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Internal Medicine > Thyroid > Flashcards

Thyroid Flashcards

1
Q

What hormones does dopamine inhibit?

A

Prolactin and TRH and TSH.

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2
Q

What increases thyroxine-binding globulin (TBG)?

A

Estrogen increases (e.g. OCP, pregnancy)
Hepatitis
Opioids
Hereditary

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3
Q

What decreases thyroxine-binding globulin (TBG)?

A 
Androgens
Glucocorticoids
Nephritic syndrome
Cirrhosis
Acromegaly
Antiepileptics 
Hereditary
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4
Q

In which situation do we want to see if reverse T3 is high?

A

Sick euthyroid syndrome

It’s an inactive molecule

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5
Q

Antithyroid peroxidase antibodies (TPO Ab) are seen in which thyroid conditions?

A

Hashimotos (high titre)
Painless thyroiditis
Graves’ disease (low titre)

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6
Q

In which conditions will thyroglobulin be increased above normal?

A

Goiter
Hyperthyroidism
Thyroiditis

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7
Q

In which conditions is thyroglobulin decreased from normal?

A

Factitious ingestion of thyroid hormone

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8
Q

What do we use thyroglobulin for clinically?

A

Detecting thyroid cancer recurrence, relapse or metastasis . Need to measure antibodies to thyroglobulin as well to help interpret.

It is a tumor marker after total thyroidectomy and radioiodine therapy

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9
Q

Which conditions will there be increased uptake on a radioactive iodine uptake scan?

A

Used to differentiate causes of hyperthyroidism.

Increased in:
Graves (homogenous)
Multinodular goiter (hererogenous)
Hot/toxic nodule (focal uptake, suppression of rest of gland)

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10
Q

In what conditions is there no uptake on RAIU but there is clinical hyperthyroidism?

A

Thyroiditis (subacute painful aka de Quervain’s or painless)
Exogenous thyroid hormone
Recent iodine load
Struma ovarii (rare ovarian tumor/teratoma comprised of >50% thyroid tissue so thyroid gland is less active/suppressed)
Antithyroid drugs

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11
Q

Primary hypothyroidism comprises what % of hypothyroid cases?

A

> 90%

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12
Q

List the causes of primary hypothyroidism

A

Goitrous:

  • Hashimoto’s thyroiditis
  • Iodine deficiency
  • Lithium
  • Amiodarone

Non-goitrous:

  • surgical destruction
  • after RAI
  • after radiation therapy
  • Amiodarone
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13
Q

What % of patients with Hashimoto’s thyroiditis have anti-TPO

A

> 90%

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14
Q

What menstrual abnormalities occur in hypothyroidism?

A

Menorrhagia

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15
Q

What type of hypertension does hypothyroidism cause?

A

Diastolic hypertension

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16
Q

What are the characteristics of a myxedema coma?

A

Hypothermia (<35 degrees)
Hypotension
Hypoglycaemia
Hypoventilation and hypercarbia and hypoxemia
Bradycardia
Mental status changes like coma (lethargy, obtundation, stupor, seizures)
Hyponatremia
GI findings (abdo pain/constipation, decreased gut motility, paralytic ileus)
EKG changes (long QT, low voltage, bundle branch blocks, other heart blocks, or other ST changes)
Pericardial or pleural effusion
Pulmonary edema
Cardiomegaly
AKI

Has a precipitating factor usually like infection or neurological illness or cardiopulmonary issue

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17
Q

What meds or nutrients decrease synthroid absorption?

A 
Iron
Calcium
Cholestyramine
Sucralfate
PPI
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18
Q

What medications accelerate thyroxine catabolism?

A

Phenytoin

Phenobarbital

19
Q

If giving someone estrogen or if someone is pregnant and hypothyroid, how do you tell them to increase their thyroid hormone due to increased need?

A

J

20
Q

Why does pregnancy increase synthroid need and by how much (%)?

A 
30-50% increase
Due to combination of:
-estrogen stimulating TBG so less free hormone
-increased volume of distribution 
-T4 cleared by placental deiodinases
-HCG competitively binds at TSH receptor
21
Q

What is the goal TSH during pregnancy?

A

Lower targets
<2.5 first trimester
<3.5 thereafter

22
Q

How often do you need to check TSH in pregnancy?

A

Every 4-6 weeks in first and second trimester and then no need to check in third trimester

23
Q

When does a fetus begin thyroid function

A

20 weeks and above

24
Q

How do you treat myxedema coma?

A

Load 5-8 microgram/kg IV levothyroxine (T4) then 50-100 micrograms daily because peripheral conversion is impaired.
Uptodate states 200-400 mcg bolus then 50-100 daily. It should raise levels by 2-4 McG/dL. Choose lower end of dosing range for those who are at higher risk for cardiac complications (MI, arrhythmia) and older patients.

Also give T3 (some people only do either T3 or T4 alone and some do combination) because greater biologic activity and faster onset.
IV T3 5-20 mcg then 2.5-10 q8h

ALSO give empiric stress steroids because decreased adrenal reserves in severe illness but also because you cannot exclude underlying adrenal insufficiency (primary or secondary)

25
Q

In myxedema coma how often should labs be monitored?

A

Serum free T3 and T4 q 1-2 days measure at least an hour after doses to avoid false highs.

26
Q

When should you expect clinical and biochemical improvement in myxedema coma after initiation of therapy?

A

Within a week.

TSH falls by 50% in a week of full thyroid hormone replacement so if TSH isn’t falling the therapy is inadequate

27
Q

1/2 of people with subclinical hypothyroidism with what two features usually become euthyroid in 2 years?

A

TSH <7 or negative anti TPO

28
Q

What is the progression per year (%) in subclinical hypothyroidism if increased titers of antithyroid antibodies?

A

4% per year

29
Q

What situations would you treat subclinical hypothyroidism rather than observing?

A

TSH>10, goiter, pregnancy, infertility or TSH 5-10 and age less than 60 (because if over 60 more risk of CV complications)

Sometimes for tsh 4-10 with symptoms he sends off tpo ab and then if positive you can consider treating depending on circumstances like pregnancy.

30
Q

What are the possible etiologies of hyperthyroidism?

A

Graves’ disease
Thyroiditis: subacute (granulomatous) or painless (lymphocytic)
Toxic adenoma or multinodular goiter

Less common include:
TSH secreting pituitary tumor
Pituitary resistance to thyroid hormone

Miscellaneous:
Amiodarone, iodine-induced, thyrotoxicosis factitious, stroma ovarii, hcg secreting tumors (choriocarcinoma), large deposits of metastatic follicular thyroid cancer

31
Q

How is hyperthyroidism related to bone health?

A

Leads to osteoporosis

32
Q

What are the characteristics of a thyroid storm?

A 
Delirium
Fever 
Tachycardia
Systolic hypertension with wide pulse pressure and low MAP
GI symptoms

20-50% mortality

33
Q

When can you not order an RAIU because the results won’t be accurate?

A

Recent IV contrast or amiodarone load. Check autoantibodies instead.

34
Q

What are the etiologies of thyroiditis?

A

Acute: rare, usually post surgical these days. Due to bacterial infection with staph/strep

Subacute: painful and silent and other

Painful -> viral, granulomatous or de Quervains

Silent -> postpartum, autoimmune or lymphocytic

Other -> meds like Amiodarone, lithium and TKIs, palpation thyroiditis and post-radiation

35
Q

How is subacute painful thyroiditis treated?

A

Nsaids, ASA, steroids

36
Q

What medications decrease the peripheral conversion of T4 to T3?

A

Beta blockers like propranolol
And steroids
And Amiodarone

37
Q

What medication can cause both hyperthyroidism and hypothyroidism?

A

Amiodarone

And to some effect lithium

38
Q

Does lithium cause hypothyroidism or hyperthyroidism or both?

A

Both

For hyperthyroidism it is through thyroiditis

39
Q

Describe the mechanism and treatment of Type 1 Amiodarone-induced hyperthyroidism

A

Occurs in underlying multinodular goiter or autonomous thyroid tissue.
Jod-Basedow effect when iodine load there is increased synthesis of T4/T3 in autonomous tissue

treatment: methimazole

not absolutely necessary to discontinue Amiodarone because amio will decrease peripheral conversion

Usually occurs earlier after start of Amiodarone (median of 3.5 months)

40
Q

Describe the mechanism and treatment of Type 2 Amiodarone-induced hyperthyroidism

A

Destructive thyroiditis
Increased release of preformed T4 and T3 leads to hyperthyroid then hypothyroid then recovery

Treat with steroids (eg 40 mg daily pred)

Usually occurs later in course of Amiodarone (median 30 months)

41
Q

What does Doppler ultrasound show for type 1 and 2 Amiodarone-induced hyperthyroidism?

A

Type 1 - Increased thyroid blood flow

Type 2 - decreased thyroid blood flow (it’s destructive process releasing stored hormone..kaboom)

42
Q

How does hypothyroidism lead to hyperprolactinemia?

A

TRH is increased and it stimulates prolactin secretion

43
Q

What is the Jod-basedow phenomenon?

A

Hyperthyroidism following iodine intake (supplementation, iodinated contrast, Amiodarone) in someone with underlying thyroid disease.

Either entire gland or autonomous nodule (more common) affected.

Lack of adequate feedback control from pituitary.

44
Q

What is the Wolff-Chaikoff effect?

A

Auto regulatory phenomenon whereby large ingestion of iodine actually inhibits thyroid hormone synthesis within the follicular cells irrespective of TSH levels.

Transient, returns to normal in 26-50 hours

Can lead to hypothyroidism in susceptible patients with underlying thyroid disease who can experience a delayed “escape” from the Wolff-Chaikoff effect

Internal Medicine (5 decks)

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