Download Subclinical hypothyroidism

MINISTRY OF HEALTH PROTECTION OF UKRAINE
Vynnitsa national medical university named after M.I.Pyrogov
«CONFIRM»
on methodical meeting of
endocrinology department
A chief of endocrinology
department, prof. Vlasenko M.V.
_________________
“_31_”_august___ 2012 y
METHODOLOGICAL RECOMMENDATIONS
FOR INDEPENDENT WORK OF STUDENTS
BY PREPARATION FOR PRACTICAL CLASSES
Scientific discipline
Мodule № 1
substantial module №1
Topic
Course
Faculty
Internal medicine
Basis of Internal medicine
“Diagnostic, treatment and prophylactic basis of
main endocrinology diseases”
Topic №9: Hypothyroidism. Classification. Clinics.
Diagnostics. Laboratory and instrumental investigations.
Differential diagnosis. Treatment. Features of hypothyroidism
in patient with ischemic heart disease.
4
Medical № 1
Vynnitsa – 2012
METHODOLOGICAL RECOMМENDATIONS
for the students of 4-th course of medical faculty for preparation to the practical
classes from endocrinology
1.Тopic №9: Hypothyroidism. Classification. Clinics. Diagnostics. Laboratory and instrumental
investigations. Differential diagnosis. Treatment. Features of hypothyroidism in patient
with ischemic heart disease.
2. Relevance of topic: Hypothyroidism is the condition resulting from a lack of the effects of
thyroid hormones on body tissues. Hypothyroidism is a common condition. Congenital
hypothyroidism is diagnosed in 1 of every 4000 newborns by screening methods, in adults over 0,5
the frequency is approximately 2 - 4%. The overall frequency in the population is approximately 0,5
– 1,0 %. Hypothyroidism is a complex of sympthoms that arises in an organism at insuffciency of
thyroid hormones or decline of sensitiveness to them by peripheral organs and tissues. A lot of
thyroid gland diseases are accompanied by hypothyroidism. The large variety of clinical symptoms,
atypical displays of hypothyroidism determine certain diffculties in diagnostics and differential
diagnostics. Untreated or unsatisfactorily treated hypothyroidi-sm results to disability of patient, and
untreated in-born hypothyroidism – to cretinism.
At hypothyroidism a lot of organs and systems are struck, and just cardiovascular and respiratory
systems, digestive tract, speed of metabolic processes changes in an organism, atherosclerotic
processes are accelerated, obesity and hypertensive illness occur. That is why adequate substitutive
therapy of hypothyroidism and its prophylaxis are important
3. Aim of lesson:
- to learn etiology, pathogenesis, diagnostic criteria of hypothyroidism
- to be able to fnd out the symptoms of hypothyroidism from anamnestic data and information of
objective inspection.
- to be able to differentiate an edematous syndrome at pathology of the cardio-vascular system,
kidneys, hypothyroidism, syndrome of Parkhon and allergic diseases.
- to be able to differentiate thyroid gland enlargement of different ethiology.
- to be able to interpret the results of lipid, albuminous, carbohydrate and hormonal researches,
ultrasonic diagnostics of thyroid gland.
- to master skills of diagnostics of hypothyroidism, establishment of localization of basic process
(primary, secondary, tertiary hypothyroidism).
- to prescribe an adequate pathogenetic and symptomatic treatment of hy-pothyroidism and
thyroiditis, to estimate its effciency.
- to defne the working capacity of patient, tactic of clinical supervision.
4. References
4.1. Main literature
1. Endocrinology. Textbook/Study Guide for the Practical Classes. Ed. By Petro M. Bodnar: Vinnytsya: Nova Knyha Publishers, 2008.-496 p.
2. Basіc & Clіnіcal Endocrіnology. Seventh edіtіon. Edіted by Francіs S. Greenspan, Davіd G.
Gardner. – Mc Grew – Hіll Companіes, USA, 2004. – 976p.
3. Harrison‘s Endocrinology. Edited J.Larry Jameson. Mc Grew – Hill, USA,2006. – 563p.
4. Endocrinology. 6th edition by Mac Hadley, Jon E. Levine Benjamin Cummings.2006. –
608p.
5. Oxford Handbook of Endocrinology and Diabetes. Edited by Helen E. Turner, John A. H.
Wass. Oxford, University press,2006. – 1005p.
4.2. Additional literature
6. Endocrinology (A Logical Approach for Clinicians (Second Edition)). William Jubiz.-New
York: WC Graw-Hill Book, 1985. - P. 232-236. Pediatric Endocrinology. 5th edition. –
2006. – 536p.
7. Thyroid Disordes (Aclevelend Clinic Guide) by Mario Skugor, Jesse Bryant Wilder
Clevelend Press,2006. – 224p.
Basic Level.
1. Anatomy and physiology of thyroid gland.
2. Regulation of thyroid gland function.
3. Influence of thyroid hormones on different tissues and organs.
Students’ Independent Study Program
You should prepare for the practical class using the existing text books and lectures. Special
attention should be paid to the following:
1. Primary, secondary, tertiary hypothyroidism: etiology and pathogenesis.
2. Pathogenesis of main symptoms of hypothyroidism in children and adults.
3. Classifcation of hypothyroidism.
4. Main symptoms and syndromes of hypothyroidism in children and adults
5. Changes of the skin and subcutaneous adipose tissue in patients with hypothyroidism.
6. Changes of cardiovascular system, nervous system and gastrointestinal tract in patients with
hypothyroidism.
7. Clinical features of course of in-born hypothyroidism.
8. Criteria of diagnostics of hypothyroidism. Subclinical hypothyroidism.
9. Differential diagnostics of hypothyroidism in children and adults. Clinical peculiarities of
congenital hypothyroidism.
10. Syndrome of galactorhea - amenorhea.
11. Atypical forms of hypothyroidism.
12. Laboratory and instrumental signs of hypothyroidism.
13. Differential diagnosis of hypothyroidism.
14. Pathogenetic and symptomatic treatment of hypothyroidism.
15. Prognosis and estimation of working capacity of patients with hypothy-roidism .
16. Myxedema coma: etiology, diagnostic criteria, emergency.
Short content of the theme.
Hypothyroidism (myxedema).
It is the characteristic reaction to thyroid hormone deficiency. The spectrum of hormone
ranges from a few non – specific symptoms to overt hormone, to myxedema coma. Hypothyroidism
occurs in 3 to 6 for the adult population, but is symptomatic only in a minor of them. It occurs 8 to
10 times more often in woman than in men and usually develops after the age of 30.
Classification
1.Congetial.
2. Acquired: 1. Primary (thyroid gland disturbances).
2. Secondary (due to pituitary disease).
3.Tertiary (due to hypothalamic disease).
4.Peripheral.
Etiology
A cause is usually evident from the history and physical examination.
1.Primary (thyroidal) hypothyroidism.
1) surgical removal, total thyroidectomy of thyroid carcinoma, subtotal thyroidectomy
(hypothyroidism occurs from 25 to 75 of patients in different series);
2) irradiation (hypothyroidism results from external neck irradiation therapy in doses 2000 rads or
more such as are used in the treatment of malignant lymphoma and laryngeal carcinoma); I131
therapy for hyperthyroidism (it results in hyperthyroidism in 20 % to 60 % of patients within the
first year after therapy and in 1 % to2 % each year there after);
3) during or after therapy with propylthyouracil, methimazole, iodides or beta-blockers;
4) autoimmune processes (hypothyroidism usually occurring as a sequel to Hashimoto’s thyroiditis
and results in shrunken fibroid thyroid gland with a little or no function and infiltrative diseases
(tuberculosis, actynomycosis);
5) trauma;
6) iodine deficiency.
2.Secondary and tertiary hypothyroidism
It occurs due to either deficient secretion of TSH from the pituitary or lack of secretion of TRH
from the hypothalamus.
- Tumor;
- Infarction;
- Infiltrative process;
- Trauma;
- Drugs (reserpin, parlodel).
3. Peripheral hypothyroidism:
- peripheral tissue resistance to thyroid hormones;
- decreasing of T4 peripheral transformation into T3 (in liver or in kidneys) ;
- production of antibodies to thyroid hormones.
Congenital:
- Maldevelopment –hypoplasia or aplasia;
- Inborn deficiencies of biosynthesis or action of thyroid hormone;
- Atypical localization of thyroid gland;
Classification.
B. 1. Laboratory (subclinical) hypothyroidism.
2. Clinical hypothyroidism, which can be divided on stages of severity: mild, moderate, severe.
C. 1. Compensation.
2. Subcompensation.
3. Decomposition.
D. 1. Without complications.
2. With complications (myopathy, polyneuroparhy, encephalopathy, coma).
Clinical features
The major symptoms and signs of hypothyroidism reflect showing of physiologic function.
Virtually every organ system can be affected. The onset of symptoms may be rapid or gradual,
severity varies considerably and correlates poorly with biochemical changes. Because many
manifestations of hypothyroidism are non-specific, the diagnosis is particularly likely to be
overlooked in patients with other chronic illnesses and elderly.
Nervous system
Most of hypothyroid patients complain of fatigue, loss of energy, lethargy, forgetfulness,
reduced memory. Their level of physical activity decreases, and they may speak and move
slowly. Mental activity declines and there is inattentiveness, decreased intellectual function, and
sometimes may be depression.
Neurological symptoms include also hearing loss, parasthesias, objective neuropathy,
particularly the carpal tunnel syndrome, ataxia.
Tendon reflex shows slowed or hung-up relaxation.
Skin and hair.
Hypothyroidism results in dry, thick and silk skin, which is often cool and pale.
Glycosoamynoglicanes, mainly hyaluronic acid accumulate in skin and subcutaneous tissues
retaining sodium and water. So, there is nonpitting edema of the hands, feet and periorbital
regions (myxedema). Pitting edema also may be present. The faces are puffy and features are
coarse. Skin may be orange due to accumulation of carotene. Hair may become course and
brittle, hair growth slows and hair loss may occur. Lateral eyebrows thin out and body hair is
scanty.
Cardiovascular system.
There may be bradycardia, reduced cardiac output, quiet heart sounds, a flabby myocardium,
pericardial effusion, cardiac wall is thick, it is increased by interstitial edema. (These findings,
along with peripheral edema, may simulate congestive heart failure). Increased peripheral
resistance may result in hypertension. The ECG may show low voltage and/or non-specific ST
segment and T wave changes. Hypercholesterolaemia is common. Whether or not these is an
increased prevalence of ischemic heart disease is controversial. Angina symptoms, when present,
characteristically occur less often after the onset of hypothyroidism, probably because of
decreased activity.
Gastrointestinal system.
Hypothyroidism does not cause obesity, but modest weight gain from fluid retention and fat
deposition often occurs. Gastrointestinal motility is decreased loading to constipation and
abdominal distension. Abdominal distension may be caused by ascities as well. Ascitic fluid, like
other serous effusions in myxedema, has high protein content. Achlorhydria occurs, often
associated with pernicious anemia.
Renal system.
Reduced excretion of a water load may be associated with hyponatriemia. Renal blood flow and
glomerular filtration rate are reduced, but serum creatinine is normal. May be mild proteinuria
and infections of urinary tract.
Respiratory system.
Dyspnea of effort is common. This complaint may be caused by enlargement of the tongue and
larynx, causing upper airway obstruction, or by respiratory muscle weakness, interstitial edema
of the lungs, and for plural effusions which have high protein content. Hoarseness from vocal
curt enlargement often occurs.
Musculoskeletal system.
Muscle and joint aches, pains and stiffness are common. Objective myopathy and joint swelling
or effusions are less often present. The relaxation phase of the tendon reflexes is prolonged.
Serum creatine phosphokinase and alanine aminotransferase activities are often increased,
probably as much to slowed enzyme degradation as to increased release from muscle.
Hemopoetic system.
Anemia, usually normocytic, caused by decreased red blood cell production, may occur. It is
probably from decreased need of peripheral oxygen delivery rather than hematopoetic defect.
Megaloblastic anemia suggests coexistent pernicious anemia. Most patients have no evidence
iron, folic acid or cyancobalamin deficiency.
Endocrine system.
There may be menorrhagia (from anovulatory cycles), secondary amenorrhea, infertility and
rarely galactorrhea. Hyperprolactinemia occurs because of the absence of the inhibitory effect of
thyroid hormone on prolactine secretion (and causes galactorrhea and amenorrhea or Van – Vik
– Cheness – Ross’s syndrome).
Pituitary-adrenal function is usually normal. Pituitary enlargement from hyperplasia of the
thyrotropes occurs rarely in patients with primary hypothyroidism –such enlargement also may
be caused by a primary pituitary tumor, which resulting TSH deficiency.
Enlargement of thyroid gland in young children with hypothyroidism suggests a biosynthetic
defect. Hypothyroidism in adults is caused by Hashimoto thyroiditis.
Secretion of growth hormone is deficient because thyroid hormone is necessary for synthesis of
growth hormone. Growth and development of children are retarded. Epiphyses remain open.
Metabolic system.
Hypothermia is common. Hyperlipidemia with increase of serum cholesterol and trigliceride
occurs because of reduced lipoprotein lipase activity.
Main symptoms of hypothyroidism
System of
organism
Skin, its
appendages and
mucuses
Pulmonary system
Symptoms
Yellowness and pallor of skin, loss of hair,
including and lateral parts of eyebrows,
myxedema,
fragility
of nails development of
Decline
of lung
vital capacity,
syndrome of apnea during sleeping. An
accumulation of liquid in pleural cavity within
the limits of myxedematic polyserositis
Cardiovascul
ar system
Gastrointestin
al system
Syndrome of “myxedematic” heart, arterial
hypotension or arterial hypertension
Macroglossia, loosing of taste, decline of appetite,
but weight increasing, gallstone illness,
dyskinesia of biliary tract
Renal system
Reproductive
system
Musculoskelet
al system
Decline of fltration and reabsorption
Menstrual cycle disorders, decline of libido,
sometimes – lactorrhea, fertility disorders
Arthritises, osteoporosis, in children –
deceleration of bone age, delay of growth
Hemopoesis
Anemia: hypo- or normochromic iron
defciency, megaloblastic, erythrocyte
sedimentation rate disorders, anemia of pholeydefcit
Decline of memory, somnolence, depressions,
psychical attacks, elongation of tendinous refex
Hypothermia, obesity,
hypercholesterolemia, xanthelasmas
Worsening of hearing, low voice, severity of
the nasal breathing
Nervousmental sphere
Exchangemetabolic
changes
ORL-organs
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 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. The therapy may provide
the patient with more energy, a feeling of well being, desirable weight reduction, improved
bowel function or other signs of better health even though the patient is not aware of these
symptoms before therapy.
Diagnostic of hypothyroidism is based on:
1) history;
2) clinical features;
3) blood analysis: anemia; hypercholesterolemia;
4) 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);
5) ECG;
6) examination of tendon reflexes;
7) ultrasonic examination;
Differential diagnosis of primary and secondary hypothyroidism:
1) clinical features:
Secondary hypothyroidism is not common, but it often involves other endocrine organs affected
by the hypothalamic – pituitary axis. The clue to secondary hypothyroidism is a history of
amenorrhea rather than menorrhagia in a woman with known hypothyroidism.
In secondary hypothyroidism, the skin and hair are dry but not as coarse; skin depigmentation is
often noted; macroglossia is not prominent; breasts are atrophic; the heart is small without
accumulation of the serous effusions in the pericardial sac; blood pressure is low, and
hypoglycemia is often found because of concomitant adrenal insufficiency or growth hormone
deficiency.
2) laboratory evaluation:
shows a low level of circulating TSH in secondary hypothyroidism, whereas in primary
hypothyroidism there is no feedback inhibition of the intact pituitary and serum levels of TSH
are very high. The serum TSH is the most simple and sensitive test for the diagnosis of pituitary
hypothyroidism.
Serum cholesterol is generally low in secondary hypothyroidism, but high in pituitary
hypothyroidism.
Other pituitary hormones and their corresponding target tissue hormones may be low in
secondary hypothyroidism.
The TSH test is useful in distinguishing between secondary and tertiary hypothyroidism in the
former; TSH is not released in response to TRH; whereas in the later, TSH is released.
Criteria of diagnostics of in-born hypothyroidism
Period
Signs
Neonates
– High body mass of new-born child (more than 3
kg)
–500
Prolonged
icterus
– Pale, dry skin
– Dense edema on the back surfaces of hands, foot,
insupra-clavicular
fossa
– Edema of face
Older than
3 months
Teenagers
– Half-opened mouth, enlarged tongue and lips
– Rough, low voice timbre at weeping
– Signs of immaturity of new-born are at term
pregnancy
– Lately cadence of umbilical cord, an umbilical
wound
heals slowly – Weak sucking refex – Slowness
of motions, refexes – Meconium departs lately
- Delay of mental and motor development
– Fontanels are closed lately
– Flatulence, constipations
– Dryness, pallor of skin
– Fragile, dry hairs
– Cold hands, foot
– Wide hollow bridge of the nose
– Late erupting and replacement of teeth
– Muscles: hypotonia, hypertrophy, cramps are
possible
– Delay of growth (nanism)
- Decline of intellect of different degree
– Delay of growth (nanism)
– Delay or superpassing of sexual development
– Dryness, pallor of skin
– Fragile, dry hairs
– Edema of face, limbs, tongue
– Bradycardia
Diagnostics of in-born hypothyroidism:
1 stage. Blood examination (TSH screening) in term new-borns is conducted on 4–5 day of age, in
premature- on 7–14 day: – TSH < 20 mIU/l is a variant of norm
– At TSH > 20 mIU/l is conducted the repeated research from the same blood sample.
a. If TSH > 50 mIU/l – probable hypothyroidism.
b. If TSH > 100 mIU/l – hypothyroidism that needs treatment.
c. It TSH of 20–50 mIU/l – the repeated research from the same blood sample, at
saving of high TSH – research of Thyrotropin and T4 in blood serum.
a. At Thyrotropin > 10 mIU/l and T4 < 120 nmol/l – thyroid prepa
rations are urgently appointed.
b. At Thyrotropin of 20–50 mIU/l and T4 > 120 nmol/l – treatment
is not appointed, repeated research of Thyrotropin and T4 – in 7
and 30 days. In the case of increasing level of Thyrotropin – vi
carious therapy is appointed.
– At Thyrotropin of 50–100 mIU/l – high authenticity of presence of inborn hypothyroidism. To
conduct the repeated research of Thyrotropin and T4 from the same blood sample and in blood
serum, taken from a child ambulatory. At once, not expecting results, appoint thyroid
preparations treatment.
a. In case if the indexes of Thyrotropin and T4 appeared normal –
treatment is stopped.
b. If Thyrotropin exceeded a norm – treatment is continued under a
regular supervision of pediatrician-endocrinologist.
– At Thyrotropin > 100 mIU/l – is quickly reported in a policlinic of child. Conduct repeated
blood examination for research of Thyrotro-pin and T4 in serum. At once (not expecting
results) appoint thyroid preparations treatment.
a. In case if the indexes of Thyrotropin and T4 appeared normal –
treatment is stopped.
b. If Thyrotropin exceeded a norm – treatment is continued under a
regular supervision of pediatrician-endocrinologist.
2 stage. Policlinic.
Control blood analysis (Thyrotropin, T4, T3) – in 2 weeks and 1,5 months from the beginning
of vicarious therapy. It should be oriented in children up to 1 year old on the level of T4. The
adequate one is considered to be the dose of L-thyroxine, at which a normal level of T4 is or fT4 is
kept at normal or relativele high indexes of Thyrotropin.
Degrees of hypothyroidism severity
Criteria
Complaints
Signs of
myopa-thy
Signs of
neuropathy
Skin dryness
Edema
Mild
Inexpressive:
general
weakness, increased
fatigability,
decline of
mental and
physical capacity, increasing
Easy
body mass,
dyspnea during
numbness,
walking
pares-thesia of
extremities
Moderate
Severe
Clear: edema of Demonstrative: sig-ni f
face, of limbs, cantly reduced memory,
sensitiveness to the depression, psychoses,
cold, somnolence, permanent somnolence
reduced memory
Expressly expressed
Presen
On elbows
Dry and dense
Puffness of face Edema are
widespread
Adynamia
Expressed, all types of
sensitiveness are
disturbed
Dry and dense
Edema are widespread,
liquid in internal
cavities
Pulse (for 1 min.) to 60
Dystrophy of
ECG signs
myocardium
60–50
50–40
A voltage, waves
Myxedemic heart,
of R- and T-fatten, hypertrophy signs of
signs of coronal in- conductivity disorders
suffciency
General
lipids (g/l)
Cholester
ol
(mmol/l)
Triglyceri
ds
(mmol/l)
Anemia
To 10,5
To 12,6
More than 12,6
To 8,4
To 10,4
More than 10,4
To 2
To 2,5
More than 2,5
Normo-, hypo-or
hyperchromic
T3, T4 of
Norm or moder- Reduced
blood
ately reduced
Thyrotropin of Increased to 10 More than 10
mIU/ìl
Complication Absent
Present
Signifcantly reduced
Signifcantly increased
Cardiac insuffciency,
psychosis, cretinism,
polyserositis of the
Laboratory indexes Improvement
After
All symptoms
treatment state disappear on a are normalized,
state, but there are the
there
is
dryness
of
background of
considerably expressed
skin, inclinations,
adequate
decline of memory, clinical signs
vicarious thyroid mental and
Treatment of hypothyroidism.
hormones
physical capacity
1. Diet №10.
therapy
2. Regimen is not restricted.
3. 1) replacement therapy:
- desiccated animal thyroid (this is an extract of pig and cattle thyroid glands, which
standardized based on its iodine content but they are too variable in potency to be reliable
and should be avoided);
- synthetic preparations of :
T4 (l-thyroxine)
- T4 is preparation of choice, because it produces stable serum levels of both T4 and T3.
-
Absorption is fairly constant 90 to 95% of the dose. T3 is generated from T4 by the liver.
The initial dosage can be 1.6 mkg/kg of ideal weight or 12.5-25 mkg in older patients and
25-50 mkg in young adult.
- The dosage can be increased in 25-50 mkg increments at 4 to 6 week intervals until clinical
and biochemical euthyroidism is achieved. In older patients more gradual increments are
indicated. Cautious replacement is particularly warranted in patients with ischemic heart
disease, because angina pectoris or cardiac arrhythmia may be precipitated by T4 therapy.
- The average maintenance dosage is 100 to 150 mkg/day orally, only rarely is a larger dosage
required. In general, the maintenance dose may decrease in the elderly and may increase in
pregnancy.
- The dosage should be minimum that restores TSH levels to normal (though this criterion
cannot be used in patients with secondary hypothyroidism).
- Patient takes the whole dose of T4 once a day (in the morning), in the summer the dose may
be decreased and in the winter should be increased.
T3 (liothyronine sodium) should not be used alone for long-term replacement because its rapid
turnover requires that it be taken. T3 is occasionally used mainly in starting therapy because the
rapid excretion is useful in the initial titration of a patient with longstanding hypothyroidism in
whom cardiac arrhythmia may occur early in replacement therapy. The risk of jatrogenic
hyperthyroidism is therefore greater in patients receiving these preparations.
In addition, administering standard replacement amounts of T3 (25 to 50 mkg/day) results in
rapidly increasing serum T3 levels to between 300 and 1000 mkg within 2 to 4 h, these levels return
to normal by 24 h. Therefore, when assessing serum T3 levels in patients on this particular regimen,
it is important for the physician to be aware of the time of prior administration of the hormone.
Additionally, patients receiving T3 are chemically hyperthyroid for at least several hours a day and
thus are exposed to greater cardiac risks. Similar patterns of serum T3 concentrations are seen
when mixtures of T3 and T4 are taken orally, although the peak levels of T3 are somewhat lower.
Replacement regimes with synthetic preparations of T4 reflect a different pattern of serum T3
response increases in serum T3 occur gradually over weeks, finally reaching a normal value about 8
wk. after starting therapy.
Synthetic T3 and T4 combinations (liotrix, thyreocomb). These preparations were developed before
it was appreciated that T4 is converted to T3 outside of the thyroid. These preparations should not
be used.
2) Symptomatic therapy:
- beta-blockers (should be used in patients with tachycardia and hypertension) in the dose of
20 – 40 - 60 mg/day;
- hypolypidemic agents;
- vitamins (A, B, E);
- diuretics and others.
Subclinical hypothyroidism
Many endocrinologists would treat such patients with T4, especially if hypercholesterolemia
were present. Even in the absence of hyperlipidemia, a trial of therapy might be varianted to
determine if the patient experiences improvement presumably the normal serum T4
concentrations before therapy did not reflect adequate tissue effects of thyroid hormones in
such patients. Unfortunately, it is also reasonable to follow these patients without T4 therapy
by surveying thyroid function at 4-to 6 months intervals to determine whether thyroid failure
has occurred, as indicated by the serum T4 falling to subnormal levels along with a greater
increase in serum TSH and the appearance of clear symptoms.
Age
Premature
newborns
0–3
months
3–6 months
6–12 months
1–3 years
3–10 years
10–15 years
> 15 years
Doses of L-thyroxine for treatment of in-born hypothyroidism
Daily dose, mkg/kg
8–10
10–15
8–10
6–8
4–6
3–4
2–4
2–3
Myxedema coma.
It is a life-threatening complication of hypothyroidism, which is extremely rare in warm climates
but not uncommon in cold areas.
Precipitating factors include:
- exposure to cold;
- infection;
- trauma;
- drugs that suppress the CNS.
Myxedema coma characteristics include a background of long-standing hypothyroidism with
extreme hypothermia (temperatures 24 to 32), areflexia, seizures, CO2 retention, and respiratory
depression caused by decreased cerebral blood flow. Severe hypothermia may be missed unless
special low reading thermometers are used. Rapid diagnosis (based on clinical judgement, history,
and physical examination) is imperative because early death is likely.
Treatment of myxedema coma.
It is treated with 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.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.
Tests and Assignments for Self-assessment.
Multiple Choice.
Choose the correct answer/statement:
1. What is the most important in treatment of anemia in patients with hypothyroidism:
A. Iron containing preparations;
B. B12 containing preparations4
C. Thyroid preparations;
D. Androgens;
E. Correction of autoimmune disorders.
2. What we can’t use in patients with myxedema coma:
A. Thyroid hormones.
B. Glucocorticoids.
C. Rehydration.
D. Symptomatic therapy.
E. Decreasing of hypoventilation.
3. The student of 23-years-old age complains of surplus fatigue ability, itch and dryness of skin
appeared in spring, that considerably increase after swimming in a pool. At a review: athletic build.
A skin by touch is dry. A thyroid gland is not enlarged. Pulse - 62/min, diminished sonority of tones
of heart. There is the symmetric languor of tendon refexes. Cholesterol of plasma of blood - 6.8
mmol/l, glucose of capillary blood in 2 hours after the use of a 75 г glucose - 6.2 mmol/l, TSH of
plasma of blood - 10.92 mU/l. What is the most credible diagnosis?
A. Hypothyroidism
B. Spring hypovitaminosis
C. Impared of tolerance to glucose
D. Allergy to the chlorine in a pool
E. Fatigue from the surplus trainings
4. At the girl of 23 days, born on 42 weeks of pregnancy with weight 4200 g, adynamia, decline of
appetite, strydor breathing take place. A mother is ill a diffuse toxic goiter; during pregnancy
adopted mercazo-lilum. Objectively: temperature of body 35 °С, a skin is dry with a yellow tint.
There is the edema on extremities. Tones of heart are muffed. Pulse -100/min. Abdomen is enlarged
in a size, liver +3 cm, umbilical hernia. What methods of research are the most informing for raising
of diagnosis?
A. Determination of TSH level in the serum of blood
B. To limit fats in the diet of child
C. Determination of level of the iodine related to the albumen
D. Determination of bone age
E. Determination of cholesterol level of blood
Answer: 1 – C. 2 – C. 3 – A. 4 – A.
Real-life situations to be solved:
Patient D., 38 years old, 3 month ago has subtotal thyroidectomy. She complaints on fatigue,
somnolence, constipation, edema on the face, changing of the voice. During examination was
found: skin pale, thick and cold, face enlarged, pulse – 58/minute, blood pressure is decreased. Put
previous diagnosis and make the plan of examination.
Answer: Primary, postoperative hypothyroidism. Level of T4, T3, TSH, cholesterol.
Students Practical Activities.
Work 1 : Students’ group is divided into 2 sub-groups, that work near the patients’ bed: ask the
patients on organs and systems, take anamnesis of the disease , anamnesis of life, make objective
exam. With the teacher’s presence. In the class-room they discuss the patients, learn data of
laboratory and instrumental exam. of these patients.
1.To group the symptoms into the syndromes.
2.To find out the leading syndrome and make differential diagnosis.
3.To formulate the diagnosis.
4.To make a plan of treatment.
Methodological recommendation prepared assistant, c.m.s. Chernobrova O.I.
It is discussed and confirm on endocrinology department meeting
" 31 " august 2012 y. Protocol № 1.