Pharmacology: Units 1-5
Unit 1: Introduction to Pharmacology
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Targeted Drug Discovery: The researcher knows that target molecule that they want to affect,
and then finds or creates a compound that would work on that target molecule.
Phonotypical Drug Discovery: The target molecule is not known however, the researchers know
what the final effect should be.
FDA: Food and Drug Administration approves all new prescription drugs. 15 years for a drug to
reach the market. First tested on cells inn cultures, then on animals, then phase one on humans
(given to healthy individuals-acute affects/toxicity are tested here), phase two the drug is given
to individuals with the target disease (small sample size), phase three the drug is given to a large
sample size of individuals with the targeted disease.
Chronic care model: treats symptoms only, unable to cure the actual cause
Unit 2: Pharmacokinetics
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Pharmacokinetics: The study of factors that are involved in getting the drug to its target body
Pharmacodynamics: The study of mechanism of the action of the drug, the therapeutic and
toxicological effects, and the chemical structure-activity relationship.
Absorption: The ability of the drug to enter the blood stream (usually from the GI tract
ENTERAL) (Parenteral administration –non alimentary routes such as IV or through respiratory
system)
o Influence in the rate of absorption by: route of administration, dosage forms, circulation
at the site of absorption, and concentration of the drug.
o Most common way drugs pass through the GI and enter blood stream is through simple
diffusion (rate of transfer is directly proportional to the concentration gradient across
the membrane)
o More lipid soluble the faster the drug will pass through the membrane
o Active transport: solute crosses the membrane against the concentration gradient and
requires ATP to pass across the membrane. (Small percentage occurs this way)
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Distribution: the movement of the drug throughout the body to various tissues.
o Vd= amount of drug administered/concentration of drug in plasma, if the Vd is low then
the drug is being retained in the bloodstream, if the Vd is high then the drug is being
concentrated in the tissues
o Rate of blood flow severely limits the distribution of the drug
Biotransformation: the chemical alteration of the drug.
o Mostly occurs in the liver
o Chemical alterations that take place in the liver which are responsible for
biotransformation: oxidation, reduction, hydrolysis, conjugation
Excretion or Elimination: the ability of the body to remove the drug and its products.
o Liver is the primary site for drug excretion
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GI tract and lungs may act as sites for drug elimination
If the drug is administered faster than it is eliminated, the drug will accumulate in the
body and reach toxic levels
o Clearance and half life are used to indicate the rate at which a drug is eliminated
Drug concentrations are usually measured by the plasma levels.
Drug storage sites: Adipose tissue-primary site for storage, Bone- stores heavy metals and
toxins, Muscles- muscle cells in particular, Organs- The liver and kidney
Albumin is the principal circulating protein that binds drugs non-specifically (Albumin levels
decline with age thus more free active drugs in the blood stream as one ages)
Changes noted in distribution of a drug as a person ages: decrease in lean muscle mass, increase
in total body fat, decrease on body water, changes in albumin concentrations
Clearance is the ability of organs, specifically the kidneys to eliminate drugs
Creatinine clearance rates are used to determine if a patient has a renal problem of
Half life of a drug is defined as the amount of time required for 50% of the drug remaining in the
body to be eliminated or inactivated
Module 3: Pharmacodynamics
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The cellular endpoint is the final effect that the drug was intended to have
Efficacy: the ability of a drug to initiate a response subsequent to binding to its target
When comparing two drugs, the drug that reached the greatest magnitude, on the Y axis of the
dose response curve is the drug that is considered the most efficacious
Potency- is the dose of the drug that produces a given response ( lowest value for a given effect
on the X axis)
ED50 or TD50= the dose of the drug at which 50% of the people resort that they had a positive
response to the drug
LD50= lethal dose of a drug also known as the toxic dose , this the known as the level and or the
dose of the drug in which 50% of the animals tested die
Therapeutic index(TI)= The ratio of LD 50/ED50 this is calculated as the dose required to
produce toxic effects divided by the dose required to achieve the desired therapeutic effects.
The attraction and binding of a drug to a receptor is called the association while the removal is
called the disassociation
A drug with high affinity binds readily to the receptor, even if the concentration of a drug is low
Ka and Kd are not good indicators of drug efficacy
Selectivity= how much affinity an agonist has on one receptor versus another
Nonselective binding- a drug will bind to any receptor
Ligand- compound that binds to a receptor
Ligand that is an angonist will bind to a receptor and activate it while a ligand that is an
antagonist will bind to a receptor and deactivate it (inhibit it form becoming active)
Whooping cough and cholera are disease of G proteins---- don’t need to remember G protein
pathway
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Tyrosine Kinase Receptor- plasma membrane receptor that transmits the signal into the
membrane of the cell (can cross multiple times)
Channel receptors- FAST no signaling cascade, this is typical in the nervous system
Intracellular Receptors- hormones induce a slow response, in order for a drug to bind to an
intracellular receptor it must either be lipid soluble so that it can diffuse through the membrane,
or it must have a specific transporter within the plasma membrane that carries the drug
molecule into the cell
Nuclear Receptors- targeted specifically to the nucleus, slower and graded response (hormones
usually use this receptors)
Desensitization- rapid decrease in responsiveness of a cell to a drug
Down regulation – slower process and involves reduction of a number of receptors on the
membrane
Module 4: Neurological Pharmacology
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Neurotransmitters:
o Acetylcholine: Important in the basal ganglia which controls movement and is
implicated in Alzheimer’s disease
o Monoamines: Dopamine, histamine, nor epinephrine, serotonin, loss of dopamine is
associated with Parkinson’s disease; serotonin may be involved in temperature
regulation, sensory perception, sleep control, and mood changes.
o Nitric Oxide: transmitter of the GI tract smooth muscle cells and the neurotransmitter
in the central nervous system.
o Peptides: Substance P, Neurotensin, Endorphin, Bradykinin, Vasopression, Dynorphin,
Neuropeptides may act as neurotransmitters or hormones. Neurpeptodes are usually
inactive until they are cleaved, their actions are long lasting. Peptides modulate pain
perception, regulate temperature, and stimulate contraction of the smooth muscle cells
of the gut.
o Amino Acids: Glycine, Aminobutyric Acids, GABA, Glutamate, Asparate,
Glycine is the simplest amino acid and is an inhibitory neurotransmitter released by
interneurons in the spinal cord, GABA is produced from glutamate and is the most
common transmitter of the brain, it is an inhibitory transmitter, Glutamate and
Aspartate strongly excite the neurons in the brain.
Cholinesterase Inhibitors (Aricept, Exelon, Reminyl) – Used for treatment of Alzheimer’s
disease, prevents the breakdown of acetylcholine, memory and reasoning
Memantine- used for Alzheimer’s disease , binds to neurotransmitter glutamate, antagonist of
the NMDA receptor on post synaptic neurons , may be neuro- protective
Betaseron-Multiple Sclerosis, inhibits the immune system from attacking itself, sloes
progression of the disease and decreases silent lesions
Novantrone: immunosupressor, blocks immune system from attacking itself, can only take this
drug for three years
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Leva-Dopa /Carbidopa –Parkinson’s Disease, chemically modified molecule of dopamine which
can cross the blood brain barrier where it is then converted into dopamine, given in very high
doses , usually given together to decrease the amount of breakdown that might occur
Sinemet-Parkinsons Disease, combined drug of Leva-Dopa and Carbidopa, allows more
dopamine to reach the brain
Amantadine- Parkinsons Disease , facilitates the endogenous release of dopamine
Rasagiline- Parkinsons Disease, antioxidant drug which prevents the breakdown of dopamine by
inhibiting monoamine oxidase
Seligiline- Parkinson’s Disease, antioxidant drug which prevents the breakdown of dopamine
Lithium- Bipolar Disorder, an ion that directly decreases the release of amine neurotransmitters
and increases their reuptake
Depakote-Bipolar disorder, anticonvulsant, most helpful during manic phases
Thioxanthenes, Phenothiazines, Butyrophenones(Haldol)- Anti-psychotic drugs, block the
central dopamine receptors
Serotonine reuptake inhibitors ( Luvox, Prozac, Zoloft)- block the reuptake of the
neurotransmitter serotonin
Trycyclic Antidepressants: effect the concentration of both serotonin and nor epinephrine
Nonbenzodiazepines (Ambien, Estorra, Indiplon)- Insomnia, effects the benzodiazepines
receptor
MOI Inhibitors- Antidepressants , cause the receptors to become down regulated, acts on
enzymes that normally degrade the amine neurotransmitter
Paxil- Antidepressant, serotonin reuptake inhibitor
Carbamazepine- Epilepsy
Vigabatrin- Epilepsy, enhances the effects of GABA
Valporic Acid – Epilepsy, blocks high frequency brain activity
Ethosuximide- Epilepdy, acts on calcium, sodium, and potassium channels
Barbiturates (Lyrica)- Epilepsy, decreases GABA function
Benzodiazepines (Diazepam, Valium, Klonopin)- Epilepsy, works on GABA, hyperpolarizes the
neuronal membrane
Dilantin- Epilepsy, interferes with the movement of sodium across the membrane, stabilizes the
membrane of the neuron , decreases the potassium and calcium movement
Unit 5: Cardiovascular
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Parasympathetic- rest digest, Sympathetic- fight or flight
Beta Blockers( Labetolol, Corgard, Inderal, Zebeta) –treats angina, hypertension, cardiac
arythmias, slows heart rate and decreases force of contraction, binds to the beta andregenic
receptors THIS DRUG HAS NEGETIVE EFFECTS ON GLUOSE/INSULIN
STATINS(Lipitor, Crestor, Zocor, Lovastatin, Cauduet)-inhibits cholesterol biosynthesis,
decreases LDL and increases HDL
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Asprin( Anti Platelet Drug)- Works through the arachodonic pathway to clock production of
thromboxine, blood thinning effects last for 1 week
Heparin (Anti-coagulant)- inhibits clot formation, binds all free calcium in blood
Nitroglycerin- treats angina pectoris, dilates coronary arteries, prevents ischemia, minimize left
ventricle remolding, reduces mortality in patients with acute heart attacks
Diuretics- LOOP=BUMEX AND LASIX works on ascending limb of the loop of henle,
THIAZIDE=DIURIL, K+ SPARING= ALDACTONE both thiazides and K+ work on distal tubule – all
treat hypertension due to a decrease in blood volume then a decrease in peripheral resistance
Angiotension-Converting enzyme inhibitor ACE( Lotensin, Vasotec, Altace, Avapro)antihypertensive drugs, they decrease blood pressure, decreases pheriperal resistance and
indirectly allows an increase in cardiac output
Thrombolytic Agents ( Activase, TPA, Streptokinase)-facilitates the breakdown of clots, usually
given 3-6 hours after incident
Digitalis(Digoxin)- used to treat heart failure patients, increases myocardial contractility by
inhibiting the NA/K+ pump in cardiac cells, thus increasing calcium and increasing contractility,
given a very low dose because it can become toxic.
Alpha 1 blocker( Cardura)- decrease blood pressure and increases blood flow, very potent and
dramatically decreases blood pressure, decreases insulin resistance and improves glucose
tolerance, decrease serum triglycerides
Bile Acid Sequestrants (Questran)- promotes the excretion of bile acid, lowers LDL, has no
effect on HDL
Fibric Acid Derivatives- treats high triglycerides levels, decreases LDL and triglycerides as well as
raises HDL
Nicotonic Acid ( Niacin B3,Niaspan) – Lowers LDL and increases HDL, increases plasma glucose
levels and decreases glucose tolerance
Anti-Dysarhthymia Drugs ( Sodium Channel Blockers= Norpace, Tambocor, Quinidine) (
Potassium Channel Blockers= Cordarone, Amidarone) ( Calcium Channel Blockers) These drugs
treat dysrthymias, these drugs alter membrane potentials of cells, decrease membranes
automatically, slow impulse conduction through myocardium thus prolonging refractory
periods
Calcium Channel Blockers ( Cardizeum, Procardia, Verapamil, Diltiazem)- treats moderate
hypertension, decreases resting and contraction concentration, decreases tone of artery,
prevents and resolves remodeling of arteries, inhibits plaque formation, decreases contractility
of the heart, can cause severe hypotension
Module 6: GI Pharmacology
 The primary function of the GI tract is the absorption and elimination of fluids and nutrients
from the diet, separating useful nutritional factors from potential toxins. Many different disease
processes act upon the gut, but the symptoms and clinical effects are often similar and not
specific to any disorder
o Antacids (Maalox, Mylanta, Phillips, Rolaids, Tums)
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Antacids attempt to neutralize excess stomach acid in the case of heartburn or
acid reflux. They are taken by mouth. These drugs typically contain a base such
as carbonate with aluminum, magnesium, or calcium. Some types of antacids
also contain additional drugs to relieve excess gas.
 Antacids are frequently used to treat minor GI discomfort after overeating or
eating foods that are not appropriate for the person.
 A common problem with the antacids is feedback to the body that acid in the
stomach is too low, thus the body produces more acid to accommodate. This
situation does not present a problem while the antacid is in the body, but will
create a negative environment when the antacid is passed from the GI tract.
o H2 Receptor Antagonists (Tagament, Pepcid AC, Zantac)
 Works to decrease the amount of acid in the stomach. Histamine is a major
regulator of acid secretion in the stomach. The binding of histamine to its
receptor activates a cellular proton pump that releases HCl into the stomach.
The exact subtype of histamine receptor in the stomach is the H2 receptor.
Thus, an H2 antagonist will prevent the histamine-activated release of acid
under resting conditions and during stimulation with food.
o Proton-Pump Inhibitors (Prilosec, Prevacid, Nexium)
 They block the hydrogen pump producing stomach acid. PPIs are more effective
in reducing acid (up to 90% reduction) than H2 blockers, but they are also more
expensive.
 Possess antibacterial effects against helicobacter pylori infection.
o Antibiotics
 The most common antibiotics prescribed for peptic ulcers are metronidazole,
tetracycline, clarithromycin, amoxicillin.
 In general, antibiotics are only known by their generic name.
o Acetylcholine M1 Receptor Antagonists (Pirenzepine/ Gastrozepin)
 They work by blocking the M1 subtype of muscarinic receptors.
 Laxatives
o Laxatives are prescribed to promote elimination from the bowel and defecation
 Bulk Forming Laxatives (Methylcellulose/Citrucell, Metamucil)
 These drugs absorb water and swell within the lower GI tract. The
increased size of the compounds stretches the bowel, and stimulates
peristalsis.
 Stimulant Laxatives (Ex-Lax, Dulcolax)
 They increase fluid accumulation in the small intestines. They should be
taken if the bowel is full, but the person feels that they can’t empty it.
Also, these drugs should be prescribed when a bulk-forming laxative is
inappropriate.
 Hyperosmotic Laxatives (Epsom Salt, Phillips Milk of Magnesia)
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Osmotically active substances produce a gradient that draws water into
the bowel and small intestines. This gradient increases fluid content and
stimulates excretion.
 Lubricants and Stool Softeners (Colace, Doxidan)
 Products like mineral oil bring water into the fecal mass, thus softening
the stool and permitting easier elimination. They are used on a shortterm basis to relieve constipation. A stool softener is usually taken
before bedtime, with the anticipated result occurring in the morning.
They work best if the person drinks a lot of water. Side effects are
uncommon, but include stomach cramps.
 Antidiarrheal Agents
o Stool Thickeners (Kaplin, Pectin)
 Prolonged use will be dangerous, as the bacteria that are inhibited by stool
thickeners are also necessary for normal digestion. Thus, they should not be
taken for more than 2 days.
o Bulking Drugs
 Bulking agents thicken the stool. They tend to be made of natural fibers from
seed that form a gelatin when inside the GI tract. Bulking agents are just high
doses of fiber, which you would normally get in the diet, so they are relatively
safe, even for children. Metamucil is a common example of a bulking agent.
o Anti-Spasmodic Drug (Imodium)
 They are thought to produce a local effect directly on the gut wall. By slowing
down the speed at which the bowel travels through the intestines, more water
can be absorbed from the stool producing fewer and firmer stools. These
medications should not be taken for more than 3 days and should relieve all
diarrhea by that time. These drugs should not be given to children. Side effects
include nausea, abdominal pain and distention, dry mouth, constipation,
drowsiness, fatigue and dizziness.
Module 7: Musculoskeletal Pharmacology
 Analgesics – pain relief
o Opioids
 Provided euphoria and depress respiration (rate)
 Enkephalins and endorphins also bind to opiate receptors
 Opioid peptides are widely distributed throughout the CNS and GI tract
 Synthesized and stored in neurons
 Tolerance = effectiveness of drug decreases overtime if taken for an extended
period of time
 Classic problem when taking opioids
 Develops in first dose with opioids but is not clinical until after 2-3
weeks
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Cross-tolerance – May develop tolerance to other opoids even if you are
taking a different one
 Theories:
o Down-regulation (less receptors) – need to take more drug for
the same effect (should switch to a different drug instead of
increase the amount taken of the current drug)
 Physical dependence = will have withdrawal syndrome if they suddenly stop
taking the drug (lacrimation, rhinorrhea, yawning, sweating, gooseflesh, chills,
diarrhea, nausea)
 Accompanies tolerance
 As early as 8 hours after last dose and may last 7 days
 Short-acting opiates have more severe withdrawal syndrome
 Hypothesis: opioids inhibit release of some neurotransmitters and thus
receptors for these neurotransmitters are up-regulated (more
receptors). If opiates are discontinued then normal neurotransmitter
release will occur with more receptors present and thus more binding to
those receptors. This leads to negative effects and withdrawal
syndrome
o Have tried blocking neurotransmitters to reduce symptoms
o Non-Steroidal Anti-Inflammatory Drugs (NSAID)
 Anti-inflammatory, anti-pyretic (reduces temp), analgesic, anti-coagulating
(decreases blood clotting)
o COX-2 Inhibitors
 COX = cycloxygenase enzyme
 Subclass of NSAID
 These drugs are only specific to the COX-2 subtype of the enzyme so don’t block
action of the entire enzyme
 Pain relief
o Local Anesthetics
 Can block MS pain although site of action is not the muscles
 Block Na+ channel and thus action potentials of neurons
 If sensory neuron block this results in pain relief
 Applications include: topical (skin), transdermal (IOP – electrical potential across
skin), infiltration (injection into selected tissue), peripheral nerve block
(injection close to nerve trunk), central neural blockade (injection within
membranes surrounding SC)
 Analgesics can be given for long period of time and are for broader level of pain
but anesthetics are given for sensation block in a specific area
 Anti-Inflammatory Drugs
o Solely bock inflammation
o Corticosteroids
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Skeletal Muscle Relaxants
 Spasticity = increased tone due to exaggerated muscle stretch reflexes
 Muscle spasm = increased tone usually after skeletal muscle injury
 Goal = decrease tone without decreasing function
 Helpful if injury is in muscle or nerve
Baclofen
Barbiturates
 Low TI
 May directly inhibit transmitter release from presynaptic terminals
(independent of GABA effect) and may have antagonistic effect on postsynaptic
receptors
Benzodiazepines
 Enhance effect of GABA but do not replace the effect
 Safer than barbiturates but still cause tolerance and physical dependence
 Diazepam (Valium)
Dantrolene
Botunlinum Toxin (Botox)
Module 8: Endocrine Pharmacology
 Based around hormones – exogenous hormones given as drugs if endogenous deficiency is
present
 Adrenocorticosteroids
o Glucocorticoids
o Mineralcorticoids
 Thyroid Pharmacology
o A lot of innervations from SNS
o Synthesizes thyroxin (T4) and tri-iodothyronin (T3)
o TSH from anterior pituitary stimulations T3 and T4 production
o T3 and T4 provide negative feedback for their own production (like glucocorticoids)
o Physiological effects: temperature regulation (increase heat production by increasing
BMR), growth and development (stimulate GH release), CV effects (increase HR and
contractility), metabolic effets (enhances lipolysis and increase response of fat cells to
other liplytic hormones)
o Long-term administration of thyroid hormones for hypothyroidism may lead to
overdosage if the correct dosage is not used
 Parathyroid Gland
o Produces PTH
o Most important job = control Ca2+ concentrations
o Released when plasma Ca2+ levels decrease
o Raises blood Ca2+ level by affecting bone, kidneys, and GI
o When levels increase PTH stops being released (negative feedback)
o Increase PTH = bone breakdown; decrease PTH = bone synthesis and remodeling
o Vit D increases serum Ca2+ and phosphate levels
o Calcitonin
 Pancreatic Hormones
o Pancreas = endocrine (insulin and glucagon regulation) and exocrine (digestive enzymes
through pancreatic duct) gland; primarily responsible for glucose control!
o DM = due to insufficient insulin secretion (Type I – beta cell function loss) or decrease in
peripheral effects (Type II – lack of insulin sensitivity)
o Action of drugs for DM
 Improved glycemic control – focuses on the hormone GLP-1 which stimulated
insulin production
 Reduce insulin resistance in type 2 diabetes – target skeletal muscles
 Lower CV risk factors of both types of DM
 Treat peripheral neuropathy
o Hypoglycemia
 Initial symptoms = headache, fatigue, hunger, tachycardia, sweating, anxiety,
confusion
 Severe symptoms = loss of consciousness, convulsions, death
o Oral Hypoglycemic Drugs
Module 9: Pulmonary Pharmacology
 Goals of these drugs: bronchodilation, facilitate removal of secretion from lungs, improve
alveolar ventilation or oxygenation, optimize breathing pattern
 Pulmonary Physiology
o Airway obstruction occurs with asthma, chronic bronchitis, lung infections, CA, or
emphysema
 Some charachteristics = bronchospasms, mucous in airways, airway
inflammation
 Asthma = imbalance of ANS, PNS is predominant, increased bronchomotor tone
leading to narrow airways
o Bronchodilators = most common treatment
o Bronchoconstriction can be caused by inflammation, abnormal bronchomotor tone,
mechanical obstruction (ex: mucous)
o Smooth muscle in airways have adrenergic beta-2 receptors that cause smooth muscle
relaxation
 Receptors activated adenylcyclase which produces AMO which causes the
relaxation and inhibits degranulation of mast cells using a G protein (amplifies
the downstream action)
 Myosin is phosphorylated and inhibited from interacting with actin thus the
muscle relaxes
 Asthma
o Inflammed airways
o Airways overly sensitive which leads to allergic reactions and narrowing
o Main symptoms = wheezing, coughing, tightening in chest, trouble breathing (esp. night
and early morning)
o Goal with drugs = reduce frequency and severity of attacks
o Attacks and triggers unique to individual
o Quick acting drugs: take at first sign of asthma attack, relieve symptoms within minutes
o Long acting drugs: taken daily, long-term control of attacks to help decrease frequency
o Bronchodilators
 For asthma, COPD, infections
 Inhalers
 Prime by spraying in air twice
 Breath out slowly to the end of a normal breath
 Spray so it does not hit roof of mouth or tongue
 Breath in slowly
 Allows drug to be administered directly to the lungs and allows higher
dosage to reach lungs
 Few side effects
o Glucocorticoids
o Methylxanthine
o Mediator-release inhibitors
 Allergies
o Caused by overactive immune system
o No cure
o During allergy attack histamine is released from mast cells causing local inflammation
and swelling followed by leakage on the wall
o Antihistamines
o Decongestants
o Corticosteroids – decrease inflammation, need to be taken daily to have an effect
o Bronchodilators –
o Leukotriene blockers
o Mediator release inhibitors
o Immunotherapy – allergy shots – gradually increase level of allergen to prevent allergy
attacks
 Other Obstructive Lung Diseases
o Expectorant
o Mucolytics
o Antitussives
Module 10: Oncological Pharmacology
 Chemotherapy = chemical given as therapy
o Goal is to selectively kill the cancerous cells while leaving the healthy cells intact
o Currently not overly specific
o Severe side effects
 Common side effects include:
 Myelosuppression (bone marrow depression) – decreased production
of all blood components; low WBC and susceptible to infections; know
pt’s blood count and wash hands; take proper precautions if you are
sick; may have increased pulse and RR if anemic
 Cardiac toxicity – Adriamycin or daunomycin ay cause irreversible
cardiac damage; check vitals frequently, monitor for SOB, chest pain
and increased pulse with little activity
 Pulmonary fibrosis – Bleomycin, methotrexate, or cisplatin may cause
this and result in restrictive lung disease
 Peripheral neuropathy – Vincrisine can cause weakness and
paresthesias distally, tumor invasion can cause neuropathy, weakness
such as foot drop should subside after chemo treatment
 Fibrosis – hard edema and fribrotic tissue that can limit joint
movement, AROM ex to prevent contractures
 GI toxicity – nausea, vomiting, diarrhea, and ulcerations of mucosal
lining can occur
 Alopecia (hair loss) – temporary side effect of certain drugs, re-growth
may begin during or after all chemotherapy
 Oncological drugs = drugs to treat cancer
 Tyrosine kinase receptor is important in transformation of normal cells to cancerous cells
o Phosphorylate other intracellular proteins when activated
o Receptor normally involved in the cellular growth and division, but when altered
somehow it can induce cancerous changes in the cell
Module 11: Immunological Pharmacology
 Usually inhibit bacterial or fungal cell wall synthesis, leaving organism with damaged outer
membrane
 May target ribosome’s involved in protein synthesis or enzymes involved in DNA replication
 Overuse and inappropriate use has led to drug resistance organisms
 Antibacterial Agents
o Penicillin
 Penicillins are the most widely prescribed and effective classes of antibiotics.
They are used to treat gram positive bacteria including streptococci,
meningococci, enterococci,
o Vancomycin
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Vancomycin resistance has become a major clinical problem in recent years.
Vancomycin-resistant enterococi are frequently resistant to all other antibiotics,
leaving no pharmacological tool for treating the infections. These resistant
bacteria are clear examples of Darwin's natural selection at work.
Tetracyclines
 They inhibit gram-positive and negative bacteria, including chlamydiae,
mycoplasmas, rickettsiae, and some protozoa and amebas. These drugs are no
longer prescribed for gonococcal disease, because of wide-spread resistance to
them. Active against both gram negative and gram positive organisms.
Chloramphenicol
 It is taken orally, and is taken up by cells quickly. It is a fairly toxic drug so its is
prescribed sparingly for serious rickettsial infections, such as typhus and Rocky
Mountain spotted fever. It can cause GI problems with diarrhea and vomiting. It
is toxic for infants with the drug accumulating resulting in the "gray baby
syndrome" in which the baby actually takes on a gray color and is accompanied
with vomiting, flaccidity and shock.
Sulfonamides
 Sulfonamides are given to treat bacterial infections and are also used for
diabetes mellitus, and edema and gout. These drugs inhibit bacterial folic acid
synthesis
Isoniozid
 Isoniozid drugs are the first line of defense to treat active tuberculosis in
combination with other agents.
 Antiviral Agents
o These drugs have been most important in the intervention for HIV.
o Acyclovir
 Is used to treat herpes simplex virus and vericell-zoster virus
o AZT
 Azidothymidine, also known as AZT or Zidovudine, was one of the first drugs
designed to fight HIV infections.
o Indinavir
 Indinavir is an inhibitor of a protease specific to HIV-1. It is typically given to HIV
positive patients in combination with reverse transcriptase inhibitors.
Combination of the two is more effective and greatly reduces the risk of the
virus mutating to become resistant to one line of drug.
o Interferons
 Interferons are endogenous proteins that are inserted into the membrane of a
cell after viral infection. This blocks subsequent viral infection by other
particles. By artificially giving interferon to a person, it inserts itself into the
membrane and fools the invading virus leaving the impression that the cell has
already been infected.
 Antifungal Agents
o Amphotercin
 Amphotericin attacks the unique lipids in fungi compromising the stability of the
fungus. It can be taken orally, topically and by IV.
o Azoles
 These drugs are particularly important in fighting fungal infections on a systemic
level or topically
 They may cause minor GI problems but side effects are few and minor