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The Thyroid
Prof. Sophia Ish-Shalom MD
The Thyroid
Thyroid Anatomy
Thyroid Hormones
Thyroid Axis
T3
T3
Thyroid Hormone Biosynthesis
Thyroglobulin
Large glycoprotein
5496 AA
MW 660000
Thyroid peroxydase
• Membrane bound
glycoprotein
• Mediates oxydation of
iodide ions and
incorporation iodine into
thyrosine residues on
thyroglobulin
Thyroid Hormones- Metabolic Actions
Nuclear receptor activation   RNA and
 protein synthesis:
 Na/K ATPase   ATP turnover
 oxygen consumption  calorigenic
effect
• Tissue growth
• Brain maturation
Laboratory Evaluation of Thyroid Function
Serum TSH the most sensitive screening test of
thyroid function
Most of the circulating T4
and T3 is bound to TBG
TT3
0.2% free
0.02% free
FT4
Agents/Conditions that 
Thyroxine-Binding Globulin (TBG)
• pregnancy
• oral contraceptives
• other estrogen
sources
• tamoxifen/SERMs
• genetics
• perphenazine
• Newborn
• infectious/chronic
active hepatitis
• biliary cirrhosis
• acute intermittent
porphyria
Agents/Conditions that 
Thyroxine-Binding Globulin (TBG)
• Androgens
• Glucocorticoids in high dosage
• Chronic liver disease
• Severe systemic disease
• Active acromegaly
• Nephrosis
• Genetics
‫מחלות בלוטת התריס‬
‫•‬
‫שנוי בצורת הבלוטה‬
‫– הגדלת כל הבלוטה ( זפק‪)goiter ,‬‬
‫– הגדלת חלק מהבלוטה (קשרית‪,‬‬
‫‪)nodule‬‬
‫•‬
‫שנוי בתפקוד הבלוטה‬
‫– תת פעילות הבלוטה‬
‫– פעילות יתר של בלוטת התריס‬
‫•‬
‫שילוב של שניהם‬
Goiter Due to Iodine Deficiency
‫קשרית בבלוטת התריס‬
‫• הינה ההפרעה השכיחה ביותר בבלוטת התריס‬
‫• שכיחותה באוכלוסיה היא ‪ 4 %‬ועולה עם הגיל‬
‫• שכיחה יותר בנשים‬
‫• ממצאי נתיחה שלאחר המוות‪:‬‬
‫ב‪ 50 %-‬מהמבוגרים נמצאו קשריות‬
‫רובן בלתי משישות (קשרית משישה <‪1‬ס”מ)‪.‬‬
‫קשרית בבלוטת התריס‬
‫• רב הקשריות הן שפירות‬
‫• רק כ‪ 20 % -15 %-‬מהקשריות הן‬
‫ממאירות‬
‫• קרצינומה בבלוטת התריס מהווה ‪ 1 %‬מכלל‬
‫הממאירויות ו‪ 0.5 % -‬מכלל מקרי התמותה‬
‫שקשורים בממאירות‬
‫אנמנזה‬
‫‪ .1‬גיל‬
‫‪ .2‬מין‬
‫‪ .3‬הקרנת הצוואר או הראש בילדות‬
‫‪ .4‬התגלתה לאחרונה צמחה במהירות‬
‫‪ .5‬אינה כואבת‬
‫‪ .6‬תלונות של צרידות‪ ,‬דיספגיה או דיספנאה‬
‫‪ .7‬תלונות שמחשידות להיפו או היפרתירואידזם‬
‫‪ .8‬תלונות ססטמיות‪ :‬חום‬
‫‪ .9‬סיפור משפחתי‬
‫בדיקה גופנית‬
‫‪ .1‬קשרית בודדת‪/‬קשרית דומיננטית בבלוטה מרובת‬
‫קשריות‬
‫‪ .2‬מאפייני הקשרית‪ :‬גודלה‪,‬‬
‫קונסיסטנציה ‪ -‬קשה‬
‫אינה מובילית‬
‫אינה רגישה‬
‫‪ .3‬הגדלת בלוטות לימפה צוואריות‬
‫‪ .4‬צרידות‬
‫‪ .5‬סימני היפו‪/‬היפרתירואידזם‬
‫אבחנה‬
‫• לבדיקות מעבדה אין ערך באבחנה בין קשרית‬
‫ממאירה לשפירה‪.‬‬
‫• עם זאת מומלץ לבדוק את תפקודי בלוטת‬
‫התריס‪ :‬היפרתירואידזם יכול להצביע על קיומה‬
‫של ‪( autonomous toxic adenoma‬שהינה‬
‫שפירה ברב המקרים)‪.‬‬
‫בדיקת הבחירה היא‪FNAC:‬‬
‫• בדיקה רגישה (‪)5% - 2% FALSE NEGATIVE‬‬
‫וספציפית (‪ )1% - 0% FALSE POSITIVE‬בטוחה‬
‫מהימנה ומדויקת לאבחן בין קשרית ממאירה לשפירה‬
‫• תשובת ה‪ :FNAC-‬ממאיר‪ ,‬שפיר‪ ,‬חשוד‬
‫• חסרונה‪ :‬חוסר יכולת להבדיל בין גידול פולקולרי‬
‫ממאיר ושפיר‬
‫• ל‪ %20 - %11 -‬מהחולים נמצאת קשרית חשודה‬
‫בבדיקת ה‪ ,FNAC-‬מתוכן ל‪ %20 -‬יש ממאירות‬
‫בבלוטת תריס‬
‫מפוי בלוטת התריס‬
‫‪Technecium99m Tc O4‬‬
‫•‬
‫• נשאר בבלוטה ‪ 6‬שעות‬
‫• זמן מחצית חיים ‪ 6‬שעות‪ ,‬קרינה ‪‬‬
‫עובר ‪ Trapping‬ולא אורגניפוקציה‬
‫– ‪100 mr  1mCi‬‬
‫– ‪ 5mCi‬לבדיקה ‪500mr ‬‬
‫מיפוי‬
‫•‬
‫•‬
‫•‬
‫•‬
‫•‬
‫‪TECNECIUM‬‬
‫למיפוי יש ערך רק בזיהוי ‪autonomous‬‬
‫‪toxic adenoma‬‬
‫עיקר השמוש במיפוי הוא במקרים של קשרית‬
‫פולקולרית‬
‫תוצאות המיפוי הן‪:‬‬
‫‪ 85% - 80%‬מהקשריות הן קרות מתוכן‬
‫כ‪ 25% - 10%-‬הן ממאירות‬
‫‪ 10 %‬הן ‪ warm‬מתוכן ‪ 10 %‬ממאירות‬
‫‪ 5 %‬הן ‪ hot‬ומתוכן ‪ 5 % -1 %‬ממאירות‬
Thyroid Scan – Cold Nodule
‫שמושי ה‪:U.S-‬‬
‫‪ .1‬אבחנה בין קשרית ציסטית לסולידית‬
‫‪ .2‬מעקב אחר גודלה של קשרית שלא הוצאה‬
‫‪ .3‬גילוי קשריות שאינן משישות (‪ 0.3‬מ”מ)‬
‫‪ .4‬חסר יכולת לאבחן בין קשרית ממאירה לשפירה‪.‬‬
‫ציסטה‬
‫• ‪ FNAC‬מהווה כלי אבחנתי וטיפולי במקרה של ציסטה‪.‬‬
‫• אינדיקציות ל‪ lobectomy-‬במקרה של ציסטה הן‪:‬‬
‫‪ .1‬ציסטה שחוזרת לאחר ‪ 3‬אספירציות‬
‫‪ .2‬ציסטה שקוטרה גדול מ‪ 4-‬ס”מ‬
‫‪ .3‬צי סטה מורכבת (‪)complex cyst‬‬
‫• ‪ U.S‬חסר יכולת לאבחן בין קשרית ממאירה לשפירה‪.‬‬
Thyroid Nodule Evaluation Algorithm
TSH  TSH
TSH -Normal

 thyroid scan
Thyroid Carcinoma
Papillary
• 50% of malignant tumors of the thyroid
• Metastasis to local lymph nodes
Follicular
• 25% of malignant tumors of the thyroid
• Metastasis to local lymph nodes, lung,
bone, liver
• Metastasis taking up I131
Thyroid Carcinoma
Medullary carcinoma
• 10% of malignant tumors of the thyroid
• Neuroendocrine
– Originates from parafollicular cells
– Functional – calcitonin producing
• Metastasizes early
• Some patients with distant metastasis
may live for many years
MEN IIb
Thyroid Carcinoma
Anaplastic
• 10% of malignant tumors of the thyroid
• 75% mortality in 1 year
Hyperthyroidism – Causes
Disorders associated with thyroid
hyperfunction
• Abnormal thyroid stimulator
– Graves’ disease
– Trophoblastic tumor
Intrinsic thyroid autonomy
• Hyprfunctionning adenoma
• Toxic multinodular goiter
Excess production of TSH (very rare)
Hyperthyroidism – Causes
Disorders not associated with thyroid
hyperfunction
• Disorders of hormone storage
– Subacute thyroiditis
– Chronic thyroiditis with transient
thyrotoxicosis
• Extrathyroidal source of hormone
– Thyrotoxicosis facticia
– Ectopic thyroid tissue
–Struma ovarii
–Functional follicular carcinoma
Hyperthyroidism
Skin - appendages
Warm, moist skin; sweating; fine, thin hair; pretibial
dermopathy (Graves' disease)
Eyes, face
Upper lid retraction (wide stare); periorbital edema;
exophthalmos, diplopia (Graves' disease)
CNS
Nervousness, hyperkinesia, variable emotional
states
Hyperthyroidism
Cardiovascular
peripheral resistance
cardiac output, stroke volume, heart rate, pulse
pressure, contractility
congestive heart failure (high-output);
arrhythmogenic; angina
Respiratory
Dyspnea; vital capacity
Hyperthyroidism
Hematopoietic
Anemia ( RBC turnover); erythropoiesis
Reproductive
fertility; menstrual irregularity; gonadal steroid
metabolism
Metabolic
basal rate; negative nitrogen balance,
hyperglycemia; free fatty acids, cholesterol and
triglycerides; hormone degradation;
requirement for fat-and water-soluble vitamins;
enhanced drug detoxification
Hyperthyroidism
Gastrointestinal
appetite; bowel movement frequency;
hypoproteinemia
Musculoskeletal
Weakness; fatigue; hypercalcemia,
osteoporosis,
deep tendon reflex
Renal
renal blood flow;
GFR; mild polyuria
Graves' disease
• Lymphocytes: release TSH
receptor-stimulating antibody
(TSH-R ab [stim]) {thyroidstimulating immunoglobulin} )TSI)
• TSH-R ab [stim] binds to the TSH
receptor and activates the thyroid
• Duration of activation is longer
than with physiological TSH
Graves' disease
Four major presentations:
• Hyperthyroidism
• Diffuse goiter
• Ophthalmopathy
• Dermopathy
Ophthalmopathy
Characterized by:
• Inflammatory orbital content infiltrate
(lymphocytes, mast cells, plasma cells)
• Enlargement of orbital musculature
(lymphocytes infiltration,
mucopolysaccharides, edema, fat)
• Eventually - muscle fiber degeneration;
Loss of striations; Fibrosis
Stare
Left Exophtalmus
Graves’
Ophtalmopathy
Pretibial Mixedema
Treatment of Thyrotoxicosis
• Antithyroid drugs – Thioamides
• Betablockers – Propranolol
• Radioactive iodine
• Surgery
Thioamides
Major drugs for thyrotoxicosis:
Propylthiouracil
• rapidly absorbed
• bioavailability: 50 - 80% (incomplete
absorption/large first-pass effect)
• metabolism: glucuronidation by the
liver; excreted by the kidney
• short half-life (1.5 hours) but
accumulated by the thyroid
Propylthiouracil
Crosses placental barrier (increased
protein binding compared to methimazole
makes propylthiouracil preferable for use
in pregnancy since less free drug is
available to cross into the fetus)
Methimazole
• about 10 times more active than
propylthiouracil
• well absorbed
• accumulated by the thyroid
• crosses the placental barrier
Mechanism of Action: thioamides
• Major action: inhibits thyroidal
peroxidase-catalyzed reactions, blocking
iodine organification: thus preventing
hormone synthesis.
Mechanism of Action: thioamides
• Propylthiouracil and methimazole (too
a much reduced degree) inhibit
peripheral deiodination of T4 and T3
thioamides
Mechanism of Action: thioamides
• Slow onset of pharmacological effect:
(since synthesis, not release is affected,
a month may be required before T4
stores are depleted.)
Toxicity: thioamides
Frequency of adverse effects: 3-12%.
• Most common: maculopapular pruritic
rash
• Rare: urticarial rash, vasculitis,
arthralgia, lupus-like reaction, hepatitis,
lymphadenopathy, cholestatic jaundice,
hypoprothrombinemia, polyserositis.
Toxicity: thioamides
•
•
Most serious potential reaction:
agranulocytosis - risk 0.3% - 0.6 % of patients;
reversible upon discontinuation; cross
sensitivity between propylthiouracil and
methimazole
possibly increased risk in:
• elderly
• patients receiving high-dose methimazole
Radioactive Iodine Treatment
• 131I is the radioactive isotope used for
treating thyrotoxicosis.
Mechanism of Action:
• Rapidly absorbed, concentrated in the
thyroid
• Incorporated into thyroid follicles
• Beta emission is the basis for therapeutic
efficacy
• Thyroid parenchymal destruction occurs
within a few weeks.
Radioactive Iodine - Pathology
• epithelial swelling, necrosis
• follicular disruption
• leukocyte infiltration
• edema
Radioiodine -Therapeutic Advantages
• good efficacy
• easy to administer
• low expense
• pain free treatment
Contraindications
• 131I- not administered to pregnant women
or nursing mothers
• 131I crosses placental barrier and
excreted in breast milk
Adrenergic receptor blocking drugs
• Rationale: reduction of sympathetic
manifestations in thyrotoxicosis:
• Agent of choice: propranolol
(nonselective beta-receptor
antagonist)
Subacute Thyroiditis
• Subacute thyroiditis - granulomatous or
De Quervain's thyroiditis
• Spontaneously remitting inflammatory
condition of the thyroid gland that may
last for weeks to several months
• It has a tendency to recur
SAT - Characteristics
• The gland is typically involved as a whole
• Thyroidal RAIU 
• Transient hyperthyroxinemia
• Elevation of the serum Tg concentration
• Erythrocyte sedimentation rate 
• Sometimes the WBC  during the early
acute phase
FT4, Thyroglobulin and TSH During
SAT
days
Thyroid Storm
Fulminating  in symptoms of thyrotoxicosis
• "Medical storm" is now likely to be
seen in undertreated patients
• Precipitated by surgery or
complicating illness, often sepsis
Presenting syndrome
•
•
•
•
•
extreme irritability
high fever, 41oC
tachycardia
supraventricular
arrhythmia
ventricular arrhythmia
•
•
•
•
•
hypotension
vomiting
diarrhea
delirium
coma
Thyroid Storm - Treatment
•
•
•
•
•
Manage dehydration: IV Saline
Glucocorticoids - dexamethasone (possible
reduction in adrenal reserve, blockage of
peripheral conversion of T4  T3)
Block hormone synthesis by large dose
propylthiouracil; Followed by large doses of
iodine, oral or parenteral; Sodium ipodate may
be used instead of iodine
Propranolol - in the absence of CHF
Digitalis may be required to control elevated
ventricular rates in the presence of atrial
fibrillation
‫‪Iodine‬‬
‫‪I - - Iodide ion‬‬
‫‪Iodine - Iodine molecule in any organic form‬‬
‫‪I2 - Molecular Iodine‬‬
‫•‬
‫•‬
‫•‬
‫‪Intake‬‬
‫•‬
‫•‬
‫•‬
‫•‬
‫•‬
‫‪ 10‬מקג'‪/‬יום ‪ -‬באזורי חסר‬
‫מ‪ 100-150 1960-‬מקג‪/‬יום‬
‫‪ 200-500‬מקג‪/‬יום ‪ -‬כעת‪ ,‬מזון‪ ,‬תרופות‬
‫במלח בישול‪ ,‬ויטמינים‪0.01-0.005 % - I- :‬‬
‫‪cretinism‬‬
‫תרופות‪ :‬אקספקטורנטים ‪ ,‬חומרי ניגוד – ‪ 1-3‬גר' ‪ Iodine‬ליום‬
Iodides
Actions on the thyroid:
• Inhibit organification
• Inhibit hormone release - major action
• Mechanism: perhaps inhibition of
thyroglobulin proteolysis
•  thyroidal size and vascularity
• May induce hyperthyroidism
(jodbasedow)
• May precipitate hypothyroidism
Iodides - Therapeutic Uses
• Short-term management of thyroid storm
• Preoperative preparation for surgery
(due to reduction in gland vascularity,
size, and fragility)
Iodides - Major Disadvantages
•
•
•
•
•
•
Iodide therapy increases intraglandular iodine
concentration
May delay initiation of thioamides treatment
May delay use of radioactive iodine treatment
Avoid in pregnancy: iodide crosses the
placenta and may cause fetal goiter
Iodide as monotherapy: not appropriate;
Iodide block lasts only 2-8 weeks; Withdrawal
at this time may exacerbate thyrotoxicosis
Iodide use should be initiated only after
thioamide treatment and not used if
radioactive iodine therapy is planned
Etiology of Hypothyroidism
Primary
• Hashimoto thyroiditis
– with goiter
– Idiopathic thyroid atrophy
• RAI therapy for Graves’
• S.p thyroidectomy
• Excessive iodine intake
• Subacute thyroididtis
• Rare
– Iodine defficiency
– Lithium therapy
– Inborn error of hormone synthesis
Etiology of Hypothyroidism
Secondary
• Pituitary defects
• Adenoma
• Irradiation
Tertiary
• Hypothalamic
Peripheral resistance to thyroid hormone
‫‪Hypothyroidism‬‬
‫•‬
‫תת פעילות של בלוטת התריס היא מחלה שכיחה‬
‫באוכלוסיה מבוגרת‪ ,‬פוגעת ב ‪ 8% -‬מהנשים וב ‪-‬‬
‫‪ 2%‬מהגברים > גיל ‪50‬‬
‫•‬
‫הסיבות השכיחות ביותר לתת פעילותשלל בלוטת‬
‫התריס בארץ‪:‬‬
‫– ‪autoimmune thyroid disease‬‬
‫– ‪thyroid ablation therapy‬‬
‫– מצב אחרי כריתה כירורגית של בלוטת התריס‬
Hypothyroidism
Hypothyroidism
Hypothyroidism in the Elderly
Hypothyroidism - Treatment
• Levothyroxine - synthetic
tetraiodothyronine sodium salt
• Synthetic T4 is identical to that produced
in the human thyroid gland
• Single, fasting, daily dose
Myxedema - crisis
‫‪Myxedema Coma/Crisis‬‬
‫•‬
‫•‬
‫•‬
‫סיבוך נדיר של תת פעילות של בלוטת‬
‫התריס‬
‫מתרחשת בד"כ בנשים קשישות הסובלות‬
‫מתת פעילות של בלוטת התריס‬
‫– שאינן מקבלות טיפול‬
‫– מקבלות טיפול חלקי או בלתי מספיק‬
‫כאשר מתוסף גורם דחק •חדש‬
‫טראומה‬
‫• זהום‬
‫• קור סביבתי‬
‫• מחלה סיסטמית‬
‫• דימום‬
‫• ארוע מוחי‬
‫• טיפול תרופתי ‪hypnotics :‬‬
‫‪anesthetics, analgesics‬‬
‫‪sedatives‬‬
‫• אי ספיקת לב‬
Myxedema Coma – Clinical Presentation
• Hypothermia
usually, but not always
Special thermometers that record << 32°C may
have to be used to determine the patient's
actual temperature and to monitor rewarming
• Absence of fever in the presence of infection
•  pulse pressure, normal systolic pressure,
 diastolic pressure,  pulse and respiration
• Coarse or thinning hair; facial swelling or
coarseness; periorbital nonpitting edema;
macroglossia; enlargement of tonsils,
nasopharynx, larynx
Myxedema Coma – Clinical Presentation
•
•
•
•
•
Thyroid - enlarged, not palpable, or a scar
may suggest previous thyroidectomy
Lungs - Slow respirations, congestion,
pleural effusions, consolidation
Heart - Soft or distant heart sounds,
diminished apical impulse, enlarged heart,
pericardial effusion
Abdomen - Distension secondary to ileus
and/or ascites,  or absent bowel sounds
Extremities - Cold, nonpitting edema of
hands and feet
Myxedema Coma – Clinical Presentation
• Skin/nails - Pale, dry, scaly, thickened
skin; dry brittle nails; ecchymoses,
purpura, sallow due to carotenemia
• Neuromuscular - Confusion, stupor,
obtundation, coma, slow speech, seizures,
reflexes with slow relaxation
• Drugs
• Tranquilizers
• Sedatives
• Anesthetics
• Analgesics
• Narcotics
• Amiodarone
• Lithium
• Phenytoin
•
Laboratory Evaluation
If myxedema coma is suspected, treatment
must be initiated immediately without waiting
for the results of lab tests
• Free T4 and (TSH)
o Free T4 and T3  
o TSH level may be   primary thyroid disorder
If not 
o secondary hypothyroidism
o severe illness
o and/or drugs: dopamine or high dose
glucocorticoids  TSH  
•
Laboratory Evaluation
If myxedema coma is suspected, treatment
must be initiated immediately without waiting
for the results of lab tests
• Free T4 and (TSH)
o Free T4 and T3  
o TSH level may be   primary thyroid disorder
If not 
o secondary hypothyroidism
o severe illness
o and/or drugs: dopamine or high dose
glucocorticoids  TSH  
Laboratory Evaluation
•
•
•
•
•
Serum electrolytes and serum osmolality:
Hyponatremia with  serum osmolality
Serum creatinine usually is  due to decreased
renal perfusion
Serum glucose: Hypoglycemia is common but
also may suggest adrenal insufficiency
Creatine phospho kinase (CPK): CPK levels often
are , and fractionation will indicate the source
to be skeletal muscle, not cardiac, unless a
myocardial infarction was the precipitating event
Hematocrit < 30%
Laboratory Evaluation
•
•
•
•
•
•
•
Arterial blood gases:  PCO2 and  PO2
Random serum cortisol should be determined
before beginning intravenous steroids
Imaging Studies:
Chest x-ray - Cardiomegaly, pericardial effusion,
congestive heart failure, pleural effusion
Other Tests:
Electrocardiogram - Sinus bradycardia,
 amplitude QRS complexes,  QT interval,
flattened or inverted T waves
Procedures
•
•
•
Temperature monitoring requires use of a rectal
probe to determine true core temperature and to
monitor rewarming
Blood transfusion: Transfuse packed red blood
cells if the hematocrit < 30% to prevent
myocardial ischemia
Pan-culture for sepsis. All patients should have a
chest x-ray and be cultured for a source of
infection. It is recommended to initially treat all
patients with myxedema coma with broadspectrum antibiotics with modification of the
antibiotic regimen based on culture results
Procedures
•
•
•
•
Endotracheal intubation:  ventilatory drive, CO2
retention, and hypoxemia all necessitate
mechanical respiratory assistance to prevent
cardiovascular collapse and worsening of
hypoxia and hypercapnia
Cardiac monitoring in an intensive care unit
Patients are at risk of myocardial ischemia
Central venous pressure or Swan-Ganz catheter
monitoring: Hypotension is a sign of loss of
blood volume, either from bleeding or vascular
redistribution, and must be corrected immediately
Treatment
Volume status
• IV glucose and normal saline
• Volume should be limited because
patients usually are volume-overloaded
and prone to congestive heart failure
from reduced cardiac function of
hypothyroidism
• If Na <120 mEq/L  small amounts of
hypertonic saline  by intravenous
furosemide to improve volume status
Treatment
For hypotension that does not improve with
fluid replacement
• Whole blood transfusion
• Cautious administration of dopamine
• Generally, hypotension is resistant to
the usual drugs until thyroid hormone
and glucocorticoids (if insufficient) are
given
Treatment
• Levothyroxine 200-500 mcg IV loading
dose  50-100 mcg/d IV  to 50-200
mcg/d PO when patient is ambulatory
• Steroid therapy: Hydrocortisone at 100
mg every 8 hours , after a baseline
cortisol level is drawn and continued
unless the random cortisol drawn on
admission indicates adrenal function
without abnormalities, at which time
hydrocortisone may be stopped without
tapering
‫‪Euthyroid Sick Syndrome‬‬
‫•‬
‫הפרעות בתפקודים מעבדתיים של בלוטת‬
‫התריס המופיעות תוך מחלה (בד"כ‬
‫קשה)‪ ,‬ללא עדות למחלה ראשונית או‬
‫משנית של בלוטת התריס‬
‫•‬
‫• לעתים מהווים סימן פרוגנוסטי‬
‫השינויים חולפים לאחר החלמה‬
Euthyroid Sick Syndrome
Sick euthyroid syndrome (SES) - probably
more common cause of thyroid hormone
level abnormalities than intrinsic thyroid
disease
Changes in thyroid hormone economy
• thyroid hormonal synthesis
• hormone transport in circulation
• action and metabolism in peripheral
tissues
• regulatory mechanisms (TSH)
•
•
ESS classification
Normal-T4 variant -  T3 production secondary
to  peripheral 5'- monodeiodination of T4
 serum T3 levels-reflecting disease severity
Low-T4 variant - serum T4 levels  sufficiently
to attain hypothyroid concentrations,
secondary to significantly  T4 production
rates and  serum total & free T3
Typically associated with  TSH secretion
(unknown cause)
•
High-T4 variant - Unusual (frequency = 1% of
SES)
Most frequently observed in elderly women
‫חשיבות ‪ESS‬‬
‫•‬
‫אין לפרש שנוי ברמות הורמוני בלוטת התריס במצב‬
‫זה כמחלה של בלוטת התריס‬
‫•‬
‫עדיין לא ידוע אם מצב זה הוא מצב הסתגלות מגן‬
‫או מצב הגורם נזק‬
‫•‬
‫טיפול בהורמוני תריס בחולים עם ‪ T4 & T3 ‬אינו‬
‫משפר את מצבם‬
‫•‬
‫תפקודי תריס חוזרים לנורמה לאחר החלמה‬
‫מהמחלה‬