aging and disease Flashcards

1
Q

explain the negative feedback in the hypothalamic pituitary thyroid axis

A

thrytrophin releasing hormone (TRH) from hypothalamus.
stimulates production and secretion of thyroid stimulating hormone (TSH) from anterior pituitary.
TSH stimulates production of thyroid hormones (T4 and T3) from the thyroid.
T4 and T3 have a negative feedback on the pituitary and hypothalamus reducing the production of TRH and TSH.

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2
Q

what is somatopause in aging and endocrine system
- effects
-cure

A

gradual decline of growth hormone secretion with age.

effects- decreased production of insulin like growth factor (IGF-1)

cure- no long term benefits proven for growth hormone replacement.

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3
Q

what is hypothyroidism in aging.
who and why does it occur

A

reduction in production of T3 hormone (while T4 remains the same
cause- elderly females or lack of dietary iodine.

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4
Q

why does menopause occurs?

A

depletion of primordial follicles in ovaries and decline oestrogen levels.
no developing granuloma cells to produce oestrogen.

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5
Q

function of different ovarian follicles?
-theca cells
-granulosa cells

A

during menstrual cycle the supporting cells develop into two layers (theca and granuloma cells)

theca cells= responds to LH and produce androgen hormone (which are precursors for oestrogen)

granuloma cells= respond to FSH and convert androgen hormone to oestrogen.

one follicle becomes dominant while the other degenerates (undergo atresia).
at ovulation the dominant follicle releases the oocyte

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6
Q

the role of oestrogen in positive feedback before ovulation

A

high oestrogen levels = positive feedback by increase in LH. stimulates granuloma cells to produce even more oestrogen = ovulation
also increase in GnRH

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7
Q

what are the 2 abnormal lesions in alzehimers disease?

A

beta-amyloid plaques- accumulates extracellular around neuron’s (main driver of AD)
neurofibrillary tangles- tau protein that builds up intracellular inside neurons

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8
Q

two forms of Aβ peptides

A

Aβ40 and Aβ42 (most toxic)
aggravate together in hippocampus

penicillin 1 mutation= more Aβ42

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9
Q

Tau tangles phosphorylation in normal and alzehimers

A

normal- contently phosphorylated and dephosphorylated

AD- always phosphorylated

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10
Q

what is cholinergic hypothesis

A

exposure to irreversible acetylcholine esterase (AChE) inhibitors can activate symptoms of AD.
in AD there is a lack of acetyl choline

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11
Q

what are the two hallmarks of Parkinson’s disease

A

loss of dopaminergic neurons in the brain
Lewy bodies- occurs in surviving substantial nigra (SNpc) (controls body movements)
contains α-synuclein inside neurons

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12
Q

explain dopamine loss pathway results in motor systems

A

normal againg- 5% dopamine loss in dorsal SNpc

PD- selective loss of substantial nigra neurons,
degeneration of the dopaminanic nigrostritatal pathway,
depletion of dopamine release in the striatum,
=motor symptoms

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13
Q

what is Braaks hypothesis of sporadic PD

A

that sporadic PD is caused by a pathogen that enters via the nasal cavity and reaches the gut

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14
Q

treatment drugs for PD

A

no cure
most common treatment is to replace dopamine because of neuron death in the substantial nigra as this controls motor control

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