Bio Flashcards
4 segments of spinal cord are:
Cervical
Thoracic
Lumbar
Sacral
fibers on dorsal side of spinal cord are
sensory
fibers on ventral side of spinal cord are
motor
name layers of meninges from the brain to the skull
pia
arachnoid
dura
what is falx cerebri
extension of dura mater, goes between 2 hemispheres of brain
name the ventricles
2 lateral ventricles
3rd ventricle
4th
what is cytoarchitecture
6 layers of cells in the cerebrum, differs in different areas. Brodmann areas are defined by their differences in cytoarchitecture
frontal lobe responsible for
primary motor cortex: movement
premotor cortex: imitation, empathy
prefrontal/orbitofrontal: EFs, attention, reasoning, planning (esp dorsolateral PFC)
inferior lateral L frontal lobe: Broca’s area
temporal lobes responsible for
primary auditory processing (Superior temporal gyrus)
auditory association cortex (aka Wernicke’s area)
what is the pathway for auditory language comprehension
vestibulocochlear nerves
MGN of thalamus
Heschl’s gyrus (superior temporal gyrus)
the parietal lobe is responsible for
primary somatosensory processing
sensory integration (heteromodal cortex)
dorsal and ventral visual pathways go thru parietal lobe
the occipital lobe is responsible for
primary visual cortex
ventral visual pathway is from occipital lobe to ___
temporal regions
Ventral pathway = WHAT
dorsal visual pathway is from occipital lobe to ___
parietal regions
Dorsal pathway = WHERE
limbic system includes
hippocampus
amygdala
septum
hypothalamus
+ Limbic cortex, which incl cingulate gyrus and parahippocampal gyrus
role of hippocampus
formation of long term memories
role of amygdala
olfactory processing
processing emotions
role of thalamus
relays info btwn cortex and brain stem
sensory information relay system
list parts of the basal ganglia
- Striatum (includes caudate nucleus and putamen)
- globus palllidus
- subthalamic nucleus
- substantia nigra
what are the primary inputs and outputs of basal ganglia
input: cerebral cortex
output: thalamus
what do motor abnormalities due to basal ganglia dysfunction look like?
problems with coordination and rhythm of mvmt
extrapyramidal symptoms (EPS) include:
and are related to:
Akathisia (inability to remain still)
Acute dystonia (involuntary muscle contractions)
Parkinsonism (muscle rigidity, tremor, bradykinesia)
Neuroleptic malignant syndrome (NMS; rigid muscles, fever, drowsiness, confusion)
Tardive dyskinesia is a late-onset EPS
EPS are side effects from first-gen antipsychotics
2 mvmt disorders associated with abnormal activity in the basal ganglia
Parkinsons disease
huntingtons disease
Basal ganglia is involved in
motor output, emotions, cognition, eye mvmts
Brainstem includes (3)
medulla
pons
midbrain
role of brainstem
control and regulation of autonomic functions, maintaining homeostasis
role of cerebellum
coordination of mvmt
also lots of connections to cortex broadly
parts of the brain most susceptible to MS
brain stem, cerebellum, spinal cord, optic nerves, WM in brain
axons range in length from:
1 mm to 1 meter
Which neurotransmitters are amines:
serotonin (SE)
acetylcholine (ACh)
Which neurotransmitters are catecholamines?
Dopamine (DA)
Norepinephrine (NE)
Epinephrine (Epi)
Which neurotransmitters are amino acids?
GABA
Glutamate
norepinephrine
catecholamine
involved in sympathetic NS - also a hormone released by adrenal gland
primarily excitatory
dopamine
catecholamine
both E and I
most dopaminergic neurons are in substantia nigra
overactivity: schizophrenia
loss of DA-ergic neurons: parkinsons
underactivity: ADHD
serotonin
5HT
biogenic amine
primarily inhibitory
originates in raphe nuclei of brainstem
involved in regulation fo mood, anger, aggression, anxiety, appetite, learning, sleep, sex, consciousness, pain
low 5HT in dep, OCD, anx
acetylcholine
biogenic amine
plays large role in parasympathetic NS and autonomic NS
primary neurotransmitter at neuromuscular junction
degeneration of ACh in striatum involved in Huntington’s disease
GABA
amino acid
major inhibitory NT
widely distributed in CNS but most concentrated in striatum, hypothalamus, spinal cord, temporal lobes
involved in emotion, balance, sleep
**many AEDs increase GABA activity
Glutamate
amino acid
primary excitatory NT
widely distributed throughout brain
excessive glu causes excitotoxicity (in TBI and stroke)
inverse agonist
binds to same receptor site, but has OPPOSITE effect of full agonists (reduces overall efficacy of a NT system)
important thing to remember about antagonists
they BLOCK, so have no effect when the agonist is not present
what is pharmacodynamics
biochemical and physiological effects of drugs on the body
what is pharmacokinetics
how the body handles the drug thru absorption, distribution, metabolism, elimination
therapeutic window
range of a drug dose that can result in desired effect without unsafe side effects
therapeutic index
ratio of the amt of drug that causes desired effect to the amt that produces dangerous side effects
high therapeutic index = safer
primary type of anxiolytic
benzodiazepines, incl:
alprazolam/Xanax
clonazepam/Klonapin
diazepam/Valium
lorazepam/Ativan
how do benzos work
enhance action of GABA (inhibitory)
benzodiazepines side effects include:
drowsiness
confusion
feelings of detachment, dizziness, imbalance,
**high potential for dependence
other drugs used as anxiolytics
Buspirone (BuSpar)
Gabapentin (Neurontin): anticonvulsant
Hydroxyzine (Vistaril, Atarax): antihistamine (VERY sedating)
SSRIs
5 main types of antidepressants
Monoamine oxidase inhibitors (MAOIs)
Tricyclic antidepressants (TCAs)
SSRIs
NDRIs
SNRIs
list some tricyclic antidepressants
Trimipramine
imipramine (Tofranil)
amitriptyline (Elavil)
desipramine (Norpramin)
nortriptyline (Pamelor, Aventyl)
tricyclic antidepressant side effects
cardiac/autonomic (e.g., orthostatic hypertension)
anticholinergic
neurobehavioral
list monoamine oxidase inhibitors (MAOIs)
phenelzine (Nardil)
isocarboxazid (Marplan)
moclobemide (moclobamine)
tranylcypromine (Parnate)
problems with using MAOIs
serious interactions with drugs or food. MUST avoid tyramine - can lead to hypertensive crisis
list some SSRIs (mnemonic)
Effective – Escitalopram
For – Fluoxetine, Fluvoxamine
Sadness – Sertraline
Panic – Paroxetine
Compulsions – Citalopram
what are SSRI side effects
7 S’s:
Stomach upset (GI upset)
Sexual dysfunction
Serotonin syndrome – with other serotonergic agents (i.e. MAOs) – hyperthermia, muscle rigidity, flushing, diarrhea
Sleep difficulties (insomnia)
Suicidal thoughts ( esp. in patients age 24 and under)
Stress (agitation, anxiety)
Size increase / Weight gain
what kind of drug is buproprion, and what is it indicated for?
NDRI
antidepressant, smoking cessation
sold as Zyban or Wellbutrin
SNRI example
venlafaxine (Effexor)
desvenlafaxine (Pristiq)
levomilnacipran (Fetzima)
what are some OTC products for depression
St John’s Wort
S-adenosyl methionine
5-HTP
omega-3 fatty acids
folic acid
what is action of 1st generation vs 2nd gen antipsychotics?
and how do these drugs differ?
1st: block DA
2nd: block DA and 5HT
2nd tend to have fewer extrapyramidal side effects
Trazodone is used for
is an atypical antidepressant often used for insomnia
list some first gen antipsychotics
haloperidol (Haldol)
thioridazine (Mellaril)
chlorpromazine (Thorazine)
molinidine (Moban)
thiothixene (Navane)
what are metabolic side effects of atypical antipsychotics?
weight gain
diabetes
dyslipidemia
list some atypical antipsychotics
olanzapine (Zyprexa)
quetiapine (Seroquel)
ziprasidone (Geodon)
aripiprazole (Abilify)
paliperidone (Invega)
iloperisone (Fanapt)
asenapine (Saphris)
clozapine (Clozaril)
risperidone (Risperdal)
tell me more about clozapine
one of most efffective atypical antipsychotics, but also the most dangerous due to fatal agranulocytosis (so need to closely monitor white blood cell count)
common side effect of risperdal
hyperprolactinemia -> gynecomastia
lithium side effects
nausea, diarrhea, vomiting, thirst, excessive urination, weight gain, hand tremor
after CHRONIC use: kidney damage, hypothyroidism, goiter
psychopharmacological tx for bipolar disorder includes
lithium
antipsychotics (like Abilify)
anticonvulsants (like divalproex (Depakote), lamitrogine (Lamictal), carbamazepine (Tegretol), topiramate (Topamax)
first line treatment for opiate addiction
opioid replacement therapy
ADHD treatments
psychostimulants (increase PFC levels of NE, DA)
non-stimulant options:
antidepressants
Strattera (NE reuptake inhibitor)
Guanfacine + clonidine reduce HI sxs of ADHD
first line tx for PTSD
psychotherapy
what is dark vs light on CT?
WHITE = very dense (like skull) - called Hyperdensities
BLACK = less dense (like air)
white matter shows up a little darker than grey matter
CT is most useful for
identifying hemorrhage or skull fracture immediately after injury
what is WADA test
inject sodium amobarbital into 1 carotid artery at a time to test cog functions of contralateral hemisphere
tell me about Wernicke’s aphasia
sxs: fluent nonsensical & meaningless speech. often have poor insight. impaired repetition
lesion in L temporal lobe
tell me about transcortical sensory aphasia
poor comprehension, but repetition is intact
lesion in border zones between temporal and parietal lobes
tell me about Broca’s aphasia
poor grammar, limited prosody, slow and effortful speech. few connecting words and verbs. Repetition impaired, writing effortful and slow.
Lesion in Broca’s area (L frontal lobe)
tell me about transcortical motor aphasia
like Broca’s, see problems with verbal epxression, but pt can repeat.
usually associated with lesion near/around Broca’s area, not impacting arcuate fasciculus
tell me about conduction aphasia
sole deficit is in repetition
associated with damage to arcuate fasciculus
tell me about anomic aphasia
focal deficit in naming objects
can be due to lesion in angular gyrus
tell me about alexia
acquired inability to read
lesion in posterior region of L hemisphere, impacting posterior corpus callosum (disconnecting visual and language centers)
tell me about agraphia
acquired disorder of writing
can be due to lesion in parietal or frontal lobe, corpus callosum, or subcortical structures
tell me about apraxia
acquired disorder of skilled purposeful mvmt
lesion usually in Left hemisphere
dementia (NCD) diagnosis requires
decline in 2 or more areas of cog functioning, impacting ADLs
alzheimer’s disease
most common cause of dementia in people over 65 yrs
insidious decline in memory, often 1st apparent sx
pathological changes: plaques and tangles
*is a CORTICAL dementia (MTL)
psychopharmacological tx for alzheimer’s disease
cholinesterase inhibitors (to prevent breakdown of ACh): galantamine, rivastigmine, donepezil
memantine (Namenda) works by regulating glutamate to prevent cell death
genetics of alzheimer’s
greatest risk factor is age, not genetics
most cases are sporadic. strongest gene influence is from APOE-e4, which is likely a factor in 20-25% of alz cases
there’s also a rare form of early onset alz (before age 60)
Pick’s disease
degeneration of frontal and temporal lobes (a type of FTD)
pathologically diagnosed by Pick’s bodies in frontal and anterior temporal lobes
first sx often behavioral dysinhibition or personality change
2nd leading cause of acquired dementia
cerebrovascular disease
vascular cognitive impairment
tends to have a stepwise progression
variable presentation depends on where lesions are.
may have focal deficits, gait disturbance, or psychomotor retardation. Depression and mood changes are common. Slow processing speed, attn problems, EF probs.
parkinsons disease
progressive neurodegenerative condition (subcortical dementia.
sxs: tremor (+ sx), rigidity (+ sx), bradykinesia, postural instability. often see gait disturbance, blank facial expression
mvmt disorder caused by degeneration of substantia nigra (in basal ganglia), and loss of DA
sxs incl: exec dysufnction, learning and memory probs, slowed PS, bradyphrenia (slowed thinking)
treatment for parkinsons disease
meds to boost DA in brain, like L-DOPA
meds to REDUCE acetylcholine to achieve better balance
Deep brain stimulation
Huntington’s disease
degenerative loss of (GABA and NE) neurons in caudate nucleus of the basal ganglia
hereditary (50% of offspring inherit)
sxs emerge in 30s - 50s. 1st sx is often behavioral disturbance. Others: uncontrolled mvmts, unusual posturing, memory and EF probs, decline in IQ as disease progresses
dementia due to HIV
subcortical dementia
diffuse, multifocal destruction of WM and subcortical structures
common sxs:
cog: forgetfulness, slow PS, concentration probs
bx: apathy, social withdrawal
motor: tremors, balacne probs, impaired rep mvmts, ataxia, hypertonia
becoming less and less common with good HIV care
chronic traumatic encephalopathy
name neuropathology
neurodegenerative disorder associated with repetitive head trauma
neuropathology: hyperphosphorylated tau protein, esp in periventricular regions
broad range of psychiatric, behavioral, and cog changes
pseudodementia
incl how to differentiate from true dementia
complaint of memory problems in context of a psychiatric illness (esp depression)
1) cortical signs (aphasia, apraxia, agnosia) uncommon in pseudo
2) in pseudo see slowing or inconsistent effort in testing
mild cognitive impairment
decline in one cog domain (usually memory)
course can last up to 5 yrs
Norepinephrine
catecholamine
is both a hormone (released by adrenal gland into blood) and a NT. is involved in fight or flight
created in locus coeruleus
active in sympathetic nervous system and CNS
Basal ganglia is involved in
motor output, emotions, cognition, eye mvmts
