Other info on HTN and more Flashcards
(17 cards)
How is BP calculated?
Cardiac output x Total peripheral resistance
V = I x R
How is the short term response to BP controlled and what does it affect?
CNS response
Baroreceptors
Chemoreceptors
Affects the cardiac output and total peripheral resistance
How does the CNS raise arterial pressure?
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)
How do baroreceptors affects BP?
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
Where are baroreceptors found?
Nerve endings in all large thoracic and neck arteries
2 major populations: carotid (body) sinus and arch of aorta
How do chemoreceptors work?
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
Where are chemoreceptors found?
2 carotid bodies (one on each bifurcation)
1-3 aortic bodies (adjacent to aorta)
How is BP controlled long term?
RAAS (renin angiotensin aldosterone system)
Vascular remodelling and contractility
Angiotensin II is the main effector of the RAAS system, what are its effects?
↑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
What is Primary Hyperaldosteronism?
High aldosterone -> low K+ and low H+ = hypokalaemia alkalosis
Unilateral aldosterone producing adenoma or Conn’s syndrome (50-60%)
Bilateral adrenal hyperplasia (40-50%)
How does hypokalaemia present?
Muscle weakness, cramping, palpitations
Induced nephrogenic diabetes insipidus
Complications of long-standing hypertension
What is Addison’s disease?
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
What are the sign and symptoms of Addison’s disease?
Lethargy, weight loss, fainting
Hyperpigmented skin creases (due to high ACTH), postural hypotension & dehydration
How is Addison’s disease investigated?
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
How is Addison’s disease treated?
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
How does vascular remodelling affect BP?
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
Why does increased peripheral resistance lead to less blood flow to the kidneys?
- 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
