2900958
| Pregunta | Respuesta |
| Primary hypertension is the most common type of hypertensive patients: true or false? | TRUE |
| You can also find an underlying disease for secondary hypertension: true or false? | True! |
| Secondary hypertension can be reversed by ________________________ | treatment of the underlying cause |
| malignant hypertension is manifested intense spasm of arteries: true or false? | true! |
| What 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 |
| The clinical manifestations normally appear quite early in patients with hypertension: true or false? | False |
| Low stroke volume can be caused by what types of shock? | Hypovolemic Cardiogenic Obstructive |
| Shock due to vasodilation can be seen in conditions such as __________________________________ | septic shock anaphylactic shock and neurogenic shock |
| What are the clinical manifestations of non-progressive shock? | SNS reflexes - hormonal and renal responses compensate |
| In patients with progressive shock, blood pressure can be maintained: true or false | False |
| In patients with irreversible shock, tachycardia may lead to cardiac arrest: true or false | True! |
| Urine output is normally reduced in patients with shock: true or false? | True! |
| Stenosis is the condition where the ________________________ | heart valve with not open fully (it is harder to force blood through) |
| Regurgitation is the condition that the _______________________________ | Heart valve will not close fully (it leaks when it should close) |
| What are the complications that may results from mitral (bicuspid) valve stenosis? | Palpations Chest pain Weakness Fatigue AF |
| The heart murmour occurs after S2, is a typical characteristic of _____________________ | aortic regurgitation |
| This condition in the heart valve is commonly caused by ________________ | Rheumatic fever |
| Aortic valve stenosis can lead to a decrease in systolic pressures, and in the long-term angina, syncope, dyspnoea: true or false? | True! |
| Aortic valve regurgitation can lead to: a. Systemic oedema b. Pulmonary oedema c. Angina d. Atrial fibrillation | b. Pulmonary oedema |
| An "artificial pacemaker" is commonly used in patients with tachycardia or bradycardia? | Bradycardia |
| This is a __________ block | Sino-Atrial |
| This is an ____________ block | Atrioventricular block |
| Atherosclerosis 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 flow | narrowing plaque decrease |
| In the atherosclerotic necrotic core, the accumulation of cholesterol crystals in the macrophages form the _____ cells | Foam cells |
| Angina is chest pain due to ___________ due to _____________________ | ishaemia due to cells deprived of O2/lack of O2 in heart tissues |
| Heart attack is when __________ myocardial damage leads to _________ | irreversible myocardial damage leads to cell death (necrosis) |
| Conduction defects are problems in _____ that carry _____________ to the heart | fibres that carry electrical signals to the heart |
| Heart failure is the _______________________________________ | inability of the heart to supply sufficient blood flow to meet the needs of the body |
| What are factors that can lead to ischaemic injury? | Atherosclerosis Vasospasm Thrombosis Cold |
| Stable plaques can easily rupture or burst, leading to blood clotting inside the artery: true or false? | False |
| Stable plaques partially block vessels: true or false? | True! |
| Stable angina is due to _______ | an increased demand of oxygen |
| Unstable angina can occur at _____ with sudden onset of pain | rest |
| Silent myocardial ischaemia is a type of myocardial ischaemia ________ | without pain |
| Variant/Prinzmetal angina is due to ______________________ | vasospasm rather than directly by atherosclerosis (cause of spasm is unknown) |
| Ischaemia is a restriction on blood supply to tissues, causing a shortage of ______ and ______ needed for cellular metabolism | oxygen and glucose |
| Infarction is ________ due to _____________________ | cell death due to long starvation of oxygen |
| What'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 |
| What tests would provide biochemical evidence of myocardial necrosis? | Troponin Creatinine kinase myocardial band (CK-MB) |
| Dilated cardioMYOPATHY is a condition in which the heart becomes _________________ without any obvious cause and hence cannot ___________________ | weakened and enlarged pump blood efficiently |
| What are the possible causes (CVS disorders) of dilated cardiomyopathies? | Coronary heart disease Heart attack Hypertension |
| Hypertrophic cardiomyopathy is a __________________ | genetic disorder that involves excessive ventricular growth or hypertrophy |
| RESTRICTIVE cardiomyopathy is due to abnormally _____ walls and ventricles lack the ________________ as they fill with blood | rigid flexibility to expand |
| Heart failure denotes ______________________________ | the failure of the heart to pump enough blood to meet the metabolic needs of the body |
| Heart 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 |
| Heart 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 |
| Heart 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 |
| Heart 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. |
| In patients with Class I Heart failure, the physical activities are limited: True or false? | False |
| Usually the LEFT heart failure can cause pulmonary oedema: true or false? | TRUE |
| Usually the RIGHT heart failure can cause systemic oedema: True or false? | TRUE! |
| Productive cough with pink frothy sputum is usually observed in patients with left or right heart failure | LEFT |
| Low output heart failure is caused by disorders that impair pumping ability of the heart and characterised by _______ skin | cold, clammy and sometimes cyanotic |
| High output failure is __________, with function of the heart supernormal but _______________________________ | uncommon inadequate owing to excessive metabolic needs |
| Urine output is normally _________ due to low cardiac output in patients with HF. This is normally due to ___________ ADH release from the posterior pituitary | decreased increased |
| Right heart failure usually occurs as a result of left heart failure: true or false? | True! |
| Left 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 |
| Right 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 |
| 3 manifestations of left heart failure: | Pulmonary fluid overload Cyanosis Activity intolerance |
| 4 manifestations of right heart failure: | Fatigue ^ peripheral venous pressure Peripheral oedema Enlarged liver |
| What 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 |
| What are common side effects of organic nitrates? | TOLERANCE Postural hypotension Headache Methaemoglobinaemia (rare) |
| Aspirin inhibits _____ irreversibly and blocks conversion of ____________ to ______________ | COX-1 arachidonic acid (AA) to thromboxane A2 |
| Clopidogrel blocks ____________ thus preventing ________________ and conformational change in __________________ | ADP receptors on platelets platelet activation GpIIb/IIa receptors |
| Tirofiban blocks receptor for _____________ which forms bridges between platelets | fibrinogen |
| Heparin inhibits _____________ to prevent activation of ________ | IIa (thrombin), IXa, Xa, XIa, XIIa and Xa thrombin |
| Fibrinolytic drugs (e.g. Streptokinase) converts __________ to _______ which breaks fibrin threads, which is associated with the risk of bleeding | plasminogen to PLASMIN |
| ___________ 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 |
| Please 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 |
| Percutaneous coronary intervention is performed within _________ upon patient presentation | 90 minutes |
| Which is the most commonly prescribed 'first line' therapy in younger (under 55y/o) patients with hypertension? | ACE inhibitors |
| A 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 |
| Describe the RAAS pathway | Renin (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 |
| Which 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. hyerplasia | a. vasodilation would actually cause vasoconstriction |
| Release 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 |
| What is the safest hypertensive drug to use in pregnancy? | Methyldopa - centrally acting agent |
| What 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) |
| ACE is present in the lungs: true or false | TRUE |
| ACE is inhibited by captopril: true or false? | TRUE |
| ACE is inhibited by losartan: true or false | FALSE |
| ACE converts angiotensin I to angiotensin II: true or false? | TRUE |
| ACE degrades bradykinin: true or false? | TRUE |
| What 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 |
| Can all the following induce/aggravate hypertension? pseudoephedrine, MOA's, excessive salt intake, nifedipine, cocaine | YES |
| An 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 |
| Activation 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 B | e. both A and B |
| Digoxin inhibits the Na/K ATPase pump: true or false | TRUE |
| Digoxin increases the force of contraction of the heart: true or false? | TRUE |
| Digoxin is a cardiac glycoside: true or false | TRUE |
| Digoxin increases intracellular calcium levels | TRUE |
| Digoxin decreases cardiac output: true or false? | FALSE It increases cardiac output |
| Which class of drugs is used in the treatment of angina and promotes redistribution of coronary blood flow towards ischaemic areas via collaterals? | Organic Nitrates |
| What 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 |
| What 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 |
| What is the Coronary Steal phenomenon? | Blood is "stolen" from one region of the coronary tree by another and may aggravate ischaemia |
| Which drug produces the coronary steal phenomenon and thus can aggravate ischaemia? | Dipyidamole |
| Why 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 |
| Which clotting factors are inhibited by unfractionated heparin? | Inhibits IIa (thrombin), IXa, Xa, XIa and XIIa |
| Which clotting factors are inhibited by low-molecular weight heparin? | Inhibits Xa |
| What clotting factors are inhibited by Warfarin? | Inhibits II (prothrombin), VII, IX, X |
| Which vitamin cofactor is required by clotting factors? | Vitamin K cofactor |
| What is the advantage of rTPA over streptokinase? | rTPA is not antigenic, therefore can be given to pt's who have antibodies to streptokinase |
| Differentiate antiplatelets, anticoagulants and fibrinolytic's | Antiplatelets: stop platelet formation Anticoagulants: prevent new thrombin Fibronolytics: dissolve existing thrombin |
| What 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 |
| What 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 |
| What 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 |
| Tolerance develops with long-acting nitrates: true or false? | True |
| Organic nitrates increase cyclic AMP: true or false? | True! |
| The anti platelet effect of aspirin is reversible: true or false? | True! |
| Heparin requires antithrombin III to inhibit clotting factors: true or false? | True! |
| Anti platelets prevent platelet adhesion, activation and aggregation: true or false? | True! |
| Warfarin blocks the extrinsic pathway of coagulation: true or false? | False, it blocks both |
| Warfarin 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 |
| Fibrinolytic drugs inhibit conversion of plasminogen to plasmin: true or false? | False: It converts plasminogen to PLASMIN which breaks fibrin threads |
| Organic Nitrates: Example Action Side Effects | Glyceryl 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) |
| Calcium channel blockers Diltiazem, verapamil Action Side effects | Action: block :-type voltage-gated calcium channels Side effects: flushing, headache and ankle oedema due to vasodilation |
| Beta-adrenoceptor antagonists (bete-blockers) atenolol, metoprolol Action Side effect | Action: 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 |
| ACE inhibitors "pril's" Action Side effects | Action: 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 |
| Antiplatelet drugs: Aspirin Action Side Effects | Action: Inhibits COX-1 irreversibly to prevent conversion of arachidonic acid (AA) to thromboxane A2 Side effects: |
| Anti platelet drugs: Clopidogrel Action: | Irreversibly blocks ADP receptors on platelets, thus preventing platelet activation and conformational change in GpIIb/IIIa receptors |
| Antiplatelet drugs: Tirofiban Actions | Action: blocks receptor for fibrinogen which forms bridges between platelets |
| Antithrombin drugs: Unfractionated heparin | Action: relies on antithimbin III to inhibit IIa (thrombin), IXa, Xa, XIa, XIIa Side effects: haemorrhage, thrombosis, osteoporosis, hyoldosteronism, hyperkalaemia, hypersensitivity |
| Antithrombin drugs: Low-molecular weight heparins e.g. enoxaparin (Clexane) Action | Action: requires antithrombin III, inhibits Xa longer half-life, longer acting Side effects: haemorrhage, thrombosis, osteoporosis, hyoldosteronism, hyperkalaemia, hypersensitivity |
| Antithrombin drugs: Warfarin Action | Action: inhibits II (prothrombin), Vii, IX, X, vitamin K dependent, slow onset, long lasting |
| Fibrinolytic drugs (thrombolytics) Streptokinase Dissolve existing thrombi | Action: 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 |
| Fibrinolytic 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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