Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Neuro Quiz 5 > Pharmacology of Meds Used to Treat Dementia > Flashcards

Pharmacology of Meds Used to Treat Dementia Flashcards

1
Q

NonPharm Treatment of AD

A

 Behavioral symptoms
 Calm environment
 Removal of stressors or triggers
 Education, communication and planning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Successful pharm treatment of AD =

A

short term improvement of symptoms and less decline in behavioral, functional and cognitive abilities over a longer period of time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

AD Pathophysiology

A

 Loss of cholinergic neurons esp muscarinic and nicotinic
 Loss of cholinergic activity correlates with severity of AD
• Up to 90% reduction in cholinergic markers (ACh)
 Loss of nicotinic receptors
• Presynaptic nicotinic receptors control the release of ACh and other NT important for memory and mood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Even though there is a loss of cholinergic transmission:

A

• Increasing cholinergic transmission does not improve memory because cell loss is caused by the disease and not what causes the disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Define M1

A

Excitatory on postsynaptic

Activation increases cognitive function!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Define M2

A

Inhibitory on presynaptic

Limits excess release of ACh

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

M1 and M2 in AD

A

M1 is preserved but M2 are reduced

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Nicotinic Receptors MOA

A

Enhance release of DA and NE which have cognition-enhancing properties

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Nicotinic Receptors in AD

A

Beta-amyloid bind them and reduce function and they indirectly cause damage through oxidative species (ROS)
So, they are reduced

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Muscarinic ACh receptors agonists Drugs

A

Arecoline and Xanomeline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Cholinesterase Inhibitors Drugs

A

Tacrine (Cognex)
Donepezil (Aricepf)
Rivastagmine (Exelon)
Galantamine (Razadyne)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Cholinesterase Inhibitor MOA

A

Prevent the hydrolysis of ACh, which increases the concentration of ACh in the synaptic cleft; BuChE also hydrolyzes ACh (increased in AD)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Cholinesterase Inhibitor Side Effects

A

GI disturbances
Muscle Cramps
Weird dreams

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Cholinesterase Inhibitor Things to Remember

A
  • Abrupt discontinuation should be avoided
  • Not with other anticholinergic agents
  • Only 1/3 of patients show clear improvement
  • Doses must be titrated in and out
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Advantages to Cholinesterase Inhibitor

A

More natural
Activate receptors all over the brain
Both muscarinic and nicotinic transmission is enhanced

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Disadvantags to Cholinesterase Inhibitor

A

Inactive in advanced AD

17
Q

Tacrine (Cognex)

A
  • Reversible, non-selective (AChE and BuChE)
  • Acts upon M1 and M2
  • WITHDRAWN
18
Q

Donepezil (Aricepf)

A
  • Specific and reversible inhibitor of AChE
  • Highly lipophilic
  • Well tolerated
  • Long half-life (3 days)
19
Q

Rivastigimine (Exelon)

A

• Inhibits BuChE and AChE
Pseudo-irreversible inhibitor (stays bound for a really long time)
Lots of GI side effects

20
Q

Galantamine (Razadyne)

A

• Reversible and selective AChE inhibitor(Enhances action of ACh on nicotinic receptors- allosteric modulator of nicotinic receptors but no difference in effectiveness)
Metabolized 3A4 and 2D6
Well tolerated

21
Q

BuCHE Inhibition in AD

A

 Neuronal AChE disappears during Alzheimer’s disease progression
 Inhibition of BuChE might be effective in late-stage Alzheimer’s disease

22
Q

NMDA Receptor Antagonists Drug

A

Memantine (Namenda)

23
Q

Normal MOA of NMDA Receptors

A

Glutamate major excitatory NT in the hippocampus and cortex
o Plays an essential role in learning and memory by triggering NMDA receptors to let a controlled amount of calcium into a nerve cell
o Excess glultamate overstimulates NMDA receptors leading to increased Intracellular Ca and free radicals → toxic
o Usually Mg blocks the receptor from excess Ca influx

24
Q

AD MOA of NMDA Receptors

A
  • There is increased Ca influx → progressive deficit in cognitive functions → leads to neuronal death
  • Blocking the NMDA receptor will decrease activity of glutamate in the synapse
25
Q

Memantine

A 
NaMenDA
•	Blocks glutamatergic NT by antagonizing NMDA receptor (more effective than Mg)
Urine excretion
60-80 hour half life
Wel tolerated
Monotherapy or combo with AChE inhibitor
26
Q

What is Namzaric?

A

Memantine ER + Donepezil

27
Q

Ginkgo Biloba MOA

A

o Increased blood flow by decreasing blood viscosity
o Inhibits MOA oxidase
o Anti-infective properties
o Prevents ROS damage

28
Q

Ginkgo Biloba Use and caution

A
  • May increase M receptors and serum levels of ACh and NA
  • CAUTION WITH ANTICOAGULANTS, ANTIPLATELETS, OR NSAIDS
  • Guidelines do NOT recommend use in AD
29
Q

Hyperzine A use in AD

A

• MOA: reversible AChE inhibitor
o Symptomatic treatment
• NOT with other AChE inhibitor
• Safety issue

30
Q

Vitamin E use in AD

A

• Antioxidant properties
• Adjunctive treatment
o Mixed evidenced
o Said to not benefit cognition (selegiline too)

31
Q

What should you monitor for brain vascular health?

A

High BP
High cholesterol
Glucose levels

32
Q

Lipid lower agents in AD

A
  • Only use if the pt has another reason for taking statins
  • There is some evidence showing a correlation between elevated mid-life cholesterol and AD
  • Mixed results
33
Q

Estrogen in AD

A
  • Promoting neuronal growth and preventing oxidative damage

* Post menopause = lower incidence of AD with estrogen replacement but also increase CV risk

34
Q

NSAIDs in AD

A
  • Long treatment (2 years) lowers the risk of AD maybe…?

* NSAIDs and prednisone are NOT recommended

35
Q

Antipsychotics in AD for non-cognitive symptoms

A
  • Adverse effects offset the usefulness

* Modest expectation of benefit

36
Q

Antidepressants in AD for non-cognitive symptoms

A
  • 50% of AD pts exhibit depression
  • SSRI (sertraline, citalopram, fluoxetine, paroxetine)
  • SNRI (venlafaxine)
  • NOT TCA’s
37
Q

What should never be used in AD

A

Benzodizepines

38
Q

Encenicline in AD

A

ACh co-agonist
MOA: Sensitizes alpha 8 nicotinic receptors and makes it possible for smaller amounts of naturally occurring ACh to activate the receptor
• MEMORY DEFICITS CAN BE MINIMIZED OR ENTIRELY REVERSED

Neuro Quiz 5 (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions