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HYPERTHYROIDISM: DIAGNOSTIC CRITERIA, TREATMENT

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HYPERTHYROIDISM: DIAGNOSTIC CRITERIA, TREATMENT Department of Internal Medicine 2 as.-prof. Martynyuk L.P. Congenital hypothyroidism Children are born with ... – PowerPoint PPT presentation

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Title: HYPERTHYROIDISM: DIAGNOSTIC CRITERIA, TREATMENT


1
HYPERTHYROIDISM DIAGNOSTIC CRITERIA, TREATMENT
  • Department of Internal Medicine ?2
  • as.-prof. Martynyuk L.P.

2
Plan of lecture
  • Anatomy of thyroid gland.
  • Physiologic effects of thyroid hormones.
  • Definition of the term Hyperthyroidism (DTG) .
  • Frequency of DTG .
  • Etiology and predisposing factors.
  • Pathogenesis of DTG.
  • Changes of the nervous system.
  • Changes of the cardiovascular system.
  • Changes of the gastrointestinal tract.
  • Changes of the endocrine system.
  • Changes of the urinary system.
  • Changes of the pulmonary system.
  • Degrees of thyroid gland enlargement(WHO, 1986,
    1994).
  • Degrees of severity of DTG.
  • Diagnostic criteria of DTG.
  • Treatment of DTG.
  • Thyroid storm diagnostic criteria and treatment.

3
Plan of lecture
  • Definition of the term Hypothyroidism.
  • Frequency of hypothyroidism .
  • Etiology of hypothyroidism .
  • Pathogenesis of hypothyroidism.
  • Classification of hypothyroidism.
  • Skin and hair.
  • Changes of the nervous system.
  • Changes of the cardiovascular system.
  • Changes of the gastrointestinal tract.
  • Changes of the endocrine system.
  • Changes of the urinary system.
  • Changes of the pulmonary system.
  • Congenital hypothyroidism.
  • Diagnostic criteria of hypothyroidism.
  • Treatment of hypothyroidism.
  • Myxedema coma diagnostic criteria and treatment.
  • Thyroiditis classification, diagnostic criteria,
    treatment.

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Physiologic effects of thyroid hormones
  • Increasing of protein metabolism in virtually
    every body tissue
  • Increasing of O2 consumption by increasing the
    activity of Na H ATPase (Na pump), primarily in
    tissues responsible for basal O2 consumption
    (i.e., liver, kidney, heart and skeletal
    muscle).)
  • Stimulation of erythropoesis
  • Positive chrono- inotropic effects on myocardium
  • Achievment of formation of nervous system and
    skeleton in perinatal perion

7
Hyperthyroidism (thyrotoxicosis) Toxic diffuse
goiter.
  • Graves disease - is the condition resulting
    from the effect of excessive amounts of thyroid
    hormones on body tissues.
  • Thyrotoxicosis is a main syndrome
  • Enlargment of thyroid gland

8
Epidemiology
  • At one time or another, approximately 0,5 of
    the population suffers from hyperthyroidism.
  • Graves disease is the most common cause of
    hyperthyroidism and is fairly common in the
    population.
  • It is responsible for over 80 of hyperthyroid
    cases.
  • It occurs most often in young women, but it may
    occur in men and at any age.

9
Etiology and predisposing factors
  • Genetic predisposition, conferred by genes close
    proximity to the major histocompatibility complex
    (HLA DR3, B8)
  • Autoimmune disorders, which can be provoked by
  • insolation
  • stress
  • acute infections
  • hormone disbalance (pregnancy and others)
  • Defect of T lymphocytes suppressors

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Pathogenesis
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Clinical manifestations
  • The clinical presentation may be dramatic or
    subtle.
  • Dysfunction of
  • the nervous system
  • the cardiovascular system
  • the gastrointestinal system
  • the pulmonary system
  • the endocrine organs
  • katabolic syndrome
  • ectodermal changes

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Degrees of thyroid gland enlargement(WHO, 1986,
1994)
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Degrees of severity
19
Treatment
  • 1. Antithyroid drugs.
  • 2. Drugs to ameliorate thyroid hormone
    effects .
  • 131I - therapy
  • Surgery.

20
Thyroid storm
  • Thyroid storm is a life- threatening emergency
    requiring prompt and specific treatment.
  • In is characterized by abrupt onset of more
    severe symptoms of thyrotoxicosis, with some
    exacerbated symptoms and signs atypical of
    uncomplicated Graves disease
  • fever
  • marked weakness and muscle wasting
  • extreme restlessness with wide emotional swings
  • confusion
  • psychosis or even coma
  • hepatomegaly with mild jaundice
  • the patient may present with cardiovascular
    collapse or shock.

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  • Thyroid storm results from- untreated or
    inadequately treated thyrotoxicosis
  • It may be precipitated by
  • infection
  • trauma
  • surgery
  • embolism
  • diabetic acidosis
  • fright
  • toxemia of pregnancy
  • labor
  • discontinuance of antithyroid medication
  • radiation thyroiditis.

22
Treatment of thyroid storm
  • Iodine-30 drops Lugols solution/day orally in
    30g 4 divided doses or 1 to 2 gr. sodium iodide
    slowly by i/v drip
  • Propylthiouracil (merkazolil) - 900 to 1200
    mg/day orally or by gastric tube.
  • Propranolol - 160mg/day orally in 4 divided
    doses or 1mg slowly i/v g 4h under careful
    monitoring a rate of administration should not
    exceed 1mg/min a repeat 1mg dose may be given
    after 2 min i/v glucose solutions .
  • Correction of dehydration and electrolyte
    imbalance cooling blanket for hypertermia.
  • Digitalis if necessary.
  • Treatment of underlying disease such as
    infection.
  • Corticosteroids-100 to 300mg hydrocortisone/day
    i/v.
  • Iodine in pharmacological doses inhibits the
    release of T3 to T4 within hours and inhibits the
    organification of iodine, a transitory effect
    lasting from a few days to a week (escape
    phenomenon.)

23
Hypothyroidism (myxedema)
  • is the characteristic reaction to thyroid
    hormone deficiency.

24
Historical perspective
  • The first full clinical description of the
    hypothyroidism and mixedeme was made in 1874 by
    Gull (by the cretinoid state supervening in adult
    life in women)
  • Term myxedeme first used by Ord in 1978

25
Epidemiology
  • - Hypothyroidism occurs in 3 to 6 for the adult
    population, but is symptomatic only in a minor of
    them.
  • Usually develops after the age of 30
  • It occurs 8 to 10 times more often in women than
    in men

26
Classification
  • 1. Primary (thyroid gland disturbances).
  • 2. Secondary (due to pituitary disease).
  • 3.Tertiary (due to hypothalamic disease).
  • 4.Peripheral.
  • I. Congenital
  • II. Acquired
  • A.Transient
  • B.Permanent

27
Classification
  • 1. Primary (thyroid gland disturbances).
  • 2. Secondary (due to pituitary disease).
  • 3.Tertiary (due to hypothalamic disease).
  • 4.Peripheral.
  • I. Congenital
  • II. Acquired
  • A.Transient
  • B.Permanent

28
Classification of hypothyroidism
  • Stages of compensation
  • 1. Compensation.
  • 2. Subcompensation.
  • 3. Decomposation.
  • Presence of complications
  • 1. Without complications.
  • 2. With complications (myopathy,
    polyneuropathy, encephalopathy, coma).
  • 1. Subclinical (laboratory) hypothyroidism.
  • 2. Clinical (overt) hypothyroidism
  • Degrees of severity
  • Mild
  • Moderate
  • Severe

29
Pathogenesis
  • Clinical signs develops due to decreased
    metabolism in the organism

30
Clinical features
  • Hypothyroidism can be presented in many different
    ways and can mimic other disorders
  • Because many manifestations of hypothyroidism
  • are non-specific,
  • the diagnosis is particularly
  • likely to be overlooked
  • in patients with other
  • chronic illnesses and elderly
  • and can lead to significant
  • morbidity and even mortality

31
Clinical manifestations
  • The clinical presentation may be dramatic or
    subtle.
  • Dysfunction of
  • the nervous system
  • the cardiovascular system
  • the gastrointestinal system
  • the pulmonary system
  • the endocrine organs
  • metabolic syndrome
  • musculosceletal changes

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Congenital hypothyroidism
  • Children are born with increased weight
  • Subcutaneous edema
  • Hypotermia
  • Prolonged jaundice
  • Physical (dwarfism) and
  • mental retardation (cretinism)
  • Treatment
  • lt 3 month 25 mkg/day
  • 3 -12 month 37,5 mkg/day
  • 1 5 years 75 mkg/day
  • 5 7 years 75 100 mkg/day
  • gt 7 years 100 mkg/day

37
Subclinical (laboratory) hypothyroidism
  • It is a state in which we cant find clinical
    features of hypothyroidism and euthyroidism is
    reached by compensatory increasing of TSH
    secretion and thats why synthesis and secretion
    of such level of thyroid hormone that will be
    enough for organism.
  • It is an asymptomatic state in which serum T4
    and free T4 are normal, but serum TSH is
    elevated.

38
Diagnostic of hypothyroidism
  • History
  • Clinical features
  • Blood analysis anemia hypercholesterolemia
  • Levels of thyroid hormone both serum T4 and T3
    are decreased (but in 25 of patients with
    primary hypothyroidism may be normal circulating
    levels of T3), TSH hormone disturbances (in
    primary hypothyroidism serum levels of TSH are
    very high (feedback), low level of circulating
    TSH in secondary)
  • ECG
  • Examination of tendon reflexes
  • Ultrasonic examination

39
Treatment of hypothyroidism
40
Replacement therapy
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Myxedema coma
  • It is a life-threatening complication of
    hypothyroidism

43
Precipitating factors include
  • exposure to cold
  • infection
  • Trauma
  • Surgery
  • Myocardial infarction
  • Bleeding
  • Stress situation
  • Drugs that suppress the CNS

44
Clinical signs of myxedema coma
  • Slow development (weakness, somnolence, coma)
  • extreme hypothermia (temperatures 24 to 32)
  • Areflexia
  • Seizures
  • Bradycardia, hypotension
  • Polyserositis
  • CO2 retention, and respiratory depression caused
    by decreased cerebral blood flow, nonreversible
    brain changes
  • Rapid diagnosis (based on clinical judgment,
    history, and physical examination) is imperative
    because early death is likely.

45
Treatment of myxedema coma
  • large doses of T4 (250-500 mkg i/v bolus 3 4
    times a day) or T3 if available (40 100 mkg I/v
    bolus 3 times a day), because TBG must be
    saturated before any free hormone is available
    for response.
  • The maintenance dose for T4 is 50 mkg/day i/v and
    for T3 10 20 mkg/day I/v until the hormone can be
    given orally.
  • Corticosteroid therapy (hydrocortisone 200 400
    600 mg/day i/v dr.
  • The patient should not be rewarmed rapidly
    because of the threat of cardiac arrhythmia.
  • Hypoxemia is common, so PaO2 should be measured
    at the outset of treatment. If alveolar
    ventilation is compromised, immediate mechanical
    ventilatory assistance is required.

46
Thyroiditis
  • The various types of thyroiditis encompass a
    heterogeneous group of inflammatory disorders of
    diverse etiologies and clinical features.

47
Classification
  • Acute thyroiditis.
  • Subacute thyroiditis
  • subacute granulamatous thyroiditis
  • subacute lymphocytous thyroiditis.
  • Chronic thyroiditis
  • Hashimoto thyroiditis
  • Ridel struma.
  • Specific thyroiditis.
  • Thyroiditis caused by mechanical or physical
    factors.

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References
  • The Merck Manual of Diagnosis and Therapy
    (fourteenth Edition)/ Robert Berkow and others.
    published by Merck Sharp Donhme Research
    Laboratories, 1982. P.997 1010.
  • Manual of Endocrinology and Metabolism (Second
    Edition)/ Norman Lavin. Little, Brown and
    Company.- Boston-New York-Toronto-London, 1994. -
    P. 357 - 380.
  • Endocrinology (A Logical Approach for Clinicians
    (Second Edition)). William Jubiz.-New York WC
    Graw-Hill Book, 1985. - P. 68 100.
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