Psych Conference III Flashcards
Paranoid delusion definition and example
Fixed, false fear/belief, not bordered in reality and not consistent with cultural beliefs. I.e. pt believes eagle is going to shoot her
Definition and example of auditory hallucinations
hearing perceptions int he absence of external stimuli (i.e. hearing jesus telling her to do things. a visual one would be seeing a ligh that is not actually there(
pt treated with perphenazine for Undifferentiated shizophrenia. What’s the drug act on, what are the side effects seen with it?
Typical neuroleptic that blocks 5HT2 receptors (agitation, nervousness, insomnia, sexual dysfunction), blocks D2 receptors, and alpha1 blockers.
Side effect of these medium potenency antispychotis (and in high potency) is Extrapyramidal Side Effects (EPS). exp,anation in another card.
What are the 4 main EPS signs?
Acute Dystonia: acute face, heck, torso muscle spasms/contractions. Very dangerous if throat shuts.
Akinesia: Parkinsonian symptoms (tremor, bradykinesia, cogwheel rigidty)
Akathisia: subjectives and objective motor restlessness
Tardive Dyskinesia: involuntary movements of the face, mouth, and tongue
In addition to EPS, what are two other important side effects of antispychotics, specifically the high potency generation?
- EPS
- Neuroleptic Malignant Syndrome: Rigidity, myoglobinuria, autonomic instability, hyperpyrexia (really high fever), increased CK, can be fatal
- Endocrine effects due to prolactin release since dopamine is inhibited and thus no longer inhibiting prolactin: galactorrhea and amenorrhea in women, gynecomastia and impotence in men
What drug can be used to treat EPS side effects? What class of drugs DOESNT work to treat EPS?
Beta blocker (propranolol) often provide dramatic relief, especially for Akathesia. Benzodiazapines also help relax them.
Anti-cholinergics DO NOT work.
While anti-cholinergics dont work to treat EPS, what is one sign from EPS that you treat with anticholinergics?
Dystonia: if throat shuts, treat with IM anti-cholinergic. (side effect often seen from haloperidol).
In terms of drug classes, what is the relationship bewteen anticholinergic and EPS?
low potency drugs: higher anticholinergic, less EPS
high potency drugs: lower anticholinergic, more EPS.
In terms of treating schizo, how does a drug like perphanazine help?
While it treats positive symptoms (hallucinations), negative symptoms usually persist (withdrawn, reduced corns for appearance and hygiene, poverty of speech, apathy, flat affect)
Typical antispychotics (high potency) produce pseudoaprkininan akinesia, including mask-like facial expressions, and reduced motivations, which are similar in appearance to core negative symptoms of schizophrenia. What is they hypothesis of endogenous negatve symptoms in schizophrenia and how typical antipsycotics contribute to them? What atypical antipsychotic also has this effect?
Risperidone at higher doses also produce this pseudoparkinian akinesia side-effect.
Hypothesis: deficit in frontal dopaminergic activity; typical antipsychotics further reduce frontal lobe dopaminergic activity
What are extrapyramidal structures? What do they do?
Basal ganglia, caudate, substantia nigra.
Control voluntary movement outside of pyramidal tracts: restlessness/akathesia, parkinsonian gait, masked face, tardive dyskinesia, dystonia (suddent stiffening/spasm)
Ratio of what neurotransmitters is associated with akathesia/restlessness? It’s treatment?
Ratios of what is assocaited with other EPS i.e. dystonia? Treatment?
Akathesia: Dopamine/NE; treat with beta blocker or benzos
Dystonia: Dopamine/Ach; treat with anti-cholinergic
The atyipcals (i.e. olanzapine) are called “big shotgun drugs.” What are some pharmacologic differences between olanzapine and perphenazine (typical) that are thought to give olanzapine a broader spectrum of action?
- Olanzapine has both broader and more focused pharm effects comapred to typical agents
- broader receptor activity: 5HT-2 receptor blocker is thought to ENHANCE dopamine release in the frontal lobes, helping to reduce the negtive symptoms
- Focal effects: dopamine bockate, more targeted effects on the meso-limbic system instead of the nigro-striatial system (which is responsible for parkinson-like symptoms)
Dysfunction of what brain region(s) can produce an apathetic clinical picture?
Dysfunction of the frontal lobe (where initiations of voluntary movement is)
- especially the anterior cingulate gyrus
- damage to any of the interconnected components of the cortical-striatal-thalamic-cortical loop associated with anterior cingulate gyrus are similarily produce apathetic clinical syndrome
*striatum = putamen + caudate