Pharmacology

Rationalisation: Prelim Platings

Jumbo hotdog, kaya mo ba ‘to? | First Semester | AY 2018-2019
INTRODUCTION TO PHARMACOLOGY 10. This phase 1 drug metabolising enzyme acts primarily on acidic
1. Any genetic variation in the DNA drugs including S-warfarin, phenytoin, and NSAIDs
A. Indel A. UGT1A1
B. Allele B. TPMT
C. Haplotype C. G6PD
D. Polymorphism D. CYP2C9
E. Copy number variation 11. It is defined as the study of substances that interact with living
2. Phase 1 enzymes systems through chemical processes to produce an effect
A. Conjugate endogenous molecules A. Pharmacotherapeutics
B. Convert glucuronic acid into small lipophilic molecules B. Pharmacogenomics
C. Deactivate thiopurine drugs C. Pharmacognosy
D. Biotransformation rxn mediated by cytochrome p450 D. Pharmacology
E. All of the above 12. The study of the relation of the individual’s genetic makeup to his
3. One of 2 or more alternative forms of a gene that arise by response to specific drugs is:
mutation and are found at the same genetic locus A. Pharmacotherapeutics
A. Polymorphism or variant B. Pharmacogenomics
B. Synonymous SNP C. Pharmacognosy
C. Indels D. Pharmacology
D. Allele 13. The branch of pharmacology that deals with the undesirable
E. Haplotype effects of chemicals on living systems
4. Phase 1 enzymes EXCEPT A. Pharmacognosy
A. CYP ZC19 B. Toxicology
B. Dihydropyrimidine dehydrogenase C. Pharmacogenomics
C. CYP 2D6 D. All are correct
D. Thiopurine S-methyltransferase 14. Which of the following chemical bonds is very strong and is usually
E. None of the above irreversible?
5. Pharmacogenomics A. Aqueous
A. Study of the toxic side effects of drugs B. Covalent
B. Study of drugs in its unaltered form C. Electrostatic
C. Study of drugs preparation and medical uses of drugs D. Hydrophobic .
D. Study of individual’s genetic make-up to his/her response to 15. The actions of this drug on the body is termed:
specific drugs A. Pharmacokinetics
E. None of the above B. Pharmacodynamics
6. The following statements regarding Phase 2 enzymes are correct C. Medical pharmacology
EXCEPT D. Pharmacognosy
A. Typically conjugate endogenous molecules
B. Polymorphism may diminish drug elimination and increase
risk of toxicity Safety Tests and Its Approaches and Goals
C. Approximately 10% of European populations are Use the given choices to answer the following numbers
homozygous carriers of the *28 allele A. Acute toxicity
D. Typically modify functional group of endogenous and B. Subacute toxicity
xenobiotic compounds resulting in a lateration of the biologic C. Chronic toxicity
activity of the compound D. Carcinogenic potential
7. The majority of polymorphic G6PD deficient genotypes are E. Mutagenic potential
associated with this class of severe deficiency ( < 10% enzyme
activity); risk of acute haemolytic anaemia and intermittent may 16. Usually 2 species, 2 routes
occur: 17. Two weeks to 3 months of testing may be required before clinical
A. Class I trials
B. Class II 18. Rodent and at least one nonrodent species for ≥ 6 months
C. Class III 19. Two years 2 species
D. Class IV 20. Determine gross and histologic pathology
8. HLA-B *57:01 polymorphism has been shown to be associated in
producing this drug adverse effect: RATIONALE
A. Abacavur-induced skin toxicity
1. D. Polymorphism- Any genetic variation in the DNA
B. Allopurinol-induced skin toxicity
A.Indel- Insertion or deletion of base pairs which may occur in coding and
C. Amoxycillin clavulanate-induced liver injury
noncoding regions
D. Carbamazepine-induced skin toxicity
B.Allele – is one of two or more alternative forms of a gene that arise by
9. Gilbert’s Syndrome-affected individuals may have 60-70%
mutation and are found at the same genetic locus.
increased levels of circulating unconjugated bilirubin due to a 30%
C.Haplotype – A series of alleles found in linked locus on chromosome
reduction in this enzyme activity:
E.Copy number variation- a segment of DNA in which a variable number of
A. Glucose-6-phosphate dehydrogenase
that segment has been found.
B. Cytochrome P40 2D6
C. Uridine 5’-diphosphoglucuronosyl transferase
2. D. Biotransformation reaction mediated by cytochrome P450. The rest
D. Thiopurine S-methyltransferase
of the choices are the characteristics of Phase 2 enzymes

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PHA211 RATIONALISATION: PRELIM PLATINGS

3. D. Allele- One of 2 or more alternative forms of a gene that arise by

mutation and are found at the same genetic locus
A. Polymorphism or variant- - Any genetic variation in the DNA
B.Synonymous SNP- Single Nucleotide polymorphisms: base-pair
substitutions that occur in the genome.
C.Indels- is one of two or more alternative forms of a gene that arise by
mutation and are found at the same genetic locus.
E.Haplotype- series of alleles found in linked locus on chromosome
4. D. Thiopurine S- Methyltransferase – Phase 2 enzymes
The rest of the choices are Phase 1 enzymes
5. D. Pharmacogenomics- study of individual’s genetic make-up to his/her
response to specific drugs
A. Toxicology- study of the toxic side effects of drugs
B. Study of drugs in its unaltered form
C. Medical Pharmacology-study of drugs preparation and medical uses of
drugs
6. D. Typically, modify functional group of endogenous and xenobiotic
compounds resulting in a lateration of the biologic activity of the
compound- Phase 1 enzymes. The rest of the choices are the characteristics
of Phase 2 enzymes
7. B. Class II- severe deficiency (< 10% enzyme activity); risk of acute
haemolytic anaemia and intermittent
A. Class I – severe deficiency ( <10% enzyme activity) ; Chronic (non-
spherocytic) haemolytic anemia
C. Class III- Moderate deficiency (10-60 % enzyme activity); Risk of acute
hemolytic anemia; hemolysis with stressors
D. Class IV- None deficiency
(60-150% enzyme activity);Normal
8. A. Abacavur-induced skin toxicity – HLA-B *57:01
B. Allopurinol-induced skin toxicity –HLA-B * 58:01
C. Amoxycillin clavulanate-induced liver injury- HLA- DRB1* 15:01
D. Carbamazepine-induced skin toxicity- HLA-B* 15:02
12. B. Pharmacogenomics- study of individual’s genetic make-up to
his/her response to specific drugs
A. Pharmacotherapeutics- - branch of Pharmacology, which is the study of
the therapeutic uses and effects of drugs
B. Pharmacognosy- the branch of pharmacology that is concerned with
medicinal drugs obtained from plants or other natural sources.
C. Pharmacology- - study of substances that interact with living systems
through chemical processes to produce an effect
13. B. Toxicology- branch of pharmacology that deals with the
undesirable effects of chemicals on living systems
A.Pharmacognosy- the branch of pharmacology that is concerned with
medicinal drugs obtained from plants or other natural sources.
C. Pharmacogenomics- study of individual’s genetic make-up to his/her
response to specific drugs
14. B. Covalent – very strong and many cases not reversible under biologic
conditions
A. Aqueous-movement of molecules through the water extracellular and
intracellular spaces.
C. Electrostatic- vary from relatively strong linkages between permanently
charged ionic molecules to weaker hydrogen bonds. Weaker than covalent
bond
D. Hydrophobic- quite weak and are probably important in interactions of
highly lipid soluble drugs
15. B. Phamacodynamics- denotes the actions of the drug on the body
A.Pharmacokinetics- describes the effects of the body on drugs
C. Medical Pharmacology-study of drugs preparation and medical uses of
drugs
D. Pharmacognosy- the branch of pharmacology that is concerned with
medicinal drugs obtained from plants or other natural sources.

9. C. Uridine 5’-diphosphoglucuronosyl transferase – Gilbert’s Syndrome-

affected individuals may have 60-70% increased levels of circulating
unconjugated bilirubin due to a 30% reduction in this enzyme activity
A. Glucose-6-phosphate dehydrogenase- is the first and rate limiting step in
the pentose phosphate pathway and supplies a significant amount of reduced
NADPH in the body. In red blood cells where mitochondria are absent, G6PD
is the exclusive source of NADPH and reduced glutathione which play a
critical role in the prevention of oxidative damage.
B. Cytochrome P40 2D6- Codeine converted to morphine. Increased function
associated with increased toxicity; decreased function associated with
decreased analgesia.
C. Thiopurine S-methyltransferase- is important in the inactivation of
chemotherapeutic purine derivatives.

10. D. CYP2C9 - acts primarily on acidic drugs including S-warfarin,

phenytoin, and NSAIDs
A. UGT1A1- increased irinotecan toxicity
B. TPMT- is important in the inactivation of chemotherapeutic purine
derivatives.
C. G6PD- - is the first and rate limiting step in the pentose phosphate
pathway and supplies a significant amount of reduced NADPH in the body. In
red blood cells where mitochondria are absent, G6PD is the exclusive source D D
of NADPH and reduced glutathione which play a critical role in the prevention D B
of oxidative damage. D B
D B
11. D. Pharmacology- study of substances that interact with living systems D B
through chemical processes to produce an effect D A
A. Pharmacotherapeutics- branch of Pharmacology, which is the study of the B B
therapeutic uses and effects of drugs A C
B. Pharmacogenomics- study of individual’s genetic make-up to his/her C D
response to specific drugs D D
C. Pharmacognosy- the branch of pharmacology that is concerned with
medicinal drugs obtained from plants or other natural sources.

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PHA211 RATIONALISATION: PRELIM PLATINGS
Carbamazepine Chlorpromazine
PHARMACOKINETICS / PHARMACODYNAMICS Chlorcyclizine Cimetidine
1. An example of phase II reaction: Ethchlorvynol Dicumarol
a. Deamination Glutethimide Diethylpentenamide
Griseofulvin Disulfiram
b. Glucoronidation Phenobarbital and other barbiturates Ethanol
c. Water conjugation Phenylbutazone Grapefruit juice
d. A and B Phenytoin Itraconazole
Rifampin Ketoconazole
e. B and C Ritonavir Nortriptyline
PHASE II REACTIONS: St. John’s Wort Oral contraceptives
PHASE I REACTIONS:
- Glucoronidation Phenylbutazone
- Oxidations
- Cytochrome P450-dependent Oxidation - Acetylation Ritonavir
o Aromatic hydroxylations - Glutathione Conjugation
Saquinavir
o Aliphatic hydroxylation - Glycine Conjugation
o Dechlorination - Sulfation Secobarbital
- Cytochrome P450-independent oxidations: - Methylation Spironolactone
o Flavin monooxygenase (Ziegler - Water Conjugation
Enzyme) troleandomycin
o Amine Oxidases DISCUSSION:
o Dehydrogenation Phase II reaction are DISCUSSION:
- Reductions reaction that forms covalent linkages RIFAMPIN and ST. JOHN’S WORT are both drug that enhances
o Azo reductions between functional group on the metabolism. CIMETIDINE is a drug that inhibit metabolism.
o Nitro reductions parent compound for form a highly *(please refer to table 4-5 (Partial list of drugs that enhance drug metabolism in
o Carbonyl reductions polar conjugates. This is involves humans) table 4-6 (Partial list of drugs that inhibit drug metabolism in humans)
- Hydrolyses th
GLUCORONIDATION AND WATER chapter 4, pp. 71 , katzung 14 ed.
o Esters
CONJUGATIONS.
o Amides
Phase I reactions ANSWER: E.) A and B
- Epoxidation
- Oxidative dealkylation involves the introduction or
o N-dealkylation unmasking of functional group like – 4. This drug is a rapidly metabolized drug whose hepatic
o O-dealkylation OH, -NH2, and –SH. An example of
clearance is blood flow limited:
o S-dealkylation which is DEAMINATION.
- N-Oxidation a. Itraconazole
o Primary amines ANSWER: E.) B and C b. Propranolol
o Secondary amines
o Tertiary amines c. Ethanol
- S-Oxidation d. All
- Deamination
- Desulfuration
e. A and C only
RAPIDDLY METABOLIZED DRUGS WHOSE HEPATIC CLEARANCE
IS BLOOD FLOW-LIMITED.
ALPRENOLOL LIDOCAINE
2. A type of genetic polymorphism that confers a poor
AMITRIPTYLINE MEPERIDINE
metabolizer (PM) phenotype that correlates with a higher risk CLIMETHIAZOLE MORPHINE
of relapse in patients with breast cancer treated with DESIPRAMINE PENTACOZINE
tamoxifen involve this enzyme: IMIPRAMINE PROPOXYPHENE
ISONLAZID PROPRANOLOL
a. CYP2D6 LABETALOL VERAPAMIL
b. CYP2C19
DISCUSSION:
c. CYP2C9 Capacity-Limited Elimination also known as mixed-order, saturable,
d. CYP2B6 dose- or concentration-dependent, nonlinear, and Michaelis-Menten elimination.
Clearance varies depending on the concentration of the drug achieved and if dosing
DISCUSSION:
rate exceed elimination capacity, steady state cannot be achieved: the concentration
CYP2D6. This is a debrosiquin-sparteine oxidation type of polymorphism that will keep on rising as long as dosing continues. Capacity-limited elimination is
expresses defect on the P450 protein that result to little or no isoform -catalyzed drug observed on ETHANOL, PHENYTOIN, AND ASPIRIN.
metabolism and thereby conferring a poor metabolizer (PM) phenotype. This correlates
Blood-flow limited elimination depends primarily on the rate of drug
with a higher risk of relapse in patients with breast cancer treated with tamoxifen.
delivery to the organ of elimination. Such drugs are called “high-extraction” drugs
CYP2C19. Involves the the stereo selective aromatic (4)-hydroxylation of the
since they are almost completely extracted from the blood by the organ.
anticonvulsant mephenytoin. PMs of mephenytoin show signs of profound sedation and PROPRANOLOL is an example.
ataxia after doses of the drug that are well tolerated by normal metabolizer. On the other
hand , the PM phenotype can notably increase the therapeutic efficacy of omeprazole. ANSWER: B.) PROPRANOLOL

CYP2C9 phenotype has reduced tolerance for the anticoagulant

warfarin (specific for CYP2C9*3). These individuals have a much higher risk of 5. An example of a drug that inhibit drug metabolism in humans:
adverse effect of warfarin (e.g. bleeding) and other CYP2C9 substrates like a. Itraconazole
phenytoin, losartan, tolbutamide, and some nonsterordal anti-inflammatory drugs. b. Propranolol
CYP2B6 has become noteworthy as one of the mosty polymorphic
P450 genes. This CYP2B6 polymorphism may have a significant impact on the c. Ethanol
CYP2B6-dependent metabolism of several clinically relavant drugs such as d. All
cyclyphosphamide, S-methadone, efavirenz, nevirapine, buproprion, selegiline, and e. A and C only
propofol. Women express considerably higher levels of CYP2B6 protein than men.
DISCUSSION:
th
(please refer to Table 4-4, chapter 4 pp.66-67, Katzung 14 . Ed. for the tabulated ITRACONZAOLE and ETHANOL are both inhibitors of drug
form of genetic polymorphism in phase I and phase II drug metabolism). metabolism.
*please refer ot he table in no.3 question.
ANSWER: A.) CYP2D6
ANSWER: E.) ITRACONAZOLE AND ETHANOL
3. An example of a drug that enhances drug metabolism:
a. Rifampin 6. Phase 1 reaction include:
b. St. John’s Wort a. Acetylation
c. Cimetidine b. Glucoronidation
d. All c. Reduction
e. A and B only d. All of the above
INDUCERS (ENHANCERS) INHIBITORS
Benzo[a]pyrene Allopurinol, chloramphenicol, isoniazid

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PHA211 RATIONALISATION: PRELIM PLATINGS

DISCUSSION: DISCUSSION:
In the options above, ACETYLATION AND GLUCORONIDATION are UDP-glucoronyl transferases
both Phase II reactions, while REDUCTION is a Phase I reaction. (UGTs) is the most dominant
(please refer to the table on NO. 1) microsomal enzyme.

ANSWER: C.) REDUCTION. ANSWER: A. UDP-

GLURONOSYL TRANSFERASE
7. The principal organ of drug metabolism: (UGTs)
a. Liver
b. GIT
c. Lungs
d. Kidneys
DISCUSSION:
“.. the liver is the principal organ of drug metabolism.” Other than the
liver there are also tissues that exhibit drug metabolizing capabilities like the GIT, the
lungs, the skin, the kidneys, and the brain.
11. Which of the following statement is true regarding
ANSWER: A.) LIVER pharmacodynamics?
8. The process wherein absorbed drugs are transported via the a. Deals with the process of absorption, distribution, and
portal system to the liver where they undergo extensive elimination of drug determine how rapidly and for how
long the drug appear at target organs
metabolism is called:
a. Zero order metabolism b. The concept of maximum response and sensitivity
b. First order metabolism determine the magnitude of the effect of particular
c. First pass effect concentration
c. Deals with the dose-concentration of the drug
d. None
d. Deals with the metabolism of the drug
DISCUSSION:
Zero order metabolism – indicates that the rate of elimination is DISCUSSION:
proportional to the concentration (i.e, the higher the concentration, the greater the PHARMACOKINETICS deals with what the body does to drugs. This
amount of drug eliminated per unit time). Have a characteristic half-life elimination deals with the “drug-concentration” relationship. it involves 4 processes, absorption,
that is constant. Drug concentration in plasma decreases exponentially with time. distribution, metabolism, and elimination.
First order metabolism – implies that the rate of elimination constant PHARMACODYAMICS deals with what the drug does to the body.
regardless of concentration occurs with the drugs that saturate their elimination This involves the concept of maximum response and sensitivity that determine the
mechanism at concentrations of clinical interest. Concentration of these drugs in magnitude of the effect of particular concentration.
plasma decreases in linear fashion over time. Do not have a constant half-life
First pass effect – happens after oral administration of drugs are ANSWER: B.) THE CONCEPT OF MAXIMUM RESPONSE AND SENSITIVITY
absorbed intact from the small intestine and transported first via the portal system to DETERMINE THE MAGNITUDE OF THE EFFECCT OF PARTICULAR
the liver, where they undergo extensive metabolism. CONCENTRATION.

ANSWER: C.) FIRST PASS EFFECT

12. It relates to the amount of drug in the body to the
9. Drugs that enhance the rate of synthesis or reduce the rate of concentration of drug in the plasma:
degradation of chemically dissimilar P450 substrate drugs are: a. Clearance
a. Enzyme inducer b. Bioavailability
b. Enzyme inhibitors c. Volume of distribution
c. Substrate stabilizers d. Half-life
d. Mixed function oxidases DISCUSSION:
DISCUSSION: CLEARANCE is the ability of the body to eliminate a drug. This is the
ENZYME INDUCERS - An enzyme inducer is a type of drug that single most important factor determining drug concentrations.
increases the metabolic activity of an enzyme either by binding to the enzyme and
activating it, or by increasing the expression of the gene coding for the enzyme. It is
BIOAVAILABITLITY is the fraction of unchanged drug reaching the
the opposite of an enzyme repressor. They “induce” cytochrome P450 by enhancing
circulation; extent of absorption varies.
the rate of its synthesis or reducing its rate of degradation.
VOLUME OF DISTRIBUTION is the amount of apparent space in the
ENZYME INHIBITORS - Enzyme inhibitors are substances which
alter the catalytic action of the enzyme and consequently slow down, or in some body able to contain a drug (homogeneously in the blood, plasma, or water)
cases, stop catalysis. There are three common types of enzyme inhibition -
competitive, non-competitive and substrate inhibition.
HALF-LIFE – the time required to change the amount of drug by ½
SUBSTRATE STABILIZERS – they induced cytochrome P450 by
decreasing its degradation.
MIXED FUNCTION OXIDASES – these enzymes requires both a
ANSWER: C.) VOLUME OF DISTRIBTUTION
reducing agent (NADPH) and molecular oxygen; in a typical reaction, one molecule
of oxygen is consumed (reduced) per substrate molecule, with one oxygen atom
appearing in the product and the other in the form of water. • In this oxidation- 13. It is the time required to change the amount of the body by ½
reduction process, two microsomal enzymes play a key role. The first of these is a during elimination or during a constant infusion:
flavoprotein, NADPH-cytochrome P450 reductase. a. Drug accumulation
ANSWER: A.)ENZYME INDUCER b. Half-life
c. Clearance
10. Most dominant microsomal enzymes that catalyze the d. Volume of distribution
coupling of an activated endogenous substance with a drug:
DISCUSSION: Please refer to the definition of terms in no. 12 .
a. UDP-glucoronosyl transferase ANSWER: B.) HALF-LIFE
b. Sulfotransferases (SULTs)
c. Epoxide hydorlases (EHs) 14. A drug was given to a 80kg patient with palpitation and chest
d. Glutathione Transferases (GSTs) pain. The VD of the drug is 50L, the target concentration is
5mg/L, and the clearance is 8L/hr. when will the concentration
of the drug be reduced to 50%?
a. 2 hours

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PHA211 RATIONALISATION: PRELIM PLATINGS

b. 3 hours DISCUSSION:
c. 4 hours TACHYPHYLAXIS – This is when responsiveness diminishes rapidly
d. 5 hours after administration of a drug.
TOLERANCE – the intensity of response to a given dose may
SOLUTION: change during the course of therapy; in these cases, responsiveness usually
decreases as a consequence of continued drug administration
HYPERSENSITIVITY – refers to allergic or other immunologic
response to drugs.
HYPERREACTIVITY – intensity of effect of a given dose of drug is
increased compared with the effect seen in most individuals.
T ½ = 4.375 HYPOREACTIVITY – Intensity of effect of a given dose of drug is
diminished compared with the effect seen in most individuals.

ANSWER: C.) 4 HOURS ANSWER: A.)TACHYPHYLAXIS

15. J.S is admitted at FUMC due to exacerbation of bronchial 18. Mechanism that may contribute to variation in drug
asthma secondary to community acquired pneumonia. A responsiveness among patients or within an individual patient
bronchodilator IV is to be given at the ER with a target plasma at different times:
concentration of 5mg/L to relieve the dyspnea. The CL is a. Alteration in concentration of drug that reaches the
70ml/min and the VD is 50L. What is the maintenance dosage receptor
should be administered every 8 hours to obtain a steady state b. Variation in concentration of an endogenous receptor
plasma concentration of 5mg/L? ligand
a. 208mg/dose c. Alteration in number or function of receptors
b. 168mg/dose d. Changes in components of response distal to the receptor
c. 188mg/dose e. All of the above
d. 198mg/dose DISCUSSION:
VARIATION IN DRUG RESPONSIVENESS
SOLUTION: A. Alteration in concentration of drug that reaches the receptor
MAINTENANCE DOSE – this is the dose that is given at regular B. Variation in concentration of an endogenous receptor ligand
interval to maintain a steady state. C. Alterations in number or function of receptor
D. Changes in components of response distal to the receptor
th
*for a more detailed explanation pls. read 37-38 of Katzung 14 edition chapter 2.

ANSWER: E. ALL OF THE ABOVE

19. A maximal biological response at a concentration of agonists

Md = 168mg/dose that does not result in occupancy of all the available receptors
may be seen with:
ANSWER: B.) 168mg/dose
a. Spare receptors
16. Dose at which 50% of individuals exhibit the specified quantal b. Desensitization
effect: c. Tolerance
a. Median effect dose d. Tachypylaxis
b. Median toxic dose e. Hyperreaction
c. Median lethal dose DISCUSSION:
d. LD50 SPARE RECEPTORS – are receptors that can elicit a maximal
e. TD50 biologic response at a concentration of agonist that does not result in occupancy of
all of the available receptors.
DISCUSSION: DESENSITIZATION – after reaching an initial high level, the
Median effect dose [ED50] – is the dose at which 50% of individuals response diminishes over seconds or minutes, even in the continued presence of
exhibit the specified quantal effect. the agonist. Attenuation of receptors through time.
Median toxic dose [TD50] – the dose required to produce a
particular toxic effect in 50% of animals. *please refer to question 17 for the definition of tolerance, tachyphylaxis, and
Median lethal dose [LD50] – THIS IS the dose that kills hyperrection.
approximately 50% of the animals in a test group.
ANSWER: A.)SPARE RECEPTORS
ANSWER: A.) MEDIAN EFFECT DOSE [ED50]
20. The dose required to produce a particular toxic effect in 50% of
17. This occurs when responsiveness diminishes rapidly after animal is:
administration of a drug: a. TD50
a. Tachyphylaxis b. LD50
b. Tolerance c. ED50
c. Hypersensitivity d. Therapeutic index
d. Hyperreactivity e. Therapeutic window
e. Hyporeactivity DISUSSION:
THERAPEUTIC INDEX – relates the dose of a drug required to
produce a desired effet to what which produces an undesired effect. It is also
defined as the ratio of the TD50 to the ED50 for some therapeutically relevant
effect.
THERAPEUTIC WINDOW – the range between the minimum toxic
dose and the minimum therapeutic dose.

*please refer to question no. 16 for the definition of TD50, LD50 and ED50

ANSWER: A.)TD50

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INTRODUCTION TO THE AUTONOMIC NERVOUS SYSTEM 64. Which of the following is considered as the treatment for MG?
(SET BBB – August 30, 2018) a. bethanecol
** A- if TRUE; B – if FALSE b. pilocarpine
c. nicotine
___51.The sympathetic preganglionic fibers leave the thoracic, lumbar, d. edrophonium
and according to new information, even sacral spinal nerves. 65. A long-acting cholinesterase inhibitor:
___52.Nicotinic receptors are also known as inotropic receptors because a. edrophonium
they simply work as ion channel. b. neostigmine
___53.Dopamine is converted to norepinephrine in the vesicle by c. physostigmine
dopamine-B-hydroxylase. d. echothiopate
___54.Stimulation of M3 will cause relaxationof bronchiolar smooth 66. This drug affects Ach transmitter storage:
muscle. a. Hemicholinium
___55. Vascular smooth muscle in skeletal muscle has sympathetic b. Vesamicol
cholinergic dilator fibers. c. Botulinum Toxin
d. TCA
**MULTIPLE CHOICE 67. Which is NOT a parasympathetic effect on the eye?
56. Antimuscarinic effects on the GIT EXCEPT: a. contraction of the ciliary muscle
a. decreased basal gastric acid secretion b. accommodation for near vision
b. decreased GI motility c. papillary constriction
c. increased gastric emptying time d. increase IOP
d. increased GI smooth muscle tone 68. A muscarinic receptor that is predominantly found on the
57. Therapeutic applications of antimuscarinic agents EXCEPT: myocardium:
a. parkinson’s disease a. M1
b. COPD b. M2
c. vasovagal attack c. M3
d.atropine poisoning d. M4
58. Which of the following antimuscarinic agents is NOT USED to relieve e. M5
bladder spasms and urinary incontinence? 69. A parasympathetic activity:
a. aclidinum a. bronchiolar smooth muscle - contract
b. oxybutynin b. heart contractility - decrease
c. darifenacin c. bladder wall - contract
d. tolterodine d. all of the above
59. A compound which is capable of regenerating the active enzyme e. A and C only
cholinesterase used in organophosphate? 70. A result of ligand binding to M1 receptor results to:
a. atropine a. Formation of IP3 & DAG, increase intracellular Ca
b. pralidoxime b. Opening of K channels, inhibition of adenylyl cyclase
c. physostigmine c. Opening of Na & K channels, depolarization
d. muscarine d. Inhibition of adenylyl cyclase
60. Which of the following is NOT an organ system effect of ganglionic
blockers? RATIONALE
a. sedation tremors 51. The answer is A (True). It is directly mentioned in Katzung (14th ed),
b. marked meiosis page 91.)
c. hypotension 52. The answer is A (True). The ion channel the question is referring to is
d. reduced GI motility the Na-K channels found truly in the nicotinic receptors.
61. Which of the following agents is susceptible to cholinesterase? 53. The answer is A (True). Dopamine-B-hydroxylase (DBH) is the
a. methacholine enzyme responsible for converting dopamine to norepinephrine.
b. acetylcholine 54. The answer is B (False). M3 receptors (parasympathetic) will make
c. carbachol the bronchiolar smooth muscles to contract. It is the B2 receptor that will
d. reduced GI motility make these muscles relax. (Refer to Table 6-3, Baby Katzung, p.63)
62. A patient received direct acting cholinoreceptor stimulant. Which of 55. The answer is A (True). Specifically M3 receptors wherein it relaxes or
the following effects is expected in the heart? makes the skeletal vessels dilate in response to nitric oxide (NO) and
a. reduced contractile strength endothelial-derived relaxing factor (EDRF). (Showcased classification in
increased refractory period in the atria Table 6-3 below)
c. increase HR 56. The answer is C (increased gastric emptying time). The choice of
d. decrease refractory period in the AV node elimination is towards a parasympathetic response. All the remaining
63. Myasthenia Gravis (MG) is an autoimmune disease affecting skeletal options showcase a sympathetic behaviour of the GIT.
muscle neuromuscular junction (NMJ) that affects nicotinic receptor 57. The answer is D (Atropine Poisoning). Physostigmine (an indirect-
function by: acting cholinomimetic drug) is used for atropine poisoning. All the other
a. causing lysis of the presynaptic membrane options are parasympatholytic effects.
b. cross-linking receptors that stimulate degredation 58. The answer is A (Aclidinum). All of the remaining options have direct
c. stimulating nicotinic receptor function effect on the genitourinary system. Aclidinum is a non-selective
d. increase nicotinic acid synthesis antimuscarinic drug are used in asthma and COPD patients.
59. The answer is B (Pralidoxime) because of its oxime group that has an
extremely high affinity for the phosphorous atom in organophosphate
insecticides, therefore, these agents are able to bind the inhibitor and
displace the enzyme.
60. The answer is B (marked meiosis).

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PHA211 RATIONALISATION: PRELIM PLATINGS

61. The answer is B (Acetylcholine – ACh). “Eventually, and usually very

rapidly, ALL OF THE ACh released diffuses within range of an
acetylcholinesterase (AChE) molecule.” – (Katzung, 14th ed; p.95)
62. The answer is A (reduce contractile strength). If you’ll base this on
Table 6-3, options B,C and D oppose the ideal cholinomimetic effects in
the heart. (Baby Katzung, p.63)
63. The answer is B (cross-linking receptors that stimulates
degredation). This is much observed in MG. The target is the post-
synaptic area, not the presynaptic membrane. This is just how ‘auto-
immunity’ in MG is explained.
64. The answer is D (Edrophonium). Edrophonium is a short-acting and
indirect – acting cholinesterase inhibitor therefore, its rapid reversal for
neuromuscular blockade is used in the diagnosis of MG, as well as
differentiating myasthenia crisis from cholinergic crisis. (Baby Katzung,
p.64)
65. The answer is D (Echothiophate). All of the choices are indirect-
acting cholinesterase inhibitors. Edrophonium is the most short-acting
one. Both Neostigmine and Physostigmine are under Carbamates which
only has an intermediate to long-acting inhibitory effect.
ECHOTHIOPHATE is the best answer because it is classified under the
indirect action of the organophosphates which has a very long acting
duration because of its irreversible inhibitory effect. (Baby Katzung –
Chapter 7)
66. The answer is B (Vesamicol). Please refer to Baby Katzung p.48
67. The answer is D (increase IOP). Be mindful of the cues hidden in the
question. This item requires for a behaviour towards a sympathetic
response, and of all the options, the one in D is reflecting towards
sympathetic response.
68. The answer is B (M2 receptor). Refer to the Table 6-1 below. (Baby
Katzung, p.51)
69. The answer is D (all of the above). Refer to Table 6-3. A B
(Baby Katzung, p.53) A A
70. The answer is A (Formation of IP3 & DAG, increasing intracellular A B
Ca). Refer again to Table 6-1. (Baby Katzung, p.51) B D
A D
C B
D D
A B
B D
B A

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R
PHA211 RATIONALISATION: PRELIM PLATINGS

SYMPATHETIC DRUGS Timolol is a nonselective beta antagonist that has excellent

1. Non-selective alpha receptor antagonist used for erectile ocular hypotensive effects when administered topically in
dysfunction administered by injecting it into the penis the eye.
A. Phentolamine
B. Tolozoline – used in peripheral vasospasm 9. A 30-year-old patient with hyperthyroidism has palpitations
(acrocyanosis) and tremors. Which of the following beta blocker is indicated
C. Phenoxybenzamine- oral treatment of in this case?
pheochromocytoma E. carvedilol
D. Prazosin- selective alpha 1 antagonist used as a F. atenolol
treatment for hypertension and BPH G. propranolol
2. Non selective alpha blocker used for peripheral vasospasm H. betaxolol
(actocyanosis) Excessive catecholamine action is an important aspect of
F. Phentolamine the pathophysiology of hyperthyroidism; beta antagonists
G. tolazoline are beneficial in this condition. Propranolol has been used
H. phenoxybenzamine extensively in patients with severe hyperthyroidism.
I. prazosin
Refer to #1 10. A beta blocker indicated for migraine headache
E. metoprolol
3. Alpha 1 blocker used for oral treatment of pheochromocytoma F. labetalol
F. phentolamine G. propranolol
G. tolazoline H. carvedilol
H. phenoxybenzamine Propranolol reduces the frequency and intensity of migraine
I. prazosine headache.
Refer to #1
11. Mechanism of action of amphetamine
4. Alpha 1 blocker used as antihypertensive E. Direct interaction with and activate adrenoceptors- MOA
F. phentolamine of norepinephrine and epinephrine
G. tolazoline F. Induce the release of catecholamines by displacing them
H. phenoxybenzamine from adrenergic nerve endings
I. prazosin G. Decrease the clearance of catecholamines by inhibiting
Other choices are non-selective alpha receptor antagonist, their neuronal reuptake-MOA of cocaine and tricyclic
for functions refer to #1 antidepressants
H. Prevent enzymatic metabolism of norepinephrine- MOA
5. Alpha 1 blocker used as antihypertensive of monoamine oxidase and catechol-o-
F. prazosin methyltransferase inhibitors
G. terazosin
H. doxazasin 12. Receptor signalling mechanism of alpha 1 receptors
I. all E. Gq->phospholipase C-> increase in IP3 and DAG
All are selective alpha 1 receptor antagonists which block F. Gs-> decreases adenylyl cyclase->decreases cAMP
vasoconstriction effects of catecholamines thereby G. Gi-> increases adenylyl cyclase->increases cAMP
lowering BP. H. Gs-> increases adenylyl cyclase->increases cAMP
Alpha 1 receptor is coupled via Gq protein family to
6. Which of the following agents is beta 1 selective agent? phospholipase C leading to formation of IP3 and DAG.
E. Propranolol- non-selective beta antagonist
F. Carvedilol- non selective alpha and beta antagonist 13. An alpha 2 selective agonist
G. metoprolol E. Phenylephrine-alpha 1 agonist
H. sotalol- non-selective beta antagonist F. clonidine
G. dobutamine-beta 1 agonist
7. A patient with angle closure glaucoma is treated with a drug H. albuterol-beta 2 agonist
that decreased aqueous secretion by inhibiting carbonic Clonidine is the only alpha 2 selective agonist among the
anhydrase. Which of the following agents has the same given choices.
mechanism of action?
E. acetazolamide 14. absence of 1 or both –OH groups on the phenyl ring results to
F. pilocarpine this effect on catecholamines:
G. apraclonidine E. reduce the potency of a drug
H. latanoprost F. increases the bioavailability after oral administration
Acetazolamide is a drug used in open angle glaucoma with G. prolongs the duration of action
same mechanism of inhibiting carbonic anhydrase. H. all of the above
I. B and C only
8. It is a beta blocker used in the management of open angle All are results of the absence 1 or both –OH groups on the
glaucoma. phenyl ring.
E. metoprolol
F. timolol 15. TRUE statement of NE removal by NET:
G. atenolol E. Heart-90% is removed by NET
H. propranolol F. Vasculature-60% is removed by NET
G. Brain dopamine-80% is removed by NET
H. All of the above

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PHA211 RATIONALISATION: PRELIM PLATINGS

I. A and B only
16. Which of the following responses is observed when
sympathomimetic drug selectively acts on alpha 1 adrenergic
receptor?
A. Decreases insulin release
B. Vasoconstriction
C. Increase cardiac contractility
D. Bronchodilatation
Alpha 1 adrenoceptor agonists bind to alpha receptors on
vascular smooth muscle muscle and induce smooth muscle
contraction and VASOCONSTRICTION, mimicking the
effects of sympathetic adrenergic nerve activation to blood
vessels.

17. Commonly used in treatment of asthma:

A. Fenoldopam
B. Oxymetazoline
C. Isoproterenol
D. Albuterol
Albuterol activates adenylyl cyclase causing bronchial
smooth muscle dilation.

18. Supine hypertension and urinary retention are common

adverse effects of
A. Beta 1 selective agonists
B. Alpha 1 selective agonists
C. Beta 2 selective agonists
D. Alpha 2 selective agonists
Alpha 1 agonists activate phospholipase C resulting in
increased intracellular calcium and vasoconstriction. Net
effect is vascular smooth muscle contraction increasing
blood pressure. Toxic dose of these drugs could lead to
supine hypertension and urinary retention. (they mimic the
effects of sympathetic adrenergic nerve activation)
19. Midodrine and phenylephrine are:
A. Beta 1 selective agonists
B. Alpha 1 selective agonists
C. Beta 2 selective agonists
D. Alpha 2 selective agonists
Both are classified as alpha 1 selective agonists.
20. Which of the following pairs (drug and clinical indication) is
incorrect?
A. Modafinil-narcolepsy
B. Methylphenidate-ADHD
C. Atomoxetine- local anesthetic
D. Duloxetine-antidepressant
Atomoxetine is used in the treatment of attention deficit
disorders.

A B
B A
C B
D D
D D
C B
A D
B B
C B
C C

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PHA211 RATIONALISATION: PRELIM PLATINGS

AUTACOIDS 11. With the presence of nitric oxide during heightened sexual
1. A histamine receptor subtype distributed in the smooth stimulation. the following is/are TRUE
muscle, endothelium, and the brain A. stimulation of guanyl cyclase
A. H1 B. increased cyclic GMP
B. H2 C. stimulation of phosphodiesterase enzyme type 5
C. H3 D. A and B only
D. H4 E. all of the above
2. It is a partially selective antagonist to histamine-2 receptors 12. Role of nitric oxide in disease, EXCEPT
(H2) A. vasodilatation
A. cetirizine B. stimulates synthesis of inflammatory PGs
B. ranitidine C. contraction of smooth muscle in the corpora cavernosa
C. thioperamide D. dilates pulmonary vessels, reducing pulmonary arterial
D. mepyramine pressure
3. A patient on antipsychotic agent developed rigidity and 13. The following is/are TRUE of nitric oxide
catatonia. Which of the following agent can significantly A. platelet aggregator
reverse this extrapyramidal side effect? B. smooth muscle relaxant
A. promethazine C. vasodilator
B. cetirizine D. A and B only
C. cyproheptadine E. all
D. diphenhydramine 14. Nitric oxide affects the vascular system
4. Which of the following agents has a significant activity in A. inhibits proliferation and migration of vascular smooth
preventing motion sickness? muscle
A. chlorpheniramine B. it has antithrombotic effect
B. dimenhydrinate C. it stimulates LDL oxidation
C. loratadine D. A and B only
D. fexofenadine E. all of the above
5. Which of the following has less sedating effect among 15. Nitric oxide gas inhalation can play an important role in the
antihistamines? following
A. desloratadine A. pulmonary hypertension
B. diphenhydramine B. septic shock
C. hydroxyzine C. cyanide poisoning
D. cyclizine D. A and B only
6. This vasoactive peptide is a vasoconstrictor E. all
A. angiotensin II 16. This eicosanoid is released through non-enzymatic
B. substance P oxygenation
C. adrenomedullin A. prostaglandins
D. bradykinin B. leukotrienes
E. neurotensin C. epoxyeicosatrienoic acid
7. This vasoactive peptide is a vasodilator D. isoprostanes
A. vasopressin 17. A cysteinyl leukotriene
B. neurotensin A. LTC4
C. neuropeptide Y B. LTD4
D. urotensin C. LTE4
E. endothelin D. all of the above
8. Nonpeptide renin inhibitor used for hypertension treatment E. A and B only
A. losartan 18. True combinations, EXCEPT
B. aliskiren A. PGE2 – bronchodilation
C. captopril B. PGF2α – bronchoconstriction
D. aprotinin C. PGI2 – lower pulmonary vascular resistance
E. urantide D. TXA2 – inhibits platelet aggregation
9. This selective antagonist of Kinin B2 receptor is indicated for 19. A topically active PGF2α derivative used in ophthalmology to
hereditary angioedema reduce intraocular pressure in open angle glaucoma or ocular
A. icatibant hypertension
B. aprepitant A. alprostadil
C. bosentan B. misoprostol
D. conivaptan C. latanoprost
E. valsartan D. iloprost
10. This substance P antagonist is indicated for the prevention of 20. EP2, EP4, IP, and DP1 receptors activate
chemotherapy-induced nausea and vomiting A. Gs – ↑adenyl cyclase, ↑cAMP
A. aprepitant B. Gi – ↓adenyl cyclase, ↓cAMP
B. omapatrilat C. Gq – ↑IP3, ↑Ca
C. nesiritide D. G12/13 – Rho activation
D. compound 21
E. aliskiren

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PHA211 RATIONALISATION: PRELIM PLATINGS

ANSWER KEY
131. A. H1 136. All of them are vasoactive peptides.
132. B. ranitidine  Angiotensin II is a vasoconstrictor.
133. D. diphenhydramine  Substance P, adrenomedullin, bradykinin, and neurotensin
134. B. dimenhydrinate are vasodilators.
135. D. cyclizine Refer to par1 on Katzung B&CP Ch17 p300.
136. A. angiotensin II 137. All of them are vasoactive peptides.
137. B. neurotensin  Neurotensin is a vasodilator.
138. B. aliskiren  Vasopressin, neuropeptide Y, urotensin, and endothelin are
139. A. icatibant vasoconstrictors.
140. A. aprepitant Refer to par1 on Katzung B&CP Ch17 p300.
141. D. A and B only 138. All of them are vasoactive peptides. Losartan, Captopril, and
142. C. contraction of smooth muscle in the corpora cavernosa aliskiren are inhibitors of renin-angiotensin system. Aprotinin
143. A. platelet aggregator is an inhibitor of kallikrein-kinin system. Urantide is an
144. D. A and B only urotensin antagonist.
145. A. pulmonary hypertension  Losartan is an angiotensin II receptor blocker.
146. D. isoprostanes  Aliskiren is the first approved nonpeptide renin inhibitor for
147. D. all of the above the treatment of hypertension.
148. D. TXA2 – inhibits platelet aggregation  Captopril is an ACE inhibitor.
149. C. latanoprost  Aprotinin is a kallikrein inhibitor.
150. A. Gs – ↑adenyl cyclase, ↑Camp  Urantide (urotensin antagonist peptide) is a penicillamine-
substituted derivative of urotensin II.
RATIONALISATION Refer to Renin Inhibitors on Katzung B&CP Ch17 p305.
139. All of them are drugs that interact with vasoactive peptide
131. Distributions are as follows:
systems.
 H1 – smooth muscle, endothelium, brain
 Icatibant is a kinin inhibitor and is indicated for hereditary
 H2 – gastric mucosa, cardiac muscles, mast cells, brain
angioedema.
 H3 – presynaptic autoreceptors and heteroreceptors in
 Aprepitant is a substance P antagonist.
brain, myenteric plexus, other neurons
 Bosentan is an endothelin antagonist.
 H4 – eosinophils, neutrophils, CD4 T cells.
 Conivaptan is a vasopressin antagonist.
Refer to Table 16-1 of Katzung B&CP Ch16 p279.
 Valsartan is an angiotensin receptor antagonist.
132. All of them are partially selective antagonists for histamine
Refer to Kinin Inhibitors in Mechanism of Action and Clinical
receptors.
Applications in SUMMARY Drugs That Interact with
 H1 – cetirizine, mepyramine
Vasoactive Peptide Systems on Katzung B&CP Ch17 p317.
 H2 – ranitidine
140. All of them are drugs that interact with vasoactive peptide
 H3 – thioperamide.
systems.
Refer to Table 16-1 of Katzung B&CP Ch16 p279.
 Aprepitant is a substance P antagonist and is indicated for
133. All of them (maybe except cetirizine) are H1-receptor
the prevention of chemotherapy-induced nausea and
antagonists.
vomiting.
 Promethazine has adrenoceptor-blocking actions.
 Omapatrilat is a vasopeptidase inhibitor.
 Cetirizine has histamine-blocking actions, but its relation to
 Nesiritide is a natriuretic peptide.
H1 is unclear.
 Compound 21 is an angiotensin receptor antagonist.
 Cyproheptadine has serotonin-blocking actions.
 Aliskiren is a renin inhibitor.
 Diphenhydramine has antiparkinsonism effects i.e.
Refer to Kinin Inhibitors in Clinical Applications in SUMMARY
significant acute suppressant effects on extrapyramidal
Drugs That Interact with Vasoactive Peptide Systems on
symptoms associated with certain antipsychotic drugs.
Katzung B&CP Ch17 p317.
Refer to 3. Antiparkinsonism effects on Katzung B&CP Ch16
141. The presence of nitric oxide (NO) during heightened sexual
p282.
stimulation relates to their mechanism of action in the vascular
134. All of them are antihistamines. Only dimenhydrinate is
smooth muscles.
indicated for motion sickness.
 NO activates soluble guanylyl cyclase.
 Chlorpheniramine is indicated for allergic rhinitis and
 Activation/Stimulation of guanylyl cyclas elevates cGMP
chronic urticaria.
levels in vascular smooth muscle
 Dimenhydrinate is a salt of diphenhydramine and has
 Inhibitors of type 5 phosphodiesterase such as sildenafil
similar efficiency.
allow NO-induced cGMP elevations to achieve higher
 Loratadine and fexofenadine are indicated for IgE
cytosolic levels and result in prolongation of the duration of
immediate allergies and urticaria.
the cGMP elevations in a variety of tissues.
Refer to B. Motion Sickness and Vestibular Disturbances and
Refer to Nitric Oxide (NO) in Mechanism of Action in
Table 16-2 on Katzung B&CP Ch16 p284.
SUMMARY Nitric Oxide on Katzung B&CP Ch19 p345.
135. All of them (except desloratadine) are first-generation
142. Nitric oxide carries various roles in disease.
antihistamines, characterized by sedating effects.
 NO diffuses to vascular smooth muscle, leading to
 Desloratadine is a second-generation antihistamine,
vasorelaxation [vasodilation].
characterized by absence of sedating effects.
 NO also stimulates the synthesis of inflammatory
 Diphenhydramine and hydroxyzine have marked sedating
prostaglandins by activating cyclooxygenase isoenzyme 2
effects.
(COX-2).
 Cyclizine has a slight sedating effect.
 NO promotes relaxation of the smooth muscle in the
Refer to Table 16-2 of Katzung B&CP Ch16 p283.
corpora cavernosa—the initiating factor in penile erection.

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 NO inhalation dilates pulmonary vessels, resulting in 149. The eicosanoids have a broad clinical pharmacology.
decreased pulmonary vascular resistance and reduced  Alprostadil is a second-line treatment for erectile
pulmonary artery pressure. dysfunction, administered via intracavernosal injection or
Refer to The Peripheral Nervous System on Katzung B&CP transurethral suppository.
Ch19 p344.  Misoprostol is a cytoprotective PGE1 derivative
143. Nitric oxide carries various roles in disease. prostaglandin used in preventing peptic ulcer and in
 NO has antithrombotic effects. combination with mifepristone for terminating early
 NO elicits smooth muscle relaxation. pregnancies.
 NO diffuses to vascular smooth muscle, leading to  Latanoprost is a topically active PGF2α derivative used in
vasorelaxation [vasodilation]. ophthalmology to reduce intraocular pressure in open-angle
Refer to Vascular Effects in Nitric Oxide in Disease on Katzung glaucoma or ocular hypertension.
B&CP Ch19 p342.  Iloprost is a prostacyclin analog that lowers peripheral,
144. Nitric oxide carries various roles in disease. pulmonary, and coronary vascular resistance.
 A major anti-atherogenic mechanism of NO involves the Refer to Products of Prostaglandin Endoperoxide Synthases
inhibition of proliferation and migration of vascular smooth (Cyclooxygenases) on Katzung B&CP Ch18 p323.
muscle cells. 150. All of them relate to receptor mechanisms of eicosanoids.
 NO has antithrombotic effects.  EP2, EP4, IP, and DP1 receptors activate adenylyl cyclase
 The anti-atherogenic effect of NO may also involve an via Gs, which increases intracellular cAMP levels, and in turn
antioxidant effect, blocking the oxidation of low-density activating specific protein kinases.
lipoproteins [inhibits stimulation of LDL oxidation] and thus  The DP2 receptor couples through a Gi-type G protein and
preventing or reducing the formation of foam cells in the leads to inhibition of cAMP synthesis and increases in
vascular wall. intracellular Ca2+ in a variety of cell types.
Refer to Vascular Effects on Katzung B&CP Ch19 p342.  CysLT1 and cysLT2 couple to Gq, leading to increased
145. Nitric oxide is significant for pulmonary hypertension and \intracellular Ca2+.
septic shock only, but it asks for the important role nitric oxide  TP couples to multiple G proteins, including G12/13 and G16,
gas inhalation plays. to stimulate small G protein signaling pathways, and may
 NO gas inhalation results in reduced pulmonary artery activate or inhibit adenylyl cyclase via Gs or Gi respectively.
pressure [decreased pulmonary hypertension] and Refer to par2 of Receptor Mechanisms in Mechanisms &
improved perfusion of ventilated areas of the lung. Effects of Eicosanoids of Basic Pharmacology of Eicosanoids
 Widespread generation and build-up of NO from inducible on Katzung B&CP Ch18 p326.
NO synthase (iNOS) in macrophages, neutrophils, T cells,
hepatocytes, smooth muscle cells, endothelial cells, and
fibroblasts causes septic shock.
 Cyanide poisoning results from complexing of cytochrome
iron by the CN− ion, and not NO.
Refer to 4. NO Gas Inhalation on Katzung B&CP Ch19 p342.
146. All of them are derivatives of arachidonic acid. All of them
(except isoprostanes) are released through enzymatic
oxygenation:
 prostaglandins through cyclooxygenase (COX)
 leukotrienes through 5-lipoxygenase (5-LOX)
 epoxyeicosatrienoic acid through microsomal cytochrome
P450 monooxygenase
 isoprostanes through direct free radical-based action on
arachidonic acid and related-lipid substrates
Refer to Isoeicosanoids on Katzung B&CP Ch18 p326.
147. All of them are leukotrienes. Leukotriene C4 (LTC4), LTD4,
and LTE4 are cysteinyl leukotrienes.
 The unstable epoxide LTA4 is conjugated with glutathione
to yield LTC4.
 Sequential degradation of the glutathione moiety by
peptidases yields LTD4 and LTE4.
 These three products, LTC4, D4, and E4, are called cysteinyl
leukotrienes.
Refer to par1 on Katzung B&CP Ch18 p324.
148. The eicosanoids have a broad clinical pharmacology.
 PGE2 is a powerful bronchodilator when given in aerosol
form
 PGF2α is a strong bronchoconstrictor and was once thought
to be a primary mediator in asthma
 PGI2 lowers peripheral, pulmonary, and coronary vascular
resistance
 TXA2 promotes platelet aggregation
Refer to Blood on Katzung B&CP Ch18 p335.

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