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					Pharmacology: Units 1-5
Unit 1: Introduction to Pharmacology

      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

      Pharmacokinetics: The study of factors that are involved in getting the drug to its target
      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
      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
          o GI tract and lungs may act as sites for drug elimination
         o   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
         o   Drug concentrations are usually measured by the plasma levels.
         o   Drug storage sites: Adipose tissue-primary site for storage, Bone- stores heavy
             metals and toxins, Muscles- muscle cells in particular, Organs- The liver and
         o   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)
         o   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
         o   Clearance is the ability of organs, specifically the kidneys to eliminate drugs
         o   Creatinine clearance rates are used to determine if a patient has a renal problem of
         o   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

     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
     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
      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

Module 4: Neurological Pharmacology

      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

      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
      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
      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
      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

      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
      STATINS(Lipitor, Crestor, Zocor, Lovastatin, Cauduet)-inhibits cholesterol
       biosynthesis, decreases LDL and increases HDL
      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)
                    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.
      H2 Receptor Antagonists(Tagament, Pepcid AC, Zantac)
          o 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.
      Proton-Pump Inhibitors(Prilosec, Prevacid, Nexium)
          o 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
          o Possess antibacterial effects against helicobacter pylori infection.
      Antibiotics
          o The most common antibiotics prescribed for peptic ulcers are metronidazole,
              tetracycline, clarithromycin, amoxicillin.
          o In general, antibiotics are only known by their generic name.
      Acetylcholine M1 Receptor Antagonists(Pirenzepine/Gastrozepin)
          o 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)
                            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)
          o Products like mineral oil bring water into the fecal mass, thus softening the stool
              and permitting easier elimination. They are used on a short-term 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
      Stool Thickeners(Kaplin, Pectin)
          o 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.
      Bulking Drugs
          o 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.
      Anti-Spasmodic Drug(Imodium)
          o 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

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
                          Cross-tolerance – May develop tolerance to other opoids even if
                              you are taking a different one
                  Theories:
                          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
                           Have tried blocking neurotransmitters to reduce symptoms
      Non-Steroidal Anti-Inflammatory Drugs (NSAID)
          o Anti-inflammatory, anti-pyretic (reduces temp), analgesic, anti-coagulating
              (decreases blood clotting)
      COX-2 Inhibitors
          o COX = cycloxygenase enzyme
          o Subclass of NSAID
          o These drugs are only specific to the COX-2 subtype of the enzyme so don’t block
              action of the entire enzyme
          o Pain relief
      Local Anesthetics
          o Can block MS pain although site of action is not the muscles
          o 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

                    Solely bock inflammation
                    Corticosteroids
      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
          o Low TI
          o May directly inhibit transmitter release from presynaptic terminals (independent
              of GABA effect) and may have antagonistic effect on postsynaptic receptors
      Benzodiazepines
          o Enhance effect of GABA but do not replace the effect
          o Safer than barbiturates but still cause tolerance and physical dependence
          o 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
        o Thyroid Pharmacology
                A lot of innervations from SNS
                Synthesizes thyroxin (T4) and tri-iodothyronin (T3)
                TSH from anterior pituitary stimulations T3 and T4 production
                T3 and T4 provide negative feedback for their own production (like
                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)
                Long-term administration of thyroid hormones for hypothyroidism may
                   lead to overdosage if the correct dosage is not used
        o Parathyroid Gland
                Produces PTH
                Most important job = control Ca2+ concentrations
                Released when plasma Ca2+ levels decrease
                Raises blood Ca2+ level by affecting bone, kidneys, and GI
                When levels increase PTH stops being released (negative feedback)
                Increase PTH = bone breakdown; decrease PTH = bone synthesis and
                Vit D increases serum Ca2+ and phosphate levels
                Calcitonin
        o Pancreatic Hormones
                Pancreas = endocrine (insulin and glucagon regulation) and exocrine
                   (digestive enzymes through pancreatic duct) gland; primarily responsible
                   for glucose control!
                DM = due to insufficient insulin secretion (Type I – beta cell function
                   loss) or decrease in peripheral effects (Type II – lack of insulin sensitivity)
                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
                        Lower CV risk factors of both types of DM
                        Treat peripheral neuropathy
   Hypoglycemia
        o Initial symptoms = headache, fatigue, hunger, tachycardia, sweating, anxiety,
        o Severe symptoms = loss of consciousness, convulsions, death
   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
                    Asthma = imbalance of ANS, PNS is predominant, increased
                       bronchomotor tone leading to narrow airways
      Bronchodilators = most common treatment
      Bronchoconstriction can be caused by inflammation, abnormal bronchomotor tone,
       mechanical obstruction (ex: mucous)
      Smooth muscle in airways have adrenergic beta-2 receptors that cause smooth muscle
           o Receptors activated adenylcyclase which produces AMO which causes the
               relaxation and inhibits degranulation of mast cells using a G protein (amplifies the
               downstream action)
           o Myosin is phosphorylated and inhibited from interacting with actin thus the
               muscle relaxes
           o Asthma
                    Inflammed airways
                    Airways overly sensitive which leads to allergic reactions and narrowing
                    Main symptoms = wheezing, coughing, tightening in chest, trouble
                       breathing (esp. night and early morning)
                    Goal with drugs = reduce frequency and severity of attacks
                    Attacks and triggers unique to individual
                    Quick acting drugs: take at first sign of asthma attack, relieve symptoms
                       within minutes
                    Long acting drugs: taken daily, long-term control of attacks to help
                       decrease frequency
                    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
      Glucocorticoids
      Methylxanthine
      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
          o   Other Obstructive Lung Diseases
                   Expectorant
                   Mucolytics
                   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
                         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
                                     Phosphorylate other intracellular proteins when activated
                                     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
      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,
      Vancomycin
           o 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.
      Tetracyclines
           o 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
           o 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
           o 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
           o Isoniozid drugs are the first line of defense to treat active tuberculosis in
               combination with other agents.

Antiviral Agents

      These drugs have been most important in the intervention for HIV.
      Acyclovir
          o Is used to treat herpes simplex virus and vericell-zoster virus
      AZT
           o   Azidothymidine, also known as AZT or Zidovudine, was one of the first drugs
               designed to fight HIV infections.
      Indinavir
           o 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.
      Interferons
           o 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
      Antifungal Agents
                     Amphotercin- Amphotericin attacks the unique lipids in fungi
                        compromising the stability of the fungus. It can be taken orally, topically
                        and by IV.
      Azoles
           o These drugs are particularly important in fighting fungal infections on a systemic
               level or topically

They may cause minor GI problems but side effect

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