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Internal Medicine > Geriatrics- Dementia > Flashcards

Geriatrics- Dementia Flashcards

1
Q

What is dementia?

A

1 an acquired deficit of cognition
2 multiple domains of cognitive impairment (2 or more) affected
3 often includes memory impairment
4 cognitive impairment not due to disturbance of arousal / wakefulness / consciousness
5 deficits sufficient to interfere with social and work activities
6 can be reversible

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2
Q

dementia syndrome

A
  • deterioration from a prior level of intellectual function
  • interferes with activities of daily living
  • > 1 category of intellectual performance affected
  • independent of level of consciousness
    -deterioration supported by historical evidence
  • documented by cognitive tests that are quantifiable, reproducible & for which normative data are available
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3
Q

the dementia syndrome

A

cognitive decline

behavioural & psychological symptoms

impairment in activities of daily living

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4
Q

What are the primary neurodegenerative diseases that cause dementia?

A

Alzheimer’s Disease
Vascular Dementia
Lewy Body Disease
Frontotemporal Dementia

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5
Q

What are some secondary systemic and potentially treatable causes of dementia?

A

Vitamin B-12 Deficiency
Hypothyroidism

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6
Q

What structural brain lesions can lead to dementia?

A

Tumors
Subdural Hematomas
Large Strokes
Hydrocephalus

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7
Q

What infections of the nervous system can cause dementia?

A

Neurosyphilis
HIV Infection

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8
Q

Differential diagnosis of dementia

A

anxiety / depression (“depressive pseudo-dementia”)

delirium

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9
Q

Clinical approach

A

is there cognitive impairment?
- history from patient & informant
- mental state exam incl. cognitive test such as MMSE
- physical exam: any systemic or other neurological abnormalities to account for symptoms?
- could the symptoms & signs be explained by delirium, anxiety or depression?
-investigations

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10
Q

investigations

A
  • cognitive tests e.g. MMSE
  • haematology: FBC, ESR
  • biochemical U&E, Cr, liver tests, cholesterol, glucose
  • serum B-12, serum & red cell folate
  • thyroid function
  • syphilis serology
  • CT scan brain

HIV test
MRI scan
Cerebral perfusion SPECT scan
EEG
lumbar puncture CSF

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11
Q

What are the types of cortical dementias?

A

Alzheimer’s Disease
Multi-Infarct Vascular Dementia
Frontotemporal Dementia (Pick’s Disease)
Lobar / Focal Dementias:
- Primary Progressive Aphasia
- Semantic Dementia
- Posterior Cortical Atrophy

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12
Q

What are the types of subcortical dementias?

A

Small Vessel Subcortical Ischaemic Vascular Disease
HIV Dementia
Lewy Body Disease
Parkinson’s Associated Dementia
Other Parkinsonian Syndromes
Huntington’s Disease
Normal Pressure Hydrocephalus

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13
Q

What types of dementia involve both cortical and subcortical regions?

A

Prion Diseases (e.g., Creutzfeldt-Jakob Disease)

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14
Q

What are the key differences between cortical and subcortical dementia?

A

Location of Damage:

Cortical Dementia: Primarily affects the cerebral cortex, leading to impairments in higher cognitive functions.

Subcortical Dementia: Involves damage to the subcortical structures (e.g., basal ganglia, thalamus), affecting motor control and emotional regulation.

Cognitive Symptoms:

Cortical Dementia: Often presents with significant memory loss, language difficulties (aphasia), and perceptual deficits. Common examples include Alzheimer’s disease and frontotemporal dementia.

Subcortical Dementia: Typically features slower cognitive processing, executive dysfunction, and changes in mood or behavior, rather than prominent memory loss. Examples include Lewy Body Disease and Huntington’s disease.

Progression:

Cortical Dementia: Symptoms may progress steadily over time, with clear changes in cognitive function.

Subcortical Dementia: Progression can be more variable, often linked to the underlying disease process (e.g., Parkinson’s).

Physical Symptoms:

Cortical Dementia: Less emphasis on physical symptoms; may see changes in motor function in later stages.

Subcortical Dementia: Often associated with motor symptoms (e.g., tremors, rigidity) early in the disease course.

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15
Q

What are the key features of cortical dementias?

A

Higher Cortical Functions Affected:
Amnesia: Memory impairment, particularly short-term memory loss.
Dysphasia: Difficulty with language, including speaking or understanding speech.
Dyspraxia: Impaired ability to plan and execute coordinated movements.
Agnosia: Inability to recognize objects, faces, or sounds despite intact sensory function.
Other Cognitive Impairments: Problems with reasoning, judgment, and problem-solving.

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16
Q

What are the key features of Alzheimer-type pathology?

A

Plaques and Tangles:
- Senile (Neuritic) Plaque:
Thick Arrow: Characterized by the accumulation of beta-amyloid peptides, contributing to neurodegeneration.
- Diffuse Plaque:
Small Arrow: Less dense, more widespread accumulation of beta-amyloid.

Neurofibrillary Tangles:
Star: Composed of hyperphosphorylated tau protein, leading to neuronal dysfunction and cell death.

Beta-Amyloid Angiopathy:
The deposition of beta-amyloid in the walls of blood vessels, increasing the risk of hemorrhage

Brain Atrophy:
Generalized shrinkage of brain tissue, particularly in the hippocampus and cerebral cortex, correlating with cognitive decline.

17
Q

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

A

Definition:

Braak staging is a classification system based on the progression of neurofibrillary tangle pathology in the brain.

Stages:
Stage I: Tangles begin in the entorhinal cortex, which is involved in memory processing.
Stage II: Tangles spread to the limbic system, affecting emotional responses and memory.
Stage III: Tangles extend into the neocortex, impacting higher cognitive functions.

Progression:
The disease typically progresses from the entorhinal area through the limbic system and into the neocortex, correlating with increasing cognitive impairment.

18
Q

Cognitive symptoms

A
  1. amnesia (dysnesia)
    amnestic MCI = prodromal clinical phase. Episodic memory loss. Limbic (hippocampal) disease. R vs. L hippocampus. Ribot’s law (“last in, first out”)
    2 aphasia (dysphasia)
    3 apraxia (dyspraxia)
    4 agnosia
    5 frontal executive function impairment
    6 other – dyslexia, dysgraphia, acalculia, L  R disorientation
19
Q

non-cognitive symptoms

A
  • psychotic – delusions, misidentifications, hallucinations
  • mood – depression, anxiety, euphoria.
  • behavioural – apathy (70%), agitation (30%), wandering (20%), physical & verbal aggression.
  • changes in sleep pattern
  • feeding & eating difficulties
  • sexual disinhibition
  • personality changes
20
Q

physical symptoms & signs

A

neurological – primitive reflexes, gait & balance disturbances, stooped posture, myoclonic jerks, seizures, bilateral pyramidal & extrapyramidal signs (late).

incontinence – urinary & faecal

general – weight loss

21
Q

natural history & progression

A

episodic & autobiographical memory  language deficits  visuo-spatial deficits (topographical memory & dressing apraxia)  frontal defects.

varies from person to person

difficult to give accurate individual predictions

time to institutionalization:
mild AD: 12% by 1 year; 35% by 2 years
severe AD: 39% at 1 year; 62% by 2 years
time to death: 1 to 16 years. median survival: 5 – 6 years
cause of death? Often systemic infection e.g. pneumonia, UTI

22
Q

management (I)

A
  • no specific treatment
  • explanation to family
  • drugs: cholinesterase inhibitors: donepezil, galantamine, rivastigmine; NMDA–R antagonist: memantine
  • support for carersgroups e.g. dementia SA
  • management of behavioural symptoms: non-pharmacological
  • use of anti-psychotics e.g. haloperidol, risperidone, quetiapine
  • treatment of intercurrent systemic illnesses
  • driving
  • testamentary capacity
  • placement
23
Q

What cognitive speed change is commonly seen in subcortical dementias?

A

Bradyphrenia: This refers to slowness of cognitive processing speed

24
Q

What emotional state is often observed in patients with subcortical dementia?

A

Apathy: Patients may show a lack of motivation or interest in activities

25
Q

How is attention affected in subcortical dementias?

A

Impaired Attention: Individuals may struggle to focus or sustain attention on tasks.

26
Q

What type of cognitive function is commonly impaired in subcortical dementias?

A

Executive Impairment: This includes difficulties with planning, organizing, and problem-solving.

27
Q

How does memory function present in subcortical dementias?

A

Memory Impairment: Patients often have poor spontaneous recall but can encode and store information well.

Recollection Aided by Cues: Recognition memory is typically preserved, allowing patients to remember with prompts.

28
Q

What mood disorder is frequently associated with subcortical dementias?

A

Depression: Many patients experience depressive symptoms.

29
Q

What physical signs are often associated with subcortical dementias?

A

Motor Signs: Patients may display various motor symptoms, such as tremors or rigidity.

30
Q

Features of subcortical dementias

A

[ frontal-subcortical connections and basal ganglia structures affected ]

  • bradyphrenia (slowness of cognitive speed)
  • apathy
  • impaired attention
  • executive impairment
  • memory impairment – poor spontaneous recall but preserved encoding and storage. Recollection aided by cues. Good recognition memory
  • depression
  • often associated motor signs
31
Q

What is vascular dementia commonly characterized by?

A

Multi-Infarct Dementia: It often presents with classical step-wise deterioration in cognitive function.

32
Q

What type of brain changes are more commonly seen in vascular dementia?

A

Small Vessel Ischaemic Changes: These typically occur in the periventricular and deep white matter of the brain.

33
Q

What underlying health conditions are often associated with vascular dementia?

A

Poorly Controlled Hypertension and Type II Diabetes: Both are significant risk factors that contribute to the development of vascular dementia.

Internal Medicine (14 decks)

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