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Pharmacology (BN517) > Cue cards > Flashcards

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1
Q

Whats 1 g (gram) in mg (milligrams)

A

1 g (gram) = 1000mg (milligrams)

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2
Q

Whats 1 mg (milligrams) in mcg/ug (micrograms)

A

1 mG = 1000mcg/ug (micrograms)

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3
Q

Whats the main drug equation

A

What you want / what youve got x (1 tablet or volume of stock solution)

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4
Q

What is the APLS formula for weight?

A

weight = (age (years) +4) x 2

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5
Q

Do you round paediatric calculations?

A

No

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6
Q

Define the term ‘drug’

A

‘Any substance or product that is used or intended to be used to modify or explore physiological systems or pathological states for the benefit of the recipient

A drug is defined as “any substance other than food that affects living systems.

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7
Q

Where do we get our drug information?

A

Medsafe, New Zealand Formulary & New Zealand Formulary for children, The Cochrane Collaboration, Poisons centre, Drug company information

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8
Q

What are the thre Characteristics of drugs

A

Potency Selectivity Specificity

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9
Q

What are the three states drugs can be in?

A

Solid, liquid, gas

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10
Q

What are Enteral drugs

A

These can be solid or liquid, and are absorbed in the stomach and intestine.

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11
Q

What are Parenteral drugs

A

Drugs that are given by routes other than the digestive tract.

IV infusions, Topical drugs, intradermal implants, Mucous membrane drugs

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12
Q

How do drugs work?

A

Drugs act by stimulating or inhibiting the function of certain cells or organisms

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13
Q

Where do drugs act on?

A

Chemical interaction
Act on receptors

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14
Q

Define Pharmacodynamics

A

What the drug does to the body to produce its effect. How it affects the GI tract e.g.

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15
Q

Define Pharmacokinetics

A

What the body does to the drug
 Absorption
 Distribution
 Metabolism
 Excretion

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16
Q

What are the nine rights?

A

1.Right patient
2.Right drug
3.Right route
4.Right time
5.Right dose
6.Right documentation
7.Right action
8.Right form of drug
9.Right response

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17
Q

What should you know before giving a drug (12)

A

What is the substance or chemical?
What are the main effects?
What are the side effects?
What if there is an adverse reaction?
What other substances are being taken?
*Drug interactions, polypharmacy

◦ The usual dose
◦ Frequency and route of administration
◦ Indications and contraindications
◦ Significant adverse reactions
◦ Major drug interactions
◦ Dietary implications
◦ Appropriate monitoring techniques and interventions

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18
Q

When should you take drugs in terms of food?

A

½ - 1 hour before or 2–3 hours after meals (depending on drug specifications).

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19
Q

Whats a psychoactive drug

A

A psychoactive drug is one which affects a person’s mood and/or behaviour.

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20
Q

What are the 8 purposes of drugs?

A

Diagnosis, Curative, Supportive, Palliative, Prophylaxis, Restorative, Substitutive, Recreation

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21
Q

What is the purpose of Diagnosis drugs?

A

To diagnose or study the pathology of medical conditions, diseases, or syndromes

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22
Q

What is the purpose of Curative drugs?

A

Curative: antibiotics

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23
Q

What is the purpose of supportive drugs?

A

Supportive drugs are sometimes used to lessen the harmful side effects. Paracetamol (↓body temperature)

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24
Q

What is the purpose of Palliative drugs?

A

NSAIDs for pain

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25
Q

What is the purpose of Prophylaxis drugs?

A

Prevention of numerous infectious diseases. vaccinations

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26
Q

What is the purpose of Restorative drugs?

A

Restore function. Vitamins

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27
Q

What is the purpose of Substitutive drugs?

A

Substituting something that is lacking. Insulin, iron

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28
Q

What is the purpose of Recreation drugs?

A

Methamphetamine, alcohol, nicotine, caffeine

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29
Q

Define Drug use

A

Taking a substance for an intended beneficial purpose with minimum hazard.

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30
Q

Define Drug misuse

A

Drug misuse: drug is used in such a way to significantly increase the potential hazard.

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31
Q

Define drug abuse

A

Drug abuse: occurs when a drug is repeatedly used for other than its intended effects.

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32
Q

What are the categories of drug (6)

A

1) Herbal
2) Over the counter (OTC)
3) Prescription
4) Tobacco
5) Alcohol
6) Illicit

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33
Q

What classifies a good drug (9)

A

1) Unlikely to produce serious unwanted effects.
2) Easy to administer.
3) Pleasant to take.
4) Of the suitable duration of action. (Shortes time taken possible, less likely for side effects)
5) Chemically stable. (able to be stored)
5) Cheap
6) Potent.
7) Selective.
8) High therapeutic index
9) Not highly protein-bound in the blood plasma.

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34
Q

Whats an example of Mucous membrane drugs

A

For example, nasal sprays and asthma drugs.

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35
Q

What are less common but other routes of administration

A

Intramuscular
Intraosseous (bone)
Subcutaneous
Per vagina
Per rectum
Dermal (on the skin but penetrates)
Inhaled

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36
Q

What are some situations where oral medications wouldn’t be administered?

A

If a person is having difficulty swallowing, is unconscious, nil by mouth, vomiting or in an emergency

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37
Q

In order for a drug to have an action it needs to …

A

Be free in the blood/ circulatory system and bound to a receptor to some description

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38
Q

What should the person and their family be able to tell you about the drug their taking?

A

What medications they are taking.

How and when to take each medication.

Expected side effects and adverse reactions.

When to notify someone of any problems with medications.

What follow-up appointments are needed to monitor progress or dosage.

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39
Q

You have several medications to give to your patient. How should you offer them to your patient and why?

A

You should offer them separately so that you can identify any medications that are refused or need to be replaced or dropped.

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40
Q

What does QID mean?

A

To give the medication four times a day.

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41
Q

What does QD mean?

A

meaning to give medication once a day.

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42
Q

What does BID mean?

A

meaning to give medication twice a day.

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43
Q

What does TID mean?

A

meaning to give medication three times a day.

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44
Q

What does PRN mean?

A

Meaning to give medication as the situation demands or according to need.

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45
Q

What does Mane mean?

A

means a medication should be given in the morning.

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46
Q

What is the best way to avoid giving the wrong drug to a patient?

A

Ensure that the generic name is used

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47
Q

What are the three different types of drug names

A
  • the chemical name
  • the approved (generic) name
  • the proprietary (trade) name or names
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48
Q

What are ethical Issues Related to Medicines

A

 Animal testing
 Use of technology
 Advertising of medicines
 Clinical trials
 Drug company and prescriber relationship
 Pharmacoeconomics – rationing of care

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49
Q

Who are the people that are most at risk groups

A
  • Elderly
  • Children
  • Pregnant women and their foetus
  • Those with altered mental abilities
  • Psychiatric
  • Developmental
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50
Q

What must prescriptions be

A
  • Clear, concise and correct
  • With the five basic nursing rights of medication administration
  • bears the signature, name and address of the prescriber
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51
Q

What are the rules for Telephone orders and standing orders

A

Can be taken if the doctor cannot be present. Must be through to a nurse entitled to administer it. The doctor must ASAP, write out the drug order & sign it

Faxed prescription can confirm an oral order but is not legally acceptable, as the signature has to be original

Standing orders’ are sometimes left by doctors. These have no legal validity unless properly written, dated
and signed as for any normal prescription

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52
Q

When fill out a hostipital drug chart you must

A

to use approved names for drugs

not to alter existing orders

to record all instances when drugs are administered, or when the drug was not administered, giving reason

that nurse-initiated therapy (e.g. mild analgesics, laxatives, antacids) is to be countersigned by a doctor

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53
Q

What are the benefits to electronic prescribing

A

Improved legibility

improved access to patient’s past history

Access to prescribing guidelines and drug information

Warnings as to potential adverse reactions, allergies and drug interactions

Possibility of accumulating epidemiological and prescribing patterns data

Improved efficiency in the health-care system

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54
Q

What drug packages are advisory

A

Advises use how to use, affects of drugs, etc

THIS MEDICINE MAY CAUSE DROWSINESS

DISCARD CONTENTS AFTER dd/mm/yyyy

RINSE MOUTH WITH WATER AFTER EACH USE

REFRIGERATE: DO NOT FREEZE

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55
Q

What drug packages are explanatory or reminders

A

CERTAIN FOODS AND DRUGS SHOULD NOT BE TAKEN WITH THIS MEDICINE

SHAKE THE BOTTLE

THIS PRESCRIPTION MAY BE REPEATED… TIMES

KEEP OUT OF REACH OF CHILDREN

TAKE IMMEDIATELY BEFORE FOOD

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56
Q

How are dangerous drugs kept?

A
  • All opiates are kept in double locked cupboard
  • Drug keys should be carried by RN
  • Must be counted
  • Must be signed for by 2 nurses (at least 1 RN) and the count noted in
    the drug register
  • Both nurses must go to the bedside and check patient
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57
Q

How are non controlled drugs kept?

A

Other drugs in single locked cupboard
* Benzodiazepines, codeine, DHC
* Not counted
* Need to be monitored

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58
Q

What are some rules to follow when documentation

A
  • Signing of register and medication charts
  • Provide a specimen signature
  • Never sign before giving a drug
  • Different forms in all institutions so a need to familiarise
  • Write in notes also to confirm meds given
  • Blister packs - check the drugs don’t just assume they are correct
  • the person who gives the drug
    is legally accountable if error occurs
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59
Q

Where should you report medication errors

A

Must be reported on a institutional and national level

MEDSAFE is responsible for regulation of therapeutic products in NZ and administering the Medicines Act 1981 and Regulations 1984

CARM – Centre for Adverse Reactions and Monitoring

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60
Q

When should you notify MEDSAFE and CARM

A

Notify of all near misses
Notify of all errors

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61
Q

What are the problems with advertising drugs on TV?

A

They do not show all the risks but show all the benefits. Patients often think the drug works better than it does.

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62
Q

What is the Medicines Act 1981

A

The Act ensures that the medicines and products used in New Zealand are safe and effective.

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63
Q

Whats the Medicines Act Amended 2005

A

The principal Act is amended by omitting the word “drugs”, and substituting the word “medicines” .

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64
Q

Whats the Misuse of Drugs Act 1975

A

An Act to consolidate and amend the Narcotics Act 1965 and to make further provision for the prevention of misuse of drugs

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65
Q

What is the Misuse of Drugs Amendment Regulations 2014

A

Pursuant to section 37 of the Misuse of Drugs Act 1975.

provide for nurse practitioners to prescribe (and therefore also to supply and administer) any controlled drug, subject to the same restrictions as currently apply to other prescribers:

provide for midwives to prescribe (and therefore also to supply and administer) the controlled drugs listed in new Schedule 1C, subject to the same restrictions as currently apply to other prescribers:

provide that prescriptions for Class A controlled drugs, Class B controlled drugs, and specified Class C controlled drugs may be either on a handwritten form or on a form electronically generated by a system approved for the purpose by the Director-General of Health and notified in the Gazette.

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66
Q

What are restricted medicines

A

Medicines that are sold by retail only by a pharmacist in a pharmacy or a hospital. Going to Chemist warehouse getting some meds

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67
Q

What are restricted medicines

A

Medicines that are sold by retail only by a pharmacist in a pharmacy or a hospital. Going to Chemist warehouse getting some meds

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68
Q

What are prescription medicines?

A

Sold by retail only under prescription from an authorised prescriber. Supplied by retail sale only under a prescriber.

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69
Q

What are pharmacy-only medicines

A

Sold in retail at only pharmacies or hospitals.

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70
Q

What are general sale medicines

A

May lawfully be sold in New Zealand. All drugs other than prescription medicines, restricted medicines or pharmacy-only medicines

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71
Q

What are controlled drugs

A

Defined in the Misuse of drugs act and has three classes. Class A, B and C

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72
Q

What are some Class A (severely restricted) drugs

A

Heroin, lysergide, thalidomide

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73
Q

What are some Class B (high- medium abuse level) drugs

A

Morphine, fentanyl, opium, methadone, pethidine, amphetamine, pseudoephedrine

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74
Q

What are some Class C, Part I (ministerial approval needed) drugs

A

Weed, ketamine, coca leaf

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75
Q

Why do drug calcs need to be accurate?

A

Too little could see the patient not recovering in the manner that would be expected; too much could have potentially harmful or even fatal consequences.

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76
Q

What are some Adverse reactions to drugs

A

Hypotension
Constipation
Nausea and vomiting

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77
Q

What’s the thought process order before prescribing drugs? (9)

A

First, do no harm.
1. What is the problem?
2. Is there a drug-based solution? What other sorts of therapy could help?
3. What does the drug do and how does it act?
4. How long will the patient be treated?
5. How will you monitor therapy?
6. How much drug should be given?
7. What is special about this patient?
8. Are there any warnings for the patient or staff?

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78
Q

What causes poor compliance

A

Complicated drug regimens.

Bad taste or pain on administration.

Adverse effects.

Not wanting to disturb or wake the patient for night-time doses.

Poor communication and lack of information.

Lack of support and monitoring of therapy.

Cost or difficulty in obtaining medicines.

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79
Q

What does poor compliance lead to

A

Drug levels in the body may fall below the therapeutic range, leading to inadequate responses and lack of effect. Monitoring and adjustment of therapy may not occur, leading to:

Revising the diagnosis.
Increasing doses.
Adding more drugs.
Sending the patient for more tests.
Poor compliance with therapy may result in pregnancy (oral contraceptives), convulsions (antiepileptic drugs), or strokes or heart attacks (anticoagulant or antithrombotic drugs).

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80
Q

Whats Polypharmacy

A

Polypharmacy is defined as ‘the concurrent use of multiple medications’.

Polypharmacy is a situation in which multiple drug interactions can occur, and is potentially harmful to the patient.

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81
Q

How can you reduce the effects of Polypharmacy

A

Prevention: avoid prescribing or administering drugs for minor complaints.

Medication review: assess appropriateness and need for therapy, dosage, formulation, ADRs, drug interactions, and compliance.

Non-pharmacological approaches: use lifestyle measures whenever possible.

Communication: with the patient, about concerns, expectations and difficulties with compliance.

Simplification: reduce regimens to essential drugs, at the lowest effective doses and frequencies.

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82
Q

Whats the definition of potent in terms of drug

A

If a drug is potent less of it is required to achieve a therapeutic range.

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83
Q

What does a selective drug mean

A

A highly selective drug will target the desired receptor or drug and not other undesired receptors or cells

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84
Q

Why might it be bad for a drug to be highly protein-bound in the plasma?

A

If more of the drug is bound to proteins then less of it is available to diffuse into tissues and have therapeutic effects.

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85
Q

Why do we need to know about pharmacokinetics?

A

To maximize beneficial effects:
We must achieve concentrations that are high enough to elicit a desired response (do not fall below the minimum effective concentration).

To minimize harm:
We must avoid concentrations that are too high (do not exceed the minimum toxic concentration).

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86
Q

What’s the definition of the therapeutic range

A

The therapeutic range is the range of plasma concentrations at which a drug is effective with minimal toxicity to most patients.

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87
Q

What’s the minimum toxic concentration = MTC (upper limit)

A

The minimum amout of drug to produce an effect

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88
Q

The minimum effective concentration = MEC (lower limit)

A

The minimum effective concentration = MEC (lower limit)

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89
Q

Whats the Therapeutic index

A

The therapeutic index is the ratio between the toxic dose (minimum toxic concentration) and the therapeutic dose (minimum effective concentration) of a drug. It is used as a measure of the relative safety of the drug for a particular treatment.

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90
Q

What does a high therapeutic index mean

A

a high therapeutic index so that a change in dose will most likely not cause any harm.

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91
Q

What does a low therapeutic index mean

A

a very low therapeutic index and serious harm or death can result if the wrong dosage is given.

92
Q

Define Clearance

A

Clearance is the ability of the body’s excretory organs to eliminate drugs from the blood. Clearance is expressed as a volume per unit of time (usually mL/min), that is, the volume of blood which is completely cleared of a drug in a period of time.

93
Q

Whats the clearance unit?

A

Clearance is expressed as a volume per unit of time (usually mL/min), that is, the volume of blood that is completely cleared of a drug in a period of time.

94
Q

What’s Half-life and how do you calculate it?

A

A drug’s half-life is the time taken for the drug concentration in the plasma to decrease to half of its original value.
The half-life is the time between 100% of maximum drug concentration and 50% of maximum. Another half-life later, concentration is at 25% of maximum.

95
Q

Whats Steady state

A

This is the condition where the concentration of a drug in a body fluid – usually the plasma – reaches a steady state (neither increasing or deceasing). That is, the rates of drug administration and drug elimination are equal.

96
Q

Whats Loading Dose

A

A high dose known as a loading dose is given to reach the therapeutic range rapidly.

97
Q

Role of the nurse in prescribing and
administration of drugs

A

Taking a drug history.
* Assessing the patient.
* Noting the prescription, checking dosage and calculations, and ensuring correct administration (‘five rights’).
* Signing the patient record after administering a dose.
* Identifying problems relating to drug therapy.
* Ensuring compliance with therapy.
* Ensuring safe storage of drugs.
* Following institutional procedures and maintaining documentation.
* Advocacy and education.

98
Q

Why is taking drugs while pregnant harmful?

A

During pregnancy, any chemical or drug that is absorbed may reach the fetus via the maternal circulation.

99
Q

If it is necessary to administer drug therapy during pregnancy, what factors should be considered

A

Fetal gestational age at the time of exposure.
Any other drugs administered concurrently.
The drug dose, intervals, and duration of treatment.

100
Q

How is Absorption of drugs affected in pregnant women

A

Pregnancy does not directly affect drug absorption from the GI tract. However, there are some GI changes that affect drug absorption:

Delayed gastric emptying.
Decreased gastric motility, which can increase or decrease drug absorption.
Drug absorption from other sites may be increased during pregnancy. For example:

Increased pulmonary drug absorption.
Increased cutaneous or topical drug absorption.

101
Q

What might cause increased cutaneous or topical drug absorption in pregnant women?

A

Pregnancy causes an increase in blood flow and surface area

102
Q

What might cause increased pulmonary absorption in pregnancy?

A

Pregnancy increases breathing rate

103
Q

Would an increase in body fat increase or decrease the volume of distribution of a fat-soluble drug?

A

increase

104
Q

How does pregnancy affect Excretion

A

Maternal renal blood flow and glomerular filtration rate increase during the first 8 months of pregnancy. This causes an increased elimination rate for drugs excreted by the kidneys.

105
Q

Whats a Teratogen

A

Teratogen: a substance that causes transient or permanent physical or functional disorders in the fetus without causing toxicity in the mother.

106
Q

Whats a Mutagen

A

Mutagen: a physical or chemical agent that causes genetic material (DNA) to undergo a detectable and heritable structural change. This may affect mother and fetus.

All mutagens are teratogens, but not all teratogens are mutagens.

107
Q

Whats a Carcinogen

A

Carcinogen: any agent that by either direct or indirect actions causes a normal cell to become a neoplastic cell (cells that grow abnormal tumours/growths). If a mutagen causes mutations that lead to cancer, they are also carcinogens.

108
Q

What kind of drug transfer occurs across the placenta

A

simple diffusion

109
Q

Transfer across the placenta depends on several factors such as

A

The physicochemical properties of the drug. For example, low molecular weight drugs freely cross the placenta, while drugs of molecular weight over 1000 (e.g. heparin) cross very poorly.

Protein binding. Drugs bound to maternal blood proteins won’t cross the placenta.

Lipid solubility. Lipid soluble drugs cross membranes more easily.

In the mother:
In late gestation, blood flow increases, and the membranes that separate mother and fetus become thinner. This results in increased placental transfer of un-ionised lipid-soluble non-protein-bound drugs.

Disease states such as hypertension or diabetes mellitus can also affect drug transfer.

110
Q

Why are the affects of drugs more harmful for the fetus than the mother

A

As the fetus has an immature liver and drug-metabolising enzymes.

Drugs and drug metabolites may accumulate in amniotic fluid, resulting in increased exposure.

Drugs that are ‘excreted’ by the fetal kidneys may pass into the amniotic fluid and be reabsorbed by the fetus increasing its exposure.
Because the only connection to the environment is via the placenta, the fetus has a slower overall rate of drug excretion. This can enhance exposure to drugs.

111
Q

What is the timeline of liver maturation for fetuses

A

Activity can be detected at 5–8 weeks.
By 12–14 weeks, the fetus has about 30% of the capacity of adults.
Full maturation of drug-metabolising capacity is not evident until 1 year after birth.

112
Q

What are signs of neonate withdrawal symptoms

A

Hyperactivity
Increased irritability
Persistent crying
Convulsions
Sudden death

113
Q

Why are newborns vulnerable

A

Their skin is thin and permeable.
Their stomachs lack acid.
Their lungs lack much of the mucous barrier.
They regulate body temperature poorly.
They become dehydrated easily.

114
Q

What are the differences between children and adults in terms of pharmacokinetic

A

Liver drug-metabolising enzyme activities are increased, so children metabolise drugs at a faster rate.

Drugs primarily eliminated by hepatic (liver) metabolism may require dosage or frequency adjustments because of a shorter plasma half-life.

Although renal function is low in the newborn, this rapidly increases. Later in childhood, renal function may exceed adult parameters, and if ignored, may result in drug underdosing.

115
Q

What are the main issues for elderly and taking drugs

A

polypharmacy and difficulty swallowing medications.

116
Q

What are Physiological Changes with Aging

A

1) An increase in sensitivity to drugs and drug-induced adverse reactions may occur. See the section below.

2) Loss in body weight (decreased volume of drug distribution) may require a lower adult dose or re-evaluation of dosages.

3) Conversely, a proportional increase in body fat in the elderly may cause an increased volume of distribution for fat-soluble drugs.

4) Pharmacokinetics are altered because of decreased gastric acid and slowed gastric motility, and unpredictable rates of dissolution and absorption.

5) A decrease in renal excretion.

6) A decrease in drug metabolism in the liver.

Therefore, higher blood and tissue levels of drugs may lead to an increased incidence of adverse drug reactions.

117
Q

Why do the elderly have a greater sensitivity to drugs?

A

The problems of decreased body size, altered body composition (more fat, less water), and decreased liver and kidney function cause many drugs to accumulate in older people’s bodies at dangerously higher levels and for longer times than in younger people.

Changes in target-organ or receptor sensitivity may result in a greater or lesser than normal drug effect.
The number of receptors may change (increase or decrease) as we age.

118
Q

The half-life of fat-soluble diazepam increases from 20 hours in a 20-year old to 90 hours in 80-year old. What might explain this?

A

diazepam is a fat-soluble drug. The elderly have a higher fat percentage and therefore have a higher percentage of distribution.

In addition, elderly people have slower drug metabolism in the liver and slower excretion by the kidneys meaning that it takes longer for them to eliminate the drug

119
Q

Can you crush pills for the elderly?

A

Crushing tablets or opening capsules is one way to make this easier. However, this may change the way the drug is absorbed, releasing a drug in 5–10 minutes.

Do not crush tablets without checking first.
Consider using a liquid alternative.

120
Q

What is bioavailability

A

The amount of drug that is free in the blood, available to bind with receptors and cause therapeutic changes.
The amount of drug reaching the systemic circulation

121
Q

What are two routes of elimination

A

metabolism and excretion.

122
Q

What is the primary organ for drug metabolism

A

The liver

123
Q

What are the main organs for drug metabolism?

A

Liver, gallbladder, oesophagus, stomach, duodenum, pancreas, illum

124
Q

What is the primary organ for excretion?

A

Kidney

125
Q

Define Metabolism in terms of drugs

A

This is the process in which a parent drug compound is transformed to different compound called a metabolite.

126
Q

What is Phase I of drug metabolism

A

Chemical modification of the drug (oxidation, reduction, hydrolysis). This is carried out by the cytochrome P450 (CYP450) family of enzymes (see this table for examples of CYP450 enzymes).

127
Q

What is Phase II of drug metabolism?

A

conjugation of the drug (addition of other molecules such as sugars, sulfate)

128
Q

What vein takes the nutrient-rich blood to the liver?

A

hepatic portal vein

129
Q

Why are the CYP450 enzymes so important for drug metabolism?

A

CYP enzymes catalyse the reaction for phase 1. These are the chemicals that modify the drug and make it ready for excretion

130
Q

Is a drug metabolite more water-soluble than the parent drug

A

yes

131
Q

What is meant by “first pass metabolism”?

A

First-pass metabolism refers to the biotransformation (breakdown) of drugs in the liver prior to the drug reaching the systematic circulation

A phenomenon of drug metabolism at a specific location in the body which leads to a reduction in the concentration of the active drug, specifically when administered orally, before it reaches the site of action or systemic circulation.

Reduces any loss

This means drug metabolism that occurs in the liver before the drug reaches the systemic circulation.

132
Q

What is filtration in the kidneys

A

The water from the blood, together with all substances dissolved in this water (including drugs) is collected by the nephron into the Bowman’s capsule.

133
Q

What is reabsorption in the kidneys

A

Water is then reabsorbed back into the bloodstream as well as ions, glucose, and other nutrients. Drugs or drug metabolites present become concentrated inside the kidney fluid, or ‘filtrate’, which then becomes urine.

134
Q

What is secretion in the kidneys

A

Some drugs are secreted by special transporters from the blood (peritubular capillaries) into the filtrate. For example, penicillin.

135
Q

What is excretion in the kidneys

A

Drugs and drug metabolites are eventually excreted by the body in the urine.

136
Q

What is glomerular filtration rate (GFR)

A

The GFR is the amount of blood filtered by the kidneys each minute. GFR represents the sum of the contributions of the individual nephrons from both kidneys. You have around 2 million nephrons in your two kidneys! Each nephron will filter approximately 0.1 mL per day.

137
Q

Drugs usually work in one of four ways What are those ways?

A

1) Replace or act as a substitute for missing substances.
2) Stimulate or increase cellular activity.
3) Depress or slow cellular activity.
4) Interfere with function of foreign cells. For example, bacteria or neoplasms.

138
Q

Drugs do not confer any new function to cells, tissue or organs. They modify existing functions. What can they modify?

A

Physiological
Biochemical
Biophysical

139
Q

Whats an Agonist

A

A drug, hormone or transmitter substance that binds a receptor and causes a cellular response

For example, salbutamol is an agonist at β2 receptors on bronchiole smooth muscle which causes bronchodilation.

140
Q

Whats a Full agonist

A

A drug that is capable, at sufficiently high concentration, of producing a maximal cellular response. For example, adrenaline is a full agonist at β1 receptors in the heart.

141
Q

Whats a Partial agonist:

A

An agonist whose maximum effect is less than the maximal response of which the receptor is capable of eliciting. For example, tramadol is a partial agonist of opioid receptors.

Only produces a submaximal response

142
Q

What is an Antagonists

A

Can only produce pharmacological effects by opposing the action of agonists.

interferes with or inhibits the physiological action of another

143
Q

What is Affinity

A

Affinity is a measure of how avidly a drug binds to its receptor. However, just because a drug binds to a receptor doesn’t mean it can activate it.

144
Q

What is Efficacy

A

Efficacy is the ability of the drug-receptor complex to elicit a physiological response. For example, morphine and naloxone both have significant affinity for opioid receptors, but:

Morphine is a full agonist therefore has high efficacy.
Naloxone is an antagonist therefore has zero efficacy.

145
Q

What is Potency

A

Potency is the amount of drug required to produce 50% of the maximal effect. That is, the more potent the drug the lower the dose required.

146
Q

Usually, for a drug to produce an effect on a tissue or system there has to be some receptor with which it can interact. What are the four primary drug targets

A

Enzymes
Carrier molecules
Ion channels
Receptors

147
Q

Where can drugs be located?

A

Free in plasma.
Bound to plasma proteins.
Bound to a receptor.
Bound to tissue.

148
Q

What are Enzymes

A

Enzymes are biological catalysts that speed up chemical reactions.

149
Q

How do Non-steroidal anti-inflammatory drugs (NSAIDs) work

A

These drugs block the cyclo-oxygenase (COX) enzymes that produce prostaglandins. Hence, they reduce pain and inflammation. However, they may have other effects

150
Q

What can be some side effcts of taking Non-steroidal anti-inflammatory drugs (NSAIDs)

A

NSAIDS decrease production of all types of prostaglandins. Some prostaglandins protect the gastric mucosa and maintain renal blood flow, so these positive effects are lost.

Gastric ulceration may occur, especially with aspirin.

Kidney (renal) function may be impaired (however, this is rare).

NSAIDS also decrease production of thromboxane A2 levels in platelets, leading to impaired platelet aggregation (especially aspirin), which prevents blood from clotting.

151
Q

What are ACE inhibitors

A

ACE inhibitors are important blood pressure-lowering drugs (antihypertensives)

152
Q

How do ACE inhibitors work?

A

ACE (angiotensin-converting enzyme) is found in blood vessels of the lungs and kidney.

ACE converts angiotensin I to the potent vasoconstrictor, angiotensin II.

ACE inhibitors decrease the activation of this enzyme. This prevents the conversion of angiotensin I to II, inhibiting vasoconstriction, and lowering blood pressure.

153
Q

Whats a side effect of taking ACE inhibitors

A

ACE inhibitors also inhibit the release of anti-diuretic hormone (ADH, also known as “vasopressin”), which increases the amount of water lost in urine.

154
Q

What is Furosemide used for

A

Furosemide is used to treat oedema and hypertension.

155
Q

How does the Furosemide drug work

A

Furosemide is a diuretic that inhibits the Na-K-Cl transporter in the kidneys. This reduces the ability of the kidneys to reabsorb sodium ions, leading to increased water loss in the urine (diuresis).

156
Q

How do Tricyclic antidepressants (TCAs) work

A

These drugs block the reuptake of noradrenaline (and to a lesser degree serotonin) from the neural synapse into the presynaptic neuron. This results in more of these neurotransmitters being available in the synapses of the brain to act on receptors, which increases mood (this is a bit of an oversimplification).

157
Q

How do Selective Serotonin Reuptake Inhibitors (SSRIs) work

A

These work similarly to TCAs but selectively inhibit serotonin (5HT) reuptake. For example, fluoxetine (Prozac).

158
Q

What drugs work on carriers?

A

Furosemide and both kinds of antidepressants

159
Q

What drugs work on ion channels

A

Local anaesthetics, Antiepileptic drugs, Calcium channel blockers, Antiemetics

160
Q

How does Local anaesthetics work

A

Local anaesthetics work by blocking the sodium channels in neurons. This stops the neuron from firing action potentials, and prevents pain and sensory signals from being sent to the brain. Examples of local anaesthetics are lignocaine, bupivicaine, and marcaine.

161
Q

How does Antiepileptic (anti seizure) drugs work

A

Although there are a range of different antiepileptic drugs, many of them work by blocking channels that cause excitation in the brain, or by increasing the action of channels that inhibit neural activity. Examples of these include:

Phenytoin (Dilantin)
Carbamazepine (Tegretol)
Lamotrigine

162
Q

How do Calcium channel blockers drugs work

A

Blocking calcium release in smooth muscle around blood vessels causes the muscle to relax, and the blood vessel to dilate, lowering blood pressure. Examples of calcium channel blockers include:

Nifedipine
Felodipine
Verapamil – this also may be used to treat some arrhythmias.

163
Q

How do Antiemetics drugs work

A

Antiemetics reduce nausea and vomiting. One example is ondansetron, which blocks serotonin (5HT3) receptors in the chemoreceptor trigger zone and gut (the 5HT3 serotonin receptor is an ion channel).

164
Q

What receptors can be targeted by drugs?

A

G protein-coupled receptors
β1 adrenergic receptors
β2 adrenergic receptors
α1 adrenergic receptors
Oxytocin receptors

165
Q

Where are G protein-coupled receptors located and what do they do?

A

These receptors are located in the cell membrane. They do not open or close in response to a hormone, neurotransmitter or drug binding. Instead, they change shape.

When activated they are able to “switch on” intracellular enzymes which produce second messengers such as cAMP and IP3. These “second messengers” are then able (via various means) to produce intracellular effects.

166
Q

Where are β1 adrenergic receptors located and what do they do?

A

These are located on the SA and AV nodes of the heart, as well as ventricular muscle cells.

β1 adrenergic receptors increase the activity of these cells. They are activated by adrenaline, noradrenaline, isoprenaline, dopamine, and dobutamine.

Effects of these drugs include:

Increased heart rate.
Increased cardiac output.
Increased blood pressure.
β1 adrenergic receptors are blocked (antagonised) by beta-blockers, for example, metoprolol and propranolol.

These drugs will decrease heart rate, cardiac output, and blood pressure.

167
Q

Where are β2 adrenergic receptors located and what do they do?

A

These receptors are located on various tissues:

Bronchiole smooth muscle
Coronary arteries
Skeletal muscle arteries
Uterus
When activated, β2 adrenergic receptors cause muscle relaxation. They are activated by adrenaline and salbutamol.

β2 adrenergic receptors are blocked (antagonised) by some beta-blockers, for example, propranolol and labetalol. This is why asthmatics should not usually be on these drugs.

168
Q

Where are α1 adrenergic receptors located and what do they do?

A

These receptors are located in various smooth muscle tissues, and have different effects in different places:

Contraction:
Some blood vessels
GI sphincters
Internal bladder sphincter
Seminal tract
Other effects:

Relaxation in the gastrointestinal tract.
Glycogenolysis in the liver.

169
Q

Oxytocin receptors

A

Oxytocin receptors are located in smooth muscle tissues, including in the uterus. When oxytocin binds these receptors during childbirth, it causes contraction of the uterine muscle.

170
Q

What are the roles dopamine has on the CNS

A

Nigrostriatal pathways: control of movement.

Mesolimbic/mesocortical pathways: emotion, perception and motivation.

Tuberoinfundibular pathways: inhibits secretion of prolactin.

Chemoreceptor trigger zone (CTZ): promotes vomiting.

171
Q

What are Antipsychotics (affecting dopamine signalling) drugs

A

Antipsychotics are all antagonists of the D2 family of receptors (D2, D3 and D4). Because dopamine receptors are found so widely in the brain, antipsychotics can have many side effects:

Movement disorders
Increased prolactin levels
Gynaecomastia, impotence, irregular menses, infertility, etc.

172
Q

What do Bromocriptine drugs do

A

This drug is a D2 receptor agonist used to treat many different medical problems, for example, Parkinson’s disease, type 2 diabetes, pituitary tumours, and hyperprolactinaemia.

173
Q

What do Levodopa drugs do

A

Levodopa is a dopamine precursor. This means it is metabolised into dopamine in the body. This drug is used to treat Parkinson’s disease, which is caused by the loss of dopaminergic neurons in the substantia nigra. Increasing dopamine levels can partially compensate for the loss of these neurons.

174
Q

Where are steroids recepors located?

A

Unlike most other types of receptors, steroid receptors are not on the cell membrane. They are found in the cytoplasm of the cell!

175
Q

What are some examples of steroid hormones

A

Estrogen
Progesterone
Testosterone

176
Q

What are examples of steroid drugs

A

Hydrocortisone
Prednisone
Dexamethasone
Beclomethasone
Budesonide
Fluticasone

177
Q

What does Desensitisation and tolerance mean in terms of drugs

A

Desensitisation and tolerance describe the observation that the effect of a drug gradually diminishes when it is given continuously or repeatedly. This may make it necessary to increase the dose to achieve the same therapeutic effects. This phenomenon may occur rapidly in the course of a few minutes, or more gradually over a period of days or weeks.

178
Q

How does the desensitisation and tolerance phenomenon occur

A

Change in receptors (altered sensitivity). With repeated activation, receptors become less able to cause cellular changes.
Loss of receptors (downregulation). Receptors may be internalised by a cell in response to a drug. This means there are less available receptors, and more drug is required to get a cellular response.
Increased metabolic degradation of the drug.
Physiological adaptation.
Behavioural adaptation.

179
Q

What happens to a pill inside your body after swallowing it?

A

The pill dissolves in the stomach, the active ingredient moves through the digestive tract and enters the bloodstream and travels around the body in the bloodstream.

180
Q

Define Receptor

A

Protein on the surface of a cell (or inside a cell) that selectively binds a specific substance (drug, neurotransmitter, or hormone) and delivers a signal to the cell.

181
Q

Define Receptor

A

Protein on the surface of a cell (or inside a cell) that selectively binds a specific substance (drug, neurotransmitter, or hormone) and delivers a signal to the cell.

182
Q

Define Substrate

A

A substance that binds to and gets changed in some way by an enzyme.

183
Q

What does distribution of drugs around the body depend on

A

Physiological factors. For example, cardiac output and regional blood flow.

Chemical factors. For example, lipid solubility of a drug, drug binding to plasma proteins or tissue components.

184
Q

What are variables that affect drug absorption

A

Nature of the absorbing surface (cell membrane) that the drug must traverse
Blood flow
Solubility of the drug
Ionisation

185
Q

How does the absorbing surface (cell membrane) that the drug traverses through affect drug absorption

A

Thickness: a single layer of cells (e.g. intestinal epithelium) is faster to traverse than several layers of cells (e.g. skin).

Surface area: a larger surface area will absorb drugs faster than a smaller one:

For example, anaesthetics are absorbed immediately from the pulmonary epithelium because of the vast surface area of the lung.
Absorption from the small intestine is more rapid than from an equivalent smaller absorbing surface, such as the stomach.

186
Q

How does Blood flow affect drug absorption

A

A rich blood supply (e.g. the sublingual route) enhances absorption, whereas a poor vascular site (e.g. the subcutaneous route) delays it.

Shock: IM drugs may be poorly absorbed due to poor peripheral circulation.

Drugs injected intravenously are placed directly into the circulatory system and are available immediately.

Food increases splanchnic blood flow and increases absorption of orally administered drugs. This is one reason why it’s best to take some oral drugs after eating.

187
Q

How does the Solubility of the drug affect how it’s absorbed

A

To be absorbed, a drug must be in solution; the more soluble the drug, the more rapidly it will be absorbed. Lipid solubility is important in drugs absorbed from certain areas (e.g. the gastrointestinal tract). If a drug is lipid soluble, it can cross cell membranes more easily.

188
Q

How does Ionisation affect how a drug is absorbed

A

Generally, drugs are either ionised or unionised. The ionised (charged) form is usually water-soluble (lipid-insoluble) and does not diffuse readily through the cell membranes of the body. The un-ionised (uncharged) form is more lipid-soluble (less water-soluble) and readily crosses cell membranes.

189
Q

What are Factors That Influence Bioavailability

A

First Pass Metabolism, Solubility of Drug, Chemical Instability, Drug Formulation

190
Q

What are Factors affecting distribution of drugs

A

Blood supply, Drug solubility

191
Q

How does blood supply affect the distribution of drugs

A

Drugs are distributed more slowly to organs with poor blood supply, which include skeletal muscles and fat.

The rate at which a drug enters depends on the permeability of capillaries and perfusion. Drugs enter well-perfused tissue more quickly.

Cardiovascular function also affects the rate and extent of distribution of a drug - specifically cardiac output.

192
Q

How does Drug solubility affect the distribution of drugs

A

Lipid-soluble drugs can readily cross membranes to enter most tissues and fluid compartments.

Lipid-insoluble drugs require more time to arrive at their point of action.

193
Q

How can Plasma Concentration help you see the distribution and concentration of drugs

A

the plasma concentration rises as absorption takes place, reaches a peak concentration, then plasma concentration starts to fall as the drug is eliminated from the blood stream (most drugs are excreted in the urine).

194
Q

Define the Volume of distribution

A

The volume of distribution (Vd) is defined as the (imaginary) volume of liquid a drug would need to be dissolved in to see the observed concentration of the drug in the plasma.

195
Q

What’s the drug concentration formula

A

Concentration = Amount ÷ Volume

196
Q

What is an adverse drug reaction?

A

“Any response to a drug which is noxious, unintended and occurs at doses used in man for prophylaxis, diagnosis or therapy”.

197
Q

Who are more at risk when developing ADR’s (Adverse drug reactions)

A

Age: the elderly and neonates have a higher incidence.

Gender: women appear to be more susceptible.

Concurrent disease: association between viral infections, drug use, and skin reactions has been described.

Genetic factors: deficiency of an enzyme involved in the metabolism of a drug may increase the risk of an ADR.

History of prior drug reaction: some individuals appear to be more susceptible to allergic drug reactions.

198
Q

Drug factors that can contribute to ADR’s

A

Chemical characteristics: large molecules such as heparin can be immunogenic, and smaller drug molecules or their metabolites can combine with body proteins to form antigens that elicit an allergic response.

Route of drug administration: topical and oral routes generally involve a lower incidence of drug allergy.

Dose: many ADRs are dose-related.

Duration and frequency: prolonged and frequent therapy can increase the likelihood of an ADR.

199
Q

What is a Type A (augmented) ADR?

A

Type A ADRs are characterised by:

Predictability from the known pharmacology of the drug. These are often an exaggeration of the desired effect (for example, bleeding when using an anticoagulant).

Relationship to dose (ADRs are more likely at higher doses, and may be a result of an inappropriately high dose).

Common occurrence (about 80% of ADRs).

Usually mild.

High morbidity and low mortality.

Reproducibility in animals.

Minor Type A reactions are often referred to as side effects.

200
Q

What are factors predisposing to type A reactions

A

The dose.

Pharmaceutical variation in drug formulation.

Pharmacokinetic variation (e.g. renal failure), pharmacodynamic variation (e.g. altered fluid balance).

Drug–drug interactions (e.g. inhibition of metabolism of one drug by another drug).

201
Q

How can type A ADRs be caused by withdrawal.

A

Withdrawal reactions are due to adaptations that have occurred at the receptor level during the course of the drug therapy. For example, a drug that blocks a receptor may cause an adaptation where more receptors are moved into the cell membrane. If the person suddenly stops taking the drug, there are more receptors in the membrane than before the drug was administered, and this can cause adverse reactions.

202
Q

In general, drugs with a low volume of distribution have…

A

Low lipid solubility.

A high degree of plasma protein binding.

A low degree of tissue binding.
For example, heparin and enoxaparin stay in plasma.

203
Q

Drugs with a high volume of distribution have..

A

High lipid solubility.

A low degree of plasma protein binding.

A high level of tissue binding.
For example, amiodarone and lead can move into fat and bone.

204
Q

What kind of drugs pass the Placental barrier

A

Passage from placenta to fetus is non-selective, and lipid-soluble substances diffuse easily across the placenta. Some molecules are metabolised and inactivated by enzymes in the placenta.

205
Q

What kind of drugs can pass through the Blood-brain barrier

A

The blood-brain barrier allows distribution of only lipid-soluble drugs (e.g. general anaesthetics, ethanol) into the brain and cerebral spinal fluid (CSF).

206
Q

What per cent of drugs go through metabolism to some extent

A

Most drugs (around 70%) undergo metabolism to some extent.

207
Q

What does metabolism do to drugs

A

In general, metabolism results in the formation of a more water-soluble metabolite, which can then be excreted. Metabolism clears the compound and promotes urinary excretion.

208
Q

How many half-lives does it generally take to reach steady state?

A

it takes 3-5 half lives to reach a steady state with repeated dosing.

209
Q

How many half-lives does it generally take for the drug to be fully eliminated

A

In general, it takes 4-5 half lives to eliminate a drug from the body

210
Q

Whats the equation of elimination

A

Elimination = metabolism + excretion

211
Q

A drug is taken orally and absorbed in the small intestine. Describe the path it takes from the small intestine to the systemic circulation.

A

Drugs that are taken orally are absorbed through the lumen of the SI into the hepatic portal vein, which drains into the liver. drugs may be processed by the enzymes in the liver before being released into the systematic circulation

212
Q

What are examples of Type A ADRs include

A

Sedation with the use of antihistamines.

Bleeding with anticoagulants.

Hypoglycaemia from the use of insulin.

Hypokalaemia with the use of diuretics.

213
Q

What is a Type B ADR?

A

Type B ADRs are characterised by:
Unpredictability
No relationship to dose
Uncommon occurrence – about 20% of ADRs
Increased severity
High morbidity and high mortality
Lack of reproducibility in animals

214
Q

What factors contribute to type B reactions

A

Pharmaceutical variation.
Receptor abnormalities caused by disease (e.g. insulin receptors).
Genetic/biological deficiency (e.g. glucose-6-phosphate dehydrogenase deficiency).
Abnormalities in drug metabolism (e.g. slow acetylators of the antituberculosis drug isoniazid).
Drug allergies.
Drug–drug interactions.

215
Q

What are some examples of Type B ADRs

A

Anaphylaxis, skin rashes with antibiotics

NSAIDs can cause interstitial nephritis. This is inflammation of the interstitium surrounding the tubules of the kidney.

Anticonvulsants such as carbamazepine and phenytoin can cause eosinophilia. This is a condition where there is an elevated level of eosinophils (a type of white blood cell involved in fighting infections) in the blood.

216
Q

What are Type C (continuous) ADR’s

A

This type of ADR occurs as a consequence of long-term use.

Examples include:
Adaptive changes: development of drug tolerance and physical dependence.

Appearance of tardive dyskinesia in persons treated long-term with neuroleptic drugs for schizophrenia.
Rebound phenomena: acute adrenal insufficiency after abrupt withdrawal of corticosteroids.

217
Q

What are type D (delayed) ADRs

A

This type of ADR is characterised by the appearance of delayed effects. In general these are considered unacceptable. However, these may be acceptable if the benefit of drug therapy outweighs the risk. For example, in the case of irreversible infertility in young persons receiving cytotoxic drugs for malignancies.

Examples include:

Carcinogenesis: the association of lymphoma with immunosuppressive drugs.
Teratogenesis: thalidomide.

218
Q

Why do genetics play a role in drug ADR’S

A

Some drug reactions are caused by genetic factors. Often these involve differences in enzymes that metabolise the drug differently, or that affect the system the drug is targeting.

219
Q

Whats a Glucose-6-phosphate dehydrogenase (G6PD) deficiency

A

The G6PD enzyme is involved in a metabolic pathway that helps protect red blood cells from oxidative damage. Deficiency in this enzyme can predispose someone to hemolytic anemia.

220
Q

Whats a Pseudocholinesterase deficiency

A

have low levels of an enzyme found in the plasma called pseudocholinesterase (also called butyrylcholinesterase). This slows down the metabolism of some muscle relaxant drugs, including suxamethonium (also called succinylcholine).

These patients may suffer from a neuromuscular blockade for several hours (or even days!) following surgery. Eventually they will metabolise the drug in their bodies; however they will need supportive therapy and sometimes mechanical ventilation while they recover from the paralysis

221
Q

What is Neuroleptic malignant syndrome

A

A potentially fatal (15–30% mortality) reaction seen in people who have recently been withdrawn from antipsychotic drugs, as well as people who are taking antiparkinsons medications.

Symptoms include a noticeable change in mental status, altered consciousness, rigidity, fever, and a loss of normal autonomic function (known as “dysautonomia”).

222
Q

Whats kind of ADR is a drug allergy, or hypersensitivity

A

Type B ADR

223
Q

How are drug allergies are characterised by

A

Occurrence in a small number of individuals.
The requirement for previous exposure to either the same or a chemically related drug.
The rapid development of an allergic reaction after re-exposure.
The production of clinical manifestations of an allergic reaction.

224
Q

What is a drug–drug interaction

A

A drug–drug interaction (drug interaction) occurs when the intensity of a drugs pharmacological effect is altered by another drug. That is, the effect(s) of a drug are increased or decreased by the concurrent or previous administration of another.

Drug interactions are a concern because they may result in loss of efficacy (diminished effect) or the development of toxicity (enhanced effect). Drug interactions are often unanticipated or go unrecognised. The exact frequency of drug interactions is unknown, although they are reported frequently.

225
Q

Who is at risk of drug–drug interactions

A

The severely ill, who typically receive multiple drugs.

Individuals receiving chronic therapy, often comprising a cocktail of drugs (e.g. in the treatment of either HIV infection or cancer).

The elderly, who tend to have multiple pathologies and often receive multiple drugs concurrently.

226
Q

How to limit Limiting adverse drug reactions

A

Communication with patient, Drug choice, Medical knowledge, Dosing

Pharmacology (BN517) (1 decks)

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