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145 Cards in this Set
- Front
- Back
What is the most common cause of infective endocarditis?
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Strep viridans
IVDU - Staph aureus NB: Strep bovis associated with colorectal cancer |
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Which bacteria is commonly involved in IE associated with prosthetic valves
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staph epidermidis
|
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Which rises first following a MI
Troponin or CK-MB? |
CK-MB rises after 2-6 hours
Troponin rises after 4-6 hours NB: myoglobin rises first 1-2 hours |
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Which takes the longest to go down troponin or CK-MB
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troponin takes 7-10 days
CK-MB takes 2-3 days |
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Which disease causes
shortened PR interval, wide QRS with a slurred upstroke seen in lead II? |
Wolf Parkinson White syndrome
|
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Management of Wolf Parkinson White syndrome
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radiofrequency ablation of accessory pathway
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Which coronary artery supplies the inferior area of the heart? Which leads will it be in?
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right, leads II, III, aVF
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Which coronary artery supplies the anteroseptal area of the heart? Which leads will the problem be in?
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left anterior descending, V1-4
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Which coronary artery supplies the lateral side of the heart? Which leads will the problem be in?
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I, aVL +/- V5-6
Left circumflex |
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Which coronary artery supplies the posterior side of the heart? Which leads will the problem be in?
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all R waves V1-2
Usually left circumflex, also right coronary |
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Which coronary artery supplies the anteriolateral side of the heart? Which leads will the problem be in?
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V4-6, I, aVL
Left anterior descending or left circumflex |
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First line therapy for uncomplicated hypertension
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ACEi
|
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Pharmacological treatment of hypertension in diabetics
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ACEi
thiazides may increase glucose intolerance |
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What does a long QT interval predispose someone to?
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ventricular tachycardia specifically vulnerable to torsades de points
|
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Pathophysiology of long QT
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Prolonged ventricular repolarisation
Different parts of myocardium repolarising at different times Set up circuit tachycardia |
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What typically triggers torsades de points in someone with congenital long QT syndrome?
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stress, physical exertion, fright
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How do you manage congenital long QT syndrome
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Beta blockers - abolish symptoms in 80% of cases but will produce significant bradycardia which does increase the long QT interval - give pacing then
ICD Pacing Mexiletine |
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What are the most common causes of acquired long QT syndrome?
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hypocalcaemia
Hypomagnesemia Hypokalaemia Drugs - sotalol, amiodarone, procainamide, lithium, TCAs, Quinines |
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What is brugada syndrome?
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Rare syndrome characterised by sudden death due to VF in anb otherwise structurally normal heart
Associated with mutations in the sodium channel gene |
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How long is a normal QT interval?
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2 large squares
460ms |
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What ECG changes do you see with hyperkalaemia?
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peaked T waves
P waves eventually flatten short QT interval |
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What ECG changes do you see with hypokalaemia
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Prolonged QT interval
Low T waves Prominent U waves |
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In what condition do you see osborne J waves on the ECG?
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= hump like waves at the junction of the j point and the ST segment
Seen in hypothermia |
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What ECG changes do you see in pericarditis?
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Diffuse ST segment elevation +/- PR depression
upright T waves |
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What is the definition of low voltage ECG?
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Total QRS height in precordial leads < 10mm and limb leads < 5mm
NB: each large square = 5mm |
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What can give you a low voltage ECG?
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Myocardial disease
Pericardial effusion Thick chest wall/barrel chest Generalised oedema |
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What ECG changes do you see with digitalis?
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ST downsloping or scooping "reversed tick"
T wave depression or inversion QT shortening +/- U waves |
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What is the characteristic sign of PE on ECG?
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Often will only show tachycardia BUT:
S wave in lead I Q wave and inverted T wave in lead III Can also show RVH |
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How do you define pathological ST elevation
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At least 1mm in 2 adjacent limb leads
OR at least 1-2mm in adjacent precordial leads |
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When is a q wave pathological?
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if QRS > 1 small square
OR > 25% height of R |
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What happens in Type I and Type II second degree heart block?
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Type I = wenckebach's
Gradual prolongation of the PR interval precedes the failure of conduction of a p wave Type II PR interval is constant, then there is an abrupt failure of conduction of a p wave |
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What are the causes of wide QRS?
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SVT with aberrancy/BBB
VT |
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What is wolff parkinson white syndrome?
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Congenital defect resulting in an acessory conduction tract (bundle of kent) that allows electrical communication between the atria and the ventricles
|
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What ECG findings do you see in WPW?
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Shortened PR interval < 120 msec (AV node is bypassed)
Delta wave (slurred upstroke of the QRS) Widening of the QRS complex |
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What arrhythmias are associated with WPW?
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AF
AV re-entrant tachycardia |
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What is AVRT
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AV re-entrant tachycardia
Seen in WPW Re-entrant loop via accessory pathway and normal conduction system usually iniaited by a premature atrial or ventricular complex |
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How do you manage AVRT?
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Avoid AV nodal blockers e.g., digitalis and verapamil
For recurrent - ablation of bypass tract is recommended |
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What is the pathophysiology behind an AV nodal re-entrant tachycardia?
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Fast and slow pathways to AV node
Usually AV node is primarily depolarised by fast pathway making it refractory to impulse from slow pathway BUT a critically timed ectopic can reach AV node when fast pathway is refractory and so jump to slow pathway but by time impulse has travelled along slow pathway fast pathway is not available again and so conducts this beat back to the atrium. If this reaches atrial insertion of slow pathway can lead to re-entrant circuit between slow and fast pathways - an AV nodal re-entrant tachycardia |
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Features of AVNRT on ECG?
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Tachycardia
Narrow QRS complex |
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What is the first choice of pharmacological management of AVNRT?
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adenosine
|
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What is the most common bacterial cause of infective endocarditis?
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Strep viridans
NB: staph epidermidis for prosthetic valves < 2months after surgery |
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What is the MOA of clopidegrel?
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Blocks platelet ADP receptors
NB: platelets release ADP and thromboxane A2 which stimulate aggregation |
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What is the MOA of enoxaparin?
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Activated antithrombin III
Inhibition of coagulation facotrs Xa |
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What is the MOA of tirofiban, abciximab?
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Blocks fibrinogen to Gp IIb/IIIa
Therefore prevents aggregation Monoclonal antibody |
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Features of stable angina
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pain lasts 5-15 minutes
exacerbated by stress/exercise ECG MAY show ST change and flat or inverted T waves OR can be normal |
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Features of unstable angina
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ECG has ST changes and inverted or flat T waves
pain at rest accelerating new onset angina angina post MI or post procedure |
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Diagnostic triad of pericarditis
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chest pain, friction rub, diffuse elevated ST ECG changes
ST change is concave upwards |
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Commonest cause of acute pericarditis
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idiopathic, usually presumed to be viral
Coxsackie virus B is most common |
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Signs and symptoms of pericarditis
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triad of chest pain, friction rub, ECG changes
pleuritic chest pain - alleviated by sitting up and leaning forward +/- fever and malaise |
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What has been shown to improve prognosis in heart failure?
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ACEi and spironolactone
|
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Which drugs have been shown to improve mortality in patients with chronic heart failure?
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* ACE inhibitors
* spironolactone * beta-blockers * hydralazine with nitrates |
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What are the ECG changes in hypokalemia?
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flattened T waves
U waves prolonged PR interval ST depression long QT |
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In Hypokalaemia...
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U have no Pot and no T, but a long PR and a long QT!
|
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What waves are seen in hypothermia?
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J waves
|
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What is the classical triad in cardiac tamponade?
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muffled heart sounds
increased JVP hypotension |
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Management of pericarditis
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1. treat underlying cause
2. pain relief - NSAIDs |
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What is the MOA of adenosine?
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works via adenosine A1 receptor
causes transient heart block in AV node |
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When is adenosine CI?
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asthma, use verapamil
|
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How do you treat SVT?
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1. vagal manoeuvres, Valsalva
2. IV adenosine 3. electrical cardioversion |
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How do you control rate in AF?
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beta blockers preferable to digoxin
|
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Does sotalol control rate or rhythm?
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both!
it's a beta blocker AND class III anti arrhythmic (K channel inhibitor) in the same class as amiodarone |
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When is digoxin indicated in AF?
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AF with coexistent heart failure
|
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What is a normal ejection fraction?
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55 - 70%
|
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What is MOA of aspirin?
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inhibit production of thromboxane A2
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What is mechanism of action of clopidogrel?
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inhibits ADP binding to its platelet receptors
|
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MOA of GP IIb/IIIa inhibitors
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blocks GP IIb/IIIa receptors --> fibrinogen and vWF binding --> decreased platelet aggregation
|
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What is Marfan's syndrome?
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AD mutation of fibrolin 1 gene
aortic root dilatation long limbs dislocation of lenses high arched palate |
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When is verapamil CI?
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in VT
may ppt VF in pts with VTW |
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What is BNP?
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hormone produced mainly by the left ventricular myocardium in response to strain
high levels are associated with a poor prognosis in HF |
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What anti-anginal drug do patients develop tolerance to?
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nitrates
|
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Nitrates are used to control anginal attacks. What is first line as prevention/treatment?
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Beta blocker or CCB
|
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Which drugs should not be described with beta blockers?
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Verapamail
Risk of 3rd degree heart block |
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Which statin is stronger simvastatin or atorvastatin?
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simvastatin
|
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When do you go on a statin when you have diabetes?
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>40 with type 2 diabetes, should be started on a statin if they have risk factors or CV disease
|
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Is diltiazem a positive or negative inotrope?
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negative inotrope
|
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What ECG finding is consistent with 3rd degree heartblock?
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p waves not related to QRS comlpex
regular bradycardia (30-60) |
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What ECG finding is consistent with 1st degree heartblock?
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prolonged PR interval (>5 small boxes)
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What ECG finding is consistent with 2nd degree heartblock?
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Type 1 (Weckenbach): progressive prolonged PR, then absent QRS and PR interval resets
Type 2: intermittent absence of QRS |
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Which cardiac drug should be given to pts with left ventricular impairment?
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ACEi
|
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What are the clinical features of patent ductus arteriosus?
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acyanotic heart defect, connection btwn pulmonary trunk and descending aorta
collapsing pulse machinery murmur left subclavicular thrill wide pulse pressure |
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How many blood cultures should you take from a patient suspected of endocarditis?
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3, not from the same site
|
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Most common pathogen for infective endocarditis
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strep viridans
IVDU: Staph aureus prosthetic valve: staph coagulase-neg |
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Duke criteria for endocarditis
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2 major, 1 major + 3 minor, 5 minor
major: 2 separate + blood cultures evidence on echo minor: fever >38.3 vascular phenomena: septic emboli and infarcts, mycotic aneurysm, janeway lesions immunologic phenomena: GN, osler's nodes, roth's spots 1 + blood culture |
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Empirical treatment of endocarditis
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benzylpenicillin PLUS flucoxacillin PLUS gentamicin
|
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Which other cardiac drug is contraindicated when taking bisoprolol?
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verapamil
causes heart block |
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What electrolyte imbalances cause ventricular tachycardia?
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hypocalcemia
hypokalemia hypomagnesia |
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What drug is firstline for stable angina?
|
beta blocker
is they have asthma or PVD, diltiazam |
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If a TOE is performed w someone in AF, and it shows a clot (or it isn't done at all), what should you do?
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1. anticoagulate with heparin followed by warfarin for 4 weeks
INR should be 2-3 |
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Pharm and later Mx of cardioversion in AF
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1. flecainide OR amiodarone
sotalol used, but no evidence 2. if no cardioversion, 100 joules of DC shock |
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MOA and Side effects of amiodarone
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K+ channel blocker - class III anti-arrhythmic
pulmonary fibrosis hypo/hyperthyroidism hepatotoxicity long QT |
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What is a bad side effect of a beta blocker (in diabetics)?
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may mask hypoglycemia
|
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Characteristic ECG finding in Wolf-Parkinson White Syndrome
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delta wave
|
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Mx of STEMI
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1. aspirin
2. clopidogrel 3. either PCI or fibrinolytic therapy **given if symptoms >20 minutes, symptoms have been happening w/in 12 hours, ST elevation on ECG, no CI to reperfusion |
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MOA of alteplase
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alteplase = tPA
catalyzes rxn btwn plasminogen and plasmin --> breaks down fibrin |
|
Absolute contraindications to fibrinolytic therapy
|
Risk of bleeding:
- active bleeding or bleeding diathesis (excluding menses) - significant closed head or facial trauma within 3 months - suspected aortic dissection (including new neurological symptoms) Risk of intracranial haemorrhage: - any prior intracranial haemorrhage ischaemic stroke within 3 months known structural cerebral vascular lesion (eg arteriovenous malformation) - known malignant intracranial neoplasm (primary or metastatic) |
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What is hyperhomocystinemia caused by and why is it important in cardio?
|
genetic defect, diet low in folate, B6, B12
ppl are more prone to endothelial injury --> more likely to clot |
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Rx of acute limb ischemia
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1. unfractionated heparin
2. if thrombolysis is appropriate, tPA 3. long term therapy = warfarin, at least 3-6 months |
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Management of critical limb ischemia aka ischemic ulcers, ischemic pain
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1. vascular reconstruction
2. regular analgesia, 3. cage and heel pad 4. elevation of head in bed 5. maintain high to normal BP |
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Side effects of GTN
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hypotension
tachycardia headaches |
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side effects of ACEi
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cough - 15% and may occur 1 year after
angioedema - may occur 1 year after hyperkalemia 1st dose hypotension- common if taking diuretics |
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Pts CI and cautioned for ACEi
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1. pregnancy and breastfeeding
2. renovascular disease - bilateral renal artery stenosis 3. aortic stenosis 4. high dose diuretics 5, hereditary idiopathic angioedema |
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MOA of atropine
|
competitive antagonist of muscarinic ACh receptors
increases firing of SA node and conduction thru AV node lowers parasympathetic activity |
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First line hypertensive medication
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CCB
|
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What is a gallop rhythm and why is it important?
|
S3
early and specific sign of LV failure caused by diastolic filling of ventricle and increased filling pressure normal if <30 yrs old also heard in constrictive pericarditis |
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MOA of digoxin
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cardiac glycoside: positive ionotrope and stimulates vagus nerve
inhibits Na/K/ATPase --> inhibits Na/Ca exchange --> increases Ca blocks AV node conduction and depresses SA node ionotrope AND rate control |
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SEs and CIs for digoxin
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SEs: increases PR, scooping ST, T wave inversion, blurred vision, N&V
CI: Wolf-Parkinson-White, hypokalemia (increased digoxin because it binds where K+ should be), 2nd or 3rd degree AV block |
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Uses for digoxin
|
CHF
not first line for AF |
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MOA of frusemide
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at thick ascending limb, inhibits NK2Cl co transporter --> diuresis
|
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SEs of loop diuretics
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hypocalcemia
hypokalemia meatbolic alkalosis |
|
MOA of thiazide
|
at distal tubule, inhibits NaCl co tranporter
|
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SEs of thiazide
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hypercalcemia
hypokalemia hypomagnesium metabolic alkalosis hyperlipidemia, hyperglycemia - dont give to diabetics hyperuricemia - dont give in gout |
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MOA of spironalactone and amiloride
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aldosterone antagonist --> less eNAC
amiloride blocks eNAC |
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SEs of spironolactone
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hyperkalemia
anti-androgen - gynecomastia |
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Allergy you need watch out with thiazide and loop diuretics
|
sulfa
|
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MOA of clopidogrel
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inhibits ADPr --> blocks gIIb/IIIa expression --> inhibits fibrinogen
|
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SE of clopidogrel
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TTP
|
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SE of aspirin
|
gastric bleeding
|
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MOA of warfarin
|
vitamin K antagonist also takes out protein C and S
increased PT |
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Caution for warfarin
|
teratogen
|
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MOA of heparin
|
catalyzes activation of antithrombin III, decreases thrombin and factor Xa
|
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How do you reverse heparin?
|
protamine sulfate
|
|
What is heparin induced thromboycytopenia?
|
heparin binds to platelets --> develop Ab to platelets, platelets that are not attacked by Ab become overactive and thrombotic
thrombocytopenic, hypercoaguable state |
|
Cautions in beta blockers
|
asthma, verapamil, bradycardia, 2nd or 3rd degree heartblock, WPW syndrome
don't give in decompensated CHF |
|
SEs of beta blockers
|
exacerbate reynauds, claudication
impotence |
|
When do you use adenosine for rhythm control?
|
SVT: re-entrant SVT, not atrial fib
|
|
Which beta blockers are only beta 1 and which ones are beta 1 + 2?
|
Beta 1 blockers: atenolol, bisoprolol, metoprolol
Beta 1 + 2 blockers: propanolol, labetolol, carvedilol |
|
Difference between non-DHP and DHP CCBs
|
non-DHP (verapamil and diltiazem): work more on heart mm, not as peripheral
DHP (nifedipine and amlodipine): work peripherally, used more for HTN |
|
SEs of verapamil and diltiazem
|
verapamil: hypotension, HF, constipation, bradycardia
diltiazem: same + peripheral edema, but not constipation |
|
arrhythmia that verapamil treats
|
SVT
|
|
SEs of DHP CCBs
|
flushing, ankle swelling, headache
|
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CI to DHP CCBs
|
severe aortic stenosis, liver failure
|
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CIs of ACEi
|
pregnancy, renal artery stenosis
|
|
SEs of ACEi
|
cough, hyperkalemia
reduced GFR by preventing constriction of efferent arterioles (aka vasodilating efferents) |
|
MOA of nitrates
|
NO relaxes smooth mm, reduces preload
dilates veins > arteries |
|
SEs of nitrates
|
reflex tachycardia, flushing, headache, tolerance
|
|
MOA of statin
|
HMG CoA reductase inhibitor
lowers LDL significantly, not as much effect on HDL or triglycerides |
|
SEs of statins
|
reversible increase in LFTs
myalgia rhabdomyolysis |
|
MOA of fibrates
|
upregulates LPL, activates PPARalpha --> increases Triglyceride clearance
significantly reduces triglycerides |
|
SEs of fibrates
|
dyspepsia, gallstones, myositis, increased LFTs
use with statin --> risk of rhabdomyolysis |
|
Which drugs causes long QT syndrome?
|
anti-histamines, anti-psychotics, anti-depressants, quinine, chloroquine
|
|
When do you do carotid endarterctomy?
|
asymptomatic: <70% medical mx, >70% surgery
symptomatic: <80% medical mx, >80% surgery |
|
Treatment of stroke without AF
|
aspirin, DO NOT give warfarin
if pt has second stroke on aspirin, then put pt on warfarin |
|
Medical mx for carotid stenosis
|
aspirin or clopidogrel (2nd line)
|
|
What do you NOT use in unstable angina?
|
tPA
|
|
Rx of unstable angina
|
1. heparin
2. send to cath lab |