Glossary of Pharm Devna II

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volatile liquid
moderate blood solubility, very potent inhalational anaesthetic
muscle relax-minimal
CNS=increases intracranial pressure
can cause hypotension,
Adverse effects: liver necrosis-rarely progressive
Main uses: limited use cuz of liver toxicity

liquid inhalant anesthetic
moderate blood solubility, potent
analgesia:yes muscle relaxation: yes
airway irritation= yes!
CNS= decreases intracranial pressure, can cause hypotension
Can cause potent respiratory depression
Uses: most widely used inhalation agent, good for neurosurgery-reduces cerebral blood flow

inhalant liquid anesthetic
very insoluble in blood, potent
analgesia: yes
Muscle relax: yes, no airway irritability
Potent bronchodilator, decreases tidal vol, increase resp rate, decreases resp to hypoxia/hypercarbia
uses: replaces halothane for peds

barbiturate, intravenous gen. anaesthetic
solid form
lipid solubility and potency are high
Analgesia: No
Muscle Relaxation: Yes
CNS: decreases intracranial press
not irritating to the airway, but cn cause coughing, larygospasm,brochospasm
can cause hypotention, can cause dose dep respiratory depression
Adverse effects: extravascular injection, causes severe pain, necrosis
Main uses: used for induction, not maintenance

phenol intravenous gen anesthetic, lipid solubility and potency are high
Analgesia: No
Muscle Relax: Yes
CNS: possible seizures in epilep
Airway irritation: none
produces moderate hypotension, profound respiratory depression
Adverse effects: alllergy to phenol, injection pain
Main use: very versatile and widely used, verypotent so good induction agent, suitable for maintenace, easy to titrate
used for conscious and deep sedation

intravenous gen anesthetic, related to PCP, more lipophilic than thiopental and more potent than thiopental
Analgesia: yes
CNS: disorientation, excitation, hallucinations
main use: not used commonly, has apps for specific patients such as those at risk for hypotension and bronchospasm

water soluble phosphate ester prodrug of propofol
Analgesia: no
muscle relaxation: no
CNS: sedative hypnotic
airway irritability: none
cvs: moderate hypotension
respiratory system: profound respiratory depression
adverse effects: paresthesias
main use=sedation

First generation H1 antagonist, highly sedating
(Atarax) 1st generation H1 antagonist
(Antivert) 1st generation H1 antagonist, used for vertigo, motion sickness

H1 antagonists; antiallergic, antiinflammatory, muscarinic receptor--decreased cough, dry mouth

alpha adrenergic-hypotension

serotonin receptor= increased appetite

cardiac ion channels: prolonged qt interval, arrythmias

peripheral nerves : local anesthetic if injected

Zyrtec 2nd generation H1 receptor antagonist, cn sedate, dizziness, dry mouth,

Claritin, 2nd generation H1 receptor antagonist
Allegra, 2nd generation H1 receptor antagonist
Zantac H2 receptor antagonist

relatively nontoxic

rare adverse effects

Tagamet- H2 receptor antagonist, --inhibit acid secretion
adverse effects: CNS: hallucinations, agitation, confusion


iterferes with several important Cytochrome P450 pathways in the liver (-->drug interaction)
need dose adjustment in renal failure

H2 receptor antagonist--Pepcid
indicated for use in gastroesophageal reflux disease
cromolyn sodium
poorly absorbed, used only topically as inhaler, nasal spray, eye drops, or oral soln for GI allergies

Uses: to prevent bronchoconstriction caused by allergen exp, exercise, or aspirin
prevents allergic rhinoconjunctivitis

rare side effects, can be used in children

nitrogen mustards
alkylating chemo agent

resistance to alkylating agents include--decreased drug uptake, increased DNA repair, cytoplasmic sulfydryls like GSH, and GST can increase resistance to alkylating agents

mech of action-cross-linking of DNA, creates a depurination of DNA

cyclophosphamide (Cytoxan)
nitrogen mustard

use: for broad general activity, most widely used alkylating agent, a prodrug that must be first metabolized by P450 system

Ifosfamide (Ifex)
nitrogen mustard chemo agent
used to treat testis cancer, sarcoma
platinum-based chemo agent
Mech: binds covalently to DNA bases and disrupts DNA fxn
Metabolism: inactivated by sulfhydryl groups, binds to glutathione, metallothioneins and thiosulfate

Toxicity: hypokalemia!, nausea, vomiting, auditory prob

Precaution: use with caution with other nephrotoxic drugs, monitor Mg, K, Ca

platinum-based chemo agent
Mech: covalent binding to DNA
Toxic: myelosupression!! thrombocytopenia (WBC supression)!!!
nausea, vomiting, much less nephrotoxic than cisplatin
precaution-reduce dose for reduce GFR
use: ovarian, lung bladder
cisplatin use lung testis, ovarian, bladder

Doxorubicin (Adriamycin)
natural antibiotic product- chemo agent
Use: broad activity but not colon or lung
Mech of action: inhibit topoisomerase II, causing DNA damage

Elimination: liver
Toxic: myelosuppression, Cardiac toxicity!!--free radical formation creates this--cn lead to CHF
Precaution: patients with heart disease, radiation sensitization, extravasation of drug

natural chemo agent
Uses: lung cancer, testis cancer, lymphomas

mech: inhibits topoisomerase II

Toxic: include myelosuppression and GI toxicity

natural chemo agent
Use: colon
Mech: targets topoisomerase I, relaxes DNA by creating double stranded DNA damage

Toxic: diarrhea, myelosuppression also seen

Paclitaxel (Taxol)
natural product (from yew tree) chemo agent
Mech: binds to tbuline, microtubles less susceptible to depolymerization, may affect apoptosis

Mech of resistance: presence of p-glycoprotein, mutations in alpha or beta subunits of tubulin

Activity: ovarian cancer, non-small cell lung cancer, breast cancer, prostrate cancer, bladder

Toxic: myelosuppression, neutropenia, thrombocytopenia, alopecia, nausea, vomiting, major neurologic toxicities!

Docitaxel (Taxotere)
natural chemo agent
Use: breast prostrate
Mech: binds to tubulin, microtubules less likely to depolymerize, may affect apoptosis

resistance; p-glycoprotein, muations in a or beta subunits of tubulin, has limited water solubility

toxic: myelosuppression, esp neutropenia and thrombocytopenia, alopecia, nausea and vomiting
less neurotoxicity than taxol but causes capillary leak syndrome instead

5 Fluorouracil
antimetabolite- pyrimidine analog chemo agent
Use: breast, all GI esp colon, bladder, premalignant lesions

Mech: inhibits thymidylate synthetase, an enzyme needed for synthesis of dTMP and DNA

must be converted to a nucleotide for activity, activity is increased by combining with leucovorin

folic acid analog chemo agent
Mech: inhibition of dihydrofolate reductase leads to partial depletion of reduced folates, inhibits pure and thymidylate biosynthesis

Metabolism: converted to polyglutamates

it is polar and large, so poorly transported across blood brain barrier
high dose toxicity rescued by leucovorin-methotrexate cannot be reversed by folate but only by folate metabolate

toxicity: myelosuppresion, renal injury, neurtoxicity, phenumonitis, mucositis

precautions; reduce dose for decrease in creatine clearance, not for those with abnormal renal function

hormone chemo drug
acts to deplete estrogen receptors in breast cancer cells, DNA polymerase activity, and thymidine incorporation, blocks cells in mid-G1, stimulates production of TGF-beta

Toxicity: bone pain, hot flashes, endometrial carcinoma, venous thrombosis, anovulation,intraretinal opacities

Leuprolide (Leupron)
hormone based chemo therapy
Use: prostate cancer LHRH antagonist)

also GnRH (inhibit gonadotropin release. Short term admin of these produce surges in FSH and LH) After 2 weeks, FSH and LH levels are reduced
Toxicity: hot flashes, libido loss, impotence

In men creates a fall in testosterone

Flutamide (Eulexin)
hormone based chemo therapy
Used to treat prostate cancer (non-steroidal antiandrogen)

binds to androgen receptors in the prostrate

cn cause liver toxicity

a derivative of tetrahydrofolic acid

used as an adjuvant chemo therapy with methotrexate to allow for normal DNA synthesis to occur in the presence of dihydrofolate reductase inhibition

immunosuppressor agent
deriv of 6 mercaptopurine (not oral), blocks de novo purine synthesis--incorp fake nucleotides into DNA, inhibiting division of all cells

Use: used with glucocorticoids to block tissue transplant rej, for rheum athritis, systemic lupus erythematosus

blocks cell med and humoral immunity

toxic: GI intolerance, leukopenia, susp to infection/malignancy

immunosuppressor T cell specific
decreased production of IL-2 and gamma interferon and binds cyclphilins which prev the complx forming that usually blocks the generation of cytoplasmic phosphatase, calcineurin--activates T cell specific txn factor, NF-AT

Use: transplants, hypersens (Type I diabetes, psoriasis, uveitis)

Toxicity: nephrotoxicity, hypertension, hepatotoxicity, encephalopathy, hypertrichosis,

toxicity assoc with low cholesterol

immunosuppressor, bacteria derived prod
prevents rej in liver + kidney transplant,

Decreases T cell synthesis of IL-2 and inhibits calcineurin phosphatase
much more potent than cyclosporine
Toxicity-neurological--headache,same as cyclosporine- nephrotoxicity, hypertension

antagonist of pro-inflamm cytokine, TNF

one end binds TNf and the other to phagocytic cells-removing TNF and preventing its action

use: treat adult/kid rehum arthr and psoriatic arthr

Toxic: worsening infections, sepsis deaths

immunosuppresant- humanized monoclonal ab against IgE

treatment: inj given every 2-4 weeks for asthma

IV gamma globulin
used to passively immunoze ind esp those lacking immunoglobulins
interferon beta (Avonex and Betaseron)
anti-viral and immunomodulaity activiy
used for multiple sclerosis
interferon gamma (Actimmune)
made only by activated T cells, no homology with alpha/beta types
induces macrophage activation
so used to treat diseases with inadeq macrophage killing: chronic granulomatous disease, visceral leishmaniasis

Interlukin 2 (Proleukin Aldesleukin)
immunostimulator-T cell growth factor used to treat renal cell carcinoma
Toxic: hypothyroidism and capillary leak syndrome (pulmonary edema)
phenylimidothiazole, anti-helminthic drug--enhances T-cell and macrophage function

used to treat colon cancer

non-pathogenic mycobacterium related to TB
stimulates macrophages and T cell fxn

used to treat bladder malignancies

corticosteroid, 4x potent as cortisol, given orally
Uses: autoimmune disorders, tumors

toxicity:increased blood sug for diabetics,abdominal pain, infections

methyl prednisolone (Medrol)
corticosteroid, oral, injectable, topical,
5x stronger than cortisol

Use: arthritis, bronchial inflamm

toxicity: weight gain, glaucoma, osteoporosis,

Long acting corticosteroid
25-40x stronger than cortisol, oral, injectable, topical

uses: skin irritation like eczema, psoriasis

toxic: can cross placenta

intermediate acting corticosteroid
5x as strong as cortisol, oral injectable, topical

uses: eczema, psoriasis, arthritis, allergies, ulcerative colitis, lupus, asthma attacks

toxic: sore throat, nosebleeds, increased coughing, headache, and runny nose

Acetyl-salicylic acid- NSAID
moderately analgesic, antinflammatory, anti-pyretic action, requires freq. dosage though

irreversibly and nonselectively inhibits COX 1 and 2, analgesic effect from inhibit of COXIII in CNS

Toxic: gastritis, tinnitus/hearing loss, hepatotoxicity, hypersensitivity

Contraindications-active peptic ulcer disease, hemophilia, allergy

beneficial for CVD
used for low-mod pain, osteoarthritis, rheumatoid arthritis

sodium salicylate
cation salicylate NSAID, minimal GI side effects
irreversibly acetylates cyclooxygenases I and II, thereby inhibiting prostaglandin synthesis and associated inflammation and pain. This agent may also activate mitogen-activated protein kinase (p38MAPK), thereby inducing apoptosis in cancer cells
Acetaminophen (Tylenol)
analgesic-antipyretic, but little antiinflamm action
rapidly abs from GI, t1/2=1-3 hrs
weak inhibitor of Cox1, 2, and 3
well tolerated, but >7g/day-liver damage
renal tubular necrosis also, methemoglobinemia (rare, oxygen delivery impaired),hemolytic anemia (rare)

excreted after hepatic glucoronide conj and sulfate conj

selectively inhibits COX-2

reduced risk of GI effects

Risks: renal damage, increased risk of MI/stroke, thrombosis

nonselective COX inhibitor (similar to ibuprofen)
long duration, analgesic and antiinflamm, antipyretic

t1/2= 12-17hrs
used for gout, migraine, osteoarthritis, pain, acute tendonitis, bursitis, rheumatoid disorders

toxicities: GI, renal, hepatic rash

potent (toxic) nonselective COX inhibitor
analgesic, antipyretic, anti-inflamm

Side effects: GI, CNS-headache,vertigo, somnolence

historical use-gout, rheum arth, osteoarth, bursitis, tendonitis, patent ductus arteriosus

used in acetaminophen overdose, helps synthesize glutathione
combines with NAPQ1 as a glutathione substitute
enhances nontoxic sulfate conj

N-acetylcysteine modulates inflammation in cystic fibrosis
prevents mucous from accumulating

cardiac glycoside, inhibits Na/K ATPase, intracellular Na increases resulting in increased ventricular ejection, decreased end-systolic and end diastolic size, increased CO and renal perfusion, decrease in sympathetic tone, incrased PR interval, slow ventricular rate

toxic: arrthymias with increased intracellular calcium

a long acting benzodiazepine favored for acute anxiety states for control of panic attacks

lower doses needed in elderly patients because of the CNS depressant effects

short acting Benzodiazepines
anxiolytic, amnesic, sedative/hypnotic, anticonvulsant and muscle relaxant.[4][5] Lorazepam is used for the short-term treatment of anxiety, insomnia, acute seizures including status epilepticus, sedation of hospitalised patients as well as sedation of aggressive patients.
bleomycin ADR
anti-tumor agent, causes pulmonary damage
codeine ADR
conversion to morphine in the absence of P450 2D6 enzyme
aminoglycosides (streptomycin, neomycin, kanamycin, tobramycin) ADR
notorious for auditory and vestibular damage (accumulate in perilymph and endolymph)
amphotericin ADR
antifungal agent
has severe side effects
hypotension, anorexia, nausea, vomiting, headache, dyspnea, and tachypnea, drowsiness, generalised weakness

also nephrotoxic esp with diuretics

local anesthetic, an ester
metabolized into PABA (allergic rxn)
primarily used in dentistry
used for infiltration and field block

amide local anesthetic
used for nerve block, epidural block, infiltration, and field block
used topically also to relieve itching, burning, and pain.

half-life: 90–120 minutes

ester local anesthetic
constricts blood vessels resulting in reduced blood loss

used in surgery and labor
used for nerve block

ester local anesthetic
used in spinal anesthesia
used topically in opthalmology

local anaesthetic drug-- amino amide group

spinal anesthesia and epidural block and nerve block, for infiltration and field block as well

local anesthetic commonly used as a topical pain reliever
cholestyramine (drug interaction)
drug used to lower cholesterol, not absorbed it binds bile salt so it is a bad idea to give it with other drugs since it is a binding resin that can bind digoxin, thyroxine, etc to prevent its absorption.
Warfarin (drug interaction)
inhibits the synthesis of Vit K dep. clotting factors.
Interacts with aspirin-pharmodynamic effect increases bleeding time and aspirin also displaces warfarin from plasma protein so it increases the dose of warfarin, increasing its drug distribution
Rifampin (drug interaction)
(antituberculosis agent) can activate CYP 3A4 and CYP2D6 and can shorten half life of digoxin, cyclosporine, sedative benzodiazepines, methadone, and beta antagonists
quinidine/digoxin drug interaction
both are bond to muscle binding sites so quinidine cn displace digoxin, thus increasing toxic digoxin blood levels
barbiturates interact with warfarin
-alkaloid drug, lipid soluble can induce CYP3A4, CYP2B, and CYP1A2, accelerates metabolism of warfarin, so need to give fore warfarin
Cimetedine drug interaction
inhibits metabolism of many drugs: procaineamide, lidocaine, codeine

it also effects gastric pH so can affect the absorption of other drugs

omeprazole drug interaction
proton pump inhibitor
competitive inhibitor of the enzymes CYP2C19 and CYP2C9, and may interact with drugs that depend on them for metabolism, such as diazepam, escitalopram, and warfarin
can also effect on drugs that are absorbed in the acidic stomach

Allopurinol (drug interaction)
can cause increased absorption of iron
inhibits xanthine oxidase needed to metabolize methotrexate
MAO inhibitors
blocks metabolism of catecholamines, tyramine, amphetamines, methyl-dopa
halothane ADR
converted by P4502E1 to a reactive intermediate, as haptene elicits formation of ab to liver tissues
acetaminophen ADR
usually detoxified through glucoronidation and sulfation, minor metabolite is detoxified by GSH and excreted. If too much acetaminophen, GSH levels fall and the mebolite reacts with tissues causing necrosis.

in chronic alcoholism-decreased liver glycogen leads to less gluoronic acid for detox

Coumadin/Heparin (derm side effect)
causes necrosis as a result of overdose
aspirin another anticoagulant can cause purpura and antihemorrhaging
hydrochlorathiazide (derm reaction)
can cause type II cytotoxic immune hypersensitivity, specifically thrombocytopenic purpura
lithium (derm reaction)
non-immune mediated reaction, aggravates or unmasks a previous existing dermatologic disease--psoriasis, acne
methotrexate (adverse skin reaction)
drug intereactions with sulfonamides or probeneicid to result in displacement from binding and altered drug excretion respectively
orthotricyclin (derm reaction)
can cause Melasma, a pharmological side effect, darkening of skin (photosensitivity)
penicillin (derm reaction)
Type-1 Anaphylactic reaction,
occurs within minutes after exposure, angioedema wheals, uriticaria
phenobarbital (derm reaction)
an anticonvulsant that can lead to DRESS , facial edema is a common feature
phenytoin (Dilantin)--derm effects
another anticonvulsant that can cause DRESS
sulfonamides (derm effects)
causes allergic contact dermatitis (delayed hypersensitivity) and can react with MTX to have displacemeent from binding-pharmalogical side effect
tetracycline (derm reactions)
a severe cutaneous reaction, hypersensitivity syndrome reaction, serum sickness-like reaction,
prednisone (derm effect)
delayed type hypersensitivity after topical use
DRESS (derm)
drug rash with eosinophils and system symptoms Hypersensitivity syndrome, caused by anti-convulsants, more common in african americans
develops 2-6 weeks after drug was started
features: rash, facial edema, arthritis, myocarditis, interstitial pneumonitis, interstitial nephritis, hepatitis, infiltration of the brain by eosinophils

Stevens Johnson Syndrome (toxic epidermal necrolysis)
rare drug-induced skin reaction, , begins within 4 weeks after drug exposure, fever mucous membrane erosions, eruption on face and upper trunk, skin rubs off (positive Nikolsky sign)

caused by antibacterial sulfonamides, anticonvulsants, NSAIDs, allopurinol

erythema nodosum
most common cause: sulfonamides, bromides, gold, sulfonylureas, oral contraceptives

formation of immune complexes and their deposition in and around venules of CT septa of subcutaneous fat, typical eruption is suddenonset of symmetrical tender, erythematous, warm nodules and raised plaques around shins ankles and knees

fixed drug eruption
cutaneous reaction to an ingested drug that recurs at the same site each time the offending drug is taken.
The most common offending agents include anti-microbials, non-steroidal anti-inflammatory drugs (NSAIDs), and anti-epileptics. Fixed drug eruptions classically present as a single, sharply demarcated, round erythematous patch or plaque, occasionally with localized bullae. Generalized bullous FDEs, however, are relatively rare and can be confused with Stevens-Johnson Syndrome.
vincristine and vinblastine
plant alkaloids, bind to tubulin dimers of microtubules acting in M phase of cancer cell cycle

pyrimidine analog, inhibits DNA synthesis,
myelosuppression is mild, flu like systems, increased toxicity

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