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Y4 > Cardiology > Flashcards

Cardiology Flashcards

1
Q

MOA of ACEi

A

Prevent the conversion of angiotensin I to II in the lungs
No aldosterone secreted from the adrenal glands

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2
Q

side effects of ACEi

A

cough
angioedema
hyperkalaemia
first dose hypotension (more common in patients taking diuretics)

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3
Q

monitoring required for ACEi

A

U&Es before initiating treatment & after increasing the dose
acceptable rise of creatinine up to 30% from baseline, and potassium up to 5.5mmol/L

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4
Q

when starting ACEi, significant renal impairment may be a sign of what

A

bilateral renal artery stenosis

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5
Q

interaction of ACEi

A

high dose diuretic therapy e.g 80mg of furosemide
increases risk of hypotension

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6
Q

cautions & contraindications of ACEi

A

pregnancy and breastfeeding
aortic stenosis (hypotension)
renovascular disease (renal impairment)
hereditary angioedema
potassium >5 mmol/L before initiating treatment

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7
Q

role of anticoagulation in AF

A

preventing a stroke

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8
Q

what is the CHA2DS2-VASc mneumonic?

A

C – Congestive heart failure
H – Hypertension (including treated HTN)
A2 – Age >75 (Scores 2)
D – Diabetes
S2 – Stroke or TIA previously (Scores 2)
V – Vascular disease (ischaemic heart disease, peripheral vascular disease)
A – Age 65-74
S – Sex (female)

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9
Q

what happens if CHA2DS2-VASc score shows no need for anticoagulation

A

need to do a transthoracic echocardiogram to exclude valvular heart disease
valvular heart disease + AF = absolute indication for anticoagulation

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10
Q

how to formalise the risk of anticoagulation therapy?

A

ORBIT score

Haemoglobin <130 g/L for males and < 120 g/L for females, or haemtocrit < 40% for males and < 36% for females = 2

> 74 years = 1

previous bleeding event = 2

renal impairment <60ml/min = 1

antiplatelet therapy = 1

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11
Q

anticoagulation used in AF

A

first line = DOACs
then warfarin

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12
Q

advantages of DOACs

A

no monitoring required
no major interactions
shorter half life than warfarin

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13
Q

reversal agents of DOACs & warfarin

A

apixaban & rivaroxaban = Andexanet alfa

dabigatran = Idarucizumab

warfarin = vitamin K

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14
Q

what is the target INR for AF

A

2-3

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15
Q

MOA of warfarin

A

inhibits epoxide reductase, preventing the reduction of vitamin K to its active hydroquinone form

prevents carboxylation of clotting factor II, VII, IX and X (mnemonic = 1972) and protein C.

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16
Q

what is warfarin

A

a vitamin K antagonist
Vitamin K is essential for the functioning of several clotting factors, warfarin blocks vitamin K and prolongs the prothrombin time

has a long half life, can take several days to achieve a stable INR (international normalised ratio)

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17
Q

inducers of P450 system

A

decrease INR

rifampicin
smoking
chronic alcohol intake
antiepileptics: phenytoin, carbamazepine
barbiturates: phenobarbitone

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18
Q

inhibitors of P450 system

A

increase INR

antibiotics e.g. ciprofloxacin, erythromycin, clarithromycin
isoniazid
omeprazole
amiodarone
SSRIs
fluconazole, ketoconazole
allopurinol

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19
Q

what can potentiate warfarin

A

warfarin is affected by the cytochrome P450 system in the liver, where this system is normally involved in the metabolism of warfarin

general potentiators:
liver disease
cranberry juice
P450 enzyme inhibitors
NSAIDs

green leafy vegetables containing vitamin K

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20
Q

what to do if BP is >180/20mmHg

A

admit for specialist assessment if signs of retinal haemorrhage/papilloedema or life threatening symptoms e.g. heart failure, AKI, new onset confusion

referral if phaechromocytoma suspected

if none of the above, arrange urgent end organ damage investigations e.g. urine dipstick & ACR, bloods (HbA1c, lipids, U&Es), ECG

21
Q

lifestyle advice for lowering BP

A

reduce caffeine
lower salt intake <6g a day
lose weight
exercise
stop smoking & drinking alcohol

22
Q

MOA of thiazide diuretics

A

work by inhibiting sodium reabsorption at the beginning of the distal convoluted tubule (DCT) by blocking the thiazide-sensitive Na+-Cl− symporter

23
Q

side effects of thiazide diuretics

A

hypotension
dehydration
hyponatremia, hypokalaemia, hypercalcemia
gout
impotence

rare:
thrombocytopenia
pancreatitis
agranulocytosis

24
Q

what do thiazide diuretics decrease the incidence of

A

kidney stones due to hypocalciuria

25
Q

MI secondary prevention

A

dual antiplatelet therapy
statin
ACEi
beta blocker

post ACS = ticagrelor + aspirin, stop ticagrelor after 12 months
post PCI = prasugrel/ticagrelor to aspirin, stop 2nd antiplatelet after 12 months
*** this period of time can be altered

if signs of heart failure e.g. reduced ejection fraction and physical signs, start eplerenone 3-14 days after

Mediterranean diet
exercise (20-30 mins a day until slightly breathless)
stop smoking

26
Q

management of angina pectoris

A

aspirin & statin in the absence of any contraindication

beta-blocker or calcium channel blocker first line
CCB as monotherapy = use rate limiting one e.g. diltiazem, verapamil
**if used in combination use a long-acting dihydropyridine calcium-channel blocker (nifedipine)

if poor response, titrate drug up to maximum dose
then add CCB/beta-blocker

only add a 3rd drug whilst a patient is awaiting assessment for PCI or CABG

27
Q

beta blockers should not be concurrently prescribed with what

A

rate limiting CBB e.g. verapamil, diltiazem
risk of complete heart block

28
Q

surgical options for angina pectoris

A

Percutaneous coronary intervention with coronary angioplasty

coronary artery bypass graft with great saphenous vein
** used in severe stenosis

29
Q

what to look for when examining a patient you think may have coronary artery disease

A

midline sternotomy scar
brachial/femoral scars
inner calves scar (great saphenous vein harvesting scar)

30
Q

what are the secondary causes of HTN

A

ROPE

renal disease = renal artery stenosis
obesity
pregnancy induced hypertension/pre-eclampsia
endocrine e.g. hyperaldosteronism

31
Q

investigations for stable chest pain

A

first line = CT coronary angiography
second line = non-invasive functional imaging (looking for reversible myocardial ischaemia)
e.g. myocardial perfusion scintigraphy with single photon emission computed tomography (MPS with SPECT) OR stress echocardiography

3rd line = invasive coronary angiography

32
Q

criteria for anginal chest pain

A
  1. constricting discomfort in the front of the chest, or in the neck, shoulders, jaw or arms
  2. precipitated by physical exertion
  3. relieved by rest or GTN in about 5 minutes

all 3 = typical angina
2 = atypical
1 = non-anginal chest pain

33
Q

presentation of cor pulmonale

A

hypoxia
cyanosis
raised JVP
peripheral oedema
hepatomegaly
third heart sound
murmurs (pan-systolic in tricuspid regurgitation)

34
Q

causes of cor pulmonale

A

COPD
interstitial lung disease
PE
CF
primary pulmonary hypertension

35
Q

side effects of statins

A

myopathy: myalgia myositis, rhabdomyolysis, asymptomatic raised creatine kinase
** risk increased if advanced age, female, low BMI, multi-system disease e.g. DM

liver impairment: check baseline, 3 months, and 12 months

36
Q

contraindications for statins

A

macrolide antibiotics
pregnancy
intracerebral haemorrhage history

37
Q

MOA of statins

A

inhibit the action of HMG-CoA reductase, the rate-limiting enzyme in hepatic cholesterol synthesis

should be taken at night, as this is when majority of cholesterol synthesis occurs

38
Q

who gets the primary & secondary prevention of statins

A

primary = 20mg
QRISK >10%
T1DM who were diagnosed >10 years ago OR >40 OR have established nephropathy

secondary = 80 mg
established CVD e.g. prior stroke, TIA, MI
peripheral vascular disease

39
Q

what should you do with the dose with antihypertensive medication before adding another medication?

A

prescribe maximum dose

40
Q

MOA of clopidogrel

A

antagonist of the P2Y12 adenosine diphosphate (ADP) receptor, inhibiting the activation of platelets

41
Q

what concurrently prescribed with clopidogrel is a cause for concern

A

omeprazole & esomeprazole - might reduce the effectiveness of clopidogrel
lansoprazole should be okay

42
Q

what are the reversible causes of cardiac arrest?

A

Hs & Ts

Hypoxia
Hypovolaemia
Hypothermia
Hypoglycaemia
Hyper/hypokalaemia
Acidosis

Tension pneumothorax
Tamponade
Toxins
Thrombosis (coronary/pulmonary)

43
Q

causes of RBBB

A

normal variant - increasing age
PE
right ventricular hypertrophy
cor pulmonale
MI
cardiomyopathy/myositis

44
Q

indications of warfarin

A

mechanical heart valves

second line after DOACs in VTE and AF

45
Q

target INR for warfarin in VTE and AF

A

VTE: 2.5, recurrent 3.5
AF = 2.5

46
Q

side effects of warfarin

A

haemorrhage
teratogenic
purple toes
skin necrosis
*** when warfarin first started protein C is reduced, putting the body into a procoagulant state
normally avoided by concurrent heparin administration
thrombosis may occur in venules leading to necrosis

47
Q

causes of chronic heart failure

A

hypertension
ischaemic heart disease
valvular disease e.g. aortic stenosis
arrythmias e.g. AF

48
Q

presentation of chronic heart failure

A

breathlessness on exertion
cough (frothy white/pink sputum)
orthopnoea
paroxysmal nocturnal dyspnoea
peripheral oedema

49
Q

when do you offer ambulatory BP monitoring/home BP monitoring

A

when clinic BP is >140/90mmHg

Y4 (16 decks)

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