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Histopathology > Endocrine Pathology > Flashcards

Endocrine Pathology Flashcards

1
Q

Normal thyroid histology

A
  • Colloid-filled acini lined by follicular epithelial cells
  • Vascular organ
  • Hormone thyroxine is secreted directly into blood
  • Regulates basal metabolic rate
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2
Q

**Hypothyroidism **- causes

A
  • Hashimoto’s thyroiditis - commonest
    • Auto-immune: production of anti-thyroid antibodies –> lymphocytic destruction of thyroid
    • Females 10:1 Males
  • Removal of thyroid
  • Radioiodine treatment
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3
Q

**Hypothyroidism **- symptoms

A
  • Myxoedema = slowing of mind and body:
    • Weight gain
    • Constipation
    • Cold intolerance
    • Tiredness
    • Depression
    • Big tongue, deep voice - deposition of matrix substances in viscera and skin
    • Thin hair
    • Weak heartbeat
    • Slow reflexes
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4
Q

**Hyperthroidism **- causes

A
  • Grave’s disease: 85% of cases
  • Hyperfunctional multinodular goitre (usually euthyroid)
  • Hyperfunctional adenoma (benign follicular tumour) - rare
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5
Q

**Hyperthyroidism **- symptoms

A
  • Increased basal metabolic rate:
    • _​_Sweating
    • Heat intolerance
    • Weight loss despite increased appetite
    • Diarrhoea
    • Tachycardia, arrhythmias (often AF)
    • Tremor, anxiety, hyperactivity
    • Brist reflexes
    • Staring gaze
    • Lid lag
    • Exopthalmos
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6
Q

**Graves disease **- diffuse toxic goitre

A
  • Female 10:1 Male
  • Autoimmune - due to thyroid stimulating antibodies
  • Symmetrical enlargement of thyroid
  • Exopthalmos - due to deposition of connective tissue behind eyeball
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7
Q

Multinodular goitre

A
  • Usually euthyroid - if active and –> hyperthyroidism then ‘toxic’
  • May be due to uneven responsiveness of areas of thyroid to fluctuating TSH over years
  • Development of well circumscribed nodules of various sizes –> irregular hyperplastic enlargement of entire thyroid gland.
  • Larger nodules filled with brown gelatinous colloid
  • Large goitres may lead to tracheal compression or dysphagia
  • Significant cosmetic effect
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8
Q

Adenoma (follicular)

A
  • Benign tumour
  • Colloid-containing microfollicles and columns of larger cells in alveolar arrangement
  • Usually euthyroid
    • Rarely hyperfunctional = “toxic” nodule –> thyrotoxicosis
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9
Q

Adenoma vs. Hyperplastic Nodule

A
  • Adenoma = solitary follicular nodule with normal background gland
    • Treatment - thyroid lobectomy
  • Disproportionate nodule = hyperplastic follicular nodule in *nodular *background gland i.e. multinodular goitre
    • Treatment - thyroidectomy or no surgery
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10
Q

**Papillary adenocarcinoma ** - thyroid cancer

A
  • Well differentiated tumour
  • Commoner in younger patients
  • Slow-growing, non-encapsulated mass
  • Histology
    • Epithelial papillary projections +/- calcified spherules between
    • Epithelial cell nuclei large with clear area centrall = ‘Orphan Annie nuclei’
    • Psammoma bodies
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11
Q

**Follicular adenocarcinoma **- thyroid cancer

A
  • Well differentiated, single, encapsulated lesion
  • Histology
    • Similar to papillary adenocarcinoma but with invasion of capsule/blood vessels
  • Haematogenous spread to:
    • Bone
    • Lungs
    • Brain
  • Good uptake of radioactive iodine (131I) - susceptible to post throidectomy radiotherapy
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12
Q

**Anaplastic carcinoma **- thyroid cancer

A
  • Highly malignant, poorly differentiated adenocarcinoma:
    • Local invasion
    • Metastases
  • Elderly patients - presents as diffusely infiltrative mass
  • Very poor prognosis - does not respond to treatment and invades the trachea –> respiratory obstruction
  • Histology
    • Spindle cell tumour +/- giant cell areas or small cell pattern
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13
Q

**Medullary carcinoma **- thyroid cancer

A
  • Rare neuroendocrine tumour
  • Arises from parafollicular ‘C’ cells which secrete calcitonin
    • Raised serum calcitonin useful diagnostically (no effects)
  • Histology
    • Amyloid stroma
    • Positive calcitonin staining
  • Incidence
    • Sporadic - 70%
    • MEN 2A/2B or familial medullary thyroid carcinoma (30%)
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14
Q

**Histology of Thyroid **- overview

A
  • Hyperplastic epithelium
    • Graves’ disease
    • Iodine deficiency
    • Goitrogen/PUT effect
  • Colloid-filled follicles
    • ‘Idiopathic’ nodular goitre
  • Anaplastic cells
    • Cancer
  • Lymphocytes
    • Hashimoto’s thyroiditis
  • Foreign-body granulomas
    • DeQuervain’s
  • Fibrous tissue
    • Riedel’s
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15
Q

**Parathyroid Glands **- function

A
  • Four glands - one in each lobe of the thyroid (superior and inferior)
  • Parathormone (PTH) is secreted in response to low serum calcium levels by the chief cells
  • PTh increases serum Ca2+ and decreases serum phosphate by:
    • Bone
      • Stimulating osteoclastic bone resorption
      • Inhibiting osteoblastic bone deposition
    • Kidney
      • Increasing Ca2+ reabsorption
      • Decreaseing phosphate reabsorption
      • Activation of Vit D by 1-hydroxylation of 25-hydroxyvitamin D
    • Gut
      • Increased Ca2+reabsorption
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16
Q

**Primary Hyperparathyroidism **- aetiology

A
  • Hypersecretion of PTH and thus elevates serum calcium from
    • Adenoma 85-95%
    • Hyperplasia 5-15%
    • Carcinoma <1%
  • Usually sporadic causes
  • Adenomas and hyperplasia may be related to MEN1, 2A or 2B
17
Q

**Primary Hyperparathyroidism **- symptoms

A
  • Due to effects of PTH and hypercalcaemia
    • *Painful bones *-
      • osteoporosis
      • osteitis
      • fibrosa cystica
    • Renal stones
    • *Abdominal groans *
      • ​Anorexia
      • Constipation
    • *Pyschic moans *
      • depression
      • lethargy
      • seizures
18
Q

**Secondary Hyperparathyroidism **- etiology

A
  • Compensatory hyperplasia of the parathyroid in response to chronic low serum calcium or increased phosphate
  • Causes:
    • Chronic renal failure - most common
    • Vit D or calcium deficiency
    • Malabsorption
    • Low serum magnesium
    • Tissue resistance to Vid D
    • Pseudohypoparathyroidism (genetic resistance to PTH)
19
Q

**Hyperparathyroidism **- investigation

A
  • Ultrasound
  • Sestamibi scan
    • Radioactive tecnetium-99 injected
    • Taken up preferentially by hyperactive glands
      • Just one - implies tumour
      • All four - implies hyperplasia
20
Q

Parathyroid Carcinoma

A
  • Rare
  • Causes very high hypercalcaemia >3.5 mmol/l
  • Rapid
    • Bone disease
    • Kidney stones
    • Metastases
  • May damage recurrent larangeal nerve
  • Adherent at surgery
21
Q

**Adrenal Gland **- function

A
  • Cortex - produces 3 types of steroids
    • Glucocorticoids - mainly cortisol from the zona fasciculata
    • Mineralocorticoids - mainly aldosterone from the zona glomerulosa
    • Sex steroids - oestrogens and androgens from the zona reticularis
  • *Medulla - *produces catecholamines mainly adrenaline
22
Q

Primary Adrenocortical Insufficiency (Addison’s disease) - Causes

A
  • Autoimmune destruction
  • Tuberculosis - bilateral adrenal (caseous necrosis)
  • Surgical remocal
  • Metastatic cancer
  • AIDs - CMV, Mycobacterium, Kaposi’s sarcoma
  • Congenital hypoplasia
23
Q

**Addison’s Disease **- clinical features

A
  • Glucocorticoid insufficiency
    • Vomiting and loss of appetite
    • Weight loss
    • Lethargy and weakness
    • Postural hypotension
    • Hypoglycaemia
  • Mineralocorticoid insufficiency
    • ​Lowered serum Na+, raised serum K+
    • Chronic dehydration
    • Hypotension
  • Increased ACTH secretion
    • ​Hyperpigmentation of skin and buccal mucosa
  • Loss of adrenal androgen
    • Decreased body hair - especially in females
24
Q

**Acute (Addisonian) Adrenal Crisis **- Addison’s disease

A
  • Preciptated by sudden stress demanding raised output from chronically failing glands:
    • Infection
    • Trauma
    • Surgery
  • Symptoms of:
    • Vomiting
    • Abdominal pain
    • Hypotension
    • Coma
  • Rapidly fatal! - unless Rx - corticosterioids (IV hydrocortisone) + fluids
25
Q

**Cushing’s Syndrome **- Clinical Features

A
  • Clinical feautres due to exposure to raised free cotricosteroid levels:
    • Central obesity and moon face
    • Plethora and acne
    • Menstrual irregularity
    • Hirsutism and hair thinning
    • Hypertension
    • Diabetes/glucose intolerance
    • Muscle wasting and peakness
    • Thin skin, easy bruising and striae
    • Osteoporosis
26
Q

**Cushing’s syndrome **- aetiology

A
  • ACTH-dependent
    • Pituitary adenoma (Cushing’s disease) –> excess ACTH secretion and bilateral diffuse adrenal hyperplasia
    • Ectropic ACTH (or corticotrophin releasing hormone) production by a non-endocrine neoplasm e.g. small cell lung Ca+
  • ACTH independent
    • Iatrogenic steroid therapy - most common cause overall
    • Adrenal cortical adenoma - majority are non-functional
    • Adrenal carcinoma - rare
      • Usually functional
      • Generally associated with overporduction of glucocorticoids and sex steroids
      • Virilization common symptom especially in women
      • Often large and invasive
    • Nodular hyperplasia
27
Q

Pheochromocytoma

A
  • Tumour arising from the adrenal medulla
  • Produces catecholamines - mostly adrenaline
  • Rare cause of surgically correctable hypertension
    • HTN paroxysmal
  • Diagnosis based on raised level of catecholamines in urine
  • Rule of 10s
    • 10% extra-adrenal (paragangliomas)
    • 10% bilateral
    • 10% malignant (no histological features predict behaviour
    • 10% not associated with hypertension
28
Q

Multiple Endocrine Neoplasia (MEN) Syndromes

A
  • Genetically inherited diseases
  • Lead to proliferative lesions of multiple endocrine glands - hyperplasia, adenoma or carcinoma
  • MEN I (Wermer) –> parathyoid adenoma/hyperplasia + hyperplasia/carcinoid tumours of other endocrine glands
    • Caused by abnormal tumour suppressor gene - chromosome 11q
  • MEN IIa –> medullary carcinoma of thyroid and/or pheochromocytoma and/or parathyroid adenoma/hyperplasia
    • Caused by abnormality on chromosome 10q
  • MEN IIb –> medullary carcinoma of the thyroid and/or pheochromocytoma
    • Caused by abnormality of *ret *oncogene - chromosome 10q

Histopathology (3 decks)

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