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EPPP kirsty > Bio > Flashcards

Bio Flashcards

1
Q

4 segments of spinal cord are:

A

Cervical
Thoracic
Lumbar
Sacral

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2
Q

fibers on dorsal side of spinal cord are

A

sensory

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3
Q

fibers on ventral side of spinal cord are

A

motor

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4
Q

name layers of meninges from the brain to the skull

A

pia
arachnoid
dura

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5
Q

what is falx cerebri

A

extension of dura mater, goes between 2 hemispheres of brain

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6
Q

name the ventricles

A

2 lateral ventricles
3rd ventricle
4th

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7
Q

what is cytoarchitecture

A

6 layers of cells in the cerebrum, differs in different areas. Brodmann areas are defined by their differences in cytoarchitecture

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8
Q

frontal lobe responsible for

A

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

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9
Q

temporal lobes responsible for

A

primary auditory processing (Superior temporal gyrus)
auditory association cortex (aka Wernicke’s area)

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10
Q

what is the pathway for auditory language comprehension

A

vestibulocochlear nerves
MGN of thalamus
Heschl’s gyrus (superior temporal gyrus)

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11
Q

the parietal lobe is responsible for

A

primary somatosensory processing
sensory integration (heteromodal cortex)

dorsal and ventral visual pathways go thru parietal lobe

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12
Q

the occipital lobe is responsible for

A

primary visual cortex

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13
Q

ventral visual pathway is from occipital lobe to ___

A

temporal regions

Ventral pathway = WHAT

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14
Q

dorsal visual pathway is from occipital lobe to ___

A

parietal regions

Dorsal pathway = WHERE

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15
Q

limbic system includes

A

hippocampus
amygdala
septum
hypothalamus

+ Limbic cortex, which incl cingulate gyrus and parahippocampal gyrus

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16
Q

role of hippocampus

A

formation of long term memories

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17
Q

role of amygdala

A

olfactory processing
processing emotions

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18
Q

role of thalamus

A

relays info btwn cortex and brain stem

sensory information relay system

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19
Q

list parts of the basal ganglia

A
  1. Striatum (includes caudate nucleus and putamen)
  2. globus palllidus
  3. subthalamic nucleus
  4. substantia nigra
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20
Q

what are the primary inputs and outputs of basal ganglia

A

input: cerebral cortex
output: thalamus

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21
Q

what do motor abnormalities due to basal ganglia dysfunction look like?

A

problems with coordination and rhythm of mvmt

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22
Q

extrapyramidal symptoms (EPS) include:

and are related to:

A

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

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23
Q

2 mvmt disorders associated with abnormal activity in the basal ganglia

A

Parkinsons disease
huntingtons disease

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24
Q

Basal ganglia is involved in

A

motor output, emotions, cognition, eye mvmts

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25
Q

Brainstem includes (3)

A

medulla
pons
midbrain

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26
Q

role of brainstem

A

control and regulation of autonomic functions, maintaining homeostasis

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27
Q

role of cerebellum

A

coordination of mvmt
also lots of connections to cortex broadly

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28
Q

parts of the brain most susceptible to MS

A

brain stem, cerebellum, spinal cord, optic nerves, WM in brain

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29
Q

axons range in length from:

A

1 mm to 1 meter

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30
Q

Which neurotransmitters are amines:

A

serotonin (SE)
acetylcholine (ACh)

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31
Q

Which neurotransmitters are catecholamines?

A

Dopamine (DA)
Norepinephrine (NE)
Epinephrine (Epi)

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32
Q

Which neurotransmitters are amino acids?

A

GABA
Glutamate

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33
Q

norepinephrine

A

catecholamine
involved in sympathetic NS - also a hormone released by adrenal gland
primarily excitatory

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34
Q

dopamine

A

catecholamine
both E and I
most dopaminergic neurons are in substantia nigra
overactivity: schizophrenia
loss of DA-ergic neurons: parkinsons
underactivity: ADHD

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35
Q

serotonin

A

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

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36
Q

acetylcholine

A

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

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37
Q

GABA

A

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

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38
Q

Glutamate

A

amino acid
primary excitatory NT
widely distributed throughout brain

excessive glu causes excitotoxicity (in TBI and stroke)

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39
Q

inverse agonist

A

binds to same receptor site, but has OPPOSITE effect of full agonists (reduces overall efficacy of a NT system)

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40
Q

important thing to remember about antagonists

A

they BLOCK, so have no effect when the agonist is not present

41
Q

what is pharmacodynamics

A

biochemical and physiological effects of drugs on the body

42
Q

what is pharmacokinetics

A

how the body handles the drug thru absorption, distribution, metabolism, elimination

43
Q

therapeutic window

A

range of a drug dose that can result in desired effect without unsafe side effects

44
Q

therapeutic index

A

ratio of the amt of drug that causes desired effect to the amt that produces dangerous side effects

high therapeutic index = safer

45
Q

primary type of anxiolytic

A

benzodiazepines, incl:

alprazolam/Xanax
clonazepam/Klonapin
diazepam/Valium
lorazepam/Ativan

46
Q

how do benzos work

A

enhance action of GABA (inhibitory)

47
Q

benzodiazepines side effects include:

A

drowsiness
confusion
feelings of detachment, dizziness, imbalance,
**high potential for dependence

48
Q

other drugs used as anxiolytics

A

Buspirone (BuSpar)
Gabapentin (Neurontin): anticonvulsant
Hydroxyzine (Vistaril, Atarax): antihistamine (VERY sedating)
SSRIs

49
Q

5 main types of antidepressants

A

Monoamine oxidase inhibitors (MAOIs)
Tricyclic antidepressants (TCAs)
SSRIs
NDRIs
SNRIs

50
Q

list some tricyclic antidepressants

A

Trimipramine
imipramine (Tofranil)
amitriptyline (Elavil)
desipramine (Norpramin)

nortriptyline (Pamelor, Aventyl)

51
Q

tricyclic antidepressant side effects

A

cardiac/autonomic (e.g., orthostatic hypertension)
anticholinergic
neurobehavioral

52
Q

list monoamine oxidase inhibitors (MAOIs)

A

phenelzine (Nardil)
isocarboxazid (Marplan)
moclobemide (moclobamine)
tranylcypromine (Parnate)

53
Q

problems with using MAOIs

A

serious interactions with drugs or food. MUST avoid tyramine - can lead to hypertensive crisis

54
Q

list some SSRIs (mnemonic)

A

Effective – Escitalopram
For – Fluoxetine, Fluvoxamine
Sadness – Sertraline
Panic – Paroxetine
Compulsions – Citalopram

55
Q

what are SSRI side effects

A

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

56
Q

what kind of drug is buproprion, and what is it indicated for?

A

NDRI

antidepressant, smoking cessation

sold as Zyban or Wellbutrin

57
Q

SNRI example

A

venlafaxine (Effexor)
desvenlafaxine (Pristiq)
levomilnacipran (Fetzima)

58
Q

what are some OTC products for depression

A

St John’s Wort
S-adenosyl methionine
5-HTP
omega-3 fatty acids
folic acid

59
Q

what is action of 1st generation vs 2nd gen antipsychotics?

and how do these drugs differ?

A

1st: block DA
2nd: block DA and 5HT

2nd tend to have fewer extrapyramidal side effects

60
Q

Trazodone is used for

A

is an atypical antidepressant often used for insomnia

61
Q

list some first gen antipsychotics

A

haloperidol (Haldol)
thioridazine (Mellaril)
chlorpromazine (Thorazine)
molinidine (Moban)
thiothixene (Navane)

62
Q

what are metabolic side effects of atypical antipsychotics?

A

weight gain
diabetes
dyslipidemia

63
Q

list some atypical antipsychotics

A

olanzapine (Zyprexa)
quetiapine (Seroquel)
ziprasidone (Geodon)
aripiprazole (Abilify)
paliperidone (Invega)
iloperisone (Fanapt)
asenapine (Saphris)
clozapine (Clozaril)
risperidone (Risperdal)

64
Q

tell me more about clozapine

A

one of most efffective atypical antipsychotics, but also the most dangerous due to fatal agranulocytosis (so need to closely monitor white blood cell count)

65
Q

common side effect of risperdal

A

hyperprolactinemia -> gynecomastia

66
Q

lithium side effects

A

nausea, diarrhea, vomiting, thirst, excessive urination, weight gain, hand tremor

after CHRONIC use: kidney damage, hypothyroidism, goiter

67
Q

psychopharmacological tx for bipolar disorder includes

A

lithium
antipsychotics (like Abilify)
anticonvulsants (like divalproex (Depakote), lamitrogine (Lamictal), carbamazepine (Tegretol), topiramate (Topamax)

68
Q

first line treatment for opiate addiction

A

opioid replacement therapy

69
Q

ADHD treatments

A

psychostimulants (increase PFC levels of NE, DA)
non-stimulant options:
antidepressants
Strattera (NE reuptake inhibitor)
Guanfacine + clonidine reduce HI sxs of ADHD

70
Q

first line tx for PTSD

A

psychotherapy

71
Q

what is dark vs light on CT?

A

WHITE = very dense (like skull) - called Hyperdensities

BLACK = less dense (like air)

white matter shows up a little darker than grey matter

72
Q

CT is most useful for

A

identifying hemorrhage or skull fracture immediately after injury

73
Q

what is WADA test

A

inject sodium amobarbital into 1 carotid artery at a time to test cog functions of contralateral hemisphere

74
Q

tell me about Wernicke’s aphasia

A

sxs: fluent nonsensical & meaningless speech. often have poor insight. impaired repetition

lesion in L temporal lobe

75
Q

tell me about transcortical sensory aphasia

A

poor comprehension, but repetition is intact

lesion in border zones between temporal and parietal lobes

76
Q

tell me about Broca’s aphasia

A

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)

77
Q

tell me about transcortical motor aphasia

A

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

78
Q

tell me about conduction aphasia

A

sole deficit is in repetition

associated with damage to arcuate fasciculus

79
Q

tell me about anomic aphasia

A

focal deficit in naming objects

can be due to lesion in angular gyrus

80
Q

tell me about alexia

A

acquired inability to read

lesion in posterior region of L hemisphere, impacting posterior corpus callosum (disconnecting visual and language centers)

81
Q

tell me about agraphia

A

acquired disorder of writing

can be due to lesion in parietal or frontal lobe, corpus callosum, or subcortical structures

82
Q

tell me about apraxia

A

acquired disorder of skilled purposeful mvmt

lesion usually in Left hemisphere

83
Q

dementia (NCD) diagnosis requires

A

decline in 2 or more areas of cog functioning, impacting ADLs

84
Q

alzheimer’s disease

A

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)

85
Q

psychopharmacological tx for alzheimer’s disease

A

cholinesterase inhibitors (to prevent breakdown of ACh): galantamine, rivastigmine, donepezil

memantine (Namenda) works by regulating glutamate to prevent cell death

86
Q

genetics of alzheimer’s

A

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)

87
Q

Pick’s disease

A

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

88
Q

2nd leading cause of acquired dementia

A

cerebrovascular disease

89
Q

vascular cognitive impairment

A

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.

90
Q

parkinsons disease

A

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)

91
Q

treatment for parkinsons disease

A

meds to boost DA in brain, like L-DOPA

meds to REDUCE acetylcholine to achieve better balance

Deep brain stimulation

92
Q

Huntington’s disease

A

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

93
Q

dementia due to HIV

A

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

94
Q

chronic traumatic encephalopathy

name neuropathology

A

neurodegenerative disorder associated with repetitive head trauma

neuropathology: hyperphosphorylated tau protein, esp in periventricular regions

broad range of psychiatric, behavioral, and cog changes

95
Q

pseudodementia

incl how to differentiate from true dementia

A

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

96
Q

mild cognitive impairment

A

decline in one cog domain (usually memory)

course can last up to 5 yrs

97
Q

Norepinephrine

A

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

98
Q

Basal ganglia is involved in

A

motor output, emotions, cognition, eye mvmts

EPPP kirsty (9 decks)

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