Cardio1- CVS Pathology

  1. In what 7 ways can the heart respond to injury?
    hypertrophy, necrosis/degeneratoin, fibrosis, thrombosis, inflammation, inflammation, neoplasia, mineralization
  2. Hypertrophy occurs when ___________; it is considered a change in _________, but cardiomyocytes do not ____________, hence hypertrophy.
    synthesis of cell components> breakdown; cardiac mass; multiply postnatally
  3. What are the 3 categories of cardiac hypertrophy?
    concentric, eccentric, mixed
  4. Concentric hypertrophy is a response to __________; 2 causes can be...
    increased afterload; aortic or pulmonic stenosis, systemic hypertension.
  5. Describe concentric hypertrophy grossly.
    more mass (thicker wall) and lumen is compressed or smaller
  6. Eccentric cardiac hypertrophy occurs in response to __________; 2 possible causes of this include...
    increased preload; valve regurgitation (extra blood flow), volume overload
  7. Describe eccentric hypertrophy grossly.
    chamber is dilated, increased mass, circumference of wall increased
  8. Describe mixed cardiac hypertrophy grossly.
    wall is thicker, chamber is dilated, more mass
  9. Mixed cardiac hypertrophy occurs in response to __(2)__; possible causes of this include... (2)
    increased afterload and preload; pulmonary hypertension and tricuspid regurgitation, pulmonic/aortic stenosis and valve insufficiency [end stage heart]
  10. With concentric hypertrophy, there is __________ dysfunction; sarcomeres are added ___________.
    diastolic (heart cannot relax to accommodate volume); in parallel
  11. With eccentric hypertrophy, there is ___________ dysfunction; sarcomeres are added ____________.
    systolic (heart cannot contract very well); in series (along their long axis as opposed to along their width)
  12. What kind of hypertrophy do you see with end stage heart disease?
    mixed cardiac hypertrophy
  13. Hypertrophic cells have impaired __(2)__ over time, and _________ density does not keep up with hypertrophy, leading to... (4)
    contraction and compliance; capillary density; degeneration, necrosis, or apoptosis, and replacement fibrosis
  14. What morphologic changes are associated with cardiac degeneration? (2)
    sarcoplasmic vacuolation (distended SR), myofibrillar lysis
  15. Delivery of intracellular components to lysosomes for degradation in order to generate energy so it can stay alive.
  16. Uncontrolled cell death that is ALWAYS considered pathologic, stimulating tissue reaction.
  17. Programmed cell death that can either be pathologic or physiologic.
  18. What are causes of necrosis? (4)
    ischemia, hypoxia,  oxidative injury (toxins, inflammatory mediators- membrane damage), mitochondrial excitotoxicity (too much Ca2+- catecholamines)
  19. Accumulation of intracellular calcium with hypercontraction of cardiomyocytes.
    contraction band necrosis (histopath change)
  20. Coronary blood flow is determined by... (3)
    pressure gradient, time in diastole, coronary vascular resistnace
  21. Ischemic injury often manifests in the _____________.
    subendocardial myocardium
  22. Ischemic damage is usually _________ than hypoxic damage.
    worse than
  23. What nutritional deficiencies cause myocardial necrosis in cattle, sheep, and pigs? Even if these nutrients are adequate in diet, what else can lead to the same effects?
    Vit E and Selenium; exposure to oxidative agents (drugs or Se agonists)
  24. What are causes of nutritional myocardial necrosis? (3)
    Vit E/Se deficiency/ exposure to antagonists, free radical injury, rapid postnatal growth
  25. Toxic myocardial degeneration/necrosis can be caused by... (7)
    Doxorubicin, Ionophores, Cardial glycosides, Gossypol (plant), Saccharated iron, Thallium, Blister beetle (cantharidin)
  26. Myocardial fibrosis is deposition of __________; it is a non-specific response to... (4)
    type I collagen; cell death, senescence, inflammation, direct stimulation of fibroblasts
  27. What are important mediators of myocardial fibrosis? (2)
    angiotensin II, TGF-beta
  28. Replacement fibrosis is when collagen ____________; reactive fibrosis is ___(3)___.
    replaces cardiomyocytes; perivascular, interstitial, and/or subendothelial
  29. Fibrosis impacts... (4)
    contractile function, compliance, electrical conduction, cardiomyocyte perfusion
  30. More important than amount of fibrosis is __________ of fibrosis.
    location (within the heart)
  31. What are the components of Virchow's triad for thrombosis?
    endothelial damage, altered blood flow, hypercoaguability
  32. What is the difference between a pale and a hemorrhagic infarct?
    • pale: artery is occluded, so no blood can enter
    • hemorrhagic: vein is occluded, so blood can enter but cannot leave
  33. __________ is sequelae of thrombosis, which consists of activation of ___________, including __(2)__.
    Thrombolysis; fibrinolytic (plasmin) system; plasminogen activators and factor XII dependent pathway
  34. How is thrombus recanalization used to stage lesions? (3)
    • no evidence of thrombus recanalization- less than 3 days
    • hypercellularity- a few days old
    • recanalization- more chronic lesion
  35. What are causes of myocardial infarctions? (3)
    primary vascular disease (atherosclerosis- humans and pigs, vasculitis), thrombosis, thromboembolic disease
  36. With feline hypertrophic cardiomyopathy (HCM), there is __________ dysfunction, __________ hypertrophy, and maybe __(2)__ of the _________.
    diastolic; concentric; infarction or thinning; LV apex
  37. What breed has heritable feline hypertrophic cardiomyopathy (HCM)?
    Maine Coon
  38. What must you rule out before you can diagnose feline HCM? (2) Why?
    r/o hyperthyroidism (T4 is tropic for heart muscle--> hypertrophy) and systemic hypertension (heart muscle is working harder--> hypertrophy)
  39. What are lesions commonly associated with feline HCM? (6)
    thickened LV, myofiber disarray, dilated LA--> turbulent blood flow--> +/- LA thrombus--> +/- saddle thrombus
  40. What histologic findings are associated with canine dilated cardiomyopathy (DCM)? (5)
    fibrosis, attenuated wavy myofibers, fatty infiltration, fibrofatty replacement, cardiomyocyte atrophy
  41. What causes secondary dilated cardiomyopathy in cats? (6)
    ischemia, cellular infiltration (inflammatory, neoplastic), nutritional (taurine deficiency), toxic, volume overload (compensation), sustained tachycardia
  42. How is ARVC definitively diagnosed?
  43. What breeds are at risk for arrhythmogenic RV cardiomyopathy?
    Boxers and Bulldogs
  44. With arrhythmogenic RV cardiomyopathy, there is _________ hypertrophy and __________ dysfunction; it is caused by...
    eccentric; systolic; an intrinsic defect in cardiac muscle (intercalated discs)
  45. Mixed hypertrophy is seen with __________; on histology, there is...
    end stage heart; extensive fibrous replacement of myocardium (cardiomyopathy of volume overload)
  46. Myocarditis is hard to distinguish from __(2)__ grossly; they are distinguished by _________.
    necrosis and fibrosis; histopathology
  47. Suppurative myocarditis:
    Gross appearance:
    Specific examples: (4)
    • Suppurative myocarditis:
    • Gross appearance: red- hemorrhage/congestion
    • Pathogenesis: hematogenous spread of pathogens
    • Specific examples: Clostridium chaveoi (cattle), Histophilus somni (cattle), Erysipelothrix (swine), Streptococcus (pigs)
  48. What is the gross appearance of necrotizing myocarditis?
    small white foci [need histo to confirm necrosis]
  49. Viral myocarditis is __(2)__; specific examples include... (5)
    necrotizing, lymphoplasmacytic; [birds] WNV and polyoma virus, [ruminants] foot and mouth dz, [dogs] parvovirus and CHV
  50. Trypanosoma cruzi causes ___________ myocarditis.
  51. What is eosinophilic myocarditis associated with? (2)
    parasitic (Trichinella, Cystiercus), immune mediated
  52. What is pyogranulomatous and granulomatous myocarditis associated with? (5)
    macrophages, higher order bacteria, immune mediated, fungal, +/- toxic
  53. Describe the gross morphology of endomyocardial fibrosis in cats? (3)
    band of fibrous tissue bridging LV, severe LA enlargement, +/- diffuse endomyocardial scarring
  54. How is endomyocardial fibrosis in cats thought to occur?
    stressful event--> post-inflammatory--> death
  55. What systemic lesions occur with right-sided heart failure? (3)
    hepatic congestion, splanchnic congestion, effusions
  56. What systemic lesion is associated with left sided heart failure?
    pulmonary edema
  57. Pulmonary edema associated with left-sided heart failure leads to... (4)
    occludes airspaces, impairs perfusion, decreased lung compliance, dilation of pulmonary veins leading to bronchoconstriction
  58. Degenerative valve disease is most frequently associated with the _________ valve; grossly, it appears...
    mitral; raised, smooth, white, glistening nodules.
  59. What causes degenerative valve disease?
    multifactorial: thought to have a genetic component
  60. What is the "jet lesion" associated with?
    linear endocardial proliferation and fibrosis due to degenerative valve disease
  61. What is the gross pathology associated with endocarditis? (3) Histological appearance? (4)
    thickened, roughened valve, vegetative projection; fibrin, neutrophils, necrotic debris, bacteria
  62. What are causes of endocarditis? (5)
    recurrent bacteremia, sepsis, thromboembolic disease, immune mediated disease, cardiac disease
  63. Endocarditis is usually associated with the ________ valve in cattle and _________ valve in dogs.
    tricuspid/pulmonic; mitral/aortic
  64. What are specific etiologic causes of endocarditis? (6)
    T. pyogenes (cattle), Erysipelothrix (pigs), Strep equi (horses), Staph/Strep/Bartonella (dogs)
  65. What is endocardial ulceration and mineralization associated with?
  66. Acute infectious pericarditis has ____________; chronic manifests as ____________.
    fibrinosuppurative exudate; fibrous adhesions
  67. What are specific etiologic causes of infectious pericarditis? (3)
    T. pyogenes (cattle), Strep/Actinobacillus (horses)
  68. Describe hemangiosarcoma clinically. (5)
    endothelial neoplasia, mets widely, aggressive [rupture, hemopericardium, tamponade]
  69. What are predilection sites for hemangiosarcoma? (2)
    right atrium and auricle, spleen
  70. What is you top differential for white infiltrating tissue in the myocardium of a cow? How about in a cat?
    • Cow: BLV--> lymphosarcoma
    • Cat: spontaneous, FeLV
  71. Describe the gross appearance of heart base tumors? (3)
    solid white mass around aorta, pericardial effusion, indistinguishable grossly from ectopic thyroid carcinoma
  72. Where would mesothelioma occur in the heart?
    lining pericardial cavity and epicardium
  73. How does mesothelioma of the heart appear grossly? (2)
    velvety mesothelial surface, solid white nodules
Card Set
Cardio1- CVS Pathology
vetmed cardio1