102595
Description
Flashcards by tanitia.dooley, updated more than 1 year ago
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Created by tanitia.dooley
almost 11 years ago
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| Question | Answer |
| Arteriole are innervated by what? | The sympathetic nervous system via a1 receptors |
| What vasoactive mediators does the endothelium synthesise? | Prostaglandins- PGI2 & PGE2=vasodilation, PGG2 & PGH2=vasoconstriction, NO, ACE, C natriuretic peptide |
| How does NO cause vasodilation? What other effects does it cause? | Via guanylate Cyclase. Inhibits platelet aggregation and SMC proliferation |
| How do vasodilators affect enzymes that control Ca2+ sensitivity? | By increasing cGMP and cAMP |
| How do vasodilators block Ca2+ channels? | By hyper polarisation of the cell indirectly using K+ channel activators and directly by blocking voltage gated Ca2+ channels |
| Name some vasoconstrictors | A1 agonists, sympathomimetic amines (release of NA or inhibit it's reuptake), eicosanoids, peptides (angiotensin and endothelin) |
| What is renin released from the kidney in response to? | Decreased renal Na, reduced renal perfusion pressure, renal sympathetic nerve activity, b agonist and PGI2 |
| What does renin do? | Cleaved angiotensinogen into angiotensin which is then converted into angiotensin II by ACE. Angiotensin II then acts on AT1 and AT2 receptors |
| What does activation of AT1 cause? | Aldosterone secretion from adrenal cortex, directly causes vasoconstriction, increases NA release from sympathetic nerves which causes vasoconstriction and increases the force and rate of contraction, increases Na absorption from proximal tubule |
| What is the synthesis of endothelin stimulated by? | Activated platelets, endotoxin, cytokines, growth factors, angiotensin II, insulin, adrenaline |
| What is endothelin synthesis inhibited by? | PGI2, NO, natriuretic peptides, stress on endothelial cells |
| Where does endothelin act and what does it cause? | GPCR (ETA) on SMC |
| A blood pressure above what should be treated? | 160/100 |
| What is the difference between primary and secondary hypotension? | Primary- no unknown cause- 90-95% of cases, secondary: known cause such as kidney disease, drug induced or phaechromocytoma |
| What is severe hypertension? | Left ventricle enlargement, impairment of renal function. Untreated malignant hypertension can lead to death from uraemia, cardiac failure or stroke |
| What drugs are used to treat hypertension? | Thiazide diuretics, beta antagonists, vasodilators, ACE inhibitors, AT1 receptor antagonists, a1 antagonists |
| What are directly acting vasodilators used to treat hypertension? | Ca blockers, K+ agonists, nitroprusside |
| How do K+ agonists treat hypertension? | Hyper polarisation and reduction in Ca2+ transport |
| How do Ca blockers treat hypertension? | Block Ca entry in response to depolarisation |
| What are the indirectly acting vasodilators used to treat hypertension? | Renin inhibitors, ACEI, AT1 antagonist |
| How do beta blockers treat hypertension? | Decreased sympathetic activity and increased vagal, decreased renin release, decreased heart rate and myocardial contractility which reduces CO and BP |
| What is cardiac failure? | When the heart is not able to maintain adequate cardiac output to perfuse tissues and organs. Fluid builds up in the pulmonary and systemic circulation and can cause oedema |
| What causes cardiac failure? | Pressure overload (narrowed valves, hypertension), circ favtors eg leaky valves, ischaemic heart disease (angina, MI) |
| Why does cardiac failure lead to fluid build up? | Increased venous pressure, reduced renal flow and activation of the renin-angiotensin system causing Na retention and therefore reduced urine outpur |
| What is preload? | The pressure stretching ventricle of the heart after passive filling of ventricle and subsequent atrial contraction |
| What is after load? | Pressure chamber of the heart has to eject blood out of the chamber-consequence of aortic pressure |
| What is the effect of increased preload in a normal person? | Increased CO and increased after load which then causes decreased CO |
| In heart failure patients why is preload already elevated? | Due to ventricular dilation and or increased blood volume |
| What is the therapeutic aim of drugs used to treat cardiac failure? | Decreased after load and hence increase SV |
| How do beta blockers treat cardiac failure? | Reduce heart rate so increased filling time and myocardial performance |
| How do cardiac glycosides treat cardiac failure? | Increase myocardial contraction by inhibiting Na/K pump which leads to increased intercellular calcium. |
| How are ACEI used to treat cardiac failure? | Renin angiotensin system usually over active in cardiac failure patients so counteract this by blocking angiotensin II formation which reduces vascular resistance and increased perfusion and decreases cardiac load |
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