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mpharm year 3 sem 1 > MP321 week 3 > Flashcards

MP321 week 3 Flashcards

1
Q

HIV viral replication steps

A

1- fusion of HIV to the host cell surface
2- HIV RNA reverse transcriptase , integrase and other viral proteins enter the host cell
3- viral DNA is formed by reverse transcription
4- viral DNA is transported across the nucleus and integrates into the host DNA
5- new viral RNA is used as genomic RNA and to make viral proteins
6- new viral RNA and proteins move to the cell surface and a new, immature, HIV forms
7- the virus matures by protease releasing individual HIV proteins

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2
Q

key HIV enzymes

A

protease
reverse transcriptase
integrase
inhibit these and stop HIV (viral) replication

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3
Q

define NRTIs

A

nucleoside reverse transcriptase inhibitors

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4
Q

how do NRTIs work

A

mimic the natural nucleosides that are incorporated into the double helix chain formation of DNA-RNA and DNA

NRTI prodrug and activated only viral kinase

target polymerase during transcription

prodrugs metabolised to give non-functional nucleosides

when NRTIs are incorporated into growing chain it causes chain termination

no more HIV can be made and CD4 cells not further compromised

to incorporate the nucleoside into the chain it needs to be converted to a nucleotide

the hydroxyl group enables the molecule to be seen and incorporated into the chain, the changes from hydroxyl to N3 in structure leads to chain termination

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5
Q

define prodrug

A

a biologically inactive compound which can be metabolized in the body to produce a drug

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6
Q

what is remdesivir used to treat

A

acute, severe covid-19, works differently to other NRTIs

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7
Q

chemistry of remdesivir

A

3’ hydroxyl group present - so a nonobligate chain terminator
although theoretically may bond to another nucleoside, it does not
note how others have this functional group removed to be active
it still works because it has a bulky group which hides and blocks the hydroxyl group
adenosine like most involved in base pairing with uracil
as this is very similar to how adenosine makes base pairs, this possibly is why it gets incorporated by viral polymerase - enables transcriptase to see and recognise

as it has a carbon - carbon bond it is more stable against nucleases as not a semi-aminal bond

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8
Q

define NNRTIs

A

non-nucleoside reverse transcriptase inhibitors

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9
Q

NNRTIs

A

Non-nucleoside reverse transcriptase inhibitors
Known as allosteric inhibitors (holy grail of inhibitor type)
Bind to a lipophilic pocket at the base of the “thumb” area of the RT enzyme
Conformationally prevents the enzyme from allowing the single strand of RNA to be transcribed
Prevents replication and protects CD4 cells
useful as they don’t block natural active site
targets polymerase during transcription as allosteric inhibitors

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10
Q

protease inhibitors (PI)

A

large proteins made following transcription and translation
proteases are inhibited by other small molecules
processed into smaller proteins to make virion
protease cleaves the larger proteins
hydrolysis of the protein peptide bond
HIV protease is a much smaller enzyme than the equivalent host aspartate proteases
Cleaves substrates N-terminal to proline residues unlike mammalian proteases (selectivity)
Tyr-Pro was identified as a cleavage site for the HIV protease
Rationale for inhibitor design was based on Phe-Pro or Tyr-Pro motif
mimic substrate with non hydrolysable functionality

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11
Q

hydrolysis of amide bond

A

split into amine and carboxylic acid and get rid of water

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12
Q

how does saquinavir work

A

when it is in the active site it won’t get cleaved and prevents the natural substrate binding, need to make the drug more favourable to get into site first

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13
Q

name 5 properties an ideal anti-microbial formulation should be

A
  • effective against targeted infection
  • able to reach (specifically) site of action
  • rapid onset
  • controllable duration
  • free of side effects
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14
Q

name 2 things that will influence the route of administration and dosage form for antimicrobials

A
  • site of infection
    -severity of infection
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15
Q

topical administration- used for ?

A

mild infection

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16
Q

IV/IM administration- used for?

A

severe infections

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17
Q

name one advantage of topical administration onto the skin

A

local action- drug retained in the skin

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18
Q

to be suitable for topical drug delivery the drug should be (3)

A
  • low MW (less than 500 Da)
  • moderately lipophilic (log P between 1 and 4)
  • effective at low dose (less than 10mg/day)
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19
Q

name the three formulation types for skin

A
  • liquid
  • semi-solid
  • solid
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20
Q

name the 2 principles of formulation for the skin

A
  • formulation should be stable but allowing drug to be released after application
  • vehicle should allow some solubility of the drug but should not retain the drug by being a very good solvent
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21
Q

name one advantage and 2 disadvantages of a liquid formulation for the skin

A

ad- rapid short term input of permeant into the skin
dis- low drug delivery
dis- treatment of surface infection only

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22
Q

name 2 advantages and one disadvantage of ointments

A

ad- increase of transdermal drug flux (the number of molecules moving through a given cross- sectional area during a given period of time)

ad- prolonged drug delivery

dis- messy to use due to greasy nature

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23
Q

name 2 advantages and one disadvantage of creams

A

ad- easier to apply than ointments
ad- can be washed off skin surface
dis- less occlusive than ointments, therefore less beneficial in dry skin conditions

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24
Q

name an example of a solid formulation for skin application

A

spray powder

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25
Q

name one of the challenges with topical application to the nail

A

nail has a hard keratinised structure- need keratolytic components to increase diffusion of drug through nail plate

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26
Q

name one important must have property of topical formulae for the eyes

A

formulation must be sterile

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27
Q

one average what is the range (%) of drug in topical formulations that reaches the aqueous humour in the eye

A

1-5%

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28
Q

name 2 advantages and one disadvantage of eye drops

A

ad- easy to administer
ad- homogenous (better dose uniformity)

dis- rapidly drained out of the eye (90% in first 30s)

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29
Q

name 3 advantages and 3 disadvantages of eye ointment formulations

A

ad- reduced drug drainage caused by tear flow
ad- sustained drug release (2-4h)
ad- incorporation of drugs with poor aqueous solubility

dis- more difficult to administer than drops
dis- more variation in dosing
dis- blurs the vision

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30
Q

name 2 advantages of ear drop formulations

A

ad- easy to administer
ad- dose uniformity

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31
Q

name 2 considerations for topical applications for the nose

A

-need of increasing nasal residence time (bioadhesion, increased formulation viscosity
-mucocilliary clearance

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32
Q

define mucocilliary clearance

A

removal of the drug from the nasal cavity

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33
Q

name 4 oropharyngeal formulations

A

-solutions
-gels
-suspensions
-mucoadhesive buccal tablets

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34
Q

name 4 vaginal formulations

A

gels
creams
pessaries
ovules

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35
Q

define pessary

A

vaginal suppository- solid, single-dose formulations of ovoid shape

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36
Q

define ovules

A

vaginal capsules, shell pessaries- solid, single dose formulations similar to oral soft capsules but shape is often elongated and larger

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37
Q

name 2 advantages and 1 disadvatange of topical formulations for the vagina

A

ad- treatment of local infections with a much lower dose than with oral administration
ad- no need of absorption of the drugs for local action

dis- release of the drugs influenced by varying volumes of vaginal fluid

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38
Q

oral administration types (2)

A

solid
liquid

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39
Q

parenteral administration types (2)

A

injections and infusions
liposomes

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40
Q

name one advantage and one disadvantage of oral administration (general)

A

ad- the simplest, most convenient and safest means of drug administration
dis- possibility of irregular absorption of certain drugs

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41
Q

name 4 advantages and 2 disadvantages of tablet formualtions

A

ad- accurate dosing
ad-convenient to handle and carry
ad- easy to take
ad- controlled release of the drug

dis- poor bioavailability of some drugs
dis- local irritant effects to GI mucosa

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42
Q

name 3 advantages and 3 disadvantages of capsule formulations

A

ad- accurate dosing
ad- drug release faster than tablets
ad- shell masks taste of unpleasant drugs

dis- bulky materials can result in a large capsule
dis- susceptible to moisture
dis- not suitable for drugs that are inactivated in the stomach

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43
Q

name 2 advantages and 2 disadvantages of powder formulations

A

ad- reconstituted just before use to avoid chemical degredation
ad- fast drug release compared to tablets and capsules

dis- not suitable for drugs that are inactivated in the stomach
dis- less convenient to carry and self-administer

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44
Q

name 2 advantages and 1 disadvantage of suspensions

A

ad- drug absorption fast than tablets or capsules
ad- convenient when drug is not soluble in water and when non-aqueous solvent cannot be used

dis- risk of sedimentation

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45
Q

can a suspension with caking be redispersed ?

A

no

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46
Q

can a suspension with settling at the bottom be redispersed

A

yes

47
Q

name 2 advantages and 2 disadvantages of syrup formulations

A

ad- drug already dissolved
ad- easy to a just dose for Childs weight

dis- risk of deterioration fast than solid dosage forms
dis- inaccuracy with patients measuring doses

48
Q

name 2 advantages and 2 disadvantages of suppositories

A

ad- good route when vomiting
ad- indicated for drugs inactivated in the liver after oral administration

dis- patient acceptability (cultural influence)
dis- irregular drug absorption

49
Q

name 2 advantages and 2 disadvantages of suppositories

A

ad- good route when vomiting
ad- indicated for drugs inactivated in the liver after oral administration

dis- patient acceptability (cultural influence)
dis- irregular drug absorption

50
Q

principles of parenteral administration

A

Administration by injection
- Intramuscular and intravenous administrations of anti-microbials (only solutions injected IV !)
- All parenteral products must be sterile
- Preferred route when rapid absorption is essential (emergency, unconscious patients)
- Generally sterile solutions or suspensions of drugs in water

51
Q

difference between injections and infusions

A
  • Injections
    = sterile solutions, emulsions or suspensions, in water or non-aqueous liquid
  • Injected in less than 15 min
  • Infusions
  • Aqueous solutions
  • Large volumes: 100 ml -1000 ml
  • Injected in more than 15 min
52
Q

depot parenteral administration

A
  • Depot preparation
  • Dispersion of the drug in an oily vehicle
    Slow release of the drug
  • IM injection deep into skeletal muscles
  • Viscous formulation, large volume (5 mL maximum) injected
    Need to be injected in large muscles to decrease pain and swelling
  • Slow release of the antibiotic for weeks
53
Q

name one advantage and one disadvantage of depot injection

A

ad- long lasting effects- 2-4 weeks

dis- negative patient acceptance- very painful

54
Q

what are liposomes

A

spherical vesicles in which a lipid bilayer membrane delimitates a central aqueous compartment

can carry hydrophilic and lipophilic drugs

liposomes form when the phospholipids are exposed to an aqueous environment

55
Q

downfall of fungizone

A

not specific - releases drug too quickly which is toxic on mammalian cells

can cause renal toxicity, haematological toxicity and cardiovascular toxicity

56
Q

name the 2 branches of antibiotic resistance

A

intrinsic and acquired

57
Q

define intrinsic antibiotic resistance

A

nothing we can do about it- natural

58
Q

name the 2 branches of resistance within acquired resistance

A

horizontal and vertical transfer

59
Q

how many cytoplasmic membranes do gram negative bacteria have

A

2

60
Q

how many cytoplasmic membranes do gram positive bacteria have

A

1

61
Q

can vancomycin be used against gram negative bacteria ?

A

no- it is too big to fit through porins in the membrane

62
Q

can vancomycin be used against gram positive bacteria?

A

yes it works well on these but is only used as a last resort

63
Q

explain why vancomycin cannot be used on gram negative bacteria

A

vancomycin is very large and very hydrophilic (due to sugars, OH and carbonyl groups)
even though porins let through hydrophilic molecules - only small ones this is too big to fit

all gram negative bacteria are intrinsically resistant to vancomycin

64
Q

explain acquired resistance - vertical transfer

A

bacteria have small genetic mutations
these are passed from parent cell to daughter cell- this is also true for mutations that make then resistant to antibiotics
because bacteria divide and multiply so quickly these are passed down many generations very quickly

natural selection also plays a part here- only bacteria resistant to the antibiotic survive to pass on their genetic material

65
Q

explain acquired resistance- horizontal transfer

A

this is where genetic material is transferred between bacteria of the same generation
it can even be transferred between bacterial species

66
Q

name and explain the three possible ways of horizontal transfer

A

conjugation
- close contact
-facilitated by pili
- genetic material transferred from one plasmid to another

transduction
-done by a virus
-virus incorporates genetic material from bacteria into its own, then leaves that bacterium and enters a new cell- this infects the new bacteria with the old bacterias genetic information

transformation
-bacteria die, then through lysis cell opens up and genetic information is then loose, other near by bacteria can then pick this up

67
Q

what do efflux pumps do

A

efflux pumps are proteins synthesised by bacteria
these want to eject anything that goes into the cell
antibiotics are ejected out of the cell by these profile pumps
can target these pumps by using an inhibitor although there is nothing on the market for this yet

68
Q

AMR- how does it translate

A

efflux pumps

antibiotic altering enzyme

change in structure of porins
- some small molecules which normally work through porins on gram negative no longer work

change in ribosomes
- if ribosomes are changed even 1 or 2 amino acids, the antibiotic no longer works

penicilli binding protein

69
Q

how does antibiotic altering enzyme work

A

antibiotic is changed (not degraded) functionalities change and it no longer functions in the same way

70
Q

why is AMR a global health issue

A
  • antimicrobial misuse/ over use leads to a high AMR
  • resistant microbes increase severity and duration of infection (high costs)
  • rapid spread (ease of transfer between species)
    -decline in antibiotic research
71
Q

what percentage of S.aureus roughly are now resistant to benzylpenicilin

A

90%

72
Q

what is MRSA

A

methicillin resistance to staphylococcus aureus

methicillin-type drugs (like flucloxacillin) developed target B-lactasmase resistant bacteria

but MRSA can produce a new penicillin binding protein that is not inhibited by flucloxacillin

73
Q

what do we use to treat MRSA

A

vancomycin

74
Q

B-lactamases-producing gram negative bacteria

A

Extended Spectrum Beta Lactamases degrade penicillins (except temocillin) + cephalosporins + monobactams
Metallo-b-lactamase (NDM 1) degrades penicillins + cephalosporins + carbapenems
Metallo-b-lactamase (KPC) degrades penicillins + cephalosporins + monobactams +carbapenems
Some metallo-b-lactamases are neither inhibited by clavulanic acid nor tazobactam

75
Q

how can we tackle AMR

A

-Use antibiotics in the right way (right drug/right dose/right time/right duration. As prescribed and full course completion
-Don’t keep/share antibiotics
-Never use antibiotics for viral sore throats
-Select most appropriate antibiotic (narrow vs broad-spectrum)
-Reserve highly effective antibiotics for severe infections
-Provide appropriate advice on management of ATB use (e.g. AMR clinical surveillance)
-Develop local antimicrobial guidelines/policies (e.g. SAPG & antimicrobials pharmacists) to encourage wise/prudent use of antibiotics
-Prevent transmission (infection control)
-Develop quicker diagnostics
-Support drug discovery efforts
-Develop further education/training
-Raise awareness
-Be PROACTIVE

76
Q

define clinical governance

A

a framework which the NHS have in place for improving the quality of their services and safeguarding high standard of care

77
Q

name the three components of the healthcare quality strategy for Scotland

A

person-centred
clinically effective
safe

78
Q

name the four components of the medication process

A

prescribing
dispensing/ preparation
administration
monitoring

79
Q

name some ways to create a safe and reliable system

A

simplify
standardise
use protocols and checklists
access to information at point of need
effective communication

80
Q

what kind of molecules can liposomes carry

A

hydrophilic and lipophilic

81
Q

how do liposomes form

A

when phospholipids are exposed to a aqueous environment

82
Q

which of fungizone and ambizome are specific

A

ambizome

83
Q

what is the main barrier to topical application to the skin

A

stratum corneum

84
Q

types of patients at higher risk of infection

A
  • immune compromised (drug or disease)
  • patients in intensive care or post op
    -malnourished
  • patient with cancer(chemo drugs)
    -diabetics
    -elderly or infirm
    -infants and neonates
85
Q

appropriate use of antibiotics

A

Correct diagnosis
Known or presumed site of infection
Likely causative organism
Antibiotic culture & sensitivity
May take 2 – 3 days to get this
Local variations in sensitivity
Patient factors
Site and severity
SIRS, MEWS, SEWS
Route of administration
Serious infection cannot wait for culture and sensitivity results
Antibiotic sensitivity is different in different areas ie what works in Edinburgh may not work in glasgow

86
Q

selection and use of antibiotics

A

Pharmaceutical
Clinical efficacy
Route of administration
Oral / IV / IM / topical / inhaled
Absorption, distribution, metabolism, excretion (ADME)
Toxicity
Knowledge of drug properties
Drug interactions
With other treatments or with foods / fluids
Cost of treatment
oral easiest most common
IV reliable- 100% bioavailability, however breaching skin, this poses its own risks
IM- less predictable, may not work
Topical- minor- not systemic infection, hard to reach high enough concentration to kill microbe
ADME- important for antimicrobials too
Tetracycline- cant have with milk- interactions

87
Q

pharmaceutical assessment (antibiotics)

A

Check patient factors
Contraindications
Interactions
Medicines, food, fluids
Allergies
Renal function
Hepatic function
Double check any other meds- OTC, prescription, herbal etc
Allergies- lactose intolerance,
Excretion- liver, kidney function

88
Q

choice of route for antibiotics

A

oral administration with adequate doses is preferred if possible
topical should be avoided where suitable oral alternatives- exceptions- cold sores, athletes foot etc
Intravenous therapy
Required for
Clinical symptoms / signs of infection and deteriorating clinical condition; febrile with neutropenia / immunosuppression; meningitis / CNS infection; infective endocarditis; bronchiectasis; bone / joint infection; deep abscess; cystic fibrosis; Staphylococcus aureus bacteraemia; skin and soft tissue infection; IV therapy if sepsis or 2 or more of heat, erythema or induration / swelling; oral route compromised - vomiting, nil-by-mouth, reduced gastrointestinal absorption; mechanical swallowing disorder; unconscious; no oral formulation available; initial therapy for biliary sepsis / intra-abdominal infection.
Use until there is clinical control of the infection
Indicators of infection returning to reference range
IM is less reliable than IV

89
Q

IV to oral switch therapy

A

In patients who have been on IV for 24 – 48 hours and who have
Settling temperature
Falling indicators of infection
Able to take oral therapy
Oral therapy available
review patient after 24 hours
If they are improving or now able(ie stopped vomiting, feeding tube removed etc)- switch to oral

90
Q

general penicillin dose

A

500mg-1g four times daily

91
Q

general gentamicin dose

A

5-7mg per kg once daily

92
Q

management of infection

A

Suggested empirical therapy
Should be modified based on
Patient factors
Results of culture & sensitivity (if taken)
Patient response to therapy
Therapeutic drug monitoring

93
Q

pharyngitis

A

upper respiratory tract infection
majority viral – no antibiotic or antiviral recommended
<20% bacterial
Streptococcus pyogenes
Narrow spectrum penicillin
Macrolide

94
Q

otitis media

A

upper respiratory tract infection
Usually viral or self limiting
Haemophilus influenzae
Penicillin
Macrolide
- delayed prescribing to see cultures

95
Q

exacerbation of COPD

A

lower respiratory tract infection
Diagnostic criteria
Increased wheeze, increased shortness of breath, increased sputum volume and purulence
Strep pneumoniae
Haemophilus influenzae
Moraxella catarrhalis
Penicillin
Tetracycline
Macrolide
IV therapy if severe infection
Patient factors
Possibility of a recurrent infection due to underlying condition
Previous therapy likely to be effective
Route of therapy – orally normally
Patient age – likely to be older: has ADME been affected
Other diseases – possibility of drug interactions

96
Q

what is the minimum age for tetracyclines

A

12

97
Q

name one common interactant of tetracyclines

A

milk

98
Q

community acquired pneumonia (CAP)

A

lower respiratory tract infection
Strep pneumoniae
Haemophillus influenzae

Non-severe CAP (C(U)RB-65 score 0 or 1)
Penicillin such as amoxicillin
tetracycline
macrolide
Moderate CAP (C(U)RB-65 score = 2 and no sepsis syndrome)
Ask about foreign travel
Possibility of Legionella (especially if the patient is confused)
Penicillin such as amoxicillin and either
Tetracycline or macrolide
Still water or showers that haven’t been used for a while - legionella is they are confused- need to use macrolide best for legionella infections

99
Q

severe community acquired pneumonia

A

lower respiratory tract infections
Severe Community Acquired Pneumonia (CURB-65 > 3 or any C(U)RB-65 score and sepsis syndrome)
Consider Legionella especially if patient confused

Macrolide (oral or IV as appropriate) and either
Penicillin or penicillin with beta lactamase inhibitor.
Quinolone may be used in a patient with true penicillin allergy

100
Q

hospital acquired pneumonia (HAP)

A

Within four days of hospital admission – treat as CAP
Within 7 days of discharge or after 5 days of hospital admission and CURB-65 less than 2
Penicillin with beta lactamase inhibitor
Tetracycline
Within 7 days of discharge or after 5 days of hospital admission and CURB-65 less than 3 or more
Penicillin and aminoglycoside
Extended spectrum penicillin

101
Q

pneumonia patient factors

A

Patient age – adult or child
Severity of infection – need for IV therapy
Severe infection may affect absorption
Comorbidities – other medicines may interact
May need to withhold other meds while the patient has sepsis (eg antihypertensives if the patient is hypotensive)

102
Q

UTI

A

Uncomplicated UTI in men and non-pregnant women
E coli
Proteus spp
Enterococci
trimethoprim
nitrofurantoin
Pregnant women
nitrofurantoin
penicillin

103
Q

upper UTI without sepsis

A

Women
trimethoprim
nitrofurantoin
Men
trimethoprim
Penicillin with beta lactamase inhibitor
Pregnant women
Penicillin with beta lactamase inhibitor
trimethoprim last trimester only can cause teratogenicity

104
Q

upper UTI with sepsis

A

Women and men
Penicillin with beta lactamase inhibitor and aminoglycoside
Pregnant women
Penicillin with beta lactamase inhibitor and aminoglycoside

most likely IV
aminoglycosides- very good at treating UTIs but can only be given via IV

105
Q

UTI patient factors

A

Anatomy
Length of urinary tract (men have longer)
Pregnancy
Possibility of teratogenicity
Which trimester of pregnancy?
Severity of infection
May need IV therapy
Does the patient have a catheter?
Difficult to eradicate infection
Length of treatment
3 days may be enough
Additional counselling
Avoid perfumed wipes, hygiene, post coital infections, fluids, avoid coffee, etc

3 days of treatment in women= 5 days in men

106
Q

skin and soft tissue infections

A

Cellulitis
Staph aureus, Strep pyogenes
Mild cellulitis /erysipelas
Narrow spectrum penicillin
tetracycline
macrolide
Moderate cellulitis
Narrow spectrum penicillin
glycopeptide IV
Human or animal bite
Penicillin with beta lactamase inhibitor
tetracycline and metronidazole

107
Q

skin and soft tissue patient factors

A

Site of infection
Comorbidities eg diabetes
Age of the patient
Is it a bacterial infection only?
Possibility of viral or fungal infection at the same time
Is topical treatment possible – some mild infections

108
Q

Necrotising fasciitis

A

Rapidly spreading infection
Strep pyogenes
benzylpenicillin 2.4g every six hours and flucloxacillin 2 g every four to six hours and gentamicin IV and clindamycin IV 600mg every six hours and metronidazole IV 500mg every eight hours
Surgical treatment may be needed
could need amputation

109
Q

pyrexia of unknown origin (PUO)

A

Sepsis or severe sepsis
Broad spectrum cover required
Penicillin and aminoglycoside IV
metronidazole
Glycopeptide IV and aminoglycoside IV
Patient factors
Age
Other treatments eg steroids, chemotherapy
Comorbidities
IV access may be difficult if hypotensive

110
Q

Clostridium difficle

A

Antibiotic associated diarrhoea
Related to broad spectrum antibacterial therapy

Non-severe
metronidazole 400mg every eight hours
vancomycin 125mg every six hours
Severe
vancomycin 125mg every six hours
Severe / complicated
vancomycin 125mg every six hours +/- metronidazole 400mg every eight hours

Relapsing – consider faecal transplant, re-establishing the microbiome

only time we use oral vancomycin but needs to be capsules

111
Q

common viral infections

A

Herpes simplex (cold sores)
aciclovir topically
Herpes zoster (chickenpox, shingles)
aciclovir 800mg five times a day
valaciclovir 1g every eight hours
Patient factors
Age
Time of onset of symptoms
Formulation of treatment – topical, eye ointment, tablets, liquids, IV
Immunocompromised or very serious infection need treatment
Most people with viral infection will get better on their own
If shinges rash for less than 72 hours- treat- if more than 72 hours- don’t treat- it makes no difference to recovery time

112
Q

common fungal infections

A

Tinea
athletes foot
Antifungal powders / ointment
Ringworm (anywhere on the body including scalp and groin)
Topical antifungal
Patient advice – sharing towels,
Candida
Oral infections
Vaginal infections
Azole antifungals – usually oral
Patient factors, age, other treatments eg inhaled or oral steroids,

113
Q

prescribing factors

A

Allergies
Sensitivities
Under dosing
Over dosing
Resistance local differences
Side effects

114
Q

name one counselling point on using tetracyclines

A

cause sun sensitivity

mpharm year 3 sem 1 (10 decks)

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