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thyroid Flashcards

1
Q

what does t4 and t3 stand for?

A

T4: Thyroxine or Tetra-iodothyronine
T3: Tri-iodothyronine

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2
Q

tell me about thyroid perioxidase (TPO)

A

Used for initial synthesis of TH

  • Found within thyroid gland
  • Faciliate iodination of tyrosine residues on thyroglobulin
  • coupling of MIT and DIT to form TH
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3
Q

tell me about deiodinases

A

Used to regulate levels of T3 to maintain tissue-specific TH balance

  • Found in various tissues (liver, kidneys, skeletal muscle, brain, other peripheral tissues)
  • Conversion of TH and inactivation of TH for body’s specific needs
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4
Q

what is Hyperthyroidism (thyroid disorder)?

A

Too much thyroid hormone (T3, T4)

Symptoms: Hot, energetic, elevated heart rate, sweaty, diarrhoea, cant sleep well, tremors, moody, affect menstrual cycle

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5
Q

what is Hypothyroidism (thyroid disorder)?

A

Too little TH

Symptoms: Cold, low energy, think slow, heart rate slow, low bp, obesity, depressed, move slowly, fatigue

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6
Q

what is the meds for hyperthyroidism?

A

Carbimazole

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7
Q

what is the meds for hypothyroidism?

A

Levothyroxine (L-Thyroxine)

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8
Q

how does carbimazole help with hyperthyroidism?

A

Inhibits thyroid peroxidase which is crucial in the synthesis of TH

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9
Q

how does carbimazole work to treat hyperthyroidism?

A
  • Inhibit TH synthesis by inhibiting thyroid peroxidase which normally iodinates tyrosyl residues in thyroglobulin to give precursor of T3 and T4 —> Reduce overall TH production —> Reduce symptoms of thyrotoxicosis (aka excess of TH)
    • T3 formed by MIT and DIT
    • T4 formed by DIT and DIT
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10
Q

what is carbimazole used for?

A
  • Hyperthyroidism, to control disease before surgery
    • Surgical removal last resort as irreversible, and may accidentally cut away parathyroid gland
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11
Q

how is the absorption like for carbimazole?

A
  • Oral once daily, well absorbed
  • Prodrug carbimazole converted into active metabolite aka methimazole in liver
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12
Q

how is the distribution like for carbimazole?

A
  • Methimazole t1/2 = 4-6h
    • Short half life but concentrate in thyroid gland (carbimazole also) so clinical effects can last a day
    • Not highly bound to plasma proteins so more drug available for action
    • Large (>90%) inhibition of thyroid organification of iodine within 12h after admin (rapid onset)
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13
Q

how is the metabolism and excretion like for carbimazole?

A
  • Broken down in liver by CYP450 and FMO enzymes
  • Well absorbed where >90% of orally admin carbimazole is excreted in urine as methimazole or further conjugated compounds, rest in faeces via enterohepatic circulation
  • 7% of methimazole excreted unchanged in urine
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14
Q

what is the adr for carbimazole when treating for hyperthyroidism?

A
  • Rashes
  • Joint pains
  • Nausea
  • Jaundice
  • Agranulocytosis (rare): Severe decrease in WBC
  • Hypothyroidism due to over treatment
    • So need to monitor thyroid size and serum TSH level, once size is reduced and normal TSH level is achieved, titrate (reduce) carbimazole dose
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15
Q

how long to see clinical response upon initiation of carbamizole for hyperthyroidism? why?

A
  • Clinical response may take several weeks (3-6weeks) to see effect after initiation
    • Carbimazole inhibits synthesis of NEW TH, not existing TH —> So need to wait for existing TH to get degraded and T4 has a long half life…
    • Good counselling point
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16
Q

what does levothyroxine (L-thyroxine) do?

A

treats hypothyroidism. it is a Synthetic TH to restore body to normal T4 levels

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17
Q

what are the types of hypothyroidism?

A
  • Primary Hypothyroidism
    • Reduction in T3 and T4 synthesis in thyroid gland
  • Secondary Hypothyroidism
    • Reduction in TSH by pituitary gland
  • Tertiary Hypothyroidism
    • Reduction in thyrotropin-releasing hormone (TRH) by hypothalamus
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18
Q

how does levothyroxine work when treating hypothyroidism?

A

Absorbed into bloodstream —> Transported to various tissues to be converted into T3 via removal of one iodine atom by deiodinases —> T3 bind to thyroxine/ thyroid hormone receptor (THR) in nucleus which heterodimerise with retinoid X receptor (RXR) to create a heterodimer important for gene regulation —> Complex binds to specific DNA sequences in cell —> mRNA transcription and translation for protein synthesis (for TH functional effects and maintenance of cell viability)

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19
Q

what is the absorption like for levothyroidism when treating for hypothyroidism?

A
  • Oral, take on empty stomach with water 30min before meal as dietary fiber can cause erratic absorption of L-thyroxine
  • Fast to increase absorption
  • Good bioavailability 70-80%
  • Onset 3-5 days, so if want faster do via IV (6-8h onset)
  • Mainly absorbed in small intestine so drugs that affect gastric pH (like antacids, PPIs) may affect absorption of Levothyroxine in small intestine
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20
Q

what is the distribution like for levothyroidism when treating for hypothyroidism?

A
  • t1/2: 7 days, so once a day dosing
  • Highly plasma protein bound
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21
Q

what is the metabolism like for levothyroidism when treating for hypothyroidism?

A
  • 80% T3 is from T4
  • Liver is a major site for degradation of TH through phase 2 glucuronidation and sulphation
  • Kidney to a smaller extent through deiodination of T4 to T3 (remove one iodine atom)
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22
Q

what is the excretion like for levothyroidism when treating for hypothyroidism?

A
  • Kidney primary excrete TH
  • Metabolites excreted in urine and faeces
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23
Q

what are the adr for levothyroxine when treating hypothyroidism?

A
  • Reduced appetite
  • Anxiety
  • Diarrhoea
  • Difficulty sleeping
  • Hair loss
  • Rare and serious: Heart issues (arrhythmias, high BP, pain), Seizures —> So avoid in patients with heart problem, epilepsy and hyperthyroidism (obv)
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24
Q

what is a life threatening case to take note of for hypothyroidism?

A

Myxoedema coma

  • Severe form of hypothyroidism
  • Reduced blood flow to GI —> Affects gut absorption of oral levothyroxine —> Insufficient TH still
  • Treatment: IV Liothyronine (synthetic T3) or IV levothyroxine
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25
Q

how to monitor for serum tsh?

A
  • During initiation to check if treatment is working
  • 6-8weeks after initiation or when dose is change to establish baseline
  • Persistent elevated TSH levels due to inadequate dosing (not properly titrated), poor compliance, malabsorption (myxoedema coma), drug (cause broken down in liver) or food interaction
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26
Q

what is the thyroid gland?

A
  • Endocrine gland
  • Located in the middle of the lower neck
  • Shaped like a “butterfly”
  • Releases thyroid hormones (TH) that regulates development, growth, metabolism
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27
Q

what is the thyroid hormones?

A

Released into circulation in a 4:1 ratio of T4:T3

  • Mostly protein-bound to Thyroxine binding globulin (TBG)
    • Unbounded are the ones free to exert biological effects
    • Preggos or being on estrogen will increase TBG levels —> More TH bind to TBG —> Lesser FTH —> TSH released to stimulate thyroid gland to release more TH —> Increase FTH
      • If thyroid gland not working, need to replace TH externally
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28
Q

what is t3?

A
  • T3 is more potent
  • 80% of T3 is produced from the peripheral conversion of T4 by deiodination via deiodinases
    • Iodine consumption (aka only exogenous from diet like seaweed, seafood, diary) is essential to produce TH
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29
Q

does t3 or t4 have a longer half life?

A

T4!

Longer t1/2 of 6-7d: Can be converted into active T3 when needed
- Free T4 (FT4) routinely measured with TSH to assess thyroid status as it reflects active and unbound TH levels

meanwhile, t3 has a Shorter t1/2 of 2d: More responsive to changes in TH needs
- Not routinely ordered for evaluation cos half life very short so may not be a good rep of the TH stores in body

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30
Q

what is the normal homeostasis of thyroid hormones?

A
  1. Low TH detected by and hence stimulates Hypothalamus to release thyrotropin-releasing hormone (TRH)
  2. TRH stimulates pituitary to release thyroid stimulating hormone (TSH aka Thyrotropin)
  3. TSH stimulates thyroid gland to secrete TH
  4. Elevated levels of circulating TH in blood —> Hypothalamus senses and stops releasing TRH
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31
Q

what does it mean when there is Elevated levels of TSH in Primary hypothyroidism?

A
  • Primary: Gland not functioning well
    • VS Secondary: Gland is functioning well
  • Hypothalamus will detect persistently low levels of TH so will secrete TRH —> Pituitary stimulated to secrete TSH —> But wont be able to stimulate thyroid gland to secrete TH so TH levels will keep being low
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32
Q

what does it mean when there is low levels of TSH in Primary hyperthyroidism?

A

Hypothalamus will detect persistently elevated levels of TH so will not secrete TRH —> Pituitary will not secrete TSH —> Thyroid gland is functioning independently of TSH levels

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33
Q

what are the tests for autoimmune thyroid disease? note: fella says fyi but to know the tests so ?

A

Hashimoto’s have ATgA & TPO
Graves’ have ATgA & TPO

  • ATgA (Thyroglobulin antibodies)
    • Thyroglobulin is a protein produced by thyroid gland
    • ATgA target thyroglobulin
  • TPO (Thyroperoxidase antibodies)
    • Thyroperoxidase is an enzyme involved in production of TH
    • TPO target thyroperoxidase
    • Strongly associated with hypothyroidism
  • TRAb (Thyrotropin/ TSH receptor IgG antibodies)
    • Specific to TSH receptor on thyroid cells
    • Antibodies keep attacking and triggering receptor —> Triggers thyroid gland to keep producing TH
    • Elevated levels are indicative of Graves’ disease
    • Expensive
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34
Q

what are the screening indications for thyroid disorders?

A
  • Presence of autoimmune disease (eg. T1DM, cystic fibrosis)
  • First-degree relative with autoimmune thyroid disease
  • Psychiatric disorders
    • Possible symptom of thyroid disease
  • Taking Amiodarone or Lithium
    • Affects thyroid hormones
  • Hx of head/ neck radiation for malignancies
  • Symptoms of hypothyroidism/ hyperthyroidism
  • Routine screening required for pediatric patients and pregnant women
    • To prevent developmental issues
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35
Q

What is hypothyroidism?

A

Decreased activity of thyroid gland

note: TH obviously low —> so TSH is high due to feedback loop

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36
Q

what causes primary hypothyroidism?

A
  • Iodine deficiency*
  • Hashimoto disease (Chronic autoimmune thyroiditis)
    • Most common hypothyroid disorder in areas with iodine sufficiency
    • Immune system attacks thyroid gland to cause damage
    • Indicated by presence of ATgA and TPO antibodies
    • Affects women more
  • Iatrogenic
    • Thyroid resection or radioiodine ablative therapy for hyperthyroidism
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37
Q

what causes secondary hypothyroidism?

A
  • Central hypothyroidism
    • Hypothalamus unable to secrete TRH
    • Pituitary unable to secrete TSH
  • Drug induced (e.g. Amiodarone, Lithium)
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38
Q

what are the signs and symptoms of hypothyroidism?

A

just rmb: Everything is slowing down

  • Cold intolerance
  • Dry skin
  • Fatigue, lethargy, weakness
  • Weight gain
  • Bradycardia
  • Slow reflexes
  • Coarse skin and hair
  • Periorbital swelling
  • Menstrual disturbances (more frequent, more blood)
    • Slowing down clearance of estrogen
  • Goiter (enlarged thyroid gland) to try to produce more TSH
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39
Q

what is the clinical manifestations of hypothyroidism?

A
  • Increase in Total cholesterol, LDL, Triglycerides
    • No more TH to regulate lipid metabolism
  • Increase in Atherosclerosis, MI risk
    • Consequence of build up of fatty deposits in arteries
  • Increase in Creatine phosphokinase (CPK) levels —> Weakness and Muscle disease
  • Increase in Miscarriage risk
    • No more TH to aid in fetal development
  • Impaired fetal cognitive development
    • No more TH to aid in fetal development
40
Q

what is the diagnosis of hypothyroidism ?

A
  • Adults that are symptomatic —> Screen
    • Primary hypothyroidism: Low T4 so high TSH and positive antibodies (TPO, ATgA)
    • Central hypothyroidism: Low TSH so low T4
  • Labs (will be given the ranges in exam)
    • TSH: Cheapest method
      • 12-22pmol/L
    • Free T4
      • 0.4-4.2mIU/L
41
Q

what is the Goals of therapy of hypothyroidism?

A
  • Minimize or eliminate symptoms —> Improve QOL
  • Minimize long-term damage to organs (eg. Myxedema (severe hypothyroidism) coma, heart disease)
  • Prevent neurologic deficits in newborns and children
  • Normalize free T4 and TSH concentrations
42
Q

what is the pharmacology of hypothyroidism?

A
  1. levothyroxine
  2. liothyronine
43
Q

what is levothyroxine?

A

Synthetic T4 (bc autoimmune disease so just give replacement)

44
Q

why is levothyroxine the drug of choice?

A

Relatively good adverse effect profile, cost, lack of antigenicity, uniform potency

45
Q

what is the initial dosing of levothyroxine?

A
  • Young, healthy adults: 1.6mcg/kg/d (normally start with 100mcg OD)
  • 50-60 years of age and no cardiac issues: 50mcg OD
  • With CVD: 12.5-25mcg/d and titrate up
    • Start at even lower dose so as to not put too much stress on the heart so abruptly
46
Q

how long does titration of levothyroxine take? why? can change how much?

A
  • Takes a couple of weeks due to negative feedback
  • Depends on response (control of symptoms, normalization of TSH and T4)
  • Can increase or decrease in 12.5-25mcg/day increments, or in 10–15% of weekly dose
47
Q

when and how can i take levothyroxine for hypothyroidism?

A
  • On empty stomach!!: 30-60 minutes before breakfast or 4 hours after dinner
    • Includes other medications
  • Space at least 2 hours apart from Ca or Fe supplements and antacids
48
Q

how to monitor after taking levothyroxine for hypothyroidism?

A
  • 4-8 weeks to assess response in TSH after initiating or changing therapy
    • General target TSH: 0.4 to 4 mIU/L
    • Symptomatic relief in 2-3 weeks
    • Normal FT4 but TSH still high —> Possible non-adherence as maybe took right before coming to get tested so not enough time to stimulate feedback loop
49
Q

monitor what after taking levothyroxine for hypothyroidism?

A

Use free T4 rather than TSH if central hypothyroidism as upstream got problem so wont be produced

50
Q

is the treatment of taking levothyroxine for hypothyroidism lifelong?

A
  • Treatment is lifelong
    • After a euthyroid state (stable) is achieved, thyroid function tests (TFT) are recommended semiannually to annually in non-preggo adults
51
Q

what happens in older adults upon tkaing levothyroxine for hypothyroidism?

A
  • TSH level rises over time but age-based normal ranges for TSH not implemented
  • > 70yo: TSH can be still WNL up to 6.9 mIU/L
52
Q

what are the adr or signs of over replacement for levothyroxine for hypothyroidism?

A
  • Cardiac abnormalities: Tachyarrhythmias, angina, MI
    • Risk of fractures
    • Signs of hyperthyroidism
53
Q

what is liothyronine?

A

Synthetic T3

54
Q

why is liothyronine not really reco for hypothyroidism?

A
  • Not really recommended due to shorter half life (1-2.5d) and more expensive
  • 😖😖High incidence of ADR
55
Q

what is the starting dose for liothyronine?

A
  • Starting Dose
    • Young, healthy adults: 25mcg
    • Elderly or CVD: 5mcg
56
Q

when to take liothyronine for hypothyroidism?

A
  • Combination T4 with T3 can be considered if normalized TSH but still symptomatic
  • Can be considered in myxedema coma since more potent, and for surgery since short half life (rapid onset and wears off quicker)
57
Q

how does maternal th help fetus?

A

Maternal TH provides fetus with TH for up to 12 weeks before fetus forms own thyroid gland

58
Q

what is the effect of maternal hypothyroidism?

A
  • Miscarriage, spontaneous abortion
  • Congenital defects, impaired cognitive development
59
Q

what happens if mom is on levothyroxine for maternal hypothyroidism?

A
  • If mom on levothyroxine, may need a 30-50% increase in pre-pregnant dosage to maintain euthyroid status
    • Due to more TBG, so need more TSH to stimulate more TH release to increase free TH levels
    • Target TSH
      • 1st trimester: < 2.5 mIU/L
      • 2nd trimester: < 3.0 mIU/L
      • 3rd trimester: <3.5 mIU/L
60
Q

what is subclinical hypothyroidism?

A

Elevated TSH with normal T4 —> Possible Initial phase of hypothyroidism like Hashimoto disease

61
Q

when to treat subclinical hypothyroidism?

A

If not symptomatic, dont need to treat

  • Consider treating
    • TSH > 10 mIU/L —> still ok, no need to treat
    • TSH = 4.5–10 mIU/L and
      • Symptoms of hypothyroidism
      • TPOAb present
      • History of cardiovascular disease, heart failure, or risk factors
62
Q

what are the risks associated for subclinical hypothyroidism?

A
  • TSH > 7.0 mIU/L in older adults: Elevated risk of heart failure
  • TSH > 10 mIU/L: Elevated risk of coronary heart disease

If untreated, screen regularly for possible development of overt hypothyroidism

63
Q

how to treat subclincal hypothyroidism?

A

Starting dose: 25–75mcg OD

64
Q

What is hyperthyroidism

A
  • Overabundance of TH
    • Mimics effects of activated sympathetic nervous system
65
Q

what causes hyperthyroidism?

A
  • Toxic diffuse goiter (Graves disease)*
    • Immune system produces antibodies (eg. TRAb) that mimic action of TSH
      • TSI subtype stimulates TH production
  • Pituitary adenomas (Tumor)
  • Toxic adenoma (Hot nodule)
    • Solitary functioning (single, hyperactive) nodule that secretes excess T3
  • Toxic multi-nodular goiter (Plummer’s Disease)
    • Multiple nodules that secrete excess T3
  • Drug-induced (e.g. Amiodarone, Lithium)
  • Subacute thyroiditis
    • Due to Infections, drug-induced, early Hashimoto’s disease
    • Release of stored hormone
66
Q

what are the Signs and symptoms of hyperthyroidism?

A

just rmb: Everything speeds up

  • Weight loss or increased appetite
  • Heat intolerance
  • Goiter
  • Fine hair
  • Heart palpitations or tachycardia
  • Nervousness, anxiety, insomnia
  • Menstrual disturbances (lighter or more infrequent menstruation, amenorrhea)
  • Sweating or warm, moist skin
  • Exophthalmos (protruding eyeball) in Graves disease
67
Q

how to diagnose hyperthyroidism?

A
  • Signs and symptoms
  • Lab tests
    • Elevated free T4 serum concentrations
    • Suppressed TSH concentrations due to negative feedback
      • Except in TSH-secreting adenomas
    • Radioactive iodine uptake (RAIU)
      • Measures thyroid gland’s ability to take up and trap radioactive iodine, which is a precursor to TH synthesis
      • High RAIU: Gland is actively secreting TH
        • Graves disease
        • TSH -secreting adenoma
        • Toxic adenoma
        • Multinodular goiter
      • Low RAIU: Disorders caused by thyroiditis or cancer
    • Presence of TRAb, ATgA, TPO to identify autoimmune causes of hyperthyroidism
    • Biopsy to identify any thyroid nodule that may be associated with cancer
68
Q

what are the Goals of therapy of hyperthyroidism?

A
  • Minimize or eliminate symptoms —> Improve QOL
  • Minimize long-term damage to organs (Heart disease, arrhythmias, sudden cardiac death, bone demineralisation, fractures)
  • Normalize free T4 and TSH concentrations
69
Q

need lifelong treatment for hyperthyroidism?

A

Might not need lifelong treatment

70
Q

what are the surgical ways to treat hyperthyroidism?

A
  • Thyroidectomy
    • SUPER SUPER HIGH RISK OF hypothyroidism as remove thyroid gland
  • Surgical resection
    • BUTBUTBUT high risk of hypothyroidism
  • Radioactive iodine (RAI) ablative therapy
    • BUTBUTBUT high (tho lesser than surgery) risk of hypothyroidism due to destroying parts of thyroid gland
    • First line option if no contraindications for Graves Disease
    • Colourless, tasteless liquid in a capsule that will concentrate in thyroid tissue
      • Destroys overactive thyroid cells
      • NOT FOR PREGGOS if not will travel to fetus
71
Q

what are the antithyroid pharmacology for hyperthyroidism?

A
  1. Thionamides: Carbimazole & Propylthiouracil
  2. Non-selective beta-blockers: Propranolol
  3. Iodides
72
Q

how does Antithyroid pharmacotherapy for hyperthyroidism work?

A
  • Reduces production of TH
  • Depletes stored hormone
73
Q

when to use Antithyroid pharmacotherapy for hyperthyroidism?

A
  • Awaiting ablative (extremely high or low temp to destroy (ablate) abnormal tissue) therapy or surgical resection
    • Minimizes risk of post-ablation hyperthyroidism caused by thyroiditis since ablative therapy can trigger temporary increase in TH release
  • Alternative option for Non- ablative or surgical candidates or failed to normalize thyroid
  • Mild disease/ small goiter/ low or negative antibody titers /women
  • Limited life expectancy so used to manage for the remainder of life
74
Q

how does Thionamides: Carbimazole & Propylthiouracil for treatment of hyperthyroidism?

A
  • Acts as substrate for TPO to inhibit iodination and synthesis of TH
  • Bonus: High dosed PTU blocks T4/T3 conversion in the periphery
75
Q

what is the dosing for carbimazole for treatmennt of hyperthyroidism?

A
  • Preferred for Graves
  • Longer half life so can take lesser doses
  • Initial: 15-60mg OD in 2-3 divided doses
  • Once euthyroid, reduce to 5-15mg OD
76
Q

what is the dosing for Propylthiouracil for treatmennt of hyperthyroidism?

A
  • Initial: 50–150mg PO TDS
  • Once euthyroid, reduce to 50mg BD or TDS
77
Q

what are the adrs for Thionamides: Carbimazole & Propylthiouracil for treatmennt of hyperthyroidism?

A
  • Hepatotoxicity risk!!!
    • Boxed warning for PTU so carbimazole first line
  • Rash
    • Risk for SJS
  • Agranulocytosis (neutrophil insufficiency) early in therapy (usually within 3 months)
  • Fever
78
Q

how is the onset for Thionamides: Carbimazole & Propylthiouracil for treatmennt of hyperthyroidism?

A
  • Slow onset (weeks) in reducing symptoms
    • Maximal effect may take 4–6 months as inhibiting synthesis of TH, so dont do anything about stored TH
79
Q

how is the efficacy for Thionamides: Carbimazole & Propylthiouracil for treatmennt of hyperthyroidism?

A
  • Remission rates low: 20%–30%
  • Remission: Normal TSH and T4 for 1 year after discontinuing antithyroid therapy
80
Q

how are the dosage titrations done for Thionamides: Carbimazole & Propylthiouracil for treatmennt of hyperthyroidism?

A
  • Monthly dosage titrations as needed (based on symptoms and free T4 conc)
    • TSH may remain suppressed for months after therapy begins
    • Early in therapy: Total T3 may be better marker of efficacy than free T4
81
Q

how does Non-selective beta-blockers: Propranolol work for treatment of hyperthyroidism?

A
  • Blocks many hyperthyroidism manifestations mediated by beta-adrenergic receptors
  • High dosed blocks T4/T3 conversion in the periphery
82
Q

when is Non-selective beta-blockers: Propranolol used for in the treatment of hyperthyroidism?

A
  • Symptomatic relief
  • Bridging therapy for thionamide effects to kick in/ before ablation/ surgery
  • PRN for high risk patients (eg. elderly with CV disease)
  • Treatment of thyroiditis (though self-limiting)
83
Q

what is iodides made of when used in the treatment of hyperthyroidism?

A

Lugol’s solution, saturated solution of potassium iodide

84
Q

how does iodides work when used in the treatment of hyperthyroidism?

A
  • Inhibits release of stored TH by saturating thyroid gland with iodine
  • Minimal effect on TH synthesis
  • Helps decrease vascularity (blood flow) and size of gland
85
Q

when is iodides used in the treatment of hyperthyroidism?

A
  • Before surgery (7–10 days) to shrink gland
  • After ablative therapy (3–7 days) to inhibit thyroiditis-mediated release of stored TH
    • Because after surgery thyroid gland is normally hyperactive for awhile
  • Thyroid storm (severe hyperthyroidism)
86
Q

why is there limited efficacy for iodides when used in the treatment of hyperthyroidism?

A

Limited efficacy after 7–14 days of therapy as body will overcome the drugs effects… sigh

87
Q

why dont use ablative rai before taking iodines when used in the treatment of hyperthyroidism?

A
  • Do not use before ablative RAI as may reduce uptake of radioactive iodine which is needed to destroy thyroid tissue
88
Q

what are the main symptoms of Pregnancy: Maternal hyperthyroidism

A
  • Failure to gain weight despite good appetite
  • Tachycardia
89
Q

what if dont treat materinal hyperthyroidisM?

A
  • Fetal loss if untreated (miscarriage)
    • BUT NOTE THAT thionamides have risk of embryopathy (abnormality)
90
Q

how to treat maternal hyperthyroidisM?

A
  • Treatment: Use lowest possible dose; keep T4 at
    upper-normal limit
    • 1st Trimester: Use PTU as Carbimazole has
      higher risk of congenital malformations
    • 2nd and 3rd Trimesters: Use Carbimazole as
      PTU has higher risk of hepatotoxicity
91
Q

what is subclinical hyperthyroidisM?

A

Low or undetectable TSH with normal T4

92
Q

what is the risk of subclinical hyperthyroidism?

A
  • Elevated risk of AF in patients >60 years old
  • Elevated risk of bone fracture in postmenopausal women

If untreated, screen regularly for the development of overt hyperthyroidism

93
Q

how to treat subclinical hyperthyroidism?

A
  • Similar to overt hyperthyroidism except oral therapy over ablative therapy for young patients
  • More compelling if TSH < 0.10 mIU/L
  • Beta blocker especially if AF
94
Q

what are the 3 drugs that cause drug induced thyroid disease?

A
  1. amiodarone*
  2. lithium
  3. interferon alfa
95
Q

how does amiodarone cause drug induced thyroid disease?

A
  • Structure contains iodine
  • MOA
    • Affects iodine uptake, secretion, production of hormones
    • Causes thyroiditis (inflammation of thyroid gland)
  • May cause hypo- or hyperthyroidism
96
Q

how does lithium cause drug induced thyroid disease?

A
  • MOA
    • Inhibits TH secretion and release —> Signalling an increase in TSH and possible goiter development (hypo)
  • Thyroiditis (hyper)
97
Q

how does interferon alfa cause drug induced thyroid disease?

A

Thyroiditis (hyper then hypo)

finals (8 decks)

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