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Met2 > Adrenals > Flashcards

Adrenals Flashcards

1
Q

Which cells in the adrenal medulla release catecholamines?

A

Chromaffin cells

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2
Q

What stimulates aldosterone release from the zona glomerulosa?

A
  • potassium (increase in)
  • reduced BP (angiotensin II)
  • ACTH secretion
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3
Q

What type of receptor is the mineralocorticoid receptor?

A

Nuclear receptor

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4
Q

What changes occur when aldosterone binds to the mineralocorticoid receptor?

A 
Na/K ATPase stimulated 
Increased expression of ENaC
Additional ENaC
Stimulates H+ ATPase
- result = loss of H+ = metabolic alkalosis
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5
Q

What are the potential causes of primary hyperaldosteronism?

A
  1. Conn’s syndrome
  2. Aldosterone producing adenoma
  3. Bilateral adrenal hyperplasia
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6
Q

What are the signs of Conn’s syndrome?

A
  • hypertension
  • suppressed plasma renin activity
  • increased aldosterone secretion
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7
Q

How can primary hyperaldosteronism be diagnosed?

A
  • aldosterone:renin ratio
  • saline suppression test
  • CT adrenal
  • adrenal venous sampling
  • metomide PET
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8
Q

How can primary hyperaldosteronism be treated?

A

MR antagonists, e.g.:

  • spironolactone
  • eplerenone
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9
Q

What is Liddle’s syndrome? What are the signs?

A 
It's overexpression of eNaC
Signs:
- hypertension 
- hypokalaemia 
- metabolic alkalosis (increased H+ secretion)
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10
Q

What do glucocorticoids inhibit?

A
  • CRH secretion + RNA transcription
  • AVP secretion + RNA transcription
  • ACTH secretion
  • POMC transcription
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11
Q

What are the main causes of Cushing’s syndrome?

A
  1. Iatrogenic - steroid creams/inhalers/tablets
  2. corticotrophin adenoma of pituitary
  3. ectopic ACTH secreting neuroendocrine tumour
  4. cortisol secreting adrenal adenoma
  5. bilateral adrenal hyperplasia
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12
Q

How is Cushing’s syndrome diagnosed?

A
  1. overnight dexamethasone suppression test
  2. 24 hour urine free cortisol
  3. LDDST (low dose dexamethasone suppression test): 0.5mg dexamethasone every 6 hours for 2 days
  4. cortisol day urine and midnight sleeping control
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13
Q

What imaging can be done for Cushing’s syndrome?

A
  • MRI pituitary
  • CT adrenals
  • Inferior petrosal sinus sampling
  • Nuclear medicine: octreotide uptake scan
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14
Q

What is the treatment for Cushing’s syndrome?

A

Pituitary:

  • transsphenoidal surgery
  • external beam radiotherapy
  • stereotactic radiosurgery

Adrenal:

  • adrenalectomy
  • metyrapone/ketoconazole/etomidate
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15
Q

What are the main reasons for primary adrenal failure/insufficiency?

A
  • autoimmune

- tuberculosis

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16
Q

What are the symptoms of Addison’s?

A
  • fatigue
  • weakness
  • myalgia
  • anorexia
  • weight loss
  • hyper pigmentation
17
Q

What is an Addisonian crisis?

A
  • low BP (can’t respond to hypotension)
  • low glucose (can’t respond to hypoglycaemia)
  • low Na+ (no/lack of aldosterone)
  • high K+ (no/lack of aldosterone)
18
Q

How is Addison syndrome diagnosed?

A
  • low 9am cortisol
  • high ACTH
  • short synacthen test (see if corticotrophs react to stimulation with synthetic ACTH)
19
Q

How is Addison syndrome treated? How is an Addisonian crisis treated?

A
  • replacement steroid (hydrocortison, fludrocortisone)

Addisonian Crisis: IV fluid resuscitation, IM hydrocortisone

20
Q

What causes congenital adrenal hyperplasia?

A

due to 21-hydroxylase deficiency

= no conversion to aldosterone and cortisol

21
Q

What is changes result from congenital adrenal hyperplasia?

A
  • excess ACTH will be secreted (no -ve feedback)

- stimulate cholesterol uptake in adrenal gland –> instead of being converted to cortisol –> converted to testosterone

22
Q

What are catecholamines made from?

A

L-tyrosine

23
Q

What are the different types of chromaffin cell tumours?

A
  1. phaeochromacytoma: arising from within the adrenal medulla
  2. paraganglioma: extra-adrenal tumour
24
Q

What are alpha 1 receptors responsible for?

A

vascular and smooth muscle contraction

25
Q

What are alpha 2 receptors responsible for?

A

presynaptic, inhibitory to noradrenaline release –> suppress BP

26
Q

What are beta 1 receptors responsible for?

A
  • positive inotropic and chronotropic in heart
  • increase renin
  • increase lipolysis
27
Q

What are beta 2 receptors responsible for?

A
  • bronchodilation
  • vascular dilation
  • uterine smooth muscle relaxation
  • glycogenolysis
28
Q

What are beta 3 receptors responsible for?

A
  • lipolysis

- energy expenditure

29
Q

What are D1 receptors responsible for?

A

cerebral, renal, mesenteric, coronary vasculature dilation

30
Q

What are D2 receptors responsible for?

A

presynaptic inhibition of noradrenaline + prolactin release

31
Q

What are the symptoms of catecholamine excess?

A
  • impending doom
  • diaphoresis
  • dyspnea
  • headache
  • hypertension
  • palpitation
  • tremor
  • N+V
  • fatigue
  • orthostatic hypotension
  • hyperglycaemia
  • weight loss
  • epigastric + chest pain
  • congestive heart failure
32
Q

What are the signs of phaemochromocytoma and paraganglioma (PPGL)?

A
  • hyperadrenergic spells
  • resistance hypertension
  • familial syndrome
  • incidentally discovered adrenal mass
  • pressor response during general anaesthesia
  • early onset hypertension
  • dilated cardiomyopathy
33
Q

How is PPGL diagnosed?

A
  • 24hour urine metanephrines
  • plasma metanephrines
  • CT/MRI adrenals and abdomen
  • I-MIBG scintigraphy
34
Q

How is PPGL treated?

A
  • surgical resection
  • pre-operative alpha and beta blockade –> phenoxybenzamine and propanolol
  • acute crisis: IV phentolamine or nircardipine
  • avoid opiates
  • I-MIBG therapy for malignant disease
35
Q

What would happen if you treated a patient with a pheochromocytoma with beta-blockers alone?

A

will lead to more vasoconstriction –> will block beta-2 receptors causing vasodilation

Met2 (26 decks)

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