Drugs Flashcards

1
Q

Atracurium Mechanism

A

Isoquinoline Derivative

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2
Q

Atracurium Pharm

A

Intermediate-acting
-hepatic met. + hofmann elimination
main product (laudanosine) causally related to seizures
-cisatracurium<histamine

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3
Q

Succinylcholine Pharm

A
  • short duration (5-10min)
  • rapid hydrolysis by butyrlcholinesterase (liver) and high capacity pseudocholinesterase (plasma)
  • neuromuscular junction -sees only small percentage of IV dose, action terminated by diffusion from cleft, plasma cholinesterase strongly influences durability
  • genetically variants of plasma cholinesterase
  • increased risk for abnormally long effect
  • dibucaine test used for identification (inhibits normal enzyme by 80% and abnormal enzyme by only 20%)
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4
Q

Succinylcholine Toxicity

A
  • Hemodynamic changes:brady/tachycardia, ventricular arrythmias, HTN
  • hyperkalemia in: large burn injuries, trauma/crush, upper/lower motor neuron injuries, muscular dystrophies, prolonged immobilization
  • Prolonged neuromuscular blockade: phase II blockade, atypical pseudocholinesterase
  • Increased intraocular or intercrainial pressure
  • Muscle Pain
  • Myoglobinuria
  • Malignant HTN
  • Anaphylaxis
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5
Q

Malignant Hyperthermia

A

treat with dantrolene to correct hyperkalemia/acidosis/cool core temp
-avoid Ca2+ channel blockers

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6
Q

Neostigmine Mechanism

A

AchE inhibitor

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7
Q

Neostigmine Pharm/Toxicity

A

Doesn’t cross BBB

  • lasts 1.5 hr
  • anticholinergic: glycopyrrolate
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8
Q

Pyridostigmine Mechanims

A

AchE inhibitor

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9
Q

Pyridostigmine Pharm/Toxicity

A

Doesn’t cross BBB

  • lasts 1-2hr
  • anticholinergic: glycopyrrolate
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10
Q

Methotrexate Mechanism

A

-inhibition of AICAR transformylase (which catalyzes the last step in the de novo biosynthesis of inosine monophosphate)
-leads to AICAR riboside accumulation, which inhibits adenosine deaminase, increasing circulation adenosine conc.
-adenosine inhibits lymphocyte proliferation & suppresses secretion of IL-1, INF gamma, TNF, increases IL-4, impairs histamine release, decreases chemotaxis of neutrophils
IMMUNOSUPPRESSION

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11
Q

Methotrexate Pharm

A
  • undergoes polyglutamation-drug stays intercellular
  • Elimination: kidney
  • Metabolism: hepatic
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12
Q

Methotrexate Toxicity

A

-Bone marrow suppression/anemia
-Pulmonary toxicity-acute/chronic interstitial pneumonitis, pulmonary fibrosis
Contrindication: HIV, Pregnancy (CAT X), no breastfeeding
-avoid vaccine
-malignant lymphomas, fatal dermatologic rxns, GI toxicity with PUD/ulcerative colitis

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13
Q

Sulfasalazine Mechanism

A
  • metabolized to active - sulfapyridine and mesalamine by bacteria in the colon
  • absorbed sulfapyridine is acetylated an dhydroxylated in the liver
  • anti-inflammatory properties of mesalamine (inhibitor of PF and LT production)
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14
Q

Sulfasalazine Pharm

A

Elimination: Renal

Oral

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15
Q

Sulfasalazine Toxicity

A

Hematotoxicity-fatal blood dyscrasias infrequent

Contraindications: known hypersensitivity to 5-aminosalicylate, salicylate, or sulfonamide drugs

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16
Q

Leflunomide Mechanism

A

active primary metabolite A77 1726 that inhibits dihydroorotate dehydrogenase (enzyme located in cell mitochondria that catalyzes a key step in de novo pyrimidine synthesis.

  • in T&B cell cycle progression is arrested & their collaborative interaction interrupted
  • Immunoglobulin production is suppressed
  • cytostatic at normal doses
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17
Q

Leflunomide Pharm

A

Elimination: feces, other metabolites, flucuronide
uricosuric effect
Oral drug

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18
Q

Leflunomide Toxicity

A

-Hepatic (no alcoholics)
Contraindicated: immunodeficiency, bone marrow dysplasia, uncontrolled infection
CAT X

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19
Q

Hydroxychloroquine Mechanism

A
  • increases intracellular vacuole pH and alters processes (protein deg by acidic hydrolases in lysosome, assembly of macromoleules in endosomes, post-translation modification of proteins in the Golgi apparatus)
  • decreases immune response against autoantigenic peptides
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20
Q

Hydroxychloroquine Pharm

A

Elimination: extensive and slow renal elimination, following partial hepatic metabolism
Oral

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21
Q

Hydroxychloroquine Toxicity

A

Hepatic disease (alcoholism)
Blood dyscrasias
CNS toxicity: polyneuritis, ototoxicity, seizures, neuromyopathy
Contraindications: ocular disease b/c drug can cause corneal opacities, keratopathy, retinopathy

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22
Q

Abatacept Mechanism

A

Binds CD80 and CD86 prevents T-cell co-stimulatory signal engaging with CD28
(fusion protein: human CTLA4/IgG1 Fc fragment)

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23
Q

Adalimumab Mechanism

A

Binds TNF-alpha, blocks its interaction with the p55 and p75 cell surface receptors
(TNF-alpha monoclonal ab)

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24
Q

Anakinra Mechanism

A

Competitively inhibits IL-1 alpha & IL-1 beta binding to interleukin-1 type 1 receptor (IL-1R1)

25
Q

Certolizumab pegol Mechanism

A

Neutralizes membrane-associated and soluble human TNF alpha (Fab fragment of humanized TNF-alpha ab)

26
Q

Etancercept Mechanism

A

Endogenous p75 acts as a TNF antagonist. As a recomninant TNFR p75 bound to the Fc fragment of the human IgG1, etanercept binds to and inactivates TNF but does not affect TNF production or serum levels

27
Q

Golimumab Mechanism

A

Binds to and neutralizes both soluble and transmembrane TNF-alpha

28
Q

Infliximab Mechanism

A

Binds to and neutralizes both soluble and transmembrane TNF-alpha

29
Q

Rituximab Mechanism

A

Fab domain binds CD20 & Fc domain recruits immune effector functions to mediate B-cell lysis (complement-dependent cytotoxicity, antibody dependent cellular cytotoxicity and induction of apoptosis are possible mechanisms) Sensitizes drug-resistant human B-cell lymphoma cell lines to cytotoxic chemotherapy

30
Q

Tocilizumab Mechanism

A

binds to both soluble (serum & synovial fluid) & membrane-bound IL-6 receptors & inhibit signaling

31
Q

Abatacept Toxicity

A

-Immunosuppression
-complicate blood glucose tests (has maltose)
INJECTION SITE ROTATION

32
Q

Adalimumab Toxicity

A

-Immunosuppression
-Malignancy
-CHF/hypotension/angina/dysrhythmia
-Lupus-like syndrome
INJECTION SITE ROTATION

33
Q

Anakinra Toxicity

A

-Immunosuppression
-Blood Dyscarsias
INJECTION SITE ROTATION

34
Q

Certolizumab Toxicity

A

-Immunosuppression
-Malignancy
-Blood Dyscarsias
-Lupus-like syndrome
INJECTION SITE ROTATION

35
Q

Etancercept Toxicity

A

-Immunosuppression
-Malignancy
-Lupus-like syndrome
INJECTION SITE ROTATION

36
Q

Golimumab Toxicity

A

-Immunosuppression
-Malignancy
-CHF/hypotension/angina/dysrhythmia
Liver function test
INJECTION SITE ROTATION

37
Q

Infliximab Toxicity

A

-Immunosuppression
-Malignancy
-CHF/hypotension/angina/dysrhythmia
Contrindication: moderate-severe CHF
-Lupus-like syndrome
Liver function test

38
Q

Rituximab Toxicity

A
  • Immunosuppression
  • CHF/hypotension/angina/dysrhythmia
  • Blood Dyscarsias
  • Stevens-Johnson Syndrome (toxic epidermal necrolysis)
  • shouldn’t get pregnant during or 4-6 months after (B-cell depletion b/c IfG crosses placenta)
39
Q

Tocilizumab Toxicity

A
  • Immunosuppression

* need serum lipid profile*

40
Q

Celecoxib Mechanism

A

NSAID

COX-2 selective

41
Q

Ketorolac Mechanism

A

NSAID

COX-1»COX-2`

42
Q

Ibuprofen Mechanism

A

NSAID

COX-1=COX-2

43
Q

Ketorolac Toxicity

A

highest GI risk

44
Q

Ibuprofen Toxicity

A

lowest GI risk
high vascular risk
Acute hepatitis, ductopenia

45
Q

Diclofenac Mechanism

A

NSAID

46
Q

Diclofenac Toxicity

A

high vascular risk
Acute and Chronic Hepatitis
Mixed damage & pure cholestasis (liver)

47
Q

Celecoxib Toxocity

A

GI risk

48
Q

Acetaminophen Mechanism

A

NSAID

49
Q

Acetaminophen Toxicity

A

IV or oral
IV-constipation/diarrhea
hepatic failure

50
Q

Aspirin Mechanism

A

NSAID

irreversibly inhibits COX-1 in platelets

51
Q

Aspirin Toxicity

A

GI risk
Acute & Chronic hepatitis
Reye’s Syndrome
Renal Toxicity
Salicylate poisoning (resp. alkalosis, met. acidosis)
-central respiratory depression & CV collapse

52
Q

Indomethacin Mechanism

A

NSAID

53
Q

Indomethacin Toxicity

A

GI risk

54
Q

Ketoprofen Mechanism

A

NSAID

55
Q

Ketoprofen Toxicity

A

GI risk

56
Q

Naproxen Mechanism

A

NSAID

57
Q

Naproxen Toxicity

A

Cholestatic, mixed damage (liver)

58
Q

Piroxicam Mechanism

A

NSAID

59
Q

Piroxicam Mechanism

A

GI risk