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Pharmacy 201 > CVS > Flashcards

CVS Flashcards

1
Q

what are the 4 types of CVD?

A
  • coronary heart disease
  • strokes & transient ischaemic attacks
  • peripheral arterial disease
  • aortic disease
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2
Q

what is primary prevention?

A

strategies that identify & alter modifiable risks to reduce incidence in disease-free pop.

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3
Q

what is secondary prevention?

A

strategies that target individuals w/ established disease, usually have already had an event

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4
Q

what is risk stratification?

A

• strategies used in primary care to identify potential patients
• estimate regularly >40s
• full formal assessment when risk 10% or higher
• use Q-risk

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5
Q

what is coronary heart disease?

A

when arteries become narrowed by an atheroma

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6
Q

what is acute coronary heart syndrome?

A
  • when rupture/erosion of atherosclerotic plaque & subsequent thrombus formation
  • thrombus because of platelet aggregation under high stress
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7
Q

what is an ischaemic stroke/transient ischaemic attack?

A

when blockage because blood clot lodge in vessel narrowed by atheroma

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8
Q

what is peripheral arterial disease?

A
  • when build up of fatty deposits in arteries & restrict blood flow to leg muscles
  • cause intermittent tiredness = claudication
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9
Q

what treatments are required for arrhythmias?

A
  • to control heart rhythm & rate to prevent cardiac arrest
  • prophylactic to prevent stroke
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10
Q

what is different in treatment of AF compared to treating arrhythmias?

A
  • stagnation of blood in atria & incomplete ventricular emptying = clot formation
  • strokes affect larger part of the brain & more likely fatal/leave bed ridden
  • antiplatelets less effective = use anticoagulants
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11
Q

what are 3 examples of ACS?

A
  • unstable angina
  • NSTEMI
  • STEMI
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12
Q

what is unstable angina?

A
  • partial/transiently obstructive thrombus
  • ischaemia, no necrosis
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13
Q

what is an NSTEMI?

A
  • partial/transiently obstructive thrombus
  • ischaemia w/ necrosis
  • partial thickness damage
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14
Q

what is a STEMI?

A
  • complete obstruction by intracoronary thrombus
  • ischaemia w/ necrosis
  • full thickness damage
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15
Q

what are some symptoms of ACS?

A
  • chest pain & pain in other parts
  • sweating
  • SOB
  • lightheaded & dizzy
  • nausea & vomiting
  • anxiety & panic
  • coughing & wheezing
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16
Q

angina can be exacerbated and alleviated by?

A
  • worse after food, cold winds, exercise, stress
  • better after GTN, rest
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17
Q

what are some ACS symptoms only found in women?

A
  • heartburn
  • cold sweats
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18
Q

what are some ACS red flags?

A
  • chest pain >15-20 mins
  • recent onset unstable angina
  • unresponsive GTN, w/ nausea, vomiting & sweating
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19
Q

what are the differences between electrocardiograms taken for ACS conditions?

A

[ unstable angina & NSTEMI ]
- ECG can be normal
- may see ST depression/T-wave inversion
- no ST elevation

[ STEMI ]
- elevation ST

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20
Q

what is cardiac troponin & what levels are considered?

A
  • biological marker of cardiac muscle death
  • normal = <14 ng/L
  • if >14 ng/L = myocardial damage/necrosis
  • if elevate 1st sample, repeat >3hrs later & rise >7 ng/L is likely MI
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21
Q

what are some differential diagnosis for ACS?

A
  • acid reflux
  • pulmonary embolism
  • anaemia
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22
Q

what is treatment for angina for symptom relief?

A

[ 1st line ] - GTN spray
[ 2nd line ] - GTN sublingual spray

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23
Q

what is treatment for angina for symptom prevention?

A

[ 1st line ] - BB or CCB
- if persist - BB + CCB
- if CI BB & CCB = add 2nd agent
[2nd line ] - long-acting nitrate/ Ivabradine/ Nicorandil

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24
Q

what is treatment for angina for 2ndary prevention?

A
  • aspirin
  • statin
  • ACEi
  • hypertension treatment & lifestyle advice
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25
Q

what is used as initial management to treat unstable angina & NSTEMI?

A
  • aspirin
  • ticagrelor/ clopidogrel/ prasugrel
  • LMWH = enoxaparin/ fondaparinux
    [ to consider ] - O2 therapy, pain management, anti-sickness, hyperglycaemia
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26
Q

what is used as 2ndary prevention to treat unstable angina & NSTEMI?

A
  • aspirin
  • ticagrelor/ clopidogrel/ prasugrel
  • ACEi
  • statin
    [ to consider ] - GTN spray for prophylaxis, hypertension treatment & lifestyle advice
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27
Q

what are the 3 types of circulation?

A
  • systemic
  • pulmonary
  • coronary
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28
Q

describe the steps of haemodynamic control?

A
  • ventricular filling = AV valves open & aortic valves closed
  • ventricular systole = AV valves closed & aortic valves open
  • early diastole = AV valves open & aortic valves closed
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29
Q

what parts of the heart are involved in electrical flow?

A
  • sino atrial node = sends signal to ventricular cardiac myocytes in AV node (auto stim.)
  • bundle of HIS = collect & carry signal to R&L ventricles
  • Purkinge fibres = specialised myocardium for electrical conduction to cardiac myocytes
  • fibrous mid line = no electrical conduction
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30
Q

what are the key features of the heart?

A
  • auto-rhythmicity
  • excitability
  • conductivity
  • contractility
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31
Q

what are the sinus rhythms?

A
  • P to Q = atria systole
  • Q to T = ventricular systole
  • P-wave = atria depolarisation
  • QRS complex = ventricle depolarisation
  • T-wave = ventricle repolarisation
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32
Q

what is the equation for blood pressure?

A

BP = CO x PR
BP = HR x SV x PR

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33
Q

what is the process of autoregulation?

A

decrease O2 :
- increase CO2/K+/H+; increase lactic acid; increase histamine and body temp.
- stimulate endothelial cells release endothelin & platelets secretions & prostaglandins ( NO release in dilation)
- vasoconstriction pre capillary sphincters

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34
Q

what is the process of neural regulation?

A

via baroflex mechanisms
- baroreceptors in aorta send signal CV centre in brain = control vagus nerve
- brain send signal = change cardiac activity
- change heart contraction, HR & CO

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35
Q

what is the process of hormonal regulation w/ low BP?

A
  • release renin = angiotensinogen to angiotensin I
  • release ACE = angiotensin I to angiotensin II
  • angiotensin II = potent vasoconstrictor & stimulate release aldosterone from adrenal cortex
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36
Q

what factors are affected by hormonal regulation?

A
  • Na+ reabsorption
  • osmotic pressure
  • H2O reabsorption
  • intravascular volume
  • venous return
  • CO
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37
Q

what is the process of hormonal regulation w/ high BP?

A
  • stop release renin = block conversion angiotensinogen & no aldosterone release
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38
Q

what effect has erythropoietin w/ low BP?

A
  • low O2 = trigger EPO release
  • stimulate red bone marrow to produce RBC = increase O2 transport
  • EPO is a vasoconstrictor = blood viscosity, resistance and pressure
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39
Q

what effect do catecholamines have w/ low BP?

A
  • release by adrenal medulla
  • vasoconstriction = increase HR & force of contraction
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40
Q

what effect do ADH and AUP w/ low BP?

A
  • ADH secreted by hypothalamus & transporter to posterior pituitary = store until nervous stimuli
  • ADH signal kidney reabsorb H2O & increase fluid level = constrict peripheral vessels & restore blood volume and pressure
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41
Q

what effect does ANP/ANH have w/ high BP?

A
  • extreme stretching cardiac cells trigger ANP release; secreted atria cells
  • natriuretic hormones = angiotensin II antagonists & promote Na+/H2O loss from kidneys; suppress renin, aldosterone & ADH release
  • promote fluid loss = decrease blood volume & BP
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42
Q

what kind of information does the pulse give?

A
  • heartbeat rhythm & heartbeat contraction; pulsatile volume and strength
  • regular; regular irregular; irregular irregular
  • weak, faint, strong and bounding
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43
Q

how is blood pressure measured?

A
  • relaxed, temperate setting w/ person seated, arm outstretched and supported
  • use both arms if significant difference > 15mmHg & use higher side for readings
  • in-clinic > 140/90 = take other reading; if different again, take 3rd reading & record lower 2nd & 3rd
  • 140/90 to 180/20; offer ABPM/HBPM
  • BP > 180/20 = urgent treatment
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44
Q

what are some extra tests used for hypertension diagnosis?

A

assess for target organ damage
- haematuria & HbA1C for diabetes
- urine albumin:creatinine & examine fundi
- electrolytes, creatinine & eGFR for chronic kidney disease
- 12-lead ECG for left ventricular hypertrophic & assess CVD-risk w/ Q-risk

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45
Q

what should the patient be informed of when diagnosed for hypertension?

A
  • absolute CVD risk & benefits/harms intervention in 10-year period
  • present absolute event risk numerically
  • use diagrams & text
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46
Q

what are the steps of full history taking?

A
  • introduction
  • presenting complaint
  • history of presenting complaint
  • past medical/surgical history
  • family history
  • social history
  • drug history
  • systems review
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47
Q

what should be involved in social history?

A
  • alcohol intake
  • tobacco use
  • recreational drug use
  • employment history
  • home situation
  • travel history
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48
Q

what is involved in drug history?

A
  • confirm name & dose = prescribed, OTC, vitamins, supplements & herbal medicines
  • borrowed, recently started, stopped & changed
  • compliance
  • allergies
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49
Q

what are the different types of metabolisers?

A
  • poor metabolisers
  • normal metabolisers
  • rapid metabolisers
  • ultra-rapid metabolisers
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50
Q

what are some BBs side effects?

A
  • fatigue
  • cold extremities
  • low pulse
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51
Q

what are factors that affect ADME?

A

[ genetic polymorphisms ]
- SNPs
- tandem repeats
- micro-satellites
- insertions & deletions

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52
Q

what are some drugs to be avoided with ACEi?

A

[ Aliskiren ]
- risk of renal impairment

[ Allopurinol ]
- risk hypersensitivity & haematological reactions

[ Azathioprine ]
- risk anaemia & leukopenia

[ Everolimus ]
- increased risk angioedema

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53
Q

what are some adverse effects of thiazide-like diuretics?

A
  • postural hypotension
  • hyperglycaemia
  • hypokalaemia
  • cardiac arrhythmias
  • metabolic alkalosis
  • dehydration
  • hyponatremia
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54
Q

what are some contraindications of thiazide-like diuretics?

A
  • refractory hypokalaemia
  • hyponatraemia
  • hypercalcaemia
  • Addison’s disease
  • pregnant women
  • severe liver & renal impairment
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55
Q

what are some contraindications of CCBs?

A
  • uncontrolled HF
  • AV block
  • unstable angina/recent MI
  • hepatic & renal impairment
  • pregnant/breastfeeding
  • grapefruit
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56
Q

what are ACE inhibitors?

A
  • target production angiotensin II = act on AT1 receptor; adrenergic innervations; release ADH
  • block vasoconstriction & aldosterone release
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57
Q

what are the effects of ACEi?

A

[ arterial & venous vasodilation ]
- decrease arterial & venous pressure
- decrease ventricular preload & after load

[ decrease blood volume ]
- natriuresis
- diuresis

  • down regulation sympathetic activity & suppression hypertrophy
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58
Q

what are some rare adverse effects of ACEi?

A
  • hyperkalaemia = aldosterone
  • taste disturbance = zinc in ACEi
  • hypotension
  • renal impairment
  • angioedema
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59
Q

what are some clinical considerations with ACEi?

A
  • cough = class effect
  • hypotension = combine low-dose diuretics
    [ dehydration ] = suspend
  • diarrhoea & vomiting
  • postural hypotension
  • acute kidney disease
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60
Q

what are some renal risk assessments for ACEi?

A
  • beneficial chronic kidney failure & hypertension
  • monitor serum creatinine, electrolytes & eGFR
  • periodically assess renal function
  • discontinue bilateral renal artery stenosis
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61
Q

when are ACEi avoided?

A
  • 55 or less
  • caribbean/black african origin = decrease response renin-dependent BP regulation
  • pregnant & breastfeeding
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62
Q

what are some adverse effects of ARBs?

A
  • hyperkalaemia = aldosterone
  • renal impairment
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63
Q

how do BBs work?

A
  • block sympathetic effect
  • adrenaline bind B-1 receptor & increase heart activity = BB block receptor
  • prolong PR interval = decrease SA & AV nodes automaticity
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64
Q

what are the effects of BBs?

A

[ cardiac ]
- contractility
- relaxation rate
- HR & conduction velocity

[ vascular ]
- mild smooth muscle contraction

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65
Q

what are some adverse effects of BBs?

A
  • bradycardia
  • bronchoconstriction
  • cardiac depression
  • hypoglycaemia
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66
Q

what are some cautions w/ BBs?

A
  • pre-existent bradycardia
  • conduction defect
  • HF
  • cardio-selective CCBs
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67
Q

how do CCBs work?

A
  • block Ca2+ channels
  • reduce contraction force & smooth muscle contraction
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68
Q

what is the effect of dihydropyridines and non-dihydropyridines?

A

[ dihydropyridines ] = amlodipine
- vascular effect
- vascular smooth muscle relaxation

[ non-dihydropyridines ] = verapamil & diltiazem
- cardiac effect
- reduce contraction force & HR
- reduce conduction velocity

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69
Q

what are some side effects of dihydropyridines?

A

[ oedema ]
- CCB dilate arteries but veins constricted
- capillary overload forces fluid into surrounding tissue

[ reflex tachycardia ]
- baroreceptor reflex

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70
Q

what are some side effects of non-dihydropyridines?

A
  • bradycardia
  • AV node block = impaired electrical conduction; Ca2+ channels located in electrical nodes
  • contractility = cardiac depression
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71
Q

what are some clinical considerations for thiazide-like diuretics?

A
  • potassium supplements
  • potassium-sparing diuretics
  • avoid ACEi = hyperkalaemia
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72
Q

how do thiazide-like diuretics work?

A
  • moderately powerful = indapamide
  • block Na+/Cl- symporter of early DCT = inhibit Na+ active reabsorption & Cl- transport = H2O reabsorption
  • promote natriuresis & diuresis
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73
Q

how do aldosterone receptor antagonists work?

A
  • antagonise mineral corticoid receptors
  • prevent insertion Na+/K+ ATPase pumps & ENAC channels in late DCT & CD
  • spironolactone & eplerenone
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74
Q

how do Na+ channel blockers work?

A
  • block apical ENAC in late DCT & CD
  • decrease influx Na+
  • Na+ not retained at expense K+
  • amiloride & triamterene
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75
Q

what are the 2 states of solid?

A

[ crystalline ]
- polymorphous; solvates & hydrates; co-crystals
- molecules packed in defined order
- cool slowly to below melting point & between melt and freeze

[ amorphous ]
- unstructured ice
- molecules packed in random order
- rapid solidification/precipitation & glassy and rubbery
- moisture sensitive

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76
Q

what is polymorphism?

A
  • different molecular arrangements in crystal lattice
  • difference = molecule orientation/conformation in lattice sites
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77
Q

how is x-ray diffraction used to differentiate between crystals?

A
  • characteristic pattern of diffraction angles & intensity diffracted beam = planes of crystal
  • crystalline = high intensity & narrow peaks
  • amorphous = low intensity & broad peaks
  • polymorphic = median intensity & narrow peaks
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78
Q

how does hydration occur in crystal lattices?

A
  • small molecular size H2O
  • multi-directional H-bonding capability
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79
Q

how is the salt form better than other crystal forms?

A
  • increase solubility
  • increase dissolution
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80
Q

what is a co-crystal?

A
  • 2 or more molecules in same crystal lattice in definite stoichiometric ratio
  • not based ionic bonds
    = sildenafil & aspirin
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81
Q

what are some primary powder properties and their effects?

A

[ particle size ] & [ shape ]
- content uniformity
- flow & mixing

[ surface area ]
- dissolution rate

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82
Q

what are some secondary powder properties and their effects?

A

[ density ]
- tablet/capsule size
[ porosity ]
- compressibility
- permeability/H2O uptake
[ flowability ]
- content uniformity
[ compressibility ]

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83
Q

how are small & irregular particles measured?

A
  • 3D size impractical
  • only 1 dimension used
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84
Q

how is the surface area of irregular particles measured?

A
  • Brunauer-Emmett-Teller theory (BET theory)
  • powder filled into vacuum-sealed chamber
  • small amounts N2 added & adsorb to powder surface until entire surface and pores covered
  • pressure transducers sense gas amount adsorbed = used calculate SA
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85
Q

what are 4 equivalent diameters for sedentary particles?

A
  • projected perimeter diameter & projected area diameter
  • feret’s diameter & martin’s diameter
  • sieve diameter
  • diameter of equivalent volume/SA/mass sphere
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86
Q

what are 3 equivalent diameters for moving particles?

A

[ stoke’s diameter ]
- sphere w/ same density & settling velocity as particle

[ aerodynamic diameter ]
- sphere w/ same density & terminal velocity in air/any relevant fluid as particle

[ hydrodynamic diameter ]
- sphere w/ same density & settling velocity that diffuses at same rate in liquid as particle

87
Q

what are the different dimensions and types of particle shapes?

A
  • 1D = acicular & rod-shaped
  • 2D = flaky & dendritic
  • 3D = porous, angular/irregular; spherical & rounded
88
Q

how good is the flowability of each type of particle shape?

A
  • spherical & rounded = good & easy mix
  • acicular; rod-shaped & angular/irregular = tend interlock = increased mechanical strength
  • flaky = cohesive effect because greater SA
89
Q

what drugs often cause interactions?

A

[ problematic ]
- enzyme inducers & inhibitors
- PGP protein inducers/inhibitors & chelating agents

[ long half lives ]

[ overdose/underdose ]
- narrow therapeutic windows
- therapeutic drug monitoring
- critical medications

90
Q

what are some resources used for drug interactions?

A
  • BNF = paper, mobile & web app
  • drug SPC
  • Stockleys
91
Q

what are some drugs that cause absorption issues?

A
  • calcium-containing products = Adcal & Calchichew
  • aluminium-containing antacids = Gaviscon & Peptac
  • chelating agents = doxycycline, alendronic acid & levothyroxine
92
Q

what are some drugs that affect distribution?

A
  • sodium valproate
  • phenobarbital
  • phenytoin
  • carbamazepine
  • warfarin
93
Q

what are the steps of phase 2 in metabolism?

A
  • conjugation
  • acetylation
  • sulfation
94
Q

what are some metabolism inducers?

A
  • carbamazepine
  • rifampicin
  • phenobarbitone
95
Q

what are some metabolism inhibitors?

A
  • sodium valproate
  • ketoconazole
  • erythromycin/clarithromycin
96
Q

how is excretion affected by drug interactions?

A
  • via glomerular filtration & active tubular secretion
  • site competition = interactions when eliminated via same active transport mechanism in PT
  • elim. w/ low affinity to transport protein = drug accumulation
  • urine pH can also affect reabsorption
97
Q

what are some PGP inducers/inhibitors?

A
  • apixaban
  • colchicine
  • ciclosporin
  • dabigatran
  • digoxin
  • tacrolimus
98
Q

what affects warfarin effect?

A

[ increase ]
- grapefruit/pomegranate/cranberry
- large acute alcohol

[ decrease ]
- green leafy vegetables/egg yolks/chickpeas
- chronic heavy alcohol

99
Q

what are MAOI?

A
  • monoamine oxidase inhibitors
  • antidepressant w/ frequent interactions
100
Q

what should be avoided w/ MAOI?

A
  • tyramine-rich & dopa-rich foods
    = mature cheese; salami & alcohol
  • only fresh food products
  • continue 2-3 weeks after stopping = long half life
101
Q

how does grapefruit juice affect ADME?

A
  • inhibit CYP 3A4 isoenzyme
  • statins; CCBs & antibiotics
102
Q

what are patients at higher risk of interactions?

A
  • elderly = less renal & liver function
  • children = underdeveloped metabolising systems
  • w/ co-morbidities
  • polypharmacy
103
Q

what is heart failure diagnosis based on?

A
  • signs & symptoms
  • patient history
  • blood levels NT-proBNP
  • ECG
  • exercise tolerance test
  • transthoracic echocardiography
104
Q

what are some other tests used to confirm HF?

A
  • full bloods
  • thyroid function tests
  • chest x-ray
  • peak flow test
105
Q

what is HF?

A
  • increased pressure in heart & inadequate cardiac output
  • due to left ventricular & myocyte dysfunction from MI
  • progressive & no cure
106
Q

what are the features of HF?

A

[ fatigue ]
- low CO = low O2

[ oedema ]
- pulmonary & peripheral
- fluid retention; increase heart pressure affect pulmonary vessels & failing kidneys

[ breathlessness ]
- dyspnoea & orthopnea
- lying down redistribute oedema on lungs
- patient sleep w/ multiple pillows (3+)

107
Q

what is NT-proBNP and its function?

A
  • released response pressure changes in heart
  • less 400ng/L = less likely HF
  • more 2000ng/L = poor prognosis
  • used monitor progress HF
108
Q

what may decrease levels of NT-proBNP?

A
  • obesity
  • african-caribbean
  • current treatment ACEi/ARBs/mineral corticoid receptor antagonists
109
Q

what may increase levels of NT-proBNP?

A
  • age > 70
  • LV hypertrophy
  • renal dysfunction
  • sepsis
  • COPD
  • diabetes
  • ischaemia
110
Q

how is severity of HF graded?

A
  • NYHA functional classification system
  • symptoms alone & show effect functional ability & QoL
111
Q

what is preserved EF?

A
  • preserved Ejection Fraction
    = more 40%
  • preserving EF = slow deterioration
112
Q

how is HF with preserved EF treated?

A
  • loop diuretic & titrate
  • relieve congestive symptoms & fluid retention
  • 1st line = ACEi & BB
  • add in = mineralcorticoid receptor antagonists
113
Q

what is the future treatment for HF?

A
  • SGLT2 inhibitors = dapaglifozin/empaglifozin
  • symptomatic HF w/ reduced EF

[ only add optimised care by HF specialist ]
- ACEi/ARB & BB & MRA
- Entresto & BB & MRA

114
Q

what is used to control symptoms in palliative care?

A

[ breathlessness ]
- repeated small dose opioids
- oramorph

[ pain ]
- opioids PO or SC
- morphine/oxycodone

[ anxiety ]
- midazolam = help agitation

[ N&V ]
- depends trust & other meds = cyclizine

[ secretions ]
- prevent death rattle = hyoscine hydrobromide

115
Q

what is palliative care?

A
  • optimise QoL & reduce suffering in patients w/ life-threatening conditions
  • symptom control = make comfortable
  • honour patient wishes & family informed trajectory
116
Q

how is acute/decomposed HF treated in 2ndary care?

A
  • IV diuretics = bolus/infusions furosemide
  • risk ototoxicity & renal impairment
  • stable 48 hours = stop IV & re-start meds
  • monitor renal function, electrolytes, HR & BP
117
Q

what is some lifestyle advice for HF patients?

A
  • regular exercise & physically active
  • sleep & careful hidden salts
  • balanced diet & health weight
  • lower alcohol & smoking
  • eligible flu vaccine
118
Q

what is a cardiac rehab programme for HF patients?

A
  • personalised, exercise-based programme for stable HF
  • exercise training = increase tolerance & QoL
  • include psychological & education component
119
Q

how is HF treatment monitored?

A
  • assess functional capacity; fluid status; cardiac rhythms
  • cognitive & nutritive status
  • assess renal function & other Us and Es
  • monitor NT-proBNP
  • teach patient recognise symptoms change & alert HP
120
Q

what if optimal drug management doesn’t work for a HF patient?

A
  • w/ severe refractory symptoms = cardiac transplant
  • if older & co-morbidities = unlikely consider
  • referral specialist centre & waiting list
  • complications = life-long immunosuppression; risk rejection & graft failure
121
Q

what is the CVS disease continuum?

A
  • endothelial dysfunction
  • atherosclerosis
  • ischaemia
  • coronary artery disease
  • thrombosis & lesion rupture
  • myocardial infarction
  • reduced contraction
  • ventricular dilation & remodelling
  • heart failure
  • death
122
Q

what can affect endothelial dysfunction?

A
  • hypertension
  • dyslipidemia
  • diabetes mellitus
  • smoking
123
Q

how does ischaemia occur?

A
  • thicken internal surface arteries & atherosclerotic lesions
  • block & affect O2 supply heart muscles
124
Q

what are the troponin levels for angina, NSTEMI & STEMI?

A

stable & unstable = no change troponin
NSTEMI = changes troponin
STEMI = rise troponin

125
Q

how does NO cause vasodilation?

A
  • endothelial cells release NO
  • NO stim. cytoplasmic guanylyl cyclase
  • elevate intracellular cGMP
  • activate protein kinase G
  • smooth muscle relaxation = vasodilation
  • PDE isoform breaks down cGMP
126
Q

what are the features of systemic circulation?

A
  • venous dilation > arterial dilation
  • decreased venous pressure
  • decreased arterial pressure = small effect
127
Q

what are the features of cardiac circulation?

A
  • reduced preload and afterload = decreased wall stress
  • decreased O2 demand
128
Q

what are the features of coronary circulation?

A
  • prevent/reverse vasospasm
  • vasodilation epicardial vessels
  • improve subendocardial perfusion
  • increased O2 delivery
129
Q

what are nitrates used for and what types are there?

A
  • acute attacks/ preventative measures
  • direct = nitroglycerin & sodium nitroprusside
  • organic = isosorbide dinitrate & mononitrate
130
Q

what are some conditions that involve thrombosis in the veins?

A
  • deep vein thrombosis
  • varicose vein
131
Q

what are the 2nd line antianginal drugs?

A
  • IF current inhibitors = ivabradine
  • Class ID sodium-channel blocker = ranolazine
  • Potassium channel activator = nicorandil
132
Q

how does ivabradine work?

A
  • selectively block hyperpolarization-activated cyclic nucleotide-gated channels in SA nodes
  • lower heart rate without affecting contractility of cardiac muscle
133
Q

how does ranolazine work?

A
  • block late inward sodium currents in phase 2 ventricular action potentials
134
Q

how does nicorandil work?

A
  • activate ATP-sensitive K+ channels
  • enhance K+ efflux & hyperpolarization vascular smooth muscle cells
  • reduce Ca2+ entry & reduce cardiac contraction
135
Q

what are the 3 phases of haemostasis?

A
  • vascular spasm
  • platelet activation
  • coagulation
136
Q

how does a vascular spasm work?

A
  • pain reflux = constriction vascular smooth muscle
  • trigger clotting factors needed & directed to injury site
137
Q

how does platelet activation work?

A
  • endothelial damage & exposed collagen
  • platelets stick to exposed collagen
  • platelets stimulate ADP; thromboxane A2 & serotonin
  • von willebrand factor = bridge w/ collagen exposed in damaged blood vessels & glycoprotein receptors GPIIb/IIIa expressed in activated platelets = stabilise collagen-platelet adhesion
  • glycoprotein receptor bind fibrinogen & form platelet-fibrin plug
138
Q

how does coagulation work?

A
  • coagulation factors in liver (ex: vitamin k) and biosynthesis clotting factors (ex: plasma proteins I to XIII)
  • X-A (prothrombin activator) ⇒ activate X (prothrombin)
  • prothrombin converted to thrombin & fibrinogen (soluble) = fibrin (insoluble) = fibrin mesh
139
Q

what are the 2 steps of clot & vessel healing?

A
  • clot retraction w/ vessel repair
  • fibrinolysis
140
Q

how does fibrinolysis work?

A
  • plasminogen = plasma protein trapped in clot
  • converted plasmin & digested to fibrin
141
Q

how does clot retraction & vessel repair work?

A
  • actin & myosin in platelets contract and pull fibrin strands
  • platelet-derived growth factor stimulate smooth muscle & fibroblast division
  • vascular endothelial growth factors rebuild endothelial lining = multiplying endothelial cells
142
Q

what are the 3 types of antithrombotic drugs and their functions?

A
  • anticoagulants = prevent thrombus formation
  • antiplatelets = prevent platelet aggregation
  • fibrinolytics = clot retraction
143
Q

what are the 2 types of oral anticoagulants?

A
  • vitamin K antagonist = warfarin
    [ direct oral anticoagulant ]
  • reversible factor Xa inhibitor = apixaban; edoxaban & rivaroxaban
  • reversible thrombin inhibitor = dabigatran
144
Q

what are fibrinolytics & their functions?

A
  • plasminogen activators = digest fibrin mesh of clot
  • plasminogen = plasma protein trapped in clot
  • activated by tissue plasminogen activator = plasmin & digest fibrin
145
Q

what class is aspirin and its function?

A
  • COX-inhibitor
  • low dose irreversibly inhibit thromboxane in platelets = decrease platelet aggregation
  • in endothelial cells, aspirin inhibit prostaglandins = increase platelet aggregation
146
Q

what are glycoprotein IIb/IIIa inhibitors and 2 example types?

A
  • prevent platelet aggregation by block binding fibrinogen to receptor on platelet
  • abciximab
  • eptifibatide & tirofiban
  • specialists only & administer i.v. hospital & high risk bleeding
147
Q

what is the function of abciximab?

A
  • monoclonal antibody bind to glycoprotein IIb/IIIa receptors & other related sites
  • adjunct HUF & aspirin for prevention ischaemic complications = high risk pts percutaneous transluminal coronary intervention
  • use once only = risk thrombocytopenia
148
Q

what is the function of eptifibatide and tirofiban?

A
  • inhibit glycoprotein IIb/ IIIa receptors
  • use prevent early MI in pts w/ unstable angina/ NSTEMI
149
Q

what are the 2 example types of tissue plasminogen activators?

A
  • streptokinase
  • alteplase; reteplase & tenectplase
150
Q

what is the features of streptokinase?

A
  • natural bacterial protein
  • limited use/rare use
  • pts develop antibodies & inactive streptokinase
151
Q

what are the features of alteplase, reteplase & tenectplase?

A
  • synthetic recombinant
  • highly-selective fibrin-bound plasminogen = clot selective
  • reteplase & tenectplase = longer half-life alteplase
152
Q

what are some adverse effects of tissue plasminogen activators?

A
  • allergic reactions
  • haemorrhage
  • hypotension
153
Q

which drugs does warfarin interact with?

A
  • macrolide antibiotics; azole antifungals; H2 receptor antagonists = breakdown warfarin
  • NSAIDs; broad-spectrum antibiotics = kill gut flora and vitK synthesis = potentiate warfarin
154
Q

what are some adverse effects of warfarin?

A
  • bleeding
  • skin necrosis
155
Q

what is the features and function of warfarin?

A
  • slow onset action & preferred venous thromboembolic disorders
  • inhibit vitk-dependent protein C = natural anticoagulant = procoagulant effects before anticoagulant effects
  • vitK in excess overcome warfarin binding reductase enzyme = manage warfarin overdose w/ vitK
156
Q

how does warfarin work?

A
  • warfarin inhibit reduction vitK = decrease activated clotting factors in blood = competitive antagonist)
  • unmodified coagulation factors II, VII, IX and X = y-carboxylation = activated
  • y-carboxylation need reduced vitamin K = converted oxidised vitamin K
  • vitamin K reductase = oxidised vitK = reduced vitK
157
Q

what are functions of oral anticoagulants?

A

[ apixaban; edoxaban; rivaroxaban ]
- direct & reversible inhibitors factor Xa
- inhibition factor Xa prevent thrombin generation & thrombus development

[ dabigatran ]
- reversible inhibitor of free thrombin; fibrin-bound thrombin & thrombin-induced platelet aggregation

158
Q

what is the function of unfractionated heparin and LMWH?

A
  • HUF & LMWHs bind anti-thrombin III = inhibit thrombin activity + block thrombin-mediated platelet activation
  • inhibit factor Xa = compliment anticoagulant effect
  • rapid onset action
159
Q

what is the differences between HUF and LMWH?

A
  • HUF = non-spec. plasma protein & tissue binding
  • LMWHs = no non-spec. binding w/ LMWHs = predictable dose-dependent response = offer better-sustained clinical effect
160
Q

what are the adverse effects of HUF & LMWH?

A
  • haemorrhage
  • heparin-induced thrombocytopenia/ low platelet
  • hyperkalaemia
161
Q

how is haemorrhage stopped for HUF & LMWH?

A
  • withdraw HUF/ LMWH
  • if rapid reversal of heparin effects needed = protamine sulfate
  • spec. antidote = neutralise/inactivate heparin but only partially reverse effect LMWH
162
Q

how is heparin-induced thrombocytopenia stopped for HUF & LMWH?

A
  • immune-mediated & complicated by thrombosis
  • signs = 30% reduction platelet count, thrombosis & skin allergy
  • use alternative coagulant = danaparoid
163
Q

how is hyperkalaemia stopped for HUF & LMWH?

A
  • inhibition aldosterone secretion result
  • diabetes mellitus; chronic renal failure; acidosis; raised plasma K+ & K+ sparing drugs = more susceptible
  • risk increase duration therapy
164
Q

what is the function of clopidogrel & prasugrel?

A
  • irreversibly inhibit ADP binding to P2Y12 receptors
  • reduce platelet aggregation
  • use prevention recurrence arterial ischaemic disease & ACS
  • combine aspirin enhance outcome & reduce CV risk but increase haemorrhage risk
165
Q

what is the function of ticagrelor?

A
  • directly act P2Y12 receptors & reversibly inhibit
  • reduces ADP-mediated platelet aggregation
  • non-competitive inhibitor = alternative clopidogrel & prasugrel
166
Q

how do ADP-receptor antagonists work?

A
  • activated platelets stimulate ADP release
  • act P2Y12 receptors in platelets
  • activate +ve feedback = more platelet plug formation
167
Q

what are the types of parenteral anticoagulants?

A
  • HUF & LMWH = dalteparin; enoxaparin & tinzaparin
  • heparinoids = danaparoid
  • argatroban
  • hirudins = bivalirudin
  • heparin flushes
  • epoprostenol
  • fondaparinux
168
Q

what are the functions of heparinoids & argatroban?

A

[ heparinoids ]
- high affinity for Xa
- i.v. use

[ argatroban ]
- direct thrombin inhibitor
- i.v. use

169
Q

what is the function of hirudins & heparin flushes?

A

[ hirudins ]
- thrombin inhibitor licensed for unstable angina/ NSTEMI & anticoagulant for pts undergoing percutaneous coronary intervention (PCT)

[ heparin flushes ]
- maintaining the patency artery & venous catheters

170
Q

what is the function of epoprostenol?

A
  • prostacyclin
  • inhibit platelet aggregation in renal dialysis when heparins unsuitable/CI
  • epoprostenol = potent vasodilator
171
Q

what is the function of fondaparinux?

A
  • synthetic polysaccharide
  • selective factor Xa inhibitor
  • similar efficacy LMWH & rapid onset action
  • 1st line ACS
172
Q

do CCB block Ca2+ channels?

A
  • no, they just stop influx of Ca2+
  • bind to specific and different allosteric sites
173
Q

what are the 3 classes of drugs used to treat hyperlipidaemia?

A
  • HMG-CoA reductase inhibitors = statins
  • cholesterol absorption inhibitors = ezetimibe
  • fibrates = fenofibrate & gemfibrozil
  • anion exchange resins = colestyramine
174
Q

how do statins lower plasma cholesterol levels?

A
  • inhibit cholesterol biosynthesis
  • inhibit HMG-CoA reductase = block access to active site
  • to compensate, liver recruit more LDL from blood
175
Q

what are lipids?

A
  • free fatty acids, cholesterol & triglycerides
  • synthesised in cell = endogenous
  • derived from dietary fat = exogenous
176
Q

what is cholesterol?

A
  • makes cell membrane & moderate fluidity
  • cell growth & viability
  • precursor steroid hormones, vitD and bile salts
177
Q

what are triglycerides?

A

supply energy to muscle & other tissues

178
Q

what is HMG-CoA reductase?

A
  • membrane-bound enzyme
  • catalyses rate-limiting step in sterol biosynthesis
  • primary target hypercholesterolemic drug therapy
179
Q

what is the process of cholesterol absorption into the blood?

A
  • enters micellar membrane in intestine
  • absorbed & transported to liver & mix w. hepatic cholesterol
180
Q

how is cholesterol absorbed from micelles into intestinal wall?

A
  • through Niemann-Pick C1 Like 1 protein on enterocyte plasma membrane
  • bile emulsify dietary lipids & facilitate absorption
  • bile salts recycle via hepatic portal vein
181
Q

what is the Niemann-Pick C1 Like 1 protein?

A
  • gateway for dietary cholesterol enter into circulation
  • target for modulating cholesterol level
182
Q

what are lipoproteins?

A
  • complex particles mobilise cholesterol & TGs
  • central core = cholesterol esters = hydrophobic
  • TGs surrounded by free chol & phospholipids = amphophilic
183
Q

what are the functions of apolipoproteins?

A
  • serve structural role
  • act as ligand for lipoprotein receptors
  • guide formation lipoproteins
  • serve activators/inhibitors of enzymes involved in metabolism of lipoproteins
184
Q

what’s the difference between LDLs and HDLs?

A
  • LDL = higher lipids at the core
  • HDL = low lipids at the core
185
Q

what are the 4 types of lipoproteins?

A
  • chylomicrons
  • chylomicron remnants
  • very low density lipoproteins
  • intermediate-density lipoproteins
186
Q

what are chylomicrons?

A
  • large triglyceride-rich particles made by intestine
  • involve in transport of dietary triglycerides & cholesterol to peripheral tissues & liver
187
Q

what are chylomicron remnants & VLDLs?

A

[ remnants ]
- removal of TGs by peripheral tissues
- becomes smaller particle

[ VLDLs ]
- produced by liver
- TGs rich

188
Q

what are IDLs?

A
  • removal TGs from VLDLs by muscle & adipose tissue
  • form enriched in cholesterol
189
Q

what are LDLs?

A
  • derived VLDLs & IDLS & enriched in cholesterol
  • carries majority chol in circulation
  • contains Apo B-100 molecule
  • high Apo B-100 = high risk atherosclerosis
190
Q

what are high number of small LDLs associated with?

A
  • hypertriglyceridemia
  • low HDL levels
  • obesity - type 2 diabetes
  • infectious & inflammatory states
191
Q

what are HDLs?

A
  • cholesterol & phospholipids
  • Apo A-1 = core structural protein
  • high Apo A-1 levels = low risk atherosclerosis
192
Q

how are HDL particles important?

A
  • role in reverse cholesterol transport from peripheral tissues to liver
  • potential mechanism HDL = anti-atherogenic
193
Q

what are the 4 pharmacological options for lipid lowering?

A
  • cholesterol synthesis inhibition
  • intestinal absorption
  • lipoprotein lipase activity
  • HDL
194
Q

what are adverse reactions due to statins?

A
  • GI disturbances
  • skeletal muscle myopathy
  • myalgia
  • myositis w/ rhabdomyolysis
195
Q

how do anion exchange resins work?

A
  • bind with bile salts = insoluble complex
  • lower intestinal cholesterol absorption
196
Q

what are some issue with anion exchange resins?

A
  • unpalatable & digestive problems
  • interfere with fat-soluble nutrients & drugs
  • limited use
197
Q

how does ezetimibe work and what are some issues?

A
  • block transport protein NPC1L1 in gut wall
  • digestive problems; myalgia; fatigue & headache
198
Q

what is thromboxane?

A
  • potent vasoconstrictor & inducer platelet aggregation
  • COX-1 convert from arachidonic acid = prostaglandin H2 = Thromboxane A2
199
Q

what role does P2Y12 play in platelet aggregation?

A
  • ADP bind P2Y12
  • inhibit adenyl cyclase
  • decrease intracellular cAMP
200
Q

how are antiarrhythmic drugs classed?

A
  • based on electrophysiological effect
  • I = NA+ channel blockers =rapid depolarisation
  • II = B-adrenergic blockers
  • III = K+ channel blockers = repolarisation
  • IV = CCB = plateau
201
Q

how do K+ channel blockers work?

A
  • block outflow K+
  • prolong QT interval = prolong refractory period & AP duration
202
Q

what are the 2 considerations before attempting retrosynthesis?

A

[ percent yield ]
- number of single steps minimised & simple
- yield each step maximised = avoid side products

[ type of synthesis ]
- linear synthesis
- convergent synthesis

203
Q

why is convergent synthesis almost always the best choice?

A
  • lower amount of steps
  • shorter time & higher yields
  • better carbon economy
204
Q

what are synthons & synthetic equivalents?

A
  • synthons = not real molecules = representation of separation charges
  • SE = actual substrates for forward synthesis
205
Q

what is the pathophysiology of atherosclerosis?

A
  • endothelial dysfunction
  • formation lipid layer/fatty streak in intima
  • migration leukocytes & smooth muscle cells into vessel wall
  • foam cell formation
  • degradation extracellular matrix
206
Q

what are the 3 types of familial hyperlipidaemia?

A
  • combined hyperlipidaemia
  • hypercholesterolaemia & polygenic hypercholesterolaemia = high chol. content
  • hyperapobetalipoproteinemia = high levels apolipoprotein B
207
Q

what is familial combined hyperlipidaemia?

A
  • high levels LDL cholesterol & TGs
  • young age
  • high risk early coronary heart diseases
208
Q

what are the three arrhythmias that are treated with anti-arrhythmic drugs?

A
  • supraventricular arrhythmias
  • both supraventricular & ventricular arrhythmias
  • ventricular arrhythmias
209
Q

what are the reasons for granulation?

A
  • prevent segregation of constituents
  • improve flow properties
  • improve compaction properties & uniformity
  • reduce toxic dust &caking of hygroscopic materials
  • increase bulk density = reduce storage volume
210
Q

what are the limitations of wet granulation?

A
  • cost = labour, time, equipment, energy & space
  • stability = moisture-sensitive & thermolabile
  • loss of materials
  • multiple processing steps
  • incompatibilities = b.w formulation components
211
Q

what are the steps of wet granulation?

A
  • blend powder & add binder = sucrose/gelatin
  • sieve moist mass
  • dry the moist agglomerates
  • sieve the dried granules = sized granules
212
Q

what are the steps of dry granulation?

A
  • compress blended powder
  • mill the slug/tablet from compression chamber
  • sieve the granules = sized granules
213
Q

what are the limitations of dry granulation?

A
  • high force/pressure involved in compaction
  • greater chances generation dust & environmental contamination

Pharmacy 201 (4 decks)

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