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Pharm > Add, Headache, Bipolar > Flashcards

Add, Headache, Bipolar Flashcards

1
Q

ADHD

Occurs in-
Funct impairment-

A
  • 6-9% of children aged 5-12 yrs (b:g=4-8:1)
  • 60-80%
  • 50%: symp in adulthood (b:g=1:1)
  • only preschool children w moderate to severe dysfunction are considered for drug treatment
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2
Q

Goals of therapy

A
  • improv in core symp
  • reduc in associated symp
  • impr functional outcomes
  • incr ability of child to exert control when desired as opposed to controlling child
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3
Q

Medication can

A
  • imp short term learning
  • prolong attention span
  • imp concent
  • redu impulsiveness, hyperactivity, aggressive
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4
Q

Stimulant medications

A
  • sche II (monthly prescr)
  • dopamine & NE reuptake inhibitor (prolonging dopamine receptor effects)
  • efficacy> 70%
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5
Q

Methylphenidate-MOA

A

Immediate
Intermediate
Long acting

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6
Q

Methylphenidate-application

A

Patch- for 9 h

DexMethylphenidate- focalin (4-5 h)

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7
Q

Methylphenidate-AD

A
  • headache (12-14%)
    -loss of appetite
  • insomina
  • abdominal pain

Emotional lability & dysphoria seen at beginning of therapy
1-4% pts discontinue due to ADRs

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8
Q

Amphetamines

A

Enters CNS, affects mood n alertness
Study aid in 60’s, appetite suppressant

  • dextroamphetamine
  • addrall
  • lisdexamphetamine
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9
Q

dextroamphetamine

A
  • amphetamine
  • short
  • intermediate
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10
Q

Adderall (racemic mis of amphetamine salts)

A

-amphetamine

  • intermediate
  • long acting
  • racemic mix of amphetamine salts
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11
Q

Modafinil

A
  • amphetamine substitute
  • use in narcolepsy

ADs:

  • less mood changes
  • less insomnia
    -less abuse (than amphetamines)
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12
Q

Lisdexamphetamine

A
  • amphetamine
    -long acting
  • prodrug of dextro-amphetamine (activated in GI)
    -1st pass metabolism

enters CNS to affect mood & alertness

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13
Q

Lisdexamphetamine- application

A
  • noninjectable
    -not ADHD diagnostic
  • study aid in 60s
  • appetite suppressant in 70s
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14
Q

Lisdexamphetamine- ADs

A

misuse
abuse
tolerance

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15
Q

TCA

A

Impramine

Desipramine

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16
Q

Imipramine/ Desipramine (TCA)

A

given to pts who cannot tolerate amphetamines

ADHD (low dose); not comorbid depression or anxiety

ADs: develop tolerance w long term use

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17
Q

SSRIs

A

used alone or given in combo with Methylphenidate

ADs: fewer ADs & reduced toxicity (than TCAs)

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18
Q

Stimulant medi for adhd

A 
Methylphenidine
Dextroamphetamine
Adderall
Lisdexamphetamine
Modafinil
Imipramine, desipramine
Ssri
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19
Q

Non stimulant medi

A

Atomoxetine

Clonidine

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20
Q

Atomoxetine

A
  • inhibits reuptake of presynaptic NE
    -not effective when combined with amphetamines: delayed therapeutic effect
  • works well for adolescents
  • AD: decreased appetite, N/V, fatigue
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21
Q

Clonidine

A
  • regulates NE release from locus ceruleus
  • reduces symptoms alone or in combo with stimulants
    -reduces symptoms of aggression & insomnia with stimulants
  • most frequently prescribed for ADHD
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22
Q

Guanfacine (intuniv)

A

-alpha 2 ago (for ADHD)
- 6 yrs -adolescents (oral: extended release)
(ADs)
Cardiovascular- bradycardia, hypo, ortho,syncope
CNS- sedation, drowsiness
Dermatological- skin rash w exfoliation (d/c)

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23
Q

ADHD

Charac-
Symp-
Risk for-

A
  • impulsiveness, heightened distractibility & short atten
  • symp: before 7yrs ( >6 mon)
  • at risk for developing new psychiatric disorders
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24
Q

Migraines

Gender
Onset
Pain location
Type of pain
Duration
A 
f (3:1)
Onset-Variable
Loca-Unilateral
Type-Pulsating, N,V, photo, phonophobia aura
Dur- 2h, 3 d
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25
Q

Cluster

Gender
Onset
Pain location
Type of pain
Duration
A 
Gender- M (10:1)
Onset- During sleep
Pain location- behind, around eye
Type of pain- stabbing, boring, sweating, flushing, nasal congestion
Duration- 15-90 m
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26
Q

Tension

Gender
Onset
Pain location
Type of pain
Duration
A 
Gender- f(2:1)
Onset- variable
Pain location- bilateral in band
Type of pain- non-pulsating, mild photo, phono
Duration- 30 m, 7d
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27
Q

MIGRAINE: 2 TYPES

A
  1. ) Common: without aura. Severe unilateral, pulsating. Can be aggravated by physical activity. Accompanied
    by N and V, photo and phonophobia. Approx 85% of migraine sufferers do not have aura.
  2. ) Classic: with aura. The aura can be visual, sensory, may cause speech or motor problems
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28
Q

TREATMENT AND PREVENTION OF MIGRAINES

A

Goals: be realistic
Treatment: with oral meds, relief and normal function within 2 hours
Prevention: total prevention unrealistic

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29
Q

GENERAL PRINCIPLES OF MIGRAINE MANAGEMENT

A

-Individual management
-Treatment choice depends on:
Attack frequency and severity
Presence and degree of disability Associated symptoms
Prior response and patient preferences
Coexistent conditions
-Establish dosing limits (2 days/week)

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30
Q

TREATMENT: ABORTIVE THERAPY (tries to stop headache)

-Must begin at onset to get full effect: 50-80% achieve significant relief Simple analgesics:

A

Acetominophen-Tylenol
NSAIDs: PG inhibitors (decrease serotonin release)
Ergotamine
‘Triptans: serotonin system
Memantine
Misc. agents: Midrin, Metoclopramide, Chlorpromazine, Prochiorperazine

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31
Q

TREATMENT: PROPHYLACTIC THERAPY (increase time between headaches)

A

Beta blockers, Clonidine, Antidepressants, Cyproheptadine, Topiramate (anticonvulsant), Calcium channel blockers, Valproate, Anticonvulsants, NSAIDs, Methysergide

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32
Q

CLUSTER HEADACHE

A

Short, severe, episodic, clustering pain over the eyes and the forehead. Clustering is the predominant feature with cluster periods lasting between 2-3 months in most patients. Remission may last from 2 months to 20 years (usually 2 years). Episodes more common in the spring and fall. A family history is not usually present. Usually at night.

33
Q

TREATMENT

A

1.) Abortive therapy: Ergotamine, Oxygen, Topical anesthetics, Misc agents-Capsaicin, Prednisone, leuprolide
2.) Prophylactic therapy: Lithium, Ergotamine, Methysergide, Misc agents-non Rx analgesics, B-blockers,
antidepressants, Cyproheptadine, Calcium channel blockers, anticonvulsants

34
Q

Migraine- cortical spreading depression

A
  • most common cause of migraine- self propagating wave of depolarizing cortical neurons associated w a large efflux of K ions
  • dilates middle meningeal artery
  • opens blood brain barrier
  • cause aura in susceptible pt
35
Q

ERGOT ALKALOIDS/METHYSERGIDE

MOA

A

action at several types of Rs including agonist, and antagonist actions at alpha adrenergic and serotonin Rs and agonist actions at CNS dopamine Rs. (Can make histamine, ACh)
(LSD is an Ergot alkaloid)

36
Q

ERGOT ALKALOIDS/METHYSERGIDE

Pharmacokinetics

A

variably absorbed from the GI tract; aided by administration with caffeine (100mg/mg of ergot). The ergot alkaloids are extensively metabolized in the body (caffeine increases absorption) (Inhaler)

37
Q

ERGOT ALKALOIDS/METHYSERGIDE

Effects

1.) CNS: hallucinogenic, bromocriptine and pergolide are best at suppressing prolactin secretion

A
  1. ) Vascular Smooth M: drug, species, vessel dependent. Ergotamine constricts human blood vessels; assoc’d w partial alpha agonist effects; prolonged vasospasm possible(also contract uterine smooth m)
  2. ) Uterine Smooth M: alpha agonist +serotonin effect+others. Ergovine most selective in this effect (can be used after delivery to decrease blood loss)
38
Q

ERGOT ALKALOIDS/METHYSERGIDE

ADs

A

1.) GI: NVD
2.) Prolonged vasospasm: especially after overdose
3.) Fibroplastic changes
4.) Ergot Poisoning: often from infected grain (claviceps purpurea) dementia

39
Q

DRUG INTERACTIONS

A

-Propranolol (+ Ergot): vasoconstriction with pain and cyanosis
-Macrolides (Erythromycin, Clarithromycin, Azithromycin) may exacerbate ergot toxicity

40
Q

CLINICAL USES OF ERGOT

1.) Migraine

A
  • Ergot decreases inflammation
    -Most effective when given during prodrome of an attack
  • May be repeated; no more than 6mg/attack and 10mg/week
  • Not usually as prophylaxis
41
Q

CLINICAL USES OF ERGOT

2.) Hyperprolactinemia

A

: usually seen with anterior pituitary tumors and antipsychotics

-Bromocriptine is the drug of choice
-Suppress lactation also

42
Q

CLINICAL USES OF ERGOT

3.) Postpartum Hemorrhage:

A

3.) Postpartum Hemorrhage: never give before delivery; increases mortality of mom and baby

43
Q

SEROTONIN AGONISTS (CHECK THESE TO MAKE SURE)

A

ADR: taste alterations, N, V, chest tightness, nasal discomfort, increased BP

Contraindicated in ischemic heart disease, uncontrolled hypertension, coronary heart disease

Don’t take with ergot (b/c additive side effects)

44
Q

1.) THE TRIPTANS

A

Sumatriptan, Zolmitriptan, Rizatriptan, Naratriptan, Eletriptan, Almotriptan, Frovatriptan

These agents have been shown to be effective for the treatment of migraine with or without aura, but
have not been studied well in the management of other types of headache. (Zolmitriptan has been shown to be a more potent agonist)

45
Q

TRIPTANS

Moa

A

MOA: selective serotonin-like R agonists (5HT-1D subtype)

Structurally similar to serotonin

Pharmacokinetics: Sumatriptan is rapidly absorbed after oral or subQ injection. Significant 1st pass effect
-Available in Nasal spray, injection, tablets

46
Q

TRIPTANS

Pharmacodynamics:

A

Onset of relief 10-90 minutes after subQ administration, 1.5 to 2 hours after oral and nasal administration (don’t need to know these times)

Duration of action shorter than migraine: may need several doses before headache is over. Doesn’t decrease length of headache, makes pain go away.

47
Q

TRIPTANS

Adverse Effects/Overdose:

A

tingling, dizziness, muscle weakness, neck pain, 5% ches pain, >10% hot flashes

48
Q

TRIPTANS

Drug Interactions

A
  • May exacerbate prolonged vasospasm if used with other anti-migraine drugs (ergot, propranol, etc), or MAOI’s and SSRIs
  • Inhibitors of CYP450-3A4 may decrease metabolism of many of these agents
49
Q

The ‘Triptans’: Advantages over Ergot

A

-More selective pharmacology (so more narrow in focus)
-Simple and consistent pharmacokinetics (get where they’re going to) -Evidence based prescribing instructions
-Well established efficacy and safety
-Fewer and less severe ADR

50
Q

2.) MIDRIN

A

2.) MIDRIN
-A combo product for patients who can’t take ergot or don’t respond to it (less effective)

MOA: Isometheptane 65mg: vasoconstrictor
Dichlorphenazone 100mg: mild sedative
Acetaminophen 325mg: pain relief (not enough; most pt’s need 500-600mg)

51
Q

Midrin

ADs

A

Adverse Effects/Overdose: dizziness, insomnia, N,V, transient numbness

Less Effective than ergot

52
Q

EXCEDRIN MIGRAINE

A

Acetominophen, aspirin and caffeine
May be as effective as sumtriptan for treatment of acute migraine in some patients Most useful in patients with infrequent, mild to moderate headaches without nausea

53
Q

SEROTONIN AGONISTS

A

TRIPTANS

Midrin

54
Q

Bipolar Disorder

A
  • This disorder, previously know as manic depressive illness, is a cyclical disorder with recurrent fluctuations in mood, energy and behavior encompassing the extremes of human experiences.
  • This disorder is genetically based,
    environmentally influenced, and the clinical presentation differs from individual to individual.
55
Q

Bipolar disorder

-Lifetime prevalence rate of a manic episode 1.6% for men, 1.7% for women

A
  • Rare before puberty and after 65, Usual age range of onset 18-44 yrs
  • Genetics
    higher genetic risk than do major
    depressivedisorders. Approximately80 90% of bipolar patients have a relative, parent, sibling, or child with a mood disorder.
56
Q

Bipolar disorder

Bipolar is characterized by mood swings (mania and depression) that are outside the range of normal mood changes.

A

Patients usually experience periods of mood elevations (called mania or hypomania) that alternate with normal mood states

-Individuals can differ in symptoms, course, severity, and response to treatment

57
Q

Bipolar disorder

Bipolar I,II,Cyclothymic disorder

A

Bipolar I-at least one manic episode, major
depression is common
Bipolar II- major depression along with hypomania
Cyclothymic disorder- non major depression and hypomania
Bipolar NOS (not otherwise specified) usually milder features

58
Q

BIPOLAR DISORDER

Clinical presentation

A

Clinical presentation- Does not require a history of depression, but mania or
hypomania that is not caused by any other medical condition, substance, or mental disorder.

Several medications and withdrawal syndromes can mimic manic and hypomanic symptoms.

59
Q

Acute Bipolar Depression

Mood stabilizer

A

Lithium, valproic acid, extended release carbamazepine

60
Q

Acute Bipolar Depression

Antipsychotics

A

Olanzapine, aripiprazole, riseridone, quetiapine

61
Q

Acute Bipolar Depression

Antidepressants

A

Combo mood stabilizer (olanzapine n fluoxetine)

62
Q

Long term treatment

A

Monotherapy w lithium, valproic acid, lamotrigine, aripiprazole

Combinatioon w olanzapine

Extended release cabamazepine

63
Q

Treatment

Medication/ psychotherapy, thyroid work up needed

A

Manic episode

  • 1st episodes: lithium plus benzodiazepines (clonazepam) for sleep
  • if no response in 2-3 wks add a 2nd agent
64
Q

Treatment

Recurrent or severe episodes
- Prophylactic therapy/ or maintenance

A

Prophylactic therapy/ or maintenance

  • If 2 major episodes try maintenance therapy
  • For breakthrough episodes add antipsychotics, benzodiazepines (check for Li induced hypothyroidism)
65
Q

Lithium
1st truly antimanic drug for bipolar
depression

A

Efficacy- 70-80% :prevents and treats both mania and depression

Long term- more effective

Other uses- schizophrenia, migraine impulse control, steroid induced mania, aggressive disorders

66
Q

Pharmacokinetics

A

Solutions absorbed better than regular or slow release formulations

Not affected by food

Renally excreted- not metabolized
Renal dysfunction can double T 1/2

67
Q

Pharmacodynamics

Onset 5/7 d

A

Affects synthesis, storage, release, uptake of NE, serotonin, dopamine, ACH, and GABA

Competes with Ca, Mg, K, Na in body tissues and binding sites

Stabilized post synaptic receptor sensitivity
Antimanic effect 10 after 28 days;antidepressant after 21 days;

68
Q

Adverse Effects
Lithium

-early

A

Gi upset, nausea, polydipsia, polyuria, nocturia, dry mouth, fine hand tremor, leukocytosis, m weak, difficulty concentrating, impaired memory

69
Q

Adverse Effects
Lithium

  • long term
A

Weigt gain, rash, acne, hypothyroidism, psoriasis, alopecia,

70
Q

Lithium

Adverse effect
Overdose problems

A

Toxicity- severe drowsiness, coarse hand tremor, m twitching, myoclonus, choreoathetosis, cogwheel rigidity, vomiting, hyperreflexia, nystagmus, seizures, coma

Mid toxicity- dec memory n concentration

71
Q

Lithium

Adverse effect
Overdose problems

A

> 1.5mEq
agitation, confusion, headache,nystagmus, tremors

>3 mEq/L
tonic/clonic twitching, seizures,
irreversible brain damage, respiratory complications, coma death

72
Q

Lithium

Adverse effect
Overdose problems

A

Dialysis can help but need to correct fluid and electrolyte abnormalities

73
Q

Monitoring

Decrease dose in elderly and those on diuretics, with renal disease, dehydration, or poor cardiac output.

A

ECG-every 6-12 m ( >50 yrs), cardiac ds

Vital signs, CBC with differential, weight, thyroid functions, renal function and urinalysis

74
Q

SERUM CONCENTRATION MONITORING

A

-Narrow therapeutic index
-Levels every 2-3 days in patients prone to toxicity- range is 0.6-1.2mEq/L 12 hours
after the last dose
-In acutely manic patients levels should be at least 0.8mEq/L and as high as 1.5mEq/L toxicity

75
Q

Lithium

Use
Cautions

A

Acute mania, maintenance

Narrow therapeutic index, thyroid tox

76
Q

Valproate

Use
Cautions

A

Acute mania

Liver, pancreas tox, sedation wt gain

77
Q

Lamotrigine

Use
Cautions

A

Maintenance

Rash

78
Q

CBZ

Use
Cautions

A

Acute mania

Sedation, heme effects

Pharm (19 decks)

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