Pharmacology Unit 6 CNS DRUGS

Card Set Information

Author:
Leon
ID:
247856
Filename:
Pharmacology Unit 6 CNS DRUGS
Updated:
2013-11-19 15:17:54
Tags:
Pharmacology Unit CNS Drugs
Folders:

Description:
Pharmacology Unit 6 CNS Drugs
Show Answers:

Home > Flashcards > Print Preview

The flashcards below were created by user Leon on FreezingBlue Flashcards. What would you like to do?


  1. 1) Memorize the Continum Chart
    • a) Stimulation – “+” sensation acuity (greater awareness of environment); “+” motor activity (restlessness)
    • i) Death
    • ii) Convulsions or seizures
    • iii) Tremors & hallucinations
    • iv) Anxiety, nerviousness
    • v) Euphoria (feeling of well-being)
    • b) Normal
    • i) Neutral
    • c) Depression – “-” sensation acuity (lack of perception, drowsy, not alert); “-” motor activity (lethargic)
    • i) Sedation (drowsy)
    • ii) Hypnosis (sleep)
    • iii) General anesthesia (loss of consciousness)
    • iv) Coma
    • v) death
  2. 2) Understand the 2 types of tolerance
    • a) –state where one must increase the dose of a drug in order to achieve or maintain the desired effect
    • i) (all narcotics, barbiturates, alcohol, tobacco)
    • b) May be “metabolic” or “receptor” based
    • c) Tolerance always occurs in process of becoming physically addicted to a drug
    • i) May get tolerance to drugs that are not addicting, but this is usually “metabolic” tolerance and does not deal w/ the CNS
    • d) “Addiction” implies “compulsion” involving CNS drugs &/or endogenous CNS compounds
  3. 3) Factors contributing to drug dependence
    • a) Addiction deals w/ “compulsion” to “self-administer” a drug
    • i) Many agents that have strong psychological “hooks” are very addicting even though their degree of physical dependence is not that high
    • b) Physical dependence
    • i) –an adaptive physiological state that occurs after administration of a drug that manifests itself by physical disturbances when the drug is withdrawn (withdrawal syndrome)
    • (1) Compulsion to take the drug to maintain well-being (no choice)
    • ii) Characteristics
    • (a) Also known if abstain = withdrawal symptoms
    • (2) “receptor” tolerance always occurs, must increase dose to maintain effectiveness
    • (3) Detrimental effects do occur
    • (a) Preoccupation w/ obtaining & using drug
    • (b) Harmful side effects
    • (i) (Drowsiness, ulcers, high BP, etc.)
    • (c) Chronic use of some drugs can cause permanent damage
    • (i) Even tobacco does this – other drugs damage kidneys, liver, etc.
    • iii) Note: Degree of physical dependence is NOT synonymous w/ degree of “addiction.
    • c) Psychological dependence
    • i) –a state of emotional reliance upon a drug in order to maintain a state of well-being
    • (1) Tolerance, if it does occur, is of the “metabolic” type so there are no withdrawal symptoms
    • (a) In reality, dependence causing drugs are usually both types at a same time
    • (b) They are on a continuum between the 2 extremes w/ some features of both
    • ii) Characteristics
    • (1) Same compulsion but no withdrawal symptoms
    • (2) Often, little or no tendency to increase dose
    • (a) (may have “metabolic” tolerance)
    • (3) Detrimental effects do occur
    • (a) Preoccupation w/ obtaining & using drug
    • (b) Harmful side effects
    • (i) (Drowsiness, ulcers, high BP, etc.)
    • (c) Chronic use of some drugs can cause permanent damage
    • (i) Even tobacco does this – other drugs damage kidneys, liver, etc.
  4. 4) CNS Stimulants – how do they work? What are the main types we talked about in class the main indications for use. (amphetamines, xanthines, cocaine)
    • a) General Stimulants: substances which generally increase the excitability of the CNS
    • b) Amphetamines: d-amphetamine (Dexedrien®), methylphenidate (Ritalin®)
    • i) - stimulates all area of the brain
    • ii) Responses observed upon administration:
    • (1) Increased alertness, wakefulness, decreased fatigue
    • (2) Mood elevation or euphoria, increased initiative
    • (3) Decreased appetite, but little effect in reducing food intake if eating for psychological reasons
    • iii) MOA:
    • (1) Increase the release of NE in the brain
    • (a) (responsible for CNS stimulation)
    • (2) BUT also, increases dopamine release
    • (a) (causes side effects)
    • iv) Therapeutic uses: Schedule II (high potential for abuse)
    • (1) Narcolepsy- uncontrollable urge to sleep
    • (2) Weight control (probably will not be approved by FDA in future)
    • (a) –this is highly abused drug
    • (b) Doesn’t control psychological eating
    • (c) Tolerance occurs (must keep increasing dose) – too dangerous a drug
    • (3) AD-HD “hyperkinetic” children
    • (a) Methylphenidate or Ritalin ® used most often
    • (i) Classroom improvement in 70-80%
    • (ii) Active
    • (iii) Learning and discipline problems
    • (iv) Short attention span
    • 1. Paradox- give stimulant to child who seems overstimulated
    • (b) MOA in AD-HD:
    • (i) + NE = + attention span
    • (ii) Perhaps dopamine helps
    • 1. (1996 study found abnormal D4 in 21% AD-HD)
    • (c) Note: Strattera® approved Nov 2 is non-stimulant
    • (i) (A selective NE Reuptake Inhibitor)
    • (ii) 2005 “black box” warning: suicidal thoughts (similar to antidepressant)
    • v) Side/Toxic Effects:
    • (1) CNS- nervousness, anxiety, sleeplessness
    • (a) High dose- schizophrenic behavior (+ dopamine), hallucinations, paranoia
    • (2) Cardiovascular- + HR, BP, & possibly arrhythmias
    • (3) Weight loss & malnutrition
    • (4) In hyperkinetic child- sleeplessness, excessive crying, etc.
    • (a) *Suppresses growth (reversibly if quit before bone closure)
    • (b) Some experts recommend drug holiday’s
    • (5) Possible (but rare) bone marrow suppression
    • (a) (do periodic blood checks)
    • vi) Contraindications:
    • (1) Insomnia or psychological disorders (suicidal, schizophrenia, etc)
    • (2) Hypertension, cardiac arrhythmias
    • (3) Anorexia
    • vii) Caution: potential for abuse
    • (1) Drug interactions: All the ANTI
    • (a) Anticholinergic, anticoagulants, anticonvulsants, tricyclic antidepressants
    • (i) Usually requires a dosage adjustment
    • c) Xanthines (more stimulants): caffeine, theobromine, theophylline
    • i) From plants found all over the world:
    • (1) Caffeine- coffee beans, tea leaves, kola nuts
    • (2) Theophylline- tea leaves
    • (3) Theobromine- cocoa
    • (a) (Cocaine also in kola nuts –taken out of coke)
    • (4) Common beverages
    • (a) Coffee: 100-150 mg caffeine
    • (b) Tea: 40-100 mg caffeine + theophylline
    • (c) Coke: 35-55 mg caffeine
    • ii) Responses observed:
    • (1) CNS stimulation
    • (a) + alertness, - fatigue
    • (i) Caffeine > theophylline > theobromine
    • (2) Cardiac stimulant (rate & force of contraction)
    • (a) Theophylline > theobromine > caffeine
    • (3) Constricts blood vessels in brain
    • (a) Coffee may help headache (if cause – dilated blood vessels)
    • (4) Diuresis
    • (a) Theophylline > theobromine > caffeine
    • (5) Bronchiorelaxation
    • (a) Requires higher dose than CNS effects
    • (i) Theophylline > theobromine > caffeine
    • (ii) Aminophylline = a more water-soluble version of theophylline
    • 1. –a drug used for asthma
    • iii) MOA:
    • (1) Inhibits breakdown of cyclic AMP
    • (2) + CNS activity
    • (3) Dilates bronchioles
    • (4) Dilates pulmonary blood vessels, but constrict cerebral vessels
    • (5) Note: Activates P450 enzymes after metabolism of many drugs
    • iv) Therapeutic Uses:
    • (1) Pain from headache
    • (a) Caffeine often over the counter
    • (i) Conflicting evidence over effectiveness
    • (ii) No activity alone
    • (iii) But is potentiator of other analgesics
    • (2) Asthma, bronchitis, emphysema
    • (a) Aminophylline
    • (3) Counter drowsiness
    • v) Side Effects:
    • (1) + HR, cardiac arrhythmias
    • (2) + gastric secretion
    • (a) Caffeine worst culprit
    • (3) Diuresis (not usually used as diuretics)
    • (4) Excess CNS stimulation
    • (a) Convulsion, insomnia
    • (5) Withdrawal
    • (a) Headache & irritability
    • vi) Cautions:
    • (1) Cardiac arrhythmia
    • (2) Ulcers
    • (3) Possibly pregnancy
    • (a) Birth defects in small animals w/ large doses caffeine
    • (4) So far no sign of birth defects in humans
    • (a) No correlation w/ caffeine intake
    • (b) A retrospective correlation study (Dec 1993 JAMA)
    • (i) Links + caffeine consumption to an increased rate of miscarriages ( more than 321 mg/day = 2.62x risk of miscarriage).
    • d) Cocaine: Schedule II drug- from cola leaves (Peru)
    • i) Compared to amphetamines in:
    • (1) Similarity
    • (a) Responses observed
    • (b) Mechanism of action in CNS
    • (c) Many side or toxic effects
    • (d) Cautions and contradictions
    • (2) Differences
    • (a) Cocaine not approved by FDA except as local anesthetic
    • (b) Used only in hospital or clinic
    • ii) Abuses:
    • (1) Cocaine like amphetamine, but more INTENSE
    • (2) If sniff cocaine, side effect may be: nosebleed
    • iii) Uses:
    • (1) Local Anesthetics- Cocaine or cocaine-like derivatives (Procaine, Benzocaine, Lidocaine, etc.)
    • (2) There are not general depressants as are the general anesthetics
    • iv) MOA:
    • (1) Unknown but seem to elevate threshold for neuron excitement by decreasing permeability to all ions
    • v) Side Effects:
    • (1) CNS
    • (a) Early signs of CNS stimulation (anxiety, restlessness, confusion, dizziness, tremors, convulsions)
    • (b) Later may get depression, unconsciousness, and death
    • (2) Cardiovascular
    • (a) Early central stimulation
    • (i) Like amphetamines, may begin w/ central stimulation causing + HR & BP
    • (b) Later depressant action directly on heart (bradycardia, hypotension, cardiac arrest)
    • (i) Different form amphetamines soon see depression
    • (3) Allergic reactions
    • (a) Not common but are possible
  5. 5) Treatment of ADHD & side effects of treatment
    • a) AD-HD “hyperkinetic” children
    • i) Methylphenidate or Ritalin ® used most often
    • (1) Classroom improvement in 70-80%
    • (2) Active
    • (3) Learning and discipline problems
    • (4) Short attention span
    • (a) Paradox- give stimulant to child who seems overstimulated
    • ii) MOA in AD-HD:
    • (1) + NE = + attention span
    • (2) Perhaps dopamine helps
    • (a) (1996 study found abnormal D4 in 21% AD-HD)
    • iii) Note: Strattera® approved Nov 2 is non-stimulant
    • (1) (A selective NE Reuptake Inhibitor)
    • (2) 2005 “black box” warning: suicidal thoughts (similar to antidepressant)
  6. 6) CNS depressants – how do they work? Differences between barbiturates and benzodiazepines. What are the main clinical uses we discussed for each type and main side effects.
    • a) General Depressants:
    • i) CNS depressant: agent which decreases excitability of tissue in CNS
    • (1) Produces sedation, hypnosis, general anesthesia, coma, death
    • (2) All drugs in this category can act as sedatives, hypnotics, or general anesthetics
    • (a) – depends upon given
    • ii) Sedatives: drugs to cause mild drowsiness or sedation or to reduce restlessness or anxiety
    • (1) Ideally, shouldn’t interfere w/ person’s ability to function normally
    • iii) Hypnotics: drug to induce sleep or allow an individual to stay asleep
    • (1) Usually dosage range is 3-4 times that of sedative
    • (2) By definition, a person can be aroused from a sleep
    • iv) General anesthetics: drug to depress the CNS to degree that causes loss of consciousness (unarousable sleep), as well as analgesia
    • (1) Person unarousable
    • (2) Abolishes perception of and reaction to pain
    • (3) Compare:
    • (a) Analgesic: drug that relieves pain w/out loss of consciousness
    • b) Sedative-hypnotics may be classified as:
    • i) Useful Therapeutic Responses- for all: Note that these responses follow the continuum chart
    • (1) As dose increases:
    • (a) Reduced anxiety -> sedation (drowsiness) -> hypnosis (sleep) -> general anesthesia
    • (2) Note: all activate P450 enzymes & so increase metabolism of many drugs
    • ii) Barbiturates- about 15 kinds commonly available in the US (50 or so FDA approved)
    • (1) Differ in:
    • (a) Speed w/ which effect occur
    • (b) Duration of action (absorbed in bloodstream at same rate, usually, but enter brain at different rates)
    • (2) All barbiturates may be taken orally (Kinds not Tested)
    • (a) Phenobarbital (Luminal®)
    • (i) Slow onset, long acting (all day)
    • (ii) Broadest spectrum of use medically (ex. Taken for epilepsy)
    • (b) Secobarbital & pentobarbital (Nembutal®)
    • (i) Intermediate acting (2-4 hours)
    • (c) Thiopental (Pentothal®)
    • (i) Short acting (onset in seconds, duration in minutes)
    • (ii) Given IV
    • (3) MOA- general depressant: mechanism unclear
    • (a) Do depress all areas of brain
    • (b) Seem to inhibit reticular activating system
    • (i) Depress synapse activity in some way
    • (ii) Probably enhance GABA receptor complex
    • (iii) & enhance Cl- entrance to neurons and hyperpolarize cells
    • iii) Non-barbiturates: “minor tranquilizers”- A CNS depressant that doesn’t have barbiturate structure
    • (1) Benzodiazepines such as: flurazepam (Dalmane®), diazepam (Valium®), chloriazepoxide (Librium®)
    • (a) MOA- all general depressants:
    • (i) Bind to special receptor that decrease activity of brain
    • (ii) Also increase activity of GABA (inhibitory transmitter)
    • (2) Ethyl alcohol-
    • (a) MOA- general depressant: unsure of mechanism-
    • (i) Seems to increase GABA short term use
    • 1. However, long term use (alcoholics) decreases GABA
    • a. Decreases antianxiety effects of alcohol (Drinks to relieve anxiety)
    • (ii) Large ingestion releases dopamine (“reward”)
    • (iii) Avoid alcohol w/ head trauma (vasodilator)
    • iv) Therapeutic uses: Generally true for all
    • (1) Relieves anxiety (most common use) – 2 kinds of anxiety
    • (a) Situational anxiety (exam, new job, dentist, etc.) – temporary
    • (b) Neurotic anxiety- no rational reason – should use psychotherapy as well (drugs do not cure)
    • (2) Sleep disorders – should only be used temporarily (highly abused drugs)
    • (a) If trouble to sleep initially, use drug w/ quick onset (& short duration)
    • (b) If trouble staying asleep, use slower onset but longer duration (try to avoid “hangover” effect)
    • (i) Note: sleep promoting properties are lost in 3-14 days
    • (ii) Few benzodiazepines are more long term – flurazepam (Dalmane®), temazepam (Restoril®), triazolam (Halcion®)
    • (3) Anticonvulsant (e.g. epilepsy) – will discuss later
    • (a) Note: Epilepsy is a major therapeutic reason to use barbiturates over benzodiazepines
    • v) Side/Toxic Effects:
    • (1) Drowsiness(if not primary use)
    • (a) Perhaps less likely w/ benzodiazepines
    • (2) Impaired performance/ or decreased perception or judgment
    • (a) Incl. psychomotor activity (lethargic, walk slowly)
    • (b) Often changes in EEG observed – long term use
    • (3) Hangover effect – dizziness & fatigue, diarrhea and nausea
    • (a) Slightly less true of benzodiazepines
    • (i) Does not repress REM sleep
    • (4) Hyperalgesia (increase sensitivity to pain)
    • (a) Only true of barbiturates- barbiturates increase sensitivity to pain
    • (i) Benzodiazepines are a better choice as sleep aid if patient can’t sleep because of pain (give analgesic like morphine or codeine first, however)
    • vi) Overdose:
    • (1) Depress respiratory (main cause of overdose death)
    • (a) Benzodiazepines are less likely to be fatal in overdose, but only if no other depressant is involved (alcohol, barbiturates…)
    • (2) Note: flumazenil (Romazicon®) a competitive antagonist for benzodiazepines may be used in overdose
    • vii) Cautions:
    • (1) Additive w/ others of sedative-hypnotics group
    • (2) Drug abuse & habituation
    • (a) Addiction occurs w/ daily use for 2 months
    • (i) All sedative-hypnotics are additive.
    • (ii) Non-barbiturates have no advantages over barbiturates
    • (3) Withdrawal state – most severe symptoms possible
    • (a) Mild- restless, insomnia
    • (b) Severe – anorexia, nausea, vomiting, hypotension, hallucinations, seizures, convulsions, death
    • (i) Take off drugs slowly – symptoms can last up to 6 weeks or longer
    • 1. Usually only 2 weeks
    • (4) Alcohol during pregnancy
    • (a) Very serious!
    • (b) As little as 2 ounces of alcohol daily during pregnancy increases chances of child having birth defects
    • (c) Women who have 3+ drinks daily are at 2-3x risk of aborting fetus as women having <1 drink per day
    • (d) Even drinking 2x/week increases risk of miscarriage
    • (e) Fetal alcohol syndrome possible
    • (i) Characteristics
    • 1. CNS dysfunction (low IQ, microcephaly)
    • 2. Slowness in growth
    • 3. Facial abnormalities
    • 4. Impaired immune system
    • 5. Variable set of additional features
    • (ii) Occurrence depends upon the population
    • 1. In from 1 in 300 to 1 in 2k live births
    • 2. 1 in 3 infants of alcoholic mothers
    • a. Smallest amount reported w/ syndrome is 75 ml (2.5 oz) alcohol daily
    • b. A glass of wine contains about 15 ml (0.5 oz) of alcohol
  7. 7) What is a general anesthetic?
    • a) –drug causes loss of consciousness (unarousable sleep), as well as analgesia
    • i) Person unarousable
    • ii) Abolishes perception of and reaction to pain
    • iii) Compare:
    • (1) Analgesic: drug that relieves pain w/out loss of consciousness
    • b) Goals:
    • i) Analgesia (particularly upon emergence form anesthesia)
    • (1) –narcotics, Ketamine used to supplement
    • ii) Loss of consciousness and amnesia
    • (1) –gases, nitrous oxide do quite well
    • iii) Muscle relaxation
    • (1) –curare used as an adjunct
    • c) Inhalation Anesthetics – administered by inhalation (enflurane, halothane, methoxyflurane, isoflurane, -nitrous oxide)
    • i) Responses upon administration:
    • (1) Work too rapidly to see all stages –see:
    • (a) Loss of consciousness
    • (b) Amnesia
    • ii) Toxic:
    • (1) Depress respiration, lower BP, and decrease HR
    • (2) Arrhythmias (especially w/ adrenergic agents)
    • (3) Nausea & vomiting – postoperatively
    • iii) Caution: malignant hyperthermia
    • iv) Note: Nitrous oxide differs from other inhalation anesthetics
    • (1) Adjunct only. Not potent enough to induce full anesthesia when alone
    • (2) When used w/ others get less hypotension and respiratory depression for level
    • d) Intravenous Anesthetics – liquids
    • i) Thiopental (barbiturate)
    • (1) Responses upon administration of thiopental
    • (a) Loss of consciousness
    • (b) Quick onset (works in seconds)
    • (2) Toxic of thiopental
    • (a) All of above except arrhythmia
    • (i) i.e. depress vitals & some nausea (less)
    • (b) Plus increased sensitivity to pain
    • (i) Usually give analgesic (narcotic) as well
    • ii) Ketamine – (not a depressant, related to PCP)
    • (1) Responses upon administration
    • (a) No depressed vitals
    • (i) May even increase respiration and HR – acts as a stimulant
    • (b) Causes analgesia without loss of consciousness at a low dose
    • (c) Loss of consciousness at higher dose
    • (d) No skeletal muscle relaxation
    • (2) Toxic of ketamine
    • (a) Upon emergence from loss of consciousness
    • (i) Nightmares, hallucination, frightening experiences
    • (b) Used in children (accept nightmares) and for minor manipulations (i.e. remove burn dressings)
    • iii) Other IV Anesthetics
    • (1) Considerably variety
    • (2) Most similar characteristics to inhalation anesthetics because they are general depressants, though of different chemical structure than those discussed
    • (a) Some more prominent examples include
    • (i) Propofol or diprivan
  8. 8) What are the goals of anesthesia? (Note: no one drug meets all 3 goals)
    • a) Analgesia (particularly upon emergence form anesthesia)
    • i) –narcotics, Ketamine used to supplement
    • b) Loss of consciousness and amnesia
    • i) –gases, nitrous oxide do quite well
    • c) Muscle relaxation
    • i) –curare used as an adjunct

What would you like to do?

Home > Flashcards > Print Preview