Question Bank 2: Cardiovascular system

b.graham
Flashcards by b.graham, updated more than 1 year ago
b.graham
Created by b.graham about 6 years ago
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Pathophysiology and Pharmacology 1 2015 Flashcards on Question Bank 2: Cardiovascular system, created by b.graham on 07/06/2015.

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Question Answer
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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