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MBBS VI Medicine > Teaching Clinic - Hypothyroidism > Flashcards

Teaching Clinic - Hypothyroidism Flashcards

1
Q

Where is T3 and T4 from?

A

• All the T4 in the circulation is derived from thyroid secretion whereas only 20% to 30% of circulating T3 is of thyroidal origin
• Normal mean daily T4 secretion is between 100 and 125 nmol (80 - 100 ug) which is entirely derived from the thyroid
• At least 2/3 of daily mean T3 production is derived from peripheral conversion of T4
• In situations of environmental iodine deficiency or diseases causing a lowered intrathyroidal iodine pool, thyroidal secretion of T3 is increased

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2
Q

Thyroid function test and what is the most important hormone tested?

A
  • Approx 99.98% T4 and approx 99.7% of T3 bound to specific plasma proteins (TBG, TBPA and albumin)
  • Log/linear inverse relationship between serum TSH and free T4 concentration produced by -ve feedback inhibition of TSH secretion by thyroid hormones
  • If free T4 is slight lowered, TSH will be increased greatly (TSH is very sensitive)
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3
Q

What is used to screen for primary thyroid dysfunction? What are the limitation of using TSH as a screening test?

A

TSH is used to screen for primary thyroid dysfunction

Limitations:
Assume that hypothalamic pituitary function is intact and normal
Assume that patient’s thyroid status is stable

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4
Q

What thyroid test should be used for patients with stable vs unstable thyroid status?

A

STABLE thyroid status:
- TSH more sensitive indicator of thyroid status than FT4

UNSTABLE thyroid status:
- FT4 is a more reliable indicator of thyroid status than TSH

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5
Q

How to classify hypothyroidism based on TSH and T4?

A
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6
Q

Hypothyroidism in adults: S/S

A

Slow relaxation phase in reflexes

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7
Q

Risk factor of hypothyroidism

A
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8
Q

Case 1
Secondary amenorrhoea for 8 months to private gynaecologist
No visual disturbance
Mild weight loss = intentional (ACEi) vs unintentional
Weight gain = rapid -> thinking Cushing’s; (PCOS)
Hyperprolactinemia

A

Hypothalamic problems
Pituitary problems
Thyroid problems
Medications which may interfere with hormonal cycle (HRT)
R/O pregnancy

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9
Q

Menarche 12, regular cycle
Uncomplicated pregnancy at 28
Barrier method for contraceptives
PMH: nil
DH: Nil
FH: mother ?hx of thyroid problem

Private blood tests in gynaecologist showed prolactin 1080 mIU/L

What are the pathological DDx for hyperprolactinemia?

A
  1. Drugs-induced - first thing to r/o:
    a. Dopamine: anti-psychotics, antiemetics, H2, methyldopa
    b. Antiemetics: metoclopramide, cimetidine, domperidone
    c. Others: estrogen
  2. Prolactinoma
  3. Stalk effect
  4. Renal failure (decreased prolactin clearance)
  5. Hypothyroidism
  6. Chest trauma
  7. Physiological: Pregnancy / lactation
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10
Q

How do we take a non-stress prolactin level?

A

Take the blood 15 minutes after putting needle in as prolactin may be raised during stress

This is important as venipuncture may cause stress = increase in prolactin

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11
Q

Aetiology of hyperprolactinemia

A
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12
Q

● Pulse 68, SR
● Dry skin
● No galactorrhea
● Small firm goiter
Ix

● PRL raised 1100 mIU/1 (up to 500)
● Thyroid function
○ Elevated TSH
○ Low T4

What type of hypothyroidism is this? What could be the cause?

A
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13
Q

How do we diagnose hypothyroidism?

A

Dx of HypoT
● Elevated TSH and low fT4 suggest primary hypoT
● Check anti-TPO and anti-Tg Ab
● USG is NOT required in absence of additional clinical indications (goiter or palpable nodule)
● Thyroid scan is NOT useful and not necessarily: primarily used in hyperthyroidism

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14
Q

What is Hashimoto Thyroiditis?

A
  • Leading cause of hypothyroidism in iodine sufficient areas
  • Autoimmune
  • M/F 1:15
  • May present with or w/o goitre, usually painless
  • Thyroid Ab titres usually measurable
  • Histology: Diffuse lymphocytic infiltration with lymphoid follicles, plasma cells and disruption of thyroid follicles
  • May be associated with other autoimmune diseases
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15
Q

What is thyroperoxidase autoantibody?

A

Initially described as anti-microsomal autoantibody
• TPO is involved in thyroid hormone synthesis at the apical pole of the follicular cell
• The most sensitive test for detecting autoimmune thyroid disease
• Present in >95% of subjects with Hashimoto’s thyroiditis and around 85% subjects with Graves’ disease

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16
Q

What is thyroglobulin autoantibody (TgAb)?

A
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17
Q

What is the function of TRAb (thyroid releasing antibody)?

A
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18
Q

What is the treatment of hypothyroidism?

A

Levothyroxine
Generally first-line:
- Low cost
- Dose consistency
- Low risk of allergic reactions
- Potentially fewer cardiac adverse effects than T3 production

Life-long replacement with thyroid hormones
Exceptions: transient hypothyroidism due to subacute thyroiditis and drug-induced hypothyroidism
- Plasma half-life of T4 is ~7 days, once daily dosing results in a steady state being reached in about 6 weeks

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19
Q

Practical tips on giving thyroxine replacement

A

Practical tips on giving thyroxine replacement
• Typical full replacement doses in adults are 1.6 mcg/kg/day
• Lower starting doses (25-50 mcg/day) might be used in older individuals, those with mild hypothyroidism or those with untreated cardiovascular disease
• T4 primarily absorbed in jejunum
• About 70% of the dose administered is absorbed on an empty stomach
• Should be taken on an empty stomach about 30 minutes before breakfast
• Bioavailability can vary between different brands of T4 formulations
• Calcium, iron, antacids, proton pump inhibitors, anticonvulsants, rifampicin increase T4 requirement by different mechanisms (absorption or metabolism)

When taking calcium, separate the timing for 4 hours as it may affect absorption of T4

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20
Q

Hypothyroid patient with thyroxine replacement
BW = 60 kg
Started T4 at 100 mcg daily
How will you monitor her treatment response?

A

Monitoring of T4 Replacement (T4 half life is 7 days)
* Adequacy of treatment monitored by TSH
* Measure FT4, TSH 4-6 weeks after commencing treatment and monitor and titrate T4 dose until a normal TSH is reached.
E.g. increase T4 dose by 12.5025ug/day if TSH remains above target
* Aim to keep TSH 0.5 to 2.5 - 3 mlU/I.
* Stable patients, measure TSH and FT4 annually.

21
Q

Hypothyroid patient with thyroxine replacement
Thyroid function normalised and remained normal for 2-3 years

Recent blood tests showed

TSH 15 mIU/L (N: 0.35-4.8)
FT4 12 pmol/L (N: 12-23)

What happened? What are the common reasons for abnormal TSH levels on a previously stable dosage of thyroid hormone?

A

Common reasons for abnormal TSH levels on a previously stable dosage of thyroid hormone
* Non-adherence to thyroid hormone regime
* Decreased absorption of thyroid hormone
* Taking thyroid hormone with food
* Taking thyroid hormone ≤4 hours of calcium, iron, soy products, or aluminum-containing antacids
* Given medication that decreases absorption of thyroid hormone e.g. cholestyramine, colestipol, orlistat, or sucralfate
* Significant weight change
* Pregnancy
* Changing in the formulation of thyroid hormone replacement
* Started on medications e.g. some anti-epileptics

22
Q

Hypothyroid patient on thyroxine replacement. Patient is pregnant, what do you need to monitor and manage?

A

Issues around pregnancy
* Goal of preconception TSH: lower reference limit to 2.5mlU/L
* Early dosage adjustment: preemptively increase T4 dose by 30% and inform their clinicians promptly upon confirmation of pregnancy
* Typical strategy: increasing dose from once daily to nine doses per week (doubling the daily dose two days each week)
* Regular monitoring of TFT every 4 weeks with dosage adjustment
* For women during pregnancy: aim
* TSH <2.5mlU/L (1st trimester)
* TSH <3.0mlU/L (2nd-3rd trimester)
* Return to pre-pregnancy dosage of T4 after delivery

23
Q

Case 2:
● 45/M non-smoker, non-drinker
● Referred by GP because of impotence
● Diagnosed T2DM for 7mo
● FBG 11 mmol/L, HbA1c 8.5

  • Investigations
  • WBC 11.951 ; ANC 8.76 T
  • LRFT, CaP04, RG unremarkable
  • ESR 88 mm/hT; CRP 7.6 ng/mLT
  • CXR clear; XR neck - no abnormal soft tissue or gas density
  • Blood culture, urine culture and NPA for resp virus all negative
  • TSH 0.1 mIU/L (N: 0.35 - 4.8)
  • fT 26 pmol/L (N: 12 - 23)
  • What was the likely clinical diagnosis? What further investigation may support your diagnosis?
A

Biochemical picture: Primary hyperthyroidism

Is it from increased production from thyroid or due to increased release of pre-formed thyroid hormones due to thyroid destruction?

Technetium thyroid scan: Primary increase in synthesis (toxic nodule, TMG, Grave’s (diffuse increase vascularity on U/S), destructive thyrotoxicosis (no increase in vascularity on U/S)

24
Q

What is subacute thyroiditis?

A
25
Q

Painless thyroiditis DDx

A
  • Hashimoto thyroiditis
  • Atrophic thyroiditis - Atrophic thyroid
  • Post-partum thyroiditis
  • Variable prognosis depending on residual thyroid reserve
26
Q

How does the thyroid hormone change along with subacute thyroiditis?

A
27
Q

What is subclinical hypothyroidism?

A

Subclinical hypothyroidism
• High TSH with normal fT4 levels
• Investigations: thyroid antibodies
• Management in non-pregnant adults
• Assess lipid levels and hypothyroid symptoms
• Regular TFT monitoring
• Start T4 replacement if persistent TSH >10 mlU/L

28
Q

When do we treat hypothyroidism?

A

Normal TSH: no need for intervention

TSH >10 mIU/L: treat with T4

29
Q

Case 3:
48/F non-smoker
Presented to A&E with ankle swelling for several months
Mild shortness of breath on exertion; no chest pain
Malaise and lethargy; generalised aches and pains in muscles

● DH: Adalat retard 20 mg qd (nifedipine)
● FH: brother has IHD
● PMHx: HT x 1 year, hyperthyroidism x 15 years treated with RAI
○ Ask hypothyroidism hx

PE
● P 58/min, SR, BP 100/70
● JVP not elevated
● Apex displaced lateral 2 cm
● HSDNO, chest clear
● Bilateral ankle edema

ECG: Sinus bradycardia
CXR: cardiomegaly
Creatinine kinase 1080 u/L

What is the approach to elevated creatinine kinase?

A
  • Heavy exertion recently
  • Fall
  • Intramuscular injection
  • Hypothyroid myopathy (CK is elevated)
  • Inflammatory myositis (far-fetched)

Check troponin T to rule out cardiac disease (causes elevated CK)

30
Q

What are the DDx for generalised aches and pains in muscles?

A
31
Q

Patient with Hx of radioiodine
Blood test
TSH 88 mIU/L (N: 0.35-4.8)
fT4 5 pmol/L (N: 12-23)

What is the Dx? What should be done?

A

Post-radioiodine hypothyroidism
Started thyroxine replacement

32
Q

Post-radioactive hypothyroidism

A

Transient: 3.5 to 28%
Pre anti 10 to 15% in first 2 years, then around 3% per year

Requires long-term follow-up

33
Q

Post-thyroidectomy hypothyroidism
- What are considerations in the management plan?

Do you just check T4 replacement?

A

Post-op parathyroidism: (Calcium phosphate)

Patients with differentiated cancer of thyroid, we try to suppress T4 so they have a lower chance of recurrence (clarify TSH target, whether they need T4 suppressive therapy?)

34
Q

Case 4
• M/45; non-smoker and non-drinker
• Referred by private practitioner for erectile dysfunction
• Type 2 diabetes dx 7 months ago: FG 11 mmol/L, HbA1c 8.5%

A

Test testosterone (gonadal status)

35
Q

HbA1c 7.4%
LH 0.3 mIU/L, FSH 0.5 mIU/L, Testosterone 5 mmol/L (N: 10-35)
Defect is in hypothalamus

Pituitary / hypothalamus is abnormal
If high LH, FSH = gonads are abnormal
TSH, fT4, central hypothyroidism, 9 am cortisol level (50) = low
Short synacthen test
Baseline ACTH 6 pg/mL
Cortisol = 30 mmol/L (0’); 75 nmol/L (30’); 100 nmol/L (60’)

What is the cause of this hormonal profile? What are the likely MRI findings?

A

Hypopituitarism
MRI: empty sella (due to damage from RT)

36
Q

Post-radiotherapy Hypopituitarism
- Treatment
- Monitoring

A

Commenced on cortisol, thyroxine & testosterone replacement

Start cortisol replacement first before thyroxine!!!!
- Rate of turnover of cortisol is decreased in hypothyroidism because of reduction in 11 beta hydroxysteroid dehydrogenase activity = may precipitate adrenal crisis if you do it the other way round (exaggerate cortisol insufficiency)

Monitor T4, don’t monitor TSH since the pituitary is gone (aim T4 to mid-level or even higher)

37
Q

Case 5
M/74
Admitted for non-specific dizziness in the recent few months, worsened in the recent 1-2 weeks
Blood test on admission
- Na 111 mmol/L
- K 3.8 mmol/L
- Cr 83 umol/L

How do you approach the investigation of hyponatremia?

A

R/O triggers
Volume status: Hypervolemic then treat
Plasma Osm and urine Osm
Want to r/o hypocortisol and hypoACTH

Pseudohyponatremia:
- Hypertriglyceridemia
- Hyperlipidemia
- High protein

Rule out:
- GI causes, e.g. vomiting / diarrhoea
- Renal causes, e.g. diuretics

Clinically euvolemic

38
Q

Plasma osmo 235; urine Osm 542; urine Na 32 mmol/L
9am cortisol 37 nmol/L
TSH 0.51 mIU/LL (N: 0.35-4.8), fT4 9.5 pmol/L (N: 12-23)

What Ix should be done?

A

LH, FSH, Testosterone, Prolactin, Cushingoid, acromegaly

MRI pituitary

39
Q

What was seen on MRI pituitary

A

Tenting of optic chiasm
Suprasellar extension
Pituitary macroadenoma

Do a visual field perimetry = bitemporal hemianopia

40
Q

What is non-thyroidal illness syndrome (NITS)?

A
41
Q

Case 6
• F/65
• CA vulva (melanoma) requiring radical vulvectomy and lymph node dissection
• Put on nivolumab since Dec 2023
• Baseline TSH, T4 normal
• Developed fever, tachycardia and painful neck swelling in the same month

What Ix to do?

A

Thyroid scan

42
Q

Case 6
* F/65
* CA vulva (melanoma) requiring radical vulvectomy and lymph node dissection
* Put on nivolumab since Dec 2023
* Baseline TSH, T4 normal
* Developed fever, tachycardia and painful neck swelling in the same month

What is the possible cause?

A

Thyroid will be destroyed by immune-checkpoint inhibitors –> destructive thyroiditis (with presentation of mostly hypothyroidism, some having preceding transient thyrotoxic phase)

Could lead to hypophysitis

ICI = upregulates T-cell response

43
Q

Classes of ICI

A

Classes of ICl
• First FDA approval in 2011: ipilimumab for melanoma
• Anti-cytotoxic T lymphocyte antigen 4 (anti-CTLA4):
ipilimumab
• Anti-programmed cell death-1
(anti-PD-1): nivolumab, pembrolizumab

44
Q

What causes immune related adverse events

A

Traditional cytotoxic chemotherapy or molecular target therapies rarely cause endocrine dysfunction

Thyroiditis, hypophysitis, DM, primary adrenal insufficiency, hypoparathyroidism

Most commonly thyroid and pituitary:
- Rich vascularisation: more suspecitivle to contact with activated T lymphocytes
- Direct expression of CTLA-4 in the pituitary or of PD-1/PD-L1 in the thyroid

45
Q

How to differentiate between thyroiditis and Graves’ disease

A

Anti-TSHR (Only in graves)
Technetium-99m thyroid scan (increased uptake = graves, decreased uptake = thyroiditis)
Presence of thyroid eye disease (Only in graves)

46
Q

Why will there be increased endocrine IRAEs?

A

More and more cancers
More patients are prescribed immune-checkpoint inhibitors

47
Q

Routine monitoring for endocrine IRAEs

A
  • Glucose (immune-checkpoint associated DM), electrolytes (Na, K, Ca), TSH, fT4, 8-9 am coristol
  • At baseline
  • Every drug infusion for 6 months
  • Every 2-3 months for next 6 months
  • Every 6 months thereafter
  • Clinical investigation of symptoms suggestive of endocrine IRAEs
48
Q

Central hypothyroidism: common causes

A
  • Pituitary adenoma
  • Infiltrative disease
  • Radiotherapy
  • Immune-checkpoint inhibitors
49
Q

In primary hyperthyroidism how can technetium thyroid scan be used to differentiate the cause?

A

MBBS VI Medicine (93 decks)

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