ENDOCRINOLOGY > THYROID > Flashcards

THYROID Flashcards

(55 cards)

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1
Q

CAUSES OF GOITER (enlarged thyroid gland)

A
  1. Biosynthetic defects: associated with reduced efficieny of thyroid hormone synthesis —> increased TSH —> thyroid growth
  2. Iodine deficiency
  3. Autoimmune disease: Grave’s (from TSH-R mediated effects of TSI and Hashimoto’s thyroiditis (due to acquired defects in hormone synthesis —> elevated TSH —> thyroid growth
  4. Nodular disease: disorder growth of thyroid cells (hyperplasticity or neoplastic)
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2
Q
  • Nodules replace normal thyroid parenchyma
  • More common in areas of borderline iodine deficiency
A

MULTINODULAR GOITER

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3
Q

DIFFUSE NONTOXIC (SIMPLE) GOITER / COLLOID GOITER

A
  • Absence of nodules and hyperthyroidism
  • Presence of uniform follicles that are filled with colloid
  • Most commonly caused by iodine deficiency (ENDEMIC GOITER)
  • SPORADIC GOITER (non endemic regions)
  • JUVENILE GOITER (in teenagers
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4
Q

ENVIRONMENTAL GOITROGENS

A

> Cassava root which contains thiocyanate
Vegetables of cruciferae family (Brussels sprouts, cabbage, cauliflower)
Milk

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5
Q

PEMBERTON’S SIGN

A

facial and neck congestion due to jugular venous obstuction when arms are raised above the head

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6
Q

SUBCLINICAL THYROTOXICOSIS

A

low TSH and normal FT3, FT4 -> suggest thyroid autonomy or undiagnosed Grave’s disease

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7
Q

DIAGNOSIS OF IODINE DEFICIENCY

A

Low urinary iodine <50 yg/L

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8
Q

TREATMENT OF DIFFUSE NON TOXIC (SIMPLE) GOITER / COLLOID GOITER

A

IODINE REPLACEMENT

SUBTOTAL or NEAR TOTAL THYROIDECTOMY —> if with tracheal compression or obstruction of thoracic inlet
FOLLOWED BY LEVOTHYROXINE

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9
Q
  • Nodules in a thyroid of normal size
  • Women > men, increase prevalence with age
  • Iodine deficient regions
A

NON TOXIC MULTINODULAR GOITER

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10
Q

NON TOXIC MULTINODULAR GOITER HISTOLOGY

A
  • Spectrum: hypercellular, hyperplasticity regions to cystic areas filled with colloid
  • Extensive fibrosis, hemorrhage or lymphocytic infiltration
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11
Q

NON TOXIC MULTINODULAR GOITER DIAGNOSIS

A
  • Distorted thyroid architecture
  • Varying size of multiple nodules
  • TFTs usually normal
  • PFTs to assess functional effects of compression
  • CT or MRI to evaluate anatomy of goiter and extent of substernal extension or tracheal narrowing
  • Barium swallow reveal extent of esophageal compression
  • Ultrasound identify nodules should be biopsied based on size and sonographic pattern
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12
Q

NON TOXIC MULTINODULAR GOITER TREATMENT

A

Conservative management
T4 suppression
- is rarely effective for reducing goiter size and risk of subclinical or overt thyrotoxicosis

Radiodine
- used when surgery is contraindicated, decrease MNG volume and selectively ablate regions of autonomy
- Usually 3.7 MBA (0.1 mCi) per gram of tissue

Glucocorticoids or surgery
- When acute compression occurs

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13
Q
  • Presence of functional autonomy
  • Subclinical or mild overt hyperthyroidism
  • Elderly with atrial fibrillation or palpitations, tachycardia, nervousness, tremor or weight loss
  • Precipitators: exposure to iodine, contrast dyes
A

TOXIC MULTINODULAR GOITER

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14
Q

TOXIC MULTINODULAR GOITER

A

> TSH low, Free T4 normal or minimal increase, T3 elevated > T4
Thyroid scan: heterogenous uptake with multiple regions of increased and decreased uptake
24 hour uptake of radioidine: in the upper normal range
Ultrasound: assess prescreens of discrete nodules corresponding to areas of decreased uptake (cold nodules)

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15
Q

TREATMENT OF TOXIC MULTINODULAR GOITER

A

Antithyroid drugs
- Normalized thyroid function
- Useful in elderly or ill patient with limited life span
- Spontaneous remission does not occur and long term treatment needed

Radioidoine
- Treatment of choice
- Treat areas of autonomy as well as decreasing mass of goiter by ablating functioning nodules

Surgery
- Provide definitive treatment of underlying thyrotoxicosis as well as goiter
- Should be EUTHYROID PRIOR SURGERY

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16
Q
  • solitary, autonomously functioning thyroid nodule
  • Functional effects of mutations that stimulate TSH-R signaling pathway or the GsA subunit genes
  • Thyrotoxicosis is mild
  • Only detected when nodule is >3 cm
  • Subnormal TSH level
  • Thyroid nodule without clinical features of Grave’s disease or other causes of thyrotoxicosis
A

HYPERFUNCTIONING SOLITARY NODULE/ TOXIC ADENOMA

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17
Q

DEFINITIVE DIAGNOSTIC TEST FOR TOXIC ADENOMA / HYPERFUNCTIONING SOLITARY NODULE

A

THYROID SCAN

-Focal uptake in hyperfunctioing nodule and diminished uptake in remainder of gland as activity of normal thyroid is suppressed

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18
Q

TREATMENT TOXIC ADENOMA / HYPERFUNCTIONING SOLITARY NODULE

A

Radioiodine ablation
- Treatment of choice
- 370-11100 MBA [10-29.9 mCi} 131I

Surgical resection
- Effective and limited to lobectomy, preserving thyroid function and minimize risk of hypoparathyroidism and damage to recurrent laryngeal nerves

Antithyroid drugs and beta blockers
- Normalized thyroid function but not optimal long-term treatment

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19
Q

Common cause of hypothyroidism worldwide

A

IODINE DEFICIENCY

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20
Q

Most common cause of hypothyroidisim in Iodine sufficient areas

A

HASHIMOTO and IATROGENIC (Treatment of Hyperthyroidisim)

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21
Q

Causes of Neonatal HYPOthyroidisim

A

> Thyroid gland dysgenesis 60%
Inborn errors of thyroid hormone synthesis 30%
TSH-R antibody mediated 5%

Clinical Manifestations
> prolonged jaundice
> feeding problems
> hypotonia
> enlarged tongue
> delayed bone maturation
> umbilical hernia
> permanent neurologic damage
> cardiac malformations

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22
Q

AUTOIMMUNE HYPOTHYROIDISIM

A
  • women > men
  • Japanese
  • Mean age: 60 years
  • Risk factors: high iodine, low selenium intake, decreased exposure to microorganisms in childhood
  • Smoking cessation (transiently increase incidence)
  • Alcohol intake (protective)
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23
Q

CLASSIFICATION OF AUTOIMMUNE HYPOTHYROIDISM

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A
  1. Hashimoto’s or goitrous thyroiditis: associated with goiter
  2. Atrophic thyroiditis: minimal residual thyroid tissue
  3. Subclinical hypothyroidism: normal thyroid hormone levels maintained by a rise in TSH
  4. Clinical hypothyroidism or overt hypothyroidism: unbound T4 levels fall an TSH levels rise further, symptoms are apparent, TSH >10 miU/L
24
Q

best documented genetic risk factors for autoimmune hypothyroidism

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A

HLA-DR (3,4,5) polymorphisms

25
Clinically used markers of thyroid autoimmunity
Antibodies to TPO and Thyroglobulin (Tg)
26
- Steroid-responsive syndrome associated with TPO antibodies, myoclonus, slow-wave activity on EEG
Hashimoto's encephalopathy
27
Laboratory Evaluation for Autoimmune Hypothyroidisim
1. NORMAL TSH —> Excludes primary (but not secondary) hypothyroidism 2. ELEVATED TSH —> do FT4 to confirm clinical hypothyroidisim 3. T4 —> inferior to TSH when used as screening test, will not detect subclinical hypothyroidism 4. Increased creatine phosphokinase, elevated cholesterol, triglycerides, anemia
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IATROGENIC HYPOTHYROIDISM
- Detected by screening before symptoms develop - 1st 3-4 months after radio iodine treatment for Grave’s disease —> transient hypothyroidism may occur due to reversible radiation damage - Low dose thyroxine may be withdrawn if recovery occurs - Unbound T4 levels —> better measure of thyroid function than TSH in months following radio iodine treatment
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IODINE DEFICIENCY
- Responsible for endemic goiter and cretinism - Uncommon cause of adult hypothyroidism unless iodine intake is very low or if with thiocyanates in cassava or selenium deficiency - Tx: Iodized salt or bread or a single bolus of oral or intramuscular iodized oil
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CHRONIC IODINE EXCESS
- Induce goiter and hypothyroidism - Patients treated with amiodarone, lithium
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SECONDARY or CENTRAL HYPOTHYROIDISM
- In the context of anterior pituitary hormone deficiencies’ - Diagnosis: low unbound T4 - Goal of treatment: maintain T4 levels ini upper half of the reference interval because TSH levels cannot be used to monitor therapy
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TREATMENT OF HYPOTHYROIDISM: No residual thyroid function
Levothyroxine 1.6 ug/kg body weight (100-150 ug)
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TREATMENT OF HYPOTHYROIDSIM: After treatment of Grave’s disease
Levothyroxine 75-125 ug/day
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TREATMENT OF HYPOTHYROIDISM: <60 years old without evidence of heart disease
Levothyroxine 50-100 ug/day
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TREATMENT OF HYPOTHYROIDISM: elderly with CAD
12.5-25 ug/day with similar increments every 2-3 months until TSH is normalized
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MISSED DOSES OF T4 MANAGEMENT
- Due to long half life (7 days) , can take two doses of skipped tablets at once
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OTHER CAUSES OF INCREASE LT4 REQUIREMENT
1. Malabsorption (Celiac disease, small-bowel surgery, atrophic or H.pylori gastritis) 2. Oral estrogen containing medications 3. SERMS 4. Ingestion with a meal 5. Bile acid sequestrates 6. Ferrous sulfate, calcium supplements, sevelamer, sucralfate 7. PPI, Lovastatin, Aluminum hydroxide 8. Rifampicin, Amiodarone, Carbamazepine, Phenytoin, TKIs
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SUBCLINICAL HYPOTHYROIDISM IN PREGNANCY: Target TSH
Target TSH: maintain in normal range but <2.5 mIU/L prior to conception
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SUBCLINICAL HYPOTHYRODISM IN PREGNANCY: Monitoring
Monitoring: 1. Immediately after pregnancy is confirmed, 2. Every 4 weeks during 1st half of pregnancy 3. Every 6-8 weeks depending on whether LT4 dose adjustment after 20 weeks of gestation LT4 dosage: increase from once daily to nine doses per week as soon as pregnancy is confirmed
40
MYXEDEMA COMA
- Reduced consciousness, seizures, hypothermia 23C - History of treated hypothyroidism with poor compliance or undiagnosed - Almost always occurs in elderly - Precipitated by: drugs that impair respiration: sedatives, anesthesia, antidepressants, pneumonia, CHF, MI, GI bleed, CVA, sepsis, exposure to cold
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TREATMENT OF MYXEDEMA COMA: MEDICAL
1. LEVOTHYROXINE single IV bolus 200-400 ug LT4 as loading dose Daily oral dose of 1.6 ug/kg/day reduced by 25% if administered IV as maintenance dose 2. Liothyronine(T3) IV or via NGT since T4 —>T3 conversion is impaired in myxedema coma - Loading dose: 5-20 ug liothyronine - maintance: 2.5-10 ug every 8 hours
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TREATMENT OF MYXEDEMA COMA: SUPPORTIVE
1. External warming: if temp <30 2. Space blankets to prevent heat loss 3. Hydrocortisone 50 mg every 6 hours - due to impaired adrenal reserve in profound hypothyroidism 4. Treat underlying: antibiotics, 5. Ventilatory support with regular ABG during 1st 48 hours 6. Hypertonic saline or IV glucose if with severe hyponatremia or hypoglycemia AVOID HYPOTONIC IV FLUIDS -> Exacerbate water retention secondary to reduced renal perfusion and inappropriate vasopressin secretion AVOID SEDATIVES
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- Most valuable tool for diagnosis and evaluation with nodular thyroid disease - Guidelines recommend for ALL PATIENTS SUSPECTED OF HAVING THYROID NODULES
THYROID ULTRASOUND
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ULTRASOUND FINDINGS BENIGN vs MALIGNANT THYROID NODULES
A. MALIGNANCY - Hypoechoic sold nodules - Infiltrative borders - Micro calcifications (>90% cancer risk) B. NON MALIGNANT - Isoechoic solid nodules (5-10% cancer risk) - Spongiform nodules (multiple small internal cystic areas or simple cysts (<3% cancer risk)
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- Not used routinely if with thyroid nodules - Performed if serum TSH is SUBNORMAL - Determine if functioning or non functioning thyroid nodules
THYROID SCINTIGRAPHY
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HOT vs COLD THYROID NODULES
A. FUNCTIONING or HOT NODULES - Almost never malignant - FNA not indicated B. NON FUCTIONING or COLD NODULES - Do not produce thyroid hormone - Malignant
47
- anti bodies that stimulate the TSH-R in Grave’s disease - Used to predict both fetal & neonatal thyrotoxicosis caused by transplacental passage of high maternal levels of TRAb or TSI (3x upper limit of normal) in last trimester
TRAb (TSH receptor antibody)
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- detect autoimmune thyroid disease. Anti-Tg less common - 80% of Graves and almost all patients with autoimmune hypothyroidism have TPO antibodies
Antibodies against TPO and Tg
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- increased in all types of thyrotoxicosis EXCEPT thyrotoxicosis factitia - Reflect thyroid tissue destruction and released of Tg - Main role: follow up of thyroid in cancer patients -After total thyroidectomy and radio ablation, Tg should mbe <0.2 ng/ml in absence of anti-Tg antibodies - If measurable levels —> incomplete ablation or recurrent cancer
Serum Tg
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CAUSES OF ELEVATED TSH
1. Hypothyroidism - most common 2. TSH secreting pituitary tumor 3. Thyroid hormone resistance 4. Assay artifact
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HYPEREMESIS GRAVIDARUM
- Severe nausea, vomiting and risk of volume depletion - Antithyroid drugs not indicated unless concomitant Grave’s disease is suspected - Tx: parenteral fluid replacement
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CHANGES IN THYROID FUNCTION during PREGNANCY
1. Increase in hCG during 1st trimester —> weakly stimulate TSH-R —> reciprocal fall in TSH 2. Estrogen induced rise in TBG during 1st trimester (sustained during pregnancy) 3. Alteration in immune system —> onset, exacerbation or amelioration of underlying autoimmune thyroid disease 4. Increased thyroid hormone metabolism by placental type III deiodinase 5. Increase urinary iodide excretion —> impaired thyroid hormone production in areas of marginal iodine sufficiency
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WOLF-CHAIKOFF EFFECT
- Excess iodide transiently inhibits thyroid iodide organification
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Recommended Dietary Allowance (RDA) IODINE
> Pregnant women: 220 ug/day > Breastfeeding women: 290 ug.day
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ENDOCRINOLOGY
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