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Adv Pharm 1 > Neuro (pt 4/4) Anti-Depressants & Parkinson's Dz > Flashcards

Neuro (pt 4/4) Anti-Depressants & Parkinson's Dz Flashcards

1
Q

What is Major Depressive Disorder (MDD)?

A

(unipolar) Often totally disabling, interfering with work, sleep, and eating

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2
Q

What is Dysthymia?

A

Less severe than major depression and involves long term chronic symptoms that do not disable but keep a person from functioning at their highest level

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3
Q

What is Bipolar Disorder?

A

(manic depressive disease) Characterized by cycles of severe highs and gut-wrenching lows, often develops into psychotic states

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4
Q

What are discontinuation symptoms of SSRIs, SNRIs, and TCAs?

A

Dizziness and paresthesias beginning 1-2 days after sudden d/c of the drug
-May persist for 1 wk or longer

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5
Q

What are discontinuation symptoms of MAOIs?

A

Delerium like state with psychosis, excitement and confusion

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6
Q

What are the general pharmacokinetics of Anti-Depressants?

A

-PO absorption is rapid (Peak 2-3 hours)
-Tightly bound to plasma proteins (bad for malnourished, low albumin, anorexic patients)
-Hepatic metabolism
-Cleared renally
-Inhibit CYP metabolism (!!!!)…beware of drug-drug interactions when patients are on anti-depressants

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7
Q

What are the therapeutic uses for Anti-Depressants?

A

-Psychological depression (Major; Dysthymia)
-Anxiety Disorders: PTSD, OCD, General Anxiety Disorder, Panic Disorders, Phobias
-Pain Disorders
-Premenstrual Dysphoric Disorder
-Smoking Cessation
-Eating Disorders
-Bipolar disorder: Lithum +/- anticonvulsant medications

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8
Q

What is Monoamine Oxidase?

A

Enzyme that breaks down catechols.
Two types:
-MAO-A = present in the NE and Dopamine neurons (Primarily in the brain, gut, placenta, liver)
-MAO-B = present to a greater extent in Serotonin and Histamine neurons

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9
Q

What do you give if patient is hypotensive and takes MAOI?

A

If hypotensive, need to give a direct acting vasopressor (not one that increases levels of catechols - would cause exaggerated response)

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10
Q

How do Monoamine Oxidase Inhibitors (MAOIs) work?

A

-Allows for neurotransmitters to accumulate over a period of weeks
-induces down regulation of adrenergic and serotonin receptors
-Currently rarely used due to toxicity and potentially lethal food/drug interactions
-Reserved for tx of depression unresponsive to newer drugs
-Some benefit in Parkinson’s

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11
Q

What are the potentially lethal food interactions with MAOIs?

A

Tyramine - smoked meats, wine, cheeses

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12
Q

What are the adverse effects of MAOIs?

A

Orthostatic hypotension
Weight gain
High incidence of sexual dysfunction
Sedation vs. insomnia or restlessness

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13
Q

A first generation anti-depressant
-Tricyclic Antidepressant
-Non selective axon terminal reuptake inhibitor of NE and Serotonin

A

Imipramine (Tofranil)

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14
Q

What are the adverse effects associated with Imipramine (Tofranil)?

A

-Increased BP & HR
-Insomnia, anxiety, agitation, sedation
-Anti-cholinergic effects: Dry mouth, constipation, urinary retention, blurry vision, confusion
-Potential for orthostatic hypotension
-Weight gain
-Sexual dysfunction

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15
Q

A selective serotonin reuptake inhibitor (SSRI) (SSRIs are the most common anti-depressant in use)
-Primary action is the inhibition of the serotonin transporter
-Less SE than Tricyclic

A

Fluoxitine (Prozac)

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16
Q

What are the adverse effects associated with Fluoxitine (Prozac)?

A

GI upset
Diminished sexual function/disinterest
HA, insomnia or hypersomnia
Most SSRI’s are Category C Drugs (fetal effects in animal studies)

17
Q

An atypical - heterogenous drug.
-Second/third generation anti-depressants
-Tetracyclic structure
-A pre-synaptic Alpha2 Adrenergic receptor antagonist on NE and serotonin neurons
-Inhibitor of these auto-receptors increases the release of NE and serotonin
-Not associated with sexual side effects
-Not commonly used – reserved for MDD that is unresponsive to other agents

A

Mirtazapine (Remeron)

18
Q

An atypical - heterogenous drug.
-Treatment for an acute exacerbation as well as prevention
-Ill defined mechanism
-Sustained lithium exposure stimulates Glutamate reuptake (Reducing the effects of the excitatory transmitter)
-Inhibits second messenger formation (IP3 & DAG) and glycogen synthase kinase-3
-Not metabolized – excreted entirely in the urine

A

Lithium – for Bipolar Disorder

19
Q

What are the Adverse Effects associated with Lithium?

A

Tremor, choreoathetosis, motor hyperactivity, ataxia, dysarthria, aphasia
Hypothyroidism
Polyuria, polydipsia, loss of responsiveness to ADH
Edema
C/I in Sick Sinus Syndrome b/c of SA node depression
Questionable teratogenicity

20
Q

Overall, toxicity and SEs are the least in which class of anti-depressants?

A

SSRIs

21
Q

How is MAOIs effect on BP diet dependent?

A

MAOIs can cause orthostatic hypotension.
-MAOIs inhibit the catabolism of dietary amines
-Tyramine is found in aged cheese, red wine, and beer
-Tyramine is a catecholamine releasing agent
↑NE = ↑BP ⟹ HTN Crisis
-MAO also metabolizes histamine therefore MAOI’s are also antihistamine antagonists

22
Q

What are the ANS effects of Lithium toxicity?

A

Nephrogenic Diabeties Insipidous
(Blocks ADH effects)

23
Q

What is the cause of Parkinsonism?

A

Lack of dopamine in the brain
-Muscle rigidity, bradykinesia, tremor, postural instability
-Cognitive declination as the disease advances
-Affective disorders – anxiety or depression
-Personality changes
-Autonomic dysfunction (Sphincter or sexual dysfunction, choking, sweating abnormalities, sensory issues)
-Progressive
-Treatment – essentially D2 stimulation, symptom management only

24
Q

What is the treatment for Parkinsonism?

A

-D2 Stimulation
-Symptom management
-Levodopa/Carbidopa
-Dopamine Agonists
-MOAI
-COMT Inhibitors

25
Q

Why do you give Levodopa/Carbidopa for Parkinsonism instead of IV Dopamine?

A

IV Dopamine cannot cross the blood-brain barrier. Levodopa can cross BB barrier. Carbidopa is given to reduce dose of Levodopa needed.
-Give Levodopa on an empty stomach; food decreases absorption

26
Q

The immediate metabolic precursor to dopamine.
-Rapidly absorbed from the small intestine (food decreases absorption)
-1-3% of dose enters the brain = High doses needed. The rest is metabolized to dopamine in the periphery and does not cross the BBB.
-Drug alone, benefits diminish after 3-4 years

A

Levodopa

27
Q

Why do you administer Levodopa with Carbidopa?

A

-1-3% of dose enters the brain = High doses of Levodopa needed.
-The rest is metabolized to dopamine in the periphery and does not cross the BBB
-Peripheral metabolism is reduced when administered with a dopa decarboxylase inhibitor (Carbidopa) that does not cross the BBB
-Plasma levels are higher, half-life of Levodopa is increased – more is available to reach the brain (reduce doses of Levodopa needed).

28
Q

What are the adverse effects associated with Levodopa?

A

-Anorexia, N/V
-Avoid phenothiazines (Ex. Compazine) due to Reduce effectiveness of levodopa
-Cardiac arrhythmias (tachycardia, afib)
-Postural Hypotension
-Behavioral effects more common in combo therapy
-Depression, anxiety, agitation, insomnia, somnolence, confusion, delusions, hallucinations, nightmares, euphoria
-Tardive Dyskinesia (80% of patients on Levodopa for >10 years)

29
Q

What are the symptoms of Tardive Dyskinesia?

A

Grimacing
Tongue movements
Lip smacking
Lip puckering
Pursing of lips
Excessive eye blinking

30
Q

-Dopa decarboxylase inhibitor that does not cross the BBB
-Decreases peripheral metabolism of Levodopa
-Plasma level of Levodopa is higher
-Half-life of Levodopa is increased → more Levodopa is available to reach the brain
-Levodopa + Carbidopa = decrease the daily dose of Levodopa by 75%

Adding Carbidopa prevents adverse effects r/t inc NE, more levodopa gets into the CNS.
-Can give much less Levodopa

A

Carbidopa

31
Q

A dopamine agonist.
-high affinity for D3
-Monotherapy for parkinsonism
-Can be used in pts with advanced disease allowing for Levodopa dose to be reduced
-Rapidly absorbed
-Excreted mostly unchanged in the urine

A

Pramipexole

32
Q

A dopamine agonist.
-high affinity for D2
-Monotherapy for parkinsonism
-Can be used in pts with advanced disease allowing for Levodopa dose to be reduced
-Metabolized in the liver by CYP450 system

A

Ropinirole

33
Q

A dopamine agonist.
-skin patch
-Provides more continuous dopaminergic stimulation than oral meds in early disease
-Localized reactions at application site

A

Rotigotine

34
Q

What are the adverse effects associated with Dopamine Agonists (Pramipexole, Ropinirole, and Rotigotine)?

A

Anorexia, N/V
Constipation, dyspepsia, reflux, peptic ulcer bleeding
Postural hypotension
Cardiac arrhythmias (d/c therapy)
Peripheral edema
Tardive dyskinesia
Confusion, hallucinations, delusions

Adv Pharm 1 (28 decks)

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