAPSULE WHICH IS A FLIMSY OR THIN FIBROELASTIC CONNECTIVE TISSUE. THIS DIGS INTO AND DIVIDES THE GLAND INTO LOBULES. * A FALSE CAPSULE WHICH IS THE DEEP CERVICAL FASCIA OTHERWISE CALLED THE PRE-TRACHEAL FASCIA.  STRAP MUSCLES THE THREE STRAP MUSCLES ARE: STERNO THYROID STERNOHYOID AND SUPERIOR BELLY OF OMOHYOID THE LIGAMENT THAT HOLDS THE THYROID GLAND TO THE TRACHEAL POSTERORLY IS CALLED LIGAMENT OF BERRY The posterolateral borders relate to the Carotid sheath ; The posterior border of each lobe harbours the superior and inferio parathyroid glands within that pretracheal fascia.  BLOOD SUPPLY ARTERIAL SUPPLY: - 3 ARTERIES SUPERIOR THYROID ARTERY FROM THE EXTERNAL CAROTID ARTERY INFERIOR THYROID ARTERY FROM THE THYRO-CERVICAL TRUNK THYROIDEA IMA FROM THE BRACHIO- CEPHALIC ARTERY OR AORTIC ARCH. THYROID ARTERIES  3 VENOUS DRAINAGES: SUPERIOR THYROID VEIN DRAINS TO THE INTERNAL JUGULAR VEIN MIDDLE THYROID VEIN DRAINS INTO THE INTERNAL JUGULAAR VEIN and INFERIOR THYROID VEIN DRAINS TO THE INNOMINATE VEIN. There is an abberant VEIN OF KOCHER. It is actually the posterior external jugular vein originating as a tributary of the common facial vein. THYROID VEINS  NERVE SUPPLY SUPERIOR LAYNGEAL NERVE INFERIOR LARYNGEAL NERVE RECURRENT LARYNGEAL NERVE SUPERIOR LARYNGEAL NERVE INFERIOR LARYNGEAL NERVE RECURRENT LARYNGEAL NERVES  PHYSIOLOGY TRH>>>>>>TSH>>>>>>T4 (then T3) THEN NEGATIVE FEED BACK PARAFOLLICULAR – C- CELLS>>>CALCITONIN  GOITRE DEFINITION. GOITRE IS SIMPLY AN ENLARGEMENT OF THE THYROID GLAND. (It is a diseased state) The normal thyroid is not visible and weighs 7- 25g (in Africans) and 15-25g in caucasians. For the gland to be palpable, it must be at least 2x its normal size or 40g. For the gland to be visible, it would be thrice its normal size.  CAUSES OF GOITRE This could be CONGENITAL or ACQIURED. 1. CONGENITAL = DYSHORMONOGENESIS BY ENZYMES DEFICIENCY Organic iodine in diet is reduced to inorganic iodine in the blood. So, If in the gut, the absorption of inorganic iodine is low OR There is Deficiency of enzymes necessary for oxidising iodine; coupling iodine and Tyrosine to MIT/DIT; OR There is interrruption of Binding of these to thyroglobulin and releasing them into the blood stream. Congenital goitre will result.  PHYSIOLOGY THE IODINES IN FOOD: (ORGANIC)IODINE >>> (INORGANIC) IODINE IN BLOOD: TRAPPED AND CONCENTRATED INTO IODIDES Thyocyanates and perchlorates inhibit this. OXIDISED INTO MIT AND DIT (MONO- AND DIO – IODO THYROSINES MIT+DIT= T3 (TRI-IODO THYRONINE) DIT+DIT = T4 (TETRA-IODO THYRONINE) (Carbimazole, Methimazole, Propyl & Methyl- thiouracil, block this binding and coupling)  2. ACQUIRED (i) – DIETARY (Pathological goitre). Deficiency of iodine in food and water as in Rocky mountainous regions due to washing-out of iodine content of the water supply and the soil. (a) Mountaneous areas with plenty of granite, there is a high calcium content in the water and this has goitrogenic effect. (b) Cassava contains cyanogenic glucosides which yield thyocyanates as a metabolic by- product which inhibit iodine uptake by the thyroid.  ABOUT ENDEMIC GOITRE Endemic goitre is described as a situation in which more than 10% of any community has goitre. This population also has more of Follicular cancer of the thyroid. These places are found around the mountaneous regions of the world that leach iodine out of the soil, Insufficient iodine in the diet – e.g.cassava, cabbage and in their water.  ABOUT SPORADIC GOITRE SPORADIC GOITRE OCCOUR IN A SMALLER NUMBER OF PEOPLE THEY MAY BE CAUSED BY GENETIC FACTORS ALSO (dyshormonogenesis). THEY OCCOUR LATE – 20-39 YEARS. PAPILLARY THYROID CARCINOMA IS COMMONER IN THIS GROUP (ii) IATROGENIC A. EXCESS IODINE INTAKE CAN PRODUCE ACUTE BLOCK OF IODINE BINDING TO TYROSINE RESIDUES IN THYROGLOBULIN PRODUCING “IODINE GOITRE”. THIS IS CALLED THE WOLFF-CHOIKOFF BLOCK (Iodine Goitre). THIS CAN OCCOUR DURING EXCESSIVE INTAKE OF IODINE IN COUGH PREPARATIONS AND ASTHMA MIXTURES OVER A PROLONGED PERIOD.  B. IN PATIENTS WITH LONG-STANDING NODULAR GOITRE, PERSISTENT USE OF LARGE DOSES OF IODINE TO ATTEMPT TO SHRINK THE TUMOUR CAN RESULT IN THYROTOXICOSIS CALLED JOD- BASEDOW THYROTOXICOSIS C. THYROTOXICOSIS FACTITIA (OR ALIMENTARY THYROTOXICOSIS or Exogenous Thyrotoxicosis). This is thyrotoxicosis caused by either (a) mistakenly ingesting exogenous thyroid hormone (e.g Laevothyroxine used as replacement therapy after thyroidectomyand tri-iodothyronone; Or (b) due to Munchesen syndrome  (iii) DIETARY. This is the basis of endemic goitre.  IN BLOOD – TBG, ALBUMIN,PRE- ALBUMIN  ABOUT SPORADIC GOITRE iv. PHYSIOLOGICAL GOITRE. This is goitre that arises from increased need of thyroid hormones e.g Puberty, Menstruation, Pregnancy and Lactation. This explains why goitre is commoner in females than in males. This type of goitre involutes when enough hormones are released in sufficient amounts or the need for increased amount is over  DRUGS: Trapping and Concentration of iodine are inhibited by Thyocyanate and Perchlorates, Nitrates, chlorpropamide etc are goitrogenic Excessive iodine intake (as in cough mixtures) causes acute block in binding of iodine to tyrosine residuesof thyroglobulin. This is called Wolff- Choikoff block. Excessive iodine intake also blocks release of hormones from the thyroid.  OTHER CAUSES OF GOITRE (v) INFLAMMATION (Thyroiditis) This may be * ACUTE (SUPPURATIVE) THYROIDITS (BACTERIAL) SUB-ACUTE GranulomatousTHYROIDITIS, Giant cell thyroiditis (DE-QUARVAINS, Non-suppurative thyroiditis) Giant-cell thyroiditis. It is of viral origin. (a). Hashimoto’s (Autoimmune)Thyroiditis – This is of Autoimmune origin (acute phase>>>hyperthyroidism; chronic phase>>>hypothyroidism) * CHRONIC THYROIDITIS. (a) Riedel’s thyroididits also called Ligneous thyroiditis because it is fibrosed and hard. It is an invasive fibrous thyroiditis.  Other causes of goiter (vi) NEOPLASIA – BENIGN AND MALIGNANT.  (vii) TOXICITY GOITRE MAY BE SIMPLE OR TOXIC (a) SIMPLE GOITRE IS GOITRE THAT IS A NON-TOXIC NON HYPOTHYROID AND NON-MALIGNANT GOITRE.  (viii) NEONATAL GOITRE THIS MAY PERESNT AS NEONATAL THYROTOXICOSIS AS IN A MOLAR PREGNANCY STRUMA OVARII. THIS IS AN OVARIAN TERATOMA IN WHICH MORE THAN 50% OF THE OVERALL MASS IS THYROID TISSSUE IT MAY ALSO COME AS PENDRED’S SYNDROME: CONGENITAL DEAFNESS IN CONJUNCTION WITH NEONATAL EUTHYROID GOITRE HISTOLOGICALLY, GOITRE MAY BE DISCRIBED AS PARENCHYMATOUS (Diffuse) GOITRE - (Felt like the body of an orange) It is due to hypertrophy and hyperplasia of the parenchyma AND THIS IS CAUSED BY PERSISTENT INCREASE IN TSH STIMULATION OR COLLOID GOTRE – IF IT IS DUE TO INCREASE IN PRODUCTON COLLOID WITHIN THE THYROID FOLLICLE. WHEN THIS PRODUCTION IS IRREGULAR, DUE TO WAXING AND WANING OF TSH, IT PRODUCES A MULTINODULAR GOITRE - (felt like the body of a corn hub). GOITRE  CLINICALLY Goitre whether parenchymatous or colloidal, may be described as diffuse goitre if it is uniformly enlarged due to persistent TSH stimulation or nodular or multinodular goitre if the stimulation of TSH waxes and wanes. ANY OF THESE MAY BE SIMPLE (I.E NON- TOXIC) [DESCRIBED AS “SIMPLE DIFFUSE GOITRE; SIMPLE NODULAR GOITRE”]: OR TOXIC DIFFUSE GOITRE , TOXIC MULTINODULAR GOITRE, TOXIC NODULE IN A GOITRE.  NATURAL HISTORY OF SIMPLE GOITRE DIFFUSE HYPERPLASIA (colloid goitre) NODULAR (waxing and waning of TSH stimulation) MAY BECOME BIGGER>> PRESSURE SYMPTOMS (hoarseness, dyspnoea, dysphagia) + COSMETICS FIBROSIS CALCIFICATION CYSTIC CHANGES HAEMORRHAGE  MAY BECOME TOXIC – especially nodular goitre) INFECTION MALIGNANCY  b. TOXIC GOITRE (Goitre associated with thyrotoxicosis) Thyrotoxicosis is due to the stimulating effect by (i) TSH (Thyroid Stimulating Hormone) causing excess thyroid hormones – T3 and T4, In a few cases, (10% of cases) only T3 is increased – described as T3-Thyrotoxicosis. (ii) The gland may also be stimulated by TSI to produce excess hormones BUT, The eye symptoms and the pretibial myxoedema are NOT related to these thyroid hormones. Features of Toxicity: HYPERMETABOLISM – anxiety, irritability, heat intolerance, nervousness, tremulousness, emotional instability, sleeping pulse tachycardia, heart failure, The hypermetabolism is caused by an autoimmunne protein called Thyroid Stimulating Immunoglobulin (TSI). They are antibodies produced by lymphocytes to a thyroid plasma antigen. They stimulate the thyroid even longer than TSH causing hyperplasia and hypertrophy of the cells with increase in production of T3 and T4  EYE SIGNS The TSI also causes infiltration of the retro-orbital tissues by lymphocytes producing Proptosis. EXOLPHTHALMOUS ( causes spasm of the lid presenting as: lid-lag, lid- retraction, starring gaze; (different from proptosis) This is an extra-ocular thyroid disease. It is caused by an Exolphthalmos Producing Substance (EPS). It may be non-infiltrative and mild or infiltrative and malignant exolphthalmous. EPS causes thyroid autoimmunity because the thyroid and the extra-ocular muscles share an auto-antigen. By a fibroblast stimulation, a cytokine is released that activates the T-cells and macrophages accumulate in the muscles. 90% of these cases develop Graves disease while another 5% develop the reverse – auto-immune hypothyroidism!  Pre-tibial myxoedema This is when the pretibial skin and the dorsum of the foot are infiltrated by a mucin-like substance –giving rise to irregular thickening of the skin, coarse hair, clubbing of fingers and toes – Thyroid acropachy.  GRAVES DISEASE ‘HYPERPLASTIC GOITRE (DIFFUSE GOITRE) THYROTOXICOSIS – TOXICITY IN A PREVIOUSLY HEALTHY GLAND IS CALLED PRIMARY THYROTOXICOSIS EXOLPHTHALMOUS PRETIBIAL MYXOEDEMA THUS TOXICITY IN A DIFFUSELY ENLARGED GLAND ESPECIALLY IF ASSOCIATED WITH EYE SIGNS, IS CALLED GRAVE’S DISEASE EXOPHTHALMOS PRETIBIAL MYXOEDEMA  PLUMMER’S DISEASE NATURAL HISTORY MAY BECOME BIGGER MAY BLEED RETROSTERNAL CROWDING – (HENCE C.T. THORACIC INLET) INFECTED MAY BECOME MALIGNANT MAY BECOME TOXIC. [TOXICITY IN A PREVIOUSLY DISEASED GOITRE IS CALLED SECONDARY THYROTOXICOSIS OR PLUMMER’S DISEASE  PLUMMER’S DISEASE (THYROTOXICOSIS IN A DISEASED GLAND) SIMPLE MULTINODULAR GOITRE TOXIC MULTINODULAR GOITRE SOLITARY NODULE TOXIC NODULE/ADENOMA HASHIMOTO’S DISEASE DEQUARVAINS THYROIDITIS MALIGNANT THYROID.  3. HYPERTHYROIDISM (THYROTOXICOSIS) A CLINICAL STATE OF HYPERMETABOLISM TYPES:- 1. PRIMARY THYROTOXICOSIS FEATURES: PRE-TIBIAL MYXOEDEMA- DIFFUSE GOITRE +/- THRILL OR BRUIT EVIDENCE OF THYROTOXICOSIS EYE SIGNS RAISED T3/T4 LOWERED TSH  2. SECONDARY THYROTOXICOSIS (Thyrotoxicosis in a previously unhealthy gland – eye signs not usual. MULTINODULAR GOITRE SOLITORY NODULE (SIMPLE OR TOXIC) HASHIMOTO’S DISEASE DEQUARVAINS DISEASE MALIGNANCY  AETIOLOGY OF THYROTOXICOSIS THYROID STIMULATING IMMUNOGLOBULIN EXOLPHTHALMOS LARGE DOSES OF IODINE (JOD- BASEDOW’S DISEASE) LARGE DOISES OF THYROXINE – THYROTOXIC FACTITIA GENETIC FACTORS  4. NEOPLASMS (of the Thyroid) BENIGN AND MALIGNANT BENIGN NEOPLASMS ADENOMA (Follicular, Papillary, Atypical) TERATOMAS  MALIGNANT NEOPLASMS DIFFERENTIATED (PAPILLARY, FOLLICULAR, MEDULLARY) UNDIFFERENTIATED (ANAPLASTIC) SQUAMOUS CELL OTHERS (Lymphomas, Sarcomas, Teratomas, Metastatic deposits)  PAPILLARY TUMOURS COMMONEST (80%) SLOW GROWING METASTASISE VIA LYMPHATICS (Lateral aberrant thyroid) THENCE TO THE LUNGS. USUALLY RESULTS FROM RADIATION THERAPY OCCURS AT 30-40 YRS OF AGE FEMALES>MALES (2:1) CONTAINS PSAMMOMA BODIES  FOLLICULAR (10%) METASTASISES VIA VASCULAR ROUTE WELL ENCAPSULATED DIFFICULT TO DIAGNOSE VIA FNAC because tissue is difficult to get. MAY CAUSE OSTEOLYTIC LESIONS (SKULL) FEMALES>MALES (3:1)  MEDULLARY CARCINOMA (5%) ARISES FROM THE PARAFOLLICULAR – C, CELLS THEY ARE NEUROCHRISTOPATHIES therefore APUDOmas MAY BE SPORADIC (80%) OR ENDEMIC AFFECTS ONLY ONE LOBE MAY PRESENT AS MEN IIA OR MENIIB OR NON- MEN familial (MCT). Therefore secrete SEROTONIN, PROSTAGLANDIN, CALCITONIN - causing,watery diarrhoea achloryhydria THEY SPREAD BY BOTH LYMPHATICS AND BLOOD VESSELS FEMALE>MALES 1.5:1  HURTLE CELL THROID CANCER (5%) THIS CANCER IS ALSO FROM FOLLICULAR CELLS. SPREADS BY LYMPHATIC>BLOOD ROUTE  ANAPLASTIC CANCERS (2%) 75% FROM PREVIOUS DIFFERENTIATED TUMOURS – ESPECIALLY FOLLICULAR F>M THEY ARE RADIOSENSITIVE  CLINICAL FEATURES OF THYROID CANCERS SUDDEN AND RAPIDLY ENLARGING THROID GLAND RECENT PAIN IN GOITRE DYSPNOEA HOARSENESS FIXITY AND DYSPHAGIA HORNER’S SYNDROME (Ptosis, Miosis, Anhydrosis) MALENESS SECONDARIES TO THE BONE  INVESTIGATIONS FOR THE THYROID THYROID FUNCTION TESTS – T3, T4, TSH X-RAYS :- NECK,(for tracheal posn); THORACIC INLET, CT SCAN (NECK, CHEST, THORACIC IN- LET) USG, MRI DIRECT/INDIRECT LARYNGOSCOPY FNAC  TREATMENT FOR THYROTOXICOSIS 1. MEDICAL: ANTI-THYROID DRUGS – CARBIMAZOLE(METHIMAZOLE) PROPYL/METHYL THIOURACIL SEDATIVES (PHENOBARBITONE, DIAZEPAM) B-BLOCKERS. PROPANOLOL; NADOLOL  INDICATIONS FOR MEDICAL TREATMENT RECURRENCE OF THYROTOXICOSIS ATHYROTIC THYROTOXICOSIS THYRO-CARDIAC CHILDREN, ADOLESCENTS, FEMALE PATIENTS DRUG THYROTOXICOSIS  TREATMENT FOR GOITRE. RADIO ACTIVE IODINE CONTRAINDICATIONS PATIENTS