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PPP II > PPP Quiz III > Flashcards

PPP Quiz III Flashcards

1
Q

Describe the pain pathway

A

Action potential travels along the 1st neuron, meets the synapse, and transacted to the second order neuron, and then to the brain.

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2
Q

Where does the Spinothalamic tract go to?

A

PAIN to the higher centers

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3
Q

MOA of NSAIDS

A

Inhibit COX to decrease synthesis of prostaglandins

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4
Q

Describe the physiology of Eicosanoids

A

PG sensitive AFFERENT nerves to pain; Increase of prostaglandins lead to increase sensitivity to pain fibers by altering the phosphorylation status of the neuron

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5
Q

Where do NSAIDS block?

A

COX; Conversion of Arachidonic acid to prostaglandins

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6
Q

What does Ibuprofen block?

A

COX1 & COX2

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7
Q

What does aspirin block (81mg)?

A

COX1

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8
Q

Name the housekeeping functions of PG: Stomach

A

COX1 to PGE2: Decrease of gastric acid secretion; Increase of mucus and bicarbonate secretion

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9
Q

Name the housekeeping functions of PG: Renal

A

COX2 to PGE2, PGI2: Increase renal blood flow; Increase glomerular filtration rate

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10
Q

Name the housekeeping functions of PG: Platelet

A

COX1 to TXA2; Increase of platelet aggregation

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11
Q

Name the housekeeping functions of PG: Endothelial Cells

A

COX2 to PGI2: Decrease platelet aggregation

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12
Q

AE of NSAIDS

A

Abdominal pain, ulcers, GI bleeding, Decrease renal blood flow, decrease glomerular filtration rate

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13
Q

AE of Aspirin

A

COX1: Increase risk of bleeding; ANTITHROMBOTIC effect; Used for CV benefits

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14
Q

AE of Celecoxib

A

COX2: Increase risk of MI and Stroke

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15
Q

AE of Acetaminophen

A

Liver toxicity (4g/day)

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16
Q

MOA of Opioids in Midbrain

A

Block release of GABA; Increase activation of noradrenergic descending pain modulation systems; At spinal level, NE and 5HT2 acting through a2 adrenergic and serotonergic receptors, inhibit spinal pain input.

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17
Q

MOA of Opioids in Dorsal Horn

A

Presynaptic action: Decrease release of neurotransmitter (substance P); Postsynaptic: Hyperpolarization of postsynap. neuron

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18
Q

Describe Opioid AE: Reward

A

Opioid action leads to sensation of reward (endorphins): Increase substance use disorder

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19
Q

Describe Opioid AE: Drowsiness

A

Decrease wakefulness and drowsiness (inhibition of excitatory drive from ascending reticular activating system)

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20
Q

Describe Opioid AE: Respiratory depression

A

Chemosensitive area in brainstem: Block rise of CO2; dependent on fall in O2 (periphery)

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21
Q

Describe Opioid AE:GI

A

Increase segmental (nonpropulsive) contractions –> constipation; Decrease peristaltic (propulsive) contraction (contraction below, relaxation above)

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22
Q

Describe Opioid AE: N/V

A

Nausea and emesis: stimulate u-R in CTZ (chemoreceptor trigger zone)

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23
Q

Describe Opioid AE:Urinary retention

A

Inhibit voiding reflex (opioid naive pt only)

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24
Q

Describe Opioid AE: CV

A

Bradycardia –> Increase parasympathetic
Hypotension –> Morphine can release histamine from mast cells –> decrease SVR –> Decrease BP

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25
Q

Describe opioid MOA

A

Opioids stimulate u receptor –> Less GABA, more ACh –> Parasympathetic

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25
Q

Describe Opioid AE: Pruritus (itching)

A

Morphine can release histamine from mast cells

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26
Q

Describe Opioid AE:Miosis

A

Results from inhibition of inhibitory GABA interneurons –> Increase para –> miosis
Important sign of opioid intoxication

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27
Q

Describe Opioid AE: Cough suppression

A

Morphine suppresses cough reflex: Not well understood ?

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28
Q

Clinical uses of Morphine (Full u agonist)

A

Chronic pain (cancer): PO (1st pass metabolism), intrathecal, epidural
Postoperative Pain: IV, inthrathecal,epidural)
Works in 15-30 min

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29
Q

Morphine AE

A

Releases histamine from mast cell –> vasodilation, allergic symptoms (pruritus)

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30
Q

Clinical uses of Methadone (Full u agonist)

A

Chronic Pain
Maintenance drug for opioid-dependent pt (heroin)
Long 1/2 life

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31
Q

Clinical uses of Fentanyl (Full u agonist)

A

Induction agent of anesthesiology
Chronic pain (transmuscosal, transdermal)
Transmucosal lozenge –> quick onset

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32
Q

Clinical uses of Codeine (Full u agonist)

A

Mild to moderate pain (ceiling effect)
Dependent on conversion of codeine to morphine by CYP2D6 (liver)
10% population have polymorphism in CYP2D6 –> makes codeine ineffective as analgesic

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33
Q

Clinical uses of Buprenorphine (Partial u agonist)

A

Post-Op pain
Maintenance drug for opioid-dependent patients
Long 1/2 life
Acts as an agonist in presence of antagonist

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34
Q

MOA of Naloxone (u Antagonists)

A

Blocks all opioid receptors
Used for opioid overdose
IM, IV, auto-injector
Short 1/2 life

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35
Q

Naloxone auto-injector

A

Narcan
Evzio –> approved for emergency treatment of OD

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36
Q

MOA of Naltrexone (u Antagonists)

A

Blocks all opioid receptors
Used for opioid dependence (alcohol dependence)
Administer by PO
CANNOT GIVE FOR AN OVERDOSE!!

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37
Q

MOA of Tramadol

A

Weakly stimulate u opioid receptors
Weakly inhibit NET and SERT
DONT GIVE WHILE ON AN SSRI
Used for mild to moderate pain (PO)

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38
Q

AE of Tramadol

A

Risk of causing seizures
CAUTION WITH PT PREEXISTING SEIZURE DISORDERS
DONT GIVE WHILE ON AN SSRI (serotonin syndrome)

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39
Q

Opioid interactions/Tolerance

A

CYP interactions = Codeine
CNS depressants = BZD, etc.
Tolerance –> Need more of drug to see same effect
Cross tolerance
Degree of tolerance

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40
Q

Clinical uses of Clonidine (a2 agonist)

A

Used as analgesic and neuropathic pain
Postop and neuropathic pain
MOA: Gi couple (less cAMP, less phos. Ca channel, less exocytosis of SP, less transported to 2nd neuron)

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41
Q

AE of Clonidine

A

Hypotension
Sedation
Dry mouth (a2 receptors on parasympathetic postgang nerve terminals)
Decrease Ach

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42
Q

Clinical uses of Gabapentin

A

MOA: Uncertain
Neuropathic pain
Seizures (adjunct therapy)

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43
Q

What drugs prolong the inactivated state of Na and what are the clinical uses?

A

Carbamazepine, Phenytoin, topiramate
Seizures
Neuropathic pain

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44
Q

Which antidepressants can you use for neuropathic pain? What is the MOA?

A

Amitriptyline, duloxetine (SNRI)
Inhibit NET –> More NE, binds to a2 –> Less SP –> Less signal transduction

45
Q

How does Lidocaine treat neuropathic pain?

A

Blocks VG Na channels
Anesthetic
Neuropathic pain (But lower dose)

46
Q

What is a seizure?

A

Excessive and hyper-synchronous neural activity

47
Q

Name the events that a seizure could alter

A

Consciousness, motor, sensory , psychic

48
Q

What is epilepsy?

A

Chronic disorder that requires the occurrence of two or more seizures that are NOT provoked by other illness (Eg. pt has seizure but then finds a brain tumor, not seizure)

49
Q

Describe the focal onset seizure

A

One hemisphere

-Normal awareness –> consciousness NOT impaired, clonus on right side of face and in right arm

-Impaired awareness –> consciousness impaired, lip smacking, repeating words

MAY SPREAD TO BECOME BILATERAL TONIC-CLONIC SEIZURE (focal onset –> generalized)

50
Q

Describe the generalized onset seizure

A

Both hemispheres

-Tonic (stiffen) clonic (jerky movement) described as (“grand mal”) –> motor movement
-Body rigid, limbs extended, head back, grimace

-Other motor–> Tonic OR Clonic

-Absence –> Primarily in children, brief loss of consciousness, NO MOTOR symptoms

51
Q

Levels of neurotransmitters during a seizure

A

Excitation: Glutamate is too HIGH
Inhibition GABA is too LOW

52
Q

Name the 4 ways to treat a seizure.

A

1) Prolong inactivated Na
2) Inhibit excitatory
3) Enhance inhibitory
4) Ca-Channel blockade (T-Type)

53
Q

Describe the stages of prolonging the inactivated Na state

A

1) Resting
2) Activated
3) Inactivated (PROLONG HERE)

Recycles from 3–>1

54
Q

Which drugs prolong inactivated state?

A

VG-Na Channel blockade

Phenytoin
Carbamazepine
Lamotrigine
Topiramate
Valproic Acid

“Please call Larry to Vaccinate”

55
Q

Which drugs block excitatory glutamatergic synapse?

A

Blocks SV2A proteins –> Less glutamate released

Levetiracetam (Keppra)

56
Q

What drugs block straight glutamate receptor?

A

BLOCK AMPA

Topiramate
Perampanel

57
Q

What drug blocks the release of Glutamate

A

Lamotrigine

58
Q

Which drugs enhance inhibitory GABA?

A

Tiagabine

Doesn’t let in the GABA (targets GAT-1)

59
Q

Which drug block the breakdown of GABA?

A

Valproic Acid (GABA-T)

60
Q

Which drugs act at GABA(A) receptor?

A

Barbiturates
BZD
Topiramate

61
Q

Which drugs block T-type Ca Channel?

A

USED IN ABSENCE SEIZURES

Valproic acid
Ethosuximide
Lamotrigine

62
Q

Which drugs are involved in Glutamate transmission?

A

Lamotrigine
Topiramate
Gabapentin?
Levetiracetam
Perampanel

“Larry took ‘good’ lab precaution”

63
Q

Which drugs are involved in GABA transmission?

A

Valproic acid
Topiramate
Gabapentin
Tiagabine
Levetiracetam
Phenobarbital
Diazepam

“Larry took ‘good’ peaceful talented violinists dancing”

64
Q

What drugs are used for absence seizures?

A

Blocking Ca T Type channels

Lamotrigine
Valproic Acid
Ethosuximide

“Larry eats vegetables”

65
Q

What seizure drugs cover the most?

A

Valproic Acid
Ethosuximide

“Eats vegetables”

66
Q

Name 5 considerations of seizure treatment

A

Social
Drivers license
Career
Avoid triggers (light, sleep, noise)
Long term treatment (counseling side effects)

67
Q

What’s the MOA/PK/AE of Phenytoin?

A

Prolong inactivated state of Na

-Used for ANY seizure except for absence
-Particularly effective against focal onset and generalized tonic clonic

-High protein binding
-Induces CYP3A4 (metabolism of oral contraceptives, other anti seizure drugs eg. carbamazepine)
-Teratogenicity (when prego its fine): cleft lip and palate
-Nonlinear –> Constant amount is eliminated, so it could be hella toxic
-Iv form: fosphenytoin

AE
-CNS: Nystagumus (“dancing eye”), ataxia (can’t walk a straight line when drunk), diplopia (double vision), sedation (can limit dose)
-Endocrine: Osteomalacia (soft bones) with hypocalcemia (altered metabolism of vitamin D and inhibition of Ca absorption)
-Hematologic: megaloblastic anemia (due to folate deficiency; blocks folate absorption)
-Gingival hyperplasia (too much connective tissue)
-Facial coarsening (large lips n tongue)
-Hirsutism (when girls look like dudes)

68
Q

What’s the MOA/Clinical Use/AE of Carbamazepine?

A

Similar to phenytoin!

-Any seizure except for absence seizures
-Effective for foal onset with or without spread to bilateral tonic-clonic seizure
-Trigeminal neuralgia(specific neuropathic pain) –> DRUG OF CHOICE
Bipolar disorders
-Induction of CYP3A4,CYP2CP (induces its own metabolism–> auto inducer)

-might have to adjust dose

-CNS: Diplopia, ataxia, drowsiness
-Hypersensitivity (BBW): Rash, steven johnson, NO ASIANS)
-Hematologic effects (BBW): Leukopenia (reversible), aplastic anemia (rare)
-Endocrine: Stimulates ADH secretion (control water and salt in body–> dilution hyponatremia)

69
Q

What’s the MOA/Clinical Use/AE of Ethosuximide?

A

-Block T-type Ca channels in thalamic neurons
-Absence seizures (DOC)
-Hepatic metabolism

AE
-GI tract: anorexia, N/V, used in kids
-CNS: Sedation, dizziness, ataxia

70
Q

What’s the MOA/Clinical Use/AE of Valproic acid?

A

-Prolongs inactivated state of Na
-Inhibition of GABA –> increase GABA
-Blockage of T-type Ca Channels
-Used for any seizures except absence)
-Migraine prophalaxais
-Bipolar

PK: High protein binding, hepatic metabolism
Inhibition of CYP2C9 (decrease metabolism of phenytoin and phenobarbital)
-caution pt with liver disease
-caution in children –> increase risk of fatal hepatotoxicity
-Teratogenicity: spina bifida (BBW PREGO USE PROTECTION REQUIREMENT)
-TAKE PREGO OFF OF DRUG!!!!

AE
Weight gain, hepatotoxicity
Tremor, dizziness, sedation, alopecia

71
Q

What’s the MOA/Clinical Use/AE of Lamotrigine?

A

Prolongs inactivated state of Na channels
CNS: diplopia, headache, ataxia
Hypersensitivity: steven johnson (BBW)

72
Q

What’s the MOA/Clinical Use/AE of Topiramate?

A

Prolong inactivated state of Na channels
-Enhances GABA
-Blocks AMPA

Any seizure except absence
-Good for primary and secondary generalized tonic-clonic seizures, focal seizures

Hepatic metabolism
CNS: memory, speech, language, headache, fatigue, dizzy, weight loss (phentermine together Qsymia)

-Induces CYP3A and Inhibits CYP2C19
-Precaution teratogenicity: cleft lip/palate

73
Q

What’s the MOA/Clinical Use/AE of Gabapentin?

A

Enhances GABA effects/block Ca channels?

-Focal onset seizures and focal onset that spends to bilateral tonic clonic (adjunct)
-neuropathic pain

-Absorbs via :L-amino acid transporter –> saturable –> decrease F with dose
-RENAL EXCRETION

AE
Sedation, dizziness, ataxia, weight gain

74
Q

What’s the MOA/Clinical Use/AE of BZD?

A

Diazepam
Lorazepam

GABA A receptor
-used for status epileptics (greater than 5 min!)

75
Q

What’s the MOA/Clinical Use/AE of Barbiturates?

A

Phenobarbital

GABA A receptor
-used for status epileptics (greater than 5 min!)

Sedation, cognitive issues, ataxia
can be used for kids

76
Q

What is status epilepticus?

A

Prolonged/repeated seizures without recovery of consciouness

Treatment
-IV Lorazrpam
-Wait 1 min, if no response, lorazepam again
-Even if seizure stops, administer non BZD (fosphenytoin)

77
Q

What’s the MOA/Clinical Use/AE of Levetiracetam?

A

MOA: Binds to SV2A modified release of glu and gaba

-Used for any seizures (adjunct)
-Renal elimination

AE
-Minor CVS effects (sedation, psych)

78
Q

What’s the MOA/Clinical Use/AE of Perampanel?

A

Blocks AMPA receptor

-Used for any seizures (primary or adjunct)
AE: CNS, Neuropsych (BBW)

79
Q

Which drug cannot be given to a pregnant woman?

A

Valporic acid

80
Q

What drug causes gingival hyperplasia?

A

Phenotoyin

81
Q

What drug causes hirsutism?

A

Phenotoyin

82
Q

What drug causes Osteomalacia?

A

Phenotoyin -vit D activation

83
Q

What drug causes weight gain?

A

Valporic acid/ Gabapentin

84
Q

What drug causes weight loss?

A

Topiramate(Weight loss drug approved)

85
Q

What drug causes alopecia?

A

Vaporic acid

86
Q

What drug causes rash?

A

Lamotrigine (BBW-Life threat)
Carbamazepine

87
Q

What drug causes anemia?

A

Phenotoyin and carbamazepine

88
Q

What drug causes cognitive changes?

A

topiramate

89
Q

What drug is approved for neuropathic pain?

A

Gabapentin, Phenyotonin

90
Q

What drug is approved for trigemninal neuralgia?

A

Carbamazepine

91
Q

Which drugs are approved for bipolar?

A

Carbamazepine, valproic acid, and lamotrigine

92
Q

Which drugs are approved for migraine?

A

Valporic acid

93
Q

Phenytoin AE

A

P450 Inducer
Hinutism
Enlarged gums
Nystagmus (dancing eye)
Teratogenic
Osteomalacia (softening of bone)
Interferes with folate
Neural

94
Q

Carbamazepine AE

A

Cyp Inducer (own metabolism)
ADH Increase (Hyponatremia)
Rash
Blood dysgraias –> aplastic anemia dis. bone ma
Amazepine

95
Q

Valproic acid

A

V weight gain
Alopecia
Liver toc
Procic acid

96
Q

Lamotrigine AE

A

Rash

97
Q

Topiramate AE

A

Cognitive impairment, weight loss

98
Q

What is sleep onset insomnia?

A

Difficulty falling asleep

99
Q

What is sleep maintenance insomnia?

A

difficulty staying asleep

100
Q

Name the MOA/Clinical Use/AE of a BZD.

A

Bind to “ALLOSTERIC MODULATOR” site off GABA(A)–> the BZD specific binding site

-Phase I reaction –> CYPS (Liver)
Phase II reaction –> Glucuronidation –> elimited by kidney

Consider AGE and HEPATIC function

101
Q

Name the drugs that skip phase I CYP activation

A

Lorazepam
Oxazepam
Temazepam

” a LOT of drugs skip phase I”

102
Q

What do you use to treat a BZD overdose?

A

Flumazenil

103
Q

Name the MOA/Clinical Use/AE of Z-Compounds

A

Zolpidem

Same as BZD –> Bind to allosteric modulated

-Sleep onset and maintenance insomnia

fewer ae of BZD

104
Q

Name the MOA/Clinical Use/AE of RaMELteon

A

Agonist at MT1 and MT2
-Sleep onset insomnia
-ONLY SEDATIVE HYPNOTIC DRUG APPROVED

105
Q

Name the MOA/Clinical Use/AE of Suvorexant

A

Antagonist at OX1 and OX2 orexin receptors

-Sleep onset and sleep maintenance

Sedation, impaired driving, SUD

106
Q

Name the MOA/Clinical Use/AE of Barbiturates

A

ALLOSTERIC MODULATORS (different binding site )

Insomnia, seizures

Tolerance, physical dependence, high addition potential, LTI

107
Q

Name the MOA/Clinical Use/AE of Antihistimines

A

Antagonist at H1

insomnia

Anticholinerigc effects, daytime sedation

108
Q

Amphetamine AE

A

Increase NE –> Increase Bp, arrhythmias, insomnia

-Increase dopamine –> growth inhibition

5HT–> anorexia

109
Q

Ritalin MOA

A

Blocks NET and DAT to increase
-ADHD/sleepiness

110
Q

Modafanil Indirect sympathomimetics

A

Block NET and DAT to increase
-excessive sleepiness
less AE

PPP II (3 decks)

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