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

Caldwell and Randolph - (all) Flashcards

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?

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?

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?

A

no rebound insomnia or withdrawal symptoms

24
Q

Describe the 2 components of Sinemet and their functions?

A
  • L-dopa + carbidopa
25
Q

Give 1 reason daily doses of L-dopa are decreased over time?

A

More gets to brain and decrease negative cardiovascular symptoms

26
Q

Explain the “on-off phenomenon” and give 1 treatment for it?

A
  • “off” periods marked by akinesia which alternate with “on” periods improved mobility but marked dyskinesia. Off periods are treated with apomorphine (subQ)
27
Q

Give 2 reasons COMT inhibitors entacapone and tolcapone improve
responsiveness to L-dopa?

A
  • decreases metabolism of L-dopa in the periphery and decreases competitive 3-O-methyldopa
28
Q

Give the 3 components of Stalevo?

A
  • L-dopa + carbidopa + entacapone
29
Q

Give 2 advantages of DA agonists over L-dopa?

A

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
Q

Give 2 indications for pramipexole

A
  • monotherapy for mild Parkinsons, or adjunctive therapy for advanced PD.
31
Q

Give the specific indication for apomorphine?

A

-Temporary relief of off-periods of akinesia in patients on dopamine therapy.

32
Q

Give the symptoms of PD that improve with treatment with Ach blockers

A
  • Improvement of tremor and rigidity ( little effect on bradykinesia)
33
Q

Give the class of drugs given for postural tremor and one in this class not to give?

A
  • Beta blockers can be given for postural tremor but not metoprolol ( cause it’s a beta blocker)
34
Q

Give 4 drugs to be given for essential tremor?

A
  • B-blockers (propranolol), Antiepiletics ( primidone, topiramate), Alprazolam.
35
Q

Give 3 drugs used to treat Huntington’s Disease?

A
  • Dopamine receptor antagonists ( perphenazine and haloperidol), reserpine, tetrabenzine.
36
Q

Give the MOA of tetrabenzaine and an advantage it has over reserpine?

A
  • inhibits vesicular monoamine transporter 2 (depletes central monoamines) – fewer adverse effects compared to reserpine.
37
Q

Give one drug approved for ALS?

A
  • Riluzole
38
Q

Explain the inherent difficulty in treating tardive dyskinesia?

A
  • Drug should be tapered off, reducing the dopamine receptor blocker often worsens the dyskinesia.
39
Q

Give one drug used to treat restless leg syndrome?

A
  • ropinirole
40
Q

What is ethosuximide used for?

A

First line therapy in uncomplicated absence seizures. No use in focal or secondarily generalized seizures.

41
Q

What should you expect with any drug that effects the CNS?

A

Behavior adverse effects

42
Q

What is Felbamate used to treat?
What is an major freaking adverse effect?
What is a good alternative

A
  • Treats refractory epilepsy.
  • Aplastic anemia - failure to make all cells ( will have thrombocytopenia, leukopenia, and anemia)
  • Rufinamide
43
Q

When ethosuximide is ineffective for absence seizures what is the next alternative?

A
  • Valproic acid
44
Q

When phenytoin or carbmazepine is not working for focal seizures what is the next alternative?

A
  • Valproic acid
45
Q

Pregabalin-

A

more potent than gabapentin and metabolized by the kidneys

46
Q

What is benzodiazepines MOA?

A

increase the affinity of GABA for GABAa receptors thereby increasing CL- influx causing hyperpolarization and suppresses seizure.

47
Q

What are some benzos and what are they used for?

A

Diazepman, Lorazepam, and midazolam; used for focal and tonic-clonic seizures

48
Q

In the order of choice what is Benzodiazepine for absence seizures?

A
  • 4th
49
Q

What really negative AE is valproic acid associated with?

A
  • Spina bifida
50
Q

What are drugs that inhibit the T-type Calcium channels specifically used to treat?

A
  • absence seizures
51
Q

Compare phenobarbital to benzos?

A
  • 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
Q

What are the prime targets for amphetamines?

A

Locus ceruleus (pons) and NAc

Clinical Neuro General (3 decks)

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