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PHAR 123 > Neurodegenerative disease > Flashcards

Neurodegenerative disease Flashcards

1
Q

In broad terms, what is Dementia?

A

-Describes cognitive, memory, communication impairments associated with Neurodegenerative Disease.

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2
Q

How are Dementias diagnosed?

A

-Memory / Language / Math / Mental Function tests
-Lab Tests (due to Vit. deficiencies, hormones???)
-Brain Scans (PET, MRI, CT)
-Psychiatric (to rule out depression, other disorders)

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3
Q

When does Alzheimer’s Disease develop?

A

Mid-Late Adulthood (usually > 65yrs)

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4
Q

T or F: Women are at higher risk of suffering from Alzheimer’s Disease.

A

True!

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5
Q

What are some factors that increase risk of getting Alzheimer’s?

A

-Age
-Family History
-Genetic Predisposition (2 APOe-4 genes = Higher risk)
-Previous Stroke
-Depressive
-Diabetic
-Metal Exposure (ie. Arsenic, Lead, Copper, Mercury)
-Smoke / Pesticide Exposure

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6
Q

Alzheimer’s Disease involves atrophy of the cortical parts of the _______ & ______ regions of the brain.

A

Frontal ; Temporal

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7
Q

In an Alzheimer’s brain, the Gyri ______ & the Sulci ______.

A

narrow ; widen

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8
Q

The major pathological brain change associated with Alzheimer’s is the development of what?

A

Neurofibrillary Tangles that contain Amyloid proteins

-This abnormal material induces toxicity, compression & destruction of surrounding brain tissues.

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9
Q

What areas of the brain are particularly susceptible to the effects of Neurofibrillary Tangles?

A

-Hippocampus (new memory formation)
-Frontal Lobe (behavior, cognition, judgement)
-Parietal Lobe (language)

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10
Q

How does Alzheimer’s progress?

A

Early: Recent memory loss, mild coordination problems, mood swings. Need reminders for daily activities.

Middle: Persistent memory loss (including past memories)… Rambled speech, lost in familiar places, sleep disturbances, confusion, slow / rigid / tremored movements. Need reminders & some degree of assistance.

Late: Loss of ability to remember, communicate, process information. Immobile, falls likely, incontinence / swallowing issues, extreme issues with mood (can appear delirious). Round the clock management needed.

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11
Q

What two classes of drugs are approved for Alzheimer’s treatment?

A

1) Cholinesterase Inhibitors (ie. Donepezil, Rivastigmine, Galantamine)
2) NMDA Receptor Antagonists (ie. Memantine)

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12
Q

How does Memantine work?

A

-Blocks NMDA receptor, preventing chronic activation from Soluble Beta Amyloid oligomers (less excitotoxicity to neurons).

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13
Q

What roles do the following drugs have as adjunct Alzheimer’s therapies:

Escitalopram
Mirtazapine
Carbamazepine
Levetiracetam
Lithium
Methylphenidate

A

Escitalopram / Mirtazapine: Antidepressants
Carbamazepine / Levetiracetam: Anticonvulsants
Lithium: Mood Stabilizer
Methylphenidate: Stimulant

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14
Q

Aducanumab & Lecanumab work how? Side effects?

A

-Target Beta Amyloid (reduce cognitive decline)

Adu: Edema & small brain bleeds (imaging abnormalities).
Lecan: Same as above & infusion related things such as chills, flushing, rash.

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15
Q

How does Gantenerumab work?

A

-Binds aggregated amyloid & subsequent Fc Gamma Receptor binding of Microglia with the MAB promotes Microglial phagocytosis of Beta Amyloid particles.

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16
Q

What is Pick’s Disease?

A

-Tau Protein accumulation in swollen neurons, which induces cortical atrophy, gliosis (particularly in Frontal Lobe), & cortical neuron loss.

-Primarily affects Frontal & Temporal Lobes (speech & behavior affected).

17
Q

What are the primary ages of patients affected by Pick’s Disease?

A

40-60yrs

18
Q

Pick’s Disease (ie. Frontotemporal Dementia) manifests clinically how?

A

-Impulsive speech or behavior
-Loss of empathy & interpersonal skills
-Reduced self-awareness & hygiene
-Sudden & frequent mood changes
-Difficulties with speech & language
-Balance / movement issues

19
Q

Lewy Bodies (found in Lewy Body Disease) are comprised of clumps of Alpha-Synuclein & _________ proteins in neurons.

A

Ubiquitin

20
Q

Which brain regions are affected by Lewy Bodies?

A

-Cerebral Cortex (info processing, perception, thought, language)
-Limbic Cortex (emotions & behavior)
-Hippocampus (new memory formation)
-Midbrain & Basal Ganglia (movement)
-Brain Stem (sleep & alertness)

21
Q

T or F: Women are at higher risk of suffering from Lewy Body Dementia.

A

False… Men are at higher risk!

22
Q

How does Lewy Body Dementia clinically manifest?

A

-Intermittent memory problems
-REM Sleep Disorder (acting out dreams)
-Balance / Motor ctrl issues
-Emotionless face
-Hallucinations
-ANS effects (dizzy, hypotensive, falls)

23
Q

What do we treat Lewy Body Dementia with?

A

-Is no direct treatment for the disease itself… Treat symptoms.

Cognitive: Alzheimer’s Drugs
Motor: Carbidopa / Levodopa
Behavior: AD’s / Antipsychotics
Sleep: Melatonin / Clonazepam
ANS: Fludrocortisone / Midodrine

24
Q

Onset of Parkinson’s is what? Who’s most affected (M or W)?

A

50-70yrs ; Men more affected

25
Q

How does Parkinson’s occur?

A

-Melanin production in Substantia Nigra induces oxidative stress on neurons, leading to misfolded Alpha Synuclein & formation of filamentous inclusions.

26
Q

What happens to Dopaminergic projecting neurons in Parkinson’s Disease?

A

DIEEEEEEEE (so no projection from Substantia Nigra to Striatum)

27
Q

What happens to neurons contained within the Substantia Nigra in Parkinson’s?

A

DIEEEEEEEEE (depigmentation of this brain region)

28
Q

How do movement defects manifest clinically in Parkinson’s?

A

-Resting Tremor
-Rigid Movements
-Bradykinesia (Slow Movements)
-Shuffling Gait

29
Q

Response to what pharmacological agent would help confirm Parkinson’s diagnosis?

A

Levodopa / Carbidopa

30
Q

What other clinical manifestations would show up with Parkinson’s (aside from movement-related defects)?

A

-Expressionless Face
-Postural Instability
-Soft Voice
-Small Writing
-Hallucinations / Delusions (advanced disease)

31
Q

What is the role of Carbidopa in Parkinson’s?

A

Reduces the systemic metabolism of Levodopa (so that it is able to reach the brain)

32
Q

Which agents block Dopamine breakdown at the neuron?

A

Tolcapone
MAO-B Inhibitors (Selegiline, Rasagiline)

33
Q

What agent reduces neuronal reuptake of Dopamine?

A

Amandatine

PHAR 123 (18 decks)

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