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Pharmacy 201 > RES > Flashcards

RES Flashcards

1
Q

what are the main signs of cystic fibrosis?

A
  • pulmonary disease
  • recurrent lung infections
  • production & accumulation of viscous sputum
  • malabsorption due to pancreatic insufficiency = poor growth/weight gain
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2
Q

what are the aims of treatment for CF?

A
  • prevent & manage lung functions
  • loosen & remove thick, sticky mucus
  • prevent & treat intestinal obstruction
  • provide nutrition & hydration
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3
Q

what are the aims of drug treatment for CF?

A
  • prevent & maintain lung function
  • patients w/ evidence of lung function = frequency of routine reviewed
  • adults review at least 3 months; more frequent immediately after diagnosis
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4
Q

what are the mucolytics used to treat CF?

A

[ dornase alfa ]
- DNA forms polymer & thicken mucus
- Dornase alfa break down DNA
- lower mucus viscosity

[ hypertonic NaCl ]
- disrupt ionic bonds supporting entanglements
- disassociates DNA from mucus proteins & break down clot
- improved access to endogenous proteolytics

[ mannitol dry power for inhalation ]
- hydrate mucus through osmotic mechanisms
- when dornase alfa unsuitable; lung function rapidly decline & other osmotic drugs inappropriate

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5
Q

what is cystic fibrosis?

A
  • inheritable autosomal recessive disease
  • mutation CFTR gene = transport sweat, digestive fluids & mucus
  • ion transport abnormalities dehydrate mucus = pulmonary & GI systems affected
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6
Q

what are some long term issues w/ CF?

A
  • difficulty breathing
  • coughing up sputum
  • poor growth & fatty stool
  • clubbing fingers & toes
  • infertility in males
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7
Q

what body systems are affected by CF?

A
  • sweat gland = elevated Cl- concentration in sweat
  • liver cirrhosis & dysfunction of hormones in pancreas
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8
Q

how does the mutation in CFTR gene affect patient with CF?

A
  • Cl- not transported through channels
  • Cl- levels reduced on epithelial surface = affect mucus consistency
  • Na+/Cl- lack affect H2O retention & HCO3- reduced = acidify layer & more viscous
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9
Q

how is CF diagnosed?

A
  • larger number CF mutations limit utility DNA tests
  • sweat test levels > 60mM in adults
  • nasal transepithelial potential difference = potential more negative
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10
Q

what is required for the management of CF?

A
  • professional diverse team
  • lifestyle & psychological support
  • poly pharmacy & stratification of treatment to disease severity
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11
Q

what are the most common CF lung infections?

A
  • Staphylococcus aureus
  • Haemophilus influenzae
  • Pseudomonas aeruginosa
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12
Q

what is involved in pulmonary mucus clearance?

A
  • airway surface liquid
  • periciliary layer
  • mucus
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13
Q

what is a non-medical intervention for CF?

A

chest physiotherapy

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14
Q

what are some extra drug treatments for CF?

A

[ inhaled bronchodilators ]
- salbutamol & ipratropium
- used for acute relief of obstruction

[ corticosteroids ]
- decrease rate decline lung function
- decrease infection frequency
- unwanted effect long term & inhaled doesn’t improve lung function w/out airway hyper reactivity

[ pancreatic enzyme supplements ]
- protease, lipase & amylase
- inactivated by stomach acid

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15
Q

what are the lungs’ advantages for pulmonary drug delivery?

A
  • massive absorptive surface area & good blood supply
  • increased permeable membrane
  • decreased mucociliary clearance = increased residence time
  • low enzymatic environment
  • rapid onset for local effect
  • low doses required = economical & less SE
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16
Q

what is a non-pressurised MDI and how does it work?

A
  • Respimat = nebuliser & pMDI
  • aerosol cloud released after mechanically actuated
  • drug forced through narrow channels & create must
  • particle generated small & low velocity
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17
Q

what are the advantages of electronic cigarettes?

A
  • disposable & refillable design
  • aerosols decrease number & level of toxicants
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18
Q

what is scintigraphy and it’s advantages?

A
  • radiation-emitting substances to patients = emissions captured by gamma camera & deposition of drug imaged
  • lung scintigraphy = diagnostic tool to evaluate new formulations
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19
Q

what are some general tips for inhalers and spacers?

A
  • turbohaler, Respimat & pMDI = primed before 1st time
  • Respimat = cartridge loaded in device
  • pMDI shaken & DPI no shaken
  • chin up for effectiveness & after use, wipe mouthpiece w/ cloth
  • corticosteroids = rinse mouth w/ water
  • dose counters = check sufficient doses remaining
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20
Q

what are some examples of spacers?

A
  • volumatic
  • aerochamber plus device
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21
Q

what is an example of pMDI?

A

ventolin

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22
Q

what are some example of DPIs?

A
  • accuhaler/easyhaler/turbohaler
  • NEXThaler
  • Ellipta
  • Spiromax
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23
Q

what are some breath-actuated metered dose inhalers?

A
  • easi-breathe
  • autohaler
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24
Q

when should steroid cards be issued?

A
  • MHRA 2006
  • prolonged high doses ICS
  • inhaled corticosteroids & drugs inhibit metabolism = CYP450; HIV protease
  • early recognition & treatment adrenal crisis in adults
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25
Q

what are some diagnostic tests for asthma and COPD?

A

[ fractional exhaled nitric oxide ]
- 40 ppb or more = adults
- 35 ppb or more = children & young

[ obstructive spirometry ]
- FEV1:FVC < 70% or below lower limit normal

[ bronchodilator reversibility test ]
- improvement FEV1 12% or more & volume 200ml or more = adults
- improvement FEV1 12% or more = children & young

[ peak flow variability ]
- over 20%

[ direct bronchial challenge test w/ histamine or metacholine ]
- decrease 20% FEV1 of 8mg/ml or less

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26
Q

what is a cough reflex?

A
  • forceful movement respiratory muscles
  • link afferent sensory stimulus to efferent motor response
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27
Q

what are some causes of cough?

A
  • irritants, smokes, fumes & dusts
  • disease & infections
  • pressure on respiratory tracts
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28
Q

what are the components of the cough reflux?

A
  • cough receptors
  • afferent nerves
  • cough centre in medulla
  • efferent nerves
  • effectors nerves
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29
Q

what are the roles of a cough?

A
  • final pathway mucociliary response
  • defense mechanisms against inhaled particles/noxious substances
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30
Q

what are the phases of a cough?

A

[ irritation ]
- stimulus irritate upper airways

[ inspiration ]
- optimum thoracic gas volume

[ compression ]
- glottis closed; abdominal muscles & thoracic cage actively contract
- increase intrathoracic pressure

[ expulsion ]
- glottis open = increase airflow = explosive decompression

[ relaxation ]
- decrease intrathoracic pressure & expiratory muscles relax
- transient bronchodilation

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31
Q

what are the classifications of cough?

A
  • dry or chesty
  • acute = less 3 weeks
  • subacute = 3-8 weeks
  • chronic = more 8 weeks
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32
Q

what are some chronic cough causes?

A
  • lung conditions
  • upper airway conditions
  • chest cavity conditions
  • digestive causes
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33
Q

how do antitussives work?

A
  • codeine & pholcodine
  • pain relief and act on cough centre & suppress cough in low doses
  • clinical use = opioid analgesics
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34
Q

how do cough drugs work?

A

increase bronchial secretion & decrease viscosity to facilitate removal by cough

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35
Q

what are some types of cough drugs?

A

[ expectorants/secretion enhancers ]
- sodium citrate & potassium iodide

[ mucolytics ]
- acetylcysteine
- actively break disulphide bonds in mucus = thinning

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36
Q

what are the advantages of spacers?

A
  • don’t need coordination between breathing & actuation of pMDI
  • reduces initial droplet velocity & time for propellant evaporate
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37
Q

what are some patients that may require spacers?

A
  • limited dexterity
  • partially-sighted/reduced vision
  • cognitive impairment
  • elderly
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38
Q

what is a breath-actuated pMDI?

A
  • assists coordination of inspiration & actuation of inhaler
  • inspiration trigger drug release
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39
Q

what is a DPI? what are some advantages/disadvantages?

A
  • no propellant = rely patient inspiration carry drug

[ advantages ]
- deliver large doses

[ disadvantages ]
- required insp. flow rate 30-90L/min
- higher upfront cost
- more exposed ambient air = stability issues

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40
Q

how are DPIs formulated?

A
  • drug micronised = smaller 5nm
  • micronised = poor flow properties because static/adhesive
  • mix w/ large carrier particles = lactose adhere micronised
  • uniform filling & improve liberation drug
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41
Q

what are the two types of multi-dose DPIs?

A
  • multiple unit dose device = diskhaler & accuhaler
  • reservoir-based device = turbohaler & clickhaler
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42
Q

how is the drug liberated from a hard capsule DPI?

A
  • drug & carrier loaded in hard-shelled gelatin capsule
  • patient puncture w/ 2 metal needles in device
  • inspiration = rotor rotate
  • turbo vibratory air pattern disrupt powder
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43
Q

what is a nebuliser? what are its advantages & disadvantages?

A
  • large device = aerosol from content unit dose nebules
  • drug inhaled in normal breathing via mask
  • used hospital & domiciliary settings

[ advantage ]
- large volume drug administered

[ disadvantage ]
- not portable size & power requirements

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44
Q

how are nebules formulated?

A
  • drug dissolved normal saline
  • solution = Ventolin
  • suspension = flixotide
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45
Q

how do jet nebulisers work?

A
  • compressed air from cylinder/hospital airline/electrical compressor
  • baffle stop large/non-resp. particles inhaled = recycled
  • compressed air pass through Ventori nozzle
  • decreased pressure draw liquid up from reservoir through feed tube
  • aerosol droplet size & drug delivery determined by compressed gas flow rate
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46
Q

how do ultrasonic nebulisers work?

A
  • energy generate aerosol from vibrating piezoelectric crystal
  • large aerosol droplet emitted from apex
  • smaller droplets in lower areas
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47
Q

how do mesh nebulisers work?

A
  • aerosol generated by vibrating mesh
  • mesh/perforated plate = 7000 holes w/ laser
  • vibrational energy from piezoelectric crystals transfer energy to mesh via transducer

[ advantage ]
- new design = aerosol release w/ patient breath
- reduces drug wastage

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48
Q

what is an arrhythmia?

A
  • abnormal rate or rhythm heartbeat
  • too fast = tachycardia
  • too slow = bradycardia
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49
Q

what are some common arrhythmias?

A
  • ectopic beats
  • atrial fibrillation
  • atrial flutter
  • ventricular tachycardia
  • ventricular fibrillation
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50
Q

what are the 4 types of AF?

A

[ paroxysmal ]
- episodes come and go
- stop in 48 hours without treatment

[ persistent ]
- episode longer 7 days
- less when treated

[ long-standing persistent ]
- continuous AF for year or more

[ permanent ]
- present all the time

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51
Q

what are some symptoms of AF?

A
  • can be asymptomatic; esp. older & suspect if had stroke or TIA
  • palpitations
  • dyspnoea
  • dizziness
  • chest pain/discomfort
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52
Q

what are the management goals of AF?

A
  • establish diagnosis
  • identify & manage underlying causes & triggers
  • control & prevent symptoms = ventricular rate/atrial rhythm
  • prevent stroke
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53
Q

how can AF cause HF and lead to stroke?

A

ventricles work too hard & enlarge

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54
Q

what are the 3 targets of management of AF?

A
  • rate control
  • rhythm control
  • stroke prevention
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55
Q

what medications are used to treat rate control in AF?

A
  • BBs = propranolol; atenolol & bisoprolol
  • rate-limiting CCBs = verapamil & diltiazem
    [ digoxin monotherapy ]
  • only non-paroxysmal & sedentary
  • blurred vision; diarrhoea & conduction disturbances
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56
Q

what is cardioversion and when is it used?

A
  • rhythm control
  • new onset AF within 48 hours present
  • in specialist care
  • pharmacological, electrical (if longer 48 hours) & surgical
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57
Q

what is electrical cardioversion?

A
  • similar external defibrillation
  • patient sedated short time
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58
Q

what is used for pharmacological cardioversion?

A

[ flecainide ]
- IV loaded then oral dosing
- dizziness; dyspnoea & asthenia

[ amiodarone ]
- bradycardia; hyperthyroidism & jaundice

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59
Q

what is surgical cardioversion?

A
  • when medication not tolerated/effective
  • heart area causing abnormal electric discharges destroyed w/ radiofrequency energy
  • if AV node, pacemaker restore sinus rhythm
    = catheter ablation via groin vein/wrist vein
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60
Q

what is Virchow’s Triad?

A
  • changes in vessel wall
  • changes blood constituents
  • changes blood flow pattern
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61
Q

other than virchow’s triad, what else can cause a stroke?

A
  • stagnation in atria
  • incomplete ventricular emptying
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62
Q

what are the 3 ways to stratify risk in AF?

A
  • CHA2DS2-VASc
  • HAS-BLED
  • ORBIT risk score
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63
Q

how is the scoring on CHA2DS2-VASc?

A
  • score >=2 =anticoagulant recommended
  • score 1 & male = consider anticoagulant
  • score 0/1 & female = anticoagulant not recommended
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64
Q

how does HAS-BLED benefit the patient?

A
  • balance risk stroke vs. risk bleeding
  • address reversible risk factors
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65
Q

what are the 2 main classes of anticoagulants?

A

[ direct-acting oral anticoagulants ]
- direct thrombin inhibitor = dabigatran
- direct factor Xa inhibitor = apixaban, edoxaban & rivaroxaban

[ vitamin K antagonists ]
- warfarin & phenindione

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66
Q

what are some points to remember with vitamin K antagonists?

A
  • counselling important
  • closely monitor INR
  • common AE = bleeding
  • effect reversible w/ vitamin K
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67
Q

what monitoring is required for DOACs?

A
  • bloods at least annually
  • 75 years or more/on dabigatran = 6-monthly
  • according to creatinine clearance
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68
Q

how are different levels of creatinine clearance monitored when using DOACs?

A
  • > =60 ml/min = yearly/current condition impacted by renal function
  • 50-59 ml/min = every 5 months
  • 40-49 ml/min = every 4 months
  • 30-39 ml/min = every 3 months
  • 20-29 ml/min = minimum every 2 months
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69
Q

what are the patient counselling points at annual review for DOACs?

A
  • adherence
  • specific dosing advice = dabigatran in packet & rivaroxaban w/ food
  • missed doses
  • monitoring
  • alcohol
  • bleeding & warning card
  • OTC = avoid NSAIDs & St. John’s Wort
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70
Q

what are the fundamentals of pulmonary drug delivery?

A
  • drug physicochemical properties
  • formulation
  • patient
  • delivery system
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71
Q

what is inertial impaction and what does it depend on?

A
  • velocity & mass particles cause impact airway surface in upper airway

[ depends on ]
- particle momentum
- position particle in airstream of parent branch
- angle of bifurcation

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72
Q

what is sedimentation?

A
  • particle suspended gas = subject gravitational force
  • dominant mechanism particles deposit lower/peripheral airway
  • less relevant when particle size less
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73
Q

what is diffusion?

A
  • dominant mechanism particles < 0.5nm
  • smaller particles deposit more via diffusion in peripheral lung & alveolar space
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74
Q

what are some drug delivery devices?

A
  • pMDIs
  • DPIs
  • nebulisers
  • electronic cigarettes
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75
Q

how are medical gases administered?

A
  • in cylinders/generated in situ
  • O2 gases under pressure & flow control w/ regulated tap
  • Continuous Positive Airway Pressure Ventilation (CPAP) = air via mask/hood/nasal canula
  • Ventilator = air via breathing tube
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76
Q

what are pMDIs?

A
  • drug dispersed in liquid propellant = solution (2-phase) /suspension (3-phase)
  • dose = set volume = released actuation of metering valve
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77
Q

what are the 2 types of pMDI filling?

A
  • cold filling
  • pressure filling
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78
Q

how does cold filling for pMDIs work?

A
  • drug, excipients & propellant chilled -60C & added canister
  • further chilled propellant added & canister sealed w/ valve
  • QC = leak tested = H2O bath & weighed
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79
Q

how does pressure filling for pMDIs work?

A
  • drug, excipients & propellant added canister under pressure via valve
  • can add ethanol before valve crimped in place
  • further propellant added under pressure
  • QC = leak tested = H2O bath & weighed
80
Q

are pMDIs interchangeable?

A
  • salbutamol pMDIs largely bioequivalent
  • beclometasone not interchangeable
  • small particles more potent = Qvar>Clenil
81
Q

what are the advantages of pMDIs?

A
  • portable & low cost
  • drug protected from environment in canister
  • multiple dose in 1 device & efficient delivery
  • disposable
82
Q

what are the disadvantages of pMDIs?

A
  • incorrect use by patients
  • inefficient at drug delivery
  • disposable
83
Q

are pMDIs sustainable?

A
  • bulky dosage forms use plastics & aluminium
  • both recyclable but no national recycling schemes
    = salamol given instead of Ventolin
84
Q

what are CFCs and what has replaced them in pMDIs?

A
  • CFCs damages ozone layer
  • replaced by HFAs
85
Q

are HFAs good solvents?

A
  • low relative permittivity values
  • surfactants required as suspending agents/valve lubricants
  • co-solvents = ethanol = aid drug solubility & excipients; but can increase droplet size
86
Q

what is Dispensing Doctors?

A
  • exception to the rules in certain rural areas = controlled localities
  • GPs dispense w/out pharmacist present
  • no prejudice to existing services
87
Q

what are the requirements of a Switzerland & EEA prescription?

A
  • patient DOB and address
  • prescriber full name, address & contact details
  • if can’t confirm registration status; use professional judgement
88
Q

what are private prescriptions?

A
  • outside of the NHS
  • patient charged item cost & markup and fee
  • record sale & supply in POM book
89
Q

what are the requirements of a private prescription?

A
  • patient details & indication
  • medicine details
  • prescriber signature & details
  • prescriber type
90
Q

what is involved in NHS repeat prescriptions?

A
  • authorise prescription w/ RA on it & doctor signature = kept pharmacist & 1st repeat issue
  • valid for 1 year
  • associated RD form
91
Q

what is involved in private repeat prescriptions?

A
  • written/printed statement on prescription
  • 1st dispensing in 6 months; no time limit remaining repeats
  • audit trail if dispense at different pharmacies
92
Q

what are the requirements of school supply?

A
  • school name
  • medicine strength & total quantity needed
  • medicine details & purpose required
  • signature of principal/head teacher
93
Q

what is involved in the supply of naxolone?

A
  • supply by people employed/engaged in provision of recognised drug treatment services
  • Human Medicines (Amendment) (No. 3) Regulations 2015
  • NHS body, local authority, Public Health England & Public Health Agency
  • by appropriately trained staff w/out RP present
94
Q

what is used to make an asthma diagnosis?

A
  • spirometry
  • peak expiratory flow
  • asthma control questionnaire (ACQ)
  • Asthma control test
  • FeNO
  • Eosinophil differential count
  • structured clinical assessment
95
Q

what is the BTS/SIGN adult guidelines?

A
  • monitored initiation low dose ICS
  • regular preventer = ICS
  • initial add-on w/ lose dose ICS = LABA (fixed dose or MART)
  • add controller therapies = increase to medium dose ICS/ + LTRA
  • no response to LABA, consider stopping
96
Q

what is part of a clinical assessment for asthma?

A
  • recurrent episodes of symptoms
  • symptom variability
  • absence of symptoms of alternative diagnosis
  • recorded observation of wheeze
  • personal history of atopy
  • historical record of variable PEF or FEV
97
Q

how is uncontrolled asthma?

A
  • 3 or more days/week w/ symptoms
  • 3 or more days/week w/ required use SABA for symptomatic relief
  • 1 or more nights/week awakening asthma
98
Q

what are some MART examples?

A
  • pMDI = Fostair 100/6 beclometasone/formoterol
    [ DPI ]
  • Symbicort 100/6 or 200/6 budesonide/formoterol
  • Duoresp Spiromax 160/4.5 budesonide/formoterol
99
Q

what are some cautions & counselling for LTRAs?

A
  • risk neuropsychiatric reactions = speech impairment & obsessive-compulsive symptoms
  • avoid pregnancy, unless essential
100
Q

what are some symptoms/SE of using LTRA w/ churg-strauss syndrome?

A
  • eosinophilia
  • vasculitic rash
  • worsening pulmonary symptoms
  • cardiac complications
  • peripheral neuropathy
101
Q

what is some advice for using LABAs?

A
  • add only if regular use ICS fail control asthma
  • not initiate w/ rapidly deteriorating asthma
  • low dose introduce & discontinue w/ no benefit
102
Q

what are some cautions w/ SABAs & LABAs?

A
  • tachycardia
  • prolonged QT & hypotension
  • risk hyperglycaemia & ketoacidosis in diabetes
  • hypokalaemia = potentiated by theophylline, corticosteroids, diuretics & hypoxia
103
Q

what is some monitoring for SABAs & LABAs?

A
  • plasma-potassium conc. in severe asthma
  • blood glucose in diabetes
104
Q

what is some monitoring for ICS?

A
  • weight & height children w/ prolonged treatment monitor annually
  • if growth slowed = refer paediatrician
105
Q

what are some cautions for ICS?

A
  • systemic absorption follow inhaled administration
  • candidiasis
  • paradoxical bronchospasm = use bronchodilator before or ICS discontinued
106
Q

how does ICS work and what can reduce its effectiveness?

A
  • reduce airway inflammation and oedema & secretion mucus into airway
  • current/previous smoking reduce effectiveness ICS = higher dose may need
107
Q

what are the overdose symptoms for theophylline?

A
  • severe vomiting
  • agitation
  • restlessness
  • dilated pupils
  • sinus tachycardia
  • hyperglycaemia
  • convulsions
  • severe hypokalaemia
108
Q

what is theophylline’s drug class?

A

xanthine bronchodilator

109
Q

what is the concentration for which theophylline is aimed?

A

10-20mg/L or 55-110micromol/L

110
Q

when should a sample be taken for someone on theophylline oral?

A

after 4-6 hours

111
Q

when is the plasma concentration of theophylline decreased?

A
  • smoking started
  • alcohol consumption
  • enzyme inducers
112
Q

when is the plasma concentration of theophylline increased?

A
  • HF
  • hepatic impairment
  • viral infection
  • elderly
  • enzyme inhibitors
113
Q

what are theophylline’s cautions?

A
  • cardiac arrhythmias & diseases
  • elderly
  • epilepsy
  • peptic ulcer
  • risk hypokalaemia increase w/ B-2 agonists
114
Q

what is a MART a combination of?

A
  • inhaled steroid & long-acting bronchodilator w/ fast onset of action = formoterol
  • both daily maintenance therapy & symptom relief
115
Q

what are some counselling points for MART?

A
  • total regular dose ICS shouldn’t decrease
  • regular once daily or more rescue doses of combi inhaler = treatment review
  • use separate reliever inhaler = SABA = not required
  • education about spec. issues around management strategy
116
Q

who is MART appropriate for?

A
  • personalised asthma action plan (PAAP)
  • able self-manage & compliant w/ treatment
  • uncontrolled symptoms on maintenance-only treatment w/ ICS/ LABA + SABA as reliever
117
Q

what are the steps of GOLD assessment?

A
  • spirometrically confirmed diagnosis
  • assessment airflow limitation
  • assessment symptoms/risk of exacerbations
118
Q

what are the diagnosis stats for COPD?

A
  • FEV1/ FVC <0.7
  • mMRC 0-1 & ≥ 2
  • number of exacerbations
  • CAT <10 or ≥10
119
Q

what are the GOLD groups and their treatments?

A
  • Group A = bronchodilator
  • Group B = long-acting bronchodilator = LABA or LAMA
  • Group C = LAMA
  • Group D = LAMA / LAMA + LABA / ICS + LABA
  • LAMA & LABA = consider highly symptomatic = CAT>20
  • ICS & LABA = consider if eos ≥ 300
120
Q

what are the fundamentals of COPD?

A
  • offer treatment + support stop smoking
  • offer pneumococcal and influenza vax.
  • offer pulmonary rehab if indicated
  • co-develop personalised self-management plan
  • optimise treatment co-morbidities
121
Q

when should inhaled therapy be started in COPD?

A
  • interventions offered if appropriate
  • inhaled therapy still need relieve breathlessness & exercise limitation
  • pt trained use inhalers & demonstrate satisfactory technique
122
Q

what are some asthmatic features?

A
  • previous secure diagnosis asthma/atopy
  • high blood eos count
  • variation FEV1 over time (at least 400ml)
  • diurnal variation PEF (at least 20%)
123
Q

what are the steps in the NICE guidelines for COPD?

A
  • confirmed diagnosis COPD
  • fundamentals COPD
  • offer SABA or SAMA
  • depend on whether asthmatic features or not
  • if diurnal symptoms affect QoL/1 severe or 2 moderate exacerbations in 1 year = LABA+LAMA+ICS
124
Q

what is given for asthmatic and non-asthmatic features in COPD exacerbations?

A
  • asthmatic = LABA + ICS
  • non-asthmatic = LABA + LAMA
125
Q

what are some inhaled antimuscarinics?

A
  • SAMA ⇒ ipratropium bromide
  • LAMA ⇒ tiotropium, umeclidinium & glycopyrronium
126
Q

what are some cautions for inhaled antimuscarinics?

A
  • bladder outflow obstruction
  • paradoxical bronchospasm
  • prostatic hyperplasia
  • angle-closure glaucoma
  • CF
127
Q

what are some side effects for inhaled antimuscarinics?

A
  • constipation
  • arrhythmias
  • cough
  • dizziness
  • dry mouth
  • headache
  • nausea
  • CI pts hypersensitivity to atropine
128
Q

what are the symptoms of a COPD exacerbation?

A
  • increased dyspnea
  • increase sputum volume
  • increase sputum purulence
129
Q

what is the treatment for COPD exacerbations?

A
  • SAMA/SABA at high dose thru nebuliser
  • hydrocortisone = severe life-threatening asthma
  • short course prednisolone + other therapy
  • antibiotics if signs infections, immunocompromised & co-morbidities
130
Q

what is the O2 aim for COPD patients?

A
  • 94-98%
  • 88-92% for pts risk of hypercapnic resp. failure
131
Q

what are the 3 steps of exacerbation prevention for COPD?

A
  • pulmonary rehab
  • education & self-management
  • integrated care program
132
Q

what are the advantages of pulmonary rehab?

A
  • improve dyspnea, health status & exercise tolerance
  • reduce hospitalisation w/ pt recent exacerbation
  • reduce symptoms anxiety & depression
133
Q

what is the dyspnea pathway for GOLD COPD?

A
  • LABA or LAMA
  • LABA & LAMA or LABA & ICS
  • LABA & LAMA & ICS
134
Q

what are the therapeutic goals of asthma?

A
  • minimal symptoms day & night
  • minimal need for reliever meds
  • no exacerbations/ limitation of activity
  • normal lung function
135
Q

what are the 2 types of drug treatments for asthma and their functions?

A
  • reliever = bronchodilators = open airways of patients suffering asthma attack
  • preventer = corticosteroids = intervene in remodelling process
136
Q

what is late phase bronchoconstriction?

A
  • continuation of inflammatory process
  • oedema more prominent
  • sensory nerve fibres release inflammatory agents & cause bronchoconstriction
  • increased parasympathetic activation ACh and M3 receptors = bronchoconstriction
137
Q

what are the steps of the early phase bronchoconstriction in asthma?

A
  • bronchoconstriction
  • mucous plugging and hyperinflation
  • vasodilation and increased permeability
138
Q

what does vasodilation & increased permeability cause in asthma?

A

inflammation cause swelling tissue due to oedema

139
Q

what is a summary of an asthma attack?

A
  • mast cell activation/ degranulation
  • immediate inflammatory responses
  • late inflammatory responses
  • inflammation-induced airway remodelling
140
Q

what are the 2 phases of an asthma attack?

A
  • early phase
  • late phase
141
Q

what are the steps of the early phase of asthma?

A
  • increase in resistance to airflow
  • peaks 30-60 min after allergen exposure & subsides 30-90 min later
  • immediate response to release inflammatory mediators from mast cells
142
Q

what are the steps of late phase in asthma?

A
  • can occur long time after allergen exposure
  • +6 hours & night-time asthma
  • driven by continuation of inflammation characterised by influx eosinophils into the lungs
143
Q

what is involved in bronchoconstriction in asthma?

A
  • increase mucous; decreases airway diameter
  • air trapping = hyperinflation
  • smooth muscle contraction narrows airway
  • narrow airway makes harder to breath = increased resistance
144
Q

what is involved in mucus plugging and hyperinflation in asthma?

A
  • inspiration air allowed into alveolus
  • in exhalation, mucous plug pivot = impeding exhalation air flow
  • increase volume alveoli = hyperinflation
  • turbulent airflow around blockage = characteristic wheezing
145
Q

what is the difference between specific & non-specific trigger factors in asthma?

A
  • specific = extrinsic asthma = allergens
  • non-specific = intrinsic asthma = all the rest
146
Q

what are the 3 main factors of asthma?

A
  • airway constriction
  • airway hypersensitivity and responsiveness
  • mucous hyper-secretion
147
Q

how is acute severe asthma different from regular asthma?

A
  • not easily reversed
  • causes hypoxaemia
  • may require hospital treatment
148
Q

what are some trigger factors for asthma?

A
  • allergens = dust mite, pollen, moulds, animals
  • chemicals = paints, hair sprays
  • drugs = aspirin, BB, NSAIDs
  • foods = colourings, nuts, preservatives
  • environmental chemicals = cigarette smoke, wood dust
  • infections
149
Q

what are the symptoms of asthma?

A
  • dyspnoea
  • wheezing during exhalation
  • tight chest/ pain
  • chronic and unproductive cough
  • night-time wakening with breathlessness
  • significant diurnal variability
150
Q

what is asthma?

A
  • obstructive disease= chronic inflammatory disorder of airways
  • resistance to airflow through airways during inspiration and expiration & airflow limitation is widespread
  • variable and reversible
  • degree depends on airway diameter and laminar/turbulent flow
151
Q

what is atopy and how is it used to diagnose for asthma?

A
  • propensity to develop antibodies to common antigens
  • associated with susceptibility develop asthma, allergic rhinitis and eczema
  • early onset asthma ⇒ 98% +ve skin tests; likely to have eczema PHx or asthma FHx
  • late onset asthma ⇒ 76% +ve skin tests
152
Q

what can cause asthma?

A
  • host factors and environmental exposures
  • genetic factors = cytokine response profiles
  • environment = allergens, pollutants, infection & stress
  • with age = altered innate and adaptive immune responses
  • genetic predisposition/intrinsic vulnerability = atopy/allergy infection
153
Q

what are the steps of first exposure in asthma?

A
  • antigen presented on dendritic cells = activates T-helper cell
  • cells secrete Th2 cytokines = activates B-cell
    = plasma cell secretes antibodies Ige = driven by Th2 cytokines
  • memory B-cells and T-cells formed
  • Ige binds to Fc receptor on mast cells = release mediators
  • Fc tail region binds to mast cells in lung w/ Ige on surface
154
Q

what is a pharmacophore?

A
  • section of drug structure responsible for drug activity
  • binds to receptor
155
Q

what are hydrophobicity & lipophilicity?

A
  • hydrophobicity = tendency non-polar groups aggregate to minimise exposition to surrounding polar solvent = water
  • lipophilicity = affinity of a molecule for non-polar solvent in a biphasic system = polar and non-polar
156
Q

what are groups that increase hydrophilicity?

A
  • carboxylic acid
  • basic
  • hydroxy
157
Q

what are groups that increase lipophilicity?

A
  • methylene
  • ring system = hydrophobicity
  • halogen
  • methyl
158
Q

what are the mechanisms of action of methylxanthines?

A
  • reverse resistance to corticosteroids
  • PDE4 inhibition = maintain high cAMP levels
  • MLCK inactivated
  • bronchial smooth muscle relaxation
159
Q

do SAMAs and LAMAs affect specific muscarinic receptor subtypes?

A
  • SAMAs = don’t discriminate
  • LAMAs = greater selectivity for M3 receptor
160
Q

what are some mechanisms of action for corticosteroids?

A
  • inhibit PGE2 & PGI2
  • inhibit leukotrienes
  • upregulate B2 receptors
161
Q

what is chirality?

A
  • non-superimposable mirror images
  • chiral center = cause = atom bonded to 4 diff. groups
  • physical properties all the same, but chemical not
162
Q

what is polarimetry?

A

used to measure observed specific rotation of chiral molecules

163
Q

how are enantiomers separated via chromatography?

A
  • dissolve mixture in solvent
  • pass solution through packed column
  • use chiral material to absorb compound
  • enantiomers = diff. affinity for chiral material
  • one emerge before other
164
Q

why bother separating chiral drugs?

A
  • receptors are chiral
  • some enantiomers have therapeutic effect or better effect than the other
165
Q

how else can chiral drugs be separated and why?

A
  • separation = expensive & wasteful
  • use chiral catalysis instead
166
Q

describe the innervation of the lungs, using the control of bronchioles by ANS.

A
  • PNS activation trigger bronchoconstriction
  • Predominantly VAGAL nerve
  • SNS activation trigger bronchodilation = increased lung capacity & preparation for exercise
167
Q

describe smooth muscle contraction.

A
  • Ca2+ ions increase & bind to calmodulin
  • Ca2+/calmodulin complex activate myosin light chain kinase
  • MLCK phosphorylates myosin
  • myosin heads bind to actin
  • Fibres contract
168
Q

what effect do M3 receptors produce?

A
  • mostly stimulatory
  • glands = secretion
  • smooth muscle airway = contraction
169
Q

what are some neurotransmitters released due to excitatory & inhibitory non-adrenergic non-cholinergic nerves?

A
  • substance P = constriction
  • nitric oxide = dilation
170
Q

what are other mediators can be found in bronchial smooth muscle?

A

histamine & leukotrienes = constriction

171
Q

what are some anti-inflammatory classes?

A
  • glucocorticoids
  • cromoglicate & nedocromil
  • anti-IgE
172
Q

what is the mechanism for B2-receptor agonists?

A
  • Gs activate adenylyl cyclase
  • increase intracellular levels cAMP
  • cAMP activate protein kinase A
  • PKA phosphorylate = dilation & reduction intracellular Ca2+
173
Q

how does PKA cause bronchodilation?

A

[ MLCK activity reduced ]
- myosin not phosphorylated
- Less smooth muscle contraction

[ activation of K+ channels ]
- hyperpolarisation
- reduces numbers open Ca2+ channels
- reduces entry rate extracellular Ca2+
- less intracellular Ca2+ = less contraction

174
Q

what are some unwanted effects for B2 receptor agonists?

A
  • systemic = tremor
  • high doses = hypokalaemia & tachycardia
  • other = headache, peripheral vasodilation & muscle cramps
175
Q

what are other mechanisms for xanthines?

A
  • adenosine receptor antagonism = A1 & A2 stim. = bronchoconstriction asthmatics
  • anti-inflammatory effect = via high cAMP
  • CNS stimulation = stim. respiratory control centre
176
Q

what are some unwanted effects for xanthines?

A
  • nervousness & insomnia
  • seizures & cardiac dysrhythmia
  • drug interaction CYP 450 inhibitors/inducers
177
Q

what receptor do LTRAs act on?

A

CysLT1 receptor in respiratory mucosa

178
Q

what is the mechanism of action for leukotrienes?

A
  • synthesised from arachidonic acid via 5-lipoxygenase pathway & bind receptors on target
    tissues
  • formed in mast cells and leukocytes
  • inflammatory response
    [ activation cysteinyl leukotriene receptor ]
  • leukocyte recruitment
  • mucus secretion
  • vascular permeability
  • smooth muscle proliferation
179
Q

what is the mechanisms of LTRAs?

A
  • prevents bronchiolar contraction mediated by LTs
  • inhibit early & late phase responses to irritants
  • generally taken orally with inhaled corticosteroid
  • few side effects & not used widely
180
Q

what are phosphodiesterase type 4 inhibitors and their mechanism of action?

A
  • roflumilast
  • inhibition of PDE = cAMP accumulation
  • PDE isozyme 4 = airways smooth muscle & inflammatory cells
181
Q

how do glucocorticoids work?

A
  • prevent progression of chronic asthma
  • effective in acute severe asthma
  • add-on therapy in asthma when
    bronchodilator is used more than once daily
182
Q

what is caused by an inhibitory glucocorticoid response element?

A
  • pro-inflammatory gene products
  • COX-2 & iNOS
183
Q

what is caused by a stimulatory glucocorticoid response element?

A
  • anti-inflammatory gene products
  • IL-10
184
Q

what are some unwanted effects?

A
  • uncommon with inhaled
  • oropharyngeal candidiasis =suppress T-lymphocytes important against fungal infection
  • poor absorption from GI tract
  • regular high doses = adrenal suppression
185
Q

what is an immunotherapy?

A
  • omalizumab
  • anti-IgE antibody
  • risk of anaphylaxis with injection
  • very expensive
186
Q

what are mast cell stabilisers?

A
  • chromoglicate and neodocromil
  • off-label use in childhood asthma
    [ weak anti-inflammatory effects ]
  • reduce immediate & late-phase responses
  • reduce bronchial hyper-reactivity
187
Q

what are the 2 therapeutic effects of glucocorticoids?

A
  • immunosuppression
  • anti-inflammatory
188
Q

how do glucocorticoid suppress the immune system?

A
  • IL-10 decreases cytokine formation
  • decreases recruitment & activation of inflammatory T cells
189
Q

how are glucocorticoids anti-inflammatory?

A

[ induces lipocortin-1 synthesis ]
- inhibits phospholipase A2
- decreased inflammatory mediators = prostaglandins & eicosanoids

[ suppress COX-2 induction ]
- reduce inflammatory prostanoid production
– reduce severity of early phase response and prevent late phase response

190
Q

what is the mechanism of COPD?

A
  • toxins stimulate macrophages & epithelial cells
    [ macrophage ]
  • secrete cytokines = attract immune cells to lungs & activate neutrophils and macrophages
  • neutrophils release protease = break down elastin in alveolar wall

[ epithelial cells ]
- toxins stimulate fibrosis
- fibroblasts grow in smooth muscle cells
- lead scarring & thickening

191
Q

what are Patient Group Directions?

A
  • name prescriber
  • name of condition
  • specific group patient & specific label
192
Q

what are Patient Specific Directions?

A
  • name patient & identifiers
  • med details
  • route administration
  • date of treatment/number doses
193
Q

what are the wholesale license requirements?

A
  • wholesaler license from WDA
  • comply good distribution standards
  • responsible person
194
Q

what are written requisitions?

A
  • not wholesale distribution
  • small quantity meds & occasional basis
  • not for profit basis
  • not for onward wholesale distribution
195
Q

what are written requisitions requirements?

A
  • formulation, name, quantity drug
  • name & address of person
  • signature prescriber & date
196
Q

what are the requirements of emergency supply from a prescriber?

A
  • relevant prescriber
  • within 72 hours
  • emergency
  • record kept
  • correct labelled & directions

Pharmacy 201 (4 decks)

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