Endocrinology Flashcards

1
Q

Define endocrinology

A

Study of hormones (+ their gland of origin), receptors, intracellular signalling pathways, + associated diseases

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2
Q

Describe insulin activation

A
  1. Binds to insulin receptors
  2. Results in phosphorylation of receptor + activation of secondary messenger - TYROSINE KINASE
  3. Phosphorylation of signal molecules
  4. Cascade of effect
  5. Glucose uptake
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3
Q

Give 3 examples of amine hormones

A

Dopamine, adrenaline, noradrenaline

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4
Q

Is T3 or T4 more active?

A

T3

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5
Q

Is T3 or T4 more abundant in the body?

A

T4

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6
Q

Where do peptide hormones bind?

A

Receptors on cell membrane

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7
Q

Where do steroid hormones bind?

A

Cytoplasmic receptors

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8
Q

Normal blood glucose?

A

3.5-8.0 mmol/L

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9
Q

Why is the brain the MAIN consumer of glucose?

A

FFAs can’t cross the BBB so the brain can’t convert them into ketones (–> acetyl-CA for Krebs)

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10
Q

Pathophysiology of DKA

A
  1. Hyperglycaemia –> osmotic diuresis
  2. More peripheral lipolysis –> more FFAS
  3. More acetyl-CoA –> more ketones
  4. Metabolic acidosis –> vomiting
  5. Dehydration impairs renal excretion of H+ + ketones
  6. pH-dependent processes impaired
  7. Worsened by ‘stress hormones’
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11
Q

Define ketoacidosis

A

A state of uncontrolled catabolism associated with insulin deficiency

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12
Q

What is hyperosmolar hyperglycaemia?

A

Life-threatening emergency characterised by marked hyperglycaemic, hyperosmolality, + mild/no ketosis

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13
Q

What is the metabolic emergency characteristic of uncontrolled T2DM?

A

Hyperosmolar hyperglycaemic state

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14
Q

Give 3 possible presentations of pituitary tumour

A

Pressure on local structures - e.g. bitemporal hemianopia
Pressure on normal pituitary - HYPOpituitarism
Functioning tumour - HYPERpituitarism

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15
Q

List 3 functioning tumours (hyperpituitarism)

A

Prolactinoma
Acromegaly
Cushing’s

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16
Q

Give 5 possible causes of hyperthyroidism

A

Grave’s disease
Toxic multinodular goitre
Solitary toxic adenoma (benign)
De quervain’s thyroiditis (post-viral)
Drug-induced hyperthyroidism

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17
Q

Treatment of Graves’ opthalmopathy?

A

IV methylprednisolone

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18
Q

Causes of primary hypothyroidism?

A

Primary atrophic hypothyroidism (PAH)
Hashimoto’s thyroidits
Postpartum thyroiditis
Iatrogenic (thyroidectomy, radioactive iodine therapy)
Drugs (e.g. carbimazole, lithium, amiodarone)
Iodine deficiency

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19
Q

Cause of secondary hypothyroidism?

A

Hypopituitarism

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20
Q

Most common cause of hypothyroidism?

A

Primary atrophic hypothyroidism (PAH)

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21
Q

What drug can cause both hyperthyroidism + hypothyroidism?

A

Amiodarone

22
Q

Main complication of hypothyroidism?

A

Myxoedema coma

23
Q

Most common type of thyroid carcinoma?

24
Q

Clinical presentation of thyroid carcinoma?

A

Thyroid nodules
Thyroid gland increases in size, becomes hard, + is irregular in shape
Dysphagia
Hoarse voice

25
Q

Treatment of thyroid carcinoma?

A

Levothyroxine (T4)
Thyroidectomy

26
Q

What is the most common hormonal disturbance of the pituitary?

A

Hyperprolactinemia

27
Q

Causes of hyperprolactinemia?

A

Prolactinoma
Pituitary stalk damage
Drugs
Pregnancy
Stress

28
Q

What is hyperprolactinemia?

A

Too much prolactin in the blood of women who aren’t pregnant + in men

29
Q

Treatment for adrenal crisis?

A

IV hydrocortisone

30
Q

What is serum calcium controlled by?

A

PTH + vitamin D

31
Q

Is hypercalcaemia or hypocalcaemia more common?

A

Hypercalcaemia

32
Q

What is calcitriol stimulated by?

A

Low plasma calcium
Low plasma phosphate
PTH

33
Q

K+ levels for hypokalaemia?

A

Serum K+ <3.5 mmol/L
(>2.5 mmol/L is a MEDICAL EMERGENCY)

34
Q

Describe carcinoid tumours

A

These tumours originate from the enterochromaffin cells (neural crest) + are capable of producing serotonin

35
Q

What is carcinoid crisis?

A

When a caricnoid tumour outgrows its blood supply mediators flow out + this is LIFE-THREATENING

36
Q

Treatment of carcinoid crisis?

A

High dose somatostatin analogue (e.g. octreotide)

37
Q

Sulphonylureas: examples + indications

A

Gliclazide
T2DM

38
Q

Glitazones: examples

A

Pioglitazone

39
Q

Glitazones: mechanisms

A

Activates PPARs which bind FFAs + induce genes that enhance insulin action

40
Q

Antithyroid drugs: examples + indications

A

Carbimazole
Grave’s + before thyroid surgery

41
Q

Antithyroid drugs: mechanisms

A

Prevents thyroid peroxidase from iodinating tyrosine residues so reduces production of T3 + T4

42
Q

GH receptor antagonists: examples + indications

A

Pegvisomant
Acromegaly

43
Q

GH receptor antagonists: mechanisms

A

Blocks action of GH at its receptor to reduce production of IGF-1

44
Q

Vasopressin antagonists: examples + indications

A

Tolvaptan
Euvolemic/Hypervolemic hyponatraemia

45
Q

Vasopressin antagonists: mechanisms

A

Inhibits V2 so increases fluid excretion

46
Q

Vasopressin analogue: examples + indications

A

Desmopressin
DI + distinguish cranial from nephrogenic DI

47
Q

Adrenal corticosteroid inhibitors: examples

A

Metyrapone
Cushing’s + diagnose adrenal insufficiency

48
Q

Adrenal corticosteroid inhibitors: mechanisms

A

Blocks cortisol synthesis by reversibly inhibits the enzyme that stimulates ACTH secretion

49
Q

Adrenal corticosteroid inhibitors: SEs

A

GI disturbances
Headache
Dizziness
Drowsiness

50
Q

What is a NFPA?

A

Benign tumour of the pituitary which doesn’t produce excess hormones