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Clin Med3: Endocrine > disorders of the thyroid - waldron > Flashcards

disorders of the thyroid - waldron Flashcards

1
Q

what is the largest endocrine organ in the body

A

thyroid

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2
Q

what hormones does the thyroid produce

A

calcitonin
thyroxine (T4)
tri-iodothyronine (T3)

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3
Q

what makes up the thyroid

A

follicular cells

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4
Q

how is the thryoid hormone regulated

A

negative feedback loop
high TSH - is a slow thyroid
low TSH - fast thyroid

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5
Q

what is Goiter

A

an enlarged thyroid or abnormal growth of thyroid gland
depending on cause: may be associated with normal, decreased or increased thyroid hormone production

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6
Q

what is the most common causes of Goiter

A

worldwide: iodine deficiency
US: multi-nodular goiter, chronic autoimmune thyroiditis (Hashimoto’s), Graves disease
physiological (puberty/pregnancy), dysmorphogenesis (sporadic), radiation exposure, TSH release from pituitary gland, autoimmunity, infection, granulomatous disease

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7
Q

what types of food may affect thyroid function

A

broccoli, kale, cauliflower, peaches, strawberries, mustard, teas, red wine, soy products

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8
Q

what synthesizes the thyroid hormone

A

iodine

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9
Q

what is sporadic goiter

A

dysmorphogenesis and endemic goiter (iodine deficiency) mostly occur during childhood; thyroid gland increases more in size with age

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10
Q

what is the presentation of Goiter

A

most asymptomatic
swelling may be discovered incidentally
concern for compressive symptoms: dysphagia, dyspnea, hoarseness
may compress neck veins causing facial congestion, discomfort
pain is rare

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11
Q

what is seen on PE with Goiter

A

central neck swelling
cervical LA think malignancy: workup accordingly
vocal cord exam if hoarseness or before surgical intervention
pemberton maneuver

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12
Q

what is Pemberton maneuver

A

elevating arms may lift goiter into thoracic inlet and cause stridor, dyspnea or enlargement of neck veins

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13
Q

how do you workup/diagnose Goiter

A

TSH, free T4, T3
US to assess nodules - FNA cytology under US guidance
CXR
CT/MRI
radionuclide scanning

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14
Q

If a TSH below normal when Goiter is suspected what needs to be assessed next

A

check serum free T4 and T3
- hyperthyroidism: graves disease, multinodular goiter, toxic adenoma

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15
Q

if a TSH is above normal when Goiter is suspected what needs to be assessed next

A

check T3 and T4
hypothyroidism: hashimoto’s thyroiditis most likely, ecept areas of endemic goiter due to iodine deficiency

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16
Q

what is the usual TSH range

A

0.45 - 4.5

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17
Q

What is the treatment of non-toxic goiter

A

no tx: annual follow up
medical therapy is controversial
if intervention: usually surgery (thyroidectomy = mainstay tx)
radioiodine ablations

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18
Q

what is the etiology of hypothyroidism

A

autoimmune thyroiditis
previous thyroid surgery
radiation therapy
lithium
PTU

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19
Q

what is the etiology of hyperthyroidism

A

Grave’s disease
toxic nodule (toxic adenoma)
toxic multi-nodular goiter (Plummer’s disease)
thyroiditis
silent, post-partum, deQuervains thryoiditis (subacute)

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20
Q

what is the presentation of hypothyroidism

A

anorexia
fatigue, depression, lethargy
cold intolerance
constipation
dry, coarse hair
anemia
muscle stiffness and or cramps
memory impairment
bradycarida
hypo-reflexia
(slows them down)

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21
Q

what is the presentation of hyperthyroidism

A

nervousness
heat intolerance
sweating
increased appetite, weight loss (some gain)
loose stools
irritability/anxiety
fatigue
muscle weakness
tachycardia, afib, palpitations, PACs
hyper-reflexia
(speeds them up)

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22
Q

What is graves disease

A

most common cause of hyperthyroidism
autoimmune disease: usu +FHx, F>M, associated with HLA
precipitated by environmental factors: stress, smoking, infection, iodine, exposure, post-partum
TSH-receptor antibodies (TRAb) stimulate thyroid hormone production

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23
Q

what causes graves disease

A

thyroid stimulating immunoglobulin (TSI)

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24
Q

what stimulates TSH

A

TRab binding with TSH receptor on the thyroid

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25
Q

what causes hyperthyroidism and thyromegaly

A

TRab stimulating both thyroid hormone synthesis and thyroid gland growth

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26
Q

What is the process of Graves (toxic goiter, thyrotoxicosis)

A

stimulating antibodies to TSH-R (TRab) -> diffuse enlargement of thyroid gland -> increasing levels of thyroid hormones suppress TSH at anterior pituitary -> low TSH, normal or high T3, T4

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27
Q

What is the presentation of Graves disease

A

most patients present with signs and symptoms of hyperthyroidism
rare presentation of graves orbitopathy (TED)
depends on age of onset, severity, duration

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28
Q

how do the elderly present with graves disease

A

symptoms may be subtle/masked
may have non-specific: fatigue, weight loss, new onset Afib
atypical: “apathetic thyrotoxicosis”

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29
Q

what is the presentation of younger patients with graves disease

A

common presentation: heat intolerance, sweating, fatigue, weight loss, palpitation, hyperdefecation, tremors
other possible: insomnia, anxiety, hyperkinesia, dyspnea, muscle weakness, pruritus, polyuria, loss of labido
eyes: lid swelling, ocular pain, conjunctival redness, dipolopia

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30
Q

what are physical signs of hyperthryoidism

A

tachycardia, HTN with increased PP, signs of heart failure, afib, fine tremors, hyperkinesia, hyperreflexia, warm/moist skin, palmar erythema, hair loss, diffuse palpable goiter, AMS

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31
Q

what are the extrathyroidal manifestation signs

A

thyroid eye disease
marked thickening of skin, mainly over tibia
bone: sub-periosteal bone formation and swelling in metacarpal bones
onchyolysis (plummer nails), clubbing: rare

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32
Q

what is thyroid storm

A

sudden on set with severe symptoms of thyrotoxicosis
medical emergency - high mortality rate d/t cardiac arrhythmias
HTN, tachy, fever, mental status changes, N/V/D

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33
Q

what is graves ophthalmopathy

A

proptosis, conjunctival irritation, eye pain, eye dryness, double vision -> refer to ophtho

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34
Q

how do you diagnose/work up graves disease

A

most pts: usually clear signs/symptoms
diagnostic tests: TSI, TSH (low), T3 and T4 (elevated), TRab (elevated), tyroid radioavtive iodine uptake (i131), US to assess thyroid BF, CT/MRI of orbits

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35
Q

what is the treatment of hyperthyroidism

A

consider endocrine referral (strongly)
medications: propylthiouracil (PTU), methimazole
-radioactive iodine (RAI) tx
-total thyroidectomy
propranolol PO -supportive until thyrotoxicosis is resolved

36
Q

what is the recommended first line treatment for graves disease

A

radioactive iodine
advantages: permanent resolution, non-invasive
disadvantages: results in hypothyroidism, delay of onset (6-8weeks)

37
Q

when is radioactive iodine contraindicated

A

pregnant or breast-feeding women

38
Q

what is the advantages/disadvantages of thiourea drugs (propylthiouracil (PTU) or methimazole)

A

weeks to control hyperthryoidism, usu. 12-24 months
advantages: if spontaneous resolution, now euthyroid on no meds
dis: difficult to control thyroid hormone levels, neurotpenia, liver enzyme elevation, rash, arthralgia, possibility of relapse

39
Q

what is the drug of choice for graves disease with pregnancy

A

PTU (propylthiouracil)

40
Q

what are the advantages/disadvantages with total thryoidectomy

A

advant: fast resolution of hyperthyroidism
dis: invasive, full anesthesia, post-op hypothyroid
consider in pregnant women intolerant to PTU

41
Q

what is the treatment of thyroid storm

A

referral to endocrine via ER
block thyroid hormone action: beta blocker
block thyroid hormone release and conversion from T4 to T3:
- PTU, postassium iodine, ipodate sodium (iodinated contrast), hydrocortisone IV
supportive

42
Q

What is Plummers disease

A

toxic nodular goiter (TNG)
autonomously functioning thyroid nodules, with resulting hyperthyroidism
second most common cause of hyperthyroidism in western world

43
Q

What is the pathophysiology of TNG

A

spectrum of single hyperfunctioning nodule (toxic adenoma) within a multinodular thyroid to a gland with multiple areas of hyperfunctioning
hyperthyroidism usu. occurs with single nodules > 2.5cm in diameter

44
Q

What is the Jod-Basedow effect

A

initial iodine supplementation can lead to hyperthyroidism

45
Q

What is the epidemiology for TNG

A

W>M
women and men >40, prevalence rate of palpable nodule is 5-7% and 1-2%
most patients with TNG > 50yo
toxicity usu. peaks in 6th and 7th decade of life

46
Q

what are the TNG thyrotoxic symptoms

A

signs of hyperthyroidism: heat intolerance, palpitations, tremor, weight loss, hunger, hyperdefication (usu. younger patients)

47
Q

what are the symptoms for elderly patients with TNG

A

weight loss: m/c complain in elderly
anorexia and constipation
dyspnea or palpitations
tremor: may be confused with essential tremor
CV concerns: Hx AFib, HF, angina

48
Q

what are obstructive symptoms of TNG

A

sx related to mechanical obstruction
large substernal goiter: dysphagia, dyspnea, or frank stridor - rarely a sx emergency
involvement of recurrent or superior laryngeal nerve may result in complains of hoarseness or voice change

49
Q

what are the common lab findings with TNG

A

low TSH with NORMAL free T4

50
Q

what is seen on PE with TNG

A

more subtle than graves
widended, palpebral fissues; tachycardia; hyperkinesis; moist, smooth skin; tremor; proximal muscle weakness; brisk DTR

51
Q

what is a positive Pemberton sign

A

mechanical obstruction may cause SVC syndrome

52
Q

what is the diagnosis/work up for TNG

A

thryoid function test
TSH: best initial screening tool; will be low
free T4: elevated or normal
nuclear scintigraphy (radioactive iodine - 123 - preferred)
US or CT neck
FNA

53
Q

what is seen on nuclear scintigraphy with TNG

A

patchy with areas of increased and decreased uptake

54
Q

what is the diagnosis/work up for TNG

A

thyroid function test
TSH: best initial screening tool; will be low
free T4: elevated or normal
nuclear scintigraphy (radioactive iodine - 123 - preferred)

55
Q

when is FNA indicated for TNG

A

autonomously functioning (hot) thyroid nodule
dominant cold nodule present in mutinodular goiter
clinically significant nodule >1cm max diameter
non-palpable nodules; FNA with US assistance

56
Q

what is the treatment for TNG

A

optimal tx remains contraversial
autonomously functioning nodules should be treated definitively with radioactive iodine or surgery
monitor
meds/surgery
endocrinology consult*

57
Q

what are medication treatment options for TNg

A

anti-thyroid drugs (thioamides - PTU, methimazole) and beta blockers used for short courses

58
Q

what is included within thyroiditis

A

spectrum of diseases: asymptomatic, hypothyroidism, with or without diffuse goiter, atrophic, occasionally painful, occasionally nodular, silent thyroiditis, postpartum thyroditis, thyrotoxicosis (rare)

59
Q

What is Hashimoto’s thyroiditis

A

autoimmune dx that destroys thyroid cells by cell and antibody-mediated immune process
aka chronic autoimmune thyroiditis and chronic lymphocytic thyroditis
formation of anti-thyroid antibodies that attack thyroid tissue causing progressive fibrosis

60
Q

what is the m/c lab findings with hashimotos thyroiditis

A

elevated TSH, low free thyroxine (T4), increased anti-thyroid peroxidase (TPO) antibodies

61
Q

what is the most common cause of hypothyroidism in iodine -suffieicne world (after age 6)

A

hashimotos thyroiditis

62
Q

what is the conventional treatment of Hashimotos

A

levothyroxine at 1.6-1.8 mcg/kg/day

63
Q

what is the patho of hashimotos thyroiditis

A

autoimmune origin with lymphocyte infiltration and fibrosis
current dx based on clinical symptoms with lab results of elevated TSH and normal to low T4

64
Q

what is the presentation of hashimotos

A

initially hyperthryoid sx
skin: myxedma (dry and brittle hair and skin)
cardiac: increased PVR, bradycardia, most present with pre-existing CV conditions
fatigue, exertional dyspnea, exercise intolerance
muscle weakness and myopathy

65
Q

what are the early symptoms of Hashimotos

A

constipation, fatigue, dry skin, weight gain

66
Q

what are teh advanced symptoms of hashimotos

A

cold intolerance, decreased sweating, nerve deafness, peripheral neuropathy, decreased energy, depression, dementia, memory loss, muscle cramps, joint pain, hair loss, apnea, menorrhagia, pressure symtpoms in neck

67
Q

what are urgent presentation concerns with hashimotos

A

accumulation of fluid in pleural and pericardiac cavities: admission and drainage
myxedema coma is the most severe clinical and must be managed as medical emergency

68
Q

what is the workup for hashimotos

A

TSH- slightly increased to high
T3 and T4 - low
positive anti-TPO and TGab
US and radioactive iodine untake helps distinguish from graves
FNA if malignancy concern
CK, prolactin, total cholesterol, LDL, TG - usu. elevated

69
Q

what is the mainstay of treatment for hashimotos/hypothyroidism

A

thyroid hormone replacement
DOC: Titrated levothyroxine sodium PO QD
half life of 7 days - early morning on empty stomach

70
Q

what should be avoided when taking titrated levothyroxine sodium

A

iron or calcium supplements, aluminum hydroxide, proton pump inhibitors, grapefruit or orange juice: causes suboptimal absorption

71
Q

what are other treatment options for hypothyroidism

A

crtomel (liothyronine) - synthetic T3
armour thyroid (“biologic thyroid replacement”)

72
Q

What is Myxedema coma

A

extreme form of hypothyroidism - medical emergency, rare, high mortality
clinical dx

73
Q

what is the presenatation of myxedema coma

A

weakness, stupor, hypoventilation, hypothermia, hyponatremia, shock and death

74
Q

what is the treatment of myxedema coma

A

ICU admission, IV levothyroxine, supportive care for respiratory and fluid status

75
Q

What is chronic autoimmune gastritis (CAG)

A

partial or complete loss of parietal cells leading to impairment of hydrochloric acid and intrinsic factor production
develop iron-deficient anemia (micro), leading to pernicious anemia (macro), then severe gastric atrophy

76
Q

What is Cretinism

A

iodine deficiency

77
Q

What is congenital hypothyroidism from Cretinism

A

due to a deficiency in thyroid hormone during early fetal development (maternal hypothyroidism during preg), usu. secondary to iodine deficiency

78
Q

What determines iodine deficiency

A

iodine intake chronically < 20 /day

79
Q

what are signs and symptoms of congential hypothyroidism

A

intellectual disability, deaf, mute, gait disturbances, short stature, puffy hands and feet, spasticity

80
Q

what are diagnostic tests for thyroid nodule

A

thyroid ultrasound, TSH, T4
if TSH low: thyroid uptake and scan
if nodules > 0.6cm, strongly consider biopsy

81
Q

what are the most common thyroid cancers

A

papillary thyroid cancer (m/c)
follicular thyroid cancer
medullary thyroid cancer
anaplastic thyroid cancer (ATC) (RARE)

82
Q

what are the risk factors for developing thyroid cancer

A

F>M
radioactive iodine exposure, fhx, childhood head and neck radiation (20-25 years later)

83
Q

what is the clinical presentation of thyroid cancer

A

painless neck swelling
non-tender firm nodule
hoarseness
neck discomfort
dysphagia (compressive symptoms)
palpable thyroid nodule, gland may be stony and hard
single nodule

84
Q

how do you diagnose/work up thyroid cancer

A

contingent on cytologic or histologic findings on biopsy
childhood radiation hx
TSH, T3, T4, TSH may be normal (t3/4 may be elevated)
US - anatomic eval - best first step
i131 uptake study= functional evaluation
FNA

85
Q

what is the treatment of thyroid cancer

A

surgical resection
RAI ablation
TSH suppression

86
Q

What is the treatment for ATC CA

A

little to no role for surgery - local invasion into trachea or vasculature - unresectable
5 year mortality near 100%

87
Q

what are complications of thyroid cancer

A

locally invasive if untreated - airway, esophagus or neurovascular structures
metastatsis: lung, bone, soft tissue
surgical complications

Clin Med3: Endocrine (7 decks)

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