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endo y3s1 > IC15 Thyroid disorders > Flashcards

IC15 Thyroid disorders Flashcards

1
Q

Physiologic functions regulated by TH

A

Main: Oxygen consumption by tissues, basal metabolic rate, lipid metabolism, uptake & utilisation of glucose

Others: Body temperature, CNS, sleep, cardiac & GI functions, muscle strength, breathing, menstrual cycle, skin dryness

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2
Q

TSH
causes of change in levels

A

Primary causes of conditions → involves thyroid gland pathology
Secondary ⇒ glands work normally; other factors causes hyper/ hypothyroidism

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3
Q

TSH
primary hypothyroidism

Level & reasons

A

Hypothalamus detect persistently low levels of THs & secretes TRH

TRH instructs pituitary to secrete TSH
* Elevation of TSH supposed to increase TH levels
* However, thyroid gland dysfunction does not allow for stimulation & secretion of THs

TSH continuously increase ⇒ elevated levels

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4
Q

TSH
primary hyperthyroidism

Levels & reasons

A

Hypothalamus detect persistently elevated levels of THs & no longer secretes TRH

No TRH to instruct pituitary to secrete TSH
* Drop in TSH supposed to decrease TH levels
* However, thyroid gland is functioning independently of TSH → not affected by low TSH

TRH not secreted due to high TH ⇒ TSH low levels

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5
Q

TH: T3

how its derived, t1/2, protein binding

A

derived from peripheral conversion of T4 by de-ionidination via deiodinases

t1/2 = 2 days; highly protein bound

Irregular, may not be representative of TH stores in body

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6
Q

TH: T4

t1/2, FT4

A

t1/2 = 6-7 days; highly protein bound

FT4 → unbound & routinely ordered with TSH to evaluate thyroid status

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7
Q

elevated TBG & effects

A
  1. lower free T3 [FT3] & free T4 [FT4] levels due to more T3 & T4 binding to extra TBG
    (Due to pregnancy/ on oestrogen)
  2. TSH released will instruct thyroid glands to release more THs
  3. Hence levels of FT3 & FT4 return to normal ⇒ achieve new equilibrium
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8
Q

Antibodies for testing

non-specific & specific

A

non-specific
ATgA: thyroglobulin Ab
TPO: thyroperoxidase Ab (significantly associated with hypothyroidism)

Diseases with (+) ATgA & TPO ⇒ 95% of Hashimoto; 60-70% of Graves’

Specific
TRAb: thyrotropin receptor IgG Ab
Confirmatory for graves’ disease but expensive
Ab continuously trigger receptors ⇒ TG continuously produce TH

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9
Q

screening
compelling indications

A
  • Presence of autoimmune disease (eg. T1DM, cystic fibrosis)
  • First-degree relative with autoimmune thyroid disease
  • Psychiatric disorders:
    Thyroid abnormalities can induce mood, anxiety, psychosis etc
    Important to determine root causes of psychiatric conditions
  • Taking amiodarone (anti-arrhythmic) or lithium (psychiatric drug)
  • Hx of head / neck radiation for malignancies
  • Symptoms of hypothyroidism / hyperthyroidism
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10
Q

screening
individuals recommended

A

paediatrics & pregnant women
thyroid hormones required for growth & development

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11
Q

hypothyroidism
causes: primary

A

Iodine deficiency → most common
Hashimoto disease (chronic autoimmune thyroiditis)
Most common in areas with iodine sufficiency

(+) ATgA & TPO Ab → disproportionately affects women

Latrogenic: thyroid resection/ radioiodine ablative therapy for hyperthyroidism
Removing too much thyroid glands; lesser TH produced now

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12
Q

hypothyroidism
causes: secondary

A

Central hypothyroidism
* hypothalamus unable to secrete TRH
* Pituitary unable to secrete TSH

Drug induced: amiodarone, lithium

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13
Q

hypothyroidism
signs & symptoms

CD, G, FWB, SCMP

A

General: Slowing down of body functions

Cold intolerance, Dry skin

Fatigue, lethargy, weakness, Weight gain, Bradycardia

Slow reflexes, Coarse skin and hair, Menstrual disturbances (more frequent, more blood), Periorbital swelling [edema]

Goiter

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14
Q

clinical manifestations of hypothyroidism

increased risks

A

Total cholesterol, LDL & triglycerides
ASCVD & MI
Miscarriage
impaired fetal development

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15
Q

cases of concern in hypothyroidism

A

pregnancy
subclinical hypothyroidism

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16
Q

diagnosis of hypothtyroidism

primary & secondary (labs)

A

Primary hypothyroidism
↑TSH, ↓ T4
Positive antibodies (TPO, ATgA)
Central hypothyroidism (secondary)
↓TSH, ↓ T4

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17
Q

cases of concern in hypothyroidism
pregnancy

risks, maternal TH, women on levothyroxine

A

Effects:
* Miscarriage, spontaneous abortion
* Congenital defects, impaired cognitive development
* Maternal THs provide fetus with TH for up to 12 weeks
Fetus TH production only occurs after formation of own thyroid glands
Important for metabolism

Pregnant women on levothyroxine → may need 30-50% increase in pre-pregnant dose to maintain euthyroid status

Target TSH
1st tri: <2.5 mIU/ L
2nd tri: <3.0 mIU/ L
3rd tri: <3.5 mIU/ L

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18
Q

cases of concern in hypothyroidism
subclinical hypothyroidism

increases risks, when to start therapy

A

Elevated risk
TSH >7.0 mIU/L in older adults → heart failure
TSH >10 mIU/L → coronary heart disease
Considerations for treatment for 25-75 mcg OD:
* TSH >10 mIU/L
* TSH 4.5-10 mIU/L and
Symptoms of hypothyroidism
TPO Ab present
History of CVD, HF or risk factors

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19
Q

hypothyroidism drugs

A
  1. Levothyroxine
  2. Liothyronine
20
Q

hypothyroidism drugs
levothyroxine

initial dosing & titration

A

Initial dosing
* Young, healthy adults: 1.6 mcg/ kg/ day
Usually just start at 100 mcg OD
* With CVD: 12.5-25 mcg OD & titrate up
Should be lower, if not may cause cardiac stress ⇒ start low & go slow
Titration
* Depends on response → control of symptoms, normalisation of TSH & TH
Takes weeks to reduce symptoms & improve physiologically
Can increase/ decrease in 12.5 - 25 mcg OD or in 10-15% of weekly dose

21
Q

hypothyroidism drugs
levothyroxine

when to take

A

30-60 mins before breakfast OR 4 hours after dinner ⇒ on empty stomach

Note: Ca or Fe supplements & antacids ⇒ to space at least 2 hours apart

22
Q

hypothyroidism drugs
levothyroxine

monitoring, ideal TSH, euthyroid state

A
  • 4-8 weeks to assess response in TSH after initiating/ changing therapy
  • General target TSH (younger adults): 0.4-4 mIU/ L
  • For central hypothyroidism: use FT4 levels
  • TSH target for older adults: higher TSH can still be WNL (>70 yo: up to 6.9 mIU/L)
  • Symptomatic relief (in 2-3 weeks)
  • Normalisation of FT4 with consistently increasing TSH → likely non-adherence

Euthyroid state: Thyroid function tests (TFT) → recommended semi annually - annually in non-pregnant adult patients

23
Q

hypothyroidism drugs
levothyroxine

AE

A

Cardiac abnormalities → tachyarrhythmias, angina, MI
Risks of fractures
Signs of hyperthyroidism

24
Q

hypothyroidism drugs
liothyronine

indication

A

if deiodination not working properly
if TH required in short time frame (ie surgery)
If patient in myxedema coma ⇒ drug is more potent

25
Q

hypothyroidism drugs
liothyronine

t1/2

A

t1/2 = 1-2.5 days
Much shorter than T4; more difficult to achieve stable state

26
Q

hypothyroidism drugs
liothyronine

initial dosing

A

Young, healthy adult: 25 mcg
elderly/ CVD patients: 5 mcg

27
Q

hypothyroidism drugs
liothyronine

AE

A

High incidence of hyperthyroid symptoms

28
Q

hyperthyroidism Causes

A

Graves disease (toxic diffuse goiter) → most common
* TSH receptor Ab [TRAb; aka TSI] mimic TSH binding ⇒ TSI subtype stimulates TH production

Pituitary adenomas: increased TSH ⇒ stimulates more TH
Toxic adenoma (hot nodule): Solitary functioning nodule that secrete T3
Toxic multinodular goiter (Plummer’s Disease): multiple nodules that secrete T3
Drug induced: amiodarone, lithium
Subacute thyroiditis: infections, drug induced, early Hashimoto’s disease
* Results in the release of stored hormone; large amounts at once

29
Q

hyperthyroidism signs & symptoms

THYROIDISM E

A

Tremor
Heart rate up
Yawning (fatigability)
Restlessness
Oligomenorrhea & amenorrhea
* Menstrual disturbances; lighter/ more infrequent menstruation

Intolerance to heat
Diarrhoea
Irritability
Sweating
Muscle wasting & weight loss
Exophthalmos (protruding eyeballs) → in Graves disease

30
Q

hyperthyroidism lab results

A
  • Elevated free T4 serum concentrations
  • Suppressed TSH concentrations (except in TSH-secreting adenomas)
  • Radioactive iodine uptake (RAIU) → used for better etiology
    Uptake elevated if gland is actively secreting TH: Graves disease, TSH-secreting adenoma, toxic adenoma, multinodular goiter
    Requires more iodine for formation of more TH
    Uptake suppressed in disorders caused by thyroiditis/ cancer
  • Presence of TRAb, ATgA, TPO
31
Q

hyperthyroidism causing elevated risks

A

AF in patients > 60 years
Bone fracture in postmenopausal women

32
Q

hyperthyroidism goals of therapy

A

Minimise/ eliminate symptoms; improve quality of life
Minimise long-term damage to organs
Normalise free T4 and TSH concentrations

33
Q

hyperthyroidism non-pharmacological treatments

A
  1. Surgical resection
  2. Radioactive iodine (RAI) ablative therapy
  3. Thyroidectomy
34
Q

hyperthyroidism
purpose of radioactive ablation

indication, c/i

A

First line option if no contraindications for Graves Disease
Destroys part of thyroid
Decreases signs of hyperthyroidism

Colourless, tasteless liquid in a capsule; concentrates in thyroid tissue
Destroys overactive thyroid cells

Pregnancy = absolute contraindication (can cross to fetus)

34
Q

hyperthyroidism indication for pharmacological therapy

A
  • Those waiting for ablative therapy/ surgical resection
    Depletes stored hormones
    Minimises risks of post-ablation hyperthyroidism caused by thyroiditis
  • Those cannot have ablative/ surgery/ failed to normalise thyroid
  • Mild disease/ small goiter/ low or negative Ab titres/ women
  • Limited life expectancy
34
Q

hyperthyroidism types of pharmacological therapy

A
  1. thionamides (carbimazole & PTU)
  2. non-selective BB (propanolol)
  3. iodine (lugol’s solution)
35
Q

hyperthyroidism therapy
thionamides (carbimazole & PTU)

MOA

A

Inhibits iodination & synthesis of TH by acting as substrate for TPO
PTU → also blocks T4/ T3 conversion in periphery at high doses

35
Q

hyperthyroidism
thionamides (carbimazole & PTU)

dosing: initial & euthyroid

A

Carbimazole
Initial: 15-60 mg daily in 2-3 divided doses
Euthyroid: reduce to 5-15 mg OD
Once physiological function & symptoms improve, may be able to stop treatment → requires ~ 1 year

PTU
Initial: 50-150 mg PO TDS
Euthyroid: reduce to 50 mg BD-TDS

35
Q

hyperthyroidism
thionamides (carbimazole & PTU)

AE

A
  • Hepatotoxicity risk (boxed warning for PTU → carbimazole first line)
  • Rash → risks for SJS
  • Agranulocytosis early in therapy (usually within 3 months)
  • Fever
35
Q

hyperthyroidism
thionamides (carbimazole & PTU)

efficacy, remission rates, dose titration (&monitoring)

A

Maximal effect may take 4-6 months
* Due to TH being stored in TG that still can be released & cause high levels of TH
* Important to clear first, which takes time

Remission rates low

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

36
Q

hyperthyroidism
thionamides (carbimazole & PTU): pregnancy

symptoms, importance & choice based on trimester

A

Symptoms:
* Failure to gain weight despite good appetite
* Tachycardia

Will have fetus loss if remain untreated → note that thioamides have risks of embryopathy

Important to use lowest possible dose & keep T4 at ULN
1st tri: use PTU, carbimazole ⇒ higher risks of congenital malformations
2nd & 3rd tri: use carbimazole, PTU ⇒ higher risks of hepatotoxicity

36
Q

hyperthyroidism
propanolol

MOA

A

Blocks hyperthyroidism manifestations mediated by b-adrenergic receptors
May block T4/ T3 conversion when used at high dose

37
Q

hyperthyroidism
propanolol

place in therapy

A
  • Symptomatic relief (ie: tachycardia)
  • Bridging therapy for thioamide effects to take place
  • Before ablation/ surgery
  • PRN for high risk patients → elderly with CVD, AF
  • Treatment for thyroiditis (usually self-limiting)
38
Q

hyperthyroidism
iodine solution

MOA

A

Inhibits release of stored THs
Helps decrease vascularity & size of gland

39
Q

hyperthyroidism
iodine solution

place in therapy

A

Before surgery (7-10 days) ⇒ shrink gland
After ablative therapy (3-7 days) ⇒ inhibit thyroiditis-mediated release of stored TH
Thyroid storm

40
Q

hyperthyroidism
iodine solution

efficacy duration, what to avoid

A

Limited efficacy after 7-14 days → TH release will resume

Do not use before ablative RAI
May reduce uptake of RAI

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