Home CPD Skin Cancer

Skin Cancer

CPD

September 30, 2018

CPD credits

Accreditation Code : CAP1809D

Group 1 : 0.75 CPD credits

Group 2 : 1.5 CPD credits

This activity has been accredited for 0.75 hours of Group 1 CPD (or 0.75 CPD credits) suitable for inclusion in an individual pharmacist's CPD plan, which can be converted to 0.75 hours of Group 1 CPD (or 1.50 CPD credits) upon successful completion of relevant assessment activities.

Case scenario

David, a 71-year-old retired construction worker, had many non-melanoma skin cancers removed. These are healing well, however he would like to look after his skin from now on to prevent any further skin cancers. He has been doing some reading on the internet regarding the use of vitamin B which can prevent skin cancers. He has walked into the pharmacy today and would like to know more. He asks the pharmacist for some advice.

Learning objectives

After successful completion of this CPD activity, pharmacists should be able to:

Describe different types of skin cancer
Discuss the potential role and evidence for nicotinamide for non-melanoma skin cancer and its place in therapy
Identify counselling points that pharmacists should discuss with patients enquiring about nicotinamide for skin cancer.

Competencies (2016) addressed: 1.1.1, 1.1.3, 1.2.1, 1.3.2, 2.1.2, 2.3.1, 3.1.2, 3.2.2, 3.2.5, 3.3.1, 3.6.1.

Competencies (2010) addressed: 1.1.1, 1.1.2, 1.2.1, 1.3.1, 2.1.3, 6.1.2, 6.2.1, 6.2.2, 6.3.3, 7.1.2, 7.1.4.

Accreditation code: CA1809D

Already read the CPD in the journal? Scroll to the bottom to SUBMIT ANSWERS.

Different types of skin cancer

There are thre

THIS IS A CPD ARTICLE. YOU NEED TO BE A PSA MEMBER AND LOGGED IN TO READ MORE.

CPD LOGIN

Click here to become a member

MODIFIABLE RISK FACTOR	STROKE DEATHS (%)	TYPE OF STROKE MOST LIKELY CAUSED	FIRST-LINE TREATMENTS
Hypertension	28	I or H	ACEI, CCBs
Atrial fibrillation	11	I	Anticoagulants
Carotid artery stenosis	Unclear	I	Antiplatelets, Statins
Hypercholesteroleamia	Unclear	I	Statins
Current tobacco use	Unclear	I or H	NRT, buproprion, varenicline
Diabetes	Unclear	I	Metformin, SGLT2 Inhibitors
Poor diet	Unclear	I or H	Non-drug treatments preferred
Physical inactivity	Unclear	I	Non-drug treatments preferred
Increase in waist to hip ratio	Unclear	I or H	Non-drug treatments preferred
Excessive alcohol	Unclear	I or H	Non-drug treatments preferred

	WARFARIN	APIXABAN	RIVAROXABAN	DABIGATRAN
Mechanism	Vitamin K antagonist	Factor Xa inhibitor	Factor Xa inhibitor	Direct thrombin inhibitor
Dosing frequency	Daily	Twice daily	Daily	Twice daily
Oral bioavailability (%)	100	50	>80	6.5*
% excreted unchanged in urine	0	34	36	85
Half-life in healthy volunteers (hours)	Highly variable 20-60	12	5-15 (mean=7)	13.4
Potential for drug interactions	CYP2C9, CYP1A2, CYP3A4 plus many others	PGP, CYP3A4	PGP, CYP3A4	PGP, PPIs
Antidote	Vitamin K (phytomenadione)	Andexanet alfa	Andexanet alfa	Idarucizumab

TRIAL	TRIAL TYPE	PATIENTS	STUDY LOCATION	DURATION (YEARS)	HR FOR ALL-CAUSE MORTALITY (95% CI)	HR FOR STROKE (95% CI)	HR FOR BLEEDING (95% CI)
ASPREE	Double blind placebo controlled RCT	n = 19,114	Australia/US	Median follow up 4.7	1.14* (1.01–1.29), NS	0.89 (0.71–1.11), NS	1.38* (1.18–1.62), P<0.001
ARRIVE	Double blind placebo controlled RCT	n = 12,546	Mainly Germany/UK	Median follow up 5	0.99 (0.80– 1.24), NS	1.12* (0.80–1.55), NS	2.11* (1.36–3.28), p=0·0007
ASCEND	Double blind placebo controlled RCT	n = 15,480	UK	Mean follow up 7.4	0.94 (0.85– 1.04), NS	1.12* (0.70–1.77), NS	1.29* (1.09–1.52), p=0.003

TRIAL	PATIENTS	INTERVENTION	CONTROL	OUTCOME	P-VALUE
MONOTHERPY
ATT	n = 40,821 with acute IS	Any antiplatelet	Placebo	11% RRR composite of IS/MI/death in patients with acute stroke	P= 0.00002
ATT	n = 23,020 with prior IS/TIA	Any antiplatelet	Placebo	22% RRR composite of IS/MI/death for long term secondary prevention	P=0.0003
ESPS-2	n = 6,602 with prior IS/TIA	Aspirin with dipyridamole (A+D)	Either drug alone or placebo	18% RRR IS, aspirin vs placebo 37% RRR IS, (A+D) v placebo	P=0.013 P<0.001
CAPRIE	n = 12,033 with prior IS	Clopidogrel	Aspirin	7% RRR in composite outcome of any stroke /MI/ death from any cause 8.7% RRR in IS, MI or vascular death	P=0.26 P=0.043
SOCRATES	n = 13,199 with IS/TIA	Ticagrelor	Aspirin	11% RRR in composite outcome of IS/MI/death 14% RRR stroke	P = 0.07 P = 0.046
DUAL ANTIPLATELET THERAPY
ESPIRIT	n = 2,739 with prior IS/TIA	Aspirin with dipyridamole (A+D)	Aspirin	20% RRR in a composite of CV death non-fatal stroke, non-fatal MI, bleeding complication 16% RRR in IS	p-value not stated 95% CI 0.66–0.98 p-value not stated 95% CI (0.64-1.10)
ESPS-2	n = 6,602 with prior IS/TIA	Aspirin with dipyridamole	Either drug alone or placebo	18% RRR IS Aspirin vs placebo 37% RRR IS (A+D) v placebo	P = 0.013 P<0.001
PROFESS	n = 20,332 with IS	Aspirin with dipyridamole	Clopidogrel	No difference in recurrent IS (HR = 1.01)	P value not stated 95% CI (0.92-1.11)
MATCH	n = 7,599 with IS/TIA	Aspirin with clopidogrel	Clopidogrel	No difference in IS (HR = 1.00) 6.4% RRR in composite end point of IS, MI, vascular death or rehospitalisation for ischemic events	P value not stated 95% CI (-4.6% to 16.3%)
CHANCE	n = 5,170 with IS/TIA	Aspirin with clopidogrel	Aspirin	32% RRR in IS (8.2% vs 11.7%) after 90 days	P<0.001
POINT	n = 4,881 with stroke or TIA	Aspirin with clopidogrel	Aspirin	25% RRR in IS (5% vs 6.5%) after 90 days	P = 0.02
TRIPLE ANTIPLATELET THERAPY
TARDIS	n = 3,096 with IS/ TIA	Aspirin + Dipyridamole + clopidogrel	Clopidogrel OR Aspirin + Dipyridamole	RRR=10% but stopped early due to significantly increased risk of bleeding (RRI 154%)	P = 0.47 P = 0.0001

DIAGNOSTIC CATEGORY*	SYSTOLIC (mmHg)		DIASTOLIC (mmHg)
Optimal	<120	and	<80
Normal	120–129	and/or	80–84
High-normal	130–139	and/or	85–89
Grade 1 (mild) hypertension	140–159	and/or	90–99
Grade 2 (moderate) hypertension	160–179	and/or	100–109
Grade 3 (severe) hypertension	≥180	and/or	≥110
Isolated systolic hypertension	>140	and	<90

CLASS	PHARMACODYNAMICS	PLACE IN CLINICAL PRACTICE
ACE Inhibitors Captopril Enalapril Fosinopril Lisinopril Perindopril Quinapril Ramipril Trandolapril	Reduce blood pressure by reducing vasoconstriction, sodium reabsorption and aldosterone release through inhibition of conversion of angiotensin-1 to angiotensin-2, and subsequent reduction of angiotensin-2-induced effects.¹⁴ ACE inhibitors also inhibit the breakdown of bradykinin, commonly resulting in a persistent dry cough.¹⁴	ACE inhibitors are considered a suitable first-line option for the treatment of hypertension that is uncomplicated by other co-morbidities.³ ACE inhibitors (or ARBs) are recommended as first-line hypertension therapy in patients with chronic kidney disease (CKD) with micro or macro albuminuria.³ ACE inhibitors are recommended for secondary prevention of ischaemic heart disease (IHD) in patients with certain concurrent indications, including hypertension.³² ACE inhibitors are recommended in patients with heart failure (HF) with reduced left ventricular ejection fraction (LVEF), in order to reduce mortality and hospitalisation.³³
ARBs Candesartan Eprosartan Irbesartan Losartan Olmesartan Telmisartan Valsartan	Reduce blood pressure by reducing vasoconstriction, sodium reabsorption and aldosterone release through competitive antagonism of type 1 angiotensin-2 receptors, and subsequent reduction of angiotensin-2-induced effects.¹⁴ ARBs do not inhibit bradykinin breakdown and are therefore often used as an alternative to ACE inhibitors if a patient experiences a persistent, dry cough with ACE inhibitor therapy.¹⁴	ARBs are considered a suitable first-line option for the treatment of hypertension that is uncomplicated by other co-morbidities.³ ARBs (or ACE inhibitors) are recommended as first-line hypertension therapy in patients with CKD with micro or macro albuminuria.³ ARBs are inferior to ACE inhibitors in the prevention of IHD,²² and in reduction of mortality in patients with HF.³⁴ However, it is reasonable to use ARBs instead of ACE inhibitors in this population if there is an intolerance to ACE inhibitors (caution in angioedema).^3,14
Thiazide diuretics Hydrochlorothiazide Thiazide-related diuretics Chlortalidone Indapamide	Induce diuresis via inhibition of sodium and chloride reabsorption in the distal convoluted tubule of the nephron, with additional increased potassium excretion.¹⁴ Antihypertensive effects at low doses are hypothesised to be the result of various direct and indirect vasodilatory actions, with no clear consensus for the mechanism thiazide-induced vasodilation.³⁵	Thiazide (and thiazide-related) diuretics are considered a suitable first-line option for treatment of hypertension that is uncomplicated by other comorbidities.³ However, thiazide diuretics are associated with an increased risk of diabetes onset, requiring careful consideration of this risk against the benefit gained from managing hypertension in the context of patient age.^3,36 In practice, thiazide diuretics do not often end up being first-line agents in treating hypertension in co-morbid conditions such as CKD, IHD, HF and atrial fibrillation. This is due to the preference of other agents (such as ACE inhibitors, ARBs and beta blockers) for the treatment and secondary prevention of the co-morbid condition.^3,32,33,37
Calcium channel blockers Dihydropyridines: Amlodipine Clevidipine Felodipine Nifodepine Nimodepine Non-dihydropyridines: Diltiazem Verapamil	Reduce blood pressure by reduction of peripheral vascular resistance through reduction of calcium influx into smooth muscle.¹⁴ This effect is seen in arteriolar smooth muscle with dihydropyridine calcium channel blockers, and, to a lesser extent, diltiazem.¹⁴ Non-dihydropyridine calcium channel blockers (diltiazem and verapamil) also have this effect on cardiac smooth muscle, resulting in; reduction of heart rate, cardiac contractility, myocardial oxygen requirements and angina symptoms.¹⁴	Calcium channel blockers are considered a suitable first-line option for the treatment of hypertension that is uncomplicated by other co-morbidities.³ The combination of calcium channel blockers with ACE inhibitors is superior to either ACE inhibitors with diuretics or beta-blockers with diuretics for the reduction of cardiovascular events and mortality in the treatment of uncomplicated hypertension.^38,39 In practice, calcium channel blockers do not often end up being first-line agents for monotherapy in treating hypertension in co-morbid conditions such as CKD, IHD and HF. This is due to the preference of other agents (such as ACE inhibitors, ARBs and beta blockers) for the treatment and secondary prevention of the co-morbid condition.^3,32,33 Conversely, non-dihydropyridine calcium channel blockers are a first-line option for rate control in the treatment of atrial fibrillation (in patients without heart failure).³⁷ Thus, treatment of hypertension in this population should be balanced with and account for the antihypertensive effects of rate control agents already employed.
Beta-blockers Atenolol Bisoprolol Carvedilol Labetalol Metoprolol Nebivolol Oxprenolol Pindolol Propranolol	Reduce blood pressure mainly by reduction of cardiac output via antagonism of beta-1 adrenoreceptors on cardiac tissue. Antagonism of beta-1 adrenoreceptors causes reductions in heart rate, cardiac contractility, cardiac conduction and relaxation rate.¹⁴ Additionally, beta-blockers can antagonize peripherally located beta-2 adrenoreceptors accounting for a myriad of additional, non-cardiac physiological effects.14 Finally, carvedilol and labetalol also antagonize peripheral alpha-1 receptors, causing additional antihypertensive effects from vasodilation.¹⁴ Differences in the selectivity of individual beta-blockers for the different types of adrenoreceptors account, for the most part, for the preference of certain betablockers in certain clinical conditions, and the variation in side-effect profiles.	Beta-blockers are not recommended as a first-line option for the treatment of hypertension that is uncomplicated by other co-morbidities, due to the unfavourable balance between safety and efficacy.³ However, selected beta-blockers are recommended for: secondary prevention of ischaemic heart disease in patients with reduced LVEF.³² management of heart failure in patients with moderately or severely reduced LVEF (may be considered in patients with mildly reduced LVEF).³³ a first-line option for rate control in the treatment of atrial fibrillation with co-morbid heart failure (alternative beta-blockers are considered suitable in the absence of heart failure).³⁷ Thus, the treatment of hypertension in the co-morbid populations listed above should be balanced with and account for the antihypertensive effects of agents used for management and secondary prevention of the relevant co-morbid condition. Selected beta-blockers: carvedilol, bisoprolol, slow-release metoprolol and nebivolol.³

MEDICATION	BRAND NAME	MEDICATION	BRAND NAME	MEDICATION	BRAND NAME
Angiotensin Receptor Blocker Combinations		Angiotensin Converting Enzyme Inhibitor Combinations		Other Combinations
Olmesartan	Olmetec	Enalapril	Multiple brands	Triamterene	Not available
+amlodipine	Sevikar	+hydrocholorthiazide	Enalapril/HCT, Sandoz, Renitec Plus	+Hydrocholorthiazide	Hydrene
+hydrocholorthiazide	Olmetec Plus	+lercanidipine	Zan-Extra	Amiloride	Kaluril
+amlodipine +hydrochlorothiazide	Sevikar HCT	Fosinopril	Monopril Fosipril	+Hydrocholorthiazide	Moduretic
Valsartan	Diovan	+hydrochlorothiazide	Fosetic
+amlodipine	Exforge	Perindopril	Coversyl
+hydrochlorothiazide	Co-Diovan	+Amlodipine	Coveram
+amlodipine +hydrochlorothiazide	Exforge HCT	+Indapamide	Coversyl Plus
Candesartan	Atacand	Quinapril	Accupril
+hydrochlorothiazide	Atacand Plus	+hydrochlorothiazide	Accuretic
Eprosartan	Teveten	Ramipril	Tritace
+hydrochlorothiazide	Teveten Plus	+felodipine	Triasyn
Irbesartan	Avapro, Karvea	Trandolapril	Gopten
+Hydrochlorothiazide	Avapro HCT, Karvezide	+verapamil	Tarka
Telmisartan	Micardis
+Amlodipine	Pritor/Amlodipine, Twynsta
+Hydrochlorothiazide	Micardis Plus

A rural focus

Key points

Local situation

International developments

Investing in prevention

Key points

How does 2019-nCoV cause severe illness?

Update for pharmacists

Advice on face masks

Local measures

Medicine safety in aged care

Rural and remote practice

Opioid overuse

Pollutants

Air pollution and cardiac events

What are the symptoms of a coronavirus infection?

Tips for prevention

Local breakthrough

Combined response needed

Case study

Discussion

Case study cont.

Recommendations for practice

Mechanism of Action

Use in Australia

Case scenario

Learning objectives

Already read the CPD in the journal? Scroll to the bottom to SUBMIT ANSWERS.

Introduction

Classification

Causes of acne

Acne myths and what patients can do to help their condition

Systemic treatment options

Oral antibiotics

Counselling

Combined oral contraceptive pill

Spironolactone

Oral isotretinoin

FIGURE 5 – Acne treatment progression from mild to severe disease

Contraindications

Adverse effects of oral isotretinoin

Counselling

Emerging therapies for acne and acne scarring

Conclusion

Case scenario continued

Key points

Learning objectives

Already read the CPD in the journal? Scroll to the bottom to SUBMIT ANSWERS.

Burden of Influenza

Advantages of implementing a pre-influenza season strategy – advice for community pharmacy

Logistical considerations

TABLE 1 – Annual Australian influenza statistics

FIGURE 1 – Australian influenza notifications 2019

TABLE 2 – State-based 2019 influenza notifications

Committing to growth

System focuses

Clinical considerations – from vaccine hesitancy to herd immunity advocates

Work force capacity – availability of pharmacists during opening hours

Maintain accreditation and improve immunisation skills

Refresh your injection technique – avoiding shoulder injury from vaccine administration

BOX 1 – Shoulder injury related to vaccine administration (SIRVA)

Keeping abreast of changes in immunisation

Clinical considerations – looking to the 2020 influenza season with 2019 vision

The 2019 influenza season

BOX 2 – Egg allergies and the influenza vaccine

TABLE 4 – 2020 Pharmacist vaccination by state, current 23 January 2020

Annual influenza vaccine timing

Managing consumer expectations

Community pharmacy immunisations

Key points

Case scenario

Learning objectives

Already read the CPD in the journal? Scroll to the bottom to SUBMIT ANSWERS.

Test your knowledge on this CPD topic prior to completion to monitor your learning experience:

Introduction

The cycle and level of addiction

Figure 1 – Cycle of addiction

Benefits of quitting

Figure 2 – Benefits of quitting

Supporting smokers on their quit journey

TABLE 3 – Important aspirin trials for primary prevention of stroke^3-5