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In Ohm's Law Flow = Pressure/
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In Poiseulle's Law Flow is = to Delta P/ [blank_start]R[blank_end]
Where R= 8Ln/ pi r^4.
Therefore Flow = delta P x r^4, so Flow is proportional to both [blank_start]driving pressure[blank_end] and radius but is inversely proportional to both the [blank_start]length[blank_end] and viscosity of the fluid.
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R
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driving pressure
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length
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Aneuryms result in laminated thrombus formation because the velocity of flow is quicker at the edges of a vessel, which creates the impotence for viscous blood and therefor aggregation of platelets and thrombus formation.
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Velocity = Flow/ [blank_start]cross sectional area[blank_end]. This means when the radius of a vessel [blank_start]decreases[blank_end] such as during atherosclerosis there will be more damage occur as the Velocity will increase [blank_start]inversely[blank_end] to the reduction in cross sectional area. This may lead to increased damage to the endothelium of vessels.
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cross sectional area
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Resistance
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Length
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decreases
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increases
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inversely
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proportionately
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The [blank_start]microcirculation[blank_end] extends from the arterioles to the [blank_start]venules[blank_end]. Its main roles are:
-[blank_start]Nutrition[blank_end] of tissues, with density being proportional to the metabolic activity of the organ
-Non-[blank_start]nutritional[blank_end] e.g. glomerular capillaries of kidneys, temperature regulation, [blank_start]signalling[blank_end], host-defence
[blank_start]Arterioles[blank_end] are single layers of SMC's and are innervated
Meta-arterioles are larger than a capillary and short cut through the vascular bed
[blank_start]Pre-capillary sphincters[blank_end]--> important for regulating blood flow
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microcirculation
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venules
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Nutrition
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nutritional
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signalling
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Arterioles
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Pre-capillary sphincters
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How many types of capillaries are there?
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Which of these is not the role of a pericyte?
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The Resistance of the micro-circulation is the sum of the pre, capillary and post capillary resistance
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Smooth Muscle Contraction:
Ca2+ entry through voltage gated calcium channels
Ca2+ release from SR ([blank_start]poorer[blank_end] here than in cardiac tissue)
Ca2+ entry through voltage independent channels e.g. NT binding receptors or stretch activated channels
Increased calcium activated calmodulin
The calcium-[blank_start]calmodulin[blank_end] complex activates myosin light chain kinase
Phosphorylation of myosin light chain allows the myosin to interact with the actin, producing contraction.
Relaxation occurs when MLC phosphatase dephosphorylaes MLC.
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poorer
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greater
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calmodulin
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phosphatase
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Apart from myogenic stretch, activating stretch channels, local factors which can impact arteriole resistance are?
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The equation for net filtration pressure = delta P - delta (colloid osmotic pressure)
If the hydrostatic pressure is 52 and the albumin levels are 36 in the plasma and the tissue pressure is -2 but the albumin levels are 13, what is the filtration.
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The mechanism of vasculitis is infection leading to antigen-antibody complexes and complement activation, which causes a dense infiltration of acute and chronic inflammatory cells. Common symptoms are
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Which of these describes essential hypertension?
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Due to a causative agent i.e. essential such as OSA, Renal artery disease, Hyperaldosteronism, Parenchymal Renal Disease, Cushing's Syndrome or Drugs.
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Unknown cause and is believed to be a byplay between genetic, lifestyle factors, diet, obesity, smoking, reduced exercise and stress.
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Renal HTN involves changes in systemic system caused by [blank_start]RAAS[blank_end] activation.
Endocrine disorders such as Cushing's causes excess production of cortisol which has the action of maintain vascular responsiveness to circulating vasoconstrictors.
Primary aldosteronism refers to a non-suppressible hypersecretion of aldosterone which promotes sodium reabsorption in the [blank_start]cortical collecting duct[blank_end] and therefore volume expansion.
Pheochromocytoma is a [blank_start]catecholamine[blank_end] secreting tumor that arises from chromaffin cells of the adrenal medulla and increases NA, A.
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RAAS
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ADH
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cortical collecting duct
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proximal tubules
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catecholamine
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endothelin
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Which of these is not a common end artery?
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Splenic
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Renal
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Pulmonary
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Opthalmic
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ACE-Inhibitors end in pril and are used to treat HTN, CHF, post AMI, Diabetic nephropathy. Main mechanism is to inhibit conversion of ANG 1 to ANG 2. This will lead to all but the following. They are contra-indicated in pregnancy.
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The reason people take sartans such as Candesartan and Ang 2 receptor blocker is that they cause less of a cough than ACE-Inhibitors
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[blank_start]Thiazide[blank_end] Diuretics (cholothalidone and Indapamide), inhibit the reabsorption of [blank_start]Na[blank_end]+ at the proximal segment of the DCT, which means more Na+ is maintained in the collecting duct and less H20 will [blank_start]reabsorb[blank_end] here, thus reducing plasma volumes. [blank_start]Low doses[blank_end] in HTN, [blank_start]higher doses[blank_end] in CCF. They have more of a vasodilatory effect in HTN.
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Thiazide
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Na
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reabsorb
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Low doses
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higher doses
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Ca2+ channel blockers such as amlodipine inhibit the entry of Ca2+ ions through a subset of voltage gated calcium channels which promotes smooth muscle relaxation.
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Olol- B-blockers competitively [blank_start]antagonise[blank_end] B-adrenergic receptors throughout the body.
They reduce BP by inhibiting [blank_start]rate[blank_end] and contraction of myocardium (B1) without reducing TPR. They also exert an effect on the CNS to decrease RENIN secretion. They reduce myocardial O2 demand by lowering HR, BP & Preload.
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antagonise
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agonise
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rate
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speed
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What type of diet and activity regime would you recommend to a patient with HTN?
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high sodium, low potassium, moderate exercise
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low sodium, high potassium, moderate exercise