PRESENTED BY
THUSHARA C
PHARMACY PRACTICE
Schizophrenia is a chronic
heterogeneous syndrome of disorganized and
bizarre thoughts, delusions, hallucinations,
inappropriate affect, cognitive deficits, and
impaired psychosocial functioning
• It is a psychotic disorder marked by
severely impaired thinking, emotions and
behaviours. Schizophrenic patients are
unable to filter sensory stimuli and may
have enhanced perception of sounds,
colours and other features of their
environment.
• Most schizophrenics, if untreated can
gradually withdraw themselves from the
interactions with other people and lose their
ability to take care of personnel needs
TYPES OF SCHIZOPHRENIA
CATATONIC
Motor symptoms are most notable. The
patient may either demonstrate rigid
immobility or excessive purposeless
movement. The patient may be silent
and withdrawn or may become loud and
shout.
Bizarre voluntary movements such as
posturing may also occur.
The patient may fluctuate between the
two extremes.
DISORGANISED
The patient tends to have
disorganized speech and
behavior with a fl at affect.
Hallucinations
and delusions are not well
formed and fragmented. The
patient may also have bizarre
mannerisms and grimacing.
PARANOID
The most common type of
schizophrenia. Patients are
usually preoccupied with
paranoid delusions or auditory
hallucinations. Cognitive
function is usually preserved; if
thought disorder is present, it
does not prevent description of
delusions or hallucinations.
RESIDUAL
The patient does not have
acute psychosis, but some
symptoms of
schizophrenia remain.
Largely negative
symptoms are seen, such
as flat affect, social
withdrawal, and loose
associations. Prominent
delusions or hallucinations
are not present.
UNDIFFERENTIATED
The patient meets the criteria for a diagnosis
of schizophrenia but does not meet the
criteria for a specific type, or the patient may
meet the criteria for multiple types of
schizophrenia. No one type appears to be
dominant.
EPIDEMIOLOGY
Lifetime prevalence of schizophrenia ranges from 0.6% to
1.9%, with an average of approximately 1%.
The worldwide prevalence of schizophrenia is remarkably
similar among all cultures.
Schizophrenia most commonly has its onset in late
adolescence or early adulthood and rarely occurs before
adolescence or after the age of 40 years.
The prevalence of schizophrenia is equal in males and
females.
SYMPTOMS OF
SCHIZOPHRENIA
POSITIVE SYMPTOMS
DELUSION
HALLUCINATION
COMBATIVENESS
INSOMNIA
NEGATIVE SYMPTOMS
Affective flattening
Alogia
Anhedonia
Amotivation
Apathy
Asocial behavior
DISORGANIZED SYMPTOMS
Disorganized speech
Thought disorder
Disorganized behavior
Poor attention
ETIOLOGY
• No one knows the exact causes of
Schizophrenia, but multiple possible
factors have been discovered.
• These factors include:
1. Genetics
2. Brain chemical imbalance
3. Environmental factors
4. Family history
PATHOPHYSIOLOGY
Genetic Theory:
• A strong genetic link exists for the development of
schizophrenia.
 Occurs in 1% of general population, however this increases to
10% if a 1st degree relative has a history of schizophrenia.
 Risk of developing schizophrenia further increases to 40%
when both parents have a history of schizophrenia.
 Monozygotic twins have demonstrated a 48% risk of
developing schizophrenia if one twin has the disease.
 Studies are going to locate specific genes to the development
of schizophrenia.
Dopamine Theory:
• The dopamine hyperactivity in the brain is responsible for
psychotic symptoms present in schizophrenia.
 While dopamine hyperactivity is present in mesolimbic
pathway, other areas of the brain such as the prefrontal, frontal
and temporal cortices have decrease activity during acute
psychosis.
 Other neurotransmitters thought to be involved in
schizophrenia include 5-HT, glutamate. The role of glutamate
is also being evaluated because one of its major functions is to
regulate dopamine activity. Glutamate deficiency has been
found to cause similar effects to that of dopamine
hyperactivity.
Neurodevelopmental Theory:
• Schizophrenia occurs as a result of an in
uterodisturbance during pregnancy. Potential
causes of this disturbance include upper
respiratory infection, obstetric complication and
neonatal hypoxia.
Psychosocial Theories:
• These theories propose that situation such
as stress, poor interpersonal skills,
conflicting family, communication and
various socio-economic influences are
linked to development of schizophrenia.
Neurotransmitter Abnormalities
• Abnormalities in the dopaminergic system
– Hypodopaminergic activity in the mesocortical
system, leading to negative symptoms
– Hyperdopaminergic activity in the mesolimbic
system, leading to positive symptoms
• The Diagnostic and Statistical Manual of Mental Disorders,
4th ed., text revision, specifies the following criteria for the
diagnosis of schizophrenia:
✓ Persistent dysfunction lasting longer than 6 months
✓ Two or more symptoms (present for at least 1 month),
including hallucinations, delusions, disorganized speech,
grossly disorganized or catatonic behavior, and negative
symptoms
✓ Significantly impaired functioning (work, interpersonal, or
self-care)
DIAGNOSIS
• Duration: Continuous signs of the disturbance persist for at least six
months. This six-month period must include at least one month of symptoms
(or less if successfully treated) that meet Criterion A.
• Exclusion of schizoaffective disorder and mood disorder with psychotic
features.
• E: Substances/general medical condition exclusion: the disturbance is not
due to the direct physiological effects of a substance (eg, a drug of abuse, a
medication) or a general medical condition.
• F: Relationship to a pervasive developmental disorder: If there is a history
of autistic disorder or another pervasive development disorder, the diagnosis of
schizophrenia is made only if prominent delusions or hallucinations are also
present for at least a month (or less if successfully treated).
• Schizophrenic patients appear to have small brains with large
ventricular volumes, indicating a relative deficit of neurons.
Structural and functional brain imaging studies have strongly
suggested that regions of the medial temporal lobe (e.g.,
hippocampus) have diminished numbers of neurons and also
have demonstrated the inability of individuals with
schizophrenia to activate the frontal cortex and successfully
execute tasks that require frontal cortical function.
IMAGING
Ventricular enlargement and cortical atrophy, as seen on CT scan, have
been correlated with chronic course, severe cognitive impairment, and non
responsiveness to neuroleptic medications. Decreased frontal lobe activity seen
on PET scan has been associated with negative symptoms.
TREATMENT
GOALS AND OBJECTIVES:
There is currently no known cure for schizophrenia. Treatment
options include psychotherapy as well as pharmacotherapy.
The goals and objectives of treatment are as follows:
A. Minimize symptoms of schizophrenia
B. Improve quality of life and social/occupational functioning
C. Prevent relapse and hospitalization
D. Minimize adverse effects of medications
E. Prevent suicide attempts or self-harm
NON-PHARMACOLOGICAL
TREATMENT
• Psychotherapy
• Family therapy
PHARMACOLOGICAL
TREATMENT
• Antipsychotic medications:
Two generation of antipsychotic medications are available for
treatment:
1. First generation or typical antipsychotics
2. Second Generation or Atypical Antipsychotics:
First generation or typical antipsychotics:
Chlorpromazine
Trifluperazine
Thioridazine
Perphanazine
Fluphenazine
Haloperidol
Loxapine
• Mechanism of Action:
The antipsychotic effect of these medications
is primarily mediated through the blockade of
dopamine type 2 (D2 receptors).
Adverse effects:
Sedation,
anticholinergic effects,
EPS
hyperprolactemia,
moderate weight gain
Photosensitivity
Second Generation or Atypical
Antipsychotics
Clonazapine
Risperidone
Olanzapine
Quetipine
Ziprasidone
• Mechanism of action:
Atypical antipsychotics are dopamine
antagonists but also block 5-HT2A-receptors
Adverse effects:
Sedation, anticholinergic effects
(Clonazapine, Olanzapine), EPS,
DM, hyperprolactemia
(Risperidone), hypercholestremia
THANK YOU……..

Schizophrenia

  • 1.
  • 2.
    Schizophrenia is achronic heterogeneous syndrome of disorganized and bizarre thoughts, delusions, hallucinations, inappropriate affect, cognitive deficits, and impaired psychosocial functioning
  • 3.
    • It isa psychotic disorder marked by severely impaired thinking, emotions and behaviours. Schizophrenic patients are unable to filter sensory stimuli and may have enhanced perception of sounds, colours and other features of their environment. • Most schizophrenics, if untreated can gradually withdraw themselves from the interactions with other people and lose their ability to take care of personnel needs
  • 4.
    TYPES OF SCHIZOPHRENIA CATATONIC Motorsymptoms are most notable. The patient may either demonstrate rigid immobility or excessive purposeless movement. The patient may be silent and withdrawn or may become loud and shout. Bizarre voluntary movements such as posturing may also occur. The patient may fluctuate between the two extremes. DISORGANISED The patient tends to have disorganized speech and behavior with a fl at affect. Hallucinations and delusions are not well formed and fragmented. The patient may also have bizarre mannerisms and grimacing.
  • 5.
    PARANOID The most commontype of schizophrenia. Patients are usually preoccupied with paranoid delusions or auditory hallucinations. Cognitive function is usually preserved; if thought disorder is present, it does not prevent description of delusions or hallucinations. RESIDUAL The patient does not have acute psychosis, but some symptoms of schizophrenia remain. Largely negative symptoms are seen, such as flat affect, social withdrawal, and loose associations. Prominent delusions or hallucinations are not present.
  • 6.
    UNDIFFERENTIATED The patient meetsthe criteria for a diagnosis of schizophrenia but does not meet the criteria for a specific type, or the patient may meet the criteria for multiple types of schizophrenia. No one type appears to be dominant.
  • 7.
    EPIDEMIOLOGY Lifetime prevalence ofschizophrenia ranges from 0.6% to 1.9%, with an average of approximately 1%. The worldwide prevalence of schizophrenia is remarkably similar among all cultures. Schizophrenia most commonly has its onset in late adolescence or early adulthood and rarely occurs before adolescence or after the age of 40 years. The prevalence of schizophrenia is equal in males and females.
  • 8.
    SYMPTOMS OF SCHIZOPHRENIA POSITIVE SYMPTOMS DELUSION HALLUCINATION COMBATIVENESS INSOMNIA NEGATIVESYMPTOMS Affective flattening Alogia Anhedonia Amotivation Apathy Asocial behavior DISORGANIZED SYMPTOMS Disorganized speech Thought disorder Disorganized behavior Poor attention
  • 9.
    ETIOLOGY • No oneknows the exact causes of Schizophrenia, but multiple possible factors have been discovered. • These factors include: 1. Genetics 2. Brain chemical imbalance 3. Environmental factors 4. Family history
  • 10.
    PATHOPHYSIOLOGY Genetic Theory: • Astrong genetic link exists for the development of schizophrenia.  Occurs in 1% of general population, however this increases to 10% if a 1st degree relative has a history of schizophrenia.  Risk of developing schizophrenia further increases to 40% when both parents have a history of schizophrenia.  Monozygotic twins have demonstrated a 48% risk of developing schizophrenia if one twin has the disease.  Studies are going to locate specific genes to the development of schizophrenia.
  • 11.
    Dopamine Theory: • Thedopamine hyperactivity in the brain is responsible for psychotic symptoms present in schizophrenia.  While dopamine hyperactivity is present in mesolimbic pathway, other areas of the brain such as the prefrontal, frontal and temporal cortices have decrease activity during acute psychosis.  Other neurotransmitters thought to be involved in schizophrenia include 5-HT, glutamate. The role of glutamate is also being evaluated because one of its major functions is to regulate dopamine activity. Glutamate deficiency has been found to cause similar effects to that of dopamine hyperactivity.
  • 12.
    Neurodevelopmental Theory: • Schizophreniaoccurs as a result of an in uterodisturbance during pregnancy. Potential causes of this disturbance include upper respiratory infection, obstetric complication and neonatal hypoxia.
  • 13.
    Psychosocial Theories: • Thesetheories propose that situation such as stress, poor interpersonal skills, conflicting family, communication and various socio-economic influences are linked to development of schizophrenia.
  • 14.
    Neurotransmitter Abnormalities • Abnormalitiesin the dopaminergic system – Hypodopaminergic activity in the mesocortical system, leading to negative symptoms – Hyperdopaminergic activity in the mesolimbic system, leading to positive symptoms
  • 16.
    • The Diagnosticand Statistical Manual of Mental Disorders, 4th ed., text revision, specifies the following criteria for the diagnosis of schizophrenia: ✓ Persistent dysfunction lasting longer than 6 months ✓ Two or more symptoms (present for at least 1 month), including hallucinations, delusions, disorganized speech, grossly disorganized or catatonic behavior, and negative symptoms ✓ Significantly impaired functioning (work, interpersonal, or self-care) DIAGNOSIS
  • 17.
    • Duration: Continuoussigns of the disturbance persist for at least six months. This six-month period must include at least one month of symptoms (or less if successfully treated) that meet Criterion A. • Exclusion of schizoaffective disorder and mood disorder with psychotic features. • E: Substances/general medical condition exclusion: the disturbance is not due to the direct physiological effects of a substance (eg, a drug of abuse, a medication) or a general medical condition. • F: Relationship to a pervasive developmental disorder: If there is a history of autistic disorder or another pervasive development disorder, the diagnosis of schizophrenia is made only if prominent delusions or hallucinations are also present for at least a month (or less if successfully treated).
  • 18.
    • Schizophrenic patientsappear to have small brains with large ventricular volumes, indicating a relative deficit of neurons. Structural and functional brain imaging studies have strongly suggested that regions of the medial temporal lobe (e.g., hippocampus) have diminished numbers of neurons and also have demonstrated the inability of individuals with schizophrenia to activate the frontal cortex and successfully execute tasks that require frontal cortical function. IMAGING Ventricular enlargement and cortical atrophy, as seen on CT scan, have been correlated with chronic course, severe cognitive impairment, and non responsiveness to neuroleptic medications. Decreased frontal lobe activity seen on PET scan has been associated with negative symptoms.
  • 20.
    TREATMENT GOALS AND OBJECTIVES: Thereis currently no known cure for schizophrenia. Treatment options include psychotherapy as well as pharmacotherapy. The goals and objectives of treatment are as follows: A. Minimize symptoms of schizophrenia B. Improve quality of life and social/occupational functioning C. Prevent relapse and hospitalization D. Minimize adverse effects of medications E. Prevent suicide attempts or self-harm
  • 21.
  • 22.
    PHARMACOLOGICAL TREATMENT • Antipsychotic medications: Twogeneration of antipsychotic medications are available for treatment: 1. First generation or typical antipsychotics 2. Second Generation or Atypical Antipsychotics:
  • 23.
    First generation ortypical antipsychotics: Chlorpromazine Trifluperazine Thioridazine Perphanazine Fluphenazine Haloperidol Loxapine
  • 24.
    • Mechanism ofAction: The antipsychotic effect of these medications is primarily mediated through the blockade of dopamine type 2 (D2 receptors). Adverse effects: Sedation, anticholinergic effects, EPS hyperprolactemia, moderate weight gain Photosensitivity
  • 25.
    Second Generation orAtypical Antipsychotics Clonazapine Risperidone Olanzapine Quetipine Ziprasidone
  • 26.
    • Mechanism ofaction: Atypical antipsychotics are dopamine antagonists but also block 5-HT2A-receptors Adverse effects: Sedation, anticholinergic effects (Clonazapine, Olanzapine), EPS, DM, hyperprolactemia (Risperidone), hypercholestremia
  • 28.