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Pathophysio Test 2

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Question
Answer
Atherosclerosis symptoms   Blocks extremity- leg cool & pale Edema when sitting, layers of artery walls separated & filled with fluid- leg warm when sitting, Skin shinier & without hair pain  
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Atherosclerosis caused by   High caloric diet: Chylomicrons taken, leave behind intermediate-density lipoproteins Float around in blood until liver can take them & turn them into HDL Extras IDL taken by macrophages, get oxidized & hurt wall → clot  
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Atherosclerosis biggest problem   Small emboli, thrombosis → myocardial infarction  
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Deep Vein Thrombosis   occurs if immobilized for a long time  
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Anatomy of Heart   Right side- deoxygenated Left side- oxygenated  
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Systole   AV valves close, 1st heart sound, ventricular contraction Semilunar valves open  
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Diastole   Semilunar valves close, 2nd heart sound Ventricles relax  
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Layers of heart   Visceral pericardium Myocardium: middle muscle layer Endocardium  
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effects of diuretics   Elevate urination→ dehydrated Can cause hypoalkemia  
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Skeletal/ Cardiac muscle differences   Cardiac does not need stimulus Cardiac is all or none  
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Blood Pressure =   cardiac output x peripheral resistance  
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Cardiac Output   amount of blood pushed by heard in one minute  
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Peripheral Resistance   depends on viscosity, diameter of vessels  
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Vasoconstricting Factors   • Bradykinin • Angiotensin II • Heparin (blood thinner)  
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Vasodialating Factors   ACE inhibitor  
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Beta Blockers   Reduce norepinepherine & epinephrine → slow heart rate Vasodilator  
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Stages of Cardiac Contractility   o Resting membrane potential o Threshold potential o Action Potential o Plateau  
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De/ Repolarization   De- more positive charge, Na+ diffuses in Re- more negative charge, K+ diffuses out  
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Cardiac Tamponade   Rapid accumulation of pus (exudate) compress the heart  
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Vagus Nerve   Parasympathetic for heart, lowers heart rate When hyperstimulated can have AV blocks  
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Normal Rate for Heart   60-100 beats/ min  
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SA Node   pacemaker in right atrium  
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AV Node   between ventricles & atria coordinates heart rate  
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Purkingi Fibers   in ventricular walls, stimulate to contract  
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Bundle Branch   sends info from AV node to apex  
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Stab Wound in Lungs   Air enters → restrict lung expansion → partial/ complete collapse of lung Tension: air enters pleural cavity on inhalation but cannot leave on exhalation Open: air enters pleural cavity through the wound on inhalation and leaves on exhalation  
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Bronchial Asthma   Obstructive airway disorder Inflammatory disease  
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Hypoxemia   less oxygen  
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Hypercapnia   more co2  
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Cystic Fibrosis   Recessive disorder in chloride transport proteins High NaCl in sweat Thick fluids → obstruct airways, obstructs pancreatic & biliary ducts  
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Embolism   Blockage Decrease perfusion (blood vessel to capillary) → decrease diffusion  
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Isovolumetric Contraction   o No change in blood volume Contraction although small AV valves closed  
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Ventricular Ejection   Amount of blood out to vessels from ventricle from each heart beat  
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Preload   stretching ventricle, filling ventricle with blood  
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Postload   tension created in order to have heart contract  
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Factors to get blood back to heart (negative pressure)   oRelaxation of heart oInhale Air in Lungs oMuscles to milk blood to heart oValves in veins  
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Lung Compliance   Ability of lungs to stretch from a change in pressure  
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Lung compliance depends on   •Elastin & collagen fibers •Water content •Surface tension  
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Heart failure   oHeart can no longer pump enough blood to rest of body… •Ventricles too thick •Ventricles too stiff •Ventricles too weak  
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Created by: brit24