hyperthyroid Flashcards

1
Q

2 broad groups of disorders

A

-Abnormal function
-Abnormal growth (nodules) in the gland

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2
Q

thyroid diseases

A

-Common problems in the general population -> Older people and women
-Functional disorders
-Related to the gland producing too little thyroid hormone (hypothyroidism)
-Or too much thyroid hormone (hyperthyroidism)
-Benign nodules in the thyroid gland are common; do not USUALLY cause serious health problems
-Occur when the cell growth within the nodule is abnormal
-Nodules can occasionally put pressure on the neck -> cause difficulty swallowing, breathing or speaking

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3
Q

testing for different disease

A

-screening- TSH (most sensitive for primary hypo and hyper) and T4
-hypothyroidism- TSH (high in primary and low in secondary) and anti-TPO

-hyperthyroidism:
-TSH (suppressed except in TSH secreting pituitary tumor or pituitary hyperplasia)
-T3 or free T4 - elevated
-123-I uptake and scan- increase uptake, diffuse versus hot foci on scan
-anti-TPO- elevated in graves
-TSI- 65% + in graves

-thyroid nodules:
-FNA bx- best dx for thyroid cancer
-123-I uptake and scan- cancer is usually cold, less reliable than FNA
-99m-Tc scan- vascular versus less vascular
-U/S- assist with FNA bx, assesses risk of malignancy , monitor nodules and pts after thyroid surgery for carcinoma

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4
Q

hyperthyroidism types

A

-Graves’ Disease
-Thyroiditis
-Acute Thyroiditis
-Subacute Thyroiditis
-Hashimoto’s Thyroiditis- small period before when its hyper and then becomes hypo
-Toxic adenomas
-Multi nodular goiter
-Thyrotoxicosis factitial (abusing levothyroxine for wt loss) vs. Struma ovarii (teratoma)
-Pituitary tumor
-Pregnancy & trophoblastic tumors
-Thyroid carcinoma – rare cause of thyrotoxicosis
-Jodbasedow disease
-Amiodarone-induced thyrotoxicosis

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5
Q

thyrotoxicosis vs hyperthyroidism

A

-Thyrotoxicosis
Is defined as the state of thyroid hormone excess
Is not synonymous with hyperthyroidism??? -> she said in class they are the same thing

-Hyperthyroidism is result of excessive thyroid function
-However, the major etiologies of thyrotoxicosis are hyperthyroidism -> Caused by Graves’ disease, toxic multinodular goiter, and toxic adenomas

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6
Q

hyperthyroidism

A

-Refers to conditions caused by excessive thyroid hormone produced by the thyroid gland
-Signs and symptoms generally result from stimulation of the adrenergic nervous system
-hx of radiation on the neck? lymphoma?
-nodules are usually non-tender (dont hurt)

-The MC causes of hyperthyroidism
-Graves’ disease
-Toxic multinodular goiter
-Toxic uninodular goiter
-Thyroiditis

-Less common causes
-Thyroid-stimulating hormone producing tumors
-Pituitary resistance to thyroid hormone
-Trophoblastic disease
-Iodine ingestion

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7
Q

graves disease

A

-toxic diffuse goiter
-MC cause, familial predisposition
-autoimmune disease
-thyroid gland is being stimulated by Thyrotropin receptor antibodies
[also known as thyroid-stimulating immunoglobulin]
-60 to 80% of thyrotoxicosis
-Prevalence varies among populations -> Typically occurs between 20-50 years of age, but also in elderly
-Genetic factors and environmental factors contribute to susceptibility to GD; Indirect evidence - stress - important environmental factor
-Smoking:
-minor risk factor for Graves’ disease
-major risk factor for ophthalmopathy
-Sudden increases in iodine intake may precipitate Graves’ disease
-3-fold increase in the occurrence of Graves’ disease in the postpartum period

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8
Q

toxic multinodular goiter

A

-toxic several nodules
-Multiple areas in the thyroid gland are overproducing thyroid hormone independently of TSH

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9
Q

toxic unimodular goiter

A

-adenoma
-A solitary nodule in the thyroid gland overproducing thyroid hormone independently of TSH

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10
Q

subacute thyroiditis

A

-often idiopathic
-but sometimes virally mediated inflammation and destruction of the thyroid gland
-Consequently, the stored thyroid hormones are released into the circulation, causing a transient hyperthyroid state

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11
Q

rare causes

A

-TSH-secreting pituitary adenoma or pituitary resistance to thyroid hormones
-Pituitary adenoma - benign neoplasms of the anterior pituitary
-Functioning trophoblastic tumors - this includes hydatidiform mole, choriocarcinoma, or metastatic embryonal carcinoma of the testis
-Iodine-induced hyperthyroidism (Jod-Basedow’s disease) - occurs when supplemental iodine is given to patients with iodine-deficiency goiter

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12
Q

epidemiology

A

-Genetics- Graves’ disease has a familial predisposition and can overlap clinically and immunologically with Hashimoto’s disease
-Graves’ disease has a genetic predisposition that is polygenic in nature
-Increased frequency in human leukocyte antigen (HLA)
-Geography- Iodine-induced hyperthyroidism - outbreaks of thyrotoxicosis have occurred when thyroid supplements added into diets of previously iodine-deficient populations

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13
Q

iodine

A

-give radioactive iodine
-whole gland lights up- graves
-overactive thyroid
-if its a nodule- only that nodule shows up
-radioactive iodine can be a treatment to kill overactive thyroid cells (last resort before removal) -> can make you hypothyroid

-Five different scintigrams taken from thyroids with different syndromes: (A) Normal thyroid; (B) Graves disease, diffuse increased uptake in both thyroid lobes; (C) Plummer disease (toxic multinodular goiter); (D) Toxic adenoma; (E) Thyroiditis (marker 99Tc).

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14
Q

thyroid nodule

A

-<1mm - monitor
-1-2mm - monitor, bx

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15
Q

symptoms

A

-Nervousness
-Sweating
-Sensitivity to heat
-Palpitations
-Fatigue
-Dyspnea
-Increase in appetite
-Eye irritation
-Swelling in legs
-Increased frequency of bowel movement, or diarrhea
-pretibial myxedema ** (dont confuse myxedema)

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16
Q

signs

A

-Cardiovascular manifestations
-Fever
-Warm, moist skin
-Tremor
-Bruit over thyroid
-Goiter
-Dermopathy (GD)
-Weight loss (although weight gain can occur in 5% of patients due to increased appetite)
-Splenomegaly
-Gynecomastia
-Oligomenorrhea/amenorrhea/menorrhagia
-Thymic hyperplasia can rarely occur
-Palmar erythema
-Onycholysis
-Less commonly:
-Pruritus
-Urticaria
-Diffuse hyperpigmentation

-Hair texture may become fine
-Diffuse alopecia occurs in up to 40% of patients
-Persisting for months after restoration of euthyroidism

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17
Q

graves ophthalmopathy

A

-Eye signs (erythema, lid retraction, stare)
-The earliest manifestations:
-Usually a sensation of grittiness
-Eye discomfort
-Excess tearing

-In severe cases - corneal exposure and damage can occur, especially if the lids fail to close during sleep
-Periorbital edema, scleral injection, and chemosis are also frequent
-Exophthalmos: Thyroid stare and Lid lag
-These are due to adrenergic stimulation, not infiltrative disease
-About 1/3 of pts have PROPTOSIS
-Best detected by visualization of the sclera between the lower border of the iris and the lower eyelid, with the eyes in the primary position
-Can be measured using an exophthalmometer
-Unilateral exophthalmos should not be attributed to Graves’ disease (tumor)
-Lid retraction, causing a staring appearance, can occur in any form of thyrotoxicosis -> result of sympathetic over activity
-eye symptoms are also called thyroid-associated ophthalmopathy -> Most of these pts have autoimmune hypothyroidism or thyroid antibodies
-onset of Graves’ ophthalmopathy occurs within year before or after dx of thyrotoxicosis in 75% of pts -> Can sometimes precede or follow thyrotoxicosis by several years, accounting for some cases of euthyroid ophthalmopathy

18
Q

graves: dermopathy

A

-Almost always in the presence of moderate or severe ophthalmopathy
-Most frequent over the anterior and lateral aspects of the lower leg (hence the term pretibial myxedema), skin changes can occur at other sites, particularly after trauma
-The typical lesion is a noninflamed, indurated plaque with a deep pink or purple color and an “orange-skin” appearance

19
Q

graves: thyroid acropachy

A

-Refers to a form of clubbing
-It is so strongly associated with thyroid dermopathy that an alternative cause of clubbing should be sought in a Graves’ patient without coincident skin and orbital involvement

20
Q

neurologic manifestations

A

-Common neurologic manifestations include
-Hyperreflexia (brisk), muscle wasting, and proximal myopathy without fasciculation
-Chorea is a rare feature
-Sometimes associated with a form of hypokalemic periodic paralysis -> This disorder is particularly common in Asian males with thyrotoxicosis

21
Q

other effects: graves

A

-The direct effect of thyroid hormones on bone resorption leads to osteopenia in long-standing thyrotoxicosis
-Mild hypercalcemia occurs in up to 20% of patients
-Hypercalciuria is more common
-There is a small increase in fracture rate in patients with a previous history of thyrotoxicosis

22
Q

presentation and Mx in the elderly and children

A

-In the elderly:
-Congestive heart failure
-Atrial fibrillation - Digoxin, beta-blockers, and anticoagulants, may be required
-Management of these complications need to be done early or in conjunction with treatment of GD

-Proximal muscle weakness

-In children:
-Accelerated linear growth
-Eye signs are more common

23
Q

differential dx

A

Anxiety
Thyroiditis
Pheochromocytoma
Autoimmune Deficiency Syndrome (AIDS)
Malignancy
Accelerated Hypertension
Orbital Tumors
Cushing’s Syndrome

24
Q

lab studies

A

-TSH level is suppressed and total and unbound T3 & T4 levels increased.
-In 2–5% of patients (and more in areas of borderline iodine intake), only T3 is increased (T3 toxicosis).
-Measurement of TPO antibodies is useful in differential diagnosis.
-Associated abnormalities that may cause diagnostic confusion in thyrotoxicosis include elevation of bilirubin, liver enzymes, and ferritin.
-Microcytic anemia and thrombocytopenia may occur

25
Q

management of hyperthyroidism

A

-For hyperthyroidism include
-Antithyroid medications
-Radioactive 131-iodine
-Subtotal thyroidectomy

-Each choice has disadvantages and advantages

-Therapy should be individualized for each patient

26
Q

antithyroid medications

A

-Thioureylene
-
Propylthiouracil (PTU); methimazole; carbimazole -> Decrease output of thyroid hormone from thyroid gland and
Inhibits thyroperoxidase; Inhibit thyroid hormone biosynthesis

-They offer patients a chance of permanent remission and their advantages include:
-No risk of permanent hypothyroidism
-Low cost, and only minor adverse effects
-They may be used as monotherapy in patients with mild disease, or to treat symptoms before patients are treated with radioactive iodine or surgery
-Pregnancy – Category D

27
Q

adjunctive therapies

A

-Beta-blockers - reduce adrenergic manifestations of hyperthyroidism
-Propanolol - often beta-blocker of choice
-Thought to have the additional benefit of blocking the peripheral conversion of T4 to T3
-due to afib

-Educate patient about relevant lifestyle changes
-Such as iodine consumption
-Avoidance of tobacco, especially in the setting of Graves’ disease

28
Q

follow up

A

-Therapy with antithyroid can continue for 6 months to 2 years for Graves’ disease
-Monitor - CBC, LFT’s & thyroid function tests every 3 months
-Maintain thyroid function tests in the high-normal range
-Patients free from symptoms

-Beta-blockers - discontinue when tachycardia abates
-Patients receiving radioactive 131-iodine should be seen 6 weeks after therapy was received, at which time thyroid function tests need to be checked for hypothyroidism
-TFT’s need to be monitored again at 3 months, 6 months, one year, and annually thereafter

29
Q

radioactive 131-iodine

A

-Very effective at ablating hyperthyroidism
-Is generally the treatment of choice except in- Pregnant women and children
-It achieves permanent hypothyroidism
-Has lower costs and complications when compared to surgery
-However, there is a risk of permanent hypothyroidism and thyroiditis, as well as the usual risks associated with radiation
-Contraindicated in pregnancy or breast-feeding
-Safety not yet established in children <10 years of age
-Elderly patients should receive antithyroid drugs prior to radioactive iodine and for several weeks after to decrease any risk of worsening hyperthyroidism from post radiation thyroiditis

-Moderate orbitopathy may worsen
-Avoid in: Patients with active orbitopathy (and especially cigarette smokers)
-Associated with aggravating the eye disease

30
Q

chart

A

-T3 thyrotoxicosis is rare

31
Q

subtotal or total thyroidectomy

A

-Rarely the treatment of first choice
-Often recommended in
-Young children
-Pregnant women who have had an adverse reaction to pharmacotherapy
-Patients with compressive symptoms
-Patients in whom there is a concern about the possibility of thyroid cancer
-When rapid control of hyperthyroidism is needed or avoidance of exacerbation of symptoms is required (i.e. cardiac patients)

-Risk of permanent hypothyroidism and severe adverse effects
-Cost may also be an issue with surgery

32
Q

goiter rx

A

-Patients with toxic uninodular and multinodular goiter
-Do not go into remission
-Require surgery
-Or radioactive 131-iodine after stabilization with -> Thioureylenes and/or beta-blockers

33
Q

management of pregnancy and hyperthyroidism

A

-Hyperthyroidism in pregnancy results in increased rates of fetal loss
-Propylthiouracil is the drug of choice initially -> Crosses the placenta less than methimazole
-In 2nd trimester – often methimazole may be preferred
-Frequently, pregnancy has an ameliorative effect - can be maintained on a low dose
-Thyroid-stimulating antibodies can be checked at the end of the pregnancy -> Will help predict neonatal hyperthyroidism
-Patients should be seen 6 weeks postpartum because Graves’ is likely to worsen then

34
Q

foods to monitor

A

-iodized salt
-cauliflower

35
Q

thyroid storm

A

-A life-threatening condition
-Characterized by
-Exaggerated signs and symptoms of -hyperthyroidism:
-A fib./shock
-Fever»>104
-Hypotensive
-Altered mental status

-Usually precipitated by a concurrent illness or injury
-Also occurs following withdrawal of antithyroid medications

-Treatment requires
-Aggressive therapy for the concurrent illness
-Bring temperature down [cold fluids, cool them down]

-Aggressive antithyroid therapy
-Beta-blocker, a thionomaides (PTU or methimazole) glucocorticoids

36
Q

toxic adenomas

A

-Single - Plummer’s disease
-Multiple – toxic multinodular goiter
-No infiltrative ophthalmopathy or dermopathy
-Tests
-Antithyroid antibodies – negative
-TSH-R -negative

37
Q

pituitary tumor

A

-Pituitary adenoma →TSH hypersecretion→ hyperthyroidism
-Rare cause
-Neoplastic inappropriate secretion of thyrotropin vs. non-neoplastic
-Symptoms of Thyrotoxicosis
AND
-TSH assay – normal or elevated
-No ophthalmopathy
-Antithyroid antibodies TSH-R Ab – normal

-Management
-Sphenoidal surgery – if large tumor
-Propranolol
-Radioactive iodine/thyroid surgery

38
Q

jodbasedow disease

A

-Iodine-induced hyperthyroidism
-Multinodular goiters:
-after large amount of iodine in diet
-or in radiographic contrast material

-Or drugs – e.g. amiodarone

39
Q

thryotoxicosis factitia

A

-Due to ingestion of excessive amount of exogenous thyroid hormone
-Contaminated ground beef
-‘hamburger thyrotoxicosis’

40
Q

struma ovarii

A

-Thyroid tissue in: 3% of ovarian dermoid tumors
-Teratomas
-Autonomous secretion of hormones due to a toxic nodule
-Or in addition to a woman’s thyroid gland in Graves’ disease
-Or toxic multinodular goiter

41
Q

pregnancy and trophoblastic tumors

A

-Post partum thyroiditis
-Mild gestational hyperthyroidism – in first 4 months when hCG levels are very high
-More likely to have thyrotoxicosis and hyperemesis gravidarum
-Molar pregnancy
-Chorio-carcinoma
-Testicular malignancies

42
Q

referrals

A

-Patients with significant ophthalmopathy require urgent referral
-Patients suspected of thyroid storm should be referred for specialist care in an ICU
-Infiltrative orbitopathy of Graves’ disease may follow an independent course; may be uninfluenced by treatment -> Nonsurgical therapies
-Significant hyperthyroidism in the elderly is poorly tolerated and may lead to psychosis, cardiac ischemia, or arrhythmia, which can be difficult to manage with conventional therapies unless hyperthyroidism is controlled
-(e.g. weakness in the extraocular muscles, diplopia, corneal ulcerations, papilledema, venous congestion, and visual field defects)