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Neurologic & Psych > EXAM 5 Antipsychotics Dr. Pond > Flashcards

EXAM 5 Antipsychotics Dr. Pond Flashcards

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1
Q

Symptoms of Psychoses

A

-false beliefs (delusion)
-hallucinations (abnormal sensation)

-antipsychotics are not specific for the type of psychoses - only treat the symptoms of the disorder

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2
Q

Symptoms of Schizophrenia
(particular type of psychoses)

A

-positive symptoms: hallucinations and delusions

-negative symptoms (depressive symptoms):
alogia (not being verbal with others)
anhedonia (no pleasure)
avolition (not able to plan or do things)
asociality
blunted effects

-cognitive symptoms:
deficit with working memory
attention deficit
deficit with processing speed of information

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3
Q

Which anatomical changes are associated with schizophrenia?

A

-enlarged ventricles

-widening of sulci -> reflecting a reduction of cortical tissue in the frontal lobe

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4
Q

Which neural pathway in the brain is associated with hyperfunction? Describe the symptoms.

A

Mesolimbic pathway
-> Positive symptoms due to hyperactivity of Dopamine neurons: hallucinations

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5
Q

REMINDER: pathway of the mesolimbic pathway

A

VTA to nucleus accumbens

Dopamine REWARD pathway

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6
Q

Which neural pathway in the brain is associated with hypofunction? Describe the symptoms.

A

Mesocortical pathway

Loss of activation of dopamine neurons -> negative symptoms: depression, problems with working memory and attention

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7
Q

REMINDER: pathway of the mesocortical pathway

A

VTA to the prefrontal cortex

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8
Q

Which pathway is responsible for motor control?

A

nigrostriatal: nigra to caudate-putamen

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9
Q

Which pathway is responsible for prolactin secretion?

A

tuberoinfundibular

arcuate nucleus of the hypothalamus to median eminence

DA acts as the inhibiting NT for prolactin secretion

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10
Q

What is the effect of Dopamine antagonists on the nigrostriatal pathway?

A

responsible for motor function -> disorder of motor function

Parkinsonian symptoms

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11
Q

What is the effect of Dopamine antagonists on the tuberoinfundibular pathway?

A

DA inhibits prolactin

-> DA antagonist block DA -> more prolactin secretion, also disrupts fertility

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12
Q

What is the effect when 5-HT-2A agonists are activated and what is the MOA of atypical (new gen) antipsychotics?

A

Hallucinations (postsynaptic, excitatory)

5-HT2A antagonist or inverse agonist (opposite effect of agonist)

modulate release of DA in the cortex, limbic, and striatum -> there may be an interplay with the dopamine pathway

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13
Q

Glutamate is involved in which neuron pathway?

A

VTA to the prefrontal cortex

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14
Q

Which antipsychotics are considered “old”?

A

-Chlorpromazine
-Thioridazine
-Perphenazine
-Haloperidol

P*TCH

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15
Q

Which Dopamine receptor in the limbic system is thought to be responsible for the psychotic symptoms?

A

D2 receptor

older antipsychotics are mainly Dopamine antagonists -> help with positive symptoms (since hyperfunctional), less with negative symptoms (since hypofunctional and antagonist is not helpful here)

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16
Q

Antipsychotics also hit which receptors?

A

-5-HT2A -> Antagonism/inverse agonism
-block muscarinic receptors
-block alpha-adrenergic receptors
-block histamine receptors

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17
Q

Side effects that come with blocking different receptors

A

M1 muscarinic blockage:
-loss of accommodation (cant focus between near and distant object), dry mouth, difficulty urination, constipation

alpha-1 blockage:
orthostasis, impotence, failure to ejaculate

blocking antihistamine R:
weight gain, sedation

18
Q

Which side effects are associated with antipsychotics?

A

-Infertility, impotence, amenorrhea-galactorrhea (lack of menstrual periods and increased milk production)
-sedation

Movement:
-rare neuroleptic malignant syndrome (hyperthermia)
-acute dystonia (involuntary muscle contraction- twisting movements)
-inner restlessness – RLS
-Parkinsonism

Long-term (months to years):
-Tardive dyskinesia and perioral tremor

19
Q

Which drugs may help with motor dysfunctional side effects of antipsychotics?
???

A

Anticholinergics, drugs that naturally hits muscarinic receptors ???
-Benztropine for example

20
Q

What are the key symptoms of Neuroleptic malignant syndrome?

A

Heat, acidosis, Rigidity

also:
-high fever
-sweating
-unstable BP
-stupor
-autonomic dysfunction

21
Q

Which drugs treat Neuroleptic malignant syndrome?

A

Dantrolene

22
Q

Repitive, involuntary, purposeless movements, often in the face

A

Tardive dyskinesia

15-20% with older antipsychotics
-may be irreversible

23
Q

What is the BBW for antipsychotics

A

increased risk of death in elderly patients with dementia-related psychotics

24
Q

What is the key difference between the newer atypical antipsychotics and the older ones?

A

higher potency at blocking 5-HT2A than D2 receptors (10x)
except for quetiapine

->less EPS (Parkinson-like) symptoms and tardive dyskinesia, little to no increase in prolactin secretion

-significant improvement in treating the negative symptoms

25
Q

Which drugs are considered atypical (new gen)?

A

-clozapine
-risperidone
-olanzapine
-quetiapine
-aripiprazole
-lurasidone
-ziprasidone
-cariprazine

-> Significant weight gain may cause other problems like diabetes, hyperlipidemia, heart disease

26
Q

What is the BBW for Clozapine (atypical)

A

-agranulocytosis (have to monitor WBC)
-Seizures
-orthostatic hypotension
-myocarditis, and cardiomyopathy

highly associated with weight gain

27
Q

Advantage of Clozapine

A

it reduces the risk of suicide (which is higher in schizophrenia patients)

28
Q

Which atypicals are mostly associated with weight gain?

A

Clozapine
Olanzapine

29
Q

Which antipsychotic is associated with less weight gain?

A

Ziprasidone

-blockade of NE and 5-HT uptake, and
5HT1a agonism - so more 5-HT

30
Q

Target of Cariprazine

A

High affinity for D3
D2 antagonist/partial agonist
low affinity for 5-HT2A, 5-HT2C

31
Q

Which drug causes fewer EPS side effects?

A

Aripiprazole
because it is a partial D2 agonist, rather than a D2 antagonist like the older ones

32
Q

How does the drug Samidorphan work?

A

mu-opioid antagonist: on the POMC neuron

POMC is a precursor for ß-endorphin and alpha-MSH

alpha-MSH binds to MC4R -> loss of appetite -> weight loss

ß-endorphin binds to MOR causing neg feedback of alpha-MSH release (we don’t want that)

Samidorphan blocks MOR AUTORECEPTORS (neg feedback) -> more release of alpha-MSH binding to MC4R -> loss of appetite

33
Q

Role of Lithium in bipolar disorder

A

used for Bipolar disorder, has delayed onset - so used for prophylaxis rather than acute manic episodes

34
Q

MOA for Lithium

A

-Substitutes for Na+ -> effects on electrolytes and ion transport

-Increases GABA inhibition, decreases NMDA excitation

-inhibits DAergic neurotransmission

-also affects second messenger and intracellular enzymes after NT hits the receptor

35
Q

Which enzymes are blocked by Lithium?

A

-Inositol monophosphatase
-Inositol polyphosphate 1-phosphatase
->thereby blocking the inositol recycling (conversion of IP2 to IP1 and IP1 to inositol)

-Glycogen synthase kinase-3 (inhibits neurotrophic and neuroprotective processes - so inhibiting it will increase neurotrophic effects)

36
Q

Which molecules are important second messengers and are involved in manic episodes?

A

IP3 and DAG

-> causes α adrenergic and muscarinic transmission (may be hyperactive in mania)

37
Q

Which enzyme produces IP3 and DAG?

A

Phospholipase C (PLC)
-cleaves the sugar-phosphate head off the inositol phospholipid -> generating IP3 and DAG

38
Q

What are the effects of IP3 and DAG?

probably don’t need to know the details

A

IP3 binds channels on the endoplasmatic reticulum and causes Ca2+ release in the cell

-DAG stays in the plasma membrane and gets attached to the activated PKC -> newly released Ca2+ binds to PKC and starts a cascade that contributes to manic episodes

-blocking this pathway results in mood stabilization

KNOW That Lithium inhibits two enzymes in the recycling pathway that prevent the formation of IP3 and DAG

39
Q

What effect does Lithium have on second messenger systems?

Side effects

A

it uncouples receptors from their G-proteins and thereby preventing second messenger action

-TSH binds to TSH-R on thyroid -> release of T3, T4
blocked by Lithium -> Hypothyroidism

-ADH (antidiuretic hormone): for water reabsorption -> blocked, so more urine output
-> nephrogenic Diabetes insipidus, Polydipsia, Polyuria

Others:
-Tremor
-Edema
-Ance
-Joint or muscle pain
-brittle nails/or hair

40
Q

How is Lithium excreted?

A

entirely in the urine

-clearance is about 20% of creatinine

-Plasma half-life is about 20 hours

41
Q

What are the signs of toxicity?

A

-vomiting, profuse diarrhea
-severe tremor, ataxia
-coma, and convulsions

can be caused by diuretics: sodium depletion can increase Lithium levels
-NSAIDs: decreases clearance
-Antipsychotics: more EPS

-narrow therapeutic index (2-3), monitor of Lithium levels needed

Neurologic & Psych (36 decks)

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