Mrc C Flashcards
Outline the mechanisms that the body uses to regulate blood pressure.
RAAS. Starts with the live. The liver produces a pre-enzyme called Angiotensinogen. This gets converted into Angiotensin I (ANGI). This gets converted by Renin an enzyme produced in the kidneys when this is low fluid volume flowing through the nephrons..
ANGI and ANGII are flowing through the blood. When the pass through the lungs they meet an enzyme called Angiotensin Converting Enzyme (ACE). ACE lives in the lungs. ACE converts AGNI to ANGII.
ANGII acts on the adrenal gland. This causes the Adrenal gland to release Aldosterone. Aldosterone acts on the kidneys. Aldosterone aids in the reabsorption of sodium, which causes the nephrons to retain water (water follows salt). This causes an increase in blood pressure due to more blood volume.
Describe the concepts of preload and afterload and how they influence blood pressure, myocardial workload and myocardial oxygen demand.
Preload- is the stretching of the ventricles just before contraction. Preload is the pressure volume relationship at the end diastolic volume. Measures the elasticity of the heart.
Afterload- Left ventricular wall stress during ejection.
The amount of blood volume (venous return) can influence preload and afterload. If there is more blood volume, which is typically the cause of increased blood pressure, the amount of wall stress and myocardial workload would be increased. More force would be required during contraction to eject blood out of the heart. This will influence myocardial oxygen demand due to increased workload.
Mrs C uses GTN (Glyceryl trinitrate) spray for relief of angina. How does this act to relieve chest pain?
GTN reacts with tissue enzymes to release nitric oxide (NO).
NO binds to and activates guanylate cyclase (enzyme on cell membranes).
Guanylate cyclase converts guanosine triphosphate (GTP) to cyclic guanosine mono-phosphate (cGMP) second messenger system.
cGMP activates a protein kinase inside the cell and through a series of steps this triggers relaxation of smooth muscle fibres in the cell.
cGMP is inactivated by the enzyme phosphodiesterase.
Relaxation of smooth muscle in the blood vessels occurs with therapeutic doses of GTN:
- Relaxation of large veins leads to venous pooling of blood. This reduces venous return to the heart decreased preload decreased stroke volume decreased cardiac workload. Thus oxygen demand is reduced.
- Relaxation of large arteries decreases afterload (and systemic blood pressure). This decreases cardiac workload decreased oxygen demand.
- Relaxation of coronary arteries and diversion to collateral circulation at the area of ischaemia increased blood and oxygen flow to the myocardium increased oxygen supply.
Cilazapril
- RAAS. Starts with the live. The liver produces a pre-enzyme called Angiotensinogen. This gets converted into Angiotensin I (ANGI). This gets converted by Renin an enzyme produced in the kidneys when this is low fluid volume flowing through the nephrons..
ANGI and ANGII are flowing through the blood. When the pass through the lungs they meet an enzyme called Angiotensin Converting Enzyme (ACE). ACE lives in the lungs. ACE converts AGNI to ANGII.
ANGII acts on the adrenal gland. This causes the Adrenal gland to release Aldosterone. Aldosterone acts on the kidneys. Aldosterone aids in the reabsorption of sodium, which causes the nephrons to retain water (water follows salt). This causes an increase in blood pressure due to more blood volume.
Cilazapril is an ACE inhibitor. The means it stops ANGI getting converted to ANGII.
This means there is a decresed stimulis of the adrenal gland,
Which leads to decreases aldosterone produced,
Which means that less sodium (and subsequently water) is reabsorbed.
Means that there is a decrease in blood pressure, as there is a decrease in blood volume.
Two potential adverse effects of cilazapril and explain their causative mechanisms.
Hyperkalaemia - Inhibition of aldosterone. Aldosterone acts via Na/K pump to reabsorb sodium from collecting ducts and DCT in exchange for potassium. Decreased aldosterone means decreased excretion of potassium
ADR: First dose hypotension
Loss of RAAS-mediated support of blood pressure. Risk increased with HF, older age, renal impairment, strong diuretics
Why is furosemide selected as a diuretic in preference to a thiazide diuretic?
frusemide is a potent diuretic acting on loop of henle while thiazide is a weaker diuretic (less response) & requires good renal func to be effective; it acts at the distal convoluted tubules.
Furosemide – acts on loop of henly, to create a strong osmotic gradient for the reasbsorbition of water, therefore get a strong diuretic better theraptuic response
Thiazide -Distal convoluted tubual- rely on good renal function to have a effect, weak theraptic effect
Furosemide
Furosemide is a potent diuretic. It inhibits sodium and chloride absorption in the ascending limb of Henle’s
loop and in both the proximal and distal tubules. The high degree of efficacy is due to this unique site of
action. The action on the distal tubule is independent of any inhibitory effect on carbonic anhydrase or
aldosterone.
Furosemide works to relive blood volume by decreasing fluid overload.
Fursimide works on the thick segment of the ascending limb of heels loops to block reabsorption of sodiume and chloride
