Home - Australian Pharmacist

Inquiry reveals the depth of Australia’s sleep deficit problem

Mikaela Dery - 3 May 2019

Clinical

The recently released government inquiry into sleep health identified the extent of the nation's sleep deficit and its impact on health, risk of accidents...

Aged care antimicrobial prescribing on the rise

Ruth Cooper - 29 October 2019

Theresa Flavin, a 57-year-old mother of five, was diagnosed with dementia at just 46. She says RACFs need a pharmacist ‘on the team’.

Industry

Data released last month shows an increase in the number of aged care residents prescribed antimicrobials, highlighting the need for pharmacists to use their...

2019: A watershed year for Australian medicine safety

Dr Chris Freeman FPS - 10 December 2019

Industry

I am enormously proud of how our work has contributed to medicine safety and the quality use of medicines finally receiving the attention it warrants.

From the President: An exciting time to be a pharmacist

Dr Fei Sim FPS BPharm (Hons) PhD FHEA GAICD FPS - 29 March 2023

The President of the Pharmaceutical Society

Industry

I often tell the story of The Starfish, the Little Boy and the Old Man. This is one of my favourite childhood stories.

Young minds, meds and moods: youth mental health in focus

AP Staff - 11 December 2000

CPD

Links to resources See journal p28 and p29: Decision aid: Minding your mental wellbeing –<a href="https://go.medcast.com.au/decision-aid-minding-your-mental-wellbeing?utm_id=701Oa0000

‘Conservative’ King Review response

Thea Cowie - 3 May 2018

Industry

Health Minister Greg Hunt hints at no major shake-up, but trade-offs will be made. Attempting to allay fears of a major pharmacy sector shake-up, the...

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Causes of dementia	Descriptions
Alzheimer’s disease	The amyloid cascade hypothesis suggests that the deposition of amyloid-β (Aβ) plaques leads to neurofibrillary tangles, cell loss, vascular damage and dementia.3 For decades, this hypothesis has been the primary target for developing therapies for Alzheimer’s disease. In light of new evidence, several iterations of the theory have been proposed, highlighting a more complex aetiology involving polygenic, epigenetic, environmental, vascular, neuroinflammatory and metabolic factors.4 Today, the aetiological complexity surrounding the pathogenesis of Alzheimer’s disease has not been fully established.
Vascular dementia	Vascular dementia results from impaired blood supply to the brain, which damages brain tissue and subsequently leads to cognitive decline.5 Common neuropathological findings include multiple infarcts or single strategic infarcts caused by atherothromboembolic events or small vessel disease.5
Mixed dementia	It is common for individuals to present with more than one type of dementia. The term ‘mixed dementia’ refers to the co-occurrence of more than one subtype of dementia, most commonly Alzheimer’s disease and vascular dementia. However, the use of this term is increasingly discouraged due to its ambiguity.6
Lewy body dementia	Lewy body dementia is an umbrella term describing two forms of dementia: dementia with Lewy bodies (DLB) and Parkinson’s disease dementia (PDD). DLB is characterised by the accumulation of α-synuclein in Lewy bodies and Lewy neurites in the brain, as well as neuronal loss in the substantia nigra, although typically less severe than that observed in Parkinson’s disease.6 PDD and DLB are both α-synucleinopathies.6 There is considerable clinical overlap between DLB and PDD.6 Generally, DLB presents at an older age, while PDD is preceded by a long period of motor symptoms.6 The arbitrary ‘1-year rule’ is commonly applied in clinical practice, whereby DLB is diagnosed when cognitive symptoms appear before or within 1 year of motor symptoms, whereas PDD is diagnosed when cognitive decline occurs in the context of established Parkinson’s disease.6
Frontotemporal dementia	Frontotemporal dementia (FTD) is a common cause of early-onset dementia, typically affecting individuals aged 45–65 years.7 FTD is categorised as three variants: 1) behavioural-variant FTD (associated with behavioural and executive deficits), 2) non-fluent variant primary progressive aphasia (progressive deficits in speech, grammar and word output), and 3) semantic-variant primary progressive aphasia (impaired naming and single-word comprehension).8 As the name suggests, FTD involves progressive degeneration of the frontal and/or temporal lobes associated with characteristic protein inclusions.6 Genetic mutations and family history of dementia play an important role in its pathogenesis.6
Other causes of dementia	Other less common causes of dementia are associated with9,10: Huntington’s disease traumatic brain injury posterior cortical atrophy infectious disease (e.g. human immunodeficiency virus [HIV], Creutzfeldt-Jakob disease) toxicity (e.g. hazardous alcohol consumption).

Causes of dementia	Descriptions
Alzheimer’s disease	The amyloid cascade hypothesis suggests that the deposition of amyloid-β (Aβ) plaques leads to neurofibrillary tangles, cell loss, vascular damage and dementia.3 For decades, this hypothesis has been the primary target for developing therapies for Alzheimer’s disease. In light of new evidence, several iterations of the theory have been proposed, highlighting a more complex aetiology involving polygenic, epigenetic, environmental, vascular, neuroinflammatory and metabolic factors.4 Today, the aetiological complexity surrounding the pathogenesis of Alzheimer’s disease has not been fully established.
Vascular dementia	Vascular dementia results from impaired blood supply to the brain, which damages brain tissue and subsequently leads to cognitive decline.5 Common neuropathological findings include multiple infarcts or single strategic infarcts caused by atherothromboembolic events or small vessel disease.5
Mixed dementia	It is common for individuals to present with more than one type of dementia. The term ‘mixed dementia’ refers to the co-occurrence of more than one subtype of dementia, most commonly Alzheimer’s disease and vascular dementia. However, the use of this term is increasingly discouraged due to its ambiguity.6
Lewy body dementia	Lewy body dementia is an umbrella term describing two forms of dementia: dementia with Lewy bodies (DLB) and Parkinson’s disease dementia (PDD). DLB is characterised by the accumulation of α-synuclein in Lewy bodies and Lewy neurites in the brain, as well as neuronal loss in the substantia nigra, although typically less severe than that observed in Parkinson’s disease.6 PDD and DLB are both α-synucleinopathies.6 There is considerable clinical overlap between DLB and PDD.6 Generally, DLB presents at an older age, while PDD is preceded by a long period of motor symptoms.6 The arbitrary ‘1-year rule’ is commonly applied in clinical practice, whereby DLB is diagnosed when cognitive symptoms appear before or within 1 year of motor symptoms, whereas PDD is diagnosed when cognitive decline occurs in the context of established Parkinson’s disease.6
Frontotemporal dementia	Frontotemporal dementia (FTD) is a common cause of early-onset dementia, typically affecting individuals aged 45–65 years.7 FTD is categorised as three variants: 1) behavioural-variant FTD (associated with behavioural and executive deficits), 2) non-fluent variant primary progressive aphasia (progressive deficits in speech, grammar and word output), and 3) semantic-variant primary progressive aphasia (impaired naming and single-word comprehension).8 As the name suggests, FTD involves progressive degeneration of the frontal and/or temporal lobes associated with characteristic protein inclusions.6 Genetic mutations and family history of dementia play an important role in its pathogenesis.6
Other causes of dementia	Other less common causes of dementia are associated with9,10: Huntington’s disease traumatic brain injury posterior cortical atrophy infectious disease (e.g. human immunodeficiency virus [HIV], Creutzfeldt-Jakob disease) toxicity (e.g. hazardous alcohol consumption).

Causes of dementia	Descriptions
Alzheimer’s disease	The amyloid cascade hypothesis suggests that the deposition of amyloid-β (Aβ) plaques leads to neurofibrillary tangles, cell loss, vascular damage and dementia.3 For decades, this hypothesis has been the primary target for developing therapies for Alzheimer’s disease. In light of new evidence, several iterations of the theory have been proposed, highlighting a more complex aetiology involving polygenic, epigenetic, environmental, vascular, neuroinflammatory and metabolic factors.4 Today, the aetiological complexity surrounding the pathogenesis of Alzheimer’s disease has not been fully established.
Vascular dementia	Vascular dementia results from impaired blood supply to the brain, which damages brain tissue and subsequently leads to cognitive decline.5 Common neuropathological findings include multiple infarcts or single strategic infarcts caused by atherothromboembolic events or small vessel disease.5
Mixed dementia	It is common for individuals to present with more than one type of dementia. The term ‘mixed dementia’ refers to the co-occurrence of more than one subtype of dementia, most commonly Alzheimer’s disease and vascular dementia. However, the use of this term is increasingly discouraged due to its ambiguity.6
Lewy body dementia	Lewy body dementia is an umbrella term describing two forms of dementia: dementia with Lewy bodies (DLB) and Parkinson’s disease dementia (PDD). DLB is characterised by the accumulation of α-synuclein in Lewy bodies and Lewy neurites in the brain, as well as neuronal loss in the substantia nigra, although typically less severe than that observed in Parkinson’s disease.6 PDD and DLB are both α-synucleinopathies.6 There is considerable clinical overlap between DLB and PDD.6 Generally, DLB presents at an older age, while PDD is preceded by a long period of motor symptoms.6 The arbitrary ‘1-year rule’ is commonly applied in clinical practice, whereby DLB is diagnosed when cognitive symptoms appear before or within 1 year of motor symptoms, whereas PDD is diagnosed when cognitive decline occurs in the context of established Parkinson’s disease.6
Frontotemporal dementia	Frontotemporal dementia (FTD) is a common cause of early-onset dementia, typically affecting individuals aged 45–65 years.7 FTD is categorised as three variants: 1) behavioural-variant FTD (associated with behavioural and executive deficits), 2) non-fluent variant primary progressive aphasia (progressive deficits in speech, grammar and word output), and 3) semantic-variant primary progressive aphasia (impaired naming and single-word comprehension).8 As the name suggests, FTD involves progressive degeneration of the frontal and/or temporal lobes associated with characteristic protein inclusions.6 Genetic mutations and family history of dementia play an important role in its pathogenesis.6
Other causes of dementia	Other less common causes of dementia are associated with9,10: Huntington’s disease traumatic brain injury posterior cortical atrophy infectious disease (e.g. human immunodeficiency virus [HIV], Creutzfeldt-Jakob disease) toxicity (e.g. hazardous alcohol consumption).

Causes of dementia	Descriptions
Alzheimer’s disease	The amyloid cascade hypothesis suggests that the deposition of amyloid-β (Aβ) plaques leads to neurofibrillary tangles, cell loss, vascular damage and dementia.3 For decades, this hypothesis has been the primary target for developing therapies for Alzheimer’s disease. In light of new evidence, several iterations of the theory have been proposed, highlighting a more complex aetiology involving polygenic, epigenetic, environmental, vascular, neuroinflammatory and metabolic factors.4 Today, the aetiological complexity surrounding the pathogenesis of Alzheimer’s disease has not been fully established.
Vascular dementia	Vascular dementia results from impaired blood supply to the brain, which damages brain tissue and subsequently leads to cognitive decline.5 Common neuropathological findings include multiple infarcts or single strategic infarcts caused by atherothromboembolic events or small vessel disease.5
Mixed dementia	It is common for individuals to present with more than one type of dementia. The term ‘mixed dementia’ refers to the co-occurrence of more than one subtype of dementia, most commonly Alzheimer’s disease and vascular dementia. However, the use of this term is increasingly discouraged due to its ambiguity.6
Lewy body dementia	Lewy body dementia is an umbrella term describing two forms of dementia: dementia with Lewy bodies (DLB) and Parkinson’s disease dementia (PDD). DLB is characterised by the accumulation of α-synuclein in Lewy bodies and Lewy neurites in the brain, as well as neuronal loss in the substantia nigra, although typically less severe than that observed in Parkinson’s disease.6 PDD and DLB are both α-synucleinopathies.6 There is considerable clinical overlap between DLB and PDD.6 Generally, DLB presents at an older age, while PDD is preceded by a long period of motor symptoms.6 The arbitrary ‘1-year rule’ is commonly applied in clinical practice, whereby DLB is diagnosed when cognitive symptoms appear before or within 1 year of motor symptoms, whereas PDD is diagnosed when cognitive decline occurs in the context of established Parkinson’s disease.6
Frontotemporal dementia	Frontotemporal dementia (FTD) is a common cause of early-onset dementia, typically affecting individuals aged 45–65 years.7 FTD is categorised as three variants: 1) behavioural-variant FTD (associated with behavioural and executive deficits), 2) non-fluent variant primary progressive aphasia (progressive deficits in speech, grammar and word output), and 3) semantic-variant primary progressive aphasia (impaired naming and single-word comprehension).8 As the name suggests, FTD involves progressive degeneration of the frontal and/or temporal lobes associated with characteristic protein inclusions.6 Genetic mutations and family history of dementia play an important role in its pathogenesis.6
Other causes of dementia	Other less common causes of dementia are associated with9,10: Huntington’s disease traumatic brain injury posterior cortical atrophy infectious disease (e.g. human immunodeficiency virus [HIV], Creutzfeldt-Jakob disease) toxicity (e.g. hazardous alcohol consumption).

Case scenario

Introduction

Learning outcomes

Pathophysiology

Box 1 – Common symptoms of dementia

Differential diagnosis

Diagnosis

Risk factors

Management

Non-pharmacological treatment

Pharmacological treatment

Additional support

Knowledge to practice

Conclusion

Case scenario continued

Key points

Our authors

References

Day one: clinical insights and celebrating talent

Day two: expanding scope and emerging technologies

Day three: practical insights and professional reflection

1. Diphtheria is back

2. Vaccination rates keep declining

3. Pharmacist's busiest flu-vaccine week on record!

4. HPV vaccination success

5. Maternal and infant RSV vaccination rates have already improved

6. What does the future hold for vaccination?

Practical guidance

Box 1: Practical advice for communicating with autistic patients

Box 2: Using AAC to support communication

Case 1

Case 2

Box 3: Tips for conducting HMRs with autistic patients

1. Who is now funded under the NIP?

2. Which RSV vaccine is funded for older Australians?

3. When does the NIP listing commence?

4. Will booster doses be required?

5. What was the reason behind the decision?

6. What does ATAGI have to say?

Case scenario

Introduction

Learning outcomes

Pathophysiology

Box 1 – Common symptoms of dementia

Differential diagnosis

Diagnosis

Risk factors

Management

Non-pharmacological treatment

Pharmacological treatment

Additional support

Knowledge to practice

Conclusion

Case scenario continued

Key points

Our authors

References

Day one: clinical insights and celebrating talent

Day two: expanding scope and emerging technologies

Day three: practical insights and professional reflection

1. Diphtheria is back

2. Vaccination rates keep declining

3. Pharmacist's busiest flu-vaccine week on record!

4. HPV vaccination success

5. Maternal and infant RSV vaccination rates have already improved

6. What does the future hold for vaccination?

Practical guidance

Box 1: Practical advice for communicating with autistic patients

Box 2: Using AAC to support communication

Case 1

Case 2

Box 3: Tips for conducting HMRs with autistic patients

1. Who is now funded under the NIP?

2. Which RSV vaccine is funded for older Australians?

3. When does the NIP listing commence?

4. Will booster doses be required?

5. What was the reason behind the decision?

6. What does ATAGI have to say?

Case scenario

Introduction