CPR Exam 1

103 flashcards · Other · by Jared Blackwell

1. Describe unique functions of arteries, arterioles, and veins

   Arteries have highest velocity and pressure. Arterioles are resistance vessels. Veins have highest capacitance/volume and compliance.

2. 1) Where does the Aorta arise from? 2) Where does the Smooth RA arise from? 3) Where does the Pulmonary Trunk arise from?

   Aorta & Pulmonary Trunk arise from Truncus Arteriosus. The Smooth RA (and coronary sinus) arise from Sinus Venosus.

3. Where do the pulmonary veins arise from embryologically?

   Pulmonary veins arise from the Lungs.

4. Where do the smooth left and right ventricle arise from?

   Smooth L/R Ventricle arise from Bulbos Coridis.

5. A- Fibroblast nuclei B- Purkinje Fiber C- Tunica Intima D- Myocardium

6. B- Purkinje Fibers or Intercalated disk? C- Cardiac muscle nuclei D- Nerve cell

7. What does the atrium embryologically develop into?

   Atrium--> Trabeculated Left and Right Auricles of Atrium. Smooth L/R ventricles from Bulbos Cordis. Smooth RA from Sinus Venosus, also coronary artery.

8. Lymphocytic Myocarditis Most common Typical of viral etiology, transplant rejection.

9. Parasitic Myocarditis: Chagas Disease Affects up to 1/2 of endemic areas of S. America. Myofiber filled with trypanosomes at arrow.

10. Dilated Cardiomyopathy Systolic dysfunction. Mitral & Tricuspid regurgitation. 90% of cases. Alcohol abuse, wet Beriberi, Coxsackie B viral myocarditis, Cocaine, Chagas disease. MICROSCOPIC: Myocyte hypertrophy, patch fibrosis. MORPHOLOGY: Large, heavy and flabby. Dilation of all 4 chambers.

11. Hypertrophic Cardiomyopathy Mutations in sarcomere. 60% genetic. Decreased CO and syncope w/ exercise. MORPHOLOGY: Thick walled, heavy. NO dilation. "Banana" shaped LV. MICROSCOPIC Myofiber disarray. Extreme hypertrophy of myocytes.

12. Cardiac Amyloidosis Usually leads to restrictive physiology. Morphology: Small semitranslucent nodules "drops of wax" on atrial surface. Microscopic: Rings around myocytes and capillaries. Can cause vascular compression and occlusion.

13. Antischkow Cells Derived from cardiac macrophages. Sign of acute rheumatic heart disease. Do NOT involve cardiac myocytes. Aschoff bodies

14. Aschoff cells Multinucleated Anitschokow cells. Sign of acute rheumatic heart disease. "Granuloma of the heart." Do NOT involve cardiac myocytes.

15. Describe chronic rheumatic fever

    Most common cause of mitral stenosis. Always involves the mitral valve sometimes aortic valve. Years-decades after exposure it clinically manifests. Repeated episodes of valvulitis & scarring results in cumulative damage to valves.

16. Describe Mitral Stenosis

    Most commonly associated with Rheumatic Fever. Increase in LA pressure, dilation of LA. Decrease in EDV due to impaired ventricular contraction. Decrease ESV & SV. Pulmonary edema RV hypertrophy, failure.

17. Aortic Stenosis Calcified leaflets at base with NO FUSION. Post-inflammatory aortic stenosis caused by chronic rheumatic fever. Fusion of leaflets, calficiations on margins.

18. What is the most common cause of mitral insufficiency?

    Myxomatous degeneration of leaflets: mitral valve prolapse. young women (3:1).

19. Describe ECG leads

    Inferior: II, III, avF "2-3 Feet" Lateral: I, V5, V6, aVL "1 hand, 5-6 fingers) Anterior: V1 & V2 Septal: V3 & V4 "3-4 boogers in nasal septum"

20. Describe the differences in NE and EPI

    NE acts on alpha1/2 and beta 1. Increases BP Decrease HR, reflex bradycardia. Large increase in TPR. EPI as on alpha1/2 and beta1/2. Increases HR Increases Systolic BP Decreases diastolic BP Widens PP Decrease TPR.

21. Pulmonary Tuberculosis Right upper lobe. CT Pulmonary TB.

22. Dextracardia- Heart on right side.

23. Pulmonary Edema Perihilar Bat-winged

24. Interstitial Pulmonary Edema.

25. Pleural Effusion Don't see diaphragm. No CP angles. Lateral cxray pleural effusion. NORMAL

26. Pneumothorax

27. Tension pneumothorax. Trachea deviates to the left.

28. Pneumoperiotneum

29. Left pulmonary embolus NORMAL

30. Aortic dissection NORMAL

31. Saddle Pulmonary Embolus "V-shaped thing."

32. Describe Bernard-Soulier Syndrome

    Congenital defect in GPIb. Poor adhesion. GPIb binds platelets to vWF. Labs: Large platelet size. Normal/decrease in platelet count. Treat w/ platelet transfusion.

33. Describe Glanzmann

    Congenital defect in GPIIb/IIIa. Poor aggregation. Normal PC & size. Labs: No platelet clumping. Treat w/ platelet transfusion.

34. Describe TTP/HUC

    TTP: Defect in ADAMTS13 which cleaves ULvWF. Long strings of vWF leads to platelet clumping and thrombus. Fever, Neuro issues, Schistocytes, thrombocytopenia, Renal failure. Common in healthy, adult females. Begins with flu symptoms. HUS: Shiga toxin. Children. Bloody diarrhea. BOTH have Hemolytic anemia. Schistocytes, Increase LDH. Treat with plasma exchange. Remove ADAMTS13 inhibitor or replenish ADAMS13.

35. Immune Thrombocytopenia/ Idipathic Thrombocytopenia Puppura (TTP)

    IgG attack platelets and platelets removed by spleen. Impaired production of platelets by megakaryocytes. Secondary: Lupus, drugs, immunodeficiency. Large/giant platelets. Treat w/ steroids, rituxan (anti-CD20 Ab),

36. Hemophilia A

    Deficiency in F VIII. X-linked recessive. Severe present before age 1. Spontaneous hemorrhage. Prolonged aPTT

37. What is Factor V Leiden?

    Gene mutation in factor V. Protein C Resistance. Protein C&S inactivate FV 10x slower. DNA test to confirm.

38. Describe a Protein S and C deficiency.

    PC & S are synthesized in liver and are vit. K dependent. Develop venous thrombosis before 50yr. Antigen assay: how much protein is present? Functional assay.

39. What occurs with a prothrombin gene mutation?

    Gene mutation leads to increased levels of prothrombin factor II. Prothrombin increases thrombin generation--> Fibrin formation. Test with mutation analysis.

40. What is an Antithrombin deficiency?

    AT inactivates F 2, 10, 9,11,12. Leads to thrombosis. Homozygous deficiency=death in utero. Test: Ag and functional assay.

41. Clinical features of malignancy and thrombosis

    Abnormal BF, Endothelial injury, Hypercoagulability. 20% of VTE occur with malignancy. Common cause of death in cancer patients. GI, pancreas, ovary, prostate, lung.

42. Describe antiphospholipid antibody/Lupus anticoagulant

    Autoantibody against protein phospholipid complex. i.e. FX --> FXa blocked One of the most common causes of prolonged aPTT. Causes inhibitor pattern on mixing study. Mixing study NOT CORRECTED. Need thrombus OR pregnancy morbidity AND Ab on 2 or more occasions 12 weeks apart.

43. Describe what DIC is

    Widespread activation of clotting --> deficiency of clotting factors --> bleeding state. Acute is worse. Manage with plasma and platelets if bleeding. Heparin if predominately thrombotic. Prolonged PT Elevated D-dimer Bleeding Microvascular thrombi LOW fibrinogen

44. What type of murmur is present with mitral regurgitation?

    Holosystolic murmur that radiates to left axilla. Diminished S1 sounds. May cause A-Fib.

45. What type of murmur is present with aortic stenosis?

    Crescendo-Decrescendo systolic murmur. Radiates to carotid. Old people- SAD (syncope, angina, dyspnea).

46. What complications may arise 5-7 days after an anterior MI?

    Interventricular septal rupture. Left ventricular free wall rupture. Sudden cardiac death. 2-7 days papillary muscle rupture.

47. What complications may arise weeks after an anterior MI?

    Ventricular aneurysm. A fibrous scar forms and the pressure results in aneurysm.

48. What is Libman-Sacks endocarditis associated with?

    Patients with SLE may be affected with libman-sacks endocarditis. Vegetations on both sides of mitral or aortic valves. May become embolus. May have photosensitivy, rash anemia.

49. How do statins work and side effects?

    They decrease cholesterol by increasing LDL receptors on liver. Side Effects: Liver toxicty ALT/AST Muscle myalgia, cramps, rhabdomylsis.

50. Familial Hyperlipidemia I

    Deficient LPL; can't convert TGs to FFA. Increase TGs & chylomicrons Pancreatitis & Xanthomas.

51. Familial Hyperlipidemia IIA

    Only one with PURE cholesterol increase. Defective LDL-R.

52. Familial Hyperlipidemia IIB

    Increase in LDL & VLDL and TGs & cholesterol.

53. Familial Hyperlipidemia III

    Defective Apo-E2 can't remove TG from VLDL-->IDL can't bind liver. Increase in IDL & TGs. DECREASE in LDL. Palmer lipid creases. Common in diabetes (like type V).

54. Familial Hyperlipidemia IV

    High VLDL & TGs. Acute pancreatitis. Hepatic overproduction of VLDL.

55. Familial Hyperlipidemia V

    Increase in VLDL. Increased chylomicrons (like type I). Associated with diabetes.

56. Describe what ITP is.

    IgG directed to platelets and removed by spleen. Acute ITP in children with viral infection. Large platelets. Chronic ITP in adults.

57. What is prolonged in Vitamin K deficiency and Liver Disease?

    PT is prolonged first because F VII has shorter half-life. Then aPTT.

58. What do Argatroban and Bivalirudin do?

    Direct thrombin inhibitor.

59. What do apixaban and edoxaban do?

    They are direct Xa inhibitors. Have Xa (10a) in name -> apixaban

60. What does Ezetimibe do?

    Decreases cholesterol absorption in GI, increasing LDL-R in liver. - Reduces LDL and TGs.

61. How do you monitor Heparin and Warfarin?

    Use aPTT to monitor Heparin. Use PT to monitor Warafrin.

62. What does clopidogrel do?

    Clopidogrel blocks ADP and inhibits platelet function. May cause TTP.

63. Which blood disorder will have schistocytes?

    DIC, TTP, HUS. TTP in adult female begins with flu-symptoms. ADAMTS13 deficient. Creates large blood clots.

64. What does abciximab do?

    Inactivates GpIIb/IIIa for fibrinogen. Antiplatelet & antithrombotic.

65. What causes right sided murmurs to be louder?

    Inspiration RINspiration

66. What causes left sided murmurs to be louder?

    Expiration LEXspiration.

67. Increased preload makes murmurs louder or softer?

    Increased preload--> LOUDER murmurs. Exception is hypertrophy & MVP

68. What is the pulse pressure in septic shock?

    Septic shock = Wide PP. aortic regurg has wide PP too.

69. What is pulse pressure in hypovolumic shock?

    Narrow PP.

70. What occurs with an Aspirin overdose?

    Metabolic acidosis and respiratory alkalosis. Hyperventalation blow out CO2 causes respiratory alkalosis.

71. What would cause this?

    Hypovolumic shock.

72. What would cause this?

    Left ventricular heart failure.

73. What does amiodarone do?

    Class III Treats arrhythmia. Blocks K+ channels. Also sodium & calcium. Side effects: pulmonary fibrosis, hypo/hyperthyroidism, corneal deposits.

74. Notching of ribs in adult coarctation of aorta. Have hypertension in upper extremities and hypotension in lower. Infants have lower extremity cyanosis. Left ventricular hypertrophy.

75. Abdominal aortic aneurysm Palpable, pulsatile, abdominal mass.

76. What does phentolamine do?

    Alpha 1 & 2 antagonist. Decrease BP. Pheochromocytoma

77. What does phenoxybenzamine do?

    Alpha 1 & 2 antagonist. Decrease BP. Pheochromocytoma

78. How does EDV change in heart failure with systolic dysfunction?

    Increased EDV.

79. Describe preload, CO, and afterload in cardiogenic and obstructive shock.

    Preload increase CO decrease Aferload increase

80. What are tests and treatments for vWF disease?

    Test: vWF antigen level. vWF multimer assay. Treatment: DDAVP & vWF concentrates.

81. Mitral stenosis Aortic stenosis Mitral regurgitation Aortic regurgitation

82. What causes a machine like murmur in the upper left sternal border?

    Patent Ductus Arteriosus Blood goes from aorta to pulmonary trunk.

83. What is the most common cause of an atrial septal defect (ASD)?

    Secundum anomaly - 90%. Endocardial cushion defect.

84. What drug is contradicted with amiodarone?

    Warfarin because amiodarone potentiates warfarin. amiodarone treats ventricular arrhythmia.

85. Aortic dissection is associated with what imaging finding?

    Widened mediastinum. Weakened distal pulses.

86. What is a common infection that causes patent ductus arteriosus?

    Rubella.

87. What congenital heart defects are common in trisomy 21?

    Infants have endocardial cushion defects from neural crest cells causing AV valve regurgitation and ASD.

88. What is a cause of acquired long QT syndrome?

    Hypokalemia or Hypomagnesemia LOW K+ & Mg2+

89. What drugs cause long QT syndrome?

    Amiodarone Quinidine Erythromycin & azithromycin Ciprofloxacin & levofloxacin Odanestron Methadone

90. What murmur does mitral valve prolapse cause?

    Midsystolic click murmur.

91. What congenital heart defects are common in maternal diabetes?

    Transposition of great arteries. Cyanosis Poor Feeding.

92. Acute left-sided heart failure presents with what?

    Pulmonary edema with dyspnea and hemoptysis.

93. Liver with hemorrhage and necrosis is evident of what heart issue?

    Congestive Heart Failure. CHF results in blood stasis in central veins and central sinusoids causing hemorrhage & necrosis.

94. High pitched, blowing, early diastolic murmur located in the left sternal border is what?

    Aortic regurgitation. Diastolic murmur, left sternal border.

95. A third heart sound S3 heard at apex suggests what?

    Heart Failure.

96. What would an increase in cAMP cause?

    Smooth muscle relaxation via EPI acting on Gs beta-2 receptors.

97. What would an increase in IPE3 cause?

    Vasoconstriction via EPI acting on Gq alpha-1 receptors.

98. What does nitroglycerin do to EDV and ESV?

    Nitroglycerin decreases preload and afterload; Decreased EDS & ESV.

99. What drug do you administer to a 76-year-old female after A-fib?

    Heparin and Warfarin. The altered flow in the fibrillating atrium can cause clot formation.

100. When would you use Niacin?

     Patients with high TGs. Niacin decreases VLDL and LDL production.