Other info on HTN and more

Question 1

How is BP calculated?

Answer 1

Cardiac output x Total peripheral resistance

V = I x R

Question 2

How is the short term response to BP controlled and what does it affect?

Answer 2

CNS response
Baroreceptors
Chemoreceptors

Affects the cardiac output and total peripheral resistance

Question 3

How does the CNS raise arterial pressure?

Answer 3

SNS release NA from nerve terminals
NA acts on the alpha-adrenergic receptors of the VSMC (vascular smooth muscle)
All arterioles remain in state of partial constriction in homeostasis
Heart is directly stimulated
(Not innervated - capillaries, pre-capillary sphincters and met arterioles)

Question 4

How do baroreceptors affects BP?

Answer 4

Activation on stretch
If baroreceptors sense increased BP -> secondary signals from tracts solitarius -> inhibition of vasoconstrictor centre and excitation of vagal parasympathetic centre

Important in maintaining postural BP, strong sympathetic discharge when standing up

Question 5

Where are baroreceptors found?

Answer 5

Nerve endings in all large thoracic and neck arteries

2 major populations: carotid (body) sinus and arch of aorta

Question 6

How do chemoreceptors work?

Answer 6

Sensitive to low O2, high CO2 and acidosis

Reduction in blood flow (e.g. reduction in pressure < 80 mmHg) causes metabolic stimulation excitatory effect on vasomotor centre

Question 7

Where are chemoreceptors found?

Answer 7

2 carotid bodies (one on each bifurcation)

1-3 aortic bodies (adjacent to aorta)

Question 8

How is BP controlled long term?

Answer 8

RAAS (renin angiotensin aldosterone system)

Vascular remodelling and contractility

Question 9

Angiotensin II is the main effector of the RAAS system, what are its effects?

Answer 9

↑sympathetic activity of the ANS
↑Na, Cl reabsorption and K+, H+ excretion and H2O retention
↑aldosterone secretion from the adrenal gland (which does the same as above)
↑ADH secretion from the posterior pituitary gland, which increases H2O resorption
↑systemic arteriolar vasoconstriction

Question 10

What is Primary Hyperaldosteronism?

Answer 10

High aldosterone -> low K+ and low H+ = hypokalaemia alkalosis

Unilateral aldosterone producing adenoma or Conn’s syndrome (50-60%)

Bilateral adrenal hyperplasia (40-50%)

Question 11

How does hypokalaemia present?

Answer 11

Muscle weakness, cramping, palpitations
Induced nephrogenic diabetes insipidus
Complications of long-standing hypertension

Question 12

What is Addison’s disease?

Answer 12

aka Primary Adrenal Insufficiency
Failure of glucocorticoid and mineralocorticoid hormone release
Leads to low circulating volume, high levels of K+ (hyperkalaemia), hyponatraemia (low Na+) and acidosis

Question 13

What are the sign and symptoms of Addison’s disease?

Answer 13

Lethargy, weight loss, fainting

Hyperpigmented skin creases (due to high ACTH), postural hypotension & dehydration

Question 14

How is Addison’s disease investigated?

Answer 14

Short synACTHen test - stimulates the adrenal gland

• Tetracosactide (synacthen) 250 micrograms IV/IM
• Check blood cortisol at time 0 and after 30 mins
• In healthy person: cortisol at 30 mins should be >600 mol/l -> suggestive of Addisons disease if that’s NOT the case

Question 15

How is Addison’s disease treated?

Answer 15

Remember that: glucocorticoid, mineralocorticoid and sex steroid production are reduced
Wear a bracelet to say you’ve got Addison’s
Acutely ill -> give hydrocortisone IV

Question 16

How does vascular remodelling affect BP?

Answer 16

In response to essential hypertension → inward increase in wall thickness, reduction in lumen diameter and increase in wall:lumen ratio → preservation or mild impairment of endothelial function

Question 17

Why does increased peripheral resistance lead to less blood flow to the kidneys?

Answer 17

• Causes kidneys to release renin -> leads to renin-angiotensin system activation
• Renin causes angiotensinogen (released by liver) to be converted to angiotensin I -> ACE coverts this into angiotensin II
• Angiotensin causes increased vasoconstriction -> leads to increased peripheral resistance
• Renin also causes increased aldosterone (from adrenal gland) > increased Na+ and H2O retention:
• Increased blood volume -> increases cardiac output + BP
• Increased BP damages blood vessels -> further reduction in blood flow to kidneys -> this vicious cycle