Chemotherapeutic Drugs Flashcards

1
Q

Competitively inhibit the incorporation of PABA (para-aminobenzoic acid) into folic acid

A

Sulfonamide

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2
Q

first clinical use of sulfonamide

A

1936

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3
Q

mass production of penicillin

A

1941

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4
Q

Harmful effects of chemotherapeutic drugs have resulted from _____________ or _____________.

A

allergic reactions or inadvertent IV overdose

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5
Q

competitive enzyme inhibitor, blocks the synthesis of folic acid in bacterial cell

A

Sulfonamide

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6
Q

Sulfonamide inhibits the enzyme

A

Dihydropteroate synthase

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7
Q

Trimethoprim inhibits the enzyme

A

Dihydrofolate reductase

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8
Q

After acute overdose of antimicrobials, most agents cause only

A

nausea, vomiting, and diarrhea

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9
Q

Biological origin of Streptomycin

A

Streptomyces griseus

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10
Q

Biological origin of Gentamicin

A

Micromonospora purpurea

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11
Q

Biological origin of Tobramycin

A

Streptomyces tenebrarius

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12
Q

Biological origin of Kanamycin

A

Streptomyces kanamyceticus

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13
Q

Biological origin of Neomycin

A

Streptomyces fradiae

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14
Q

Active against Pseudomonas aeruginosa

A

Amikacin, Gentamicin, Tobramycin

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15
Q

Most ototoxic aminoglycosides

A

Neomycin, Kanamycin, Amikacin

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16
Q

Most vestibulotoxic aminoglycosides

A

Streptomycin, Gentamicin

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17
Q

Most nephrotoxic aminoglycosides

A

Neomycin, Tobramycin, Gentamicin

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18
Q

Trimethoprim poisoning can cause:

A

Megaloblastic anemia
Leukopenia
Granulocytopenia

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19
Q

Trimethoprim poisoning antidote

A

Leucovorin

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20
Q

Leucovorin other names

A

● Wellcovorin ● Citrovorum factor ● Folinic acid

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21
Q

Chemical name of Leucovorin

A

5-formyltetrahydrofolate

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22
Q

Used to treat unintentional folic acid antagonist overdose

A

Leucovorin

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23
Q

Aka Diamino-diphenyl-sulfone (DDS)

A

Dapsone

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24
Q

Dapsone is combined with

A

Clofazimine & Rifampin

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25
Q

Average elimination half-life of dapsone

A

30 hours

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26
Q

Average elimination half-life of dapsone overdose

A

77 hours

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27
Q

Disorder characterized by the presence of a higher-than-normal level of methemoglobin

A

Methemoglobinemia

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28
Q

clamps of damaged hemoglobin

A

Heinz-Erlich bodies

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29
Q

Dapsone is metabolized by 2 primary routes

A

● Acetylation
● CYP450 Oxidation

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30
Q

Dapsone toxic effects are caused by the p-450 metabolites, including

A

–Methemoglobinemia
–Sulfhemoglobinemia
–Heinz body hemolytic anemia

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31
Q

may occur owing to depletion of intracellular glutathione by oxidative metabolites

A

Hemolysis

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32
Q

Dapsone therapeutic ranges from

A

50-300 mg/d

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33
Q

Death has occurred with dapsone overdose of

A

1.4 g and greater

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34
Q

Px with ____________________ may experience greater dapsone toxicity at lower doses.

A

G6PD deficiency, congenital hemoglobin abnormalities, and underlying hypoxemia

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35
Q

form of hemoglobin that does not bind oxygen.

A

Methemoglobin

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36
Q

Decreases oxyhemoglobin saturation

Unresponsive to methylene blue

A

Sulfhemoglobinemia

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37
Q

A reducing agent and is employed as a medication for the treatment of methemoglobinemia

A

METHYLENE BLUE

38
Q

Effective in the treatment of Parkinson’s disease

A

Amantadine

39
Q

Prophylaxis against parkinsonian side effects of neuroleptic agents

A

Amantadine

40
Q

Used in therapy of cocaine addiction

A

Amantadine

41
Q

4 cardinal features of Parkinsonism

A

a. Bradykinesia
b. Muscular Rigidity
c. Resting Tremor
d. Postural Instabilit

42
Q

BN of Amantadine

A

Symmetrel

43
Q

•Enhance the release of dopamine
•Prevent dopamine reuptake in the peripheral and CNS
•Has anticholinergic properties, especially in overdose

A

Amantadine

44
Q

Amantadine intoxication causes:

A

✓Agitation
✓Visual hallucinations
✓Nightmares
✓Tremor
✓Disorientation
✓Delirium
✓Slurred speech
✓Ataxia
✓Myoclonus
✓Seizures
✓Heart failure
✓Rarely, ventricular arrhythmias

45
Q

Amantadine withdrawal may result in:

A

✓Hyperthermia
✓Rigidity

46
Q

Amantadine serum level associated with toxicity

A

> 1.5 mg/L

47
Q

Neuroleptic malignant syndrome (NMS) antidote

A

Dantrolene

48
Q

NMS is characterized by

A

a. Fever
b. Muscular Rigidity due to muscle contraction
c. Altered mental status
d. Autonomic dysfunction

49
Q

not effectively removed by dialysis because the volume of distribution is very large

A

Amantadine

50
Q

Amantadine volume of distribution

A

5 L/kg

51
Q

Optical isomer of quinidine

A

Quinine

52
Q

Once used for treatment of malaria and for chloroquine-resistant cases

A

Quinine

53
Q

Treatment of nocturnal muscle cramps (idiopathic and common to older patients)

A

Quinine

54
Q

Banned due to its toxic effect and also used as an abortifacient

A

Quinine

55
Q

Toxic dose of quinine in adults

A

3-4 g

56
Q

Fatal dose of quinine in children

A

1 g

57
Q

Mild intoxication of quinine produces

A

✓Nausea
✓Vomiting
✓ Cinchonism

58
Q

Clinical presentation of cinchonism includes

A

Tinnitus
Deafness
Vertigo
Headache
Visual disturbances

59
Q

Severe intoxication of quinine may cause

A

• ataxia
• obtundation
• convulsions
• coma
• respiratory arrest
•with massive intoxication quinidine-like cardiotoxicity

60
Q

Retinal toxicity of quinine occurs _______ hours after ingestion

A

9-10

61
Q

Retinal toxicity of quinine

A

 blurred vision
 impaired color perception
constriction of visual fields
blindness
macular edema
disk pallor
pupils are fixed and dilated
retinal artery spasm

62
Q

previously been recommended for quinine-induced blindness

A

Stellate ganglion block

63
Q

Plasma quinine levels above ________ have been associated with visual impairment

A

10 mg/L

64
Q

87% of patients with levels above _________ reported blindness.

A

20mg/L

65
Q

Levels with have been associated with cardiac toxicity.

A

16mg/L

66
Q

an injection of local anesthetic in the sympathetic nerve tissue of the neck

A

stellate ganglion block

67
Q

used in the treatment of rheumatoid arthritis

A

Chloroquine and hydroxychloroquine

68
Q

blocks the synthesis of DNA and RNA and also has some quinidine-like cardiotoxicity

A

Chloroquine

69
Q

oxidizing agents and can cause methemoglobinemia or hemolytic anemia (especially in patients with G6PD deficiency)

A

Primaquine and quinacrine

70
Q

Lethal dose of chloroquine for an adult is

A

30-50 mg/kg

71
Q

Therapeutic dose of chloroquine phosphate for malaria prophylaxis

A

500 mg once a week

72
Q

Therapeutic dose of chloroquine phosphate for malaria treatment

A

2.5 g over 2 days

73
Q

Primaquine and quinacrine intoxication cause:

A

•GIT upset
•Severe methemoglobinemia
•Hemolysis
•Ototoxicity
•Retinopathy

74
Q

Amodiaquine can cause:

A

Fatal neutropenia

75
Q

Mefloquine in therapeutic dose or overdose can cause:

A

• Dizziness
• Vertigo
• Hallucinations
• Psychosis
• Seizures

76
Q

Treat cardiotoxicity as for quinidine poisoning with ______________

A

sodium bicarbonate 1-2 meq/kg IV

77
Q

may be useful in treating hypotension via combined vasoconstrictor and inotropic actions

A

Epinephrine infusion

78
Q

has been reported to reduce mortality in animals and to ameliorate cardiotoxicity in human cases

A

High-dose diazepam (2 mg/kg IV, given over 30 mins)

79
Q

Hydrazide derivative of isonicotinic acid

A

ISONIAZID (INH)

80
Q

Known to cause hepatitis on chronic use

A

ISONIAZID (INH)

81
Q

Acute overdose of INH causes

A

seizures and metabolic acidosis

82
Q

Active form of Vit. B6

A

pyridoxal 5-phosphate

83
Q

INH Acute ingestion of as little as _____ can produce toxicity

A

1.5 g

84
Q

Chronic therapeutic INH use may cause:

A

✓Peripheral neuritis
✓Hepatitis
✓Hypersensitivity reactions

85
Q

Do not induce emesis because of the risk of rapid onset of coma and seizures.

A

Isoniazid

86
Q

Gastric lavage for massive ingestions

A

Isoniazid

87
Q

Enhanced Elimination of isoniazid

A

Forced diuresis and dialysis

88
Q

A __________ dose produces a peak INH concentration of 3 mg/L at 1 hour.

A

5 mg/kg

89
Q

Other toxic effects of quinine

A

✓Hypokalemia
✓Hypoglycemia
✓Hemolysis
✓Congenital malformations

90
Q

May aggravate cardiotoxicity of quinine

A

Acidification of the urine