Week 4 Pathology - Endocrine Flashcards
What is the clinical triad of Grave’s Disease?
1) Hyperparathyroidism (hyper functional enlargement of thyroid
2) Exophthalmos
3) Pretibial myxoedema
What is the pathogenesis of Grave’s disease?
Stimulatory autoantibody formation against TSH receptor, and then these activate thyroid hormone release/follicular cells outside of normal feedback mechanisms
What is the typical TFT pattern in Grave’s?
Low TSH, High T3 and T4
What is the pathogenesis of Hashimoto’s thyroiditis?
formation of autoantibodies against TSH receptors, thyroglobulin, thyroperoxidase –> all causing reduced functionality of follicular cells and thyroid hormone –> hypothyroidism
Also causes immune cell migration and tissue damage
What two factors will increase PTH secretion?
Low ECF calcium
High ECF Phosphate
What is the mechanism by which PTH hormone is released/not released?
GPCR on parathyroid cells are constantly sampling ECF, and when Ca2+ is bound, there’s chronic inhibition of PTH release.
When tonic inhibition is removed –> PTH release
What are the 4 ways that PTH serve to increase Ca2+ in plasma?
- Bone resorption via osteoclasts
- Vitamin D activation
- Increased renal absorption of Ca2+
- Reduced phosphate reabsorption renally
What is primary hyperparathyroidism?
Autonomous overproduction of PTH by the Parathyroid gland.
Majority of hyperparathyroidism.
Usually due to single adenoma.
What is the classical biochemical findings of primary hyperparathyroidism?
Inappropriately elevated
What is secondary hyperparathyroidism?
Caused by disorders that result in hypocalcaemia, which will lead to increased PTH levels.
Commonly CKD and Vit D deficiency, malabsorption syndrome.
What is the classical biochemical findings of secondary hyperparathyroidism?
Low Calcium
high PTH
What tertiary hyperparathyroidism?
Excessive PTH secretion after longstanding secondary hyperparathyroidism, which remains after the cause of the secondary hyperparathyroidism has been corrected –> often needs surgery to correct
What is the pathogenesis of T1DM?
Genetic susceptibility, autoimmunity, and environmental triggering (i.e. viral infection) –> formation of autoantibodies against beta islet cells
What is the pathogenesis of T2DM?
Focal atrophy and amyloid deposition after persistent islet cell stimulation leading to beta cell depletion.
Also genetic susceptibility.
What are macrovascular complications of DM?
CAD
PVD
Cerebrovascular disease
HTN
What are the microvascular complications of DM?
Nephropathy
Retinopathy
Neuropathy
What trophic hormones are secreted by the anterior pituitary?
LH
FSH
ACTH
TSH
Prolactin
GH
What are some causes of pan-hypopituitarism?
Ischaemic injury
Trauma
Non functioning pituitary adenoma
What is Cushing’s syndrome? What is Cushing’s Disease?
Syndrome of effects of pathologically elevated levels of cortisol, from whatever cause.
Cushing’s Disease is an ACTH secreted pituitary tumour, causing increased cortisol secretion from adrenals.
Other than Cushing’s disease, what are the other aetiologies of cushing’s syndrome?
- Iatrogenic (exogenous steroid use)
- Autonomous cortisol production
- Ectopic ACTH secreting tumour (SCLC, carcinoids)
What is the clinical presentation of Cushing’s syndrome?
Weight gain, central adiposity
Moon face
Abdominal striae
Proximal wasting
Easy bruising/thinning of the skin
Infertility
What are associated metabolic complications of Cushing’s syndrome?
HTN
Diabetes
Osteoporosis
Dyslipidaemia
How does each type of cushings respond to dexamethasone testing?
- Pituitary: high ACTH, doesn’t respond to low, but does to high dose dexamethasone
- Ectopic ACTH: high ACT, insensitive to high dose Dex
- Adrenal tumour, high urine cortisol despite low ACTH, insensitive to high dose dex
