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  1. what are lipoproteins?
    any complex of lips with proteins usually formed in the liver or intestine
  2. how are plasma proteins classified?
    • by density (lip content)
    • High: HDL, 50% lips/50% proteins
    • Low: LDL, large amts of cholesterol
    • Very Low: VLDL: 25% cholesterol
  3. what is the number 1 killer in the US?
  4. what is atherosclerosis
    • a response to injury where cholesterol-rich fat (plaques) accumulate in the intima of large and medium sized arteries
    • plaques occludes (can be slow build up or quick rupture of plaques) arteries causing ischemic hrt disease, myocardial infarction, stroke, and gangrene of the extremities
  5. what are the 4 types of arteriosclerotic lesions?
    • atherosclerosis
    • arteriosclerosis
    • hypertensive arteriosclerosis
    • calcific sclerosis
  6. what are the risk factors for atherosclerosis?
    • high LDL level
    • cigarette smoking (oxidizes LDL)
    • high blood pressure (intima damage)
    • lack of exercise (change in lipoprotein receptor count)
    • heredity
    • low HDL levels (keep LDL from binding to plaques)
  7. what are the risk factors for atherosclerosis that we cannot do anything about?
    • heredity
    • male sex
    • advancing age
  8. what is the deadly quartet for arteriosclerosis?
    • hypertension
    • hyperlipidemia (cholesteral and LDL)
    • cigarette smoking
    • diabetes mellitus
  9. what are the "soft" factors of arteriosclerosis that are of uncertain importance?
    • obesity
    • inactivity
    • personality characteristics
  10. what artery is used to monitor a pt who is likely to develop any form of arteriosclerosis?
    the ocular fundus (bottom of the eye)
  11. why is vascular smooth muscle an important factor in atherosclerosis?
    • has receptors for LDL
    • can get into intima through holes in the internal elastic membrane
  12. what is the progression from injury to occlusion in the atherosclerosis "response to injury hypothesis"?
    • development of areas of endothelial injury
    • smooth muscle proliferation in the intima
    • insudation of lipproteins (oxidized LDL)
    • accumulation of macrophages and platelets
    • formation of fibrous cap and atheroma
  13. what is hypertension?
    • a consequene of arteriosclerosis
    • bp of 160/90
    • results from imbalance in
    • --- cardiac output
    • --- renal function
    • --- peripheral resistance
    • --- sodium homeostasis
  14. what are the different stages of atherosclerosis development?
    • fatty streaks, diffuse intimal fibrosis: early lesions of the endothelial surface of large arteries:
    • fibrolipid plaque: intimal changes not reversible
    • complicated plaque: causes signs and symptoms of the disease
  15. what are fatty streak lesions (atherosclerosis)?
    • the early stage of atherosclerosis
    • begin in children in all populations
    • collections of foamy lipid-laden macrophages and smooth muscle cells just beneath the intimal surface of the arteries
  16. what are diffuse intimal fibrosis lesions (atherosclerosis)?
    • part of the early stage of atherosclerosis
    • develops over the first few decades
    • may be related to the development of atheroma
  17. what is the fibrolipid plaque stage of atherosclerosis?
    • the 2nd stage
    • intimal changes are no longer reversible
    • intimal surface shows a layer of fibrosis ("fibrous cap") which encloses a zone of fatty, necrotic, and partly calcified debris full of elongated smooth muscle cells, fibroblasts, and macrophages
  18. what is the complicated plaque stage of atherosclerosis?
    • 3rd (maybe final?) stage
    • the further progression of plaque build up that can take many forms (confluent, calcific, ulerative)
    • causes signs and symptoms of disease
  19. what can happen to athersclerotic plaques once they form in the arteries?
    • become
    • - confluent (merge)
    • - calficied (eggshell aorta)
    • - ulcerated (may lead to atheroembolism / thromboembolism)
    • - hemorrhagic
  20. what can happen if athersclerotic plaques expand?
    • the internal layer of the intima may break up and the lesion puts pressure on tunica media
    • media damange leads to formation of atherosclerotic aneurysm (fusiform or saccular) which could rupture
  21. what is an aneurysm?
    • an abnormal dilation of arteries or veins
    • develope as a result of weaking of the wall of a vessel (tunica media)
    • more frequent in aorta
  22. what causes aneurysms?
    • congenital factors (atherosclerosis)
    • infections (syphilis)
    • trauma
  23. what are the different types of aneurysms?
    • dissecting
    • berry
    • syphilitic
    • pseudoaneurysms
  24. what are dissecting aneurysms?
    • occurs when blood is forced through an intimal defect into the wall of an artery, under arterial pressure
    • may result in a column of blood traveling along the tunica media dissecting the wall
    • associated w/ hypertension but can also occur with wall degeneration seen in cystic medial necrossis or Marfan's syndrome
  25. what are the two types of dissecting aneurysms?
    • based on aortic location
    • type A: if ascending part
    • type B: if descending part
  26. what are berry aneurysms?
    • tend to develop at branch points of arteries in the basal cerebral circulation
    • saccular outpouchings of the arterial wall - may fill w/ thrombus, may bleed (subarachnoid bleeding)
    • impt cause of intracranial bleeding in young pt
    • unclear pathogenesis
  27. what are pseudoaneurysms?
    • occur w/ injury to arterial wall allows escape of blood to form a hematoma confined by arterial adventitia
    • (not a true aneurysm)
  28. what are varicose veins?
    • abnormally dilated twisted veins caused by increased vessel intraluminal pressure
    • any vein may be affected but superficial veins of the legs are the most common
  29. what are the risk factors for varicose veins?
    sex, age, heredity, posture, obesity
  30. what is a deep venous thrombosis?
    • aka thrombophlebitis and phlebothrombosis
    • a thrombus formation in deep viens (usually the legs)
    • may have coinciding infection or inflammation
    • associated w/ prolonged bed rest
    • can be life threatening due to risk of PE
  31. what is vasculitis?
    • inflammation and necrosis of blood vessels (aortitis)
    • types:
    • -- raynaud phenomenon
    • -- polyarteritis nodosa
    • -- thromboangiitis obliterans (Buerger disease)
  32. what is a hemangioma?
    • benign tumor of a blood vessel usually located in the skin but can be found in internal organs
    • composed of mases of capillary like channels filled w/ blood
  33. what is a hemangiosarcoma?
    • rare, highly malignant
    • usually begins as small, painless red nodule located in the skin/liver
  34. what is the general description of heart failure?
    • clinical syndrome
    • the heart does not pump enough blood to meet the needs of the body
    • usually associated w/ defective myocardial function, inc resistance, inadequate ventricular fillling or inc ventricular blood vol
  35. what changes occur in a failing heart?
    • dilatation (enlargement) of one or more chambers
    • ventricular hypertrophy (long standing failure)
  36. signs and symptoms of heart failure are due to what?
    hypoxic and congestive effects on organse and tissues and depends on whether the hrt failure is L sided or R sided
  37. what happens in other organs due to heart failure?
    • dimished tissue perfusion
    • venous congestion / fluid retention
  38. what is left sided heart failure?
    • left ventricle unable to maintain adequate CO and congestion builds up in the lungs
    • generally due to ischemic hrt disease and systemic hypertension
  39. with what is left heart failure usually associated?
    • (CHF)
    • inc hydrostatic presure in pulm venous circulation, pulmonary congestion and respiratory symptoms like dyspnea,orthopnea and cough that progress to pulmonary edema
    • renal ischemia and activation or renin-angiotensin-aldosterone make it worse
  40. CHF implies what of the left ventricle?
    significant infarction (30-40% of ventricular mass)
  41. what is right heart failure?
    R side of the hrt is unable to overcome an increase in pulm arterial pressure due to pulm arterial hypertension that results from parenchymal or vascular disease (PE) of the lungs or long lasting L side hert failure (cor pulmonale)
  42. what are the clinical manifestations of R sided hrt failure?
    • distention of neck veins
    • congestion of liver and ascites
    • pitting edema
  43. what does right heart failure usually cause?
    • chronic passive congestion of the liver, spleen, and gut
    • peripheral edema and ascites
    • liver venous congestion may cause necrosis and destruction of normal liver tissue
    • edema of the gut may lead to cardia cachexia
  44. what is cor pulmonale?
    • right ventricular enlargement and associated heart failure
    • develops secondary to pulmonary disease associated w/ pulmonary hypertension
    • can be acute (w/ PE) or chronic (w/ COPD)
  45. what is the most common type of heart disease in the US?
    ischemic hrt disease aka coronary hrt disease (80% of deaths from hrt disease)
  46. what are the risk factors for ischemic hrt disease?
    • diabetes mellitus
    • obesity
    • age
    • sex
    • family hx
    • personality
    • life habits
    • contraceptives
  47. what is ischemic heart disease?
    • (IHD) aka coronary heart disease is a consequence of atherosclerosis of coronary arteries
    • develops when blood flow to the hrt is inadequate
    • describe a group of clinical syndromes
    • -- angina pectoris
    • -- myocardial infarction
    • -- chronic ischemic heart disease
    • -- sudden death
    • the under lying leasion is usually due to atherosclerotic stenosis or occlusions of the coronary arteries
  48. what is angina pectoris?
    pain in the chest, neck, left jaw, left shoulder and arm due to transient ischemic myocardial injury
  49. what are the characteristics of an angina attack?
    • begin suddenly
    • intense compression
    • burning
    • tightness
    • pain sometimes radiating to the jaw or left arm
    • usually triggered by physical activity
  50. what causes angina?
    imbalance btwn myocardial O2 supply and demand which leads to myocardial ischemia
  51. what are the major forms of angina?
    • stable angina (not enough O2 when demand increases w/ physical activity)
    • variant angina (random vasospasms due to hypersensitivity to endogenous vasoconstriction agents reducing O2 supply)
    • unstable angina (vnot enough O2 when demand inc along w/ random vasospasms)
  52. what is the most common form of ischemic heart disease?
    stable angina
  53. what is the primary characteristic of stable angina?
    myocardial O2 demand greatly exceeds O2 supply w/ attacks brought on by physical activity
  54. what is the treatment of stable angina?
    • beta blockers and organic nitrates (dilation of coronary arteries)
    • calcium channel blockers too bc of effect on myocardium and peripheral vasculature
  55. what is the primary problem with variant angina?
    • O2 supply to myocardium decreases bc of coronary artery vasospasm (emotional and environmental triggers due to hypersentivity to endogenous vasoconstrictors)
    • can occur even when pt at rest
  56. what is the tx for variant angina?
    calcium channel blockers w/ long lasting nitrates
  57. what is unstable angina?
    • combination of stable and variant: demand increases but the supply does not along w/ further compromise from vasospasms
    • serious and potentially life-threatening form of myocardial ischemia
    • associated w/ thrombosis in the coronary arteries
  58. what happens physiologically w/ unstable angina?
    • coronary vasoconstriction is superimposed on an increase in myocardial oxygen reqs
    • may begin w/ minimal levels of physical activity or spontaneously when pt at rest
  59. what is a myocardial infarction?
    • irreversible necrosis of a portion of heart muscle due to occluded coronary artery and reduced blood flow - associated w/ high cholesteral, hypertension, smoking
    • typically related to thrombosis of a coronary artery (usually formed at the site of an ulcerated and ruptured atheromatous plaque)
    • rarely caused by prolonged arterial spasm or arteritis
  60. what are typical symptoms of a myocardial infarction?
    • severe persistent chest pain unrelieved by rest or nitroglycerin
    • nausea
    • vomiting
  61. what are the different types of myocardial infarctions?
    • transmural infarcts
    • subendocardial infarcts
  62. in what ways can arteries vary from each other?
    • can be elastic (aorta & beginning of branches)
    • can be muscular ( thick smooth muscle t. media)
    • can be small (autonomic blood flow regulation)
    • can be arterioles (fewer than 5 layers of muscle)
  63. what is a transmural infarct?
    • a type of myocardial infarction resulting from occlusion of a coronary artery involving the full thickness of the ventricular wall (usually L) and is greater than 2.5 cm in diameter
    • 90% are associated w/ a hx of thrombosis
    • usually develop from the endocardium outward as a wave of advancing necrosis
  64. where are the most common sites for thrombosis?
    • descending left anterior arter
    • right coronary artery
    • left circumflex artery
    • (3:2:1 ratio)
  65. what is a subendocardial infarct?
    • type of myocardial infarction where the necrotic area is only partially through the thickness of the myocardium (1/3 to 1/2 of the L ventricle)
    • not associated w/ regional thrombosis
    • due to hypoperfusion
  66. subendocardial infarction is also called what?
    non-Q-wave infarction bc it is only associated w/ ST elevation and T wave inversion
  67. what are the differences between transmural and subendocardial infarctions
    transmural: "Q-wave infarctions", ST segment progressive elevation is combined w/progressively deeper & wider Q-waves (hallmark, vectors are moving around dead/bad tissue)-- necrotic tissue though myocardium

    subendocardial: ST elevation, T wave inversion -- necrotic tissue only 1/3 or 1/2 through myocardium
  68. what is the gross appearance w/ a myocardial infarction?
    • 12-24hr: infarcted area begins to show a gray/brown pallor that progresses to a soft yellow brown
    • 10-14 days: granulation tisssue appears
    • lesion becomes gray white as scaring develops
  69. what microscopic appearance changes occur w/ a myocardial infarction?
    • begin after 6 hrs: myocytolysis followed by inflammatory response
    • 6-12 hrs: coagulative necrossis starts
    • 12-24hrs: infiltrated by neutrophils, mm cells begin to lose nuclei
    • days: mm cells replaced by macrophages and fibroblasts *critical bc most hrt wall has lowest degree of mechanical integrity and most prone to rupture*
  70. what complications can occur post myocardial infarction?
    • cardiac arrhythmia (w/in first week post-infarct)
    • left ventricular dysfunction (leads to CHF)
    • myocardial rupture (L ventricle, 10-14 days post-infarct "cardiac tamponade")
    • ventricular aneurysm or rupture
  71. what is the definition of sudden death (in regards to ischemic heart disease)?
    • when death occurs instantaneously or within 24hrs of the onset of acute sx or signs
    • most due to acute arrhythmia or acute myocardial failure, both associated w/ myocardial infarctions
  72. during embryogenesis, what is the blood flow like through the heart?
    • shunted btwn R and L atrium through foramen ovale
    • these must close after birth to allow for normal functioning of the hrt
    • ductus arteriosus exists btwn aorta and pulm artery too
  73. what are the two types of defective shunts in the heart after birth?
    • R to L: like tetralogy of Fallot
    • L to R: like atrial or ventricular septal defect
  74. what tends to be the problem in congenital heart disease (most commone problem?)
    the shunts that exist in the hrt or btwn hrt and lungs do not close
  75. what happens w/ a R to L shunt as a congential heart defect?
    • blood containing reduced hemoglobin is diverted away from pulmonary circulation to systemic circulation
    • reduces O2 saturation of the arterial blood
    • causes cyanosis
  76. what is Tetralogy of Fallot?
    • a congenital hrt disease
    • an example of a R to L heart shunt that also has:
    • -- pulmonary stenosis
    • -- ventricular septal defect
    • -- dextroposition of aorta (moves to the R)
    • -- R ventricular hypertrophy
  77. CHD is divided in to what (based on the shunt)
    those with cyanosis and those without cyanosis
  78. what CHD result in cyanosis?
    • tetrology of Fallot
    • transposition of great vessles (R ventricle to aorta, L ventrical to pulm artery -- req surgery)
    • patent ductus arteriosus
  79. what CHD do NOT result in cyanosis?
    • atrial septal defect (more common)
    • ventricular septal defect
    • coarctation of aorta
    • R ventricular hypertrophy
  80. what happens w/ a L to R shunt as a congential heart defect?
    oxygenated blood is diverted from systemic circ to pulmonary circ
  81. what physiological changes occur w/ a L to R heart shunt?
    • inc blood volume, inc demands on the R side of the hrt and pulm ciruclation
    • hypertrophy of pulm arterioles walls, increased pulm circ resistance (pulm hypertension) which cause R ventricle hypertrophy (may reverse the shunt)
  82. what is coarctation of the aorta?
    • local constriction of the aorta below the origin of subclavin a.
    • a type of CHD that does not cause cyanosis
    • more freq in males
  83. what happens clinically w/ a coarctation of the aorta?
    • inc BP in UE (L ventricular hypertrophy)
    • dec BP in LE w/ diminished pulses, pallor, coldness and possibly intermittent claudications in calf muscles
  84. what is transposition of great vessels (TGA)?
    • a CHD that causes cyanosis
    • blood doesn't move from any chamber to the correct place
    • fatal
    • occurs when the aorta and pulmonary artery are transposed
  85. what is observed in a child with TGA?
    • tires w/ any activity
    • further complicated with chest infections, breathlesness, pulmonary HTN
  86. what are ventricular and atrial septal defects (VSD/ASD)?
    • an opening btwn the walls of the ventricles or atria
    • causes a L to R shunt so more blood gets into the lungs causing breathing difficulties and less blood to the tissues
    • can be small/med/large or simple/complex
    • large may cause hrt failure
  87. what are compensation mechanisms for CHF?
    • inc hrt rate and contractility
    • hypertrophy of the mm or dilation of hrt ventricles
    • create an additional burden on the compromised hrt so heart will decompensate
  88. how does a person w/ heart failure present?
    • Dyspnea (breathlessness due to vascualar constriction)
    • Orthopnea (gauged by # of pillows used)
    • Paroxysmal nocturnal dyspnea (sudden, wakes the pt)
    • Nocturia (inc renal blood flow during sleep)
    • Cardiac edema (R side hrt failure)
  89. what are the physical signs of heart failure?
    • Tachycardia (compensatory to maintain CO)
    • Pulmonary Rales (inc hydrostatic pressure -> inc fluid into alveoli)
    • Abnormal hrt sounds (atrial and ventricular gallop/3rd & 4th hrt sounds)
    • Neck vein distension (incr central venous pressure bc of R side hrt failure)
    • Pitting edema & ascites (sign of R side hrt failure)
  90. through what examinations is heart failure diagnosed?
    • ECG (presence of Q wave helps confirm MI)
    • X-ray (cardiac chamber enlargement & congestion - objective evidence)
    • Echocardiogram (identify chamber enlargement, quantify ventricular & valvular function)
    • Cardiac catheterization (invasive, evals cardiac pressure, chamber size, valvular stenosis & regurg, and hrt anatomy)
  91. what is acute rheumatic fever?
    • systemic immunologically mediated disease (anti-streptoco-ccus antibodies)
    • symptoms develop 2 weeks after streptococcus A pharingeal infection.
  92. what are the clinical sx of rheumatic heart disease?
    • migratory polyarthritis (arthritis that progressively affects a multiple joints)
    • carditis in all 3 layers
    • erythema (redness of the skin)
  93. What happens with valvular heart disease?
    • calcific aortic stenosis
    • mitral valve prolapse
    • nonbacterial and bacterial endocarditis
    • systemic lupus erythematosis
  94. valvular heart disease can result in what?
    • blood flow obstruction due to valve stenosis/failure
    • backward flow of blood bc valve cannot close properly
  95. what is myocarditis?
    • any inflammatory condition that involves the myocardium
    • usually associated w/ necrosis of myocytes
    • can be an acute process (hrt failure, tachycardia, AV block, fever)
    • can be asymptomatic
  96. what causes myocarditis?
    • possibly
    • microbiological agents (50% of cases are viral myocarditis)
    • hypersensitivity reactions
    • radiation
    • etc
  97. what is cardiomyopathy?
    • a general "catch all" term when drs cannot identify a specific problem
    • non-inflammatory myocardium disorders w/ 3 possible clinical patterns (dilated, hypertrophic, restrictive)
  98. what is dilated cardiomyopathy?
    • aka congestive cardiomyopathy
    • results from a variety of previously undiagnosed cardiac diseases (idiopathic)
    • characterized by dilatation and hypertrophy of hrt chambers and congesitve hrt failure
  99. what is hypertrophic cardiomyopathy?
    • aka obstructive cardiomyopathy
    • inherited condition w/ hypertrophied myocardium and mitral insufficiency
  100. what is restrictive cardiomyopathy?
    rare condition w/ restriction of ventricular filling
  101. what is the accumulation of excess fluid btwn the cardiac sack?
    • pericardial effusion
    • if the fill up is very slow, the hrt can continue to pump formally even if there's a large amt of fluid
  102. what is pericarditis?
    inflammation of the visceral or parietal pericardium
  103. how is pericarditis classified?
    • according to gross appearance
    • - serous
    • - fibrinous
    • - purulent
    • - hemorrhagic
  104. what causes serous acute pericarditis?
    • usually due to a bacterial, viral or immunologically mediated inflammation of the epicardium and pericardium
    • results in serous effusion into pericardial space (usually <200mL)
  105. what is fibrinous acute pericarditis?
    • most common
    • usually non-infectious in origin
    • seen after a myocardial infarct or trauma to pericardium
    • produces a loud pericardial friction rub w/ adhesions that may persist
  106. what is purulent acute pericarditis?
    • seen most freq in young males
    • associated w/ infectious agents (bacteria and fungi)
    • produces thick, creamy exudate (up to 500mL) that accumulates w/in pericardial cavity
    • often becomes chronic adhesive constrictive pericarditis
  107. what is hemorrhagic acute pericarditis?
    • fibrinous or suppurative effusion mixed w/ blood
    • often due to injry, TB, or neoplasm
  108. are primary tumors of the heart common or rare?
  109. what is the most common cardiac neoplasm?
    • myxomas (benign)
    • most likely to arise in the left atrium (foramen ovale area)
    • tumor appears as a gelatinous, polypoid mass
    • may cause valve obstruction depending on size
  110. what is the most common malignant cardiac neoplam?
    • angiosarcoma
    • (but, malignant cardiac tumors are rare)
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