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30 Cards in this Set
- Front
- Back
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outline the types of arteries from large into small vessels |
Elastic arteries > muscular arteries > arterioles > capillaries |
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How is smooth muscle of the walls of arteries, arterioles, venules and veins controlled? |
The contraction of smooth muscle is controlled by the mediators released locally from sympathetic nerve terminals, circulating hormones and endothelial cells parasympathetic nerves are not generally important in controlling the vascular smooth muscle tone |
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what are the three layers of blood vessels? draw a cross section of elastic artery, musclar artery and arteriole |
- tunica intima - tunica media - tunica adventitia check moodle |
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what is tunica intima? |
an inner lining of endothelial cells and a thin layer of fine connective tissue dominated by elastic fibres
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what is tunica media |
the middle layer: larger elastic arteries (e.g. aorta) have a high proportion of elastic tissue, while the smaller muscular arteries have a large amount of smooth muscle.
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what is tunica adventitia? |
composed mainly of collagen fibres and elastic tissue. Nerves and lymphatic vessels are found within this layer.
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what are the physical differences of veins compared to arteries? |
veins carry deoxygenated blood from the tissue (except pulmonary veins) veins also have three layers - lower BP - thinner walls - they contain less elastic, collagenous and smooth muscle tissue - easily distensible and compressible - blue colour (lack of O2) - consist of semilunar biscupid valves - contraction of skeletal muscles assist the blood flow - high blood volume |
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what is atherosclerosis? |
changes in the endothelial lining and can lead to occlusion of blood vessels (e.g. coronary arteries) by plaques. This narrows the blood vessels and decreases the perfusion of the tissue (e.g. myocardium).
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what are the risk factors of atherosclerosis? |
smoking diabetes obesity high blood cholesterol diet high in fats personal or family history of heart disease |
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outline the steps of forming atherosclerosis |
1. Plaque formation is initiated by endothelial damage (e.g. caused by hypertension)
2. Platelets, macrophages and low-density lipoprotein (LDL; high proportion of cholesterol) adhere to the damaged epithelium 3. The macrophages release free radicals; these cause peroxidation of the LDL, which is then ingested by the macrophages 4. Macrophages release inflammatory cytokines and growth factors, which cause proliferation of smooth muscle and fibroblasts 5. Thrombi can form on the plaque, which can narrow or even block the blood vessel |
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what is anuerysm? |
a bulge or weakness in the arterial wall, which can be caused by disease, injury or an abnormality present at birth.
• An aneurysm looks like a bubble in the wall of an inner tube, and like an inner tube the artery involved may suffer a puncture/blow-out. If the aneursym bursts, as the massive blood loss is usually fatal |
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what is varicose veins? |
unsightly distended blood vessels With age, the walls of the veins become less resilient, and become distended on the heart side of each valve. Swelling occurs (due to pooled blood), which makes the valves less effective. Blood flow decreases further and the vessels become more distended. Often observed in veins of the arms and legs, where blood flow opposes gravity |
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what are the risk factors of varicose veins? |
women age 30-60 lack of exercise occupation requiring long hours of standing or sitting |
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Why is controlling the resistance of individual vascular beds important? |
The resistance of individual vascular beds determines the distribution of blood flow to individual organs and is relevant to the treatment of angina chest pain; due to plaque-mediated decreases in myocardial perfusion |
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How is total peripheral resistance controlled? why is it important? |
PR (peripheral resistance) is controlled mainly by the arterioles and one of the main determinants of arterial pressure. control PR is important for the treatment of hypertension |
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How is vascular smooth muscle tone controlled? |
Like other muscle cells, vascular smooth muscle contracts when the intracellular calcium concentration [Ca2+]i rises.
Vasoconstrictors and vasodilators act by increasing or reducing [Ca2+]i and/or by altering the sensitivity of the contractile machinery to [Ca2+]i. |
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what are the three mechanisms regulating the concentration of [Ca2+]i |
• Entry/exit of Ca2+ across the plasma membrane • Sequestration of Ca2+ within the cell • Linking [Ca2+]i and smooth muscle contraction |
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how does Entry/exit of Ca2+ across the plasma membrane occur? |
Entry occurs through i) voltage-gated Ca2+ channels which open when the cell is depolarised, and ii) receptor-operated channels. The opening probability of voltage-gated channels can also be influenced by second messengers produced by G-protein coupled receptors. Ca2+ exit is mediated by Na+/Ca2+-ATPase and by Na+/Ca2+ exchange.
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how does Sequestration of Ca2+ within the cell occur? |
Intracellular Ca2+ in vascular smooth muscle is contained in the sarcoplasmic reticulum, which is the main storage site of releasable Ca2+. Many vasoconstrictors activate membrane-bound phospholipase C, which increases levels of IP3. This acts on receptors on the sarcoplasmic reticulum to release Ca2+ into the cytoplasm. Recapture of the released Ca2+ occurs by an ATPdrivenactive transport system, which is modulated by cAMP and cGMP.
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how does Linking [Ca2+]i and smooth muscle contraction occur? |
Smooth muscle differs from striated and cardiac muscle in that it contains no troponin. In smooth muscle, Ca2+-calmodulin regulates myosin light-chain kinase (MLCK) which phosphorylates myosin light-chains, enabling myosin to interact with actin, so initiating contraction. A fall in Ca2+ leads to dephosphorylation of myosin light-chains by myosin phosphatase (MP) leads to relaxation.
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what are the components of vasoconstrictors? |
Agents causing contraction (vasoconstrictors) might:
• Release intracellular Ca2+ secondary to receptor-mediated IP3 formation. • Depolarise the membrane allowing Ca2+ entry through Ca2+ channels. • Allow Ca2+ entry through receptor-operated channels. |
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what are the possible components of vasodilators? |
• Agents causing relaxation (vasodilators) might:
• Inhibit Ca2+ entry through voltage-gated Ca2+ channels (Ca2+ channel inhibitors) either directly or indirectly by hyperpolarising the membrane (K+ channel activators). • Increase intracellular cAMP or cGMP concentration: cAMP causes inactivation of myosin lightchainkinase (MLCK), and also enhances Ca2+ efflux; cGMP opposes agonist-induced increases in [Ca2+]i. |
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what are the types of vasodilators? |
- ACE inhibitors - ATI (angiotensin Ⅱ subtype Ⅰ) receptor antagonists - Drugs that interfere with sympathetic transmission - calcium antagonist - K+ channel activators - Nitrates - Agents causing Ca+ release from or re-uptake into the sarcoplasmic reticulum |
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what are the examples of ACE inhibitors? what is the mechanism of action? |
(e.g. captopril, enalapril) prevent conversion of inactive Angiotensin I to the potent vasoconstrictor Angiotensin II by ACE, a membrane-bound enzyme found in endothelial cells
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what are the examples of ATI receptor antagonist? mechanism of action? |
(e.g. losartan, valsartan) prevent the actions of angiotensin II, which include generalized vasoconstriction, but especially in the afferent arterioles of the kidney. Also block other effects of angiotensin II such as increased release of noradrenaline from sympathetic nerve terminals (which would also reinforce vasoconstriction).
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what are the examples of drugs that interfere with sympathetic transmission |
(e.g. α1 adrenoreceptor antagonists, such as prazosin).
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what are the examples of calcium antagonists? mechanism of action? |
act by blocking Ca2+ entry into response to depolarisation;
these compounds dilate both resistance and capacitance vessels. These include dihydropyridines (e.g. nifedipine, amlodipine), which act preferentially on vascular smooth muscle, whereas verapamilacts on the heart. Dihydropyridines usually produce a transient reflex tachycardia as a result of the lowering of BP. Verapamil do not because they also slow the cardiac pacemaker. |
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what are the examples of K+ channel activators? mechanism of action? |
K+ channel activators relax smooth muscle by increasing membrane permeability to K+.
This hyperpolarises the membrane, switching off voltage-dependent Ca2+ channels. These include cromokalim, pinacidil, minoxidil and diazoxide. These drugs open a high-conductance K+ channel, which is ATP-sensitive. In normal circumstances, ATP closes these K+ channels, causing the cell to depolarise. K+ channel activators work by antagonising the action of ATP on these channels, opening them and causing relaxation, when ATP would normally have kept them closed. |
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what are the examples of nitrates? mechanism of action? |
(e.g. glyceryl trinitrate, isosorbide dinitrate) are powerful vasodilators thatspontaneously break down under physiological conditions to form nitric oxide (NO), which activates soluble guanylate cyclase
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what are the examples of agent causing Ca2+ release from or re-uptake into the sarcoplasmic reticulum? |
(drugs that influence the cytoplasmic [cAMP] and [cGMP]).
These include β2 adrenoreceptor agonists, adenosine and prostacyclin all increase [cAMP] via adenylate cyclase. |
