Andrenal Glands

Question 1

what is the order of the 4 adrenal gland layers?

Answer 1

zona glomerulosa, zona fasiculata, zona reticularis, medulla

Question 2

what does the memory tool “go find rex - make good sex” mean?

Answer 2

glomerulosa, fasiculata, raticularis, mineralocorticoids, glucocorticoids, sex hormones

Question 3

what does the medulla secrete?

Answer 3

catecholamines - adr and noradr

Question 4

which part of the adrenal gland is the only area to receive secretomotor innervation from SNS? And what nerves innervate this?

Answer 4

medulla - and T8-T11 splanchnic nerve

Question 5

what innervates the blood vessels?

Answer 5

preganglionic fibres synapsing in the coeliac ganglion giving rise to post-gang fibres

Question 6

what do preganglionic neurons secrete and onto what receptor ?

Answer 6

acetylcholine and nicotinic acetylcholine receptors

Question 7

what do postganglionic neurones secrete and onto what receptor?

Answer 7

sympathetic - secrete noradrenaline and a1, a2, b1 and b2 adrenoceptors (except for sweat glands - acetylcholine and muscarinic receptors). parasympathetic - secrete acetylcholine and muscarinic receptors

Question 8

what % adrenaline:noradrenaline does the medulla secrete?

Answer 8

80%:20%

Question 9

what fibres directly innervate chromaffin cells?

Answer 9

preganglionic cholinergic sympathetic fibres

Question 10

what’s the role of the adrenals in the fight or flight response? how fast is their response?

Answer 10

follows on from the SNS response which cannot be continued over long periods due to the ATP demand. recretion of catecholamines sustains the fight or flight response. not as fast as SNS - usually minutes and not so demanding on energy as adrenaline released continuously if needed from the activation of a single fibre.

Question 11

is the medullary fight or flight response targetted?

Answer 11

no

Question 12

what is a pheochromocytoma?

Answer 12

tumour of the chromaffin cells which releases excess adrenaline and noradrenaline

Question 13

what are the clinical signs of a pheochromocytoma?

Answer 13

cholinergic - heat intolerance, tachycardias, hypertension, panic attacks, pallor, hyperglycaemia

Question 14

how is aldosterone secreted? how is it related to the RAAS system?

Answer 14

from the ZG - in response to low sodium and low blood volume -> juxtaglomerular cells produce renin and from the liver - angiotensin. angiotensin I converts to angiotensin II by ACE and heads to the ZG. this stimulates the release of aldosterone which reduces K+ levels alongside.

Question 15

what is the juxtaglomerular apparatus? what cells make up this? which ones secrete rein?

Answer 15

specialised collection of cells around the afferent arteriole and DCT in the kidney. made up of juxtaglomerular cells (renin) and macula densa cells

Question 16

what is a pre-hormone?

Answer 16

secreted from gland as inactive but becomes active in the tissues

Question 17

where in the kidneys does aldosterone work?

Answer 17

collecting ducts and DCT to increase Na reabsorption

Question 18

what are the two main functions of aldosterone on the kidney?

Answer 18

binds to the mineralocorticoid receptors in the nucleus and increases expression of epithelial sodium channels and also increases expression of na-k-atpase. both of these work to reabsorb Na back into the blood

Question 19

how do we get aquaporins?

Answer 19

inserted by vassopressin in response to low blood volume and pressure. influx of Na also leads to influx of H2O threfore reabsoption of Na and H2O

Question 20

so how is sodium reabsorbed by aldosterone?

Answer 20

aldosterone binds to the mineralocorticoid receptor on the nucleus. this causes the epithelial sodium channels to increase expression and increase amount of sodium into the cell. mineralocorticoid receptors also increase expression of na-k-atpase pumps, increasing amount of sodium being pushed into interstitial fluid and in turn into the blood. resorbing more K into the cells.

Question 21

what is conn syndrome? what does it manifest as?

Answer 21

adrenal aldosteronoma. anifests as hypertension and hypokalemia

Question 22

what is the treatment for conn syndrome?

Answer 22

surgical resection or aldosterone receptor antagonist therapy

Question 23

why can you get alkalosis with conn syndome>

Answer 23

in the collecting duct and DCT K-H+ exchange channels prevent the body losing too musch potassium by shuffling K back out of the cel and into extraceullar fluid in exchange for H. when aldosterone production is really high and therefore the Na-K-ATPase is high then the exchange of hydrogen ions with increase = alkalosis

Question 24

what is renovascular HTN?

Answer 24

narrowing of arteries supplying kidneys therefore increased renin = increases aldosterone

Question 25

what is cortisol’s -ve feedback role?

Answer 25

CRH tells ant pituitary to release ACTH to the zona fasiculata. when theres a surge in cortisol this signals to the hypothalamus and pituitary that there is enough cortisol thanks and we dont need no more so it stops producing it

Question 26

what are the direct effects of cortisol?

Answer 26

mobilisation of amino acids and fatty acids from muscle and adipose (respectively) and leads to increases in circulating plasma

Question 27

how does cortisol increase glucose levels?

Answer 27

by increasing the expression of the enzymes necessary for gluconeogenesis in the liver, leading to increased circulating glucose

Question 28

how does the physiological effects of cortisol counteract the effects of tissue damage?

Answer 28

in high levels it has anti-inflammatory properties and is the basis for corticosteroid injections. prevents lysosome release, reduced capillary permeability, reduced WBC migration, reduced lymphocyte production, reduced cytokine production

Question 29

does cortisol have an equal affinity to mineralocorticoid receptors>

Answer 29

yes

Question 30

what is the role of 11B-HSB enzyme?

Answer 30

chills in the cytoplasm and converts cortisol to inactive cortisone therefore minimising the effects on the sodium balance.

Question 31

what happens if you eat too much liquorice?

Answer 31

antagonist of 11b-hsd, therefore the enzyme doesnt convert cortisol so it is free to have an effect on the receptor causing further sodium reuptake and therefore cause HTN and hypokalemia

Question 32

what is the difference between cushing’s disease and cushing’s syndrome?

Answer 32

disease - too much ACTH produced by pituitary. syndrome - too much cortisol from adrenal gland. both will present with weight gain, bruising, thin arms and legs, pundulous abdomen, stretchmarks, red cheeks and a buffalo hump

Question 33

a patient presents with cushing;s symptoms and an increase in acth - is this the disease or the syndrome>

Answer 33

disease

Question 34

what controls the release of sex hormones?

Answer 34

ACTH and other things such as possibly the cortical androgen stimulating hormone

Question 35

what are the pre androgens?

Answer 35

dehydroepiandrosterone (DHEAS) and androstenedione

Question 36

where does the conversion to testosterone occur?

Answer 36

in the extra adrenal tissues such as adipose tissue

Question 37

what are the physiological effects of androgen release?

Answer 37

?pubic hair growth and in males external sex characteristics in development

Question 38

does the adrenal also produce oestrogen?

Answer 38

yes a little