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thyroid disorders Flashcards

1
Q

what are the physiological functions regulated by THs

A
  • cardiac functions
  • GI function
  • muscle strength
  • menstrual cycle
  • sleep
  • CNS
  • body temperature
  • breathing
  • skin dryness
  • increase lipid metbaolism
  • increase uptake and utilisation of glucose
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2
Q

what is the correlation between oxygen uptake and basal metabolic rate

A

increase oxygen consumption by most tissues increases basal metabolic rate

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3
Q

what is the negative feedback

A

when there are low levels of circulating TH, the hypothalamus will secrete TRH to signal the pituitary to secrete TSH, TSH signals the thyroid gland to increase TH

once there are elevated levels of circulating TH in the blood, hypothalamus senses and stops releasing TH

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4
Q

compare the thyroid levels in primary hyperthyroidism and hypothyroidism

A

primary hyperthyroidism
- elevated circulating TH –> hypothalamus stops producing TRH, not stimulating release of TSH and subsequent TH
- thus low TSH, high TH

primary hypothyroidism
- low circulating TH –> hypothalamus tries to increase TH by releasing TRH and pituitary releases TSH but unsuccessful in stimulating thyroid gland to release TH
- thus high TSH, low TH

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5
Q

what is the ratio of TH production

A

4:1 of T4:T3

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6
Q

how is T3 formed

A

80% of T3 is formed from peripheral conversion of T4 by deiodination via deiodinases

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7
Q

what are the mechanisms to regulate TH

A
  1. negative feedback
  2. peripheral conversion of T4 to T3
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8
Q

compare the PK characteristics between T3 and T4 and clinical signifcance

A
  • T3 has half life of 2 days while T4 has a half life of. 6-7 days, thus the shorter half life makes T3 not an accurate representation of thyroid status
  • free T4 levels are measured as only unbound T4 can diffuse into cells to carry out metabolic functions
  • both T3 and T4 are >99% protein bound (most commonly bound to thyroxine-globulin protein TBG)
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9
Q

what is important for T3 and T4

A

iodine consumption is essential for production of THs and must be obtained exogenously

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10
Q

what are the tests of autoimmunity for thyroid disorders

A
  • thyroglobulin antibodies (ATgA)
  • thyroperoxidase antibodies TPO)
  • thyrotropin receptor IgG antibodies (TRAb)

ATgA and TPO target thyroglobulin protein and thyroperoxidase enzyme respectively that can lead to inflammation and destruction of the thyroid tissue thus leading to release of stored TH and if destruction is excessive, it can eventually result in hypothyroidism as the thyroid gland becomes less able to produce TH

TRAb mimics the action of TSH and binds to TSH receptors on thyroid cells, stimulating the thyroid gland to release TH, leading to hyperthyroidism

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11
Q

what are some compelling indications to test for thyroid disorders

A
  • routinely screened in pediatrics and pregnant women
  • presence of autoimmune diseases (T1DM, cystic fibrosis)
  • first degree relative with history of thyroid disorder
  • psychiatric disorder
  • taking amiodarone or lithium
  • hx of head or neck radiation for malignancy
  • symptoms for hyperthyroidism or hypothyroidism
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12
Q

what are the s/sx of hypothyroidism

A
  • cold intolerance (lack of TH causes the inability to generate and maintain body heat)
  • weight gain
  • bradycardia
  • slow reflexes
  • dry skin
  • coarse skin and hair
  • fatigue, lethargy, weakness
  • periorbital swelling
  • menstrual disturbances (more freq and larger volumes as low TH decreases metabolism of estrogen)
  • goiter
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13
Q

what are the s/sx of hyperthyroidism

A
  • heat intolerance
  • weight loss or increased appetite
  • fine hair
  • goiter
  • heat palpitations or tachycardia
  • sweating or warm, moist skin
  • anxiety, nervousness, insomnia
  • menstrual disturbances (lighter and more infrequent)
  • exophthalmos ie. bulging eyes (in Grave’s)
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14
Q

what are the primary and secondary causes of hypothyroidism

A

primary
- iodine deficiency
- hashimoto’s (+ ATgA and TPO)
- iatrogenic causes (radioactive ablative therapy, surgical resection of thyroid gland)

secondary
- central hypothyroidism (dysfunction of hypothalamus/ pituitary)
- drug-induced (amiodarone/ lithium)

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15
Q

what are the causes of hyperthyroidism

A
  • toxic diffuse goiter in grave’s ((+)TRAb)
  • pituitary adenomas (refers to non cancerous tumors)
  • toxic adenoma (solitary functioning nodule secreting T3)
  • toxic multi-nodular goiter in Plummer’s (multiple nodules secreting T3)
  • drug induced (amiodarone, lithium)
  • subacute thyroiditis (infections, drug induced, early Hashimoto’s where there’s temporary spike)
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16
Q

what are the clinical manifestations of hypothyroidism

A
  • elevated total cholesterol, LDL and TG (decreased total cholesterol clearance due to lower metabolic rate, decreased LDL clearance due to reduced expression of LDL receptors, decreased TG breakdown due to reduced lipoprotein lipase activity)
  • elevated risk of atherosclerosis and MI (due to elevated lipids, and other metabolic abnormalities)
  • increased CPK levels (due to muscle pain and weakness)
  • increased risk of miscarriage
  • impaired fetal development
  • labs (for primary hypothyroidism, low T4 high TSH; for central hypothyroidism, low T4 low TSH)
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17
Q

what are the clinical manifestations of hyperthyroidism

A
  • elevated FT4, suppresed TSH
18
Q

what are the goals of therapy for hypothyroidism

A
  • minimise or eliminate symptoms, improve QoL
  • minimise long term damage to organs (myxedema coma, heart disease)
  • normalise free T4 and TSH concentrations
  • prevent neurologic deficits in newborns and children
19
Q

what are the goals of therapy for hyperthyroidism

A
  • minimize or eliminate symptoms, improve QoL
  • minimise long term damage to organs (heart disease, arrhythmias, sudden cardiac death, bone demineralization, fractures)
  • normalise FT4 and TSH concentrations
20
Q

what is the pharmacological management for hypothyroidism

A
  • levothyroxine (synthetic T4)
  • liothyronine (synthetic T3)
21
Q

what is the place in therapy of levothyroxine for hypothyroidism (dose, titration, monitoring, s/e, PK)

A
  • drug of choice
  • initial dose for young, healthy adults: 1.6mcg/kg/day; for 50-60yo w/o CVD: 50mcg/day; for established CVD: 23.5-25mcg/day
  • titrate in 12.5-25mcg/day or in 10-15%
  • monitoring in 4-8w to assess levels of TSH (normal FT4 levels but high TSH indicates non-adherence since FT4 levels easier to normalize) but assess FT4 levels for central hypothyroidism (since TSH levels will always be low)
  • f/b TFT monitoring q6-12m for nonpregnant adults after euthyroid state achieved
  • symptomatic relief in 2-3w
  • s/e includes anxiety, diarrhea, sleep ifficulties, hair loss, reduced appetite (rarely cardiac abnormalities, seizures)
  • onset 3-5d
  • > 99% protein bound
  • metabolized in liver through glucoronidation and sulfation
  • eliminated in urine and feces and as metabolites in bile
22
Q

what to counsel patients on for levothyroxine

A
  • take 30-60mins before breakfast or 4hrs after dinner
  • also same spacing interval for other medications
  • space 2hrs apart from calcium or iron supplements, and antacids
23
Q

what is the place in therapy of liothyronine for hypothyroidism

A
  • much shorter half life than T4
  • high incidence of s.e
  • generally not recommended
  • can be considered in myxedema coma (though usually IV levothyroxine is usually given instead)
24
Q

what is myxedema coma and how is it managed

A

myxedema coma is a severe form of hypothyroidism

managed by IV liothyroxine (or IV thyronine)

25
Q

what is the key concepts in managing pregnant patients with hypothyroidism

A
  • need 30-50% increase in pre-pregnant dosage since maternal TH provide fetus with THs for up to 6w, up until fetus forms their own thyroid gland
  • maternal hypothyroidism can cause miscarriage or spontaneous abortions, congenital defects and impaired cognitive development
26
Q

what are the management strategies for hyperthyroidism

A
  • surgical resection
  • radioactive ablative therapy (colorless, tasteless liquid that concentrates in thyroid tissues to destroy overactive thyroid cells)
  • thyroidectomy
  • pharmacological management is last line
27
Q

for whom are pharmacological management suitable for to manage hyperthyroidism

A
  • not candidates for ablative therapy or surgery
  • failure to normalise
  • limited life expectancy
  • mild disease, small goiter, negative or low Ab
28
Q

what are the pharmacological management for hyperthyroidism

A
  • thionamides (carbimazole, propylthiouracil)
  • iodides (lugol’s solution)
  • nonselective BB (propranolol)
29
Q

what is the moa of thionamides

A

carbimazole and PTU works by inhibiting thyroid peroxidase (TPO) which usually iodinates to form precursors of T4 and T3, thus reducing synthesis of THs

at higher doses, PTU can inhibit T4/T3 conversion in the periphery

30
Q

what is the place in therapy for thionamides in managing hyperthyroidism

A
  • carbimazole preferred for grave’s
  • carbimazole initiated at 15-60mg then once euthyroid become 5-15mg OD; PTU initiated at 50-150mg TDS then once euthyroid become 50mg BD/TDS
  • FT4 levels will take 3-6w to show changes due to its long half life and stores of T4 need to be depleted
  • TSH levels likely to remain elevated for months
  • efficacy assessed through symptomatic improvement and FT4 levels
31
Q

what are the s/e of thionamides

A

rash, nausea, joint pain, jaundice, aggranulocytosis (rare)

32
Q

what are the key concepts in managing hyperthyroidism in pregnancy

A
  • in first trimester, PTU > carbimazole since carbimazole more assoc w congenital malformation
  • in second and third trimester, carbimazole since PTU is more hepatotoxic and also less potent
33
Q

what is the moa if NSBB to manage hyperthyroidism

A

propranolol blocks many hyperthyroidism manifestations mediated by beta adrenergic receptors

also blocks T4/T3 conversion at high doses

34
Q

what is the place in therapy of NSBB for hyperthyrodism

A
  • for sx relief
  • bridging therapy before thionamide effects kick in/ before ablative therapy/ before surgery
35
Q

what is the moa of iodides

A

lugol’s solution is a saturated solution of potassium iodide
- inhibits release of stored THs
- minimal effect on TH synthesis
- helps decrease vascular and size of thyroid gland

36
Q

what is the place in therapy of iodides in managing hyperthyroidism

A
  • shrink thyroid gland before surgery, take 7-10d prior
  • prevent thyroiditis-mediated release of stored THs after RAI, take 3-7d after
  • limited efficacy after 7-14d of treatment as TH release will resume
  • do not take before RAI as may reduce uptake of radioactive iodine
37
Q

how does drug-induced hypo/hyperthyroidism occur

A
  • amiodarone contains iodine in its structure thus affects iodine uptake, secretion and production, causing thyroiditis
  • lithium inhibits THs secretion and release
38
Q

what is the clinical significance of subclinical hypothyroidism

A

elevated TSH with normal T4
- likely early Hashimoto’s
- elevated risk of HF in older adults
- elevated risk of coronary heart disease

39
Q

what is the clinical significance of subclinical hyperthyroidism

A

low or undetectable TSH with normal T4
- increased risk of AF in ≥60yo
- increased risk of bone fracture in postmenopausal women

40
Q

when to consider treating if subclinical hypothyroidism and subclinical hyperthyroidism

A
  • treat subclinical hypothyrodism if TSH >10mIU/L
  • treat subclinical hyperthyroidism if TSH <0.10mIU/L

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