Adrenal glands Flashcards

1
Q

what are the layers of the adrenal gland structure and what so they produce?

A

CORTEX
- zona glomerulus : mineralocorticoids like aldosterone SALT.
- zona fasiculata : Glucocorticoids like cortisol SUGAR.
- zona reticularis : glucocorticoids and androgen SEX.
MEDULLA
- chromaffin cells : adrenaline and noradrenaline.

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2
Q

what are some characteristics of steroid hormones?

A
  • synthesised from cholesterol in adrenal glands and gonads.
  • lipid soluble.
  • binds to nuclear receptor family receptors to modulate gene transcription.
  • eg : gluco/mineralocoticoids, androgens, oestrogens, progestins.
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3
Q

how do corticosteroids exert action by regulating gene trasncription?

A
  • diffuse across plasma membrane and binds to glucocorticoid receptor causing dissociation of chaperone proteins.
  • receptor ligand complex translocated to nucleus.
  • receptor binds to glucocorticoid response element GRE or other transcription factors.
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4
Q

describe aldosterone and its effects.

A
  • mineralocorticoid which is a steroid lipophilic hormone carried with albumin.
  • receptors intracellular and regulated gene transcription.
  • in nephron promoted NA+/K+ pump expression so reabsorption of Na+ and excretion of K+ influencing water retention, increasing Blood vol and pressure.
    RAAS system!!! LOOK OVER SLIDE.
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5
Q

what causes hyperaldosteronism?

A
  • primary defect in adrenal cortex : bilateral idiopathic adrenal hyperplasia, Conn’s syndrome (adenoma), low renin.
  • secondary overactive RAAS : renin producing tumour, renal artery stenosis, high renin levels.
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6
Q

how does hyperaldosteronism present and how would you treat?

A
  • signs : high BP, low ventricular hypertrophy, stroke, hypernatraemia, hypokalamia.
  • treatment : adenomas removed by surgery, spironolactone which is a mineralocorticoid receptor antagonist.
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7
Q

describe the features and actions of cortisol.

A
  • most abundant corticosteroid counting for 95% of glucocorticoid activity,
  • steroid hormone carried in plasma by transcortin.
  • negative feedBack to hypothalamus inhibits CRH & ACTH.
  • regulates gene transcription, synthesised in response to ACTH.

actions : increased protein breakdown, lipolysis of fat, gluconeogenesis, anti-inflammatory, depression of immune response, resistance to stress by increasing available glucose.

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8
Q

describe briefly the pathway of stress in the hypothalamic-pituitary-adrenal axis.

A
  • stress –> hypothalamus –> CRH –> anterior pituitary –> ACTH –> adrenal cortex –> cortisol –> target tissue.
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9
Q

what are the overall glucocorticoid actions on metabolism?

A
  • increased glucose production.
  • breakdown of proteins.
  • redistribution of fats in abdomen, buffalo hump, moon face.
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10
Q

what external and endogenous causes of cushing’s syndrome?

and what are the signs?

A
  • external : prescribed glucocorticoids.
  • endogenous : cushing’s disease and adenoma secreting ACTH, cortisol producing adrenal tumour (adrenal cushing’s), non-pituitary adrenal tumours producing ACTH like small cell cancer.
  • signs : moon face, buffalo hump, abdominal obesity, purple striae, acute weight gain, hyperglycaemia etc.
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11
Q

what is the significance of steroid drugs?

eg: prednisolone, dexamathasone.

A
  • anti-inflammatory and immunomodulatory.
    used to treat inflammatory disorders like asthma, inflammatory bowel disease, RA, auto immune diseases.
  • suppress immunity in organ transplantation.
  • side effects : high cortisol effects.

SHOULD BE GRADUALLY REDUCED NOT STOPPED IMMEDIATELY.

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12
Q

what is addison’s disease?

A
  • chronic adrenal insufficiency commonly caused by destructive atrophy from autoimmune response (used to be TB complication).
  • presents as postural hypotension, lethargy, weight loss, anorexia, increased skin pigmentation (decreased cortisol causing increased POMC & MSH) hypoglycaemia.
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13
Q

what is an addisonian crisis?

A
  • life threatening emergency due to adrenal insufficiency precipitated by severe stress, salt depravation, infection, trauma, abrupt steroid drug withdrawal.
  • symptoms nausea, vomiting, pyrexia, hypotension.
  • treatment being fluid replacement, cortisol.
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14
Q

describe importance of androgens.

A
  • DHEA which is an androgen is converted to testosterone in testes pre-pubery release of testosterone alone.
  • in females these are converted to oestrogen by other tissue which is the only source after menopause. or purely used to promote libido.
  • promotes axillary and pubic hair growth in both sexes.
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15
Q

describe the special structure of the adrenal meduall.

A
  • modified sympathetic ganglion on ANS with chromaffin cells that lack axons but act as postganglionic nerve fibres to release AD & NAD to blood.
    LOOK AT SLIDES.
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16
Q

what are the hormonal actions of adrenaline?

A
  • heart : increases HR (B1), contractility (B1).
  • lungs : bronchodilation (B2).
  • vessels : vasoconstriction (a1) and vasodilation (B2).
    LOOK OVER SLIDES.
17
Q

what is a phaeochromocytoma?

A
  • a chromaffin cell tumour which is tumour that stains dark with chromium salts.
  • may precipitate severe hypertension.
  • characteristics : severe hypertension, headaches, palpitations, anxiety, weight loss.