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EPPP Ingrid > Biological Bases > Flashcards

Biological Bases Flashcards

1
Q

What are the major divisions of the spinal chord?

A

Cervical (C1-C8), Thoracic (T1-T12), Lumbar (L1-L5), Sacral (S1-S5).

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2
Q

Dorsal pathways are ____ and relay ____ information, ventral pathways are ____ and relay ____ information. (motor, sensory, ascending, descending)

A

Dorsal pathways are ascending and relay sensory information (to the brain), ventral pathways are descending and relay motor information (to the muscles).

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3
Q

Damage to spinal chord leads to weakness (paresis) or immobility (paralysis)
a) at and above the site of damage
b) at and below the site of damage

A

b) at and below the site of damage

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4
Q

Name and describe the cranial meninges from most external to most internal.

A

Dura: hardest layer, also forms the falx cerebri (extends into longitudinal fissure and divides the 2 hemispheres).
Arachnoid: thinner than dura, veins pass through it.
Pia: thinnest and most delicate, lots of vascular tissue.

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5
Q

Where is cerebrospinal fluid (CSF) formed?

A

In the choroid plexus (linings of the lateral ventricles).

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6
Q

Describe the pathway of the flow of CSF.

A

It flows from the lateral ventricles, to the third ventricle, down the cerebral aqueduct, into the fourth ventricle, and into the subarachnoid space around the brain and spinal chord.

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7
Q

What are the purposes of CSF?

A

Provides buoyancy and structural support, protects from infection, regulates cerebral bloodflow.

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8
Q

How many cell layers is the cerebral cortex made of?

A

Six.

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9
Q

Describe the Frontal Lobe’s
a) location/boundaries
b) subdivisions from posterior to anterior
c) function

A

a) anterior to the central sulcus
b) primary motor cortex, premotor cortex, prefrontal cortex, orbitofrontal cortex.
c) initial motor movements, imitation, empathy, higher level cognitive functions (EF), speech production.

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10
Q

Location and function of Broca’s area

A

Located in the inferior lateral region of the dominant frontal lobe (left for most people). Involved in speech production (oral and written), grammar, and syntax comprehension.

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11
Q

Describe the temporal lobes’
a) location
b) subdivisions
c) function

A

a) inferior to the lateral sulcus
b) superior temporal gyrus (primary auditory cortex), middle temporal gyrus (auditory association cortex???), inferior temporal gyrus
c) auditory processing, speech comprehension

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12
Q

Location and funciton of Wernicke’s area

A

Located in the dominant temporal lobe in the auditory association cortex. Its function is language comprehension.

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13
Q

Describe the parietal lobes’
a) location
b) subdivisions
c) function

A

a) posterior to the central sulcus
b) primary somatosensory cortex, heteromodal cortex.
c) sensory processing, visual processing pathways that receive inputs from occipital lobes.

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14
Q

Describe the occipital lobes’
a) location
b) subdivisions
c) function

A

a) posterior to the temporal and parietal lobes
b) primary visual cortex, visual association cortex
c) visual processing, integration of visual information

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15
Q

Location and function of the hippocampus

A

Located in the medial temporal lobes, forms part of the limbic system. Invovled in memory formation and storage.

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16
Q

Location and function of the amygdala

A

Located anterior to the hippocampus and part of the limbic system. Invoved in processing emotions, fight or flight, and olfactory processing. Also involved in flashbulb memories (emotionally salient).

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17
Q

Location and function of the thalamus

A

Located superior to the brain stem, made up of several nuclei. It functions as the relay center between the cortex and the brain stem.

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18
Q

Location, components and function of the basal ganglia.

A

Located in the subcortical region. Made up of several nuclei including the striatum (caudate nucleus, putamen, nucleus accumbens), globus pallidus, subthalamic nucleus, & substantia nigra. They receive input from the cortex and send outputs to the thalamus, they are involved in coordination and rhythm of movement.

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19
Q

Huntington’s Disease and Parkinson’s Disease are associated with abnormalities in which brain structure?

A

Basal Ganglia

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20
Q

What are the subdivisions of the brain stem (from rostral to caudal) and its functions?

A

The midbrain, the pons, and the medulla. The brainstem is involved in regulating autonomic functions and maintaining homeostasis.

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21
Q

What is the location and function of the reticular formation?

A

Located in the brainstem, invovled in alertness, consciousness, pain and regulating respiratory and cardiac systems.

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22
Q

Location, subdivisions and function of the cerebellum.

A

Attached to the posterior brainstem. Divided into superior, middle and inferior cerebellar peduncles. Involved in regulating movement, rhythm, balance, coordination and posture. Also involved in learning and attention.

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23
Q

Are most neurons multipolar or unipolar?

A

Multipolar.

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24
Q

Describe the process of neuronal firing.

A

A presynaptic neuron will release neurotransmitters into the synapse, which may be excitatory or inhibitory. When post-synaptic neurons reach a threshold of excitation, the neuron fires. The strenght of the firing does not depend on the strenght of the input (all or nothing).

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25
Q

List neurotransmitters that are biogenic amines.

A

Acetylcholine (ACh) and serotonin.

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26
Q

Norepinephrine
a) type of neurotransmitter
b) functions
c) excitatory or inhibitory

A

a) catelcholamine
b) found in sympathetic nervous system, regulates mood, memory, alertness, hormones. Underlies “fight or flight”.
c) excitatory (primarily)

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27
Q

Dopamine (DA)
a) type of neurotransmitter
b) function and location
c) excitatory or inhibitory
d) disorders involved with

A

a) catelcholamine
b) found mostly in the substantia nigra, involved in emotions, movement, endocrine functioning, attention, reward-driven learning, desire, pleasure.
c) both excitatory and inhibitory
d) schizoprehnia (positive sx’s due to DA hyperactivity in subcortical regions, negative sx’s due to DA hypoactivity in cortical esp PFC), underactivity of DA –> ADHD, loss of DA producing neurons–> Parkinson’s disease.

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28
Q

Serotonin (5-HT)
a) type of neurotransmitter
b) functions
c) excitatory or inhibitory
d) disorders involved with

A

a) biogenic amine
b) regulates mood, appetite, sleep, sexual functioning, consciousness and pain.
c) primarily inhibitory
d) low levels involved with depression, OCD, anxiety

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29
Q

Acetylcholine (ACh)
a) type of neurotransmitter
b) functions
c) excitatory or inhibitory
d) disorders involved with

A

a) biogenic amine
b) major role in parasympathenic nervous system, involved in muscles and movement, alertness and attention (thru reticular formation), memory.
c) ???
d) Degeneration of ACh in striatum involved in Huntington’s disease

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30
Q

Gamma-aminobutyric acid (GABA)
a) type of neurotransmitter
b) functions
c) excitatory or inhibitory
d) disorders involved with

A

a) amino acid
b) emotion, balance, sleep patterns; concentrated in striatum, hypothalamus, spinal cord, temporal lobes.
c) inhibitory (primary inhibitory NT)
d) high levels assoc with anxiety

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31
Q

Glutamate
a) type of neurotransmitter
b) functions
c) excitatory or inhibitory
d) disorders involved with

A

a) amino acid
b) building block of proteins, learning and memory.
c) excitatory (primary excitatory NT)
d) implicated in cell death following TBI and stroke

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32
Q

What is an agonist?

A

A chemical that binds to a receptor site and mimics the activity of a neurotransmitter (boosts)

Partial agonist does the same thing but < 100% of full effect.

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33
Q

What is an inverse agonist?

A

A chemical that binds to the receptor site but decreases the efficacy of the neurotransmitter.

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34
Q

What is an antagonist?

A

A chemical that blocks or reverses the effects of agonists or inverse agonists but has not effect of its own.

35
Q

What organs metabolize drugs?

A

Kidneys and liver.

36
Q

What is the therapeutic window of a drug?

A

Range of dose that is effective without unsafe side effects.

37
Q

What is the therapeutic index of a drug?

A

Dose that causes benefits divided by dose that causes dangerous side effects.

38
Q

What are anxiolytics primarily prescribed for, and what are the two types of anxiolytics?

A

Primarily prescribed for anxiety. The two types are benzodiazepines and non-benzodiazepines.

Benzo: diazepam, lorazepam, clonazepam Non-benzo: buspirone, gabapentin

39
Q

What are the pros and cons of benzodiazepines?

A

Pros: They act rapidly and have sedative, muscle-relaxing and anxiolytic effects.
Cons: They have several side effects including high potential for dependence, dizziness, confusion, etc.

40
Q

What neurotransmitters and hormones do benzodiazepines impact?

A

They enhance GABA (inhibitory NT) and block rapid release of stress hormones.

41
Q

What are barbiturates and why are they no longer used?

A

Non-benzos used for sedation and sleep induction, no longer used due to extreme side effects (tolerance, physical dependence, severe withdrawal).

42
Q

What are the classes of antidepressants?

A

Monoamine oxidase inhibitors (MAOIs), tricyclic antidepressants (TCAs), selective serotonin reuptake inhibitors (SSRIs), norepinephrine-dopamine reuptake inhibitors (NDRIs), serotonin-norepinephrine reuptake inhibitors (SNRI’s)

Typical antidepressants include MAOIs, TCAs & SSRIs.

43
Q

Describe the mehcanisms and side effects of tricyclic antidepressants (TCAs) and list some examples of TCAs.

A

They block the reuptake of serotonin and norepinephrine. Side effects include cardiac/autonomic, anticholinergic and neurobehavioral, have been discontinued. Examples include: desipramine, amitriptyline, nortriptyline, imipramine.

44
Q

Describe the mehcanisms and side effects of monoamine oxidase inhibitors (MAOs) and list some examples of MAOs.

A

Block reuptake of monoamine neurotransmitters by blocking transporters. Rarely used because of drug-drug and drug-food interactions, such as hypertensive crisis. Examples include phenelzine, tranylcypromine.

45
Q

Describe the mehcanisms and side effects of SSRIs and list some examples of SSRIs.

A

Block reuptake of serotonin by selective binding (don’t block other monoamines). Side effects include GI symptoms, headache, insomnia, agitation. Examples include escitalopram, citalopram, fluoxetine, sertraline, paroxetine, fluvoxamine.

Serotonin syndrome when 2 SSRIs taken simultaneously or excessively.

46
Q

List the atypical antidepressants and examples of each.

A
  • NDRIs such as bupropion, used for smoking cessation.
  • SNRIs such as venlafaxine & desvenlafaxine
  • Miztrazapine/remeron
  • Trintellix/vortioxetine- improves cognitive x’s of depression
  • Trazodone- often used for insomnia
47
Q

Describe mechanisms and side effects of conventional antipsychotics (1st gen) and list examples.

A

They block dopamine receptors. Side effects include extrapyramidal symptoms like parkinsonism, acute dystonia (muscle spasms), akathisia (restless movements, anxiety), tardive dyskinesia (stereotyped movements). Other side effect is neuroleptic malignant syndrome (rare but life-threatening). Examples: haloperidol, thioridazine, molinidine, chlorpromazine, loxipine.

48
Q

Describe mechanisms and side effects of atypical antipsychotics (2nd gen). List some examples.

A

They block dopamine and serotonin receptors. Side effects include metabolic effects (weight gain, diabetes, dyslipidemia). Examples: olanzapine, quetiapine, ziprasidone, aripiprazole, clozapine, risperidone.

49
Q

Which drug is the first-line treatment for new onset schizophrenia?

A

Risperidone.

50
Q

Purpose and mechanism of lithium and its side effects.

A

Lithium is a mood stabilizer used to treat mania/hypomania. Mechanism thought to involve serotonin and NE. It has a narrow therapeutic index; and many side effects both short-term (GI x’s, weight gain, hand tremor) and long-term (hypothyroidism, goiter, rarely kidney damage). Toxicity may result in death.

51
Q

What are first-line treatments for bipolar disorder?

A

Antipsychotics (e.g., aripriprazole) and anticonvulsants (e.g., divalproex, lamotrigine, carbamazepine, topiramate).

52
Q

What is opioid replacement therapy?

A

First-line treatment for addiction that involves replacing opioid of use with a less addictive opioid.

53
Q

Describe mechanisms and side effects of stimulants and list examples.

A

Stimulants increase levels of NE and DA in the prefrontal cortex. Side effects include insomnia, headache, tic increase, irritability, weight loss, slow growth in children. Examples: amphetamine, methylphenidate, lisdexamfetamine, dexmethylphenidate.

54
Q

Describe how CT scan works and what it’s used for.

A

Uses x-ray to look at slices of the brain and shows density of tissue (more dense = whiter). Can detect enhancing lesions when done with contrast. Used often in ER.

55
Q

Describe how MRI works and its clinical use.

A

Uses magnetic fields to show the intensity/brightness of tissue (hyperintense = brighter area). Provides more detail than CT and used to detect small lesions.

56
Q

What is neuroangiography used for?

A

Used to see lesions of blood vessels (e.g., AVMs) by injecting contrast material into vasculature.

57
Q

Describe how Wada Testing works and what it is used for.

A

Type of neuroangiography for localizing language functioning. Pharmaceutical is injected into each carotid artery (putting to sleep the contralateral hemisphere) to assess cognitive functions in that hemisphere.

58
Q

Describe how PET scans work and their clinical use.

A

Radioactive material is injected to measure regional cerebral bloodflow (more active uses more glucose and becomes more radioactive). Used for mapping distribution of NTs and identifying brain dysfunction.

59
Q

Describe how fMRI works and its clinical uses.

A

fMRI detects functional changes from blood oxygenation. Used to measure real-time response to motor activities and neuropsych testing.

60
Q

What is Wernicke’s aphasia? What is the pathology?

A

Inability to understand language, speech is usually fluent but nonsensical and meaningless. Lesion in temporal lobe.

Also known as sensory aphasia or receptive aphasia.

61
Q

What is transcortical sensory aphasia? What is the pathology?

A

Similar to Wernicke’s aphasia (poor comprehension but fluent speech), but can repeat what other’s say. Lesion between parietal and temporal lobe.

62
Q

What is Broca’s aphasia? What is the pathology?

A

Difficulty with speech production (slow, halting), poor grammar, slow writing, impaired repetition but intact auditory and reading comprehension. Lesion in frontal lobe.

Also known as motor or expressive aphasia.

63
Q

What is transcortical motor aphasia? What is the pathology?

A

Similar to Broca’s aphasia but person can repeat what others say. Lesion in frontal areas surrounding Broca’s area.

64
Q

What is conduction aphasia? What is the pathology?

A

Inability to repeat what others say (but fluent speech production and comprehension otherwise). Lesion thought to be in arcuate fasciculus (white matter tract connecting Broca’s and Wernicke’s areas).

65
Q

What is anomic aphasia? What is the phathology?

A

Focal deficit in naming objects. Lesion thought to be in the angular gyrus.

66
Q

What is alexia? What is the usual pathology?

A

Acquired inability to read. Pathology is usually a stroke in the posterior dominant hemisphere, including posterior corpus callosum (disconnects visual and language centers).

67
Q

What is agraphia? What is the pathology?

A

Acquired disorder of writing, may affect several components of writing (spelling, grammar, letter orientation). Lesions can be in parietal lobe, frontal lobe, corpus callosum, or subcortical structures.

68
Q

What is apraxia? What is the pathology?

A

Inability to carry out skilled, purposeful movement (e.g., brushing teeth) without primary motor or sensory impairments. Lesion usually in left (dominant?) hemisphere.

69
Q

What is demetia (aka neurocognitive disorder)?

A

Umbrella term for decline in two or more areas of cognitive funcitoning that results in significant functional impairments. Many etiologies.

70
Q

What is Alzheimer’s Disease? What is the pathology? What are the treatments?

A

Disease that causes dementia (most common cause) and involves a decline n memory and at least one other cognitive domain. Pathology involves beta-amyloid plaques and neurofibrillary tangles (primarily in limbic cortex) as well as acetylcholine deficiency and glutamate excitotoxicity. Treatments include medications (cholinesterase inhibitors, glutamate regulators) that slow the progression of AD.

Medications do not restore lost cognitive functions.

71
Q

Describe the progression of symtpoms of Alzheimer’s disease through the early, intermediate and later stages.

A

Early stage: memory impairments, particularly new learning, sometimes visual-spatial deficits and word-finding or naming difficulties. Intermediate stage: Increased impairments in memory, visualspatial skills, word-finding, naming and emergence of apraxia, acalculia, ahpasia or agnosia.
Later stage: may include severe intellectual impairment, minimal verbal abilities, gait and motor problems.

72
Q

What is Pick’s disease?

A

A type of frontotemporal dementia that involves degeneration of frontal and temporal lobes. Symtpoms include behaivoral disinhibition, executive dysfunction, and langauge difficulties.

Currently no treatment.

73
Q

What is cerebrovascular disease (aka vascular dementia)?

A

Second most common cause of demetia with variable deficits that occurs when people suffer multiple strokes.

74
Q

Describe Parkinson’s dementia.

A

Dementia associated with Parkinson’s disease, “subcortical dementia”, involves deficits in EF, processing speed, memory.

75
Q

What is Parkinson’s disease? What is the pathology? What is the treatment?

A

A progressive neurodegenerative disease that causes tremor, rigidity, bradykinesia (slowed movement) and posture instability. Pathology includes degeneration of the substantia nigra and loss of dopamine. Treatment includes medications that boost dopamine.

76
Q

What is Huntington’s disease? What is the pathology? What is the treatment?

A

A degenerative disease and movement disorder that causes jerky movements, clumsiness, cognitive deficits (memory, concentration) and behavioral/emotional x’s. Dementia almost always occurs. Pathology is a loss of neurons in the caudate nucleus (basal ganglia) and loss of GABA and NE resulting in overactive dopamine system. There is no treatment, just genetic counseling.

77
Q

What is chronic traumatic encephalopathy (CTE)? What is the pathology?

A

Neurodegenerative disorder linked to history of brain trauma. Pathology includes hyperphosphorylated-tau protein (p-tau) distributed irregularly around the ventricles. Involves psychiatric, behavioral and cognitive x’s.

New diagnosis. Only studied by restrospective family member reports.

78
Q

What is pseudodementia?

A

Dementia-like presentation in psychiatric disorders, such as cognitive problems reported in depression. Typically characterized by slow processing speed and inconsistent attention/effort, but intact memory and visual-spatial skills.

79
Q

What is mild cognitive impairment? How long is the course?

A

Impairment in at least one cognitive domain greater than expected for age, but no functional impairment. Usually transitional time between normal aging and dementia (course usually 5 years).

80
Q

What is delirium?

A

Acute confusional state with disturbance in consciousness with an abrupt onset. It is usually associated with a medical condition, substance intoxication/withdrawal, or toxin exposure.

81
Q

What is concussion?

A

Mild traumatic brain injury with at least some alteration (not necessarily loss) of consciousness, posttraumatic amnesia, or focal neurlogical deficit.

82
Q

What is the difference between a simple partial seizure and a complex partial seizure?

A

Both involve only one part of the brain but a complex partial seizure involves alteration and/or loss of consciousness.

83
Q

What are the general effects on mood/affect from lesions to the left and right hemispheres?

A

Negative emotions are processed primarily in the right hemisphere, and damage to this hemisphere can produce inappropriate indifference or euphoria.
In contrast, positive emotions are processed primarily in the left hemisphere, and damage to this hemisphere can produce depression or emotional volatility.

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