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
Treatment of thyroid carcinoma?
Levothyroxine (T4) Thyroidectomy
26
What is the most common hormonal disturbance of the pituitary?
Hyperprolactinemia
27
Causes of hyperprolactinemia?
Prolactinoma Pituitary stalk damage Drugs Pregnancy Stress
28
What is hyperprolactinemia?
Too much prolactin in the blood of women who aren't pregnant + in men
29
Treatment for adrenal crisis?
IV hydrocortisone
30
What is serum calcium controlled by?
PTH + vitamin D
31
Is hypercalcaemia or hypocalcaemia more common?
Hypercalcaemia
32
What is calcitriol stimulated by?
Low plasma calcium Low plasma phosphate PTH
33
K+ levels for hypokalaemia?
Serum K+ <3.5 mmol/L (>2.5 mmol/L is a MEDICAL EMERGENCY)
34
Describe carcinoid tumours
These tumours originate from the enterochromaffin cells (neural crest) + are capable of producing serotonin
35
What is carcinoid crisis?
When a caricnoid tumour outgrows its blood supply mediators flow out + this is LIFE-THREATENING
36
Treatment of carcinoid crisis?
High dose somatostatin analogue (e.g. octreotide)
37
Sulphonylureas: examples + indications
Gliclazide T2DM
38
Glitazones: examples
Pioglitazone
39
Glitazones: mechanisms
Activates PPARs which bind FFAs + induce genes that enhance insulin action
40
Antithyroid drugs: examples + indications
Carbimazole Grave's + before thyroid surgery
41
Antithyroid drugs: mechanisms
Prevents thyroid peroxidase from iodinating tyrosine residues so reduces production of T3 + T4
42
GH receptor antagonists: examples + indications
Pegvisomant Acromegaly
43
GH receptor antagonists: mechanisms
Blocks action of GH at its receptor to reduce production of IGF-1
44
Vasopressin antagonists: examples + indications
Tolvaptan Euvolemic/Hypervolemic hyponatraemia
45
Vasopressin antagonists: mechanisms
Inhibits V2 so increases fluid excretion
46
Vasopressin analogue: examples + indications
Desmopressin DI + distinguish cranial from nephrogenic DI
47
Adrenal corticosteroid inhibitors: examples
Metyrapone Cushing's + diagnose adrenal insufficiency
48
Adrenal corticosteroid inhibitors: mechanisms
Blocks cortisol synthesis by reversibly inhibits the enzyme that stimulates ACTH secretion
49
Adrenal corticosteroid inhibitors: SEs
GI disturbances Headache Dizziness Drowsiness
50
What is a NFPA?
Benign tumour of the pituitary which doesn't produce excess hormones