complete dementia Flashcards

1
Q

What is dementia?
A:

A

Dementia is a syndrome that refers to a progressive decline in intellectual functioning, severe enough to interfere with a person’s normal daily activities and social relationships.

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2
Q

How many disorders can cause dementia?
A:

A

Over 60-70 disorders can cause dementia.

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3
Q

What are the most prevalent forms of dementia?
A:

A

The most prevalent forms of dementia are Alzheimer’s disease, vascular dementia, Lewy body dementia, and frontotemporal dementia.

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4
Q

What are some rarer forms of dementia?
A:

A

Some rarer forms of dementia include pre-senile dementia, Picks disease, Korsakov dementia, pseudo-dementia, endocrine related dementia, Parkinson’s disease, Huntington’s chorea, posterior cortical atrophy, normal pressure hydrocephalus, and neurosyphilis.

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5
Q

What is vascular dementia?
A:

A

Vascular dementia refers to the pathology of many different types. Early symptoms include memory difficulties and executive difficulties. There is often a history of stroke/falls, and there are usually vascular risk factors present.

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6
Q

What is Lewy body dementia?
A:

A

Lewy body dementia is under the umbrella of diseases related to Parkinson’s disease. Early symptoms include executive difficulties, visuospatial problems, and hallucinations.

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7
Q

What is frontotemporal dementia?
A:

A

Frontotemporal dementia is an umbrella term that includes many different variants, including Picks disease, semantic dementia, and primary progressive aphasia (PPA). The main cognitive deficits are in executive functioning and attention, and memory and visuospatial abilities are mostly spared.

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8
Q

What is the main cognitive deficit in frontotemporal dementia?
A:

A

The main cognitive deficits in frontotemporal dementia are in executive functioning and attention.

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9
Q

What are some early symptoms of Lewy body dementia?
A:

A

Some early symptoms of Lewy body dementia include executive difficulties, visuospatial problems, and hallucinations.

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10
Q

How many types of vascular dementia are there?
A:

A

There are many different types of vascular dementia.

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11
Q

What is perception, and what are some common perception-related symptoms in dementia?

A

Perception is the process of making sense of information from the external environment and the body. In dementia, common perception-related symptoms include difficulty recognizing objects, judging the position of people or objects, and ignoring one side of the world.

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12
Q

What is executive functioning, and what are some common executive functioning-related symptoms in dementia?

A

Executive functioning refers to the cognitive processes involved in planning, decision-making, problem-solving, and self-monitoring. In dementia, common executive functioning-related symptoms include difficulty initiating tasks, getting stuck on tasks or repeating actions, and not thinking through the consequences of actions.

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13
Q

What is language, and what are some common language-related symptoms in dementia?

A

Language refers to the cognitive processes involved in understanding and expressing information. In dementia, common language-related symptoms include difficulty understanding words, concepts, and complex sentences, difficulty finding words, and reduced vocabulary.

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14
Q

What are some non-cognitive symptoms of dementia?

A

Non-cognitive symptoms of dementia include delusions, hallucinations, agitation/wandering, depression/dysphoria, anxiety, euphoria/elation, apathy/indifference, disinhibition, irritability/lability/aggression, aberrant motor behavior, night-time behavior, and appetite/eating changes.

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15
Q

What is the Mini-Mental State Exam (MMSE), and what does it test for?

A

The MMSE is a series of questions and tests that assess a person’s cognitive abilities, including memory, attention, and language. It is often used as part of the diagnostic criteria for dementia.

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16
Q

What are the key diagnostic criteria for dementia?

A

To be clinically diagnosed with dementia, a patient needs to show memory impairment, impairment in one or more cognitive domains (language, motor activity, recognition, executive function), and continuing cognitive decline.

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17
Q

How is the subtype of dementia determined?

A

A histopathological diagnosis is required to determine the subtype of dementia.

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18
Q

What is the amyloid hypothesis, and how does it relate to Alzheimer’s disease?

A

The amyloid hypothesis proposes that the accumulation of beta-amyloid protein outside the cell leads to the formation of plaques that kill neurons, causing Alzheimer’s disease.

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19
Q

What are beta-amyloid and tau proteins, and how do they relate to Alzheimer’s disease?

A

Beta-amyloid is a fragment of the amyloid precursor protein that accumulates outside the cell and is thought to be involved in the development of plaques in Alzheimer’s disease. Tau proteins help stabilize microtubules in neurons, and abnormal phosphorylation of tau proteins causes them to clump together and form neurofibrillary tangles, another hallmark of Alzheimer’s disease.

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20
Q

What is the tau hypothesis, and how does it relate to Alzheimer’s disease?

A

The tau hypothesis proposes that abnormal phosphorylation of tau proteins causes them to clump together and form neurofibrillary tangles, leading to impaired axonal transport and cell death in Alzheimer’s disease.

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21
Q

What are some current theories about the development of Alzheimer’s disease?

A

Current theories propose that Alzheimer’s disease is multifactorial, involving several pathways and dependent on life experience. Other proposed factors include protein accumulation, inflammation, and oxidative stress.

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22
Q

What is oxidative stress, and how does it relate to Alzheimer’s disease?

A

Oxidative stress refers to the development of free radicals, which can lead to cellular death. It is thought to play a role in the development of Alzheimer’s disease.

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23
Q

What is inflammation, and how does it relate to Alzheimer’s disease?

A

Inflammation refers to an overactive immune response, particularly from microglia in the brain. It is thought to play a role in the development of Alzheimer’s disease.

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24
Q

What are some common symptoms of neurofibrillary tangles in Alzheimer’s disease?

A

Common symptoms of neurofibrillary tangles include impaired axonal transport and cell death.

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25
Q

What are the cognitive domains? language, motor activity, recognition, executive function

A

To be diagnosed with dementia, patients must show memory impairment, impairment in one or more cognitive domains (language, motor activity, recognition, executive function), and continuing cognitive decline.

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26
Q

What are amyloid plaques and what role do they play in Alzheimer’s disease?

A

Amyloid plaques are structures that contain large amounts of a 42 amino acid peptide called “β-amyloid” or Aβ42. They are a hallmark of Alzheimer’s disease and are thought to be involved in the death of neurons.

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27
Q

What are neurofibrillary tangles and what role do they play in Alzheimer’s disease?

A

Neurofibrillary tangles are clumps of tau protein that accumulate inside neurons, disrupting their normal functioning and contributing to their death. They are another hallmark of Alzheimer’s disease.

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28
Q

What is the amyloid hypothesis of Alzheimer’s disease?

A

The amyloid hypothesis suggests that the accumulation of beta-amyloid protein (BAP) outside the cell leads to the formation of amyloid plaques, which then kill neurons and contribute to the development of Alzheimer’s disease.

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29
Q

What is the tau hypothesis of Alzheimer’s disease?

A

The tau hypothesis suggests that abnormal phosphorylation of tau proteins causes them to become “sticky,” leading to the breakdown of microtubules, which are responsible for axonal transport. This breakdown leads to cell death and contributes to the development of Alzheimer’s disease.

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30
Q

What is the pathophysiology of Alzheimer’s disease?

A

The pathophysiology of Alzheimer’s disease involves the accumulation of Tau and Aβ proteins in the brain, which leads to synapse loss and neuronal death.

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31
Q

What are some current theories of dementia?

A

Current theories suggest that dementia is multifactorial, involving several pathways and dependent on life experience. They also suggest that inflammation and oxidative stress may contribute to the development of dementia.

32
Q

What is the role of microglia in inflammation-related theories of dementia?

A

Microglia are immune cells in the brain that can become overactive and contribute to inflammation in the brain. Inflammation is thought to be a contributing factor to the development of dementia.

33
Q

What is oxidative stress and how does it contribute to the development of dementia?

A

Oxidative stress refers to the development of free radicals, which can cause cellular damage and death. This damage is

34
Q

How do neurofibrillary tangles form in Alzheimer’s disease?

A

Neurofibrillary tangles are one of the hallmarks of Alzheimer’s disease. They’re formed by a protein in the brain called tau. Normally, tau helps with the structure and function of neurons.

However, in Alzheimer’s disease, tau becomes abnormal and starts to clump together. These clumps eventually form twisted structures called “neurofibrillary tangles.” This process is believed to damage neurons and disrupt communication between them, which can contribute to the symptoms of Alzheimer’s disease.

35
Q

What is the role of amyloid precursor protein (APP) in Alzheimer’s disease?

A

APP is a membrane protein that sits in the membrane and extends outward. It is thought to be important for neuronal growth, survival, and repair. Enzymes cut the APP into fragments, the most important of which for AD is called β-amyloid or Aβ.

36
Q

What is the primary early symptom of Alzheimer’s disease?

A

The primary early symptom of Alzheimer’s disease is a deficit in recent memory.

37
Q

How early can changes in the brain associated with Alzheimer’s disease begin before symptoms appear?

A

Changes in the brain associated with Alzheimer’s disease can begin 10-20 years before symptoms appear.

38
Q

What are the histopathology signs of Alzheimer’s disease that are first noticed in the brainstem?

A

The histopathology signs of Alzheimer’s disease that are first noticed in the brainstem are in noradrenergic neurons.

39
Q

What brain regions are associated with memory changes in the early stages of Alzheimer’s disease?

A

The entorhinal cortex and hippocampus are associated with memory changes in the early stages of Alzheimer’s disease.

40
Q

What is the primary basis for emotional changes in Alzheimer’s disease?

A

The decreased level of brain Ach is the primary basis for emotional changes in Alzheimer’s disease.

41
Q

What are the primary symptoms of moderate stage Alzheimer’s disease?

A

The primary symptoms of moderate stage Alzheimer’s disease include significant memory loss, personality and behavioral changes, disorientation in time and space, inability to undertake simple tasks, reduced range of thinking, and language problems.

42
Q

What is the primary symptom of severe stage Alzheimer’s disease?

A

Dysphasia with disordered and fragmented speech is the primary symptom of severe stage Alzheimer’s disease.

43
Q

What physical changes occur in the brain during the moderate stage of Alzheimer’s disease?

A

The cerebral cortex begins to shrink as more neurons die during the moderate stage of Alzheimer’s disease.

44
Q

What physical changes occur in the brain during the severe stage of Alzheimer’s disease?

A

Extreme shrinkage occurs in the brain during the severe stage of Alzheimer’s disease, and the ventricles may become expanded.

45
Q

What is the main drug class currently approved for treating Alzheimer’s disease?

A

Acetylcholinesterase inhibitors (AchEIs)

46
Q

What is the recommended use of AchEIs in Alzheimer’s disease treatment?

A

AchEIs are recommended for the treatment of mild to moderate AD.

47
Q

How well do AchEIs delay progression to the severe stage of AD?

A

AchEIs delay progression to the severe stage of AD by 6 to 12 months in 30% of patients.

48
Q

What are the improvements observed with AchEI treatment in AD patients?

A

Improvements in cognitive function, behavioral symptoms, and daily activities.

49
Q

What are some significant side effects of AchEIs?

A

Significant side effects due to peripheral actions of the drugs include nausea, vomiting, and hepatic toxicity.

50
Q

What is the MOA of Tacrine?

A

Tacrine is a long-acting AchEI that blocks M1, M2, and nicotinic receptors, increases the release of Ach from nerve endings, inhibits MAO, and increases the release of NA, 5HT, and DA from nerve endings.

51
Q

What are some significant side effects of Tacrine?

A

Significant side effects of Tacrine include nausea, vomiting, increased peripheral Ach levels, and life-threatening hepatic toxicity.

52
Q

What is the MOA of Donepezil?

A

Donepezil is a reversible centrally active AchEI.

53
Q

What are some side effects of Donepezil?

A

Side effects of Donepezil include nausea and vomiting, hallucinations, aggression, agitation, urinary incontinence, and gastric and duodenal ulcers.

54
Q

What is the MOA of Rivastigimine?

A

Rivastigimine is a reversible AchEI.

55
Q

What are some side effects of Rivastigimine?

A

Side effects of Rivastigimine include nausea, vomiting, hallucinations, aggression, agitation, confusion, insomnia, and worsening of Parkinson’s disease symptoms.

56
Q

What is the MOA of Galantamine?

A

Galantamine is a reversible AchEI and an allosteric modulator/agonist at nicotinic Ach receptors, which stimulates further Ach release.

57
Q

What are some side effects of Galantamine?

A

Side effects of Galantamine include nausea and vomiting, hallucinations, aggression, agitation, confusion, insomnia, muscle spasms, bradycardia, and syncope.

58
Q

What is the MOA of Memantine?

A

Memantine is a medication used to treat moderate to severe Alzheimer’s disease. It works by blocking NMDA (N-methyl-D-aspartate) receptors in the brain.

In Alzheimer’s, overactivity of these receptors can lead to an excess of calcium in nerve cells, contributing to cell damage.

59
Q

What are some side effects of Memantine?

A

Balance impaired; constipation; dizziness; drowsiness; dyspnoea; headache; hypersensitivity; hypertension

60
Q

What is the proposed mechanism of action of Glutamate NMDA receptor antagonists in Alzheimer’s disease treatment?

A

Glutamate NMDA receptor antagonists, such as Memantine, are effective in improving cognitive, functional, behavioral, and daily activity scores in moderate-to-severe AD patients by blocking the overactivity of glutamatergic synapses, which can cause excitotoxicity.

61
Q

What is the recommended use of Memantine in Alzheimer’s disease treatment?

A

Memantine is indicated for moderate-to-severe AD and is generally added to the AchEI regimen during the progression of the disease.

62
Q

What are some advantages of Memantine over AchEIs in terms of side effects?

A

Memantine is generally better tolerated than AchEIs, with fewer gastrointestinal side effects.

63
Q

What are some pharmacotherapeutic approaches for treating associated symptoms of Alzheimer’s disease, such as depression and anxiety?

A

SSRIs, such as Citalopram and Sertraline, and AEDs, such as Carbamazepine and Oxcarbazepine, can be used to treat depression and anxiety in AD patients.

64
Q

What are some pharmacotherapeutic approaches for treating aggression and agitation in Alzheimer’s disease?

A

AEDs, such as Sodium Valproate, and antipsychotics, such as Risperidone and Quetiapine, can be used to treat aggression and agitation in AD patients.

65
Q

What are some non-pharmacological interventions for treating Alzheimer’s disease?

A

Non-pharmacological interventions for treating AD include cognitive and behavioral therapies, physical exercise, and social engagement.

66
Q

What is the role of diet in Alzheimer’s disease prevention and treatment?

A

A healthy diet, such as the Mediterranean diet, rich in fruits, vegetables, whole grains, and fish, can help reduce the risk of AD and improve cognitive function in AD patients.

67
Q

What is the role of physical exercise in Alzheimer’s disease prevention and treatment?

A

Regular physical exercise can help reduce the risk of AD and improve cognitive function in AD patients.

68
Q

What are some potential future pharmacotherapeutic approaches for treating Alzheimer’s disease?

A

Potential future pharmacotherapeutic approaches for treating AD include immunotherapy, tau protein-targeted therapies, and neuroinflammation-targeted therapies.

69
Q

What is the role of genetics in Alzheimer’s disease?

A

Genetics plays a significant role in AD, with certain genetic mutations, such as the APOE4 allele, increasing the risk of developing AD.

70
Q

What is the relationship between sleep disturbances and Alzheimer’s disease?

A

Sleep disturbances, such as insomnia and sleep apnea, have been linked to an increased risk of developing AD and may contribute to the progression of the disease.

71
Q

What is the relationship between cardiovascular disease and Alzheimer’s disease?

A

Cardiovascular disease has been linked to an increased risk of developing AD, with risk factors such as hypertension, high cholesterol, and diabetes contributing to the progression of the disease.

72
Q

What is the relationship between traumatic brain injury and Alzheimer’s disease?

A

Traumatic brain injury has been linked to an increased risk of developing AD, particularly in individuals with a history of repetitive head trauma.

73
Q

What is the role of inflammation in Alzheimer’s disease?

A

Chronic inflammation has been implicated in the development and progression of AD, with neuroinflammation playing a significant role in the pathology of the disease.

74
Q

What are some potential biomarkers for diagnosing and monitoring Alzheimer’s disease?

A

Potential biomarkers for diagnosing and monitoring AD include amyloid beta and tau protein levels in cerebrospinal fluid, neuroimaging techniques such as PET scans, and genetic testing for AD risk alleles.

75
Q

What are some potential risk factors for developing Alzheimer’s disease?

A

Potential risk factors for AD include age, genetics, cardiovascular disease, traumatic brain injury, sleep disturbances, and lifestyle factors such as diet and exercise.