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PAPOM > Neuropharm- Comp 1 > Flashcards

Neuropharm- Comp 1 Flashcards

1
Q

A1 Receptor binding effects

A
  • increased vascular smooth muscle contraction
  • mydriasis (increased contraction of pupillary sphincter m.)
  • increased intestinal and bladder spincter contraction

Gq protein class

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2
Q

a2 R binding effects

A
  • inhibition of NT release ( - NE from nerve endings, Ach from adjacent PS neurons)
  • decreased sympathetic outflow
  • increased platelet aggregation
  • decreased lipolysis
  • decreased insulin release
  • decreased aqueous humor production

Gi protein class

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3
Q

B1 R effects

A
  • increased hr, contractility
  • increased renin release –> which increases BP
  • increased lipolysis

Gs protein class

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4
Q

B2 R effects

A
  • Smooth m. Relaxation (vasodilation in skeletal m., bronchodilation, uterine smooth m., GI smooth m.)
  • CNS: presynaptic Rs stimulate NT release
  • increased aqueous humor production
  • increased HEart contraction
  • increased platelet aggregation
  • increased insulin secretion, increased lipolysis, increased glycogenolysis
  • increased K+ uptake

Gs protein class

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5
Q

NSAIDs
(Aspirin, ibuprofen, naproxen)

Mechanism of Action

A

Cox inhibition

Aspirin is irreversible, others are reversible

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6
Q

NSAIDs
(Aspirin, ibuprofen, naproxen)

Use

A
  • Decrease PGE2 synthesis, stops pain nerve sensitization
  • Early intervention
    against platelet action.
    Acute pain suppression.

Tension headache & Migrane Acute action

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7
Q

NSAIDs
(Aspirin, ibuprofen, naproxen)

Toxicity

A

Bleeding, GI irritation, erosions, and ulcers

  • salicyclism, increased leukotrienes (asthma, allergies) with aspirin
  • -> with allergy to ASA, avoid NSAIDs
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8
Q

Acetaminophen

Mechanism of action

A

Weak COX inhibition

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9
Q

Acetaminophen

Use

A
  • Decease PGE2 synthesis
  • Stops pain nerve sensitization
  • Less GI effects than NSAIDs

Tension headaches

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10
Q

Acetaminophen

Toxicity

A

Liver toxicity at high doses Or EtOH consumption

N-acetylcysteine is the antidote

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11
Q

Benzodiazepines

Examples and Mechanism

A

Estazolam, Flurazepam. Temazepam

Potentiate GABA
at Cl-channel (increase frequency)

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12
Q

Benzodiazepines

Use

A

Muscle relaxant; Anxiolytic
Status epilepticus seizures

Tension headaches

EtOH withdrawal, muscle relaxant, sedative, preop-sedation/induction of mechanically ventillation

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13
Q

Benzodiazepines

Toxicity

A
  • Drowsiness
  • Impaired judgement
  • Depressed motor skills
  • Anterograde amnesia
  • Tolerance
  • Dependence
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14
Q

Antimuscarinics

Examples and MOA

A

Cyclobenzaprine
Methocarbamol
Orphenadrine
Amitriptyline

M3 Block; Amitriptyline (tricyclic antidepressant) inhibits reuptake of 5HT and NE

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15
Q

Antimuscarinics

Use

A

Local Strain, muscle spasm

Tension headaches

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16
Q

Tizanidine

Mechanism of Action

A

Centrally acting α2 adrenergic agonist (reduced norepinephrine outflow)

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17
Q

Tizanidine

Use

A

Muscle relaxant

-Migraine prophylaxis
Multiple sclerosis, amyotrophic lateral sclerosis (ALS)

Also for tension headaches

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18
Q

Tizanidine

Toxicity

A 
Drug interactions (fluoroquinolones) with CYP1A2 
raises tizanadine levels

Results in enhanced CNS effects

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19
Q

“Ergots”

Mechanism of Action, Drugs

A
  • Ergotamine
  • Ergotamine Tartrate and Caffeine (Cafergot)
  • Dihydroergotamine

Vasoconstrictor at
5-HT1B/1D receptor

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20
Q

“Ergots”

Toxicity

A

Vasoconstriction in

coronary arteries. Avoid coronary artery disease, atherosclerosis

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21
Q

“Ergots”

Use

A

Counteracts the early

vasodilating phase of Acute Migrane

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22
Q

“Triptans”

MOA, Drugs

A
  • Sumatriptan
  • Almotriptan
  • Rizatriptan
  • Zolmitriptan
  • Naratriptan
  • Eletriptan
  • Partial Agonist at
    5HT1D/1B receptors
  • Vasoconstriction to reverse vasodilatory phase
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23
Q

“Triptans”

Use

A

Migraine (acute) and cluster
headaches

Oral, Nasal, SQ administration; short duration requires multi-dose, but must limit daily dosing

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24
Q

“Triptans”

Toxicity

A

All Drugs:
Paresthesias, dizziness, muscle weakness, coronary vasoconstriction, chest pain. Not for coronary artery disease patients.

Serotonin syndrome: SSRIs, MAOIs, tricyclic antidepressants, St John’s Wort, linezolid

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25
Q

Propranolol

MOA

A

Nonselective Beta

Blocker

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26
Q

Propanolol

Use

A

Prevents trigeminal
nerve excitement

Migrane Prophylaxis

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27
Q

Propanolol

Toxicity

A
  • Hypoglycemia
  • Bronchoconstriction via beta2 blockade
  • Vasoconstriction
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28
Q

Amitriptyline

MOA

A

Tricyclic blocks

reuptake of 5-HT

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29
Q

Amitriptyline

Use

A

Maintains serotonin
against vasodilating phase

Migrane prophylaxis

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30
Q

Amitriptyline

Toxicity

A
  • Anticholinergic (M3) effects
  • Alpha1 block (orthostasis)
  • H1 block (sedation)
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31
Q

Calcium channel Blockers

Examples and MOA

A

E.g. Verapamil
Diltiazem

Block vascular calcium channels; Vasodilation

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32
Q

Calcium channel Blockers

Use

A

Prevent onset of vasoconstrictive
ischemic phase

Migrane prophylaxis

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33
Q

Ca2+ Channel blockers

Toxicity

A

Hypotension
Constipation
Gingival hyperplasia

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34
Q

Valproic Acid and Valproate

MOA

A
  • Mixed action:
    1. Sodium and calcium channel blocker
    2. Increase GABA synthesis
    3. Reduce GABA degradation
    4. Decreases glutamate at NMDA receptor
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35
Q

Valproic Acid and Valproate

Use

A

Migrane Prophylaxis

Absence Seizures, Myoclonic Seizures, Specific Myoclonic Seizures, Generalized Tonic- Clonic Seizures.

Manic phase of bipolar disorder

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36
Q

Valproic Acid and Valproate

Toxicity

A 
Birth defects (blocks
folate absorption), severe hepatitis, weight gain, GI upset

Inhibitor of CYP

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37
Q

Topiramate

MOA

A

Potentiate GABA

Blocks sodium channels and Glutamate

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38
Q

Topiramate

Use

A

Migrane prophylaxis

Partial Seizures,
Generalized Tonic- Clonic Seizures
Adjunct therapy for headache

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39
Q

Topiramate

Toxicity

A
  • CNS effect
  • Teratogen
  • Reduced oral contraceptive effect
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40
Q

Phenothiazines
Prochlorperazine

MOA

A

Dopamine receptor antagonists. Also M3 and histamine H1 blockade.

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41
Q

Phenothiazines
Prochlorperazine

Use

A

Antiemetic

Used in migrane prophylaxis

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42
Q

Phenothiazines
Prochlorperazine

Toxicity

A

EPS symptoms and Parkinson’s like effects, increase in prolactin, muscarinic (M3) and histamine (H1) blockade.

Elevated QT interval.

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43
Q

Botulinum toxin

MOA

A

Cleavage of Snap-25 protein, which prevents vesicle fusion, release of Ach vesicles

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44
Q

Botulinum toxin

Use

A

Migraine prophylaxis

Blepharospasm
Focal hand dystonia
Cervical dystonia

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45
Q

Botulinum toxin

Toxicity

A

Absence of muscarinic actions, loss of muscle tone, fatigue, paralysis, respiratory arrest

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46
Q

Carbamazepine
Oxcarbazepine (prodrug)

MOA

A

Sodium channel blockade

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47
Q

Carbamazepine
Oxcarbazepine (prodrug)

Use

A

Trigeminal neuralgia

Partial Seizures,
Generalized Tonic-Clonic Seizures, Manic episodes

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48
Q

Carbamazepine
Oxcarbazepine (prodrug)

Toxicity

A

Drowsiness, Ataxia, Agranulocytosis, SIADH (hyponatremia), Teratogen, Nausea, diplopia, headache

Potent inducers of CYP isoenzymes (e.g. CYP3A4); induces own metabolism

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49
Q 
Lorazepam
Diazepam
Midazolam
Clorazepate
Clobazam

Use

A

Status epilepticus initial treatment, anxiolytic, EtOH withdrawal, muscle relaxant, sedative, preop-sedation/induction of mechanically ventillation, tension headaches

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50
Q 
Lorazepam
Diazepam
Midazolam
Clorazepate
Clobazam

MOA

A

Enhance GABA-mediated Cl- influx, increased membrane polarization

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51
Q 
Lorazepam
Diazepam
Midazolam
Clorazepate
Clobazam

Adverse effects

A

Sedation

Tolerance can occur with chronic use

Interactions minimal

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52
Q

Ethosuximide

Use

A

Absence seizures

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53
Q

Ethosuximide

MOA

A

Blocks T-type (low-threshold) Ca2+ channels thus reducing pacemaker current underlying thalamic rhythm in spikes and waves seen in generalized seizures.

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54
Q

Ethosuximide

Adverse effects

A

Nausea, headache, dizziness, hyperactivity

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55
Q

Felbamate

Use

A

Refractory to other seizure treatments; typically used for partial and Lennox-Gastault syndrome

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56
Q

Felbamate

MOA

A
  • Blocks glycine activation of NMDA-type glutamate receptors

- GABAa receptor potentiation

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57
Q

Felbamate

Adverse effects

A

Aplastic anemia and hepatotoxicity limit its use (must obtain informed consent)

Also: Nausea, vomiting, headache, dizziness, somnolence, insomnia

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58
Q

Gabapentin,
Pregabalin
MOA

A

Blocks presynaptic voltage-gated Ca2+ channels possessing α2δ subunit

May may modulate the release of excitatory neurotransmitters that participate in epileptogenensis and nociception

59
Q

Gabapentin,
Pregabalin
Use

A

Adjunct therapy for partial seizures, also for neuropathic pain & bipolar disorder

60
Q

Gabapentin,
Pregabalin
ADEs

A

Somnolence, dizziness, ataxia;
Favorable pharmacokinetic profile; dosage adjustment necessary in renal impairment

  • Interactions are minimal
61
Q

Lamotrigine

MOA

A

Prolong inactivation of voltage-gated Na+ channels, decreases ability of neurons to fire at high frequency

Acts on voltage-gated presynaptic Ca2+ channels– decreases glutamate release

62
Q

Lamotrigine

Use

A

Partial seizures, primary general epilepsy, Lennox-Gestault Syndrome (can be adjunct or monotherapy)

Also for bipolar disorder maintenance

63
Q

Lamotrigine

ADEs

A

Dizziness, headache, diplopia, rash including potentially life-threatening Stevens-Johnson syndrome

Slow dose titration required to reduce risk of rash (over 6-8 weeks)

64
Q

Levetiracetam

MOA

A

Assumed to act on synaptic protein SV2A, a/w antiseizure activity in mice

65
Q

Levetiracetam

Use

A

Broad spectrum drug, focal seizures, primary general tonic/clonic seizures; off label for status epilepticus

66
Q

Levetiracetam

ADEs

A

Nervousness, dizziness, depression, seizures
Pregnancy: animal studies show teratogenic effects

**No CYP or UGT metabolism

67
Q

Phenobarbital
(Barbituates)
MOA

A

Enhances GABA-mediated Cl- influx

68
Q

Phenobarbital
(Barbituates)
Use

A

Partial seizures, primary general tonic/clonic seizures; Status epilepticus alternative

69
Q

Phenobarbital
(Barbituates)
ADEs

A

Sedation, decreased cognition, ataxia, hyperactivity

**Potent inducer of CYP isoenzymes

t½ 75-110h

70
Q

Phenytoin, Fosphenytoin

MOA

A

Prolong inactivation of voltage-gated Na+ channels , decreased glutamate release

71
Q

Phenytoin, Fosphenytoin

Use

A

Complex partial seizures, general tonic/clonic seizures, status epilepticus, prevention or treatment of seizures during neurosurgery

Nonseizure: ventricular arrythmias, sometimes from digitalis intodication

72
Q

Phenytoin, Fosphenytoin

ADEs

A

Diplopia, ataxia, hypotension, bradycardia, gingival hyperplasia, hirsutism, neuropathy, nystagmus, jaundice, osteomalacia, skin coarsening, purple glove syndrome (IV), SJS/TEN/DRESS
- Teratogenic (interference with folic acid absorption)

  • Nonlinear elimination kinetics at therapeutic doses;
  • Potent inducer of CYP isoenzymes
73
Q

Topiramate

MOA

A

Likely:
Prolonged inactivation of voltage-gated Na+ channels

Increased GABA synthesis and decreased GABA degradation

Blocks kainite and AMPA glutamate receptors

Weakly inhibits carbonic anhydrase

74
Q

Topiramate

Use

A

Partial seizures, Primary General Tonic/Clonic seizures, Lennox-Gestalt syndrome (adjunctive)

Nonseizure: Migrane prophylaxis, cluster headaches, neuropathy, weight loss with phenteramine

75
Q

Topiramate

ADEs

A
  • Somnolence
  • cognitive slowing
  • confusion
  • paresthesias
  • Hyperthermia most commonly in children; metabolic acidosis; renal calculus

Use with caution in patients with renal impairment and those with hepatic impairment

-Inhibits CYP2C19 and a weak inducer of CYP3A4

76
Q

Valproate

MOA

A

increased GABA synthesis, increased GABA transport from synapse, and decreased GABA degradation, or may mimic GABA actions at postsynaptic receptor sites

Possibly blocks voltage-gated Na+ channels

Possibly blocks T-type Ca2+ channels thus reducing pacemaker current underlying thalamic rhythm in spike and waves seen in generalized seizures

Possible histone deacetylation

Possible block of NMDA receptors

77
Q

Valproate

Use

A

Generalized tonic/clonic seizures,
Focal seizures,
Absence seizures,
Status Epilepticus (off-label)

Nonseizure: Acute mania with bipolar disorder, migrane prophylaxis, diabetic neuropathy

78
Q

Valproate

ADEs

A

Nausea, tremor, weight gain, hair loss, teratogenic, thrombocytopenia, hyperammonia, hepatotoxic, rare acute pancreatitis (Boxed warning)

Inhibits CYP isoenzymes

79
Q

Aspirin

MOA

A

Irreversible acetylation of serine on COX-1and 2. Blocks Thromboxane (TXA2)

80
Q

ASA

Use

A

Analgesic, Antipyretic, Anti-inflammatory, Low dose antiplatelet

81
Q

ASA

Toxicity

A
  • Bleeding, GI irritation, erosion, ulceration, allergic reactions (leukotriene mediated)
  • Compensated resp. alkalosis. (Manage by ion trapping)
  • salicylism (ringing ears), Reye’s syndrome
82
Q

Dipyridamole

MOA

A
  • Phosphodiesterase inhibitor -blogs PGI2 binding (increases cAMP, cGMP, and NO
  • –>Vasodilator (PGI2).
  • Inhibits TXA2 synthesis and receptors; Antiplatelet
83
Q

Dipyridamole

Use

A

Combine with aspirin for stroke and TIA prevention

84
Q

Dipyridamole

Toxicity

A

Bleeding, hypotension, vasodilation

85
Q

Cilostasol

MOA

A

Phosphodiesterase inhibitor (increases cAMP). Acts to stabilize platelets; Antiplatelet

86
Q

Cilostasol

Use

A

Intermittent claudication.
Thrombosis in peripheral vascular disease.
Prevents stroke.

87
Q

Cilostasol

Toxicity

A

Vascular headache, tachycardia (secondary to vasodilation)

88
Q

Clopidogrel

MOA

A

Irreversible ADP receptor blocker. Stops expression of surface GPIIb/IIIa.
Prodrug; Antiplatelet

89
Q

Clopidogrel

Use

A

Angioplasty, stent, CAD, Stroke
vascular ischemia with atherosclerosis.
Acute coronary syndrome.

90
Q

Clopidogrel

Toxicity

A

Bleeding.
Alternative if patient has aspirin contraindication.
Safer than Ticlopidine.

May lose effect due to inactive CYP2C19.
14% of population is variant and cannot convert clopidogrel to active form. These patients are at risk for MI stroke and death.

91
Q

Ticlopidine

MOA

A

Irreversible ADP receptor blocker. Stops expression of surface GPIIb/IIIa.
Prodrug; Antiplatelet

92
Q

Ticlopidine

Use

A

Angioplasty, stent, CAD, Stroke
vascular ischemia with atherosclerosis.
Acute coronary syndrome.

93
Q

Ticlopidine

Toxicity

A

Bleeding.
**Neutropenia,
agranulocytosis, thrombotic thrombocytopenic purpura (TTP) and aplastic anemia

94
Q

Prasugrel

MOA

A

Irreversible ADP receptor blocker. Stops expression of surface GPIIb/IIIa.
Prodrug; Antiplatelet

95
Q

Prasugrel

Use

A

Angioplasty, stent, CAD, Stroke
vascular ischemia with atherosclerosis.
Acute coronary syndrome.

Faster onset, more consistent action than clopidogrel.

96
Q

Prasugrel

Toxicity

A

Multi-enzyme conversion to active metabolite, therefore less problems with enzyme inactivity.
Conversion by CYP3A4 and CYP2B6; not CYP2C19.
Bleeding.

97
Q

Ticagrelor

MOA

A

Reversible ADP receptor blocker

Direct acting; Antiplatelet

98
Q

Ticagrelor

Use

A

Angioplasty, stent, CAD, Stroke
vascular ischemia with atherosclerosis.
Acute coronary syndrome.

Faster action than clopidogrel
Prevents thrombotic events

99
Q

Ticagrelor

Toxicity

A

Drug inhibits CYP3A4 (so will increase concentrations of drugs such as statins).

Bleeding

100
Q

Abciximab

MOA

A

High affinity for GPIIb/IIIa receptors

Blocks the glycoprotein IIb/IIIa pathway involved in cross-linking platelets

Long-acting (7-10 days)

101
Q

Abciximab

Use

A

Angioplasty, stent, CAD, Stroke

102
Q

Abciximab

Toxicity

A

Bleeding

103
Q

Eptifibatide
Tirofiban
MOA

A

Short-acting,
reversible, binds GPIIb/IIIa receptors

Antiplatelet

104
Q

Eptifibatide
Tirofiban
Use

A

Angioplasty, stent, CAD, Stroke

105
Q

Eptifibatide
Tirofiban
Toxicity

A

Bleeding

106
Q

Heparin
Unfractionated
MOA

A

Binds Antithrombin III to reduce active clotting factors (II and Xa)

107
Q

Heparin
Unfractionated
Use

A

IV anticoagulant.
Rapid acting, t1/2 1.5 hrs.
Does not cross placenta (safe in pregnancy)

108
Q

Heparin
Unfractionated
Toxicity

A 
Bleeding
- Use protamine to bind heparin (antidote).
Thrombocytopenia
Osteoporosis
Hyperkalemia
Hypersensitivity
109
Q

Low Molecular Weight Heparins

MOA

A

Enoxaparin, Dalteparin, Tinzaparin

Binds Antithrombin III to reduce active clotting factors

110
Q

Low Molecular Weight Heparins

Use

A

SQ anticoagulant. Rapid acting t1/2 4-6 hrs

111
Q

Low Molecular Weight Heparins

Toxicity

A

Bleeding, less thrombocytopenia

112
Q

Fondaparinux
Idraparinux
MOA

A

Synthetic pentasaccharide of heparin which binds to antithrombin III.
Selective for factor Xa vs II

113
Q

Fondaparinux
Idraparinux
Use

A

Anticoagulant

Fondaparinux: s.c., t1/2 17-21 hrs (dosed once daily)

Idraparinux: s.c., t1/2 80 hrs (dosed once per week)

114
Q

Fondaparinux
Idraparinux
Toxicity

A

Bleeding, but minimal thrombocytopenia

115
Q

Warfarin

MOA

A

Blocks vitamin K epoxide reductase. Stops clotting factor synthesis.

116
Q

Warfarin

Use

A

Delay of 4-5 days for anticoagulant benefit. - Check INRs

Hypercoagulopathy, vascular necrosis, and protein C deficiency can be controlled by heparin.

Crosses placenta (teratogen)

117
Q

Warfarin

Toxicity

A

Bleeding.

Add vitamin K or replace clotting factors (severe bleed).

Drug interactions (protein 
binding and CYP mediated)
118
Q

Bivalirudin
Argatroban
Dabigatran
MOA

A

Hirudin-like Direct Thrombin Inhibitors (DTI)

119
Q

Bivalirudin
Argatroban
Dabigatran
Use

A

Alternative to heparin in HIT. Rapid injectable, short-acting. Angioplasty, stent.

Dabigatran to prevent stroke in nonvalvular atrial fibrillation–Oral formulation

120
Q

Bivalirudin
Argatroban
Dabigatran
Toxicity

A

Bleeding, but no thrombocytopenia.

Idarucizumab is the antidote.

All require dose adjustment in renal impairment.

121
Q

Rivaroxaban
Apixaban
Edoxaban
MOA

A

Direct factor Xa inhibitor
(oral drugs)
Rapid onset

122
Q

Rivaroxaban
Apixaban
Edoxaban
Use

A

DVT, prevent strokes in patients with atrial fibrillation
VTE prophylaxis and treatment

Little monitoring, unlike warfarin

123
Q

Rivaroxaban
Apixaban
Edoxaban
Toxicity

A

Bleeding risk especially with drugs that inhibit CYP3A4.

No antidote, use antifibrinolytics for severe bleed

Impaired renal or hepatic function result in increased drug effect.

124
Q

Streptokinase
Urokinase
MOA

A

Natural tissue plasminogen activator (tPA); a protease which targets plasminogen to plasmin

125
Q

Streptokinase
Urokinase
Use

A

Infused in thrombosed vessel to lyse clot. (Fibrinolytic)

Streptokinase is a bacterial protein, can induce allergic reactions.
Replaced with newer drugs (alteplase)

126
Q

Streptokinase
Urokinase
Toxicity

A

All drugs increase bleeding.

Contraindications: Prior intracranial hemorrhage and malignant intracranial neoplasms

Reversed by aminocaproic acid tranexamic acid.

Block plasmin interaction with fibrin

127
Q

Anistreplase

MOA

A

(Streptokinase
plus plasminogen)
Activates plasminogen to plasmin

128
Q

Anistreplase

Use

A

Infused in thrombosed vessel to lyse clot.

129
Q

Anistreplase

Toxicity

A

All drugs increase bleeding.

Contraindications: Prior intracranial hemorrhage and malignant intracranial neoplasms

Reversed by aminocaproic acid tranexamic acid.

Block plasmin interaction with fibrin

130
Q

Alteplase
Reteplase
Tenecteplase
MOA

A

Human Recombinant tissue plasminogen activators tPA

Faster onset of action than alteplase

Longer t1/2 than alteplase or reteplase

131
Q

Alteplase
Reteplase
Tenecteplase
Use

A

Infused in thrombosed vessel to lyse clot.

Use IV asap, within 3 hrs for optimal benefit

Use: MI, acute ischemic stroke, pulmonary embolism, central venous catheterization.

132
Q

Alteplase
Reteplase
Tenecteplase
Toxicity

A

All drugs increase bleeding.
Contraindications: Prior intracranial hemorrhage and malignant intracranial neoplasms

Reversed by aminocaproic acid tranexamic acid.

Block plasmin interaction with fibrin

133
Q

Nifedipine

MOA

A

Calcium channel blocker

134
Q

Nifedipine

Use

A

Common to all CCBs; antianginal, antihypertensive

Arterioles relax, TPR and afterload decrease.
BP falls, heart works less for systole.

Stroke prevention

135
Q

Nifedipine

Toxicity

A

Arteriole action only
Decreases TPR, BP.
May elicit the SANS reflex and tachycardia.
Common to all “dipines”

136
Q

Labetalol

MOA

A

Alpha and Beta 1,2 antagonist, antioxidant potential

137
Q

Labetalol

Use

A

Hypertensive crisis, congestive heart failure, cocaine withdrawal

138
Q

Labetalol

Toxicity

A

Bronchoconstriction, masking hypoglycemia (beta-2), orthostasis (alpha-1)

139
Q 
“Statin” drugs MOA
Lovastatin
Atorvastatin
Pravastatin
Simvastatin
Rosuvastatin
A

Competitively inhibit HMG CoA reductase.

140
Q 
“Statin” drugs use
Lovastatin
Atorvastatin
Pravastatin
Simvastatin
Rosuvastatin
A

There is an increase in the number of LDL receptors
LDL decreases 25-45%.

Stroke prevention

141
Q 
“Statin” drugs Toxicity
Lovastatin
Atorvastatin
Pravastatin
Simvastatin
Rosuvastatin
A

Hepatic toxicity, Myopathy, rhabdomyolysis

Drug interactions: enzyme inhibitors

142
Q

Cytochrome P450 Enzyme inhibitors

A
  • grapefruit juice
  • protease inhibitors,
  • amiodarone
  • cimetidine
  • azole antifungals (e.g. ketoconazole)
  • erythromycin
  • sulfonamides
  • isoniazid
  • valproic acid
  • quinidine
  • acute alcohol abuse
143
Q

Cytochrome P450 Enzyme inducers

A
  • St John’s wort
  • phenytoin, phenobarbital, carbamazepine
  • griseofulvin
  • rifampin
  • chronic alcohol abuse
  • nevirapine
144
Q

B3 R effects

A

Gs

Increased lipolysis, increased thermogenesis, increased bladder relaxation

PAPOM (3 decks)

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