HYPERTHYROIDISM: DIAGNOSTIC CRITERIA, TREATMENT.

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Transcript HYPERTHYROIDISM: DIAGNOSTIC CRITERIA, TREATMENT.

HYPERTHYROIDISM:
DIAGNOSTIC CRITERIA,
TREATMENT
Department of Internal Medicine №2
as.-prof. Martynyuk L.P.
Plan of
lecture
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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.
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.
34. Thyroiditis: classification, diagnostic
criteria, treatment.
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Physiologic effects of thyroid hormones
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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
Hyperthyroidism (thyrotoxicosis)
Toxic diffuse goiter.
Grave’s 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
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.
Etiology and predisposing factors
• Defect of T
lymphocytes
suppressors
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)
Pathogenesis
Insufficiency of T suppressors
Increasing function of B lymphocyte
Toxic influence of lymfocytes
Secretion of thyroid – stimulating
immunoglobulin (TSI)
The thyroid
Secretion of T4, T3
Thyrotoxicosis
Pathologic changes in different organs and systems
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
Degrees of thyroid gland
enlargement
(WHO, 1986, 1994)
0-we can’t see or palpate thyroid gland;
IA- we can palpate but can’t see;
IBthyroid gland can be seen when patient
put head back;
II –thyroid gland can be seen in normal
position of the head.
III – thyroid gland can be seen from the
distance of 5 meters or more
0 –goiter is
absent
1- we
can
palpate but
can’t see
2 – thyroid gland
can be
palpated and
seen
Degrees of severity
Mild
Moderate
Severe
Heart beat under 100 100 - 120
less than 10 – 20 %
Weight
10 %
loss
over 120
rare
Changes
from
organs and
systems
- ophthalmopathy
- signs of heart
failure І – ІІ А
-ophthalmopathy
-dystrophic
changes from
inner organs
-thyroid storm
decreased
patients cant
work
Work
capacity
normal
more than 20 %
Treatment
I.
1. Antithyroid drugs.
2. Drugs to ameliorate thyroid hormone
effects .
II. 131I - therapy
III. Surgery.
Thyroid storm
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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.
Thyroid storm results from:- untreated or
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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.
Treatment of thyroid storm
- Iodine-30 drops Lugol’s 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”.)
Hypothyroidism (myxedema)
is the characteristic reaction to thyroid
hormone deficiency.
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
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
Classification
I. Congenital
II. Acquired
A.Transient
B.Permanent
1. Primary (thyroid gland
disturbances).
2. Secondary (due to
pituitary disease).
3.Tertiary (due to
hypothalamic disease).
4.Peripheral.
Classification
I. Congenital
II. Acquired
A.Transient
B.Permanent
1. Primary (thyroid gland
disturbances).
2. Secondary (due to
pituitary disease).
3.Tertiary (due to
hypothalamic disease).
4.Peripheral.
Classification of hypothyroidism
1. Subclinical (laboratory)
hypothyroidism.
2. Clinical (overt)
hypothyroidism
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Degrees of severity:
Mild
Moderate
Severe
Stages of compensation
1. Compensation.
2. Subcompensation.
3. Decomposation.
Presence of complications
1. Without complications.
2. With complications
(myopathy,
polyneuropathy,
encephalopathy, coma).
Pathogenesis
• Clinical signs develops due to decreased
metabolism in the organism
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
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
Congenital hypothyroidism
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Children are born with increased weight
Subcutaneous edema
Hypotermia
Prolonged jaundice
Physical (dwarfism) and
mental retardation (cretinism)
Treatment
< 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
> 7 years – 100 mkg/day
Subclinical (laboratory)
hypothyroidism
It is a state in which we can’t find clinical features of
hypothyroidism and euthyroidism is reached by
compensatory increasing of TSH secretion and that’s
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.
Diagnostic of hypothyroidism
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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)
5. ECG;
6. Examination of tendon reflexes
7. Ultrasonic examination
Treatment of hypothyroidism
Diet №10.
Regimen is not restricted
etiologic
Therapy of
the cause
Pathogenetic
replacement therapy
Thyroid
hormones
symptomatic
Treatment
of complications
Replacement therapy
Myxedema coma
It is a life-threatening complication of
hypothyroidism
Precipitating factors include
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exposure to cold
infection
Trauma
Surgery
Myocardial infarction
Bleeding
Stress situation
Drugs that suppress the CNS
Clinical signs of myxedema coma
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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.
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.
Thyroiditis
The various types of thyroiditis encompass a
heterogeneous group of inflammatory disorders
of diverse etiologies and clinical features.
Classification
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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.
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-TorontoLondon, 1994. - P. 357 - 380.
• Endocrinology (A Logical Approach for
Clinicians (Second Edition)). William Jubiz.-New
York: WC Graw-Hill Book, 1985. - P. 68 – 100.