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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
Indications and contraindications of thiazides
Contraindications: gout and potentially diabetes
26
Indications and contraindications of beta blockers
Indications: MI, IHD, CHF Contraindications: asthma, COPD, heart block
27
Indication of alpha blockers
Resistance to other drugs Prostatic hypertrophy
28
What are the heart protection study findings
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
29
What is the mode of action of statins
They inhibit HMG-CoA reductase which catalyses the production of cholesterol
30
What do statins do
Reduce plasma cholesterol Reduction in hepatic cholesterol synthesis leads to an up regulation of hepatic LDL receptors, promoting LDL uptake in the liver
31
When are statins less effective in hypercholesterolaemia
In homozygous familial hypercholesterolaemia as a statin can’t make an LDL receptor Sometimes atorvastatin is effective
32
What were the findings of the 4S study (Scandinavian simvastatin survival study)
35% reduction in LDL Over 5 years, 30% reduction in mortality, 42% reduction in death from CAD
33
What are some other effects of statins
Regression of atherosclerosis Lipid depletion leading to stabilisation of plaques Reduce progression of carotid disease, reduced risk of stroke Improve endothelial function
34
What were the findings of the heart protection study
40mg simvastatin to high risk patients 25% reduced MI / stroke / revascularisation / in all patients even with low cholesterol levels
35
What is rosuvastatin used for mainly
Healthy patients with normal cholesterol but elevated C-reactive protein Reduced risk of MI and stroke by 50%
36
Why should statins be taken at night
Because main cholesterol synthesis occurs at night so this offsets that
37
Explain some adverse effects of statins
- 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
How can statins be used as a preventative measure
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
What are some key interactions of simvastatin
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
What is ezetimibe
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
What is alirocumab
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
How can nitrates be used in ischaemic heart disease
Via release of NO Cause venodilation, leads to a decrease in preload and a reduction in cardiac work Coronary vasodilation
43
Describe nitrate tolerance
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
What drugs are used for prevention of angina
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
How are CCIs used in ischaemic heart disease
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
Mode of action of nicorandil (K+ channel activator)
Combined NO donor and activator of ATP- sensitive K-channels Potassium leaves cell causing hyperpolarisation
47
How is aspirin 75mg used as an anti platelet drug
Used to treat MI in patients who have previously had an MI - secondary but not primary prevention Also used in prevention of strokes
48
Describe the mode of action of aspirin
Inhibits cycle-oxygenase enzyme which is responsible for converting endoperoxides into thromboxane
49
What happens a few hours after taking aspirin
MRNA reproduces cycle-oxygenase enzyme which reforms the prostacyclin
50
How long does it take to reform platelets after taking a 75mg aspirin
7 days as requires the bone marrow to synthesis more platelets
51
What is dipyridamole
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
What does GP IIb/IIIa do
Binds fibrinogen which leads to cross linking of platelets
53
What is the mode of action of clopidogrel
Inhibits ADP induced expression of GP- similarly effective and safe as aspirin Clopidogrel + aspirin greatly reduced MIs in patients at risk
54
What is abciximab
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
Describe the fibrinolysis system
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
Mode of action of warfarin
Inhibits coagulation
57
What are the low molecular weight heparins (LMWHs)
Enoxaparin, tinzaparin Activate antithrombin III in the body Antithrombin- inactivates some clotting factors and thrombin by complexing with serine protease of the factors
58
Why is heparin chosen over warfarin in hospital
Heparin acts immediately, warfarin takes a few days to have an effect
59
What are heparins mainly used for
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
Describe symptoms and diagnosis of DVT
Painful swelling in 1 calf Diagnosed by US, D-dimer blood test
61
Mode of action of warfarin
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
Why is warfarin a difficult drug to prescribe
Narrow therapeutic window - can cause risk of bleed (intracranial) Many ADRs (
63
What is the activity of warfarin monitored by
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
How to calculate warfarin dose
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
What are some common counselling points for warfarin
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
What should patients report to dr if they experience while on warfarin
Haemoptysis Blood in faeces / urine Nose bleeds that last 20-30 mins Easy bruising Necrosis D&V for more than 2 days
67
What are the DOACs
Prevent thromboembolism - less bleeding than warfarin - fewer drug interactions - does not require monitoring
68
What are the goals of managing heart failure
Identify / treat any cause Reduce cardiac workload Increase cardiac output Counteract maladaptation Relieve symptoms Prolong quality of life
69
What types of drugs worsen heart failure
Rate limiting CCI (verapamil / diltiazem) NSAIDs due to fluid retaining properties Pioglitazone
70
How to calculate ACEi dose
Low dose then titration up Monitor eGFR and K+ before and during treatment
71
What are the risks of using ACEi
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
What causes CHF
Overactivity of the sympathetic nervous system
73
What is eplenerone
Mineralocorticosteroid Aldosterone receptor antagonist Oppose cardiac fibrosis Risk of hyperkalaemia, increased with ACEi/AT1 receptor antagonist
74
How does digoxin act in AF
Impairs AV conduction and increases vagal activity via the CNS The heart block and bradycardia is beneficial in heart failure with AF
75
Define sepsis
Microbial invasion and systemic inflammation resulting in organ dysfunction Death from multi organ failure
76
What is a clinical definition of sepsis
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
What is bacteraemia
Presence of micro-organisms in blood stream May be transient eg dental procedures May be terminated by host immune system
78
What is septicaemia
Bacteraemia + sepsis
79
Why is rapid treatment so important in sepsis
With every hour delayed, mortality risk increases by 8%
80
What is the cytokine cascade
Increased endothelial permeability Oxidative stress Clotting activation Autonomic NS activation.
81
What causes the systemic inflammatory response (SIRS)
Cytokine release Therefore not specific for infection. Can also be caused by: - trauma - burns - pancreatitis - intra cranial haemorrhage
82
What are common causes of community onset sepsis
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
What are the risk factors of infective endocarditis
Valvular disease Prosthetic valve IV drug use Central lines Implantable cardiac devices
84
How does s. Aureus cause infective endocarditis
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
What is rheumatic fever
Antibody cross-reactivity following s.pyogenes infection Damage to connective tissue Causes fever, poly arthritis, carditis Untreated repeat attacks can cause valvular disease
86
Describe the presentation and signs of infective endocarditis
- fever - lethargy - embolic infection - new murmur - skin lesions from emboli - classic signs include roths spots and Osler’s nodes
87
Describe the diagnosis and management of infective endocarditis
Dukes criteria Usually either: - microbiology: persistent bacteraemia - cardiology - vegetations on echocardiograms Treated with high dose IV antibiotics May need valve replacement
88
How does hospital onset sepsis usually arise
Central and peripheral lines Urinary catheters Pneumonia Post op wound infections Neutropenic sepsis (often caused by chemotherapy)
89
What are the risk factors for resistant organisms
- frequent hospital admissions - prolonged stay in ICU - hospital stays overseas - nursing home residents - previous carriage - previous antibiotic use
90
How should sepsis be followed up
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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