PHARMACOLOGY study of drugs

PHARMACOTHERAPEU refers to the use of specific drugs to

study of how ROUTE
TICS prevent, treat,the
or body dealsa with
diagnose the
disease
PHARMACOKINETICS drug –its absorption, distribution,
analysis of what the drug does to the
PHARMACODYNAMICS and
body,elimination
and how the drug exerts its ORAL
deals
effect with the preparation and
PHARMACY SUBLINGUAL
dispensing
the study ofofthe medications
harmful effects of
TOXICOLOGY (also known as the brand name) is RECTAL
chemicals (drugs)
TRADE NAME assigned to the compound
“nonproprietary” name) often byderived
the
GENERIC NAME pharmaceutical
from the chemical company
name; INHALATION
prophylaxis, diagnosis, orthe easiest
therapy of
ADVERSE DRUG and most effective way to refer to a
disease orand
expected for known
the modification
effect of aofdrug INJECTION
REACTION
SIDE EFFECTS physiologic
that is not the function. An adverse
intended drug
therapeutic TOPICAL
outcome Genetics TRANSDERMAL
Disease KIDNEYS
Factors responsible for Drug interactions PRESCRIPTION
variations in response to
drugs Age
Diet
Sex
 ROUTES OF DRUG ADMINISTRATION
ADVANTAGES DISADVANTAGES EXAMPLES
ENTERAL
absorption of some
analgesics; sedative-hypnotics;
easy, safe, convenient drugs; chance
drugs must beof first-
easily
rapid onset; not subject to first-pass pass inactivation in many others
absorbed from
poor or incomplete oral nitroglycerin
alternative toinactivation
oral route; local effect mucosa laxatives; suppository forms of other
absorption' chance of
on rectal tissues drugs
PARENTERAL rectal irritation
rapid onset; direct application for
irritation; patient general anesthetics; anti-asthmatic
respiratory disorders; large surface chance of infection if
provides more direct administration compliance is agents anti-cancer
insulin; antibiotics;
area for systemic absorption sterility is notin
to target tissues; rapid onset only effective drugs; narcotic anelgesics
maintained antibiotic ointments; creams used to
local effects on surface of skin treating
drug must outerbelayers
able toof treatnitroglycerin; motion sickness
without braking the skin; can minor skin irritation and injury
pass throughskin dermal medications; drugs used with
provide steady, prolonged delivery primary location for drug
primary sites for drug excretion layers
LIVER intact phonophoresis and iontophoresis
metabolism
an order, especially by a physician, for the preparation and administration of a medicine,
therapeutic regimen, assistive or corrective device, or other treatment
 LATIN LATIN
ABBREVIATIO
ABBREVIATION MEANING TRANSLATIO MEANING TRANSLATI
N
a.c. before meals N
ante cibum ml milliliter ON
b.i.d. twice a day bis in die noct at night
b.i.n. twice a night bis in noctus O.D. right eye oculo dextro
c with cum O.S. left eye oculo sinistro
cap capsule capsula O.U in each eye oculo utro
d day dies p.c. after meals post cibum
(no substituting
daw p.o. by mouth per os
generic or brand
gtt drop gutta p.r.n. as needed pro re nata
h.s. bedtime hora somni pil pill pilula
I.M. into the muscle qh every hour quaque hora
I.V. into the vein q3h every 3 hours quaqe 3 hora
 LATIN
ABBREVIATIO
MEANING TRANSLATI
N every
qAM ON
morning
qd daily quaque die
every other quaque altera
qod
day die
s without
under the sine
s.l. tongue;
tab sublingual
tablet tabella
three times a
t.i.d. ter in die
day
tsp teaspoon
tbsp tablespoon
as directed
ut dict
by doctor
 INFLAMMATION
injury/infection/trauma
attacks the cell membrane of the cell
cell membrane contains phospholipids
activation of phospholipase occurs
causes formation of arachidonic acid (AA); from phospholipase A2
COX: prostaglandins (PGs), prostaglandins, thromboxanes, and leukotrienes
thromboxane A2 (TXA2) are eicosanoids derived from arachidonic acid
arachidonic acid is further metabolized by; cyclooxygenase pathway and lipoxygenase pathway
which are ingested in the diet and stored as
LO: leukotrienes (LTs) phospholipid in the cell membrane

EFFECTS OF EICOSANOIDS ON THE DIFFERENT SYSTEMS

CARDIOVASCULAR REPRODUCTIVE
RESPIRATORY SYSTEM GI TRACT
SYSTEM LTC4 and LTD4: SYSTEM
PGE2 + LT's contract smooth muscle
bronchoconstriction + PGE2 and PGF2:
TXA2: vasoconstrictor, increased mucus secretion contract pregnant
+ increased vascular PGE2: watery diarrhea, vomiting and cramps (↑cAMP) uterus
prothrombotic
permeability
PGI2 and PGE2: Role in promoting labor;
inhibit gastric acid secretion and increase mucus production in miscarriages
bronchodilation no interaction of leukocyte with (premature labor);
endothelial cells inducing abortions
inhibits leukocyte endothelial capillary obstruction
PGE2 + PGI2 protective effects interction ischemic injury CONSEQUENCES
PGE2 and PGI2: Leukotriene Inhibitors - on GIT OF BLOCKING
mucosal ulceration Role in maintaining
vasodilators bronchodilation, for asthma PGI2 & PGE2
inhibits the activation of protease and oxygen radicals FROM NSAID INTAKE patent ductus arteriosus
neutrophils endothelial injury
(↑ mucosal blood flow; ↑cAMP; ↑ mucus
cytoprotective effects secretion; ↑ protein synthesis)
are 1 and COX-2) catalyze the conversion of arachidonic acid to
COX-1 and COX-2: enzymes that synthesize
PHARMACOLOGICAL/PHYSIOLOGICAL EFFECTS NON-SELECTIVE INHIBITION nonselective cyclooxygenase COX-1 COX-2 prostaglandin (PG) H2, the precursor of PGs and
prostaglandins,prostaglandins
while sparing synthesis of
EFFECTS ON PAIN AND INFLAMMATION inhibitors; they inhibit both the that regulate by cytokines thromboxane. These lipid mediators play important roles in
COX-2 INHIBITORS or COX-2 SELECTIVE DRUGS Celecoxib (Celebrex) decrease pain
beneficial and inflammation
prostaglandins with regulate
that help minimal or
sensitize nerve endings to physiologic ▪ Synthesizes PGs
PGE2, PGI2, LTB4 no adverse effects
PGE2: (1) increases heat production, (2) shuts down heat on the stomach
NSAIDs andPGE2
inhibit other
painful stimuli
Promotes aggregation and processes that mediate
LTB4 FEVER losing mechanism; therefore raising body temperature tissues = synthesis = reducing ▪ Especially important inflammation, pain,
degranulation
Hyperemia, edema, hotness of
due to increased Peripherally: PGs sensitize the nerve endings to NSAIDs block these
fever fever produces prostaglandins
eicosanoids at inflammation sites. PAIN bradykinin and
Centrally: PGshistamine
lower the threshold for central pain effects = reducing the
PGD2 vasodilation
affect the hypothalamus •circuits
activates kininogens cyclooxygenase
intensity of pain
temperturewater
increases regulating INFLAMMATION • vasoconstriction in capillaries enzyme & reduces
PGE2 - causes pain system and andproduces
electrolytes mucusfever • vasodilation
Decrease in some vascular
activation beds of neutrophils
and function prostaglandin
produces contraction
secretion in GIT of
PGF2α PROSTAGLANDINS Stabilization of lysosomal membranes
uterine smooth
vasodilation andmuscles
inhibition ANTI-INFLAMMATORY ACTION
PGI2 vasoconstriction and Inhibits mucopoly saccharide biosynthesis
of platelet aggregation
TXA2 stimulates platelet Reduce edema, pain and inflammation
aggregation Inhibition of TXA2 by
bronchoconstriction PGI2: prevents platelet aggregation Aspirin at LOWER
LTC4, LTD4 increased capillary ANTIPLATELET ACTION TXA2: promotes platelet aggregation DOSES (75-150 mg) →
permeability Platelets aggregate lead to coagulation and thrombosis reduce platelet
aggregation.

OPIOIDS (narcotics) - for

LOW & SLOW; no anti-pyretic and anti-inflammatory effects Codeine, Morphine
moderate to severe pain
similar to aspirin and other NSAIDs
in its ability to decrease pain (analgesic) and fever (anti-pyretic)
ANALGESICS no anti-inflammatory and anticoagulant properties
ACETAMINOPHEN / advantage: not associated with upper gastrointestinal tract
NON-OPIOIDS PARACETAMOL irritation
has anti-pyretic and analgesic effects
important and useful medication in the treatment of fever and mild
NSAIDs (Ibuprofen. Aspirin, to moderate pain NSAIDinflammation)
(without is aspirin (given as
temperature associated with fever
Mefenamic Acid, COXIBS, antiplatelet) acetylsalicylic acid
(antipyresis), and
cortisolNaproxen,
and other Ketoprofen)
glucocorticoids increase blood glucose and liver glycogen (ASA) - blood thinner and may
cortisol facilitates the breakdown of muscle into amino acids and lipids into free fatty acids, which can be transported to the liver to
GLUCOCORTICOIDS - glucose that is synthesized in the liver: can beform glucose
stored (gluconeogenesis)
as glycogen or released back into the bloodstream to increase blood
given as anti-inflammatory glucose levels
glucocorticoids = effective and potent anti-inflammatory agents
increasd risk of GI bleeding
Suppress the transcription of genes involved in inflammation
CORTICOSTEROIDS - Stabilize lysosomal membranes, Inhibit the phospholipase
thereby making themA2 lesswhich release
fragile AA from the cell
and susceptible membrane
to rupture. Lysosomes are organelles that
inhibit phospholipase A2 contain degradative enzymes. When lysosomes are ruptured, these enzymes begin to digest cellular components contributing to
inflammation.
Decrease vascular permeability that helps control swelling and erythema at the site of inflammation.
 GENERIC NAMES RECEPTORS MECHANISM causesEFFECTS
muscle AR/SE COMMON S.E. BRAND NAMES
inhibits reflexes in the nausea, sedation,
weakness, used to
spinal cord and blocks somnolence, dizziness,
manage spasticity, has
release of excitatory fatigue, confusion,
Baclofen GABA B sedative effects, works Lioresal, Trilaxant
neurotransmitters muscular
Centrally Acting through GABA, somnolence, sedation
(e.g.: norepinephrine, pain/weakness,
increase the affinity of anxiolytic, sedative-
glutamate) feeling of calm, muscle hypotension
and concentration, and Valium, Valzepam,
Diazepam GABA A GABA that increases hypnotic
relaxant, anti-spasticity,
antispastic, muscle impairment of motor Trankil
Tizanidine ALPHA 2 the influx of chloride Sirdalud
Anti-Spasticity/Muscle not popularly given for
relaxant muscle
reticulum, which leads
Relaxants Dantrolene RYANODINE-1 spasticity, causes weakness, hepatotoxic Dantrium
to the inhibition
neurotoxic of the
protein muscle weakness
produced by the
bacterium Clostridium generalized weakness,
Peripherally Acting (inhibits) not considered
botulinum, given fatigue, flu-like
Botulinum Toxin ACETYLCHOLIN anxiolytic and sedative- Botox, Dysport
through injection symptoms, pain/bruising
E hypnotic
(cannot be taken orally at injection site
due to risk of
hypnotics GABA that increases
respiratory depression) relaxation, anxiolytic addictive, withdrawal Clonazepam (Rivotril)
• central nervous system Benzodiazepine CHLORIDE the influx of chloride causing much hypnotic
(anti-anxiety), anti- symptoms Diazepam (Valium,
depressants Non- chloride channel
ions at the
CHLORIDE anxiety effect, hypnotic Zolpidem (Stilnox)
• enhancing the effects of Benzodiazepene opening with resulting drowsiness, dizziness,
(sleep-inducing)/Z a small barbiturate
the gamma-aminobutyric Enhance the effect of overdose can result in decreased alertness Pentobarbital (GABA
Anxiolytics/Sedative- anxiolytic (anti-anxiety),
acid GABA. May cause coma or death due to and concentration, B) (Nembutal)
Hypnotics hypnotic (sleep- Phenobarbital
(GABA) Barbiturate profound central respiratory depression, and impairment of
•resulting in anxiolytic inducing), motor coordination (Luminal)
nervous system bradycardia, syncope,
(anti-anxiety), hypnotic anticonvulsant Secobarbital
depression hypotension,
(sleep-inducing), (Seconal)
respiratory depression
anticonvulsant, and
TRUE resistance to passive
Baclofen can cause muscle
Glutamate SPASTICITY movement
Anweakness
excitatory FALSE
GABA
neurotransmiters Ry2 receptors
A and onB cardiac
Anti-spastic /acts
Dantrolene on
muscle MS
muscle
relaxants are used to treat CP
spasticity found GABAALS B
Pentobarbital actsinon
Centrally acting muscle Ca recpetors
Botulinum toxin
relaxants include GABA Eperisone
A receptors
Diazepam acts
Benzodiazepines canoncause GABA True
B receptors
withdrawal symptoms in
botulinum toxin use
inhibits the False
norepinephrine
chronic
Zolpidemrelease
is alsoofknow as serotonin
True
Alprazolamvalium
is also known as False
True
rivotri
Botulinum toxin can be given False
True
Benzodiazepines
orally increase False
K
the affinity of GABA that
increases theacts
influx GABA ACl receptors
Tizanidine onof
GABA B receptors
tizanidine
Trilaxant is
valium
 once information
BACTERIOSTATI BACTERICIDA regarding
TARGETED
EMPERIC causative agent PROPHYLAXIS TREATMENT
drugs used to treat bacterial C L medical treatment THERAPY
infections inhibit the growth and the used to prevent an
kill bacteria based on experience or susceptibility of
of bacteria drugs that educated guess in the infection
should befrom occurring
based on the antibiotics given in
occurring antibiotics DNA replication the bacteria to
inhibit cell wall recommendation
high probability ofofana
discovered by Alexander and proteinhas no significant absence of complete or
classification various
the presence of an
synthesis
relevance with outcome of perfect information medical specialist
infection infection
do not treat infections due antibiotics, injection after a surgery,
(if occurs) can
(result of culture and
to virus bothtreatment
are effective physician can instrumentation,
cause or
death with existing
sensitivity testing)
TYPES ACCORDING TO now shift to a conditions
ANTIBIOTICS MECHANISMdrug that is AR/SE
MECHANISM OF ACTION
effective
INHIBITION OF CELL Penicilins (-cilin) Beta-Lactam Antibiotics, blocks function hypersensitivity reactions, allergy
WALL SYNTHESIS of cell wall enzymatic proteins which
(bactericidal) Cephalosporins (ceph-) cause cell wall breakdown hypersensitivity reactions, allergy, GI problems
nephrotoxicity, ototoxicity (hearing or balance
INHIBITION OF PROTEIN Aminoglycosides (-micin)
act at bacterial ribosomes problems), hypersensitivity
ANTIBIOTIC SYNTHESIS Macrolides (-mycin) GI reactions, allergic reactions
S (bacteriostatic) act at bacterial ribosomes, not given to 8 (photosensitivity), teeth discoloration because
Tetracyclines (-cycline) DNA synthesis, both
INHIBITION OF NUCLEIC year olds andofyounger
which are DNA of tetracycline-calcium, hypersensitivity, GI
ACID SYNTHESIS Fluoroquinolones (-acin) topoisomerases
do not directly inhibitthat human
DNA/RNA cellssynthesis,
lack and
(DNA/RNA) Sulfonamides (sulfa-) theythat are essential
inhibit folic acidforsynthesis
bacterial DNAneeded
(bacteriostatic) by bacteria for replication
Rifampicin: RMP or R suppresses RNA synthesis hepatotoxicity, GI and autoimmune reactions
inhibits the synthesis of mycolic acid,
Isoniazid: INH or H mechanism of action is unknown; hepatotoxicity, peripheral neuritis
required for the mycobacterial cell wall
ANTI-TB DRUGS (RIPES) Pyrazinamide: PZA or Z converted to pryanozoic acid which is hepatotoxicity and hypereuricemia, joint pains
the active form (PRO DRUG) optic neuritis, color blindness, GI and allergic
Ethambutol: EMB or E suppresses RNA synthesis
reactions, hypereuricemia
vestibular dysfunction, deafness, nephrotoxicity,
Streptomyocin: STM or S inhibit bacterial cell membrane synthesis
cause increased skin sensitivity to neuromuscular blockade, peripheral neuritis
Tetracyclines ultraviolet light • If the patient
DRUGS CAUSING is receiving UV treatments: therapists
SENSITIVITY TO UV Fluoroquinolones must be careful to adjust the ultraviolet
LIGHT light treatments in accordance with
Sulfonamides changes in the dosage of the antibacterial
drug
ANTIBIOTIC occurs when microbes evolve and develop mechanisms to protect themselves against the antibiotics used to treat them
RESISTANC more difficult to treat requiring higher doses or different agents that might be more toxic
E a microbe can be resistant to multiple drugs (multidrug resistant)
Broad
Spectrum used when giving an empirical antibiotic therapy
Antimicrobia
Antibiotics an infection that does not respond to the usual antibiotic used to treat it.
l Resistance
inhibits Cefalen
What acid
nucleic is
effectsCiprofloxacin
of antibiotic therapy
antimicrobial
recommende because of under dosing
Chloramphenicol
dresistance?
to children
following Gentamicin
because is it Penicillin
mostpains.
joint likely Tetracycline
Pyrazinamide
What woulddrugbe is accident
Rifampicin
needing
following
prophylaxis Chloramphenicol
A 12 year old boy with
inhibits cell health care staff
fight Ofloxacin
wall
following
antimicrobial Levofloxacin
Prevent getting an
inhibits
inhibits folic Erythromycin
Cefazolin
protein
acid True
Clofazimine
more
used when
effective than antibiotics
False
givinganti-
Which an
empirical PZA
TB drug is a
TBprodrug?
drugs are RMP
Ethambutol
drugs
hepatotoxic Isoniazid
Rifampicin
complains of
Ethambutol
hearing
 90-95% collagen fibers and
CORTICAL/COMPACT
BONE Organic Matrix (30%)
provides elasticity/tensile strength gelatinous medium (ground 85% of the skeleton
Inorganic Minerals, composed of calcium and BONE
CANCELLOUS/ spongy bone, metabolically active (prone to osteoporotic
COMPOSITION provides compressional strength substance)
Calcium Salts (70%) phosphate TRABECULAR BONE fracture, specifically: hip, wrist, spine)
Osteogenic Cells stem cells, develop into osteoblasts
attach to the destroyed bones and then coat the bone with collagen, the calcium from the
Osteoblast forms bone tissue, bone building
blood will attach to form new bone tissue
BONE CELL Osteocyte mature bone cells, maintains bone tissue
TYPES Osteoclast
functions in resorption (destruction of bone matrix), bone crushing attach to old bones and release enzymes and acids that dissolve the bone
BONE REMODELING BONE RESORPTION bone resorption takes 4-5 times longer than bone absorption
CYCLE osteoblasts lay down collagen and mineral deposits over the area remodeled by osteoclass,
BONE FORMATION
this isinvital
released when there is a high calcium level in the blood, facilitates calcium deposition thefor maintaining
bone, reduces bone
calciummineral
uptake density
in the and bone
kidney, strength calcium in
normalizes
Calcitonin
low calcium levels in the blood, increases calcium uptake in the the blood
controls bone absorptive activity of osteoclasts, may cause osteoporosis if too much is
Parathyroid
intestines and kidneys, stimulates calcium release from the bone taken
HORMONAL Osteocytes slows down apoptosis (cell death) = decreases activation of bone remodelling
INFLUENCE Estrogen Osteoblasts slows down aopotosis, decreases oxidative stress = maintains bone formation
Osteoclasts increases apoptosis, decreases RANKL-induced differentiation = decreases bone resorption
Vitaminskeletal
systemic D/Calcitriol
diseases characterized by: increases calcium
low bone mass,absorption in the intestine, increases calcium reabsorption in theadvancedkidney, normalizes
age, female,calcium levels in the blood
white/asian
microarchitectural deterioration of bone tissue, increased bone NON-MODIFIABLE race, family
smoking, history ofcalcium
inadequate osteoporosis,
intake, inadequate vitamin D, low
fragility, RISK FACTORS
females are at susceptible
risk at a lowerto fracture
age than men MODIFIABLE personal history of
BMI, estrogen fragility fracture
deficiency, hypoganadism, chronic steroid
Dual-Energy X-ray golden standard for diagnosing therapyosteoporosis, scans bone
Central
Absorptiometry (DEXA) - T-Score results are only mineral density
applicable to of
thethe whole body
extremities scanned and is
DIAGNOSIS is used Peripheral
only used as a screening tool
X-ray used to rule out fractures and not for diagnosing osteoporosis in patients with bone loss
Primary due to post-menopause (decreased estrogen levels), senility (aging), and idiopathic causes
CLASSIFICATION
facultySecondary
process of bone due to diseases and other factors
• epiphyseal cartilage cells continue to be produced but don’t degenerate
mineralization, deficient or impaired Rickets
BONE SOFTENING • causes demineralization and softening • bones of stay soft and do not ossify
bones
OSTEOPOROSI metabolism of Vitamin D, Osteomalacia Etidronate• (Didronel),
similar
S Phosphate, and Calcium formation, used to normalize bone
Biphisphonates Ibandronate (Bonviva),
slows down rate of bone loss, turnover (taken with or without
calcitonin and increase bone eating, Cibacalcin (Human),
Calcitonin Pamidronate (Aredia),
Anti-resorptive Agents preserves bone mineral women that
formation, lack
given asendogenous
an intranasal Miacalcic estrogen,
(Salmon)
Esterified
density Estrogen estrogen as a result of menopause or
because of removal
the decreased level of Estradiol, Estropipate,
PHARMACOLOGIC Denosumab surgical of ovaries,
MANAGEMENT estrogen, RANKL enhances
promote bone formation, Teriparatide given as an injection Forteo
Anabolic Agents stimulate osteoblastic activity
more than osteoclastic activity Strontium given orally Protaxos
REHABILITATION
weight bearing exercises, coordination, balance, and proprioceptive exercises, postural awareness and proper body mechanics, fall precautions and techniques
MANAGEMENT
dose of calcium
1200 mg once a day
for women
following 60
is given Calcitonin
ascalcium in the
an intranasal Teriparatide
Estrogen
bone from
following the
contains Calcitonin
Compact
circulation
the in the
metabolically
only one that Trabecular
active part of can
the True
Whichhaveof the False
Strontium
following is a
diagnosing Risedronate
Z-score
Bisphosphonate
Which of the
osteoporosis T-score
Ibandronate
following
following is mayan
Estrogen
Calcium
anabolic
give rise agent
to
of vitamin D inif Estrogen
osteoporosis
Where is the
calcium Intestine
precursor of
estrogen in the Kidney
calcification
vitamin D located
What
the is the role
prevention of from bone
of RANKL
following siteinis
osteoporosis Hips bone
Activates
prone toin
softening Arms
Osteopenia
osteoporotic
adults due to
Myeloma
deficiency of
 RESPIRATORY DRUGS MECHANISM OF ACTION AR/SE DRUGS
common cold, seasonal allergies, and upper Drugs used to treat Respiratory Tract Irritation
from the and Control
upper Respiratory
respiratory tract Secretions (Strepsils Dry Cough)
and gastrointestinal
respiratory tract infections. ANTITUSSIVES • alpha-1–adrenergic agonists bind to alpha-1 receptors • antitussives may
located on the headache, dizziness, •(Flemex)**
Phenylephrine
upset
ACUTE AND MINOR • over-the-counter preparations DECONGESTANTS reduce
blood the ability of coughing to raise secretions. •(Dimetapp)**
Diphenhydramine
certainvessels of the
physiologic nasal mucosa
functions (gastricand stimulate
secretion, CNSvasoconstriction,
neural modulation), nervousness, nausea
PROBLEMS (nasal • different agents are combined drying dizziness, blurred •• Dimenhydrinate
ANTIHISTAMINES as wellup
asthe mucosal
various vasculature and
hypersensitivity decreasing nasal congestion
(allergic) inflammation
Pseudoephedrine
congestion, coughing, • a decongestant, an antitussive, and an combination with congestion,
other agentsmucosal
(e.g., antitussives, decongestants, vision, and of the (Dramamine)
• Ambroxol (Mucosolvan)
MUCOLYTICS • decrease nasal irritation and discharge (rhinitis, oral mucosa
allergies) expectorant may be combined and identified by bronchodilators). gastrointestinal Expectorant) (Robitussin)
(Ambrolex) (Strepsils
a specific trade name. • guaifenesin is the only expectorant (stomatitis), and
EXPECTORANTS upset (Flemex)**(Ventolin
• Certain antihistamines, may also have acknowledged by the FDA to have evidence of therapeutic effects.
Drugs used to maintain patency in expectorant)**
theObstructive
myocardium.Pulmonary Disease F UDV)**
• Chronic obstructive pulmonary disease BETA-ADRENERGIC cardiac irregularities,
• Inhalation--the drug is applied directly to the respiratory tract Salmeterol
CHRONIC AND (COPD). Asthma and COPD are characterized BRONCHODILATO AGONISTS
XANTHINE •• potent CNS stimulants → CNS- excitation nervousness, cardiac
restlessness, Theophylline (Nuelin SR)
drugs (formoterol, salmeterol) long-acting beta-adrenergic agonists. Terbutaline (Bricanyl)
SERIOUS AIRWAIY by bronchospasm, airway inflammation, RS DERIVATIVES • Theophylline enhances bronchodilation by inhibiting the can also be constipation,
arrhythmias and urinary
ANTICHOLINERGIC • these drugs Ipratropium (Atrovent)
OBSTRUCTIONS and mucous plugging of the airways. inflammatory response in bronchial muscosa, reducing retention, tachycardia,
DRUGS used to supplement treatment of moderate to severe asthma.bronchial administration. Tiotropium
Mometasone (Spiriva)
(bronchial asthma, • primary goals of drug treatment is to prevent GLUCOCORTICOIDS hyperresponsiveness by: reducing mucosal edema and mucus blurred vision,
retardation and
of growth
ANTI- and upper respiratory Cromolyn Nedocromil
Beclomethasone
chronic bronchitis, and or reverse the bronchial constriction and CROMONES/MAST •production,stabilize antigen-sensitive
decreasing local mast cells by reducing
generation calcium influxand
of prostaglandins and in children,(inhalation);
cataracts,
INFLAMMATORY passages (Tilade) Sodium
emphysema) subsequent obstruction of the airways in CELL STABILIZERS (glucocorticoids,
LEUOKOTRIENES subsequent releae of inflammatory
beta mediators
agonists) to provide optimal management in (Singulair)
AGENTS free of serious cromoglycate (example)
these disorders by using bronchodilators INHIBITORS specific patients with asthma and COPD. In particular, it appears that Zileuton (Zyflo)
RESPIRATORY
CHARACTERISTICS
characterized by: bronchial smooth-muscle spasm, airway inflammation, mucous plugging of TREATMENT/Tx
PROBLEM
the airways preferred drug: Glucocorticoids
leukotriene inhibitors, beta agonists, and theo-phylline can be used to
exaggerated bronchoconstrictor response of the airways to various stimuli
BRONCHIAL ASTHMA complex interaction between several different these cells release proinflammatory chemical supplement glucocorticoids as needed
mediators
the (e.g.:
chemicals leukotrienes,
irritate the bradykinin,
respiratory epithelium prolonged and excessive use of beta-2 agonists may ctually increase
cells (macrophages, neutrophils, eosinophils, histamine, and platelet activating factor)
and stimulate the contraction of bronchiole airway hyperresponsiveness, thus increasing the risk of attacks
platelets, and epithelial cells)
chronic bronchitis is a clinical diagnosis applied to a long-standing
smooth muscle inflamation of the bronchial goal of Tx: maintain patency and prevent airflow restriction
REVERSIBLE tree
BRONCHOSPASM IN emphysema is a pathologic condition marked by the destruction of alveolar walls and preferred drug: Anticholinergics
COPD enlargement of the terminal air spaces followed by bronchodilators - long acting B2 agonists
cystic fibrosis is one of the most common hereditary diseases that affects all the major
RESPIRATORY exocrine glands; resulting in very thick, viscuous secretions Tx goal: maintain airway patency
PROBLEMS IN CYSTIC mucous plugs obstruct various organs
FIBROSIS leads to pulmonary problems such as pneumonia, bronchiectasis, pulmonary fibrosis, and preferred drug: Bronchodilators and mucolytic and/or expectorant
various pulmonary infections drugs which may help limit the formation of mucous plugs
Survanta, exosurf - decreases surface tension of the lungs permitting alveoli to open readily
 ORAL ANTIDIABETIC AGENTS
peripheral tissues (Diabinese) Glimepiride
with hepatic & renal
SULFONYLUREAS production (gluconeogenesis) - (Amara)
impairments,
disturbances,onVitamin
multiple
BIGUANIDES increased
- increase insulin release
sensitivity helps
of peripheral Glipizide(Glucophage)
Metformin (Glipdin)
GI
B12disturbances,
deficiency;
ALPHA-GLUCOSIDASE Inhibit
tissues sugar
(muscle)breakdown
to insulin in the Acarbose (Glucobay)
increased AST edema,
disturbances, and ATL Pioglitazone
INHIBITORS intestines and delay
- increased glucose of
sensitivity Miglitol(Actos)
THAZOLIDINEDIONES levels
weight gain, fractures, Rosiglitazone
BENZOIC ACID peripheral tissues
other than site used tobyinsulin
sulfonylureas
DERIVATIVES/MEGLITINI -decrease
Stimulates insulinpressure
secretionand hepatotoxic, teratogenic; Repaglinide
Hypoglycemia Sitagliptin (NovoNorm)
(Januvia)
in blood respiratory tract Nateglinide
(Saxenda) (Starlix)
INCRETIN DESMIMETICS changes in lipid profile.
symptoms, headache, Exenatide (Byetta)
Sitagliptine - DPP4 inhibitor
TYPES OF DIABETES
TYPE I TYPE II (Non-Insulin DIAGNOSIS INSULIN THERAPY
effective as human insulin but with less
CHARACTERISTIC (Insulin-Dependent/Juvenile- Dependent/Adult- SYMPTOMS Analogue Insulin
Lipohypertrophy due to postprandial
leads to poorhyperglycemia andand
insulin absorption delayed
may
Onset) Onset) polyueria, polydipsia,
AGE AT ONSET Usually before 20 Usually after 30 repeated injections of insulin hypoglycemia
cause earlywith
associated postprandial
decreasedhyperglycemia
weight gain,
polyphagia,
Random weight
plasma loss
glucose Metformin (Glucophage)
TYPE OF ONSET Abrupt; often severe Gradual; usually subtle in the same area and/orinsulin
lower delayed hypoglycemia
dose, less hypoglycemia
Fasting>200mg/dl
plasma glucose Oralcombined withshould
medications insulinnot be abruptly discontinued when starting insulin
compared with insulin alone
BODY WEIGHT Normal Overweight
(75g) >126mg/dl
plasma glucose therapy because of the risk of rebound hyperglycemia
BLOOD INSULIN Markedly reduced Normal or increased Fasting glucose readings = titrate basal insulin
PERIPHERAL RESPONSE >200mg/dl, confirmed
caloric intake by
for at least
Normal Decreased HbA1C - amount Insulin can cause rapid reduction in blood glucose
TO INSULIN antidiabetics if diet 8 hours before of blood
blood
CLINICAL MANAGEMENT Insulin and diet sugar attched to
production secondary to control
by the alone tissue
peripheral is Insulin use does not mean that the patient has a severe disease
SUMMARY hemoglobin (6.5% or
autoimmune dysfunction in or reduced insulin above)
 ANTI-HYPERTENSIVE DRUGS - increase renal blood flow, vasodilation of blood vessels, prevention
Doxazocin of aldosterone
(Alfadil XL) secretion may cause reflex AR/SE RENIN-ANGIOTENSIN-ALDOSERONE SYSTEM
vasoconstriction, therefore vessels decrease sympathetic activity on the delivery of blood to other organ systems is
Terazocin (Hytrin) tachycardia asasthma,
well as
remain dilated =
vasodilation = decrease blood the heart and/or peripheral
reduce blood Labetalol
patients with compromised.
Renin As a response,
is an enzyme that travelsthe kidneythe
through willblood
produce
and
vasculature, lowers intravascular Benazepril (Lotensin)Prazocin (Minipress) orthostatic
and hypotension
depression of heart headache,
pressure, reduces heart rate, used to prevents
volume, conversion of Bisoprolol (Bisoten) dizziness, converts angiotensinogen
travels through the lungs, thein the liver into Iangiotensin
antiotensin is I Increases blood pressure and prevents
ACE INHIBITORS Captopril (Capoten) rate
may and
causemyocardial
a persistent dry further blood loss
Angiotensin Valsartan (Diovan) excretion,
converted and water retention therefore increases
BLOCKERS - ACE is a nonspecific the effects ofI Angiotensin
to Angiotensin II the
II on Ennalapril (Hypace) cough
and to angiotensin II in the lungs through the
DIURETICS - decrease bloodwith itvasculature
water fromand yourvarious
blood, other e Candesartan
(Micardis plus) electrolyte imbalance such orthostatic blood volume, (3) facilitates the release of
enzyme, preferrable for patients
volume, decrease cardiac output = - decreasing the amount of fluid Furosemide Olmesartan
Hydrochlorothiazide Aldosterone from the adrenal gland, this is also a
CALCIUM CHANNEL BLOCKERS Verapamil (Isoptin)+ Quinapril as sodium
may causedepletion
reflex hypotension
decrease bood pressure myocardial and vascular smooth-
facilitates vasodilation
Ticlodipine = decreases flowing through your veins and
– for secondary
(Lasix) (Accuzide)
Amlodipine (Norvasc) (hyponatremia)
tachycardia and as
as well
muscle cells causing
Epinephrine it to
- drug of relax,for
choice Clonidine - centrally acting anti-hypertensive drug that Ezetimibehypotension
- anti-lipid drug acts in the
blood pressure
prevention of Felodipine (PLendil) orthostatic
ventricular fibrillation reduces sympathetic nervous system activity intestine
thrombotic stroke intolerant of Aspirin ANTI-HYPERLIPIDEMIA AR/SE CHOLESTEROL SYNTHESIS GOOD CHOLESTEROL BAD CHOLESTEROL
disease and stroke
• Decrease bile acid absorption and increase LDL receptors on hepatocytes HMG-CoA reductase = facilitates eventual production the body of excess cholesterol by
STRATEGIES IN MANAGEMENT steps of cholesterol synthesis), VLDL - produced in the liver
HMG-CoA REDUCTASE • Increase lipoprotein lipase activity to increase peripheral clearance
Lovastatinof lipoproteins Increase serum transaminases, muscle of cholesterol absorbing it and carrying it back to the
decreasing cholesterol synthesis and released in to the bloodstream to supply body
INHIBITORS (statins) increases LDL receptors on Pravastatin tenderness, myopathy vessel and remains there
BILE ACID SEQUESTRANTS in the liver, decrease LDL, Cholestyramine vasoconstriction = reduces blood volume and flow,
hepatocytes, decrease LDL, Constipation, flatulence (utot)
FIBRIC ACID (resins)
DERIVATIVES -increase
decrease LDL, increase HDL. Colestipol
Clofibrate increases blood=pressure
vasocdilation increases blood volume and flow, Platelet aggregation: The clumping
HDL, decrease Flushing, rash, itchiness embolism - clot that travels from the site
(Fibrates) decrease triglycerides
decrease triglycerides Benzafibrate reduces vlood pressure together of platelets in the blood.
NICOTINIC ACID Niacin Flushing, rash, itchiness
- Least
DRUGS DIRECTED TO BLOOD FLOW • Action against Factor Xa AR/SE
clotting factors; used primarily to
ANTICOAGULANTS –Aspirin
Warfarin (Coumadin)
(blood-thinner)
prevent and
ANTITHROMBOTICS OR ANTI- platelet-induced clotting; used treat venous
• Action against vitamin K(Plavix)
Clopidogrel dependent clotting increased risk of bleeding
PLATELET AGGREGANTS dissolution
primarily to of clots, emergency
prevent arterial Alteplase (Actilyse)
THROMBOLYTICS treatment of arterial thrombosis Dypiridamole
Streptokinase (Streptokin)
CARDIAC DRUGS Urokinase AR/SE
by inhibiting activity ofDRUG
enzymeUSED IN CONGESTIVE HEART FAILURE (CHF)
DIGITALIS ATPase
amount of that controls
blood the to the
returning Digoxin (Lanoxin) CHF such as diuretics, calcium channel
Nitrates Headache, nausea, dizziness, vomiting,
movement of calcium, blockers, ACE
VASODILATORS heart (cardiac preload)sodium
and and (isosorbide inhibitors, beta blockers, angiotensin
diarrhea
decreases the pressure the heart dinitrate)
Releases nitric oxide leading to DRUGS FOR ANGINA PECTORIS
Nitroglycerin headache, dizziness, and orthostatic
ORGANIC NITRATES dilation of coronary arteries,
Isosorbide dinitrate (Isordil, Isoket) hypotension
myocardial muscle relaxation
 DRUGS FOR
PARKINSON'S DISEASE DOPAMINE
impaired balance PARKINSON'S
REPLACEMENT
DOPA
- caused
coordination by a decrease
of motor movement, in
THERAPY
DECARBOXYLASE
(Basal
inhibitsGanglia) Substantia
acetlycholine releaseNigra:
dopamine producing cells, inhibits (DDC) INHIBITORS
DOPAMINE AGONISTS
coordination of motor movement,
unwanted
increase motor activities
in acetylcholine production ANTICHOLINERGICS
since dopamine itself cannot cross
(muscles become too excited = NMDA RECEPTOR
the blood-brain
Treatments: barrier, L-DOPA
medications is
to increae MONOAMINE OXIDASE
ANTAGONIST
converted
dopamine in to the
dopamine INSIDE(deep
brain, surgery the TYPE B (MAO-B)
CATECHOL-O-
Rehabilitation:
brain stimulation)improve strength, INHIBITORS
METHYLTRANSFERASE
coordination, balance, endurance
(COMT) INHIBITORS
EPILEPSY between
Glutamate - messenger CATEGORY
pre-synaptic and post-synaptic ion-channel modulator
before starting a PT session
neuron ion-channel modulator
transmission - enhance
inhibitory
inhibitors of excitatory
neurotransmission -
modulators of pre-
reduce excitatory
synaptic machinery
ion-channel modulator

ion-channel modulator
resolve dopamine MOA deficiency by DRUGS
brain)
being converted to dopamine of
prevent peripheral conversion Levodopa + Benserazide
Carbidopa (Madopar)
after
L-DOPA into dopamine bybarrier
crossing blood-brain
Cabergoline
Benserazide
directly
inhibitingstimulate
(DOPA)dopamine
decarboxylase
inhibit excessive
receptors in basalacetylcholine
ganglia BiperidenPergolide
(Akidin) (Apiden)
influence caused by dopamine Pramipexole (Ramipex)
Diphenhydramine* (Sifrol)
(Benadryl)
-deficiency
Unclear: said to increase Trihexyphenidyl (Artane)
down dopamine in the basal Amantadine (PK-Merz)
release of dopamine and to
ganglia; enables dopamine to Entacapone (Comtan)
the brain.
remain active for longer periods Tolcapone
- Useful as an adjunct to

MOA EFFECT ON NEURONAL TRANSMISSION

sodium channel blockade (fast
Slowed recovery from inactivated state
inactivation)
calcium channel blockade post-synaptic inhibitory action
GABA agonism/potentiation inhibitory activity by permitting hyperpolarization
NMDA (N-methyl-d-aspartate)
receptor blockade
AMPA receptor blockade decreased excitatory synaptic activity
SV2a (synaptic vesicle protein 2a)
sodium vesicle
channelinhibition
blockade (slow recovery of neurons from prolonged
inactivation) depolarization
potassium channel blockade
potassium channel activation
 AR/SE
Cardiovascular: orthostatic hypotension (postural
movements
hypotension), ofcardiac
the face, arms, legs or trunk.
arrhythmias.
They are often fluid and
Cardiovascular: orthostatic dance-like, but they
hypotension may
(postural
also cause
hypotension),rapid jerking or slow
cardiac arrhythmias. and extended
(including exacerbation of pre-existing psychotic
Psychiatric
symptoms, symptoms (especially
disorientation, the memory
confusion, elderly)
insomnia, anxiety, nightmares, inability to
impairment,
concentrate,visual
mood hallucinations, nervousness,
changes, psychotic reactions,
psychosis, hallucinations,
hallucinations, confusion, agitation, nausea,
palpitations,
dizziness, nightmares,
vomiting, diarrhea, insomnia,dry
constipation, hallucinations,
mouth, sore
confusion, fatigue, increased sweating,
behavioral disturbances; urine, skin, hair, beard
FIRST-GEN
Phenytoin AEDs
(Dilantin) SECOND/THIRD-GEN AEDs
Oxcarbazepine
Carbamazepine (Tegretol) Valproate Zonisamide (T-type)
Lamotrigine
(Depakene)
Ethosuximide (T-type) Valproate Gabapentin (Neurontin)
Benzodiazepines
Topiramate
Lamotrigine
Barbiturates
Vigabatrin
Valproate Felbamate
Topiramate
Levetiracetam
Lacosamide
Oxcarbazepine Topiramate
 AEDs UNDER
AR/SE
DEVELOPMENT hyponatremia Vigabatrin:
visual field loss Phenytoin
Retigabine and Lamotrigine: double vision
Neurosteroids Phenytoin: gingival hyperplasia and hirsutism
Topiramate
sedation, and Zonisamide: cognitive problems
Seletracetam diziness Topiramate: weight loss
Brivaracetam Valproic acid, Gabapentin and
Pregabalin: weight gain
Gabapentin and Pregabalin: peripheral edema
Retigabine Valproic acid and Felbamate: liver toxicity
 (according to the
SYMPTOMS
Diagnostic andbehave
feel, think, and Statistic
weight gain
and can lead to a variety
of emotional and
norepinephrine, • Anxiety, agitation or
dopamine (increased restlessness
• Slowed thinking, speaking or body
movements
• Feelings of worthlessness or guilt,
fixating on past failures or self-blame

unusual shifts in mood, energy,

BIPOLAR DISORDER activity levels, concentration, and
ability to carry out day-to-day tasks

SCHIZOPHRENIA SYMPTOMS
the patient’s thoughts
with
causeda patient’s ability toof
by overactivity
participate in
hallucinations, social
• Negative: social withdrawal,
events and tospeech
disorganized foster or
emotional flattening, anhedonia,
deficits)
behavior,and andcognitive
impaired disturbance in the thought process
symptoms,
symptoms, such such as as (bizarre delusions, auditory
multiple factors,
suspiciousness, hallucinations), decreased level of
including genetic function in work, social relations and
susceptibility and
substances from the bloodstream
Blood Brain Barrier
from
has entering
a higher the CNS despite
concentration in the
Acetylcholine
movement of the trunk cerebral cortex
and extremities. Upon Tardive dyskinesia
associated
consultationwithwiththetheuse EPS
of antipsychotic
Primary neurochemical Increased dopamine activity
change
delusions in and
schizophrenia
auditory
characterized Schizophrenia
hallucinations by marked
along
thought disturbance and Psychosis
management of mood
an impaired perception Lithium
swings in bipolar
Major problem with
Antidepressant that Sedation
tricyclic antidepressants Second-generation
have a lower
synapses andsidehelpeffect antidepressants
profile
remove TRUE
chemicalreleased
structure and
transmitters through
work by blocking the TRUE
hormone
reuptake of that play a role
amine Cortisol
in the pathogenesis of
Neurotransmitter(s) Serotonin, Norepinephrine,
Most prevalent
affected mental
in depression Dopamine
illness in the US and the Depression
Which
world. neurotransmitter Acetylcholine
has
that afunction
excitatory effect
to prevent
Blood Brain Barrier
certain substances from
 ANTI-DEPRESSANT DRUGS - enhance stimulation of post & presynaptic
SYMPTOMS
activities. receptors
DRUGS FOR DEPRESSION
SSRIs, but their more troublesome
- blocks
side-effects lead toreuptake
patients of
being
norepinephrine and other
Depression can affect
monoamines
INHIBITORS to decrease
(MAOIs) -receptor
have
people of any age,
sensitivity
dangerous interactions with some
including children.
However, clinical foods and ATYPICAL
drugs, and should be
Manic - talking
depression symptoms,
excessively, racing
thoughts, hostility, less
sleep, delusions LITHIUM
Depression - extreme
fatigue, prolonged
sadness

ANTI-PSYCHOTIC
DRUGS - block central
ANTIPSYCHOTICS (D2 MOA
dopamine receptors block the release of dopamine and are
ANTAGONISTS) -
associated with higher risk of
tendency to bind to other
extrapyramidal
associated withsymptoms (EPS)
lower risk of
CNS dopamine receptors
PSYCHOTICS) - more
extrapyramidal symptoms (EPS) but
selectove to certain
with higher risk of metabolic side
dopamine receptor
effects
drug-induced psychosis risk is very high with drugs that increase synaptic dopamine availability
UGS - enhance stimulation of post & presynaptic
MOA
receptors
UGS FOR DEPRESSION
remain in the synaptic cleft)
- mainstay for treatment of depression
- three-ring structure
better tolerated and are safer in
inhibit serotonin reuptake in
overdose than other classes of
SEROTONIN-NOREPINEPHRINE synaptic cleft →reuptake
norepinephrine ↑ serotonin
in levels
antidepressants and should be
RE-UPTAKE INHIBITORS (SNRIs) synaptic cleft → ↑ serotonin and
Selective α2-adrenergic antagonist → ↑ serotonin and norepinephrine -
release 5-HT2 and 5-HT3 receptor antagonists → ↑ effect of serotonin on
free 5- HT1
inhibits certainreceptor → likely
enzymes causes neuronal
to decrease antidepressant effects
excitation and desentization
decrease release of norepinephrine and dopamine and increase effects of
serotonin acetylcholine and GABA
can accumulate in the body and reach toxic levels
monovalent cation that competes with Na, Ca, and Potassium in
can stabilizeneural
influencing neuronal excitability by decreasing sensitivity of certain
excitability
postsynaptic receptors and uncoupling these receptors from their
subcellular second messenger systems
DRUGS
NEUROLEPTICS Haloperidol - high
CONVENTIONAL/TYPICAL Perphenazine
ANTIPSYCHOTICS Prochlorperazine - high
5-HT2A/D2 ANTAGONISTS Iloperidone
SEROTONIN-DOPAMINE Lurasidone
ANTAGONISTS Olanzapine - 5-HT2C, H1
1. Cocaine
2. Amphetamines (shabu)
at increase synaptic dopamine availability
3. L-dopa (levodopa)
 DRUGS AR/SE
- mostly are liver-metabolized and renally excreted
anticholinergic activity (dry
Doxepin
- mainstay for treatment of depression
FluvoxamineImipramine mouth, constipation, urinary sexual desire and other
retention, tachychardia sexual problems, such as
Paroxetine
Duloxetine erectile dysfunction and
Sertraline - has been shown to be
Levomilnacipran and induce a hypertensive decreased orgasm, fatigue
Phenelzine Milnacipran
crisis, has drug interactions and drowsiness, insomnia,
Selegiline
Nefazodone dry mouth, blurred vision,
with tyramin-containing
Trazodone. constipation, orthostatic
Mild: free hand tremor, GI upset, uscle weakness,
fatigue, problems with memory and concentration
Lithium (Eskalith) (Lithobid) Moderate: confusion, lethargy, ataxia, dysarthria,
nsytagmus, emesis, increased deep tendon reflexes,
increased tremor, muscle
Severe: choreoathetoid fasciculations
movements, seizures,
respiratory complications, coma, death

sedation and anticholinergic effects
AR/SE
extrapyramidal symptoms,
orthostatic hypotension,
prolonged QT interval,
sedation, seizures, sexual
dysfunction, hyperglycemia,
weight gain, anticholinergic
effects, dyslipidemia,
hyperprolactinemia
 CHEMOTHERAPY DRUGS damage the MOA DNA of DRUGS
ALKYLATING de Dacarbazine
cancer
normal cells to keepof
metabolism
AGENTS
ANTIMETABOLIT Ifosfamide
mercaptopurine,
them from multiplying
cells, which make
ES Doxorubicin
Cytarabine
Antineoplastic - ANTHRACYCLINE DNA cancerduring
cells the
stopcell
multiplying, stop your Epirubicin
Paclitaxel
blocks the formation S cycle, bind with DNA
Cytotoxic - kill cells, of MITOTIC
body from making the Idarubicin
INHIBITORS attack enzymes that
which is one reason TOPOISOMERAS proteins thatcells
cancer anti-tumor
Vinca
help cancer Mitoxantrone
chemotherapy has such EANTI-TUMOR
INHIBITORS the cell cycle, which antibiotic)
divide and grow (also acts as an
severe side effects ANTIBIOTICS binds with DNA so it
anti-tumor
Dectinomycin
not a
A. c. 6 c.
chemotherapy drug
antineoplastic cells,
C. mercaptopurin
isoprinosine
except: glucocorticoids
immunosuppressan
D. c. d. vinblastine
daclizumab
ts
chemotherapy c. vincristine d. all
A. will stop cancer c.
drugs d.
B. cells from levamisole c.
drug/s and
multiplying
C. methotrexated.and colony
immunosuppressan
chemotherapy c.
E. cyclophosphamide
drugs
given in leukemia, chlorambucil c.
B.
except
Chemotherapy vincristine
c. Carmustine
A. Peripheral
drugs, except
Adverse effects of d. neuropathy
A. Enhance the C. Liver, kidney, heart
chemotherapy Glucocorticoids.
C. immune response prob d. AOTC.
rejection
except of C. D.
A stimulate C.
transplanted Interleukins.
C production of Bacillus Calmette
Cyclosporine.
For autoimmune
antibodies against Guerin.
C C. Glucocorticoids.
Given in systemic Steroids.
orders
D. lupus D.
C. Azathioprine.
erythematosus D.

AR/SE
vomiting, diarrhea, hair
loss, fatigue, fever, mouth
sores, pain, constipation,
easy bruising, bleeding,
nerve damage (peripheral
neuropathy), liver and
kidney problems, heart
problems, infertility, kidney
IMMUNODILATORS - modify the response of the immune system by
increasing (immunostimulators) or decreasing (immunosuppressives)
Imiquimod
tumors,ofprimary
the production serum or
antibodies Resiquimod
IMMUNOSTIMULANTS inhibitors
IMMUNOSUPPRESSA treat secondary
autoimmune diseases Isopronosine
IL-1
NTS such as pemphigus, lupus,
and IL-2
 As of July 15, 2021

first line of drug for

PARACETAMOL some experts raise
symptomatic treatment
IBUPROFEN concerns with the use of
Dexamethasone,
this drug helps prevent cytokine
CORTICOSTEROIDS Prednisone,
storm
TOCILIZUMAB Methylprednisolone
doses are given to
ANTICOAGULANTS stops blood from clotting hospitalized patients
REMDESIVIR rather than high doses
LOPINAVIR/
RITONAVIR
HYDROXYCHLOROQUI
do not recommend majority of the studies
NE
IVERMECTIN inconclusive in ivermectin are still in
phase 2&3
 strong
recommendation:
severe COVID case

evidence is very low

2021: not a