OHIA AD and PD Flashcards

1
Q

TorF: Carbidopa is an inhibitor of AADC

A

True

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

Carbidopa effectively prevents the conversion of levodopa to

DA in the __________ and __________ leading to an increased availability of this drug in the CNS.

A

Carbidopa effectively prevents the conversion of levodopa to
DA in the GASTROINTESTINAL TRACT and PERIPHERAL TISSUES leading to
an increased availability of this drug in the CNS.

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

What is the MOA of DA precursors?

A

-Restores dopaminergic transmission in the striatum by enhancing the synthesis of DA in the surviving neurons of the substantia nigra
pars compacta

-Decreases the rigidity, tremors and other symptoms of PD

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

Levodopa/carbidopa can be used in the tx of:

A

motor fluctuations in advanced Parkinson’s disease

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

These compounds enhance dopaminergic neurotransmission by

activating postsynaptic DA receptors:

A

Drugs in this class includes ropinirole and pramipexol.

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

TorF: DA receptor agonists have a shorter half life compared to LDOPA

A

False. They have longer durations of action than levodopa (8-24 h v. 6-8h)
and therefore, have been effective in patients exhibiting fluctuations
in their response to levodopa.

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

TorF: DA receptor agonists are peptide molecules that compete with LDOPA to cross the BBB

A

False. These drugs are non-peptide molecules, they do not compete with levodopa for transport across the blood-brain barrier.

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

TorF: DARA require enzymatic conversion by AADC and, therefore, can be effective late in the course of PD.

A

False: These drugs do not require enzymatic conversion by AADC
and, therefore, can be effective late in the course of PD.

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

TorF: DARA is associated with less risk of developing dyskinesia and motor fluctuations when compared
to patients started with levodopa therapy.

A

True

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

DARA can be used in the tx of:

A

Idiopathic PD and Restless Legs Syndrome.

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

this class include selegiline, rasagiline

A

INHIBITORS OF DA METABOLISM

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

TorF: Rasagiline is metabolized to methamphetamine and

amphetamine

A

False. Selegiline is metabolized to methamphetamine and

amphetamine. Rasagiline does not form such toxic metabolites.

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

TorF: Both selegiline and rasagiline can improve motor function in PD when used alone and both can potentiate the effectiveness of levodopa therapy

A

True

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

Selegiline and rasagiline are used:

A

as adjunct to levodopa/carbidopa in Parkinsonism.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Tolcapone and Entacapone ________ the peripheral metabolism of levodopa, thereby increasing central uptake and brain concentrations of DA.

A

They DECREASE METABOLISM of levodopa, thereby

INCREASING UPTAKE and brain concentrations of DA.

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

_____________ can cross the blood-brain barrier and inhibit COMT in the
brain

A

Tolcapone can cross the blood-brain barrier and inhibit COMT in the
brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

TorF: Entacapone is only distributed into peripheral tissues.

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

TOLCAPONE and ENTACAPONE is used in the tx of:

A

Adjunct to levodopa/carbidopa in idiopathic Parkinsonism

especially in patients who have symptom fluctuations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

ANTIMUSCARINIC AGENTS incl

A

Drugs in this class includes BENZTROPINE and TRIHEXIPHENIDYL.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

BENZTROPINE and TRIHEXIPHENIDYL block __________ receptors and reduce cholinergic tone in the CNS.

A

BLOCK MUSCARINIC RECEPTORS and REDUCE CHOLINERGIC TONE in the CNS.

These drugs are presumed to act by modifying the activity of striatal cholinergic interneurons that regulate the interactions of neurons of the direct and indirect pathways.

21
Q

TorF: BENZTROPINE and TRIHEXIPHENIDYL reduce tremor more than bradykinesia.

A

True

22
Q

How are benzotrpine and trihexiphenidyl used?

A

Adjunct in Parkinsonism

Drug-induced extrapyramidal disorders.

23
Q

An antiviral agent used in the prophylaxis and treatment of influenza.
Has an anti-Parkinson’s disease action.

A

AMANTADINE

24
Q

What are the effects of AMANTADINE on neurotransmitters?

A
  • Increases the release of DA
  • Blocks cholinergic receptors

-Blocks NMDA glutamate receptors (major pathway involved in
PD)

25
Q

TorF: Amantadine has little or no effect on tremor but is effective against
rigidity and bradykinesia

A

True

26
Q

Alzheimer’s disease (AD) refers to dementia that does
not have antecedent causes such as stroke, brain trauma
or alcohol.

A

Typically, dementia begins after age 60 with prevalence:

  • doubling approximately every 5 years thereafter
  • in persons aged 85 or older, around 50% have this disease.
27
Q

Two microscopic features are characteristic of AD:

A

-EXTRACELLULAR AMYLOID PLAQUES, consisting of amorphous extracellular
deposits of β-amyloid protein (known as Aβ).

-INTRANEURONAL NEUROFIBRILLARY TANGLES, comprising filaments of a
phosphorylated form of a microtubule-associated protein (Tau).

28
Q

Aβ accumulation is an upstream event that triggers tau pathology resulting in:

A

Aβ accumulation is an upstream event that triggers tau pathology resulting in impaired neuronal function and cell loss.

29
Q

The most prominent feature of AD is:

A

deficiency of acetylcholine

30
Q

Anatomical basis of ACh deficit is due to:

A

-Atrophy and degeneration of subcortical cholinergic neurons
especially those in the nucleus basalis of Meynert NBM).

-NBM is a pivotal cholinergic relay system projecting widespread innervation to the cortex and medial temporal lobe structures.

31
Q

TorF: donepezil is an irreversible inhibitor of acetylcholinesterase (AChE) with preference for the enzyme located in the brain.

A

False. It Is a REVERSIBLE inhibitor of acetylcholinesterase (AChE) with
preference for the enzyme located in the brain.

32
Q

Donepezil drug intx:

A

Antagonizes anticholinergics.

May potentiate succinylcholine-type muscle relaxants, cholinergic agonists.

Concomitant NSAIDs may increase risk of GI bleeds.

33
Q

Rivastigamine inhibits:

A

reversible inhibitor of AChE.

Also inhibits butyrylcholinesterase (serum and hepatic
cholinesterase that is upregulated in AD brain).

Active orally or transdermally.

34
Q

Rivastigamine intx:

A

Antagonizes anticholinergics

 May potentiate succinylcholine-type muscle relaxants

 Concomitant metoclopramide, beta-blockers not recommended

35
Q

Rivastigamine uses:

A

Mild to moderate dementia for AD

Mild to moderate dementia associated with Parkinsonism

36
Q

What class of medication is Galantamine apart of:

A

CHOLINESTERASE INHIBITORS

37
Q

Galantamine intx:

A

Potentiates neuromuscular blockers, cholinesterase inhibitors, cholinergic agonists.

Antagonizes anticholinergics

May be potentiated by substrates for CYPs (ketoconazole, paroxetine, cimetidine.)

38
Q

Memantine drug class:

A

NMDA RECEPTOR ANTAGONIST

39
Q

TorF: memantine is a competitive NMDA-type glutamate receptor antagonist

A

False. a noncompetitive of the NMDA-type glutamate receptor.

40
Q

Memantine interacts with the _______ binding site of the channel to prevent its excessive activation

A

Interacts with the Mg2+ binding site of the channel to prevent its
excessive activation.

41
Q

Memantine MOA:

A

noncompetitive of the NMDA-type glutamate receptor.

Interacts with the Mg2+ binding site of the channel to prevent its
excessive activation.

Reduces the rate of clinical deterioration in patients with moderate
to severe AD.

42
Q

TorF: Urinary disorders is a SE of memantine

A

True

43
Q

Memantine drug intx:

A

Drug Interactions:

Caution with other NMDA antagonists (e.g., amantadine,
ketamine)

May affect renally-excreted drugs (e.g., triamterene, cimetidine,
metformin, nicotine, ranitidine)

Plasma levels may be increased by urinary alkalinizers.

44
Q

Parkinson’s disease (PD) is a progressive neurological disorder of muscle movement characterized by

A

Bradykinesia (slowness and poverty of movement)

Muscular rigidity

Resting tremor (which usually abates during voluntary movement)

An impairment of postural balance leading to disturbances of gait and to falling.

45
Q

Nonmotor manifestation of PD include:

A

depression,anxiety, psychosis, cognitive changes, fatigue, sleep disorders and autonomic disorders.

46
Q

TorF: Dementia or mild cognitive impairment will eventually develop in most patients.

A

True

47
Q

PD has been correlated with the destruction of ______ neurons in the ___________ that provides innervation to the striatum (caudate and putamen)

A

PD has been correlated with the destruction of DA neurons in the
SUBSTANTIA NIGRA PARS COMPACTA that provides innervation to the
striatum (caudate and putamen), parts of the basal ganglia
system involved in motor control.

48
Q

Indirect pathway:

A

PUTAMEN—>GPe—>STN—>GPi—>THALAMUS—>cortex

The net effect of stimulating the indirect pathway at the level of the
striatum is to reduce the excitatory outflow from the thalamus to the cerebral cortex.

49
Q

Direct pathway:

A

Signals from putamen to GPi to thalamus and then to cortex

The net effect of stimulation of the direct pathway at the level of the
striatum is to increase the excitatory outflow from the thalamus to
the cortex.