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05 Endo > Thyroid Gland Disorders > Flashcards

Thyroid Gland Disorders Flashcards

1
Q

most common cause of hypothyroidism world wide

A

iodine deficiency

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2
Q

most common cause of hypothyroidism in iodine sufficient areas

A

autoimmune disease and iatrogenic causes

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3
Q

common complaint for hypothyroidism

A

weight change

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4
Q

first line test performed if thyroid disorder is highly suspected

A

tsh

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5
Q

most useful physiologic marker of thyroid hormone action

A

tsh

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6
Q

when is thyroid hormone requested

A

tsh is abnormal

suspected or known pituitary disease (measure both tsh and ft4)

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7
Q

diagnostic hallmark for autoimmune thyroid disorders

A

thyroid autoantibodies

can contribute to its development and chronicity

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8
Q

normal values to thyroid ab

A

Tg-Ab 5-20
TPO-Ab 8-27
TSHR-Ab 0

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9
Q

modality that can confirm presence of a nodule

A

uts

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10
Q

uses of uts

A 
confirm nodule
size
benign or suspicious features
cervical lymphadenopathy
>50% cystic (anechoic, usually benign)
posterior location
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11
Q

what is subclinical hypothyroidism

A

biochemical evidence of hormone deficiency in patients who have few or no apparent clinical features of hypothyroidism

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12
Q

biochem of subclinical hypothyroid

A

elevated serum tsh and normal ft4

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13
Q

indications for treatment of subclinical hypothyroidism

A

woman who wishes to concieve or is pregnant
tsh >10 mlU/l
tsh <10 mlU/l with symptoms of hypothyroidism, positive tpo-ab, or evidence of heart disease

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14
Q

treatment for subclinical hypothyroidism

A

starting treatment: low dose levothyroxine (25-50 ug/d), target normal tsh
not starting treatment: monitor annually

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15
Q

queen anne’s sign

A

thinning of outer third eyebrows

NOT A SPECIFIC SIGN OF HYPOTHYROIDISM

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16
Q

classification of autoimmune hypothyroidism

A

hashimoto’s or goitrous thyroiditis: early stage

atrophic thyroiditis: late stage

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17
Q

pathogenesis of autoimmune hypothyroidism

A

lymphocyte infiltration and fibrosis

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18
Q

risk factors for autoimmune hypothyroidism

A

hla-dr polymorphisms
female preponderance
environmental factors (5)

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19
Q

clinical manifestations of autoimmune hypothyroidism

A

initial stages: goiter > hypothyroid
hashimoto’s thyroiditis: irregular, firm consistency, small goiter with mild symptoms
autoimmune thyroiditis: overt symptoms with atrophic thyroid

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20
Q

treatment for hypothyroidism

A

levothyroxine
no residual thyroid fn: 1.6-1.7 ug/kg or 100-150 ug/d
<60 yo without cvd: 50-100 ug/d
after treatment of graves’: 75-125 ug/day

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21
Q

treatment for hypothyroidism for elderly

A

20% less levothyroxine

with cad: 12.5-25 ug/d

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22
Q

monitoring of hypothyroidism

A

check tsh levels, 2 mos after start of treatment

target tsh: lower half of reference range

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23
Q

expected results for hypothy treatment

A

until 3-6 mos

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24
Q

t/f patients can double the dose after a skipped dose in hypothyroidism

A

true

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25
Q

other causes of hypothyroidism

A

amiodarone-induced hypothyroidism
secondary hypothyroidism
sick euthyroid syndrome

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26
Q

confirmation of secondary hypothyroidism

A

low ft4 level

tsh can be low, normal, or slightly increased

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27
Q

treatment for secondary hypothyroidism

A

elevated tsh, normal ft4 = subclinical hypothyroidism
(+) tpo-ab or symptomatic = t4 treatment
(-) tpo-ab or asymptomatic = annual follow up

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28
Q

major cause of sick euthyroid syndrome

A

release of cytokines (ex. il-6)

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29
Q

patterns of ses

A 
*low t3, normal t4 and tsh
low t4 (decreased tissue perfusion)
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30
Q

thyrotoxicosis vs hyperthyroidism

A

thyrotoxicosis: classic physiologic manifestations of excessive quantities of thyroid hormones
hyperthyroidism: disorders that result from sustained overproduction and release of hormone by the thyroid

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31
Q

causes of thyrotoxicosis

A

primary hyperthyroidism
thyrotoxicosis without hyperthyroidism
secondary hyperthyroidism

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32
Q

common symptoms of thyrotoxicosis

A

hyperactivity, irritability, dysphoria, heat intolerance and sweating, palpitations, fatigue and weakness, weight loss with increased appetite, diarrhea, polyuria, oligomenorrhea

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33
Q

signs of thyrotoxicosis

A

tachycardia, tremor, goiter, warm moist skin, muscle weakness, proximal myopathy, lid lag, gynecomastia

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34
Q

t/f only tsh will suffice to check for thyrotoxicosis

A

false, also request t3 and t4

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35
Q

t/f grave’s disease accounts for 40-60% of thyrotoxicosis

A

false, 60-80%

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36
Q

pathophysiology of grave’s disease

A

thyroid stimulating immunoglobulins leading to thyroid hormone synthesis and gland growth

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37
Q

PE for grave’s disease

A

symmetric enlargement of thyroid up to 2-3x
soft to firm and rubbery
smooth or lobular

severe: thrill/bruit

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38
Q

what is a true bruit

A

auscultated bruit should be louder over the thyroid than upper left sternal area

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39
Q

signs and symptoms of grave’s disease

A

graves’ opthalmopathy
thyroid dermopathy
thyroid acropachy

40
Q

natural history of graves’ opthalmopathy

A

rapid onset and deterioration (worsens in initial 3-6 mos) and then gradual improvement (plateau in next 12-18 mos)

41
Q

most frequent lesion in thyroid dermopathy

A

pre-tibial myxedema

42
Q

associated with long-standing thyrotoxicosis

A

clubbing

43
Q

clinical manifestations of graves disease

A

apathetic thyrotoxicosis (elderly)
hypokalemic periodic paralysis (asian males)
sinus tachy*/a fib

44
Q

diagnostic test for graves disease

A

radioactive iodine uptake and scan (discriminates high uptake of gd vs low/no uptake of thyroiditis)

45
Q

factors that increase uptake in rai

A 
hyperthyroidism
response to glandular hormone depletion
excessive hormone loss
normal hormone synthesis with deficiencies
hormone biosynthetic defect
46
Q

factors that decrease uptake in rai

A 
primary hypofunction
secondary hypofunction
exogenous thyroid hormones
increase availability of iodine
increased hormone release (rare)
47
Q

treatment for gd

A

antithyroid drugs: thioamides carbimazole or methimazole

propylthiouracil

48
Q

monitoring for gd

A

every 4-6 weeks, based on thyroid function tests and clinical manifestations
euthyroidism is achieved in 6-8 weeks

49
Q

other drugs for gd

A

propanolol for adrenergic symptoms

anticoagulation for a fib

50
Q

t/f older patients, females, non-smokers and patients with allergy, severe hypothyroid or large goiters are most likely to relapse

A

false, should be younger patients, males, and smokers. [sic]

51
Q

____ can be initial treatment for gd in relapses after trial of anti-thyroid drugs

A

radioiodine

52
Q

t/f if first dose of rai fails, give second dose

A

true, can be done after 6 months

53
Q

indications for surgery

A

relapse after antithyroid drugs

very large goiter

54
Q

t/f clinical features of gd worsen without treatment and lead to death

A

true

55
Q

what is the diagnosis? tsh low, unbound t4 normal, unbound t3 high

A

t3 toxicosis

56
Q

possible diagnosis/differentials for primary thyrotoxicosis without features of graves disease

A

toxic adenoma

multinodular toxic goiter

57
Q

pathogenesis of multinodular toxic goiter

A

similar to non-toxic multinodular goiter but difference is presence of functional autonomy

58
Q

diagnosis/test for mtg

A

thyroid scan showing areas of increased uptake with decreased uptake in surrounding areas

uts can assess “cold nodules”
fine needle aspiration

59
Q

pathogenesis of toxic adenoma/ hyperfunctioning solitary nodule

A

most have acquired somatic, activating mutations in tsh-receptor

subnormal tsh, thyroid nodule, absence of clinical features of gd or other toxicoses

60
Q

diagnostic test for toxic adenoma

A

thyroid scan showing focal uptake in the hyperfunctioning nodule and diminished uptake in the remainder of thyroid gland

61
Q

management for toxic adenoma

A

rai, thyroid drugs, surgery

62
Q

preferred therapy for toxic mng/ta in pregnancy

A

anti thyroid drugs

63
Q

when is rai preferred therapy for toxic mng/ta

A

elderly
px previously operated or externally irradiated necks
no access to thyroid surgeon

64
Q

when is surgery preferred therapy for toxic mng/ta

A
  • symptoms/signs of neck compression
  • thyroid malignancy confirmed or suspected
  • large goiter/nodule
  • goiter/nodule with substernal or retrosternal extension
  • coexisting hyperparathyroidism requiring surgery
65
Q

labs for subclinical hyperthyroidism

A

subnormal tsh, normal free t3/t4

66
Q

t/f tpo-ab can be used to predict risk of autoimmunity in px with subclinical hyperthyroidism

A

true

67
Q

management for subclinical hyperthyroidism

A

rai

> 65 yo / < 65 yo with comorbidities + TSH <0.1 mU/L = TREAT
<65 yo asymptomatic = consider treating or observe

68
Q

other diseases associated with thyrotoxicosis

A 
multinodular toxic goiter
hyperfunctioning solitary nodule
subclinical hyperthyroid
thyroiditis
amiodarone-induced thyrotoxicosis
69
Q

subacute thyroiditis is thought to be caused by ___

A

viral infection of thyroid gland (mumps, influenza, adenovirus)

70
Q

pathogenesis of subacute thyroiditis

A

apoptosis -> release of t3 and t4 = 1. thyrotoxicosis and suppression of tsh -> (6wks) t3 and t4 run out = 2. hypothyroidism + elevated tsh -> 3. recovery

71
Q

_____ is the usual outcome of subacute thyroiditis

A

complete resolution

72
Q

management for subacute thyroiditis

A 
antithyroid drugs
aspirin/nsaids
prednisone
tsh and ft4, monitor every 2-4 wks
levothyroxine
73
Q

pathophysiology of acute thyroiditis

A

suppurative infection of the thyroid

children and ya: presence of piriform sinus

74
Q

clinical presentation of acute thyroiditis

A

abrupt, thyroid pain that radiated to throat or ears, small tender asymmetric goiter

fever, dysphagia, erythema over thyroid

75
Q

diagnosis of acute thyroiditis

A

esr and wbc increased
normal thyroid fn
fna biopsy infiltrated by pmns

76
Q

management of acute thyroiditis

A

antibiotics

surgery to drain abscess

77
Q

pathophysiology of silent thyroiditis

A

underlying autoimmune thyroid disease

78
Q

phases of postpartum thyroiditis

A

2-4 wks: thyrotoxicosis
4-12 wks: hypothyroidism
resolution

79
Q

diagnosis of silent thyroiditis

A

normal esr with tpo-ab

80
Q

management for silent thyroiditis

A

propanolol to relieve adrenergic symptoms
levothyroxine
annual follow up

81
Q

types of chronic thyroiditis

A

hashimoto’s thyroiditis*

riedel’s thyroiditis

82
Q

type 1 vs type 2 amiodarone induced thyrotoxicosis

A

table 8

83
Q

t/f in general thyroid nodules are malignant, however there is a 5-15% benign rate

A

false, generally benign, 5-15% chance malignant

84
Q

evaluation of thyroid nodules

A

tsh -> uts -> fna

85
Q

features that are bad in uts for thyroid nodules

A 
microcalcifications
hypoechogenicity
irregular margins
taller than wide
presence of lateral lymph nodes
86
Q

thyroid biopsy indications

A

solid, >1 cm
cyst >2 cm
<1 cm with high suspicious features

87
Q

management for patients with benign thyroid neoplasms

A

tsh suppression therapy

88
Q

most common malignancy in the endocrine system

A

thyroid cancer

89
Q

method of spreading well differentiated follicular epithelial cell thyroid cancers

A

papillary (ptc) = lymphatics

follicular (ftc) = hematogenous

90
Q

most common type of thyroid cancer

A

well differentiated papillary tc

91
Q

indicators for poor prognosis of ftc

A 
distant metastases
>50 yo
primary tumor >4 cm
hurthle cell histology
marked vascular invasion
92
Q

treatment for well differentiated tcs

A

surgery, radioiodine (more beneficial in more severe), levothyroxine-tsh suppression therapy (MAINSTAY)

93
Q

monitoring for well differentiated tcs

A 
serum tg (normal: < 1 ng/ml)
whole body scan for px with known iodine-avid metastases or elevated tg + (-) imaging
94
Q

t/f anaplastic (undifferentiated) carcinoma has poor prognosis

A

true

95
Q

t/f all patients with medullary thyroid ca should be tested for ret mutations

A

true

96
Q

treatment for medullary thyroid carcinoma

A

mainstay: surgery
monitoring: serum calcitonin

05 Endo (16 decks)

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