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Phase 2a - Systems > Cardio 2 > Flashcards

Cardio 2 Flashcards

1
Q

list 3 viral causes of acute pericarditis

A 
Coxsackie B
Influenza
EBV
Mumps
Varicella
HIV
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2
Q

list 3 bacterial causes of acute pericarditis

A 
Pneumonia
Rheumatic fever
TB
Streps
Staphs
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3
Q

list 5 causes, other than bacterial/viral infection, of acute pericarditis

A

Fungi, MI, uraemia, rheumatoid arthritis, SLE, myxoedema, trauma, surgery, malignancy, radiotherapy, sarcoidosis, idiopathic + drugs

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4
Q

describe the pain seen in acute pericarditis

A

sharp, central chest pain - worse on inspiration or lying flat, relieved by leaning forward

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5
Q

what might be heard on auscultation of a patient with pericarditis?

A

pericardial friction rub

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6
Q

what investigation would you carry out to diagnose acute pericarditis? what would you see?

A

ECG - concave upwards (saddle-shaped) ST segment elevation in all leads

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7
Q

how would you treat acute pericarditis?

A

treat underlying cause.
NSAIDs for analgesia.
colchicine if relapsing.

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8
Q

what is constrictive pericarditis?

A

heart is encased in a rigid fibrotic pericardium - prevents diastolic filling of ventricles.

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9
Q

what causes constrictive pericarditis?

A

most common in UK = idiopathic.
globally = TB.
also occurs after any pericarditis.

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10
Q

what are the clinical features of constrictive pericarditis?

A

those of right-sided heart failure - raised JVP, oedema, hepatomegaly, ascites, pulsus paradoxus, diffuse apex beat

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11
Q

what two investigations would you carry out in constrictive pericarditis and what would you find?

A

CXR - normal/small heart + pericardial calcification.

CT/MRI - pericardial thickening/calcification

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12
Q

how would you treat constrictive pericarditis?

A

surgical excision of pericardium

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13
Q

what is the definition of hypertension?

A

> 140/90mmHg based on 2+ readings on separate occasions

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14
Q

what are the criteria for treating hypertension?

A

ALL with sustained >160/100mmHg.

those with sustained >140/90 that are at high risk of coronary events, have diabetes or end-organ damage

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15
Q

list 3 causes of secondary hypertension

A

renal disease - diabetic nephropathy, chronic glomerulonephritis, PKD, chronic tubulointerstitial nephritis.
endocrine disease - Conn’s, phaeochromocytoma, Cushing’s, acromegaly.
Coarctation of the aorta.
pregnancy.
steroids.
the Pill.

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16
Q

give 3 risk factors for hypertension

A

age, FHx, male gender, African or Caribbean origin, high salt intake, sedentary lifestyle, overweight/obese, smoking, excess alcohol intake.

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17
Q

what investigations would you carry out on a patient presenting with a high blood pressure reading?

A

take blood pressure again, on at least 1 other occasion.

24h ambulatory BP monitoring (ABPM) - exclude white coat effect

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18
Q

give 3 examples of non-pharmacological measures you would encourage a patient with hypertension to take

A 
weight reduction.
Mediterranean diet - oily fish, low saturated fat, low salt.
limit alcohol consumption.
exercise.
smoking cessation.
increase fruit and veg intake.
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19
Q

what drug would you prescribe for a 45yo caucasian patient with hypertension with no other medical history?

A 
ACE inhibitor - ramipril.
if CI (cough) - ARB - losartan
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20
Q

what drug would you prescribe a 67yo Afro-Caribbean man with hypertension?

A

calcium channel blocker - amlodipine

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21
Q

if first line treatment is failing to control a patient’s hypertension, what drug regime would you prescribe them? and if this fails?

A

ACE inhibitor + CCB or ACE inhibitor + thiazide.

all 3 if a combination of 2 fails to control.

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22
Q

how do calcium channel blockers work to reduce hypertension?

A

decrease calcium entry into vascular smooth muscle cells - vasodilation of arterial smooth muscle, lowering arterial pressure.

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23
Q

what are the side effects of CCBs?

A

bradycardia, headaches, flushing

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24
Q

what is the most common cardiac arrhythmia?

A

atrial fibrillation

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25
Q

what is AF?

A

chaotic, irregular atrial rhythm at 300-600bpm.
AV node is conducting some of the atrial impulses - irregular ventricular response.
irregularly irregular pulse.

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26
Q

list 4 causes of atrial fibrillation

A

heart failure/ischaemia, hypertension, MI, PE, mitral valve disease, pneumonia, hyperthyroidism, caffeine, alcohol, hypokalaemia, hypomagnaesaemia

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27
Q

what ECG features would you see in atrial fibrillation?

A

absent P waves
irregular QRS complexes
atrial rate 300bpm

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28
Q

give 3 forms of treatment you would give a patient with atrial fibrillation

A

warfarin - anticoagulation.
beta blockers/CCBs - rate control.
Cardioversion - rhythm control.

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29
Q

describe what you would see on an ECG trace in atrial flutter

A

saw tooth flutter waves between QRS complexes

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30
Q

what is the difference between atrial fibrillation and atrial flutter?

A

atrial fibrillation = irregular ventricular conduction of atrial beats.
atrial flutter = atrial rate of 300bpm (same as AF), but ventricles conduct every other atrial beat - 150bpm

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31
Q

name 2 common causes of heart block

A

coronary artery disease, cardiomyopathy, fibrosis of conducting tissue

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32
Q

what is first degree AV block? how does it appear on ECG?

A

delayed AV conduction.

prolonged PR interval (>0.22s).

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33
Q

how does Mobtiz type I (second degree) AV block appear on ECG? aka Wenckebach phenomenon

A

progressive PR interval prolongation until a P wave fails to conduct - PR interval then returns to normal, then begins to get longer again.

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34
Q

how is Mobitz type II (second degree) AV block seen on ECG?

A

dropped QRS waves aren’t preceded by progressive PR prolongation. wide QRS complex.

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35
Q

what is 2:1 or 3:1 advanced second degree AV block?

A

every second or third P wave conducts to ventricles

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36
Q

what is third degree AV block? how are ventricular contractions maintained?

A

all atrial activity is failing to conduct to ventricles - atrial and ventricular activity completely dissociated (shown in P and QRS waves).
ventricular contractions are being maintained by spontaneous escape rhythms from below site of block.

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37
Q

describe the ECG features seen in RBBB

A

secondary R waves in V1.

slurred S in V5 and V6

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38
Q

list 2 causes of RBBB

A

PE, RVH, IHD, congenital heart disease, idiopathic

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39
Q

describe the ECG features seen in LBBB

A

opposite to RBBB.
secondary R waves in left ventricular leads (I, AVL, V4-V6).
slurred S in V1 and V2.

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40
Q

list 2 causes of LBBB

A

IHD, LVH, aortic valve disease, post-op

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41
Q

give 3 causes of sinus tachycardia

A

physiological - exercise/excitement.

fever, anaemia, heart failure, thyrotoxicosis, acute PE, hypovolaemia, drugs.

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42
Q

what causes atrioventricular junctional tachycardias?

A

re-entry circuits - two separate pathways for impulse conduction

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43
Q

what are the ECG changes seen in supraventricular tachycardia?

A

absent or inverted P wave after QRS

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44
Q

name 2 things that may aggravate a supraventricular tachycardia

A

exertion, coffee, tea, alcohol

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45
Q

what is the 1st line management of a supraventricular tachycardia?

A

vagal manoeuvres - breath holding, valsalva manoeuvre, carotid massage

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46
Q

what drugs may be used to treat a supraventricular tachycardia?

A

IV adenosine.

if fails - verapamil/atenolol.

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47
Q

what is the long-term management of a supraventricular tachycardia?

A

radiofrequency ablation of accessory pathway via catheter.

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48
Q

what are ventricular ectopic premature beats?

A

a premature beat arising from an ectopic focus in the ventricles - this focus depolarises before the SAN, leading to a premature and inefficient beat.

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49
Q

describe the clinical and ECG features of a premature ventricular ectopic beat

A

broad, abnormal QRS complex before you would expect it.

patient complains of extra/missed beats/heavy beats - palpitations

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50
Q

how would you treat a symptomatic ventricular ectopic beat? what are patients with ventricular ectopic beats at a higher risk of?

A

beta blockers.

ventricular fibrillation.

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51
Q

what are the ECG features of a ventricular tachycardia?

A

rapid ventricular rhythm with broad abnormal QRS complexes

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52
Q

list 3 causes of prolonged QT

A

congenital, hypokalaemia, hypocalcaemia, hypomagnesaemia, tricyclics, macrolides

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53
Q

what causes Wolff-Parkinson-White?

A

congenital accessory conduction pathway between atria and ventricles

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54
Q

describe the features of a resting ECG in a patient with WPW

A

short PR interval, wide QRS complex due to slurred upstroke (delta wave)

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55
Q

what is an aneurysm? how might they cause symptoms?

A

permanent localised dilation of an artery.
pressure effects on local structures, or vessel rupture.
can be a source of emboli.

56
Q

how might an abdominal aortic aneurysm be discovered?

A

a pulsatile mass palpated on abdo exam.
calcification on a plain XR.
rupture.
epigastric or back pain due to pressure effects.

57
Q

what is the difference between a true and false aneurysm?

A

true aneurysm has the wall of the artery forming a capsule around the aneursym.
false aneurysm wall is made up of surrounding tissue.

58
Q

how would a ruptured AAA present?

A

sudden severe epigastric pain radiating to back leading to hypovolaemic shock - collapse

59
Q

how would a ruptured AAA be repaired?

A

endovascular repair with stent insertion, or surgical replacement of aneurysmal section

60
Q

describe the pain of a dissecting aortic aneurysm

A

abrupt onset of severe, tearing central chest pain radiating through back

61
Q

how is a dissecting aortic aneurysm managed?

A

urgent BP control - lanetalol IV.

surgical repair.

62
Q

give 3 risk factors for peripheral arterial disease

A

hypertension, smoking, diabetes, diet, sedentary lifestyle, obesity, hyperlipidaemia, age, male gender, FHx

63
Q

what causes peripheral artery disease?

A

atherosclerosis causing stenosis of arteries

64
Q

describe the clinical features of intermittent claudication

A

cramping pain in calf/thigh/buttock after walking a given distance (shorter=more severe) - relieved by rest

65
Q

describe the clinical features of critical ischaemia

A

ulceration, gangrene, pain at rest.

burning foot pain at night relieved by hanging legs over the side of the bed

66
Q

what are the 4 stages in the Fontaine classification of peripheral artery disease?

A

asymptomatic - intermittent claudication - ischaemic rest pain - ulceration/gangrene (critical ischaemia)

67
Q

give 3 signs of peripheral artery disease

A

absent femoral, popliteal or foot pulses.

cold, white leg(s), atrophic skin, punched out ulcers, postural colour change, capillary refill prolonged

68
Q

what are the 5 Ps of acute limb ischaemia?

A 
Paraesthesia
Perishingly cold
Pallor
Paralysis
Pain
69
Q

what diagnostic tests would be performed in peripheral artery disease?

A

Ankle-brachial pressure index (ABPI) - ratio of ankle and brachial systolic pressures.
colour duplex USS.
MR/CT angiography.

70
Q

describe conservative treatment of limb ischaemia

A

exercise, quit smoking, lose weight, manage diabetes and hypertension.
clopidogrel (antiplatelet) to prevent progression and reduce risk.

71
Q

how would intermittent claudication be managed, beyond conservative risk reduction treatments?

A

revascularisation - percutaneous transluminal angioplasty (PTA) or surgical reconstruction/arterial bypass graft.

72
Q

what are some risk factors for infective endocarditis?

A 
congenital - valve defects, VSD, PDA.
prosthetic valves.
IVDU.
poor dental hygiene.
soft tissue infections.
73
Q

name the most common causative organism in infective endocarditis?

A

Streptococcus viridans

74
Q

give 3 organisms (apart from Strep viridans) that can cause infective endocarditis

A

enterococci, staph aureus/epidermidis, diphtheroids, Haemophilus, actinobacillus, Coxiella burnetii, chlamydia.
fungi - Candida, aspergillus, histoplasma.

75
Q

what is an infective endocarditis patient at risk of?

A

stroke - vegetations.

destruction of valve - regurgitation - worsening heart failure.

76
Q

describe the clinical features of infective endocarditis

A

systemic features of infection - malaise, fever, night sweats, weight loss, anaemia.
heart failure + new murmurs.
vascular events - embolism ± metastatic abscesses.
immune complex deposition - petechial haemorrhages under skin, splinter haemorrhages under nails, Roth’s spots, arthrlagia, acute glomerulonephritis.

77
Q

what investigations should you carry out in suspected endocarditis?

A

3 sets of blood cultures, at different times and sites.
bloods - anaemia, neutrophilia, high ESR/CRP.

transthoracic echocardiography (TTE) - just standard echo.

78
Q

describe the Duke criteria for diagnosis of IE

A

2 major or 1 maj + 3 min, or 5 min.
Major criteria - persistently +ve blood culture. endocardium involvement seen on +ve echo, new murmur.
Minor criteria - fever, vascular/immunological signs, +ve blood culture/echo that doesn’t meet major.

79
Q

how would you treat infective endocarditis?

A

before results of culture - IV benzylpenicillin + gentamicin.
then tailor to cultures and sensitivity.

80
Q

what is shock?

A

acute circulatory failure with inadequate or inappropriately distributed tissue perfusion - prolonged oxygen deprivation leads to necrosis, organ failure and death

81
Q

list the different types of shock

A

hypovolaemia, cardiogenic, sepsis, anaphylaxis, neurogenic shock

82
Q

give 3 causes of hypovolaemia shock

A

haemorrhages - GI bleed, trauma, AAA dissection etc.

fluid loss - burns, diarrhoea, intestinal obstruction.

83
Q

give 3 causes of cardiogenic shock

A

(= pump faillure).

ACS, arrhythmias, aortic dissection, PE, tension pneumothorax, cardiac tamponade, endocarditis

84
Q

give 3 signs of hypovolaemic shock

A

pale grey skin, slow capillary refill, sweating, weak pulse, tachycardia

85
Q

name 2 precipitating factors of anaphylactic shock

A

penicillin, contrast, latex, dairy, nuts, insect stings

86
Q

describe the clinical features of anaphylactic shock

A

onset within 5-60mins of exposure.

warm peripheries, hypotension, urticarial, angio-oedema, wheezing, upper airway obstruction.

87
Q

how would you manage septic shock?

A

take blood cultures before abx - then co-amoxiclav and tazocin IV

88
Q

how would you manage anaphylactic shock?

A

remove cause. O2. IM adrenaline. IV chlorphenamine and hydrocotisone.

89
Q

how would you manage hypovolaemic shock?

A

raise legs. fluid bolus - repeat if shock improves.

90
Q

what risk score is used to determine stroke risk in AF patient?

A 
CHA2DS2-VASc score:
Congestive heart failure.
Hypertension.
Age >75yrs. (2 points, that's why it's A2).
Diabetes mellitus.
S2 - prior stroke (2pts).
V - vascular disease
Age - 65-74.
Sex category - female sex.
91
Q

what is the enzyme that breaks down bradykinin?

A

angiotensin converting enzyme - excess bradykinin (since it’s not being broken down) is the reason why some patients on ACEi get a persistent dry cough

92
Q

explain how ACE inhibitors work

A

ACE inhibitors inhibit conversion of angiotensin I to angiotensin II in the lungs - this prevents it from acting on the adrenals to increase aldosterone secretion and thus cause water and sodium retention at the kidneys.
angiotensin II is also a vasoconstrictor, so ACEi act as vasodilator, and causes sodium and water excretion - lower blood volume, lowers BP.

93
Q

how do angiotensin receptor blockers produce a similar effect to ACEi? give two examples of ARBs

A

by blocking angiotensin II receptors, so its actions cannot be exerted.
losartan, candesartan.

94
Q

give 2 examples of ACEis

A

ramipril, lisinopril

95
Q

why do you get hyperkalaema as a side effect of angiotensin 2 receptor blockers?

A

ARBs cause a direct effect on aldosterone production in the adrenals - aldosterone works on the distal convoluted tubules of kidney by causing sodium to be reabsorbed in return for potassium excretion - ARBs reverse this transfer, so there’s potassium retention.

96
Q

calcium channel blockers are negatively inotropic and negatively chronotropic, what does this mean?

A

inotropic - reduces the contraction.

chronotropic - lowers the heart rate.

97
Q

how do calcium channel blockers work? give some examples.

A

decrease calcium entry into vascular and cardiac cells. intracellular calcium is lower - relaxation and vasodilation of arterial smooth muscle.
reduce myocardial contractility and suppress cardiac conduction, particularly at AV node.
this reduces myocardial oxygen demand - important in angina.

dihydropyridines (amlodipine, nifedipine) - selective for vasculature.
non-dihydropyridines (diltiazem, verapamil)- selective for heart

98
Q

what clotting factors does warfarin work on?

A

2, 7, 9, 10 by inhibiting vitamin K synthesis - so anticoagulates by inhibiting coagulation factor synthesis

99
Q

statins are given to correct hyperlipidaemia, what enzyme do they act on? name 2 statins.

A

HMG-CoA reductase - involved in making cholesterol.
so they reduce the cholesterol production in liver and increase clearance of LDL-cholesterol from blood.

simvastatin, atorvastatin, pravastatin.

100
Q

amiodarone is used for pharmacological cardioversion, but it also chemically resembles a hormone made naturally by the body - what is this and what can this cause?

A

thyroxine - can cause hyperthyroidism

101
Q

in supraventricular tachycardia, adenosine is administered IV to bring the heart back into normal rhythm, how does it work on the heart? what type of arrhythmias should it be used for?

A

it works via the A1 receptor, which reduces cAMP - so causes cell hyperpolarisation by pushing potassium out of the cell.
also relaxes the smooth muscle of the heart causing vasodilation.

only used for ventricular tachycardias.

102
Q

why do you need to warn the patient that they may get a sense of ‘impending doom’ after you administer adenosine?

A

because it induces transient heart block in the AV node so the heart stops for a beat or so

103
Q

atropine is derived from the deadly nightshade, but what heart arrhythmia is it used for and how does it help?

A

it is used for any severe bradycardia - it blocks the action of the vagus nerve/parasympathetic system by being a competitive antagonist of muscarinic ACh receptors.
dilates pupils, increases heart rate and reduces salivation.

104
Q

if you have a patient that comes in with unstable angina but tells you he is allergic to aspirin, what is then your first line of treatment after giving GTN?

A

clopidogrel monotherapy

105
Q

give an example of a short and a long acting nitrate

A

short - glyceryl trinitrate (GTN).

long - isosorbide mononitrate

106
Q

how do nitrates work to reduce the pain of angina?

A

converted to NO, which is a vasodilator - relaxation of capaticance vessels reduces cardiac preload + LV filling, which reduces cardiac work and myocardial oxygen demand.

107
Q

give 2 possible side effects of nitrates

A

flushing, headaches, light headedness, hypotension

108
Q

name 3 beta blockers

A

bisoprolol, atenolol, propranolol, metoprolol

109
Q

how do beta blockers work to improve symptoms of ischaemic heart disease?

A

they reduce force of contraction and speed of conduction in the heart via beta 1 receptors - reducing cardiac work and oxygen demand.

110
Q

how do beta blockers work as a treatment for AF?

A

slow the ventricular rate by prolonging the refractory period at the AV node

111
Q

list the indications for beta blockers

A

IHD - symptoms and improve prognosis.
chronic heart failure.
AF and other SVTs - reduce rate, maintain sinus rhythm.
hypertension - only if other medicines are insufficient.

112
Q

how do beta blockers work as a treatment for hypertension?

A

reduce renin secretion from the kidney, which is mediated by beta1 receptors.

113
Q

give some possible SEs of beta blockers

A

fatigue, cold extremities, headache, nausea, sleep disturbance, ED in men.

114
Q

what major disease is a contraindication to the use of beta blockers?

A

ASTHMA - can cause life-threatening bronchospasm due to blockade of beta2 adrenoreceptors in airways

115
Q

name an aldosterone antagonist

A

spironolactone, epleronone

116
Q

what cardiac indication do aldosterone antagonists treat?

A

chronic heart failure - as an addition to beta blocker and ACEi/ARB

117
Q

name a LMWH. name a drug that is very similar to LMWHs

A

dalteparin, enoxaparin.

similar drug - fondaparinux.

118
Q

how do LMWHs work?

A

inhibit factor Xa by inhibiting antithrombin

119
Q

how does fondaparinux work?

A

inhibits factor Xa.

120
Q

how does aspirin work in prevention of thrombosis?

A

it irreversibly inhibits cyclooxygenase (COX) to reduce production of pro-aggregation factor thromboxane from arachidonic acid - reduces platelet aggregation and risk of arterial occlusion.

121
Q

give some examples of antiplatelet drugs, apart from aspirin

A

clopidogrel, new oral anticoagulants, glycoprotein IIb/IIIa inhibitors

122
Q

how does clopidogrel work?

A

prevents platelet aggregation by binding irreversibly to adenosine diphosphate receptors on surface of platelets

  • independent of COX pathway, so can be taken with aspirin
123
Q

how do glycoprotein IIb/IIIa inhibitors work?

A

prevent platelet aggregation by inhibiting the GPIIb/IIIa receptor on platelet surface

124
Q

name 2 fibrinolytic (thrombolysis) drugs

A

alteplase, streptokinase

125
Q

how do fibrinolytic drugs work?

A

catalyse the conversion of plasminogen to plasmin which acts to dissolve fibrinous clots and re-canalise occluded vessels.
- allows reperfusion of tissues, preventing/limiting tissue infarction.

126
Q

name a loop diuretic

A

furosemide, bumetanide

127
Q

give a cardiac indication of loop diuretics

A

symptomatic treatment of fluid overload in chronic heart failure

128
Q

describe the mechanism of loop diuretics

A

act on ascending limb of loop of Henle to inhibit the Na/K/2CL cotransporter that transports the ions into the cell - water follows these ions, so they have a potent diuretic effect.

also - cause dilation of capaticance vessels - reduces preload + improves contractile function of the heart.

129
Q

what are potassium sparing diuretics used for? name an example.

A

used as part of combination therapy, to treat hypokalaemia arising from loop/thiazide diuretic use.

amiloride.

130
Q

how do potassium sparing diuretics work?

A

weak diuretics.
act on distal convoluted tubules in kidney - inhibit sodium and water reabsorption by acting on epithelial sodium channels - causes potassium retention.

131
Q

give an example of a thiazide/thiazide like diuretic

A

bendroflumethiazide, indapamide, chlortalidone

132
Q

describe the mechanism of action of thiazide diuretics

A

inhibit the Na/Cl cotransporter in the distal convoluted tubule of the nephron, preventing reabsorption of sodium and water.
also cause vasodilation.

133
Q

how does digoxin work in AF/atrial flutter?

A

reduces heart rate and increases force of contraction (-vely chronotropic, +vely inotropic).

works via indirect pathway - increased vagal tone, reduced contraction at AVN and preventing dome impulses travelling to the ventricles.

134
Q

for what cardiac problem might sildenafil be prescribed? what class of drug is this?

A

primary pulmonary hypertension.

phosphodiesterase type 5 (PDE5) inhibitor

135
Q

how does sildenafil work as a treatment of pulmonary hypertension?

A

causes arterial vasodilation by increasing cGMP (normally broken down by PDE5).

Phase 2a - Systems (18 decks)

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