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Chemistry lectures (Sun) > Exam 5 > Flashcards

Exam 5 Flashcards

1
Q

Routes for administering a drug

A

Oral, Rectal, transcutaneous, subcutaneous, intramuscular, intravenous

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2
Q

Absorption is affected by

A

The formulation of the drug (tablet, capsule etc.) and the chemical natures of the drug (weak acid vs weak base, ionized vs nonionized) May be subjected to first-pass metabolism

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3
Q

Transportation of drugs

A

Transported as a free drug which can interact with its receptor and correlates with both the therapeutic and toxic effects or as a drug-protein complex

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4
Q

Distribution

A

Depends on the lipid solubility of the drug, with volume distribution characteristics of a drug and expressed mathematically

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5
Q

Volume distribution equation

A

Vd = D / Ct

Vd = volume of distribution
D = an injected dose
Ct = concentration of the drug in plasma

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6
Q

Metabolism of drugs

A

Undergo oxidation, reduction, hydroxylation and conjugation in liver, facilitated by microsomal cytochrome P-450 which can be influenced by drugs such as barbiturates, alcohol, smoking and diet, generation of the metabolite or metabolites of the parent drug, which may have significant or comparable therapeutic effects

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7
Q

Excretion

A

With the kidneys as the primary route of excretion which is affected by water solubility and pH of urine, the biliary tract, lungs and sweat glands in the event of severe renal failure

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8
Q

Pharmacokinetics

A

The quantitative study of drug disposition in the body, describe mathematically the fate of a drug after administration of a given dosage form by a given route of admission

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9
Q

The therapeutic window

A

Range between minimum toxic concentration and minimum effective concentration

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10
Q

Decay of serum drug concentration equation

A

Ct = C0e-^kdt for many drugs

Ct = the serum concentration of a drug at time t
C0 = the initial dose divided by the volume of distribution
Kd = a disposition or elimination constant

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11
Q

First order of kinetics of drug elimination

A

A constant fraction is eliminated per unit of time, This causes an exponential decrease in the concentration as a function of time

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12
Q

Decline of plasma concentration versus time for a drug obeying zero-order kinetics

A

Elimination rate is constant, independent of concentration, capacity limited

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13
Q

Zero-order kinetics equation

A

Ct = Co - kt

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14
Q

Half-life of the drug

A

The period of time during which the concentration of a drug decays in half, may be determined for phase II of the dose response curve

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15
Q

Half-life equation

A

Ct = C0e -kdt, T1/2 = 0.693/Kd

T1/2 doesn’t vary with plasma concentration of a drug which follows 1st order

T1/2 changes with plasma concentration of a drug which follows zero order kinetics

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16
Q

Multiple oral dose-response curve

A

The dose interval is T1/2, steady state after 5 half lives

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17
Q

Antiepileptic drugs

A

High protein binding and interindividual variation for the protein binding, liver enzyme induction, active metabolite, various toxic effect with different drugs, use therapeutic ranges, interpret plasma concentration, determined by immunoassays

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18
Q

Valproic acid

A

Used for petite mal, administered orally, GI absorption rapid, highly protein bound, eliminated by hepatic metabolism, toxic >120 ug/ml

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19
Q

Carbamazepine

A

Used for variety of seizures, less common, 70-80% protein bound, eliminated by hepatic metabolism, toxic >120 ug/ml

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20
Q

Phenytoin

A

Used for variety of seizures, orally, highly protein bound, zero-order kinetics

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21
Q

Phenobarbital

A

active form of primidone, used in several types, 50% bound to protein, eliminated by liver metabolism and kidney excretion, dosage adjustment required

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22
Q

Tricyclic antidepressants

A

imipramine, amitriptyline, doxepin and fluoxetine. first-pass effect, high protein binding, half-life varies

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23
Q

Therapeutic drug monitoring of antidepressants

A

No improvement after 4 weeks of therapy, question on noncompliance, measured by HPLC

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24
Q

Immunosuppressants

A

Used to prevent rejection of transplants, require establishment of individual dosage regimens to optimize therapeutic outcomes and minimize toxicity

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25
Cyclosporine
Antirejection therapy in organ transplants, 5-50% absorption, distributed through RBCs and plasma, 98% protein bound, toxic >400 ng/mL, measured by FPIA or EMIT
26
Toxic effects of cyclosporine
Renal dysfunction, hypertension, hirsutism, tremors
27
Tacrolimus (FK-506)
Immunosuppressive drug, orally, more potent than cyclo, eliminated by hepatic metabolism, whole blood correlation, measured by immunoassays or HPLC/MS
28
Toxic effects of tacrolimus
Similar to cyclo in renal toxicity, thrombus formation
29
Aminoglycosides
Gentamicin, tobramycin, amikacin, streptomycin, neomycin and kanamycin, used in combination with beta-lactam antibiotics, require IV, IM, or intrathecal administration
30
Toxic effects of aminoglycosides
Nephrotoxicity and ototocixity
31
Therapeutic monitoring of aminoglycosides
Serum drug level upon initiation, serum drug level and serum creatinine level during therapy, measured by FPIA or EMIT
32
Vancomycin
Used for infection with staph epi and staph aureus, IV administration, eliminated by renal filtration and excretion, no established relationship between serum level and toxic effect
33
Toxic effects of vancomycin
Phlebitis, neutropenia, nephrotoxicity, nephritis and ototoxicity, measured by FPIA or EMIT
34
Cardioactive drugs
Significant toxic side effects, narrow therapeutic windows, active metabolites
35
Digoxin
improve cardiac contraction in CHF and correct supraventricular tachycardia, orally administered, highly bound to skeletal muscle and myocardial muscle, long half-time, eliminated through kidney
36
Toxic effects of cardioactive drugs
Cardiac dysfunction, CNS toxicity, GI toxicity, measured by FPLA or EMIT
37
Procainamide
Used to correct atrial and ventricular arrhythmias, orally, liver metabolized, kidney eliminated, active metabolite NAPA generated
38
Toxic effects of procainamide
Hypotension, bradycardia, prolongation of ECG intervals, SLE
39
Lidocaine
Used for ventricular arrhythmias and prevention of ventricular fibrillation, considerable overlap of therapeutic and toxic ranges, IV and IM administration, eliminated by hepatic metabolism
40
Toxic effects of lidocaine
CNS toxicity, atrioventricular node blockage
41
Lidocaine drug monitoring
Initial serum drug concentration, every 12 hours in patient with CHF, every 24 hours on prophylaxis after MI, measured by FPIA or EMIT
42
Salicylates
Used as analgesic, antipyretic and anti-inflammatory drug, function by decreasing thromboxane and prostaglandin formation through inhibiting cyclooxygenase
43
Toxic effects of salicylates
Stimulation of the respiratory system which causes an initial respiratory alkalosis, gastric irritation, conversion of pyruvate to lactate and stimulation of mobilization of free fatty acid, resulting in excess ketone body formation which can cause metabolic acidosis
44
Salicylates detection and treatment
Trinder method or forced alkaline diuresis
45
Trinder method
Salicylate is combined with an acidic ferric chloride to form a blue complex, which can be measured colormetrically
46
Acetaminophen
Analgesic drug, eliminated by hepatic uptake, biotransformation, conjugation and excretion, involve the formation of reactive intermediates that are then conjugated with reduced glutathione, which can be depleted in overdoses
47
Toxic effects of acetaminophen
Delayed hepatocytic necrosis due to the accumulation of reactive intermediates
48
Detection and treatment of acetaminophen
Immunoassays, HPLC, treated with N-acetylcysteine which may function as glutathione substitute
49
Ethanol
Most often used and abused substance
50
Ethanol toxic effect
Dose-dependent gradient in CNS depression
51
Ethanol absorption
Poor absorption by stomach affected by fullness of stomach, rapid absorption from small intestine
52
Ethanol distribution
Readily penetrate cell membrane, distribute to all tissues
53
Ethanol metabolism
2-10% excreted by lung and kidney, 90-98% metabolized by ADH and ALDH
54
Ethanol elimination
if BAC <20 mg/dL, elimination is first order, between 20-300 mg/dL, kinetics are zero order, BAC decreases at 18 mg/dL/hr, chronic alcoholics can eliminate at rates of 30-40 mg/dL/hr
55
Ethanol detection
Enzymatic analysis and GC (headspace analysis)
56
Enzymatic analysis
ADH Eth. + NAD+ -> Ald. + NADH+ + H+ The reaction is driven almost completely to the right by use of excess NAD+ and ADH, and the amount of NADH+, measured at 340 nm is proportional to the amount of ethanol in specimen
57
GC (headspace analysis)
Utilize the principle that alcohols and acetone are sufficiently volatile to be present in easily measurable concentrations in the air space in a closed system, inject a portion of this headspace into a gas chromatograph for analysis
58
Methanol metabolism
Converted to formaldehyde by liver alcohol dehydrogenase, which is then rapidly oxidized by aldehyde dehydrogenase to formic acid
59
Methanol toxic effects
Less severe CNS than ethanol, serious acidosis (formic acid), optic neuropathy and blindness (formic acid)
60
Detection and treatment of methanol
Gas chromatography, treated by administration of ethanol to competitively inhibit metabolism, sodium bicarb to alleviate metabolic acidosis, folate administration to enhance folate-mediated metabolism of formate, hemolysis
61
Ethylene glycol
Antifreeze, short half life (3 hours)
62
Ethylene glycol toxic effects
Neurological abnormalities, severe metabolic acidosis, acute renal failure, cardiopulmonary failure
63
Detection and treatment of ethylene glycol
Gas chromatography, treated by ethanol to saturate alcohol dehydrogenase, forced diuresis
64
Isopropanol
Converted by alcohol dehydrogenase to acetone which is eliminated slowly
65
Isopropanol toxic effects
CNS depression, coma
66
Detection and treatment of isopropanol
Gas chromatography, not treated by ethanol
67
Lead
From industrial waste, lead-based paint, lead pipes, mainly from ingestion, absorption rate varies with age
68
Lead toxicity
Inhibit enzymes for the heme synthesis which often leads to anemia and accumulation of zinc protoporphyrin in RBC and ALA in urine, forms bonds with the sulfhydryl group of cysteine in proteins
69
Toxic effects of lead
Neurological, gastrointestinal, renal, hematopoietic, calcium metabolism
70
Lead measurement
Whole blood lead, hair and urine levels, 10 ug/dL as cut off in children and 30 ug/dL in adults, chelation therapy required if level is above 60 ug/dL, measured by graphite furnace atomic absorption analysis
71
Lead treatment
Avoidance of continued exposure, chelation therapy to allow removal of lead from soft tissue and bone by forming LMW complexes that can be cleared by renal filtration
72
Mercury
Major sources are industrial uses, fungicide, dental amalgams, fish
73
Mercury toxic effects
Exposed by inhalation or ingestion, mostly from contaminated foods, inhalation and accidental ingestion, nontoxic in elemental form, moderately toxic in ionized form, highly toxic in organic form
74
Basis for toxicity of mercury
React with sulphydryl groups of protein, causing a change in tertiary structure of the protein with subsequent loss of the biological activity, binds to proteins in lipid0rich tissues, such as neurons, eliminated primarily through renal filtration
75
Toxic effects of mercury
CNS abnormalities: tremors, incoordination, irritability, depression Renal disorder: disputation of renal function GI: salivation, diarrhea, stomatitis Other: increase in congenital abnormalities
76
Mercury measurement
Blood, urine and hair mercury measurement, 50 ug/dL is significant exposure in blood, 200 ug/dL is significant in hair, 50 ug/dL is significant exposure in urine, measured by cold vapor atomic absorption spectrophotometry
77
Mercury treatment
Chelation therapy
78
Arsenic
Major sources from air and water in industrialized areas, agriculture and smelting industries, homicide and suicide agent, absorbed rapidly by passive diffusion, eliminated by renal filtration
79
Arsenic measurement
Atomic absorption spectrophotometry
80
Arsenic toxic effects
Many organ systems affected due to high-affinity binding to the thiol groups in proteins GI distress, renal failure, hemopoietic effects, vascular disease, CNS system
81
Cadmium
Major sources: paints and plastics, nickel-cadmium batteries, exposed by inhalation of cadmium particulates in industry and by ingestion of contaminated food
82
Cadmium detection
Atomic absorption spectrophotometry
83
Cadmium toxic effects
Binds to proteins and other cellular components, renal toxicity
84
Amphetamine
CNS stimulation due to enhancement of neurotransmitter release, can be used to treat narcolepsy, obesity and ADHD
85
Amphetamines abuse potential
The initial euphoria, restlessness, irritability and paranoid psychosis
86
Amphetamines metabolism
Unchanged (30%) or go through oxidative deamination in liver
87
Amphetamines overdose effects
Dizziness, tremor, hypertension, cardiac arrhythmia, convulsion and coma
88
Amphetamines immunoassays
Variable cross-reactivities with other sympathomimetic amines, GC/MS
89
Cannabinoids
Can treat anorexia and nausea, abuse potential to feel high
90
Cannabinoids absorption and metabolism
Consumed by smoking marijuana, absorbed through the lungs, reach peak blood concentration within minutes followed by rapid declines in THC concentration due to rapid tissue distribution, metabolized to a large number of compounds with THC-COOH as the major urinary metabolites
91
Cannabinoids method of detection
Immunoassays calibrated with THC-COOH, GC/MS
92
Cocaine
Alkaloid present in the leaves of the coca plant, stimulate CNS system by blocking uptake of dopamine and norepinephrine, can be used as local anesthetic for nasal surgery
93
Cocaine abuse potential
increased alertness and euphoria
94
Cocaine absorption and metabolism
Administered by nasal insufflation or smoking, metabolized to ecgonine methyl ester and benzoylecgonine, excreted as parent compound or metabolites
95
Cocaine effects of overdose
Seizure, arrhythmias, MI, hypertension, hyperthermia, sudden death
96
Cocaine method of detection
Immunoassays designed for the detection of its metabolites, GC/MS
97
Opiates
Naturally occurring or semisynthetic analgesic alkaloids derived from opium, used clinically due to their analgesic properties
98
Semisynthetic derivatives or morphine
Heroin, oxycodone, hydromorphone
99
Opiates absorption and metabolism
Administered by IV injection or subcutaneous injection, smoking or nasal insufflation less frequent, converted to 6-acetalmorphine which is hydrolyzed to morphine, inactivated by glucuronide conjugation
100
Codeine
combined with non-opiate analgesic agents for clinical use, have 10% of the analgesic potency of morphine, can be converted to morphine
101
Opiates and codeine abuse potential and overdose
Sedation, euphoria, respiratory depression, orthostatic hypotension, diminished intestinal motility, nausea and vomiting, coma, pulmonary edema
102
Codeine and opiates methods of detection
Immunoassays designed primarily for the detection of morphine and codeine, variable cross-reactivity with morphine-3-glucuronide and with other opiates among the immunoassays, GC/MS
103
Frequency histogram
Frequency (y) vs the values of the clinical results (x), bell shaped, described by mean, median, mode, standard deviation, and coefficient of variable
104
Mode
Most frequent observation
105
Standard deviation
Dispersion of single observations
106
Coefficient of cariation
CV (100%) = (SD/mean) x 100

Chemistry lectures (Sun) (5 decks)

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