Cns Key Points

Front 1

The 3 Neurotransmitters of the PNS

Back 1

Acetylcholine, Norepinephrine, and Epinephrine

Front 2

Motor symptoms of Parkinson's Disease are mainly treated with drugs that activate ___________ receptors.

Back 2

Dopamine

Front 3

Motor symptoms of Parkinson's disease are treated with drugs that block ________________ receptors.

Back 3

Cholinergic

Front 4

Most effective treatment for motor symptoms of Parkinson's.

Back 4

Levodopa

Front 5

Enzyme that converts Levadopa to Dopamine

Back 5

decarboxylase

Front 6

These drugs block dopamine receptors in the striatum and can negate the effects of Levodopa

Back 6

First-generation antipsychotics

Front 7

These second-generation antipsychotics can be used to treat levodopa-induced psychosis

Back 7

Clozapine and Quetiapine

Front 8

Levodopa with an MAOI can result in

Back 8

hypertensive crisis

Front 9

What is the effect of taking levodopa with a high protein meal?

Back 9

Reduced therapeutic effects. Amino acids compete with levodopa for absorption from the intestine and transport across the BBB

Front 10

How does Carbidopa enhance the effects of Levodopa?

Back 10

It prevents the decarboxylation of levodopa in the intestine and peripheral tissues, and since it cannot cross the BBB, it does not prevent the conversion of levodopa to dopamine in the brain

Front 11

Can Carbidopa cross the blood-brain barrier?

Back 11

No. All of its actions take place in the intestine and peripheral tissues.

Front 12

Pramipexole is an oral ______________ agonist

Back 12

nonergot dopamine

Front 13

_________________ is a first-line drug for motor symptoms in Parkinson's disease and can be used for mono therapy early on.

Back 13

Pramipexole

Front 14

Mechanism by which dopamine agonists relieve motor symptoms of Parkinson's:

Back 14

They cause direct activation of dopamine receptors in the striatum

Front 15

Nausea, dyskinesia, postural hypotension, and hallucinations result from excessive activation of _____________ receptors.

Back 15

Dopamine

Front 16

Entacapone is a __________________________.

Back 16

COMT inhibitor

Front 17

This drug is combined with levodopa to inhibit metabolism by COMT in the intestine and peripheral tissue, thereby making more levodopa available to the brain.

Back 17

Entacapone

Front 18

MAO-B inhibitors that can enhance responses to levodopa (name 2)

Back 18

Selegiline and Rasagiline

Front 19

Which BRAIN enzyme inactivates dopamine?

Back 19

MAO-B

Front 20

Spherical, extracullar bodies that consist of a beta-amyloid core surrounded by remnants of axons and dendrites

Back 20

Neuritic plaques

Front 21

In patients with Alzheimer's ________________ is present in high levels and may contribute to neuronal injury.

Back 21

beta amyloid

Front 22

Neurofibrillary tangles result from production of a faulty form of this protein, that in healthy neurons serves to maintain the orderly arrangement of neurotubules

Back 22

tau

Front 23

Alzeheimer's dementia can be treated with _______________ or ____________________.

Back 23

cholinesterase inhibitors; memantadine (Namenda)

Front 24

Donepezil is an example of a

Back 24

cholinesterase inhibitor

Front 25

Cholinesterase inhibitors increase the availability of __________ at synapses?

Back 25

acetylcholine

Front 26

Peripheral cholinergic side effects include:

Back 26

nausea, vomiting, dyspepsia, diarrhea

Front 27

Cardiac cholinergic side effects include:

Back 27

bradycardia

Front 28

First generation antihistamines, tricyclic antidepressants, and conventional antipsychotics can reduce responses to these drugs:

Back 28

cholinesterase inhibitors

Front 29

Memantadine modulates the effects of glutamate at _____________ receptors.

Back 29

NMDA

Front 30

The only drug approved for severe Alzheimer's Disease

Back 30

Memantadine

Front 31

Significant side effects of Memantadine

Back 31

no clinically significant adverse effects

Front 32

In this type of seizure, excitation undergoes limited spread from the focus to adjacent cortical areas

Back 32

partial

Front 33

In this type of seizure excitation spreads widely throughout both hemispheres of the brain

Back 33

generalized

Front 34

Phenytoin is active against ___________ and ___________ seizures but not ___________ seizures.

Back 34

tonic-clonic;partial;absence

Front 35

therapeutic phenytoin range

Back 35

10-20 mcg/mL

Front 36

If phenytoin levels rise above _______ mcg/mL, CNS toxicity develops

Back 36

20

Front 37

Phenytoin toxicity signs:

Back 37

nystagmus, sedation, ataxia, diplopia, cognitive impairment

Front 38

Gingival hyperplasia is caused in 20 percent of patients on this drug

Back 38

phenytoin

Front 39

Carbamezapine is active against ____________ and _________ seizures.

Back 39

partial;tonic-clonic

Front 40

Often the preferred seizure drug

Back 40

Carbamezapine

Front 41

When initiating carbamezapine and periodically, this should be checked.

Back 41

CBC (can cause leukopenia, anemia, and thrombocytopenia; and RARELY, fatal aplastic anemia)

Front 42

Seizure drug that can sometimes cause hematologic toxicity

Back 42

Carbamezapine

Front 43

This drug has activity against all types of seizures

Back 43

Valproate

Front 44

In children under 2 taking valproic acid, especially when taking other AEDs, this is a risk

Back 44

Fatal liver injury

Front 45

This AED can cause potentially fatal pancreatitis

Back 45

Valproate

Front 46

Phenobarbitol is sometimes used for seizures in contrast other barbiturates because

Back 46

it does not cause generalized CNS depression at these doses

Front 47

These three AEDs INDUCE the synthesis of hepatic drug-metabolizing enzymes and accelerate inactivation of other drugs (oral contraceptives;warfarin)

Back 47

Phenytoin, carbamezapine, phenobarbitol

Front 48

What is the deal with AEDs and pregnancy

Back 48

All are potentially dangerous, but not as dangerous as having seizures during pregnancy

Front 49

How to minimize fetal risk while taking AEDs?

Back 49

AVOID VALPROATE; use just one AED if possible at lowest effective dose

Front 50

We know initial treatment of status epilepticus is with a benzodiazapine, but follow-up treatment usually consists of:

Back 50

phenytoin or fosphenytoin

Front 51

3 drugs used for spasticity:

Back 51

Baclofen, diazepam, and dantrolene

Front 52

These two muscle relaxants relieve spasticity by mimicking the inhibitory actions of GABA in the CNS

Back 52

Baclofen and diazepam

Front 53

This drug acts directly on muscle to promote relaxation

Back 53

Dantrolene

Front 54

Abrupt discontinuation of intrathecal baclofen can lead to ________________, organ failure, and fatality.

Back 54

rhabdomyolysis

Front 55

Prolonged use of dantrolene can cause

Back 55

liver damage (monitor LFTs and minimize dose)

Front 56

This CNS muscle relaxant can be used to treat malignant hyperthermia

Back 56

dantrolene

Front 57

First-generation antipsychotics carry a higher risk than second-generation for

Back 57

EPS

Front 58

Second-generation antipsychotics carry a higher risk than first-generation for

Back 58

metabolic effects

Front 59

Thought to relieve symptoms of schizophrenia by causing strong blockade of D2 receptors:

Back 59

First-generation antipsychotics

Front 60

Thought to relieve the symptoms of schizophrenia by causing moderate blockade of D2 receptors and strong blockade of 5-HT3 receptors

Back 60

Second-generation antipsychotics

Front 61

Anticholinergic drugs are effective against these particular extrapyramidal side effects

Back 61

acute dystonia; parkinsonism {akathisia is harder to treat but may respond to anticholinergics, beta blockers, or benzodiazapines)

Front 62

Although there really is no treatment for tardive dyskinesia, this could POSSIBLY help:

Back 62

switching to a second-generation antipsychotic

Front 63

Is the risk of EPS higher with high or low potency first-generation antipsychotics?

Back 63

high-potency

Front 64

Of the first-generation antipsychotics, do high or low potency have a greater risk of tardive dyskinesia?

Back 64

equal with both groups

Front 65

The risk of sedation, orthostatic hypotension, and anticholinergic effects is greater with ________ potency FGAs.

Back 65

low

Front 66

If a person on a FGA is experiencing muscle rigidity, high fever, and autonomic instability, they could be experiencing this potentially fatal adverse effect.

Back 66

neuroleptic malignant syndrome

Front 67

These two drugs are used to treat neuroleptic malignant syndrom

Back 67

dantrolene and bromocriptine

Front 68

How do antipsychotics affect circulating levels of prolactin?

Back 68

They increase it by blocking the inhibitory actions of dopamine on prolactin release

Front 69

This drug can counteract the beneficial effects of FGA drugs and vice versa (dopamine receptors)

Back 69

levodopa (levodopa activates them, FGAs block them)

Front 70

Haldol is a ________________.

Back 70

high-potency FGA

Front 71

These two SGAs carry the greatest risk of metabolic effects

Back 71

Clozapine and Olanzapine

Front 72

This is the most effective antipsychotic drug available.

Back 72

Clozapine ( second-generation antipsychotic)

Front 73

The major adverse effect of Clozapine

Back 73

agranulocytosis

Front 74

In general, antidepressant therapy should continue for how long after symptoms resolve?

Back 74

4 to 9 months

Front 75

Agitation, confusion, hallucinations, hyperreflexia, tremor, and fever are a sign of:

Back 75

serotonin syndrome

Front 76

TCAs block reuptake of:

Back 76

NE and 5-HT

Front 77

Most common side effects of TCAs

Back 77

sedations, orthostatic hypotension, anticholinergic effects

Front 78

Most serious adverse effect of TCAs

Back 78

cardiotoxicity

Front 79

TCAs and MAOIs taken concurrently can cause:

Back 79

a hypertensive crisis

Front 80

How do TCAs affect responses to direct-acting sympathomimetics (e.g. epinephrine)?

Back 80

They intensify response

Front 81

How do TCAs affect responses to indirect-acting sympathomimetics (eg, amphetamine)

Back 81

diminish response

Front 82

With antidepressants, it's not the inhibition or accumulation of MAOs that causes the antidepressant effect, but:

Back 82

the adaptive cellular responses that relieve depression

Front 83

What do MAOIs do?

Back 83

Increase neuronal stores of NE and 5-HT and intensity transmission at noradrenergic and serotonergic synapses

Front 84

main neurotransmitters MAOIs and TCAs work on

Back 84

NE and serotonin (5-HT)

Front 85

MAOIs are first-line drugs for this condition ONLY

Back 85

atypical depression

Front 86

This class of antidepressants does NOT cause direct CNS stimulation

Back 86

TCAs (SSRIs and MAOIs do cause direct CNS stimulation)

Front 87

_________ and ___________ cause orthostatic hypotension.

Back 87

TCAs and MAOIs

Front 88

If a patient taking an MAOI is admitted with a hypertensive crisis, treatment is:

Back 88

an IV vasodilator (nitroprusside, labetalol, phentolamine) or sublingual nifedepine

Front 89

MAOIs and ___________-acting sympathomimetics can result in hypertensive crisis

Back 89

indirect (amphetaine, cocaine)

Front 90

MAOIs plus SSRIs could equal

Back 90

serotonin syndrome

Front 91

The three types of drugs used to treat bipolar disorder:

Back 91

mood stabilizers, antipsychotics, antidepressants

Front 92

Lithium trough levels should be less than :

Back 92

1.5 mEq/L

Front 93

When should lithium level be measured?

Back 93

12 hours after evening dose

Front 94

common side effects of lithium at therapeutic doses:

Back 94

tremor, goiter, polyuria

Front 95

Reduction in sodium levels will_________ lithium excretion.

Back 95

reduce (causing lithium to accumulate, possibly to toxic levels) Maintain normal sodium intake levels.

Front 96

Lithium levels can be increased by _________ and ___________.

Back 96

diuretics (thiazides, especially) and NSAIDs

Front 97

Barbiturates often _____________ hepatic drug-metabolizing enzymes, and benzodiazapenes do not.

Back 97

induce

Front 98

Selection of a particular benzodiazapene relies heavily on a preference for

Back 98

time-course

Front 99

This drug can be used to treat benzodiazapene overdose

Back 99

Flumazenil (benzodiazapene receptor antagonist)

Front 100

Benzodiazapines, Buspar, and these four antidepressants are first-line drugs for generalized anxiety disorder

Back 100

Venlafaxine, Paroxetine, Escitalopram, Duloxetine

Front 101

Buspirinone levels can be increased by:

Back 101

erythromycin, ketoconazole, and grapefruit juice

Front 102

The best treatment for PTSD

Back 102

exposure therapy

Front 103

These drugs are approved for PTSD, although there isn't proof that drugs are particularly effective:

Back 103

Paroxetine and Sertraline

Front 104

Amphetamines work primarily by promoting neuronal release of ______ and ________, and partly by blocking their reuptake.

Back 104

NE and dopamine

Front 105

How do amphetamines cause vasoconstriction and cardiac effects (increased heart rate, increased AV conduction, increased contractility)?

Back 105

by promoting release of norepinephrine from peripheral neurons

Front 106

These are the only three non-stimulants approved for ADHD:

Back 106

atomoxetine, guanfacine, and clonidine

Front 107

Caffeine is a

Back 107

methylxanthine

Front 108

Caffeine and other drugs in its class act primarily by

Back 108

blocking adenosine receptors

Front 109

Two principal uses of caffeine:

Back 109

treatment of apnea in premature infants and reversal of drowsiness