Flashcards in 29 Neurodegenerative diseases Deck (50):
Neuro-degenerative diseases are characterized by?
premature, primary death of specific nerve cells
T/F For Neuro degenerative diseases, drugs are curative and help to prevent further degeneration?
False. Drugs generally only help with symptoms and quality of life. Some drugs may help retard degeneration only.
An example of a hypokinetic ND disease is?
An example of a hyperkinetic ND disease is?
Both parkinsons and Huntingtons have malfunctions involving what?
The extrapyramidal system. (primarily substantia nigra and striatum)
which type of neurons are degenerative in huntingtons disease?
striatal neurons only.
Which ND disease is characterized by degeneration of motor neurons in the spinal cord and cerebral cortex?
Which ND disease is characterized by degeneration to the hippocampus and cerebral cortex?
I forgot.....Oh Alzheimers.
T/F Parkinsons disease can be attributed partially to pesticides and insecticides?
true to some degree
Blocking NMDA is a good treatment for?
superoxide dismutase does what?
O2 radical to H2O2
If you exhaust your antioxidant stores what generally happens inside the cell?
1) DNA damage
2) Protein damage
3) Lipid peroxidation of membranes
What is the fourth most common ND disease among the elderly? What is its incidence rate among those over 65?
Name some of the characteristics of parkinsons disease (5 major ones)?
3) abnormal posture
4) shuffling gait
5) impaired speech
what degenerates in parkinsons disease?
The nigrostriatal pathway. These neurons project to the putamen and caudate nucleus.
How many of the neurons in the nigrostriatal pathway have to be destroyed before you see parkinsonian signs?
What do you see remaining in the living neurons of parkinsons patients? What is it made of?
1) Lewy bodies
2) alpha synuclein
What are 4 things that resemble parkinsons disease due to the parkinsonian movements?
1) encephalitis lethargica
2) small strokes
3) traumatic brain injury
4) anti-psychotic drugs
(Review basal ganglia pathway) If you inhibit the Globus pallidum externa, will this help or worsen parkinsons disease symptoms?
It will worsen the symptoms because the sub thalamic nucleus can be activated which activates the globus pallidus interna. The GP interna inhibits the thalamus, therefore not allowing normal movements.
How dopamine/epi form?
what breaks down dopamine?
COMT =Dopamine to 3-methoxytyramine
MAO= 3 methoxytyramine to HVA
What is so significant of L-DOPA?
It acts as a precursor for dopamine and is able to cross the BBB.
What percentage of L-DOPA reaches the brain?
Why do you see a lot of side effects when using levadopa?
because of the conversion of dopamine to Norepi.
what are some of the signs/symptoms of using levadopa?
5) anxiety, depression, psychosis
what is the drug of choice for treatment of parkinsons patients with symptoms?
Levodopa and carbidopa combination
What does carbidopa do?
prevents the metabolism of L-Dopa to Dopamine in the periphery before it reaches the brain.
What does entacapone do?
why does it matter if L-DOPA is converted to dopamine in the periphery?
because dopamine cannot cross the BBB
Selegiline and Rasagiline are both inhibitors of MAO b. What is the biggest difference between these two drugs?
Selegiline is metabolized into methamphetamine and amphetamine products and rasagiline is not.
Bromocriptine acts a?
dopamine receptor agonist:
D1 partial agonist.
Ropinirole and pramipexole are both dopamine agonists that act on which receptors?
D2 and D3 receptors (agonists)
when should you not give a patient dopamine agonists?
in patients with heart and mental problems.
(causes arrhythmias, hypotension, confusion, etc)
what is apomorphine? when do you give it? How is it given?
1) Dopamine receptor agonist
2) advanced patients with "off disease"
3) given be sub Q injections only.
why would you give a parkinsons patient Benztropine or trihexyphenidyl?
They are muscarinic antagonists that help reduce tremor and rigidity. This occurs because with parkinsons disease, loss of the nigrostriatal neurons leads to increased firing of the striatal cholinergic inter-neurons and over stimulation of the muscarinic receptors.
What is amantadine? What are some side effects?
1) Block NMDA (glutamate) receptors and cholinergic muscarinic receptors.
2) Rash on lower extremities, worsening of CHF, and glaucoma.
what is the most common cause of dementia in adults?
what are 2 major signs/symptoms of alzheimers? what are 2 major histological findings?
amyloid plaques with NF tangles
loss of neurons in the cerebral cortex and hippocampus
which two pathways are majorly affected by the brain?
1) nucleus basalis cholinergic pathway
2) septohippocampal cholinergic pathway
what are the 3 major things that predispose you to getting alzheimers?
2) gender (2x more women)
T/F 6% of the age group 65-85 have alzheimers, and 45% of the over 85 have alzheimers?
10% of the Alzheimers cases are inherited. Which 4 genes are primarily responsable for alzheimers?
APP (amyloid precursor protein gene)
PS1 & PS2 (presenilin gene, 1 being worse)
APOe4 (Apolipoprotein E gene)
Which gene is the primary genetic risk factor for late onset AD?
T/F There is no cure and no way to slow the progression of alzheimers?
True. You can only treat the symptoms.
what affect does a NMDA receptor inhibitor have?
It decreases glutamate activation.
Doneprazil, galantamine, tacrine, and rivastigmine are all ACh esterase inhibitors. How long do each of these act?
1) 70 hours
2) 7 hours
3) 3 hours
4) 1.5 hours
what degrades rivastigmine?
what degrades donepezil, galantamine, and tacrine?
CYP3A4 and CYP2D6
ACh inhibitors are relatively safe except for tacrine which causes?