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Cardio Block > 1- common drugs for CVD > Flashcards

1- common drugs for CVD Flashcards

1
Q

what are examples of drug types that are for preventing things causing risk factors?

A
  • anti-cholesterol drugs
  • anti-hypertensive drugs
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2
Q

what are examples of anti-cholesterol drugs?

A
  • statins (simvastatin, atorvastatin)
  • fibrates
  • PCSK 9, inhibitors (evolocumab, alirocumab)
  • siRNA of PCSK 9 (inclisiran)
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3
Q

what are examples of anti-hypertensive drugs?

A
  • thiazide diuretics
  • beta blockers
  • vasodilators = calcium antagonists, alpha blockers, ACE inhibitors, angiotensin receptor blockers (ARB)
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4
Q

what are some examples of other drugs that impact hyperlipidaemia & hypertension?

A
  • Mineralocorticoid antagonists
  • alpha 2 agonists/imidazoline modulators
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5
Q

what are examples of statins?

A

simvastatin and resovostatinand atorvastatin(1st choice)

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6
Q

what is function of statins?

A

blocks HMG CoA reductase (rate-limiting enzyme for cholesterol synthesis)

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7
Q

what are statins used for?

A
  • hypercholesterolaemia
  • diabetes (who are at risk of CVD)
  • angina/MI (who survive heart attack or have angina)
  • CVA (cerebral vascular accident - stroke) / TIA (transient ischaemic attack)
  • High Risk of MI and CVA
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8
Q

what are side effects of statins?

A
  • myalgia/myopathy = achiness usually in upper arms
  • rhabdomyolysis = breakdown of muscles (rarely and if occurs can cause renal failure)
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9
Q

what is an example of fibrates?

A

bezafibrate

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10
Q

when are fibrates used?

A
  • hypertriglyceridemia
  • low HDL cholesterol
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11
Q

what are some signs of familial hypercholesterolemia?

A
  • development of xanthomas which are fatty deposits that build up under skin often around eyes, elbows, knees, hands & feet
  • Xanthelasma: Yellowish deposits of cholesterol under the skin around the eyes
  • arcus senilis (corneal arcus) = white or greyish ring around the cornea of the eyes
  • cholesterol deposits in tendons = can cause tendon thickening and may be noticeable in areas like achilles tendons
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12
Q

what do patients with familial hypercholesterolemia require?

A

additional lipid lowering agents as well as statins like PCSK 9 inhibitors & inclisiran

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13
Q

what are PCSK 9 inhibitors?

A

they are extra lipid lowering agents that can be given in addition to statins
- work by inhibiting the binding of PCSK9 to LDL receptor, PCSK9 inhibitor increases number of LDL receptors available to clear LDL, thereby lowering LDL cholesterol levels

(PCSK9 usually internalises LDL receptors so less receptors to bind to LDL)

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14
Q

what is inclisiran?

A

new class of drugs (gene silencing) that turns off gene for PCKS 9 so acts like PCSK 9 inhibitor
= this boosts the liver’s ability to remove harmful cholesterol from body as PCSK 9 isn’t there to internalise LDL receptors

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15
Q

what is action of PCSK 9 protein?

A
  1. produced using mRNA
  2. binds to LDL receptor
  3. degrades LDL receptor
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16
Q

what is action of inclisiran? (gene silencing drug for hyperlipidaemia)

A
  1. binds to ASGPR receptor and endocytosed
  2. endosome degraded releasing siRNA (small interfering RNA)
  3. siRNA loaded into RISC complex (RNA induced silencing complex)
  4. complex binds to PCSK 9 mRNA and destroys it
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17
Q

what can hypertension lead to if not controlled?

A

→atherosclerosis →heart failure, stroke, blindness, kidney failure

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18
Q

what are numbers for
a) possible hypertension
b) severe hypertension

A

a) systolic: between 140-180 mmHg
diastolic: between 90-110 mmHg (should do home checks too as white coat theory)

b) systolic: higher than 180 mmHg
diastolic: between 90 - 110 mmHg
(medical emergency)

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19
Q

what is numbers for low blood pressure?

A

systolic: lower than 90 mmHg
diastolic: lower than 60 mmHg

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20
Q

what are types of anti-hypertensive drugs?

A
  1. thiazide diuretics
  2. beta blockers
  3. vasodilators
    • calcium antagonists
    • alpha 1 blockers
    • ACE inhibitors
    • angiotensin receptor blockers (ARB)
  4. mineralocorticoid antagonist e.g. spironolactone
  5. alpha 2 or imidazoline receptor agonist e.g. clonidine, moxonidine
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21
Q

what is function of diuretics?

A

they are antihypertensives that block sodium reabsorption in kidneys

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22
Q

what are 2 types and examples of diuretics?

A
  1. thiazide diuretics e.g. bendrofluazide
    • mild
    • used in hypertension
  2. Loop diuretics e.g. furosemide
    • stronger
    • used in heart failure
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23
Q

what are side effects of diuretics?

A
  • hypokalaemia = a lower than normal potassium level in your bloodstream
    • tiredness
    • Arrhythmias = heart beats with anirregular or abnormalrhythm
  • hyperglycemia = high blood sugar →diabetes
  • increased uric acid →gout & impotence
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24
Q

what are cardioselective beta blockers examples and when are they used?

A
  • only block beta 1 receptors e.g. atenolol, bisoprolol
  • used in angina, acute coronary syndrome, myocardial infarction, hypertension and heart failure
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25
Q

what are some non-selective beta blockers examples and when are they used?

A
  • block beta 1 and beta 2 e.g. propranolol, carvedilol (alpha & beta blocker)
  • used as with cardioselective beta blockers but also thyrotoxicosis (hyperthyroidism), migraine
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26
Q

what are some side effects of beta blockers?

A

= asthma →contraindicated in brittle/severe asthma (can use carefully with mild asthma)

= tired

= heart failure (beta blockers can worsen heart failure in short term especially cardiogenic shock)

= cold peripheries

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27
Q

what are types of calcium antagonists and what is their general purpose?

A
  1. dihydropyridines
  2. rate limiting calcium antagonists
  • they are vasodilator anti-hypertensives
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28
Q

what is
a) an example of dihydropyridines (calcium antagonists)
b) what are they used for
c) their side effects

A

a) amlodipine (calcium channel blockers)
b) hypertension & angina
c) ankle oedema (swelling)

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29
Q

what is
a) an example of rate limiting calcium antagonists
b) what are they used for
c) what drug should be avoided when both on

A

a) verapamil, diltiazem
b) used in hypertension & angina - also supraventricular arrhythmias as acts on AV node
c) avoid use with beta blockers since acts on AV node

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30
Q

what is mechanism of ACE inhibitor
a) lisinopril
b) losartan

A

angiotensin converting enzyme inhibitor
a) block angiotensin I becoming angiotensin II
b) block angiotensin II receptors

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31
Q

when are ACE inhibitors used?

A

hypertension and heart failure

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32
Q

what are ACE inhibitors
a) good for?
b) bad for?

A

a) good for kidneys in diabetic nephropathy (common complication for diabetes which can damage blood vessels in the kidneys that filter waste from the blood)
b) bad for kidneys in renal artery stenosis (narrowing of the one or both of renal arteries - cause kidney failure)

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33
Q

should you use ACE inhibitors in pregnancy induced hypertension?

A

NO - NEVER USE

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34
Q

what are side effects ACE inhibitor
a) lisinopril?
b) losartan?

A

a) cough, renal dysfunction, angioneurotic oedema - rapid swelling of deep layers of skin, often face (because increases bradykinin levels)
b) renal dysfunction (no cough)

*losartan is one without cough side effect!

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35
Q

what do alpha blockers
a) do
b) an example
c) when are they used
d) what are the side effects

A

a) block alpha adrenoceptors to cause vasodilation (as antihypertensives)
b)doxazosin
c) used in hypertension & prostatic hypertrophy
d) postural hypotension (dizzy when stand)

36
Q

for mineralocorticoid antagonists
a) what is their function
b) example
c) when are they used
d) side effects?

A

a) block aldosterone receptors
b) spironolactone & eplerenone
c) heart failure & resistant hypertension
d) enlargementof a man’s breasts (gynaecomastia), hyperkalaemia, renal impairment

37
Q

what drug should be used if resistant hypertension?

A

mineralocorticoid e.g. spironolactone, eplerenone

38
Q

what are alpha 2 adrenoceptor agonist/ imidazoline receptor modulator drugs?

A
  • centrally acting drugs e.g. clonidine or moxonidine
  • reduces release of norepinephrine in renal in the nerves
  • causes blood relaxation and lowering of blood pressure
39
Q

what are clonidine & moxonidine examples of?

A

alpha 2 adrenoceptor agonist/ imidazoline receptor modulator drugs

40
Q

what are general types of anti-anginal drugs?

A

= you want to reduce workload of heart

  • vasodilators (decreases preload & afterload)
  • slows heart rate (decreases workload)
  • metabolic modulators (metabolically reduce demand of heart for energy)
41
Q

what are examples of anti-anginal vasodilators?

A
  • nitrates (slow down heart rate so decreases workload)
  • nicorandil (K ATP channel opener)
  • calcium antagonists (dihydropyridine)
42
Q

what are examples of anti-anginal drugs that slow heart rate?

A
  • beta blockers
  • calcium antagonists (diltiazem, verapamil)
  • ivabradine
43
Q

what are examples of drugs that are anti-anginal drugs that are metabolic modulators?

A

ranolazine (late sodium channel modulator)

44
Q

for nitrates:
a) what is their function
b) example
c) when are they used
d) side effects
e) what is a problem?

A

a) venodilators to decrease preload & afterload as anti-anginal drug
b) isosorbide mononitrate
c) used in angina & acute heart failure
d) headache & hypotension/collapse
e) tolerance is common so you have to leave 8hr a day nitrate free to avoid tolerance

45
Q

what is nicorandil? and what are side effects?

A

= vasodilator anti-anginal drug
- K ATP channel blocker
side effects = headache & mouth/GI ulcers (not uncommon and can be serious - GI ulcers can cause harmful fistulas)

46
Q

what is Ivabradine? how does it work? what is problem with it? what is side effect?

A

= anti-anginal drug that slows heart rate by acting on If (funny current) channel modulator in the sinus node
- slows heart rate only in sinus rhythm - doesn’t work in atrial fibrillation
- side effect = altered visual disturbance

47
Q

what is Ranolazine?

A

= anti-anginal drug that is a metabolic modulator
- it’s a late sodium channel modulator
- decreases calcium load on heart (due to Na/Ca exchanger)
- effective in refractory angina (stubborn)

48
Q

what drug is good for stubborn angina?

A

ranolazine (a metabolic modulator)

49
Q

what is
a) NSTEMI
b) STEMI

A

a) thrombosis →if not blocking whole vessel then NSTEMI
b) thrombosis →if blocking whole vessel then STEMI

50
Q

what are anti-thrombotic drugs general types?

A
  1. anti-platelet
  2. anti-coagulants
  3. fibrinolytics
51
Q

what is aspirin mechanism?

A

acts on COX (cyclooxygenase) pathway - prevents formation of thromboxane A2

52
Q

what anti-thrombotic drugs act on ATP receptor P2Y12?

A

clopidogrel, ticlopidine, prasugrel (these can be used alongside aspirin - dual anti platelet therapy)

53
Q

if huge thrombus load - what drugs can be used and where do they act on?

A

in addition to other drugs - abciximab, eptifibatide, tirofiban

  • act on glycoprotein IIb, IIIa (final pathway)
54
Q

what are examples of anti-platelet agents?

A

aspirin, clopidogrel, Ticagrelor, Prasugrel
= all prevent thrombosis

55
Q

what are anti-platelet drugs prescribed for and what are their side effects?

A

used in: angina, acute MI, CVA/TIA, patients at high risk of MI & CVA

side effects: haemorrhage anywhere, peptic ulcer →haemorrhage, aspirin sensitivity →asthma

56
Q

a) what is purpose of anti-coagulants?
b) examples?
c) when are they used?
d) side effects?

A

a) prevent new thrombosis
b)
- heparin, Fondaparinux (subcutaneously)
- warfarin, rivaroxaban, dabigatran, edoxaban (oral)
c) deep vein thrombosis, pulmonary embolism, NSTEMI, atrial fibrillation
d) haemorrhage anywhere (warfarin needs very carefully controlled by INR - international normalised ratio)

57
Q

what clotting factors does warfarin block?

A

2, 7, 9, 10

58
Q

what anti-coagulant drugs are now more commonly used than warfarin and why?

A
  1. rivaroxaban (factor X inhibitor)= 1st choice
  2. Dabigatran (thrombin factor IIa inhibitor)*Xa converts prothrombin (II) to Thrombin (IIa)
  • they are more effective than warfarin as warfarin risky of bleeding
59
Q

how can patient bleed due to excessive warfarin be reversed?

A

vitamin K

60
Q

for fibrinolytic drugs:
a) what do they do?
b) example
c) when are they used?
d) side effects
e) when to avoid?

A

a) dissolve formed clot
b) streptokinase tissue plasminogen activator (tPA)
b) used for STEMI, pulmonary embolism, CVA (stroke) - selected cases only for CVA & pulmonary embolism
c) haemorrhage serious risk
d) avoid in: recent haemorrhage (some CVAs), trauma, bleeding tendencies, severe diabetic retinopathy (diabetes complication →damage to retina) , peptic ulcer

61
Q

what are some anti-arrhythmic drugs?

A
  1. Atrial fibrillation. rate control with
    - beta blockers
    - Digoxin
    - rate limiting calcium channel blockers
    - chemically cardiovert with amiodarone (which is Vaughan Williams Class III), or Flecainide (which is Vaughan Williams Class Ic )
  2. Ventricular tachycardia (amiodarone)
62
Q

what are some general types of heart failure drugs? (lots)

A

Heart Failure Drugs (4 pillars drug)

  1. ARNI = ACE Inhibitors/ ARBs & Neprilysin inhibitors (sacubitril valsartan)
  2. Beta-blockers
  3. Mineralocorticoid antagonists (Spironolactone, eplerenone)
  4. Sglt2 inhibitors (Dapagliflozin / Empagliflozin)

also:

  • Diuretics
  • Digoxin
63
Q

what is digoxin function? why is it good & bad?

A

blocks atrioventricular (AV) conduction which means good for atrial fibrillation

bad if excessive as the heart falls too much giving bradycardia & heart block.
also bad as increases ventricular irritability which produces ventricular arrhythmias (can be narrow window)

64
Q

what does digoxin toxicity cause?

A
  • nausea, vomiting
  • yellow vision
  • bradycardia, heart block
  • ventricular arrhythmias

*why it’s often avoided until last resort or atrial fibrillation

65
Q

how does neprilysin inhibitor work? whats an example?

A

it’s a heart failure drug - works by angiotensin receptor blocker (ARB) and endopeptidase inhibition

sacubitril valsartan
- (valsartan = ARB therefore blocks angiotensin II receptor) (sacubritil = a neprilysin so blocks breakdown of natriuretic peptide products and therefore increases vasodilation, more natriuresis which is beneficial)

66
Q

how does neprilysin inhibitor compare to ACE inhibitor or angiotensin receptor blocker (ARB)?

A

it’s better than ACEi or ARB

67
Q

what are side effects of neprilysin inhibitor?

A
  • Hypotension
  • Renal impairment
  • Hyperkalaemia
  • Angioneurotic oedema
68
Q

what is SGLT2 inhibitors?

A

heart failure drug that was initially developed for diabetes to prevent glucose reabsorption but in this process they have other effects

examples = Dapagliflozin / Empagliflozin

69
Q

how does SGLT2 inhibitors work as heart failure drug?

A

reduced CV risk factor
- lowers blood glucose levels
- lowers blood pressure via osmotic diuresis
- increases urinary caloric loss with reductions in body weight
- reduces albuminuria possibly due to alterations in tubuloglomerular feedback

70
Q

what are the 4 pillars of therapy in heart failure?

A

ARNI’s = angiotensin receptor-neprilysin inhibitors

BB = beta blockers

MRA = mineralocorticoid receptor antagonists

SGLT2i = sodium-glucose co-transporter 2 inhibitors

71
Q

what can obesity lead to?

A
  • natriuretic peptides, inflammatory adipocitokines, oxidative stress
  • sympathetic nervous & RAAS
  • hermodynamic changes →dilated LA, dilated RV, right ventricular hypertrophy

these all lead to:
- interstitial fibrosis
- increased LV stiffness
- impaired relaxation
- increased LV filling pressure
- increased pulmonary pressure

all leads to HFpEF (Heart Failure with Preserved Ejection Fraction)

72
Q

what are some characteristics of arterial thrombosis?

A
  • low in RBC’s (red blood cells)
  • high platelets
  • low fibrin
  • high shear flow
  • main reason behind MI & stroke
  • white clot
73
Q

what are some characteristics of venous thrombosis?

A
  • high in red blood cells (RBC’s)
  • low platelets
  • high in fibrin
  • low shear flow
  • main reason behind deep vein thrombosis & pulmonary embolism
  • red clot
74
Q

what are antiplatelet drugs general function?

A

drugs that interfere with normal function of blood platelets and reduce to form platelet plugs

75
Q

what is general function of anticoagulants?

A

slow down clotting, thereby reducing fibrin formation & preventing clots from forming & growing

76
Q

what is general function of fibrinolytics?

A

drugs that act as thrombolytics by activating plasminogen to form plasmin, which degrades fibrin and so breaks up thrombi

77
Q

what effect do drugs that block HCN channels have?

A

drugs that block HCN channels hence block funny current so slow heart rate in sinus rhythm (SA node)

78
Q

what is function of organic nitrates?

A

relaxes smooth muscle via their metabolism to nitric oxide

  • decreases preload (via dilation of veins) & afterload (via dilations of arteries)
  • increases coronary blood flow
79
Q

what is an example of organic nitrate?

A

glyceryl trinitrate (GTN) and isosorbide mononitrate (ISMN)
- useful in treatment of angina

80
Q

what are natriuretic peptides?

A

Peptide hormones synthesised by heart (also brain and other organs)

= they provide a counter-regulatory system for the Renin-Angiotensin-Aldosterone System (RAAS)

81
Q

when are natriuretic peptides released?

A

in response to cardiac distension (stretching/enlargement of heart chambers) or neurohormonal stimuli (signals from nervous system & hormones that influence cardiovascular system)

82
Q

what do natriuretic peptides cause?

A
  1. They cause excretion of salt and water in the kidneys, thereby reducing blood volume and blood pressure
  2. they inhibit renin release (Decrease renin release - decrease blood pressure)
  3. Act as a vasodilators - decrease SVR and blood pressure
83
Q

what are the 2 types of natriuretic peptides released by heart?

A

Atrial Natriuretic Peptide (ANP) and Brain-type Natriuretic Peptide (BNP)

84
Q

for ANP (atrial natriuretic peptides)
a) how many amino acids
b) where are they stored
c) when are they released

A

a) 28 amino acid peptide
b) atrial muscle cells (atrial myocytes)
c) released in response to atrial distension (hypervolemic states - increased blood volume)

85
Q

for BNP (brain natriuretic peptides) a) how many amino acids & what are they?
b) what are they synthesised by?

A

a) 32 amino acid peptide - BNP is first synthesised as pre pro-BNP, which is then cleaved to pro-BNP (108 amino acids) and finally BNP (32 amino acids)

b) heart ventricles, brain (where it was originally identified) and other organs

*Medications which inhibit the degradation of BNP has been developed = to increase blood pressure?

86
Q

what natriuretic peptides can be measured in patients with suspected heart failure?

A

Serum BNP and the N-terminal piece of pro-BNP (NT-pro-BNP, 76 amino acids)

Cardio Block (34 decks)

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