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Unit 19 > From T's Review: Part 1 > Flashcards

From T's Review: Part 1 Flashcards

1
Q

Where do neurons releasing NE come from?

A

Locus coeruleus, lateral tegmental area

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2
Q

What would low levels of NE lead to?

A

depression, BP issues

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3
Q

Where are the nuclei of neurons that release 5HT?

A

Raphe nuclei, pons, medulla

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4
Q

What does 5HT do?

A

Regulate mood, sex, sleep, appetite

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5
Q

Ach nicotinic receptors are linked to which type of channels? Where are these receptors located?

A

Ionic ligand-gated

Motor end plate of a skeletal muscle fiber

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6
Q

Ach muscarinic receptors are linked to which type of channels? Where are these receptors located?

A

2nd messengers via g proteins

Basal ganglia for motor control

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7
Q

Where are the neurons that release GABA?

A

Striatopallidal pathway interneurons

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8
Q

What do the interneurons that release GABA do?

A

Suppress repetitive firing so that the CNS is in a state of tonic inhibition

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9
Q

The ascending arousal system is implicated in arousal and wakefulness and has two pathways: the thalamic pathway and the extrathalamic pathway. What is the main difference?

A

Thalamic pathways release Ach whereas extrathalamic release monoamines

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10
Q

Gray matter contains…

A

mostly cell bodies (very little myelin).

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11
Q

White matter contains…

A

axons (lotsa myelin)

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12
Q

What kind of TBIs lead to increased risk of hematomas and CN damage?

A

Low velocity

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13
Q

What are two types of diffuse (widespread) TBI?

A
  1. Diffuse axonal injury (dBI)

2. Pressure wave (blast injury) (bTBI)

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14
Q

What is created by an Acceleration-Deceleration TBI? What is a common cause of this?

A

MVA

Coup & Contracoup (the hit @ the anterior, the hit from the rebound posterior) (brain “hicky”)

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15
Q

Contusion of the orbital surfaces often manifests in what kind of memorable patient presentation?

A

raging w/o language

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16
Q

Basal skull fractures can lead to varying levels of cranial nerve damage - what CN can be damaged by an ethmoid bone fx?

Howsabout a longitudinal fx @ the temporal bone? What if it’s transverse?

A

CN I

CN VII
CN VIII

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17
Q

What kind of damage can a temporal blow to the head create?

A

conduction & sensorineural hearing loss (EVEN w/o fx)

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18
Q

What is the difference bw a subdural hematoma and an epidural hematoma?

A

Subdural hematoma = bw dura and brain, venous - develop over a longer period of time

Epidural hematoma = above dura, typically arterial bleed (surgical emergency)

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19
Q

What TBI can cause third nerve palsy (i.e. an Egyptian figure?)

A

A herniation through the foramen magnum

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20
Q

Selective attention is a common cognitive impairment post TBI. What is a relatively common pathology that is an example of this deficit in selective attention?

A

Neglect

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21
Q

What is the cognitive quality of strategic control defined as?

A

ability to sustain attn over time / concentration / ability to divide attention

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22
Q

What are the 3 attention related networks?

A
  1. Vigilance
  2. Orienting
  3. Executive Attention
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23
Q

Where is the vigilance network located and what NT controls this?

A

brainstem, RIGHT frontal lobe, noradrenergic control (NE)

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24
Q

Where is the orienting network located and what NT controls this?

A

primarily superior colliculus (eye fx), thalamus under cholinergic control (Ach)

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25
Q

Where is the executive attention network located and what NT controls this?

A

Orbitofrontal cortex, dorsolateral pre-frontal cortex, dopaminergic control (DA)

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26
Q

What is amantadine?

A

Used to treat tonic arousal in disorders of arousal and attn (can also help w/ faster recovery from TBI)

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27
Q

How is impaired phasic arousal treated?

A

Frequent task changes (behavioral) and alerting cues (adaptive)

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28
Q

What does SOS stand for in an TBI context?

A

Structure, organize, systematize: turn the new into the routine (errorless learning)

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29
Q

What are the 3 types of DS?

A
  1. Nondisjunction Trisomy 21
  2. Translocation
  3. Mosaicism
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30
Q

If every cell has 47 chromosomes, which type of DS does the pt have?

A

Nondisjunction Trisomy 21

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31
Q

If addtl or partial chromosome 21 attaches to another chromosome (14, usually), what type of DS does the pt have?

A

Translocation

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32
Q

If some cells have an extra chromosome 21 and some cells have 46, what type of DS does the patient have?

A

Mosaicism

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33
Q

What test is ordered is DS is suspected at birth?

A

Karyotype

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34
Q

What cardiac abnormalities are common in DS?

A

Atrial or ventricular septal defects

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35
Q

What orthotic is typically recommended for a pt w/ DS?

A

Sure-step SMO (supra-malleolar orthosis) -> UCBL (basically high trimline @ foot and heel) / shoe insert

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36
Q

How common is DS?

A

1 in 700 babies

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37
Q

What precautions should be taken for a patient w/ DS in light of atlanto-axial instability?

A
  1. Watch for gait changes of any kind.
  2. Avoid any head trauma of any kind in sports.
  3. DO NOT HYPEREXTEND NECK
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38
Q

What brain pathology would discriminate AD from MCI? What differentiates MCI from “normal”?

A

whole brain atrophy (bc normal aging involves shrinking of the pre-frontal cortex)

hippocampal atrophy

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39
Q

What kinds of long-term memory are there?

A

Explicit / Declarative and Implicit / Non-declarative

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40
Q

What kinds of explicit /declarative long-term memories are there?

A

Episodic - ya member events

Semantic - ya know facts

41
Q

What part of the brain is thought to contribute to explicit / declarative memory?

A

hippocampus, polymodal association areas, medial temporal lobe

42
Q

What kinds of implicit / non-declarative long-term memories are there?

A

Procedural
Non-associative (Habituation and Sensitization)
Associative (Emotional Response and Skeletal Muscle)

43
Q

Where is procedural memory thought to originate?

A

Striatum
Motor Cortex
Cerebellum

44
Q

Where are non-associative memories thought to originate from?

A

Reflex pathways

45
Q

Where is associative learning thought to originate from?

A

Emotional responses: amygdala

Skeletal muscle: cerebellum, premotor cortex

46
Q

What is the key difference bw mild cognitive impairment and dementia?

A

MCI does NOT interfere w/ everyday function

47
Q

In pts w/ dementia what are the 3 As that are affected?

A

Aphasia
Agnosia (ability to recognize objects)
Apraxia

48
Q

What are some distinguishing features of vascular dementia w/ reference to alzheimer dementia?

A

Biggest difference: Planning / decision making more impacted than memory loss.

Also, less apathy and depression.

Difficulty w/ motor fx, slow gait, and poor balance.

THERE IS A LESS STEADY DECLINE (in a good way!)

49
Q

What are 3 common screening tools for pts w/ dementia? What are norms for these?

A
  1. Mini Cog (higher score = less likely to have dementia, 3-5)
  2. Clock in the box
  3. Montreal Cognitive Assessment (MOCA) (30 point max, > 26 = normal)
50
Q

Where are short term memories stored? How bout long-term?

A

Front Lobe

Medial Temporal Lobe

51
Q

What is the general flow of memory?

A

Memories begin in the unimodal/polymodal association areas -> parahippocampal cortex -> through the entorhinal cortex before going to various areas in the hippocampus where eventually -> retrieval occurs and they move back through the entorhinal cortex -> through perirhinal cortex and back to the unimodal/polymodal association areas

52
Q

What is the hippocampus responsible for and what is a famous clinical case that illustrates this?

A

Object recognition, spatial representation

HM, had no hippocampus so had no ability to store memories but could improve implicit memories.

53
Q

What is the etiology of AD? What is one proposed mechanism for this?

A

Cholinergic neurons to the neocortex and hippocampus are destroyed.

Abnormal TAU proteins accumulate and become entangled in neurons while Beta-amyloid plaques build up between neurons. Microglia can’t clean these.

54
Q

What are the stages of pre-clinical AD?

A

Stage 1 = asymptomatic amyloidosis
Stage 2 = amyloidosis + neurodegeneration
Stage 3 = MCI leading to dementia
SNAP = suspected non-alyzheimer pathology w/o amyloids

55
Q

Does Tau accumulate extracellularly or intracellularly?

A

intracellularly

56
Q

Why is long-term potentiation important for this unit?

A

LTP is required to consolidate memory via the hypothalamus - (nerves that wire together, fire together)

57
Q

What percent of people over 65 have MCI?

A

20%

58
Q

Which part of the brain does priming come from?

A

The neocortex

59
Q

What is the CAM?

A

Confusion Assessment Method - used for assessing for Delirium

60
Q

What distinguishes delirium from other cognitive change pathologies?

A

acute onset, fluctuating course

61
Q

What is the mechanism of action for stimulant meds such as Ritalin, Concerta, Adderall, and Vyvanse?

A

Block reuptake of NE, 5HT, and DA.

62
Q

What is the mechanism of action of stimulants such as levodopa/carbidopa? What is this called?

A

Replace dopamine depletion. A memetic.

63
Q

What are the side effects of levodopa/carbidopa?

A

postural hypertension, dyskinesia, insomnia, hallucinations

64
Q

What are some side effects of Ritalin, Concerta, Adderall, and Vyvanse?

A

Confusion, Insomnia, Weight Loss

65
Q

Mirapex and ReQuip are some examples of dopamine agonists. Are these MORE or LESS potent than Levidopa/Carbidopa? And what is one side effect that you will NOT see w/ these that you WILL with L/C?

A

LESS

Postural hypotension

66
Q

What is the main mechanism of action of an anticholinergics?

A

inhibit central cholinergic activity, sedate vestibular system, ANTI PNS.

67
Q

Cogentin, Benadryl, and Dramamine are all examples of what type of drug?

A

Anticholinergics

68
Q

What is the difference between adverse side effects of anticholinergics vs. acetylcholinesterase inhibitors?

A

anticholinergics are ANTI PNS so everything dries out: confusion, agitation, palpitation, blurred vision, dry mouth, constipation.

vs. acetylcholinesterase inhibitors have WET side effects: urination, diarrhea, agitation, sweating.

69
Q

What age group will have the most intolerable side effects when taking an anticholinergic?

A

Patients over 65

70
Q

What kind of drug is Elavil and what might a patient take it for? What is a significant side effect of this drug for PTs to be aware of?

A

Tri-cyclic Antidepressant (TCA) - not great for depression, usually better for sleep

AmiTRIPtyline - effect on ambulation is significant

71
Q

What are 3 SSRIs and what are these commonly prescribed for? What makes SSRIs particularly effective for these populations?

A

Celexa, Prozac, Zoloft

Depression, PTSD, Eating Disorders

High affinity for 5HT transporters

72
Q

What are some common side effects of SSRIs?

A

Weight gain, sexual dysfunction.

Watch for signs of suicidal ideation.

73
Q

What kind of drugs are the following: Cymbalta, effexor, wellbutrin?

A

atypical compounds used as antidepressants.

74
Q

Name 4 Benzodiapines.

A

Ativan
Klonopin
Valium
Xanax

75
Q

What are Benzos typically used for?

A

Sleep, Muscle Relaxers, Alcohol w/drawal, anxiety

76
Q

What are common side effects of taking Benzos?

A

cause and effect w/ falls

can cause anterograde amnesia

77
Q

What is the mechanism of action of Benzos?

A

Make inhibitory system more inhibitory AKA facilitate GABA.

78
Q

What classes of drugs both have as their side effects: drowsiness, ataxia, psychomotor impairment, and disorientation?

A

Benzos and Opioids

79
Q

What are some side effects of antihistamines?

A

Sedation, confusion, dryness, and ataxia.

80
Q

What type of neurons projecting to the neocortex and hippocampus are destroyed in AD and why is this relavant pharmacologically?

A

cholinergic, which is why we use acetylcholinesterase in the treatment of AD (to INCREASE Ach by decreasing its breakdown)

81
Q

What is the main mechanism of action for stimulants?

A

block reuptake of monoamines (NE, 5HT, DA)

82
Q

What are 2 common uses of anticholinergics?

A
  1. Tx for PD tremors (congentin)

2. Allergic rxns (benadryl)

83
Q

What are antihistamines used for BESIDES what you think :) ?

A

Vertigo and balance disorders

84
Q

Which drug is NOT a stimulant but has similar effects and is taken by folks that can’t tolerate the cardiac effects of stimulants?

A

Straterra

85
Q

On the Glasgow Coma Scale, a severe TBI corresponds to which scores?

A

3-8

86
Q

On the Glasgow Coma Scale, a moderate TBI corresponds to which scores?

A

9-12

87
Q

On the Glasgow Coma Scale, a mild TBI corresponds to which scores?

A

13-15

88
Q

On the Rancho scale (8 pt) a severe TBI corresponds to which scores?

A

1-3 (highest response is localized)

89
Q

On the Rancho scale (8 pt) a moderate TBI corresponds to which scores?

A

4-6 (highest response is confused-appropriate)

90
Q

On the Rancho scale (8 pt) a mild TBI corresponds to which scores?

A

7-9 (highest response is purposeful appropriate)

91
Q

What does a 1 vs. 2 on the Rancho scale indicate?

A 
1 = no response / coma
2 = response to noxious stim via w/drawal
92
Q

Why do we use the CRS - Revised?

A

To differentiate bw coma, vegetative state, and minimally conscious in SEVERE TBI

93
Q

What are four mechanisms of Implicit Memory learning?

A
  1. Priming
  2. Associative Learning (classical and operant conditioning)
  3. Non-associative Learning (habituation and sensitization)
  4. Motor Learning/Procedural Learning
94
Q

What’s the difference between classical and operant conditioning?

A

Classical = learn to pair 2 stimuli together (Pavlov’s dog)

Operant = pair behavior and consequence

95
Q

What are the 4 quadrants of operant conditioning as explained by training a dog?

A

Positive Reinforcement: dog walks well, gets treat!

Negative Reinforcement: holding the remote in front of Mable - I am NOT hitting it, but I am getting good behavior bc she is aware of the negative

Positive Punishment: hitting the button when Mable yanks on her leash

Negative Punishment: not letting Mable have a treat until she’s fully laying down.

96
Q

In what context does unsupervised learning normally occur? And where is this process based in the brain?

A

constant practice, primary motor cortex

97
Q

In what context does reinforcement learning typically occur? And where is this process based in the brain?

A

Basal Ganglia - especially w/ action selection, reward influenced

98
Q

In what context does supervised learning typically occur? And where is this process based in the brain?

A

Cerebellum - error-based learning

99
Q

What are the three stages of learning?

A

Cognitive (verbal/motor)
Associative (motor)
Autonomous (automatic)

Unit 19 (2 decks)

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