Cardiology Flashcards

(74 cards)

1
Q

what kind of drug is aspirin

A

antiplatelet

COX inhibitor preventing production of TXA2

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2
Q

what kind of drugs are warfarin and DOACs

A

anticoagulants

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3
Q

anticoagulants work of fibrin/platelet rich clots

A

anticoagulants work on fibrin rich venous clots

antiplatelets work on platelet rich arterial clots

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4
Q

how do B blockers work

A

block B adrenoceptors, therefore antagonise sympathetic activity
B1 found in the heart
B2 found in the lungs

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5
Q

what effect does blocking B1 receptors have on the heart

A

negative inotropy and chronotropy (contractility and rate)

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6
Q

propranolol is non/cardioselective

A

propranolol is non-selective

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7
Q

examples of cardioselective B blockers

A

atenolol

bisoprolol

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8
Q

indications for B blockers

A

angina
arrhythmias and HR
heart failure (at low dose)

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9
Q

contraindications for B blockers

A

asthma / COPD

heart block

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10
Q

side effects of B blockers

A
cold peripheries 
exacerbate heart failure 
bronchoconstriction 
sleeping problems 
tiredness 
bradycardia
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11
Q

how do loop diuretics work

A

inhibit the Na/K/Cl channel in the ascending limb of the loop of Henle

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12
Q

examples of loop diuretics

A

furosemide

bumetanide

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13
Q

how to thiazide diuretics work

A

inhibit the Na/Cl channel in the DCT of the nephron

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14
Q

examples of thiazide diuretics

A

bendroflumethiazide

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15
Q

side effects of loop diuretics

A

dehydration
nocturia / frequency
electrolyte imbalances - low K, Ca
ototoxicity

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16
Q

side effects of thiazide diuretics

A

low K, Mg
high Ca
^ urate - gout
impotence

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17
Q

examples of vasodilatory drugs

A

nitrates
alpha blockers
hydralazine

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18
Q

how do CCB work

A

inhibit calcium channels in smooth muscle causing coronary and peripheral vasodilatation

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19
Q

where do dihydropyridine CCB mainly work

give examples

A

peripherally

amlodipine, nifedipine

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20
Q

where do non-dihydropyridine CCB mainly work

give examples

A

SAN and AVN
verapamil
diltizaem

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21
Q

how does digoxin work

A

block AVN NA/K ATP pump

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22
Q

digoxin side effects / toxicity

A
arrhythmia 
nausea 
confusion 
reverse tick sign on ECG 
yellow vision 
gynaecomastia
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23
Q

how do statins work

A

inhibit HMG-CoA reductase which is responsible for synthesis of cholesterol in the liver

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24
Q

at what time of day should statins be taken

A

night

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25
side effects of statins
``` myalgia LFT derangement abdominal discomfort ^CK myositis rhabdomyolysis ```
26
how do ACEI work
blocking the action of ACE which converts AgI to AgII
27
side effects of ACEI
``` dry cough hypotension taste disturbance hyperkalaemia renal impairment angioedema (very rare) ```
28
ACEI are one of the sick day rule drugs?
yes
29
what is stable angina
a disease caused by myocardial ischaemia where a patient experiences chest pain on exertion and is relieved by rest
30
cause of stable angina
atheroma
31
clinical features of stable angina
chest pain on exertion relieved by rest relieved by GTN spray central chest pain, radiating to jaw, left arm, neck
32
investigations for stable angina
history ECG CT coronary angiography
33
management of stable angina
lifestyle: smoking, alcohol, diet, weight loss, exercise, stress, triggers aspirin + statin drugs: SL GTN PRN 1. B blocker or CCB 2. swap 3. long acting nitrate, nicorandil, ivabradine
34
a patient should call 999 after ?min following a second dose of GTN in angina
5 min after 2nd dose
35
drugs for secondary prevention in stable angina
antiplatelet - low dose aspirin ACEI statin DM control
36
what is prinzmetals angina
coronary artery spasm
37
what is ACS
acute coronary syndrome | comprises of unstable angina, NSTEMI and STEMI
38
features of ACS
new onset chest pain >15 min associated with N+V, radiation, sweating, SOB, haemodynamic instability does not respond to GTN
39
investigations for ACS
ABCDE 12 lead ECG Bloods: troponin I+T, FBC, U+E, LFT, CRP, glucose, lipids
40
ECG features suggestive of ACS
new ST elevation or depression Pathological Q waves new LBBB T wave inversion
41
causes of a raised troponin
``` ACS arrhythmias PE pericarditis myocarditis ```
42
management of ACS
``` ambulance into hospital ABCDE 12 lead ECG troponin levels Oxygen if hypoxic GTN, morphine (vasodilators) + antiemetic aspirin 300mg crushed and ticagrelor 180mg PCI if within 120min thrombolysis if >120min ```
43
long term pharmacological management after ACS
``` dual antiplatelet therapy for 6 months - aspirin (lifelong) and clopidogrel statin B blocker (ACEI DM control) ```
44
who might have an atypical MI
elderly diabetics females
45
describe which leads are abnormal and the vessel affected in an inferior MI
leads 2, 3, aVF | right coronary artery
46
describe which leads are abnormal and the vessel affected in an anterior MI
leads V1-4 | left anterior descending (LAD) artery
47
describe which leads are abnormal and the vessel affected in a lateral MI
leads 1, aVL, V5 and V6 | circumflex artery
48
complications of MI
``` death cardiac arrest cardiogenic shock arrhythmia - VF, heart block papillary muscle rupture ventricular thrombus ventricular aneurysm VSD mitral regurgitation Dressler's syndrome ```
49
what is Dressler's syndrome
thought to be an autoimmune pericarditis becoming evident several weeks post MI
50
what criteria is used for infective endocarditis
Duke criteria
51
what score is used to stratify NSTEMI patients
GRACE score
52
IV adenosine needs to infused in a large venous cannula?
yes
53
adenosine has a short/long half life
short half life
54
indication for adenosine
to terminate SVT where valsalva manoeuvre has failed
55
side effect of adenosine
sense of impending doom | bronchospasm (avoid in asthmatics)
56
how does adenosine work
transient AVN blockade
57
what is a reversible cause of PEA
tension pneumothorax
58
what is PEA
pulseless electrical activity | a rhythm that should produce a pulse but doesnt
59
what are the 4H and 4T reversible causes of cardiac arrest
``` Hypoxia Hypothermia Hyper/hypokalaemia Hypovolaemia Tension pneumothorax Tamponade Toxins Thrombosis ```
60
a right coronary infarct supplies the AVN and can cause arrhythmia after infarction, true or false
true
61
describe which leads are abnormal and the vessel affected in an posterior MI
tall R waves in V1-2 left circumflex artery could also be right coronary artery
62
contraindications to ACEI/ARBs
pregnancy and breast feeding renovascular disease aortic stenosis idiopathic angioedema
63
monitoring for ACEI
U+E prior to starting
64
HTN management algorithm
``` 1. <55yr or T2DM - commence ACEI OR >55yr or Afro-Caribbean - commence CCB A or C 2. A+C OR A+D 3. A+C+D 4. if K<4.5 - commence spironolactone if K>4.5 - commence a/B blocker 5. if still uncontrolled, refer to specialist ```
65
drug management of bradycardia
IV atropine | antimuscarinic
66
causes of AF
``` SMITH Sepsis + infection e.g. pneumonia Mitral valve disease Ischaemic heart disease Thyrotoxicosis Hypertension HOCM, lung Ca, PE, alcohol, genetics, CO poisoning ```
67
drugs used in rate control of AF
B blockers | CCB
68
drugs used in rhythm control of AF
amiodarone | flecainide
69
what is thromboangiitis obliterans aka
Buerger's disease = Raynauds phenomenon with extremity ischaemia small/medium vessel vasculitis strongly associated with smoking
70
management of acute pericarditis
ibuprofen and colchicine
71
ECG features of pericarditis
widespread saddle shaped ST elevation | PR depression
72
definition of a STEMI on ECG
``` clinical symptoms consistent with ACS >20min 2mm STE in 2 contiguous leads 1mm STE in limb leads new LBBB ST depression - posterior MI raised biomarkers of ischaemia ```
73
definition of NSTEMI
ECG changes but no STE | raised biomarkers of ischaemia
74
management of bradycardia
1. IV atropine | 2. transcutaneous pacing