Cardiology Flashcards

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
Q

side effects of statins

A
myalgia 
LFT derangement  
abdominal discomfort 
^CK 
myositis 
rhabdomyolysis
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26
Q

how do ACEI work

A

blocking the action of ACE which converts AgI to AgII

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27
Q

side effects of ACEI

A
dry cough 
hypotension 
taste disturbance 
hyperkalaemia  
renal impairment 
angioedema (very rare)
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28
Q

ACEI are one of the sick day rule drugs?

A

yes

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29
Q

what is stable angina

A

a disease caused by myocardial ischaemia where a patient experiences chest pain on exertion and is relieved by rest

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30
Q

cause of stable angina

A

atheroma

31
Q

clinical features of stable angina

A

chest pain on exertion
relieved by rest
relieved by GTN spray
central chest pain, radiating to jaw, left arm, neck

32
Q

investigations for stable angina

A

history
ECG
CT coronary angiography

33
Q

management of stable angina

A

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
Q

a patient should call 999 after ?min following a second dose of GTN in angina

A

5 min after 2nd dose

35
Q

drugs for secondary prevention in stable angina

A

antiplatelet - low dose aspirin
ACEI
statin
DM control

36
Q

what is prinzmetals angina

A

coronary artery spasm

37
Q

what is ACS

A

acute coronary syndrome

comprises of unstable angina, NSTEMI and STEMI

38
Q

features of ACS

A

new onset chest pain >15 min
associated with N+V, radiation, sweating, SOB, haemodynamic instability
does not respond to GTN

39
Q

investigations for ACS

A

ABCDE
12 lead ECG
Bloods: troponin I+T, FBC, U+E, LFT, CRP, glucose, lipids

40
Q

ECG features suggestive of ACS

A

new ST elevation or depression
Pathological Q waves
new LBBB
T wave inversion

41
Q

causes of a raised troponin

A
ACS 
arrhythmias 
PE 
pericarditis 
myocarditis
42
Q

management of ACS

A
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
Q

long term pharmacological management after ACS

A
dual antiplatelet therapy for 6 months - aspirin (lifelong) and clopidogrel 
statin 
B blocker
(ACEI
DM control)
44
Q

who might have an atypical MI

A

elderly
diabetics
females

45
Q

describe which leads are abnormal and the vessel affected in an inferior MI

A

leads 2, 3, aVF

right coronary artery

46
Q

describe which leads are abnormal and the vessel affected in an anterior MI

A

leads V1-4

left anterior descending (LAD) artery

47
Q

describe which leads are abnormal and the vessel affected in a lateral MI

A

leads 1, aVL, V5 and V6

circumflex artery

48
Q

complications of MI

A
death 
cardiac arrest 
cardiogenic shock 
arrhythmia - VF, heart block 
papillary muscle rupture 
ventricular thrombus 
ventricular aneurysm
VSD
mitral regurgitation 
Dressler's syndrome
49
Q

what is Dressler’s syndrome

A

thought to be an autoimmune pericarditis becoming evident several weeks post MI

50
Q

what criteria is used for infective endocarditis

A

Duke criteria

51
Q

what score is used to stratify NSTEMI patients

A

GRACE score

52
Q

IV adenosine needs to infused in a large venous cannula?

A

yes

53
Q

adenosine has a short/long half life

A

short half life

54
Q

indication for adenosine

A

to terminate SVT where valsalva manoeuvre has failed

55
Q

side effect of adenosine

A

sense of impending doom

bronchospasm (avoid in asthmatics)

56
Q

how does adenosine work

A

transient AVN blockade

57
Q

what is a reversible cause of PEA

A

tension pneumothorax

58
Q

what is PEA

A

pulseless electrical activity

a rhythm that should produce a pulse but doesnt

59
Q

what are the 4H and 4T reversible causes of cardiac arrest

A
Hypoxia 
Hypothermia 
Hyper/hypokalaemia 
Hypovolaemia 
Tension pneumothorax 
Tamponade 
Toxins 
Thrombosis
60
Q

a right coronary infarct supplies the AVN and can cause arrhythmia after infarction, true or false

A

true

61
Q

describe which leads are abnormal and the vessel affected in an posterior MI

A

tall R waves in V1-2
left circumflex artery
could also be right coronary artery

62
Q

contraindications to ACEI/ARBs

A

pregnancy and breast feeding
renovascular disease
aortic stenosis
idiopathic angioedema

63
Q

monitoring for ACEI

A

U+E prior to starting

64
Q

HTN management algorithm

A
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
Q

drug management of bradycardia

A

IV atropine

antimuscarinic

66
Q

causes of AF

A
SMITH 
Sepsis + infection e.g. pneumonia 
Mitral valve disease 
Ischaemic heart disease 
Thyrotoxicosis 
Hypertension 
HOCM, lung Ca, PE, alcohol, genetics, CO poisoning
67
Q

drugs used in rate control of AF

A

B blockers

CCB

68
Q

drugs used in rhythm control of AF

A

amiodarone

flecainide

69
Q

what is thromboangiitis obliterans aka

A

Buerger’s disease
= Raynauds phenomenon with extremity ischaemia
small/medium vessel vasculitis strongly associated with smoking

70
Q

management of acute pericarditis

A

ibuprofen and colchicine

71
Q

ECG features of pericarditis

A

widespread saddle shaped ST elevation

PR depression

72
Q

definition of a STEMI on ECG

A
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
Q

definition of NSTEMI

A

ECG changes but no STE

raised biomarkers of ischaemia

74
Q

management of bradycardia

A
  1. IV atropine

2. transcutaneous pacing