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Question Bank 2: Cardiovascular system

b.graham Pathophysiology and Pharmacology 1 2015 Englisch 126 Karten

Question Bank 2: Cardiovascular system

Karten in diesem Stapel (126)

  1. 1Primary hypertension is the most common type of hypertensive patients: true or false?TRUE
  2. 2You can also find an underlying disease for secondary hypertension: true or false?True!
  3. 3Secondary hypertension can be reversed by ________________________treatment of the underlying cause
  4. 4malignant hypertension is manifested intense spasm of arteries: true or false?true!
  5. 5What are the impacts of Malignant Hypertension on the eye, brain and kidney?Eye: retinal haemorrhage or exudate
    Brain: increases intracranial pressure
    Kidneys: haematuria, proteinuria, acute renal failure
  6. 6The clinical manifestations normally appear quite early in patients with hypertension: true or false?False
  7. 7Low stroke volume can be caused by what types of shock?Hypovolemic
    Cardiogenic
    Obstructive
  8. 8Shock due to vasodilation can be seen in conditions such as __________________________________septic shock
    anaphylactic shock
    and neurogenic shock
  9. 9What are the clinical manifestations of non-progressive shock?SNS reflexes - hormonal and renal responses compensate
  10. 10In patients with progressive shock, blood pressure can be maintained: true or falseFalse
  11. 11In patients with irreversible shock, tachycardia may lead to cardiac arrest: true or falseTrue!
  12. 12Urine output is normally reduced in patients with shock: true or false?True!
  13. 13Stenosis is the condition where the ________________________heart valve with not open fully (it is harder to force blood through)
  14. 14Regurgitation is the condition that the _______________________________Heart valve will not close fully (it leaks when it should close)
  15. 15What are the complications that may results from mitral (bicuspid) valve stenosis?Palpations
    Chest pain
    Weakness
    Fatigue
    AF
  16. 16The heart murmour occurs after S2, is a typical characteristic of _____________________aortic regurgitation
  17. 17This condition in the heart valve is commonly caused by ________________Rheumatic feverThis condition in the heart valve is commonly caused by ________________
  18. 18Aortic valve stenosis can lead to a decrease in systolic pressures, and in the long-term angina, syncope, dyspnoea: true or false?True!
  19. 19Aortic valve regurgitation can lead to: a. Systemic oedema b. Pulmonary oedema c. Angina d. Atrial fibrillationb. Pulmonary oedema
  20. 20An "artificial pacemaker" is commonly used in patients with tachycardia or bradycardia?Bradycardia
  21. 21This is a __________ blockSino-AtrialThis is a __________ block
  22. 22This is an ____________ blockAtrioventricular blockThis is an ____________ block
  23. 23Atherosclerosis is a progressive disease characterised by __________ of arteries caused by formation of ______ that hardens with time, leading to narrowing of the blood vessel producing a _______ in blood flownarrowing
    plaque
    decrease
  24. 24In the atherosclerotic necrotic core, the accumulation of cholesterol crystals in the macrophages form the _____ cellsFoam cells
  25. 25Angina is chest pain due to ___________ due to _____________________ishaemia due to cells deprived of O2/lack of O2 in heart tissues
  26. 26Heart attack is when __________ myocardial damage leads to _________irreversible myocardial damage leads to cell death (necrosis)
  27. 27Conduction defects are problems in _____ that carry _____________ to the heartfibres that carry electrical signals to the heart
  28. 28Heart failure is the _______________________________________inability of the heart to supply sufficient blood flow to meet the needs of the body
  29. 29What are factors that can lead to ischaemic injury?Atherosclerosis
    Vasospasm
    Thrombosis
    Cold
  30. 30Stable plaques can easily rupture or burst, leading to blood clotting inside the artery: true or false?False
  31. 31Stable plaques partially block vessels: true or false?True!
  32. 32Stable angina is due to _______an increased demand of oxygen
  33. 33Unstable angina can occur at _____ with sudden onset of painrest
  34. 34Silent myocardial ischaemia is a type of myocardial ischaemia ________without pain
  35. 35Variant/Prinzmetal angina is due to ______________________vasospasm rather than directly by atherosclerosis
    (cause of spasm is unknown)
  36. 36Ischaemia is a restriction on blood supply to tissues, causing a shortage of ______ and ______ needed for cellular metabolismoxygen and glucose
  37. 37Infarction is ________ due to _____________________cell death due to long starvation of oxygen
  38. 38What's the typical pain pattern in a patient with MI? What's the typical ECG shape for such a patient?Dull chest pain, radiating up neck and left arm
    S-T elevation
  39. 39What tests would provide biochemical evidence of myocardial necrosis?Troponin
    Creatinine kinase myocardial band (CK-MB)
  40. 40Dilated cardioMYOPATHY is a condition in which the heart becomes _________________ without any obvious cause and hence cannot ___________________weakened and enlarged
    pump blood efficiently
  41. 41What are the possible causes (CVS disorders) of dilated cardiomyopathies?Coronary heart disease
    Heart attack
    Hypertension
  42. 42Hypertrophic cardiomyopathy is a __________________genetic disorder that involves excessive ventricular growth or hypertrophy
  43. 43RESTRICTIVE cardiomyopathy is due to abnormally _____ walls and ventricles lack the ________________ as they fill with bloodrigid
    flexibility to expand
  44. 44Heart failure denotes ______________________________the failure of the heart to pump enough blood to meet the metabolic needs of the body
  45. 45Heart failure is classified into 4 classes bases on level of patient activity: What is Class I heart failure?Patient with heart disease but with no limitations in physical activity
  46. 46Heart failure is classified into 4 classes bases on level of patient activity: What is Class II?Patient with heart disease but with slight limitations in physical activity.
    Ordinary physical activity results in fatigue, dyspnea, palpitations or angina
  47. 47Heart failure is classified into 4 classes bases on level of patient activity: What is Class III?Marked limitations of physical activity.
    At rest is fine
    Less than ordinary physical activity results in fatigue, dyspnea, palpitations or angina
  48. 48Heart failure is classified into 4 classes bases on level of patient activity: What is Class IV?Inability to carry on physical activity without discomfort.
    Angina may be present at rest.
    On physical activity discomfort increases.
  49. 49In patients with Class I Heart failure, the physical activities are limited: True or false?False
  50. 50Usually the LEFT heart failure can cause pulmonary oedema: true or false?TRUE
  51. 51Usually the RIGHT heart failure can cause systemic oedema: True or false?TRUE!
  52. 52Productive cough with pink frothy sputum is usually observed in patients with left or right heart failureLEFT
  53. 53Low output heart failure is caused by disorders that impair pumping ability of the heart and characterised by _______ skincold, clammy and sometimes cyanotic
  54. 54High output failure is __________, with function of the heart supernormal but _______________________________uncommon
    inadequate owing to excessive metabolic needs
  55. 55Urine output is normally _________ due to low cardiac output in patients with HF. This is normally due to ___________ ADH release from the posterior pituitarydecreased
    increased
  56. 56Right heart failure usually occurs as a result of left heart failure: true or false?True!
  57. 57Left heart failure is:the inability of heart to pump oxygenated blood into arterial circulation leading to decrease in peripheral blood flow and accumulation of blood in pulmonary circulation
    leads to pulmonary oedema
  58. 58Right side heart failure is:the inability of heart to pump blood through the pulmonary circulation with enlargement of the systemic and hepatic venous systems
    leads to systemic oedema
  59. 593 manifestations of left heart failure:Pulmonary fluid overload
    Cyanosis
    Activity intolerance
  60. 604 manifestations of right heart failure:Fatigue
    ^ peripheral venous pressure
    Peripheral oedema
    Enlarged liver
  61. 61What are the mechanisms of organic nitrates?Causes vasodilation of veins and arteries
    Reduces cardiac O2 consumption secondary to reduced cardiac preload (venous) and afterload (arteriole)
    Reduces coronary artery spasm
    Redistribution of coronary blood flow towards ischaemic areas via COLLATERALS
  62. 62What are common side effects of organic nitrates?TOLERANCE
    Postural hypotension
    Headache
    Methaemoglobinaemia (rare)
  63. 63Aspirin inhibits _____ irreversibly and blocks conversion of ____________ to ______________COX-1
    arachidonic acid (AA) to thromboxane A2
  64. 64Clopidogrel blocks ____________ thus preventing ________________ and conformational change in __________________ADP receptors on platelets
    platelet activation
    GpIIb/IIa receptors
  65. 65Tirofiban blocks receptor for _____________ which forms bridges between plateletsfibrinogen
  66. 66Heparin inhibits _____________ to prevent activation of ________IIa (thrombin), IXa, Xa, XIa, XIIa and Xa
    thrombin
  67. 67Fibrinolytic drugs (e.g. Streptokinase) converts __________ to _______ which breaks fibrin threads, which is associated with the risk of bleedingplasminogen to PLASMIN
  68. 68___________ are the first-line therapy option for patients with stable angina. If it is ineffective, it can be combined with __________ or ___________Organic nitrates
    beta-adrenoceptor blockers or Ca2+ channel blockers
  69. 69Please describe the mechanisms of the treatment options for patients with acute coronary syndromes (MI)Oxygen: restores O2 levels
    Reduce O2 demands: nitrates
    Opioids: decrease sympathetic drive
    Anti-platelets, antithrombin & thrombyltics: prevention of thrombus formation
    Beta-blockers or ACE inhibitors: reduce cardiac and metabolic needs
  70. 70Percutaneous coronary intervention is performed within _________ upon patient presentation90 minutes
  71. 71Which is the most commonly prescribed 'first line' therapy in younger (under 55y/o) patients with hypertension?ACE inhibitors
  72. 72A stepped approach, in which new medication is added to current therapy until the target blood pressure is achieved, has the advantage of ____________minimising adverse effects while increasing patient compliance
  73. 73Describe the RAAS pathwayRenin (Kidneys) -> causes Angiotensinogen (released by liver) to convert to Angiotensin I -> which is converted to Angiotensin II by ACE (released by lungs) which increases: Sympathetic activity, Aldosterone secretion --> increased tubular Na, Cl reabsorption and K excretion, H2O retention, vasoconstriction
  74. 74Which one of the following effect CANNOT be attributed to angiotensin II? a. vasodilation b. salt retension c. stimulation of aldosterone release from the adrenal glands d. hypertrophy e. hyerplasiaa. vasodilation
    would actually cause vasoconstriction
  75. 75Release of renin from the granular cells in the kidney in response to a fall in blood pressure results in?the conversion of angiotensinogen to angiotensin I
  76. 76What is the safest hypertensive drug to use in pregnancy?Methyldopa - centrally acting agent
  77. 77What are the adverse effects of Calcium Channel Blockers?Flushing ad ankle oedema (due to vasodilation)
    Constipation (due to effects on GIT nerves and smooth muscle)
  78. 78ACE is present in the lungs: true or falseTRUE
  79. 79ACE is inhibited by captopril: true or false?TRUE
  80. 80ACE is inhibited by losartan: true or falseFALSE
  81. 81ACE converts angiotensin I to angiotensin II: true or false?TRUE
  82. 82ACE degrades bradykinin: true or false?TRUE
  83. 83What would be the recommended treatment for a patient with BP of 185/115, low CV risk (<10%) and no evidence of end organ damage?Start an antihypertensive immediately
  84. 84Can all the following induce/aggravate hypertension? pseudoephedrine, MOA's, excessive salt intake, nifedipine, cocaineYES
  85. 85An elderly pt (70y/o) was given a thiazide diuretic for the treatment of hypertension. After 6 weeks, the doctor decided a second drug was required to reduce her BP to a target level. Which drug would be the most likely to be used if there were no other complications?ACE Inhibitors
  86. 86Activation of the RAAS in heart failure can be reduced by which of the following drugs? a. ACE inhibitors b. angiotensin receptor blockers c. aspirin d. diuretics e. both A or Be. both A and B
  87. 87Digoxin inhibits the Na/K ATPase pump: true or falseTRUE
  88. 88Digoxin increases the force of contraction of the heart: true or false?TRUE
  89. 89Digoxin is a cardiac glycoside: true or falseTRUE
  90. 90Digoxin increases intracellular calcium levelsTRUE
  91. 91Digoxin decreases cardiac output: true or false?FALSE
    It increases cardiac output
  92. 92Which class of drugs is used in the treatment of angina and promotes redistribution of coronary blood flow towards ischaemic areas via collaterals?Organic Nitrates
  93. 93What is stable angina?Stable angina is caused by stable plaques
    i. Thick fibrous caps
    ii. Partially block vessels
    iii. Do not tend to form clots or emboli
    iv. Myocardial ischemia occurs during periods of increased metabolic demand
    v. Pain when heart’s oxygen demand increased e.g. exercise
  94. 94What is unstable angina?Caused by unstable plaques
    i. Thin fibrous caps
    ii. Plaque can rupture and cause a clot to form
    iii. May completely block artery
    iv. Clot may break free and become an embolus
    v. Myocardial Ischemia ranging between stable angina to myocardial infarction
    vi. Can occur at rest with sudden onset of pain
  95. 95What is the Coronary Steal phenomenon?Blood is "stolen" from one region of the coronary tree by another and may aggravate ischaemia
  96. 96Which drug produces the coronary steal phenomenon and thus can aggravate ischaemia?Dipyidamole
  97. 97Why are anti platelets important?Anti platelet drugs prevent the formation of platelets at a variety steps in the coagulation process. Platelets adhere to diseased/damage areas of the vessel, therefore by preventing the formation, there is less chance of a clot forming
  98. 98Which clotting factors are inhibited by unfractionated heparin?Inhibits IIa (thrombin), IXa, Xa, XIa and XIIa
  99. 99Which clotting factors are inhibited by low-molecular weight heparin?Inhibits Xa
  100. 100What clotting factors are inhibited by Warfarin?Inhibits II (prothrombin), VII, IX, X
  101. 101Which vitamin cofactor is required by clotting factors?Vitamin K cofactor
  102. 102What is the advantage of rTPA over streptokinase?rTPA is not antigenic, therefore can be given to pt's who have antibodies to streptokinase
  103. 103Differentiate antiplatelets, anticoagulants and fibrinolytic'sAntiplatelets: stop platelet formation
    Anticoagulants: prevent new thrombin
    Fibronolytics: dissolve existing thrombin
  104. 104What are the goals in the treatment of stable angina?Relieve or prevent pain
    Slow progression of atherosclerosis
    Improve prognosis - decrease the risk of MI or death
  105. 105What are the aims of treating acute coronary syndrome?Preventing irreversible ischaemic damage
    restore O2
    Decrease O2 demand and increase delivery
    Pain management
    Prevent thrombus formation
    Reduction in cardiac work and metabolic needs of the heart
  106. 106What are the available reperfussion strategies?Preferred:
    Percutaneous coronary intervention (PCI, angioplasty with or without stunting) - within 90mins of pt presentation
    Fibrinolysis - when there are major delays to PCI
  107. 107Tolerance develops with long-acting nitrates: true or false?True
  108. 108Organic nitrates increase cyclic AMP: true or false?True!
  109. 109The anti platelet effect of aspirin is reversible: true or false?True!
  110. 110Heparin requires antithrombin III to inhibit clotting factors: true or false?True!
  111. 111Anti platelets prevent platelet adhesion, activation and aggregation: true or false?True!
  112. 112Warfarin blocks the extrinsic pathway of coagulation: true or false?False, it blocks both
  113. 113Warfarin had an early onset of action and therefore does not require an overlap with IV heparin: true or false?False - slow onset of action but long duration
  114. 114Fibrinolytic drugs inhibit conversion of plasminogen to plasmin: true or false?False:
    It converts plasminogen to PLASMIN which breaks fibrin threads
  115. 115Organic Nitrates: Example Action Side EffectsGlyceryl trinitrate (GTN), Isosorbide dinitrate, Isosorbide mononitrate
    Action: vasodilation - redistribution of coronary bloodd flow towards ischaemic areas via collaterals
    Side effects: tolerance, postural hypotension, headache, methaemoglobinaemia (rare)
  116. 116Calcium channel blockers Diltiazem, verapamil Action Side effectsAction: block :-type voltage-gated calcium channels
    Side effects: flushing, headache and ankle oedema due to vasodilation
  117. 117Beta-adrenoceptor antagonists (bete-blockers) atenolol, metoprolol Action Side effectAction: unknown but increased HR, contractility and renin release
    Side effects: cold hands and feet, tiredness and muscle fatigue, mask sympathetic response to hypoglycaemia, bad dreams
  118. 118ACE inhibitors "pril's" Action Side effectsAction: competitively inhibits the actions of angiotensin converting enzyme (ACE) in the RAAS system
    Side effects: dry cough, accumulation of bradykinin, first dose hypotension, fast disturbance (metallic), angioneurmtic oedema, neutropaenia
  119. 119Antiplatelet drugs: Aspirin Action Side EffectsAction: Inhibits COX-1 irreversibly to prevent conversion of arachidonic acid (AA) to thromboxane A2
    Side effects:
  120. 120Anti platelet drugs: Clopidogrel Action:Irreversibly blocks ADP receptors on platelets, thus preventing platelet activation and conformational change in GpIIb/IIIa receptors
  121. 121Antiplatelet drugs: Tirofiban ActionsAction: blocks receptor for fibrinogen which forms bridges between platelets
  122. 122Antithrombin drugs: Unfractionated heparinAction: relies on antithimbin III to inhibit IIa (thrombin), IXa, Xa, XIa, XIIa
    Side effects: haemorrhage, thrombosis, osteoporosis, hyoldosteronism, hyperkalaemia, hypersensitivity
  123. 123Antithrombin drugs: Low-molecular weight heparins e.g. enoxaparin (Clexane) ActionAction: requires antithrombin III, inhibits Xa longer half-life, longer acting
    Side effects: haemorrhage, thrombosis, osteoporosis, hyoldosteronism, hyperkalaemia, hypersensitivity
  124. 124Antithrombin drugs: Warfarin ActionAction: inhibits II (prothrombin), Vii, IX, X, vitamin K dependent, slow onset, long lasting
  125. 125Fibrinolytic drugs (thrombolytics) Streptokinase Dissolve existing thrombiAction: converts plasminogen to plasmin with breaks fibrin threads, this action can be blocked by antibodies that develop > 4 days after initial dose, can't be given repeatedly
    Side effect: allergic reaction if pt has antibodies, risk of bleeding
  126. 126Fibrinolytic drugs (thrombolytics) Recombinan tissue plasminogen activators (tPAs) (all plane's e.g. altePLASE)Action: activated thrombus-bound plasminogen preferentially
    Non antigenic: can be given to pt's with abs to streptokinase
    Side effects: risk of bleeding

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Pathophysiology and Pharmacology 1 2015 Karteikarten am Question Bank 2: Cardiovascular system, erstellt von b.graham am 07/06/2015.
Erstellt von
b.graham
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