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Endocrine Week 1 > ICL 1.2: Thyroid Disorders and Pharmacology > Flashcards

ICL 1.2: Thyroid Disorders and Pharmacology Flashcards

1
Q

what are the actions of the thyroid hormones?

A
  1. increase Na/K ATPase activity
  2. increase oxygen consumption
  3. increase heat production
  4. drive brain maturation
  5. allow tissue growth
  6. increase free radical production
  7. increase beta adrenergic responses
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2
Q

what condition does increased RSH, decreased free T4 indicate?

A

primary hypothyroidism

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3
Q

what condition does increased TSH and normal free T4 indicate?

A

mild thyroid failure

aka sub-clinical hypothyroidism

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4
Q

what condition does increased TSH and increased free T4/T3 indicate?

A
  1. thyroid hormone resistance

2. TSH secreting tumor

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5
Q

what condition does decreased TSH and high free T4 or T3 indicate?

A

thyrotoxicosis

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6
Q

what condition does decreased TSH and normal free T4 or T3 indicate?

A

subclinical hyperthyroidism

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7
Q

what condition does decreased TSH, low free T4 and normal or low T3 indicate?

A
  1. central hypothyroidism

2. sick euthyroid

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8
Q

what thyroid imagining techniques do you use?

A
  1. US
  2. I-131 uptake/scan
  3. Tc-99 scan
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9
Q

what is thyroid US used for?

A
  1. assessing nodular disease
  2. aids in aspiration
  3. assessing vascular flow for cancer risk
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10
Q

what is the I-131 uptake scan used for?

A
  1. differentiates causes of thyrotoxicosis
  2. determining treatment

Tc-99 scan is the same but with inferior resolution

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11
Q

what are the etiologies of hypothyroidism?

A
  1. surgical
  2. post-ablative
  3. infiltrative disease
  4. autoimmune destruction
  5. inflammatory
  6. drugs: lithium, amiodarone, interferone
  7. hreditary/congenital
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12
Q

what are the 3 clinical presentation of hypothyroidism?

A
  1. mild thyroid failure
  2. overt hypothyroidism
  3. myxedema coma
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13
Q

what are the signs and symtpoms of hypothyroidism?

A
  1. fatigue
  2. cognitive slowing
  3. weight gain
  4. cold tolerance
  5. hoarseness
  6. dry skin and hair
  7. brady cardia
  8. pericardial effusion
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14
Q

what are he lab findings for hypothyroidism?

A
  1. TSH elevated in primary diseases; low in central disease
  2. free T4 is normal or low
  3. T3 is often normal until disease is advanced
  4. elevated cholesterol
  5. hyponatremia
  6. elevated CK
  7. hypoglycemia in advanced cases
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15
Q

how do you treat hypothyroidism?

A

levothyroxine is DOC

80% of orally ingested dose is absorbed mostly in the proximal and mid small bowel so should be taken on empty stomach

peak levels occur 2-4 hours after ingestion; it’s protein bound

25-300 mcg daily

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16
Q

what drug interactions do you need to keep in mind when treating hypothyroidism?

A
  1. dose requirements decrease with age
  2. dose requirements increase with pregnancy or any cause of increased circulating estrogen
  3. phenytoin increases thyroid hormone metabolism
  4. cholesterol binding resins like calcium and soy can decrease absorption
  5. T1/2 is 7 days for T4 and 24 hours for T3
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17
Q

how do you assess if treatment of hypothyroidism is working?

A

adequacy of treatment tis assessed by measurement of TSH

TSH does not stabilize for 4-5 weeks after a dose change of T4

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18
Q

what are the considerations you give when treating hypothyroidism in elderly and pregnant patiuets?

A

elderly patients and those with coronary artery disease: start with low dose 12.5-25 mcg daily

pregnancy: requirements may increase as early as 5 weeks gestation; inadequate maternal replacement may result in reduction in fetal IQ

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19
Q

what is a myxedema coma?

A

hypothyroidism with respiratory insufficiency, hypothermia and mental status changes

an acute medical emergency

often precipitated by infection, CVA, MI and prolonged omission of levothyroxine

mortality is realted to the precipitating cause

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20
Q

how do you treat myxedema coma?

A
  1. ventilatory support
  2. fluid therapy
  3. T4 replacement given IV; initial loading dose 300 mcg followed by 50 mcg daily
  4. give hydrocortisone 100 mg every 8 hours until adequacy of adrenal cortical function is established

TREAT THE PRECIPITATING CAUSE

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21
Q

when is levothyroxine used for suppressive therapy?

A
  1. thyroid nodules

20% effective but no longer recommended

  1. thyroid cancer
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22
Q

what are the etiologies of thyrotoxicosis?

A

aka high I-131 uptake in:
1. graves disease

  1. TMNG
  2. toxic adenoma
  3. TSH secreting tumor
  4. thyroid hormone resistance syndrome
  5. struma ovaria
  6. metastatic follicular cancer (rare)
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23
Q

what are the 3 clinical syndromes of thyrotoxicosis?

A
  1. subclinical hyperthyroidism
  2. overt thyrotoxicosis
  3. thyroid storm
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24
Q

what are the signs of thyrotoxicosis?

A
  1. tremor
  2. palpitations, tachycardia, wide pulse pressure
  3. hyperdefecation
  4. heat intolerance, increased sweating
  5. weight loss
  6. muscle weakness
  7. irritability, agitation
  8. insomnia
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25
Q

what are the lab findings of thyrotoxicosis?

A
  1. low TSH; usually completely suppressed
  2. T4 is normal to elevated
  3. T3 is normal to elevated; in a critically ill patient a high normal or frankly elevated T3 is highly indicative of thyrotoxicosis
  4. low cholesterol
  5. hypercalcemia
  6. hyperglycemia
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26
Q

what is Graves disease?

A
  1. thyrotoxic symptoms
  2. goiter +/- bruit
  3. extra-thyroidal anifestations like oculopathy or dermopathy
  4. more common in women
  5. family history of other autoimmune glandular disorders
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27
Q

how do you treat Grave’s disease?

A
  1. antithyroid drugs: PTU or methimazole
  2. radioactive iodine
  3. surgery: subtotal thyroidectomy
  4. B-blockers: propranolol
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28
Q

which drugs are antithyroid drugs?

A

thiocarbamides: PTU, methimazole

they inhibit intrathyroidal peroxidase

they do not affect iodine trapping or release of stored thyroid hormone

PTU inhibits conversion of T4 to T3; propranolol also does that

remission rates are 30-60% ):

29
Q

what is the DOC for Graves in pregnancy?

A

PTU

30
Q

what are the side effects of antithyroid drugs?

A
  1. rash
  2. agranulocytosis
  3. toxic hepatitis
  4. lupus like syndrome
  5. arthralgia
  6. fever
31
Q

what is the DOC for Grave’s in nonpregnant adults?

A

I-131

24 hr uptake prior to dosing and discontinue antithyroid drugs 10-14 days prior because recent iodine exposure interferes with I-131

may flare in hyperthyroid symptoms 1 week after therapy which is indicative of radiation thyroiditis

effects may not be apparent before 6 weeks

32
Q

how effective is I-131 treatment for Graves?

A

70-80% tarted effectively with 1 dose at 1 year

permanent hypothyroidism is an expected outcome of I-131 treatment

no increased risk of malignancy in treated patients or ftal anomalies in offspring of women previously treated

women should defer pregnancy for 6 months after therapy though

33
Q

when is I-131 treatment contraindicated?

A

there is increased progression of oculopathy if it was moderate to severe

so if they have pretty bad oculopathy just refer them to surgery; don’t treat with radioactive iodine

34
Q

why are B-blockers used for hyperthyroidism?

A

they’re used as adjuvant therapy to control symptoms like arrhythmias and tachycardia

propranolol is what’s used because it inhibits T4 to T3 conversion

35
Q

what are the requirements for a subtotal thyroidectomy?

A

pretreatment with antithyroid drugs and B-blockers

90% effective

can be used in pregnancy during 2nd trimester

36
Q

what are the complications of a subtotal thyroidectomy?

A
  1. recurrent laryngeal nerve injury
  2. hypoparathyroidism
  3. permanent hypothyroidism
  4. thyroid storm
37
Q

how do you treat toxic nodular thyroid disease?

A

control symptoms with B-blcokers and antithyroid drug therapy but you will not see permanent remission with this therapy

I-131 therapy can be used if gland size and low I-131 uptake are not prohibitive

surgery is effective but is limited but he underlying health of the patient

patients often older and may present with apathetic thyrotoxicosis

38
Q

what are the causes of thyrotoxicosis?

A

thyrotoxicosis is when the uptake scan shows hyperthyroid symptoms with low I-131 uptake and this is seen in:

  1. thyroiditis (Hashimoto, subacute, postpartum)
  2. iodine induced (amiodarone, iodinated contrast)
  3. ingestion of thyroid hormone
39
Q

how do you treat subacute thyroiditis?

A

self limited problem that requires symptomatic therapy only

so give them B-blockers for tachycardia and anti-inflammatory agents for thyroid pain; occasionally give prednisone to control pain

40
Q

how do you differentiate subacute thyroiditis from ingestion of thyroid hormone?

A

thyroglobulin levels

thyroglobulin will be low if they patient is taking thyroid hormones

thyroglobulin will be detectable with thyroiditis

41
Q

what is a thyroid storm?

A

life threatening medical emergency where patients present with thyrotoxicosis, fever and mental status changes

42
Q

how do you treat thyroid storm?

A
  1. supportive measures like sedation, rehydration, oxygen, cooling and treatment of the precipitating cause
  2. propranolol 6-80 mg every 6 hrs
  3. hydrocortisone 100 mg IV every 8 hrs
  4. PTU 100-200 mg every 4-6 hrs
  5. iopanoic acid 1 g every 8 hrs after initiation of PTU
43
Q

how common is thyroid cancer?

A

it’s the most common endocrine malignancy

35,000 new cases every year and more common in females; 5th most common in women

2,000 deaths per year; 6.6% overall mortality rate

4-17% of all thyroid nodules are malignant and incidence increases with age

44
Q

what is the pathology of thyroid cancer?

A

80% from follicular epithelial cells while less than 20% from parafollicular cells, metastatic or lymphoma

45
Q

what are the follicular vs. papillary subtypes of thyroid cancer?

A

FOLLICULAR

  1. papillary
  2. follicular
  3. anaplastic

PAPILLARY

  1. follicular variant
  2. tall cell
  3. trabecular cell
  4. columnar cell
  5. clear cell
  6. solid variant
46
Q

how common is papillary thyroid cancer?

A

60-70% of thyroid cancers

F:M 2.5:1

47
Q

what is the prognosis of papillary thyroid canceR?

A

best prognosis if less than 4 cm, noninvasive and patient is under 45 years old

10 year survival is 90-95%

local LN mets are associated with increased recurrence

encapsulated papule is more favorable

TSH dependent so suppress TSH during treatment

48
Q

how common if follicular thyroid cancer?

A

10-20% of thyroid cancers

F:M 3:1

49
Q

what is the prognosis for follicular thyroid cancer?

A

encapsulated with minimal invasion and under 45 years old is an excellent prognosis \

10 year survival for minimally invasive is 86% but only 44% with highly invasive

hematogenous spread so there’s increased malignant potential over time

secreted TG; rarely secreted T3

50
Q

what are the variants of follicular cancer?

A
  1. Hurthle cell

2. insular variant

51
Q

how common is anaplastic thyroid cancer?

A

less than 10% of thyroid cancers

F:M 1.2:1

it’s basically the undifferentiated form of papillary thyroid cancer

usually seen in older patients

52
Q

what is the prognosis for anaplastic thyroid cancer?

A

highly malignant; 6-12 month survival

surgery/radiation is only palliative

may be difficult to differentiate from lymphoma or renal cell cancer metastatic to the thyroid since it’s undifferentiated

53
Q

how common is medullary thyroid cancer?

A

5%

F:M 1:1

it’s a neuroendocrine origin

54
Q

wha tis the prognosis for medullary thyroid cancer?

A

more aggressive than follicular cell but less than anaplastic

usually multifocal presentation with local and distant metastasis, even with small primary tumors

55
Q

what are the biomarkers for medullary thyroid cancer?

A
  1. calcitonin
  2. CEA
  3. chromogranin
56
Q

can you screen for medullary thyroid cancer?

A

limited usefulness of calcitonin as a screening tool in thyroid nodules

can do RET screening though and it’s associated with FMTC, MEN2a and MEN2b syndromes

57
Q

what are the paraneoplastic syndromes associated with medullary thyroid cancer?

A
  1. flushing
  2. diarrhea
  3. Cushings syndrome
58
Q

what are the symptoms of MEN1 syndrome?

A

3Ps:
1. pituitary adenoma

  1. parathyroid hyperplasia
  2. pancreatic tumors

due to MEN1 mutation on chromosome 11

59
Q

what is the clinical presentation of MEN2a?

A
  1. medullary carcinoma of the thyroid
  2. pheochromocytoma
  3. hyperparathyroidism

RET mutation

60
Q

what is the clinical presentation of MEN2b?

A
  1. medullary carcinoma of the thyroid
  2. pheochromocytoma
  3. mucosal neuromas
  4. Marfanoid body habits

RET mutation

61
Q

how do you diagnose thyroid canceR?

A

palpable mass, incidental finding, genetic screening or cervical adenopathy

they usually have normal thyroid function studies

factors suggesting malignancy: rapid growth, compressive symptoms, hoarseness, stridor, dysphagia, extremes of age, male sex, radiation, exposure, hard fixed mass, adenopathy, vocal cord paralysis

radiation and family history are the strongest factors!

62
Q

what are the fine needle aspiration results of papillary thyroid cancer?

A

large pale nuclei

prominent nucleoli

increased number of nucleoli

psammoma bodies

63
Q

what are the fine needle aspiration results of follicular thyroid cancer?

A

cannot differentiate adenoma from carcinoma of FNA

so you can’t differentiate malignant vs. benign without surgery and biopsy

64
Q

which US findings suggest benign thyroid lesions?

A
  1. hyperechoic lesions
  2. halo effect
  3. thin walled cyst
  4. egg shell calcifications
65
Q

which US findings suggest malignant thyroid lesions?

A
  1. hypoechoic
  2. thick walled cyst
  3. intralesional calcification
  4. large size
  5. lymphadenopathy
  6. LN size over 1 cm, spherical, loss of fatty hilum

however, you can’t differentiate bening vs. malignant on us, you have to do FNA or biopsy; no US criteria reliably excludes malignancy!!!!

66
Q

what srugery do you do for thyroid cancer?

A
  1. total thyroidectomy is preferred for large papillary and follicular type cancers
  2. lobectomy is sufficient for incidentally discovered microscopic papillary cancers
  3. surgery for medullary cancer should include total thyroidectomy, bilateral central node dissection and ipsilateral modified radical neck dissection

total thyroidectomyvs. lobectomy lower reucrrence risk, prevention of recurrence in contralateral lobe, use of TG as a tumor marker after I-131 for total thyroidectomy, not a lobectomy because they’ll still have TG being produced by normal tissue

67
Q

what is the goal of thyroid hormone suppressive therapy in thyroid cancer patients?

A

complete TSH suppression in high risk patients

you’ve made them hyperthyroid so you have to be careful to watch for arrhythmias and bone loss

68
Q

how do you follow up for thyroid cancer after treatment?

A

long term follow up due to risk of late recurrent

if I-131 is not give, do exam, TG, US, CXR, CT, MRI

TG should be less than 5 ng/dl in a patient with a remnant and they’re off suppressive therapy so if they got a total thyroidectomy but you didn’t do I-131 then it’s fine if they’re TG is around 5 since there’s tissue left behind; if they did the thyroidectomy and I-131 then the TG should be undetectable

IS every 6 months for 2 years to check for lymph node metastasis and do a stimulated TG twice, two years apart and then measure the baseline TG at least yearly after that

if there’s no uptake in a TG positive patient after an iodine dose, do a CT or PET scan

Endocrine Week 1 (11 decks)

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