Thyroid disorders Flashcards

1
Q

Know how to make the diagnosis of hyperthyroidism and how to investigate the differential diagnosis of hyperthyroidism

A

Diagnose by symptoms, screen with TSH, if low, then FT4 and T3. Then what is the cause? Thyroid scan or I uptake, or Abs (TSH-R or TPO)

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2
Q

Know the causes of increased and decreased iodine uptake or 99mtechnetium thyroid scan uptake

A

Increased: Graves, Toxic adenoma or toxic multinodular goiter’ decreased: Thyroiditis (subacute - viral, painless - silent, Post-partum), hashimotos’, I excess. Painless, post-partum, and Hashimoto’s has TPO Ab. Grave’s has TSH-R Ab and TPO.

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3
Q

Know the three autoimmune manifestations of Graves’ disease

A

orbitopathy (proptosis), pretibial myxedema, acropachy(finger clubbing)

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4
Q

Know thepathophysiology of the autoimmune manifestations.

A

Genetic polymorphisms: HLA-DR, CTLA-4, PTPN22. T cell regulatory defect leading to production of TSH receptor antibodies in thyroid, bone marrow, lymph nodes. TPO antibodies also produced – may lead to thyroid destruction later

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5
Q

Know the therapeutic options for Graves’ disease

A

Drugs, about 20% long term remission but 30% relapse: PTU (better in 1st 1/3 of pregnancy), methimazole (stronger, longer T1/2). Near total thyroidectomy. Radioactive I (radiation about 24-48h, possible worsening of ophthalmopathy).

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6
Q

Signs/symptoms of thyrotoxicosis

A

Nervousness, palpitations, sweating, heat intorlerance, fatige, wt loss, dyspnea, increased appetite, eye symptoms; more rare: fixable hair and nails, increased BM, diarrhea, menstrual issues. High HR, goiter, tremors, skin chages, hyperactivity, bruit, lid lag and retraction, ophthalmopathy, A fib, onycholysis (nails peeling off due to cell turnover), vitiligo

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7
Q

Apathetic thyotoxicosis

A

Atypical presentation in elderly. Missing most other signs of hyper thyroid, mostly just A fib, wt loss.

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8
Q

Percent causes of thyroid ophthalmopahty

A

80% is graves. The rest is hashimoto’s or euthyroid.

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9
Q

Signs and symptoms of ophthalmopathy

A

Symptoms: Inflammatory – irritation, gritty, pain, watering, photophobia, periorbital edema, If optic nerve compression – decreased vision, Diplopia – due to eye muscle inflammation. Signs: Periorbital edema, Conjunctival edema (chemosis), injected (redness), Opthalmoplegia (eye muscle weakness), diplopia– muscle imbalance, Proptosis, Retina: papilledema

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10
Q

What causes lid retraction?

A

Proptosis - eyelid not big enough to get over it; and TH stimulates sympathetic activity which causes the eyes to open more.

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11
Q

What causes the ophthalmopathy? How does treatment of Thyroid help?

A

Not sure how, likely T cells infiltrating and attacking antigen in eye muscles. Hyperthyroid Tx does NOT influence course of eye disease. Tx for eyes not great: lubricants, tape shut; corticosteroids, orbital radiation; surgery on lids, orbital decompression (chunk of bone to allow for room for muscles), muscle balancing.

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12
Q

What is pretibial myxoedema?

A

aka Grave’s dermopathy. On shins or top of feet. Immune infiltration under skin. Feels hard and firm but painless. Give topical corticosteroids

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13
Q

Do pretibilal myxedema and acropachy regress with Tx of graves?

A

No! Continue to progress despite that, but can be treated separately.

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14
Q

Other causes of hyperthyroidism

A

Graves is number 1. Then, Toxic (hyperfunctioning) thyroid nodule(s), Silent (autoimmune; Hashimoto’s) thyroiditis and variants; Subacute thyroiditis (de Quervain’s thyroiditis) - stupid name, it’s painful.

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15
Q

Know the differentiating features (clinical, biochemical, radiological) between Graves’ disease, thyroiditis, and toxic nodules

A

Graves: Usually diffuse symmetrical goitre, Extrathyroidal autoimmune signs. Toxic nodule(s): Single nodule or irregular, lumpy (multiple nodules) goitre, No autoimmune signs

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16
Q

Dx of toxic nodules

A

Screen: suppressed TSH, then T4 T3. Do thyroid scan to see nodules. Negative TPO and TSH-R.

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17
Q

Silent thyroiditis

A

Aka transient hyperthyroidism Variant of Hashimoto’s. May cause hyper or hypo. Self-limiting, so don’t need Tx, give ß blockers to reduce symptoms. NO neck pain or tender thyroid. No systemic symptoms. WBC and ESR normal. Positive TPO Ab. Can go back to normal or drop to hypo after being hyper (followup).

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18
Q

Subacute thyroiditis (de Quervain’s)

A

Viral cause. Self-limiting. Exquisitely tender and painful thyroid, don’t want to be touched at all. Neck pain radiating to ear or jaw. Often preceded by upper respiratory infection. Prodrome: myalgia, malaise, fatigue. Fever. ESR elevated; WBC usually normal.. WBC count can be different. Transient hyper, then maybe hypo then maybe recover. Almost never happens again. Give ß blockers, analgesics, corticosteroids.

19
Q

Postpartum thyroiditis

A

Variant of Hashimoto’s, after pregnancy. Can result from drop off of estrogen (anti-inflammation). Can be hyper, hypo, or hyper then hypo. Can get permanent hypo if no hyper phase, high TPO, or sever hypo.

20
Q

Subclinical hyperthyroidism

A

Normal T3/T4, suppressed TSH. Usually normalizes, some progress to hyper. Higher risk of A fib, aggravate CHF, angina. Same cause as hyper, same Tx.

21
Q

Know the causes of hypothyroidism

A

Endogenous: Most common: Hashimoto’s (autoimmune). Other autoimmune (painless or post-partum in the hypo phase). Subacute (viral) in hypo phase (rare). Congenital. Exogenous: overtreat Radioactive I, anti-thyroid drugs, surgery, higher I intake

22
Q

Know the symptoms and signs of hypothyroidism

A

Fatigue, apathetic face, cool dry thick skin, periorbital edema, Weight gain, Cold intolerance, Constipation, Nausea / low appetite, slower reflexes, Menorrhagia (frequent/heavy), edema, Shortness and slowness of breath, diastolic hypertension depression, psychosis, Dry skin, Brittle hair and nails, Galactorrhea (rare), loss of outer 1/3 eyebrow. Severe: heart failure, coma, generalized edema

23
Q

What is hashimoto’s?

A

Autoimmune destruction of thyroid follicles and spilling of stored TH. Can present with hyper, then euthyroid, then hypo (progressive). Goiter is common. TPO Ab. Nodules rare (from scarring). Can have some ophthalmopathy or polyglandular autoimmune syndrome.

24
Q

Most common presentation of Hashimoto’s?

A

A euthyroid goiter with TPO Ab. Then hypothyroidism, then hyperthyroid phase (least common).

25
Q

Know the diseases associated with the polyglandular autoimmune syndromes

A

hypoparathyroid, adrenal insufficiency, hypogonadism, hypothyroidism, celiac disease, vitiligo, pernicious anemia (type 1 in kids, autosomal recessive; type 2 in adults, HLA)

26
Q

Subclinical hypothyroidism

A

No or minimal symptoms. Same causes. Defined as elevated TSH and normal T4. Some will revert to normal if middle elevated TSH compared to high. Treat if TSH>10, or if has Goiter, pregnant or other symptoms (TPO). Increased risk of CVD.

27
Q

Know the causes of goiter

A

I deficiency. Nontoxic multi or single nodule goiter. Graves, Hashimotos, or other thyroid issues.

28
Q

Why do we care about nodules?

A

May cause hyperthyroidism, May be a thyroid cancer, Sometimes cause compressive symptoms if big enough

29
Q

Know the epidemiology of thyroid nodules

A

About 5% are palpable but over 60% of people have them but most are not significant. only about 50/million are cancer

30
Q

Management of thyroid nodules

A

Check TSH, then ultrasound/scan, then fine needle aspirate for nodules >1cm or suspicious of cancer. If hot nodule do radio I or surgery, if cold then decide if benign or not (surgery).

31
Q

Know the clinical features of a nodule that suggest malignancy

A

characteristics of nodule: fixed/hard; characteristics of trachea: central/deviated; vocal chord paralysis; evidence of local invasion; palpable lymph nodes/ipsilateral lymphadenopathy

32
Q

Dx and Tx of thyroid cancer

A

FNA of nodule. Total thyroidectomy +/- node removal, then radioactive iodine

33
Q

Know the types of thyroid cancer

A
  1. papillary / pap.-follicular (80% - indolent disease; cure rate 95%; neck lymph node spread common (30-50%), lung 10%); 2. follicular, Hurthle cell, anaplastic; 3. medullary ( 25 % familial; RET)
34
Q

Know the two followup tests for thyroid cancer

A

Serum thyroglobulin and antiTgb Ab every 6-12 mo; Also, Periodic TSH stimulated thyroglobulin testing and Periodic neck ultrasound

35
Q

Know how amiodarone affects the thyroid

A

Used for arrythmias. Lots of I in it, induces lower I uptake, can cause hypo (Tx: thyroxine) or hyper (hard Tx since can’t uptake I).

36
Q

Know how lithium affects the thyroid

A

used for depression. Inhibits TH synth. Sometimes cause hypo (give thyroxine), rarely hyper.

37
Q

Know how interferon affects the thyroid

A

used for hepatitis C. hypo more common than hyper. Can treat as usual, and usually resolves after stopping INF

38
Q

Know the adverse effects of hypothyroidism in pregnancy

A

Best to treat before pregnancy. Hypo (mild: neurocognitive development; overt hypo: maternal hypertension, pre-eclampsia, anemia, postpartum hemorrhage, spontaneous abortion, fetal death, low birth weight, abnormal brain development) and hyper (miscarriage or premature birth) is no good for fetus.

39
Q

Managing Hypothyroidism in pregnancy

A

Screen. Treat all hypo cases as more I needed. Give Thyroxine and/or more I

40
Q

Higher risks for hypothyroidism in pregnancy

A

prior thyroid dysfunction/surgery; Age > 30; TPO Ab +; Type 1 diabetes or other autoimmune; Hx of miscarriage or preterm delivery; Hx of head or neck radiation; Fam Hx of thyroid dysfunction; Morbid obesity (BMI > 40); Use of amiodarone, lithium, or recent contrast dye use; Infertility; Residing in an area of known moderate to severe iodine insufficiency

41
Q

Gestational hyperthyroidism

A

Due to hCG stimulating TSH-R. No Tx needed.

42
Q

Know the differences between Graves’ disease and gestational hyperthyroidism

A

Gestational doesn’t have TSH-R Ab, no ophthalmopathy.

43
Q

How to treat Grave’s during pregnancy.

A

PTU 1st trimester, then methimazole (teratogenic in 1st). target high normal or slightly hyperthyroid levels (avoid hypothyroidism!!)

44
Q

Know the common causes of postpartum hyperthyroidism and how to differentiate these

A

Graves’ disease versus post-partum thyroiditis (thyrotoxic phase of Hashimoto’s thyroiditis). Ddx with TSH-R Ab (TPO in both). Can’t do nuclear med uptake if breastfeeding