Bio 365 Final Exam

Front 1

What are the criteria for the diagnosis of depression?

Back 1

1. 2 weeks (or mania for 1)
2. Depressed mood, loss of interest in pleasurable activities, sleep disturbanes, change in appetite, loss of energy, suicidal thoughts
3. In mania, 3 of following: inflated self-esteem, decreased sleep, racing thoughts, excessive talkativeness, distractability, excessive involvement in pleasurable activities.

Front 2

What are the classes of antidepressant drugs?

Back 2

1. Tricyclic compounds
2. MAO inihibitors
3. SSRIs
4. Serotonin-norepinephrine reuptake inhibitors (SNRIs)
5. Dopamine reuptake inhibitors (DRIs)

Front 3

How long does it take for antidepressants to start working? why?

Back 3

2-4 wks. Slowness of development of biochemical adaptation in monoaminergic function.

Front 4

How do Tricyclic antidepressants work? What are some examples?

Back 4

inhibit NE and 5-HT uptake, causing downregulation of brain B-adrenoceptors and sensitization of post-synaptic serotonergic receptors. Ex: desipramine, imipramine, nortriptyline

Front 5

How do MAOIs work? What is an example?

Back 5

Inhibit functioning of monoamine oxidase (A more important), leading to elevated brain concentrations NE, DA and 5-HT (most imp). Iproniazid.

Front 6

What are the side effects of MAOIs and TCAs?

Back 6

1. excessive CNS stimulation
2. peripheral vascular effects (orthostatic hypotension)
3. atropine-like effects reflecting imbalance between sympathetic and vagal tone

Front 7

What foods/drugs must patients on MAOIs avoid?

Back 7

Those that would increase amine levels or that contain tyramine. No co-admin of TCAs and MAOIs.

Front 8

What are examples of SSRIs?

Back 8

fluoxetine (prozac), sertraline (zoloft), fluvoxamine (luvox), paroxetine (paxil)

Front 9

How does Lithium work?

Back 9

blocks Adenylyl cyclase and the inositol cycle, antagonizing second messenger systems.

Front 10

What other disorders are antidepressants used to treat?

Back 10

Panic disorder and OCD

Front 11

What are the sites of action of antibiotics and examples of drugs under each category?

Back 11

1. Cell Wall - penicillins, cephalosporins, vancomycin, bacitracin, cycloserine, isoniazid
2. Cell membrane - polymyxins, nystatin, amphotericin B
3. Cell proteins - aminoglycosides, tetracyclins, chloramphenicol, clindamycin
4. Nucleic Acids - griseofulvin, 5-fluorocytosine, rifampin, sulfonamides, trimethoprim

Front 12

What does cycloserine do?

Back 12

In cell wall formation, inhibits the conversion of L-alanine to D-alanine and the linking together of two D-alanine molecules

Front 13

What does Bacitracin do?

Back 13

Binds the carrier molecule that transports the D-alanine dipeptide/3 AAs/sugar complex to cell wall

Front 14

What does vancomycin do?

Back 14

In cell wall formation, prevents the transfer of the sugar pentapeptide from the carrier molecule to growing polymer strands

Front 15

What do penicillins and cephalosporins do?

Back 15

Bind the active site of the enzyme responsible for cell wall cross linking and thus inhibit its function.

Front 16

What do Polymyxins do?

Back 16

They are cationic detergents, so they react with phospholipid groups of cell membranes and cause disorganization and rupture of cell membranes

Front 17

What do Amphotericin B and nystatin do?

Back 17

Same thing as Polymyxins, but on fungal cells

Front 18

How is antibiotic resistance disseminated?

Back 18

1. Conjugation - sex-factor
2. Transductino - bacteriophage vector, small plasmids
3. Transformation - direct DNA transfer from solution
4. Transposition - gene hopping around among plasmids and chromosomes

Front 19

What are some products of genes on R-plasmids?

Back 19

1. Interfere w/ transport systems or pores so that antibiotics can't enter cell
2. Site of action no longer binds drug
3. Enzymes that destroy antibiotic
4. Substitute resistant enzymes
5. Active transport to remove drug

Front 20

What agents affect nucleic acid synthesis only in bacteria/protozoa?

Back 20

Pas, Sulfones, Sulfonamides

Front 21

What agents affect the synthesis of bacterial cell proteins?

Back 21

1. Aminoglycosides
2. Tetracyclines
3. Chloramphenicol
4. Macrolides

Front 22

What is the evidence that antipsychotics act on DA receptors?

Back 22

1. Reserpine (depletor of DA and NE) has antipsychotic actions
2. Amphetamines, which release DA from presynaptic terminals, induce psychosis. Antipsychotic agents block these actions.
3. Antipsychotics block the actions of DA agonists (L-dopa, apomorphine, bromocriptine)

Front 23

What are the families of DA receptors? What do they include?

Back 23

D1-like (D1, D5) and D2-like (D2, D3, D4)

Front 24

What are the side effects of antipsychotics?

Back 24

1. Parkinsonism
2. Neuroleptic malignant syndrome
3. Akathisia
4. Tardive dyskinesia
5. Pseudopregnancy
6. Seizures (high doses)

Front 25

What are galenicals?

Back 25

Natural preparations, obtained by drying or extracting plant or animal materials

Front 26

Pure Compounds

Back 26

Isolated from natural sources by physical and chemical extraction and purification.

Front 27

Drug Nomenclature

Back 27

1. Chemical Name - given by manufacturer: 1-methyl-4-etc.
2. Nonproprietary (generic) name - official name: meperidine, flunitrazepam
3. Proprietary name: Demerol, Rohypnol
4. Common Name: Demmies, Roofies

Front 28

Routes of Drug Administration

Back 28

1. Topical
2. Percutaneous
3. GI Tract: Oral mucosa, oral, rectal mucosa
4. Pulmonary epithelium
5. Injections: Subcutaneous, intramuscular, intravenous, intra-arterial, injection into body cavities

Front 29

Factors influencing a drug's ability to cross capillary walls

Back 29

1. Aqueous solubility
2. Lipid solubility
3. Molecular size and shape

Front 30

What effect does plasma protein binding have on drug action?

Back 30

Lower peak free drug concentrations at site of action, slowed elimination in kidney and metabolism in liver.

Front 31

Three stages of drug concentrations following IV admin.

Back 31

1. initial dilution and mixing
2. Distribution
3. Elimination

Front 32

Phase I reactions

Back 32

Oxidation, reduction, hydrolysis. May increase, decrease or not alter pharmacological activity of drug.

Front 33

Phase II reactions

Back 33

Synthetic or conjugation reactions. endogenous substance combines with functional group to make very polar.

Front 34

Where does biotransformation occur?

Back 34

*liver*, gi tract, lungs, skin, kidneys

Front 35

Where are drug biotransformation enzymes located?

Back 35

1. ER
2. Mitochondira
3. Cytosol
4. Lysosomes
5. nuclear and plasma membranes

Front 36

Oxidation

Back 36

uses cytochromes P450 and NADPH-cytochrome P450 reductase.

can also use: microsomal flavin-containing monooxygenases, alcohol dehydrogenase, xanthine oxidase, monoamine oxidase

Front 37

which cytochromes are important for benzodiazepine metabolism?

Back 37

3A4 and 2C19

Front 38

types of phase II reactions

Back 38

1. Epoxide hydration - oxygen inserted across C=C
2. Sulfation
3. Glucuronidation - UDPGA attached so that conjugates can be excreted by bile or urine
4. Glutathione conjugation
5. Methylation

Front 39

Pharmacokintics

Back 39

Quantitative description of the rates of the various steps of drug disposition, including:
1. absorption of drugs
2. distribution to organs and tissues
3. elimination by biotransformation and excretion

Front 40

Pharmacodynamics

Back 40

Intensites and time courses of the responses to drugs

Front 41

What are the complications in relating drug plasma concentration and effect?

Back 41

1. Irreversibly acting drugs
2. Tolerance
3. Combinations of drugs with synergistic or antagonistic actions
4. Active metabolites

Front 42

equation for half-life

Back 42

t1/2 = 0.693/k

Front 43

Bioavailability

Back 43

percentage of drug that enters systemic circulation in unchanged form after administration

Front 44

Bioequivalence

Back 44

Comparable bioavailability between related drugs

Front 45

Therapeutic equivalence

Back 45

Comparable clinical effectiveness and safety between similar drugs

Front 46

Measurements of bioavailability

Back 46

1. correlation of dose with response
2. plasma concentration measurements
3. urinary excretion

Front 47

Plateau principle

Back 47

The rate of approach to the steady state concentration only depends on the elimination rate constant (assuming first-order kinetics), even the Css depends on the rates of administration and elimination.

Front 48

In what way is the liver suited for rapid extraction of large amounts of drug?

Back 48

1. large (1.5 kg)
2. high blood flow
3. maximal blook contact with hepatic cell surfaces

Front 49

Factors affecting hepatic clearance

Back 49

1. extraction directly dependent on liver blood flow
2. clearance dependent on concentration of enzyme and affinity of enzyme that metabolizes drug

Front 50

What is total body clearance equal to?

Back 50

Clh + Clr

Front 51

extraction ratio

Back 51

E = (Ca - Cv) / Ca

Front 52

Hepatic clearance

Back 52

R * E

Front 53

What is the average GFR?

Back 53

120 ml/min

Front 54

Renal excretion of drugs

Back 54

GFR + TSR - TRR

Front 55

What type of molecules are transported in tubular secretion?

Back 55

Ionized molecules

Front 56

What compounds are used to measure GFR?

Back 56

Inulin and creatinine

Front 57

TI

Back 57

TI = TD50 / ED50 TI should be as high as possible

Front 58

Certain safety factor

Back 58

(CSF) = TD1 / ED99

Front 59

How do drugs bind to receptors?

Back 59

combination of electrostatic forces, hydrogen bonds, Van der Waals forces

Front 60

Over what concentration range to drugs compete?

Back 60

100 fold

Front 61

Example of drugs with shared selectivities as well as unique properties

Back 61

Chlorpromazine, procaine and diphenhydramine (all good local anaesthetics, H1 receptor antihistamines and myocardial antiarrythmics)

Front 62

In what ways can selectivity be achieved due to differential drug distribution?

Back 62

1. topical application
2. intra-arterial injection
3. selectivity by ionization
4. differential blood flow
5. distribution by selective carriers
6. selective concentration by excretion

Front 63

In what ways can tissue differences influence drug selectivity?

Back 63

1. Selective cellular binding
2. Selective uptake by tissues
3. Selective intracellular activation
4. Selective tissue vulnerability

Front 64

How does the cholera toxin work?

Back 64

binds ADP-ribose to guanyl nucleotide binding site, leading to persistent activation of Gs, resulting in elevated cAMP and secretion of H2O into gut

Front 65

Proof that action of a neuromodulator is through a G protein coupled receptor

Back 65

1. Intracellular GTP required
2. non-hydrolyzable GTP analog greatly prolongs action
3. high affinity GDP-B-s analog can't be displaced
4. block with pertussis toxin (inactivates subset of Ga proteins)

Front 66

Chloramphenicol

Back 66

antibiotic that affects protein sythesis. Inhibits peptidyl transferase and prevents peptide bond formation

Front 67

Cycloserine

Back 67

Antibiotic that acts at the cell wall to inhibit cell wall synthesis. Inhibits the conversion of L-alanine to D-alanine and also the linking together of two D-alanine residues

Front 68

Aminoglycosides

Back 68

Antibiotic that affects protein synthesis. Binds 30S subunit of bacterial ribosome, blocks tRNA binding and also distorts codons of mRNA resulting in misreading of genetic code

Front 69

Polymyxins

Back 69

Antibiotics that act on cell membrane. Act as cationic detergents that react with phospholipids, leading to disorganization of bacterial cell membranes and leakage of cytoplasm

Front 70

List four (4)of the seven DSM-IV criteria for diagnosing substance dependence

Back 70

1. Tolerance: Either need for markedly increased amounts of drug to achieve intoxication, or
markedly diminished effect with continued use of the same amount of drug.
2. Drug withdrawal symptoms.
3. Drug was often taken in larger amounts or over a longer period than was intended.
4. Persistent desire or unsuccessful efforts to cut down or control drug use.
5. Great deal of time spent in using drug, or recovering from drug use.
6. Important social, occupational, or recreational activities given up or reduced because of drug
use.
7. Continued drug use despite knowledge of having a persistent or recurrent physical or
psychological problem that is likely to have been worsened by drug

Front 71

Cyclophosphamide

Back 71

Alkylating agent that covalently binds DNA, interfering in cell division

Front 72

L-asparaginase

Back 72

Certain leukemic cells are deficient in enzyme L-asparagine snythetase and require exogenous asparagine. If supply is decreased, protein synthesis is slowed, killing these cells

Front 73

Tamoxifen

Back 73

hormone that slows rate of growth of breast cancers that are dependent on estrogens. Binds estrogen receptor which is internalized and translocated to nucleus. There it inhibits DNA and RNA synthesis instead of inducing synthesis as estrogens normally would.

Front 74

steady state concentration

Back 74

(Dm/Tm)/Cl

Front 75

Maintenance dose

Back 75

(Ctox-Cther) x V

Front 76

Extraction ratio

Back 76

(Ca-Cv)/Ca

Front 77

Rate of administration

Back 77

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