Neuro C Flashcards
What are the biogenic amines
Anything that turns into neurotransmitters
Glutamine, gaba glycine, serine, alanine, cystathionine, glutamine, lysine, theonine, leucine
What are the excitatory neurotransmitters
Noreepi Dopamine Epinephrine glutamate serotonin acetlychline histamine
What are the inhibitory neurotransmitters
Gaba
glycine
nitric oxidie
neurosteroids
acetyl choline
Increase: agression,depression
decreased: decreased memory, delirium, delusion
Dopamine
Increase: psychoses, anxiety, confusion, aggression
decreased: dementia, movement disorders, depression
Serotonin
Increase: anxiety
decreased: depression,dementia
Norepi
Increase: anxiety, aggression inattention
Decreased: anxiety
Gaba
Increased: affective decrease, lethargy
Decreased: anxiety
Glycine
Increased: affective decrease, lethargy
Decreased: anxiety
Nitrous oxidide
Increased: sedation, vasodiliation, visual hallucinations
decreased: vasospasm, potential hyperactivity
Histamine
Increased: mania
Decreased: depression
Where are neuro transmitters stored, how are they released
vesicles store them
actional potential comes down and causes vesicle to bind to pre-synaptic terminal which binds to the post synaptic which will cause action to happen
after binding you will have metabolism and reuptake
Pro receptor activity vs anti-receptor activity
Pro: Na or Ca opening channel
Anti: Cl- slows down nervous system
What B vitamins are required to turn cysteine into taurine.
B3 and B 6
What enzyme builds and what breaks down acetyl choline.
Builds: choline acetylase
Breaks: acetylcholine esterase
What are the three fates of tryptophan
Niacinaminde(b3)
Serotonin which converts into melatonin
Where does melatonin come from? Where and what vitamins does it need
From serotonin in the pineal gland needs B5, B12 and folate
deficiency in phenylalanine cause
what about pheny-hydroxylase
Phenylalanine: retardation
enzyme: Phenyl ketone urea
What is the pathway to make Epi
Phenylalanine-tyrosine-L-dopa-dopamine-NE-Epi
4 fates of tyrosine
Melanin production
Thyroid hormone
TCA cycle
Doapmine,Ne, Epi
What does tyrosine hydroxylase need
B3, Fe
What happens in the adrenal medulla
Ne-Epi
the only place that contains N-methyl-transferase
what is the primary breakdown product of catecholamines in the urine
Vanillamandilic acid
what two enzymes are used in the production of catecholamine breakdown
what happens if you have a genetic deficiency in them
MAO and COMT
Genetic deficiency: Increased NE and Epi= hyper and anxiety sleep disturbance and aggrivation
N-methyl-D-Aspartate (NMDA receptor)
non catecholamine receptors that mediate excitatory neurotransmission
What excites NMDA receptors
Glutamate
What does Nitric oxide do?
excites cGMP
What three things do cGMP act on
Retina: photoreception
Vascular smooth muscle: vasodilation
AMPA (excitatory receptors): probable desensitization, glutamine class to calm you down
Histamine 1 receptor
Exitatory
-increased depolarization in hypothalamic and limbic areas
Snotty nose
Histamine 2 receptors
excitatory/stimulating
central and peripheral
slows potassium conductance increasing excitation in the hipocampus, amydala and basal nuclei
runs HCL transporters
Histamine 3 receptors
Inhibitory
Blocks calcium channels in the basal nuclei decreasing histamine release
Histamine 4 receptors
Inhibitory
slows/modulates NMDA receptor complex
Histidine to histamine needs what vitamin
decarboxylase so needs B1
Histamine is reduced how and removed how
reduced: methylation
Removed MAO
what does gaba do
cl=channel activity to inhibit
Formed from glutamine in CNS
Glycine does what
also does a Cl- channel but acts like gaba without being gaba
inhibitory/calming
How does the brain know if we have night or day
the Retino-hypothalamic pathway
What is the circadian control of waking
ACTCH–creates increased adrenal cortex activity–leads to the AM cortisol surge
brain wakes up
What is the circadian control of calming the brain in PM
Light diminishes–retino-hypothalamic pathway increases activity = night–fibers communicate with the pineal gland–melatonin released
what is the filter of movement and how does it work
the basil nuclei/ganglia is the filter of output from the motor cortex
it communicates with the diencephalon and the cerebellum to make smooth motor movement
what are the three functional parts of the cerebellum and what do they do
Vestibulocerebellum: controls balance and eye movement
pontocerebellum: planning and initiation of movement
Spinocerebellum: synergy, which is control of rate, force, range and direction of movement
What inhibits and excited Basil Nuclei/Ganglia
What does it consist of
Inhibitory: Gaba
Excitatory: dopamine
allow for plan and execution of smooth movements
consists of: striatum, globus pallidus, subthalamic nuclei, substantia nigra
Huntington’s Chorea
Choreaform jerky, uncontrolled hyperkinetic movement and demntia
“purposeless movement”
gaba neuron autoimmune attack
Parkinson’s
Damage to substantia nigra (dopaminergic system)
decreased dopamine
festinating gait, cog-wheel rigidity, pill-rolling resting treamor
ALS/ Lou Gerhigs Disease
Loss of both lower and upper motor neurons
-mixed presenatition
death following respiratory complication
10% autosomal DOMINANT
Encephalitis
focal neurological deficit
infx of brain itself
headache persists even as systemic SX
Meningitis
Infection of the meninges
Most common organisms to cause bacterial meningitits
E. Coli
H.flu
Meningococcus
Most common organisms to cause brain abscess
Strep and Staff
increased risk in orbital infections
What is tabes dorsalis associated with
Neurospyhilis destroying dorsal roots, impaired sensation and ataxia, absent DTR
what can cause encephalitis
Togaviridae (bird reservoir not horse)
Measles, mumps, chicen pox, rubella = autoimmune encephalitis
HSVI and II
poliomyelitis
Poliovirus
non-soecific gastroenteritis, flaccid paralysis
What are two types of neuroglial tumors
what are the difference?
Astrocytoma and Glioblastoma
glioblastoma is a grade 4 astrocytoma
grade 3 is malignant, 1 +2 benign
Where do brain tumors tend to occur in adults?
Children?
Adults: above tentorium cerebelli
children: below tentorium
What is the most common primary brain tumor of adults
glioblastoma multiforme
Tumor of the astrocytes that is high grade and no longer like the parent tissue, very aggressive
Acoustic neuroma is what cranial nerve
CN8
what is meniers like syndrome and what is it associated with
Acoustic neruoma
vertigo, nausea vomitting
What is von recklinghausens
Neurofibromatosis, autosomal dominant and mutations
Autoimmune demyelination in the CNS
what dz and sx
Multiple sclerosis
Glove and stocking parasthesia, optic neuritis
Ascending paralysis that is self limiting after a viral illness
Guillain-Barre Syndrome
Acute idiopathic polyneuritis, polyradiculoneuropathy
+ gouers sign, walk up theighs to stand up
what bug causes descending paralysis
botulism
axonal reaction
axon damaged, cell body enlarges, becomes ascentric and increases protein synthesis
Red neurons
acute necrosis of neurons, changes before death of neuron
cowdry bodies think
herpes
negri bodies think
rabies
What syndrome do you get with thiamine B 1 deficiency due to alcoholism, what does it lead to
Wenicke-Korsakoff SYNDROME
confabulations, no short term memory
they make everything up but dont mean to
encephalopathy due to Thiamine deficiency
Pellegra
Niacin deficiency
4 D’s: Dementia, dermatitis, diarrhea, death
Vitamin B12 deficiency
Macrocytic anemia
Degeneration of spinal cord (spasticity, weakness, dementia, loss of proprioception)
some PNS symptoms
not cured by folate supplementation
Diffuse cortical atrophy, neurofibillary tangles
Alzheimers dizsease
Dementia
clinically finding not a disease
Where are plaques in alzheimers
Senile plaques in cortex
abnormal tau protein laden nerve processes, microglia, astrocytes
What are the three lysosomal storage disease
Tay-sachs
Hyrlers
Pompes
what diesase has deficicnecy in hexoaminidase A enzyme and what does that cause
Tay-Sachs
neurodegenerative disorder that leads to inability to catabolize GM 2 gangliosides
get dementia siezures parylisis and death by age 4
what disease can you not degrade mucopolysaccharides
Hurker’s
happens peripherally
Retarded growth, skeletal deformities
death by 6-10yo
What disease has alpha-glucosidase deficiency
Pompe’s
Can make glycogen but can not break it down
get muscular build up like cardiomegaly
What disease results from deficiency in phenylalanine hydroxylase
what happens
PKU
autosomal recessive
nromal at birth but build up phenylallanine and get mental retarded since they cant convert it to tyrosine
What disease has toxic levels of copper storage
what is the pathoneumonic finding
Wilson’s Disease
Toxic levels of copper storage leading to kaiser-fleisher rings in the eye, liver and brain
What disease is caused by inborn enzyme deficienies that create abnormal myelin
Leukodystrophies
