Хиперхолестеролемија: Разлика помеѓу преработките

[непроверена преработка][непроверена преработка]
Избришана содржина Додадена содржина
Создадена страница со: {{Infobox disease | Name = Хиперхолестеролемија | Image = Cholesterol.svg | Caption = Структурн...
 
Нема опис на уредувањето
Ред 14:
}}
'''Хиперхолестеролемија''' ([[American and British English spelling differences#Simplification of ae and oe|also spelled]] '''hypercholesterolaemia''' позната и како'''дислипидемија''') претставува високо ниво на [[холестерол]] во крвта.<ref name=Durrington>{{cite journal|last=Durrington|first=P|title=Dyslipidaemia|journal=[[The Lancet]]|volume=362|issue=9385|pages=717–31|date=August 2003 |pmid=12957096|doi=10.1016/S0140-6736(03)14234-1|url=}}</ref> Претставува форма на "[[хиперлипидемија]]" (покачени нивоа на [[липид]]и во крвта) и "хиперлипопротеинемија" (покачени нивоа на [[липопротеин]]и во крвта).<ref name=Durrington/>
<!--
 
Cholesterol is a [[sterol]]; see the diagrammatic structure at the right. It is one of three major classes of [[lipid]]s which all animal cells utilize to construct their membranes and is thus manufactured by all animal cells. Plant cells do not manufacture cholesterol. It is also the precursor of the [[steroid hormone]]s, [[bile acid]]s and [[vitamin D]].
 
Ред 26:
Although hypercholesterolemia itself is [[asymptomatic]], longstanding elevation of serum cholesterol can lead to [[atherosclerosis]].<ref name="BMJ2008">{{cite journal |author=Bhatnagar D, Soran H, Durrington PN |title=Hypercholesterolaemia and its management |journal=BMJ |volume=337 |issue= |pages=a993 |year=2008 |pmid=18719012 |doi= 10.1136/bmj.a993|url=}}</ref> Over a period of decades, chronically elevated serum cholesterol contributes to formation of [[atheroma|atheromatous plaques]] in the arteries. This can lead to progressive [[stenosis]] (narrowing) or even complete [[Vascular occlusion|occlusion]] (blockage) of the involved arteries. Alternatively smaller plaques may rupture and cause a clot to form and obstruct blood flow.<ref>{{cite journal |author=Finn AV, Nakano M, Narula J, Kolodgie FD, Virmani R |title=Concept of vulnerable/unstable plaque |journal=Arterioscler. Thromb. Vasc. Biol. |volume=30 |issue=7 |pages=1282–92 |date=July 2010 |pmid=20554950 |doi=10.1161/ATVBAHA.108.179739 |url=}}</ref> A sudden occlusion of a coronary artery results in a [[myocardial infarction]] or heart attack. An occlusion of an artery supplying the brain can cause a [[stroke]]. If the development of the stenosis or occlusion is gradual blood supply to the tissues and organs slowly diminishes until organ function becomes impaired. At this point that tissue [[ischemia]] (restriction in blood supply) may manifest as specific [[symptom]]s. For example, temporary ischemia of the brain (commonly referred to as a [[transient ischemic attack]]) may manifest as temporary loss of vision, [[dizziness]] and impairment of [[equilibrioception|balance]], [[aphasia]] (difficulty speaking), [[paresis]] (weakness) and [[paresthesia]] (numbness or tingling), usually on one side of the body. Insufficient blood supply to the heart may manifest as [[angina pectoris|chest pain]], and ischemia of the eye may manifest as [[amaurosis fugax|transient visual loss in one eye]]. Insufficient blood supply to the legs may manifest as [[claudication|calf pain when walking]], while in the intestines it may present as [[Abdominal angina|abdominal pain after eating a meal]].<ref name=Durrington/><ref name=Grundy1998>{{cite journal |last1=Grundy |first1=SM |last2=Balady |first2=GJ |last3=Criqui|first3=MH |last5=Greenland |first5=P |last6=Hiratzka |first6=LF |last7=Houston-Miller |first7=N |last8=Kris-Etherton |first8=P |last9=Krumholz |first9=HM |title=Primary prevention of coronary heart disease: guidance from Framingham: a statement for healthcare professionals from the AHA Task Force on Risk Reduction. American Heart Association |journal=[[Circulation (journal)|Circulation]] |volume=97 |issue=18 |pages=1876–87 |year=1998 |pmid=9603549 |url=http://circ.ahajournals.org/cgi/content/full/97/18/1876 |doi=10.1161/01.CIR.97.18.1876 |last4=Fletcher |first4=G |last10=Larosa |first10=J. |last11=Ockene |first11=I. S. |last12=Pearson |first12=T. A. |last13=Reed |first13=J. |last14=Washington |first14=R. |last15=Smith |first15=S. C. }}</ref>
 
Some types of hypercholesterolemia lead to specific physical findings. For example, familial hypercholesterolemia (Type IIa hyperlipoproteinemia) may be associated with [[xanthelasma|xanthelasma palpebrarum]] (yellowish patches underneath the skin around the eyelids),<ref name=Shields2008>{{cite book |last1=Shields |first1=C |last2=Shields |first2=J |title=Eyelid, conjunctival, and orbital tumors: atlas and textbook |publisher=Lippincott Williams & Wilkins |location=Hagerstown, Maryland |year=2008 |isbn=0-7817-7578-7 }}</ref> [[arcus senilis]] (white or gray discoloration of the peripheral [[cornea]]),<ref name=Zech2008>{{cite journal |title=Correlating corneal arcus with atherosclerosis in familial hypercholesterolemia |author=Zech LA Jr, Hoeg JM |journal=Lipids Health Dis |date=2008-03-10 |volume=7 |page=7 |pmid=18331643 |doi=10.1186/1476-511X-7-7 |pmc=2279133 |issue=1}}</ref> and [[xanthoma]]ta (deposition of yellowish cholesterol-rich material) of the [[tendon]]s, especially of the fingers.<ref name=Andrews2006>{{cite book |last1=James|first1=WD |last2=Berger|first2=TG |title=Andrews' Diseases of the Skin: Clinical Dermatology |publisher=Saunders Elsevier|year=2006|pages=530–2 |isbn=0-7216-2921-0 |url=}}</ref><ref name=Rapini2007>{{cite book |last1=Rapini|first1=RP |last2=Bolognia|first2=JL |last3=Jorizzo|first3=JL |title=Dermatology: 2-Volume Set |publisher=Mosby |location=St. Louis, Missouri |year=2007 |pages=1415–6 |isbn=1-4160-2999-0 }}</ref> Type III hyperlipidemia may be associated with xanthomata of the palms, knees and elbows.<ref name=Andrews2006/>-->