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ED Primary Exam > Week 4 Pathology - Endocrine > Flashcards

Week 4 Pathology - Endocrine Flashcards

1
Q

What is the clinical triad of Grave’s Disease?

A

1) Hyperparathyroidism (hyper functional enlargement of thyroid
2) Exophthalmos
3) Pretibial myxoedema

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2
Q

What is the pathogenesis of Grave’s disease?

A

Stimulatory autoantibody formation against TSH receptor, and then these activate thyroid hormone release/follicular cells outside of normal feedback mechanisms

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3
Q

What is the typical TFT pattern in Grave’s?

A

Low TSH, High T3 and T4

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4
Q

What is the pathogenesis of Hashimoto’s thyroiditis?

A

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

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5
Q

What two factors will increase PTH secretion?

A

Low ECF calcium
High ECF Phosphate

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6
Q

What is the mechanism by which PTH hormone is released/not released?

A

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

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7
Q

What are the 4 ways that PTH serve to increase Ca2+ in plasma?

A
  1. Bone resorption via osteoclasts
  2. Vitamin D activation
  3. Increased renal absorption of Ca2+
  4. Reduced phosphate reabsorption renally
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8
Q

What is primary hyperparathyroidism?

A

Autonomous overproduction of PTH by the Parathyroid gland.

Majority of hyperparathyroidism.

Usually due to single adenoma.

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9
Q

What is the classical biochemical findings of primary hyperparathyroidism?

A

Inappropriately elevated

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10
Q

What is secondary hyperparathyroidism?

A

Caused by disorders that result in hypocalcaemia, which will lead to increased PTH levels.

Commonly CKD and Vit D deficiency, malabsorption syndrome.

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11
Q

What is the classical biochemical findings of secondary hyperparathyroidism?

A

Low Calcium
high PTH

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12
Q

What tertiary hyperparathyroidism?

A

Excessive PTH secretion after longstanding secondary hyperparathyroidism, which remains after the cause of the secondary hyperparathyroidism has been corrected –> often needs surgery to correct

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13
Q

What is the pathogenesis of T1DM?

A

Genetic susceptibility, autoimmunity, and environmental triggering (i.e. viral infection) –> formation of autoantibodies against beta islet cells

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14
Q

What is the pathogenesis of T2DM?

A

Focal atrophy and amyloid deposition after persistent islet cell stimulation leading to beta cell depletion.

Also genetic susceptibility.

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15
Q

What are macrovascular complications of DM?

A

CAD
PVD
Cerebrovascular disease
HTN

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16
Q

What are the microvascular complications of DM?

A

Nephropathy
Retinopathy
Neuropathy

17
Q

What trophic hormones are secreted by the anterior pituitary?

A

LH
FSH
ACTH
TSH
Prolactin
GH

18
Q

What are some causes of pan-hypopituitarism?

A

Ischaemic injury
Trauma
Non functioning pituitary adenoma

19
Q

What is Cushing’s syndrome? What is Cushing’s Disease?

A

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.

20
Q

Other than Cushing’s disease, what are the other aetiologies of cushing’s syndrome?

A
  • Iatrogenic (exogenous steroid use)
  • Autonomous cortisol production
  • Ectopic ACTH secreting tumour (SCLC, carcinoids)
21
Q

What is the clinical presentation of Cushing’s syndrome?

A

Weight gain, central adiposity
Moon face
Abdominal striae
Proximal wasting
Easy bruising/thinning of the skin
Infertility

22
Q

What are associated metabolic complications of Cushing’s syndrome?

A

HTN
Diabetes
Osteoporosis
Dyslipidaemia

23
Q

How does each type of cushings respond to dexamethasone testing?

A
  1. Pituitary: high ACTH, doesn’t respond to low, but does to high dose dexamethasone
  2. Ectopic ACTH: high ACT, insensitive to high dose Dex
  3. Adrenal tumour, high urine cortisol despite low ACTH, insensitive to high dose dex

ED Primary Exam (46 decks)

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