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Post Midterm Patho > Neurological Disorders > Flashcards

Neurological Disorders Flashcards

1
Q

Degenerative Disorders a type of neurological disorder, are they usually progressive, or rapid?

A

Usually progressive decline over decades.

Some are rapid (few years)

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2
Q

Define Dementia:

A

Loss of ordered neural function (loss of cognition, memory, language etc.)

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3
Q

Is Dementia a disease?

A

No. Dementia is a manifestation of several unrelated disease

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4
Q

Alzheimer(‘s) Disease (AD) is a form of what? Explain the term ADT?

A

Form of Dementia.

Dementia of the Alzheimers Type

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5
Q

Is AD progressive? What else is it?

A

Progressive and Irreversible

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6
Q

At what age do the incidence of AD increase?

A

65 and above

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7
Q

What is the Et of AD?

A
  1. 90% idiopathic

2. 10 % familiar

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8
Q
  1. What gene does the idiopathic Et involve?

2. At what age would idiopathic AD present?

A
  1. Apolipoprotein on E gene (APOE)

3. over 65

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9
Q

What does apolipoprotein cause to form?

A

Lipoproteins

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10
Q
  1. The familiar etiology of AD usually occurs at what age?
  2. What Chrm are involved?
  3. What 3 Genes are involved?
A
  1. Before 65 years
  2. 1, 12, 14, 19, 21
  3. APP, PS1, PS2
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11
Q
  1. APP stands for what? What chrm is it on?
  2. What does this form a precurser to?
  3. If the gene is defective, what occurs?
A
  1. Amyloid Precussor Protein, Chrm 21
  2. Forms precurser to amyloid
  3. Accumulation of Amyloid
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12
Q

PS 1 /2 stands for what?

A

Presenilin Gene

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13
Q
  1. PS1 is on what Chrm?

2. PS2 is on what Chrm?

A
  1. Chrm 14

2. Chrm 1

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14
Q

Since AD has chromosome 21 involved, what does this link the disorder to?

A

Down Syndrome

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15
Q

Pathophysiology of AD involves what?

A

Atrophy of Cerebral Cortex

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16
Q

The cortex is affected in the sulci and the gyri, what does it cause to occur to each of these?

A
  1. Sulci = prominant dips

2. Gyri = Thinner tissue

17
Q

What 2 Part of the brain are affect in AD?

  1. A
  2. H

3.What are both of these? (the term for specialized ganglia in a group)

A
  1. Amygdala
  2. Hippocampus
  3. Nuclei
18
Q

Where is the Amygdala? What is it involved in?

A

Temporal Lobe, involved in response to our enviorment

19
Q

Where is the hippocampus? What is it involved in?

A

Temporal Lobe, involved in maintaining memory

20
Q

Is the sensory cortex affected in AD?

A

No, the person is still able to feel touch

21
Q

The lesions in AD develop d/t to what?

A

Accumulation of proteins in the neurons

22
Q

What are the 2 Lesions involved in AD?

A
  1. Neuritic Placques

2. Neurofibrillary Tangles

23
Q

What are the Neuritic Placques? Where are they?

A

Deposits of Amyloid Protein, usually at the terminal ends of a neuron

24
Q

What are the neurofibrillary Tangles? Where are they?

Are they resistant to breakdown? This means that what happens after you die?

A

Fibrous proteins in cytoplasm

Yes, still present after death

25
Q

The lesions cause an increase or decrease of ACH?

A

Decrease

26
Q

What does the decrease of ACH stand for?

What is it?

A

Acetylcholine

Neurotransmitter

27
Q
  1. Describe the Mnft’s of AD?

2. What are the stages based on? Over how long?

A
  1. Insidious onset

2. Based on Progression (~10 yrs)

28
Q

What are the 3 stages of AD classified as? How long does each stage last? Is there a distinct change between one stage and the next?

A
  1. Mild (2-4 yrs)
  2. Moderate (2-10yrs)
  3. Severe (2 yrs)

There is no distinct change. They overlap

29
Q

The Mnfts of mild AD are what 3 things?

A
  1. Memory problems (often family member notices this)
  2. Careless work habits
  3. Familiar routine manageable (ADL’s are not affected)
30
Q

What are the Manifestations of Moderate AD? (6)

A
  1. Declining in cognition
  2. Confusion (where am i? what am I doing?)
  3. Language problems (receptive, ability to speak, same question)
  4. Some motor disturbance (using knife/fork)
  5. Indifference (lack of interest)
  6. Problems with ADLS
31
Q

What are the manifestations of sever AD? (5)

A
  1. Severe mental impairment
  2. minimal voluntary movement
  3. no self care (requires hep with all ADLS)
  4. incontinence
  5. Rigid, flexor posturing
32
Q

Explain what a patient with sever AD would flex like?

A

Flexed at elbows and writs qlenched

33
Q

How do you Dx AD? Is it easy?

A

Very difficult to dx.

  1. Dx on clinical presentation (initially very vague in the beginning stages of the disease)
  2. Exclude the other ways that dementia can be caused (example exclude vascular or toxic dementia)
  3. EEG, CT, MRI, Labs
34
Q

Is there a difinivite test for AD?

A

No

35
Q

Explain the following:

  1. EEG:
  2. Labs:
A
  1. Electroencephalogram = test or record of brain activity

2. Ex. Vitamin B12 associated with dementia, so look for these levels

36
Q

What does the treatment for AD include?

A
  1. no cure
  2. Symptomatic
  3. Behavioral / Enviornmental Manipulations
  4. Pharmacologic
37
Q

What are the pharmacologic interventions?

A
  1. Glutamate Receptor Blocker
  2. Ach-esterase Inhibitors
  3. Low dose antipyschotic drugs (ex: risperidone)
  4. Antidepression Drugs (ex: effexor)

May also be on….

Statins (cholesterol lowering drugs), ASA (blood thinner) and symptomatic management

38
Q

What does the Glutamate Receptor Blocker do? Is it a good thing in small levels? (explain why) What is an example?

A

Blocks the receptor, therefore it cant bind because high levels of the glutamate can become neurotoxic.

It is good in small levels because it increases neurofunction, problem occurs if it builds up.
Ex: Memantine

39
Q

What does the Ach-esterase inhibitor do? What is an example?

A

Inhibits enzyme that breaks up ACh, therefore the small ammoutns that are present are not broken down.
Ex: Aricept

Post Midterm Patho (16 decks)

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