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Rheumatology > Pharm > Flashcards

Pharm Flashcards

1
Q

Skeletal muscle contraction is evoked by what receptor?

A

Nicotinic cholinergic (M receptor)

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2
Q

NON depolarizing neuromuscular blockers act as?

A

ACh antagonists

ex: Tubocrarine

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3
Q

Depolarizing neuromuscular blockers act as?

A

ACh agonists

Ex: Succinylcholine

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4
Q

Nondepolarizing neuromuscular blockers w. Renal elimination?

A

Pancuronium + tubocurarine

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5
Q

Non depol blocker w/ Hepatic metabolism and Hofman elimination to from Laudanosine?

A

Atracurium

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6
Q

AE of Laudanosine?

A

Seizures

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7
Q

Stereoisomer of atracurium and inactivated to form LESS laudanosine and one of the MC used muscle relaxants?

A

Cisatracurium

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8
Q

MOA of nondepol neuromuscular blockers?

A

Competitively prevent ACh action at skeletal muscle end plate

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9
Q

Phase of blockade by depolarizing blocker during which the end plate repolarizes but is less than normally responsive to agonists (ACh or succinylcholine)?

A

Desensitization

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10
Q

Caused by massive release of Calcium form SR leading to uncontrolled contractions and stimulation of metabolism of skeletal muscle?

A

Malignant hyperthermia

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11
Q

Made up of 2 ACh molecules linked end to end?

A

Succinylcholine

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12
Q

Where is Succinylcholine metabolized?

A

Liver and Plasma by Pseudocholinesterases

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13
Q

What is the affect of continuous depolarization of motor end plate?

A

Muscle relaxation and Paralysis

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14
Q

What is required for tension to be maintained is skeletal muscle?

A

Periodic REpolarization and Depolarization

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15
Q

What is the difference btwn Phase I and Phase II affects of Succinylcholine actions?

A

Phase I–> continuous depolarization

Phase II–> gradual repolarization

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16
Q

How does AChesteral Inhibitor affect the paralysis produced by Succinylcholine?

A

Phase I–> AChesterase I increases Succin action

Phase II–> AChE inhib Reverses Succ action

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17
Q

AE of Succinylcholine?

A

Respiratory paralysis–> asphyxiation
Stimulates Autonomic ganglia–> Histamine released
Myalagia–> Hyperkalemia
Malignant hyperthermia–> co-admin w. inhaled anesthetic

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18
Q

What is a very early sign of Life threatening malignant hyperthermia caused by Succinylcholine action?

A

Jaw muscle contractions (trismus)

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19
Q

ACh Esterase inhibitors include?

A

Pyridostigmine
Neostigmine
Physostigmine
Sugammedex –> steroidal agent only

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20
Q

MOA of Curare?

A

competitive ACh antagonist

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21
Q

Neuromuscular blockers that also affect Autonomic ganglia?

A

Tubocurarine–> weak blocker

Succinylcholine–> Stimulator

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22
Q

Neuromuscular blockers that affect Cardiac Muscarinic receptors?

A

Pancuronium–> Moderate BLOCKER

Succinylcholine–> Stimulator

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23
Q

Neuromuscular blockers w. ability to Release Histamine?

A

Atracurium–> slight
Tubocurarine–> Moderate
Succinylcholine–> Slight

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24
Q

Localized disorder of bone remodeling caused by increased osteoblastic and osteoclastic activity?

A

Pagets disease (osteotitis deformans)

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25
Q

Disease associated w. increased Hat size + hearing loss due to narrowing of auditory foremen?

A

Pagets disease

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26
Q

What are the typical levels of Alkaline phosphatase, calcium, PTH, and phosphates in Pagets disease?

A

ALP–> Elevated >10x normal
Phosphates–> W/ in normal range
Calcium–> Normal levels
PTH–> Normal levels

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27
Q

Bones with mosaic pattern of growth, increased “chalk stick fractures” + Increased risk of HF & osteogenic sarcoma?

A

Pagets

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28
Q

What are the defining characteristics of the 3 stages of Pagets disease?

A

stage 1–> Osteolytic w, increased resorption
stage 2–> Disorganized bone formation
stage 3–> sclerotic or burnt out phase

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29
Q

What is the primary abnormality in Pagets disease?

A

Over production and activity of Osteoclasts

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30
Q

Alkaline phosphatase is a marker for?

A

Bone formation

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31
Q

Hydroxyproline is a marker for?

A

Bone Resorption

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32
Q

Patient w. hypercalcemia + hypercalciuria + renal Stones + hypophosphatemia?

A

Primary HyperParathyroidism

osteititis fibrosa cystica

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33
Q

Causes increased PTH + Increased ALP + Increased cAMP in urine + weakness and Constipation?

A

Primary Hyperparathyroidism (OFC)

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34
Q

Cystic bone spaces filled with brown fibrous bone tissue causing bone pain, Stones + bones + groans?

A

Osteititis Fibrosa cystica

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35
Q

Bone lesions due to 2nd or tertiary hyperparathyroidism due to Renal failure?

A

Renal osteodystrophy

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36
Q

Pt w. bone disease caused by

Hypovitaminosis D–> hypcalcemia + hyperphosphatemia + increased ALP + PTH?

A

Renal Osteodystrophy

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37
Q

Brown bone tumors of hyperparathyroidism?

A

Osteititis Fibrosa cystica

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38
Q

Decreased bone disease?

A

Osteoporosis

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39
Q

Thickened and dense bone disease (weak)?

A

Osteopetrosis

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40
Q

Soft bone disease (not mineralizing properly)?

A

Osteomalacia + Rickets

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41
Q

Causes Abnormal bone architecture?

A

Pagets disease

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42
Q

Pt with muscle rigidity, tachycardia, increased CO2 production, and elevated core body temp?

A

Malignant hyperthermia–> Succinylcholine + sevoflurane

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43
Q

What is the treatment for Malignant hyperthermia?

A

DANTROLENE

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44
Q

Bone disorder caused by Parayxovirus infection of Osteoclasts?

A

Pagets disease

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45
Q

Radiographic lytic lesions with increased ALP?

A

Pagets disease

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46
Q

MOA of methotrexate when treating RA?

A

Block AICAR–> AICA accumulates–> Inh Adenosine Deaminase–> Increased Adenosine

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47
Q

What is the role of AICAR transformylase?

A

Catalyzes the last step of Inosine monophosphate biosynthesis (AICA–> FAICAR)

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48
Q

How does accumulating adenosine affect RA?

A 
InhibitsLymphocyte proliferation 
suppresses Secretion of IL-1, IFN, TNF
Increases IL-4 secretion 
Impairs Histamin release from basophils
Decreases PMN chemotaxis
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49
Q

What drug undergoes polyglutamation to be retained Intracellularly?

A

Methotrexate

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50
Q

MXT metabolism and elimination?

A

RENAL Elimination-> (tubular secretion)

Hepatic metabolism-> CI w/ alcoholics + hepatic Failure

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51
Q

AE of MXT?

A 
Immunosuppression-> CI w. HIV 
Pulmonary Fibrosis 
Interstitial Pneumonitis 
Teratogenic 
Less frequent: 
Malignant Lymphoma 
Fatal Derm rxn 
GI toxic (PUD + Ulcerative colitis-> w. NSAIDS)
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52
Q

Pro-drug, metabolized into sulfapyridine and melamine by Bacterial in colon?

A

Sulfasalazine

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53
Q

What metabolite of Sulfasalazine is acetylated and hydroxylated in the LIVER?

A

Sulfapyridine

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54
Q

What kind of patients experience Higher levels of Sulfapyridine?

A

POOR ACETYLATORS

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55
Q

MOA of Sulfasalazine?

A

Primarily Anti-inflammatory by MESALAMINE

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56
Q

MOA of Mesalamine?

A

Inhibits PG and LT production

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57
Q

Sulfasalazine Elimination + CI + AE?

A

Renal Elimination
CI w. Hypersensitivity to salicylates + Sulfa
AE: Fatal BLOOD dyscrasia

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58
Q

MOA of Leflunomide?

A

Prodrug–> A77 1726–> inhibits Dihydroorotate dehydrogenase

Suppresses B + T cells and Immunoglobulins

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59
Q

What is the active metabolite of Leflunomide?

A

A77 1726

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60
Q

What is the function of Dihydroorotate dehydrogenase?

A

Key step in Pyrimidine synthesis

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61
Q

MOA: inhibits Pyrimidine synthesis–> T + B cells arrested in cell cycle & collaboration interrupted?

A

Leflunomide

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62
Q

Cytostatic drug that also suppresses Immunoglobulin production?

A

Leflunomide

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63
Q

What RA drug metabolite also has a Uricosuric effect (increases Uric acid elimination)?

A

Leflunomide–> A77 1726

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64
Q

Leflunomide Elimin + AE?

A

Fecal elimination
Hepatic toxicity
Teratogenic
CI w, Immunosuppression or infections

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65
Q

MOA of Hydroxychloroquine?

A

Increases intracellular vacuole pH + alters protein degradation + and macromolecule assembly

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66
Q

Drug that diminishes formation of peptide-MHC protein complexes required to stimulate CD4+ T cells?

A

Hydroxychloroquine

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67
Q

Hydroxychloroquine Elimination + AE?

A 
Slow renal elimination 
AE: 
OCULAR disease 
Hepatic toxicity 
Blood dyscrasia 
CNA toxic
Ototoxic 
Seizures 
Neuropathy
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68
Q

AE: Ocular disease + Ototoxic + Seizures + hepatotoxic?

A

Hydroxychloroquine

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69
Q

What drug requires routine Opthalmic exams?

A

Hydroxychloroquine

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70
Q

RA drugs that are mAbs against TNF alpha?

A

Adalimunmab
Certolizumab
Infliximab
Golimumab

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71
Q

RA drugs that acts as Soluble receptor for TNF?

A

Etanercept

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72
Q

RA drugs acting as IL-1 receptor antagonists?

A

Anakinra

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73
Q

RA drug that acts as IL-6 receptor mAb?

A

Tocilizumab

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74
Q

What is the cell that is thought to be responsible for RA inflammatory process?

A

T helper 17 cells

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75
Q

What is the action of Th17 cells in RA?

A

Release IL-17–> induces IL-1 + IL-6 + TNF alpha release

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76
Q

What is the role of IL-23 + IL-6 + IL-1 in RA?

A

Induces T cell differentiation into Th17 cells

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77
Q

MOA; anti CTLA4–> binds CD80 & CD86 to prevent T-cell co-stimulatory signal engaging w, CD28?

A

Abatacept

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78
Q

MOA; binds TNF, blocks its interaction w. p55 and p75 cell surface receptors?

A

Adalimumab

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79
Q

MOA: competitively inhibits IL-1alpha + beta binding to IL-1R?

A

Anakinra

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80
Q

MOA: hmAB that neutralizes membrane associated and soluble human TNF alpha?

A

Certolizumab

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81
Q

MOA: hmAb that binds to and neutralizes both soluble & transmembrane TNF alpha?

A

Golimumab

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82
Q

MOA: chimeric (mouse) mAb that binds and neutralizes soluble & transmembrane TNFalpha?

A

Infliximab

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83
Q

MOA: anti-CD20 which mediates B cell lysis?

A

Rituximab

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84
Q

MOA: hmAb that binds to soluble (serum & synovial fluid) & membrane bound IL-6 receptors to Inhibit signaling?

A

Tocilizumab

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85
Q

What drug RA drug contains Maltose which may complicate blood glucose tests?

86
Q

What drug requires reliable contraception for upto 4-6 after use?

A

Rituximab–> IgG crosses placenta

87
Q

RA drugs inducing Lupus like syndrome?

A

Etanercept
Infliximab
Adalimumab
Certolizumab

88
Q

Describe phase I of Succinylcholine use?

A

Immediate Depolarization but rapid recovery from, with NO FADE–> muscle contractions followed by paralysis

89
Q

Describe Phase II of succinylcholine use?

A

Desensitization with slow transition

Prolonged recovery and FADE causing only flaccid paralysis (NO muscle involuntary contractions)

90
Q

Genetically variants of plasma cholinesterase causes abnormal levels of what drug? What is the test used to identify this phenomenon?

A

Succinylcholine

Dibucanine test

91
Q

AE: HTN, arrhythmias, Hyperkalemia, increased Intracranial pressures, muscle pain, Myoglobinuria, malignant hyperthermia?

A

Succinylcholine

92
Q

What are the AchE inhibitors?

A

Neostigmine
Edrophonium
Pyridostigmine

93
Q

What are the Anti-cholinergics used to terminate Neuromuscular blockade?

A

Glycopyrrolate

Atropine

94
Q

Off target actions of AchE inhibitors?

A 
Cardio--> bradycardia 
Pulmonary--> Bronchospasms 
GI--> Increased peristalsis 
GU--> increased bladder tone
Opthalmic--> pupillary constriction
95
Q

What rapidly encapsulates steroids to reverse ANY depth of neuromuscular blockade?

A

Sugammadex

96
Q

Sugammadex is inactive against what kind of neuromuscular blockers?

A

NON steroidals–> Succinylcholine + cisatracurium

97
Q

What is the main function of NMBs?

A

reversible blockade of Nm receptors

Paralysis of skeletal muscle–> NO pain or anxiety relief

98
Q

What can reverse neuromuscular blockade?

A

AchE inhibitors

Sugammadex

99
Q

What is a common AE of Nondepolarizing NMBAs?

A

Nephrotoxicity + Hepatotoxicity

100
Q

How is Hyperuricemia defined?

A

Uric acid plasma level > 7 mg/dL

Precipitation > 9 mg/dL

101
Q

What is the rate limiting step in purine metabolism?

A

Ribose –> PRPP

Enzyme: PRPP synthetase

102
Q

What enzyme is responsible for turning Hypoxanthine into Nucleic acids?

103
Q

Abnormal (decreased) HGPRT function in some Mediterranean groups leads to?

A

Increased Uric acid in serum

104
Q

What drug is effective only against Gouty arthritis and is a prophylactic agent against future attacks?

A

Colchicine

105
Q

MOA of Colchicine?

A

Depolimerization of microtubules

106
Q

How does microtubules inhibition affect GOUT?

A

prevents inflammatory cell (PMNs) proliferation + migration
Blocks immune response
STOPS phagocytosis of crystals

107
Q

AE of Colchicine?

A

GI + blood dyscrasia

108
Q

MOA: COX inhibitor + analgesic & antipyretic + inhibits leukocyte motility?

A

Indomethacin –> treat acute attacks

109
Q

AE of indomethacin?

A 
N/V 
Ulcers 
CNS--> Severe frontal headache 
Blood disorders 
Antagonizes furosemide and HCTZ
110
Q

AE: severe headache and decreased function of Diuretics?

A

Indomethacin

111
Q

MOA of Allopurinol?

A

Competitive inhibitor of Xanthine oxidase

112
Q

How is Allopurinol a suicide inhibitor of Xanthine oxides?

A

Drug is a substrate for the enzyme and its metabolite –> Oxypurinol is a NON competitive inhibitor of XO

113
Q

What are the therapeutic effects of Allopurinol?

A

Reduces plasma and Urine uric acid levels
Facilitates Dissolution of uric acid crystals
Prevents formation of uric acid kidney stones

114
Q

Tx primarily for hyperuricemia due to enzyme abnormalities, and in familial hyperuricemic nephropathy + 2nd due to heme disorders?

A

Allopurinol

115
Q

AE of allopurinol?

A

Increase incidence of acute attacks
Exfoliative dermatitis (HS rxn)
Interaction w. 6-mercaptopurine
CI w. Ampicillin and related antibiotics

116
Q

Why is Allopurinol CI with 6-mercaptopurine and Ampicillin like antibiotics?

A

6-MP–> metabolized by XO–> increases serum levels and AE–> PANCYTOPENIA
Ampicillin–> increases RISK for Exfoliative dermatitis

117
Q

MOA of Febuxostat?

A

Uloric–> Direct inhibitor of oxidized and reduced Xanthine Oxidase

118
Q

When is Febuxostat used?

A

pt with HS to Allopurinol

119
Q

What is a limitation of allopurinol that is overcome by Febuxostat?

A

Renal insufficiency–> Feb can be used in pts with mild to Moderate Renal Impairment

120
Q

AE of Febuxostat?

A

Elevated transaminases

121
Q

Where in the Kidney is Uric acid secreted?

122
Q

MOA of Probenecid?

A

Inhibits transport of organic anions across epithelial barriers
Interferes with UA reabsorption in the BRUSH boarder of PT

123
Q

What drug competes with uric acid for Brush boarder transporters?

A

Probenecid

124
Q

Clinical uses of Probenecid?

A

pt w. < 1 g of UA excretion

Dissolution of UA crystals in joints

125
Q

AE of probenecid?

A 
SJ syndrome
Aplastic anemia 
Hepatic necrosis
Hypersensitivity rxn 
Nephrotic syndrome
126
Q

Probenecid is CI with concurrent use of?

A

Salicylates–> inhibit Uricosuric actions of Probenecid

127
Q

What enzyme (not present in humans) converts Uric acid into allantoin?

A

Urate Oxidase

128
Q

MOA of Pegloticase?

A

PEGylated formulation of pig URATE OXIDASE

Converts UA–> Allantoin

129
Q

What drug rapidly lowers serum levels of Uric acid and reduces urinary excretion of UA and is used in pt with Severe Gout to Dissolve TOPHI?

A

Pegloticase

130
Q

AE of pegloticase?

A 
Gout flares--> colchicine or GCs prophylatically 
Elimination occurs in 10-12 days 
Antibodies against PEG moiety 
CV--> chest pain 
Constipation
131
Q

What is a common AE of all TNF alpha inhibitors?

A

2nd malignancies
Immunosuppression
Injection site injuries

132
Q

What drugs are associated with CHF?

A

Rituximab
Infliximab
Adalimumab
Golimumab

133
Q

What drugs are associated with Lupus like syndromes?

A

Adalimumab
Certolizumab
Entanercept
Infliximab

134
Q

What RA drug is associated with SJS?

135
Q

What drug is associated with altered LIPID profile?

A

Toclizumab

136
Q

What is the RA modifying affects of glucocorticoids?

A

Joint sparing–> inhibit erosive progression

137
Q

MOA of glucocorticoids use in RA?

A

Induce synthesis of anti-inflammatory proteins and inhibiting proinflammatory cytokines (NFkb inhibition)

138
Q

How do glucocorticoids have their anti-inflammatory affects?

A

Binding to cytosolic GCR–> binding to DNA GC response element–> upregulate anti- inflammators
Bind cGCR–> - interfere with transcription of NFkB–> reduce RANKL production

139
Q

AE of glucocorticoids?

A

Osteoporosis
PUD (concurrent use w. NSAIDS)
CV disease (impacts lipids, glucose, and insulin)
Infection

140
Q

Which glucocorticoids are associated with Salt and Water retention?

A

Hydrocortisone
Cortison
Prednisone

141
Q

What drug has a BBW for Anaphylaxis and infusion rxns?

A

Pegloticase

142
Q

AE: Torsades de pointes + Aplastic anemia + Hepatic failure + Myopathy + Seizures + Retinopathy + Hearing loss?

A

Hydroxychloroquine

143
Q

AE: SJS + pancytopenia + immunosuppression + Hepatic Necrosis+ ILD?

A

Leflunomide

144
Q

AE: SJS + aplastic anemia + hepatic failure + SLE + Renal disease + MALE infertility + Diffuse pulmonary fibrosis?

A

Sulfasalazine

145
Q

AE: HTN + atrophic skin + depression + Osteoporosis + Cataracts + TB?

A

Betamethasone

146
Q

What group of drugs decreases calcium absorption, increases Ca secretion, inhibit OSTEOBLASTS –> causing Osteoporosis?

A

Glucocorticoids

147
Q

Hydrocortison AE?

A

typical GC AE +
Adrenal insufficiency
Hyperglycemia

148
Q

Which COX selectivity causes Anti-inflammatory + analgesic + antipyretic + increase BP + reduce urine PGI2?

A

COX-2 selective + Traditional NSAIDS

149
Q

What drugs inhibit platelets + reduce urine TXA2 + increase bleeding time + GI toxic?

A

COX-1 selective and traditional NSAIDS

150
Q

What are the COX-2 selective NSAIDS?

A

Celecoxib
Diclofenac
Etodolac
Meloxican

151
Q

What are the non-selective NSAIDS?

A

Acetaminophen

Ibuprophen

152
Q

COX 1 selective NSAIDS?

A 
Ketorolac
Ketoprophen 
Indomethacin 
Aspirin 
Sulindac
Naproxen
Piroxican
153
Q

Which NSAID is associated with the HIGHEST + LOWEST risk for GI toxicity?

A

Ketorolac= highest

Ibuprophen + Celecoxib= lowest

154
Q

How can the GI toxicity of NSAIDS be reduced?

A

Concurrent admin with PPIs or H2 antagonists

155
Q

What is the mechanism by which NSAIDS cause CV toxicity?

A

NSIADS compete with aspirin for COX-1 inhibition causing a pro-aggreagry condition

156
Q

Which NSAIDS have shown cardioprotective actions by NOT competing with Aspirin?

A

Naproxen
Sulindac
Celecoxib

157
Q

Which NSAID competes with Aspirin and increase CV risk?

A

Ibuprophen

158
Q

AE of NSAIDs?

A 
GI--> Ulcers 
CV--> pro-agregarory/ infarctions 
HTN--> inhibit PGs 
Hepatotoxic 
Renal Toxic
159
Q

Which two NSAIDs are associated with HTN?

A

Piroxicam

Diclofenac

160
Q

What is the mechanism of increased BP by NSAIDs and which current BP therapies need intensifying?

A

inhibit PG formation

ONLY ACEi + ARBs

161
Q

AE: Reyes syndrome?

162
Q

Which NSAID is associated with HIGHEST + Lowest risk for Hepatic toxicity?

A 
Sulindac = highest 
Ibuprophen= lowest
163
Q

Which of the anti RA drugs is also URICOSURIC?

A

Eflunomide

164
Q

What drugs competes with Probencid for tubular secretion?

A

Methotrexate

165
Q

AE of aspirin?

A 
GI Ulcers 
Bleeding 
Macular degeneration 
Tinnitus
Bronchospasms
Angioedema 
Reyes 
Renal toxic
166
Q

Which class of drugs is associated with Respiratory alkalosis + Central respiratory depression + CV collapse + Antagonize Uricosuric drugs?

A

Salicylates

167
Q

MOA inhibits COX 1+2 in CNS producing antipyretic + analgesia?

A

Acetaminophen –> NOT anti-inflammatory

168
Q

AE of Acetaminophen?

A

N/V
Constipation/ diarrhea
Hepatic failure–> produce radicals
Renal toxic

169
Q

MOA of Duloxetine?

A

Sertonin-Norepinephrine Reuptake inhibitor–> MOSTLY Serotonin

170
Q

What receptor does Duloxetine have it actions on?

A

NONE or upon the reuptake of Dopamine

171
Q

MOA of Milnacipran?

A

Serotonin-NE repuptake inhibitor–> NE mostly

172
Q

What FM drug undergoes CYP 2D6 metabolism?

A

Duloxetine

173
Q

CI for both Duloxetine and Milnacipran?

A 
Severe Hepatic dysfunction or Chronic alcoholism 
And Pre-existing CV disease 
Uncontrolled close angled Glaucoma 
MAOis 
SIADH 
BBW: SUICIDES

*both have Hepatic metabolism

174
Q

AE of Duloxetine and Milnacipran?

A

HTN and elevated HR

175
Q

CI with Uncontrolled close angled Glaucoma?

A

Duloxetine + Milnacipran

176
Q

AE: SUICIDES + SIADH?

A

Duloxetine + Milnacipran

177
Q

MOA of Pregabalin?

A

Inhibits Pre-synaptic Alpha-2-delta subunit of L-type Calcium channels

178
Q

What drug inhibits the excitatory transmission by Glutamate?

A

Pregabalin (Inhibits L-type calcium channel)

179
Q

Elimination of Pregablin?

A

Renal + Unchanged

180
Q

AE of Pregabalin?

A 
Withdrawal= worsening symptoms 
Dependence 
Sedation 
Depression/ suicidal 
Blurred vision 
Xerostomia
181
Q

AE: Blurred vision + Xerostomia + Dependence?

A

Pregabalin

182
Q

MOA of Amitriptyline?

A

Tricyclic antidepressant

183
Q

MOA of fluoxetine?

184
Q

MOA of Carisoprodol?

A

CNS action in reticular activating system + spinal cord causing SEDATION + altered perception of pain

185
Q

How does Carisoprodol have its muscle relaxing affects?

A

NO DIRECT EFFECT–> but by affecting CNS reticular system + spinal cord

186
Q

What drug is associated with CYP2C19 metabolism?

A

Carisoprodol

187
Q

What condition cause increasing toxicity of Carisoprodol?

A

Hepatic or Renal failure

188
Q

AE of Carisoprodol?

A 
Drowsiness/ Dizziness
Insomnia 
Vertigo 
Ataxia 
Mydriasis 
Temporary Vision loss
Orthostatic Hypotension
189
Q

MOA of Cyclobenzaprine?

A

Related to TCA but action on BRAIN STEM

190
Q

Elimination of Cyclobenzaprine?

A

Enterohepatic recirculation

CYP 3A4 + 1A2 + 2D6

191
Q

AE of Cyclobenzaprine?

A

Anticholinergic–> Drowsiness + xerostomia + Fatigue + N/V + blurred vision + Confusion
Increased QT
MOST significant: GI = PARALYTIC ILEUS = constipation

192
Q

Drug causing Old people to fall and major constipation?

A

Cyclobenzaprine

193
Q

MOA of Methocarbamol?

A

Generalized sedative actions causing Altered pain perception

194
Q

What drug is Dealkylated and hydroxylated in Liver and has renal elimination?

A

Methocarbamol

195
Q

AE of Methocarbamol?

A

CNS depression –> dizziness + lightheadedness + Blurred vision + Headache + Irritable

196
Q

MOA of Tizanidine?

A

pre-synaptic Alpha 2 AGONIST–> decreases activation of motor neurons–> reduction in Muscle tone but NOT strength

197
Q

What muscle relaxer can also be used as an Anti-hypertensive drug (related to Clonidine)?

A

Tizanidine

198
Q

Tizanidine elimination?

A

Short t1/2 –> extensive Renal elimination

199
Q

AE of Tizanidine?

A 
HEPATOTOXIC 
Rebound HTN + Tachycardia 
CNS depression 
Hypotension 
Common: Asthenia + Xerostomia + dizziness + sedation
200
Q

MOA for Baclofen?

A

GABA (B) agonist–> inhibitory signals or hyperpolarize to reduce excitatory signals

201
Q

Causes pain relief from inhibition of substance P action?

202
Q

GABA b agonist?

203
Q

Baclofen elimination and AE?

A 
Renal 
Encepalopathy 
abdominal pain
seizures
respiratory depression
204
Q

BBW: rebound neural activity–> Seizures + hallucinations + increased spasticity?

205
Q

Common AE include: increase Blood Glucose + Drowsines + confusion + headache?

206
Q

MOA: directly interferes with Ryanidine receptors thus Ca++ release?

A

Dantrolene

207
Q

Uncouples excitation- contraction process by inhibiting Ca++ release?

A

Dantrolene

208
Q

Dantrolene effects what types of fibers?

A

Skeletal muscle

NO effect on CARDIAC or SMOOTH muscle

209
Q

Causes “floppy child syndrome” by crossing placenta during C-section use?

A

Dantrolene

210
Q

AE of Dantrolene?

A

Drooling
Dysarthria
Myalgias
Backache

uncommon: Vfib or cardio collapse

Rheumatology (4 decks)

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