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Detailed approach to thyroid gland and parathyroid glands

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Detailed approach to thyroid gland and parathyroid glands

  1. 1. 1 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013THYROID AND PARATHYROID DISORDERSBY DR. MAGDI AWAD SASI 2013
  2. 2. 2 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013Thyroid Gland AnatomyLargest endocrine gland; high rate of blood flowAnterior and lateral sides of tracheao Two large lobes connected by isthmusThyroid follicleso Filled with colloid and lined with simple cuboidal epithelial(follicular cells) that secretes two hormones, T3 and T4 .Thyroid Gland physiology: Synthesis and release of thyroid hormones is influenced by TSH from thepituitary. Two kinds of hormones are produce in the thyroid gland triiodothyronine(T3) and thyroxine (T4). Concern the regulation of the metabolic and oxidation rates in all thetissues of the body except the brain.
  3. 3. 3 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013 At physiological levels, they stimulate growth and development withsynthesis of many enzymes. At pharmacological levels, increased heat production and O2consumption related in part to uncoupling of oxidative phosphoryiation. Many of the effects appear to be mediated by way of sympatheticnervous system. The sympathetic overactivity seen in many patients with anxiety statesaccounts for the frequent mistakes in diagnosis. Hypothalamus - the highest control of thyroid function((TRH)). Thyroid hormoneo Body’s metabolic rate and O2 consumptiono Calorigenic effect - heat productiono heart rate and contraction strengtho respiratory rateo Stimulates appetite and breakdown CHO, lipids and proteinso Alertness, bone growth/remodeling C (calcitonin or parafollicular) cellso Produce calcitonin blood Ca2+, promotes Ca2+deposition andbone formation especially in children What is Hyperthyroidism ?Increased synthesis and production of too much thyroid hormones iscalled hyperthyroidism. This leads to thyrotoxicosis.Thyrotoxicosis is the over production of thyroid hormones withoutincreased synthesis. Thyrotoxicosis could be a result of thyroditis or toomuch intake of exogenous thyroid hormone.
  4. 4. 4 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013 What Causes Hyperthyroidism?Hyperthyroidism can be that the whole gland is producing too muchhormones or there is only a single nodule producing more than enoughhormones. When this happens, the single nodule is called "hot nodule". causes of hyperthyroidism and thyrotoxicosis:1. Too much iodine intake2. Autoimmune --Graves disease-the most commonThyroiditis-Hashimotos, DeQuervains, reidls thyroiditis.3. Noncancerous growths of thyroid or pituitary gland4. Toxic thyroid adenoma5. Toxic multinodular goiter6. Postpartum thyroiditis7. TSH-secreting tumors (pituitary)8. HCG-producing tumors9. Hyper functioning ovarian teratoma.10.Overmedicating with synthetic thyroid hormone.11.Drugs—Amidarone.12.Thyrotoxicosis factitiaSymptoms of thyrotoxicosis:Hyperthyroidism can either be symptomatic or asymptomatic. It can beacute or chronic depending on the length with which the thyroid glandhas been producing more than normal amounts of the hormones. Thesymptoms usually begin slowly and are not noticeable as can be largelyattributed to stress only. As time goes , the symptoms will become morepronounced.The paradoxical association of loss of weight with normal or increasedappetite is particularly suggestive of hyperthyroidism.
  5. 5. 5 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013D/D Diabetes mellitus--------Defective alimentary absorption.The weight is gained if increased appetite is more than the metabolic rateI. Heat production increased:Heat intoleranceincreased sweatingII. CNS--- pt can’t keep still.Undue fatigability , proximal muscle weakness( thyrotoxicmyopathy) ,hyperkinesias—exaggerated and purposelessmovements ,Difficulty concentrating ,tremors , Emotionliability.(mysthenia gravis association 10% ).III. Psychiatric:Nervousness and anxiety, Irritability, sleep disturbance,Psychosis , insomnia.IV. CVS--- palpitation , dyspnea on exertion , chest pain,CCF The elderly patient usually present with cardiovascular symptoms((predominant or alone)). Unexplained heart failure after middle age should always arousesuspicion of hyperthyroidism. Failure of digitalis in normal dosage to control the rapid heart rateis very suggestive. Many of the effects appear to be mediated by way of sympatheticnervous system sensitivity. Difficulty in stabilizing a diabetic patient is sometimes the first clueto the thyroid disorder.V. GIT---Weight loss despite an increased appetite, diarrhea,heartburn. For weight variation according to age,Young –increased weight /// Elderly- weight decreased.VI. Musculoskeletal system and growth:Pain in the back—thyrotoxic kyphosis resulting from osteoporosisHypercalcemia with its clinical squeal is very rare, arthralgia ,proximal muscle weakness.
  6. 6. 6 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013VII. Integument:Loss of hair. Nails may show recession from the nail bed.Polyuria and polydypsia—less common.NECK---- A visible enlargement of the thyroid gland in the neck (goiter)EYES---Exophthalmos - protruding eyes, diplopia, chemosis, swellingMenstrual cycle variations – lightening of menstrual flow and lessfrequent periods.CLINICAL FINDING :If there is neck swelling (GOITER) ,it is a must to pass through 4 steps.1. Inspection---site,size ,shape,skin changes,surface .ASK THE PATIENT TO SWALLOW—PATHOGNOMIC2. Palpation- contirm , temperature, borders, consistency,tendenrness3. Percussion----for retrosternal extension4. Auscultation--- for bruitExam the eyes for eye signs --is it Graves.Skin –feels warm , moist skin with fever.CVS—PULSE—collapsing , sleeping heart rate 80/min , atrial fibrillationBLOOD PRESSURE--- systolic HTN with high pulse pressure.
  7. 7. 7 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013CCF--- raised JVP , pedal edema, systolic murmursCNS---hyperactive reflexesCLINICAL SIGNS IN GRAVES DISEASE:Increase in thyroid gland sizeSoft to slightly firmNon-nodular / nodularBruit and/or thrillMobileNon-tenderWithout prominent adenopathyEYE SIGNS:Ophthalamic Graves disease:1. Swelling of the eyelids-Due to overfilling of orbit.The lids appear congested andedematous –congestiveophthalmopathy.2. Irritation of the conjunctivae:.Grittiness and soeness of the eyes..Edema of conjunctiva( chemosis)
  8. 8. 8 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013.It may ulcerate and may prolapse between the lids..Corneal Damage may occure..The appearance of prominent vessels at the lateral canthi is usually asign that the ocular manifestation are going to be trouble some.3. Exophthalmos:Appearance of sclera B/W the lower lid and limbus of cornea .Means protrusion of the eye ball.Symmetrical in Graves disease with hyperthyroidism.Caused by increased bulk of orbital contents.The fat is increased and the muscles enlarged, infiltrated withlymphocytes and contain increased amounts of water andmucopolysccharides.Usually alters little with treatment and may be remarkably persistent.In some, it is progressive and may cause loss of vision if effectivetreatment not given ((malignant exophthalmos )).Unilateral exophthalmos causes:1.Retro-orbital aneurysm2.Retro-orbital tumor3. Involvement from outside4. Chronic myopia4. Lid retraction:Recognized by the appearance of sclera B/W The upper lid and the limbus ofthe cornea when the patient is looking straight a head and not staring.2types:1.Spastic lid retraction:It is diagnostic of Graves disease.It is present in all positions of gaze
  9. 9. 9 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013It is one of the commonest eye signs of Graves diseaseIt is due to spasm of the elevator palpebrae superioros and sympatheticstimulation of the superior orbital muscle of muller.2.Paralytic lid retraction:Not specific for Graves disease.Occurs only in the presence of limitation ofupward gazeI. Disorders of the muscles-Graves disease,ocular myopathyII. Mysthenia gravisIII. Upper brain stem lesionsIt is thought to be caused by over innervationsof elevator palpebrae superioros when anattempt is made to look up.Lid retraction is the cause of a conjunctivalirritation and keratitis.5. Lid lag: NORMALLID LAGOccurs when the sclera B/Wupper eye lid and corneabecomes visible as thepatient gaze follows theexaminer fingers down wardfrom the position ofmaximum elevation.The eye moves not in closecontact with eye lid as adelay in lid movement.
  10. 10. 10 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 20136.Ophthalmoplegia:Paresis of one or more ofextraocular muscles usuallycauses diplopia.Upward and outwardsmovements reduced 4 times.Limitation of upward gaze may be due to tethering andadhesions of inferior oblique and superior rectus muscle whenthey decussate.It is pathognomic in Graves disease .It is one of the most unpleasant ocular complication of graves .7.Congestive ophthalmopathy: malignant exophthalmosIT IS A MEDICAL EMERGENCY REQUIRING IMMEDIATE ADMISSION.The patient complain of severe pain in the eye or failure of vision.It is a sever and progressive ocular changes in Graves characterized by:1. Prominent eyes2. Lids and conjunctiva swollen and inflamed3. Marked ophthamoplegia4. Retinal veins may be prominent.5. Papilloedema may develop.6. Oular tensions may be high.7. Keratitis8. Pressure on the optic nerve may be sudden and complete whichcauses loss of vision even with normal fundus.
  11. 11. 11 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013Clinical Differentiation of LidRetraction from Proptosis Measurement usingprisms or special ruler(exophthalmometer)OR with scleraseen above iris : Observing position oflower lid (sclera seenbelow iris = proptosis,lid intersects iris = lidretraction)Normal positionof eyelidsProptosis Lid retractionSKIN SIGNS---PRETIBIALMYXEDEMA5% of patients.Usually affects the shins frontalareaThe swelling often extends overthe dorsum of the feet and toeswhere it is associated with tissuegrowth.The skin is coarse ,purplish –red ,peaud orande appearance ,raised surface Thick, leathery consistency,with coarse hair in the affected area.
  12. 12. 12 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013The superficial layer of the skin is infiltrated with the mucopolysaccharidehyaluronic acid.Nodularity, sometimes.Sharply demarcatedmargins,Non-tender.It tends to develop afterhyperthyroidism has beentreated by surgery or withradioactive iodine.The latent period take 4-32months.Soft tissue swelling that ispigmented andhyperkeratotic.Thyroid AcropachyClubbing of fingers.Painless.Periosteal bone formation andperiosteal proliferation .The subperiosteal new boneformation resembles soap bubbleson the surface of bone with coarsespicules.
  13. 13. 13 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013 Onycholysis of ThyrotoxicosisDistal separation of theNail plate from nail bedPlummer’s nails) Frequency of Neuromuscular Disorders Associated with Thyrotoxicosis: Myopathy due to thyrotoxicosis >50Usually proximal and mild to moderate Hypokalemic periodic paralysis <1 Myasthenia gravis <1 Thyrotoxic Periodic Paralysis: Most common cause of hypokalemic periodic paralysis Flaccid paralysis Lower extremities affected most often Ocular and bulbar muscles uninvolved, respiratory muscles rarelyinvolved Most often starts during sleep Precipitated following exercise, high salt intake or high carbohydratediet Hypokalemia during the paralysis .
  14. 14. 14 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013 Differential Diagnosis of a Painful Thyroid: Subacute granulomatous thyroiditis Most common Hemorrhage into a goiter, tumor or cystwith or without demonstrable trauma Less common Acute suppurative thyroiditis <1% Anaplastic (inflammatory) thyroid carcinoma <1% Hashimoto’s thyroiditis <1% TB, atypical TB, amyloidosis <1% Metastatic carcinoma DiagnosisMany symptoms of hyperthyroidism are the same as those of otherdiseases, so hyperthyroidism usually cannot be diagnosed based onsymptoms alone. With suspected hyperthyroidism, you have to take amedical history and perform a thorough physical exam. Several bloodtests confirm the diagnosis of hyperthyroidism and find its cause:1. **TSH test**The first test , The most accurate measure of thyroid activity available.The TSH test is especially useful in detecting mild hyperthyroidism.Generally, a TSH reading below normal means a person hashyperthyroidism and a reading above normal means a person hashypothyroidism.2. **T3 and T4 test**With hyperthyroidism, the levels of one or both of these hormones inthe blood are higher than normal3. Thyroid-stimulating immunoglobulin (TSI) test((Thyroid stimulating antibody test)) measures the level of TSI in theblood. Most people with Graves’ disease have this antibody.
  15. 15. 15 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 20134. Ultrasound neck-U/S more sensitive than physical examination , particularly fornodules that are < 1 cm or located posteriorly in the gland.U/S also more sensitive than thyroid scanThyroid U/SBenignCharacteristicsMalignant CharacteristicsRegular borderHalo (sonolucent rim)Irregular borderNo HaloHyperechoic Hypoechoic(more vascular)Egg shell calcification MicrocalcificationN/A Intranodular vascular spots(color doppler)5. **Radioactive iodine uptake test**low levels of iodine uptake might be a sign of thyroiditis, whereas highlevels could indicate Graves’ disease.
  16. 16. 16 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013Causes of ThyrotoxicosisDivided by Degree of Radioiodine UptakeHigh I123 UptakeGraves’ diseaseToxic nodular goiterTSH-mediated thyrotoxicosisPituitary tumorPituitary resistance tothyroid hormoneHCG-mediated thyrotoxicosisHydatidiform moleChoriocarcinomaOther HCG-secreting tumorsThyroid carcinoma (very rare)I123Low I123 UptakeSubacute thyroiditisHashitoxicosisDrug-inducedIodideThyroid hormoneStruma ovariiFactitiousI1236. **Thyroid scan**A thyroid scan shows how and where iodine is distributed in thethyroid. The images of nodules and other possible irregularities help todiagnose the cause of a person’s hyperthyroidism.Thyroid ScanThyroid nodule: risk of malignancy 6.5%Coldnodule16-20%malignant“Warm”Nodule(indeterminant)5% malignantHot NoduleTc-99m < 5%malignantI123 < 1% malignantonly 5-10% of nodules
  17. 17. 17 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 20137. FINE NEEDLE ASPIRATION• 25G Needle, 10cc syringe• Done in Office• NOT INDICATED IN TOXIC PATIENTS .• +/- Local anaesthesia• 3-5 passes• SEN 95-99% (False Negative rate 1-5%)• SPEC > 95%• Benign: macrofollicular or "colloid" adenomas, chronic autoimmune(Hashimotos) thyroiditis• Suspicious or Indeterminant: microfollicular or cellular adenomas(follicular neoplasm)Treatment:Hyperthyroidism is treated with medications, radioiodine therapy, or thyroidsurgery. The aim of treatment is to bring thyroid hormone levels to a normalstate, thus preventing long-term complications, and to relieve uncomfortablesymptoms. No single treatment works for everyone.Treatment depends on the cause of hyperthyroidism and how severe it is. Whenchoosing a treatment, consider1. Patient’s age2. Side effects of the medications3. Pregnancy or heart disease4. The availability of an experienced thyroid surgeon. Medications1. Beta blockersBeta blockers act quickly to relieve many of the symptoms ofhyperthyroidism, such as tremors, rapid heartbeat, and nervousness, butdo not stop thyroid hormone production. Most people feel better withinhours of taking these medications.
  18. 18. 18 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 20132. Antithyroid medications :Treatment of hyperthyroidism Antithyroid drugs Carbimazole 10 mg tid Reduce to maintenance after 4 weeks Rash, GI, agranulocytosis Graves – withdraw drugs after course oftreatmentCarbimazole, thiouracil ,methimazolAntithyroid medications interfere with thyroid hormone production but don’tusually have permanent results. Antithyroid medications are not used to treatthyroiditis.Once treatment with antithyroid medications begins, thyroid hormone levelsmay not move into the normal range for several weeks or months. The averagetreatment time is about 1 to 2 years, but treatment can continue for manyyears.Side effects in some people, including:1. Allergic reactions such as rashes and itching2.Agranuloctosis- decrease in the number of white blood cells in the body.3. Liver failure, in rare casesAsk the patient to stop antithyroid medication if he develop:1. Fatigue & weakness3.Vague abdominal pain & Loss of appetite5. Skin rash or itching & Easy bruising7. Jaundice8. . Fever & persistent sore throat.
  19. 19. 19 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013Antithyroid medications and pregnancyRadioiodine therapy is contraindicated . propylthiouracil (PTU), isavailable for women in this stage of pregnancy or for women who areallergic to methimazole and have no other treatment options.Some women are able to stop taking antithyroid medications in the last 4to 8 weeks of pregnancy due to the remission of hyperthyroidism thatoccurs during pregnancy. However these women should continue to bemonitored for recurrence of thyroid problems following delivery.Methimazole:Advantage –1.less frequent doses , fewer pills & more convenient.2. lower incidence of acute hepatic necrosis.Complications:Serum sicknessCholestatic jaundiceHypoglycemiaLoss of tasteAlopeciaNephritic syndromeDose (10mg)30---60 mg once dailyIndications :1. Toxic Goiter2. Preparing hypetthyroid for surgery3. Preparing elderly fo RAI4. Mild toxicosis
  20. 20. 20 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 20133. Radioiodine TherapyIn radioiodine therapy, patients take radioactive iodine-131 by mouth.Because the thyroid gland collects iodine to make thyroid hormone, it willcollect the radioactive iodine from the bloodstream in the same way. Theradioactive iodine gradually destroys the cells that make up the thyroidgland but does not affect other body tissues.Treatment of hyperthyroidism Radio-iodine Inflammatory response followed byfibrosis May be used for Graves, TMG or TA ? Need for drug treatment before andafter May need retreatment Long term risk of hypothyroidismTreatment with beta blockers can control symptoms.women wait a year after treatment before becoming pregnant.4. Thyroid Surgery((least-used))Surgery may be used to treat:1.Pregnant women who cannot tolerate antithyroid medications2.Large goiters and Cancerous thyroid nodulesBefore surgery, we may prescribe antithyroid medications to temporarilybring a patient’s thyroid hormone levels into the normal range. Thispresurgical treatment prevents a condition called thyroid storm—asudden, severe worsening of symptoms—that can occur whenhyperthyroid patients have general anesthesia.
  21. 21. 21 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013Treatment of Hyperthyroidism Surgery Rarely used nowadays Need to be rendered euthyroid beforesurgery Lugol’s iodine 0.1-0.3 mls tid for 10 daysbefore surgeryDRUGS USED IN THYROTOXICITY
  22. 22. 22 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013After surgery:A. When part of the thyroid is removed, T3T4 levels may return to normalB. Some patients may still develop hypothyroidism, need thyroxine.C. If the entire thyroid is removed, lifelong thyroxine is necessary.D. After surgery, patients’ thyroid hormone levels should be monitored.Facts TO REMMEBER: Hyperthyroidism is a disorder that occurs when the thyroid gland makesmore thyroid hormone than the body needs. Hyperthyroidism is most often caused by Graves’ disease, an autoimmunedisorder. Hyperthyroidism is much more common in women than men. Hyperthyroidism is also more common in people older than age 60 and isoften caused by thyroid nodules. Hyperthyroidism in this age group issometimes misdiagnosed as depression or dementia. For people olderthan age 60, subclinical hyperthyroidism increases their chance ofdeveloping atrial fibrillation , heart failure. Hyperthyroidism is treated with medications, radioiodine therapy, orthyroid surgery. No single treatment works for everyone. Treatment by medication- antithyroid and B blockers . Hyperthyodism will not cause carcinoma. Exophthalmos is characteristic for graves disease. After RAI therapy, hypothyroidism is the rule and TR is thyroxine lifelong. Treatment of Hyperthyroidism IN USA:Make diagnosis, get RAI uptake.Beta block (inderal 40-80 mg tid).If RAI uptake is high – treat with RAI.If RAI is low – symptomatic
  23. 23. 23 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013 Graves Eye DiseaseUsually mild – Tx, protective glasses, elevate head of bed, conjunctivallubricantsHigh dose steroidsExternal radiotherapyOrbital decompression Toxic Solitary Adenoma Rare cause (< 2% of patientswith hyperthyroidism) Younger people 30’s and 40’s Scan Benign follicular adenomas
  24. 24. 24 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013Toxic solitary noduleLess than 40year more than 40year1.Make pt euthyrod by: 1.Radioactive iodinePropraolol, thiourea A.Permenant hypothyroid2.Before 10 days of O.T.Iodine therapy. 1/3 of pt by 8 yr afterRAI3.Surgery B. Nodule remain in50%C.10% of pt may grow.Post operative hypothyroidism-Trsnsiet.14% become hypothyroidBy 6 years after surgery.MULTINODULAR GOITER: Older Usually less severe hyperthyroidism May have subclinicalhyperthyroidism. May have long history of goitre A thyroid containing multiplenodules is likely to be benign MNG. Fine needle biopsy is performed onany nodule that is growing /dominant/ hard inconsistency.
  25. 25. 25 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013Larger retrosternal goiter rarely harbor a malignancy but can be followed by CT.1.Surgical resection=compression 2 .Thyroxine useful in pt TSHor Continuous growthThyroxine should not be prescribed3.Pt found be toxic may have RAI scan For pt w suppressed TSH since mayIF I123 is a therapeutic consideartion Add to autonomous secretion andcause thyrotoxicosisUss guided FNA biopsy is reserved for pts with nonpalpable nodules 1.5cm indiameter with H/O head-neck irradiation.TOXIC MULITNODULAR GOITER1.Symptomatically with propranolol/thiourea 3.PT follow a low iodine diet toEnhance thyroid uptake of RAI95% recurrence rate after they are stopped. Which may be relatively low .2. RAI should be given after stopping T.U./ 3days 4.High doses 0f RAI required.And reender patient euthyroid. 5.Pt should be followed closelyHyper and hypo are common6.SURGERY FOR COSMOTIC AND PRESSURE SYMPTOMS
  26. 26. 26 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013EMERGENCY THYROID STATUS ((THYROID STORM)) It is an exacerbation of hyperthyroidism. IT is an acute life threatening , hypermetabolic state which may be theinitial presentation of thyrotoxicosis. Less than 10% of hospitalized thyrotoxicosis. Mortality 20---30% Can be caused by all causes of hyperthyroidism but Graves the mostcommon.Precipitating event:I. Systemic insult—surgery, trauma ,myocardial infarction ,pulmonaryembolism, severe infection, DKA.II. Discontinution of antithyroid drugsIII. Excessive iodine ( amiodarone , radiocontrast dyes)IV. Radioiodine therapySymptoms:o Increased all vital signso Increased body temperature, sweatingo Tachycardia, Arrythmia, atrial fibrillationo Vomiting/ nausea, dyspnea, tacchypneao Diarrhea, epigastric discomforto Heart failure/ pulmonary odemao ConfusionLABORATORY:o Increased free T4 AND T3o Decreased TSHo Hyperglycemia , elevated alkaline phosphatase, leukocytosis, Mildhypercalcemia , and elevated liver enzymes.o Cortisol increase (( NORMAL LEVEL = ADRENAL INSUFFICIENCY))
  27. 27. 27 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013Treatment:A. TREATMENT DIRECTED AT THYROID GLAND AND HORMONES--Inhibition of new hormone synthesis with Thioamide drugs such as PTU andmethimazole.Inhibition of hormone release with Iodine & potassium iodide(Lugols solution)& Lithium carbonate.B. TREATMENT DIRECTED AT PREVENTING HORMONES AFFECTS ON THEBODYPTU , Corticosteroids ,B blockes( propanolol),Amiodarone, Plasmapheresis.C. TREATMENTS DIRECTED AT MAINTAINING HOMEOSTASIS Hyperthermia—acetaminophen , cooling , blankets Fluid and electrolyte testing / replacement Glucose Vasopressors Digoxin and diuretics if appropriate. BETA BLOCKERS—decrease adrenergic hyperactivity PTU------------------blocks the peripheral conversion of T4 TO T3. GLUCOCORTICOIDS—inhibit hormone production and decrease peripheralconversion from T4 to T3.SODIUM IODIDE SOLUTION(LUGOLS)—high levels of iodide will initiallysuppress release of thyroid hormoneTreat cardiac symptoms , fever and hypertension.“Apathetic Hyperthyroidism” Common symptoms:Weight loss, anorexiaConstipation despite thyrotoxicTachycardia, Atrial fibrillation , Heart failure, anginaCognitive Dysfunction
  28. 28. 28 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013HypothyroidismDefinition: Hypometabolic state due to deficiency of thyroid hormones . Hypothyroidism results specially from glandular destruction andunderproduction of thyroid hormones. It is characterized by Accumulation of mucopolysaccharides in the SCtissue ((non pitting edema )). Incidence : middle -50s female:male ratio → 10:1ETIOLOGYA. PRIMARY : THYROID FAILURE (95%)B. SECONDARY : PITUITARY TSH DEFICITC. TERTIARY : HYPOTHALAMIC DEFICIENCY OF TSHD. PERIPHERAL RESISTANCE TO THE ACTIONS OF THYROID HORMONES• Autoimmune hypothyroidism:-Hashimoto’s thyroiditis- Atrophic thyroiditis• Iatrogenic:-Radio-iodine therapy- Thyroidectomy- External radiation to theneck (lymphoma/CA)• Drugs :-Antithyroid drugs,amiodarone, lithium,interferon• Congenital hypothyroidism:-Thyroid agenesis- Dyshormogenesis- TSH-R mutationPRIMARY CAUSES• Iodine deficiency• Infiltrative disorderInfiltrative disorders: amyloidosis, sarcoidosis, hemochromatosis…
  29. 29. 29 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013Transient hypothyroidism:1. Silent thyroiditis , including postpartum thyroidtis2. Subacute thyroiditis3. Withdrawal of thyroxine trtB. Secondary hypothyroidism:1. Hypopituitarism: tumors, pituitary surgery or irradiation, infiltrativedisorders, Sheehan’s syndrome, traumaC.3ry -Hypothalamic disease: tumors, trauma, infiltrative disorders .Clinical manifestations:There will be systemic symptoms which may delay the diagnosis.It is diagnosed either at first sight or not at all.Myxedema enters into D/D of unexplained heart failure not responding todiuretics and digoxin.Myxedem enters into D/D unexplained ascitis(protein content high).The pituitary is often quite enlarged in 1ry hypothyrodism due to reversiblehyperpalsia of TSH- secreting cells.The concomitant hyperprolactinemia seen in hypothyrodism can lead tomistaken diagnosis of pituitary adenoma.CNS—Tiredness ,weakness, Difficulty concentrating and poor memorythought and movements are retarded, parasthesia , thyroid maddness,speech isslow , hoarse voice , depression, psychosis, confusion, Perceptivedeafness(40%)of all cases.CVS—Fatigue , Dyspnea , lose of effort , legs swelling , syncopyAngina pectoris , CCF,pericardial sffusion.GIT---lose of apetite , abdomenal distention ,constipation .
  30. 30. 30 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013SKIN- Dry skin , feeling cold , thick coarse skin.Endo----Weight gain , cold intolerance , hair lossMENSTRAUL CYCLE----menorrhagia , Dysmenorrhea.Amenorrhea may be the presenting feature in young patients.They have a tendency for fluid collection in negative spaces even in theabsence of bilateral leg swellings. The patient may present with unexpainedsymptomatic pleural effusion or ascitis or pericardial effusion .Hypothyrodismcan be subclinical for long time as the patient may be at risk of coronary heartdisease as low thyroid hormones elevate the cholestrol . Pericardial effusionmay be huge and result into cardiac tymponade with heart failure symptoms .The commonest presentation:1. Tingling and numbness in the fingers due to carpel tunnel syndrome.2. Muscular aches & pains is a prominent feature following thyrodectomy.3. Too much reliance should not be placed on thining of outer third of theeyebrows---------------uncommon in normal peopleRare presenting features:1.Hoffmans syndrome: Patient presents with stiff,aching ,swollen muscles
  31. 31. 31 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 20132.CNS disorders:Epilepsy ,drop attacks ,dementia ,cerebellar ataxia ,peripheralneuropathy.All of which may in large part recover with thyroxine treatment.3.Coma with hypothermia: Especially elder patient living alone with inadequate blanket. Precipitated by phenothiazine. In mild hypothyrodism, the symptoms are usually minor and non specific. Tiredness, Depression ,Puffiness of face , Periorbital swelling andconstipation. May be present singly or in combination with out H/O thyroid diseases.CLINICAL SIGNS: Dry skin ,coarse ,thick and rough, distinict yellowish tint. Malar flush, cool peripheral extremities &cyanosis of ears Enlarged tongue D/D Amyloidosis. Puffy face,periorbital edema,pallor. Puffy hands and feet (non pitting thickning of S/C tissue) . Diffuse alopecia-dry ,brittle, sparse,come out easily. Hands –reynauds phenomena Bradycardia Delayed tendon reflex relaxation Carpal tunnel syndrome
  32. 32. 32 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013
  33. 33. 33 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013Delayed Deep Tendon Reflex• Achilles’ tendon reflex time mostcommonly sought but may also beeffectively tested on brachioradialis orbiceps• Achilles’ tendon reflex timing is best elicited with patient kneeling.COMPLICATIONS OF HYPOTHYRODISM:1. Mostly cardiac----CAD , CCF2. Increased susceptibility to infections3. Megacolon in long standing hypothyroidism4. Organic psychosis with paranoid delusions (madness)5. Infertility (rare cause)6. Adrenal crisis may be precipitated by thyroid therapy.7. Convulsions8. Deep stupor & coma9. Refractory hyponatremia in sever myxedema.10 .Myxedematous pt are sensitive to opiates.11. Inappropriate secretion of ADH has been observed12. Sellar enlargement & TSH secreting tumors may develop in untreatedpt which decrease in size after replacement therapy.LABORATORY INVESTIGATION:Suspicion of hypothyroidism in the appropriate clinical context is the key todiagnosis.A. Family history of thyroid disease, Goiter , vitiligo ,autoimmune disease.
  34. 34. 34 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013B. H/O previous destructive therapy• Diagnosis : serum TSH: serum T4  total or free?: thyroid autoantibodies• In outpatient setting → serum TSH !!! Dyslipidemia with elevated cholesterol and triglycerides AnemiaCNOCLUSION: TSH ↑ and FT4 normal: subclinical hypothyroidism TSH ↑ and FT4↓:clinical hypothyroidism TSH normal or ↓ and FT4 ↓:secondary hypothyroidismMANAGEMENT:• Aim: to make patient euthyroid clinically & biochemically.• Treatment with L-thyroxine is life-long → ensure compliance!!Monitoring:• Clinically & biochemically• Measure TSH and free T4 2-3 month after initiation of therapy →determine maintenance dose.
  35. 35. 35 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013OVERT HYPOTHYROIDISM• Starting dose : 50-100 ug/d →→ 100-200ug/d within 2 weeks• IHD / grossly hypothyroid / elderly:• Start at 25 ug/d• ↑ slowly within 2-4/52 according to pt response• Angina: withhold / ↓ dose. Proper Management of IHD• Hypopituitarism:• Cortisol: to avoid adrenal crisisSUBCLINICAL HYPOTHYROIDISM:• L-thyroxine to ↓ risk of CAD• 50-100 ug/d →→ adjust to maintain TSH at normal level• Most asymptomatic & don’t need Rx (monitor TSH q2-5y)• Treatment Indications:A. Increased risk of progressionB. TSH > 10, Female > 50 year old.C. Anti-TPO Ab titre > 1:100,000 ?D. Goitre present ?E. Dyslipidemia?F. Total cholesterol (TC) 6-8% if TSH > 10 and TC > 6.2 nMG. Symptoms?H. Pregnancy, Infertility, Ovulatory Dysfunction.
  36. 36. 36 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013PREGNANCY:• ↑ dose, especially in 2nd/ 3rdtrimesterLevothyroxine (T4)• Eltroxin (GSK)• Synthetically made• 50 ug white pill  no dye (hypoallergenic)• Most commonly prescribed treatment for hypothyroidism• No T3 (but 85% of T3 comes from T4 conversion)• All patients made euthyroid biochemically• Most (but not all) patients feel normal• Average dose 1.6 ug/kg• Age > 50-60 or cardiac disease: must start at a low dose (25 ug/d)• Recheck thyroid hormone levels every 4-6 weeks after a dose change• Aim for a normal TSH level• Medical situations where T4 medication may be affected.ex:A. Estrogen: Pregnancy, OCP, HRTi. Need to increase T4 dose!B. Drugs that interfere with T4 absorptioni. Iron, Calciumii. Cholestyramine (cholesterol resin Rx)At least 4h between T4 and these drugs!
  37. 37. 37 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013Liothyronine (T3)• Cytomel (Theramed)• Shorter half-life• Fluctuating levels (i.e. need a slow-release pill)• Twice daily dosing often needed• 10x more potent: palpitations & other cardiac side effects• High T3 levels, low T4 levels (not physiologic either!)HYPOTHROID MEDICAL EMERGECY((MYXEDEMA COMA))• Severe, uncompensated form of prolonged hypothyroidism.• Precipitated by stress / infection / drug• Complication: signs of hypothyroidism with1 Hypoventilation2. Cardiac failure3. Fluid & electrolyte imbalance4. Coma 50% of cases
  38. 38. 38 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013PLAN OF MANAGEMENT1. Treat precipitating cause2. Gradual rewarming → blanket3. Accurate core T° → rectal thermometer– Aim for slow ↑ in core T° : 0.5 °C/hr4. Cardiac monitoring5. Correction of electrolyte abnormalities6. Adequate hydration & nutrition (dextrose)7. L-thyroxine (300-400 ug oral/iv) &tri-iodothyronine 10 ug 8 hrly8. Hydrocortisone : blood cortisolTHYROIDITISCLASSIFICATION:SUBACUTE, NONSUPPURATIVE UNKNOWN CAUSE ASSOC. WITH VIRAL URT INFECTIONSCHRONIC, HASHIMOTO’S IMMUNOLOGICAL FACTORS PRESENCE OF IMMUNOGLOBULINS &ANTIBODIES DIRECTED AGAINST THETHYROID
  39. 39. 39 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013Inflammation of the thyroid gland (thyroiditis) comprises many commondisorders of the thyroid gland. Thyroiditis affects mainly women and can occurat any age. Affected patients can be euthyroid, hypothyroid or hyperthyroiddepending on the cause. Many patients ultimately develop permanenthypothyroidism.Key learning pointsHashimoto’s thyroiditis is the most common form of thyroiditis.Subacute or De Quervain’s thyroiditis is most likely due to a viral infectionThyroiditis can often lead to hypothyroidism developing.Amiodarone can cause hyperthyroidism or hypothyroidismAn enlarging or hard thyroid could also be due to a carcinoma.Hashimoto’s Disease(( chronic lymphocytic thyroditis )): Most common cause of hypothyroidism in North America (not idodinedefeciency!)& most common form of thyroditis. Autoimmune Its frequency is increased by dietary iodine. Females > Males 6 times , Runs in Families. Antithyroid antibodies:Thyroglobulin Ab ,Microsomal Ab ,TSH-R Ab (block) First preceded by subclinical hypothyroidism with normal thyroidhormones levels and elevated TSH Later ,FT4 levels fall and TSH levels rise further Auto antibodies can be induced by amidarone, interferon ,IL 2,GCSF. Anti TPO +++ C/F:Diffusely enlarged ,firm, finely nodulesOne lobe may be asymmetrically enlarged (D/D neoplasm)Pt c/o neck tightness, pain &tenderness are not present.10% of cases are atrophic ,fibrotic particularly in elderly female.LAB.: antiperoxidase (95%) & antithyroglobulin(60%).
  40. 40. 40 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013 Treatment: Thyroid Hormone Replacement Levothyroxine (T4) No benefit to giving iodine! In fact, iodine may decrease hormone production Variety :1.Subclinical thyroditis:Very common 40% female , antibodies 13% female2.Postpartum thyroditis:Transient hyperthyroidism followed by hypothyroidism.Recovery is the rule.Subacute thyroditis:Common disorders De quervains thyroditisGranulomatous thyroditisGaint cell thyroditisPresented by acute painful enlargement of thyroid gland and dysphagia .The pain may radiate to the ears.Silent thyroditis -----no painYoung and middle aged women are most commonly affected.Viral infection has been suggested as the cause.Clinically; the manifestation may persist for weeks or months andassociated with thyrotoxicosis.LAB.:ESR increased and antithyroid antibodies decreased.I123 radioactive uptake is lowFine needle aspiration-----Gaint multinucleated cells.
  41. 41. 41 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013Suppurative thyroditis:Rare disorderC/F-Severe pain, tenderness& redness,fluctuation in thyroid gland region.Caused by pyogenic organisms.Occurs in the course of systemicinfection.Riedlels thyroditis(chronic fibrous thyroditis):It is called woody thyroiditis,ligamentous thyroiditis,riedlesstruma.It usually causes hypothyroidism andmay cause hypoparathyrodism .Age –middle age or elder women.Enlargement is often asymmetric.The gland is stony hard and adherent to the neck structures.This leads to compression signs-Dysphagia, Dyspnea& hoarsness.It is usually a manifestation of a multifocal systemic fibrosis with:1.Retroperitoneal fibrosis2.Mediastinal fibrosis3.Biliary tract sclerosisNOTES IN Thyroiditis: Painful (subacute, de Quervain’s) Painless (post partum) Hyperthyroid, hypothyroid and euthyroid phases Anti thyroid drug therapy does not work.
  42. 42. 42 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013THYROID TUMORS:1. Follicular cancer: Common , 15% of thyroid malignancies. Age-50 year Female—72% More likely to have distant metastases Invasion juxtanodal +Blood vessels +++Distant sites +++ Classified as differentiated thyroid carcinoma. Death 24% Resemble to normal thyroid +++ I 123 uptake +++ Degree of malignancy +++ C/F thyroid nodule =thyrotoxicosis LAB.----------thyroglobulin levels high in metastatic follicular carcinoma. Less common than papillary Imaging –extensive bones and soft tissue metastases may develop. Total thyroidectomy (or near total). Routine remnant ablation with RAI due to increased risk of metastaticdisease2. Papillary CancerMost common (70% of all) and least aggressive.Differentiated thyroid carcinoma.Age –40year// female --- 70%Death --- 7%Invasion --juxtanodal ++++Blood vessels +Distant sites +Resemble to normal thyroid +I123 uptake -cold nodule +C/F thyrotoxicosis with nodule
  43. 43. 43 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013LAB—thyroglobulin levels are high in most metastatic papillar ca.Imaging--- extensive bone and soft tissue metastasis may bedetected on radioisotope scans.USS neck – solid lesion // CXR-------puntate calcification.Extent of surgery (near total thyroidectomy). Follow up with sTSH,thyroglobulin exam and US.Radioactive iodine ablation for high risk tumours. Follow up withRAI scans plus the above.Anaplastic carcinomaRare ,1% thyroid carcinomaAge –57year// female 56%Deaths ---98%C/F: thyroid noduleSigns of pressure or invasion of surrounding structuresRecurrent laryngeal nerve pulsyInvasion -- juxta nodal +++Blood vessel +++++Distant sites ++++I123 uptake ODegree of malignancy +++++Highly aggressive –locally and systematicallyMedullary carcinoma: Uncommon , less than 5% of thyroid cancer Average age—50year // female 56% Death 33% Invasion –tend to metastases locally Juxta nodal ++++ Blood vessels +++ Distant ++ Of all cases- 1/3 sporadic , 1/3 familial , 1/3 MEN type II
  44. 44. 44 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013 I123 uptake O C/F: thyroid nodule --- firm non tender Anterior cervical lymph nodes may be enlarged. 1/3 Frequently secrete serotonin and PG leading to diarrhea and fatigue. LAB.:TFT--- normal except in thyroditis 2ry to cancer. Calcitonin levels may be elevated ,especially after stimulation by PGinfusion. 2/3 Familial—children and siblings of patient with MC are advised to havegenetic testing to detect RET-PROTO-ONCOGENE mutation. Imaging – tend to calcify Metastases may be detected by PET scan and MRI. Degree of malignancy--------- ++++ Worse prognosis if tissue stains heavily with calcitonin or MM AG LEUM1.Solitary Thyroid Nodule FNA Benign no further intervention Malignant or suspicious– papillary or follicular.Non-thyroidal illnesspatients may have low T3 and/or T4 usually with a normal sTSHPsychotic patients may have elevated T3 and/or T4.Simple non-toxic goiterNormal TFT’sNo treatment requiredSurgery if obstructive symptoms
  45. 45. 45 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013SOLITARY THYROID NODULECall for fine needle aspiration biopsy.1.NODULAR WITH BENIGN CYTOLOGY 2.SOLITARY THYROID NODULE IN PTIn a pt with H/O radiation therapyNeed to be followed by1.Periodic palpation At high risk of malignancy-resection2.Rebiopsied if further growth occurs3.Cystic nodules can be managed by 4.Solitary nodule in thyrotoxic ptremoval of Fluid for cytology to are an indication of RAI scandeflate the cyst.To differentiate adenoma/gravesCysts recur and need repeated aspirationsThyroxine suppression therapy is ineffectiveIn shrinking nodules unless the pt has primary a hot nodule is usually benignHypothyroidism with increased TSH but resected to cure toxicity.
  46. 46. 46 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013NON-TOXIC GOITERCOMMON INWOMEN:ADOLESCENTPREGNANTLACTATINGMENOPAUSETREATMENT:IODIZED OIL IMIODINE TABLETSSALTFORTIFICATIONWITH IODINEEDUCATE ABOUTINTAKE OF: SEAWEEDS SHELLFISH FISH- TAMBAN, HITO,DALAG
  47. 47. 47 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013
  48. 48. 48 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013PARATHYROID GLAND
  49. 49. 49 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 20134 GLANDSSECRETES PARATHORMONE (PTH) IN RESPONSE TO SERUM Ca & PhLEVELSREGULATE CALCIUM & PHOSPHORUS METABOLISMORGANS AFFECTED:BONES - resorptionKIDNEYS Ca reabsorption Ph excretionGIT – enhances Ca absorptionDIAGNOSTIC TESTS:HEMATOLOGICAL SERUM CALCIUM SERUM PHOSPHORUS SERUM ALKALINE PHOSPHATASEURINARY STUDIES URINARY CALCIUM URINARY PHOSPHATE - TUBULAR REABSORPTION OF PHOSPHATEHYPOPARATHYROIDISMDECREASED PTH PRODUCTIONHYPOCALCEMIACALCIUM IS:
  50. 50. 50 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013 DEPOSITED IN THE BONE EXCRETEDCAUSE:HEREDITARYIDIOPATHICSURGICAL - most common (transient, permenant)PARATHYROID ADENOMA RESECTION suppression of PTHAND accelerated remineralization of skeleton(Hungry bone syndrome)CONGENITALLY ABSENTHEAVY METALS- hemochromatosis, hemosiderosis, wilson diseaseDYSEMBRYOGENESIS---Dogeorgs syndromeINFECTION , GRANULOMA , SECONDARYFUNCTIONAL DECREASE PTH BY MG DEFICIENCY—maabsorption.NECK RADIATIONPOLYGLANDULAR AUTOIMMUNE Type1-----APECEDAutoimmune poly endocrinopathy Candidiasis Ectodermal DystrophyPresent in childhood with 2/3:1.Candidiasis 2.Addison disease 3. HypoparathyrodismPT may develop cataract ,vitiligo, alopechia, uveitis, immune thyroid disease.
  51. 51. 51 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013S/SX:It is ionized calcium which under physiological regulation , is necessary formuscle contraction and nerve function.Hypocalcemia is a manifestation of reduced rate of bone resorption in theabsence of sufficient PTH.Ca in blood Neuro excitibility and Tetany Ca in ECFAffect the neuromuscular and cardiovascular sites.It can manifested acutely as a medical emergency or chronic cold case.Hypocalcemic tetany is manifested by:1. Numbness and tingling in the fingers and toes and around the lips2. Laryngeal stridor with crowing inspiration.3. Dyspnea and cyanosis.ACUTE HYPOCALCEMIA TINGLING OF THE FINGERS CHEVOSTEK’S, TROUSSEAU’SIn sever tetany , cramps of individual musclegroups occurs in the hands and feet ascarpopedal spasm.
  52. 52. 52 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013There may be convulsions , abdominal pain , nausea and vomiting.The seizures are of :Grand mal type/ no aura / no loss of consciousness /no incontinence& traumaEpileptiform attacks are striking and frequently described symptoms ofhypocalcemia.CHRONIC HYPOCALCEMIA Mental abnormalitiesIRRITIBILITY & CONFUSIONPERSONALITY CHANGESEMOTIONAL LIABILITY- DEPRESIONMEMORY IMPAIREMENT.
  53. 53. 53 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013Papilloedema and increase intracranial pressure may accompany it. CARDIAC ARRHYTHMIA FATIGUE, WEAKNESS CATARACTCataract is a characterized consequence of chronic hypoparathyrodism.Ectopic calcifications –lens, subcutaneous tissues, thickened calvarium.XRAY: INCREASED BONE DENSITYIn idiopathic hypoparathyrodism,Abnormalities of ectoderm- nails ,teeth , hairs , dry scaly coarse skinBlunting of roots of teeth and dysplasia of tooth enamelNails- malformed ,brittle, transverse groovesD/D OF TETANY:1.HYPOCALCEMIA:Ca Po4 PHHypovitamniosis D NResistance vit D NMalabsorption Nhypoparathyroism N2.Metabolic alkalosis----normal CA, PO4 , INCRESED PTHPersistent vomitingHypokalemic alkalosisExcessive alkali treatment
  54. 54. 54 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013CRF over correction of acidosisHypokalemic alkalosis(( hyperaldosteronism/ corticosteroid analogue))3. K Deficiency4. MG DeficiencyD/D OF HYPOCALCEMIA:1. Hypocalcemia – hypercalciuria2. Acute pancreatitis3. Osteoblastic metastases-----prostate, breast4. Chemotherapy for leukemia and lymphoma.LABORATORY: Ca in blood and urineBlood phosphatePhosphate clearance1. SERUM CALCIUM: low 9mg/dlS.Ca is largely bound to albumin. The depressed level of S.Ca must becorrelated with the simultaneous concentration of serum albumin.Low albumin ==== S.Ca is depressed.(0.8—1 mg of Ca to 1gm of albumin).Corrected S.Ca = S.Ca mg/dl + (0.8 X{4---ALBUMINg/dl})Urine Ca approaches zero as the conc. Of Ca in blood less than 7mg/100ml.2.SERUM CA low, SERUM PO4 high, ALP normalWhy increased phosphate?B/C lack of hormone effect on phosphate clearance by the kidney.The rate of excretion of urinary excretion of 3 5 AMP is reduced.
  55. 55. 55 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 20133.SERUM MG --lowHypomagnesemia reduces both PTH RELEASE AND TISSUE RESPONSIVNESSTO PTH---------HYPOCALCEMIA.4. ECG-prolonged QT + T wave abnormalities.5. SLIT LAMP EXAMINATION ---post. Lenticular cataract6. IMAGING-----CT scan of skull ----basal ganglia calcificationBones denser than normalSpine showed the presence of lines parallel to the cortex of the vertebralbodies giving rise to an image of a small copy of the vertebral body within thebody, a sign called “bone within a bone”.
  56. 56. 56 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013COMPLICATION:1) Acute tetany with stridor2) Ossifications of paravertebral ligaments3) Convulsions4) Parkinsonism symptoms5) Treatment related – nephrocalcinosis and CRFD/D OF HYPOCALCEMIA:I. Decrease intake or absorption:1.Malabsorption—no diarrhea2.Small bowel bypass, short bowel3. VIT D deficiency - absorption , 25 hydroxycolecalciferolII. Loss1.Alcoholim
  57. 57. 57 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 20132.Chronic renal insufficiency3.DiureticIII. Endocrine disease1.Hypoparathyrodism2.Sepsis3.PseudohypoparathyrodismIV. Physiological1.Decrease albumin2.Decrease end organresponse to VIT D3.Indued by loop diuretic,aminoglycoside, plicamycinD/D OF HYPOPARATHYRODISM:V. Ideopathic epilepsyVI. ChoreoathetosisVII. AsthmaVIII. Brain tumors( convulsion and calcifications)MANAGEMENT:10% 20 - 30 ml 500- 1500 N/SVIT D 50,000—10,000U daily by mouth1---2 gm Ca by mouthCa SUPPLEMENTCa carbonate (40%Ca) 500mg/ 5 times a dayCa salts should be given orally as soon as possible to supply 1-2 gm Ca/d.VIT D SUPPLEMENT – LIQ FORM: WITH WATER, JUICE OR MILK.Should be started as soon as oral Ca started.
  58. 58. 58 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013Treatment of choice for chronic hypocalcemia is VIT D.Ergocalciferol—250,000-150,000U/D, slow actingToxicity takes weeks to disappear (6-18weeks).Gives more stable serum Ca level.Dihdrotachysterol—faster in onset, 3 times more potentDaily dose 0.125—1mg/d , expensiveCalcitriol (1, 5 DHCC)- RAPID , HIGH COST , TOXICITY 2 WKSUSED IN ACUTE HYPOCALCEMIA 4 MICOGM/DCalcifedrol—intermediate onset and duration of action 20mico/dSEIZURELISTEN FOR STRIDOR OR HOARSENESSTRACHEOSTOMY SET AT BEDSIDECaGLUCONATE AT BEDSIDEHYPERPARATHYROIDISMIncrease PTH production.Hypercalcemia with Hypophosphatemia.Age-50year, sex- 3times in female more than malePRIMARY – adenoma OR hyperplasia or CA of the parathyroid gland.Can be familial 5%( hyperplasia or adenoma)Multiple endocrine neoplasia MEN I IIA IIB
  59. 59. 59 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013SECONDARY – compensatory over secretion of PTH in response tohypocalcemia from : CHRONIC RENAL DISEASE RICKETS MALABSORPTION SYNDROME OSTEOMALACIATERTIARY-enlarged gland and become autonomusCRF-----bone disease ---renal dystrophy.PHYSIOLOGY OF PTH:1. Renal tubule reabsorption of CA2. Inhibits the net absorption of PO4 &HCO3 by renal tubule.3. Stimulate the synthesis of 1,25 DHCC by the kidney.4. Cause excretion of CA and PO4 by the kidneyPATHOLOGY OF INCREASED PTH:1. Calculus formation within urinary tract- 5% of renal stones.2. Diffuse parenchymal calcification (Nephrocalcinosis).3. Osteoclastic activity in bone and increase CA delivery may produce diffusedemineralization and pathological fractures cystic bone lesionsthroughout the skeleton ===Osteitis fibrosa cysticD/D OF HYPERCALCEMIA:I. Intake or absorptiona. Milk alkali syndromeb. VIT D or A excess – 25 HCC helpful to confirm DX.II. Endocrine disorders1.HPT (1RY OR 2RY)2.Acromegally
  60. 60. 60 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 20133.Adisson disease.4.HyperthyrodismIII. Neoplastic diseasesa. Tumor secreting PTH related proteins(ovary, kidney, lung)b. Metastases to bone (breast )c. Multiple myeloma ,leukemia ,lymphomad. Secretions of PG and osteolytic factors.IV. Miscellaneous1. Thiazide2. Sarcoidosis3. Pagets disease4. Immobilization5. Hypophosphatasia6. Acute ill patient (ICU)7. Renal transplant8. Familial hypocalcemic hypocalcinuriaLeprosy , Tuberculosis, Berylliosis, Cocidomycosis, Histoplasmosis.1,25Dihydrocholecalciferol---------CAS/SX:Most patients are asymptomatic.Hypercalcemia is usually discovered accidently by blood biochemistry.Nodules are almost never palpable.Polyuria and constipation are the most characteristic symptoms.1. Skeletal manifestation:1-4%of patientsOsteitis fibrosa cystic may cause brown tumors.Cysts of the jaw.Pathological fractures -back.Patients have bone pain, arthralgia ,diminished bone density (hip/radius).
  61. 61. 61 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 20132.Urinary tract manifestationPolyuria and polydypsia may be present and due to increased CAKidney stones are seen in 18% of ptsNephrocalcinosisRenal failure2. Hypercalcemic manifestationSever cases Thirst SOME PATIENT PRESENT W NEUROMUSCULARPolyuria muscle weaknessAnorexia easy fatigabilityNausea parasthesiaVomiting depressionConstipation sleeping tendencyAnemia pruritisWeight loss psychosisHTN comaCARDIAC ARRHYTHMIAS, HTNXRAY: BONE DEMINERALIZATIONIMAGING:I - To localize the gland:Preoperative processes unsuccessful B/C so small 1 cm1. USS neck2. CT scan neck3. MRI NECK4. T C- 99m seastamibi5. Thallium/technetium subtraction scanii- Angiography and selective venous sampling of PTH
  62. 62. 62 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013iii- Bone x rays are normal and not required to make diagnosis.There may be DemineralizationSubperiosteal resoption of bone (radial aspects of fingers)Loss of lamina dura of teethPathological fractureMottling of the skull(salt and pepper appearance).Chondrocalcinosis(articular cartilage calcification).Iv- patient with renal osteodystrophy:Have ectopic calcifications around joints and soft tissues.Dissiminated calcification in the X ray changesSkin, soft tissues , arteries OsteopeniaOsteitis fibrosaCalciphylaxis Osteosclerosis
  63. 63. 63 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013Painful ischemic necrosis Osteosclerosis of the vertebralOf skin and gangrene bodies is calledCardiac arrhythmia RUGGER JERSEY SPINERespiratory failureCa may precipitate in the cornea(band keratopathy) & soft tissues(calciphylaxis)COMPLICATIONS OF HYPERCALCEMIA:1. Peptic ulcer2. Pancreatitis3. Coma4. Azotemia5. Arrhythmia6. FracturesLaboratory:The hall mark of hypercalcemia is s.ca more than 10.5mg/dlIn hyperproteinemic state, total s.ca may be increased but ionized ca normalwhere as in 1ry HPT , ionized calcium increased.S O4 is often low 2.5Urinary ca excretion may be high or normal (250mg/g creatinine)An excessive loss of phosphate in urineIn 2ry HPT, s po4 is high.ALP is elevated only if bone disease is present.Plasma CL and uric acid levels may be elevated.Elevated levels of PTH confirm the diagnosis.Assay ---- immune radiometric assay (IRMA).
  64. 64. 64 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013ECG----short QTSUMMARY:S.Ca , Urinary Ca, CL & Uric acid, Urinary PO4, S.PO4 and PTH.MANAGEMENT:TX OF CHOICE : SURGICAL REMOVAL OF HYERPLASTIC TISSUEINDICATIONS-1. S.Ca 1mg above upper limit of normal / U.Ca excretion more than50mg/24hr.2.U.Ca excretion 400mg/24hr3.Cortical bone density 2SD below normal4.Relative youth 30-60year5.Symptomatic HPT6.Difficult follow upAfter surgery,pt. may develop parasthesia ,tetany as a result of rapid fall ofblood calcium .(although sCa normal).So, frequent periodic monitoring of Ca and albumin recommended.S.PTH postoperatively misleading//Transient thyrotoxicosis may occure.MEDICAL TREATMENT:Intensive hydration with normal saline.Bisphonates-Pamidronate , Alendronate30-90mg/o.9N/S over 4-12 hoursPreparing for surgery.Estrogen replacement—postmenopausalAvoid digoxin and give propranololGlucocorticoid is ineffective.Renal osteodystrophy –avoid hyperphosphatemia—Ca acetate&calcitriol
  65. 65. 65 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013LOW Ca, HIGH Ph DIETNO MILK, CAULIFLOWER & MOLASSESSTRAIN URINE FOR STONESTO AVOID1. Immobilization2. Thiazid3. VIT A/D4. Ca. antaacidsCARE FOR PARATHYROIDECTOMYFOLLOW UP:CA, ALBUMIN---twice yearlyRFT +U.Ca--------once yearlyBONE DENSITY---1-2yearFAMILIAL HYPOCALCIURIC HYPERCALCMIA:Autosomal dominantCharacterized by 1. Decrease urine CA 50 micro/24hr2.Variable increase MG3. Minimal PTH increaseDX family history + urinary Ca clearanceNo surgeryExcellent prognosis

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