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Neuro 2 Final > Pharm > Flashcards

Pharm Flashcards

1
Q

name 3 typical antipsychotic agents

A

haloperidol
chlorpromazine
fluphenazine

(haloperidol + “-azines”)

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2
Q

typical antipsychotics

mechanism of action:

A

block dopamine D2 post-synaptic receptors&raquo_space; incr [cAMP]

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3
Q

what are the 3 main side effects of low potency typical agents?

give 2 examples of low potency typical agents.

A

low potency typical agents cause:

  • sedation
  • hypotension
  • seizure-threshold reduction (i.e., incr likelihood for seizures)

chlorpromazine and thioridazine
(“CHeating THieves are LOW”)

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4
Q

high potency typical agents cause what kind of side effects?

A

movement disorders (EPS symptoms)

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5
Q

give 3 examples of high potency typical agents.

A

trifluoperazine
fluphenazine
haloperidol

(“Try to Fly HIGH”)

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6
Q

what percent of D2 receptors should be occupied to provide efficacious treatment?
at what percent would you begin to see EPS side effects?

A

60-75% D2 receptor occupancy = efficacy

≥80% = EPS

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7
Q

what 3 other receptors give non-neurologic side effects assoc w/ low potency typical agents?

A
  • anticholinergic (antimuscarinic) effects: dry mouth, constipation, urinary retention, blurred vision, sedation
  • antihistamine effects: sedation
  • alpha-adrenergic effects: orthostatic hypoT, impotency/ejac interference
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8
Q

what 2 side effects are assoc w/ anti-dopamine effects?

A
  • dopamine receptor antagonism&raquo_space; hyperprolactinemia

- extrapyramidal system SEs (EPS) / tardive dyskinesia (TD)

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9
Q

how would you treat the EPS / tardive dyskinesia assoc w/ the anti-dopamine effects of typical antipsychotic agents?

give 3 options for treatment.

A

anticholinergic agents:

  • diphenhydramine
  • benztropine
  • trihexyphenidyl
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10
Q

which atypical antipsychotic drug causes agranulocytosis?

therefore, what must be monitored while on this drug?

A

clozapine

-must monitor WBCs

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11
Q

neuroleptic malignant syndrome (NMS) is another toxicity of typical antipsychotic agents and is fatal in 10-20% of cases. what drug is given to treat NMS?

A

dantrolene

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12
Q

give the 4 main side effects assoc w/ atypical antipsychotic agents.

A

weight gain
metabolic effects (hyperglycemia, hyperlipidemia)
QT prolongation / ECG changes (only a few)
stroke

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13
Q

which agents, typical or atypical, are more commonly used for first line therapy?

A

ATYPICAL = first line therapy

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14
Q

adherence (compliance) is critical in treatment of psychotic disorders. how can non-adherence be managed?

A

long-acting injectable agents (LAIAs)

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15
Q

what typical (2) and atypical (4) antipsychotics are used as long-acting injectable agents to manage non-adherence?

A 
typical:
-haloperidol decanoate
-fluphenazine decanoate
-------------------------
atypical:
-risperidone
-olanzapine pamoate
-aripiprazole
-paliperidone palmitate
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16
Q

how long does it take to evaluate response to therapy?

A

2–3 weeks

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17
Q

what would you give as an adjunctive therapy in pts that are acutely agitated bc the therapeutic drug hasn’t kicked in yet?

A

benzodiazepines (e.g., diazepam / alprazolam / lorazepam)

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18
Q

what antipsychotic drug is used in pts with suicidal thoughts/behaviors?

A

clozapine

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19
Q 
Question:
A 35‐year‐old homeless man has been taking thioridazine for many years to control his schizophrenia and has experienced numerous typical adverse effects of treatment, including blurred vision, dry mouth, mydriasis, nausea, urinary retention, and constipation. These effects are caused by blockade of which of the following receptors?
A. Alpha adrenergic
B. Dopamine
C. Nicotinic
D. Serotonin
E. Muscarinic
A

E. Muscarinic

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20
Q

which 2 typical antipsychotics have the most antimuscarinic effects?

A

thioridazine

mesoridazine

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21
Q

which 2 atypical antipsychotics have the most antimuscarinic effects?

A

clozapine

olanzapine

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22
Q 
Question:
A 63‐year‐old man presents with social withdrawal, blunted affect and poor hygiene. After taking an antipsychotic medication prescribed for these symptoms, he developed blurry vision, weight gain and excessive salivary secretions. Laboratory results show fasting hyperglycemia. Which of the following drugs is he most likely taking?
A. Olanzapine
B. Haloperidol
C. Lithium
D. Asenapine
E. Valproic acid
A

A. Olanzaprine

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23
Q

weight gain and metabolic effects are side effects from which class of antipsychotics – typical or atypical?

A

ATYPICAL&raquo_space; weight gain, metabolic effects, stroke

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24
Q 
Question:
A highly agitated 23‐year‐old woman is admitted to a psychiatric unit complaining that “dead people” are telling her that she is going to be buried alive. She also claims that Jimmy Fallon has been reading her mind and telling everyone her intimate secrets on TV. Organic causes for the patient’s behavior are ruled out, and a thorough psychiatric evaluation indicates that her current behavior did not arise secondary to a mood disorder. The patient is treated with a drug considered to be appropriate for her condition. Two days later she complains of severe pain in the eyes and neck and is found to have a fixed upward gaze and a twisting upward torsion of the head. Treatment with which drug would most likely cause the patient’s eye and neck problem?
A. Amitriptyline
B. Chlorpromazine
C. Fluphenazine
D. Lithium
E. Risperidone
A

C. Fluphenazine

Fluphenazine (+++) > Chlorpromazine (++)

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25
Q

EPS symptoms are most likely to result as a side effect from which class of antipsychotics – typical or atypical?

A

TYPICAL&raquo_space; EPS

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26
Q

which 4 typical antipsychotic drugs are most likely to induce EPS as a side effect in a pt? (only looking at (++++) and (+++))

A

haloperidol (++++)
fluphenazine (+++)
trifluoperazine (+++)
pimozide (+++)

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27
Q

which 1 atypical antipsychotic drug may cause EPS as a side effect in a pt?

A

lurasidone (+++)

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28
Q 
Question:
A 38‐year‐old patient is being treated with clozapine for negative symptoms associated with schizophrenia. Which of the following laboratory tests is most important to monitor during initial therapy?
A. Red blood cell count
B. Platelet count
C. Serum creatinine
D. White blood cell count
E. Serum lipase
A

D. White blood cell count

“Must watch CLOZapine CLOZely!”

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29
Q 
Question:
A 31‐year‐old man with schizophrenia is evaluated because of signs of tardive dyskinesia. He has been treated with several different medications to control his schizophrenia during the past several years. His physician stops treatment with his current medication and prescribes clozapine 25mg. He is currently taking no other medications. This patient is most likely to require special monitoring and surveillance due to the potential of clozapine to cause which of the following adverse effects?
A. Agranulocytosis
B. Seizures
C. Diabetes
D. Orthostatic Hypotension
E. QT prolongation
A

A. Agranulocytosis

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30
Q 
Question:
A 22‐year‐old schizophrenic patient is unfortunately diagnosed with NMS following treatment with a high‐dose, multi‐drug regimen for his psychiatric condition. Which of the following agents is best suited for therapy of this condition?
A. Alprazolam
B. Dantrolene
C. Phenytoin
D. Aspirin
E. Valproic acid
A

B. Dantrolene

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31
Q 
Question:
A 41‐year‐old schizophrenic patient is being treated with haloperidol and chlorpromazine and develops a drug‐induced acute dystonic reaction. Which of the following is the most appropriate acute therapy?
A. Lithium
B. Diphenhydramine
C. Imipramine
D. Tranylcypromine
A

B. Diphenhydramine

May also use benztropine or trihexyphenidyl

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32
Q 
Question:
In comparing neuroleptics, which of the following is more likely associated with skeletal muscle rigidity, tremor at rest, flat facies, uncontrollable restlessness, and spastic torticollis?
A. Haloperidol
B. Clozapine
C. Olanzapine
D. Ziprazidone
E. Quetiapine
A

A. Haloperidol

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33
Q 
Question:
A 22‐year‐old, obese college student is diagnosed with schizophrenia. Which of the following medications would be most appropriate given her current weight while also effectively treating her schizophrenia?
A. Aripiprazole
B. Divalproex
C. Clozapine
D. Amitriptyline
E. Olanzapine
A

A. Aripiprazole

-Although atypical antipsychotics (like aripiprazole) usually cause weight gain, aripiprazole (0/+) is the least likely of the atypicals. If a typical antipsychotic was an answer choice, it would be a better choice.

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34
Q 
Question:
A schizophrenic patient has a history of cardiac arrhythmias due to a prolonged QT interval. Which agent should be avoided in this patient because it can cause further QT prolongation, with an associated risk of serious ventricular arrhythmias, including torsades de pointes?
A. Diazepam
B. Fluoxetine
C. Phenobarbital
D. Phenytoin
E. Thioridazine
A

E. Thioridazine

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35
Q 
ECG changes are predominantly a side effect from which class of antipsychotics - typical or atypical?
which typical antipsychotic drug is most likely to cause ECG changes in a pt?
A

TYPICAL&raquo_space; ECG changes

thioridazine

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36
Q

most atypical antipsychotics do not cause ECG changes. however, if an atypical antipsychotic is used and ECG changes (QT prolongation) result, which drug was most likely used?

A

ziprasidone

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37
Q 
Question:
A 31‐year‐old woman is treated with an antipsychotic agent because of a recent history of spontaneously removing her clothing in public places and claiming she hears voices telling her to do so. Her BP is normally 130/70 mmHg. Since being treated, she has had several bouts of syncope. Orthostatic hypotension was noted on physical exam. Which of the following drugs most likely caused the syncope?
A. Chlorpromazine
B. Fluphenazine
C. Haloperidol
D. Olanzapine
E. Ziprazidone
A

A. Chlorpromazine

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38
Q

which 2 typical and 1 atypical antipsychotics are most likely to cause hypotension as a side effect?

A

typical:
chlorpromazine
thioridazine

atypical:
clozapine

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39
Q 
Question:
A 36‐year‐old woman has had schizophrenia for several years, during which time she has received various types of medications. Her current treatment is with thioridazine, and she is experiencing amenorrhea and galactorrhea. Which of the following antipsychotic agents would be more appropriate for this patient to decrease the severity of her current adverse effects?
A. Quetiapine
B. Haloperidol
C. Paliperidone
D. Risperidone
E. Thiothixene
A

A. Quetiapine

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40
Q

hyperprolactinemia is a side effect of which class of antipsychotic drugs – typical or atypical?

A

TYPICAL&raquo_space; prolactin

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41
Q

which atypical antipsychotic drug is most likely to give hyperprolactinemia?

A

risperidone

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42
Q

which 2 atypical antipsychotics are most likely to cause weight gain, metabolic effects, and seizures?

A

clozapine

olanzapine

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43
Q

which 3 atypical antipsychotics are most likely to cause stroke?

A

olanzapine
paliperidone
risperidone

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44
Q

which 3 typical antipsychotics are most likely to cause sedation (may be used with atypical at night to induce sleep)?

A

chlorpromazine (+++)
mesoridazine (+++)
thioridazine (++/+++)

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45
Q

What are the 2 categories for ADHD meds?

A

Stimulants and non-stimulants

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46
Q

What are the stimulant drugs for ADHD?

A
  • Amphetamine (d,l), Dextroamphetamine (d) (Methamphetamine)
  • Lisdexamfetamine (pro‐drug)
  • Methylphenidate (d/d,l) & Dexmethylphenidate (d)
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47
Q

What are the non-stimulant drugs for ADHD?

A

Atomoxetine
Guanfacine
Clonidine

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48
Q

What are the MOA of stimulants (ADHD)?

A

Main effect of stimulants is to enhance neurotransmitter transmission via:

  • Inhibition of neurotransmitter pre‐synaptic reuptake (DA & NE)
  • Increase neurotransmitter release (amphetamines only)
  • Amphetamines greater impact on dopamine synthesis, storage/release, and reuptake
  • Methylphenidate’s main focus of activity is on inhibition of dopamine reuptake
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49
Q

TQ What are the Amphetamine salts* drugs for ADHD?

A
  • Adderall (IR/XR): *Amphetamine (2 different salt forms) and *Dextroamphetamine (2 different salt forms)
  • Dextroamphetamine: Dexedrine/Dextrostat
  • Methamphetamine: Desoxyn
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50
Q

TQ What are the Methylphenidate drugs for ADHD?

A
  • Ritalin (IR/SR/LA)
  • Concerta
  • Methylin
  • Metadate (IR/ER/CD)
  • **Quillivant XR (oral suspension)
  • **Daytrana (patch)
  • Dexmethylphenidate (Focalin (IR/XR))
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51
Q

What is Lisdexamfetamine a pro-drug of?

A

dextroamphetamine (vyvanse)

less risk of drug abuse because no initial high

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52
Q

TQ The onset of activity for stimulants is what?

A

Less than 24 hours

works immediately! versus non-stimulant…3 days before the school year and the kid is focused

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53
Q

TQ Are stimulants controlled substances?

A

Yes (1 month supply only, no refills, no samples)

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54
Q

Adderall is made of 2 amphetamine salts and comes in an IR and ER forms. What proportion of the long acting product is immediate release versus long acting release?

A

XR = 50% IR beads and 50% XR beads

XR Duration = 8‐12 hours (shorter for IR form) for most indiv

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55
Q

T/F: Dexedrine/dextroamphetamine doesn’t last as long as other agents

A

True

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56
Q

TQ: Vyvanse (lisdexamfetamine; pro‐drug of _______________)

A

Long acting!

dextroamphetamine

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57
Q

Longest DOA for all methylphenidate derivatives

A

Concerta (d,l‐methylphenidate)

10-12 hours

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58
Q

What separates concerta from other agents?

A

-methylphenidate (not amph.)
-not 50%/50% ratio b/c different delivery system: “Biphasic” release property (OROS)
• Phase 1: 22% IR
• Phase 2: 78% ER

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59
Q

Ritalin (d,l‐methylphenidate)

SR and LA DOA and ratio of IR to LA

A
  • SR DOA = 4‐8 hours (shorter for IR form)
  • LA DOA = 8‐10 hours
  • LA = 50% IR beads and 50% LA bead
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60
Q

TQ!!

  • Only extended‐release oral solution available (liquid)
  • Lowest IR highest ER ratio
  • Distributed as a powder requiring reconstitution prior to dispensing…comes in liquid
  • No need to refrigerate, yet do need to shake well
A

Quillivant XR (d‐methylphenidate)

20% immediate‐release and 80% extended‐release methylphenidate formulation

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61
Q

Metadate (IR/ER/CD) (d,l‐methylphenidate)

ER and CD DOA, and ratio

A
  • ER DOA = 6‐8 hours (shorter for IR form)
  • CD DOA = 8‐10 hours
  • CD = 30% IR beads and 70% CD beads
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62
Q

TQ Which stimulant drug is the patch?

A

Daytrana (patch) (d,l methylphenidate)

  • Onset of activity within 2 hours (1‐2 hours)!!
  • good for kids in the morning before school
  • benefit: removable, not re-applicable, easy application
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63
Q

Focalin (dexmethylphenidate)

IR DOA, ER DOA, and ratio

A

Focalin (dexmethylphenidate)

  • IR DOA = 4‐6 hours hours
  • XR DOA = 10‐12 hours hours
  • XR = 50% IR beads and 50% XR beads
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64
Q

MOA of non-stimulant agents for ADHD?

A

Main effect of non‐stimulants is to enhance neurotransmitter transmission via:

  • Inhibition of neurotransmitter pre‐synaptic reuptake (only NE) (atomoxetine)…Also has down‐stream impact on DA system due to overlap
  • Activation of centrally‐located (CNS) alpha‐2 adrenergic receptors (guanfacine/clonidine)…Post‐synaptic alpha‐2 inhibition in prefrontal areas
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65
Q

TQ What is the onset of activity for non-stimulant agents?

A

2-4 weeks! or longer… (much slower than stimulants)

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66
Q

Which pt groups is non-stimulant agents for ADHD good for?

A
  • Useful for patients intolerant of stimulant effects or parents resistant to stimulant class
  • Non‐scheduled, refills without visit, samples
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67
Q

Atomoxetine (straterra) and Guanfacine (Intuniv) are both….

A

long acting and once a day

18-24 hours

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68
Q

Clonidine is available in IR and ER but IR has to be taken up to 3x a day. ER duration of action is…

A

18-24 hours

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69
Q

What are some SE of stimulants?

A
  • Decreased appetite (Weight loss)
  • Insomnia
  • Headache/Stomach‐ache
  • Irritability/Aggression: (Tics, Psychoses)
  • Elevated BP/HR
  • Sudden cardiac death (rare): Cardiac structural abnormalities
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70
Q

What are some SE of non-stimulants?

A
  • Decreased appetite (Weight loss)
  • Insomnia (atomoxetine)
  • Sedation/Somnolence (guanfacine/clonidine)
  • Headache/Stomach‐ache
  • Dizziness
  • Suicidal ideation (rare; atomoxetine)
  • Liver injury (rare; atomoxetine)
  • Hypotension (guanfacine/clonidine)
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71
Q

T/F: Can be in remission in psychiatry

A

True!

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72
Q
  • ___-_______: 25-50% reduction in symptoms
  • Remission: Symptom-free or near symptom-free
  • Recovery: sustained remission for at least 8 wks w/o worsening symptoms
  • Relapse: return of symptoms 6 mo after response (depressive breakthrough)
A

Non-response

Response

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73
Q

T/F: Antipsychotics can be used to treat depression

A

True!

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74
Q

T/F: Antidepressants can be used to treat other issues, such as anxiety, PTSD, panic disorder, OCD, etc

A

True!

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75
Q

What are the SNRI’s used as antidepressants? (5)

Serotonin-Norepi Reuptake Inhibitors

A
  • TCAs
  • Desvenlafaxine
  • Duloxetine
  • Venlafaxine

-Amoxapine (SNRI + DRA)

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76
Q

What are the SSRI’s used as antidepressants? (7)

Serotonin-Selective Reuptake inhibitors

A
  • Citalopram
  • Escitalopram
  • Fluoxetine
  • Paroxetine
  • Sertraline
  • Vilazodone
  • Vortioxetine
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77
Q

What is the NDRI used as an antidepressant? (1)

Noradrenergic-Dopamine Reuptake Inhibitors

A

Bupropion

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78
Q

What are the SARA’s used as antidepressants? (3)

Serotonin-Adrenergic Receptor Antagonists

A
  • Mirtazapine (+H1 blockade)
  • Nefazodone
  • Trazodone
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79
Q

What are the MAOI’s used as antidepressants? (3)

Monoamine Oxidase Inhibitors

A
  • Phenelzine
  • Selegiline
  • Tranylcypromine
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80
Q

What is the MOA of TCAs?

A

-inhibit the reuptake of NE and serotonin (5HT)

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81
Q

TQ: What are the 3 key side effects of TCAs?

A
  • Cardiovascular (alpha): orthostatic hypotension
  • Anticholinergic (muscarinic): dry mouth, constip
  • CNS (histamine): **sedation
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82
Q

What are some additional SE’s of TCAs?

A
  • Weight gain
  • Sexual dys
  • SIADH
  • Altered glucose metab
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83
Q

TQ What are the 3 things you see with TCA overdose?

A

“Quinidine-like” effects (Na channel blockers)

  • Coma
  • Cardiotoxicity (conduction abnormalities)
  • Convulsions
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84
Q

What is the MOA of SSRIs?

A

-Selectively inhibit the reuptake of serotonin eventually resulting in down-regulation of post-synaptic receptors

(differences are kinetic and indication)

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85
Q

What are some SE of SSRI’s?

A
  • sexual dys
  • GI: N/V/D/C
  • CNS: sedation
  • weight gain
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86
Q

What is the most serious SE of SSRI’s?

A

Serotonin syndrome

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87
Q

TQ
Which SSRI has an extremely high risk of drug-drug interactions (CYP450)? Which 2 SSRI’s have the least risk of CYP450 interactions?

A

***Fluoxetine=most risk

citalopram and sertraline=least risk

88
Q

What is the MOA of SNRI’s?

A

-selectively inhibit the reuptake of 5HT and NE eventually resulting in down-regulation of post-synaptic receptors

89
Q

SNRI’s key differences are CYP450 effects and indications. SE’s are similar to…

A

SSRI’s

90
Q

ALL antidepressants either are, or can be, associated with withdrawal syndrome…therefore what is recommended?

A

slow titration downward is recommended

significant for venlafaxine

91
Q

MAOI’s MOA

A

non-selective (A & B) inhibit MAO thereby incr levels of NE, 5HT, and DA except for selegiline (patch) b/c selective

92
Q

MAOI’s key differences are pharmacokinetics and risk of ___________ _____

A

hypertensive crisis

wine and cheese assoc due to drug decr tyramine metab

93
Q

MAO’s SE? (3)

A
  • orthostatic hypotension
  • sexual dys
  • weight gain
94
Q

What are the mood stabilizers that are anti-seizure agents? (4) what is the misc mood stabilizer? (1)

A

anti-seizure agents:

  • carbamazepine
  • lamotrigine
  • divalporate
  • valproic acid

misc: Lithium

95
Q

What are the 3 key actions of lithium?

A

-inhibits calcium-dep release of NE, DA, and 5HT

96
Q

TQ What is lithium indicated for?

A

acute and maintenance treatment of mania/bipolar disorder

97
Q

TQ What is lithium similar to?

A

monovalent Na+/K+ ion

incr Na+/K+ clearance from kidneys…electrolyte issues

98
Q

TQ

What are 2 impt lithium SE?

A
  • Hyponatremia

- Nephrogenic Diabetes Insipidus!!!! (polyuria/polydipsia)

99
Q

TQ

What does lithium have drug interactions with? (3)

A
  • Diuretics (furesomide)
  • ACEIs (K+ issues)
  • NSAIDs
100
Q

TQ

T/F: Lithium is a narrow therapeutic agent: 0.4-1.5 mEq/ml

A

True!

can be toxic over 1.5

101
Q

Divalproex is used for ______ psychotic features (bipolar)

A

acute

102
Q

Carbamazepine is used for _____ and __________ (bipolar) treatment

A

acute and maintenance

103
Q

Lamotrigine is used for (bipolar) ____________

A

maintenance

104
Q

Carbamazepine is a major ________ inhibitor! drug-drug interactions!!

A

CYP450

105
Q

SE of anti-seizure mood stabilizers for bipolar disorder

A

Carbamazepine: sedation, blurred vision, hepatotoxicity

Divalproex: temor, hepatotoxicity

Lamotrigine: ataxia/tremor

106
Q

Which antidepressant has strong alpha1-adrenergic and histamine blocking effects?

A

TCAs: amitriptyline

107
Q

Which group of anti-depressants inhibits the reuptake of both serotonin and norepi but doesnt have an effect at histaminergic, muscarinic, or dopaminergic receptors?

A

SNRI’s (not TCAs!)

108
Q

Fluoxetine, Carbamazepine, Omeprazole, Cimetidine, Phenytoin/Phenobarb, Isoniazid

A

Examples of BIG CYP450-affecting agents

109
Q

TQ: Alzheimer’s disease drugs somewhat delay ________ _______ of alzheimer’s disease

A

cognitive decline

110
Q

TQ T/F: Alzheimer’s dz drugs slow the progression of the disease

A

FALSE! They do NOT slow disease progression

111
Q

What are the 4 acetylcholinesterase inhibitors used to treat AD? What are their indication level (mild mod sev)

A
  • Tacrine (rare)
  • Donepezil (mild-mod-sev)
  • Rivastigmine (mild-mod)
  • Galantamine (mild-mod)
112
Q

What is the neuroprotective agent used to treat AD?

A

Memantine

113
Q

What is the time course for AD?

A

2-3 years: symptom onset, cognitive decline, AD dx
(drugs target here)

2 years: decline, nursing home

3-4 years: Dementia & death

114
Q

T/F: Patients, families, and caregivers should NOT expect dramatic results with AD drugs

A

TRUE

  • on avg, drugs effective for 6-12 month in 50% of pts
  • modest clinical effects (1-2 pt difference in mental status exam after 2 years of tx)
115
Q

What is the cholinergic hypothesis of alzheimers dz?

A

Degeneration of basal forebrain nuclei–>deficit in central cholinergic transmission

drugs may compensate for deficit in early stage dz…AChE inhib compensate for cognitive deficits

116
Q

TQ: Tacrine is _________, not selective, poor tolerability while the other 3 AChE inhib are brain selective. However, rivastigmine isn’t AChE selective.

A

hepatotoxic

117
Q

TQ Rivastigmine interacts with BuChE (pseudocholinesterase) as well as AChE

Galantamine is a weak ______ receptor agonist

A

nicotinic

118
Q

TQ Which two AChE inhib must you take with food?

A

Rivastigmine and galantamine

119
Q 
TQ 
Which AChE inhib is this?
-long half life 60 hrs, 1 daily 
-CYP 2D6 & 3A4
-glucuronidation
A

Donepezil

less likely for drug-drug interactions

120
Q 
TQ 
Which AChE inhib is this?
-shorter half life (1/2 hr)
-Esterases-NOT CYP450
-less risk for interference by metab of other drugs
A

Rivastigmine

121
Q 
TQ 
Which AChE inhib is this?
-half life=6 hr
-CYP 2D6 & 3A4
-undergoes glucuronidation
A

Galantamine

122
Q

PNS somatic: NMJ, nicotinic

PNS autonomic: muscarinic

CNS: both _____ and ______

A

nicotinic and muscarinic

123
Q

Muscarinic receptors in the CNS are located in the….(3)

nicotinic receptors? (3)

both: corpus striatum, cerebral cortex, hippocampus, thalamus, hypothalamus, cerebllum

A

midbrain, medulla, pons

substantia nigra, locus coeruleus, septum

124
Q
  • Good CNS entry
  • Some PNS distrib=peripheral muscarinic side effects
  • use: Alheimers dz
A

Donepezil
Rivastigmine
Galantamine

125
Q

________ side effects assoc with dosing errors and fatal aspiration pneumonia when switch from donepezil to rivastigmine

A

Peripheral

126
Q 
TQ
Muscarinic AE of AChE inhib....
DUMBELLS:
-Defection
-Urination
-Muscle weakness, miosis
-**Bradycardia, bronchorrhea, bronchospasm (killer b's)
-Emesis
-Lacrimation
-Salivation, sweating

key word…

A

Discharge!

increases the discharge of feces, urine, mucus, tears, vomiting, saliva, sweat

127
Q

In which pt are AChE inhib contraindicated? What should we use instead?

A
  • sick sinus syndrome
  • AV block
  • *COPD
  • *asthma
  • peptic ulcer
  • aspiration pneumonia (bad gag reflex)
  • dehydration (electrolyte abnorm)

Use Memantine!

128
Q

Neostigmine, pyridostigmine, edrophonium have NO CNS entry, limited distrib, and are used to reverse paralysis by nicotinic R antag. Why cant they get into the CNS?

A

They are positively charged!

129
Q

__________ has widespread distrib, peripheral muscarinic and nicotinic SE, and used to reverse atropine poisoning

A

physostigmine (PNS)

130
Q

MOA of memantine?

A

NMDA receptor antag blocks Ca influx and blunts neural death

amyloidosis destruct cells via GluR (NMDAR) excitotoxicity ….leads to neural death

connected to memory..if too much glu, NMDA R activated, calcium levels incr –>cell degeneration

131
Q

SE of memantine?

A

:) HA, dizziness, cleared by kidney (fewer risk of drug-drug interactions)

132
Q

How can we fix dementia in AD? What is the risk?

A

atypical antipsychotics risperidone, olanzapine, or quetipine for agitation and psychosis in AD

risks of AE, parkinsonism, sedation, falls, stroke, mortailty

133
Q

5th leading cause of death in the US?

A

medication-related problems!

134
Q

Pts with AD are even more sensitive to CNS toxicity of other drugs with ____-______ effects (part of aging as well)

A

anti-muscarinic

ex: atropine lowers cholinergic activity of mm. and glands=blurred vision, dry mouth, flushing, confusion, hot

135
Q

Compare and contrast anti-cholinesterase inhibitors overdose with anti-cholinergic effects?

A

anti-cholinesterase:

  • defacation
  • urination
  • miosis
  • bradycardia
  • bronchospasm
  • bronchorrhea
  • salivation, sweat

anti-cholinergic/muscarinic:

  • **confusion and delirium
  • constipation
  • urinary retention
  • mydrasis
  • tach
  • bronchodil
  • anti-secretory
  • dry mouth, no sweat
136
Q

What is the “beers criteria”

A

list of drugs considered inappropriate for older pts due to ineffectiveness of high risk for AE

137
Q

OTC cold meds (antihistamines) disrupt muscarinic receptors and can cause what? (on the beers list)

A

anti-cholingeric effects

avoid in AD!!!

138
Q

As you age, renal blood flow and GFR goes down. So serum creatinine alone isn’t a proxy for GFR in elderly pts because why?

A
  • reduced lean body mass=reduced creatinine prod
  • Less creatinine prod + decr GFR=masks change in creatinine clearance

(Serum Cr appear normal while kidney function (GFR) deteriorates)

139
Q

Which drug type is preferred in the elderly and why?

Phase I or II hepatic metabolism

A

phase II hepatic metab (inactive metab, glucuronides) preferred in elderly. CYP450 phase I metab can turn some metabolites to active form. and risk of interactions increase

140
Q

Inactivated directly by phase II metab and is preferred in the elderly

A

benzodiazepam (temazapam)

141
Q

What is the antidote for benzodiazepams (benzo antag)?

A

Flumazenil

142
Q

Pt presents with generalized anxiety disorder. Do you prescribe a benzo alone or a benzo + SSRI?

A

Benzo + SSRI

benzo may be discontinued after SSRI takes effect

143
Q

A __________ is a drug that decr CNS activity, moderates excitement, and calms the recipient. They are fast-acting compared to SSRIs

A

sedative

144
Q

A ________ is a drug that produces drowsiness and facilitates the onset & maintenance of sleep and from which the recipient can be aroused easily. Involve more pronounced CNS depression which can be achieved by incr the dose

A

hypnotic

145
Q

TQ
What are the dose-response curves for these two sedative-hypnotic classes?
Drug A: barbituates, alcohols, and older sedative-hypnotics
Drug B: benzos, newer sedative-hypnotics

A

Drug A: linear
Drug B: plateau

  • barbituates: if incr dose/overdose, then sedation»coma (linear)
  • benzos: if overdose then tops off at sleep/anesthesia (plateau)
146
Q

Benzodiazepines:

Acts on which receptor and causes what to occur?

A
  • Act on GABAa receptors

- cause sedation, hypnotic effects, m. relaxation, anxiolytic, anticonvulsant

147
Q

Barbituates:

Acts on which receptor and causes what to occur?

A
  • Act on GABAa receptors

- cause mild sedation to anesthesia

148
Q
  • widely distributed: CNS, placenta, *breast milk
  • hepatic metabolism/excretion (cumulative toxicity)
  • Risk of depedence and tolerance
  • binds GABAa and enhances its effects (shifts dose resposne curve to the left)
A

Benzodiazepines

149
Q

What is the result of benzodiazepams binding to GABAa receptors?

A

-enhances GABA effects (shifts dose response curve left)
-Incr Cl influx»
Hyperpolarization»
Decr AP (CNS depression)

150
Q

When comparing benzos which drug has the longest half life (longest acting) with fast onset and which has the shortest half life (short acting)?

A

Diazepam: longest half life and very fast acting

Midazolam: shortest half life (short acting)

151
Q

Which 2 benzos do not undergo heavy hepatic metabolism and are therefore a good choice for pts with hepatic insuff?

A

Lorazepam
Oxazepam

(no active metabolites!)

152
Q

Which benzo would you choose for an outpt undergoing alcohol withdrawal?

A

Diazepam (very fast onset with long half life)

153
Q

Which benzo would you choose for pre op?

A

Midazolam (short acting!)

154
Q

Which benzos are more likely to cause cumulative toxicity?

A

those with long half lives such as diazepam*, lorazepam, and clonazepam

(shorter acting: alprazolam, oxazepam, temazepam, midazolam, triazolam)

155
Q

For a pt with addictive tendencies, should you choose a benzo that has a fast onset or slow onset of action?

A

slow! (cant seek that initial “high”)

156
Q

Which benzo has active metabolites and is highly addictive due to long duration and fast onset?

A

Diazepam

157
Q

Which benzo is good for treating acute anxiety because it is intermediate acting and intermediate onset?

A

lorazepam

158
Q

Which benzo has a slow rate of onset ?

A

Oxazepam

159
Q

Which benzo would be extremely risky when given to an addict? Why? Which benzo should you give?

A

Avoid:
*Alprazolam (very fast onset), Diazepam (fast onset)

Give:
*Lorazepam (intermediate onset & HL)
Clonazepam (intermediate onset & HL)
Oxazepam (slow onset & short HL)

160
Q

For an addict with anxiety, what is most likely prescribed?

A

Buspirone

161
Q
  • Used to treat generalized anxiety disorder
  • effects take more than a week
  • does not cause sedation, hypnotic, euphoric, anticonvulsant, or muscle relaxant effects
  • CYP450 metab!
  • unknown MOA
A

Buspirone

162
Q
  • widely distributed throughout the body: CNS, placenta, breast milk
  • Hepatic metabolism and kidney excretion
  • Inducer of CYP450!
  • Binds GABA to incr. duration
  • Risk of dependence and tolerance
  • overdose»coma
A

Barbituates

163
Q

What is the MOA of barbituates?

A 
Binds GABAa receptor >>
increases duration of GABA channel opening>>
Incr Cl influx>>
Hyperpolarization>>
Decr AP>>
CNS depression
164
Q

Which GABAa receptor agonist would help to treat insomnia?

A

Zolpidem or zaleplon

165
Q

Pt has difficulty falling asleep. Tx?

A

Zolpidem or zaleplon (short HL)

less risk than benzo/barbs

166
Q

Pt has difficulty staying asleep. Tx?

A

Eszopiclone (longer acting)

167
Q
  • Hepatic metabolism and kidney excretion
  • CYP450 interactions
  • short half lives (
A 
Newer hypnotics (sleep aids)
such as:
-eszopiclone (Lunesta)
-zolpidem (Ambien)
-zaleplon (Sonata)

(“Z-drugs”) zzzzzzz

168
Q

What are some clinical uses of sedative-hypnotics?

A
  • Relief of anxiety
  • Insomnia
  • Sedation and amnesia before and during medical surgical procedures
  • Treatment of epilepsy and seizure states
  • Component of balanced anesthesia (IV administration)
  • Control of ethanol or other sedative-hypnotic withdrawal states
  • Muscle relaxation in specific neuromuscular disorders
  • Diagnostic aids or for treatment in psychiatry
169
Q

T/F: Benzos do not help treat addiction/tolerance to benzos

A

FALSE:

Give benzos for treatment of other sedative-hypnotic withdrawal such as benzos

170
Q

What are the advantages to using benzos to treat anxiety? disadvantages?

A

:)

  • high therapeutic index
  • antidote available (flumazenil)
  • low risk of drug-drug interactions
  • minimal cardio/autonomic effects

:(

  • Risk of dependence
  • CNS depression
  • Amnestic effects
  • CNS depression when w/ alcohol (coma)
171
Q

Why would we use Z-drugs instead of benzos for treatment of insomnia?

A
  • Benzos have hangover effects such as sedation and run risk of cumulative toxicity if long acting
  • Z drugs have rapid onset with minimal hangover, no amnesia/tolerance
172
Q

Which melatonin agonist can be used for treatment of insomnia? Which pt group should we be careful giving them to?

A

Ramelteon (acts as MT1 and MT2 R)

  • Liver impairment pts: be careful because hepatic 1st-pass metabolism means that may need to change dosage
  • Risk of CYP450 interactions
173
Q

Main SE of Ramelteon?

A
  • endocrine changes (decr testosterone and incr prolactin

- other SE: dizziness, somnolence, fatigue

174
Q

All inhaled anesthetics end in what? Which drug is the exception?

A

“-ane” ex: deslurane, enflurane, etc

the exception is nitrous oxide

175
Q

All of the following are examples of what type of drug?

  • Dexmedetomidine
  • Diazepam (Valium)
  • Etomidate
  • Fentanyl
  • Fospropofol
  • Ketamine
  • Lorazepam
A

IV anesthetics

176
Q

The _______ _______ is a collection of component changes in behavior or perception that include:

  • unconsciousness
  • amnesia
  • analgesia
  • attenuation of autonomic reflexes to stim
  • Immobility in response to stim (skeletal m. relaxation)
A

anesthetic state

177
Q

T/F: All of the currently available anesthetic agents when used alone can achieve all five of the desired states of anesthesia

A

FALSE! None can do it alone! mix them up

178
Q

Where do anesthetics primarily act?

A

At the synapse

  • Presynaptic: release of neurotransmitters
  • Postsynaptic: frequency/amplitude of impulses exiting at the synapse
179
Q

MOA of general anesthetics:

-include which ion channels?

A

Inhibitory (Cl channels via GABAaR & glycineR)

Excitatory (Ach nAChRs/mAChRs, EAA/Glu via APMA, kainite, & NMDA receptors, and Serotonin 5HTR)

180
Q

______ and _______ anesthetics are administered by inhalation

A

volatile and gaseous (NO)

181
Q

For inhaled anesthetics, what are the two key determinants of PK and how quickly the CNS concentration changes?

A
  • uptake via gas exchange in the alveoli

- distribution

182
Q

TQ: What is the driving force for uptake of inhaled anesthetics?

A

alveolar concentration

driven by inspired air concentration and alveolar ventilation

183
Q

Partial pressure in the alveoli is expressed as a ratio of alveolar concentration (Fa) over inspired conc (Fi). The faster Fa/Fi approaches 1, the _______ anesthesia will occur during inhaled induction

A

faster

faster taken up=faster distrib

184
Q

The ______:____ _______ _________ defines the relative affinity of an anesthetic for the blood compared with that of inspired gas (blood solubility)

A

blood:gas partition coefficient

185
Q

What is the relationship between blood:gas coefficient and rate of anesthesia onset?

A

Inversely related

186
Q

Agents with____ solubility (NO, desflurane) reach high arterial pressure _____, which results in rapid equil with brain and fast onset of action

A

low, rapidly

(conc lung>blood...small
blood compartment (high conc) sends it into brain!)
187
Q

Agents with ____ blood solubility (halothane) reach high arterial pressure ______, which in turn results in slow equil with brain and slow onset of action

A

high slowly

(conc blood>lung…goes immediately into
blood from inhalin), blood
highly distributed so takes
longer to get it to brain )

188
Q

What determines the affinity of an anesthetic for the brain compared to the blood?

A

brain:blood coefficient

189
Q

Which inhaled anesthetic is an incomplete anesthetic with rapid onset and recovery?

A

Nitrous oxide (100% MAC with 0.47 blood:gas)

fast because 0.47 blood:gas coeff

190
Q

Which inhaled anesthetic has the lowest MAC, medium rate of onset and recovery, and is soluble in blood?

A

Halothane

191
Q

______ ______ _______ is the concentration of inhaled anesthetics that prevents movement in response to surgical stimulation in 50% of subjects

A

Minimale alveolar concentration (MAC)

192
Q

MAC is also a measure of ______

A

potency

193
Q

MAC values greater than ____% indicate that even if ____% of the inspired air at barometric pressure is the anesthetic, the MAC value would still be less than 1 and other agents must be supplemented to achieve full surgical anesthesia

A

100%

Ex: nitrous oxide 40% + 70% of volatile agent=110% MAC :)

194
Q

What are the 4 stages of increasing depth of CNS depression?

A

Stage 1: analgesia
Stage 2: excitement
Stage 3: surgical anesthesia
Stage 4: medullary depression

195
Q
  • Inhaled anesthetics ______ the metabolic rate of the brain and increase cerebral blood flow (not ok in incr ICP)
  • Risk of respiratory depression
A

decrease

196
Q

Halothane can cause bradycardia while desflurane and isoflurane _________ HR

A

increase

197
Q

What are some toxicities of inhaled anesthetics?

A
  • N/V
  • Halothane: hepatitis
  • Renal toxicity if have fluoride (enflurane, sevoflurane)
198
Q

TQ When inhaled anesthetics are used with succinylcholine, malignant hyperthermia (tach + HTN), severe m. rigidity, rhabdomyolysis, hyperthermia, hyperkalemia, and acid-base acidosis may occur. What is the antidote?

A

Dantrolene (blocks calcium release from sarcoplasmic reticulum)

199
Q

__ ________ are widely used to facilitate rapid induction of anesthesia and are the preferred method of anesthesia induction in most settings

A

IV anesthetics

200
Q

T/F IV anesthetics do not produce all the desired changes so use balanced anesthesia with inhaled anesthetics, sedative-hypnotics, opiods, and NM blockers

A

True!

201
Q

IV anesthetics are highly lipophilic and therefore prefer the brain and spinal cord. Therefore, they have a _____ onset of action

A

quick

202
Q
  • MOA: GABAa agonist IV anesthetic
  • averages 30 seconds for onset of action
  • 3-10 min duration of action (dose and rate dependent)
  • rapid rate of onset and recovery
  • half life stays about the same
  • continuos infusions and maintenance of anesthesia, sedation in ICU, conscious sedation and short-duration general anes in locations outside the OR
A

Propofol

203
Q

Since propofol is highly insoluble it is formulated as an emulsion containing soybean oil, glycerol, and lecithin/egg yolk. Therefore watch out for ______ ______. Propofol may also cause hypotension and respiratory depression

A

allergic reactions

204
Q

What is the water-soluble prodrug of propofol?

A

Fospropofol

-onset and recovery prolonged b/c prodrug must be converted to active form

205
Q
  • IV anesthetic that enhances GABA effects on GABAa R
  • produces rapid loss of consciousness with less rapid recovery rate
  • minimal cardiovascular and respiratory depression (useful in pts with impaired CV/resp. systems/heart pts)
  • extensive liver and plasma biotransformation
A

Etomidate

206
Q

Adverse effects of etomidate?

A
  • Adrenocortical suppression

- limited use for continuous infusion (bad for long term ICE pts or those in induced coma)

207
Q
  • IV anesthetic that is an NMDA receptor antag, similar to PCP
  • *Only IV anesthetic to produce profound analgesia
  • produces dissociative anesthetic state: catatonia, amnesia, analgesia, w/ or w/ out loss of consciousness
  • slow nystagmic gaze back and forth
  • stimulates symp NS
A

Ketamine

208
Q

Ketamine adverse reactions?

A

-vivid colorful dreams, hallucinations, out of body experiences, increased distorted visual, tactile, and auditory sensitivity

209
Q
  • IV anesthetic that is an alpha-2 adrenergic agonist that produces hypnosis from stim of alpha 2 in the locus caeruleus
  • analgesic effects at the level of the spinal cord
  • sedative effect resembles physiologic sleep state
  • principally used for the short-term sedation of intubated and ventilated pts in an ICU setting or as an adjunct to general anesthesia
A

Dexmedetomidine

210
Q

What are 3 classes of anesthesia adjuncts?

A

Opioids
Barbituates
Benzos

211
Q

Notes on anesthesia adjuncts:

  • Opioids: agonist at opiate receptors such as fentanyl, sufentanil, remifentanil, morphine, risk of resp dep., often used in ___
  • Barbituates: incr. dur of GABAa channel opening such as thiopental, methohexital, risk of resp dep and CYP450 induction
  • Benzos: increase GABAa receptor sensitivity to GABA, antidote=flumazenil
A

preop

212
Q

-Dose response curve for NT and NT plus midazolam shifted left. What is the NT?

A

-GABAa

(decreases sensitivity of R to GABA so
shifts dose response curve to the left…barbs interact with GABA channel and extend its opening to allow
more cl in. Benzos allow receptor to open with less GABA conc so moves curve left …this is a change in potency aka x axis)

213
Q

Pt goes in for ocular surgery. Which IV anesthetic drug is rapid in onset/recovery and antiemetic?

A

Propofol

214
Q

lower blood:gas partition=_______onset

A

quicker

215
Q

Why can nitrous oxide be used alone?

A

MAC is greater than 100%

Neuro 2 Final (5 decks)

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