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Block 6 > Week 5 > Flashcards

Week 5 Flashcards

1
Q

Donepezil, Galantamine, Rivastigmine
1. name of these drug types
2. MOA?
3. Used for what disorder?

A
  1. Cholinesterase Inhibitors
  2. Inhibits acetylcholinesterase to boost levels of ACh -> treats cognitive symptoms of Alzheimers
  3. Alzheimers
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2
Q

Donepezil, Galantamine, Rivastigmine
1. At what stage of AD are these used for?

A
  1. Donepezil - at all stages (first line drug)
  2. Rivastigmine - at all stages (first line drug)
  3. Galantamine - mild to moderate dementia of AD
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3
Q

Donepezil, Galantamine, Rivastigmine
(Cholinesterase Inhibitors)
1. What are the side effects
2. What are some contraindications

A
  1. Nausea, dizzy, insomnia; loss of appetite, weight loss; bradycardia
  2. Don’t use if taking anticholinergic drugs - opposite effect of what these drugs are trying to do
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4
Q

Memantine
1. What type of drug is this
2. MOA
3. What disease is this used for?

A
  1. NMDA receptor antagonist
  2. Blocks NMDA which are usually activated by excitatory glutamate (only treats cognitive symptoms of AD) -> too much glutamate cuases too much neural excitation which is most likely a reason for neuronal injury in alzheimers dx
  3. Alzheimer’s disease
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5
Q

Memantine
1. What stage of AD is this best used for?
2. Side effects
3. Contraindications

A
  1. moderate to severe AD patients
  2. dizziness, confusion, hallucination
  3. Hypersensitivity to memantine
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6
Q

Aducanumab
1. What type of drug is this?
2. MOA
3. What disease is this used for?

A
  1. Anti-amyloid plaque antibody
  2. monoclonal Ab against aggregated forms of amyloid beta. Ab surround aggregated amyloid beta and recruit activated microglia -> phagocytosis
  3. Alzheimers disease
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7
Q

Aducanumab
1. What stage of AD is this used for?
2. side effects

A
  1. mild AD
  2. headache, confusion, dizziness, falls, vision change
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8
Q

what is the difference between declarative and non-declarative long term memory?

A
  1. Declarative: these are facts and events
  2. Non-declarative: these are skills, doesn’t require conscious thought and allows people to do things by rote
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9
Q
  1. Describe Long term potentiation
  2. When does this happen (declarative or non-declarative)
A
  1. strengthening of a synaptic connection that happens when the synapse of one neuron repeatedly fires and excites another neuron
    -> Ca2+ flux through NMDA receptor channels initiate LTP
  2. When forming declarative long term memories
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10
Q

How do cells in the brain work together to create classical conditioning in non-declarative long term memory? (hint: pukinje cells are involved)

A
  1. Unconditioned stimulus (ex: dog food) signals come from climbing fibers in from inferior olive
  2. Conditioned stimulus (ex: bell) signals come from mossy fibers (parallel fibers to climbing fibers) in from pontine nuclei in brainstem
  3. Both signals go into purkinje fibers -> when stimuli come in at the same time eventually you get long term depression of parallel fiber EPSP after beginning to pair US and CS
    ** AMPA receptors are being removed from parallel fiber synapse (mossy fibers) and allows US to occur in response to CS alone **
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11
Q

Alzheimer’s Disease
1. Degeneration of what?
2. Loss of what NT?
3. Gross changes in brain (3)

A
  1. cortex
  2. loss of ACh cortical activity
  3. gyri narrow and sulci widen + hydrocephalus ex vacuo (image) + hippocampal atrophy
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12
Q

Alzheimer’s Disease
1. clinical features (5)

A
  1. slow-onset of memory loss
  2. loss of learned motor skills and language
  3. behavior and personality changes
  4. patient becomes mute and bedridden
  5. No focal neuro deficits
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13
Q

Alzheimer’s Disease Genetics
1. Sporadic vs Familial which is more uncommon
2. what genetic mutation in sporadic type increases risk vs which one decreases risk

A
  1. familial late onset is uncommon and familial early onset is rare
  2. ApoE - E4 allele increases risk —- ApoE - E2 allele decreases risk
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14
Q

Alzheimer’s disease
1. Familial early onset (rare) - is seen with what genetic mutations?
2. Why do those with down syndrome have higher risk of AD as well?

A
  1. mutation or duplication of APP gene on chromosome 21 OR mutation in presenilin 1
  2. three chromosome 21 is where APP gene is found - increases risk of AD by age of 40
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15
Q

Alzheimer’s Disease
1. What is found in histology of brain (2)
2. What does this lead to?

A
  1. beta amyloid plaques
  2. Neurofibrillary tangles (collection of tau proteins inside neuron cell body)
  3. Neuritic plates - amyloid core surrounded by dystrophic neurites
    –> this all leads to loss of neurons and gliosis
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16
Q

Pick Disease
1. What is it?
2. Pathophysiology?

A
  1. rare cause of dementia that degenerates frontal and temporal lobes causing changes in personality and aphasia
  2. pick bodies (spherical tau proteins) - inside neurons
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17
Q

Pick disease
1. Is it inherited?
2. Hallmark symptoms
3. Gross anatomy descriptions of brain (2 main ones)

A
  1. It is mostly sporadic
  2. changes in personality/behavior (frontal) and aphasia (temporal)
  3. Cortical atrophy in frontal and temporal lobes -> “knife-edge” appearance in these areas, ventricular dilation, etc
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18
Q

Parkinson Disease
1. What does histology show?

A
  1. Shows lewy bodies (cytoplasmic inclusions - which are deposits of alpha-synuclein) in substantia nigra of basal ganglia
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19
Q

Lewy Body Dementia
1. Pathophysiology
2. Triad symptoms?

A
  1. Collection of lewy bodies (deposits of alpha synuclein) in cortex -> the build up of this causes dementia
  2. Dementia, Parkinson symptoms, Hallucinations
    Dementia occurs before parkinson sx

In parkinson, lewy bodies are in basal ganglia

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20
Q

Chronic Traumatic Encephalopathy (CTE)
1. Sx
2. pathophysiology
3. Changes to brain (gross) (4)

A
  1. Inattention, mood and behavior disturbances, confusion, memory loss, demention, parkinsonism
  2. Brain damage due to repetitive truamatic brain injuries
  3. Cerebral atrophy, enlarged ventricles, thinning of corpus collusim, depigmentation of substantia nigra
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21
Q

Prion Disease (Spongiform Encephalopathy)
1. Types
2. Most common subtype

A
  1. sporadic, inherited (PRNP gene on chromosome 20), transmitted
  2. Creutzfeldt-Jakob Disease
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22
Q

Creutzfeldt-Jakob Disease (A type of prion disease)
1. Presentation (symptoms) (3)
2. Pathophysiology?

A
  1. Rapidly progressive dementia, Myoclonus (muscle jerk), Ataxia
  2. PrPc (normal) -> changes to PrPsc (abnormal);; with more abnormal/pathologic protein it will accumulate in neurons, damage neurons, and causes spongy holes in brain matter
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23
Q

Prion Disease
1. Changes to brain (gross and histology)

A
  1. some degree of cerebral atrophy with hippocampus spared
  2. Histo: spongiform change (holes in neuronal processes/neurites, neuronal loss, reactive gliosis, absence of inflammation
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24
Q
  1. What are association fibers in cortex
A
  1. cerebral fibers that have their origin and termination within the cortex and in the same hemisphere
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25
Q
  1. What are commissural fibers in cortex
A
  1. cerebral fibers that have their origin and termination within the cortex but in the opposite hemisphere
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26
Q
  1. What are projection fibers in cortex
A
  1. fibers connect the cortex to the subcortical regions
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27
Q

What lobes are useful in visual cortical system?

A
  1. mostly occipital but also the parietal and temporal lobe
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28
Q

Meyer’s Loop
1. Where is it found?
2. What is its function?

A
  1. temporal lobe
  2. It is made up of the dorsal and ventral stream - essential for visual sense. (as seen in image)
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29
Q
  1. Function of the Ventral stream of Meyer’s Loop
  2. Function of the Dorsal stream of Meyer’s Loop
A
  1. analyze what an object is, such as form and color
  2. where the object is, such as position, speed, and motion
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30
Q
  1. Lesion to the upper V1 of primary visual cortex causes [inferior/superior] quadrantopsia
  2. Lesion to the lower V1 of primary visual cortex causes [inferior/superior] quadrantopsia
A
  1. inferior - meaning bottom of their visual field is lost
  2. superior - meaning the top of their visual field is lost
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31
Q

Language processing
1. Speech skils that are left hemisphere dominant
2. Speech skils that are right hemisphere dominant

A
  1. understanding and producing speech (depends on wernicke and brocas areas respectively)
  2. emotion and affective elements of speech -> with lesions a person may not be able to detect these in someone else’s speech
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32
Q
  1. Dominant half of brain includes more skills for…
  2. Non- Dominant half of brain includes more skills for…
A
  1. language, skilled motor function, arithmetic
  2. prosody, visual spatial analysis, musical ability, sense of direction in space
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33
Q

Frontal Lobe Organization

  1. Dorsolateral
A
  1. working memory and selective attention
34
Q

Frontal Lobe Organization

  1. Ventrolateral
A
  1. response inhibition and goal-appropriate response
35
Q

Frontal Lobe Organization

  1. Orbitofrontal
A
  1. Cognitive process of decision making, inhibitory control, and social and emotional regulation
36
Q

Orbitofrontal syndrome
1. what sx occur

A
  1. inappropriate affect in social interactions; acquired sociopathy, aggression
37
Q

Dorsolateral syndrome
1. what sx occur

A
  1. problems with planning, inattentive, undermotivated
  2. Getting stuck on one task
38
Q

Anterior cingulate/mesial frontal lobe syndrome (green in image)
1. what sx occur

A
  1. Lack of will or motivation
  2. Akinetic mutism (person doesn’t really speak)
  3. Loss of spontaneity
39
Q

Olfactory epithelium
1. What kind of epithelium is this?

A
  1. pseudostratified (contains bipolar olfactory cells)
40
Q

Bowman’s Glands in olfactory epithelium
1. Function?

A
  1. secrete watery solvents for odorents, to flush odorants from surface of epithelium
41
Q

Olfactory tract splits into..
1. Medial olfactory stria
2. Lateral olfactory stria

what are their purpose

A
  1. travel to oflactory nucleus in the brainstem
  2. travel to primary olfactory cortex, entorhinal cortex, and amygdala (part of how smells are assoc. to memories and emotion)
42
Q

What is the path from odorant arriving to olfactory cell –> interpretation of signals
4 general steps

A
  1. Odorant binding proteins (OBP) in mucus bind odorants and carry them to sensory receptors
  2. Olfactory sensory receptors are GPCRs - with binding of OBP-odorant complex -> leads to increase of cAMP and causes AP
  3. CN I takes these AP signals through cribiform plate to olfactory bulb
  4. Olfactory tract splits into medial and lateral olfactory stria -> here odorant singals are analyzed
43
Q

Taste Buds (Neuro-epithelial cells)
1. What is the purpose of the taste pore?
2. What is found within a taste bud? (3 general cell types)

A
  1. to protect cells from abrasion
  2. sensory cells (register flavor), supporting cells, basal cells
44
Q

What CNs does a sensory cell in a taste bud synapse on? (3)

A
  1. CN VII, IX, X
45
Q

Taste analysis by what CN?
1. anterior 2/3 of tongue
2. posterior 1/3 of tongue
3. epiglottis

A
  1. CN VII
  2. CN IX
  3. CN X
46
Q

From sensory cells in taste buds how to signals arrive to gustatory cortex?

A
  1. tracts of CN VII (via chorda tympani then nervus intermeidus), IX, X travel to brainstem
  2. arrive to solitary nucleus of brainstem
  3. Medial lemniscus pathway to VPM of thalamus
  4. Projects to gustatory cortex
47
Q

How are taste receptors activated with salty flavors?

A
  1. Salt opens Na+ ion channels -> leads to change in membrane potential
48
Q

How are taste receptors activated with sour flavors?

A
  1. Sour tastants open H+ channels and Blocks K+ channels leading to change in membrane potential
49
Q

How are taste receptors activated with bitter flavors?

A
  1. Bitter tastants stimulate a single GPCRs → activates PLC → increase IP3 → opens Na and Ca channels
50
Q

How are taste receptors activated with sweet and umami flavors?

A
  1. Stimulate DUAL unit GPCrs
  2. activates PLC → increase IP3 → opens Na and Ca channels
51
Q

Dementia
1. MMSE score
2. What is the symptom triad?

A
  1. <27
  2. aphasia (affects how you communicate), apraxia (inability to perform learned movments on command-also makes it hard to speaks), agnosia (inability to interpret sensations like objects, faces, voices, etc)
52
Q

Mild Cognitive impairment vs Dementia
1. What is the difference

A
  1. Mild cognitive impairment occurs usually secondary to another process, such as intoxication, infection, etc.
  2. Dementia is significant cognitive decline over time
53
Q

What parts of the brain are affected in Alzheimer’s disease

A
  1. hippocampus, entorhinal cortex
  2. spreads to temporal and parietal cortices
  3. Then becomes generalized over whole cortex
54
Q

Vascular Dementia
1. Pathophysiology
2. what risk factors can patients have
3. acute or chronic

A
  1. Abnormalities to vascular system can lead to strokes and then cause cognitive impairment. (Multi-infarct dementia - series of small strokes that result in dementia)
  2. HTN, increased cholesterol, smoking
  3. typically acute onset and then don’t continue to deteriorate
55
Q

What neurological disease causes a person to act out their dreams (REM sleep behavior disorder)?

A

Lewy body dementia

56
Q

Normal Pressure Hydrocephalus (NPH)
1. What is it?
2. Triad of symptoms?
3. Changes to brain?
4. typical in what age ranges?

A
  1. An abnormal buildup of CSF in the brains ventricles - this occurs if the normal flow of CSF throughout the brain and spinal cord is blocked in some way
  2. wet, wobbly, whacky -> urinary incontinence, gait instability, cognitive impairment
  3. Ventriculomegaly - when CSF becomes trapped in the spaces, causing them to grow larger. (this can cause damage to brain)
  4. infants and elderly
57
Q

What findings are seen brain imaging of someone with prion disease?

A
  1. cortical ribbon - non-specific cortical atrophy
58
Q

Global ischemic injury vs focal ischemic injury

A
  1. Global -> when cerebral blood flow is reduced throughout most or all of the brain
  2. Focal -> a reduction in blood flow to a very distinct, specific brain region
59
Q

What are changes to the brain
1. early on in global ischemia
2. later on in global ischemia

A
  1. early laminar necrosis appear as linear zones of reddish hyperemia (excess of blood in vessels) that follow cortical ribbons
  2. fluid-filled slit like spaces within the grey matter of the cerebral cortex. These spaces replace the neuronal layers that have undergone necrosis eary on.
60
Q
  1. what is a watershed infarct?
  2. borders zones between what arteries? (2)
A
  1. ischemic lesions that are situated along the border zones between territories of two brain areas supplied by major arteries
  2. Infarct at ACA/MCA watershed + at PCA/MCA watershed
61
Q

timeline of change in a focal ischemia event
1. <6 hours
2. 12-24 hours
3. 24-72 hours
4. 2-3 days
5. 5-7 days
6. 7 days
7. 2 weeks
8. 3 weeks
9. 2-6 months

A
  1. no change
  2. red neurons appear
  3. neutrophilic infiltrates
  4. coagulative necrosis w/macrophage infiltration
  5. vascular proliferation at edge of injury
  6. Astrogliosis at edge
  7. Liquefactive necrosis
  8. Cavitation appears
  9. Fluid filled cavity surrounded by glial scar
62
Q
  1. are neurons or glial cells more vulnerable to ischemia
  2. What subtype is most susceptible? (2)
A
  1. neurons
  2. purkinje cells in cerebellum + pyramidal cells in CA1 region of hippocampus
63
Q

Intraparenchyma Hemorrhage
1. pathophysiology
2. locations in brain it is most likely to happen (3)

A
  1. most commonly due to HTN. HTN leads to deposition of lipid and hyaline material in the walls of small arteries which weaken the walls and cause them to be weak points of vessel rupture
  2. basal ganglia, pons, cerebellum
64
Q

What is the most common cause of subarachnoid hemorrhage?
-> due to what artery?

A
  1. berry aneurysm
  2. bleeding (cause of hemorrhage) is the anterior communicating artery
65
Q

Cerebral amyloid angiopathy
1. pathophysiology
2. Where does the hemorrhage occur?
3. Can show symptoms of what other disease?

A
  1. Deposition of beta amyloid in the cortical vessels -> making it weak and likely to rupture
  2. cerebral cortex
  3. Alzheimers
66
Q

Lacunar Strokes
1. pathophysiology
2. common locations? (4)
3. Common vessels affected?
4. risk factors

A
  1. arteriolar sclerosis in certain arteries that cause small strokes and then later leaves lacunae (empty space) in brain
  2. Internal capsule, thalamus, basal ganglia, pons
  3. Lenticulostriate arteries (deep arteries of MCA) (area it supplies in image) or ACA
    • associated with HTN, smoking, diabetes
67
Q

Charcot-Bouchard Aneurysms
1. Where do these happen?
2. What can it cause?

A
  1. microaneurysms (artery wall is weak so it balloons out) in the small branches of lenticulostriate arteries
  2. These can rupture and cause bleeding/hemorrhage -> usually in basal ganglia and thalamus
68
Q

Ateriovenous malformation
1. Pathohysiology
2. what damage to brain can it cause
3. How can it be tx?

A
  1. shunts blood flow from arterial circulation directly into veins without intervening capillary bed
  2. intracerebral hemorrhage
  3. These areas can be embolized or surgically removed
69
Q

Cavernous malformation
1. pathophysiology

A
  1. groups of tightly packed, abnormal small blood vessels with thin walls -> it can contain slow moving blood that is usually clotted
70
Q

Where is the pterygopalatine fossa found?

A
  1. behind the maxilla
  2. Between the maxilla and the pterygoid process of sphenoid bone
71
Q

Branches of Trigeminal
1. V1 (sensory, motor, or mixed?)
2. V2 (sensory, motor, or mixed?)
3. V3 (sensory, motor, or mixed?)

A
  1. sensory
  2. sensory
  3. mixed
72
Q

What parts of the nasal cavity are innervated by V1 and V2

A

look at image - this is all sensory from trigeminal nerve

73
Q

Clinical significance of Kiesselbach Plexus (what supplies blood to nasal cavity)

A
  1. Air you breathe in can dry mucosa and can crack these small vessels leading to nose bleeds - there is significant anastomoses though
74
Q

What is the significance of the submucosal venous plexus in nasal cavity?

A
  1. It gives off heat and this allows us to warm up air that we breathe in
75
Q

What arteries are Kiesselbach’s plexus formed by (3)

A
  1. facial artery
  2. maxillary artery
  3. ophthalamic artery

1,2 come from ECA and 3 comes from ICA

76
Q
  1. Sensory on anterior 2/3 of tongue is via
  2. Sensory on posterior 1/3 of tongue is via
  3. Taste on anterior 2/3 of tongue is via
  4. Taste on posterior 1/3 of tongue is via
  5. Motor innerveration on whole tongue
A
  1. V3
  2. CN IX
  3. CN VII (chorda tympani)
  4. CN IX
  5. CN XII (except palatoglossus which is via CN X)
77
Q
  1. Blood supply to tongue
  2. Venous drainage of tongue
A
  1. lingual artery (branch of ECA)
  2. Deep lingual vein (drain into IJV)
78
Q

What is the nerve supply to the hard and soft palate?

A
  1. greater palatine nerve and lesser palatine nerve (from CN V2 - sensory nerve)
79
Q

Neuromyelitis Optica (NMO)
1. What sx occur
2. What markers/identifiers are found?

A
  1. optic neuritis, myelopathy with longitudinally extensive hyper intense signal in throacic spinal cord, normal MRI brain
  2. Aquaporin 4 antibodies - confrim dx
80
Q

What tx is given to someone with NMO to avoid paralysis or blindness?

A
  1. steroids
  2. plasma exchange

Block 6 (9 decks)

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