Endocrine pathology Flashcards
in the thyroid, what do parafollicular or C cells produce?
Calcitonin
what ar ethe effects of the thyroid hormones?
upregulation of CHO, lipid metabolism and protein synthesis + an increase in metabolic rate, critical role in brain development
What are the main causes of HYPERTHYROIDISM?
Graves Disease (20-40yo, F)- > autoimmune resulting from the brak down of self tolerance of thyroid autoantigens (TRAB), importantly the TSH receptors , which results in : diffuse toxic hyperplasia, infiltrative opthalmopathy, localised dermopathy known as myoedema.
- Hyperfunctioning toxic multinodular goitre
- hyperfunctioinig toxic adenoma
- Iodine induced hyperthryoidism
- Neonatal thyrotoxicosis assoc. with maternal graves disease.
- hyperfunctioning thyroid carcinoma
- TSH secreting pituiitary adenoma (rare)
What are some causes of HYPERTHYROIDISM where you WOULDNT see low TSH levels?
- Subacute granulomatous thyroiditis (de Quervain’s)- painful thyroiditis : 40-50 yo F, post viral infection. Pain and transient hyperthyroidism
- Subacute lymphocytic thyroiditis:painless thyroiditis : anti-TPO positive-
- Struma ovarii (ovarian teratoma with ectopic thyroid)
- Factitious thyrotoxicosis (exogenous thyroxine intake)
What are the causes of hypothyroidism? PRIMARY
** associated with goitre
Hashimoto’s Thyroiditis: autoimmune (45-65, F), autoimmune destruction of the thyroid gland characterised by a lymphocytic infiltrate, autoantibodies to thyroglobulin and thyroid peroxidase (anti-TPO)
- Iodine deficiency **
- Post ablative surgery, radioiodine surgery, external radiation
- drugs (lithium)
- Developmental
Congenital **
• Drugs (lithium, iodides, p-aminosalicylic acid);
• Developmental (thyroid dysgenesis: PAX-8, TTF-2, TSH-receptor
mutations);
• Thyroid hormone resistance syndrome (TRβ mutations);
• Congenital biosynthetic defect (dyshormonogenetic goitre)
Secondary: Pituitary failure, Tertiary: hypothalamic failure
**These can be associated with goitre (please also see “causes of goitre” below)
What are secondary causes of hypothyroidism
Pituitary failure
What are tertiary causes of hypothyroidism
hypothalamic failure
What are the causes of goitre?
either diffuse or multinodular, endemic or sporadic.
cuases of endemic goitre
endemic goitre?: characterised by low intake of iodine, and sometimes the intake of goitrogens that interfere with thyroid synthesis
Iodine deficiency is a common but preventable health problem. It leads to impairment of thyroid hormone synthesis and increase in TSH causing hypertrophy of the follicular cells.
The resultant increase in the mass of the thyroid overcomes the hormone deficiency, but not always and the patient may become hypothyroid.
Causes of Sporadic goitre
SPORADIC GOITRE: has a female preponderance and a peak incidence at puberty or early adult life. Note that goitre may be physiological in adolescence and pregnancy. Sporadic goitre has many causes that include ingestion of substances that interfere with thyroid hormone synthesis, autosomal recessive conditions- dyshormonogenetic goitre or is idiopathic. Most simple goitrous presentations are euthyroid.
Causes of Multinodular goitre
Is caused by recurrent episodes of hyperplasia and involution that produce irregular enlargement of the thyroid.
All simple types of goitre can convert into multinodular goitre
The dominant clinical features are mass effects including superior vena caval syndrome.
Most multinodular presentations are euthyroid or have subclinical hyperthyroidism.
Some may develop an autonomous nodule and produce hyperthyroidism. The incidence of malignancy in long-standing goitres is <5%.
What features would you see on a HYPERPLASTIC THYROID?
Scalloping of coloid
Papillary folding
Loss of coloid ! relative icnrease in the number of cells at the expense of colloid
cells lining the coloid appear low columnar or cuboidal (instead of squamous)
What would you see in a MULTINODULAR thyroid?
- variably sized and shape follicles form irregular nodules
- follicles are distended with colloid
- cuboidal cells show regular nuclei
- haemociderin laden macrophages
- fibrosis
HASHIMOTO’s
- Atrophied follicles
- intense inflammatory cell infiltrate (germinal cells, lymphocytes, plasma cells) replacing follicles
- groups of HURTHLE CELLS
What would you see in an adenoma?
regular round nuclei and granular cytoplasym
What is the most common primary benign neoplasm of the thyroid?
Primary adenoma
what are some primary malignant thyroid neoplasms?
what is the most common
Papillary carcinoma (75% to 85% of cases)
Follicular carcinoma (10% to 20% of cases) – often appear the same as adenoma but show capsular invasion. Medullary carcinoma (5% of cases) – MEN2 Anaplastic carcinoma (<5% of cases)
WHAT IS A GOOD WAY OF EVALUATING A THYROID NODULE?
FNA BIOPSY
What does papillary carcinoma of the thyroid look like microscopically?
unencapsulate papillary structures with a branching pattern ground glass bodies PSAMMOMA BODIES- bright red infiltrating nests of tumour cells
What are the causes of primary hyperparathyroidism?
Parathyroid adenoma 80-85%
Parathyroid hyperplasia 15% (Note the association with MEN I and 2 ) and
rarely parathyroid carcinom
wht is the commmonest tumour of the pituitary gland?
Pituitary adenoma
• Commonest tumour of the pituitary gland
• 10% of all intracranial neoplasms
• 25-35% invade local tissue without the capacity to metastasize
• Young to middle aged adults
• Functioning or non-functioning determines clinical presentation
• If non-functioning macroadenoma >10mm
– visual field defects and HYPOPITUITARISM
• If functioning usually a microadenoma <10mm
In functioning adenoma’s what are common pathologies which can occura as a consequence?
– GH-gigantism or acromegaly
– TSH- hyperthyroidism
– Prolactin-galactorrhoea, amenorrhoea, infertility
– FSH/LH-ovarian cysts, oligomenorrhoea, amenorrhoea, endometrial
hyperplasia
– ACTH-Cushing’s disease
Describe CUSHING’s Syndrome
Caused by any condition that produces elevated glucocorticoid levels (cortisol).
Aetiology:
exogenous: Most commonly iatrogenic glucocorticoid administration
Endogenous :
ACTH-dependent
• Cushing disease– pituitary adenoma (70%)
• Ectopic ACTH/CRH from tumour (for example lung cancer) (10%)
ACTH-independent
• Adrenal adenoma (10%)
• Adrenal carcinoma (5%) Rarer causes
• Macronodular hyperplasia
• Primary pigmented nodular adrenal disease
• McCune-Albright syndrome
What is CONN’s Syndrome?
HIGH BP caused by excessive production of aldosterone (mineralocorticoid)
Aetiology
– Adrenal adenoma 40%
– Bilateral hypertrophy of the zona glomerulosa cells* 60%
– Glucocorticoid-remediable aldosteronism (Autosomal Dominant where
aldosterone secretion is under the control of ACTH)
– Adrenal Carcinoma