18. sedative and hypnotics 2.L-dopa can also be used in the treatment of hepatic coma.

 Diazepam Drug interaction between L-dopa and (choice) :

1.carbidopa ↑therapeutic effect of L-dopa
-Pharmacological effects
Bcuz inhibit the action of decarboxylase in PNS so L-dopa
1. sedation, relief of anxiety
entering CNS will be ↑
2. hypnosis : induce sleep rapidly 2.selegiline↑therapeutic effect of L-dopa
Diazepam can prolong the time of sleep, reduce the awake Bcuz inhibit of MAO-B, so dopamine in CNS will↑, halflife of
frequency and increase the awake threshold. Has insignificant DA will ↑
influence on REM. 3.COMT ↑therapeutic effect of L-dopa
3. anticonvulsant effects So COMT inhibitor es. Nite capone
4.Pyridoxamine (vit B6)↓therapeutic effect of L-dopa bcuz
4. antiepileptic action
of ↑the activity of dopa dehydroxylase in PNS so ↓DA in CNS,
Effective in treating grand mal seizure. Diazepam is the first
↓pass through BBB
choice used in treating status epileptics via iv. (can’t be used incombination with L-dopa)
5. muscle relaxation
-Therapeutic uses 22. Opioid analgesics
1.it is effective in treating various kinds of anxiety. Morphine
2.used before anesthesia to enforce the action of anesthetic -Pharmocological effects
drugs and to relieve the anxiety of patients. Mainly acts on opioid-receptors(µ) and is a strong agonist.
3.it is most widely used hypnotic drugs clinically, effective in (A.)central effects
treating insomnia. 1.analgesia, sedation
4.it is appropriate in treating spasticity in tetanus, rabies, 2.respiratory depression
3.antitussive action
infantile fever of high fever, puerperal convulsion.
4.miosis
5.effective in treating grand mal seizure. Diazepam is the
5.emetic action
first choice used in treating status epileptics via iv. (B.)Effects on cardiovascular system
6.diazepam is used to treat central myotonia 1.morphine causes orthostatic hypotension in some patients
their superiorities comparing with barbiturates; 2.pressure of cerebrospinal fluid↑
1.higher in therapeutic index, it is (diazepam) = 8, slighter in (C.)effects on smooth muscle
-gastrointestinal tract: causes constipation
respiratory inhibition, no anesthetic action used in larger
-biliary tract:constricts biliary smooth muscle, this may result
dose. in biliary colic
2.more insignificance in inducing drug metabolizing enzyme -therapeutic uses.
3.less unwanted action (tolerance, dependence, rebounce of (a).Pain
REM, dizziness, dysfunction of movement) The cause of morphine used to treat myocardial infarction.
1.analgesia
2.sedation, antianxietyO2 comsumption↓
19. drugs effective in Epilepsias 3.dilates blood vesselsworkload of heart↓
choose drug for different type of seizure (matching) (B.)acute pulmonary edema(Cardiac asthma)
Phenytonin sodium dilation  1st grandma seizure (C.)Diarrhea
(D.)Anesthesia
Ethosuximide  1st of absence seizure
Untoward effects(side effects)
Diazepam  1st of status epilepsia via iv
(A.)Tolerance
Clonazepam absence seizure and myoclonic seizure (B.)Dependence
Phenobarbital grand mal seizure and status epilepsia (C.) nausea, constipation and biliary colic.
Sodium valproatetreat every kind of epilepsia (D.) It is abandoned to use in women during labor and milking.
Carbamazepine partial seizure, neuralgia, diabetes Reasons:
Magnesium sulfate1st of treat puerperal convulsion ①delay labor
②depress respiration of neonates and infants
(E) It is contraindicated in patients with asthma, brain injury.
21. Antiparkinsonian drugs
L-Dopa
-Pharmacological effects
In CNS, L-dopa was converted to dopamine by decarboxylase,
and elevated the level of dopamine in the brain, therefore
restoring deficient dopamine in the striatum.
-Clinical uses
1.L-dopa can be used to correct manifestation of parkinsonism
syndrome except caused by antipsychotics
 -Supplement of K+ and treatment of arrhythmias.
23.Analgesic-Antipyretic and Anti-inflammatory drug 26.Antihypensive drugs
comparing between NSAIDs & Opioid Analgesics classification of antihypensive
NSAIDs Opioid Analgesics 1. Diuretics
1.active site PNS CNS 2. Drugs that alter sympathetic nervous system functions
2.mechanisms -inhibit the activity -stimulate the opioid ● Sympathoplegic drugs.
of cox,↓production receptor in CNS
● Adrenergic neuron blocking agents.
of PG in PNS
● Adrenoceptor antagonists.
3.intensity and -can relieve pain of -can release all kind of
characteristic in mild to moderate pain, effective in 3. Director vasodilators
relieving the pain intensity reduce both dull and 4. Ca2+ channel blocker
-reduce dull pain of sharp pain 5. Agents that block production or action of angiotensin
various causes eg. -Angiotensin converting enzyme inhibitors (ACEI).
Muscular, dental, -The angiotensin II receptor blockers
joints, neuralgiform
and menstrual pain
-ineffective relieving 27.Antianginal drugs
sharp pain cause by Nitroglycerine
trauma and visceral
-pharmacological effect
smooth muscle colic
4.side effects -no tolerance and -tolerance and ●Effects on vascular smooth muscle
addiction can be seen addiction can develop Veins usually ( low concentrations )
after a long time use after long time use Arterioles (slightly higher dose).
-no respiratory -respiratory inhibition Large coronary artery diameters↑
inhibition Venous capacitance↑
why aspirin should be used in smaller dosage when Ventricular preload and afterload ↓
used with prophylaxis of IHD and stroke? Blood flow of ischemia area↑
-due to the mechanism: The blood supply of the endocardial layer↑
1) Low doses inhibit thromboxane synthetase→ ●Effects on hemodynamics
synthesis of thromboxane A2 ↓ -Systolic and diastolic blood pressure ↓
2)high doses →PGI2 synthesis in walls of blood vessels -Cardiac output decrease ↓
↓ → accelerate thrombosis formation ●Effects on other smooth muscle
*So in treating thrombosis, aspirin should be used with -Almost all smooth muscles↓
small dose. ●Other effects
-Platelet aggregation↓
25.Congestive heart failure -therapeutic application
Treat angina pectoris (effort angina, variant angina and
cardiac glycoside unstable angina) by relieving symptoms of angina.
-pharmacological effects -adverse reaction
(a)Positive inotropic effects -Throbbing headache
↑Cardiac contractility ↓end-systolic and end-diastolic size -Tolerance to organic nitrates could rapidly develop following
+ ↑Cardiac output and renal perfusion. prolonged administration (consumed too much thiol reason).
(b)Negative chronotropic effects
This effect is secondary to the positive inotropic action.
Combination therapy of angina pectori
↑Output↑ parasympathetic activity↓heart rate.
1.Organic nitrates and β-adrenergic receptor antagonists
This effect corrects the over excitement of sympathetic
●When used in combination, organic nitrates can offset
system in CHF patients, conducive to the relief of CHF
increased myocardial oxygen consumption related to
symptoms.
augmented ventricular end-diastolic volume induced by β-
(C) Electrophysiological effects
adrenergic receptor antagonists, and β-adrenergic receptor
-Therapeutic applications
antagonists can reduce the reflected increase of heart rate
● Various types of CHF.
induced by organic nitrates.
● Dosing regimens must be carefully performed.
2.Calcium channel blockers and β-adrenergic receptor
● Effectively decrease the refractory period of the
antagonists.
atrioventricular node and hence ventricular rate.
●β-adrenergic receptor antagonists can abate the reflex-
● Atrial flutter and fibrillation.
induced increase in heart rate induced by calcium channel
-Mechanisms of action blockers.
The increased contractility is caused by an increase in 3.Calcium channel blockers and Organic nitrates
intracellular free calcium concentration. ●Calcium channel blockers and organic nitrates have a
-Adverse reactions and toxicity treatment synergistic effect on reduction of myocardial oxygen. Calcium
●Adverse reactions channel blockers reduce afterload while organic nitrates
-Visual changes, gastrointestinal disturbances decrease preload.
- Cardiac arrhythmia.
●Toxicity treatment
 B. antidiuretic effect
32.Diuretic -used in patients with diabetes insipidus. They can reduce
Furosemide urine volume and eliminate thirst.
-Mechanism and pharmacological effects C. Antihypertensive effects
(a)have a prompt and strong diuretic effect. -results from their diuretic effect
-inhibit the Na+- K+-2Cl- cotransporting carrier protein in -Therapeutic uses
ascending limb of Henle’ loop resulting in a profound increase (1) Edema associated with congestive heart failure, hepatic
of Na+, K + and Cl- in urinary excretion . cirrhosis and chronic renal failure.
-Consequently, the dilution and concentration functions of (2) Hypertension
the kidney are affected, and the kidney excretes a large (3) Diabetes insipidus.
amount of nearly isotonic urine. -Adverse Effects
(b) An increase in the excretion of Na + enhances the A. Electrolytes disturbances
exchange of K+ -Na + in distal tubule and collecting duct, -low concentration of K+, Na +, Cl- and Mg2 +.
resulting in a loss of K+. B. Metabolic changes
(c) Loop diuretics increase the renin secretion due to the -result in hyperglycemia and hyperlipidemia . Hyperuricemia
reduction of blood volume, which enhances the aldosterone so should be use incaution in patient with gout.
release and consequently loss of K+.
-therapeutic uses 35.Asthma and cough
(a) severe edema: cardiac, hepatic and renal edema.
which drug is first line?
(b) acute pulmonary edema and brain edema.
-Beclomethazone (inhale) ,cromolyn
-reduces blood volume and venous return →decrease
pulmonary vascular pressure →relieve pulmonary edema which drug treat acute asthma?
-increases the excretion of water→ concentration of blood↑ -β2 agonist given subcutaneous eg.adrenaline
→osmotic pressure of plasma↑→ ameliorate the edema of which drug use in prophylaxis?
brain -cromolyn, nedocromil,beclomethasone
(c) Acute renal failure
The main problem in the early stage of acute renal failure is
short of urine.
36.Oxytocics
-Furosemide increases the urine flow rate in acute renal clinical uses of oxytocin
failure and wash out the obstructed tubules to prevent the 1.induction of term labor
necrosis of tubules. 2.controlling postpartum hemorrhage
-Lowers the resistance of renal blood vessels and increases 3.preventing postpartum uterine atony
glomerular filtration
clinical uses of Ergonovine
(d) Treatment of hypercalcemia and promote the excretion of
1.controlling postpartum bleeding and facilitate uterine
poisons
involution
-adverse effects
A.Disturbance of water and electrolytes 2.Ergotamine can be used to treat migraine, Ergonovine
Excessive diuresis can result in low blood volume, low should not be used for induction of term labor.
concentration of K+, Cl- , Na+ ,Ca2+ and Mg2 +.
B. Ototoxicity 38. Adrenocorticosteroids
It can’t be used with aminoglycosides. why should give in the morning?
C. Hyperuricemia -According to the day-night rhythm of glucosteriods,
-The time of the highest tide of the hormone secretion, the
Thiazides suppression of adrenal cortex by exogenous dosage is
-Mechanism and pharmacological effects relatively slight.
A. Diuretic effects -The advantage may increase compliance, and lower incidence
(1) The thiazide derivatives, act mainly on the distal tubule of adverse effects (HPA suppression).
to decrease the reabsorption of Na+ by inhibition of Na+-Cl- Glucocorticoid
cotransporter on the luminal membrane, resulting in increased -physiological effect
excretion of Cl- and Na+ in the tubular fluid (10% of the 1.carbohydrate metabolism
filtered load) and produce a gentle and lasting diuretic effect. ●gluconegenesis ↑liver/muscle glycogen↑
(2) Loss of K+: Thiazides increase the Na+ in the filtrate ●glucose utilization↓blood glucose↑
arriving at the distal tubule, facilitating K+-Na+ exchange, thus 2.protein metabolism
resulting in the increase of urinary excretion of K+. Also ●protein synthesis↓,protein metabolism↑negative
thiazides inhibit carbonic anhydrase →secretion of H+↓→ k+ nitrogen balance
Na+ exchange↑ excretion of k+↑. 3.lipid metabolism
(3)Thiazides facilitate Ca2+ reabsorption in the distal tubule, ●lipolysis↑,lipid synthesis↓,redistribution of body
thus decrease the concentration of Ca2+ in the urine. fat(long-term)
 -It has activity against Giardia lamblia as well as Trichomonas
4.water and electrolyte mentalism vaginalis.
-less effect on electrolytes and water balance -Metronidazole has antibacterial activity against all anaerobic
-long term use: the mineralocorticoid-like properties will bacilli.
appear 4 generations of Quinolones
-excessive glucocorticoids: lower the blood Ca2+ and the (1) First generation (nalidixic acid)
bone will be decalcified -They inhibit part of gram negative bacterium, because of narrow
5.permissive effect antibacterial spectrum, microbial resistance, poor absorption after
-many normal functions become deficient in the absence of oral administration, they are only used for urinary tract infections.
glucocorticoids. (2) Second generation (pipemidic acid)
-They have better activity against gram negative and part of gram
-pharmacological effect positive bacteria. They are effective after oral administration, low
1.anti-inflammatory properties microbial resistance and few side effects. They are used for urinary
2.immunosuppressive effects and intestinal tract infections.
3.antitoxic effects: glucocorticoids increase the endurance (3) Third generation (Fluoroquinolones)
of body tobacterial endotoxin. -They possess much higher activity against gram negative (E. coli,
4.antishock effects: large dosage is needed for treatment Salmonella, Shigella) and gram positive bacterium (staphylococci,
of all kinds of severe shock methicillin-resistant strains)
-Fluoroquinolones represents an important therapeutic advance,
5.effects on blood and hematopoietic system
since they have broad antimicrobial activity and are effective after
6.other effects of glucocorticoids oral administration for the treatment of a wide variety of infective
-GI tract: ↑gastric acid and pepsin production diseases.
-CNS: ↑excitability, eg.insomnia, irritability (4) Fourth generation (trovafloxacin, moxifloxacin)
-clinical application -They have an extensive activity against Gram-positive bacteria,
1.replacement therapy including resistant strains and anaerobic bacteria.
2.severe infection and prevention of inflammatory sequel Sulfonamide
3.autoimmune and allergic diseases
-Antimicrobial Activities
4.anti-shock therapy
Sulfonamides inhibit a wide range of microorganisms
5.hematologic disease
6.local administration including Streptococcus pyogenes, Streptococcus pneumoniae,
-adverse reactions Haemophilus influenzae, Nocardia, Chlamydia trachomatis,
1.ADR by long-term and large dosage therapy and some protozoa. Some enteric bacteria, such as E coli,
-hyperadrenalism-like syndrome(Cushings syndrome): the salmonella, and shigella are inhibited.
symptoms include moon faces, buffalo hump, central obesity, skin -mechanism reaction
atrophy, acne, adema, hypokalemia, hypertension, diabetes mellitus ●Susceptible microorganisms require extracellular para-
etc. aminobenzoic acid (PABA) in order to form dihydrofolic acid,
2.induction or aggravation of infections an essential step in the production of purines and the
-glucocorticosteriod should be comboined with effective
synthesis of nucleic acids.
antibiotics.
●The structures of sulfonamides are similar to PABA
3.Gastrointestinal reactions
-induce or aggravate the ulcers, even induce hemorrhage or ●Sulfonamides competitively inhibit dihydropteroate
perforation of the gastrointestinal tract. synthase and prevent normal bacterial utilization of PABA.
4.cardiovascular complications ●Sulfonamides are bacteriostatic. Sulfonamides do not
5.osteoporosis, amyotrophy, delayed wound healing affect mammalian cells since they require preformed folic
6.central nervous system effects acid.
42. -Clinical usage
Quinolones 1. Systemic infection
-mechanism -Sulfisoxazole (SIZ) and sulfamethoxazole (SMZ) are often
●Quinolones exert their bactericidal effect by inhibiting type II used to treat urinary tract infections.
topoisomerase (DNA gyrase, DNA) and topoisomerase IV. -SMZ given together with TMP, is used widely for respiratory
●DNA gyrase is a heterotetramer composed of two A subunits and tract infections, such as sinusitis and bronchitis, and enteric
two B subunits.  The enzyme introduces negative superhelical twists infection.
into bacterial DNA and this is essential for replication and -Sulfadiazine (SD) achieves therapeutic concentrations in
transcription cerebrospinal fluid and is a first-line therapy for treatment
●Topoisomerase IV is composed of two C subunits and two E
of epidemic cerebrospinal meningitis.
subunits .
-Inhibition of topoisomerase Ⅳprobably interferes with separation
2. Local infection
of replicated chromosomal DNA into the respective daughter cells -Sodium sulfacetamide (SA-Na) is employed effectively in the
during cell division. therapy of ophthalmic infections
advantage of combine SMZ+TMP -Mafenide sulfamylon (SML) and silver sulfadiazine (SD-Ag)
1.Antibacterial spectrum are used topically to prevent bacterial colonization and
2. Antibacterial activity double blocking of folic acid synthesis; infection of burn wounds.
similar t1/2 3. Intestinal tract infection
3. Resistance -Salazosulfapyridine (SASP) is poorly absorbed so it is used
4. Adverse reaction for intestinal tract infections.
pharmacologic effect of metronidazole
-kills trophozoites but not cysts of Entamoeba histolytica.

43. β-lactam Antibiotics
Penicillin G
-Spectrum of activity
The penicillin-susceptible organisms include
●Gram-positive cocci, e.g., Streptococcus pyogenes
(A,B,C,G,F), non-β-lactamase producing staphylococcus
aureus, sensitive streptococcus pneumoniae;
●Gram-positive bacilli, e.g., corynebacterium diphtheriae;
Anthrax bacillus; tetanus bacillus
● gram-negative cocci. e.g., nesseria meningitides  -treatment of urinary tract infection caused by G- bacillus
●spirochetes.
-Mechanism of action
1) Penicillins inhibit the formation of cell wall and are
bactericidal in action.
●Penicillin exerts its effect by binding to cellular receptors
(penicillin-binding protein) now identified as transpeptidase
which catalyzed the cross-linking reaction of cell wall.
●By binding to and inhibiting transpeptidation reactions,
it interrupts the synthesis of cell wall peptidoglycan.
●A defective cell wall allows water to enter and swell the
cell, causing membrane lysis and cell death.
2) increase the activity of cell-wall autolytic enzyme.
When the cell wall synthesis is inhibited, the bacteria
become larger and then the autolytic enzyme is triggered to
lyse the cell.
-Therapeutic uses
A wide variety of infectious diseases induced by most
cocci, gram-positive bacilli, and spirochetes, and certain
gram-negative bacilli.
• the first choice when the following
infections are indicated.
• Streptococcal infections,
infective endocarditis caused by streptococci
• Staphylococcal infections.
• Pneumococcal infections.
• Meningococcal infections, meningitis caused by
meningococi.
• gonococcal infections.
• syphilis infections.
• Diphtheria, anthrax.
-Untoward effects
Allergic reactions
• Most severe anaphylactic shock
Herxheimer reaction
compare characteristic of 4 semisynthesized penicillin
1.acid stable Penicillins (β-lac tamase unstable)
Penicillin V :
-spectrun: same as penicillin G but lower activity
-acid: acid stable, can be taken orally
-β-lactamase:unstable
2.Penicillinase-resistant Penicillin (oxacillin, methiallin,
cloxacillin)
-spectrum: same as Penicillin G
-acid: acid stable, can be taken orally, i.v., i.m.
-β-lactamase: Penicillinase-resistance
MRSAcaused by↓affinity of Penicillin bind to PBPs
3.Broad-spectrum Penicillins
Ampicillin :
-spectrum: G+, G- bacilli, E.coli, H.imfluenzae, Salmonella,
Proteus speciesG-
-acid: acid stable
-β-lactamase: Penicillinase-resistance
Carbenicillin :
-spectrum: same as Amipicillin, but is also used in sever G -
infection caused by proteus, pseudomonas, aeroginosa strains
-acid: acid stable
-β-lactamase: not penicillinase-resistance
4.Anti G- bacillus Penicillin (mecillinam, temocillin)
-spectrum: some G- organism
-β-lactamse: β-lactamse-resistance(G - bacillus)
44.Chloramphenicol and Tetracyclines
Chloramphenicol
-Untoward effects
●Bone marrow disturbances
-Reversible anemia is apparently dose-related
and occurs concomitantly with period of treatment.
（reversible suppression of red cell production)
-Aplastic anemia is idiosyncratic and usually fatal, which is
not related to dose and therapy.
●Gray-baby syndrome (short)
1.This condition is seen in neonates, especially premature
infants who have been given relatively large doses of
chloramphenicol;
2.Vomiting, hypothermia, gray color, respiratory
irregularities and shock are often observed.
3.The condition develops because of the immature hepatic
conjugating mechanism and the inadequate mechanism for
renal excretion in neonates.
def of Superinfection
is caused by overgrowing of resistant organism and yeasts in
respiratory and gastrointestinal tract. Superinfection is a
significant problem which can result in staphylococcal
enterocolitis, intestinal candidosis, and pseudomembranous
colitis. These superinfections should be treated with
vancomycin and other drugs. (intestinal flora)
46. Aminoglycoside
common characteristic
-Spectrum of activity
●Aminoglycosides are highly active againstaerobic G– bacteria, such
as Escherichia coli, Pseudomonas aeruginosa, Klebsiella, Salmonella.
●Anaerobic bacteria are resistant because aminoglycosides’
transport into cells is oxygen-dependent.
●Aminoglycosides used in combination with β-lactams to extend
coverage to G＋ microbes.
-Mechanism of action
The mechanism of Aminoglycosides is to inhibit protein synthesis by
binding to 30S subunit of the ribosome in susceptible
microorganisms .
●by interfering with the initiation complex of peptide
formation.
●inducing misreading of the code on the mRNA template, which
causes incorporation of inappropriate amino acid into peptide.
●by rupturing the polysomes into monosome, which become
nonfunctional.
-Adverse reaction
Ototoxicity-should not be use with flurosemide
Nephrotoxicity
Neuromuscular blockade
Allergic reactions
47. Antifungal Drugs& Antiviral drug
classification
A. Drugs for systemic mycotic infections
(a) amphotericin B, (b) flucytosine, (c) azoles including
ketoconazole, fluconazole, et al.
B. Drugs for superficial mycotic infections
(a) griseofulvin, (b) nystatin, (c) topical azoles
(clotrimazole, ketoconazole, et al. ).
Azole mechanism
inhibit of fungal cytochrome P450 enzymes, thereby impairing
the biosynthesis of ergosterol for the cytoplasmic
membrane.
48. AntiTB & Anti leprosy Drug
First-line agents
isoniazid, rifampin, ethambutol, streptomycin and
pyrazinamide
Isoniazid
-pharmacological
Isoniazid is bacteriostatic for resting M. tuberculosis but
bactericidal for reproducing bacilli.
-mechanism
●inhibiting the synthesis of DNA in tubercle bacillus;
●inhibiting the synthesis of mycolic acids, important
constituents of the mycobacterial cell wall.
-clinical usage
●the primary drug for the treatment of all types of
tuberculosis
●be used alone for prophylaxis or the early pulmonary
tuberculosis with slight symptom.
-adverse of reaction
●Reactions on nervous system-toxicity to CNS due to
deficiency of vitamin B6 because Isoniazid can increase the
excretion of vitamin B6.
●Hepatotoxicity
Ethambutol
-adverse effect is optic neuritis
51. Antineoplastic
classification
1.according to cell cycle divided into CCS and CCNS
2.according to mechanism action
●agents affecting synthesis of nucleic acids
●agents directly affecting structure and function of DNA
●agents interrupting transcription and RNA synthesis
●agents affecting protein synthesis
●agents affecting hormone balances.
3.according to structure and sources
(a) alkylating agents; (b) antimetabolites; (c) antibiotics;
(d) alkaloids; (e) hormones; (g) miscellanous agents :Platinum
Alkylating Agents
Mechanism of action
Alkylation of DNA results in DNA interactions, which damage
the structure and function of DNA, leading to
cell death.
Vinblastine and Vincristine
Mechanism of action
Vinblastine (VLB) and Vincristine (VCR) are CCS agents (M
phase cells specific). The two agents are spindle poisons,
which block the formation of mitotic spindle by preventing the
assembly of tubulin dimmers into microtubules.
antimetabolites
Antimetabolites are similar to necessary substances such as
folic acid , purine and pyridine in chemical structure. These
agents compete the action site on an essential enzyme and
inhibit nucleic acid synthesis. Agents of this group mainly
affect S phase cells. All antimetabolites undergo intracellular
activation.
52. Immunosuppression drug
Cyclosporin and tacrolimus
-The action of cyclosporin and tacrolimus is to inhibit T-cell
activation . They preferentially Inhibits antigen-triggered
signal transduction in T lymphocytes, blunting expression of
many lymphokines, including IL-2, as well as expression of
antiapoptotic proteins.
-Mechanisms: inhibiting calcineurin-catalyzed
dephosphorylation of nuclear factor of activated T-cells
(NFAT)
-The clinical application : organ transplantation, and
rheumatoid arthritis.
-Adverse reactions: Nephrotoxicity toxicity, induce cancer
41.Antimicrobial drug general consideration
antibiotic : A drug used to treat infections caused by bacteria and
other microorganisms. Originally, an antibiotic is a substance
produced by one microorganism that selectively inhibits the growth of
another.
antibacterial drug : any drug that destroys bacteria or inhibits
their growth
Antimicrobial spectrum :means the species of microorganisms that
the drug can inhibit or kill.
-Divided in to: Narrow spectrum, Extended spectrum,
Broad spectrum
Chemotherapy index (CI) ：To evaluate the safety of
chemotherapeutic drugs, the value is LD50/ED50 or LD5/ED95.
Minimal inhibitory concentration (MIC): MIC is the lowest
concentration of antimicrobial agents that prevents visible bacterial
growth in 18-24 hours incubation.
classification according to mechanism of action of antimicrobial
agents
1)inhibitors of cell wall synthesis :penicillin, cephalosporins
2) inhibitors of synthesis or damage to cytoplasmic
membrane:
polymyxins
3) modification in synthesis or metabolism of nucleic acids:
Quinolones, rifampin
4) inhibitors of protein synthesis:tetracyclines,
chloramphenicol, erythromycin
5) modification in energy metabolism (folic acid metabolism)
: Sulfonamides, trimethoprim trimethoprim
Antimicrobial agents’ resistance
●Enzymic inactivation: to destroy the antimicrobial such as
β-lactamase destroy many penicillins and cephalosporins
●Modification (alteration) of target sites
●Decreased accumulation: an efflux system that pumps out
the drug
 ●Genetic mutations: such as quinolones (DNA gyrase gene
mutation)

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