-
READ
- It is helpful to subdivide
- schizophrenic symptoms into three categories:
- positive symptoms, characterological traits, and negative symptoms.
- 1.
- Positive Symptoms
- (Targets for medication treatment)
- a.
- Delusions and
- impaired thinking
- c.
- Confusion and
- impaired judgment
- d.
- Severe anxiety,
- agitation, and emotional dyscontrol
- 2.
- Characterological
- Traits
- a.
- Social isolation
- and sense of alienation
- b.
- Poverty of
- thoughts (few or no thoughts and concrete thinking)
- c.
- Emptiness and
- anhedonia (no joy)
- d.
- Psychomotor
- retardation/activity
- e.
- Blunting of
- perception (e.g., insensitivity to pain)
- Although many general
- practitioners treat anxiety and depressive disorders, most patients presenting
- with psychotic symptoms should be referred to a psychiatrist. These patients are often hard to treat. Many psychotic patients can be treated on an
- outpatient basis; however, hospitalization is often necessary.
- Antipsychotic meds (also
- referred to as neuroleptics or major tranquilizers) should be started when the
- early signs of psychosis appear, since many times a more florid psychotic episode
- can be averted with appropriate early intervention.
- Positive symptoms are the
- primary target symptoms for treatment by antipsychotic meds. Such drugs do little to affect
- characterological traits or negative symptoms (some possible exceptions are clozapine
- (Clozaril) and risperidone (Risperdal).
- MECHANISM OF ACTION OF
- ANTIPSYCHOTICS
- 1.
- The primary model
- is the dopamine model, which holds that schizophrenia is caused by abnormal
- dopaminergic activity in the brain.
- Dopamine neurons, in the basal ganglia, regulate motor functioning. Dopamine neurons, in the limbic and reticular
- systems, help to control emotions and screen stimuli. In schizophrenia and
- psychoses, dopamine neurons are overactive or hyper-reactive. Excessive dopamine activity may lead to the
- inability to screen stimuli, disorganized perception and thought, and
- behavioral agitation. Antipsychotic
- drugs bind to and block postsynaptic dopamine (D2) receptors in the mesolimbic
- system. (Note that drugs that increase dopamine activity, like amphetamines,
- may produce a psychosis similar to paranoid schizophrenia. Also, drugs like amphetamines, if given to
- schizophrenics, may exacerbate psychotic symptoms.
- 2.
- A modified model
- of the dopamine model suggests that in schizophrenia, hyperdopaminergic
- activity in the mesolimbic tracts is associated with positive symptoms, and
- decreased activity in the prefrontal cortex is associated with negative
- symptoms.
- 3.
- The neurodevelopmental/neurodegenerative
- model suggests that a genetically determined defect or a defect from an event,
- such as a viral infection, during fetal or early infantile development, leads
- to abnormal development later in life, especially during the synaptic “pruning”
- during adolescence. Treatment is
- directed not just at the final psychotic symptoms, but toward correcting the
- abnormal development.
- Have a familiarity with the
- high potency dopamine blockers and with the weak (low potency) dopamine
- blockers, the latter causing minimal neurological side effects. In general, which group causes more sedation
- and anticholinergic side effects? Which
- group causes more extrapyramidal side effects?
- Know the five groups of side
- effects of all neuroleptics and know the side effects calling for medication
- reassessment.
- How are sedation, extrapyramidal
- side effects, and akathisia managed/treated?
ATYPICAL ANTIPSYCHOTICS
- 1.
- Strong serotonin
- blockers, but varying degrees of dopamine (D2) blockade.
- 2.
- reduction of
- negative symptoms
- 3.
- improved
- cognition and reduced neuro-anatomical changes (enlargement of lateral
- ventricles)
- 4.
- significantly
- reduced risk of tardive dyskinesia
- 5.
- overall better
- tolerability by patients
- 6.
- Because the
- atypicals tend to produce weight gain, alter carbohydrate metabolism similar to
- diabetes, and alter lipid metabolism, all patients on these meds should have
- their weight, blood sugar, and lipid levels monitored.
- 7.
- Clozapine—treats
- both positive and negative symptoms; up to 40% of those who have failed to
- respond to haloperidol and chlorpromazine respond to clozapine.
- b.
- low incidence of
- extrapyramidal side effects/very few cases of tardive dyskinesia
- c.
- lowers seizure
- threshold
- e.
- agranulocytosis—has
- caused several deaths
- 8.
- Risperidone
- (Risperdal)
- a.
- potent dopamine
- blocker
- b.
- increased risk of
- extrapyramidal side effects
- a.
- low incidence of
- extrapyramidal side effects
- c.
- increased weight
- gain and problems in carbohydrate metabolism
- a.
- low incidence of
- extrapyramidal side effects
- c.
- causes
- extrapyramidal side effects
- d.
- should be avoided
- in patients with cardiovascular disease because of its affect on cardiac
- conduction
- 12.
- Aripiprazole (Abilify)
- c.
- nausea and anxiety
- 13
- Paliperidone
- (Invega)—metabolite of risperidone that may be better
- Tolerated
- because of extended-release formulation.
- The choice of antipsychotic medication is
- based on patient history, motor state, and the side effect profile of the
- meds. Understand the choice of
- medication considerations on page 209.
- Review the patient education
- and psychotherapeutic issues on page 211.
-
anxiety/benzo stuff
- 1.
- Our wiring
- (nervous system)—complex network of nerve pathways, brain structures, and
- glands responsible for eliciting the fight or flight response. This response
- mobilizes the body and mind during times of potential danger. Nonessential physiological processes (such as
- digestion and reproduction) shut down, and energy is channeled into a host of
- bodily functions preparing the organism for rapid action. The nervous system shifts into a state of
- hyperarousal and vigilance.
- 2.
- As stressful
- events are perceived at the level of the cortex and also processed in a crude
- way on the subcortical level (the amygdale), lower brain areas become
- activated. In a sense, the limbic system
- is put on alert. If you should perceive
- that there is imminent danger, a burst of excitation emanates from a cluster of
- nerve cell bodies in the brain stem called the locus coeruleus (LC). The LC nerve cells, which project to the
- limbic system, are mediated by the neurotransmitter NE.
- 3.
- The limbic system
- and adjacent hypothalamus shift into high gear, and by way of the pituitary
- gland (and other downstream endocrine glands) and the sympathetic nervous
- system, many stress hormones are released into the system. The brain and body are ready for action.
- 4.
- There is another
- feature of the nervous system that plays a role in anxiety. On the surface of most nerve cells in the
- brain (including cells in the LC) are tiny gateways called chloride ion
- channels. Chloride ions, which have a
- slight negative charge, are in abundance in the fluid surrounding the nerve
- cells. The ion channel can be activated
- (opened) when stimulated by the naturally occurring neurochemical GABA.
- 5.
- As the gate
- opens, the chloride ions are drawn in.
- When the nerve cell is infused with negative ions, its electrical
- characteristics are changed, resulting in decreased excitability (it is
- hyperpolarized). This operates as a type
- of biological braking mechanism, serving to damped “limbic alert” and calm
- overall brain excitation.
- 6.
- Benzodiazepine
- molecules (antianxiety agents) also bind to the chloride ion channels, further
- facilitating the inflow of negative ions and thus producing a widespread
- calming in many areas of the brain
-
adhd stuff
- KNOW “ISSUES IN DIAGNOSING
- AND INITIATING PHARMACOLOGIC TREATMENT OF CHILDREN AND ADOLESCENTS,” PAGES
- 225-228 (EXCLUDING DRUG RESEARCH AND OUTCOME STUDIES).
ADHD
- 1.
- KNOW DIAGNOSTIC
- ISSUES AND NEUROBIOLOGY
- A.
- STIMULANTS (BE
- FAMILIAR WITH DRUGS IN THIS GROUP—SEE CHART PAGE 230; HOWEVER, YOU ARE NOT
- RESPONSIBLE FOR TYPICAL DAILY DOSES)
- 1.
- MECHANISM OF
- ACTION: INHIBITION OF
- DOPAMINE
- REUPTAKE. IN ADDITION, AMPHETAMINES INCREASE RELEASE OF DOPAMINE FROM VESICLES.
- 2.
- CATEGORIZED BY
- ONSET OF ACTION (USUALLY
- MODERATELY
- RAPID, USUALLY 30-45 MINUTES AFTER INGESTION), OR BY DURATION OF ACTION
- (USUALLY 4 TO 12 HOURS).
- 3.
- DOSING IS 2-3
- TIMES A DAY, OR ONCE-DAILY
- DOSING
- WITH LONG-ACTING PRODUCTS.
- 4.
- IMPORTANT ISSUES
- REGARDING STIMULANT
- TREATMENT
- (BOTTOM OF PAGE 230-231).
- 5.
- CONSEQUENCES OF
- MISDIAGNOSIS AND
- STIMULANT
- TREATMENT (SEE FIGURE 21-D).
- B.
- ALPHA-2
- ADRENERGIC AGONISTS
- 1.
- CLONIDINE
- (CATAPRES) AND GUANFACINE
(TENEX)
- a.
- TREAT CORE ADHD
- SYMPTOMS
- b.
- MOST EFFECTIVE IN
- REDUCING IRRITABILITY, AGGRESSION AND IMPULSIVITY AND IN PROMOTING SEDATION TO
- TREAT INITIAL INSOMNIA.
- 2.
- TREATMENT OF
- CHOICE FOR COMORBID TICS
- 3.
- COMBINED USE OF
- ALPHA-2 AGONISTS AND
- STIMULANTS
- A COMMON PRACTICE FOR TREATING ADHD AND CORMORBID ADHD AND TICS.
- 1.
- BUPROPION
- (WELLBUTRIN SR/LA) AND
- ATOMOXETINE
- (STRATTERA) ARE EFFECTIVE IN TREATING CORE ADHD SYMPTOMS
- 2.
- ONLY THOSE THAT
- INCREASE AVAILABILITY OF
- DA
- OR NE ARE USEFUL (THUS SSRIs ARE NOT USEFUL IN TREATING CORE ADHD SYMPTOMS)
- 5.
- CAN TREAT
- COMORBID DEPRESSION
- 6.
- CLINICAL EFFECTS
- SEEN 5-40 DAYS AFTER INITIATING TREATMENT, AND USUALLY LAST 24 HOURS A DAY.
DEPRESSION
- 1.
- USE OF
- ANTIDEPRESSANTS MAY BE RISKY IN BIPOLAR
- PATIENTS
- BECAUSE A MANIC EPISODE MAY BE EXACERBATED OR ANTIDEPRESSANTS MAY CAUSE CYCLE
- ACCELERATION. THUS, POTENTIAL BIPOLARITY
- IN ALL DEPRESSED CHILDREN AND TEENS MUST BE ADDRESSED AND EVALUATED.
- 2.
- KNOW THE HISTORY
- AND CLINICAL FEATURES THAT
- MAY
- SUGGEST A HIGHER RISK OF BIPOLAR DISORDER
- 3.
- KNOW THE DIAGNOSTIC
- ISSUES OF CHILDHOOD-ONSET
- MAJOR
- DEPRESSION, AND THE DIFFERENCES FROM THOSE OF ADULT-ONSET MAJOR DEPRESSION.
- A.
- SSRIs ARE MORE
- EFFECTIVE AND HAVE
- LESS
- SEVERE SIDE EFFECTS THAN TRICYCLICS
- B.
- TIME TO ONSET OF
- POSITIVE MEDICATION
- EFFECTS
- IS GREATER FOR CHILDREN THAN ADULTS.
- C.
- APATHY/AMOTIVATION
- OR EMOTIONAL
- DISINHIBITION,
- SOMETIMES SEEN IN ADULTS ON CHRONIC SSRI TREATMENT, IS MORE COMMONLY
- ENCOUNTERED IN CHILDREN.
BIPOLAR DISORDER
- 1.
- UNDERSTAND THE
- DIAGNOSTIC ISSUES, AND THE
- NEED
- TO DIFFERENTIATE CHILDHOOD-ONSET MANIA
- FROM
- ADHD (INAPPROPRIATE MEDICAL TREATMENT OF STIMULANTS OR ANTIDEPRESSANTS MAY
- CAUSE CYCLE ACCELERATION IN BIPOLAR PATIENTS)
- 2.
- PSYCHOPHARMACOLOGY
- OF BIPOLAR DISORDER
- A.
- MAJOR DEPRESSION
- IN SUSPECTED BIPOLAR
DISORDER
- 1.
- FIRST LINE
- MEDS—MOOD STABILIZERS THAT
- HAVE
- SOME ANTIDEPRESSANT ACTION (LITHIUM OR OLANZAPINE-FLUOXETINE COMBINATION). LAMOTRIGINE (LAMICTAL) NOT USUALLY FIRST LINE
- BECAUSE OF POTENTIALLY SEVERE RASHES (STEVENS-JOHNSON SYNDROME).
- 2.
- COMBINATIONS OF
- MOOD STABILIZERS
- 3.
- ANTIDEPRESSANTS
- AVOIDED AS
- MONOTHERAPY
- SINCE THEY MAY CAUSE SWITCHING OR CYCLE ACCELERATION.
- 4.
- IF NECESSARY, ADD
- AN ANTIDEPRESSANT IF
- PATIENT
- IS ALREADY BEING TREATED WITH A
- MOOD
- STABILIZER, WHICH WILL DECREASE THE RISK OF SWITCHING OR CYCLE ACCELERATION.
- 1.
- FOR VERY SEVERE
- AGITATION, USE
- BENZODIAZEPINES
- OR ATYPICAL ANTI-
- PSYCHOTICS,
- WHICH MAY BEGIN TO WORK
- IN
- SEVERAL HOURS. LITHIUM AND
- ANTICONVULSANT
- MOOD STABILIZERS OFTEN TAKE 1 TO 2 WEEKS TO BEGIN REDUCING SYMPTOMS.
- 2.
- CHOICE OF MOOD
- STABILIZER USED
- DEPENDS
- ON SIDE-EFFECT PROFILE. THE MAJORITY OF
- CHILDREN WITH MANIA MUST BE TREATED WITH TWO OR MORE MOOD STABILIZERS IN
- COMBINATION TO ACHIEVE A GOOD OUTCOME.
- 3.
- ATYPICAL
- ANTIPSYCHOTICS LIKE OLANZAPINE (ZYPREXA)
MAY BE ADDED TO MOOD STABILIZER.
- 4.
- GABAPENTIN
- (NEURONTIN) MAY BE ADDED
- ON
- TO REDUCE ANXIETY, BUT IS INAFFECTIVE MONOTHERAPY FOR MANIA.
- C.
- COMORBID ADHD AND
- BIPOLAR DISORDER
1. MOOD STABILLIZERS USED AS INITIAL
TREATMENT.
2. ONCE STABILITY ACHIEVED, STIMULANTS
- BE FAMILIAR WITH THE SIDE
- EFFECTS AND DRUG
- INTERACTIONS OF LITHIUM AND
- MOOD-STABILIZING
- ANTICONVULSANTS THAT CAN BE
- ESPECIALLY
- PROBLEMATIC FOR CHILDREN AND
- TEENAGERS (P. 239-240).
ANXIETY DISORDERS
- 1.
- BE FAMILIAR WITH THE DIAGNOSTIC ISSUES
- 2.
- PSYCHOPHARMACOLOGY OF ANXIETY DISORDERS
- A.
- OBSESSIVE-COMPULSIVE DISORDERS
- 1.
- SSRIs—FIRST LINE TREATMENT;
- ZOLOFT
- (SERTRALINE), LUVOX (FLUVOXAMINE),
- AND
CLOMIPRAMINE (ANAFRANIL) ARE FDA
APPROVED FOR USE IN CHILDREN.
2. GRADUAL IMPROVEMENT THAT USUSALLY
- PLATEAUS AT
- ABOUT 12 MONTHS.
- 3.
- TREATMENT
- RESISTANT CASES SOMETIMES RESPOND TO SSRIs AUGMENTED WITH LOW DOSES OF CLOMIPRAMINE, LITHIUM, OR ATYPICAL ANTIPSYCHOTICS LIKE
- RISPERDAL (RISPERIDONE). B.
- SEPARATION ANXIETY DISORDER, SOCIAL ANXIETY DISORDER, GENERALIZED ANXIETY DISORDER
- 1. IF SCHOOL REFUSAL IS PART OF
- THE PRESENTING PROBLEM, A BENZODIAZEPINE MAY BE HELPFUL SINCE IT CAN PROVIDE
- QUICK RELIEF
- SO THAT CHILD CAN RE-ENTER SCHOOL QUICKLY. ANTIDEPRESSANTS, WHICH TAKE SEVERAL WEEKS
- OF TREATMENT BEFORE SYMPTOMS
- ARE REDUCED, CAN BE
- COADMINISTERED. ONCE SSRIs PROVIDE BENEFITS, THE BENZODIAZEPINE CAN BE
- GRADUALLY DISCONTINUED. 2. FLUVOXAMINE (LUVOX) ESPECIALLY
- EFFECTIVE. C.
- POST-TRAUMATIC STRESS DISORDER-SSRIs FIRST-LINE AGENTS D. SPECIFIC PHOBIAS 1.
- MOST PHOBIAS CAN BE TREATED WITH WITH STANDARD EXPOSURE-BASED COGNITIVE BEHAVIORAL
- TREATMENT. 2.
- BENZODIAZEPINES CAN BE USED FOR CONDITIONS THAT REQUIRE URGENT ATTENTION (FEAR OR DENTAL PROCEDURES). E. PSYCHOTIC DISORDERS 1.
- ATYPICAL ANTIPSYCHOTICS USED MUCH MORE THAN TRADITIONAL
- ANTIPSYCHOTICS DUE TO LESSER SIDE EFFECTS (TARDIVE DYSKINESIA). 2.
- WEIGHT GAIN AND EXTRAPYRAMIDAL SIDE EFFECTS MORE COMMON IN CHILDREN AND ADOLESCENTS THAN
- IN ADULTS. F.
- AUTISM SPECTRUM DISORDERS—NO MEDS HAVE
- BEEN FOUND THAT TREAT THE CORE SYMPTOMS.
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