Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Endocrine physiology > Adrenal gland physiology > Flashcards

Adrenal gland physiology Flashcards

1
Q

What is the adrenal gland- where is it located, function - ie what hormones does it produce?

A
  • located in the posterior abdomen - between the kidneys and diaphragm
  • it is a small endocrine gland that produces** steroid hormones adrenaline and noradenaline** that function to control heart rate, blood pressure & other important body functions
  • also produces aldosterone,
  • produces cortisol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe the structure of the adrenal gland

A
  • consists of an outer connective tissue capsule - cortex and medulla
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are the 3 zones of the cortex?

A
  1. zona glomerulosa
  2. zona fasciculata
  3. zona reticularis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what hormone is associated with the zona glomerulosa?

A
  • mineralocorticoids - eg aldosterone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is the primary target of aldosterone?

A

the kidneys

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is the hormonal effect of aldosterone?

A

aldosterone increases renal absorption of Na+ and water, especially in the presence of ADH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe the hormones that are associated with the zona fasciculata ?

A

glucocorticoids - steroid hormones that effect glucose metabolism
* CORTISOL
* corticosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the target of the glucocorticoids released by the zona fasciculata?

A

the majority of cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are the hormonal effects of the glucocorticoids?

A
  • glucocorticoids **increases the rates of glucose & glycogen formation **by the liver
  • they stimulate the** release of amino acids** from skeletal muscle & lipids from adipose tissue
  • cortisol also reduces inflammation - ie an antiinflammatory effect
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what hormone is associated with the zona reticularis ?

A
  • small quantities of androgens (male sex hormones) are released from this zone
  • these may be converted to estrogens in the blood stream
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what are the targets of the androgens released by the zona reticularis?

A
  • skin
  • bones
  • other tissues

minimal effects in normal adults

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what are the hormonal effects of the adrenal androgens?

A

they stimulate the development of pubic hair in both males and females

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what hormones does the adrenal medulla produce?

A
  • adrenaline
  • noradrenaline
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are the effects of noradrenaline and adrenaline released by the medulla of the adrenal gland?

A

they increase cardiac activity, blood pressure, glycogen breakdown, and blood glucose levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is the adrenarche?

A

the maturation of the zona reticularis in late childhood associated with increased adrenal androgen DHEA secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is the adrenopause?

A

the decline in DHEA production with age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

where are the adrenocorticoids synthesised?

A

in the adrenal cortex - all 3 zones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Describe the zona glomerulosa

A
  • subcapsular
  • 10-15% of the adrenal cortex
  • mineralocorticoid synthesis - aldosterone
  • actions are mediated through mineralocorticoid receptor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe the functions of aldosterone

A
  • maintains electrolyte balance and ECF/plasma volume
  • regulates** Na+absorption and K+ excretion** in the renal distal tubule and collecting ducts
  • also has a secondary role in acid base balance - H+ excretion and HCO3- absorption
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe the action of aldosterone on the principal cells

A
  • aldosterone** increases the expression of Na+ channels and Na+/K+ ATPase pumps** in the cell membrane on the luminal membrane
  • it also increases expression of K+ channels on the apical membrane allowing the excretion into urine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Describe the action of aldosterone in intercalated cells

A
  • aldosterone increases the expression of H+ATPase pumps to stimulate the secretion of H+ into the urine
  • aldosterone also increases the activity of the apical Cl-HCO3- exchangers - which reabsorb Cl- from the lumen into the cell and excrete bicarbonate from the cell into the lumen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Describe the renin-angiotensin - aldosterone system (RAAS)

A
  • granular cells produce prorenin, after a drop in blood pressure prorenin is cleaved to form renin
  • the release of renin causes angiotensin to be produced by the liver
  • renin causes angiotensin to be converted to angiotensin I
  • angiotensin I is converted to angiotensin II by the ACE enzyme
  • angiotensin II stimulates the release of aldosterone from the renal cortex
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What effects does primary hyperaldosteronism/ conns syndrome have on renal reabsorption of electrolytes and water?

A

it causes electrolyte imbalances - increase in Na and hco3- reabsorption and increase in H+ and K+ excretion
* causing muscles cramps (hyper natremia (Na+))
* causing muscle weakness (hypokalemia (K+))
* causing metabolic acidosis
* increases water reaborption - hypertension

24
Q

what are the possible causes of primary hyperaldosteronism/ conns syndrome?

A
  • aldosterone secreting adrenal tumours
  • adrenal hyperplasia (genetic disorder)
25
Q

what are the possible treatments for primary hyperaldosteronism / conns symdrome?

A
  • surgery
  • spirinolactone - aldosterone receptor antagonist
26
Q

what is an example of a primary aldosertone deficiency?

A

addisons disease

27
Q

what is addisons disease?

A

autoimmune destruction of adrenal cortex

28
Q

what are the symptoms of hypoaldosteronism?

A
  • hyponatremia - low Na+ plasma levels
  • hyperkalemia
  • decreae in ECF/plasma volume
  • cardiac arrthymias
29
Q

Describe the** zona fasciculata**

A
  • 75% of adrenal cortex
  • contains pale cells - numerous lipid droplets
  • well developed ER and lots of mitochondria
  • synthesise cortisol in response to increased ACTH
  • actions mediated by the glucocorticoid receptor
30
Q

what are the metabolic actions of glucocorticoids?

A
  • causes an** increase in muscle protein catabolism** (breakdown)
  • increases** triglyceride breakdown**
  • increases hepatic gluconeogenesis - therefore increases plasma glucose
  • decreases** muscle insulin sensitivity**
31
Q

what are the secondary actions of cortisol?

A
  • supresses immune and inflammatory responses
  • inhibits T & B cell function
  • maintains normal blood pressure and cardiac output
  • important role in water & electrolyte balance - increases Na+ reabsorption and K+ excretion
  • stress response
32
Q

what is the cortisol awakening response?

A
  • The cortisol awakening response (CAR) is the change in cortisol concentration that occurs in the first hour after waking from sleep
  • 30-70% increase in cortisol 30 mins after rising
33
Q

what nucleus is important in the circadian rhythm of cortisol?

A
  • suprachiasmatic nucleus in the hypothalamus
34
Q

What is hypercortisolism/cushings syndrome?

A

a disorder relating to abnormally high levels of cortisol in the body

35
Q

what are the possible causes of hypercortisolism?

A
  • cortisol secreting adrenal tumours
  • ectopic tumours (tumours occuring in abnormal places) that secrete ACTH
  • primary ACTH excess - cushings disease
  • prolonged glucocorticoid therapy
36
Q

what are examples of symptoms of hypercortisolism?

A
  • insulin resistance
  • obesity
  • hyperglycemia
37
Q

what is an example of a disorder relating to hypocortisolim?

A

addision’s disease- autoimmune destruction of the adrenal xortex

38
Q

what are examples of symptoms associated with hypocortisolism?

A
  • hypoglycemia
  • ACTH excess
  • MSH excess - hyperpigmentation
39
Q

what is the function of the enzyme 11Beta hydroxysteroid dehydrogenase?

A
  • this enzyme converts active cortisol into inactive cortisone
  • prevents the glucocorticoids acting on the minerlaocorticoid receptors
  • highly active in most metabolically active tissues eg liver, adipose, skeletal muscle etc
40
Q

what does chronic ingestion of glycyrrhetinic acid lead to?

A
  • this can inhibit the 11 beta hydroxysteroid dehydrogenase activity
  • this allows the glucocorticoids (cortisol etc) to exert their effects on the mineralocorticoid receptor and produce hypertension and hypokalemia
41
Q

describe the zona reticularis

A
  • 10-15% of the adrenal cortex
  • adjacent to the renal medulla
  • not fully differentiated untiil early childhood
  • synthesis of androgens - DHEA is the most abundant
42
Q

Describe DHEA

A
  • much more abundant than gonadal androgens
  • easily converted to testosterone
  • most adundant androgen in females - plays a role in development of secondary secual characteristics
43
Q

what is adrenal androgen synthesis regulated by?

A

ACTH

44
Q

what is congential adrenal hyperplasia?

A
  • hyperplasia = enlargement of tissue/ organ due to increase in growth of cells
  • decreases cortisol production, increases male sex steroid production, increases ACTH
  • abnormal development of primary/secondary sex characterstics
45
Q

Describe the difference in the embryology of the adrenal gland

ie where are they derived from

A
  • adrenal cortex is derived from the embryonic mesoderm
  • adrenal medulla is derived from the neural crest of the embryonic ectoderm
46
Q

what are chromaffin cells?

A
  • neuroendocrine cells located in the adrenal medulla
  • they secrete adrenaline , noradrenaline etc
47
Q

what are chromaffin cells innervated by?

A

preganglionic sympathetic neurons

48
Q

What occurs if the chromaffin cells are stimulated by the pre ganglionic sympathetic neuron?

A
  • they release adrenaline (80%) and noradrenaline (20%) into blood stream in response to increased sympathetic nervous system activity
  • called the sympathoadrenomedullary system
49
Q

what receptors are NE and E associated with?

A

plasma membrane adrenoceptors - G protein coupled receptors

50
Q

what are the 4 main subtypes of adrenoceptor ?

A
  • Alpha 1
  • alpha 2
  • beta 1
  • beta 2 - ADRENALINE ONLY
51
Q

what do the alpha adrenergic receptors preferably bind to?

A

noradrenaline

52
Q

what do the beta adrenergic receptors bind to?

A
  • adrenaline
53
Q

what are the physiological effects of adrenaline?

A
  • increase in HR and CO
  • increase in the breakdown of glycogen & fat
  • increase in O2 consumption
  • increase in skeletal muscle blood flow
54
Q

what is the role of adrenaline / epinephrine VS noradrenaline in the stress response?

A
  1. adrenaline VIA ADRENAL MEDULLA increases HR, BP, peripheral vasoconstriction to increase blood flow, increase lipid breakdown and glucose for fuel
  2. noradrenaline VIA sympathetic nerves increases HR, BP and peripheral vasoconstriction
55
Q

what is an example of a disorder of the adrenal medulla?

A
  • pheochromocytoma
  • tumour of the chromaffin cells
56
Q

what are the symptoms associated with pheochromocytoma?

A
  • severe hypertension
  • hyperglycaemia
  • anxiety
  • arrthymias
  • increased metabolic rate

Endocrine physiology (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions