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Flashcards

Cardiovascular Pathology

littlebluechair English 182 cards

Cards in this deck (182)

  1. 1What disease is associated with the development of an abdominal aortic aneurysm?Atherosclerosis.
  2. 2What is the gold standard for diagnosis of traumatic rupture of the aorta?Aortogram or computed tomography (CT) angiogram.
  3. 3What is the treatment for aortic dissection?Control hypertension (descending aortic dissection); immediate surgical intervention (ascending aortic dissection)
  4. 4What is the difference between dissection and aneurysm?Dissection results when a tear in the tunica intima allows blood to penetrate into and divide the tunica media. Aneurysm is a general term for vascular wall dilation and occurs when the vessel wall is weakened (eg atherosclerosis).
  5. 5What genetic disease is associated with aortic dissection in young, particularly male patients?Marfan syndrome.
  6. 6What is the cause of aortic dissection in Marfan syndrome?Cystic medial degeneration of the wall of the aorta (highlighted by loss of elastin)
  7. 7What is the most common causes of cardiac tamponade?Trauma, iatrogenic trauma, pericarditis, myocardial rupture, hypothyroidism
  8. 8What collection of signs and symptoms would suggest that a patient is presenting with cardiac tamponade?Finding a Beck triad (low arterial blood pressure, jugular venous distention, and distant, muffled heart sounds) and/or pulsus paradoxus on physical examination.
  9. 9What is pulsus paradoxus?Decreased systemic pressure with inspiration. (>10mmHg)
  10. 10What is the treatment for cardiac tamponade?Immediate pericardial window.
  11. 11What is the difference between tension and nontension pneumothorax?In tension pneumothorax, the volume of air in the pleural cavity increases with each breath, secondary to a tissue flap that essentially creates a one way valve. due to the resulting pressure gradient and shifting of mediastinal structures, this can result in compromise of intrathoracic vessels. In nontension pneumothorax the volume of gas remains constant during breathing and there is little to no effect n mediastinal structures.
  12. 12What signs and symptoms would suggest that a patient is presenting with tension pneumothorax?Tachycardia, hypotension, decreased heart sounds, distended neck veins, and absent breath sounds on the side of the pneumothorax.
  13. 13What radiologic evidence would support a diagnosis of tension pneumothorax?Deviation of the trachea to the side of the chest opposite the pneumothorax due to unilateral increased intrathoracic pressure.
  14. 14What is the emergent treatment for tension pneumothorax?Needle thoracostomy followed by chest tube insertion.
  15. 15How can patients develop a pneumothorax?They can develop spontaneously (rupture or apical blebs)or after penetrating chest wounds. They are also associated with lung infections, parenchymal lung disease, and lung cancer.
  16. 16What are the clinical characteristics of bacterial endocarditis?Fever, anemia, murmur, emboli, osler nodules, nail hemorrhages, roth spots, Janeway lesions.
  17. 17What are the Osler nodes of bacterial endocarditis?Tender-raised lesions on toes and fingers.
  18. 18What are Roth spots of bacterial endocarditis?White retinal spots surrounded by hemorrhage.
  19. 19What are the small red lesions on palms and soles of patients with bacterial endocarditis?Janeway lesions.
  20. 20What disease is associated with notched ribs, cystic hygroma of neck, and coarctation of the aorta?Turner syndrome
  21. 21What are the cyanotic congenital heart disease?Tetralogy of Fallot, Transposition of the great vessels, Tricuspid atresia, Truncus arteriosus; Total anomalous venous return; hypoplastic left heart.
  22. 22What birth defect is associated with cyanosis, death soon after birth and maternal diabetes?Transposition of the great vessels.
  23. 23What shape is the heart in transposition of the great vessels?Egg shaped
  24. 24What congenital heart disease is associated with ventricular septal defect (VSD), pulmonary stenosis, right ventricular hypertrophy and overriding aorta?Tetralogy of Fallot
  25. 25What is the shape of the heart in tetralogy of Fallot?Boot shaped
  26. 26What congenital cyanotic heart disease is characterized by wide pulse pressure, single loud S2 and holosystolic murmur of VSD?Truncus arteriosus
  27. 27What cyanotic congenital heart disease is associated with right ventricular heave, wide fixed S2 split and a snowman shaped heart?Total anomalous venous return.
  28. 28What is the most common type of tumor involving the heart?Metastatic tumor (most are not primary)
  29. 29What is the most common primary cardiac tumor in children?Rhabdomyomas
  30. 30What is the mechanism of rheumatic fever?Cross-sensitivity between tissues and antistreptolysin antibodies.
  31. 31What is the lab test that helps diagnose rheumatic fever?Elevated antistreptolysin O (ASO) antibody titers.
  32. 32What is the rash that has central clearing in rheumatic fever?Erythema margintum
  33. 33What is the chronic consequence of fibrotic healing of valves after rheumatic fever?Chronic rheumatic heart disease
  34. 34What valve abnormality is most commonly involved with rheumatic heart disease?Mitral stenosis (MS)
  35. 35Infection of the aorta with which organism is associated with aneurysm of the aortic root and aortic arch?Treponema pallidum (tertiary syphillis)- due to the disruption of the vasa vasorum
  36. 36What is the characteristic appearance of the aorta in tertiary syphillis?The tissue is wrinkly and has a tree bark-like appearance
  37. 37What are the infectious causes of dilated cardiomyopthy?Coxsackie virus and Chagas disease (Trypanosoma cruzi)
  38. 38What cardiac abnormalities are associated with chronic infection with Trypanosoma cruzi?Cardiomyopathy, the pathogenesis of which is not well understood.
  39. 39What is the etiology of Osler nodes, Roth spots and Janeway lesions?All are caused in some way by immune complex deposition occurs in vessels leading to small vessel vasculitis.
  40. 40What valve is most commonly involved in bacterial endocarditis?Mitral valve.
  41. 41What acute necrotizing vasculitis in children may be complicated by the development of coronary aneurysms?Kawasaki disease.
  42. 42What medium-to large vessel vasculitis primarily affects young Asian females and may be referred to as pulseless disease?Takayasu arteritis- upper extremity pulses may be weak due to thickening of the aortic arch and/or proximal great vessels.
  43. 43Temporal arteritis (giant cell arteritis) primarily presents in elderly females and often affects branches of which artery?The carotid artery and in turn the temporal artery and the vascular supply to the eye; therefore temporal arteritis has diagnostic urgency to prevent blindness
  44. 44What is Dressler syndrome?An autoimmune form of fibrinous pericarditis which affects patients several weeks to months post MI. The exact etiology is unknown, but the autoimmune reaction is believed to be directed toward myocardial agents. This syndrome may also affect heart surgery patients.
  45. 45What is the treatment for Dressler syndrome?Steroids and nonsteroidal anti-inflammatory drugs (NSAIDs)
  46. 46What are the two major categories of pericarditis?Acute pericarditis
    Chronic pericarditis
  47. 47What is the cause of unstable angina?Atherosclerotic plaque disruption with subsequent platelet plug formation, possibly leading to thrombosis of a coronary vessel.
  48. 48What is the difference between unstable angina and STEMI/NSTEMI?In unstable angina, heart muscle is not damaged. In STEMI and NSTEMI, heart muscle undergoes ischemic damage and becomes infarcted.
  49. 49What is the cause of stable angina?Stable angina is a clinical scenario that can be caused by decreased blood flow to myocardium (eg due to narrowing of vessel lumen by atherosclerosis), resistance of vasculature to blood flow, and decreased oxygen carrying capacity of blood.
  50. 50What drug relieves the chest pain associated with stable angina?Usually nitroglycerin or vasodilators (ie calcium channel blockers). If there is decreased oxygen carrying capacity in the blood, the patient may need blood transfusion or other therapies.
  51. 51Which artery is the most commonly affected during acute MI?Left anterior descending (LAD)
  52. 52What are the two patterns of MI?Transmural, subendocardial
  53. 53What areas of the heart are affected with transmural infarctions?Blood flow to the entire ventricular wall is compromised. Ultimately, necrosis extends from epicardium to endocardium.
  54. 54What are the typical findings on ECG with transmural infarction?ST segment elevation or Q waves.
  55. 55What areas of the heart are affected with subendocardial infarctions?Only the inner one-third of usually the left ventricle wall.
  56. 56What are the ECG findings in acute subendocardial infarcts?Nonspecific ischemic changes, ST depression.
  57. 57What are the earliest histologic changes associated with infarction?Early features of coagulative necrosis with blurring of nuclear and cell borders.
  58. 58In general, what are the gross and microscopic changes observable in MI at autopsy?In general, observable changes will vary depending on amount of elapsed time between infarction and autopsy. Gross changes can include: pallor or hyperemia, necrotic areas, early scar formation, and old scars from previous MI. Microscopic changes can include: blurring of cardiomyocyte nuclei and striations, neutrophils,macrophages, fibrosis and scar formation.
  59. 59During healing and repair, what type of necrosis does infarcted myocardium undergo?Coagulative necrosis
  60. 60What are the first microscopic changes of coagulative necrosis of MI observable?After 12 hours.
  61. 61What are the first cells to appear in the damaged tissue about 12 hours post-MI?Neutrophils
  62. 62What is the most common cause of death within the first 24 to 48 hours post-MI?Arrhythmia
  63. 63By the third day, what gross evidence is there that tissue has been damaged by MI?Area of infarct is pale and beginning to turn yellow with surrounding hyperemia
  64. 64What cells begin to migrate to the damaged tissue between days 3 and 5 post MI?Macrophages
  65. 65What is the most common cause of death between days 3 and 7 post MI?Ventricular wall rupture leading to cardiac tamponade
  66. 66By 10 days post-MI, what gross changes to the myocardium are obvious?Yellow necrotic tissue replaced with new gray-white vascular connective tissue.
  67. 67What is the anatomic location of the carotid bodies and what is their function?The carotid bodies are located near the bifurcation of the common carotid artery (bilaterally), and they function as chemoreceptors monitoring levels of carbon dioxide and oxygen in the blood
  68. 68What is cardiomyopathy?Cardiomyopathy is a general term used to reflect a change in heart muscle structure or functional ability. There are many causes of cardiomyopathy, including acquired and inherited forms, all of which generally manifest clinically and pathologically as one of the three major types of cardiomyopathy.
  69. 69What are the major types of cardiomyopathy?Dilated, hypertrophic, restrictive.
  70. 70What cardiomyopathy are associated with alcoholic abuse and beriberi (thiamine deficiency)?Dilated
  71. 71Which cardiomyopathy is the most common?Dilated
  72. 72What therapeutic drug is associated with dilated cardiomyopathy?Doxorubicin
  73. 73What cardiac abnormality is seen at autopsy in hypertrophic cardiomyopathy?Myocardial hypertrophy (particularly of the ventricular septum)
  74. 74Mechanistically what is the major difference between dilated and hypertrophic cardiomyopathy?Dilated cardiomyopathy will result in systolic dysfunction because the heart becomes so massively enlarged that it cannot pump adequately. In contrast, hypertrophic cardiomyopathy will result in diastolic dysfunction because there is so much extra myocardium that the chambers cannot fill with an adequate quantity of blood.
  75. 75What is the characteristic shape of the left ventricle (LV) in hypertrophic cardiomyopathy?Banana shaped
  76. 76What inheritance pattern is seen in familial hypertrophic cardiomyopathy?Autosomal dominant
  77. 77What type of cardiomyopathy may result from systemic processes such as amyloidosis and hemochromatosis?Restrictive/obliterative cardiomyopathy
  78. 78Which form of restrictive cardiomyopathy is associated with eosinophilia?Loeffler obliterative cardiomyopathy
  79. 79What are the clinical findings in restrictive cardiomyopathy?Loud S3, normal chest X ray.
  80. 80What are the common cause of cardiac tamponade?Trauma, iatrogenic trauma, pericarditis, myocardial rupture, hypothyrodisim
  81. 81What is the etiology and organism involved in rheumatic fever?Immunologically mediated inflammatory response to group A beta hemolytic streptococcus infection, usually pharyngitis or tonsillitis.
  82. 82What is the Aschoff body of rheumatic fever?Focal interstitial myocardial inflammation with multinucleated giant cells.
  83. 83Do blood cultures show septicemia with streptococcus during rheumatic fever?No
  84. 84What cardiac abnormalities are associated with chronic infection with Trypanosoma cruzi?Cardiomyopathy, the pathogenesis of which is not well understood.
  85. 85What are the cyanotic congenital heart disease?Tetralogy of Fallot; Transposition of the great vessels, Tricuspid atresia, Truncus arteriosus; Total anomalous venous return; hypoplastic left heart
  86. 86What is the ductus arteriosus?It connects the pulmonary artery to the proximal aorta, effectively bypassing the lungs during fetal development.
  87. 87What happens if the ductus doesn't close after birth?If it remains patent after birth, the neonates becomes hypoxic (patent ductus arteriosus, PDA)
  88. 88The sinus venosus gives rise to which parts of the cardiovascular system?A portion of the wall of the right atrium and the coronary sinus
  89. 89The bulbus cordis gives rise to which parts of the cardiovascular system?The proximal aorta and the pulmonary arteries
  90. 90What is the function of the ductus venosus?To provide a direct passageway for nutrient-rich blood from the placenta to pass through the developing liver to supply the developing heart.
  91. 91What happens to the ductus venosus at birth?It becomes obliterated and fibrosed, forming the ligamentum venosum.
  92. 92Define the anatomic components of the cardiovascular systemHeart, macrovasculature (aorta, arteries, large arterioles, veins, microvasculature (small arterioles, postcapillary venules, capillaries, and lymphatics.
  93. 93What are the characteristics of Tetralogy of Fallot (TOF)?Pulmonary valve stenosis, Right ventricular hypertrophy, Overriding aorta, Ventricular septal defect (VSD)
  94. 94What is the treatment of TOF?Surgical repair
  95. 95How does the anatomy differ from normal in the transposition of the great arteries? (TGA)The aorta arises anteriorly from the right ventricle, while the pulmonary artery (PA) arises from the left ventricle. The aorta is posterior to the PA in a normal heart. This condition may also be referred to as transposition of the great vessels by some sources.
  96. 96Is TGA compatible with life?No, unless there is a shunt (patent ductus arteriosus (PDA), VSD, patent foramen ovale (PFO), etc present to allow mixing of blood.
  97. 97What are the five congenital heart diseases that cause cyanosis (right to left shunt) early in postnatal life?1. Truncus arteriosus
    2. TGA
    3. Tricuspid atresia
    4. Tetralogy of Fallot
    5. Total anomalous pulmonary venous connection (five words)
  98. 98Why does right-to left shunting cause cyanosis?Right to left shunting means that deoxygenated blood from the right side of the heart passes into the left side of the heart and is pumped to the systemic circulation. This bypasses the lungs, resulting in circulation of deoxygenated blood which does not meet the oxygen demand of peripheral tissues, resulting in cyanosis.
  99. 99What clinical features of cystic fibrosis is unique in males?Congenital bilateral absence of the vas deferens, azoospermia and infertility
  100. 100What is the number one cause of death in infants age 1 month to 1 year?Sudden infant death syndrome (SIDS)
  101. 101What preventative measures has been shown to reduce the incidence of SIDS?Back to bed.
  102. 102What organisms infect and may subsequently colonize the lungs of individuals with cystic fibrosis?Pseudomonas aeruginosa, Staphyloccocus aureus, Hemophilus influenza, Burkholderia cepacia
  103. 103What is the treatment of cystic fibrosis?There is no curative treatment. Systomatic treatment with N-acetylcysteine can loosen mucous plugs. Antimicrobials are given for pulmonary infections. Ultimately, lung transplant may be necessary. Pancreatic enzyme replacement is also typically needed.
  104. 104What is the pathogenesis of cystic fibrosis?The defective chloride channel causes secretion of abnormally viscid mucus that plugs the liver, pancreas and lungs. This leads to impaired food digestion and increased susceptibility to pulmonary infections leading ultimately to chronic infection and subsequent respiratory failure
  105. 105What are the risk factors for infantile respiratory distress syndrome (IRDS)?Prematurity, male gender, maternal diabetes and delivery by cesarean section.
  106. 106What is the etiology of IRDS?Insufficient pulmonary surfactant
  107. 107What does the chest x-ray of an infant with RDS show?Uniform, minute reticulogranular densities producing a diffuse "ground glass" appearance.
  108. 108What are the microscopic features of RDS?Collapsed air spaces, expanded respiratory bronchioles, and alveolar ducts lined by eosinophillic hyaline membrane.
  109. 109What is the treatment for IRDS?Surfactant replacement therapy with oxygen
  110. 110What is the treatment given to the mother to prevent IRDS?Steroids (glucocorticoids)
  111. 111What is the classic presentation of cystic fibrosis?History of meconium ileus, recurrent sinusitis, bronchitis, foul smelling stools
  112. 112How are forms of acute pericarditis classified?By the associated type of pericardial effusion: serous, fibrinous, hemorrhagic, purulent or caseous.
  113. 113What x-ray finding is helpful in diagnosing constrictive pericarditis?Calcified pericardium
  114. 114What physical finding of constrictive pericarditis is found on auscultation?Pericardial knock-the sound produced during rapid ventricular filling.
  115. 115Chest pain and echocardiogram revealing a "water-bottle" shaped heart would be associated with what diagnosis?Pericardial effusion
  116. 116What diseases are associated with hemorrhagic pericardial effusion?TB and malignancy
  117. 117What type of effusion is most common?Serous
  118. 118What are some common causes of pericarditis and pericardial effusion?Infection, renal failure, connective tissue disease.
  119. 119What type of clot has lines of Zahn?Thromboembolus or premortem clot
  120. 120What type of clot lacks lack of Zahn, is homogeneous in color, and is easily removed from vessels?Postmortem clot
  121. 121What is the triad of preeclampsia?A pregnant woman presenting with hypertension, edema and proteinuria
  122. 122What is eclampsia?Seizures, plus the triad of preeclampsia.
  123. 123What microscopic changes are seen at 10 days post MI?Granulation tissue is forming, macrophages are the predominate cell type.
  124. 124By the fifth week post-MI, what macroscopic and microscopic changes are evident?Fibrosis of infected area with scar formation.
  125. 125Which complication of MI causes a friction rub and is likely to occur between 3 days and 3 weeks after the MI?Fibrinous pericarditis
  126. 126If after MI, damaged myocardium does not regain full mobility, what complication are patients at higher risk to experience?Thromboembolic events due to blood stasis near the areas of impaired myocardial mobility.
  127. 127What tests are needed to diagnose pulmonary thromboembolus?CT-Angiogram (CTA), or less often, ventilation/perfusion (V/Q) scan
  128. 128Are emboli always blood clots?No. Embolus is a generic term used to describe a mass of substance that originated elsewhere and moved to its current position via the bloodstream. Emboli can be fat, air, thrombus, bacteria (septic emboli), amniotic fluid, or tumor cells.
  129. 129What is the treatment for eclampsia?Magnesium sulfate and delivery of the baby.
  130. 130What dangerous syndrome associated with preeclampsia is characterized by hemolysis, elevated liver function tests (LFTs) and low platelets?HELLP syndrome
  131. 131What laboratory tests may be used to assess for myocardial infarction?Troponin and/or CKMB are used to assess for cardiac function. Historically, myoglobin, LDH, AST levels were also used.
  132. 132When do cardiac troponin levels increase after a myocardial infarction and how long will the levels remain elevated?Levels will rise approximately 3 to 6 hours after infarction and may remain elevated for as long as 14 days after the event . (Note, there is a latent period, therefore if a patient presents with very acute infarction, the troponin level may initially not be elevated)
  133. 133Which laboratory test is used in diagnosis and management of congestive heart failure?B-type natriuretic peptide (BNP)
  134. 134ECG findings and electrolyte abnormalitiesPeaked T waves- Hyperkalemia
    Prolonged QT- Hypocalcemia
    Flattened T waves- Hypokalemia
    Prominent V waves- Hypokalemia
    Wide QRS- Hyperkalemia
  135. 135What is cardiac output?The volume of blood pumped by the heart per unit time. CO (mL/minute)=stroke volume (mL/beat) x heart rate (beats/minute)
  136. 136What is ejection fraction (EF)?Of the volume of blood present in the left ventricle at the end of diastole (EDV), EF is the percentage of that volume that is pumped per beat. Normal EF >55%/ EF= SV/EDV X 100
  137. 137Changes in which variables will affect cardiac output?Stroke volume and heart rate.
  138. 138Changes in which variables will affect stroke volume?Preload, afterload and contractility
  139. 139At which phase of the myocardial action potential does calcium enter the cardiomyocytes?Phase 2 (plateau)- calcium enters via voltage gated calcium channels
  140. 140What is the consequence of calcium influx on cardiomyocyte contraction?Calcium influx triggers additional calcium release from the sarcoplasmic reticulum. Calcium binds troponin C inducing a conformational change in troponin I and movement of the troponin-tropomyosin complex out of the actin filament active site. When this active site is bound by myosin, cross-bridges form and contraction can occur.
  141. 141What is the function of the three cardiac troponins?Troponin C binds calcium and is bound to both troponin T and troponin I.
    Troponin T is bound to tropomyosin.
    Troponin I is bound to actin and holds the troponin-tropomyosin complex in place.
  142. 142How is the smooth muscle contraction apparatus different from the cardiac muscle contraction apparatus?Smooth muscle contraction is dependent on calcium binding calmodulin to activate myosin light chain kinase and phosphorylate myosin leading to cross-bridge formation and contraction. Smooth muscle contraction does not involve troponins.
  143. 143Which phase of the pacemaker action potential undergoes diastolic depolarization?Phase 4-the membrane potential will spontaneously depolarize as sodium conductance is increased, this accounts for the automaticity of the sinoatrial (SA) and atrioventricular (AV) nodes and subsequently for heart rate.
  144. 144What cells compose the myocardium and to what fibrous structure are they associated?The myocardium is composed of cardiac muscle cells (aka cardiomyocytes). These cells are arranged in layers which form a complex spiral around the chambers of the heart. Many cardiomyocytes are anchored to the fibrous cardiac skeleton.
  145. 145Describe the innervation of blood vessels?In vessels containing smooth muscle cells, sympathetic nerve fibers discharge noerepinephrine to cause vasoconstriction. Vessels that supply blood to skeletal muscles also have cholinergic innervation to cause vasodilation. Density of innervations is higher in arteries than in veins.
  146. 146What histologic layer of the wall of the heart is homologous with the tunica intima of blood vesselsEndocardium
  147. 147Where do branches of the Purkinje system terminate within the heart?In the subendocardial layer, which also contains veins and other nerve branches
  148. 148Which two organs do not have lymphatic drainage?Central nervous system
    Bone marrow
  149. 149At what anatomic location does lymphatic fluid reenter the bloodstream?Either via the thoracic duct at the confluence of the left internal jugular and right subclavian veins.
  150. 150What is the anatomic location of the carotid sinus and what is their function?The carotid sinuses are dilated segments of the internal carotid artery (bilaterally), and they contain baroreceptors which detect changes in blood pressure and transmit this information to the central nervous system.
  151. 151What is the murmur associated with a patent ductus arteriosus (PDA)?Continuous machinery-like murmur.
  152. 152At birth, what is used to close a PDA?Idomethacin
  153. 153What is used to keep a PDA open?Prostaglandin E (PGE)
  154. 154What is the most common congenital cardiac anomaly?VSD
  155. 155What are the different types of VSD?Membranous (most common), infundibular, muscular (multiple: Swiss-cheese septum)
  156. 156What are three congenital heart disease that cause a left-to-right shunt and late cyanosis?PDA, VSD, Atrial septal defect (ASD)
  157. 157Why does late cyanosis occur?With persistent left to right shunting, pulmonary resistance increases, leading to pulmonary hypertension. Eventually a left to right shunt will become a right to left shunt, causing cyanosis.
  158. 158What is the name for the situation when a left to right shunt becomes a right to left shunt?Eisenmenger syndrome
  159. 159What are endocardial cushion defects?A spectrum of malformations including VSD, foramen primum, cleft anterior leaflet of the mitral valve, and atrioventricular canal defects.
  160. 160What cardiac defect is associated with Turner syndrome?Coarctation of the aorta
  161. 161What are the two type of coarctation of the aorta?Infantile type- aortic stenosis is proximal to the insertion of the ductus arteriosus (DA)
    Adult type: aortic stenosis is distal to the insertion of the DA
  162. 162Why does right to left shunting cause cyanosis?Right to left shunting means that deoxygenated blood from the right side of the heart passes into the left side of the heart and is pumped to the systemic circulation. This bypasses the lungs, resulting in circulation of deoxygenated blood which does not meet the oxygen demand of peripheral tissues, resulting in cyanosis.
  163. 163What are the clinical and radiographic characteristics of coarctation of the aorta?Higher blood pressure in the upper extremities when compared to the lower, notching of the ribs.
  164. 164What does the chest X-ray of an infant with RDS show?Uniform, minute reticulogranular densities producing a diffuse 'ground glass' appearance.
  165. 165What are the microscopic features of RDS?Collapsed air spaces, expanded respiratory bronchioles, and alveolar ducts lined by eosinophilic hyaline membranes.
  166. 166What is the treatment of IRDS?Surfactnat replacement therapy and oxygen.
  167. 167Which complication of MI causes a friction rub and is likely to occur between 4 days and 3 weeks after the MI?Fibrinous pericarditis
  168. 168If after MI, damaged myocardium does not regain full mobility, what complication are patients at higher risk to experience?Thromboembolic events due to blood stasis near the areas of impaired mobility
  169. 169What conditions are associated with Kerley B lines?Left ventricular failure (CHF) and mitral stenosis.
  170. 170What are the findings of CHF on chest radiography?Cardiomegaly, pulmonary vascular congestion and edema, Kerley B lines, and bilateral pleura effusions.
  171. 171What is an empyema?Pus within the pleural space usually as a result of primary infectious process or postsurgical/posttraumatic circumstances.
  172. 172What are the most common etiologies of anterior mediastinal masses?Thymoma, ectopic Thyroid, Teratomas, and terrible lymphomas.
  173. 173On what side do most ruptures of the diaphragm occur?On the left side because the liver usually protects the right side from damage.
  174. 174What is the most valuable imaging method for staging lung cancer?CT scan
  175. 175What are the peripherally located lung cancers?Adenocarcinomas and large cell lung carcinoma.
  176. 176What is unique about the tunica media of the carotid sinus?It is thinner than the tunica media in other vessels which allows baroreceptors in this segment of the internal carotid artery to detect changes in blood pressure and transmit this information to the central nervous system.
  177. 177What is the composition of the tunica adventitia?Type 1 collagen and elastic fibers
  178. 178Which part of the brain parenchyma does uncontrolled hypertension affect first?Basal ganglia and internal capsule.
  179. 179What is the most common identifiable etiology of hypertension?Renal disease, which accounts for less than 10% of all cases of HTN, the remaining 90% of cases are termed essential primary hypertension and the underlying cause is not well-characterized.
  180. 180What is arteriosclerosis? Arteriolosclerosis?Arteriosclerosis is a term used to describe hardening of medium to large arteries.
    Arteriolosclerosis is a term used to describe the hardening of small arteries.
  181. 181Define stable anginaA clinical term used to describe chest pain that develops with exertion or stress and is relieved with rest.
  182. 182What do fatty streaks progress into?Plaques- a nodular accumulation of fatty materials and macrophages which may be associated with cholesterol crystals and calcification.

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Flashcards on Cardiovascular Pathology, created by littlebluechair on 21/12/2013.
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