Teacher's copy

[teresa]

Hi All,
You may have found this already but if not I think it will be very handy for the end of year exam.
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Pharmacology Workshop
Nursing Adults with Complex Needs
(Teacher’s copy with answers)



Aim:

· To further develop an understanding of the principles of drug treatment by discussing pharmacological management using a variety of scenarios

Learning outcomes:

After attending the workshop and doing some further work, you should be able to:

· Discuss the role of antibiotics in the treatment of disease
· Explain the mode of action of opiates in the management of pain
· Discuss the biological basis for the use of anti-depressants
· Explain the importance of therapeutic drug monitoring in the treatment of epilepsy
· Explain how route of administration relates to drug structure, with reference to insulin
· Explain the biological basis of the unwanted effects of NSAIDs in the treatment of inflammatory conditions
· Discuss some of the risks and benefits of corticosteroids
· Explain the benefits of inhaled versus systemic administration of drugs in the treatment of asthma
· Describe the features and immediate treatment of anaphylaxis as an adverse drug reaction

Links to previous biology modules:

Nursing Essentials Introduction to Pharmacology*
Initiating Care in Adult Nursing *
Nursing Adults With Complex Needs *

* It’s important you re-read these lecture notes before the Pharmacology Workshop
Work in groups of 4-6 students and consider one of the following

Question 1. Atrial Fibrillation (AF)
A patient has been admitted to the ward after suffering a cerebral vascular accident. Previously he has been treated for AF.
1. Briefly describe the actions of digoxin
a. Rate of impulses generated by SA node is reduced thus slowing HR
b. Increased interval between atrial contraction and ventricular systole increases stroke volume
c. Both a) & b) lead to a better CO and tissue perfusion
2. Explain why a person taking digoxin may have an increased urinary output even in the absence of taking diuretics?
a. Increased renal blood flow causes a diuresis
3. Digoxin has a “narrow therapeutic window” explain what this term means and the implications for patient monitoring
a. Digoxin works within a narrow plasma concentration range
b. Plasma assays to reduce risk of toxicity
c. Checking pulse and observing for signs of toxicity
4. Digoxin toxicity occurs when plasma concentrations become excessively high. List at least four complications of digoxin toxicity
a. Arrhythmia’s, tachycardia, AV blockade
b. Nausea and vomiting
c. Diarrhoea
d. Disorientation & hallucinations
e. Visual disturbances
5. Warfarin is often used in the treatment of people with AF. Explain why this drug is needed for their condition?
a. High risk of embolism in AF that can pass into systemic circulation and cause a stroke
6. Briefly explain the therapeutic action of warfarin.
a. Warfarin interferes with the of Vit K that is necessary for the synthesis of prothrombin and other clotting factors in the liver
b. They could explain warfarin inhibits the manufacture of epoxide reductase an enzyme necessary for the oxidization of inactivated Vit K back to its active form in the liver.
7. Explain how the dose of warfarin is titrated to ensure its optimum anticoagulant action in AF.
a. INR (international normalized ratio) between 2-3 is used to reduce risk of blood clotting
8. What may be the consequences should the INR rise above 3?
a. Increased risk of bruising, haemorrhage etc.
9. Give four examples of drugs that either increase or decrease the action of warfarin.
Drugs increasing action of warfarin Drugs decreasing action of warfarin
· Aspirin · Alcohol
· Metoprolol · Oral contraceptives
· Cimetidine · Carbamazepine
· Metronidazole · Antacids/St John’s wort
10. What is the antidote to warfarin?
a. Vitamin K (reduces INR)


Question 2 Diabetes – diabetes is an increasing problem representing a challenge to nurses

1. Explain how the dose of insulin is judged to be correct for good health in a type I diabetic person.
a. Correct weight level for age/sex/height
b. Maintenance of blood glucose near normal
c. Subjective feelings of wellness
2. Why can’t insulin be administered orally?
a. Because it’s a polypeptide hormone that will be digested to its component amino acids in the GI tract
3. What is the action of insulin?
a. Facilitates uptake of glucose into liver/muscle cells
b. Promotes storage of glucose as glycogen and use of glucose for energy
c. Promotes storage of excess nutrients as fat
d. Stimulates protein synthesis
4. What other measures can be used to help control blood glucose levels in diabetes?
a. Oral hypoglycaemic drugs
b. Weight reduction
c. Reduction in carbohydrate/fat intake
d. Exercise
5. Insulin is classified as short-acting; intermediate-acting and long-acting. Complete the gaps in the following table: Teacher, please note these times are averages and will vary with different manufacturers preparations
Insulin Onset time Peak effect Duration of action
Short-acting 30-60 mins 4 hrs 6-8 hrs
Intermediate-acting 2-4 hrs 4-12 18-24 hrs
Long-acting 4-6 hrs 10-30 24-36 hrs
6. Answer the following questions about the hypoglycaemic drug Gliclazide:
a. Which group of hypoglycaemic agents does it belong to? (sulphonylureas)
b. Briefly explain Gliclazides mode of action (it lowers blood glucose levels by increasing insulin production by the pancreas)
c. Is it possible for a person taking this drug to become hypoglycaemic? (yes, if drug taken and insufficient CHO taken – tho’ less likely than with earlier sulphonylureas)
7. In an emergency situation which two substances may be used to treat hypoglycaemia?
a. IV glucose or oral glucose if awake
b. Subcutaneous glucagon




Question 3 – Antibiotics

Pneumocystis carinii pneumonia (PCP) is a fungus that causes pneumonia only in individuals with impaired immune system function such as HIV.

1. Co-trimoxazole is frequently given as a prophylaxis for PCP. Explain the mode of action of this drug:
a. Interferes with para-aminobenzoic acid, a precursor of folic acid which is necessary for cell replication
2. Which two sulphonamide (sulfonamide) drugs are contained in Co-trimoxazole giving it both a bactericidal and bacteriostatic action?
a. Trimethoprin
b. Sulphamethoxazole
3. State two adverse effects associated with sulphonamide drugs such as co-trimoxazole:
a. Diarrhoea
b. Crystalluria
c. Hypersensitivities ranging from rash through to photosensitivity and agranulocytosis and aplastic anaemia.
4. Explain what is meant by the term “contra-indication” and state two contra-indications to the drug co-trimoxazole
a. Contra-indication – a situation where the drug must not be given
i. Known hypersensitivity
ii. First 3 months pregnancy
iii. Babies <2/12 age
5. A patient with a wound infection is treated with flucloxacillin; explain how this drug destroys micro-organisms:
a. Interferes with synthesis of cell wall (bactericidal)
6. What is the purpose of swabbing a wound before commencing treatment with antibiotics?
a. Microscopy (to look at under the microscope)
b. Culture (to grow on an agar dish) and
c. Sensitivity (to ensure correct antibiotic has been given)
d. To identify the microorganism and to ensure the correct antibiotic is administered
7. How might a heavy growth of staphylococcus aureus, grown from a wound swab, have been introduced into a wound?
a. Direct contact with health care worker
b. From one patient to another
c. From the patient’s own skin


Question 4 – Pain Control

After bowel surgery a patient returns to the ward with a PCA containing a preparation of morphine
1. What does PCA stand for?
a. Patient Controlled Analgesia
2. Explain the mode of action of morphine in relieving pain.
a. Acts on pain gate in substantia gelitanosa
b. Mimics action endogenous opioids that block the release and action of substance P
c. Recent studies show it affects transmission at nociceptors
3. Why is prochlorperazine sometimes administered with opiate drugs?
a. Opiates stimulate the chemoreceptor trigger zone (CTZ) causing nausea & vomiting in 30% patients – particularly if mobile
b. Prochlorperazine suppresses the action of dopamine on the CTZ reducing nausea & vomiting
4. How may the respiratory centre be affected by morphine toxicity?
a. Suppression of the respiratory centre in the medulla
5. How does naloxone exert its action in reversing morphine toxicity and what precautions must be taken when it is used as an antidote to morphine overdose?
a. Naloxone is a morphine antagonist which competes for morphine receptor sites reversing its action
b. Naloxone has a shorter half life (about 60 mins) than morphine (4 hours) therefore patients should be kept under observation and repeat doses administered as required
c. This can be a problem in addicts treated for overdose who discharge themselves after receiving Naloxone
6. Briefly explain the consequences and nursing implications for a person taking regular doses of morphine that stimulate opioid receptors in the gastrointestinal tract.
a. Morphine decreases peristalsis resulting in increased water absorption and increased risk of constipation
b. Attention to bowel movements, use of prophylactic aperients and increased dietary fibre and fluid intake
7. Why would analgesics, such as pethidine and diclofenac, be prescribed for biliary or renal colic rather than morphine?
a. Morphine may cause spasm in the smooth muscle of the biliary ducts and ureters and possibly exacerbate pain
b. Both pethidine and diclofenac have smooth muscle relaxant properties.
8. List adverse effects you would observe for in a patient who has received an injection of morphine:
a. Respiratory depression
b. Hypotension
c. Drowsiness
d. Confusion
e. Urinary retention/constipation
f. Papillary constriction
9. What changes in vital signs would indicate to you a patient’s pain is resolving following a morphine injection?
a. Reduction in tachycardia, respiratory rate and BP
b. Better skin colour
c. Less restlessness – ability to rest
d. Patient reports less pain/non-verbal signs

Question 5. – Depression

Three types of depression are said to exist: -
· Reactive depression occurring as a response to a sad event, some life crisis or side-effect of certain drugs (i.e. some antihypertensive agents)
· Endogenous – depression occurring without any apparent trigger
· The least common is bipolar affective disorder (previously termed manic depression)

1. Name at least two drug interactions which may occur in people taking St John’s Wort (hypericum perforatum) to self-treat mild depression.
a) Drugs used to treat HIV
b) Some anti-cancer drugs
c) Cyclosporine (anti-rejection drug)
d) Digoxin & Warfarin
e) Some oral contraceptives & antidepressant drugs
2. Explain the mode of action of Prozac (fluoxetine) which is a selective serotonin re-uptake inhibitor (SSRI) prescribed for depression.
a) Blocks the re-uptake of serotonin into the pre-synaptic neurone increasing its concentration in the synaptic cleft
b) Serotonin, along with other neurotransmitters (i.e. noradrenalin) are important in regulating mood, behaviour, appetite etc.
3. Tricyclic antidepressants (TCA’s), such as doxepin, have a similar action to SSRI’s in relieving depression but have a number of side-effects. Name one adverse and one beneficial effect of TCA’s
a) Adverse – dry mouth, blurred vision, constipation, urinary retention etc.
b) Beneficial – sedative action that is useful when insomnia accompanies depression
4. How long does it take for SSRI’s and TCA’s to have any clinical effect? Why is this?
a) 10-21 days to affect mood
b) It takes this long to alter the number/sensitivity of post-synaptic receptors to the neurotransmitter i.e. increasing the amount of serotonin down-regulates the receptors.
5. What life-threatening complications and management may be required in a depressed person who takes an overdose of TCA’s?
a) Convulsions, metabolic acidosis and potentially lethal cardiac arrhythmias requiring: admission, cardiac monitoring, activated charcoal (to block absorption), diazepam (to control convulsions), correction blood pH, hypoxia and anti-arrhythmia drugs
6. What non-pharmacological interventions might also be helpful in people with depression?
a) Counseling
b) Cognitive behavioural therapy
c) Support groups etc.

Question 6. Epilepsy

A patient is admitted to the neurology ward for assessment of recurrent seizures. They have been told they have epilepsy and have been commenced on the drug phenytoin to try to control the seizures.

1. What is epilepsy? What is happening in the brain?
a. Abnormal, synchronous discharge of electrical activity in the brain. May be focal or generalized – phenytoin usually used for generalised grand mal seizures.
2. What is the mode of action of phenytoin?
a. Promotes intracellular removal sodium during the refractory period therefore causing cortical nerve stability against hyper-excitability – particularly in the motor cortex – and prevents discharging neurons from repeated firing.
3. Many anticonvulsant drugs, such as phenytoin are suspected teratogens. Explain what this means and the implications for a young woman.
a. A substance that can cause birth defects
b. The risk of foetal malformation is high in women taking phenytoin particularly when combinations of anticonvulsants drugs are used.
4. State four common adverse reactions associated with anticonvulsant drugs; look up any terms you do not understand and explain what they mean.
a. Gastrointestinal disturbances (nausea, vomiting, altered appetite etc)
b. Sedation/Ataxia (loss of coordination)
c. Headache
d. Nystagmus (rapid involuntary oscillation of the eyes)
e. Mental confusion
f. Allergies
g. Myelosuppression
h. Gingival hyperplasia
i. Hepatotoxicity
j. Hirsuitism
5. Phenytoin has a narrow therapeutic window. Explain what this means. What implications does this have for adjusting the dose?
a. Narrow therapeutic plasma concentration range of action with wide variation in metabolism between individuals
b. Easy to have either ineffective or toxic dose
c. To obtain optimum dose regular blood concentration monitoring is carried out to ensure level within therapeutic range


Question 7. - Rheumatoid arthritis (RA)

A person with RA is having their medication reviewed. She takes a combination of anti-inflammatory drugs to relieve the pain and prevent “flare ups” of the disease. One of the drugs she takes regularly is a NSAID called Ibuprofen.
1. What does NSAID stand for?
a. Non-steroidal anti-inflammatory drug
2. NSAID’s are prostaglandin inhibitors. Explain how inhibition of prostaglandin synthesis reduces the pain and inflammation associated with RA.
a. Prostaglandins are mediators of inflammation that augment the action of histamine and other chemicals responsible for vasodilation and increased permeability of blood vessels.
b. Prostaglandins also directly stimulate pain receptors. NSAID’s inhibit the enzyme cyclo-oxygenase which converts arachidonic acid to inflammatory mediators such as prostaglandins
3. Explain why NSAID’s also act as antipyretic agents.
a. Prostaglandins are found in the heat regulating centre of the hypothalamus during infections and act as pyrogens increasing body temperature.
b. NSAID’s inhibit prostaglandin activity and cause a decrease in body temperature.
4. What do you think could be a consequence in joints when mobility is increased as a result of reduced inflammation and pain when NSAID’s are taken?
a. NSAID’s may hasten degenerative changes within the joint.
5. Ibuprofen is known to have one of the lowest risks for NSAID’s. What are the main complications associated with NSAID’s? Explain why these complications may occur.
a. Gastrointestinal: most NSAID’s have an acidic action on the stomach wall but also inhibit prostaglandin secretion which is vital for the production of the protective gastric mucus.
b. Airways: Exacerbation of asthma because if cyclo-oxygenase is blocked it encourages production of leukotrienes that are involved in type I hypersensitivity reactions involving the release of histamine in the airways.
c. Renal tract: may also impair renal function.
d. NSAID’s are also linked to other allergic reactions i.e. skin rashes and very rarely suppression of the bone marrow.
6. By what other routes can Ibuprofen be administered? Will administration via these routes remove the risk of complications identified in Q 5?
a. Rectally and percutaneously. No less complications if administered rectally but fewer with percutaneous route.


Question 8 – Asthma

A patient with asthma has an inhaler to relieve bronchospasm and is being instructed in its correct use.
1. Aerosol inhaled salbutamol (Ventolin) is a â2 receptor agonist. Explain what this means; where it acts and its mode of action.
a. A drug that binds to a receptor of a cell that triggers a response by that cell
b. â2 agonists are selective for smooth muscle in the respiratory tract and stimulation leads to bronchodilation and relief of spasm; this mimics the action of the sympathetic NS on the smooth muscle of the respiratory tract (sympathomimetic)
2. Explain why inhaled salbutamol has few systemic side-effects.
a. Inhaled salbutamol acts locally with little absorption reducing systemic side-effects; this also means a much lower dose is required
3. How quickly will salbutamol relieve a wheezing attack?
a. Within minutes and continue to act for up to 4 hours
4. What potential side-effects may occur in a person who exceeds the recommended maximum 12 doses/day?
a. Fine muscle tremor (particularly in the hands); headache; palpitations (tachycardia and arrhythmias) and sleep disturbance
5. What is the mode of action of inhaled anticholinergic bronchodilators such as ipratropium?
a. Ipratropium is related to atropine and blocks parasympathetic stimulation of the airways (remember parasympathetic stimulation causes broncho-constriction) reducing broncho-constriction and excessive mucus production.
6. Ipratropium has a slower onset of action (45 minutes) than salbutamol but lasts for up to 4 hours; what does this tell you about its clinical use?
a. It is best used as a prophylactic against broncho-constriction and can be used in conjunction with â2 receptor agonists or if â2 receptor agonists are contra-indicated
7. What is the difference between inhalers that act as “relievers” such as salbutamol, and “preventers” such as beclamethasone?
a. Relievers reduce symptoms of asthma i.e. bronchoconstriction;
b. preventers (steroids)reduce inflammation and long-term damage to the airways;
c. sometimes a combined broncho-dilator and steroid may be used i.e. Seretide (fluticasone + salmeterol)


Question 9 – Inflammatory bowel disease

A patient with an exacerbation of ulcerative colitis (a common form of inflammatory bowel disease) is taking regular drugs, including prednisolone, to try to achieve remission from the disease.
1. What type of drug is prednisolone?
a. Prednisolone is a synthetic steroid (cortisol)
2. Explain the beneficial effects of prednisolone in inflammatory bowel disease.
a. Prednisolone reduces the inflammatory response in the lining of the colon in ulcerative colitis
3. List at least five other conditions where steroids are indicated.
a. Crohn’s disease; asthma; hay fever; lymphomas; leukaemia; eczema; rheumatoid arthritis; systemic lupus erythematus; polyarteritis nodosa etc.
4. Identify at least five adverse effects of steroids such as prednisolone and briefly explain why they may occur.
a. Steroid induced diabetes (effect on carbohydrate metabolism); oedema (water retention)
b. hypertension (sodium and water retention)
c. increased risk of infection (suppression of immunity & inflammation)
d. gastric ulceration/bleeding (reduced stomach mucus secretion)
e. increased risk arthritis/bone pain and #’s (osteoporosis)
f. shock (failure of steroid secretion in physiological stress)
g. Cushing’s disease
h. psychological (euphoria)
i. Amenorrhea
j. hirsuitism etc.
5. How may the adverse effects mentioned above be minimalised in some cases? Inhaled steroids (asthma)
a. foam/suppositories/enemas (ulcerative colitis)
b. topical applications in severe skin diseases
c. careful monitoring of dose
d. reduce dose carefully when condition improves.
6. Sulphasalazine (and related drugs) are prostaglandin inhibitors used in inflammatory bowel diseases to keep patients in remission. Briefly explain how these drugs work in reducing inflammation and include two possible side-effects.
a. Metabolized in the bowel to 5-ASA & sulphapyridine (therefore sulphasalazine is ae pro-drug) where they inhibit the prostaglandin synthesis necessary for inflammation
b. nausea, vomiting, watery diarrhoea and rarely agranulocytosis (suppression of the bone marrow)


Question 10 – Adverse drug reactions

A patient receives intravenous penicillin and has a severe anaphylactic reaction. Senior staff are summoned and 500micrograms of adrenaline is injected intramuscularly to be repeated at 5 minute intervals as necessary.
1. What are the features of anaphylactic shock?
a. Wheezing,
b. swelling of larynx and airway and
c. severe hypotension
2. How does adrenaline help in this situation?
a. Reverses bronchoconstriction
b. reverses vasodilatation and
c. reduces laryngeal oedema
3. Identify at least two other drugs that may have to be used in anaphylactic shock and explain their role.
a. Antihistamines such as chlorpheniramine to prevent relapse and hydrocortisone to prevent further deterioration in severe anaphylactic shock
4. What other substances, besides an adverse drug reaction, might cause anaphylaxis?
a. Insect stings; food e.g. shell fish, peanuts (virtually anything)
5. What does this scenario illustrate with regards to the administration of intravenous drugs and vaccinations in clinical settings?
a. Resuscitation equipment including drugs and oxygen must always be available; staff training to recognize and be able to manage anaphylaxis