Schizophrenia

Front 1

What structural brain abnormalities exist in pts with schizophrenia?

Back 1

Enlarged lateral and third ventricles
Reduced cortical gray matter volume (Cortex, Prefrontal Cortex, Hippocampus, amygdala, Superior temporal gyri)

*Occurs over time; caused by meds or disease

Front 2

What structural brain abnormality is associated with negative symptoms?

Back 2

Loss in frontal cortex

Front 3

What structural brain abnormality is associated with positive symptoms?

Back 3

Loss in the temporal cortex

Front 4

What structural changes exist in the medial temporal lobes of SCZ pts?

Back 4

Abnormal neuron alignment in the amygdala, entorhinal cortex, and hippocampus

Front 5

What changes occur in the sensory input of SCZ patients?

Back 5

Thalamus reduces in size - impaired sensory filtering, leading to increased stimulation of primary sensory cortical areas

*correlates with sensory overload experienced by SCZ pts*

Front 6

What is the effect of amphetamine on schizophrenic patients and why?

Back 6

Paranoid delusions
Agitation
Hallucinations
Ideas of reference

Increases DA release and blocks DA reuptake

*(so does cocaine)

Front 7

What is the role of glutamate in schizophrenia?

Back 7

Glutamatergic neurons in cortex synapse onto DA neurons in mesocortex and GABAergic neurons which inhibit DA neurons to striatum

If glutamatergic neurons impaired, mesocortical activity decreases and mesolimbic activity increases

Front 8

How can positive symptoms be decreased pharmacologically?

Back 8

Block D2 receptors in Mesolimbic pathway

60-70% of D2 receptors need to be blocked for clinical benefit

Front 9

How are negative symptoms worsened pharmacologically?

Back 9

Block D2 receptors in the Mesocortical pathway (prefrontal cortex)

Front 10

How are extrapyramidal signs (e.g. Parkinson-like movements) generated pharmacologically?

Back 10

Block D2 receptors in the nigrostriatal pathway

Ach>DA in basal ganglia

Gradual onset

Extrapyramidal signs occur when >80% D2 receptors are blocked

Front 11

What is the result of blocking D2 receptors in the tuberoinfindibular pathway and why?

Back 11

Hyperprolactinemia because DA normally inhibits prolactin (inhibit an inhibitor)

Results in hypogonadism, infertility, decreased bone density

Front 12

Are the extrapyramidal symptoms caused by anti-psychotics permanent?

Back 12

Onset early in medication course, but generally go away with time

Exception: Tardive Dyskinesia

Front 13

What is tardive dyskinesia?

Back 13

Late-onset, persistent state of involuntary, repetitive body movements; choreathetoid movements of face, trunk, or extremities

Extremely difficult to treat; instead try to avoid, although difficult because cannot predict its onset

Front 14

What is dystonia?

Back 14

Can be acute or tardive
Occurs within hours or days of starting the medication
Painful spasms

Front 15

What is the treatment for dystonia caused by anti-psychotics?

Back 15

Treat immediately with anti-cholinergic medications

Front 16

What is akathesia?

Back 16

Inability to sit still
Occurs shortly after starting anti-psych meds
Occurs in high percent of pts
Can be mistaken for exacerbated psychosis, anxiety, or depression
*Risk factor for suicide*

Front 17

How is akathesia caused by anti-psychotics treated?

Back 17

Anticholinergics or beta-blockers

Front 18

What is the treatment for extrapyramidal symptoms caused by anti-psychotics?

Back 18

1) Decrease the dose of the anti-psychotic
2) If persists, administer anti-cholinergic
3) Switch to second generation medication (atypical)

Front 19

What is Neuroleptic Malignant Syndrome?

Back 19

Muscle rigidity (more so w/ typicals)
Fever
Autonomic instability
Elevated WBC (15+)
Elevated CPK

Mostly associated with typicals (though seen with some atypicals)

Front 20

How do you treat Neuroleptic Malignant Syndrome?

Back 20

Stop taking antipsychotic
Provide supportive treatment

Front 21

Why do typical anti-psychotics have many side effects?

Back 21

In addition to binding D2, also block muscarinic, histaminic, and alpha-1 receptors

Front 22

List the anticholinergic side effects of typical anti-psychotics

Back 22

Blurry vision
Dry mouth
Constipation
Urinary Retention

Front 23

List the antihistaminic side effects of typical anti-psychotics

Back 23

Sedation
Weight Gain

Front 24

What is the alpha-1-antiadrenergic side effect of typical anti-psychotics?

Back 24

Orthostatic hypotension

Front 25

What is the effect of high potency drugs?

Back 25

More extrapyramidal signs, less anticholinergic

*will often need to give anticholinergic drug to treat side effects

Front 26

What is the dangerous side effect of Clozapine that has caused it to be prescribed less today? If prescribing, what action has to be taken?

Back 26

Agranulocytosis, which can lead to infections and death

(also seizures and myocarditis)

WBCs must be heavily monitored (weekly)

Front 27

Name some second generation, atypical anti-psychotics

Back 27

Clozapine
Risperidone (Risperdal)
Olanzapine (Zyprexa)
Quetiapine (Sereoquel)
Ziprasidone (Geodon)

Front 28

What is different about atypical drug targeting vs typicals?

Back 28

Bind 5HT2A receptors as well as D2 receptors

Increase release of DA in prefrontal cortex (<negative symptoms)

Front 29

How do the atypicals function differently than the typical anti-psychotics?

Back 29

Atypicals block 5HT2A receptors in the mesocortical, nigrostriatal, and tuberoinfindibular pathways, allowing for more DA release = less negative symptoms, EPS, and hyperprolactinemia

*Still block DA in mesolimbic pathway because D2 antagonism more robust in this pathway than 5HT2A antagonism

Front 30

What receptor is blocked by all anti-psychotics?

Back 30

D2

Front 31

What additional receptor is blocked by atypicals?

Back 31

5HT2A