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ENDO 2 Exam II (2017) > Thyroid Diseases Pales > Flashcards

Thyroid Diseases Pales Flashcards

1
Q

Thyroid hormone steps

A

iodine absorbed by GI tract
iodine distributing in ECF
iodine transported into thyrocyte
iodine oxidized by H202 with help of thyroid peroxidase (TPO)
oxidized iodine binds to thyroglobulin
T1 and T2 formed
T1 and T2 couple with help of TPO to form T3 and T4
still bound to thyroglobulin, T3 and T4 secreted into follicular lumen
T4 and T3 cleaved off thyroglobulin and released into circulation

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2
Q

Thyroid Hormone

A 
Most of the T4 and T3 are bound in the blood
Only unbound T4 and T3 are active 
T3 is 8 x  more active than T4
Most of T3 in the tissues converted from T4 peripherally by de-iodinization
TSH stimulates
- Growth of thyroid gland
 - Synthesis of T4 and T3
- Release of T4 and T3
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3
Q

Thyroid Hormone Effects

A

Regulates expression of thyroid hormone–responsive genes
– Increases expression LDL receptors accelerating LDL clearance.
Causes Positive chronotropic and inotropic effects in the heart
Increases basal metabolic rate
Increases mental alertness
Increases ventilatory drive
Increases gastrointestinal motility
Increases bone turnover.

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4
Q

Hyperthyroidism. Thyrotoxicosis. Thyroid Storm

A

Hyperthyroidism—increased function of the thyroid gland
Thyrotoxicosis—Increased level of thyroid hormone
Thyroid Storm– extreme form of Thyrotoxicosis

heat intolerance… palpitations…tachycardia… irritable…loose stools…tremor…warm moist skin…hyperreflexia…

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5
Q

types of hyperthyroidism

A 
Graves disease
toxic nodule(s)
iodine exposure (Jod-Basedow phenomenon)
ectopic thyroid tissue/struma ovarii
TSH-secreting pituitary adenoma
factitious/ iatrogenic
thyroiditis (initial stage)
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6
Q

Graves Disease

A

60-80% of patients with thyrotoxicosis
Autoimmune condition
More common among women
Most often occurs 20 – 50 years of age.
Caused by TSI, auto-atibodies activating TSH receptors on Thyroid Gland leading to overproduction of T4 and T3
Other thyroid autoantibodies in Graves disease: TPO antibodies, thyroglobulin antibodies, and TSH receptor antibodies.

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7
Q

Triad of Graves Disease:

A

Goiter, exophthalmos, and pretibial myxedema/thyroid dermopathy.

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8
Q

Eye issues and other symptoms in hyperthyroid

A

orbitopathy:
…“staring”… lid lag and
strabismus*

Fibroblast proliferation with GAG deposits, and lymphocyte infiltration in the muscles around the eyes produce proptosis and diplopia.

bruit over the thyroid
clubbing of the fingers

Increased T3 leads to increased bone turnover.

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9
Q

Clubbing – Hypertrophic Osteoarthopathy

causes

A

. Cardiac diseases, ie SBE, congenital heart

  1. Pulmonary diseases, ie PF, non-small cell lung cancer - especially adenocarcinoma, cystic fibrosis
  2. GI diseases, ie Crohns disease, cirrhosis, celiac
  3. Renal failure
  4. Thyroid disease, ie Graves (smokers with high titer TSIs)
  5. Malignancies, ie Hodgkins
  6. Idiopathic
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10
Q

Thyrotoxic cardiomyopathy

A

tachycardia induced cardiomyopathy,
AF, high output failure, and pulmonary hypertension.

Apparently due to increased free estradiol from the increased aromatase activity of thyroxine

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11
Q

Graves Disease Course

A

Mortality 10–30% without treatment
Mild Graves disease may go into remission (spontaneously or after treatment)
The clinical course of ophthalmopathy does not follow thyroid disease. Treatment of Graves thyrotoxicosis doesn’t improve ophthalmopathy.

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12
Q

Treatment of Graves hyperthyroidism:

A

1a. Antithyroid (thiourea) drugs: Block oxidation (* TPO inhibition of I- to Io) , organification (iodination) and coupling– usually used up to four days before RAI to avoid RAI induced storm.
— 1. PTU* – OK in Pregnancy (1st trimester only). Blocks T4 T3.
— 2. methimazole – less hepatic necrosis and drug of first choice.
Side effects of both: Agranulocytosis, Hepatitis, SLE?

1b. Iodine – (Iopanoic acid or Ipodate sodium) which block T4 T3
(give after starting thiourea drugs) - works via peripheral
inhibition of 5’ monodeiodination of T4. * Wolff-Chaikoff effect – stops synthesis and release.
1c. Lithium, potassium perchlorate (inhibits the sodium iodide symporter).

  1. RAI unless pregnant - may start with propranolol and
    anti-thyroid drugs (PTU qid or methimazole daily).
  2. Surgery - very rare (pregnancy)
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13
Q

Thyroiditis

A

Thyrotoxicosis without hyperthyroidism is the first stage of thyroiditis.
Due to leakage of the stored T4 and T3 through more permeable inflamed epithelium
Transient and will go into euthyroid and then hypothyroid state.

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14
Q

Thyrotoxicosis work up.

A

TSH is a screening test for thyroid abnormalities
Low TSH is suggestive of primary thyrotoxicosis. Should be confirmed by high Free T4 and/or Free T3 tests
If TSH is low, but FT4/FT3 normal –> subclinical hyperthyroidism
Total T4 and Total T3 are not done much any more because they may be affected by many factors and be falsely positive or falsely negative

Autoimmune antibodies:

  • TSI
  • Anti- TPO (anti-microsomal), - Anti-thyroglobulin antibodies

Thyroid uptake and scan

  • Uniform increase in Graves
  • Hot Nodule (s) in TN or MNTG
  • Decreased uptake in thyroiditis, factitious
  • Uptake outside of thyroid if ectopic tissues
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15
Q

Thyrotoxic Crisis or Storm

A

Severe Thyrotoxicosis
Fever(>102F)
Tachycardia (Sinus or Atrial fibrillation)
Tachypnea
All the symptoms of thyrotoxicosis
May have End Organ Damage (High Output Heart Failure)

Treatment:

  • PTU iv
  • with iodides (Ipodate or SSKI)
  • Beta Blockers
  • Corticosteroids
  • Plasmaphoresis.
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16
Q

Subclinical Hyperthyroidism

A

Decreased TSH with normal T4 and T3
Early stage of thyrotoxicosis
Usually asymptomatic but patients have an increased risk of Atrial Fibrillation and Osteoporosis.
Most often will progress to full blown thyrotoxicosis and usually requires treatment

17
Q

Apathetic Hyperthyroidism

A

Thyrotoxicosis without usual facial and behavioral features
Usually occurs in the older patients (over 60)
Depressed facial features and “apathetic” behavior without proptosis, tremors, hyperactivity
Mostly presents with cardiac toxicity (arrhythmia), myopathy and osteoporosis

18
Q

Jod-Basedow Phenomenon

A

Iodine-induced hyperthyroidism
Usually happens in a patients with
- Pre-existent but silent thyroid disease (Graves, Multinodular Goiter, Thyroiditis)
- Endemic goiter (from low Iodine content in diet) when patient moves into high iodine area)
Sometimes happens after iodinated contrast is given for CT

19
Q

Wolff–Chaikoff effect

A

Physiological and temporary decrease in thyroid function in response to large iodine exposure

20
Q

Amiodarone effect

A

39%iodine by weight.

Amiodarone-induced Thyrotoxicosis

  • Type 1. Jod Basedow Phenomenon from iodine load and pre-existant silent thyrooid desiease
  • Type 2. Amiodarone-induced thyroiditis

Amiodarone-induced hypothyroidism
Wolff-Chaikoff effect — transient from iodine load
Thyroiditis

21
Q

Euthyroid sick syndrome

A

Acute, severe illness can cause abnormalities of TSH or thyroidhormone levels in the absence of underlying thyroid disease,

The major cause of these hormonal changes is the release of cytokines, such as IL-6

Several patterns exist
- Low T3syndrome: decrease in T3levels with normal levels ofT4andTSH Peripheral conversion of T4 to T3 is replaced by conversion of T4 to rT3. It is thought to be adaptive as it may limit catabolism in starved or ill patients.
Low T4syndrome: fall in totalT4and T3levels, normal FT4 level, and TSH being either low or high, which spontaneously reverseal after recovery
The diagnosis is frequently presumptive. Only resolution of the test results with clinical recovery can clearly establish this disorder.
No Treatment required

22
Q

Hypothyroidism

A

Myxedema = really a lymphedema with
accumulation of glycosaminoglycans in the skin with doughy feeling upon palpation.

diastolic hypertension

23
Q

Hypothyroidism. Symptoms.

A 
Tiredness, weakness
Dry skin
Feeling cold
Hair loss
Difficulty concentrating and poor memory
Constipation
Weight gain with poor appetite
Dyspnea
Hoarse voice
Menorrhagia (lateroligomenorrhea or amenorrhea)
Paresthesia
Impaired hearing
24
Q

Hypothyroidism. Signs

A 
Dry coarse skin; cool peripheral extremities
Puffy face, hands, and feet (myxedema)
Diffuse alopecia
Bradycardia
Peripheraledema
Delayed tendon reflex relaxation
Carpal tunnel syndrome
Serous cavity effusions

brittle nails…thin hair…loss of the lateral 1/3 of the eyebrows…pedal edema…

25
Q

The Hypos of Hypothyroidism

A 
Hyporeflexia
Hypomentia
Hypothermia
Hypoventilation
Hypotension or diastolic HTN
Hypohemoglobinemia (anemia—macrocytic)
Hypoglycemia
Hyponatremia (decreased renal Na/K ATPase)
Hypometabolism of drugs and lipids (hyperlipidemia)
26
Q

Hashimoto Thyroiditis

A

The mean age at diagnosis is 60 years, and theprevalence of overt hypothyroidism increases with age.
Associated with positive TPO antibodies

27
Q

Adult Hypothyroidism

A

Hashimoto’s Disease – *** Chronic
Lymphocytic Thyroiditis with
HLA-DR5. (not lymphocyte mediated!)

Antibodies to TPO
and thyroglobulin.

The thyroid is usually enlarged
and boggy.

28
Q

Other autoimmune diseases associated with Hashimoto’s disease

A 
Addisons
HypoparaThyroidism, 
Type 1 DM
Sjogren’s, vitiligo
Primary Billiary Cirrhosis
IBD
29
Q

Treatment of Hypothyroidism:

A

Start with L-thyroxine 25-75 mcg/day, unless pregnant (start with 100-150 mcg) or Hx of CAD (start at 25 mcg)
Maintain clinical euthyroid state – usual dose1.6 mcg/kg/day
Keep TSH between 0.5 mU/L – 2.0 mU/L
For those still feeling tired at TSH < 2mU/mL, check for anemia, B12 deficiency, and sleep apnea. May consider low dose T3
Special considerations for emergency surgery
Monitor oral intake of drugs (ie. imatinib) and food substances (ie. omeprazole, soy milk, coffee, fiber, calcium)

30
Q

Acute Thyroiditis

A

Rare suppurative infection (bacterial or fungal) of the thyroid
When diagnosed in children and young adults, frequently associated with presence of a piriform sinus (remnant of the fourth branchial pouch that connects the oropharynx with the thyroid)
When Diagnosed in elderly, it’s usually associated with long-standing goiter and degeneration in a thyroidmalignancy.

31
Q

Symptoms and signs, treatment of acute thyroiditis

A 
Thyroid pain referred to the throat or ears
Small, tender asymmetric goiter
Fever
Dysphagia
Erythema over the thyroid 
Lymphadenopathy.
Elevated ESR and WBC
Treatment: surgery and antibiotics
Depending on the size of affected part of thyroid, hypothyroidism may develop  after resolution
32
Q

Subacute Thyroiditis

A

De Quervain’s thyroiditis,or granulomatous thyroiditis, orviral thyroiditis
Symptoms can mimicpharyngitis.
Women affected three times more frequently than men.
The peak incidence occurs at 30–50 years
Thyroid dysfunction is usually temporary

33
Q

Subacute Thyroiditis. Clinical features

A

Symptoms of URI followed in a few weeks by

  • Very painful small goiter with pain referred to ear or jaw
  • Fever
  • Complete resolution is the usual outcome, but permanent hypothyroidism can occur

Treatment

  • Large doses ofAspirin orNSAIDs
  • Occasionally glucocorticoids are required
  • Beta blockers for thyrotoxicosis (anti-thyroid medications are not required)
  • T4 replacement may be needed if the hypothyroid phase is prolonged
34
Q

Silent/Painless thyroiditis

A

Occurs in patients with underlying autoimmune thyroid disease.
Clinical course similar to subacute thyroiditis, but without thyroid tenderness.
When occurs 3–6 months after pregnancy it’s calledpostpartum thyroiditis
Associated with the presence of TPO antibodies antepartum and normal ESR
3 times more common in women with type 1diabetes mellitus.
Usually resolve over time
May recur in subsequent pregnancies.

35
Q

Riedel’s thyroiditis

A

Rare disorder of middle-aged women
Painless goiter with local symptoms due to compression of the esophagus, trachea, neck veins, or recurrent laryngeal nerves.
The goiter is hard, nontender, asymmetric, and fixed, leading to suspicion of amalignancy.
Thyroid dysfunction is uncommon
Treatment is surgical relief of compressive symptoms.
Associated with idiopathic fibrosis at other sites (retroperitoneum, mediastinum, biliary tree, lung, and orbit)

36
Q

Myxedema crisis

A
  1. Precipitated by medicine non-compliance, surgery, stress,
    infections, etc.
  2. The 10 hypos: hypothermia, hypoventilation, hyporeflexia,
    hypoglycemia, hyponatremia, hypoxemia, etc
  3. 20-50% mortality
  4. Lethargy and stupor to “myxedema coma”
  5. “myxedema madness”
  6. Hypersensitive to opiates
Treatment:
Hydrocortisone 100 mg IV followed by 
300 mcg levothyroxine(LT4) IV, over 5 
minutes, followed by LT3 20-50 mcg IV 
over 5 minutes

ENDO 2 Exam II (2017) (19 decks)

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