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CMED 311 > Trans 038 Pharma (Amil) > Flashcards

Trans 038 Pharma (Amil) Flashcards

1
Q

• Most common cause of dementia in the elderly.

A

Alzheimers Disease

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2
Q

• Manifest with an insidious loss of episodic memory followed
by slowly progressive dementia.
• Brain atrophy in the medial temporal lobes, spreading to
lateral and medial parietal, temporal lobes and lateral frontal
cortex

A

Alzheimer’s Disease

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3
Q

Histologic findings in AD?

A

• Histologically, lesions are neuritic plaques, containing beta
amyloid, neurofibrillary tangles.

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4
Q

Most important risk factor in Alzheimer’s Disease

A

• Most important risk factors: age >70 years and positive family
history

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5
Q

Major Genetic Risk in Alzheimer’s Disease

A

• Major genetic risk: e4 allele of ApoE gene

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6
Q

Forgetting of words, especially proper names, progressing to forgetting common nouns and until fluency of speech is impaired

A

Dysnomia

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7
Q

impaired facial recognition?

A

Prosopagnosia

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8
Q

Acetylcholinesterase inhibitors (3)

A

Donepezil
Rivastigmine
Galantamine

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9
Q

Target dose Donezepil?

A

10 mg daily

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10
Q

Target dose Rivastigmine?

A

6mg twice daily

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11
Q

Target dose Galantamine

A

24 mg daily, extended release

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12
Q

Acetylcholinesterase inhibitors MOA detailed?

A
  • Patient with AD reduced cerebral content of choline acetyl transferase, which leads to a decrease in acetylcholine synthesis and impaired cortical cholinergic function
  • Cholinesterase inhibitors (donepezil, rivastigmine and galantamine) increase cholinergic transmission by inhibiting cholinesterase at the synaptic cleft and provide modest symptomatic benefit in some patients with dementia
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13
Q

are considered symptomatic therapies and are not believed to be neuroprotective or to alter the underlying disease trajectory

A

AchE

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14
Q

When you give cholinesterase inhibitor there is increase cholinergic transmission. T or F?

A

T

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15
Q
  • Oldest cholinesterase inhibitor still in use

* Remains a preferred and widely prescribed drug in this class due to its once-daily dosing and ease of use

A

Donepezil

Most common because it is the oldest cholinesterase inhibitor

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16
Q

Donepezil starting dose

A

Dose: Start at 5mg/day, increased to 10mg/day after 4-6 weeks

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17
Q

Unique AE of Donepezil?

A

Unique AEs: nightly dosing can be associated with vivid dreaming or nightmares

Other AEs: GI symptoms, symptomatic bradycardia, rhabdomyolysis, neuroleptic malignant syndrome

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18
Q

mental status changes. Madalas side effect ng anti-psychotic drugs. Potentially fatal.

what syndrome?

A

Neuroleptic malignant syndrome

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19
Q

• Available as a twice-daily tablet or solution and as a once-daily extended-release capsule (US)
 When you use it in patients with only mild cognitive impairment there is increase mortality. Usually given to patients with moderate-severe cognitive impairment.
• Has been associated with increased mortality in patients with mild cognitive impairment
• Increase mortality has not been observed in patients treated for AD, mixed dementia or vascular dementia

A

Galantamine

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20
Q

Starting dose of Galantamine

A

• Starting dose: 8mg OD, increase to 16mg OD after 4 weeks then after 4 weeks maintain at target maintenance dose of 24mg OD after 4

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21
Q

what is the contraindication of Galantamine

A

DO NOT USE IN PATIENTS WITH END-STAGE RENAL DISEASE OR SEVERE HEPATIC IMPAIRMEN

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22
Q

• Available in oral and transdermal formulations
 More famous is the transdermal, the patches. More tolerable and efficacy is similar.
• Transdermal patch is preferred over the oral formulation because of better tolerability and similar efficacy

A

Rivastigmine

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23
Q

Patches can cause skin irritation and application sites should be rotated. T or F?

A

T

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24
Q

NMDA Receptor Antagonist?

A

Memantine

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25
Q

Target dose memantine?

A

10 mg BID

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26
Q

is the principal excitatory amino acid neurotransmitter in cortical and hippocampal neurons

A

Glutamate

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27
Q

One of the receptors activated by glutamate is the ______ receptor, which is involved in learning and memory

A

NMDA

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28
Q

T or F? Excessive NMDA stimulation can be induced by ischemia and lead to excitotoxicity, suggesting that agents that block pathologic stimulation of NMDA receptors may protect against further damage in patients with vascular dementia

A

T

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29
Q

More appropriately used for vascular dementia.

A

NMDA receptor antagonists: Memantine

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30
Q

MC adverse effects of memantine

A

Dizziness

Other AE: confusion, hallucinations

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31
Q

Usual dose of memantine?

A

Usual dose: 5mg OD on the 1st week, 10mg OD on the 2nd week, 15mg/day on the 3rd week and 20mg OD on the 4th week onwards
 Has been found

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32
Q

Chronic condition characterized clinically by episodes of focal disorders of the optic nerves, spinal cord and brain, which remit to a varying extent and recur over a period of many years and are usually progressive due to demyelination of nerves.

A

Multiple Sclerosis

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33
Q

Typical features include weakness, paraparesis, paresthesia, loss of sight, diplopia, nystagmus, dysarthria, tremor, ataxia, impairment of deep sensation and bladder dysfunction.

A

MS

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34
Q

Initial symptom of about half of the patients with MS?

A

• Weakness or numbness in one or more limbs is the initial symptom in about half of patients.

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35
Q

Diagnostic Criteria for MS?

A

2 or more typical attacks of CNS demyelination with objective evidence on examination for both lesions

2 clinical attacks c objective evidence on examination for only one lesion

one attack c objective evedence on examination of 2 or more lesions

one attack c objective evidence on examination for only one lesion (clinically isolated syndrome)

Progressive non relapting deficits suggesting of MS

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36
Q

MX of MS?

A

CORTICOSTEROIDS (E.G. METHYLPREDNISOLONE)

• Intravenous administration of massive doses of methylprednisolone (a bolus of 500 to 1000mg daily for 3-5 days) followed by high oral doses of prednisone (beginning with 60-80 mg daily and tapering to a lower dosage over a 12- to 20-day period) is generally effective in aborting or shortening an acute or subacute exacerbation of MS or of optic neuritis.

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37
Q

Adverse effects of corticosteroids in MS?

A

AEs: hypercortisolism, Cushing syndrome, hypertension, hyperglycemia and erratic diabetic control, osteoporosis, avascular necrosis of the head of the femur, cataracts, gastrointestinal hemorrhage and activation of tuberculosis or pneumocystis.

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38
Q

• Modestly alter the natural history of relapsing-remitting MS
 Mas mahal ng kaunti
 Delivered subcutaneously every 2 days
• Given subcutaneously every second day, long term

A

interferon Beta

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39
Q

Dose of Interferon beta for MS?

adverse effects?

A
  • Dose: 30mcg or 6.6 million units

* AEs: development of antibodies to the drug; flu-like symptoms, malaise

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40
Q
  • A.k.a COPOLYMER I

* Mimics actions of myelin basic protein (autoantigen)

A

glatiramer(glatiramer acetate)

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41
Q

Dose and Adverse effects of glatiramer

A
  • Dose: 20mg daily via subcutaneous injection

* AEs: flushing, chest tightness, dyspnea, palpitations and severe anxiety

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42
Q
  • Monoclonal antibody
  • Alters various components of the immune response
  • Directed against alpha-integrin in order to block lymphocyte and monocyte adhesion to endothelial cells and their migration through the vessel wall
  • Used in rheumatoid arthritis and fistulizing Crohn disease
  • Given monthly by IV route
A

Natalizumab

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43
Q

AEs: associated with the appearance of progressive multifocal leukoencephalopathy (PML)

which drug?/

A

Natalizumab

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44
Q

what are the agents that are used to control spasticity/

A
  • Baclofen
  • Tizanidine*
  • Dantrolene
  • Diazepam*
  • Botulinum toxin
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45
Q
  • Toxin derived from Clostridium botulinum
  • Commonly found in canned foods. Most popular use is for its aesthetic indications (improvement of wrinkles, hyperhidrosis)
A

botolinum toxin

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46
Q

MOA Botulinum Toxin

A

• Blocks the release of acetylcholine in the neuromuscular junction, resulting in temporary muscle relaxation/paralysis which improves spasticity

47
Q

route and frequency of botolinum toxin?

A

• Given via intramuscular injections to affected spastic muscles, usually every 10 to 16 weeks

48
Q

MOA baclofen?

A

• Inhibits transmission of monosynaptic and polysynaptic reflexes at the spinal cord level, possible by hyperpolarization of primary afferent fiber terminals with resultant relief of muscle spasticity

49
Q

AE of baclofen?

A

• AEs: abrupt discontinuation of intrathecal baclofen has resulted in sequelae of high fever, altered mental status, exaggerated rebound spasticity, muscle rigidity, rhabdomyolysis, multiple organ system failure and death

50
Q

MOA dantrolene?

A

• Acts directly on skeletal muscle by interfering the release of calcium from the sarcoplasmic reticulum

51
Q
  • IV form is traditionally used for the treatment of malignant hyperthermia and neuroleptic malignant syndrome.
  • Only the oral form is indicated for chronic spasticity.
A

Dantrolene

52
Q

• First-line treatment for status epilepticus (IV)

A

Diazepam IV

53
Q

Diazepam MOA?

A

binds to stereospecific benzodiazepine receptors on the postsynaptic gamma-aminobutyric acid (GABA) neuron in different regions of the central nervous system, increasing the inhibitory effects of GABA which is involved in sleep

54
Q

an α2-adrenergic agonist that acts on the spinal and supraspinal levels to block excitatory interneurons. It reduces spasticity by increasing presynaptic inhibition and has great effects in the polysynaptic pathways. It also possesses a moderate central analgesic effect.

A

Tizanidine

55
Q

• Intense paroxysm of involuntary repetitive muscular contractions

A

convulsion

56
Q

“Transient occurrence of signs and/or symptoms due to abnormal excessive or asynchronous neuronal activity in the brain

A

Seizure

57
Q

Classically, two unprovoked seizures more than 24 hours apart constitutes the diagnosis of

A

Epilepsy

58
Q

A condition resulting either from the failure of the mechanisms responsible for seizure termination of from the initiation of mechanisms which lead to abnormally prolonged seizures (after time point t1). It is a condition that can have long-term consequences (after time point t2), including neuronal death, neuronal injury and alteration of neuronal networks depending on the type and duration of seizures.

A

Status epilepticus

59
Q

Long half lives epileptic drugs?

shorter half lives?

A

Long half-lives (OD dosing): Phenytoin, phenobarbital, ethosuximide
• Shorter half-lives: Valproate, Carbamazepine

60
Q

Leads to accumulation of active Phenytoin/Phenobarbital

what drug interaction?

A

Chloramphenicol + Phenytoin/Phenobarbital

61
Q

___________ REDUCE blood Phenytoin concentration

____________ INCREASE blood phenytoin concentration

A
  • Antacids

* Antihistamines

62
Q

may cause breakthrough menstrual bleeding and failure of oral contraceptive medications in women

what 3 drugs?

A

Phenytoin, carbamazepine, phenobarbital

63
Q
  • Oldest non-sedating drug in the treatment of epilepsy
  • Sodium channel blocking antiseizure drug
  • Available in oral, IM and IV forms
A

Phenytoin

64
Q

• AEs:
o Hirsutism, gum hypertrophy and coarsening of facial features in children may be seen in prolonged use
o “Purple glove syndrome” in IV
o Symptoms of overdose: ataxia, diplopia, stupor
o Has antifolate effect and alters Vit. K metabolism

what drug?

A

Phenytoin

65
Q

• One of the most widely-used antiseizure drugs

DOC for trigeminal neuralgia

A

Carbamazepine

66
Q
  • Prototypical Na-channel blocking antiseizure drug
  • Usually used for focal to bilateral tonic-clonic seizures
  • Causes many of the side effects of phenytoin but to a slighter lesser degree
A

Carbamazepine

67
Q

o Mild leukopenia, pancytopenia, hyponatremia, diabetes insipidus (request for CBC before starting the treatment and recheck regularly)
o May exacerbate absence or myoclonic seizures
o Associated with Steven-Johnsons Syndrome in patients who have HLA-B*1502 allele (Asians are at a higher risk

which drug’s adverse effect?

A

Carbamazepine

68
Q
  • First line broad-spectrum antiseizure drug, used for myoclonic and atonic seizures as well as for generalized tonic-clonic seizures
  • Used as mood stabilizers in bipolar disorder and prophylactic treatment for migraine
  • Usually hepatotoxic in children 2 years of age and younger
A

Valproate/valproic acid

69
Q

• IV form is used in status epilepticus

A

VAlproate

70
Q

which drug’s AE?

o Weight gain in the first months of therapy
o Menstrual irregularities, PCOS
o Pancreatitis
o Tremors, slight bradykinesia

A

Valproate

71
Q

Introduced in 1912 as a sleeping aid; oldest of the currently available antiseizure drugs

A

phenobarbital

72
Q

commonly used in the treatment of epilepsy in children; primary treatment in infantile seizures

A

barbiturate

73
Q

MOA phenobarbital

A

Act as positive allosteric modulator of GABAA at higher concentrations

74
Q

Relatively new drug; broad-spectrum antiseizure agent and on of the most commonly prescribed drugs for epilepsy, primarily because of its perceived favorable pharmacokinetic properties and lack of drug-drug interactions
• No important interactions with other antiepileptic drugs; often used as first-line agent in patients taking numerous medications or those with organ failure

A

Levetiracitem

75
Q

Levetiracetem MOA

A

• Binds selectively to SV2A; which reduces the release of the excitatory neurotransmitter glutamate during trains of high-frequency activity

76
Q
  • Closely resembles phenytoin in its antiseizure activity but different in safety profile
  • Selectively blocks the slow Na-channel, thereby preventing the release od the excitatory transmitters glutamate and aspartate
  • Effective as a first-line and adjunctive drug for generalized and focal seizures
  • May be an alternative to valproate in young women because it does not provoke weight gain and ovarian problems
A

Lamotrigine

77
Q

Adverse effects of Lamotrigine

A

dermatologic eruptions, co-administration with valproate increases serum concentration of lamotrigine.

78
Q

Broad-spectrum antiseizure drug used in the treatment of focal seizures.

Primary generalized seizures and seizures in the Lennox-Gastaut syndrome

A

Topiramate

79
Q

commonly used for migraine headache prophylaxis

A

Topiramate

80
Q

MOA of topiramate

A

MOA not clear; possible sites of action relevant to its clinical activities are (1) voltage-gated Na-channels; (2) GABAA receptor subtypes; (3) AMPA or kainite receptors

81
Q

Produce their functional effects by positive allosteric modulation of GABAA receptors.

are the first-line acute treatment for seizures, either in status epilepticus or acute repetitive seizures (seizure clusters)
• Not commonly used in long-term management of epilepsy

A

Benzodiazepines

82
Q
  • First-line treatment for status epilepticus (IV)

* Rectal gel form used in acute repetitive seizures

A

Diazepam

83
Q

• Used in the treatment for status epilepticus; prolonged duration of action after bolus intravenous injection
 Ativan- drugs used as date rape drug therefore it was banned in the Philippines

A

Lorazepam

84
Q

• May be given intramuscularly; preferred in the out-of-hospital treatment of status epilepticus

A

Midazolam

85
Q
  • Long-acting benzodiazepine; one of the most potent antiseizure agents
  • Useful in the treatment of absence, atonic and myoclonic seizures
A

Clonazepam

86
Q
  • Mostly idiopathic; begins bet. Age 45-70, peaks at the 6th decade of life, affects men more than women
  • Patients manifest with decreased levels of dopamine

• Manifests as expressionless face, poverty and slowness of voluntary movement, resting tremor, stooped posture, axial instability, rigidity and festinating gait

A

PD

87
Q

Tetrad of PD?

A

bradykinesia, resting tremors, rigidity, postural instability

88
Q

Currently the most effective agent in the treatment of PD but not usually used as first drug

A

Levodopa

89
Q

pre cursor of dopamine?

A

Levodopa

90
Q

Levodopa is commonly given with?

A

Carbidopa, a decarboxylase inhibitor which prevents peripheral conversion of levodopa to dopamine

91
Q

If levodopa is given without carbidopa, anorexia, nausea and vomiting may occur. T/F?

A

T

92
Q
  • First-line therapy for PD and their use is associated with a lower incidence of the response fluctuations and dyskinesias that occur with long-term levodopa therapy.
  • Have direct dopaminergic effect on striatal neurons
  • Unlike levodopa, they do not require enzymatic conversion to an active metabolite, act directly on the postsynaptic dopamine receptors, have no potentially toxic metabolites
A

Dopamine Agonist

93
Q

contraindications of Dopamine agonists (3)

A

• Contraindicated in patients with a history of psychotic illness or recent myocardial infarction, or with active peptic ulceration

94
Q

examples of dopamine agonists

A

Bromocriptine, Pramipexole, Ropirinole

95
Q

Tolcapone and entacapone are under what drug class?

A

COMT Inhibitors

96
Q

Selegiline and Rasagiline are under what drug class?

A

Monoamine Oxidase - B Inhibitors

97
Q

MOA of Monoamine Oxidase - B Inhibitors

A

selectively prevents peripheral metabolism of dopamine
• Retards the breakdown of dopamine, thus enhancing the effect of levodopa
• Appear to have neuroprotective effects by decreasing oxidative stress in dopaminergic neurons (CONTORVERSIAL!)

98
Q

is more potent that selegiline and useful as in the early treatment of PD patients with mild symptoms

A

Rasagiline

99
Q

CO-ADMINISTRATION OF LEVODOPA and nonselective MAOI → may result in

A

hypertensive crises

100
Q

Anticholinergics in PD examples?

A

(TRIHEXYPHENIDYL, BENZTROPINE MESYLATE)

101
Q
  • Antiviral agent, given 100mg BID
  • Unknown mechanism of action in PD (NMDA antagonist)
  • Mild to moderate benefit for tremor, hypokinesia and postural symptoms
  • AEs: leg swelling, may worsen CHF, glaucoma
A

Amantadine

102
Q
  • Characterized by periodic, commonly unilateral, pulsatile headaches that begin in childhood, adolescence or early adult life and recur with diminishing frequency during advancing years.
  • Onset of attack usually upon waking up, but may occur at any time of the day
A

MIGRAINE

103
Q

AKA CLASSIC MIGRAINE

• Commonly starts with visual disturbances followed in a few minutes/hours by hemicranial headache, nausea, vomiting, lasting for hours or more

A

migraine with aura

104
Q

(AKA COMMON MIGRAINE) • Lasts for minute to hours, with increasing hemicranial headache, with or without nausea or vomiting

A

MIGRAINE WITHOUT AURA

105
Q
  • One of the most commonly used drug classes, available in both over-the-counter and prescription-only molecules/preparations
  • Anti-inflammatory and analgesic activity is mediated chiefly through inhibition of prostaglandin biosynthesis
A

NSAIDS

106
Q

MOA of NSAIDS?

A

irreversibly acetylates and blocks platelet COX, while the non-COX-selective NSAIDs are reversible inhibitors

107
Q

o Currently first-line therapy for acute severe migraine attacks in most patients
o Ineffective in preventing migraine if given during the aura of migraine
o Should not be used in patients at risk for coronary artery disease/angina because of the risk of coronary vasospasm

A

Triptans (Sumatriptan, Zolmitriptan, Rizatriptan)

108
Q

o 6mg given SQ; 25-50mg oral tablets or nasal spray
o Effective and well tolerated; reduces nausea, vomiting, photophobia, phonophobia
o Headache relief is longer with SQ and inhalation routes

A

Sumatriptan

109
Q

o Alpha agonist with strong serotonin receptor activity and vasoconstrictive action
o As effective as triptans, but notorious for causing peripheral and coronary vasoconstriction; have been associated with strokes
o Useful in cluster headaches

A

Ergot alkaloids (ergotamine)

110
Q

Some Betablockers for migraine?

A

Propranolol: 10-20mg BID/TID up to 240mg daily
• Atenolol: 40-160 mg/day
• Metoprolol: 100-200 mg/day

111
Q

Anti epileptic drugs for head ache?

A
  • Valproic acid 250mg TID to QID

* Topiramate: 23mg per day up to 100mg BID

112
Q
  • Effective in decreasing the frequency and severity of migraine attacks in some patients
  • Usually, there is a lag of several weeks from initiation of drug until benefits are attained
  • Verapamil 320-480 mg/day
  • Nifedipine 90-360 mg/day

what drug class?

A

Calcium channel blockers

113
Q

Increases synaptic concentration of epinephrine and norepinephrine in the CNS by inhibition of their reuptake by the presynaptic neuronal membrane pump

• Do not co-administer with MAOIs

A

TRICYCLIC ANTIDEPRESSANTS (TCAS) (E.G. AMITRIPTYLINE)

114
Q

has been shown to effective in preventing migraine, but not effective in the treatment of acute migraine

A

Amitriptylin

CMED 311 (47 decks)

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