Pathophysiology
P-I-12. Endocrine disorder, Case 4
内分泌疾患 症例4
Anamnesis: 52-year-old woman presents to her GP with the following symptoms: recently very weak, depressed, increased need for sleep. She complains of feeling generally unwell because she has not been able to perform as well as usual at work lately. She has poor concentration and often naps at work when she has the opportunity. She feels uncomfortable because, despite eating little, she keeps putting on weight. She has put on 8 kg in the last 2 months, even though she has been on a low-carbohydrate, low-calorie diet, eating fibre-rich foods since she noticed the weight gain (about 1 month ago), because she is constipated.
Physical examination: Female patient of medium physical development, height: 158 cm, weight: 70 kg. BMI: 28. Skin pale, cool, dry, “pasty” to touch. Blood pressure: 130/90 mm Hg, resting pulse 56/min. Respiration rate: 10/min. Chubby cheeks. Her sweater has a noticeable amount of hair loss. Physical examination reveals no thyroid gland. Faint heart sounds, bradycardia. No other abnormalities on examination of lungs and heart. Abdomen is soft, palpable, no abnormal tenderness or abnormalities. Liver and spleen not accessible. Decreased bowel sounds. The aa. dors pedis are weakly palpable. Bilaterally, reflexes are poor.
ECG: Sinus bradycardia. Low voltage in all 12 leads. ST depression marked from V1 to V4. No other abnormalities.
Laboratory tests: From the laboratory results it should be noted that the patient had a sedimentation rate of 26 mm/h, fasting blood glucose: 3.1 mmol/L, total cholesterol: 7.4 mmol/L, triglyceride: 3.4 mmol/L, fT4 and fT3 were significantly decreased, TSH 40 mIU/L ↑↑. Anti TPO: ↑↑; anti TG ↑↑.
Ultrasound: The thyroid gland is smaller than average, its structure is not typical of the thyroid gland, but has areas of what can be described as fibrotic. A fine needle aspiration biopsy is recommended.
Scintigraphy: The thyroid gland is smaller than usual. Isotope uptake is reduced throughout the thyroid area. No nodules are seen.
Results of the fine-needle biopsy: Lymphocytic and plasma cell infiltration of thyroid cells is seen in the sample. In some places fibrotic transformed cells are visible. Conclusion: chronic thyroid inflammation.
Key Quotes & What They Tell Us
| Quote / Value | Interpretation |
|---|---|
| “very weak, depressed, increased need for sleep”; poor concentration; naps at work | Slowed metabolism and CNS depression from thyroid hormone deficiency |
| “despite eating little, she keeps putting on weight” (8 kg/2 months); constipation | Reduced metabolic rate and gut hypomotility |
| Skin “pale, cool, dry, pasty”; chubby cheeks; hair loss | Myxoedematous skin changes typical of hypothyroidism |
| Pulse 56/min; RR 10/min; “reflexes are poor” | Bradycardia, slow respiration, and delayed reflex relaxation — generalized slowing |
| ECG: sinus bradycardia, “low voltage in all 12 leads” | Reduced electrical activity ± pericardial effusion typical of hypothyroidism |
| fT4 and fT3 decreased; TSH 40 mIU/L (↑↑) | Primary hypothyroidism — low hormones with compensatory high TSH |
| Total cholesterol 7.4, triglyceride 3.4 mmol/L (high); glucose 3.1 (low) | Hypothyroid dyslipidaemia (reduced clearance) and tendency to hypoglycaemia |
| Anti-TPO ↑↑; anti-TG ↑↑; FNA: “lymphocytic and plasma cell infiltration … fibrotic” | Autoimmune (Hashimoto’s) chronic thyroiditis → gland destruction/atrophy |
Key Points
- Diagnosis: Hashimoto’s thyroiditis causing primary hypothyroidism.
- Pathophysiology: Autoimmune lymphocytic destruction of the thyroid → deficient fT4/fT3 → compensatory rise in TSH; gland becomes small and fibrotic.
- Clinical picture: Generalized slowing — fatigue, weight gain, constipation, bradycardia, cold/dry skin, hair loss.
- Metabolic effects: Hypercholesterolaemia/hypertriglyceridaemia from reduced lipid clearance; hypoglycaemia tendency.
- Contrast with Graves’: High TSH with low free hormones and a small/atrophic gland — the mirror image of the hyperthyroid case.
一問一答
▶In the Case 4 patient (weight gain, bradycardia, high TSH, low fT4), what is the diagnosis?
Hashimoto's thyroiditis causing primary hypothyroidism.
▶What is the pathophysiology of Hashimoto's thyroiditis?
Autoimmune lymphocytic destruction of the thyroid → deficient fT4/fT3 → compensatory rise in TSH; the gland becomes small and fibrotic.
▶What lab pattern confirms primary hypothyroidism in Case 4?
Decreased fT4 and fT3 with markedly elevated TSH (40 mIU/L).
▶Why does the patient gain weight despite eating little in Case 4?
Reduced metabolic rate from thyroid hormone deficiency, with gut hypomotility causing constipation.
▶Which antibodies and biopsy findings confirm Hashimoto's in Case 4?
Elevated anti-TPO and anti-TG, with FNA showing lymphocytic and plasma cell infiltration and fibrotic transformation.
▶What skin changes are typical of hypothyroidism in Case 4?
Pale, cool, dry, 'pasty' (myxedematous) skin, chubby cheeks, and hair loss.
▶Why is the cholesterol and triglyceride high in Case 4?
Hypothyroidism reduces lipid clearance, causing hypercholesterolemia and hypertriglyceridemia.
▶What ECG findings are seen in hypothyroidism (Case 4)?
Sinus bradycardia and low voltage in all 12 leads (with ST depression V1–V4).
▶Why does low voltage on ECG occur in hypothyroidism?
Reduced electrical activity, sometimes with a pericardial effusion, lowers ECG voltage.
▶Which neuro/cognitive symptoms reflect thyroid hormone deficiency in Case 4?
Weakness, depression, increased need for sleep, poor concentration, and delayed (poor) reflexes.
▶How does the thyroid ultrasound appear in Hashimoto's (Case 4)?
A small thyroid with atypical, fibrotic-appearing structure (and reduced isotope uptake on scintigraphy).
▶How does Hashimoto's hypothyroidism contrast with Graves' on labs and gland appearance?
Hashimoto's: high TSH with low free hormones and a small/atrophic gland; Graves': low TSH with high free hormones and a diffusely enlarged, overactive gland — mirror images.
▶Why is fasting glucose low (3.1 mmol/L) in Case 4?
Hypothyroidism slows metabolism and reduces gluconeogenesis, giving a tendency to hypoglycemia.
▶Why is TSH elevated when thyroid hormones are low?
Reduced negative feedback from low fT4/fT3 lets the pituitary increase TSH secretion (compensatory).
▶What is the cornerstone treatment of Hashimoto's hypothyroidism?
Lifelong levothyroxine (T4) replacement.
▶Why does the patient have constipation and reduced bowel sounds in Case 4?
Decreased gut motility from thyroid hormone deficiency.
▶What is the most common cause of primary hypothyroidism in iodine-sufficient areas?
Hashimoto's (autoimmune chronic lymphocytic) thyroiditis.
▶Why does bradycardia occur in hypothyroidism?
Thyroid hormone deficiency reduces cardiac chronotropy and overall metabolic/sympathetic drive.
▶What is the most severe, life-threatening manifestation of untreated hypothyroidism?
Myxedema coma.
▶Why does hair loss occur in hypothyroidism?
Reduced thyroid hormone slows hair follicle metabolism and turnover, causing diffuse hair loss.