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![INTRODUCTION
The 4 parathyroid glands are located posterior to the
thyroid gland.
They produce parathyroid hormone (PTH), which is the
primary regulator of calcium physiology.
PTH acts directly on bone,(induces calcium resorption),
and on the kidney, where it stimulates calcium
reabsorption and synthesis of 1,25-dihydroxyvitamin D
[1,25(OH)2D], a hormone that stimulates
gastrointestinal calcium absorption.
Calcium and vitamin D, inhibit PTH release and
synthesis.](https://image.slidesharecdn.com/thyroidparathyroidkinara-160915090824/85/Thyroid-parathyroid-kinara-43-320.jpg)
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Thyroid parathyroid kinara
- 1. HYPERTHYROIDISM,HYPOTHYROIDISM AND PARATHYROID DISEASE PRESENTER:KINARA S KENYORU MED/18/11 FACILITATOR: DR. GARDNER
- 2. INTRODUCTION/ANATOMY •Thyroid gland locatedin the neck,ant to trachea btn cricoid cartilage and the suprasternal notch. (C5 and T1) •12-20g
- 4. THYROID GLAND DISORDERS Thyroid hormones: T4: (Thyroxine) is made exclusively in thyroid glandT3: (Triiodothyronine) main source is peripheral deiodination: Ratio of T4 to T3 ; 5:1 Potency of T4 to T3; 1:10 T4 is the most important source of T3 by peripheral tissue deiodination “ T4 to T3 “ T3 is the most important because more than 90% of the thyroid hormones physiological effects are due to the binding of T3 to Thyroid receptors in peripheral tissues.
- 6. THYROID HORMONEEFFECTS CALORIGENESIS GROWTH & MATURATION RATE C.N.S. DEVELOPMENT & FUNCTION CHO, FAT & PROTEIN METABOLISM MUSCLE METABOLISM ELECTROLYTE BALANCE VITAMIN METABOLISM CARDIOVASCULAR SYSTEM HEMATOPOIETIC SYSTEM GASTROINTESTINAL SYSTEM ENDOCRINE SYSTEM PREGNANCY
- 7.
- 8. DEFINITION Excess thyroidhormone Most common forms; diffuse toxic goitre(Graves dse) 80% toxic multinodular goiter 5% toxic adenoma – younger patients & in iodine- deficient areas Thyroiditis (transient <8mo, symptomatic treatment)
- 9. Epidemiology M<F 1:5. Prevalence, which is approximately 1.3 percent, increases to 4 to 5 percent in older women. Hyperthyroidism is also more common in smokers. Graves' disease is seen most often in younger women, while toxic nodular goiter is more common in older women.
- 10. Etiology 1. Graves disease 2.Multinodular goitre 3. Solitary thyroid adenoma 4. Thyroiditis 1. Sub acute (de Quervain’s) 2. Post-partum 5. Iodide-induced 1. Drugs (e.g. amiodarone) 2. Radiographic contrast media 3. Iodine prophylaxis programme 6. Extrathyroidal source of thyroid hormone 1. Factitious thyrotoxicosis 2. Struma ovarii 7. TSH-induced 1. TSH-secreting pituitary adenoma 2. Choriocarcinoma and hydatidiform mole (HCG) 8. Follicular carcinoma ± metastases
- 11. Pathogenesis ct’d InGraves dse, circulating autoantibodies against thyrotropin receptor cause release of thyroid hormones and thyroglobulin, stimulate iodine uptake, protein synthesis and thyroid gland growth. Ophthalmopathy is due to Ab reaction against the TSH receptor that results in activation of T cells against tissues in the retro orbital space that share antigenic epitopes with thyroid follicular cells.
- 12. THYROTOXICOSIS Symptoms: Hyperactivity Irritability Dysphoria Heat intolerance & sweating Palpitations Fatigue & weakness Weight loss with increased appetite Diarrhea Polyuria Sexual dysfunction Signs: Tachycardia Atrial fibrillation Tremor Goiter Warm, moist skin Muscle weakness, myopathy Lid retraction or lag Gynecomastia * Exophthalmos * Pretibial myxedema
- 13. Clinical manifestations SKIN Theskin is warm due to increased blood flow; it is also smooth because of a decrease in the keratin layer. Palms are warm,moist and hyperemic and Plummer’s nails are seen. Other changes include: Sweating-due to increased calorigenesis; often ass with heat intolerance Onycholysis (loosening of the nails from the nail bed,)& softening of the nails Hyperpigmentation; mediated by accelerated cortisol metabolism Pruritus and hives, primarily in Graves' hyperthyroidism Vitiligo and alopecia areata Thinning of the hair Infiltrative dermopathy in patients with Graves' hyperthyroidism.
- 14. Manifestations …..ctd EYES Stareand lid lag occur in all patients(Due to sympathetic overactivity) Only in Graves' disease have ophthalmopathy- inflammation of the extraocular muscles and orbital fat and connective tissue; proptosis (exophthalmos), impairment of eye-muscle function, diplopia periorbital and conjunctival edema. gritty feeling or pain in their eyes Corneal ulceration optic neuropathy and blindness from severe proptosis
- 15. Manifestations….ctd CARDIOVASCULAR increase incardiac output, due both to incr peripheral oxygen needs and incr cardiac contractility. Heart rate is increased, pulse pressure is widened, and peripheral vascular resistance is decreased Systolic hypertension High- or normal-output CHF. Atrial fibrillation 10 to 20 % more common in elderly patients Other abnormalities; mitral valve prolapse, mitral regurgitation, and an increase in left ventricular mass index.
- 16. Manifestations…ctd METABOLIC / ENDOCRINE Serum lipids — low serum total and high-density lipoprotein (HDL) cholesterol concentrations Hyperglycemia — due to antagonism to the peripheral action of insulin leading to impaired glucose tolerance in untreated patients RESPIRATORY Dyspnea and dyspnea on exertion may occur due to: a) Oxygen consumption and CO2 production increase. b) Respiratory muscle weakness. c) Tracheal obstruction from a large goiter. d) Hyperthyroidism may exacerbate underlying asthma. e) Pulmonary arterial systolic pressure is increased
- 17. Manifestations…ctd GASTROINTESTINAL Weight loss-increased metabolic rate (hypermetabolism), and secondarily to increased gut motility and the associated hyperdefecation and malabsorption; Hyperphagia. Anorexia/Vomiting/abdominal pain Dysphagia due to goiter Deranged LFTs,esp high serum ALP. Steatorrhea HEMATOLOGIC Normochromic, normocytic anemia. High Serum ferritin concentrations Graves' hyperthyroidism may be ass with ITP and pernicious anemia and antineutrophil antibodies. Hyperthyroidism may also be prothrombotic
- 18. Manifestations…ctd GENITOURINARY Urinary frequencyand nocturia/ Enuresis is common in children oligomenorrhea,/anovulatory infertility /Amenorrhea gynecomastia, reduced libido, and ED in men. BONE increased porosity of cortical bone and reduced volume of trabecular bone. NEUROPSYCHIATRIC Behavioral and personality changes, such as psychosis, agitation, depression, anxiety, restlessness, irritability, and emotional lability and Insomnia.
- 19. Investigations TFTS: -Primary: <TSH,>T3 & T4 -Secondary: Normal or > TSH, Radioiodide scan 99mTc 131I ELISA for anti –TSH receptor/TSI, antimicrosomal ab LFTS – elevated CBC- mild normocytic anemia, mild neutropenia, < Platelets Biopsy- FNA cytology Ultrasound CT/MRI – head/ chest
- 20. TREATMENT Includes: 1. Symptom relief 2.Antithyroid pharmacotherapy 3. Radioactive iodine 131 therapy 4. Thyroidectomy
- 21. 1. Symptoms relief Propranolol 40mg/6h PO for CVS and CNS symptoms Hydration of pt key before b blocker therapy CCBs may also be used for symptom relief. These therapies must be tapered and stopped once TFTs are within normal ranges.
- 22. 2. Antithyroid pharmacotherapy Thionamides methimazoleand propylthiouracil (PTU) inhibit thyroid hormone synthesis, and PTU also inhibits conversion of T4 to T3, faster onset of action. Employed for long term control in children,adolescents and pregnant women. In adult men and non-pregnant women,they control hyperthyroidism before definitive mgt with radioactive iodine or surgery. A major serious S/E is agranulocytosis. Propylthiouracil-5-10mg/kg/24 hours. Methimazole 0.25-1mg/kg/24 hours Titrate the antithyroid drug dose every 4 weeks until thyroid functions normalize, Duration 12 – 18 months.
- 23. Pharmacotherapy…ctd Sodium ipodate oriopanoic acid-lowers serum T 3 and T 4 levels and causes rapid improvement of hyperthyroidism; appropriate for acute management of severe hyperthyroidism that is not responding to conventional therapy
- 24. 3. Radioactive iodinetherapy . Radioiodine 131 (131I) Causes destruction of thyroid follicular cells Main complication is hypothyroidism If the first dose does not control the hyperthyroidism within 6 to 12 months,then administer another dose. Contraindicated during pregnancy and breastfeeding due to risk of cretinism
- 25. 4. Surgery Thyroidectomy Exopthalmos: Corticosteroids. Tarsorrhaphy. Orbital decompression. Cardiac arrythmias: ß- blockers. In euthyroid state, cardioversion is done.
- 26. THYROID STORM Rarebut life threatening sudden severe exarcerbation of hyperthyroidism. Causes: Precipitated by stress or infection with either unrecognized thyrotoxicosis inadequately treated thyrotoxicosis Following subtotal thyroidectomy/radio active iodine. Trauma. Pregnancy. Emotional stress.
- 27. Management Treatment startedimmediately with Propranolol 80mg/6hrs orally(dose of 1-5mg/6hrs given IV). Potassium iodide 60mg daily orally/ sodium iopodate 500mg daily orally. Carbimazole 60-120mg daily Dexamethasone 2mg/6hrs IV. Fluid replacement. 150ml/hr Antibiotics.
- 28.
- 29. Epidemiology Prevalence ofovert hypothyroidism is 0.1-2%. The prevalence of subclinical hypothyroidism is 4-10% percent of adults. F>M=5-8:1
- 30. Primary hypothyroidism Autoimmunehypothyroidism: Hashimoto's thyroiditis(TPO, thyroglobulin, TSH receptors), atrophic thyroiditis Iatrogenic: 131I treatment, subtotal or total thyroidectomy, external irradiation of neck for lymphoma or cancer Drugs: iodine excess (including iodine-containing contrast media and amiodarone), lithium, antithyroid drugs, p-aminosalicyclic acid, interferon- and other cytokines, aminoglutethimide Congenital hypothyroidism:1:3000-4000 absent or ectopic thyroid gland, dyshormonogenesis, TSH-R mutation. Iodine deficiency Infiltrative disorders: amyloidosis, sarcoidosis, hemochromatosis, scleroderma, cystinosis, Riedel's thyroiditis
- 31. Etiology Secondary hypothyroidism Hypopituitarism: tumors,pituitary surgery or irradiation, infiltrative disorders, Sheehan's syndrome, trauma, genetic forms of combined pituitary hormone deficiencies Isolated TSH deficiency or inactivity Bexarotene treatment Hypothalamic disease: tumors, trauma, infiltrative disorders, idiopathic
- 32. HYPOTHYROIDISM Symptoms: Tiredness Cold intolerance Weakness Sexual dysfunction Dry skin Hair loss Difficulty concentrating, forgetfulness Heavy menses Constipation Signs: Bradycardia Dry coarse skin Puffy face, hands and feet Diffuse alopecia Peripheral edema Delayed tendon reflex relaxation Carpal tunel syndrome Serous cavity effusions.
- 33. CLINICAL MANIFESTATIONS Skin Theskin is cool and pale in due to decreased blood flow. dry roughness of the skin . Sweating is decreased Skin discoloration may occur. A yellowish tinge may be present if the patient has carotenemia, while hyperpigmentation may be seen if ass with primary adrenal failure. Hair may be coarse, hair loss is common, and the nails become brittle. Nonpitting edema (myxedema) occurs in from infiltration of the skin with glycosaminoglycans with associated water retention Eyes Periorbital edema. Graves' ophthalmopathy may persist when hypothyroidism develops after treatment of Graves' hyperthyroidism.
- 34. Manifestations Hematologic Increased riskof bleeding (hypothyroidism-associated hypocoagulable state ) normochromic, normocytic hypoproliferative anemia Pernicious anemia in AI thyroiditis.(macrocytic anemia) iron deficiency anemia, secondary to menorrhagia Cardiovascular system decrease in cardiac output mediated by reductions in heart rate and contractility thus reduced exercise capacity and SOB during exercise. Other abnormalities: Pericardial effusion/hypercholesterolemia/Hypertension
- 35. Manifestations Respiratory system Fatigue, shortness of breath on exertion, rhinitis, and decreased exercise capacity may result from impaired respiratory function Hypoventilation occurs because of respiratory muscle weakness and reduced pulmonary responses to hypoxia and hypercapnia Sleep apnea mostly as a result of macroglossia. Gastrointestinal disorders Decreased gut motility results in constipation/marked ileus Decreased taste sensation. Gastric atrophy due to the presence of antiparietal cell antibodies. Pernicious anemia Celiac disease is four times more common in hypothyroid patients A modest weight gain due to decreased metabolic rate and accumulation of fluid Ascites is a rare finding.
- 36. Manifestations…ctd Reproductive abnormalities> (women) oligo- or amenorrhea or hypermenorrhea-menorrhagia, decreased fertility. If pregnancy does occur, there is an increased likelihood for early abortion, Hyperprolactinemia may occur, and is occasionally sufficiently severe to cause amenorrhea or galactorrhea. (men) Decreased libido, erectile dysfunction, and delayed ejaculation Neurological dysfunction — - Hashimoto's encephalopathy - Myxedema coma - when severe hypothyroidism is complicated by trauma, infection, cold exposure, or inadvertent administration of hypnotics or should be suspected in comatose patients who are hypothermic, hypercapnic, and hyponatremic. Musculoskeletal symptoms — Joint pains, aches and stiffness
- 37. CRETINISM Hypothyroidism datingfrom birth. Tyroxine is essential for growth and development of brain during the first three years. Earlier onset greater is the brain damage. Causes : - Congenital developmental defects. - Radio iodine/surgery. - Post radiation. - Iodine deficiency. - Drug induced. - Hashimoto’s thyroiditis. - Recurrent hypothyroidism.
- 38. Investigations Relies heavilyon lab tests. TFTs Primary: High TSH & low T4 Central (2˚ & 3˚): Low T4, TSH inappropriately normal for the low T4, coexisting hormone def. Lipid profiles – Fasting cholesterol and triglycerides may be raised U/E/Cs < Na+ Muscle enzymes (CPK) – elevated CBC- anaemia (normocytic normochromic) CXR- Effusions CT head- sellar/ suprasellar region.
- 39. Treatment Goals; Reverse clinicalprogression Correct metabolic derangements
- 40. Treatment STANDARD REPLACEMENTTHERAPY The treatment of choice is synthetic thyroxine (T4). Bioavailability 80% levothyroxine (T4) – 50-100µg/24h PO (1.6mcg/kg/day), review at 12wks. Adjust 6wkly by clinical state and to normalise but not suppress TSH (keep TSH 0.35-5.5mIU/L) should be taken on an empty stomach, an hour before breakfast not with other meds that interfere with absorption, such as bile acid resins, proton pump inhibitors, calcium carbonate, and ferrous sulfate . Older patients and pts with ischemic heart disease started at 25- 50mcg levothyroxine daily
- 41. SPECIAL TREATMENT CONSIDERATIONS Myxedemacoma Reduced level of consciousness, seizures Hypotension/shock Hypothermia Hyponatremia Usually in elderly hypothyroid pts. Usually precipitated by intercurrent illnesses that impairs ventilation An Emergency with a high mortality rate Treatment: Lyotironine(T3) or T4, Hydrocortisone, external warming, IV fluids
- 42.
- 43. INTRODUCTION The 4parathyroid glands are located posterior to the thyroid gland. They produce parathyroid hormone (PTH), which is the primary regulator of calcium physiology. PTH acts directly on bone,(induces calcium resorption), and on the kidney, where it stimulates calcium reabsorption and synthesis of 1,25-dihydroxyvitamin D [1,25(OH)2D], a hormone that stimulates gastrointestinal calcium absorption. Calcium and vitamin D, inhibit PTH release and synthesis.
- 44. HYPERPARATHYROIDISM Increased PTHsecretion leading to hypercalcemia and hypophosphatemia. Incidence 27 cases annually per 100,000 Prevalence HPT general population 0.1%-0.3% Prevalence women >60 years more than 1%
- 45. Causes Primary hyperparathyroidism Solitaryadenoma-80% Hyperplasia of all glands Parathyroid cancer Associated with hereditary syns MEN I (hyperparathyroidism, pituitary tumors, pancreatic tumors) MEN II – hyperparathyroidism, pheochromocytoma, medullary carcinoma of thyroid.
- 46. Causes…ctd Secondary hyperparathyroidism Decreasedvit D intake Chronic renal failure Tertiary hyperparathyroidism Occurs after prolonged secondary hyperparathyroidism
- 47. Clinical features andcomplications Symptom and signs: >1/2 asymptomatic Symptomatic: Stones, Bones, Groans, Thrones and Psychiatric Overtones - weakness and fatigue, depression, bone pain, myalgias, decreased appetite, joint pain, cognitive impairement - decreased appetite, nausea and vomiting, constipation, polyuria, polydipsia Complications Nephrocalcinosis, Recurrent nephrolithiasis, Urinary obstruction, infection, loss of renal function Osteitis fibrosa cystica: > giant multinucleated osteoclasts in scalloped areas on bone surface (Howship’s lacunae)
- 48. Parathyroid immunoassay PTHlevels Serum calcium levels Serum phosphate - 1˚ (low), 2˚ (elevated) Alkaline phosphatase – elevated Bone densitometry decreased Radioisotope studies
- 49. Management SURGERY VERSUSMEDICAL MANAGEMENT Symptomatic primary hyperparathyroidism -parathyroid surgery. Parathyroidectomy is an effective therapy that : cures the disease, decreases the risk of kidney stones, improves bone mineral density/and may decrease fracture risk and modestly improve some quality of life measurements.
- 50. Alternatives to surgery Preventivemeasures Avoid factors that can aggravate hypercalcemia, including thiazide diuretic and lithium carbonate therapy, volume depletion, prolonged bed rest or inactivity, and a high calcium diet (>1000 mg/day). Encourage physical activity to minimize bone resorption. Adequate hydration (at least 8 glasses of water per day) to minimize the risk of nephrolithiasis. Maintain a moderate calcium intake (1000 mg/day). A low calcium diet may lead to further increases in PTH secretion and could aggravate bone disease Maintain moderate vitamin D intake (400 to 600 International Units daily). Vitamin D deficiency stimulates PTH secretion and bone resorption and, therefore, is deleterious in patients with primary hyperparathyroidism.
- 51. Drug therapy Bisphosphonates andestrogen plus progestin inhibit bone resorption and can increase bone density and possibly lower serum calcium concentrations in patients with hyperparathyroidism Other medications,Eg calcimimetics or vitamin D analogues, suppress parathyroid hormone release or counteract the effects of hyperparathyroidism at the level of the PTH receptor.
- 52. HYPOPARATHYROIDISM Hypoparathyroidism is acondition of parathyroid hormone deficiency Primary hypoparathyroidism is a state of inadequate PTH activity Secondary hypoparathyroidism is a physiologic state in which PTH levels are low in response to a primary process that causes hypercalcemia
- 53. Etiology Primary Hereditary/genetic: Idiopathic-isolated autoimmune Ass’ with other abnormalities- thymus, thyroid, adrenal, ovary. Secondary Surgery(thyroidectomy and parathyroidectomy) Radiation Hemochromatosis
- 54. Clinical manifestations Paresthesias Muscle aches and cramps Twitching and spasms of muscles Fatigue or weakness Painful menstruation patchy hair loss Dry, coarse skin Brittle nails Anxiety and nervousness, headaches, depression, mood swings, memory problems Hypocalcemia: Chvostek, trousseau sign
- 55. Diagnosis Measurement ofcalcium, serum albumin (used to correct serum calcium levels) and PTH in blood
- 57. Treatment Medical treatment Calcium supplements Calcitriol Surgery parathyroidectomy Patientsat a higher risk of permanent primary hypoparathyroidism
Editor's Notes
- #5 Thyroid gland produces thyroxine(T4), calcitonin and triiodothyronine(T3).
- #6 Stored in thyroglobulin in follicular lumen
- #9 Thyroiditis – lymphocytic or postpartum
- #10 Disturbances of the normal homeostatic mxn can occur at the level of the pituitary,thyroid gland and the periphery.
- #13 * Only in graves
- #15 VON GRAEFE’S SIGN – Lid lag. JOFFROY’S SIGN – Absence of wrinkling of forehead on looking up. STELLWAG’S SIGN – Decreased frequency of blinking. DALRIMPLE’S SIGN – Lid retraction exposing the upper sclera. MOBIUS SIGN – Absence of convergence
- #17 Exacerbation of bronchial asthma
- #18 the red blood cell mass may be increased in hyperthyroidism, but the plasma volume is increased more, resulting in a normochromic, normocytic anemia.
- #20 Differential diagnosis: Panic attacks Psychosis Mania Pheochromocytoma Hypoglycemia Occult malignancy
- #21 The choice of radioactive iodine, antithyroid medication, or surgery for hyperthyroidism should be based on the cause and severity of the disease as well as on the patient’s age, goiter size, comorbid conditions, and treatment desires.
- #22 Treatment: Reducing thyroid hormone synthesis: Antithyroid drugs (Methimazole, Propylthyouracil) Radioiodine (131I) Subtotal thyroidectomy Reducing Thyroid hormone effects: Propranolol Glucocorticoids Benzodiazepines Reducing peripheral conversion of T4 to T3 Propylthyouracil Glucocorticoids Iodide (Large oral or IV dosage) (Wolf-Chaikoff effect)
- #23 PTU is preferred
- #24 The Wolff–Chaikoff effect is an autoregulatory phenomenon that inhibits organification in the thyroid gland, the formation of thyroid hormones inside the thyroid follicle, and the release of thyroid hormones into the bloodstream
- #25 Radio iodine ablation – Postmenopausal women and elderly men. In recurrence following surgery. Given to fertile women conception postponed to 1 year.
- #28 Administer oxygen. Monitor all vital signs. Initiate basic life support if necessary.
- #30 Worldwide iodine def is the foremost cause but in areas of adequate iodine intake autoimmune thyroid dse is the commonest cause.
- #35 HTN due to incr peripheral vascular resistance
- #39 Positive ANF.
- #41 T4 is a prohormone with very little intrinsic activity and it is deiodinated in peripheral tissues to form T3, the active thyroid hormone.
- #42 SPECIAL TREATMENT CONSIDERATIONS Elderly patients Coronary Artery Disease Poor adrenal gland reserve Childrens Pregnancy Emergency surgery (Non thyroid related)