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BIO 669 QUIZ 4 QUESTIONS & VERIFIED
ANSWERS| GRADE A| 100% CORRECT
(NEW 2024/ 2025 UPDATE)
myocardial ischemia - ANS ✓local, temporary deprivation of coronary blood supply -need O2 >50% to not decrease function of heart 3 types of myocardial ischemia - ANS ✓stable angina-specific amount of exercise ppl can do before noticing chest pain, chronic, know how far they can go before symptoms start. tx w/NTG to vasodilate -prizmetal angina-occurs unpredictably & at rest, while sleeping. transient ischemia that doesn't follow any pattern -silent iscemia-have ischemia w/out the detectable symptoms like angina acute coronary syndromes - ANS ✓include unstable & stable angina, transient ischemia, sustained ischemia, MI, myocardial inflammation & necrosis unstable angina - ANS ✓results from reversible myocardial ischemia -presents as new onset angina, angina occurring at rest, or angina that increases in severity or frequency -is a sign of impending MI or rupture so will need treated sustained ischemia - ANS ✓can lead to changes in myocardium -stunning the myocytes=ischemia leading to damage of myocardium & makes cells hypocontractible, lasting hours-days (temporary) -hibernating myocardium=myocytes adapt & stop working to prolong their survival, reversible -myocardial remodeling=mediated by RAAS that leads to myocyte hypertrophy & permanent loss of contractile function MI - ANS ✓stemi & nonstemi -nonstemi=affects only the area under endocardium & not thru entire myocardial wall (subendocardail MI) will see ST depression & T wave inversion w/out Q waves
Bio -stemi=affects entire myocardial wall (transmural MI) will see ST elevation, sudden & extended obstruction of myocardial blood supply, leads to death of cells S&S of MI - ANS ✓sudden severe chest pain that may radiate, n/v, diaphoresis, dyspnea, complications=cardiac arrest due to ischemia, L ventricular dysfunction, & electrical instability acute pericarditis - ANS ✓acute inflammation of pericardium -occurs w/anything that increases friction like an increase in proteins, transudate, or anything that causes inflammation of pericardial fluid -leads to friction rubs pericardial effusions - ANS ✓accumulation of fluid in the pericardial cavity -if it occurs slowly over time the pericardium can stretch & accommodate w/out compressing the heart -if it occurs rapidly it causes compression of heart known as cardiac tamponade- which leads to decreased blood flow & can stop it completely constrictive pericarditis - ANS ✓addition of connective tissue that leads to compression of the heart & decreased cardiac output -seen w/TB patients -as you increase metabolic demands the heart can't increase to meet those needs because its restricted -develops gradually hypertropic cardiomyopathy - ANS ✓can be hypertropic obstructive/asymmetrical septal cardiomyopathy OR hypertensive/valvular cardiomyopathy -both increase afterload, decrease EF, & cardiac output hypertropic obstructive cardiomyopathy - ANS ✓thickening of septal wall which causes outflow obstruction of LV tract hypertensive/valvular hypertropic cardiomyopathy - ANS ✓occurs b/c of increased resistance to ventricular ejection, myocytes hypertrophy trying to compensate for increased workload restrictive cardiomyopathy - ANS ✓normal systolic BP but increased diastolic BP & normal wall thickness
Bio rheumatic fever - ANS ✓systemic inflammatory disease caused by delayed immune response to pharyngeal infection by group A beta haemolytic streptococci (strep throat) -affects ages 5- -febrile illness w/inflammation of joints, skin rash, nervous system & heart inflammation -treat within 9 days, if untreated will lead to rheumatic heart disease -S&S=fever, lymphadenopathy, n/v, increased HR, epistaxis bad S&S=carditic, polyarthritis, chorea(unexpected movements), subcutaneous nodules, erythema marginatum (rash on trunk) infective endocarditis - ANS ✓infection of endocardium agents=bacteria, fungus, virus, parasites, rickettsia must have 3 components- -damaged endocardium -blood borne pathogen adherence to endocardium via adhesins -pathogens hide in thrombi, form fibrin, proliferate & vegetate dilated cardiomyopathy - ANS ✓impaired systolic function that increases intracardiac volume -HF w/decreased ejection fraction & ventricular dilation -usually results from ischemic heart disease, valvular disease, DM, alcohol, or renal failure S&S of infective endocarditis - ANS ✓fever, petechia, new or changed murmur, weight loss, back pain, night sweats, HF Osler nodes-painful red nodules on pads of finger/toes janeway lesions-painful hemorrhagic lesions on palms/soles cardiac complications of AIDs - ANS ✓myocarditis endocarditis pericarditis pericardial effusion pulmonary HTN cardiotoxicity heart failure - ANS ✓inadequate perfusion of tissues left sided HF - ANS ✓aka CHF can be HF w/preserved EF or HF w/reduced EF
Bio HF w/reduced EF (HFrEF) - ANS ✓aka systolic HF -inability of heart to generate adequate cardiac output to perfuse tissues EF<40% -decreased contractility, increased preload which will eventually increase afterload & decrease perfusion to tissues -leads to an increase in catecholamines & RAAS to increase BP, CO, & contractility -becomes a vicious positive feedback loop cycle that decreases contractility, increases preload & afterload leading to worsening of L HF HF w/preserved EF (HFpEF) - ANS ✓aka diastolic HF -pulmonary congestion despite a normal stroke volume & cardiac output -results from decreased compliance of LV leading to decreased diastolic relaxation which causes increased preload, backing up into pulmonary circulation & causing pulmonary edema S&S of L HF - ANS ✓pulmonary congestion & inadequate perfusion of systemic circulation SOB, cough w/frothy sputum, fatigue, decreased urine output, edema & pulmonary edema, crackles, pleural effusions, hypo or HTN, S3 gallop drugs to treat HF - ANS ✓+ inotropes=increase contractility diuretics=decrease preload ACE inhibitors/ARBS/aldosterone blockers=decrease preload & afterload R sided HF - ANS ✓inability of RV to produce adequate bloodflow into pulmonary circulation -caused by diffuse hypoxic pulmonary disease -caused by L sided HF that backs up to pulmonary circulation b/c it increases systemic pressure S&S=JVD, peripheral edema, cor pulmonale high output failure - ANS ✓inability of heart to supply body w/blood borne nutrients despite adequate blood volume & normal or increased contractility -the heart will increase its output but body's needs still aren't met -causes= anemia, septicemia, hyperthyroidism, beriberi (vitamin b12 deficiency) shock - ANS ✓cardiovascular system fails to perfuse the tissues adequately resulting in impaired oxygen & glucose use -decreased oxygen & glucose causes cells to use ATP faster than they can make it -increased hydrogen concentration leads to decreased pH & metabolic acidosis occurs
Bio multiple organ dysfunction syndrome - ANS ✓progressive dysfunction of 2 or more organs resulting in an uncontrolled inflammatory response to severe illness/injury -involves stress response, microvascular coagulation, release of cytokines/kinin/inflammatory processes causing decreased blood flow, increased metabolism, decreased perfusion -all organs can be affected varicose veins - ANS ✓vein in which blood has pooled producing distended, tortous, palpable vessels -caused by trauma or gradual vein distention risk factors-female, family hx, fat, pregnant, DVT, prior leg injury chronic venous insufficiency - ANS ✓inadequate venous return over a long period due to varicose veins or valvular incompetence -can lead to venous stasis ulcer thrombus formation - ANS ✓obstruction of venous flow leading to increased venous pressure -3 factors (triad of Virchow) promote thrombosis= 1)venous stasis 2)venous endothelial damage 3)hypercoagulable states -usually occurs in lower extremities & is asymptomatic superior vena cava syndrome - ANS ✓progressive occlusion of SVC that leads to venous distention in upper extremities & head -causes=tumors of lymphatics or bronchus -a low pressure vessel HTN - ANS ✓consistent elevation of systemic arterial BP -systolic > -diastolic > 90 primary HTN - ANS ✓most common, aka essential or idiopathic -genetic & environmental factors -SNS causes increased HR & vasoconstriction which increase BP -overactive RAAS causes Na & water retention, increased vascular resistance, insulin resistance & platelet aggregation -decreased renal excretion of salt=pressure-natriuresis relationship secondary HTN - ANS ✓caused my systemic disease process that raises peripheral vascular resistance or cardiac output
Bio examples=renal disease, adrenocorticoid tumors, adrenamedullary tumors, or drugs complicated HTN - ANS ✓chronic damage to blood vessels & tissues leading to target organ damage in heart, kidneys, brain, & eyes malignant HTN - ANS ✓HTN crisis -rapidly progressing HTN when diastolic is > -will cause cerebral encephalopathy & life threatening organ damage if not fixed tx of HTN - ANS ✓loop or thiazide diuretics, ACE or ARB inhibitors, Ca channel blockers -no longer beta blockers b/c they have a higher rate of stroke than those drugs orthostatic hypotension - ANS ✓decrease in systolic & diastolic BP among standing up -lack normal BP compensation in response to gravitational changes on the circulation acute & chronic orthostatic hypotension - ANS ✓acute=elderly at increased risk b/d decreased thrust mechanisms. causes=drugs, prolonged immobility, starvation, exhaustion, dehydration/volume depletion, venous pooling chronic-causes=DM, endocrine d/o, metabolic d/o, CNS or PNS d/o, cerebral infarcts, parkinsons, autonomic neuropathy=most common cause aneurysm - ANS ✓localized dilation or outpouching of a vessel wall or cardiac chamber -can be thoracic or abdominal or can occur in cerebral circle of willis -most common=abdominal causes=atherosclerosis or HTN -can lead to aortic dissection or rupture true aneurysm - ANS ✓involves all 3 layers of wall -weakening of vessel wall -can be fisuform or circumferential (circular) or saccular (spherical) false aneurysm - ANS ✓extravascular hematoma (outside of vessel) that penetrates & communicated w/intravascular space thrombus formation - ANS ✓blood clot that remains attached to the vessel wall -risk factors=injury/inflammation, obstruction of flow, stasis/pooling
Bio -will have intermittent claudication which is pain w/walking coronary artery disease - ANS ✓any vascular d/o that narrows/occludes coronary arteries leading to myocardial ischemia atherosclerosis=most common cause -risk factors=old, family hx, males, post menopausal women, dyslipidemia, HTN, smoking, DM, fat non-traditional risk factors= -increased inflammatory & thrombus markers-high sensitivity CRP, ESR, von Willebrand factor concentration, interleukin 6 & 18, TNF, fibrinogen, CD40 ligand -troponin I-identifies myocardial injury -adipokines -infection
