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SYSTEMIC PHARMACOLOGY > Endocrine - thyroid and anti-thyroid > Flashcards

Endocrine - thyroid and anti-thyroid Flashcards

1
Q

thyroid hormones function

A

liver - lipid turnover, gluconeogenesis
muscle - insulin sensitivity, glucose utilisation, oxidative metabolism
adipose - lipolysis
heart - diastolic (relaxation), increase contractility of heart
vessels - vasodilation, decrease resistance, increase venous tone

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2
Q

synthesis of T3/T4 requirements

A

Na/I symporter

  • > TPO oxidation (thyroid peroxidase)**
  • > iodination**
  • > conjugation
  • > endocytosis
  • > proteolysis
  • > D1/D2 (deiodinases) converts T4 -> T3
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3
Q

wolff-chaikoff effect

A

when there is iodine exposure, excess iodine gets transported into the gland via Na-I symporters-> inhibition of TPO -> decrease synthesis of thyroid hormones
so administer KI during emergency hyperthyroidism

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4
Q

causes of hypothyroidism

A

primary:

  • autoimmune: Hashimoto’s thyroiditis - antibodies attack TPO in thyroid gland
  • iodine def
  • drugs with high iodine (amidarone) - wolff chaikoff effect

secondary:

  • pituitary failure: decrease in TSH secretion
  • hypothalamic failure: decrease TRH

congenital hypothyroidism

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5
Q

hypothyroidism symptoms

A
  • fatigue, lethargy
  • mental slowness
  • dry skin
  • weight gain
  • irregular menses
  • hair loss/ puffy eyes
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6
Q

drugs for hypothyroidism

A

isomers of the thyroid hormones

  • levothyroxine (T4)
  • liothyronine (T3)
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7
Q

levothyroxine

  • method
  • onset
  • half-life
  • clinical use
  • monitoring
A
  • method: oral/ IV
  • onset: oral (3-5); IV (6-8)
  • half-life: 1wk
  • clinical use: (IV) myxedema coma (decreased mental status w/ hypothermia) + congenital hypothyroidism
    preferred over liothyronine
    need to monitor thyroid fn 6-8wks after therapy
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8
Q

liothyronine

  • method
  • onset
  • half-life
  • clinical use
A
  • method: oral/ IV
  • onset: 3hrs
  • half-life: 1 day
  • clinical use: (IV) myxedema coma
    for rapid onset - not to be used for chronic replacement of thyroid hormones
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9
Q

thyroid replacement therapy ADR

A

CVS: tachycardia, palpitations, hypertension, cardiac arrest
heat intolerance
hyperactivity, insomnia, irritability
bone: bone resorption, reduced bone mineral density

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10
Q

levothyroxine DDIs and food interaction

A

30-45 minutes on empty stomach
DDI w/ estrogen hormone replacement: increase thyroxine-binding globulin levels -> bind to thyroxine -> reduce free thyroxine to cure the hypotension

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11
Q

levothyroxine in subclinical hypothyroidism (normal T4, raised TSH)

A

only to be used if TSH > 10

does not reduce CVS/mortality in these pts

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12
Q

levothyroxine in elderly

A

elderly: decrease lean body mass w/ age -> decrease thyroid degradation
causes reduced bone mineral density, increasing risk of fractures
need to start with small dose then slowly titrate

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13
Q

levothyroxine in pregnancy

A

hypothyroidism can impair fetus neuropsychological development, miscarriage, premature death, low birth weight
so need to increase levothyroxine dosage (30-50%) during pregnancy + 4-6wks during pregnancy

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14
Q

levothyroxine in IHD pts

A

full dose of levothyroxine can ppt acute coronary syndrome, cause of +ve inotropic & chronotropic effects of T4 on heart
start w/ small dose then titrate up

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15
Q

hyperthyroidism signs and symptoms

A

increased metabolism -> increased appetite + weight loss
heat production - flushed, warm moist skin
tachycardia, anxiety

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16
Q

causes of hyperthyroidism

A
  • autoimmune: Grave’s disease
    thyroid stimulating ab pretends to be TSH and binds TSH receptors -> stimulates thyroid hormone synthesis + gland growth
  • hyperactive thyroid nodules
  • iodine consumption
  • thyroid hormone consumption - drugs
  • inflammation -> release of stored hormones
17
Q

Grave’s signs and symptoms

A
  • bilateral proptosis
  • periorbital edema
  • lid retraction
  • skin lesions
  • clubbing
18
Q

drugs for hyperthyroidism**

A
  • thioamides (anti-thyroid)
  • high conc of iodine
  • radioactive iodine
19
Q

thioamides drugs (2)

A

carbimazole* - more common in SG

propylthioracil (PTU) - black box warning

20
Q

thioamides MOA

A

inhibit TPO
inhibits iodination: interferes w/ incorporation of iodine into thyroglobulin
specific to each drug:
PTU - inhibits T4->T3 deionisation
Carbimazole - converted to thiamazole - anti-thyroid

21
Q 
PTU
- half life
- absorption method
- metabolism
- excretion
- dosing freq
- does it cross placenta
- affects breast milk?
difference from carbimazole
A
  • half life: ~ 1hr
  • absorption method: oral
  • metabolism: hepatic
  • excretion: urine - 35% gets excreted within a day
  • dosing freq: 1-4 times/day
  • does it cross placenta: yes
  • affects breast milk? no

used during thyroid storm: extra effect of blocking peripheral conversion of T4 -> T3

22
Q

carbimazole

  • half life
  • absorption method
  • metabolism
  • excretion
  • dosing freq
  • does it cross placenta
  • affects breast milk?
A
  • half life: ~ 4-6hrs
  • absorption method: oral
  • metabolism: hepatic
  • excretion: urine
  • dosing freq: 1/2 times/day
  • does it cross placenta: yes
  • affects breast milk? no
23
Q

thioamides clinical use

+ onset time

A
  • graves
  • thyroid storm: PTU
  • overactive thyroid gland
  • radioiodine therapy/ thyroidectomy prep
  • slow onset (3-12 wks)**
24
Q

thioamides ADR

A

quite low incidence rate

  • possible agranulocytosis**(leukopenia - decreased WBC) (first 3 mths) - watch out signs of sore throat, fever, infection -> do complete blood count
  • purpuric papular rash
  • cholestatic jaundice
  • liver failure if severe - esp if PTU: black box warning
25
Q

thioamides CI

A

pregnancy: crosses placental barrier + fetal abnormalities
PTU: children -> liver failure

26
Q

drugs w/ high iodine conc

A
  • lugol’s solution -> I2 + KI

- potassium iodide (KI)

27
Q

Lugol’s solution

  • route
  • onset time
  • peak effect
  • clearance
A
  • route: oral
  • onset time: 1-2 days
  • peak effect: 10-15 days after
  • clearance: renal
28
Q

high iodine conc MOA

A
  • limits its own transport
  • suppress iodination of tyrosine -> inhibit thyroid hormone synthesis
  • decrease thyroid gland size and vascularity
  • inhibit thyroid hormone synthesis

has to be given AFTER anti-thyroid drugs (PTU)

29
Q

high iodine conc clinical use + CI

A
  • large thyroid size
  • thyrotoxic crisis
  • endemic goitre

CI: pregnancy - cross placenta -> fetal goitre

30
Q

iodine ADR

A
  • possible allergy -> angioedema, laryngeal edema -> suffocation
  • chronic intoxication: GI intolerance, rhinorrhoea - just need to stop treatment
31
Q

radioactive iodine MOA

A
  • mimicks iodine, gets absorbed by NaI transporter into follicular cells
  • passes through tissues
  • pyknosis (necrosis/apoptosis) of follicular cells
    must be careful about the dosage - if not may actually destroy the thyroid gland
32
Q

2 isotopes of radioactive iodine + differences

A

131-I (destructive)

  • can be in solution form
  • half-life: 8 days
  • reduce enlargement of gland w/ thyroid cancer

123-I (diagnostic)

  • only in tablet
  • half-life: half a day
33
Q

radioactive iodine ADR + CI

A
  • possibly delayed hypothyroidism
  • organs with NaI transporter will have increased risk of cancer (stomach, kidney, breast)
  • worsens grave’s ophthalmopathy
    CI: pregnant women - exposes fetus to radiation
34
Q

relief of symptoms caused by hyperthyroidism

A

beta blockers (relief sympathetic symptoms of tremors/ palpitations/ sweatiness)

35
Q

drug to use if pregnant mother has graves

A

1st trimester: PTU. carbimazole can cause fetal abnormalities - 1st trimester is when organogenesis happens
2nd and 3rd trimester: carbimazole. organ development over. PTU can cross placental membranes and cause hepatotoxicity in fetus

SYSTEMIC PHARMACOLOGY (22 decks)

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