Extra notes Flashcards

1
Q

Give examples of low molecular weight heparins (LMWHs)

A

Dalteparin, Enoxaparin

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2
Q

What drug can be used to reverse dabigatran bleeding?

A

Idarucizumab - if patient has severe renal failure, haemodialyis has to be used instead of this drug

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3
Q

What drug can be used to reverse rivaroxaban/apixaban bleeding?

A

Andexanet alfa - is a form of factor Xa

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4
Q

What drug can be used to reverse heparin, dalteparin and enoxaparin bleeding?

A

Protamine sulphate

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5
Q

Management of HOCM

A
A - Amiodarone
B- beta blockers or verapamil for symptoms
C - cardioverter defibrillator
D - dual chamber pacemaker
E - endocarditis prophylaxis
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6
Q

What are the drugs to avoid in HOCM?

A

Nitrates, ACE inhibitors and ionotropes

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7
Q

When should morphine be given in ACS?

A

Severe chest pain only - mild pain use normal analgesics like paracetamol

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8
Q

Side effects of nitrates

A

hypotension
tachycardia
headaches
flushing

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9
Q

Side effects of thiazides

A
dehydration
postural hypotension
hyponatraemia, hypokalaemia, hypercalcaemia*
gout
impaired glucose tolerance
impotence
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10
Q

Very rare effects of thiazides

A

thrombocytopaenia
agranulocytosis
photosensitivity rash
pancreatitis

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11
Q

What are the two types of atrial septal defects?

A

Ostium secundum and ostium primum.

Ostium secundum are the most common

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12
Q

What is the most common atrial septal defect?

A

Ostium secundum are the most common

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13
Q

Features of atrial septal defects

A
  • ejection systolic murmur, fixed splitting of S2

- embolism may pass from venous system to left side of heart causing a stroke

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14
Q

Features of Ostium secundum specifically

A

70% of ASDs
Associated with Holt-Oram syndrome (tri-phalangeal thumbs)
ECG: RBBB with RAD

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15
Q

Features of Ostium primum specifically

A

Present earlier than ostium secundum defects
associated with abnormal AV valves
ECG: RBBB with LAD, prolonged PR interval

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16
Q

Contraindications of beta blockers

A

uncontrolled heart failure
asthma
sick sinus syndrome
concurrent verapamil use: may precipitate severe bradycardia

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17
Q

Side effects of beta blockers

A
bronchospasm
cold peripheries
fatigue
sleep disturbances, including nightmares
erectile dysfunction
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18
Q

Causes of palpitations

A

arrhythmias
stress
increased awareness of normal heart beat / extrasystoles

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19
Q

Management of major bleeding with high INR (warfarin management)

A

Stop warfarin
Give intravenous vitamin K 5mg
Prothrombin complex concentrate - if not available then FFP*

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20
Q

Management of minor bleeding with INR >8.0 (warfarin management)

A

Stop warfarin
Give intravenous vitamin K 1-3mg
Repeat dose of vitamin K if INR still too high after 24 hours
Restart warfarin when INR < 5.0

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21
Q

Management of no bleeding but INR >8.0 (warfarin management)

A

Stop warfarin
Give vitamin K 1-5mg by mouth, using the intravenous preparation orally
Repeat dose of vitamin K if INR still too high after 24 hours
Restart warfarin when INR < 5.0

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22
Q

Management of minor bleeding and INR 5.0 to 8.0 (warfarin management)

A

Stop warfarin
Give intravenous vitamin K 1-3mg
Restart when INR < 5.0

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23
Q

Management of no bleeding and INR 5.0 to 8.0 (warfarin management)

A

Withhold 1 or 2 doses of warfarin

Reduce subsequent maintenance dose

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24
Q

What ECG leads does a Left anterior descending ALONE artery affect?

A

V1-V4

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25
Q

What ECG leads does a right coronary artery affect?

A

II, III, aVF

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26
Q

What ECG leads does a left anterior descending or left circumflex artery affect?

A

V4-6, I, aVL

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27
Q

What ECG leads does a left circumflex artery ALONE affect?

A

I, aVL +/- V5-6

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28
Q

What ECG leads does a left circumflex artery + right coronary artery affect?

A

V1-V2

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29
Q

What ECG leads does posterior MI affect?

A

Tall R waves in V1-2

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30
Q

Difference between LBBB and RBBB

A

One of the most common ways to remember the difference between LBBB and RBBB is WiLLiaM MaRRoW

in LBBB there is a ‘W’ in V1 and a ‘M’ in V6
in RBBB there is a ‘M’ in V1 and a ‘W’ in V6

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31
Q

Causes of LBBB

A

New LBBB is always pathological.

Myocardial infarction
hypertension
aortic stenosis
cardiomyopathy
rare: idiopathic fibrosis, digoxin toxicity, hyperkalaemia
32
Q

What condition is associated with a short PR interval?

A

Wolff-Parkinson-White syndrome

33
Q

Causes of prolonged PR interval

A
idiopathic
ischaemic heart disease
digoxin toxicity
hypokalaemia*
rheumatic fever
aortic root pathology e.g. abscess secondary to endocarditis
Lyme disease
sarcoidosis
myotonic dystrophy
34
Q

Atherosclerosis

A

Affects the medium and large arteries. It is caused by chronic inflammation and activation of the immune system in the artery wall. This causes deposition of lipids in the artery wall, followed by the development of fibrous atheromatous plaques.

35
Q

Complications of hypertension

A
Ischaemic heart disease
Cerebrovascular accident (i.e. stroke or haemorrhage)
Hypertensive retinopathy
Hypertensive nephropathy
Heart failure
36
Q

What investigations are done to assess for end organ damage in hypertension?

A
  1. Urine albumin:creatinine ratio for proteinuria. dipstick for microscopic haematuria to assess for kidney damage
  2. Bloods for HbA1c, renal function and lipids
  3. Fundus examination for hypertensive retinopathy
  4. ECG for cardiac abnormalities
37
Q

Cardiogenic shock management

A

Ionotropes

38
Q

Statins mechanism of action

A

They act by competitively inhibiting the HMG-CoA reductase, the rate-limiting enzyme in the mevalonate pathway (cholesterol biosynthesis pathway). This competition reduces the rate at which HMG-CoA reductase is able to produce mevalonate, the next molecule in the cascade that eventually leads to cholesterol production.

39
Q

Statins side effects

A

Myopathy

Rhabdomyolysis

40
Q

Fibrates mechanism of action

A

Stimulate peroxisome proliferator activated receptor (PPAR) alpha, which controls the expression of gene products that mediate the metabolism of TG and HDL. As a result, synthesis of fatty acids, TG and VLDL is reduced, whilst that of lipoprotein lipase, which catabolises TG, is enhanced.

41
Q

Fibrates indications

A

hypertriglyceridemia

low HDL cholesterol

42
Q

Thiazide diuretics mechanism of action

A

Thiazide diuretics inhibit the reabsorption of sodium and chloride ions from the distal convoluted tubules of the kidneys by blocking the thiazide-sensitive Na+-Cl- symporter and therefore there is increased excretion of sodium.

43
Q

What kind of calcium channel blocker is Amlodipine?

A

Dihydropyridines calcium antagonists
Block of the L-type calcium channels (dihydropyridine channels) and reduced calcium entry into smooth muscle cells and cardiac cells. This leads to decreased electrical conduction within the heart and reduced contraction and thus increased relaxation. This leads to vasodilation of arteries and thus reduces blood pressure.

44
Q

Side effects of ARBs

A

Renal dysfunction
No cough
Never use in pregnancy induced hypertension

Dizziness, lightheadedness, or faintness upon rising, confusion

45
Q

Nitrates mechanism of action

A

Nitro vasodilators are prodrugs that donate NO by various mechanisms. Nitrates undergo chemical reduction, likely mediated by enzymes. NO stimulates the soluble form of the enzyme guanylate cyclase in the smooth muscle cells of blood vessels. Guanylate cyclase produces cyclic guanosine monophosphate (cGMP) from guanosine triphosphate (GTP). cGMP in turn activates cyclic nucleotide-dependent protein kinase G, which phosphorylates various proteins that play a role in decreasing intracellular calcium levels, leading to relaxation of the muscle cells and thus to dilation of blood vessels.

46
Q

Non-modifiable risk factors in CVD

A
Personal history 
of CHD
Family history 
of CHD
Age
Gender
47
Q

Hypertension definition

A

a disorder in which the sustained mean arterial blood pressure (MABP) is higher than expected for the age, gender and race of the individual – remember there are lots of different definitions of hypertension

48
Q

Endocrine disorders that cause hypertension

A

Adrenal gland hyperfunction / tumours
Conn’s syndrome - excess Aldosterone
Cushing’s syndrome - excess corticosteroid
Pheochromocytoma - excess noradrenaline

49
Q

What examination is recommended in the routine examination of hypertensive patients?

A

Fundoscopy

50
Q

Grade I hypertensive retinopathy changes

A

Slight or modest narrowing of the retinal arterioles with an arteriovenous ratio of >1:2

51
Q

Grade II hypertensive retinopathy changes

A

Modest or severe narrowing of the retinal arterioles with an arteriovenous ratio of <1:2 or arteriovenous nicking

52
Q

Grade III hypertensive retinopathy changes

A

Bilateral soft exudates or flame-shaped haemorrhages

53
Q

Grade IV hypertensive retinopathy changes

A

Bilateral optic nerve oedema

54
Q

Cardiogenic shock

A

Associated with loss of contractility of the heart, thus leads to reduced stroke volume, reduced cardiac output and decreased MABP, thus leads to inadequate tissue perfusion and ischemia.

55
Q

What is Wirchow’s triad?

A

Hypercoagulative state
Endothelial injury
Circulatory stasis

56
Q

D-dimer

A

Is a breakdown product of cross-linked fibrin

High negative predictive value for VTE.

57
Q

Peripheral arterial disease main symptoms

A
Intermittent claudication (pain on walking – cramp like pain especially in calves) and critical limb ischemia. 
Cold peripheries
Ulcers/gangrene
Hair loss, colour change
absent peripheral pulses
58
Q

Lower limb ischemia investigations

A
  1. Non-invasive investigation – via measurement of ABPI and duplex ultrasound scanning
  2. Invasive investigation – CT angiography, catheter angiography, magnetic resonance angiography
59
Q

ABPI values for normal limbs, claudication and severe limb ischemia

A

Normal – 0.9 -1.2
Claudication – 0.4 -0.85
Severe – 0 – 0.4

60
Q

Imaging method to diagnose a ruptured aortic aneurysm

A

CT

61
Q

Management of AAA

A

evaluation, surveillance, endovascular aneurysm repair/Open repair

62
Q

IN cardiac arrest, what drug is given after the 3rd shock?

A

Amiodarone 300mg and adrenaline 1mg

In non-shockable rhythms, adrenaline 1mg is given as soon as possible and every 3-5 minutes (no amiodarone)

63
Q

What murmur causes a tapping apex beat?

A

mitral stenosis

64
Q

What is a cardiac murmur?

A

Audible turbulence of blood flow

Can be Innocent and pathological

65
Q

What murmur radiates to the carotids?

A

aortic stenosis

66
Q

What murmur radiates to the axilla?

A

mitral regurgitation

67
Q

What murmur has a displaced apex?

A

mitral regurgitation

68
Q

What is congenital heart disease?

A

Abnormality of the structure of the heart

Present at birth

69
Q

What ejection systolic murmurs are louder on expiration?

A

Aortic stenosis and HOCM

70
Q

What ejection systolic murmurs are louder on inspiration?

A

Pulmonary stenosis

Atrial septal defect

71
Q

The need for anticoagulation needs to be considered in HF patients; what groups of patients need to be considered?

A
  1. Symptomatic or asymptomatic paroxsymal, persistant or permanent AF
  2. Atrial flutter
  3. A continuing risk of arrhythmia recurrence after cardio-version back to sinus rhythm or catheter ablation
72
Q

Most common ECG finding in patients with PE

A

Sinus tachycardia

- The S1, Q3, T3 pattern is often quoted in books but is actually rare.

73
Q

What tool is used to determine the need for anticoagulation in AF patients based on risk of thromboembolism and stroke?

A

CHA2DS2-VASc score

74
Q

Amiodarone side effects

A
thyroid dysfunction
corneal deposits
pulmonary fibrosis/pneumonitis
liver fibrosis/hepatitis
peripheral neuropathy, myopathy
photosensitivity
'slate-grey' appearance
thrombophlebitis and injection site reactions
bradycardia
lengths QT interval
75
Q

Causes of third heart sound (S3)

A

Congestive heart failure

Dilated cardiomyopathy