The thyroid axis is a finely tuned system that regulates metabolism, growth, and energy balance. Disturbances in this axis can present subtly or dramatically, and understanding them requires more than memorizing hormone levels, it demands clinical reasoning.
In the following 10 cases, you’ll explore a spectrum of thyroid dysfunctions, from common presentations to critical emergencies.
🧑⚕️ Case 1: Emma
Emma, a 32-year-old primary school teacher, presents with fatigue, weight gain despite unchanged diet, and increased sensitivity to cold. She reports feeling “foggy” and emotionally flat. Her periods have become heavier and more irregular over the past six months.
On examination:
- HR: 58 bpm
- BP: 110/70
- Dry skin, mild periorbital puffiness
- Palpable, firm, non-tender goitre
Investigations:
- TSH: 8.2 mIU/L (↑)
- Free T4: 11 pmol/L (low-normal)
- TPO antibodies: stron gly positive
- Tg antibodies: positive
- CBC: normocytic anaemia
- Lipids: elevated LDL
🧠 Clinical questions
✅ Diagnosis
Hashimoto’s thyroiditis with subclinical
hypothyroidism and systemic symptoms.
🩺 Management
- Start levothyroxine (e.g. 50 mcg daily, titrate to TSH)
- Recheck TFTs in 6–8 weeks
- Monitor symptoms and adjust dose
- Screen for other autoimmune conditions (e.g. coeliac, T1DM if relevant)
🧑⚕️ Case 2: Aisha
Aisha, a 26-year-old law student, presents with palpitations, weight loss despite increased appetite, heat intolerance, and tremor. She’s anxious, sleeping poorly, and has noticed her eyes feel “bulgy.” Her mother has rheumatoid arthritis.
On examination:
- HR: 112 bpm
- BP: 140/80
- Fine tremor, warm moist skin
- Lid lag and mild proptosis
- No palpable nodules, but thyroid is diffusely enlarged and non-tender
Investigations:
- TSH: <0.01 mIU/L (↓)
- Free T4: 32 pmol/L (↑)
- Free T3: 9.1 pmol/L (↑)
- TSH receptor antibodies (TRAb): positive
- ESR: mildly elevated
- ECG: sinus tachycardia
🧠 Clinical questions
1. What’s the pattern in her TFTs?
Suppressed TSH with elevated T4 and T3 confirms primary
hyperthyroidism. The pituitary is responding appropriately — but the thyroid is
overproducing hormone independently.
2. What do the antibodies tell us?
Positive TRAb confirms Graves’ disease — stimulating
autoimmunity. These antibodies mimic TSH and drive excess hormone production.
3. Why are her eyes affected?
Graves’ orbitopathy is due to autoimmune inflammation of
orbital fibroblasts. It’s not caused by excess hormone — it’s a separate immune
process.
4. Why is her thyroid enlarged but smooth?
Diffuse goitre reflects global stimulation by TRAb. No nodules or tenderness suggests Graves’, not thyroiditis or multinodular goitre.
✅ Diagnosis
Graves’ disease with thyrotoxicosis and mild orbitopathy.
🩺 Management
- Start carbimazole (e.g. 15–30 mg daily) to block hormone synthesis
- Consider propranolol for symptom control
- Monitor TFTs every 4–6 weeks
- Discuss long-term options: antithyroid drugs, radioactive iodine, or surgery
- Refer for ophthalmology for eye review
🧠 Case 3: David
David, a 52-year-old accountant, presents with persistent fatigue, weight loss, and low libido. He’s noticed increased sensitivity to cold, reduced appetite, and difficulty concentrating. His wife reports he’s become emotionally flat and withdrawn. He denies neck pain or swelling but has experienced headaches.
On examination:
- HR: 62 bpm
- BP: 95/60
- Pale, thin, dry skin with fine wrinkling
- No goitre
- Visual fields: bitemporal hemianopia
Investigations:
- TSH: 1.4 mIU/L (normal)
- Free T4: 7.8 pmol/L (↓)
- Free T3: 2.6 pmol/L (↓)
- Morning cortisol: 120 nmol/L (↓)
- Testosterone: 4.1 nmol/L (↓)
- LH/FSH: low
- Prolactin: elevated
- MRI: 2.5 cm pituitary macroadenoma compressing the optic chiasm
🧠 Clinical questions
1. Why is TSH “normal” despite low T4 and T3?
This is central hypothyroidism. The pituitary isn’t producing enough TSH. The TSH looks “normal,” but it’s inappropriately low given the low T4. Always interpret TSH in context.
2. Why check testosterone?
Low libido and fatigue in a male patient warrant checking testosterone. It’s low here, confirming hypogonadism. FSH and LH are also low, confirming secondary (central) hypogonadism.
3. What’s the broader pattern?
This is panhypopituitarism:
- ↓ TSH → central hypothyroidism
- ↓ ACTH → adrenal insufficiency
- ↓ LH/FSH → hypogonadism
- ↑ Prolactin → stalk compression (loss of dopamine inhibition)
4. Why the visual field defect?
Bitemporal hemianopia suggests optic chiasm compression — classic for a large pituitary mass.
✅ Diagnosis
Pituitary macroadenoma causing panhypopituitarism and central hypothyroidism.
🩺 Management
- Urgent endocrinology referral
- Start hydrocortisone first (before thyroxine) to prevent adrenal crisis
- Consider transsphenoidal surgery if compressive symptoms or growth
- Long-term hormone replacement: thyroxine, testosterone, hydrocortisone ± others
- Monitor visual fields and MRI regularly
🧠 Case 4: Sarah
Sarah, a 34-year-old woman, presents six months after giving birth with profound fatigue, cold intolerance, weight gain, and inability to breastfeed. Her delivery was complicated by a severe postpartum haemorrhage requiring transfusion. She reports amenorrhoea since delivery and low mood and thought she might have depression.
On examination:
- HR: 58 bpm
- BP: 90/60
- Pale, dry skin
- No goitre
- Flat affect, sparse axillary hair
Investigations:
- TSH: 0.9 mIU/L (normal)
- Free T4: 6.9 pmol/L (↓)
- Morning cortisol: 100 nmol/L (↓)
- LH/FSH: low
- Prolactin: low
- MRI: empty sella with pituitary atrophy
🧠 Clinical questions
1. What’s the significance of the postpartum haemorrhage?
Severe blood loss can cause pituitary infarction, known as
Sheehan’s syndrome. The pituitary is highly vascular and vulnerable to
hypoperfusion during obstetric shock.
2. Why is prolactin low?
Unlike macroadenomas, this is pituitary destruction, not
compression. Prolactin is low because lactotrophs are damaged, explaining her
inability to breastfeed.
3. Why is TSH “normal” despite low T4?
This is central hypothyroidism. The pituitary isn’t
producing enough TSH. The “normal” TSH is inappropriately low given the low T4.
4. What’s the broader pattern?
This is panhypopituitarism:
- ↓ TSH → central hypothyroidism
- ↓ ACTH → adrenal insufficiency
- ↓ LH/FSH → amenorrhoea
- ↓ Prolactin → lactation failure
✅ Diagnosis
Sheehan’s syndrome causing panhypopituitarism.
🩺 Management
- Start hydrocortisone first, then thyroxine
- Long-term hormone replacement: thyroxine, hydrocortisone, oestrogen/progesterone
- Monitor bone density, mood, and fertility goals
- Educate about stress dosing and sick-day rules
🧠 Case 5: George
George, a 68-year-old retired builder, presents with a visible neck lump, occasional palpitations, and mild tremor. He reports episodes of sweating and weight loss, alternating with fatigue and weight gain. No eye symptoms. No family history of thyroid disease.
On examination:
- HR: 88 bpm
- BP: 130/80
- Irregular, nodular goitre with no tenderness
- No signs of orbitopathy
Investigations:
- TSH: 0.2 mIU/L (↓)
- Free T4: 18 pmol/L (normal-high)
- Free T3: 6.1 pmol/L (↑)
- TPO antibodies: negative
- TRAb: negative
- Thyroid ultrasound: multiple nodules, some with increased vascularity
- Radionuclide scan: patchy uptake, hot and cold areas
🧠 Clinical questions
✅ Diagnosis
Toxic multinodular goitre causing mild thyrotoxicosis.
🩺 Management
- Monitor TFTs and symptoms
- Consider radioactive iodine if symptoms worsen
- Surgery if compressive symptoms or cosmetic concern
- Avoid iodine-containing medications (e.g. amiodarone)
- Regular ultrasound to monitor nodule growth
🧠 Case 6: Tom
Tom, a 56-year-old man, presents with palpitations, weight loss, and heat intolerance. He has no eye symptoms and no family history of thyroid disease. On examination, his thyroid is normal-sized but has a firm, solitary nodule in the right lobe. No tenderness or lymphadenopathy.
On examination:
- HR: 104 bpm
- BP: 135/80
- Warm skin, fine tremor
- No orbitopathy
Investigations:
- TSH: <0.01 mIU/L (↓)
- Free T4: 26 pmol/L (↑)
- Free T3: 7.9 pmol/L (↑)
- TRAb: negative
- TPO antibodies: negative
- Thyroid ultrasound: solitary 2.2 cm nodule, increased vascularity
- Radionuclide scan: focal “hot” nodule with suppressed uptake elsewhere
🧠 Clinical questions
1. What does the scan show?
A hot nodule with suppressed uptake elsewhere confirms a
toxic adenoma — an autonomously functioning thyroid nodule producing excess
hormone.
2. Why are antibodies negative?
This is non-autoimmune hyperthyroidism. The nodule is acting
independently of TSH or immune stimulation.
3. Why is TSH suppressed?
Excess T4 and T3 from the nodule suppress pituitary TSH via negative feedback. The rest of the gland is shut down.
✅ Diagnosis
Toxic adenoma causing primary hyperthyroidism.
🩺 Management
- Radioactive iodine ablation of the nodule
- Surgical lobectomy if compressive symptoms or cosmetic concern
- Beta-blockers for symptom control
- Monitor for post-treatment hypothyroidism
🧠 Case 7: Emily
Emily, a 29-year-old woman in her first trimester (9 weeks gestation), presents with fatigue, mild constipation, and increased sensitivity to cold. She has a history of autoimmune gastritis but no known thyroid disease. Her pregnancy is otherwise progressing normally.
On examination:
- HR: 72 bpm
- BP: 110/70
- No goitre
- No orbitopathy
- BMI: 23
Investigations:
- TSH: 3.8 mIU/L (↑ for pregnancy)
- Free T4: 13.5 pmol/L (normal)
- TPO antibodies: positive
- BhCG: appropriate for gestational age
🧠 Clinical questions
1. Why is her TSH “high” if it’s within the non-pregnant
reference range?
In pregnancy, especially the first trimester, TSH should be
lower due to the stimulatory effect of hCG on the thyroid. The recommended
upper limit is ~2.5 mIU/L in early pregnancy. So 3.8 is elevated for gestation,
even if it’s “normal” outside pregnancy.
2. What does a normal free T4 mean here?
This is subclinical hypothyroidism — TSH is elevated, but
free T4 is still normal. However, in pregnancy, even mild thyroid dysfunction
can affect fetal development and pregnancy outcomes.
3. Why do TPO antibodies matter?
Positive TPOAb increases the risk of progression to overt
hypothyroidism and is associated with miscarriage and other complications. It
also confirms autoimmune thyroiditis as the underlying cause.
✅ Diagnosis
Subclinical hypothyroidism in early pregnancy, likely due to Hashimoto’s thyroiditis.
🩺 Management Principles
- Start levothyroxine (e.g. 50 mcg daily), especially with positive TPOAb
- Recheck TFTs every 4–6 weeks during pregnancy
- Adjust dose to keep TSH <2.5 mIU/L in first trimester, <3.0 in second and third
- Monitor for postpartum thyroiditis after delivery
Pregnancy lowers the threshold for treatment. Even mild TSH
elevation can matter — especially with positive antibodies. Think of it as
protecting both the mother’s physiology and the developing foetal brain.
🧠Case 8 : Priya
Priya, a 38-year-old woman, presents with a 2-week history of anterior neck pain, low-grade fever, palpitations, and fatigue. She reports recent weight loss despite poor appetite, and difficulty sleeping. She had a viral upper respiratory infection three weeks ago. No eye symptoms.
On examination:
- HR: 102 bpm
- BP: 125/75
- Tender, enlarged thyroid — especially on the right
- No orbitopathy
- Mild tremor, warm skin
Investigations:
- TSH: <0.01 mIU/L (↓)
- Free T4: 28 pmol/L (↑)
- Free T3: 7.8 pmol/L (↑)
- TPO antibodies: negative
- TRAb: negative
- ESR: elevated
- CRP: elevated
- Radionuclide scan: low uptake
🧠 Clinical questions
1. What’s the pattern in her TFTs?
Suppressed TSH with elevated T4 and T3 suggests
thyrotoxicosis. But the cause isn’t stimulation — it’s destructive release of
preformed hormone.
2. Why is the thyroid tender?
Pain and fever suggest subacute thyroiditis (de Quervain’s),
often post-viral. Inflammation damages follicular cells, releasing stored
hormone into circulation.
3. Why is uptake low on the scan?
In thyroiditis, the gland isn’t making new hormone — it’s
leaking what it already stored. So iodine uptake is low. This contrasts with
Graves’, where uptake is high due to active synthesis.
4. Why are antibodies negative?
This isn’t autoimmune stimulation. It’s inflammatory destruction, usually triggered by infection or immune dysregulation.
✅ Diagnosis
Subacute (de Quervain’s) thyroiditis causing transient
thyrotoxicosis.
🩺 Management Principles
- Supportive care: NSAIDs for pain and inflammation
- Beta-blockers (e.g. propranolol) for symptom control
- Steroids if severe pain or prolonged symptoms
- No antithyroid drugs — the gland isn’t overproducing
- Monitor TFTs: may progress to hypothyroid phase before recovery
🔥 Case 9: Leanne
Leanne, a 42-year-old woman with known Graves’ disease (stable on carbimazole), presents to the emergency department with confusion, vomiting, and high fever. She has recently had a chest infection with cough and fever. She’s agitated, sweating profusely, and has had two episodes of palpitations and near-collapse.
On examination:
- Temp: 39.8°C
- HR: 142 bpm, irregular
- BP: 90/50
- RR: 28
- Diaphoretic, tremulous, confused
- No focal neurological signs
- Diffuse goitre, no orbitopathy
Investigations:
- TSH: <0.01 mIU/L (↓)
- Free T4: 55 pmol/L (↑↑)
- Free T3: 18.2 pmol/L (↑↑)
- ECG: atrial fibrillation
- LFTs: elevated transaminases
- WBC: elevated
- Chest X-ray: right lower lobe pneumonia
🧠 Clinical questions
1. What makes this more than just thyrotoxicosis?
This is thyroid storm - a life-threatening exacerbation of
hyperthyroidism. It’s triggered by physiological stressors (infection, surgery,
medication non-compliance) and causes multisystem decompensation:
- CNS: agitation, delirium
- CVS: tachyarrhythmia, hypotension
- GI: vomiting, diarrhoea
- Thermoregulation: hyperpyrexia
2. Why is T3 so high?
Graves’ disease often causes T3-predominant thyrotoxicosis.
In thyroid storm, both T3 and T4 are markedly elevated, but the severity of
illness reflects tissue sensitivity, not just hormone levels.
3. What triggered the storm?
Likely the pneumonia. The infection increased metabolic demand and immune activation overcoming the brake on hormone synthesis provided by her regular carbimazole.
✅ Diagnosis
Thyroid storm secondary to Graves’ disease, precipitated by infection.
🩺 Emergency Management
Multimodal approach — block synthesis, conversion, release,
and effect:
1. Beta-blocker:
- Propranolol IV or oral → controls symptoms and blocks peripheral T4→T3 conversion
2. Antithyroid
drug:
- Carbimazole or PTU → blocks new hormone synthesis
- PTU preferred acutely (also blocks T4→T3 conversion)
3. Iodine
(after ATD):
- Lugol’s iodine → inhibits hormone release (give 1 hour after ATD)
4. Steroids:
- Hydrocortisone → reduces T4→T3 conversion, supports adrenal axis
5. Supportive
care:
- IV fluids, cooling, treat infection, correct arrhythmia
🧠Tip
Thyroid storm is a clinical diagnosis, not just a lab
result. Always ask: Is this patient failing multiple systems? If yes, act fast.
Hormone levels alone don’t tell the whole story.
🧠 Case 10: Amira
Amira, a 44-year-old woman, presents with fatigue, weight gain, and amenorrhoea. She has a history of craniopharyngioma resection at age 12. She reports poor concentration, cold intolerance, and dry skin. No goitre or neck symptoms.
On examination
- HR: 60 bpm
- BP: 100/65
- Pale, dry skin
- No visual field defects
Investigations:
- TSH: 1.1 mIU/L (normal)
- Free T4: 7.2 pmol/L (↓)
- Free T3: 2.4 pmol/L (↓)
- Cortisol: low
- LH/FSH: low
- Prolactin: normal
- MRI: hypothalamic scarring, small pituitary
🧠 Clinical questions
1. Why is TSH “normal” despite low T4 and T3?
This is central hypothyroidism — but the problem is
hypothalamic, not pituitary. TRH deficiency leads to low TSH output, and the
TSH that is produced may be biologically inactive.
2. Why is prolactin normal?
Prolactin is under inhibitory control by dopamine, not TRH.
In hypothalamic disease, prolactin may be normal or even elevated if stalk
function is impaired.
3. What’s the broader pattern?
This is hypothalamic hypopituitarism — low TRH, GnRH, and CRH leading to secondary failure of thyroid, gonadal, and adrenal axes.
✅ Diagnosis
Central hypothyroidism due to hypothalamic dysfunction (post-craniopharyngioma).
🩺 Management
- Start hydrocortisone first, then thyroxine
- Consider oestrogen/progesterone replacement if fertility not desired
- Monitor bone density, mood, and metabolic health
- Long-term endocrine follow-up
🧠 Wrapping Up: Why Thyroid Cases Matter
From silent autoimmunity to storm-level crisis, thyroid disorders offer a masterclass in clinical reasoning. They can teach you to interpret feedback loops, recognise compensation before collapse, and listen carefully when symptoms speak louder than numbers. Each case - whether nodular, autoimmune, central, or gestational - reveals how physiology adapts, fails, and recovers. But more than that, these cases remind us that good medicine isn’t just about identifying disease. It’s about understanding systems, respecting complexity, and responding with critical thinking.
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