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Uni > Module 1 Allison > Flashcards

Module 1 Allison Flashcards

1
Q

Benefits of IP

A
  • timely access
  • speedier more accessible
  • Easier than Dr because more available, more time, more approachable
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2
Q

When was it recommended nurses prescribe?

A

1986

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3
Q

When did NPF come in?

A

1998

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4
Q

When did supplementary prescribing for nurses and pharmacists begin?

A

2003

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5
Q

When did allied health professionals start supplementary prescribing?

A

2005

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6
Q

In 2006 what happened for prescribers?

A
  • Prescribing powers extended for nurses, midwives and pharmacists
  • Independent prescribing
  • but Independent prescribing for physiotherapist and podiatrists not until 2013.
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7
Q

What is Non Medical Prescribing?

A

Prescribing of medicines, dressingsand appliances by health professionals who are not doctors.

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8
Q

What are 3 models of Non Medical Prescribing

A

Supplementary Prescribing
Independent Prescribing
Nurse Prescribers Formulary for Community Practitioners

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9
Q

What are the NHS 2000 recommended Clinical Tasks

A
  • order diagnostic investigations (pathology tests and X-rays)
  • make and receive referrals direct (to a therapist or a pain consultant)
  • admit and discharge patients for specified conditions and within agreed protocols
  • manage patient caseloads (diabetes or rheumatology)
  • run clinics (ophthalmology or dermatology)
  • prescribe medicines and treatments
  • carry out a wide range of resuscitation procedures including defibrillation
  • perform minor surgery and outpatient procedures
    to triage patients using the latest IT to the most appropriate health professional
  • take a lead in the way local health services are organised and in the way that they are run.
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10
Q

Who are IP’s

A

Nurses, podiatrists/chiropodists, physiotherapists and pharmacists

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11
Q

What do IPs have to take responsibility for?

A
  • for the clinical assessment of the patient, establishing a diagnosis and the clinical management required
  • prescribing or not, and the appropriateness of any prescribing
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12
Q

Who are IPs registered with?

A

GPhC, NMC, (Nurse and midwifery council), HCPC (Health and care professional council)

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13
Q

What is a PGD?

A

A policy written by Doctor, Senior Manager, Pharmacist, and Senior professional from Profession using the PGD.
Authority comes from the organisation – accountability also falls with organisation
It is not prescribing

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14
Q

Example of supply of PGD where?

A 
Minor Injuries clinic
Walk-In Centre
Family Planning Clinic
Genito-Urinary Clinic
Ante-Natal Clinic
Diabetic Clinic
Paramedics
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15
Q

Named Healthcare professional is authorised to do what under PGD?

A

Supply a pre-labelled, fixed quantity medicine or

Administer fixed quantity medicine

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16
Q

What are the Standards of proficiency for prescribers?

A

Standards and proficiencies for programmes of preparation
Standard of conduct
Within own level of competency

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17
Q

Introduction of NMC Standards of proficiency for nurse and midwife prescribers in what year?

A

2007

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18
Q

Change to Legislation enabling nurse prescribers to prescriber licensed drugs when?

A

2009

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19
Q

Physiotherapists and Podiatrists get independent prescribing in what year?

A

2012

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20
Q

Nurse & pharmacist independent prescribers prescribe schedule 2-5 controlled drugs with exceptions of diamorphine, cocaine & dipipanone for treatment of addictions in what year?

A

2012

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21
Q

Podiatrists & Physiotherapists given independent prescribing status when?

A

2013

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22
Q

NHS England sets out proposals for more efficient and responsive access to medicines for patients NHS England is consulting on these proposals, which cover: Independent prescribing by radiographers, Independent prescribing by paramedics, Supplementary prescribing by dietitians . Use of exemptions within the Human Medicines Regulations (2012) by orthoptists.

A

2015

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23
Q

Therapeutic radiographers get independent prescribing, dieticians & diagnostic radiographers get Supplementary Prescribing in what year?

A

2016

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24
Q

A Competency Framework for all Prescribers is published in what year?

A

2016

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25
Q

What is ethics according to Nuttal 1993

A

judging what we do and the consequences of what we do and considering the justifications that might be given for our moral position

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26
Q

What is ethics according to Jones 2008?

A

The application of the processes and theories of moral philosophy to a real situation

..It is concerned with the basic principles and concepts that guide human beings in thought and action.

..It underlines their values as individuals within a society

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27
Q

According to Purtilo, 1993, what is meta-ethics

A

Determines what is meant by good, bad or happiness and how we know that one decision is better than another
Allows us to discover reasons for moral judgements

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28
Q

What is professional ethics?

A

Term used for moral responsibilities and actions in professional settings
The codes of practice and conduct = ethical framework to which we work in practice.

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29
Q

Name some ethical theories

A
  • Deontology: Duty based care, All “duties” equal
  • Utilitarianism
  • Greatest good for greatest number
  • Ends justify means
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30
Q

Ethical principles based on?

A

Autonomy

Beneficence

Non-maleficence

Justice

Sanctity of Life

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31
Q

What is the opposite of competence?

A

Negligence (different from making mistakes)

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32
Q

legally you are not guilty of negligence if

A

if he has acted in accordance with a practice accepted as proper by a responsible body of medical men skilled in that particular art

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33
Q

The duty of care comes from

A

Neighbour principle

Donoghue v Stevenson (1932)

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34
Q

Breach of duty comes from

A

Standard of care

Bolam v Friern Hosp. Management Committee (1957)

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35
Q

Damage or injury & Assessment of damages comes from

A

Damage would not have happened but for a particular fault, then the fault is the cause of the damage
Hoston v East Berkshire AHA (1987)

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36
Q

What is Vicarious liability?

A

where someone is held responsible for the actions or omissions of another person. In a workplace context, an employer can be liable for the acts or omissions of its employees, provided it can be shown that they took place in the course of their employment.

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37
Q

What is professional accountability

A

to be answerable to oneself and others for one’s own actions

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38
Q

How to Maintain duty of care to patients

A 
Observe UK law
Operate within limits of professional competence
Maintain prof. Knowledge and competence
Ensure patient consent for treatment
Hold professional indemnity insurance
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39
Q

What is the distinction between an act or an omission to act?

A

Not acceptable to actively kill but may be permissible to let someone die

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40
Q

What is autonomy?

A

self rule. freedom from controlling influences. supporting a persons right to accept/refuse treatment and care

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41
Q

What is truth telling

A

to not lie, confuse, deceive or withhold

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42
Q

What must you consider when deciding if you are accountable?

A 
Do you have:
Sufficient knowledge base
Appropriate skills
Professional attitude
Degree of autonomy
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43
Q

What protects you when things go wrong?

A 
Vicarious libality
Employee
Acting in course of employment
Using due care and skill
Acting within role & policies
Obeying employer
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44
Q

What are the four key areas to ensure that you exercise a duty of care regarding prescribing

A
  1. Prescribing (info from pt, write clear, pad secure)
  2. Product liability (ensure monitoring and prescription use appropriate)
  3. Consent
  4. Communication (Responsible for giving sufficient information, Respect for autonomy)
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45
Q

What are the two branches of law and what do they deal with?

A

Civil (Disputes between individuals eg Negligence, Assault)

Criminal (Offences against the state so Crown brings action against the defendant)

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46
Q

What are the sources of law?

A

Statute – law enacted by parliament

Common – evolving as new cases arise (Judge-made law)

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47
Q

Name some principles as described by Beauchamp and Childress

A

Respect for autonomy (following the patient’s wishes)
Beneficence and non-maleficence (the antibiotics are unlikely to be beneficial and over prescribing could do harm by reducing their effectiveness in the future)

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48
Q

What are internal prescribing influences

A

Personal ethics
Knowledge and experience
Fear / loyalty
Convenience / effort

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49
Q

What are External prescribing influences

A 
MHRA
Patient choice
CPD
ABPI (industry)
DTC (advertising)
Professional code of practice
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50
Q

What is law according to oxford dictionary

A

A body of rules enacted or customary in a community and recognised as enjoying or prohibiting certain actions and enforced by the imposition of penalties

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51
Q

Consider what with consent and compacity

A 
Valid consent
Emergency situations
Patients who are mentally ill
Patients with learning disabilities
Children <16yrs
Young people >16yrs
Patients < 18yrs refusal of treatment
Patient capacity to consent
A patient’s best interest
What is meant by Fraser Competence? (childrens rights and wishes)
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52
Q

Statutory duty to disclose when

A 
Road Traffic Act (1998)
Prevention of Terrorism (2015)
Public Health
Misuse of drugs
Data protection Act 
Human Rights Act
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53
Q

Who can gain access to health record?

A 
Road Traffic Act (1998)
Prevention of Terrorism (2015)
Public Health
Misuse of drugs
Data protection Act 
Human Rights Act
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54
Q

Electronic record governed by?

A

Data protection act

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55
Q

Which manual records can be accessed

A

those made after 1991

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56
Q

What did the Caldicott report (1997) find

A

weaknesses in security and confidentiality of patient records
Recommended Caldicott Guardians and protocols

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57
Q

Data protection act March 2000 deals with

A

handling / storage of confidential personal data.

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58
Q

Whistle blowing came under

A

Public interest disclosure act

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59
Q

Single competency Framework for all prescribers 2014, includes

A 
Consultation
1. Knowledge
2. Options
3. Shared decision making
Prescribing effectively
4. Safe
5. Professional
6. Always improving
Prescribing in context
7. The healthcare system
8. Information
9. Self and others
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60
Q

What are the Seven Principles of Safe Prescribing

A
  1. Consider the pt
  2. Which strategy (established diagnosis, differential diagnosis, refer, Rx needed, expectation)
  3. Consider choice of product (Effective, Appropriate, Safe, cost Effective)
  4. negotiate a contract w pt
  5. review (is med safe, effective, acceptable)
  6. record keeping (local and body guidelines)
  7. reflect (peer learning, cpd, aware access points)

UPSIDE DOWN PYRAMID

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61
Q

What are the principles of prescribing?

A

Only Patients they have assessed
Only using their own pad
Only 6 repeats, or reviewed within the last 6 month

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62
Q

Ten Principles of Good Prescribing

A

Clear reasons for prescribing
Establish patient’s medication history before prescribing
Ascertain factors that may alter benefits/risks of treatment
Identify patient’s ideas, concerns, and expectations
Individual, effective, safe, and cost-effective medicines
National guidelines and local formularies
Clear unambiguous legal prescriptions
Monitor adverse & Therapeutic effects of medicines
Communicate and document prescribing decisions
Prescribe within the limitations of your knowledge, skills and experience

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63
Q

FP10P is

A

lilac

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64
Q

FP10SS is

A

green, designed for use with prescriber’s computer system

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65
Q

FP10 is

A

green

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66
Q

FP10MDA-SS is

A

(blue) – used for prescribing controlled drugs (mainly methadone) to addicts. Twice the size of standard FP10 space for pharmacist to record instalment

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67
Q

Prescription requirements are

A

Completed in black ink or computer generated
Clearly indicate the date, the name of the prescriber with professional registration number and contact details (phone number)
Name, address with postcode, age and DOB of patient. It is a legal requirement to state age if prescribing for a child under 12 years
Weight if applicable

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68
Q

Prescriptions should be written including

A 
Name of medicines should be clearly written
Dosage schedule
Route of administration
Amount prescribed
State duration of course if applicable 
Prescribe generically where possible, with no abbreviations (except approved ones in back of BNF)
line under each item
Z at end
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69
Q

Topical Rx should must include

A

the quantity to be applied and the frequency of application must be included.

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70
Q

Dressings and appliances Rx should include

A

details of how to be applied and how frequently changed are useful

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71
Q

Rules for safety Rx

A

Avoid unnecessary decimal points e.g. 3.0mg
Do not use abbreviations of units e.g. mcg
When decimals are unavoidable place a zero e.g. 0.5ml rather than .5ml
Less than 1g – use milligrams
Units for insulin not “U”
Write names and preparations clearly and not abbreviated e.g. DF118
Write directions in English without abbreviations
Unused space in the prescription area should be blocked with a diagonal line to prevent fraudulent use

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72
Q

When to not use generic name

A

Modified release preparations
Compound preparations
Same drugs but used at different doses for different indications
Same drug is formulated to give a different potency
Narrow therapeutic index

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73
Q

What does the Responsible Officer for prescription pads do

A

Only authorised personnel are able to issue and record prescription pads
Responsible for keeping records of the prescriptions
Pad destruction when leaving trust

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74
Q

Loss or suspected theft of prescriptions

A

During Office Hours - Report to the Line Manager, the Police, Non-Medical Prescribing Lead, the Local Counter Fraud Specialist and Chief Pharmacist.
Out of office Hours - Report directly to the local police station and the Manager On-Call. Local Counter Fraud Services arranges for all pharmacists to be notified of any lost or missing prescription pads
A new pad is provided by the Trust where procedures are in place for security and stock control
Following the theft or loss of the prescription pad, the Non-Medical prescriber is required to write ALL PRESCRIPTIONS IN RED INK FOR TWO MONTHS
Complete Incident Form.
Local Counter Fraud Services arranges for all pharmacists to be notified of any lost or missing prescription pads
A new pad is provided by the Trust where procedures are in place for security and stock control
Following the theft or loss of the prescription pad, the Non-Medical prescriber is required to write ALL PRESCRIPTIONS IN RED INK FOR TWO MONTHS
Complete Incident Form.

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75
Q

What type of errors are there in Rx writing

A

Transcription prescribing errors
Confusion between dosage forms
Duration of medication

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76
Q

What are good sources of information?

A 
BNF/ NPF
NICE
Local Prescribing advisors or Pharmacist
MHRA
National and local guidelines and policies
Drug Tariff
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77
Q

Name some bad sources of info?

A

MIMS
GP
Pharmaceutical Industry

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78
Q

Anti-psychotics were first developed as?

A

Anaesthetics. Then found to relax patients

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79
Q

Name first generation Antipsychotics

A

Haloperidol, Chlorpromazine, Flupentixol

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80
Q

Name second generation Antipsychotics

A

Clozapine
Risperidone, Olanzapine, Quetiapine
Aripiprazole

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81
Q

Which are typical and which atypical out of first and second generation anti-psychotics?

A

First Typical

Second Atypical

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82
Q

How do antipsychotics work

A

dopamine blockade

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83
Q

What effect will Dopamine blockade have on Mesolimbic pathway

A

↑ dopamine – psychosis

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84
Q

What effect will Dopamine blockade have on Mesocortical pathway

A

↓ dopamine – negative symptoms

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85
Q

What effect will Dopamine blockade have on Nigrostriatal pathway

A

↓ dopamine in Parkinson’s

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86
Q

What effect will Dopamine blockade have on Tuberoinfundibular pathway

A

Dopamine inhibits Prolactin release

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87
Q

Dopamine related Side effects of Antipsychotics

A

Can worsen negative symptoms
Extra pyramidal side effects (EPSE)
Hyperprolactinaemia

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88
Q

What are EPSE

A 
(extrapyridal side effects)
Dystonias
Parkinsonism
Akathisia
TD
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89
Q

Other side effects of antipsychotics

A 
Dizziness
Low blood pressure
Dry mouth
Constipation
Weight gain
Sedation
Salivation
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90
Q

Indication for antipsychotics

A 
Schizophrenia
Bipolar disorder
Psychosis in other conditions
Dementia
(Risperidone – Persistent aggression Caution!!!!!!)
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91
Q

Antipsychotics can not be used to treat which of the following:

To treat anxiety
In Huntington’s Disease
To treat heart arrythmias
To treat hiccups
To treat nausea
In Tourette’s syndrome
A

Arrythmias

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92
Q

How long does it take anti-psychotics to kick in

A

1-2 weeks

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93
Q

Why is there non compliance with Antipsychotics

A

poor insight, side effects, poor communication

therefore Depot can be useful

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94
Q

What if no response to antipsychotics?

A 
Check compliance
Review diagnosis
?Increase dose
?Augment medication
Change medication
Other types of treatment
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95
Q

How long to continue Antipsychotics?

A

1-2 years after response

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96
Q

How to stop antipsychotics

A

Gradual withdrawal
(60-70% relapse in a year, 85% in 2 years
10-30% relapse if on active medication)

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97
Q

What is Clozapine used for

A

Treatment resistant Schizophrenia

Psychosis in Parkinson’s

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98
Q

Main side effects of Clozapine

A 
Many side effects
Weight gain ++
Hypersalivation
Fits
Myocarditis
Neutropaenia and agranulocytosis (Regular blood monitoring)
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99
Q

How does Aripriprazole work?

A

Partial agonist D2 receptor

Works as antagonist in mesolimbic system
(positive symptoms of Schizophrenia)

Works as agonist in prefrontal cortex
(negative symptoms of Schizophrenia)

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100
Q

Neuroleptic Malignant Syndrome symptoms

A

Hyperthermia, autonomic instability
Fluctuating consciousness
Mutism
Severe EPSE / Rigidity

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101
Q

What to do if Neuroleptic Malignant Syndrome

A

Stop antipsychotic
Medical emergency!!!!
only 0.5%, Mortality up to 20%

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102
Q

Antidepressants were first developed to treat what

A

TB

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103
Q

How does imipramine act

A

mental and motor slowing

?effect on reuptake of serotonin and noradrenaline

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104
Q

Name some Monoamine transmitter

A

Serotonin
Noradrenaline
Dopamine

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105
Q

Name some Selective Serotonin Reuptake Inhibitors (SSRIs)

A 
Fluoxetine
Paroxetine
Citalopram
Escitalporam
Sertraline
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106
Q

SSRI side effects

A 
Nausea, GI symptoms
Insomnia, Agitation
Sexual dysfunction
??Suicidal behaviour
Low sodium (in older people)
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107
Q

Overdose in SSRIs

A

not so bad

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108
Q

Name some Serotonin & Noradrenaline Reuptake Inhibitors (SNRIs)

A

Venlafaxine

Duloxetine

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109
Q

Name a Noradrenaline Reuptake Inhibitors (NARI’s)

A

Reboxetine

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110
Q

Name some Tricyclic Antidepressants (TCAs)

A

Imipramine
Clomipramine
Amitriptyline
Dosulepin

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111
Q

Side effeccts of TCAs

A 
Dry mouth, Constipation, Drowsiness
 ↑ Heart rate, ↓ Blood pressure
ECG changes
Tremor, headache
Sexual dysfunction
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112
Q

Over dose with TCAs

A

bad. Heart defects, convulsions and death

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113
Q

Name some Monoamine oxidase inhibitors

A

Phenelzine
Isocarboxazid
Tranylcypromine
Moclobemide (reversible)

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114
Q

Side effects of MAOI

A
  • Tyramine foods (Mature cheese, pickled herring, Bovril, Marmite, “Off” foods, Alcoholic drinks etc)
    Cause hypertensive crisis
    Throbbing headache
    Subarachnoid haemorrhage
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115
Q

What is Mirtazapine

A
  1. Noradrenergic and specific serotonergic antidepressants (NaSSA)
  2. Inhibit NA a2-auto and heteroreceptors
  3. Prevent negative feedback on 5-HT and NA
  4. Block 5-HT2 and 5-HT3 enhances 5-HT1
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116
Q

Name some other Antidepressants out the main groups

A

Trazodone
Agomelatine
Bupropion

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117
Q

What are the indications for Antidepressants

A 
Depression
Anxiety Disorders
Obsessive Compulsive Disorder
Neurological pain
Insomnia
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118
Q

Prescribe in moderate/severe depression:

A

SSRIs first line medication

Don’t forget psychological treatments

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119
Q

How long do antidepressants take to work

A

Up to 6 weeks

But…Plasma levels steady within 5-7 days

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120
Q

What is the minimum continuation period for antidepressants

A

6-9 months

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121
Q

How long withdrawal with Antidepressants

A

Gradual withdrawal – at least 4 weeks

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122
Q

Can you give antidepressants as prophylaxis

A

Yes, same dose as acute treatment

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123
Q

Name some mood stabilisers

A

Lithium
Sodium Valproate
Carbamazepine
Lamotrigine

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124
Q

Indications for mood stabilisers

A
  • Bipolar disorder
    Mania
    Depression
    Prophylaxis
  • Augmentation therapy in depression
    Lithium
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125
Q

Lithium was first used to treat what

A

Gout

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126
Q

How does Lithium work

A
  1. Stabilises glutamate?
  2. Increases serotonin release?
  3. Deactivates the GSK3β enzyme?
    - Restores normal brain cycle?
  4. Interacts with nitric oxide?
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127
Q

What is the therapeutic window

A

Between 0.6 and 1.0mmol/l

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128
Q

Side effects of lithium

A 
Thirst, polyuria
Tremor
Diabetes insipidus
Arrythmias
Weight gain
Thyroid problems
Ebstein’s anomaly in foetus
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129
Q

What are symptoms of Lithium toxicity

A 
GI upset
Muscle weakness
Drowsiness
Ataxia
Tremor
Seizures
Coma / Death
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130
Q

Lithium interacts with

A

Diuretics (increase Li concentrations)
ACE inhibitors (increase Li concentrations)
NSAID’s (increase Li concentrations)

((excreted by kidneys))

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131
Q

What do we Monitor with Lithium

A 
Baseline U&amp;E’s, TSH and ECG
Blood levels  - aim for 0.6-1.0mmol/l
Levels every 5-7 days until stable
Then levels every 3-6 months
TFT’s, U&amp;E’s 6 monthly
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132
Q

How to take lithium

A

Constantly. intermittent use is bad

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133
Q

How long to stay on lithium

A

min 2-3 years

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134
Q

How long does withdrawal take with Lithium

A

3-6 months. can precipitate relapse

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135
Q

Name another mood stabiliser

A

Anticonvulsants:

Sodium Valproate (Semi-sodium Valproate, Valproic acid)
Carbamazepine
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136
Q

How do anticonvulsants work as mood stabilisers?

A

Stabilise sodium channels?? - Cells less excitable

Potentiates GABA receptors?? - Inhibitory neurotransmitter

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137
Q

Side effects of Sodium Valproate

A

Hepatic impairment

Foetal abnormalities

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138
Q

What monitoring with sodium valporate?

A

Check LFT’s at baseline and 6 monthly

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139
Q

Carbamazepine side effects

A

Agranulocytosis
Rashes
Foetal abnormalities

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140
Q

Monitoring with Carbamazepine

A

FBC closely for 1-2 months

Then 3-6 monthly

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141
Q

There are three general types of side effect. They are

A 
Effect more than desired Therapeutic effect (eg antihypertensive hypotension)
Wrong target (on ion channels, carrier proteins, enzymes and receptors like: adrenergic, cholinergic, dopaminergic, opioid and histamine)
Hazardous like chemotherapy or DNA related. These cause things like dry mouth, hair loss, gastro intestinal disturbances and neutropaenia
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142
Q

Name the five classes of ADR

A 
Type A – Augmented reaction
Type B – Bizarre
Type C – Chronic
Type D  - Delayed
Type E – End of Dose
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143
Q

What is augmented reaction ADR

A

Extended effects of drug therefore responds to dose reduction
More likely in young, old and renal and liver impairment

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144
Q

Give examples of augmented reaction ADR

A

Low blood pressure with antihypertensive
Low blood sugar with insulin
Dry mouth that is associated with tricyclic antidepressants

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145
Q

What to do with an augmented reaction ADR

A

Stopping the drug altogether
Reducing the dose of the drug
Switching to an alternative drug
Record ADR in notes

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146
Q

What are the types of Bizarre ADRs

A

Type I – Anaphylaxis e.g penicillins
Type II- cytotoxic/blood dyscrasias e.g.carbimazole
Type III- immune complex medicated (serum sickess) e.g. thiazides
Type IV- T-cell medicated (rashes) e.g. penicillins

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147
Q

What is a bizarre ADR

A

reactions are novel responses that are not expected from the known pharmacological actions of the drug.
High mortality

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148
Q

What to do with Bizarre ADR

A

Require prompt detection and rapid action
Drug suspected withheld
Medical prescriber informed immediately
Any resuscitation measures undertaken
The drug should be stopped/alternative found
Record in patient notes and easily visible to future prescribers

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149
Q

Differences between Type A and B (augmented and bizarre)

A

Type A
PredictableUsually dose dependentHigh morbidityLow mortalityResponds to dose reduction

Type B
UnpredictableRarely dose dependentLow morbidityHigh mortalityResponds to drug withdrawal

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150
Q

What are chronic ADR

A

long term effects

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151
Q

give examples of chronic ADR

A

Continued exposure – tolerance e.g. Opioids
Cumulative effects – e.g. Methotrexate – liver
Long term effects e.g. osteoporosis & steroids

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152
Q

What are long term effects, Type C ADR

A

Continued exposure – tolerance e.g. Opioids
Cumulative effects – e.g. Methotrexate – liver
Long term effects e.g. osteoporosis & steroids

153
Q

What are delayed Effects Type D ADR

A

Impaired fertility – e.g. Inadequate sperm counts from prior exposure to cytotoxics e.g. Cyclophosphamide
Impaired fetal development – e.g. Spina bifida in the fetus after maternal exposure to sodium valporate in pregnancy.

154
Q

What are End of Dose Type E ADR

A

Withdrawal effects after long term treatment

155
Q

High Risk Groups for ADR

A 
Some genetic groups
Age – very young and old
Sex – female
End organ failure – liver or renal impairment
Polypharmacy
Multiple Disease states
156
Q

What side ADR is associated with NSAIDs

A

Dyspepsia

157
Q

What side ADR is associated with Laxatives

A

Diarrhoea

158
Q

What side ADR is associated with Iron Preparations

A

Nausea and Vomitting

159
Q

What side ADR is associated with Ca Ch Blockers

A

Oedema

160
Q

What side ADR is associated with Antibiotics

A

Rash or allergy

161
Q

What side ADR is associated with Opiate Analgesics

A

Constipation

162
Q

What side ADR is associated with Diuretics

A

Hypokalemia

163
Q

What side ADR is associated with ACE Inhibitors

A

Cough

164
Q

Give examples of Absorption Interactions

A

Antacids forming complexes with them: Gaviscon & cipro

drugs affect gut transit time, affecting rate of absorption: metoclopramide or opiates

165
Q

How can absorption interactions be dealt with

A

change admin time

166
Q

What is protein binding interaction

A

Two drugs compete for the same protein binding

site and one or both is displaced. Result is increased concentration of free drug Eg phenytoin and warfarin

167
Q

What are metabolic interactions

A

When P450 enzyme is effected

168
Q

If P450 activity is increased then…

A

some drugs are metabolised more quickly ↓ bioavailability

169
Q

If P450 is inhibited then…

A

some drugs are metabolised more slowly ↑ bioavailability

170
Q

What are Enzyme inhibition of cytochrome P450 system

A

drugs that inhibit P450 reduce metabolism, increased free drug

171
Q

What are Enzyme inducers

A

drugs that induce P450 increase metabolism, reduce free drug

172
Q

Give examples of drugs that given at same time will interact due to enzyme inhibition

A 
Allopurinol
Amiodarone
Cimetidine
Ciprofloxacin 
Diltiazem
Erythromycin
Ethanol (acute)
Isoniazid
Ketaconazole
Metronidazole
Omeprazole
Sulphonamides
Oral contraceptives
Valproate
Verapamil
173
Q

Give an example of two drugs and what would happen with a renal interaction

A

Methotrexate and NSAIDs both renally excreted – if they are competing for excretion, then methotrexate may not be eliminated as quickly and may cause toxic effects

174
Q

Give examples of Drugs with narrow therapeutic margin

A

warfarin,digoxin,antiepileptics, theophylline, cyclosporin

175
Q

which Drugs require careful dosage monitoring

A

antihypertensives, antidiabetic drugs

176
Q

Give examples of Enzyme inducers

A

rifampicin,phenytoin, carbamazepine, barbiturates

177
Q

Give examples of Enzyme inhibitors

A

cimetidine,ketoconazole, ciprofloxacin, erythromycin

178
Q

What sources of info are there for interactions

A

BNF Appendix 1
Stockley’s Drug Interactions
Summary of Product Characteristics – www.medicines.org.uk

179
Q

Give example of food interaction

A

grapefruit juice interacts with diltiazem, nifedipine

180
Q

Give some examples of herbal remedies interatcing

A

Ginseng interacts with warfarin, calcium channel blockers, St Johns Wort interacts with simvastatin, HIV drugs

181
Q

How long does it take enzyme inducers to have an interactive effect

A

1-3 weeks because they stimulate the production of new metabolising enzymes

182
Q

How long does it take enzyme inhibitors to have an interactive effect

A

24 hours

183
Q

What is pharmacogenetics

A

the study of the genetic basis for variation in drug response.

184
Q

Genes for enzymes in drug metabolism include

A

CYP2D6 and CYP2C9, and thiopurine-S-methyltransferase (TPMT)

185
Q

Suspected ADR should be reported to

A

The Medicines and Healthcare products Regulatory Agency (MHRA)

186
Q

Why should ADR be reported

A

To recognise unknown hazards
To take adequate regulatory measures
To ensure safety of use of medicines

187
Q

Which ADR reported via yellow card

A

Report any serious ADR for all medicines
All Black triangle drugs
All occurring in children
New drugs and closely monitored

188
Q

How can we report ADR

A

Yellow Card Scheme
Electronic
Prepaid yellow cards
24 hour Freephone service

189
Q

What does ▼ mean

A

closely monitored by MHRA

190
Q

How can you minimize ADR

A

Prescribe good indication, esp pregnancy.
Check on all previous medication
Assess previous reactions to medicines
Verify other drug use e.g. OTC/ herbals
Take age into consideration – elderly/ children
Check for renal/hepatic disease
Complete yellow cards
Prescribe in accordance to protocols/guidelines/formularies
Give clear instructions on medication to patient esp elderly
Prescribe drugs that are familiar as side effect profiles are known and black triangle drugs with caution.
Inform the patient of possible side effects to help identify ADRs

191
Q

What are the characteristics of a bacteria cell

A

Pilus, capsule, flagellum, cell wall

and ribosomes, nucleoid (DNA), plasma membrane, cytoplasm

192
Q

What are the two types of bacteria

A

Gram positive and Gram negative

193
Q

Give an example of G +ve bacteria

A

Staphylococcus, enterococcus, streptoccous

194
Q

Give an example of G -ve bacteria

A

E coli, salmonella, psuedomonas, haemophilus

195
Q

What are the characteristics of G-ve bacteria

A

lipopolysaccharides, Porin,

and Protein, Cell wall all around

196
Q

What are the characteristics of G+ve bacteria

A

peptidoglycans surround, cell wall, protein not all way round

197
Q

Bacteria are characterised by shape give examples

A

cocci, bacilli, budding/appendaged, etc

198
Q

Where most likely to find G +ve bacteria infections

A

skin/wound, line related, gangerous wound, abdo

treat with vancomycin, teicoplanin, gentamicin
(resistant to cephlasporin, metronidazole)

199
Q

Where most likely to find G -ve bacteria infections

A

Gut, UTI, sepsis, pneumonia (cephlasporin, gentamicin, cipro, tazocin, imiprem, trimethoprim)
(Resistant to amox)
leg ulcers, CF, catheters, sepsis (aminoglycosides, cipro, tazocin, imiprem) resistant to everything else
Abdo (metronidazole, co-amoxiclav, clindamycin, tazocin, imiprem) resistant to benzylpenicilin, amox, cefruoxime, gentamicin, macrolides, quinolones

200
Q

What is the difference between Aerobic and Anaerobic bacteria

A

Aerobic get energy from food and oxygen

201
Q

What is bacteriacidal and bacteriostatic

A

Bacteriacidal kill bacteria - cell wall (faster)

Bacteriostatic stunt its growth helping immune sytem - RNA synthesis, no growth/reproduction

202
Q

Antimicrobial agents can inhibit which target zones

A

Cell wall synthesis, protein synthesis, nucleic acid synthesis, other metabolic processes (eg folic acid pathway)

203
Q

Which antibiotics target cell wall

A

penicillin, cephlasporin

204
Q

Which antibiotics target protein synthesis

A

aminoglycosides, chloramphenicol, macrolides, tetracyclines

205
Q

Which antibiotics target nucleic acid synthesis

A

quinolones, metronidazole, rifampicin

206
Q

Which antibiotics target other metabolic processes

A

sulphonamides, trimethoprim

207
Q

Difference between broad and narrow spectrum Antibiotics

A

Broad target G+ve and G-ve

Narrow primarily against a specific species anaerobic microorganism

208
Q

How do bacteria become resistant

A
  1. recognise and create enzymes to destroy the AB
  2. close contact of sick patients and extensive use of antimicrobials
  3. incorrect use of AB/wrong diagnosis
  4. gene mutation
  5. gene transfer
  6. use of broad spectrum not specific
209
Q

How do bacteria withstand AB

A
  1. change the target

2. stop from reaching target at high conc

210
Q

what are the three mechanisms of AB resistance

A
  1. change permiability
  2. enzymatic degradation - B lactamase
  3. alter targets
  4. efflux
211
Q

What is the role of Clavulanic acid?

A

B lactamase inhibitor (same structure so sacrifices itself)

212
Q

Extended Spectrum B Lactamase are resistant to

A

penicillin, cephlasporin,

213
Q

Which bacteria produce ESBL?

A

E coli, Klebsiella

214
Q

How do bacteria pass on resistance

A

Conjugation (2 fuse), transduction (virus infects bacteria and leaves DNA which is resistant), transformation (pick up from environment)

215
Q

What is Antibiotic stewardship

A

resistance growing, v little new AB, therefore public health initiative to encourage responsible prescribing and preserve what we have

216
Q

Start smar initiative says

A

No AB without clinical evidence, stick to local guidelines, document indication/review date/dosage/route, cultures if poss

217
Q

After 48 hours of AB what are options

A
  1. stop
  2. switch route
  3. continue
  4. switch AB
  5. outpatient parenteral AB
218
Q

DOH says what about AB prescribing

A

right drug, right dose, right time, right duration, for every pt

219
Q

Switch to oral IV why?

A

IV infections, no IV discomfort, faster admin, faster discharge, cost saving on drug and time.

220
Q

What is the prophylaxis policy with AB

A

reduces surgical site infections, IV AB 60 min before procedure, significant blood loss then longer treatment

221
Q

How do you prescribe gentamicin

A
  1. weight
  2. work out for obese or ideal
  3. calculate dose
  4. calculate creatinine clearance
  5. check dosing interval based on clearance
222
Q

What do chief cells secrete?

A

pepsinogen (protein to peptides) and gastric lipase (triglycerides to fatty acids/monoglycerides)

223
Q

What do parietal cells secrete?

A

HCL (pepsinogen to pepsin) and intrinsic factor (for B12 of RBC)

224
Q

What do surface mucous cells and mucous neck cells do?

A

secrete mucous and absorb

225
Q

What do G cells secrete?

A

gastrin (stimulate chief and parietal cells. contract oesophogeal sphincter, increase motility, relax pyloric sphincter

226
Q

What do Parietal cells contain receptors for?

A

acetylcholine, gastrin and histamine, all of which stimulate gastric acid production

227
Q

Acetylcholine is released by

A

vagus nerve endings in response to stimuli, such as thinking about food

228
Q

Gastrin is a hormone released by

A

the stomach and duodenum in response to food ingestion - Affects parietal cells which in turn causes gastric acid to be released in stomach.

229
Q

Histamine is released from

A

cells in the gastric mucosa and diffuses into nearby parietal cells

230
Q

Pepsin is a what enzyme

A

a proteolytic enzyme that helps digest protein foods and also can digest the stomach wall

231
Q

What is H-pylori

A

a gram negative bacterium found in the gastric mucosa of most clients with chronic gastritis

232
Q

Who usually has H-pylori

A

gastric and duodenal ulcers

233
Q

How does H-pylori spread

A

oral-fecal or iatrogenic

234
Q

The stomach secretes

A

mucous and bicarbonate

235
Q

Why does acid not harm stomach

A

diluted by food and secretions. HCL cant be reabsorbed. pancreatic juices and bile alkali the acids.
prostaglandin E

236
Q

What kind of drugs affect the GI system

A 
Laxatives
Antidiarrheal
Antiemetic's
Drugs used for acid peptide disorders
Cholinergics
Anticholinergics
237
Q

Name an associated disorder with the oral cavity

A

stomatitis

238
Q

Name an associated disorder with the oesphogus

A

GORD

239
Q

Name an associated disorder with the stomach

A

peptic ulcers, gastritis

240
Q

Name an associated disorder with the small intestine

A

malabsorption, inflammatory bowel

241
Q

Name an associated disorder with the large intestine

A

diarrhoea, constipation

242
Q

Name an associated disorder with the pancreas

A

pancreatitis, diabetes

243
Q

Name an associated disorder with the gall bladder

A

cholecystitis

244
Q

Name an associated disorder with the liver

A

hepatitis, cirrhosis

245
Q

Underlying Causes of GI Disorders

A 
Dietary excess
Stress
Hiatus hernia
Oesophageal reflux
Adverse drug effects 
Peptic ulcer disease
246
Q

Name some symptoms of digestive disorders

A 
Diarrhoea 
Constipation
Bleeding from the digestive tract (Gastrointestinal bleeding)
Regurgitation
Difficulty swallowing
247
Q

Name some symptoms of digestive disorders which could be something else

A 
Abdominal pain (Acute or Chronic or Recurring)
Passing of gas (flatulence)
Loss of appetite 
Hiccups 
Nausea
248
Q

What is GORD

A

Gastro-oesophageal Reflux. Caused by stomach acid splashing up into the oesophagus. Can be confused with heart problem

249
Q

How to treat GORD

A

Antacids – usually contain aluminium or magnesium compounds. increase the pH of chime making it less acid
Alginates – form a raft that floats on top of the stomach contents. reduces reflux and protects the oesophageal mucosa

250
Q

Give examples of H₂ Receptor antagonists

A

cimetidine, famotidine, ranitidine

251
Q

How do H2 receptor antagonists work

A

Histamine, Gastrin, acetylcholine release HCL and pepsin. H2 receptor antagonists block stimulatory effects of histamine therefore reducing gastric secretions

252
Q

How do PPI work

A

H in HCL punped into lumen by protein pumps(in parietal cells of mucosa) PPI block the pump irreversibly.

253
Q

Indications for H2 Antagonists

A
  • Short-term treatment of active duodenal ulcer or benign gastric ulcer
  • Treatment of pathological hypersecretory conditions such as Zollinger–Ellison syndrome (a condition characterised by severe peptic ulceration, gastric hypersecretion, elevated serum gastrin, and gastrinoma (a tumour) of the pancreas or duodeum)
  • Prophylaxis of stress-induced ulcers and acute upper GI bleeding in critical patients
  • Treatment of erosive gastroesophageal reflux
  • Relief of symptoms of heartburn, acid indigestion, and sour stomach (OTC preparations)
254
Q

Types of Antacids

A 
Sodium bicarbonate (Bell/Ans)
Calcium carbonate (Calciday-667, Tums, and others)
Magnesium salts (Milk of Magnesia and others) 
Aluminum salts (Amphojel and others) 
Magaldrate (Lowsium, Riopan)
255
Q

“indigestion” could mean

A

dyspepsia, regurgitation, and the sensation of having a lump in the throat (globus sensation).

256
Q

Diarrhoea is when

A

either an increase in fluid secretion into the gut or a reduction in fluid absorption from the gut – or an increase in motility

257
Q

Acute Dairrhoea can be due to

A

food poisoning
gastroenteritis (infection)
Anxiety
drugs

258
Q

Chronic diarrhoea can be due to

A 
Chronic diarrhoea –causes include: 
Irritable bowel syndrome
Inflammation of the bowel – e.g. ulcerative colitis
Chronic bowel infections
Hormonal changes
Food intolerance
259
Q

How does Kaolin Morphine work

A

Reduce gut motility e.g. opiates

Absorb excess fluid e.g. kaolin

260
Q

What is an ulcer

A

Erosions in the lining of the stomach and adjacent areas of the GI tract

261
Q

What are the symptoms of an ulcer

A

Gnawing, burning pain, often occurring after meals

262
Q

What can be the cause of an ulcer

A

Helicobacter pylori

263
Q

What do you treat an ulcer with

A

Histamine-2 (H2) antagonists
Antacids
Proton pump inhibitors
Antipeptic agents (coat injured area of stomach preventing further damage)
Prostaglandins (Inhibit the secretion of gastrin and increase the secretion of the mucous lining of the stomach, providing a buffer)

264
Q

What happens when vomitting

A

Abdominal muscles contract- increasing abdominal pressure, cardiac sphincter and oesophagus relax and gastric contents are ejected

265
Q

What can stimulate the vomiting centre

A
  • Physical stimuli from the gut (mechanical or chemical)
  • Chemical stimuli (blood) -> CTZ
  • Motion stimuli (vestibular apparatus)
  • Higher centres (cerebral cortex)
266
Q

Give examples of Antiemetic drugs

A

Histamine H₁ antagonists
Dopamine D₂ receptor agonists
Serotonin 5HT₃ receptor antagonists

267
Q

Give an example of Histamine H₁ antagonists

A

meclizine, cyclizine, promethazine and muscarinic antagonists such as hyoscine

268
Q

When are Histamine H₁ antagonists effective

A

motion sickness and vomiting caused by irritants in the stomach – but have little effect against substances that act directly on the CTZ

269
Q

Give an example of Dopamine D₂ receptor agonists

A

metoclopramide and domperidone

270
Q

When are Dopamine D₂ receptor agonists effective

A

act on the CTZ. Both also increase gut motility. Antipsychotics also act on CTZ as D₂ agonists and can be used for acute chemotherapy induced emesis

271
Q

Give an example of Serotonin 5HT₃ receptor antagonists

A

Ondansetron

272
Q

When are Serotonin 5HT₃ receptor antagonists effective

A

act on CTZ and are particularly effective for vomiting caused by radiation therapy or cytotoxic drugs

273
Q

What happens to GI when you grow old

A
  • Constipation, diverticulitis and gastritis more common
  • can be side effect of drugs
  • Stomach lining capacity to protect decreases. esp aspirin/NSAID
  • lactase levels decrease (more intolerance)
  • more bacteria (pain, bloating and weight loss) and affect absorption of folic acid, iron, calcium
274
Q

normal number of bowel movements ranges

A

2 or 3 a week to as many as 2 or 3 a day

275
Q

What in the stool may indicate a disorder.

A

Changes in the frequency, consistency, or volume of bowel movements or the presence of blood, mucus, pus, or excess fatty material (oil or grease)

276
Q

How would you treat constipation

A

lifestyle
then bulk-forming laxative (adequate fluid intake is important)
then osmotic laxative if stool hard
or stimulant laxative if soft but difficult to pass
stop treatment once soft and easy to pass

277
Q

Which drugs cause constipation

A

Aluminium antacids
Antimuscarinics (e.g. procyclidine, oxybutynin)
Antidepressants (most commonly tricyclic antidepressants, but others may cause constipation in some individuals)
Antiepileptics (e.g. carbamazepine, gabapentin, oxcarbazepine, pregabalin, phenytoin) Sedating antihistamines
Antipsychotics
Antispasmodics (e.g. dicycloverine, hyoscine)
Calcium supplements
Diuretics
Iron supplements
Opioids
Verapamil

278
Q

What are rome criteria for constipation

A

1/4 time Straining
1/4 time Lumpy and or hard poo
1/4 time sense of incomplete evacuation
2 or less bowel movements/week

279
Q

For constipation what do we monitor

A 
Frequency
Amount
Effort
Consistency
Emptying
Shape
(FAECES)
280
Q

Warning signs

A

Bleeding, palpable mass RHS abdo/pelvis, persistent unexplained change, narrowing stool, FH colon cancer/IBS. unresponsive to treatment, unexplained weight loss, iron deficiency anaemia, fever, or nocturnal symptoms

281
Q

Co-danthramer is used for what and what to watch out for

A

terminally ill patients. It may colour the urine red and can cause a characteristic red rash over the buttocks and perineum. The risk is increased if the patient is incontinent of urine or faeces.

282
Q

What to avoid in terminal cancer constipation

A

bulk forming laxatives, such as Fybogel because not suitable for patients with a poor fluid intake, or when opioids have reduced bowel motility.

283
Q

ADR of bulk forming laxatives

A 
Flatulence
Sensation of abdominal fullness
Intestinal obstruction
Faecal impaction
Oesophageal obstruction
Severe diarrhoea
284
Q

Example of bulk forming laxative

A

Fybogel®, Celvevac® Normacol®, Regulan.

acts in 24-36 hours

285
Q

Example of stimulant laxative

A

Senna, Bisacodyl, co-danthramer, co-danthrasate, dioctyl, docusol
8-12 hours

286
Q

ADR with stimulant laxative

A 
Weakness
Nausea
Abdominal cramp
Mild inflammation of the rectum and anus
Urine discolouration (especially senna)
287
Q

Give example of Hyperosmolar Laxatives

A

Lactulose, glycerin

Saline compounds - magnesium salts, polyethylene glycol (PEG) and electrolytes

288
Q

How does lactulose work

A

Act by drawing fluid from the body into the bowel by osmosis
Enters the GI tract orally and is minimally absorbed
The drug is distributed only in the intestine – metabolised by bacteria in the colon and excreted in the faeces

289
Q

How do PEG- non-absorbable solution work

A

as an osmotic – but does not alter electrolyte balance draw water into the intestine fluid accumulation distends the bowel and promotes peristalsis

290
Q

How do stimulant laxatives work

A

Stimulate an increase in colonic motility (peristalsis) and mucus secretion
Irritate intestinal mucosa or stimulate the nerve endings of the intestinal smooth muscle

291
Q

How do bulk forming laxatives work

A

Act like dietary fibre increasing water content and faecal mass – increase stool weight and frequency

292
Q

ADR lactulose

A

Abdo distension

Nausea and vomittin

293
Q

ADR Saline compounds

A

Dehydration
Hypernatraemia
Hypocalcaemia
Cardiac arrythmias

294
Q

ADR PEG/Macrogol

A

Nausea
Abdominal fullness
Explosive diarrhoea

295
Q

Centrally opioids antagonise which receptors

A

µ (mu), δ (delta), К (Kappa) and ORL-1 (opioid receptor-like 1).

296
Q

Opioid Induced Constipation is caused by which receptors

A

mu-opioid receptor agonists binding to mu-receptors in the myenteric and submucosal plexus tissues within the GI tract, this leads to inhibition of the propulsive activity of the intestine and slower gut transit time.
and centrally acting opioids may reduce intestinal peristalsis

297
Q

What is Prucalopride

A

A selective, high affinity 5-HT₄ receptor agonist, which stimulates colonic mass movement

should only be prescribed by clinicians with experience of treating chronic idiopathic constipation and review of the patient’s previous laxative treatments.

298
Q

What is Lubiprostone

A

A bicyclic fatty acid derived from prostaglandin E1 that acts by specifically activating CIC-2 cholride channels on the apical aspect of gastrointestinal epithelial cells, producing a chloride-rich fluid secretion.
Chloride channels are key regulators in the intestinal tract, which transport chloride ions into the lumen with sodium and fluids passively following, thus increasing intestinal fluid secretion
These secretions soften the stool, Increase motility and promote bowel movements.

299
Q

Naloxone is a

A

centrally and peripherally acting opioid antagonist
inhibits the stimulation of µ-opioid receptors within the GI tract
high first pass metabolism
Crosses BBB therefore opioid withdrawal and loss of analgesic effect
Naloxegol doesnt cross BBB because pegylated

300
Q

Methylynaltrexone bromide is a

A

peripheral selective antagonist of the mu receptor. Indicated for opioid induced constipation in terminally ill patients.

301
Q

What is pharmacokinetics

A

the way body affects the drug:

Absorption •Distribution •Metabolism •Excretion

302
Q

What is pharmacodynamics

A

effects of drug on body

303
Q

Give examples of enteral routes

A

oral and rectal

304
Q

Give examples of parenteral routes

A

IV, IM, SC, Intra-arterial, Intrathecal, Intra-peritoneal

305
Q

Give examples of percutaenous routes

A

ingalation, sublingual, topical, transdermal, intranasal

306
Q

Give examples of Absorption-Related Food/Drug Interactions

A

Grapefruit juice increases absorption of antihistamines, codeine, tranquilizers, cardiovascular & antiretroviral drugs
•Vegetables or vitamins with iron can decrease absorption of erythromycin
•Dairy foods or other calcium rich items decrease absorption of tetracycline

307
Q

degree of drug distribution depends on:

A

Properties of the drug (physical & chemical)

• Drugs ability to penetrate cell membranes

308
Q

Which factors determine how much of the drug reaches its target

A
  • Plasma protein binding
  • Blood flow
  • Blood brain barrier
309
Q

What are Plasma protein binding

A

Manufactured in the liver.
They contribute to osmotic pressure, help to control water balance and are involved in the transport of substances in blood including drugs

310
Q

How are drugs transported in the bloodstream

A

albumin transports Free (unbound) drug and Partially reversibly bound. Protein bound not available to exert effect.
Only “free” drug may: • Diffuse through capillary walls • Produce a therapeutic effect • Be metabolised • Be excreted
(Concentration of unbound drug determines the drug concentration and therefore efficacy of the drug )

311
Q

What is the effect of protein binding on drug action?

A
  • Changes in the concentration of plasma proteins will influence the effect of a highly bound drug
  • low plasma protein level may occur in old age or malnutrition
  • Reduced doses in both hepatic and renal failure
312
Q

What gets into the BBB

A

lipid soluble and small
E.g. Second generation antihistamines (loratadine), achieve far lower brain concentrations cf some of the first generation antihistamine (diphenhydramine), and thus are classified as non-sedating

313
Q

What is metabolism

A

enzymatic conversion of one chemical compound into another. Most drug metabolism occurs in the liver, although some processes occur in the gut wall, lungs and blood plasma.
Metabolic processes will convert the drug into a more water-soluble compound. This is an essential before the drug can be excreted in the body fluids such as urine or bile.

314
Q

What is phase 1 metabolism

A

involve reduction or hydrolysis of the drug, but the most common biochemical process that occurs is oxidation (

315
Q

How is a drug oxidised

A

Oxidation is catalysed by cytochrome P450 enzymes and results in the loss of electrons from the drug (electrons are negatively charged subatomic particles).

316
Q

What is Phase 2 metabolism

A

conjugation - attachment of an ionised group (metabolite more water soluble) to the drug. These groups include glutathione, methyl or acetyl groups. These metabolic processes usually occur in the hepatocyte cytoplasm.
This facilitates excretion as well as decreasing pharmacological activity

317
Q

Cytochrome P450 enzymes are essential for the production of

A

cholesterol, steroids, prostacyclins, and thromboxane A2

318
Q

How does cytochrome p450 effect drug metabolism

A

It can be inhibited or induced by drugs, resulting in clinically significant drug-drug interactions that can cause unanticipated adverse reactions or therapeutic failures

319
Q

What is the relation of cytochrime p450 and adverse drug reactions and interactions

A

knowing which drugs are metabolised by cP450 and which are most inhibiting/inducing helps reduce ADR and interactions

320
Q

What is an inducing agent

A

with another medication, the dosage of the other medication may need to be adjusted since the rate of metabolism is increased and the effect of the medication reduced

321
Q

What is an inhibiting agent

A

If a medication is taken with an agent that inhibits its metabolism, then the drug level can rise and possibly result in a harmful or adverse effect

322
Q

Name some cytochrome p450 inducers

A

Carbamazapine, Rifampacin, Barbiturates, Phenytoin, St Johns Wort

323
Q

Name some cytochrome p450 inhibitors

A

Sod Valporate, cipro, sulphonamide, cimitidine, omeprazole, antifungals, amiodarone, isoniazid, erthythromycin, clarithromycin, grapefruit juice

324
Q

Where does elimination mainly occur

A

Kidneys, Liver, Faeces

325
Q

How does the liver affect elimination

A

makes into more soluble for kidneys to excrete.

excreted into bile and therefore faeces

326
Q

Who has altered physiology

A

Pregnancy • Old Age • Children

327
Q

How is absorption affected in pregnancy

A

gastric emptying and SI motility reduced (progesterone) this increase Tmax, reduce Cmax
gastric pH increase, mucous production increase
N&V

328
Q

How is distribution affected in pregnancy

A

plasma volume & extravascular water content expansion. total body water increase by 8L (hydrophilic drugs can distribute)
plasma albumin conc falls so binding falls (more free drug)
placental hormones and steroids displace drugs from binding site

329
Q

How is metabolism affected in pregnancy

A
  • some drugs induced by oestrogen/progesterone. Therefore higher metabolism, inc excretion
  • some isoenzymes competitively inhibited by progesterone/estridiol imparing elimination eg theophylline
330
Q

How is elimination affected in pregnancy

A

renal elimination increased by 60-80%. GFR up by 50%. so more elimination of drugs. eg penicillin, digoxin

331
Q

How is absorption affected in elderly

A

Decrease absorption because:
decrease cardiac output, blood flow, drug abs.
reduced gastric PH. loss of intestinal surface

332
Q

How is distribution affected in elderly

A

Increase toxicity, drug effect

decreased albumin production, in blood, and how much binds to drug.

333
Q

How is metabolism affected in elderly

A

increased duration and affect of drug

reduced hepatic enzyme activity, hepatic blood flow, metaboloisation

334
Q

How is excretion affected in elderly

A

lowered renal function

335
Q

Other names for liver disease

A 
Alpha 1 antitrypsin
		Alagille syndrome
		PFIC
		Hepatitis B,C
		Autoimmune hepatitis
		Primary sclerosing cholangitis
		Budd chiari syndrome
		Veno-occlusive disease
		Fatty Liver Disease
		Primary biliary cirrhosis
		Hemochromatosis
		CF Liver disease
		Alcoholic steatohepatisis
336
Q

Name some functions of the liver

A

Production of bile
Synthetic function - plasma protein - clotting factor
Metabolism - fat - carbohydrate - protein
Storage - vitamins - glycogen
Detoxification (metabolites of drugs sometimes harmful like para)

337
Q

How is aspirin metabolised

A

Phase one - salicylic acid
Phase two - joins glucoronic acid or glycine

metabolite excreted kidneys

338
Q

Paracetamol metabolised with

A

glutathione

339
Q

prodrugs are

A

metabolised into active drug

340
Q

Symptoms of choleostasis

A 
Jaundice
Pale Stools
Coloured Urine (yellow-brown dependant on age)
Steatorrhoea
Pruritis
Fat soluble Vitamin deficiencies
341
Q

Symptoms of Cirrhosis

A 
Portal hypertension
Haematemesis
Malaena
Coagulopathy
Ascites
Encephalopathy
Hepatopulmonary syndrome
Failure to thrive
Malaise
Lethergy
Jaundice (late change)
342
Q

Symptoms of Acute Liver Failure

A 
Jaundice
Hypoglycaemia
Coagulopathy
Encephalopathy
Hepatorenal Syndrome
Electrolyte and acid base disturbance
Cerebral oedema
343
Q

Changes in drug distribution in liver disease

A

Hypoalbuminaemia- resulting in high fraction of free drug

Blood bypassing the liver – portosystemic shunting

344
Q

Changes in excretion in liver disease

A

Compounds excreted in bile via the enterohepatic circulation may reach high concentrations resulting in hepatoxicity e.g phenytoin and some antibiotics.

345
Q

After first pass metabolism the clearance of the drug is determined by

A

Extent of drug binding
Blood flow
Functional hepatocytes

346
Q

Liver Function Tests

A 
AST = Aspartate Transaminase  50 iu/l
ALT  = Alanine Transminase  40i u/l

Enzymes found in hepatocytes (particularly ALT)
Raised level = inflammation/necrosis of liver

ALP, GammaGT, glucose, albumin, prothombin time, partial thromboblastin time, 1NR

347
Q

Two types lipoprotein

A

High and low density

high HDL and low LDL good

348
Q

How do statins work

A

inhibit of enzyme (3-hydroxy-3-methylgulutaryl-Coenzymes A reductase) - HMG CoA reductase
HMG CoA reductase is involved in the production of cholesterol

As a result Hepatocytes import LDL cholesterol from the blood.
Serum cholesterol levels fall

349
Q 
What are the effects of the following on liver:
PHENYTOIN
WARFARIN
CORTICOSTERIODS
NON-STEROIDAL ANTI-INFLAMMATORY
DRUGS
HYPNOTICS/SEDATION
CIMETIDINE
A

PHENYTOIN - Hepatic clearance decreased
WARFARIN - Inhibit clotting factor synthesis
CORTICOSTERIODS/NSAIDs - Leads to excess sodium and water retention/ gastrointestinal bleeding
HYPNOTICS/SEDATION - May precipitate hepatic encephalopathy
CIMETIDINE - Enhanced risk of adverse drug reaction

350
Q

How can you deal with blood poisoning with Urine pH

A

Altering urine pH increases excretion - alkaline means acid dissolved vice versa

351
Q

What is therapeuric index

A

The therapeutic index of a drug is the ratio of the dose that produces toxicity to the dose that produces a clinically desired or effective response in a population of individuals.

Therapeutic index= (TD 50)/ED50

Where: TD50 is the dose of drug that causes a toxic response in 50% of the population and ED50 is the dose of drug that is therapeutically effective in 50% of the population.

352
Q

Which drugs have effect on the kidneys

A 
many antibiotics, 
histamine H2-receptor antagonists,
digoxin, 
anticonvulsants 
non-steroidal anti-inflammatory drugs (NSAIDs)
Drugs inc potassium potassium supplements and potassium-sparing diuretics
drugs inc sodium eg antacids
vit d because calcium inc
353
Q

Name some Drugs that have been reported to cause glomerulonephritis

A

penicillamine, gold, captopril, phenytoin and some antibiotics, including penicillins, sulphonamides and rifampicin

354
Q

Name some Drugs that may cause interstitial nephritis

A

penicillins, cephalosporins, sulfonamides, thiazide diuretics, furosemide, NSAIDs and rifampicin

355
Q

Name some drugs that cause direct toxicity to the renal tubules

A

aminoglycosides, amphotericin and ciclosporin.

356
Q

Name some drugs which causes crystalluria and could therefore cause urinary tract obstruction

A

High-dose sulfonamides, acetazolamide or methotrexate

357
Q

Name some drugs which cause urinary tract obstruction due to retention of urine in the bladder

A

Anticholinergics (eg, tricyclic antidepressants), and alcohol

358
Q

What information is needed on a Clinical Management Plan

A 
•	Pt name  
•	The illness being treated
•	Start and review date 
•	class of meds/appliances under plan 
•	Any restrictions or limitations to the strength or dose of any medicine
•	warnings/sensitivities
•	The arrangements for notification of:-
a) Suspected or known reactions
b) Incidents which might lead to death or serious deterioration
•	when SP to refer
359
Q

Can a Supplementary prescriber prescribe CDs under the CMP

A

yes since 2005 nurse and pharmacist and 2006 for physiotherapist, podiatrist, radiographer, and optometrist

360
Q

who can be a Supplementary Prescriber

A

nurse, midwife, pharmacist, physiotherapist, podiatrist, radiographer, optometrist, chiroprodists, podiastrists, dietican

361
Q

What pharmacokinetic differences are there in kids?

A

Absorption - gastric pH, intestinal transit
Skin - SA, thickness,
Less muscle
Distribution - more water, less protein binding

362
Q

Give example of rectal route good in kids

A

diazepam for epileptic seizures or analgesics eg paracetamol, may be given this way if the child is vomiting

363
Q

Give example of drugs requiring high doses in kids

A

carbamazepine,
phenytoin and
theophylline

364
Q

Child under 16 and can understand can consent to meds under

A

Gillick competence

365
Q

What does STOPP and START stand for?

A

STOPP-Screening Tool of Older Persons Prescriptions START -Screening Tool to Alert doctors to Right i.e. appropriate, indicated Treatments

366
Q

How is absorption affected in elderly

A

less motility, gastric acid, emptying

367
Q

How is distribution affected in elderly

A

less lean body mass, water in body plasma protein

more adipose tissue

368
Q

How is metabolism affected in elderly

A

liver size and mass less and less blood flow to it. therefore less proteins, less CHD transformed, less cholesterold, bile, phsospholipids,

369
Q

How is excretion affected in elderly

A

renal function less. in size, blood flow, functionality, secretion.

370
Q

What is polypharmacy

A

the practice of prescribing four or more medications to the same person

371
Q

How does antihistamine work

A

allergen on mast cell triggering histamine release (by IgE antibodies) - antihistamine blocks other side

372
Q

Name first gen antihistamines

A

diphenhydramine ( benedryl), chlorphenamine, cyclizine, hydroxyzine, promethazine (phenegran)

373
Q

Name second gen antihistamines

A

loratidine, cetirizine, desloratidine, acirvastine,

374
Q

Name some drugs used in opiate detox

A 
Lofexidine is the main drug used - withdrawal 
Adjuvent therapies can be added
Buscopan
Loperimide
Zopiclone
Diazipam
375
Q

How does Naltrexone work

A

Pt who are drug free and want the safety of not being able to use heroin
Helps people to cope with triggers and high risk situations with the knowledge that heroin use would have no effect
Works by binding tightly to opiate receptors in the brain to block the effects of heroin

376
Q

What drugs used in alcohol withdrawal

A

Chlordiazepoxide (Librium tablet) - 6-11 days, sedative, anti-anxiety effect
Disulfiram (trade name Antabuse) - producing an acute sensitivity to alcohol
Acamprosate (brand name Campral) - stabilise the chemical balance in the brain that would otherwise be disrupted by alcoholism. works with abstinance and support groups
Naltrexone

377
Q

Give example of drugs for therapeutic monitoring

A

Gentamycin
Vancomycin
Cyclosporin
Aminophylline

378
Q

How does Nalaxone work

A

binds to the opioid receptors and blocks them, preventing the body from responding to opiates. Used for respiratory depression/coma caused by opioids therefore reverses. technically anyone can give because emergency.

Uni (2 decks)

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