Which means 5% is due to: renal (renal artery stenosis) and hyperaldosteronism. \n
AWESOME!!\n
Pheochromocytoma - very rare. Causes head aches and sweating. \nRenal vascular disease - triggar RAA system. \n
“lower the pressure, the better, as long as it is not symptomatic”.\n
ALWAYS start with life style modification. \nIf not at goal, then look at drugs. \nBeta blockers and diaretics as long as they are not opposed to them.\nIf diabetic, then use ACE inhibitors.\nSometimes ACEi don’t work as well as Ca channel blockers in AA.\n
acute corronary syndrom, Marfan’s with aneurism, AAA, worry about dissection through vessel wall. \n
Pain secondary to ischemia. \nUsually seen in youn men who smoke cigarrettes. \nTx - sessations, vasodilators\n
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May be due to decreased release of vasodilation chemicals. \nImmune complex, type III\nTips of fingers, top of phylanges. Can happen more with stress. \nWhite, blue, then red. \n\n
Can become painful and lower extremity edema. Can cause hyperpigmentation and ulceration due to venus stasis. \n
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Number one Killer in us Men and Women.\n\n
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Silent MI - diabete. Based on secondary neuropathy. No sensation of chest pain. \nWomen present with atypical presentations: tierd, vague abdominal pain, be sensitive.\nVessels decrease by 50% before symptoms. \nStart with exercise induced pain. \n
Some women will just have back pain. \nEcho’s and stress tests\nACE Inhib - actually prevents remodelling that predispose heart to “floppy sloppy”.\n\n
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Q-wave - with full-thickness (transmurral).\nBlood must be blocked for 20 minutes or more. \nDysrhythmia is the most common complication resulting from an MI. \nThen remodeling, then heart failure. \n
Myosite might be stunned for a couple days. \n
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Inflammation makes exudate. \nIf infectious, then cells like PMN’s will come in. \nTampanad - enough fluid to cause contraction on heart. \nFever, Chest pain that increases when lying down!!! Slight ST segment elevation with no Q. --> acute pericarditis. \n
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SUDDEN DEATH - \n
Dilated: viral, pregnancy, drugs and etoh.\nHypertrophic: valve regurg, fatigue, dry cough at night, \nRestrictive: least common. \n\nTx - diuretics, ACEi, \n
If it occurs during diastole, it is most likely a pathologic murmur.\n
Egophany - A to E changes. Sign of consolidation. \n
Balooning at leaflett’s. \nLate systolic murmer is a back-flow murmur. \n
Usually staph, need anti bact with dental.\nLess rheumatic, more drug use.\nUnexplaned feaver and new murmur. MOST IMPORTANT signs. \nCould become emboli, bacteremic, autoimmune predisposition. \n
Takes a long time for IV-antibiotics \n
RIght sidded - due to lung disease, core pulmonaly,\nIf bad enough, can lead to left sided. \nLeft sided - due to systemic HTN, Mitral stenosis, \n