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521-Pharmacology > Exam 3 review > Flashcards

Exam 3 review Flashcards

1
Q

Preclinical AD

A

-measurable brain changes without any symptoms
-abnormal AB shown in PET and CSF
-abnormal levels of tau protein(PET) in CSF and plasma

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2
Q

early symptoms of AD

A

-language problems
-misplacing items
-getting lost on familiar routes
-losing interest in things
-difficulty preforming tasks

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3
Q

worsening AD symptoms

A

-forgetting details about life
-changes in sleep pattern
-difficulty reading or writing
-poor judgement and loss of ability to recognize danger
-hallucinations
-depression, agitation
-difficulty doing basic tasks

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4
Q

severe AD

A

-unable to understand language
-will not recognize family members
-can not perform basic activities of daily living

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5
Q

goals for treating AD

A

-slow the progression of disease
-manage behavior problems, confusion, sleep problems and agitation
-modify the home environment
-support family members and other caregivers

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6
Q

Alpha secretase

A

-cut APP in the middle of the amyloid sequence
-good cut because it does NOT generate amyloid

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7
Q

Beta secretase

A

-cuts at N terminal of APP
-no significant harm associated with this cut alone

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8
Q

Gamma Secretases

A

-Cuts APP closer to cell membrane

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9
Q

Sequential cuts by gamma, beta, and alpha secretases:

A

-Lead to the formation of a self-aggregating peptide
● Peptides aggregate to form oligomers, then fibrils
● Fibrils form extracellular amyloid plaques, a hallmark sign of Alzheimer’s disease (AD)

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10
Q

Tau protein

A

-Stabilizes microtubules
● Crucial for signal transmission from neuron cell bodies to terminals

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11
Q

Hyperphosphorylation of tau

A

-Causes tau to become adhesive, disrupting transport
● Leads to accidental degeneration of neurons
● Forms intracellular aggregates in neurons

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12
Q

Alzheimer’s disease definition

A

Characterized by intracellular aggregates of hyperphosphorylated tau (neurofibrillary tangles) and amyloid plaques

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13
Q

Familial Alzheimer’s disease

A

-mutation of amyloid precursor protein and Presenilin 1/Presenilin 2

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14
Q

Sporadic Alzheimer’s disease

A

-APOE-e4 allele: responsible for transport of cholesterol, structure.function of cells, proteolytic degradation of beta-amyloid

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15
Q

Theories about neurodegeneration in AD

A
  1. . Disruption of calcium regulation/homeostasis
  2. Damage mitochondria through oxidative stress leading to increased protein, lipid
    and DNA damage
  3. Chronic activation of an immune response/inflammatory pathways
  4. Impaired protein clearance/protein turnover
    a. Two mechanisms that work on clearing proteins: ubiquitin-proteasome system and
    autophagy-lysosome system
  5. Synaptic dysfunction
  6. Tau phosphorylation leading to NFT formation
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16
Q

mTOR

A

Inhibits autophagy, slowing down cellular cleaning processes

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17
Q

AMPK

A

Activates autophagy, promoting cellular maintenance and energy balance.

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18
Q

Sensor proteins

A

Located within the cell to identify misfolded or dysfunctional proteins

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19
Q

Vesicle formation

A

Sensor proteins bind to faulty proteins and form a vesicle (autophagosome) around
them

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20
Q

Fusion with lysosome

A

The autophagosome fuses with the lysosome

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21
Q

Lysosome action

A

Lysosome enzymes degrade the contents of the autophagosome, removing damaged
proteins.

22
Q

APP localization

A

-found at the plasma membrane

23
Q

APP turnover

A

-managed by endosomal internalization

24
Q

Autophagosome accumulation

A

Observed in neurons in
AD brains and AD mouse models

25
Q

Mutant APP Overexpression

A

-leads to accumulation of AB peptides and other APP fragments in autophagic vesicles

26
Q

Cholinesterase Inhibitors for AD

A

-Donpezil
-Rivastigmine
-Galatamine

27
Q

NMDA receptor antagonist for AD

A

memantine

28
Q

monoclonal antibodies for AD

A

-target AB
-Aducanumab
- Lecanemab
- Donanemab

29
Q

Atypical antipsychotics for agitation in AD

A

-Brexiprazole

30
Q

symptoms of parkinsons

A

-resting “pill rolling” tremor
-akinesia/bradykinesia
-rigity
-postural instability

31
Q

hereditary causes of parkinsons

A

-loss of function mutations on DJ-1, parkin, and PINK1
-gain of function mutations in alpha-synuclein

32
Q

NEUROPATHOLOGY OF PD

A
  1. Loss of dopaminergic projection neurons in substantia nigra
  2. Lewy bodies (cytoplasmic inclusion bodies)
33
Q

Pathologic Factors Contributing to Sporadic PD

A

-Oxidative stress/ environmental toxins
● Metabolic dysfunction
● Excitotoxicity (NMDA receptor involvement)
● Proteasome dysfunction (inclusion bodies)
● Autophagy dysfunction (inclusion bodies)
● Inflammation

34
Q

true or false: lewy bodies can develope in the gut, spread to vagal nerve, and cause onset of motor symptoms

A

true

35
Q

Goal of parkinson’s drugs

A

-restore dopaminergic activity

36
Q

L Dopa

A

-replace dopamine
-inhibit peripheral conversion of L-Dopa to dopamine

37
Q

Inhibit of dopamine degradation

A

COMT and MAO-B

38
Q

Carbidopa

A
  • Inhibitor of dopa decarboxylase
  • Carbidopa does NOT cross BBB
  • Reduces peripheral metabolism of L-DOPA
39
Q

COMT inhibitor

A
  • Tolcapone and entacapone
  • Prolongs action of levodopa (reduces
    peripheral metabolism)
  • Tolcapone has both central and peripheral
    effects
  • Entacapone has only peripheral effects
40
Q

MAO-A Inhibitors

A

metabolizes NE, serotonin, and DA

41
Q

MAO-B Inhibitors

A
  • Metabolizes DA selectively
  • Selegiline and Rasagiline
42
Q

Adenosine A2A Receptor Antagonist

A
  • Istradefylline
  • Inhibition of A2A enhances dopamine D2
    signaling
43
Q

Stage 1 analgesia

A

-disorientation
-altered consciousness
-amnesia
-euphoria

44
Q

Stage 2 anestetics

A

-excitement stage
-delirium, uncontrolled movement
-irregular breathing
-goal is to move through this stage as rapidly as possible

45
Q

Stage 3 anesthesia

A

-surgical anesthesia
-return of regular respiration
-plane 1: light anesthesia
-plane 2: Loss of blink reflex, regular respiration
-plane 3: Deep anesthesia. Shallow breathing, assisted ventilation needed
-plane 4: Diaphragmatic respiration only, assisted ventilation is required.
Cardiovascular impairment

46
Q

Stage 4 anestesia

A

-medullary depression
-Too deep; Depression and Respiration arrest, no eye
movement, essentially an overdose and represents anesthetic crisis. This is the
stage between respiratory arrest and death due to circulatory collapse

47
Q

Central gaze, constricted pupils, regular aspirations, and the anesthetic
depth is sufficient that noxious stimuli does not cause reflexes or excessive
autonomic effects

A

surgical anestesia

48
Q

Apnea, non-reacted dilated pupils, circulatory failure, and hypertension are
most likely associated with this stage of general anesthesia

A

medullary depression

49
Q

Four stages of general anesthesia:

A

-delirium
-analgesia/amnesia
-surgical anesthesia
-medullary depression

50
Q
A

521-Pharmacology (11 decks)

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