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Clinical Pharmacology And Therapeutics > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What are the NICE target blood pressure ranges for someone on antihypertensives

A

Systolic: <140 (140-130 in diabetics)
Diastolic <90 (<80 in diabetics)

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2
Q

What are the goals of hypertension treatment

A
  • reduction in cardiovascular damage
  • preservation of renal function
  • limitation or reversal of left ventricular hypertrophy
  • prevention of IHD
  • reduction in mortality due to stroke and MIs
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3
Q

What are some ways of treating hypertension

A

Reducing CVD risk:
- reduce alcohol consumption
- reduce weight
- reduce caffeine
- reduce fat and salt intake
- increase fruit and oily fish intake
- increase exercise
- smoking cessation

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4
Q

Who should be given antihypertensives

A

Clinical BP >140/90 or home BP >135/85

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5
Q

What are the stages of hypertension

A

Stage 1 >140/>90 - treat if the patient is under 80 and has one of: end organ damage, diabetes, CV disease of CV risk

Stage 2 >160/>100 - treat all patients

Severe >180/>120 (same day referral)

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6
Q

What do ACE inhibitors do

A

Interfere with the renin angiotensin aldosterone system
- renin is released by kidney when low level of pressure or sodium is perceived
- renin acts on angiotensinogen (liver) and converts it to angiotensin I
- ACE enzyme in lungs then converts angiotensin I to angiotensin II which is a vasoconstrictor and also stimulates release of aldosterone which causes sodium retention and K loss

ACE inhibitors therefore inhibit the conversion of angiotensin I to angiotensin II and therefore prevent vasoconstriction and sodium retention

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7
Q

Why do ACEi cause cough

A

Because they potentiate bradykinin which stimulates cough (affects 10% of patients)

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8
Q

3 adverse effects of ACEi

A

Cough (bradykinin)

May increase potassium - interaction with salt (KCI) substitute - causes cells to depolarise - abnormal electrical activity in heart (arrhythmias)

Angioedema: increased incidence in black patients

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9
Q

Why are ACEi contraindicated in renovascular disease

A

Narrowing in renal arteries means patient is very dependent on RAAS- Renin-dependent hypertension. ACEis lead to renal underperfusion and severe hypotension and kidney damage

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10
Q

How can you monitor ACEi use

A

Monitor eGFR before and during use (eGFR can drop slightly which indicates ACEi is working - if severe drop (>15), reduce dose or stop drug.

Can worsen renal function overall

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11
Q

How can ACEi be used in diabetes

A

Effective at preventing nephropathy in DM. ACEi slows this damage to the kidneys due to inhibiting RAAS

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12
Q

Mode of action of the AT1 receptor antagonists eg candesaratan, losartan, valsartan

A

Block the action of Angiotensin II at the AT1 receptor

Have similar consequences to ACEis but do not cause cough

Used equally to ACEi

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13
Q

Mode of action of calcium channel inhibitors eg amlodipine, felodipine, nifedipine

A

Inhibit voltage operated Ca2+ channels on vascular smooth muscle which leads to vasodilation and a reduction in BP

Rate-limiting eg verapamil has a greater effect on cardiac tissue

DHPs (dihydropyridines): more on vascular smooth muscle cells

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14
Q

What are diuretics (thiazide like)

A

Second line antihypertensives
- Inhibit Na/Cl in DCT (require good functioning of PCT)
- reduction in circulating volume due to naturiesis and diuresis
- causes vasodilation
- ineffective in moderate renal impairment
- measure eGFR before and during use (can’t work if patient has moderate renal impairment)

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15
Q

Side effects of thiazide like diuretics

A

Hypokalaemia (reduction in K+) - excitable cells become hyperpolarisation
Postural hypotension
Impaired glucose control
Do not use in gout

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16
Q

What are the alpha blockers eg doxazosin and prazosin

A

Competitive receptor antagonists of a-1 adrenoceptors
Last choice antihypertensives as many side effects

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17
Q

Why does NICE no longer recommend beta blockers for hypertension

A

Reduced effectiveness at preventing stroke and increased risk of diabetes

Less effective than alpha blockers

Reduce sympathetic nervous stimulation of renin release

Are contraindicated in asthma and are cautioned in COPD

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18
Q

Adverse effects of ACEis

A

Cough (10%)
Severe first dose hypotension
Renal damage

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19
Q

Adverse effects of CCIs

A

Peripheral oedema
Constipation

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20
Q

Adverse effects of thiazides

A

Urination
Diabetogenic
Hypokalaemia
Impotence
Postural hypotension

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21
Q

Adverse effects of beta blockers

A

Bronchospasm

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22
Q

Adverse effects of alpha blockers

A

Widespread
Postural hypotension

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23
Q

Indications and contraindications of ACEis (AT1 receptor antagonists)

A

Indications: heart failure, left ventricular hypertrophy, diabetic nephropathy

Contraindications: renovascular disease

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24
Q

Indications and contraindications of calcium channel inhibitors

A

Indications: Afro-Caribbean ethnicity, Dihydropyridines in isolated systolic HT

Contraindications: dilitazem/verapamil in angina but not CHF

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25
Q

Indications and contraindications of thiazides

A

Contraindications: gout and potentially diabetes

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26
Q

Indications and contraindications of beta blockers

A

Indications: MI, IHD, CHF
Contraindications: asthma, COPD, heart block

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27
Q

Indication of alpha blockers

A

Resistance to other drugs
Prostatic hypertrophy

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28
Q

What are the heart protection study findings

A

Simvastatin reduces CV events in the high risk patients even with normal cholesterol so statins should be considered for all high risk patients irrespective of cholesterol level

Atorvastatin is the first line in the UK

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29
Q

What is the mode of action of statins

A

They inhibit HMG-CoA reductase which catalyses the production of cholesterol

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30
Q

What do statins do

A

Reduce plasma cholesterol

Reduction in hepatic cholesterol synthesis leads to an up regulation of hepatic LDL receptors, promoting LDL uptake in the liver

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31
Q

When are statins less effective in hypercholesterolaemia

A

In homozygous familial hypercholesterolaemia as a statin can’t make an LDL receptor
Sometimes atorvastatin is effective

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32
Q

What were the findings of the 4S study (Scandinavian simvastatin survival study)

A

35% reduction in LDL
Over 5 years, 30% reduction in mortality, 42% reduction in death from CAD

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33
Q

What are some other effects of statins

A

Regression of atherosclerosis
Lipid depletion leading to stabilisation of plaques
Reduce progression of carotid disease, reduced risk of stroke
Improve endothelial function

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34
Q

What were the findings of the heart protection study

A

40mg simvastatin to high risk patients
25% reduced MI / stroke / revascularisation / in all patients even with low cholesterol levels

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35
Q

What is rosuvastatin used for mainly

A

Healthy patients with normal cholesterol but elevated C-reactive protein
Reduced risk of MI and stroke by 50%

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36
Q

Why should statins be taken at night

A

Because main cholesterol synthesis occurs at night so this offsets that

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37
Q

Explain some adverse effects of statins

A
  • muscle pain
    Very rarely leading to rhabdomyolysis (<1 fatal case per 1 million)
    Simvastatin better than atorvastatin
  • increased diabetes but expert view is that this is outweighed by the CV benefits
38
Q

How can statins be used as a preventative measure

A

NICE recommends to treat patients with a 10% risk of a CV event in the next 10 years

Low intensity = 20mg atorvastatin

High intensity = 80mg atorvastatin

39
Q

What are some key interactions of simvastatin

A

Contraindicated with macrolides
Interacts with CCI amlodipine, verapamil, diltiazem

For amlodipine + statin use pravastatin or 20mg simvastatin max

Also psoralen (grapefruit juice) inhibits CP450

40
Q

What is ezetimibe

A

A cholesterol absorption inhibitor

Prevents cholesterol absorption and is suggested for use on top of a statin if the statin is not controlling cholesterol

41
Q

What is alirocumab

A

Monoclonal antibody
Inhibits PCSK9 which binds to LDL receptors and leads to their degradation so the inhibition increases LDL receptors reducing LDL in body

Used in addition to max dose statins
Given by sc injection every 2 weeks

42
Q

How can nitrates be used in ischaemic heart disease

A

Via release of NO
Cause venodilation, leads to a decrease in preload and a reduction in cardiac work

Coronary vasodilation

43
Q

Describe nitrate tolerance

A

When using oral nitrates or patches, prolonged exposure can reduce effectiveness

Aim for a nitrate free period so give 2 doses (8am, 4pm) instead of 3 doses

Or use sustained release preparations once a day which doesn’t give 24 hour coverage

44
Q

What drugs are used for prevention of angina

A

B blockers
-ve inotropic anc chronotropic which reduces cardiac work and prevents symptoms

Coronary flow only occurs during diastole, by slowing the heart, the diastolic period will be increased and more time for coronary blood flow

B-blockers also have anti arrhythmic effects and reduce the risk of MI

45
Q

How are CCIs used in ischaemic heart disease

A

Rate-limiting agents eg verapamil and diltiazem

Cause vasodilation and improve coronary blood flow which prevents symptoms

Verapamil and diltiazem are myocardial depressants and reduce cardiac work. Also have anti-arrhythmic effects

46
Q

Mode of action of nicorandil (K+ channel activator)

A

Combined NO donor and activator of ATP- sensitive K-channels

Potassium leaves cell causing hyperpolarisation

47
Q

How is aspirin 75mg used as an anti platelet drug

A

Used to treat MI in patients who have previously had an MI
- secondary but not primary prevention
Also used in prevention of strokes

48
Q

Describe the mode of action of aspirin

A

Inhibits cycle-oxygenase enzyme which is responsible for converting endoperoxides into thromboxane

49
Q

What happens a few hours after taking aspirin

A

MRNA reproduces cycle-oxygenase enzyme which reforms the prostacyclin

50
Q

How long does it take to reform platelets after taking a 75mg aspirin

A

7 days as requires the bone marrow to synthesis more platelets

51
Q

What is dipyridamole

A

An anti platelet drug
Phosphodiesterase inhibitor - prevents breakdown of cAMP and cGMP. This then inhibits aggregation of platelets

Or inhibits reuptake of adenosine

Can be used in conjunction with aspirin - makes aspirin more effective

52
Q

What does GP IIb/IIIa do

A

Binds fibrinogen which leads to cross linking of platelets

53
Q

What is the mode of action of clopidogrel

A

Inhibits ADP induced expression of GP- similarly effective and safe as aspirin
Clopidogrel + aspirin greatly reduced MIs in patients at risk

54
Q

What is abciximab

A

MAb against GP IIB/ IIa
given to patients undergoing angioplasty prevents cross linking - one time use to prevent body forming antibodies against the MAb

55
Q

Describe the fibrinolysis system

A

Eg altepase drug
Breaks down clots
Endogenous system to dissolve clots
Activated in parallel with clotting system
Produces enzyme plasmin which digests fibrin of clot and promotes healing

56
Q

Mode of action of warfarin

A

Inhibits coagulation

57
Q

What are the low molecular weight heparins (LMWHs)

A

Enoxaparin, tinzaparin
Activate antithrombin III in the body
Antithrombin- inactivates some clotting factors and thrombin by complexing with serine protease of the factors

58
Q

Why is heparin chosen over warfarin in hospital

A

Heparin acts immediately, warfarin takes a few days to have an effect

59
Q

What are heparins mainly used for

A

To prevent DVT formation in veins
Mainly due to immobility in hospital as lying down blood becomes stagnant in veins

This can increase risk for PE

60
Q

Describe symptoms and diagnosis of DVT

A

Painful swelling in 1 calf

Diagnosed by US, D-dimer blood test

61
Q

Mode of action of warfarin

A

Anticoagulant
Vitamin K antagonist - vit K is essential for production of prothrombin and factors VII, IX and X
Warfarin blocks vit K reductase which is needed for vit K to act as a co-factor

62
Q

Why is warfarin a difficult drug to prescribe

A

Narrow therapeutic window - can cause risk of bleed (intracranial)
Many ADRs (

63
Q

What is the activity of warfarin monitored by

A

International normalised ratio (INR) - prothrombin time
Normal INR is around 1
INR increased by impaired clotting due to warfarin and liver disease (as the liver produces coagulation factors)

64
Q

How to calculate warfarin dose

A

Monitor INR frequently at start (2x per week) then increase interval gradually

Can be reversed with vit K if patient is bleeding, has high INR or is in warfarin overdose

65
Q

What are some common counselling points for warfarin

A

Patients must stick to their regimen
Take at 6pm
If miss a dose then dont take 2 doses together and inform dr at next blood test
Advised not to become pregnant
Alcohol in moderation
Avoid excessive consumption of green veg, beetroot and liver (vit K)

66
Q

What should patients report to dr if they experience while on warfarin

A

Haemoptysis
Blood in faeces / urine
Nose bleeds that last 20-30 mins
Easy bruising
Necrosis
D&V for more than 2 days

67
Q

What are the DOACs

A

Prevent thromboembolism
- less bleeding than warfarin
- fewer drug interactions
- does not require monitoring

68
Q

What are the goals of managing heart failure

A

Identify / treat any cause
Reduce cardiac workload
Increase cardiac output
Counteract maladaptation
Relieve symptoms
Prolong quality of life

69
Q

What types of drugs worsen heart failure

A

Rate limiting CCI (verapamil / diltiazem)
NSAIDs due to fluid retaining properties
Pioglitazone

70
Q

How to calculate ACEi dose

A

Low dose then titration up
Monitor eGFR and K+ before and during treatment

71
Q

What are the risks of using ACEi

A

May cause severe hypotension - caution with diuretic therapy, give at night

Cause deterioration of renal function in pre existing renal disease

Cough (10%)

Avoid in renovascular disease

72
Q

What causes CHF

A

Overactivity of the sympathetic nervous system

73
Q

What is eplenerone

A

Mineralocorticosteroid
Aldosterone receptor antagonist
Oppose cardiac fibrosis

Risk of hyperkalaemia, increased with ACEi/AT1 receptor antagonist

74
Q

How does digoxin act in AF

A

Impairs AV conduction and increases vagal activity via the CNS
The heart block and bradycardia is beneficial in heart failure with AF

75
Q

Define sepsis

A

Microbial invasion and systemic inflammation resulting in organ dysfunction

Death from multi organ failure

76
Q

What is a clinical definition of sepsis

A

Evidence of systemic inflammatory response + 2 of:
- temp >38 or <36
- HR >90/min
- RR >20 / min
- WBC >12 x 10^6 or <4x10^6

77
Q

What is bacteraemia

A

Presence of micro-organisms in blood stream
May be transient eg dental procedures
May be terminated by host immune system

78
Q

What is septicaemia

A

Bacteraemia + sepsis

79
Q

Why is rapid treatment so important in sepsis

A

With every hour delayed, mortality risk increases by 8%

80
Q

What is the cytokine cascade

A

Increased endothelial permeability

Oxidative stress

Clotting activation

Autonomic NS activation.

81
Q

What causes the systemic inflammatory response (SIRS)

A

Cytokine release

Therefore not specific for infection. Can also be caused by:
- trauma
- burns
- pancreatitis
- intra cranial haemorrhage

82
Q

What are common causes of community onset sepsis

A

UTI - E.coli
Pneumonia - S.pneumoniae
Skin / soft tissue / joints - S.aureus
Meningitis - N.meningitidis
Intra-abdominal infection - E.coli
Infective endocarditis - streptococci, S. aureus

83
Q

What are the risk factors of infective endocarditis

A

Valvular disease

Prosthetic valve

IV drug use

Central lines

Implantable cardiac devices

84
Q

How does s. Aureus cause infective endocarditis

A

Mainly when an IV drug user doesn’t clean their skin and they inject s. Aureus into their veins and it goes to the heart

85
Q

What is rheumatic fever

A

Antibody cross-reactivity following s.pyogenes infection

Damage to connective tissue

Causes fever, poly arthritis, carditis

Untreated repeat attacks can cause valvular disease

86
Q

Describe the presentation and signs of infective endocarditis

A
  • fever
  • lethargy
  • embolic infection
  • new murmur
  • skin lesions from emboli
  • classic signs include roths spots and Osler’s nodes
87
Q

Describe the diagnosis and management of infective endocarditis

A

Dukes criteria
Usually either:
- microbiology: persistent bacteraemia
- cardiology - vegetations on echocardiograms

Treated with high dose IV antibiotics
May need valve replacement

88
Q

How does hospital onset sepsis usually arise

A

Central and peripheral lines

Urinary catheters

Pneumonia

Post op wound infections

Neutropenic sepsis (often caused by chemotherapy)

89
Q

What are the risk factors for resistant organisms

A
  • frequent hospital admissions
  • prolonged stay in ICU
  • hospital stays overseas
  • nursing home residents
  • previous carriage
  • previous antibiotic use
90
Q

How should sepsis be followed up

A

Assess risk of recurrence

Exclude endocarditis / intravascular source if there is persistent bacteraemia, multiple signs of infection and specific signs of endocarditis

Monitor bloods

Clinical Pharmacology And Therapeutics (7 decks)

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