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Bio 252 > Nov. 25, 2019 > Flashcards

Nov. 25, 2019 Flashcards

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Biology 101 flashcards
1
Q

During CORTICAL ATROPHY, what can be observed about the SULCI and GYRI?

A

The SULCI are more prominent and the GYRI are more slender

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2
Q

What role does the HIPPOCAMPUS play in cognitive Fx?

A

Maintains memory, important part in cognition

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3
Q

What role does the AMYGDALA play in cognitive Fx?

A

Helps to interact/respond to the intermediate environment

eg writing notes, listening to Ahmed

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4
Q

What happens to the HIPPO and AMYG when a pt has AD?

A

They lose NEURONS

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5
Q

Is the SENSORY CORTEX affected during AD?

A

No

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6
Q

What is the role of Ach?

A

It is a stimulatory NEUROTRANSITTER, that helps move APs from one neuron to another one

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7
Q

Are the lesions associated w AD visible to the naked-eye?

A

They are visible under a microscope

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8
Q

T or F:

NEURITIC PLAQUES are located inside the cell

A

F, they are located outside the cell

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9
Q

What is the core of a NEURITIC PLAQUE?

A

AMYLOID BETA w/ degenerative nerve terminals

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10
Q

How is ABETA formed?

A

ABETA is produced when AMYLOID PRECURSOR PROTEIN is broken down

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11
Q

What is the role of TAU proteins?

A

Proteins that stabilize microtubules

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12
Q

What are NEUROFIBRILLARY TANGLES composed of?

A

Primarily TAU

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13
Q

Where are NEUROFIBRILLARY TANGLES found?

A

They deposit inside of the cell’s cytoplasm, and at the end of fibers (I don’t know specifically what fibers, my notes just say “fibers”)

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14
Q

What do the deposits of TAU do to the fibers in brain cells?

A

They cause them to change shape and tangle, this is how they become NEUROFIBRILLARY TANGLES

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15
Q

Are TANGLES easy to breakdown?

A

No

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16
Q

TANGLES __________ after necrosis

A

Persist

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17
Q

What are the MNFTS of AD?

A

Anything r/t l/o cognitive Fx

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18
Q

Describe the onset of AD

A

Insidious

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19
Q

Approx how long do pts w/ AD live after diagnosis?

A

~ 10 yrs

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20
Q

T or F:

Death by AD is not directly a result of AD

A

T

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21
Q

How long does the mild stage of AD last?

A

2-4 years

22
Q

How do the MNFTS of AD appear in mild AD?

A
  • Pt appears mostly normal
  • Can manage familiar tasks
  • May become slightly negligent/forgetful
  • If anyone realizes they’re sick, it will be the people around them, not the person themselves
23
Q

How long does the mod stage of AD last?

A

2-10 years

24
Q

How do the MNFTS of AD appear in mod AD?

A
  • L/o cognitive Fx
  • Substantial confusion
  • Language problems
    • Speaking and understanding
    • May have repetitive speech
    • Paraphasia (use of words in the wrong context)
  • Poor self-care
  • Depression
  • Some aggression
25
Q

How long does the severe stage of AD last?

A

~ 2 years

26
Q

How do the MNFTS of AD appear in severe AD?

A
  • Severe mental impairment
  • No self-care
  • Unable to respond to environment
  • Minimal voluntary movement
  • Flexor posturing
27
Q

What does flexor posturing look like?

A
  • Arms flexed, or bent inward on the chest
  • Hands are clenched into fists
  • Legs extended
  • Feet turned inward
28
Q

Is there a definitive test for AD?

A

No

29
Q

How is the Dx of AD done?

A
  • By excluding other possibilities eg dementia
  • Imagining to detect lesions in the brain
    • EEG
    • CT
    • MRI
  • Labs to rule out other diseases
    • B12
    • HIV, syphilis
    • CBC
    • CRP
    • Thyroid
30
Q

What is the cure of AD?

A

There isn’t one

31
Q

What is the Tx for AD?

A
  • Suppress progression

- Symptom management

32
Q

What drugs are involved in the management of AD?

A
  • Ach-esterase inhibitor
    • Aricept (Donepezil)
  • Glutamine receptor blocker
    • Memantine
  • Anti-depressants
  • Anti-psychotics
    • Risperidone (Risperdal)
33
Q

Which is normal to find in the body:

Myelinated or unmyelinated axons

A

Both!

34
Q

What causes demyelination?

A

Autoimmune destruction of myelinated axons in the CNS

35
Q

Who is most commonly affected by MS?

A
  • Young women
  • Residents of colder regions
  • Caucasians
36
Q

What is the Et of MS?

A
  • Family Hx
    • 15x more likely to have
    • Abn MHC/HLA
  • Complex trait
  • Must have preceeding infct
    • Viral trigger
    • Often EBV (infctious mononeucleosis)
37
Q

What is the effect of demyelination in the CNS?

A

Causes inflm damage -> poor conduction of AP

38
Q

What are SCLEROTIC PATCHES in MS?

A

They are hardened patches produced when myelin in destroyed

39
Q

What causes SCLEROTIC PATCHES?

A

Inflm damage caused by lymphocyte and macrophages

40
Q

What is the usual role of OLIGODENDROCYTES?

A

They myelinate, and provide support to axons in the CNS

41
Q

What areas are most affected by plaques?

A
  • Optic nerve
  • Spinal cord
  • Cerebellum
  • Brain stem
42
Q

T or F:

Only motor response is affected in MS

A

F, bot motor and sensory are affected

43
Q

What are the mnfts of MS?

A
  • Sensory deficit
  • Parasthesia
  • Fatigue
  • Uni-lateral visual impairment
  • Bowel and bladder dysfx
  • Weak muscle action
  • Change in gait
  • Chronic remissions and exacerbations
44
Q

Is there a deficiency of ATP in MS?

A

No, the l/o voluntary muscle movement is all neuro related

45
Q

How is MS Dx?

A
  • Hx and mnfts
  • MRI to view sclerotic patches
  • Serology to dectect Abs
  • Samples taken from the spinal cord
    • CFS w inc IgE indicate MS
46
Q

If protein content is elevated in CNS, what does this indicate? (3)

A
  • BBB is compromised
  • Autoimmune problem
  • Inflm w/in spine or brain
47
Q

Is MS reversible?

A

Nope

48
Q

How fast is the progression of MS?

A

Not fast, slow progression

49
Q

Why do you admin STEROIDS in MS?

A
  • To suppress the immune response

- Suppress inflm

50
Q

What can be used w STERIODS?

A

Interferons

51
Q

What is METHOTREXATE? (this is involved in Tx for MS)

A
  • An anti-CA agent
  • Immunoregulatory (for longterm)
  • Anti-folic
52
Q

What is FOLIC ACID used for in the body?

A
  • For cell division/DNA replication
  • Hepatotoxic
  • Standing orders for CBC and liver Fx

Bio 252 (24 decks)

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