CARDIOVASCULAR PATHOLOGY2

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rere_girl4ever
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CARDIOVASCULAR PATHOLOGY2
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2015-03-15 18:51:37
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CARDIOVASCULAR PATHOLOGY2
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  1. What is Jervell and Lange-Nielsen syndrome? What are patients at risk for?
    • Congenital long-QT syndrome inherited disorder of myocardial repolarization due to iron channel defects 
    • Accompanied by NEUROSENSORY/ SENSORINEURAL DEAFNESS
    • Autosomal recessive

    • Present with syncopal episodes
    • Are at risk for SUDDEN CARDIAC DEATH due to torsades de pointes (a ventricular arrythmia)
  2. This congenital long QT syndrome is associated with sensorineural deafness
    Jervell and Lange-Nielsen syndrome
  3. What is Romano-Ward syndrome and what are patients at risk for?
    • Congenital long-QT syndrome - inherited disorder of myocardial depolarization due to iron channel defects.
    • Autosomal dominant

    • Present with syncopal epidodes.
    • Are at risk for SUDDEN CARDIAC DEATH due to torsades de pointes (a ventricular arrythmia)
  4. What are the congenital long QT syndromes?
    • Jervell and Lange-Nielsen syndrome (associated with neurosensory deafness)
    • Romano-ward syndrome
  5. Patient experiences an episode of syncope (which was not provoked by any activity or circumstance). ECG reveals QT interval prolongation. What is the pathology?
    • Congenital long-QT syndrome inherited disorder of myocardial repolarization due to iron channel defects 
    • Jervell and Lange-Nielsen syndrome (associated with neurosensory deafness)
    • Romano-ward syndrome

    • Present with syncopal epioses
    • Are at risk for SUDDEN CARDIAC DEATH due to torsades de pointes (a ventricular arrythmia)
  6. Young child with a family history of sudden death shows QT interval prolongation. What is the pathology?
    • Congenital long-QT syndrome inherited disorder of myocardial repolarization due to iron channel defects 
    • Jervell and Lange-Nielsen syndrome (associated with neurosensory deafness)
    • Romano-ward syndrome

    • Present with syncopal epioses
    • Are at risk for SUDDEN CARDIAC DEATH due to torsades de pointes (a ventricular arrythmia)
  7. Describe the pathogenesis of Hyperplastic arteriolosclerosis.
    BP (malignant hypertension) ⇨  causes BASEMENT MEMBRANE duplication and SMOOTH MUSCLE hyperplasia in the renal arteries ⇨ onion skin appearance ⇨ Renal artery stenosis of hyperplastic arteriolosclerosis ⇩GFR, thus activating renin-angiotensin-aldosterone system ⇨ ⇧⇧⇧BP leads to retinal hemorrages or papilledema(optic disc swelling due to ↑intracranial pressure)
  8. Laminated smooth muscle cells and reduplicated basement membranes in renal arteries are characteristic of this cardiovascular pathology.
    Hyperplastic arteriolosclerosis
  9. Onion skin appearance in renal arterioles are characteristic of this cardiovascular pathology.
    Hyperplastic arteriolosclerosis
  10. Describe the clinical presentation and findings of hyperplastic arteriolosclerosis.
    • ⇧blood pressure - diastolic is > 120-130 mmHg
    • Retinal hemorrages/ papilledema
  11. Transmural inflammation of the arterial wall with fibrinoid necrosis is characteristic of?
    Polyarteritis nodosa
  12. Which micro organism commonly cause right sided bacterial endocarditis? What are some of the complications that can occur?
    S.aureus- often affects the tricuspid valve (IV drug abusers) septic embolization to the lungs leading to pulmonary abscesses
  13. Which patients are at risk of bacterial endocarditis caused by S.aureus?
    • IV drug abusers
    • Incision and drainage of abscess
    • Infected IV catheters such as central lines
  14. This microorganism causes the formation of large vegetations on previously normal valves.
    S.aureus (acute bacterial endocarditis)
  15. This microorganism causes the formation of small  vegetations on congenitally abnormal or diseased valves.
    Viridans group streptococci
  16. Which patients are at risk of bacterial endocarditis caused by S.bovis (gallolyticus)?
    Patients with colon cancer
  17. Patients with colon cancer are at risk of developing endocarditis caused by which organism?
    S.bovis (gallolyticus)
  18. Describe the infective endocarditis caused by S.aureus.
    • Acute
    • Large vegetations on previously normal valves.
    • Affects tricuspid valves (IV drug abusers) and mitral valve
  19. Which organisms are responsible for infective endocarditis with negative blood cultures?
    • Coxiella burtnetii ***
    • Bartonella
    • Haemophillus
    • Actinobacillus
    • Cardiobacterium
    • Eikenella
    • Kingella
  20. Describe the inheritance of hypertrophic cardiomyopathy.
    • 60-70% are FAMILIAL 
    • Autosomal dominant
  21. Who does the familial/ sporadic form of hypertrophic cardiomyopathy occur in?
    • Familial- young 
    • Sporadic- elderly
  22. What causes hypertrophic cardiomyopathy?
    • Missense mutations in cardiac sacomere proteins
    • 1. β-myosin heavy chain
    • 2. Myosin-binding protein C
    • 3. Cardiac troponin T
    • 4. Tropomyosin
  23. Describe the presentation of hypertrophic cardiomyopathy.
    Syncope during exercise and may lead to sudden death in young athletes due to VENTRICULAR ARRYTHMIA
  24. What are the causes of Restrictive/ infiltrative cardiomyopathy?
    • Sarcoidosis
    • Amyloidosis
    • Post radiation fibrosis
    • Endocardial fibroelastosis (fibroelastic tissue in endocardium of young children)
    • Infiltrative diseases: Pompe, hemochromatosis
  25. What is endocardial fibroelastosis and which cardiomyopathy is it associated with?
    Restrictive/ infiltrative cardiomyopathy
  26. Which cardiomyopathy is amyloidosis associated with?
    Restrictive/ infiltrative cardiomyopathy
  27. Which type of cardiomyopathy is sarcoidosis associated with?
    Restrictive/ infiltrative cardiomyopathy
  28. Describe the pathophysiology of Restrictive/ infiltrative cardiomyopathy.
    Decreased ventricular compliance (⇩distensibility) ⇨ Diastolic dysfunction (ventricles can't fill)
  29. ST segment elevation in the inferior leads is diagnostic of?
    An inferior myocardial infarction
  30. What causes an inferior myocardial infarction? How do we treat?
    • Due to blockage of the right coronary artery which supplies the SA and and AV node.⇨ BRADYCARDIA
    • Muscarinic antagonist- e.g. Atropine
  31. Describe the pathogenesis of an inferior MI.
    Due to blockage of the right coronary artery  ⇨  SA and and AV node perfusion ⇨ BRADYCARDIA
  32. What supplies the SA and AV nodes?
    Right coronary artery
  33. Posteromedial papillary muscle rupture is caused by?
    Inferior MI due to thrombosis of the Right coronary artery
  34. Describe the conduction velocity of cardiac tissues from the fastest conduction velocity to the slowest.
    • Purkinje
    • Atria
    • Ventricles
    • AV node
  35. Which coronary artery is responsible for ST segment elevation in leads II, III and avF?
    • Right coronary artery
    • Ischemic injury to the inferior wall of the heart
  36. Occlusion of the right coronary artery results in ST segment elevation in which leads?
    • II, III and avF
    • Ischemic injury to the inferior wall of the heart
  37. Ischemic injury to the inferior wall of the heart produces ST elevation in which leads?
    II, III and avF- Right coronary artery

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