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BRS > Endocrinology- adrenal gland > Flashcards

Endocrinology- adrenal gland Flashcards

1
Q

Which main artery and vein are close to Adrenal Gland?

A

Inferior vena cava

Abdonminal aorta

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2
Q

Which artery and vien supplies each adrenal gland?

A

left- supplied by abdonminal artery

drains into IVC

right- supplied by abdonminal artery

drains into RENAL VIEN

Both have many arteries only one vien into the gland

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3
Q

Label this histology of adrenal gland (each layer)

A
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4
Q

What hormones does each layer of adrenal gland produce?

A

Cortiocsterioids (cortisol)- adrenal cortex (zona golmerulosa, fasciculata, reticularis)

catecholamines (adrenaline)- medulla

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5
Q

Give examples of each catecholamine AND coricoesteriods

A

catecholamines - noradrenaline and adrenaline

corticosteriod - mineralocoricoids (aldosterone), glucocorticoids (corticol),

_sex steriods only in kids (_androgens and oestrogens)

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6
Q

What does each layer of cortex produce?

A

zona glomerulosa- aldosterone

(increase Na + reabsorption in blood and k+ excretion in urine and increase blood pressure as increased water retention)

zona fasiculata and reticularis- cortisol + sex hormones

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7
Q

What molecule do all corticosteriods come from?

A

cholesterol

steriod ( based on cholesterol)

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8
Q

How is progesterone (precursor) synthesized from cholesterol?

A
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9
Q

Progesterone to aldosterone?

A
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10
Q

Progesterone to cortisol?

A

FORGET aldesterone pathway on this

and enzyme is (numbers) HYDROXYLASE

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11
Q

Where do sex steriod come of on the pathway?

A
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12
Q

How does aldesterone increase blood pressure? (mechanism of action)

A

activate ATPase and Na+ channel from urine to cell.

so Na+ reabsoprted in tubules in kidney into blood so increase water retention

also K+ and H+ from cell to urine increased

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13
Q

How is it aldosterone regulated?

A

3 ways

-juxtagolermular appartus measues renal perfusion pressure (blood flow that passes through renal tissue)

  • Increase renal sympathetic activity
  • decrease Na+ load to top of loop of Henle

ALL release renin into blood

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14
Q

What does renin do?

A

Switch on cascade to convert to AT to AT 1

eventually to Angiotensin ii that regulates release of aldosterone

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15
Q

How exactly does AT 11 regulate aldosterone release?

A

Affects all enzyme in pathway to produce aldesterone from cholsterol:

side chain cleavage

3 hydoxysteriod deydro

21, 11, 18 hydroxylase IN golumerulosa

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16
Q

How is cortisol regulated?

A

By ACTH released by pit gland

17
Q

What are effects of cortisol

A

(some similar to glucagon)

stress response, increase blood glucose, lysis of protiens and fat, glucogenosis, enhances effect of glucagon and catechloamines,

excretion of water load and increase vessel permeablity

18
Q

How is there a negative feedback?

A

cortisol feedback negatively to pit gland and hypo

19
Q

How does ACTH stimulate cortisol?

A

Goes to fasiculata and reticulartis

activates enzymes in pathway from cholesterol to cortisol:

side chain cleavage, 3 hydroxysteriod dehydro

21,11,17 dehydrolase

20
Q

What is special about fluctations in cortisol levels in body?

A

diurnal rthym- tells tissues what time of day it is, important waking up

low at midnight

high at 8.30am

tells body what time of day it is

(ACTH slightly ahead)

21
Q

What is Addison’s disease?

A

Primary adrenal failure (not enough hormones).

autoimmune disease, destroys cortex.

OR

Tuberclosis-disease

22
Q

What levels in body give indication?

A

A lot of ACTH and MSH excreted

low BP

low cortisol and aldesterone

23
Q

Symptoms of addisons disease?

A

increase pigmentation, tanned looking

weakness

weight loss

low BP

diarheea

vomitting

Vitiligo (patches of white) might be autommune co-existing as well

24
Q

Why do addisons have good tan?

A

POMC is precurosr to produce ACTH, MSH and endorphonines

so when produce a lot of ACTH simulatnously produce a lot of MSH

25
Q

How can addisons lead to death?

A

Cortisol and Aldosterone deficiency

Salt loss (Na+)

low BP

death

26
Q

Treatement of addisons disease?

A

rehydrate with normal saline (as low blood volume)

Dextrose (glucose) prevent hypoglycaemia due to low glucocorticoid defi

as well as give hydrocortisone (corisol as a medication)

27
Q

What is name of condition of too much cortisol?

A

Crushing’s disease

28
Q

What chemical level changes causes crushing disease?

A

tumour in adrenal too much cortisol

tumour in pit gland too much ACTH

29
Q

Symptoms of Crushing disease

A

increase weight gain

depression

red cheeks

moon face

thin skin

myopathy

thin arms and legs

red striae- stretch marks

poor wound healing

30
Q

What other condition is commonly associated with Cushing’s syndrome? Why?

A

Diabities due to insuline resistance

as body becomes resistant to hormones

31
Q

Possible causes of crushing syndrome?

A

steriod by mouth- long term do function of cortisol

pituitary adenoma

ectopic (too much) ACTH produced by lung cancer

adrenal adenoma

32
Q

Clincal signs of crushing disease

A

thin skin

proximal myopathy- weakness of muscles

centripetal obesity- lemon on stick

hypertension

diabites

immunsupression

moon face

striae- stretch marks

33
Q

What cells of adrenal medulla derived from?

A

Ectodermal neural crest

temporary group of cells unique to vertebrates that arise from the embryonic ectoderm germ layer,

34
Q

What is precusor for catecholamines (noradrenanline and adrenal )?

A

Tyrosine - amino acid

35
Q

What trigger release of catecholamines?

A

Stored in cytoplasmic granules + released in response to ACTH from preganglionic symp neurones

36
Q

How are they synthesized from tyrosine? (pathway)

A

(dont need to know enzymes)

37
Q

What effects do catecholamines have on body?

A

Fight or flight response

tachycardia, sweating, increase blood glucose, alertness, vasocontriction

38
Q

How do they travel in blood? Do they travel freely or bound to molecule? And which one?

A

NA and Adr circulate bound to albumin

39
Q

How are the NorA and Adr degraded?

A

monoamine oxidsase and catechol-O-methyl transferase

BRS (19 decks)

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