Docstoc

Hyperthyroid Dysfunction Dr Kamal

Document Sample
Hyperthyroid Dysfunction Dr Kamal Powered By Docstoc
					“THYROID DYSFUNCTION”
OVERACTIVITY OF THYROID

Dr. Kamal Al-Shoumer
DIC (UK), PhD (UK), MRCP (UK), FRCP (UK)

Vice-Dean &Associate ProfessorFaculty of Medicine - Kuwait University Consultant & Head of Division of Endocrinology & Metabolic Medicine

OUTLINE
• • • • • • INTRODUCTION THYROID HORMONE SYNTHESIS THYROID HORMONE CONTROL ACTIONS OF THYROID HORMONE CLINICAL DISORDERS HYPERTHYROIDISM

INTRODUCTION
(Survey/Kuwait- Al-Shoumer , 1998)
(n=283 per month) % Diabetes Tops the list and was not included Hypothyroidism 27.9 Hirsutism 24.7 Hyperthyroidism 11.7 Osteomalacia 3.5 Short stature 3.2 Pituitary disease 2.1 Infertility 1.8

INTRODUCTION
(Survey/Kuwait - Al-Shoumer , 1998)
(n=283 per month) % Gynecomatsia 1.8 Hyperprolactinemia 1.8 Hypogonadism 1.4 Others (galactorrhea,hyper- 20.1 hypoparathy.,osteoporosis, delayed puberty, Addison’s, etc)

INTRODUCTION-I THYROID GLAND
- The largest endocrine gland - 20-25 g (adults) – women, menses, pregnancy - Greek thyreos = shield (dipylon) - purple brown, two lateral lobes, isthmus - 50% cases, pyramidal lobe at isthmus - lies in front upper trachea (2nd/3rd rings) - Posterior – 2 pairs of parathyroid glands

INTRODUCTION-II
- Functional unit = thyroid follicle/acinus (amorphous colloid material – thyroglobulin- in center surrounded by a layer of cubical or columner epithelial follicular cells) - Parafollicular cells (C-cells) 1% (located mainly in middle part of lateral lobes) - Aterial= superior/inferior thyroid arteries from external carotid and subclavian arteries)

THYROID GLAND HISTOLOGY

http://arbl.cvmbs.colostate.edu/hbooks/pathphys/endocrine/thyroid/anatomy.html

www.bartleby.com/107/illus1174.ht ml

Gross Anatomy of the thyroid and surroundings

http://perth.uwlax.edu/biology/faculty/maher/Jthryoid/img003.jpg

THYROID HORMONES IN THE BLOOD

• Approximately 99.98% of T4 is bound to 3 serum proteins: Thyroid binding globulin (TBG) ~75%; Thyroid binding prealbumin (TBPA or transthyretin) 15-20%; albumin ~5-10% • Only ~0.02% of the total T4 in blood is unbound or free. • Only ~0.4% of total T3 in blood is free.

Actions of thyroid Hormones-I
Increase BMR ( oxygen consumption & heat production – body temperature) Growth/development= all tissues (brain) Carbohydrate metabolism= hyperglycemia ( glucose absorption/production/utilization) Fat metabolism= decrease (Chol., TG, Phospholipids)

Actions of thyroid Hormones-II
Protein metabolism ( both protein anabolism & catabolism – excess=catabolism) Bone turnover Cardiovascular= HR, muscle contraction, cardiac output, SBP, wide pulse pressure ( DBP) GI tract= appetite, GI motility, diarrhoea CNS= essential for normal brain development : memory, mentation, reflexes, tremor Gonadal function Vitamin A synthesis stimulation from the liver

-

-

Hypothalamus-Pituitary-Thyroid axis
Stimuli from Central nervous system
-ve

Hypothalamus

Releasing (TRH)/inhibitory hormones(somatostatin)

-ve
Pituitary gland (anterior lobe)

Thyrotropin (TSH)
T3, T4 hormones

Thyroid gland

arbl.cvmbs.colostate.edu/hbooks/ pathphys/endocrine/thyroid/control .html

THYROTOXICOSIS
PREVALENCE in the community (UK) 19 per 1000 women 1.6 per 1000 men annual incidence 1-10 per 1000 Women to men 4-10 : 1 Peak age 4th-5th decade Grave’s disease 10-15 yr younger

CLINICAL MANIFESTATIONS OF HYPERTHYROIDISM:
Symptom Nervousness Increased sweating Heat intolerance palpitations Dyspnea Fatigue/weakness Weight loss Increased appetite Hyperdefecation % 69-99 45-91 41-89 63-89 66-81 44-88 52-85 11-65 12-33

CLINICAL MANIFESTATIONS OF HYPERTHYROIDISM:
SIGN Thyr. enlargement Lid retraction Hyperactivity Tremor Tachycardia >90 AF % 37-100 34-80 39-80 40-97 58-100 3-38

CAUSES OF THYROTOXICOSIS - I
1. Autoimmune: Graves’ disease (60-85%) Hashimoto’s thyroiditis

2. Autonomous: MNG (10-30%) Solitary toxic adenoma (2-10%)

CAUSES OF THYROTOXICOSIS - II
3. Transient: Postpartum thyroiditis Subacute thyroiditis Painless thyroiditis 4. Drug-induced: Iodine-induced Thyroxine or T3 (factitious) Amiodarone Interferon Lithium

CAUSES OF THYROTOXICOSIS - III
5. Secondary: TSH secreting tumour Trophoplastic tumours Syndr. of inapprop. TSH secretion

6. Ectopic: Struma ovarii Metastatic follicular carcinoma

GRAVES’ DISEASE
AI dx with hyperthyroidism, goitre (diffuse) ± opthalmopathy ± dermopathy Prevalence: 2.2% in UK Incidence: 3 per 1000 in UK F:M 7-10: 1

Figure 10-4. Classic severe Graves' ophthalmopathy demonstrating a widened palpebral fissure, periorbital edema, proptosis, chemosis, and conjunctival injection.

Figure 12-3. End stage in severe involvement of extraocular muscles in ophthalmopathy (courtesy of Prof. Wiersinga, Amsterdam).

Graves’…Ophthalmopathy

http://www.muhealth.org/~daveg/t hyroid/thy_dis.html

Graves’… Dermopathy

• http://www.ohiohealth.co m/healthreference/referen ce/3C8F3995-E45A406AB785837268AEED7B.ht m?category=questions

Figure 12-6. A case of severe pretibial myxedema showing the coarsened, nodular, infiltrated, pigmented lesions on the lower extremities.

Figure 10-8. Remarkable "pretibial myxedema", also present on feet and hands, of a patient with Graves' disease and exophthalmos.

If You Have Hyperthyroidism, You’re in Good Company

Barbara Bush 1984 Pre-treatment

Barbara Bush 1991 Post-treatment

GRAVES’ DISEASE Pathogenesis
1. Female sex preference: AI, role of sex hormones

2. Genetics: 50% with FH of AI dx (Mono-30%, dizygotic-5%) HLA DR3, B8

GRAVES’ DISEASE Pathogenesis
3. Autoimmunity: autoantibodies to thyroid tissue TSH-R Ab (TSAb, TGSI, TBAb) TPO (antimicrosomal) Thyroglobulin

4. Interacting role of T and B cells

Toxic Adenomas
• • • • • Single Nodules in any age (+/- palpable) Release excessive thyroid hormone Identified with radioactive scan “Hot Nodule” No TSH-R Ab

Toxic Multi-Nodular Goiter
• • • • • • • Develops from multinodular goiter Nodules become autonomous Plummer’s disease Usually old (+50 yrs) Present with CVS Palpable (one or more or non) No ophthal nor dermopathy

Factitious Hyperthyroidism

• Excessive intake/exposure to thyroid hormone

Transient Thyroiditis
• Caused by release of stored hormones due to inflammation- as stores are limited, it is transient • Acute • Subacute • Painless

Transient Thyroiditis
Post-partum: • 10% pregnancies • 1-6 mths after delivery • Short-lived hyperthyroid phase 2-6 weeks then hypothyroid 2-8 weeks the euthyroid • misleading sequence of symptoms • FH of AI disease is common • +ve thyroid ABS

Transient Thyroiditis
Subacute (De Quervain’s thyroiditis) • Viral in origin • Transient hyperthyroidism • Pain tenderness on thyroid tissue • Fever, myalgia, malaise and URTI may precede • Firm hard goiter • No bruiti

HYPERTHYROIDISM DIAGNOSIS Adequate history Clinical examination Remember all causes Then perform lab tests

HYPERTHYROIDISM INVESTIGATIONS MAIN:
- Raised T4 and T3 levels (free/bound) - Could be only T4 or rarely T3 raised Suppressed TSH (low) - Very rarely raised TSH - secondary thyrotoxic.

HYPERTHYROIDISM INVESTIGATIONS Others:
Thyroid antibodies antithyroglobulin & antimicrosomal, TSH-Receptor Radioisotope thyroid tests Iodine uptake (..itis versus toxicosis) Thyroid scan (etiology)

. Thyroid Scans.

a.

Normal thyroid imaged with 123I.

b.

Cold nodule in the right lobe imaged by 99mTc.

c.

Elderly woman with obvious multinodular goiter and the corresponding radioiodide scan on the right.

HYPERTHYROIDISM INVESTIGATIONS
Supplementary :
- Glucose tolerance (increased glucose/insulin) - Raised liver enzymes (transaminase, ALP) - Raised serum ca, urine ca & po4 - CXR - ECG

HYPERTHYROIDISM TREATMENT-I
1. Antithyroid medications: (block thyroid hormone synthesis) Protocol of therapy: 45 - 60 mg carbimazole OR PTU for 4-6 wks then: i) Titration: reducing the dose to a maintenance dose, or ii) Block/replace: adding thyroxine 100150µg od

HYPERTHYROIDISM TREATMENT-II
Duration of treatment: from 12 months to 2 years Outcome of antithyroid therapy: 50% or more - remission Follow-up: essential Adverse effects pruritus, rashes, urticaria, neutropenia, agranulocytosis (warn patients)

HYPERTHYROIDISM TREATMENT-III
B-Adrenoceptors blocking drugs Propranolol (inderal) - acts on B-receptors - inhibits conversion of T4 to T3 - while awaiting decision - useful for those with arrhythmia, emergency - not used in pregnancy, heart failure, asthma

HYPERTHYROIDISM TREATMENT-IV
Iodine - inhibits thyroid hormone release - effects achieved rapidly - useful in crises or before surgery to prepare pts

HYPERTHYROIDISM TREATMENT-V
2. Radioiodine therapy: - iodine - 131 - destroy thyroid cells - Patients preparation prior - Contraindicated in large goitre (tracheal compression), pregnant, lactating ± severe eye dis/some children <10y - Pregnancy deferred 3-6 months - Avoid contact with children 5-10 d - Follow up - essential (hypothyroid.)

HYPERTHYROIDISM TREATMENT-VI
Surgery – near total thyroidectomy for Graves’ disease - Patient preparation is essential - Indicated for very large goitre with severe hyperthyroidism, relapsed patients after antithyroid - Complications: of surgery, hypoparathyroidism, laryngeal nerve damage, thyroid crises, recurrent hyperthyroidism, hypothyroidism

HYPERTHYROIDISM TREATMENT-VII (pregnancy)
-Treatment of choice is antithyroid (carbimazole or propylthiouracil) - Patients seen more frequently - Dose of drug (minimum required) - Third trimester (possible dose reduction ± stopping it at 36 weeks)

Considerations with Thioamides
• Both PTU and Methimazole may be used in pregnancy • PTU and Methimazole are considered safe in breastfeeding
– Methimazole appears in higher concentrations

• Watch for agranulocytosis
– Fever – Sore throat

HYPERTHYROIDISM TREATMENT-VII (pregnancy)
- TSH-R antibodies at late pregnancy (if high , don’t stop antithyroid) - Check TSH-R antibodies, T3, T4, TSH from cord blood - Monitor mother and baby after delivery

Thyroid Storm
• Medical Emergency, with high (>50%) mortality if untrested, with treatment (10%) • PPT (infection, surgery, stress etc) • Diagnostic signs and symptoms (aggravation):
– – – – – Fever Tachycardia Altered mental status Vomiting and diarrhea Cardiac arrhythmia

More on Thyroid Storm
• If suspected, draw lab
– FT4 – FT3 – TSH

• Start treatment immediately

Management-I
• ICU monitoring • Priority treatment of hypotension, pulm edema • Adequate hydration • Cooling blanket or paracetamol • Drug therapy (PTU, propranolol, iodine, hydrocortisone, chlorpromazine, treat the cause)

ACOG Practice Bulletin, Number 37, August 2002


				
DOCUMENT INFO
Shared By:
Categories:
Stats:
views:223
posted:4/28/2008
language:English
pages:62