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competency 10/11 > endo: thyroid > Flashcards

endo: thyroid Flashcards

1
Q

thyroid hormones are impt for

A

normal growth, development and for controlling energy metabolism

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2
Q

production of thyroid hormones are dependent on

A

TSH
- secreted by the pituitary gland, in response to stimulation from hypothalamus in the brain

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3
Q

our thyroid gland secretes 3 main hormones:

A

T4: thyroxine, or tetra-iodothyronine
T3: tri-iodothyronine
Calcitonin - involved in the control of plasma Ca2+ and is used to treat osteoporosis and other metabolic bone diseases

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4
Q

T4 converted to T3 by the body

A

where it is transferred by blood to tissues of the body, where it acts

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5
Q

regulation of thyroid hormone secretion

A
  1. myrial neural inputs influence hypothalamic secretion of thyrotropin-releasing hormone (TRH)
  2. TRH stimulates release of thyrotropin (TSH, thyroid-stimulating hormone) from the anterior pituitary
  3. TSH stimulates the synthesis and release of the thyroid hormones (T3 and T4)
  4. T3 and T4 feedback to inhibit synthesis and release of TRH and TSH
  5. Low levels of I- are required for T4 synthesis, but high levels inhibit T4 synthesis and release
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6
Q

wolff-chaikoff effect

A

autoregulatory phenomenon
- during initial iodine exposure, excess iodine is transported into the thyroid gland by the sodium-iodide symporter > this transport results in transient inhibition of thyroid peroxidase and a decrease in the synthesis of thyroid hormone

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7
Q

s/sx of hypothyroidism

A
  • fatigue and lethargy
  • mental slowness
  • dry skin
  • weight gain
  • irregular menses
  • hair loss
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8
Q

when is liothyronine preferred over levothyroxine?

A

when a rapid onset of action is needed:
- less desirable for chronic replacement therapy due to short half life coupled with cost
- iv for treatment of myxedema coma (severe presentation of hypothyroidism, state of emergency)

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9
Q

overdosing of levothyroxine or liothyronine can cause

A

cardiac arrest, hypertension, palpitations, tachycardia, anxiety, heat intolerance, hyperactivity, insomnia, irritability, weight loss
- in children: insomnia, restlessness, accelerated growth and bone maturation

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10
Q

long term use of high dose levothyroxine has been associated with

A

incr bone resorption and reduced bone mineral density, esp in post-menopausal women

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11
Q

onset of action - levothyroxine vs liothyronine

A

3-5 days (oral), within 6-8hrs (iv)

VS 3hrs (oral or iv)

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12
Q

persistently elevated TSH levels despite treatment with levothyroxine may happen due to

A

inadequate dosing, poor compliance, malabsorption, drug or food interaction

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13
Q

levothyroxine should be taken (time of the day)?

A

30-45mins before breakfast, on an empty stomach

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14
Q

with estrogen hormone replacement treamtent, incr/decr in levotyroxine dose required?

A

incr, due to incr thyroxine-binding globulin levels > binds levothyroxine and reduces the amt avail for action

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15
Q

drugs and supplements that reduces absorption of levothyroxine

A

iron, calcium carbonate, cholestyramine, soya, fiber, caffeine, antacids

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16
Q

drugs and supplements that increases clearance of levothyroxine

A

phenytoin, carbamazepine, phenobarbital, rifampicin

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17
Q

drugs and supplements that increases binding of levothyroxine

A

estrogen hormone replacement therapy

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18
Q

levothyroxine enhance effects of (drugs)

A

warfarin, amitriptyline

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19
Q

levothyroxine decr effects of (drugs)

A

propranolol

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20
Q

when should we treat subclinical hypothyroidism? and w what?

A

TSH>10mIU/L, levothyroxine shown to reduce cv events and mortality

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21
Q

levothyroxine dose requirement gradually incr or decr w age? and why?

A

decr, due to age-related decr in thyroxine degradation and in lean body mass

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22
Q

levothyroxine replacement may precipitate ___ in an elderly person with asymptomatic IHD

A

severe angina or myocardial infarction

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23
Q

in people >65yo, levothyroxine should be

A

started at a small dose and dose titration should be carried out slowly

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24
Q

over-replacement of levothyroxine in the elderly population have been associated with

A

reduced bone mineral density and incr risk of fractures

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25
Q

thyroid hormone insufficiency in pregnancy can result in

A

impaired neuropsychological development of the offspring (who only starts developing thyroid hormone after 12 weeks)

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26
Q

maternal hypothyroidism is associated with

A

miscarriage, premature death, and low birth weight - can be prevented with optimum thyroid hormone replacement

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27
Q

most women with known hypothyroidism need a _____ incr/decr dose of levothyroxine during pregnancy

A

30-50% incr, as early as first 4-6 weeks of gestation
- patients will need a reduction of their levothyroxine dose after pregnancy

28
Q

general consensus that subclinical hypothyroidism in pregnant women should or should not be treated?

A

should be treated, with levothyroxine

29
Q

prolonged untreated hypothyroidism can lead to

A

persistent bradycardia, an adverse atherogenic lipid profile, and deterioration in myocardial function

30
Q

newly diagnosed hypothyroid patients with IHD should be started on

A

small dose of levothyroxine, slowly titrated up every 4-6 weeks until euthyroidism is achieved
- positive inotropic and chronotropic effects of thyroid hormone on the heart: starting full dose of levothyroxine could precipitate ACS in hypothyroid patients with silent IHD

31
Q

s/sx of hyperthyroidism

A
  • increased motor activity, metabolism
  • incr heat production (flushed, warm moist skin)
  • incr appetite, and weight loss w insufficient intake
  • incr hr, anxiety
32
Q

causes of hyperthyroidism

A
  • grave’s disease: caused by thyroid stimulating antibody (binds to TSH receptors on the thyroid glands), stimulates both thyroid hormone synthesis and thyroid gland growth resulting in hyperthyroidism and thyromegaly
  • hyperactive thyroid nodules
  • incr iodine consumption
  • incr thyroid hormone consumption
  • inflammation and release of stored thyroid hormones
33
Q

what is grave’s disease precipitated by?

A

environmental factors like stress, smoking, infection, iodine exposure, pregnancy

34
Q

moa of thioamides

A

thought to inhibit thyroid peroxidase enzyme (TPO) and interfere with incorporation of iodine into tyrosyl residues of thyroglobulin (iodination)

inhibit coupling of iodotyrosyl residues to form iodothyronines

35
Q

PTU additional MOA

A

inhibits deiodination of T4 to T3

36
Q

carbimazole is converted to active metabolite

A

thiamazole, after absorption
- anti-thyroid effects are due to thiamazole

37
Q

PTU vs carbimazole: dosing frequency

A

1-4 times daily, once or twice daily

38
Q

PTU vs carbimazole: plasma half life

A

75mins vs 4-6hrs (thiamazole: 5-13hrs)

39
Q

PTU vs carbimazole: which is preferred for treatment of thyroid storm?

A

PTU, has a small but additional effect of blocking the peripheral conversion of T4 to T3

40
Q

when can we expect improvement of grave’s disease following thioamide treatment?

A

3-6 weeks

41
Q

therapeutic uses of thioamides

A
  • grave’s disease
  • thyroid storm
  • overactive thyroid gland
  • to attain a euthyroid state rapidly in preparation for radioiodine therapy or thyroidectomy
42
Q

most serious reaction seen to develop from PTU or thiamazole

A

agranulocytosis: sore throat, fever, or other signs of infection
- more common within the first 3 months of use
- reversible upon discontinuation of the offending drug
-> STOP and have a complete blood count

43
Q

most common reaction from thioamides

A

mild, occasionally purpuric, urticarial papular rash
- often subsides spontaneously without interrupting treatment

44
Q

black box warning for PTU

A

liver failure

45
Q

hyperthyroidism in pregnancy

A

thyroid dysfunction diminishes as pregnancy proceeds
- hence, reduction of dosage of thioamides may be possible

46
Q

PTU use during pregnancy

A

readily crosses placental membranes, can induce goiter and even cretinism in the developing fetus - important that a sufficient but not excessive dose be given
- warn pt of the rare potential hazard to the mother and fetus of liver damage

*PREFERRED agent during organogenesis (first trimester of pregnancy)
BUT given potential maternal adverse effects of PTU eg. hepatotoxicity, may be preferable to switch from PTU to thiamazole for the 2nd and 3rd trimesters

47
Q

thiamazole use in pergnancy

A

may be associated with rare development of fetal abnormalities such as aplasia cutis and choanal atresia, only used in 2nd and 3rd trimester

48
Q

effect of iodide once discontinued

A

effect may not be maintained
- may produce severe exacerbations of thyrotoxicosis when the gland ‘escapes’ from iodide block, following withdrawal of the iodides

49
Q

iodide moa

A

high conc of iodide can
- suppress iodination of tyrosine and also coupling of the monoiodotyrosyl and diiodotyrosyl residue, thus inhibiting thyroid hormone synthesis
- decrease thyroid gland size and vascularity when given over 1-2 weeks
- can be used to temporarily inhibit T4 and T3 synthesis and release into the circulation (useful in thyroid storm)

50
Q

can iodide be used in pregnancy and lactation?

A

no, crosses the placenta and may cause fetal goiter

51
Q

therapeutic uses of iodide

A
  1. In the preoperative period, in preparation for thyroidectomy, as it reduces
    thyroid hormone synthesis and release, and reduces thyroid size and
    vascularity. (Consider concurrent beta-blockade (eg, propranolol) in the
    immediate preoperative period to reduce the risk of thyroid storm)
  2. Thyrotoxic crisis (An hour after Anti-thyroid drugs are administered) After a
    radioactive iodine exposure, potassium iodide can be used to block uptake
    of radioiodine by the thyroid, reducing the risk of thyroid cancer.
  3. Endemic goitre 􀂱 Endemic goitre occurs in iodine-deficient areas. Goitre is
    an adaptive process: iodine is essential for the production of thyroid
    hormones; iodine deficiency impairs thyroid hormone synthesis; to
    compensate, the thyroid gland increases in volume. Thyroid function usually
    remains normal. Iodide is used as overcome the iodine deficiency
52
Q

adr of iodide

A
  • allergic reactions: angioedema, laryngeal edema > suffocation and rashes
  • chronic intoxication with iodide (iodism): metallic taste, gi intolerance, soreness of the teeth and gums, increased salivation, irritation of the eyes, along with lacrimation and rhinorrhea, severe headache - disappear spontaneously within a few days after stopping adm of iodide
53
Q

can radioactive iodine be used in pregnancy and lactation?

A

no, c/i!
- concentration of isotope in the fetal thyroid
- exposure of fetal tissues to radiation
- only can be used 6 wk after breast-feeding has stopped

54
Q

adr of radioactive iodine

A
  • high incidence of delayed hypothyroidism
  • small but significant incr in certain types of cancer (incl stomach, kidney and breast) - these tissues express the sodium iodide transporter
  • a/w worsening graves’ opthalmopathy
    ^ adr may set in 1-2 months after treatment
55
Q

when is thyroidectomy best performed during pregnancy?

A

second trimester

56
Q

PTU dose

A

initial: 300mg in 3 divided doses
usual maintenance: 100-150mg in 3 equally divided doses

57
Q

treatment of thyrotoxic storm

A

antithyroid drugs (PTU 250mg Q4H after a loading dose of 500-100mg, or thiamazole 20mg Q6H), block thyroid hormone synthesis > inorganic iodine (saturated solution of KI 250mg Q6H or 1g IB Q12H), decr release of preformed T3 and T4, given 1 hr later

reduction of circulating thyroid hormones: cholestyramine up to 4g Q6H, enhance hormone fecal excretion

peripheral effects of thyroid hormones: BB

resolution of systemic manifestation:
- glucocorticoids (hydrocortisone, dexamethasone)l reduce T4 conversion to T3 and treat potential risk of adrenal insufficiency due to severe thyrotoxicosis (destructs effect on cortisol)
- paracetamol for fever

58
Q

goals of therapy

A
  • Preserve bone mass – stable or increasing BMD is considered a good response to treatment)
  • Correct calcium deficiency
  • Prevent future falls and fractures
  • Pain relief
  • Strengthen muscles and restore mobility and improve quality of life through physiotherapy
59
Q

risk factors for osteoporosis

A

female
ca deficiency
low body mass
elderly
drugs: PPI
conditions: RA
smoking
excessive alcohol
physical inactivity
poor nutrition

60
Q

Calcium absorption plateaus after

A

ingestion of more than 500mg-600mg elemental calcium in a single setting

61
Q

calcium carbonate vs calcium citrate: absorption

A

calcium citrate not affected by gastric pH for absorption
calcium carbonate soluble in acid, take after food

62
Q

Atypical femoral fracture: Look out for development of

A

dull aching pain in the hip, groin or thigh. Also look out for the development of severe bone, joint or muscle pain. Consult the doctor if any of those symptoms appears.

63
Q

Osteonecrosis of the jaw: After starting the medication, monitor for any

A

oral symptoms (e.g. tooth ache, loose teeth, non-healing of sores or discharge) and practice good oral hygiene. Brush your teeth twice a day, floss regularly and visit the dentist at least twice a year. Let your dentist know that you are taking this medication before any dental procedure.

64
Q

cellulitis, look out for

A

skin redness and swelling

65
Q

signs or symptoms of low calcium

A

numbness of the lips, tingling in your hands or feet, muscle cramps, muscle weakness or seizures

66
Q

Acute phase reaction:

A

For the first infusion, some patients may experience flu-like symptoms (headache, fever, muscle ache, joint pain) after the infusion, which may last for 1-7 days. This is most common after the first infusion, and less common for subsequent infusions. Take paracetamol 1g 30 minutes prior to infusion, and every 6 hours thereafter as needed for the next 2-3 days if symptoms develop. Your temperature, heart rate and blood pressure will be measured before, during and after the infusion. You will be observed for 45 minutes after the infusion to monitor for side effects.

67
Q
A

competency 10/11 (31 decks)

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