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Neuro Drugs Flashcards

1
Q 
Acyclovir, famciclovir, valacyclovir
Mechanism?
Clinical use?
Toxicity?
Mechanism of reistance?
A

Monophorphorylated by HSV/VZV thymidine kinase and not phosphorylated in uninfected cells–>few adverse effects. Guanosine analog. Triphosphate formed by cellular enzymes. Preferentially inhibits viral DNA polymerase by chain termination

HSV and VZV. Weak against EBV. No activity for CMV. USed for HSV-induced encephalitis and genital lesions. Prophylaxis in immunocompromised. No effect on latent forms.

Obstructive crystalline nephropathy and acute renal failure if not adequately hydrated

Mutated viral thymidine kinase.

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2
Q

Chromotolysis

A

Process involving the cell body following axonal injury. Changes reflect increase protein synthesis (from repair of synaptic proteins to repair of structural proteins) in effort to repair the damaged axon. 3 characteristics:

1) round cellular swelling
2) displacement of nucleus to the periphery
3) disperson of nissl substance throughout cytoplasm

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3
Q

Lipofuscin

A

yellow-brown “wear and tear” pigment associated with normal aging and found in diffferent organs as deposits

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4
Q

Neurotransmitter changes with disease

1) alzheimers
2) anxiety
3) depression
4) huntington disease
5) parkinson disease
6) schizophrenia

A

1) Decreased ACh
2) Increased NE, Decreased GABA, Decreased 5-HT
3) Decreased NE, Decreased dopamine, decreased 5-HT
4) Decreased ACh, Decreased glutamate, Increased dopamine
5) Decreased dopamine, Increased 5-HT, Increased ACh
6) Increased dopamine

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5
Q

When is B6 used as a co-factor for decarboxylation when forming neurotransmitters?

A

Tryptophan–>serotonin
Phenylalanine–>Dopa–>Dopamine–>NE–>Epi
Glutamate–>GABA

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6
Q

Wernicke Korsakoff syndrome?

A

confusion, ophthalmoplegia, ataxia (classic triad)+confabulation, personality change, memory loss (permanent). Damage to medial dorsal nucleus of thalamus

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7
Q

What does hemicholinum do?

A

Blocks reuptake of choline into axon

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8
Q

What does alpha bungarotoxin (venom from snake) do?

A

Blocks postsynaptic ACh receptor and prevents ACh binding

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9
Q

Neostigmine
Type of Drug
MOA
Clinical applications

A

Anticholinesterase
Increase endogenous ACh (no CNS penetration)
Posoperative and neurogenic ileus and urinary retention, myasthenia gravis, reversal of neuromuscular junction blockade (postoperative)

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10
Q

Pyridostigmine
Type of Drug
MOA
Clinical applications

A

Anticholinsterase

Increase endogenous ACh; increased strength. Pyridostigmine gets rid of myasthenia gravis

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11
Q

Physostigmine
Type of Drug
MOA
Clinical applications

A 
Anticholinesterase 
Increase endogenous ACh. Physostigmine "phxes" atropine overdose.
Anticholinergic toxicity (crosses BBB-->CNS)
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12
Q

Endrophonium
Type of Drug
MOA
Clinical Applications

A

Anticholinesterase
Increase endogenous ACh
Used in the tensilon test for diagnosis of myasthenia gravis (extremely short acting). Myasthenia now diagnosed by anti-AChR ab (anti-acetylcholine receptor antibody) test.

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13
Q

What are signs of organophosphate poisoning
What do organophosphates do?
How do you treat this poisoning?

A
  • DUMBELSS (Diarrhea, Urination, miosis, bronchospasm, bradycardia, excitation of skeletal msucle and CNS, lacrimation, sweating, and salivation)
  • Irreversibly inhibit AChe
  • Atropine (competitive inhibitor) + pralidoxime (regenerates AChE if given early
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14
Q

Phenobarbital, pentobarbital, thiopental, secobarbital
MOA
Clinical Use
Toxicity

A
  • Facilitate GABAA action by increasing duration of Cl− channel opening, thus decreasing neuron firing (barbidurates increase duration). Contraindicated in porphyria.
  • Sedative for anxiety, seizures, insomnia, induction of anesthesia (thiopental).
  • Respiratory and cardiovascular depression (can be fatal); CNS depression (can be exacerbated by EtOH use); dependence; drug interactions (induces cytochrome P-450). Overdose treatment is supportive (assist respiration and maintain BP).
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15
Q

Diazepam, lorazepam, triazolam, temazepam, oxazepam, midazolam, chlordiazepoxide, alprazolam.
MOA
Clinical Use
Toxicity

A

-Facilitate GABAA action by increasing frequency of
Cl− channel opening. decreasing REM sleep. Most have long half-lives and active metabolites (exceptions: triazolam, oxazepam, and midazolam are short acting–>higher addictive potential).
-Anxiety, spasticity, status epilepticus (lorazepam and diazepam), detoxification (especially alcohol withdrawal–DTs), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia).
-Dependence, additive CNS depression effects with alcohol. Less risk of respiratory depression and coma than with barbiturates.
Treat overdose with flumazenil (competitive antagonist at GABA benzodiazepine receptor).

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16
Q

MAC (minimal alveolar concentration required to prevent 50% of subjectes from moving in response to noxious stimulus) of inhaled anesthetic is proportional or inversely proportional to potency

A

Inversely proportional–> lower MAC means more potent

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17
Q

decreased solubility in blood of drug is more likely to have higher or lower induction and recovery times?

A

higher (more rapid) induction times

18
Q

Increased solubility in lipids of drugs is proportional or inversely proportional to potentcy

A

Proportional

19
Q

increase sol in lipids=increased potency=1/MAC

A

Equation for anesthetics

20
Q

Thiopentol
Class
Use
MOA

A
  • Barbiturates
  • Induction of anesthesia and short surgical procedures
  • high potency, high lipid solubility, rapid entry into brain, ultra short acting barbiturate
  • Effect terminated by rapid redistribution into tissue (i.e. skeletal muscle) and fat.
  • Decreases cerebral blood flow
21
Q 
Midazolam
Class
Use
Side effects
MOA
A
  • Benzodiazepines
  • Most common drug used for endoscopy; used adjunctively with gaseous anesthetics and narcotics.
  • May cause severe postoperative respiratory depression. Decreases BP (treat overdose with flumazenil), and anterograde amnesia
22
Q

Flumazenil
Class
Use

A

GABAa receptor antagonist

Reverse coma, used in hepatic encephalopathy/alcohol-induced coma

23
Q

Ketamine
Class
Use
Side effects

A
  • PCP analog
  • Act as dissociative anesthetics. Block NMDA receptors. CV stimulants.
  • Cause disorientation, hallucination, and bad dreams. increase cerebral blood flow
24
Q

What is unique about ketamine in terms of cerebral metabolic rate and cerebral blood flow?

A

All IV anesthetics except ketamine decrease cerebral metabolic rate and decrease cerebral blood flow. Ketamine increases cerebral blood flow.

25
Morphine and fentanyl are used with other CNS depressants during general anesthesia. What class do they come from?
Opoids
26
Propofol Class Use Side effects
GABAa potentiator Sedation in ICU (most popular i.v. anesthetic), rapid anesthesia induction, short procedures Causes hypotension
27
Halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, nitrous oxide MOA Effects Toxicity
- Mechanism unknown - Myocardial depression, respiratory depression, nausea/emesis, increased cerebral blood flow (decrease cerebral metabolic demand) - Hepatotoxicity (halothane), nephrotoxicity (methoxyflurane), proconvulsant (enflurane), expansion of trapped gas in a body cavity (nitrous oxide). Can cause malignant hyperthermia-rare, life-threatening hereditary condition in which inhaled anesthetics (except nitrous oxide) and succinylcholine induce fever and severe muscle contractions (Treatment of malignant hyperthermia: dantrolene)
28
What are neuromuscular blocking drugs used for?
Muscle paralysis in surgery or mechanical ventilation. Selective for motor (vs. autonomic) nicotinic receptor
29
Depolarizing neuromuscular blocking drug (non-competitive/short acting) What is it? What does it do? What do you generally give it with to prevent cardiac issues? How is blockade reversed? Complications?
-Succinycholine -Strong ACh receptor agonist; produces sustained depolarization and prevents muscle contraction. Prevention of repolarization can cause muscle paralysis (used for muscle paralysis in short surgical procedures). -Atropine -Phase I (prolonged depolarization)-no antidote. Block potentiated by cholinesterase inhibitors -Phase II (repolarized but blocked; ACh receptors are available, but desensitized)-antidote consists of cholinesterase inhibitors Complications include hypercalcemia, hyperkalemia, and malignant hyperthermia
30
Nondepolarizing (competitive/long acting) Tuborcurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuroncium What do these do? How is blockade reversed?
-Antagonists-compete with ACh for receptors -Neostigmine (medium acting must be given with atropine to prevent muscarinic effects such as bradycardia) Edrophonium (short acting) Other cholinesterase inhibitors
31
Bromocriptine | What does it do?
Dopamine agonist
32
Amantadine | What does it do?
May increase dopamine release; also used as an antiviral against influenza A and rubella; toxicity=ataxia
33
L-dopa/carbidopa Mechanism Clinical Use Toxicity
-Increase level of dopamine in the brain. Unlike dopamine, L-dopa can cross BBB and is converted by dopa decarboxylase in the CNS to dopamine. Carbidopa, a peripheral decarboxlase inhibitor, is given with L-dopa to increase the bioavailability of L-dopa in the brain and to limit peripheral side effects -Parkinson disease -Arrhythmias from increased peripheral formation of catecholamines. Long term use can lead to dyskinesia following adminstration ("on-off" phenomenon) akinesia between doses. First line for Parkinson treatment Can cross BBB and converted to dopamine in CNS
34
Selegiline MOA Clinical use Toxicity
Selective MAO type B inhibitor - Prevent dopamine breakdown - Adjunctive agent to L-dopa in treatment of Parkinson disease - May enhance adverse effects of L-dopa
35
Entacapone, tolcapone | What does it do?
COMPT inhibitors-prevent L-dopa degeneration-->Increase dopamine availibility)
36
Benztropine | What does it do?
Antimuscarinic Improves tremor and rigidity but has little effect on bradykinesia "Park your mercedes-benz"
37
Tetrabenazine and reserpine | What does it do?
Inhibit vesicular monoamine transporter (VMAT); limit dopamine vesicle packaging and release
38
Haloperidol | What does it do?
Dopamine receptor antagonist
39
``` Thrombolytics alteplase (tPA), reteplase (rPA), tenecteplase (TNK-tPA) MOA Clinical use Toxicity ```
- Directly or indirectly aid conversion of plasminogen to plasmin, which cleaves thrombin and fibrin clots. Increase PT, Increase PTT, no change in platelet count. - Early MI, early ischemic stroke, direct thrombolysis of severe PE. - Bleeding. Contraindicated in patients with active bleeding, history of intracranial bleeding, recent surgery, known bleeding diatheses, or severe hypertension. Treat toxicity with aminocaproic acid, an inhibitor of fibrinolysis. Fresh frozen plasma and cryoprecipitate can also be used to correct factor deficiencies.
40
Aspirin (ASA) MOA Clinical use Toxicity
- Irreversibly inhibits cyclooxygenase (both COX-1 and COX-2) enzyme by covalent acetylation. Platelets cannot synthesize new enzyme, so effect lasts until new platelets are produced: increase bleeding time, decrease TXA2 and prostaglandins. No effect on PT or PTT. - Antipyretic, analgesic, anti-inflammatory, antiplatelet (decrease aggregation). - Gastric ulceration, tinnitus (CN VIII). Chronic use can lead to acute renal failure, interstitial nephritis, and upper GI bleeding. Reye syndrome in children with viral infection. Overdose causes respiratory alkalosis initially, which is then superimposed by metabolic acidosis.
41
ADP receptor inhbitor (Clopidogrel, ticlopidine, prasugrel, ticagrelor) MOA Clinical use Toxicity
- Inhibit platelet aggregation by irreversibly blocking ADP receptors. Inhibit fibrinogen binding by preventing glycoprotein IIb/IIIa from binding to fibrinogen. - Acute coronary syndrome; coronary stenting.

Neurology (7 decks)

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