Transcript Thyroiditis

Hypothyroidism. Iodine
deficiency disorders.
Department of Internal Medicine N2
as.-prof. Svystun I. I.
Anatomy of thyroid gland
Hyoid Bone
Cricothyroid Ligament
Thyroid Cartilage
Cricoid Cartilage
Thyroid Gland
Pyramidal Lobe
Right Lobe
Isthmus
Left Lobe
Trachea
The thyroid is a firm
vascular organ lying in the
neck, caudal to cricoid
cartilage.
It is composed of two
nearly equal lobes connected
by a thin isthmus and weights
approximately 20 – 30 g.
Rests of thyroid tissue
are occasionally presents in
sublingual or retrosternal
areas.
Thyroid secrets: T3, T4,
calcitonin.
A follicle is structural and functional unit of the
thyroid gland
• The follicle contains
colloid (which consists of
thyroglobuline, a
glycoprotein, containing T3
and T4 within its matrix)
• Epithelial cells
• Parafollicle cells (C-cells)
(synthesized calcitonine)
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The thyroid hormones, thyroxine (T4) and triiodothyronine (T3)
Hypothalamus
TRH stimulation
inhibition
Pituitary
Free hormone
Liver
Thyroid
Binding
proteins
Bound hormone
T4
T3
TSH stimulation
Thyroid
are secreted under the stimulatory
influence of pituitary thyrotropin
(thyroid-stimulating hormone or
TSH). TSH secretion is primary
regulated by a dual mechanism:
• thyrotropin-releasing hormone
(TRH);
• thyroid hormone.
Thyroid hormone exits in circulation
in both free and bound formas. The
thyroid gland is the sole source of
T4 and only 20% of T3 is secreted
in the thyroid. Approximately 80%
of T3 in blood is derived from
peripheral tissue (mainly hepatic or
renal) deiodinatoin of T4 to T3.
Thyroid hormone synthesis
howmed.net
Major deiodinative and non-deiodinative pathways of thyroid hormones metabolism.
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Physiologic effects of thyroid hormones
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2.
3.
4.
5.
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
Achievement of formation of nervous system and
skeleton in perinatal period
Goitre
• is an enlargement of the thyroid gland.
GOITRE
• HYPERTHYROIDISM
• HYPOTHYROIDISM
• EUTHYROIDISM
Degrees of thyroid gland enlargement
(WHO, 1994)
0 –goiter is absent
1- we
can palpate but can’t see
2 – thyroid gland can be palpated and
seen
Hypothyroidism (myxedema)
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.
Historical perspective
• The first full clinical
description of the
hypothyroidism and
mixedema 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
1. Primary (thyroid gland
disturbances).
2. Secondary (due to
pituitary disease).
3.Tertiary (due to
1. Laboratory
hypothalamic disease).
(subclinical)
hypothyroidism 4.Peripheral.
2. Clinical
hypothyroidism
Etiology of primary hypothyroidism
•
•
-
Congenital
Maldevelopment –hypoplasia or aplasia
Inborn deficiencies of biosynthesis or action of thyroid hormone
Atypical localization of thyroid gland
Severe iodine deficiency
Acquired
iodine deficiency
autoimmune processes (Hashimoto’s thyroiditis): MAE 1 & 2
surgical subtotal removal or total thyroidectomy
irradiation therapy (organs of the neck)
I131 therapy
during or after therapy with propylthyouracil, methimazole, iodides
for hyperthyroidism
infiltrative diseases (tuberculosis, actynomycosis)
trauma
medications such as amiodarone, interferon alpha, thalidomide
Etiology of secondary and tertiary
hypothyroidism
• Congenital
- Congenital pituitary or hypothalamus disorders (anatomical or
physiological)
• Acquired
- Tumors or metastasis
• hemorrhagic necrosis (Sheehan’s syndrome)
- Inflammatory disorders (infection, infiltrative process)
- Trauma
- surgical and radiation treatment for pituitary or hypothalamic
disease
- Chemical and pharmacological intoxications (reserpin,
bromocriptine).
Etiology of 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
Skin and
hair
- Skin is dry, thick and silk, is often cool
and pale.
- Nonpitting edema of the hands, feet and
periorbital regions (myxedema). Pitting
edema also may be present.
- The faces are puffy and features are
coarse.
the loss of the lateral aspect
of the eyebrow, sometimes
termed Queen Anne's sign
Skin and hair
- 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.
- Hypothyroidism does not
cause obesity, but
modest weight gain from
fluid retention and fat
deposition often occurs
Nervous
system
Patients complain on 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.
Cardiovascular
system
Complains on: dyspnea, pain in
the region of the heart
Objective examination:
• Increased peripheral resistance
• Hypertension
• Bradycardia
• LV hypertrophy with decreased
contractility, reduced cardiac
output
• Pericardial effusion
• Congestive heart failure
- The ECG may show low voltage
and/or non-specific ST segment
and T wave changes.
- Hypercholesterolemia
Gastrointestinal system
- Gastrointestinal motility is
decreased loading to constipation
and abdominal distension,
pseudoobstruction of intestines,
paralytic ileus.
- 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
Blood disorders
- 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
- Thyroid gland: nonpalpable or enlargement.
- Adrenal glands: hypofunction
- Pituitary system: 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.
- Gonadal glands: menorrhagia (from
anovulatory cycles), secondary amenorrhea,
infertility and galactorrhea; decreased potention in men
Metabolic system
- Hypothermia is common
- Hyperlipidemia with increase of serum
cholesterol and trigliceride occurs because
of reduced lipoprotein lipase activity
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
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. This
designation is only applicable when thyroid function
has been stable for weeks or more, the hypothalamicpituitary-thyroid axis is normal, and there is no recent
or ongoing severe illness.
Diagnosing and Managing Thyroid Disease in the Nursing Home . JAMDA. Volume 9, Issue 1 , Pages 9-17,
January 2008
Recommendations of Six Organizations Regarding Screening of
Asymptomatic Adults for Thyroid Dysfunction
ORGANIZATION
SCREENING
RECOMMENDATIONS
American Thyroid Association
Women and men >35 years of age
should be screened every 5 years.
American Association of Clinical
Older patients, especially women,
Endocrinologists
should be screened.
American Academy of Family
Patients ≥60 years of age should be
Physicians
screened.
American College of Physicians
Women ≥50 years of age with an
incidental finding suggestive
of symptomatic thyroid disease should
be evaluated.
U.S. Preventive Services Task Force
Insufficient evidence for or against
screening
Royal College of Physicians of London
Screening of the healthy adult
population unjustified
Treatment of hypothyroidism
No specific diets are
required for
hypothyroidism.
Regimen is not restricted
Therapy of
the cause
Pathogenetic
replacement therapy
Symptomatic
Thyroid
hormones
Treatment
of complications
Replacement therapy
• Synthetic preparations
– T4 (l-thyroxine)
– T3 (liothyronine sodium)
•
-
Combined:
Thyrocomb
Thyrotom
Thyroidin
Novothyral
Side effects
- Allergic reactions
- Angina pectoris
- Cardiac arrhythmia
Congenital hypothyroidism
•
•
•
•
•
Children are born with increased weight
Subcutaneous edema
Hypotermia
Prolonged jaundice
Physical (dwarfism) and mental retardation
(cretinism)
Peculiarities of treatment
< 3 month – 25 mcg/day
3 -12 month – 37,5 mcg/day
1 – 5 years – 75 mcg/day
5 – 7 years – 75 – 100 mcg/day
> 7 years – 100 mcg/day
Myxedema coma - is a life-threatening
complication of hypothyroidism
Precipitating factors include
•
•
•
•
•
•
•
•
exposure to cold
infection
Trauma
Surgery
Myocardial infarction
Bleeding
Stress situation
Drugs that suppress the CNS
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.
Treatment of myxedema coma
- large doses of T4 (200-500
mcg i/v bolus 3 – 4 times a
day) or T3 if available (40 –
100 mcg 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 mcg/day i/v until
the hormone can be given
orally.
Treatment of myxedema coma
- Corticosteroid therapy
(hydrocortisone 200 –
400 – 600 mg/day i/v).
- 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.
With all forms of thyroiditis, destruction of the
normal architecture of the thyroid follicular
occurs, yet each disorder has distinctive
histologic characteristics.
Classification
1.
2.
•
•
3.
•
•
4.
5.
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.
Acute thyroiditis
is an acute bacterial inflammation
Etiology: a bacterial
pathogen:
- St. aureus,
- Str. hemolyticus,
- Str. pneumonie,
- anaerobic
organisms,
- E. coli,
- coccidiodomycosis.
Infection occurs either
- secondary to
hematogenous or
lymphatic spread,
- or direct introduction
of an infective agent
by trauma.
Clinical signs: fever, chills and other
signs of abscess formation.
Anterior neck swelling and pain
radiating to the ear or mandible.
The physical examination suggests
the presence of an abscess, with
erythema of the skin, marked
tenderness to palpation, and at
times fluctuance.
Laboratory:
Leucocytosis with a left shift,
increased ESR.
Thyroid hormone concentrations in
blood are normal, although
hyperthyroxinemia has been
reported
Treatment
- Patient should be treated at surgical department.
- Parental antibiotics should be administered according
to the specific pathogen identified.
- If fluctuance is present, incision and drainage might be
required.
- Bacterial thyroiditis must be treated early and
aggressively, since abscess formation can
occasionally dissect downward into the mediastinum.
Recurrences of the disorder are very rare.
- (Duration of the treatment must be nearly 1,5-2
month).
Subacute thyroiditis –
an acute inflammatory disease of the
thyroid probably caused by a virus with
destruction of thyrocytes
• subacute granulamatous thyroiditis;
• subacute lymphocytous thyroiditis
Subacute thyroiditis
Etiology
- Coxsackie virus
- Adenovirus
- Mumps
- Echovirus
- Influenza
- Epstein-Barr viruses
A genetic
predisposition is
likely because of the
association of HLABW 35
histocompatibility
antigens.
Clinical signs
- unilateral anterior neck pain, often
associated with unilateral radiation of
pain to the ear or mandible.
- Pain is often proceeded by a few
weeks prodrome of myalgias, lowgrade fever, malaise and sore throat.
- Dysphagia
- Symptoms of hyperthyroidism
Physical examination: an exquisitely
tender, very hard, nodular enlargement,
which is most often unilateral.
- Tenderness is often so extreme that
palpation is limited.
- Tachycardia, a widened pulse
pressure, warm skin and diaphoresis
are also observed when
hyperthyroidism is present.
Subacute thyroiditis
• Laboratory findings
- Early in the disease we can find an increase in T4, a decrease
in RAI uptake (often 0), leucocytosis and a high ESR.
- After a several weeks, the T4, is decreased and the RAI uptake
remains low.
- Full recovery is the rule; rarely, patients may become
hypothyroid.
• Treatment
- An acute phase lasts from 4-8 weeks, during which treatment is
symptomatic (aspirin 600 mg q 3-4 h, prednisolone 10-20 mg
orally tid; after 1 week prednisolone can be tapered by 5 mg
every 2-3 days; thus glucocorticoids are usually not required for
longer than several weeks.
- Symptomatic therapy due to the phase (hyperthyroid –
anrithyroid drugs, beta-blockers, hypothyroid – thyroid hormone
replacement (levothyroxine 100-150 mkg/day).
• Following the hypothyroid phase recovery occurs, and the
normal histologic features and secretory capacity of the thyroid
are restored.
Ultrasound of the right lobe of the thyroid demonstrates an ill-defined irregular region of heterogeneous
hypoechogenicity without elevation of flow on Colour Doppler examination.
http://radiopaedia.org
Chronic thyroiditis.
Hashimoto thyroiditis (chronic
lymphocytic thyroiditis) HT
• HT is an organ - specific autoimmune
disorder, a chronic inflammation of
the thyroid with lymphocytic infiltration
of the gland generally though to be
caused by autoimmune factors.
It is more prevalent (8:1) in woman than men and is most
frequent between the ages of 30 and 50 .
A family history of thyroid disorders is common, and incidence
is increased in patients with chromosomal disorders,
including Turners, Down and Klinefelters syndromes.
Histologic studies reveal extensive infiltration of lymphocytes in
the thyroid.
Clinical features
HT is characterized by a wide spectrum of clinical
features, ranging from no symptoms and the presence
of small goiter to frank myxedema.
- sensation of tightness in the area of the anterior neck
- mild dysphagia.
Physical examination usually discloses a
symmetrically enlarged, very firm goiter, a smooth or
knobby consistency. Occasionally patients present
with a single thyroid nodule.
A small group of patients have a form of HT termed
primary idiopathic hypothyroidism, goiter is usually
absent in this group (atrophic form of HT).
Yet a small subset of patients(probably 2-4%) present
with hyperthyroidism and have so-called
hashitoxicosis (hypertrophy from of HT).
Laboratory findings
1. early in the disease - high titers of antithyroid
(antimicrosomal) antibodies. Late in the disease,
the patient develops hypothyroidism with a
decreased in T4,T3 and antibodies in this stage
are usually no longer detectable;
2. the thyroid scan typically shows a irregular pattern
of iodine uptake;
3. fine-needle biopsy of
the nodule or enlarging area
should be done to rule out
a coexistent neoplasm.
Ultrasound of thyroid gland
Ultrasound reveals - hypoechoic thyroid gland with coarse or "micronodular" echotexture
of the gland - color doppler imaging reveals augmentation of the vascularity of the gland
http://radiopaedia.org
Treatment
-
-
-
treatment of HT requires lifelong replacement
with thyroid hormone to correct and prevent
hypothyroidism. The average oral
replacement dose with L-thyroxine is 100 to
150 mkg/day;
glucocorticoids have been reported to be
effective in HT when true is a rapidly enlarging
goiter associating with pressure symptoms;
symptomatic therapy
National iodine status in 2013
www.iccidd.org
• The resulting low level of thyroid hormones in the blood
(hypothyroidism) is the principal factor responsible for damage
to the developing brain and other harmful effects known
collectively as “iodine deficiency disorders” . The adoption of
this term emphasizes that the problem extends far beyond
simply goitre and cretinism.
Recommended iodine intake
UNICEF, ICCIDD, and WHO recommend
that the daily intake of iodine should be as
follows:
• • 90 μg for preschool children (0 to 59
months);
• • 120 μg for schoolchildren (6 to 12
years);
• • 150 μg for adolescents (above 12 years)
and adults;
• • 250 μg for pregnant and lactating
women.
Diagnostic procedures
Diagnostic procedures
Diagnostic procedures
Blood constituents
• TSH
• Thyroglobulin (The thyroid hyperplasia
and goitre characteristic of iodine
deficiency increases serum Tg levels, and
in this setting serum Tg reflects iodine
nutrition over a period of months or years)
• thyroxin (T4) and triiodothyronine (T3),
is usually not recommended for monitoring
iodine nutrition (the serum T4 is typically
lower and the serum T3 higher than in
normal populations)
Treatment
• Iodine Replacement (In an adult, 150
mcg/day)
• Universal salt iodization (USI)
• Iodine supplementation
• Levothyroxine
• Surgery (standard of care for large goiter
associated with obstructive symptoms
such as dough, stridor, and dysphagia is
thyroidectomy, if the goiter extends into
the anterior mediastinum)
THYROID NODULES
Benign nodular goiter
Chronic lymphocytic thyroiditis
Simple or hemorrhagic cysts
Follicular adenomas
Subacute thyroiditis
Papillary carcinoma
Follicular carcinoma
Hürthle cell carcinoma
Poorly differentiated carcinoma
Medullary carcinoma
Anaplastic carcinoma
Primary thyroid lymphoma
Sarcoma, teratoma, and miscellaneous tumors
Metastatic tumors
Indications for US of thyroid
gland:
–Patients at risk for thyroid malignancy
–Patients with palpable thyroid nodules or
MNGs
–Patients with lymphadenopathy
suggestive of a malignant lesion
Indications for FNA
• Of diameter larger than 1.0 cm that is solid and hypoechoic on
US
• Of any size with US findings suggestive of extracapsular growth
or metastatic cervical lymph nodes
• Of any size with patient history of neck irradiation in childhood
or adolescence; PTC, MTC, or MEN 2 in first-degree relatives;
• Of any size with patient history of previous thyroid surgery for
cancer;
• Of any size with patient history of increased calcitonin levels in
the absence of interfering factors;
• Of diameter smaller than 10 mm along with US findings
associated with malignancy ;
• the coexistence of 2 or more risk of thyroid cancer
• Nodules that are hot on scintigraphy should be excluded from
FNA biopsy
Suspicion of malignancy
Suspicion of malignancy
FNA Results and Recommendations
FNA Result
Benign
Nondiagnostic
Papillary thyroid cancer
Suspicious for papillary
thyroid cancer
Indeterminate
Recommendation
Observation
Repeat ultrasonographyguided FNA
Surgery with preoperative
ultrasonography
Surgery with preoperative
ultrasonography
Hürthle cell neoplasm:
Surgery
Bethesda System
Category
Risk of Malignancy
Recommended
Therapy
Nondiagnostic or
unsatisfactory
1%-4%
Ultrasonography-guided
FNA
Benign
0%-3%
Observation
Atypia or follicular lesion
of undetermined
significance
5%-15%
Repeat FNA
Follicular neoplasm or
suspicious for follicular
neoplasm
15%-30%
Thyroid lobectomy
Suspicious for
malignancy
60%-75%
Near total thyroidectomy
or lobectomy
Malignant
97%-99%
Near total thyroidectomy
An alternative method of reporting thyroid cytopathology is the Bethesda System. In The Bethesda System for
Reporting Thyroid Cytopathology (TBSRTC), it is recommended that every report begin with 1 of 6 diagnostic
categories. Clinicians can use the diagnostic category and the implied risk of malignancy to guide treatment
planning.