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Endocrinology Y2 > Hyperadrenal Disorders > Flashcards

Hyperadrenal Disorders Flashcards

1
Q

What disease is associated too much cortisol

A

Cushings

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2
Q

What is Cushings cause by

A

Too much cortisol

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3
Q

Clinical features of Cushings disease? (7)

A
  • Too much cortisol
  • Centripetal obesity
  • Moon face/buffalo hump
  • Proximal myopathy
  • Hypertension and hypokalaemia
  • Red striae, thin skin and bruising
  • Osteoporosis, diabetes (DMII)
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4
Q

Causes of Cushings? (3)

A
  • Taking too many steroids
  • Pituitary dependent Cushing’s disease
  • Ectopic ACTH from lung cancer
  • Adrenal adenoma secreting cortisol
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5
Q

Tests for Cushings? (3)

A
  • 24h urine collection for urinary free cortisol High level suggests Cushing’s syndrome
  • Blood diurnal cortisol levels Should be lowest at midnight (high at 9am)
  • Low dose dexamethasone suppression test Artificial analogue of cortisol Stops normal people making ACTH Normal people suppress their cortisol to zero, Cushings fails to do so
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6
Q

When are Blood diurnal cortisol levels tested and why

A

Mignight, cortisol should be lowest here

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7
Q

3 treatments for Cushings? (2 pharmacological methods)

A
  1. Enzyme inhibitors
  2. Receptor blocking drugs
    * Surgery is also an option
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8
Q

2 Inhibitors of steroid synthesis?

A
  • Metyrapone

- Ketoconazole

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9
Q
  • Metyrapone is an example of
A

Inhibitor of steroid synthesis

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10
Q
  • Ketoconazole is an example of
A

Inhibitor of steroid synthesis

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11
Q

MoA of metyrapone?

A
  • Inhibits 11beta-hyroxylase
  • Steroid synthesis in the zona fasciculata (and reticularis) arrested at the 11-deoxycoritsol stage
  • 11-deoxycortisol has no negative feedback effect on the hypothalamus or pituitary
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12
Q

metyrapone inhibits what enzyme

A

11beta-hyroxylase

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13
Q

Where in the adrenals is cortisol synthesised

A

zona fasciculata

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14
Q

Uses of steroid synthesis inhibitors in Cushings? (3)

A
  • Control of Cushing’s prior to surgery:
  • Adjust dose (oral) according to cortisol (aim for mean serum cortisol 150-300 nmol/L)
  • Improves patient symptoms and promotes best post-op recovery
  • Control of Cushing’s symptoms while waiting for radiotherapy to work
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15
Q

effects of 11-deoxycorticosterone when cortisol synthesis is halted at that stage?

A

: 11-deoxycorticosterone accumulates in the z. glomerulosa; it has aldosterone-like (mineralocorticoid) activity, leading to salt retention and hypertension

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16
Q

What hormone effects does 11-deoxycorticosteron have similar effects to

A

Aldosterone

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17
Q

What is ketoconazole used for

A

Cushings

18
Q

Side effects of ketoconazole?

A
  • Liver damage Possibly fatal Monitor liver function weekly, clinically and biochemically
19
Q

What is the cause of Conns syndrome

A

Benign adrenal cortical tumour (Zona glomerulosa) Primary hyperaldosteronism

20
Q

Which zone of the adrenals produce aldosterone

A

Zona glomerulosa

21
Q

Zona glomerulosa produces…

A

Aldosterone

22
Q

Zona fasciculata produces….

A

Cortisol

23
Q

Symptoms of high aldosterone

A
  • Hypertension and hypokalaemia
24
Q

How to diagnose primary vs secondary Hyperaldosteronism

A
  • Renin-angiotensin system should be suppressed (this rules out secondary hyperaldosteronism) Zero/very low renin
25
Q

renin levels in primary Hyperaldosteronism?

A

Low

26
Q

renin levels in secondary Hyperaldosteronism?

A

high

27
Q

Treatment for primary Hyperaldosteronism?

A

Mineralocorticoid receptor antagonist]

- Surgery

28
Q

Mineralocorticoid receptor antagonist example?

A

SPIRONOLACTONE/EPLERONONE

29
Q

MoA of spironolactone?

A
  • Converted to several active metabolites, including CANRENONE, a competitive antagonist of the MR
  • Blocks Na+ resportion and K+ excretion in the kidney tubules (potassium sparing diuretic)
30
Q

Effects of mineralocorticoid receptor antagonists?

A
  • Blocks Na+ resportion and K+ excretion in the kidney tubules (potassium sparing diuretic)
31
Q

RoA of mineralocorticoid receptor antagonists

A

Oral

32
Q

Side effects of of mineralocorticoid receptor antagonists

A
  • Menstrual irregularities (also an agonist of the progesterone receptor)
  • Gynaecomastia (antagonist of the androgen receptor) Painful
33
Q

Drug of choice for hyper-aldosteronism? why?

A

Epleronone ->- Less binding to androgen and progesterone receptors

34
Q

MoA of epleronone

A
  • Converted to several active metabolites, including CANRENONE, a competitive antagonist of the MR
  • Blocks Na+ resportion and K+ excretion in the kidney tubules (potassium sparing diuretic)
35
Q

what is PHAEOCHROMOCYTOMAS:

A

Tumours of the adrenal MEDULLA which secrete catecholamines (make adrenaline and noradrenaline)

36
Q

Risk of PHAEOCHROMOCYTOMAS

A

That the Tumour suddenly degranulates and produces loads of adrenaline which increases HR, anxiety and possible strokes/MRIs

37
Q

Clinical features of phaeochromocytomas (5)

A
  • Hypertension in young people
  • Episodic severe hypertension (this can also be precipitated by abdominal palpation by the doctor)
  • More common in certain inherited conditions
  • Severe hypertension can cause MI or stroke
  • High adrenaline can cause ventricular fibrillation and death Medical emergency
38
Q

Management of phaeochromocytomas?

A
  • Eventually need surgery, BUT patient needs preparation as anaesthetic can precipitate a hypertensive crisis
  • ALPHA BLOCKADE= first therapeutic step
  • Patients may need intravenous fluid as alpha blockade commences
  • Beta blockade added to prevent tachycardia
39
Q

First step in Management of phaeochromocytomas?

A

Alpha blockade

40
Q

What can happen if you give anaesthetic preop to a phaeocytochroma patient if they haven’t been given alpha blockers

A

Release of adrenaline, boom, hypertensive crisis bitches

Endocrinology Y2 (18 decks)

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