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Clinical Neuro General > Caldwell and Randolph - (all) > Flashcards

Caldwell and Randolph - (all) Flashcards

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1
Q

Explain why acyclovir is more selectively toxic than other antivirals.

A

-Because it only works on virally-infected cells since it must be phosphorylated to active form by VIRAL enzymes, that is they were made by the virus

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2
Q

List three viruses that acyclovir can be used against.

A

HSV-1, HSV-2, VZV, EBV

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3
Q

List two indications for valacyclovir

A

Recurrent HSV or VZV

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4
Q

List three indications for famciclovir

A

Acute HSV genital or VZV

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5
Q

Apply the early symptoms and DOV for herpes encephalitis to a clinically-relevant case scenario?

A

Acyclovir is DOC, will have seizures, disorientation, etc.

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6
Q

Explain how ganciclovir is metablized to an active form inside host cells?

A

Ganciclovir is phosphorylated by CMV kinases from guanosine to guanine.

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7
Q

Explain how cidofovir has selective toxicity?

A

Not as much as others because is activated in normal cells but 1000x more effective against viral polymerases than host.

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8
Q

Explain what is unique about the metabolism requirement of foscarnet?

A

It is an inorganic pyrophosphate compound not a nucleoside like others, but it inhibits viral DNA and RNA polymerases

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9
Q

List 4 viuses attacked by foscarnet

A

EBV, HSV, HBV, VZV

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10
Q

Give the CDC guideline treatments for influenza in adults?

A

Figure it the hell out!

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11
Q

Explain the MOA of neuraminidase inhibitors?

A

MOA: inhibitr viral cleavage of sialic acid, inhibit the release of newly formed viruses.

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12
Q

Explain the site of action for palivizumab?

A
  • the fusion (F) protein of RSV
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13
Q

. Expain the dosing and timing of palivizumab treatment for RSV?

A

15 mg/lg IM monthly x up to 5 doses during RSV season with 1st dose given just prior to RSV season.

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14
Q

Explain who should avoid contact with people receiving ribavirin and why?

A

Pregnant or planning to get pregnant because it’s a teratogenic.

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15
Q

Discuss the receptor site of action for barbiturates (how differ from BZs)

A

They are agonists at the GABA receptors so they act Like GABA, whereas benzo’s bind and increase the ability for GABA to bind

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16
Q

Apply the indication for phenobarbital and secobarbital to a clinically-relevant case scenario?

A

Phenobarbital is used for pre-op sedation for adults; secobarbital for short term insomnia.

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17
Q

Describe BZ withdrawal and give symptoms?

A

Restlessness, anxiety, weakness, and generalized seizures

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18
Q

Describe the general receptor type upon which zolpidem and zaleplon act?

A

GABAa

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19
Q

Describe the particular MOA for propofol?

A

Like alcohol it stimulates the release of GABA, increase GABA production.

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20
Q

Apply the population in which etomidate is useful to a clinically- relevant case scenario?

A

Good for people with low cardiovascular reserve b/c does not drop blood pressure.

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21
Q

Apple one advantage and one disadvantage in the use of buspirone for persistent anxiety to a clinically- relevant case scenario?

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A

Can be used for long term anxiety, and not cross-tolerant with many BZ so will need to taper off (also inhibit 5HT release)

22
Q

Apply switching a patient from a BZ to a Buspirone to a clinically-relevant case scenario?

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A

If on a BZ then need to taper them off ( can’t just switch from benzos to buspirone because will have withdrawal symptoms)

23
Q

Give 2 advantages to use of ramelteon as a hypnotic agent?

Study These Flashcards
A

no rebound insomnia or withdrawal symptoms

24
Q

Describe the 2 components of Sinemet and their functions?

Study These Flashcards
A
  • L-dopa + carbidopa
25
Give 1 reason daily doses of L-dopa are decreased over time?
More gets to brain and decrease negative cardiovascular symptoms
26
Explain the “on-off phenomenon” and give 1 treatment for it?
- “off” periods marked by akinesia which alternate with “on” periods improved mobility but marked dyskinesia. Off periods are treated with apomorphine (subQ)
27
Give 2 reasons COMT inhibitors entacapone and tolcapone improve responsiveness to L-dopa?
- decreases metabolism of L-dopa in the periphery and decreases competitive 3-O-methyldopa
28
Give the 3 components of Stalevo?
- L-dopa + carbidopa + entacapone
29
Give 2 advantages of DA agonists over L-dopa?
Advanced parkinson’s DA agonists smooth out fluctuations, and may reduce AFFECTive symptoms of PD, specific for D3. Used over L-dopa when L-dopa produces end of dose akinesia, “on-off” phenomenon, or lack of response to L-dopa
30
Give 2 indications for pramipexole
- monotherapy for mild Parkinsons, or adjunctive therapy for advanced PD.
31
Give the specific indication for apomorphine?
-Temporary relief of off-periods of akinesia in patients on dopamine therapy.
32
Give the symptoms of PD that improve with treatment with Ach blockers
- Improvement of tremor and rigidity ( little effect on bradykinesia)
33
Give the class of drugs given for postural tremor and one in this class not to give?
- Beta blockers can be given for postural tremor but not metoprolol ( cause it’s a beta blocker)
34
Give 4 drugs to be given for essential tremor?
- B-blockers (propranolol), Antiepiletics ( primidone, topiramate), Alprazolam.
35
Give 3 drugs used to treat Huntington’s Disease?
- Dopamine receptor antagonists ( perphenazine and haloperidol), reserpine, tetrabenzine.
36
Give the MOA of tetrabenzaine and an advantage it has over reserpine?
- inhibits vesicular monoamine transporter 2 (depletes central monoamines) – fewer adverse effects compared to reserpine.
37
Give one drug approved for ALS?
- Riluzole
38
Explain the inherent difficulty in treating tardive dyskinesia?
- Drug should be tapered off, reducing the dopamine receptor blocker often worsens the dyskinesia.
39
Give one drug used to treat restless leg syndrome?
- ropinirole
40
What is ethosuximide used for?
First line therapy in uncomplicated absence seizures. No use in focal or secondarily generalized seizures.
41
What should you expect with any drug that effects the CNS?
Behavior adverse effects
42
What is Felbamate used to treat? What is an major freaking adverse effect? What is a good alternative
- Treats refractory epilepsy. - Aplastic anemia - failure to make all cells ( will have thrombocytopenia, leukopenia, and anemia) - Rufinamide
43
When ethosuximide is ineffective for absence seizures what is the next alternative?
- Valproic acid
44
When phenytoin or carbmazepine is not working for focal seizures what is the next alternative?
- Valproic acid
45
Pregabalin-
more potent than gabapentin and metabolized by the kidneys
46
What is benzodiazepines MOA?
increase the affinity of GABA for GABAa receptors thereby increasing CL- influx causing hyperpolarization and suppresses seizure.
47
What are some benzos and what are they used for?
Diazepman, Lorazepam, and midazolam; used for focal and tonic-clonic seizures
48
In the order of choice what is Benzodiazepine for absence seizures?
- 4th
49
What really negative AE is valproic acid associated with?
- Spina bifida
50
What are drugs that inhibit the T-type Calcium channels specifically used to treat?
- absence seizures
51
Compare phenobarbital to benzos?
- Phenobarbital (binds to an allosteric site on GABAa) less specific in nature and weak agonist activity increases potential for significant side effects as compared to benzos.
52
What are the prime targets for amphetamines?
Locus ceruleus (pons) and NAc

Clinical Neuro General (3 decks)

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