PART 1- INTRODUCTION TO NURSING SELECTIVE TOXICITY- drug’s ability to attack only those found
in foreign cells w/o damaging normal human cell
PHARMACOLOGY CRITICAL CONCENTRATION- amount of drug that is needed CHAPTER 1- Introduction to Drugs to cause a therapeutic effect ABSORPTION- what happens to the drug when it enters & PHARMACOLOGY- study of the biological effects of chemicals reaches the circulation PHARMACOTHERAPEUTICS- uses drugs to treat, prevent, & SITES OF ABSORPTION: diagnose disease Oral, rectal DRUGS- chemicals that cause changes Mucous membrane THERAPEUTIC CLASS- pwd sa uban sakit Skin PHARMACOLOGIC CLASS- pero antidiuretic jud sya Lungs SOURCES OF DRUGS: Muscles PLANTS ANIMAL PRODUCTS 1. PASSIVE DIFFUSION- greater to lower concentration o GENETIC ENGINEERING- process of altering w/ no energy required; small molecule DNA 2. ACTIVE TRANSPORT- uses energy; larger molecule INORGANIC COMPOUNDS 3. FILTRATION- used in drug excretion DRUG EVALUATION: ADMINISTRATION 1. PRECLINICAL TRIALS ORAL ROUTE- most commonly used; not invasive; 2. PHASE I STUDIES less expensive 3. PHASE II STUDIES IV- fastest route 4. PHASE III STUDIES IM- least 5. CONTINUAL EVALUATION SUB-Q- least a. BRAND NAME- trade name DISTRIBUTION- movement of drug to the body b. GENERIC NAME-abbreviation of chemical Factors: name LIPID SOLUBILITY c. CHEMICAL NAME- chemical structure of a IONIZATION drug PERFUSION OF THE REACTIVE TISSUE d. ORPHAN DRUGS- drugs that have been BLOOD-BRAIN BARRIER discovered but are not financially viable BIOTRANSFORMATION (METABOLISM) e. OVER-THE-COUNTER DRUGS- products that LIVER ENZYME SYSTEMS- liver is the most important site are available w/o prescription of drug metabolism HEPATIC MICROSOMAL SYSTEM- structure of hepatic CHAPTER 2- Drugs and the Body cells’ intracellular lined up w/ enzymes EXCRETION- removal of drug from body; skin, saliva, lungs, bile & feces. PHARMACODYNAMICS- how the drug affects the body KIDNEY- plays the most important role in drug excretion PHARMACOKINETICS- how the body reacts on the drug HALF-LIFE- time it takes for the amount of drug to decrease DRUG ACTIONS: To replace substitutes for missing chemicals To increase/ decrease certain cellular activities CHAPTER 3- Toxic Effects of Drugs To interfere w/ the functioning of foreign cells, like invading neoplasms (CHEMOTHERAPEUTIC AGENTS) ADVERSE EFFECTS- undesired effects RECEPTORS SITE- specific areas on cell membranes; react w/ Reasons of occurrence: certain chemicals to cause an effect Pt is sensitive to the drug SPECIFIC CHEMICAL- the key Pt taking too much/ little of the drug PERFECT FIT- the lock ADVERSE DRUG REACTION- unintended & undesired reaction AGONIST- create response to the drug ANTAGONIST- doesn’t create response SIDE EFFECT- result of drug in addition of the desired COMPETITIVE ANTAGONIST- some drugs react w/ therapeutic effect receptor sites to block normal stimulation, producing TYPES OF ADVERSE REACTIONS: no effect 1. PRIMARY NONCOMPETITIVE ANTAGONIST-react w/ receptor 2. SECONDARY sites & prevent the reaction of another chemical w/ 3. HYPERSENSITIVITY a different receptor sire ALLERGY: 1. ANAPHYLACTIC REACTION (TYPE 1) “Immediate Hypersensitivity Reaction” RECEPTOR SITES Sudden, widespread, potentially sever & life- IDENTIFYING MARKERS- histocompatibility threatening antigens/ Human Leukocyte Antigens Appears w/in 10 min (HLAs)- identify a cell as self-cell S/S CHANNELS Hives, rash, difficulty breathing, increased 3. CYTOPLASM BP, dilated pupils, diaphoresis, increased MITOCHONDRIA heart rate, respiratory arrest ENDOPLASMIC RETICULUM 2. CYTOTOXIC REACTION FREE RIBOSOMES “Toxic to Cell” GOLGI APPARATUS Antibodies produced by the Immune system LYSOSOMES response bind to antigens on the pt own cell CELL PROPERTIES surfaces ENDOCYTOSIS- incorporation of material into the cell *Ex. ABO incompatibility o PINOCYTOSIS- cell-drinking 3. SERUM SICKNESS o PHAGOCYTOSIS- cell-eating Immune system reacts to medicines that EXOCYTOSIS- secretion of substances out of the cell contains protein HOMEOSTASIS *Ex. Vaccines, Antiserum PASSIVE TRANSPORT 4. DELAYED ALLERGIC REACTION DIFFUSION- higher to lower concentration “Cell-mediated) OSMOSIS- lower to higher solutes Takes 2-3 days o ISOTONIC Cell-mediated response (CD4 & HELPER T o HYPERTONIC- higher solutes CELLS- recognize antigen) o HYPOTONIC-lower solutes *Ex. Tuberculin test, contact dermatitis FACILITATED DIFFUSION- w/ carrier *HAPTENS- incomplete antigen ACTIVE TRANSPORT- requires energy CELL CYCLE DRUG-INDUCED TISSUE & ORGAN DAMAGE 1. GO PHASE- resting phase 1. DERMATOLOGICAL REACTIONS: 2. G1 PHASE- synthesize substances for DNA formation RASHES 3. S PHASE- actual synthesis of DNA HIVES (burning & itching) 4. G2 PHASE- produce substances for mitotic spindles 2. MUCOUS MEMBRANES: 5. M PHASE- cell division. Mitosis STOMATITIS 3. SUPERINFECTIONS (Suprainfection) New infection occurring in pt w/ preexisting CHAPTER 8- Anti-infective Agents infection 4. BLOOD DYSCRASIA/BONE MARROW DEPRESSION CHAPTER 9- Antibiotics 5. TOXICITY 6. ALTERATION IN GLUCOSE METABOLISM ANTIBIOTIC- inhibit bacteria 7. ELECTROLYTE IMBALANCES BACTERIOSTATIC- prevent growth of bacteria 8. SENSORY EFFECTS BACTERICIDAL- kill bacteria 9. NEUROLOGIC EFFECTS BACTERIA: 10. TERATOGENICITY GRAM-POSITIVE- respi & soft tissues infections GRAM-NEGATIVE- GU & GI infections CHAPTER 5- Dosage Calculations SYNERGY- given in combination 1. AMINOGLYCOSIDES PART 2- CHEMOTHERAPEUTIC AGENTS a. Treat serious infection caused by gram- CHAPTER 7- Introduction to Cell negative aerobic bacilli b. Bactericidal Physiology c. Ex. Amikacin, Gentamicin, Kanamycin, Neomucin, Streptomycin The Cell 2. CEPHALOSPORINS 1. CELL NUCLEUS a. 1960 RIBOSOMES- sites of protein synthesis b. Similar to penicillin 2. CELL MEMBRANE c. Has 4 generations (Peck, HENPeCK, LIPOPROTEIN HENPeCKS, for gram+ & -) d. Bactericidal & bacteriostatic b. PROTEASE INHIBITORS- blocks protease e. Nephrotoxicity (essential for maturation of infectious virus) f. Ex. Cephalexin activity 3. FLUROQUINOLONES c. NUCLEOSIDES- inhibits cell protein synthesis a. New class with broad spectrum d. FUSION INHIBITORS- new class of drugs, b. Ex. Ciprofloxacin, Levofloxacin, Ofloxacin prevents fusion of virus w/ human cell 4. MACROLIDES membrane a. Interfere w/ protein synthesis 4. DRUGS USED FOR HEPA B b. Bactericidal/ bacteriostatic a. Ex. Adefovir,Entecavir c. Ex. Erythromycin, Azithromycin 5. LOCALLY ACTIVE ANTIVIRAL AGENTS 5. LINCOSAMIDES a. Given locally to treat viral infection a. Similar to the macrolides but are more toxic b. Ex. Aldara, Herplex, Abreva b. Ex. Clindamycin, Lincomycin 6. MONOBACTAM ANTIBIOTICS CHAPTER 11- Antifungal Agents a. Gram-negative inhibitor b. Ex. Azactam MYCOSIS- infection caused by fungus 7. PENICILLINS & PENISILLINASE-RESISTANT ERGOSTEROL- found in cell wall of fungi ANTIBIOTICS 1. SYSTEMIC ANTIFUNGALS a. Alexand Fleming a. EX. Amphotericin B, Caspofungin, b. w/ tetracyclines, the effectiveness will Micafungin, Nystatin decrease b. AZOLES- newer drugs that treats systemic c. Ex. Amoxicillin, Ampicillin fungal infections 8. SULFONAMIDES i. Ex. Ketoconazole, Fluconazole a. Inhibit folic acid synthesis 2. TOPICAL ANTIFUNGAL b. Not used much any more a. DERMATOPHYTES- causative agent c. Competitively block para-aminobenzoic acid b. Causes tinea infections: ringworm, athlete’s (gram + & -) foot, jock itch d. Teratogenic c. Ex. Gentian violet, Butenafine, Butoconazole e. Ex. Sulfadiazine, Cotrimoxazole 9. TRTRACYLCINES a. Semisynthetic CHAPTER 12- Antiprotozoal Agents b. Inhibiting protein synthesis c. Composed of four rings PROTOZOA- thrives in tropical area d. Ex. Tetracycline, Minocycline 1. MALARIA 10. ANTIMYCOBACTERIAL ANTIBIOTICS a. ANOPHELES MOSQUITO- PLASMODIUM a. Acid-fast bacteria i. FALCIPARUM- most dangerous b. Ex.Rifampicin, Isoniazid, Ethambutol ii. VIVAX- mild, seldom 11. LEPROSTATIC DRUGS iii. MALARIAE- endemic a. Ex. Dapsone iv. OVALE- rarely seen b. LIFE CYCLE i. GAMETOCYTES CHAPTER 10- Antiviral Agents ii. SPOROZOITES iii. TROPHOZOITES VIRUSES iv. MEROZOITES INTERFERONS- signals other cell of virus invasion c. ANTIMALARIALS 1. AGENTS FOR INFLUENZA A & RESPI VIRUSES i. Ex. Quinine, Chloroquine, a. Prevent shedding of viral protein coat & Mefloquine, Primaquine entry of viruses ii. Interrupts plasmodial reproduction b. Ex. Amantadine, Ribavirin, Rimatidine, of protein synthesis in RBC stage Zanamivir iii. Risk fo cardiac toxicity & convulsions 2. AGENTS FOR HERPES & CYTOMEGALOVIRUS 2. AMEBIASIS a. Inhibit viral DNA replication a. ENTAMOEBA HISTOLYTICA b. Ex. Acyclovir, Cidofovir, Foscarnet b. CYST-TROPHOZOITE 3. AGENTS FOR HIV & AIDS c. Can cause death a. REVERSE TRANSCRIPTASE INHIBITORS- blocks 3. LEISHMANIASIS RNA & DNA, prevent transfer of information a. SAND FLIES- PROMASTIGOTE- AMASTIGOTE 4. TRYPANOSOMIASIS a. TRYPANOSOMA a. In combination therapy i. AFRICAN SLEEPING SICKNESS b. Inhibit DNA production that depend on ii. CHAGAS’ DISEASE metabolites 5. TRICHOMONIASIS c. Ex. Methotrexate, Pentostatin, Capecitabine a. TRICHOMONAS VAGINALIS 3. ANTINEOPLASTIC ANTIBIOTICS b. Cause vaginitis a. Not selective 6. GIARDIASIS b. Toxic to human cells a. GIARDIA LAMBLIA c. Toxic to rapidly multiplying cells (GI, skin, 7. PNEUMOCYSTIS CARINII PNEUMONIA marrow) a. Most common opportunistic infection in pts d. Interfere w/ DNA synthesis by inserting w/ AIDS themselves between base pairs in the CAN OTHER ANTIPROTOZOAL AGENTS chain & causing a mutant DNA molecule Ex. Metronidazole, Pentamidine e. Ex. Doxorubicin, Bleomycin, Dactinomycin 4. MITOTIC INHIBITORS CHAPTER 13- Anthelmintic Agents a. Kill cells as the process of mitosis begins b. Interfere w/ the ability of a cell to divide c. Ex. Vincristine, Vinblastine, VInorelvbine INTESTINE-INVADING WORMS 5. HORMONES & HORMONE MODULATORS NEMATODES, PINWORMS, WHIPWORMS, a. Cancer in the breast tissue, ovaries, uterus, THREADWORMS, ASCARIS, HOOKWORMS, prostate & testes PLATUHELMINTS: CESTODES b. Used to block the release of gonadotropic TISSUE-INVADING WORM INFECTION hormones 1. TRICHINOSIS c. Ex. Tamoxifen, Anastrazole, Estramustine a. TRICINELLA SPIRALIS 2. FILARIASIS a. ELEPHANTIASIS PART 3- DRUGS ACTING ON THE 3. SCHISTOSOMIASIS IMMUNE SYSTEM a. SNAIL ANTIHELMINTIC CHAPTER 15- Introduction to the Ex. Mebendazole, Praziquantel, Albendazole Immune Response & Inflammation CHAPTER 14- Antineoplastic Agents BODY DEFENSES 1. BARRIER DEFENSES NEOPLASM- cancer a. SKIN- has keratin, acidic sweat, sebum ANAPLASIA- loss of ability b. MUCOUS MEMBRANES- works like flypaper AUTONOMY- growing w/o restrictions c. GASTRIC ACID METASTASIS- travel from place d. MAJOR HISTOCOMPATIBILITY COMPLEX- ANGIOGENESIS- generate blood vessels ability to distinguish between self-cells & CAUSES OF CANCER foreign cells 2. CELLULAR DEFENSES Genetic predisposition a. LEUKOCYTES- lymphocytes & myelocytes Viral infection b. NEUTROPHILS- capable of diapedesis (to go Constant irritation outside the bloodstream), active kaau. Stress phagocytes Areas w/ carcinogenic c. BASOPHILS- histamine TYPES OF CANCER d. EOSINOPHILS- histaminase CARCINOMAS- tumors in epithelial cells e. MONOCYTES/ MACROPHAGES- antigen SARCOMAS- tumor in mesenchyme presenter ANTINEOPLASTIC DRUGS f. MAST CELLS- fixed basophils in respi & GI 1. ALKYLATING AGENTS tract. Prostaglandin a. Non-cell cycle-specific CLINICAL PRESENTATION b. Most useful in slow-growing cancers, resting CALOR- heat phase TUMOR- swelling c. Disrupts cell mechanisms that affect DNA RUBOR- redness d. Ex. Busulfan, Carboplatin DOLOR- pain e. Magka alopecia PATHOPHYSIOLOGY INVOLVING THE IMMUNE SYSTEM 2. ANTIMETABOLITES 1. NEOPLASMS IMMUNE SUPPRESSANTS 2. VIRAL INVASION OF CELLS 1. T & B CELL SUPPRESSORS 3. AUTOIMMUNE DISEASE- suppressor t cells don’t 2. INTERLEUKIN RECEPTOR ANTAGONIST suppress, genetic predisposition to develop 3. MONOCLONAL ANTIBODIES autoantibodies CHAPTER 18- Vaccines & Sera 4. TRANPLANT REJECTION- t cells are activated by the presence of the foreign cells ACTIVE IMMUNITY- body recognizes foreign protein & produces antibodies CHAPTER 16- Anti-inflammatory Agents PASSIVE IMMUNITY- antibodies are injected 1. IMMUNIZATION- exposure to weakened protein SALICYLATES- popular anti-inflammatory agents 2. VACCINES- stimulate formation of antibodies ANTIPYRETIC- fever-blocking a. Stimulate active immunity ANALGESIC- pain-blocking 3. IMMUNE SERA & ANTITOXINS NONSTEROIDAL ANTI-INFLAMMATORY DRUGS- strong anti- a. SERA-contain antibodies inflammatory &analgesic effects b. ANTITOXIN- immune sera that have ACETAMINOPHEN- antipyretic & analgesic but no antibodies that might be released by inflammatory effects of salicylates/ NSAID invading pathogens 1. SALICYLATES c. Immune sera provide passive immunity a. Oldest anti-inflammatory b. Inhibits thromboxane A, a vasoconstrictor CHAPTER 19- Introduction to Nerves & that increases platelet aggregation & clot formation the Nervous System c. Inhibits synthesis of prostaglandin d. Ex. Aspirin, Balsalazide, Mesalamine, CNS- integration Olsalazine, Salsalate PNS- bring info to cns 2. NONSTEROIDAL ANTI-INFLAMMATORY DRUGS AUTOMATIC NS-regulate automatic unconscious responses a. Ex. Ibuprofen, Celecoxib, Diclofenac ASCENDING TRACT- sensory 3. RELATED DRUGS DESCENDING TRACT- response a. ACETAMINOPHEN PHYSIOLOGY OF THE NERVOUS SYSTEM i. For pain & fever. For children 1. NEURONS ii. Ex. Acetaminophen, TYPES: Unipolar, Bipolar, Multipolar Aurothioglucose, Anakinra, SOMA- cell body Penicillamine DENDRITES- branch-like covering of neuron b. GOLD COMPOUND AXON- elongated process i. CHRYSOTHERAPY- gold salts AFFERENT- sensory ii. Inhibits phagocytosis. The release of EFFERENT- motor lysosomal enzymes is inhibited & 2. ACTION POTENTIAL tissues destruction is decreased IMPULSES & STIMULUS iii. For rheumatic inflammatory AT REST- negative inside cell conditions DEPOLARIZATION- sodium rush into cell, change is charge CHAPTER 17- Immune Modulators ACTION POTENTIAL- sudden reversal of membrane lasts less than a micro-second IMMUNE STIMULANTS- used to energize exhausted immune REPOLARIZATION- returns to resting system membrane IMMUNE SUPPRESSANTS- used to block the normal effects of 3. GLIAL CELLS immune system TYPES: i. ASTROCYTE- IMMUNE STIMULANTS: ii. MICROGLIAL 1. INTERFERONS- stimulate interferon receptor sites to iii. EPENDYMAL produce antiviral proteins iv. OLIGODENDROCYTES 2. INTERLEUKINS- chemicals produce by T cells to v. SCHWANN CELLS communicate between leukocytes. Activate cellular NODES OF RANVIER immunity & inhibit tumor growth 4. NERVE SYNAPSE 3. T & B CELL MODULATOR Where communication occurs 5. NEUROTRANSMITTERS Stimulate postsynaptic cells by exciting/ a. CEREBRAL CORTEX- associated w/ higher inhibiting them brain function such as though & ation SYNAPTIC VESSICLE- produce b. RIGHT SIDE OF THE BRAIN- artistic neurotransmitters i. Largest part of human brain MONOAMINOXIDASE- degrades c. LEFT SIDE OF THE BRAIN- analytical neurotransmitters d. ENGRAM- reverberating circuit of action 1. ACETYLCHOLINE- nerves & muscle(degrades potential that eventually becomes a long- neurotransmitters term 2. NOREPINEPHRINE & EPINEPHRINE- catecholamines i. Responsible for short-term memory (stimulants) in times of emergency(fight/fly) e. Substances affecting learning: 3. DOPAMINE- coordination of impulses & responses i. ADH-released during reaction to 4. GAMMA-AMINOBUTRIC ACID- prevent stress overexcitability like seizure ii. OXYTOCIN 5. SEROTONIN- arousal & sleep CENTRAL NERVOUS SYSTEM PART 4- DRUGS ACTING ON THE BLOOD BRAIN BARRIER CAROTIDS CENTRAL & PERIPHERAL NERVOUS VERTEBRALS SYSTEMS CIRCLE OF WILLIS CHAPTER 20- Anxiolytic & Hypnotic GANGLION- composed of nerves outside spinal & brain cord Agents ANATOMY OF THE BRAIN 1. HINDBRAIN ANXIOLYTICS- prevent feeling of tension/ fear a. BRAINSTEM-pons & medulla oblongata SEDATIVES- calm patients b. Control basic, vital functions like respiration, HYPNOTICS- cause sleep bp, swallowing reflex, & RAS ANXIETY- feeling of tension, nervousness, apprehension that c. CEREBELLUM- regulates posture, balance & usually involves unpleasant reactions to a stimulus, voluntary muscle activity whether actual/ unknown 2. MIDBRAIN fast heart rate, rapid breathing, elevated blood a. THALAMUS- sensation, cold, heat, pain, pressure touch, muscle senses- SEDATION- loss of awareness b. HYPOTHALAMUS- major sensor for activities. HYPNOSIS- extreme sedation results to cns depression Temperature, water balance, appetite & 1. BENZODIAZEPAM fluid balance. Produce hormones & store in a. Most frequently used anxiolytic drugs the posterior pituitary gland b. Act in the limbic system & the RAS to make 3. LIMBIC SYSTEM GABA more effective, causing interference a. 3 neurotransmitters: EPINEPHRINE, NOR- w/ neuron firing EPINEPHRINE, & SEROTONIN. c. For anxiety disorders, alcohol withdrawal, b. Expression of emotions- anger, pleasure, hyperexcitability and preoperative relief of motivation, stress anxiety & tension 4. FOREBRAIN d. Ex. Diazepam a. Made up of 2 cerebral hemisphere joined by 2. BARBITURATES CORPUS CALLOSUM a. Once the sedative/ hypnotic drugs of choice b. Speech & communication b. Inhibit neuronal impulse conduction in the 5. BASAL GANGLIA- extrapyramidal motor system ascending RAS ANATOMY OF THE SPINAL CORD 31 pairs of spinal nerves CHAPTER 21- Antidepressants Agents DORSALROOT- sensory fiber MOTOR FIBER- ventral root AFFECT- refer to people’s feelings in response to their FUNCTIONS OF THE CNS environment 1. SENSORY FUNCTIONS DEPRESSION- feelings of severe & long-lasting sadness, 2. MOTOR FUNCTIONS despair, hopelessness, disorganization. Little energy, sleep a. PYRAMIDAL SYSTEM “Voluntary movement” disturbances, lack of appetite, limited libido, inability to b. EXTRAPYRAMIDAL “Unconscoius” perform activities 3. INTELLECTUAL& EMOTIONAL 1. TRICYCLIC ANTIDEPRESSANTS (TCAs) a. Inhibit presynaptic reuptake of the CHAPTER 23- Antiepileptic Agents neurotransmitters which lead to an accumulation of these neurotransmitters in EPILEPSY- sudden discharge of excessive electrical energy the synaptic cleft from nerve cells b. Ex. Impiramine SEIZURES- caused by these abnormal cells called primary 2. MONOAMINE OXIDASE INHIBITORS seizures because no underlying cause can be identified. a. Inhibit MAO Leads to head injury, drug overdose, environmental b. Tyramine- thyroxine- epinephrine & exposure- secondary seizures norepinephrine GENERALIZED SEIZURE 3. SELECTIVE SEROTONIN REUPTAKE INHIBITORS Begin in one area of the brain & rapidly spread a. Newest drugs that specifically block the throughout both hemisphere of the baine reuptake of 5HT, w/ little to no effect on NE. Loss of consciousness resulting from thes massive b. Increase extracellular level of serotonin by electrical activity limiting its reabsorption into the presynaptic 1. TONIC-CLONIC SEZIRES- aura warning sign. cell Grand mal seizure 2. ABSENCE SEIZURE- petit mal seizure. Abrupt, CHAPTER 22- Psychotherapeutic Agents brief periods of unconsciousness 3. MYOCLONIC- sporadic periods of muscle SCHIZOPHRENIA- hallucinations, paranoia, delusions, speech contractions that last for several minutes abnormalities 4. FFEBRILE- related to very high fever. Self- MANIA- overactivity & excitement limited & don’t reappear NARCOLEPSY- daytime sleepiness & sudden periods of loss of 5. STATUS EPILEPTICUS- most dangerous. Rapid wakfulness reoccurring ATTENTION-DEFICIT DISORDERS- inability to concentrate on PARTIAL SEIZURES one activity for longer than a few minutes FOCAL SEIZURES 1. ANTIPSYCHOTIC/ NEUROLEPTIC DRUG Involve one area of the brain & don’t spread a. Essentially dopamine receptor blockers 1. SIMPLE PARTIAL-single muscle movement b. Used to treat disorders that involve thought 2. COMPLEX PARTIAL- complex sensory processes changes c. Known as neuroleptic & major tranquilizers d. Types: i. TYPICAL- primarily dopamine CHAPTER 24- Antiparkinsonism Agents receptor blockers CHAPTER 25- Muscle Relaxants ii. ATYPICAL- bock both dopamine & serotonin receptors CHAPTER 26- Narcotics & Antimigraine e. Common neurological effects: Agents i. DYSTONIA- hiwi liog ii. AKATHISIA- foot tapping iii. PSEUDOPARKINSONISM- slow char iv. TARDIVE DYSKINESIA- lips & tongue 2. ANTIMANIC a. Mania- opposite of depression b. Lithium salts 3. CENTRAL NERVOUS SYSTEM STIMULANTS a. Calm hyperkinetic children & help them focus on one activity for a longer period b. Excite the arousal stimuli from the RAS c. Increase release of catecholamines leading to an increase stimulation of the postsynaptic neurons d. Ex. Dexedrine e. Contraindication: anxiety, agitation, tension, dardiac disease, history of drug dependence including alcoholism