Drug treatments Flashcards
Outline the response to decreased cardiac output by the sympathetic nervous system
SNS detects decreased aortic blood flow
Stimulate release of noradrenaline which works on B1-receptors to increase cAMP
The increase in cAMP increases intranodal Ca2+ which leads to increased rate and force of contractions by nodal cells
The increase in cAMP also increases intracellular Ca2+ in ventricular conducting cells leading to increased force of contraction
INCREASE IN CYTOSOLIC CA2+ VIA IP3
IP3–> Ca2+–> constriction
It also causes arterio-constriction which increases after load via A1-receptors. This also happens to veins returning blood to heart which increases preload –> STARLINGS LAW–> INCREASED CO
Describe the effect of the parasympathetic system on the heart.
Releases actetylcholine
Decreases frequency by decreasing cAMP via M2(muscarinic)-receptors
Has no effect on SV, only HR
Side note: no muscaranic agonists as there are lots of side effects
Outline the RAAS
Decrease in renal perfusion detected
Kidney secretes RENIN
RENIN converts angiotensinogen, which is made in the liver, to angiotensin I
Angiotensin I is converted to Angiotensin II by Angiotensin-converting enzyme (ACE) in the lungs
Angiotensin II causes : increased sympathetic activity (effects due to AT1-receptors), Na/Cl reabsorption, aldosterone secretion from adrenal glands, ADH secretion from posterior pituitary gland, widespread vasoconstriction
Whats the effects on CO of Na/Cl retention as part of the RAAS response?
Water follows Na/Cl back into efferent arteriole in kidneys
More water increases hydrostatic pressure in vessels
Increased preload increased CO due to starlings law.
What are the effects of arterio-constriction and venous-constriction on BP as part of the RAAS response?
Arterio-constriction via AT1-receptors increases after load which increases BP
Veno-constriction via AT1-receptors increases preload which increases BP
Briefly outline how Increased release of Angiotensin II causes constriction of vessels
Increased Angiotensin II, increases IP3
This increases intracellular Ca2+
Constriction of vessels
How does aldosterone cause Na/Cl retention by the kidneys?
Aldosterone activates cytoplasmic receptors which bind. to the nucleus to increase expression of Na+/Cl- channels and so increases uptake which leads to increased water retention
When would vasodilators be used as a means to treat hypertension?
In patients with benign prostatic hypertrophy
Noradrenaline -> A1 antagonist
so no IP3-> Ca2+ increase -> constriction
How is coronary blood flow regulated?
Endothelium derived relaxing factor - NO
How is cardiac workload regulated?
End diastolic volume(EDV) - PRELOAD
Regulated by sympathetic system, RAAS
Heart rate (sympathetic system, Ca2+)
Contractility
Total peripheral resistance (Sympathetic system, RAAS)
Define stabile angina
What do treatments for stabile angina aim to achieve?
A predictable pattern of pain during exercise that is relieved by rest
Treatment aims to decrease work done by the heart and/or increase blood supply and treat risk factors
Outline the main and minor pathways/effects of nitrates on CO
Nitrates increase NO which increases cGMP
This decreases Ca2+
Causing veno-dilation
Which decreases preload which in turn decreases workload via starlings law
Nitrates increase NO which dilate some coronary arteries which increases O2 supply to myocardium. However the heart has its own mechanisms to dilate coronary arteries so nitrates have limited effects
What are the side effects of taking nitrates?
Postural hypotension
Reflex tachycardia
Headache (dilation of vessels in meninges)
Dizziness
What can you use to treat reflex tachycardia caused by nitrates?
Beta blockers - bisoprolol
What are the clinical signs of a myocardial infarction ?
Pain Sweating Tachycardia Cold, clammy skin All due to increased sympathetic nervous system (noradrenaline/adrenaline)
