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PR3152: Immune & Endocrine Systems > Thyroid Disorders > Flashcards

Thyroid Disorders Flashcards

1
Q

What shape is the thyroid gland?

A

Butterfly

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2
Q

Physiological functions regulated by thyroid hormone (TH)

A

Increase consumption by most tissues, increase basal metabolic rate

  1. Body temp
  2. CNS
  3. Sleep
  4. Cardiac func
  5. GI func
  6. Muscle strength
  7. Breathing
  8. Menstrual cycle
  9. Skin dryness
  10. Incr lipid metabolism
  11. Incr uptake and utilisation of glucose
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3
Q

What is the negative feedback that stops overprdtn of TH

A

1) Hypothalamus detects when circulating THs are low and will release thyrotropin-releasing hormone (TRH)
2)TRH instructs pituitary to release TSH
3) TSH instructs thyroid gland to secrete THs
4) Elevated levels of circulating THs in blood -> Hypothalamus senses and stop releasing TRH.

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4
Q

Are TSH levels elevated or low in primary hypothyroidism?

A

Elevated.

Hypothalamus will detect persistently low levels of THs and secrete TRH which will instruct pituitary to secrete TSH (which will unsuccessfully try to stimulate thyroid gland to secrete THs).

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5
Q

Are TSH levels elevated or low in primary hyperthyroidism?

A

Low

Hypothalamus will detect persistently elevated levels of thyroid hormones and no longer secrete TRH and so pituitary will not receive instructions to secrete TSH. Thyroid gland is functioning independently (of TSH levels), continue to secrete TH, leaving to symptoms.

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6
Q

What are the 2 ways which TH levels are regulated?

A

Negative feedback
Peripheral conversion of T4 to T3

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7
Q

Wha is the ratio of T4 : T3 released into circulation? Why?

A

T4:T3 = 4:1

T3 is degraded faster, shorter 1/2 than T4

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8
Q

T4 or T3 more potent?

A

T3

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9
Q

What needs to be consumed for prdtn of thyroid hormones?

A

Iodine consumption is essential for the production of thyroid hormones and must be obtained exogenously. Eg. seaweed, seafood. SG add iodine into salt to prevent iodine deficiency.

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10
Q

During routine tests, T4 or T3 is measured?

A

Free T4.

T3 is not routinely ordered as half life is short so tends to be more erratic/inconsistent and may not be representative of TH stores in body.

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11
Q

Are T4 and T3 protein bound?

A

Yes, >99%

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12
Q

When are thyroxine binding globulin (TBG) levels elevated?

A

Pregnancy or on estrogen- oral contraceptives

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13
Q

When TBG levels elevated, how will the body respond?

A
  • FT3 & FT4 levels will go down because more of T3 & T4 will bind to the extra TBG so cannot exert as much physiological effects since free lvls are decreased.
  • Hypothalamus detects this and TSH will be released and will instruct TG to release more THs Levels of FT3 and FT4 will return to normal (New equilibrium is achieved).
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14
Q

What antibodies are tested for autoimmunity (i.e immune system attacks thyroid gland causing incr/decr prdtn of TH)

A

ATgA, TPO, TRAb

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15
Q

What compelling indications calls for screening?

A

1) Presence of autoimmune disease (eg. T1DM, cystic fibrosis)
2) First-degree relative with autoimmune thyroid disease
3) Psychiatric disorders -> thyroid abnormalities can induce mood, anxiety etc so check if thyroid got problem (is this the RC?) instead of treating the psychiatric problem.
4) Taking amiodarone or lithium
5) Hx of head / neck radiation for malignancies
6) Symptoms of hypothyroidism / hyperthyroidism.

Routine screening required for pediatric patients and pregnant women as thyroid abnormalities affect developmental issues.

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16
Q

Primary causes of hypothyroidism

A
  • Iodine deficiency (most common cause worldwide) - cant form TH
  • Hashimoto disease: Most common hypothyroid disorder in areas with iodine sufficiency aka chronic autoimmune thyroiditis:
    (+) ATgA and TPO antibodies => disproportionately affects women
  • Iatrogenic: Thyroid resection (portion or completely) or radioiodine ablative therapy for hyperthyroidism
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17
Q

Secondary causes of hypothyroidism

A
  • Central hypothyroidism => hypothalamus unable to secrete TRH or pituitary unable to secrete TSH (TSH low, T4 low)
  • Drug induced (e.g., amiodarone, lithium)
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18
Q

S&S of hypothyroidism

A
  • Cold intolerance
  • Dry skin
  • Fatigue, lethargy, weakness
  • Weight gain
  • Bradycardia
  • Slow reflexes
  • Coarse/thick skin and hair
  • Periorbital swelling
  • Menstrual disturbances (more frequent, more blood)–> more painful cramps
  • Goiter
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19
Q

Clinical manifestation of hypothyroidism

A
  • ↑ Total cholesterol, LDL, Triglycerides (high CV risk)
  • ↑ Atherosclerosis, MI risk
  • Creatine phosphokinase (CPK) levels ↑ - statins also increases this so much check if its due to thyroid issue or statin use.
  • ↑ Miscarriage risk
  • Impaired fetal development.
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20
Q

How to diagnose hypothyroidism

A
  • Signs & symptoms / Screening
  • Labs:
    1° hypothyroidism: ↑TSH, ↓ T4 or Positive antibodies (TPO, ATgA)
    Central hypothyroidism (pituitary problem): ↓TSH, ↓ T4
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21
Q

Goals of therapy for hypothyroidism

A
  • Minimize or eliminate symptoms; improve quality of life
  • Minimize long-term damage to organs (myxedema coma, heart disease)
  • Prevent neurologic deficits in newborns and children
  • Normalize free T4 and TSH concentrations.
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22
Q

What is the drug of choice for hypothyroidism?

A

Levothyroxine

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23
Q

Does levothyroxine mimic T3 or T4?

A

It is synthetic T4

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24
Q

Initial Dose of levothyroxine

A
  • Young, healthy adults => 1.6 mcg/kg/d
  • 50-60 years of age and no cardiac issues => 50 mcg daily
  • With CVD (high cholesterol, Hx of MI etc) => 12.5-25 mcg/d and titrate up
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25
Q

Titration of levothyroxine

A
  • Depends on response (control of symptoms, normalization of TSH and T4)
  • Can increase or decrease in 12.5- to 25-mcg/day increments, or in 10%–15% of weekly dose.
  • Available in 25μg, 50μg, 75μg, 100μg.
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26
Q

When should levothyroxine be taken?

A
  • 30-60 minutes before breakfast (take it the moment you wake up) or 4 hours after dinner (empty stomach)
  • This includes other medications
  • Special attention to calcium or iron supplements and antacids => need to space at least 2 hours apart (milk, tofu too!)
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27
Q

When and what to monitor after starting levothyroxine

A
  • 4-8 weeks to assess response in TSH (takes time) after initiating or changing therapy
  • Symptomatic relief (2-3 weeks)
28
Q

What is the general target for hypothyroidism

A

General target TSH: 0.4 to 4 mIU/L. (FT4 = 0.8-2.7ng/dL)

29
Q

What does normalization of FT4 with consistently ↑ TSH hints at?

A

Non-adherence.

30
Q

Is levothyroxine treatment lifelong?

A

Yes esp if resection

31
Q

Does TSH levels increase in older people?

A

Yes but we still dont titrate upwards

32
Q

SE of over replacing thyroxine levels

A
  • Cardiac abnormalities (tachyarrhythmias, angina, myocardial infarction)
  • Risk of fractures
  • Signs of hyperthyroidism (duh!)
33
Q

After euthyroid state, TFT are recommended how often?

A

every 6-12months in nonpreg adults

34
Q

What is liothyronine and what is it used for?

A

Synthetic T3, Hypothyroidism

35
Q

Why is liothyronine rarely used and when is the rare case that it will be used?

A

High incidence of adverse effects eg. incr Afib

Can be considered in Myxedema coma or when pt needs to go for CT scan and need to stop replacement TH, can switch to this for the time being due to shorter t1/2

36
Q

What is the effect of hypothyroidism during pregnancy

A
  • Miscarriage, spontaneous abortion
  • Congenital defects, impaired cognitive development
37
Q

Dose of levothyroxine for pregnant women

A

30-50% increase in pre- pregnant dosage to maintain euthyroid status due to increases TBG

38
Q

What is the target TSH levels for different trimesters?

A

1st trimester: < 2.5 mIU/L
2nd trimester: < 3.0 mIU/L
3rd trimester: <3.5 mIU/L

39
Q

What is subclinical hypothyroidism?

A

“mild form of hypothyroidism”

Elevated TSH with normal T4. Usually a result of early Hashimoto disease

40
Q

Who is at risk of subclinical hypothyroidism?

A
  • TSH greater than 7.0 mIU/L in older adults -> elevated risk of heart failure
  • TSH greater than 10 mIU/L -> elevated risk of coronary heart disease
41
Q

When should you consider treating subclinical hypothyroidism?

A
  • TSH > 10 mIU/L (widely accepted)
  • TSH 4.5–10 mIU/L and:
    Symptoms of hypothyroidism
    TPO present
    History of cardiovascular disease, heart failure, or risk factors for such
  • Initial daily doses of 25–75 mcg recommend (low doses first)

If untreated, screen regularly for the development of overt hypothyroidism (actual hypothyroidism- high TSH, low T4)

42
Q

Causes of hyperthyroidism

A
  • Toxic diffuse goiter (Graves disease): Most common hyperthyroid disorder: Thyroid receptor antibodies (TRAb) that mimic TSH => stimulate TH production
  • Pituitary adenomas
  • Toxic adenoma (hot nodule): Solitary functioning nodule that secrete T3
  • Toxic multi-nodular goiter (Plummer’s Disease): multiple nodules that secrete T3
  • Drugs induced (e.g., amiodarone, lithium)
  • Subacute thyroiditis (“bursts” and lots of TH gets released)
43
Q

S&S of hyperthyroidism

A
  • Weight loss or increased appetite
  • Heat intolerance
  • Goiter (not as common but is due to nodules growing)
  • Fine hair
  • Heart palpitations or tachycardia
  • Nervousness, anxiety, insomnia
  • Menstrual disturbances (lighter or more infrequent menstruation, amenorrhea, less cramps)
  • Sweating or warm, moist skin
  • Exophthalmos in Graves disease, bulging eyes
44
Q

How to diagnose hyperthyroidism?

A
  • Signs and symptoms
  • Elevated free T4 serum concentrations
  • Suppressed TSH concentrations (except in TSH-secreting adenomas)
  • Radioactive iodine uptake (RAIU) can be used for better etiology -> ultrasound scan to check if got uptake of iodine:
    Uptake elevated if gland is actively secreting TH: Graves disease, TSH-secreting adenoma, toxic adenoma, multinodular goiter
    Uptake suppressed in disorders caused by thyroiditis or cancer (cancer cells does not need iodine anymore, just keep producing TH on its own)
  • Presence of TRAb, ATgA, TPO
  • Biopsy (invasive)
45
Q

Goals of therapy of hyperthyroidism

A
  • Minimize or eliminate symptoms, improve quality of life
  • Minimize long-term damage to organs (heart disease, arrhythmias, sudden cardiac death, bone demineralization, and fractures)
  • Normalize free T4 and TSH concentration
46
Q

Treatment option for hyperthyroidism

A
  • Surgical resection; often results in hypothyroidism (1st line)
  • Radioactive iodine (RAI) ablative therapy; often results in hypothyroidism (high doses):
    Colorless, tasteless liquid in a capsule that will concentrate in thyroid tissue:
    Destroys overactive thyroid cells
    Pregnancy = absolute contraindication -> cannot give to baby
  • Thyroidectomy; definitely results in hypothyroidism (remove completely, must be on levo for life)
  • Antithyroid pharmacotherapy (usually not LT, rare, last line):
    Thionamides
    Iodides
    Non-selective beta-blockers
  • Try to solve RC instead eg. cut off nodule/adenoma, resection etc
47
Q

What is first line for hyperthyroidism?

A

Surgical resection

48
Q

When is antithyroid pharmacotx considered for hyperthyroidism

A
  • Those awaiting ablative therapy or surgical resection:
    Depletes stored hormone (cause you gg to “burst” the TG -> can lead to hyper due to released of all the stored hormone)
    Minimizes risk of post-ablation hyperthyroidism caused by thyroiditis
  • Not ablative or surgical candidates / failed to normalize thyroid
  • Mild disease - no use gg through surgery / small goiter / low or negative antibody titers / women- tend to do btr than men
  • Limited life expectancy (too old, no point resectioning)

Surgery is CI in pregnancy and too young/old

49
Q

What is unconvenient about ablative/radioactive therapy?

A

Pts must be isolated

50
Q

What are the 2 common thionamides given for hyperthyroidism?

A

Carbimazole and Propythiouracil (PTU)

51
Q

MOA of thionamide

A

Inhibits iodination and synthesis of thyroid hormones; PTU can additionally block T4/T3 conversion in the periphery at high doses

52
Q

Dose of thionamides

A
  • PTU - Initial: 50–150 mg by mouth three times daily; once euthyroid, can reduce to 50 mg two or three times daily
  • Carbimazole (preferred for Graves for most patients) – Initial: 15-60 mg daily in 2-3 divided doses; once euthyroid, can reduce to 5-15 mg once daily
53
Q

Which thionamide is preferred in Graves disease?

A

Carbimazole

54
Q

SE of thionamides

A
  • Hepatotoxicity risk (boxed warning for PTU)
  • Rash – risk for SJS
  • Agranulocytosis (low WBC count) early in therapy (usually within 3 months)
  • Fever
55
Q

How long does thionamides take effect?

A

Slow onset in reducing symptoms (weeks) - low efficacy. Maximal effect may take 4–6 months due to their MOA

56
Q

Thionamides efficacy monitoring

A
  • Remission rates low: 20%–30%. Remission is defined as normal TSH and T4 for 1 year after discontinuing antithyroid therapy
  • Monthly dosage titrations as needed (depending on symptoms and free T4 concentrations):
    TSH may remain suppressed for months after therapy begins
    Early in therapy, total T3 maybe better marker of efficacy than free T4
    Do not look at TSH as it takes a long time (1-2yrs), look at T4 instead.
57
Q

2 main smx of hyperthyroidism in pregnancy

A

Failure to gain weight despite good appetite
Tachycardia

58
Q

How to treat hyperthyroidism in pregnancy

A

Use lowest possible dose; keep T4 at upper-normal limit:
- 1st Trimester: Use PTU as Carbimazole have higher risk of congenital malformations. 1st trimester is whr infant organs are alr formed
- 2nd and 3rd Trimesters: Use Carbimazole (Preg Class D) as PTU have higher risk of hepatotoxicity and yet less potent.

59
Q

Non-selective BB place therapy in hyperthyroidism

A
  • Symptomatic relief (not solving RC but since carbimazole takes months to work, BB provides symptomatic relief in the time being)
  • Bridging therapy for Thionamides effects to kick in / before ablation / surgery
  • PRN for high risk patients – elderly with CVS disease
  • Treatment of thyroiditis, which is usually self-limiting
60
Q

Which non-selective BB is used in hyperthyroidism? and its MOA

A

Propranolol

MOA: Blocks many hyperthyroidism manifestations mediated by β- adrenergic receptors; also may block T4 conversion to T3 when used at high dose

61
Q

Iodides place in therapy in hyperthyroidism

A
  • Before Surgery (7–10 days) to shrink the gland
  • After ablative therapy (3–7 days) to inhibit thyroiditis-mediated release of stored TH
  • Thyroid storm
62
Q

What to take note of when using iodides

A
  • Limited efficacy after 7–14 days of therapy as TH release will resume
  • Do not use before ablative RAI (may reduce uptake of radioactive iodine since both are similar).
63
Q

What is subclinical hyperthyroidism

A

Low or undetectable TSH with normal T4

64
Q

What is the risk of subclinical hyperthyroidism

A
  • Elevated risk of AF in patients older than 60
  • Elevated risk of bone fracture in postmenopausal women
  • Conflicting data about mortality risk
65
Q

How to treat subclinical hyperthyroidism

A
  • Similar to overt hyperthyroidism except oral therapy alternative to ablative therapy in young patients
  • More compelling if TSH < 0.10 mIU/L
  • BB esp if AF
66
Q

Common drugs that induce thyroid disease

A

Amiodarone: Afib
- Contains iodine in its chemical structure
- Affects iodine update, secretion, production; causes thyroiditis
- May cause hypo- or hyperthyroidism

Lithium: mood stabiliser
- Inhibits thyroid hormone secretion and release, thus signaling an increase in TSH and possible goiter development (hypo)
- Thyroiditis (hyper)

Interferon alfa: Hep C
- Thyroiditis (hyper then hypo)

PR3152: Immune & Endocrine Systems (7 decks)

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