Brainscape's Knowledge GenomeTM

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


See full index

Sophie - Applied Physiology & Pharmacology Year 2 > 52.2 Endocrine Involvement in Secondary Hypertension > Flashcards

52.2 Endocrine Involvement in Secondary Hypertension Flashcards

1
Q

Which system is in control of long term blood pressure regulation?

A

Renin-angiotensin-aldosterone axis (RAAS)

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

Describe the RAAsystem

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

What is the effect of angiotensin II on circulation?

A

Vasoconstrictor

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

What is the purpose of the RAAS system? Why is this important clinically?

A

Raise blood pressure = antagonists can be used to LOWER blood pressure

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

Which cells release renin?

A

Juxtaglomerular apparatus

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

What causes renin release from the JGA? (4)

A
  1. Reduce pressure in afferent arteriole (detected by baroreceptors in afferetn arteriole), increase renin secretion
  2. Sympathetic stimulation via beta 1 receptors, increase renin secretion
  3. Na+ enters macula densa via NKCC transporter, prostaglandins used to stimulate, adenosine to inhibit renin secretion (more sodium = less renin release, reduced sodium delivery = more renin release)
  4. Negative feedback via AT1 receptors, means antagonists or ACE-Is increase renin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the three main classes of anti-hypertensive drugs that modulate the RAA axis that you need to know about?

A
  • ACE inhibitors
  • Angiotensin receptor blockers
  • Renin inhibitors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the action of ADH?

A

Secretion controlled by nerve impulses from the hypothalamus. Hypothalamic-pituitary axis.
ADH → V1a/b + V2
*V1a in blood vessels → vasoconstriction
*V1b in pituitary → ACTH release → cortisol release
*V2 in renal CD → AQP2 insertion → ↑ water retention → ↑ circulating volume
increases blood pressure

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

What is the action of aldosterone?

A

mineralocorticoid receptors in DCT/ CD → ↑ Na+ retention/ K+ excretion mediated by ENaC/
Secreted when increased circulating ATIII

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are other neuroendocrine factors that contribute to long-term ABP control?

A

*Natriuretic peptides (ANP/ BNP) → respond to stretch in atria/ ventricles → ↑ renal Na+/ water excretion + vasodilation → ↓ systemic BP
*Insulin resistance + HT correlation
Suggested abnormal SNS activation/ Na+ retention involved
DM2 patients respond better to certain antiHTsives → imp factor to consider.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is aldosterone and where/how does it act?

A
  • Steroid hormone secreted by the adrenal cortex (zona glomerulosa)
  • Acts on the kidney through:
    • Classical steroidal pathway
      • Aldosterone binds to a cytoplasmic receptor which is then translocated to the nucleus for the transcription of proteins involved with Na+ reabsorption, including: ENaC, Na+/K+ ATPase, metabolic enzymes to generate more ATP to fuel the pump
    • Non steroidal pathway
      • Receptor activates PKC and PKD through increasing [Ca+] intracellularly, which increases the activity of a variety of transport proteins within epithelial cells
  • Aldosterone acts to promote Na+ retention (and therefore also K+ excretion)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the effects of aldosterone on:

  • Renal function
  • Vascular tone
  • Circulating volume
A
  • Renal function -> Increases sodium reabsorption and potassium excretion
  • Vascular tone -> Increases vascular tone due to endothelial dysfunction and enhances the pressor response to catecholamines and up‐regulation of angiotensin II receptors
  • Circulating volume -> Increases circulating volume
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the effects of cortisol on:

  • Renal function
  • Vascular tone
  • Circulating volume
A
  • Renal function -> Increases GFR by increasing glomerular blood flow and increases phosphate excretion by decreasing its reabsorption in the proximal tubules. In excess, cortisol has aldosterone-like effects in the kidney causing salt and water retention.
  • Vascular tone -> Increases vascular tone
  • Circulating volume -> Increases circulating volume indirectly by promoting Na+ reabsorption.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the effects of adrenaline on:

  • Renal function
  • Vascular tone
  • Circulating volume
A
  • Renal function -> Decreases flow to kidneys by increasing the resistance in all renal vascular segments, leading to antidiuresis
  • Vascular tone -> Initially vasoconstriction, with prolonged exposure leads to vasodilation.
  • Circulating volume -> Increases circulating volume through action on adrenal cortex to secrete aldosterone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Which are the main glands involved in secondary hypertension?

A

Posterior pituitary, adrenal gland

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

What does the adrenal medulla secrete?

A

The catecholamines noradrenaline and adrenaline

18
Q

What does the adrenal cortex secrete?

A

The steroid hormones: cortisol, aldosterone, androgens

19
Q

What is a phaeochromocytoma?

A

A tumour of the chromaffin cells in the adrenal medulla

20
Q

What does phaeochromocytoma cause?

A

Excess adrenaline/noradrenaline release
–> hypertension, headache, sweating, anxiety

21
Q

What are the effects of cortisol on the renal system?

A
  • Increases glomerular filtration rate (by increasing glomerular blood flow)
  • Increases phosphate excretion
  • Has aldosterone-like effects as able to bind to aldosterone receptor –> sodium and water retention
22
Q

What is the role of cortisol in terms of blood volume and blood pressure?

A

Helps maintain normal blood volume/pressure

23
Q

What is the effect of adrenaline on the renal system?

A

Decreases renal blood flow (constriction of arterioles)

24
Q

What is the effect of adrenaline on vascular tone?

A

Vasoconstriction in most blood vessels (α1)
Vasodilation in blood vessels of major muscle groups/heart/lungs/liver (β2)

25
Q

What is the effect of adrenaline on circulating volume?

A

Increases circulating volume

26
Q

What is the effect of aldosterone on the renal system?

A

Increases sodium reabsorption and potassium secretion

27
Q

What is the effect of aldosterone on circulating volume?

A

Increases circulating volume

28
Q

What is the stimulus for renin release from the kidney?

A

Decrease in renal perfusion, sensed by juxtaglomerular apparatus

29
Q

What is the role of renin in the RAA axis?

A

Converts angiotensinogen to angiotensin I

30
Q

Which enzyme converts angiotensin I to angiotensin II? Mainly where?

A

ACE (Angiotensin-converting enzyme)
In the vascular endothelium of the lungs and kidneys

31
Q

What are the 5 main actions of angiotensin II?

A
  • (Overall) Increased sympathetic activity
  • (Kidney tubule) NaCl reabsorption, K+ excretion, water retention
  • (Adrenals) Aldosterone secretion
  • (Arteries) Vasconstriction
  • (Pituitary) ADH secretion
32
Q

What receptor type and pathway does ADH act on in the collecting duct?

A

V2 receptors
Gs-coupled GPCR –> increases cAMP –> PKA activation

33
Q

What is the effect of ADH activation of V2 receptors?

A

Increases the transcription and insertion of aquaporin 2 channels into the apical membrane

34
Q

What is the effect of ADH on blood flow in the vasa recta?

A

Vasoconstriction of descending vasa recta
Slows down blood flow to allow more time for water reabsorption

35
Q

Which receptor and pathway does ADH act on in blood vessels?

A

V1 receptors
Gq-coupled –> IP3/DAG pathway –> smooth muscle contraction

36
Q

What is the effect of ADH on circulating volume?

A

Matintains circulating volume

37
Q

What is the main angiotensin receptor and its pathway?

A

AT1
Gq/Gi coupled
Activates PLC –> IP3/DAG pathway
Also inhibits cAMP

38
Q

Where are AT1 receptors mainly located?

A

Kidney
Vascular smooth muscle

39
Q

Cushing’s syndrome involves excess…

A

cortisol

40
Q

Conn’s syndrome involves excess…

A

aldosterone

41
Q

What are the main physiological characteristics of Conn’s syndrome?

A

Excessive fluid retention
Hypokalaemia
Hypertension

42
Q

What are the main physiological characteristics of Cushing’s syndrome?

A

Hypertension
Increased urination
Hypokalaemia
Hypernatremia

Sophie - Applied Physiology & Pharmacology Year 2 (32 decks)

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