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PHAL304 > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Chronotropy

A

Heart rate

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2
Q

Inotropy

A

Force of heart contraction

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3
Q

Adrenoreceptors

A

a1 - constrict vascular SM, inotropy
a2 - constrict vascular SM, reduce preganglionic NA release
B1 - chronotropy, inotropy, renin secretion (cAMP)
B2 - dilate arterioles, some chronotropy/inotropy (cAMP)
B3 - dilate coronary microvasculature, decrease inotropy

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4
Q

Propanolol

A

Inhibit B1 and B2

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5
Q

Metoprolol

A

B1 selective = no rest effects, decrease rate and force and renin secretion

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6
Q

Carvediol

A

B1, B2, a1 (some vasodilation)

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7
Q

Beta blockers activity

A

decrease cardiac output, decrease BP, decrease renal renin output, negative chronotropic (SA and AV nodes), negative inotropic, decrease work, decrease oxygen consumption
metabolised CYP2D6
Improve cardiac CA2+ storage and release via cAMP

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7
Q

B3

A

Nebivolol is agonist and B1 blocker
ARs - cardiomyocyte relaxation, decreased cAMP, eNOS activation -> relaxation of vascular smooth muscle, reduce remodelling

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8
Q

Baroreceptors

A

Detect initial drop in cardiac output with beta blockers, causing an initial increase in peripheral resistance (long term decreases)

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9
Q

Therapeutic uses of beta blockers

A

Hypertension - renin, cardiac output, decrease peripheral resistance (not used for this anymore due to low BP)
rate control - anti arrhythmic
Angina - reduce oxygen consumption
Heart failure - not a great effect, chronotropy, vasodilation
Anxiety - tremors and HR

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10
Q

beta blockers adverse effects

A

bronchospasm (B2 respiratory inhibition - asthma), withdrawal (taper), heart failure (too slow), low exercise tolerance, peripheral vasoconstriction, heart block (via conduction), CNS effects (cross BBB), worsening lipid profiles (lipoprotein lipase - increase bad cholesterol)
Type 2 diabetes - hypoglycaemia response inhibited

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11
Q

Atenolol

A

Only bblocker that is hydrophilic, does not cross BBB
Excreted in urine unchanged, longer half life

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12
Q

Ischaemic heart disease

A

Interruption of cardiac blood supply involving epicardial coronary vessels, block oxygen to heart. Caused by coronary artery disease (plaque)
Angina to myocardial infarction
chest pain, shortness of breath, exhausted, myocardial wall tissue dies
Treat decreasing ino and chrono, BP, oxygen demand, sympathetic stimulus

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13
Q

Sympathetic effect on adrenergic receptors

A

B1,2 a1 = myocyte death and increased arrhythmias
a1, B1 = vasoconstriction, sodium retention, fibrosis and scarring

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14
Q

Preload and afterload

A

Preload is the filling of the heart and is determined by the wall stretch
Afterload is down stream resistance affecting how the heart squeezes

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15
Q

Carvediol vs 2nd gen B-Blockers

A

Pros - greater drop in BP, no adverse decrease in HR, little impact triglycerides and glucose
Cons - no selectivity, bronchospasm, need twice a day dosing

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16
Q

ACE inhibitor example

A

Cilazapril
Good absorption and bioavailability 60%, half-life 9h, metabolised to active drug by liver, cleared through kidney
Decrease vascular resistance, BP, sodium retention, preload, blood volume return, decrease SM contraction, increase bradykinin vasodilator, downregulates sympathetic activity
AEs - bradykinin = leaky blood vessels, rash, hypotension, swelling of face

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17
Q

ARB example

A

Candesartan
Prodrug candesartan cilexetil via esterase in GI tract, low bioavailability, half life 9h, CYP2C9 inhibition, excreted in urine (less liver than other ARBs)
Selective to AT1, block all effects of Ang II (not just formation from one thing), no bradykinin accumulation, but lose vasodilator capability, angioedema, renin feedback loop?

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18
Q

Heart failure

A

damage decreases cardiac output and perfusion. Baroreceptors pick up drop and activate the nervous system and noradrenaline. -> salt and water retention, vasoconstriction, ion/chrono

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19
Q

RAAS

A

Release of angiotensin II and aldosterone from adrenal cortex
Control sodium excretion and fluid volume plus vascular tone
Liver -> angiotensinogen -> Ang I -> Ang II -> release aldosterone

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20
Q

Angiotension II

A

Vasoconstrictor, smooth muscle proliferator, fluid retention/hypertrophogenic, fibrogenic, apoptosis, NA and aldosterone release, remodelling via AT1 and 2 receptors

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21
Q

Aldosterone

A

mineralocorticoid receptor agonist
Anti-natriuretic peptide and fibrogenic, salt chloride and water retention, hypertrophy, damage arteries

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22
Q

RAAS inhibitors

A

Renin inhibitors - stop Ang II formation from angiotenisogen
ACE inhibitors - prevent Ang II from Ang I and bradykinin
AT1 blockers - at receptor (avoid AT2)

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23
Q

Renin

A

Released from juxtaglomerular cell on renal afferent arterioles
via stimulation of B1Rs on JG cells, low renal BP, low Na+ conc in distal tubule (glomerulus feedback)

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24
Q

ACE

A

Angiotensin converting enzyme
Ang I to Ang II
Extrinsic (vascular endothelial surface) and intrinsic (in cytosol of tissues)

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25
Q

AT1 vs AT2

A

AT1 - hypertensive effects (vasoconstriction, aldosterone, Na+ reabsorption, cell growth - fibrotic)
AT2 - beneficial (vasodilation, decrease BP, inhibit cell growth, anti-fibrotic)

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26
Q

Calcium channel blocker drug classes

A

Dihydropyridines, phenylalkylamines, benzothiazipines

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27
Q

Types of voltage gates calcium channels

A

L-type - long lasting in cardiac and vascular SM
T-type - transient in neurons and pacemaker cells

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28
Q

Heart conduction

A

SA node = pacemaker -> AV node = conduction -> cardiomyocytes
Via calcium currents, extracellular -> intracellular release

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29
Q

Phases of cardiac action potential

A

Na+ influx -> -> Ca2+ in (L-type) -> K+ out
NA/Adr causes CA2+ influx -> slow stroke
SA node -> atria -> AV node -> His bundles/Prkinje fibres -> ventricles

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30
Q

Calcium channel blockers

A

Inhibit calcium influx through L-type channels
Act on entry into vascular (vasodilation) cardiac (ino) muscle and SA/AV node (chrono)

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31
Q

CCB examples

A

Used in hypertension
Dihydropyridine = Amlodipine - vasodilator
Phenylalkylamines = Verapamil
Benzothiazipines = Diltiazem - depress cardiac contractility, SA/AV nodes (arrhythmias and angina)

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32
Q

Amlopidine

A

vasodilation in arterial smooth muscle, reduce afterload and arterial pressure, stabilises inactive L-type Ca2+ channel state (prevents change to active)
selective to arterial due to longer depolarisations in inactive channels
Good bioavailablity, peak 6-12h, CYP3A4, plasma bound = 30-50 hour half life
ADRs - decrease BP -> tachycardia, increased ino/chrono, increase oxygen demand = not used in angina

33
Q

Varapamil

A

Binds to open L-type Ca2+ channels (more likely in myocardial cells)
suppress cardiac contractility, reduce LTCC recovery from inactivation
Decrease oxygen demand (angina), not used in heart failure as may cause heart block or with B-blockers
Rapid oral absorption, CYP3A4 inhibiton, lower bioavailability

34
Q

Diltiazem

A

Cardiac LTCCs and some vascular LTCCs in sarcolemmal membrane of heart and vascular SM -> hypertension, angina (not first line) and arrhythmias
Not used in heart failure or with B-blockers, does not cause AV block, hypertension or bradycardia
Rapid, 1st pass metabolism, CYP3A4/2D6 and esterases

35
Q

CCB ADRs

A

Relaxed smooth muscle, facial flushing, constipation, bradycardia, hypotension, AV block, HF

36
Q

Anti-lipidaemics benefits

A

Dyslipidaemias -> CV disease, endothelial lesions, thrombotic occlusion
Hypercholesterolaemia -> coronary heart defects, HTN
CV disease + kidney disease cycles -> fucked

37
Q

Cholesterol synthesis

A

Acetyl coenzyme A -> HMG CoA -reductase> mevalonate (MVA) -> cholesterol
In liver and diet, LDL receptors regulate
Transported by lipoproteins

38
Q

Types of cholesterol lipoproteins

A

HDL (picks up used cholesterol), LDL, IDL, VLDL, chylomicrons
HDL 2 and 3 = ApoA-I (the rest are ApoB)

39
Q

LDL receptors

A

Bind apoplipoprotein B100 from LDL -> internalisation of LDL -> recycled receptor, LDL degraded to aas and free cholesterol
Cholesterol -> decrease HMG CoA reductase, increase ACAT, decrease LDL Rs

40
Q

Atherosclerosis

A

Increase in plasma cholesterol, deposition of fatty materials in arteries, low LDLRs, uptake of oxidised LDL by macrophages -> foam cells -> deposition in arteries, calcification, thrombus, occlusion, ulceration

41
Q

Anti hyperlipidaemics

A

Endogenous Cholesterol Esterase attenuators, LDL receptor degradation inhibitors, exogenous CE uptake inhibitors

42
Q

Endogenous CE attenuators

A

Statins - atorvastatin
Fibrates - bezafibrate
Nicotinic acid

43
Q

LDL receptor degration inhibitors

A

PCSK9 inhibitors - alirovumab

44
Q

Exogenous CE uptake inhibitors

A

Cholesterol uptake inhibitors - ezetemibe
Bile acid binding resins - colestipol and cholestyramine

45
Q

Statins

A

Atorvastatin
Treatment for dylipidaemia
Reversible, competitive HMG CoA reductase inhibitors, increase LDLR synthesis, LDL clearance = low LDL in blood, slight HDL increase
Pleiotropic = effect on mavalonic acid

46
Q

Atorvastatin

A

Decrease hepatic cholesterol synthesis
Rapid absorption, long half life - 14h, plasma protein binding, poor bioavailability, CYP3A4

47
Q

Pleiotrophy

A

Inhibit MVA pathway = no isoprenylation = decrease cell growth, increase eNOS, decrease ROS = anti-inflammatory via NFkB

48
Q

Statins adverse effects

A

myopathy and rhabdomyolysis = release of myoglobin into plasma and kidney
Pain from damage to skeletal tissue via mitochondrial function creating ROS?
Interact w CYP3A4, 2C9, OATP1B1, glucoronidation

49
Q

Ezetimibe

A

reduce reuptake of cholesterol from diet into bile

50
Q

Alirocumab

A

PCSK9 inhibition = decrease LDLR destruction via preventing binding of LDLR
2-4 weeks subcutaneous, 4-6h onset

51
Q

Types of diuretics

A

Osmotic, loop, thiazide, K+ sparing

52
Q

Kidneys

A

?

53
Q

Osmotic diuretics

A

Mannitol
Not metabolised = filtered in glomerulus -> pulls water into nephron
Causes osmotic stress in proximal tubule lumen limited water reabsorption, sodium retention in urine, draws water out of cells increase extracellular fluid volume (pulmonary oedema and increase renal blood flow)
IV for acute emergency, some hypersensitivity reactions

54
Q

Loop diuretics

A

Frusemide - most potent
Organic acid transporter (proximal tubule) -> NKCC2 transporter inhibitor on thick ascending loop (sodium/potassium channel on inner lumen surface)
Block sodium influx through NKCC2 to compensate for ATPase activity.
Hypertension (decrease BP), oedema, hyperkalaemia, hypercalcaemia

55
Q

Frusimide

A

4-6h duration, rapid absorption, plasma protein binding, CYP/glucoronidation
ADRs - hypovolemia, dizziness, syncope, hyponatraemia, hypokalaemia, Mg2+ and Ca2+ depletion, uric acid retention

56
Q

Thiazide diuretics

A

Bendroflumathiazide - mild diuretic
Inhibit Na+/Cl- transporter (eNCC1) in distal cortical diluting segment = prevent NaCl reabsorption, increase sodium and water excretion
Hypertension (decrease BP, peripheral resistance and plasma volume), can be used in renal disease if GFR is maintained

57
Q

Bendroflumathiazide

A

Oral, 1h onset, variable elimination kinetics, compete w uric acid transporters (OATs), renal elimination
Dehydration, alkalosis, uric acid retention, hypokalaemia, dehydration, hyponatremia

58
Q

K+ sparing diuretics

A

Spironolactone and amiloride
At late distal/collecting duct

59
Q

Spironolactone

A

Aldosterone antagonist at mineralocorticoid receptor (stops promotion of sodium reabsorption and potassium loss via ENaC pump synthesis)
First pass metabolism, binds to basolateral surface receptors
oral = 70% absorbed, prodrug -> canrenone
ADRs - hyperkalemia, GI disturbances

60
Q

Amiloride

A

ENaC inhibitor, inhibits sodium flux (weak effects on sodium balance)
OAT at proximal tubule
ADRs - hyperkalaemia
Use - drug resistant hypertension, chronic liver failure

61
Q

Antiarrhythmic drugs

A

Metoprolol, amiodarone, diltiazem, digoxin

62
Q

Arrhythmias

A

Abnormal rhythm can cause sudden death. Originate in atria/AV node or ventricles
Caused by defect in pulse generation via automatic tissue/ectopic beats (tacky/Brady), defect in impulse generation (drops beats)
Abnormal depolarisation - Na+ channel effect

63
Q

Classes of antiarrythmics

A

Class I - interfere with Na+ channel (lignocaine)
Class II- B blockers (metoprolol)
Class III - decrease potassium efflux (amiodarone)
Class Iv - Ca2+ blockers (diltiazem)

64
Q

Class I antiarrythmic

A

Block fast Na+ channels in use-dependant way -> upstole/phase zero -> plato phase
Lignocaine binds to Na+ channels in open and inactivated states, increasing rate and magnitude of depolarisation

65
Q

Class II antiarrythmics

A

Block NA/A
Decrease increasing firing at SA node, slow conductor velocity at AV node
Rate control, stress/exercise tachycardias, decrease mortality post-MI
Adverse = non-selective, bronchospasm, negative inotropic, fatigue, insomnia, depression

66
Q

Class III antiarrythmics

A

Block K+ efflux, increase AP duration and refractory period (to repolarisation), decrease Na+, Ca2+ flux
Decrease chance of reentry arrythmias, rate control, no pro-arrhythmic action
10-100 day accumulation, can cause pulmonary fibrosis, rashes, thyroid abnormalities

67
Q

Class IV antiarrythmics

A

Decrease Ca2+ in nodal cells and cardiomyocytes
Binds to open state -> promote inactivated channel
LTCCs = decrease rate of discharge in SA node, decrease conduction, increase refractory period in AV node and decrease myocardial contraction
Don’t use with B-blockers

68
Q

Digoxin

A

Doesn’t fit Vaughan Williams classification
Increase inotrophy and decrease chronotrophy
Cardiac glycoside = inhibit cellular Na+/K+ATPase -> increase inotrophy, decrease sympathetic tone, increase urine, decrease renin release
Increase vagal activity of ACh = decrease SA node firing rate, decrease AV conduction velocity, decrease ventricular rate
Narrow therapeutic range, oral or IV, lots of interactions, can cause arrhythmias

69
Q

Intravascular thrombi

A

Can lead to angina, MI, deep vein thrombosis, pulmonary embolism, stroke

70
Q

Prostacyclin (PGI2)

A

endothelial cells -> inhibit platelet aggregation and secretion, increase cAMP release, decrease COX activity on platelets, decrease prothrombotic trombone production

71
Q

Thrombus formation

A

Cholesterol -> endothelial boundary -> plaque -> rupture into vessel -> decreased PGI2 synthesis-> thrombin -> release collagen, TXA2, ADP -> platelets can adhere to ECM proteins

72
Q

Thrombin

A

GPCR agonist -> Ca2+ entry = change platelet shape -> ADP and TXA2 = platelet activation

73
Q

Fibrin

A

Made from fibrinogen
Stabilised platelets, forming polymers in matrix

74
Q

Antiplatelet examples

A

Aspirin and clipodogrel

75
Q

Anticoagulants examples

A

LMWH - enoxaparin
VKAs - warfarin
NOACs - dabigatran

76
Q

Asprin

A

Broken down in liver to inactive form
Inhibit COX irreversibly via acetylation (selective to COX1)
Stops COX from forming TXA2
Beneficial for vascular disease
Risk = haemorrhage and GI ulceration

77
Q

Clopigodrel

A

ADP non comp inhibitor on P2Y receptors -> prevent GPIIb/a activation
Reduce platelet activation and synergistic with aspirin

78
Q

Warfarin

A

VitK antagonist, prevent throbs from forming
Stop recycling of VitK via epoxide reductase -> can’t form prothrombin, factors VII, IX and X
CYP2C9/1A2/3A4 - lots of interactions, haemorrhage, GI tract loss, bruising, skin necrosis
1-8h peak, can’t measure blood levels have to use international normalised ratio

79
Q

Dabigatran

A

novel oral anticoagulant

80
Q

Haparin

A

Bind antithrombin III to inactivate thrombin as well as mediate factor Xa (creates thrombin)
Enoxaparin (safer_
Subcutaneous administration, half life 406h, cleared by urine
Use to treat deep vein thrombosis

PHAL304 (4 decks)

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