Nursing Pharmacology Prelim

NURSING PHARMACOLOGY

I. Fundamentals of Pharmacology
Pharmacology
Study of the biological effects of chemicals.
Drugs
Chemicals that are introduced in the body to cause some sort of change.
Pharmacokinetics
Absorption, distribution, metabolism, and
excretion of drug(s) in the body.

Pharmacotherapeutics
The use of drugs to prevent or treat a disease.
Pharmacodynamics
The biochemical and physical effect of drug(s) and the mechanism of drug action.

pharmacokinetics pharmacotherapeutics pharmacodynamics pharmacology

Sources:
Plants
Earliest drug source (leaves, roots, bulbs, fruits, blossoms, extracts)
Ex. Alkaloids – most active component in plants, reacts with acids to form a salt that easily dissolves in body fluids (caffeine, Nicotine, Atropine)
Glycosides – naturally occurring plant active components that has both toxic and good effect (lanoxin, digoxin)

Resins – local irritants and caustic agents (laxatives)
Oils – thick greasy liquids volatile:( peppermint, spearmint, juniper)/ fixed:( castor oil, olive oil)
Animals
Body fluids, glands of animals are also natural drug source
Ex. Hormones – (insulin)
Oils & Fats – (liver oils)
Enzymes – catalyst produced by living cells (pepsin)
Vaccines – suspension of killed, modified, or attenuated microorganism

Minerals
Metallic and non metallic minerals that provides inorganic materials not available in plants or animals.
Usually combined with other ingredients
Ex. ( Fe S04, Mg SO4, )
Nursing Responsibilities
Administer drug by using 10 R’s
Assessing drug effects
Intervening to make the drug treatment more tolerable
Health teaching abt. The drug
Monitoring overall px care plan to prevent medication error

Legal/Ethical Considerations
Control of Drug Development,
Evaluation {Pre clinical trials} {Phases of Drug studies I - IV} {Approval} {Continual Evaluation}
Pregnancy Category {A – X}
Production {Controlled Substance, Generic Drugs, Orphan Drugs,}
Dispensing {OTC Drugs, Generic Drugs, DAW Drugs}

R’s of Drug Administration
Right drug and patient
Right storage of drug
Right route
Right dosage
Right preparation
Right timing
Right recording/ documentation
Take complete px drug hx
Know if px has any drug allergies
Be aware of potential drug – drug or drug – food interactions
Teach your px about the drug he is receiving

Routes / Sites of Administration
Enteral:
Oral
Solid
Liquid
Meds by NGT
Enteral feedings
Rectal
Disposable Enemas

Parenteral
Intradermal
Subcutaneous
Intramuscular
Intravenous
Percutaneous
Topical
Creams, lotion, ointments
Patch testing for allergies
NTG (Transdermal)
Medication to Mucus membranes
Topical powder

PHARMACODYNAMICS - how the drug affects the body
DRUG ACTIONS:
To replace or acts as a substitute for missing chemicals.
Increase or stimulate certain cellular activities.
To decrease or slow cellular activities.
To interfere with the functioning of foreign cells such as invading microorganism or neoplasm

Receptor Sites – specified areas in the cell that allows certain chemicals to cause an effect in the cell
AGONIST – direct interaction of drug that causes same activity (Ex. Insulin-Insulin Receptor)
ANTAGONIST – has an affinity for a receptor but displays no intrinsic activity
Prevents a response from occurring

COMPETITIVE ANTAGONIST - competes c agonist for receptor sites Ex. (Curare vs. acethylcholine receptor sites)
NON COMPETITIVE – binds to receptor sites & blocks the effect of the agonist (protects / prevent another antagonist from entering)
DRUG ENZYME INTERACTIONS – drug effects by interfering c enzyme system that acts as a CATALYST for various chemical reactions
blocks the cascade effect of enzyme
SELECTIVE TOXICITY – choosy? Ex. (penicillin attacks enzyme system unique to bacterial cell death)
NON SELECTIVE TOXICITY – not so choosy? Ex. (chemotherapeutic drugs destroying normal & neoplastic cells)

PHARMACOKINETICS – how the body acts on the drug
CRITICAL CONCENTRATION – sufficient / high concentration of the administered drug working at the (molecular level ) reactive tissues
DOSAGE – based on the amount that must be given to eventually reach the critical concentration
LOADING DOSE – usually drugs that are needed to take effect quickly Ex. (Aminophylline, Lanoxin)
DYNAMIC EQUILIBRIUM – actual concentration that a drug reaches the body
FACTORS:
ABSORPTION FROM THE SITE OF ENTRY
DISTRIBUTION ON THE ACTIVE SITE
BIOTRANSFORMATION IN THE LIVER
EXCRETION FROM THE BODY

ABSORPTION- what happens to a drug from the time it is introduced to the body until it reaches the circulating fluids and tissues.
Areas of Absorption:
GI, Orally, Rectally, Skin, Mucus Membranes, Lungs, Muscles, Subcutaneous
How Drugs are absorbed:
☺ Passive Diffusion- Major process of absorption
- when there is ↑concentration in one side, drug molecules moves towards the area of ↓concentration

- movement towards the other side is faster if the molecules are smaller, soluble in water and lipid
- no electrical charge that could repel it from the cell membrane
Effortless process, passive process.
Most common in oral form of medication.
☻ Active Transport – uses energy to actively move a molecule across a cell membrane
- Molecule moves from an area of ↓ concentration to area of ↑concentration (usu. electrolytes)

☻ ADMINISTRATION & ABSORPTION ☺
Ж ORAL – most common, non invasive, practical & viable
easily broken down by the gastric juices
affected by presence or absence of food in the stomach
Ideal timing for administration ( ? )
Ψ INTRAVENOUS – drugs that cannot survive in enough quantity hen given orally
- Reaches their full strength @ the time of injection
More like ly to cause toxic effect (↑ margin for error )
Ω INTRAMUSCULAR – absorbed directly in the capillaries in the muscles & sent into circulation (1-5cc) (site of giving?)
- Takes effect faster in men than in women ( Tº? )

Ф SUBCUTANEOUS –small amt(0.5 – 1cc)usually in the upper arm, abdomen, thigh
- drugs move rapidly in vessels than in oral
ß RECTAL / VAGINAL – absorbed by the perfusion of local blood flow in the rectum/ vagina
- treatment of local irritation or infection
Ξ RESPIRATORY – available in all forms that targets the lungs
- mostly in gas or inhalation form or mist
- (ET route?)
₤ BUCCAL/SUB LINGUAL & TRANSLINGUAL – common route for certain cases of emergency
- drugs prevent destruction/transformation in the GI

 TOPICAL – superficial or external use only
- used for dermatologic, ophthalmic, otic and nasal preparation
♣ SPECIAL AREAS / INFUSIONS – given to a specific area of the body
Epidural – injected in epidural space
Intrapleural – injected in the pleural cavity
Intraperitoneal – injected in the peritoneal cavity
Intraosseus – injected in the rich vascular bone network(long bone)
Intra-articular – injected into a joint

FIRST PASS EFFECT – liver synthesizes and breakdown much of the component thereby needing a ↑ dose to have a desired effect
- ◙ drug -> stomach -> small intestine -> portal venous system (liver)-> heart(® side) -> heart (left side)-> systemic circulation-> area (affected) in need of
drug ☼
THINGS to consider in first pass effect
Px diet / food preference
Drug preparation / formulations
Liver affectation

DISTRIBUTION – movement of the drugs that survived the first pass effect thru the body tissues
FACTORS:
BLOOD FLOW - ↑ blood flow ↑distribution & absorption
SOLLUBILITY – fat soluble (easily crosses cell membrane, can cross BBB CNS) or H²O soluble
BINDING – drugs bind c plasma protein (albumin)
FREE / UNBOUNDED – exerts effectiveness, excreted quickly
BOUNDED – slow release, long duration of action, hard to dispose

METABOLISM / BIOTRANSFORMATION – Conversion of drugs by the ◙ LIVER☼ thru the use of bodily system, enzymes
Ability of the body to change a drug from its dosage form to a more water soluble form
► EXCRETION – Elimination of drugs from the body (kidneys, lungs, skin, salivary, mammary glands, GI tract)
♥ ½ LIFE♦ - The time it takes for the amt. of drug in the body to ↓ to ½ of the peak level it previously achieved
- time it takes for ½ of the drug to be excreted by the body

Factors:
Rate of absorption
Metabolism
Appropriate dose
Excretion
Variables Influencing Drug Action
Age
Gender
Weight
Physiological
Pathological
CV
Liver / Kidney dse.
Genetic
Psychological
Environmental

TOLERANCE - ↑ Resistance to a drug effect 2° to ↑ biotransformation of drug components.
DEPENDENCE – may come about if px manifest withdrawal S/Sx when drug is stopped.
DRUG – DRUG INTERACTION
SITUATIONS:
At the site of absorption (tetracycline vs. Ca & Ca products*)
During distribution (ASA* vs. methotrexate)
During metabolism (coumadin* vs. anti tb)
During excretion (Lanoxin vs. Quinidine*)
At the site of action (Anti HPN vs. AH’s*)

DRUG TO FOOD INTERACTIONS : SOME FOODS AFFECTS DRUG FUNCTION AND EFFICIENCY
TETRACYCLINES vs. Fe / Ca
DRUG TO LAB TEST : GIVING DRUGS PRIOR TO A LAB TEST CAN ALTER THE RESULT
ATB prior to sputum/ wound GS/ CS
Anti DVT (Fragmin) alters (↑) liver fxn test exams

PHARMACOTHERAPEUTICS – USE OF DRUG TO TREAT/ CURE A DISEASE
ACUTE – CRITICALLY ILL Px THAT REQUIRES INTENSIVE THERAPY Ex.(Thrombolytics for AMI px)
EMPERICAL – BASE ON PRACTICAL EXPERINCE RATHER THAN SCIENTIFIC DATA Ex.( EMPERIC ATB prior to GS / CS)
SUPPLEMENTAL – REPLENISH / SUBSTITUTE FOR MISSING SUBSTANCE IN THE BODY Ex. (Ca for Osteoporotic px. Vit. B complex for DM px)
SUPPORTIVE – DOES NOT TREAT THE CAUSE OF THE DISEASE BUT MAINTAINS OTHER BODY SYSTEMS INTEGRITY UNTIL Px CONDITION IMPROVES Ex. ( O² in a PTB px)
PALLIATIVE – FOR END STAGE / TERMINAL Dse. PROMOTION OF COMFORT IS TOP PRIORITY Ex. (Bone CA px having continous M SO4 drip)

ADVERSE EFFECTS – HARMFUL / UNDESIRABLE EFFECTS THAN HAT HAS BEEN EXPECTED OF A DRUG
KINDS:
DOSE RELATED ?
Px RELATED ?
DRUG ACTIONS:
Primary – can be caused by simple overdose Ex. (overdose of blood thinners can lead to profuse bleeding)
Secondary – good or bad effect Ex. (AH’s can promote sleeping but what if the px will drive a vehicle)
Hypersensitivity - ↑ response to 1° / 2° drug actions that can lead to a pathological condition

DRUG ALLERGY – Occurs when the body forms an antibodies to a particular drug causing an immune response upon re- exposure
TYPES
ANAPHYLACTIC –
CYTOTOXIC
SERUM SICKNESS
DELAYED RESPONSE
IDIOSYNCRATIC EFFECT – Non pharma related but can be genetic in origin
IATROGENIC EFFECT – Adverse drug reaction that tends to mimic a pathology Ex. (ASA cause GI irritation that mimics PUD)

Nursing process Asssessment Nursing Dx Planning Intervention Evaluation

DERMATOLOGICAL
RASH / HIVES - Assessment: color, turgor, pattern & other pertinent data Intervention: frequent skin care, avoid friction, rubbing, and tight clothing, hydration
STOMATITIS – Assessment: observe for gingivitis, glositis, odinophagia, halitosis Intervention: frequent, proper oral care a non irritating solution, evaluate diet tolerance
SUPER INFECTION – Assessment: S/Sx on infection(fever, diarrhea, itching, redness, pain, warmth, discharge Intervention: proper body hygiene (bathing, hand washing etc.,) DC causative meds.
BLOOD DYSCRASIA – Assessment: fever, chills, ↓Hct /Hgb (Anemia), ↓Platelet count (thrombocytopenia), ↓ WBC (leukopenia), ↓CBC (pancytopenia) Intervention: supportive tx, prevent injury, monitor all lab exam / result

TOXICITY
LIVER TOXICITY – Assessment: fever, malaise, N & V, jaundice, stool change, altered LOC, ↑ liver enzyme lab results Intervention: hygiene, frequent rest periods, DC causative drugs, monitor for bleeding and altered LOC.
RENAL TOXICITY – Assessment: URINE (color, character, amount) monitor BUN, CREA level, edema Intervention: Strict / accurate I & O ( q 1 – q shift – q 24°), DC causative meds  (gentamycin, ampothericin B)
POISONING – Occurs hen an overdose of drugs affects multiple body systems c possible or potential fatal reactions.

ALTERATIONS IN GLUCOSE METABOLISM
Hypoglycemia- OHA, Insulin
Assessment: S/Sx: fatigue, drowsiness, hunger, , anxiety, headache, cold clammy skin, shaking and lack of coordination, ↑HR, ↑BP, numbness and tingling of mouth, tongue and lips, confusion, rapid shallow respiration, seizure and coma
Interventions: Give hyperglycemic agents IV or Oral to prevent injury and falls

Hyperglycemia: Ex. (Ephedrine- bronchodilator/ Anti asthma that relieves nasal congestion causes ↑glucogenolysis
Assessment: fatigue, polyuria, ↑thirst (polydipsia), deep respirations (kausmauls), restlessness, polyphagia, nausea, dry flushed skin, fruity odor breath
Intervention: Insulin, OHA

ELECTROLYTE IMBALANCE
Hypokalemia- drug affects kidneys can cause ↓ K level in serum by altering renal exchange system (proximal tubules)
Assessment: weakness, numbness, muscles cramps, nausea and vomiting, ↓bowel sounds, Hypokalemic paralysis
Interventions: K rich diet (unless CIx, K supplements prevent injury or falls)

HYPERKALEMIA - ↑K supplements, ↑K sparing diuretics, ↑K rich diets in renal problems
Assessment: weakness, DOB, bradycardia, Ms cramps, Numbness
Intervention: Monitor px status (CV,LOC, Homeostasis) diet modification, K wasting drug regimens / protocols, monitor lab exams.

SENSORY EFFECTS
OCCULAR TOXICITY – Tiny blood vessels in the retina “END ARTERIES” are affected, occluded by some drugs Ex. ( Chloroquine) Aralen causes inflamation, retinal damage, blindness
ASSESSMENT: observe for visual acquity, color or vision changes, corneal, retinal affectation
INTERVENTION: supportive tx, prevent injury, optic care – hygiene, proper drug administration

AUDITORY TOXICITY : Tiny vessels & nerves can be affected by some drug hearing affectation / disturbance Ex. (ASA can cause tinnitus or aural fullness hen given in excessive doses)
ASSESSMENT: hearing acquity, Rine’s test, Rombergs test,
INTERVENTION: Prevent injury, monitor for perceptual losses, symptomatic drug treatment, (speak in medium tone firm voice)

Nursing process Eval Intervention/ Implementation Planning Nsg Dx Assessment

Common household measurements:
1quart= 4 cups 1pint = 2 cups
1cup= 8 ounces 1tbsp= 3tsp: 15 – 16 ml
1tsp = 60ugtts: 4-5ml
Apothecary Measurements:
60minims = 1fluidram 8fluidram=1fl oz; 480minims 16 fl oz =1 pint 2pints=1quart
4quarts = 1gallon

Metric measurements:
Units of length (meter)
1mm = .001m 1cm = .01m
1hectometer = 100 meters
Units of volume (liter)
1ml = .001L 1decaliter = 10 Liters
Units of wt (gram)
1ug/mcg = .00001gm 1mg = .001gm
1cg = .01gm 1dg = .1gm
1dg = .1gm 1kg = 1,000grams

Other unit equivalents
1gm = 15 gr. 1gr. = 60mg
1mg = 1oooug
1ml =1cc;15gtts;60ugtts;1gram
1L = 1qt;1000ml
1gal = 4L; 4qt; 4000cc
1oz = 30gm;30cc
1kg = 2.2lbs
1lb = 16 oz

Drug computations
Formulas:
VOL. OF DRUG TO BE GIVEN:
Q= Desired dose (mg) X vol of stock preparation(cc)
Stock dose
Ex: give 1000mg sulperazone iv q8 stock dose is 1500mg dillute it in 10cc
Solution:1000mg/ 1.5mg x 10cc = 6.67cc iv q 8
Ex: dormicum 7.5 mg was ordered for a px having difficulty to sleep stock dose of dormicum is 15mg/tab. How many tablet will you give?
What time will you give the drug?
Ex: glucophage tab 750mg od was started for a diabetic px. Stock dose is 500mg /tab. Ho many will you give? Nursing considerations?

IV FLUID RATE:
Macrodrops per minute(gtts/min)
= total IVF vol(cc) x 15gtts/cc #hrs(infusion time) x 60min/hr
Ex hook D5Lr 1L x 8 hrs, 16 hrs, 4 hrs.
Solution: 1000cc x 15 gtts /cc
8 hrs x 60 min/ hr
=15000 gtts / cc
480 min/hr
=31.25cc/min

cc / hour
Volume of iv fluid = cc/ hr
# hours to be infuse
Ex: start Pnss 1Liter x 8 hours for a DM patient
1000cc = 125cc/ hr
8 hour

Conversion (annex)
Conversion of T°
°C to ° F = (° C x 1.8) + 32 = °F
°F to ° C = (°F - 32) (.55) =°C
Ex. px has 39.5°c during admission.using the formula, convert it to °F
(39.5C x 1.8) + 32 = 103.°F
Ex.3y/o child has dengue,100.3 °F convert it to °C using the formula
(100.3°F - 32) (.55) = 37.5°C

Computation (annex) pediatric doses
Frieds’s rule: for a child less than 1y/old
childs dose(age ≤1y/o)= infants age(in mos.)
150 mos.
x ave. adult dose
Young’s rule: children 1-12 y/o
childs dose (age1-12 y/o) = childs age (in yrs.)
child’s age (in yrs.) +12
x ave. adult dose
Clark’s rule :
wt. in lbs x usual adult dose = safe child’s dose
150 lbs

NERVOUS SYSTEM - operates through the use of electrical impulse and chemical messengers to transmit information throughout the body and to respond into internal & external stimuli.
CENTRAL NERVOUS SYSTEM
AUTONOMIC NERVOUS SYTEM
PERIPHERAL NERVOUS SYSYTEM
NEURONS – basic functional unit of the nervous system, about 14 billion are located in the brain the rest in the SC, PNS .
PARTS:
DENDRITE – Short, branchlike projections that conveys information from one neuron towards another neuron .
CELL BODY ( SOMA ) – largest part of the neuron
AXON - Elongated, carries information away from the neuron .
EFFECTOR CELLS – Receives the signal sent by the axon(cells, muscles, glands, or another nerve)
AFFERENT FIBERS - Nerve axons that run from PNS to CNS
EFFERENT FIBERS - Nerve axons that carry impulse from the CNS to Periphery

Action potential – Electrical impulse sent by the nerves
☻ cell membranes & nerve membranes have pores or channels that controls the movement of a substance in & out of the cell
☻ some of these channels allows entry & exit of Na, K, Ca
☻ when cells are at rest, membranes are impermeable to Na but permeable to K
Depolarization – Na channels open in response to the stimulus Na ions rush inside the cell (positive rush of Ion ) ☻a nerve cannot be stimulated again during depolarized stage☻
Repolarization - return of the cellular environment to the resting membrane potential ☻stage of responding / balance bet. Na & K occurs ☻
Resting membrane potential- negative environment inside the cell

NERVE SYNAPSE – Where the communication bet.2 nerve occurs thru the release of a Neurotransmitter
NEUROTRANSMITTER - chemical that stimulates the receptor sites by exciting or inhibiting them
☻ may either be reabsorbed (reuptake) or broken down by the enzymes in the area Ex. (MAO breaks down the neurotransmitter Epinephrine) (Acetylcholinesterase breaks don the neurotransmitter acethylcholine)☻
SELECTED NEUROTRANSMITTER
Acetylcholine – communicates in the Ms & N, neurotransmitter in the ANS & Parasympathetic
Norepi / Epi – classified as catecholamines eurotransmitter released by the sympathetic branch of the ANS, released as a hormone by the adrenal medulla
Dopamine – found in ↑ amts. In the brain for coordination of impulse & responses both motor & intellectual. heart ?

Gamma amino butyric acid (GABA) – found in the brain, inhibits or stimulation nerve activity & important in preventing overexcitability or stimulation such as seizure activity
Serotonin – found in the limbic system, important for the in arousal and sleep, prevention of depression and motivation promotion
Ω limbic system – area of the brain that contains ↑ amounts of neurotransmitters ( epi / norepi / serotonin) if responsible for the expressions of emotions ( anger, pleasure, motivation, how a person learns & react to stimuli) Ω

ANXIOLYTICS & HYPNOTIC AGENTS
ANXIOLYTICS – D rugs that alter ‘s the individual’s response to the environment, prevents feelings of tension or fear
ANXIETY - a feeling of tension, nervousness, apprehension, or fear that usually involves unpleasant reactions to stimulus
HYPNOTICS – Drugs causes sleep or minor tranquilizers (provides hypnosis & sense of tranquility in anxious pxs)
HYPNOSIS – Result of extreme sedation & CNS depression / sleep.
SEDATIVES – Drugs that cause calmness, unaware of environment
SEDATION - Loss of awareness and reaction to environmental stimulus. Desirable in (restless, nervous, irritable, or overreacting to a stimulus pxs)

BENZODIAZEPINES: Most frequently used anxiolytics: prevents anxiety w/out causing much sedation
ALPRAZOLAM / XANOR
LORAZEPAM / ATIVAN
DIAZEPAM / VALIUM
Action: Acts in the limbic system & RAS to make GABA more effective causing interference in neuron firing.
Indication : anxiety d/o, AWS, hyperexcitability,agitation.
Pharmacokinetics: well absorbed in the GI,peaks30min- 2hrs, lipid soluble, crosses the placenta, enters breastmilk,
CIx : +allergy, psychosis, shock, coma, narrow > glaucoma, acute alcohol intoxication, pregnancy,
Cautions: elderly or debilitated px
Adverse effects : Mild drowsiness, depression, lethargy,fatigue, restlessness, bradycardia, changes in libido, drug dependence.
Antidote: Flumazenil / Romazicon :

BARBITURATES: former drug of choice prior to benzodiazepines, risk of addiction , and dependence
PHENOBARBITAL / LUMINAL
BUTABARBITAL/ BUTISOL
Action : CNS depressants ↓ neuronal impulse conduction in the RAS, ↓ cerebral cortex, alters cerebellar fxn, ↓motor output .
Ix : Anxiety, sedation, insomnia, seizures, acute manic reactions.
Pharmacokinetics: absorbed well, peaks20-60mins.,induces liver enzymes systems. lipid soluble, crosses placenta, enters breast milk
CIx: +allergy, hepatic / kidney / respiratory d/o dse., pregnancy.
Cautions : acute or paradoxical pain (masking?), lactating women
Adverse effects : somnolence, agitation, confusion, hyperkinesia, ↓BP, syncope, apnea, Stevens- Johnsons

OTHER ANXIOLYTICS & HYPNOTICS : does not fall to benzodiazepines or barbiturates.
AH’s: Benadryl / Dipenhydramine, Phenergan / Promethazine: can be sedating for some peoples, Tx for mild insomnia
Paraldehyde / Paral : sedates px c delirium tremens or psych conditions characterized by extreme excitement. Excreted by the lungs and urine
Buspirone / Buspar : anti anxiety agent, (-) sedative, anticonvulsant,Ms relaxant properties,

AUTONOMIC NERVOUS SYSYTEM: involuntary, visceral nervous system (hypothalamus, medulla & SC)
DIVISIONS:
PARASYMPATHETIC / CRANIO SACRAL DIVISION
SYMPATHETIC / THORACOLUMBAR DIVISION
SYMPATETHIC - fight or flight ↑ CV fxn, BP, PR, RR, dilated pupils, bronchi’s dilate, ↑blood flow to the skeletal Ms., sweating↑, piloerection ,↑RAAS, GLYCOGENOLYSIS, ↓
Adrenergic Transmission: sympathetic nerves that synthesize,stores, release Norepinephrine
RECEPTORS:
ADRENERGIC :
ALPHA ADRENERGIC : (ALPHA 1,) FOUND IN THE BLOOD VESSELS(VASOCONSTRICTORS), IRIS(DILATION), URINARY BLADDER(CONSTRICTION)
ALPHA ADRENERGIC :(ALPHA 2) LOCATED IN THE NERVE MEMBRANES, MODULATORS FOR THE RELEASE OF NOR EPI
BETA RECEPTORS :
BETA 1: FOUND IN CARDIAC TISSUE HAVING (+) INOTROPIC, CHRONOTROPIC EFFECT,↑LIPOLYSIS
BETA 2 : FOUND IN THE SMOOTH Ms.,PERIPHERY(↑Ms & LIVER GLYCOGEN BREAKDON) BLOOD VESSELS(VASODILATION), PERIPHERY, UTERINE Ms.(RELAXED UTERINE MS.

PARASYMPATHETIC - Rest & digest ↑GI motility & secretions, ↓HR, BP,RR, pupillary dilation
Cholinergic Transmission:Neurons that uses ACh
Cholinergic drugs: promotes the action of Acetylcholine
Aka parasympathomimetic drug
Major classes
Cholinergic agonist – mimics the action of acetylcholine, stimulates cholinergic receptors
Anticholinesterase – inhibits acetylcholinesterase, as a result, acetycholine is not broken down and begins to accumulate thus the effect of acetylcholine is prolonged

DIRECT CHOLINERGIC AGONIST:
URECHOLINE
PILOCARPINE
Action: Parasympathetic action that ↓HR,(-)inotropic effect, vasodialtion, bronchoconstriction, ↑mucus, GI activity, bladder tone, relaxed GI, Bladder sphincters, pupil constriction(miosis).
Indications: Acute post op, non obstructive urinary retention, bladder atony c retention
Pharmacokinetics: short half life (1-6hrs), well absorbed
CIx: (+) allergy,pregnant & lactating px’s, Bradycardia, Hypotension, CAD,asthma,
Adverse effects: N & V, cramps, diarrhea,↑salivation, Bradycardia, heart block,hypotension, Cardiac arrest , Urinary urgency.

INDIRECT CHOLINERGIC AGONIST: does not react c ACh receptor sites directly. reacts c Acetylcholinesterase(enzyme responsible for breakdown of Ach)
NEOSTIGMINE
PYRIDOSTIGMINE
Action: cholinesterase inhibitor, ↑ ACh level faciltation of nerve transmission
Indication: Myasthenia gravis , myasthenic crisis
Pharmacokinetics: duration of 2-4 hrs,must be given every few hours
(Pyridostigmine=3-6hrs), does not need to be taken frequently, Oral & Parenteral form, can be given in px that inhaled nerve gases
CIx: cholinergic crisis
(Endophonium iv=used to distinguish if the px is having w/c type of crisis is happening to the px.)

Adverse effects:Bradycardia, Cardiac arrest, tearing,dysphagia, N & V, ↑bronchial secretions, incontinence, urinary frequency.
Myasthenic Crisis – px condition improved p endophonium iv injection
Cholinergic Crisis – px condition gets worst p giving endophonium iv injection
Tensilon Test – Dx test for Myasthenia Gravis
☻ ALL MYASTHENIA GRAVIS DRUGS DOES NOT CROSS THE BLOOD BRAIN BARRIER☻

Alzheimer’s dse – progressive neural degeneration in the cortex leading to a marked memory loss & inability to do ADL’s.- ↑ loss of Ach producing hormones
TACRINE (COGNEX)- mild – mod. dementia .
GALANTAMINE (REMINYL)- mild – mod dementia
RIVASTIGMINE (EXCELON)- liquid, capsule prep
DONEZEPIL (ARICEPT)- o.d. dose only
Action:indirect cholinergic blocks Ach’ase at the cells of the cortex & crosses the BBB
Pharmacokinetics- metabolized by the liver, excreted by the kidney
CIx Cautions:(+) allergy, Liver dse. Pregnant & lactating,bradycardic, intestinal & urinary obstruction
Adverse effect:Insomnia, fatigue, rash,N&V,Ms cramps

Anticholinergic Drugs- used to block the effects of Ach & the PNS (Parasympatholytic agents)
BELLADONA:
ATROPINE ( oral, parenteral, topical )
Action : blocks the effect of PNS there by promoting SNS effects(dilate pupils, ↑HR,RR,PR, ↓GI, URINARY, BLADDER FXN,salivation,bronchial secretions,)
Ix: preop px, severe bradycardia,hyperactive bowel,pylorospasm
Pharmacokinetics: well absorbed,cross the BBB,excreted in the urine
CIx / Cautions: (+) allergy, glaucoma,GI obstruction,Prostate enlargement,bladder obstruction,tachycardia,myocardial ischemia,liver & kidney problem,breastfeeding & lactating px.
Adverse effects: blurred vision, ↑IOP °, cyclopegia,Gi disturbance,dry mouth, insomnia,heartburn, constipation etc
SCOPALAMINE, DICYCLOMINE,PROPANTHELINE

PARKINSONS DSE - progressive neurologic d/o due to marked degeneration in the brain(basal ganglia & substantia nigra) thereby affecting Corpus striatum (helps maintain Ms tone not related to any movement)
tremors leading to rigidity, weakness, bradykinesia, simian posture, difficulty in performing intentional movements, shuffling gait, slurred speech, mask face
* corpus striatum is connected to substantia nigra by series of neuron that uses inhibitory GABA
* substantia nigra sends back impulse to corpus striatum using the inhibitory neurotransmitter Dopamine

☻ higher neurons from the cerebral cortex secrete Ach in the corpus striatum as an excitatory neurotransmitter to coordinate intentional movements of the body=☻
☻↓ dopamine in the area causes imbalance that allows the cholinergic / excitatory cells to dominate = ☻
☻ affecting the fxn of basal ganglia & extrapyramidal motor system (provides coordination for unconscious Ms movements Ex. Position, posture, movement) ☻

type 1(inhibition) antiparkinsonian drug:
Dopaminergic : ↑ effects of dopa @ receptor sites,does not cross BBB proven to be much more effectve than Anticholinergics
* effective only if there’s enough intact neuron in the substantia nigra (unextensive degeneration)
Levodopa (Dopar): precursor of dopamine, crosses the BBB then converted to dopamine usually given c
Carbidopa (Sinemet)= ↓ the effect of dopa decarboxylase enzyme in the GI tract & periphery leading to ↑ dopamine converted in the brain
Amantadine(Symmetrel)- antiviral, ↑release of dopa
Bromocryptine (Parlodel)- dopa agononist acting on dopa receptor directly-does not need further metabolism(more effective than dopar & Sinnemet

Pergolide (Permax )- adjunct to carbi-levodopa.
Pramipexole (Mirapex)- effective if levodopa effect has decreased
Ropinirole (Requip) – new drug. Used in early & late stage of PD when levodopa has lost its adequate effect.
Apomorphine iv (Apokyn)- new drug.dopa agonist that manages hypomobility in PD.given SQ route
Actions: ↑ level of dopa in the substantia nigra
Pharmacokinetics: absorbed well in GI & body
CIx/ ^Cautions : (+)allergy, closed angle glaucoma,^CVD, asthma,liver, renal dse.
Adverse effects:anxiety,nervousness,arrythmias

type 2 (stimulation) antiparkinsonian drug:
Anticholinergics: opposes the effects of Ach @ receptor sites in the
Benztropine (Cogentin)- oral,im,iv for parkinsons due to phenothiazines
Biperiden (Akineton)- oral, im, adjunctive tx for PD due to phenothiazines
Dipenhydramine (Benadryl) used in px ho cannot tolerate more potent type of anti PD drugs(Old pxs)
Procyclidine (Kemadrin)- oral,for any type of parkinsonism, controls excessive salivation due to use of neuroleptics
Trihexyphenidyl ( Artane)- used c levodopa, used alone for control of drug induced Extrapyramidal d/o.

Action: ↓ tremors & rigidity, drooling assoc. c PD
Ix: Parkinsons dse., Parkinsonism(idiopathic, atherosclerotic,postencephalitic)releif of Extrapyramidal d/o due to phenothiazines
Pharmacokinetics :variable absorption in GI, 1-4 hrs, metabolized in the liver
CIx /^ Cautions: (+) allergy, closed angle glaucoma,GI, GU obstructions, prostate enlargement ^tachycardia, hypo/hypertension, pregnant & lactating px
Adverse effects : disorientation,confusion, memory loss, agitation,delirium,weakness,dry mouth, N & V, ↓ GI, GU activity

Psychotherapeutic Agents: drugs aiding in the Tx Mx of mental d/o.
Psychosis: perceptual & behavioral d/o
Schizophrenia- most common type. (hallucinations, paranoia, delusion, speech abnormality, affective problems) strong genetic predisposition
Mania- assoc. c bipolar illness (manic-depressive) periods of extreme depression followed by hyperactivity & excitement.
Narcolepsy- char. by daytime sleepiness &sudden loss of wakefulness. Problem c RAS
Attention-deficit d/o- inability to concentrate on an activity for longer than a few minutes & hyperkinesis

Antipsychotic /Neuroleptics, Major tranquilizers
Antipsychotic - eliminate S/Sx of psychosis
Neuroleptic- adverse neurobiologic effect causing abnormal body movements
Major Tranquilizers- can calm agitated patient
Major types: Typical & Atypical
TYPICAL –dopamine receptor blocker{Phenothiazines} Ex: Chlorpromazine/Thorazine, Fluphenazine/Prolixin,Haldol/haloperidol
Action: blocks dopa receptor,prevents stimulation of neuron by dopa,depress RAS

Ix : hallucination, schizophrenia, anxious/agitated px, dellusions, ADHD
Pharmacokinetics: absorbed in GI, still present 6mos, p last dose, children metabolizes drugs faster than old px
CIx/^ Cautions: (+) allergy, PD, CAD, blood dyscrasia, ^glaucoma, PUD, GI/Urinary obstruction
Adverse Reaction: weakness, EPS (dystonia, akathisia, tardive dyskinesia), hypotension, urine color turns pink to reddish brown (minor harmless effect)

Atypical- blocks dopa & serotonin receptors
Ex. Clozapine, Olanzapine, Risperidone,Quetiapine,
Action: blocks dopa & serotonin receptors, depress RAS
Ix: Schizophrenia unresponsive to typical type,
Pharmacotherapeutics: 4-12hrs, metabolized in the liver excreted in urine & feces.
Adverse effects: drowsiness, sedation, seizures, diziness

MANIC- opposite of depression, overstimulation of certain neurons in the brain
ANTI MANIC DRUGS- drugs used to treat manic d/o Ex: Lithium salt, Lamictal, Seroquel,Zyprexa
Ix: Manic d/o, Manic-depressive (bipolar)
Action: alters Na transport in Ms & Nerves;( ↓ dopa & norepi but not serotonin) Neurons; ( ↑ storage of neuronal dopa & nor epi, ↓ content of 2 nd messengers )
Pharmacokinetics- absorbed in GI,30min-3hrs peak level when px is dehydrated: lithium more absorbed than Na=toxic level,enters breastmilk.
CIx / ^Caution:(+) allergy, Renal, Liver, Cardiac Dse. Dehydration( ↓ Na ),pregnant & lactating px

Adverse effects: therapeutic level: 0.6- 1.2mEq/L
Serum level 1.5=CNS problem: lethargy, slurred speech, Ms. weakness, fine tremor,renal gastric toxicity
Serum level 1.5-2= Intensified above S/Sx +ECG changes
Serum level 2~2.5= progression of effects renal pulmonary fatalities
Serum level >2.5= Complex multi organ toxicity c significant risk of death

CNS Stimulants: Tx for attention deficit d/o & narcolepsy,
Methylpenidate/Ritalin,Concerta-both
Dexmethylpenidate/Focalin- Ix:6y/o px only
Dextroamphetamine/Dexedrine
Modafinil/Provigil-narcolepsy
Pemoline/Cylert-adhd
Action: releases catecholamines from presynaptic neuron= increase stimulation of post synaptic neurons
Pharmacokinetics: rapidly absorbed in GI,peaks 2-4hrs. Half life =2-15hrs

CIx /^Cautions : (+) allergy, anxiety, agitation,fatigue, galucoma,^hx of seizures, drug dependence,alcoholics
Adverse effects : nervousness,insomnia,dizziness, headache,blurred vision & difficulty c accomodation, anorexia, nausea, wt. loss, HPN, arrythmias, angina,

Epilepsy - sudden dc of excessive electrical energy from the cells of the brain.
Classifications:
Generalized- begins in one area of the brain & rapidly spread throughout both hemispheres.px often loses consciousness as a result of massive abnormal electrical brain activity
Tonic-clonic -aka Grand mal, loss of consciousness, confusion & exhaustion upon recovery
Absence- aka petit mal, abrupt, brief(3-5secs)loss of consciousness

Myoclonic- short, sporadic periods of Ms contraction for several minutes
Febrile-most common in children,
Status epilipticus- most dangerous type seizures recur over & over
Partial – aka focal seizures , involves one area of the brain, S/Sx depend on exactly where the abnormality occurs.
Simple partial – single area of the brain affects a single Ms.
Complex partial- hallucinations,mental distortion,involuntary urination

Drugs for tonic-clonic seizures
HYDANTOINS- stabilizes N membranes & limit the spread of excitability.
Phenytoin (Dilantin) – therapeutic level10-20ug/ml
Ethotoin (Peganone) – therapeutic level 15-50ug/ml
Fosphenytoin (Cerebyx) – short acting
Mephynytoin (Mesantoin) –sev. multi system toxicity
Ix: tonic-clonic seizures
Pharmacokinetics: 6-4hr:met. In liver,excreted by kidney
CIx ^Cautions: (+)allergy, hepatic & renal dse.
Adverse effects: nystagmus, ataxia, slurred speech, confusion, S’s J’s syndrome fatigue.

BARBITURATES & B -LIKE DRUGS
Phenobarbital( Luminal)–therapeutic level 15-40ug/ml
Primidone (Mysoline)-therapeutic level 5-12ug/ml
Mephobarbital (Mebaral)-causes ↓BP,↓HR, circulatory collapse.
Action: CNS depressants, inhibits impulse & conduction in the ascending RAS, ↓cerebellar fxn, ↓motor output
Pharmacokinetics: 79 hr: metabolism
Adverse effects: Somnolence, insomnia, vertigo, nightmares, lethargy, nervousness, bradycardia, depression, withdrawal syndrome

BENZODIAZEPINES- ↑ the effects of GABA(causes stimulation of Limbic & RAS)
DIAZEPAM (Valium)-releives tension, anxiety & Ms spasm, not used for long time Tx of seizures half life= 20-50 hrs
CLONAZEPAM (Klonopin)-usu for petit mal & myoclonic half life =18-50hrs
Ix: Anxiety d/o, AWS, Ms relaxant, Status Epilipticus
CIx ^ Cautions: allergy, pregnant, liver kidney dse.
Adverse effects: drowsiness, sedation, depression, disorientation,diarrhea, incontinence, withdrawal

PETIT MAL DRUGS
SUCCINIMIDES – supresses the abnormal elctrical activity in the brain
ETHOSUXIMIDE (Zarontin)- drug of choice for petit mals/ absence seizures,often used first. thera level=40-100ug/ml
METHSUXIMIDE (Celontin)- can cause bone marrow depression.
Pharmacokinetics: peaks 1-7 hrs, halflife: 30-60hrs, metabolized in liver, excreted in the urine & bile
CIx ^ Cautions: allergy, renal, hepatic dse, pregnancy
Adverse effects: drosiness, ataxia, headache,diarrhea

PETIT MALS DRUGS (annex)
Depakene (Valproic acid)- drug of choice in tx myoclonic seizures peaks 1-4 hrs. half life 6-16 hrs
Acetazolamide (Diamox)- for absence seizure in children, for open angle glaucoma, ↓edema in CHF px s, half life 2.5 – 6 hrs.
Zonisamide (Zonegram) – new drug. Inhibits voltage sensitive Na & Ca channels, px should be hydrated due to possibilities of renal calculi

FOCAL SEIZURE DRUGS
CARBAMAZEPINE (Tegretol) – drug of choice, ability to block Na channels to prevent repetitive action potentials in the abnormal focus
CLORAZEPATE (Tranxene) –also used for anxiety, alcohol wihtdrawal
FELBAMATE (Felbatol) – usually given if other medications fail.causes liver toxicity & aplastic anemia
GABAPENTIN (Neurontin) – adjunctive therapy for other seizure drugs
LAMOTRIGINE (Lamictal) – adjunctive therapy

LEVETIRACETAM (Keppra)- newer drug,renal toxicity
OXCARBAZEPINE (Trileptal) – for px 4-16 y/o
TOPIRAMATE (Topamax)- interferes Na channels causing stability of nerve membranes
CIx^ Cautions:(+) allergy, bone marrow supression,^pregnancy, liver & kidney dse.
Adverse effects: drowsiness, ataxia, dizziness, nausea, vomiting, hepatitis, CV complications, S’s J’s syndrome

PAIN – sensory & emotional experience assoc.w /actual or potential tse damage.
PAIN PERCEPTION:
Painful stimulus  free nerve endings (nociceptors)  release of prostaglandin  pain receptors (A-delta-small, fast,myelinated fiber / Cfiber-slow,unmyelinated)  ascending tracts (spinothalamic tracts-beginning of the gate control theory)  hypothalamus  thalamus  cerebral cortex

NARCOTICS - aka opiods.
OPIOD RECEPTORS- receptors (CNS, GI, Periphery)that respond to endogenous opiates (Endorphin, Enkephalin)
BRAINSTEM-opioid receptors helps control BP, pupil diameter.
GI- opioid receptors regulates N & V cough
SC & THALAMUS- opioid receptors help integrate & relate incoming info abt. Pain
HYPOTHALAMUS- opioid rceptors interrelate the endocrine & neural response to pain
LIMBIC SYSYTEM- opioid receptors incorporate emotional aspects of pain & response to pain.

Peripheral Nerve sites- opioid receptors may block release of neurotransmitters that are related to pain & inflammation
4 types of opiod receptors
Mu(u) - 1°pain blocking receptors (analgesia) ↓RR, GI activity, euphoria, ↑pupil constriction
Kappa (k)- assoc. c some analgesia, pupil constriction, sedation, dysphoria
Beta(ß)- reacts c enkephalins in the periphery to modulate pain transmission
Sigma( E )- pupillary dilation, maybe responsible for hallucinations, dysphoria, psychose assoc. c narcotic use

NARCOTIC AGONIST- drugs that react c opioid receptors throughout the body to cause analgesia sedation, euphoria (controlled substance)
FENTANYL (Duragesic)
MEPERIDINE (Demerol)
OXYCODONE (OxyContin)
MORPHINE (Astramorph)
Action: analgesia, antitussive, adjuncts to general anesthesia
Ix : severe acute or chronic pain, pre op meds, analgesia during anesthesia
Pharmakokinetics: fastest route is iv, greater absorption in male, most are in preg. category C (except oxyxodone –B- do not cut, crash meds!! -Fast effect)

CIx ^ Cautions: (+) allergy, pregnancy, labor, lactation,^ respiratory dysfxn, recent GI & GU surgery, head injuries, alcoholism, liver & kidney dse.
Adverse effects: respiratory depression, hypotension, shock, biliary spasm, constipation, hallucinations, anxiety, fear, ureteral spasms, dependence

NARCOTIC AGONIST – AGONIST – stimulates certain opioid receptors & blocks some. Has less abuse potential than pure narcotics
BUPRENORPHINE (Buprinex)- mild-mod. Pain
BUTORPHANOL (Stadol) – preop med mod.-sev. Pain, effective in tx of migraine headache.
NALBUPHINE (Nubain) – mod. – sev. Pain, adjunct for gen anesthesia
PENTAZOCINE (Talwin)- prefered in shifting iv- oral pain killer, highly hallucinogenic & euphoric (+ tripelannamine)
Pharmacokinetics: well absorbed iv-im, crosses placenta

CIx /^Cautions: allergy,pregnancy, lactation, ^COPD & CV dse px.
Adverse effects: respiratory depression, apnea, suppression of cough reflex, N & V, constipation, biliary spasm,psychose, lightheadedness, GU & GI affectations

NARCOTIC ANTAGONIST
NALMEFENE (Revex)
NALOXONE (Narcan)- tx & dx of narcotic use
NALTREXONE (ReVia)
Actions: blocks opioid receptors & reverse the effects of opioids.
Ix: narcotic overdose (resp. depression, sedation)
Pharmacokinetics- well absorbed p injection, passes in the placenta & breast milk.
CIx^Cautions: allergy,^ pregnant / lactating px.
Adrese effects: acute narcotic abstinence syndrome (n & v, svveating, tachycardia, hypotension, pulmonary edema.

Nsg implementation:
Maintain patent airway /provide artificial ventilation
Continous px monitoring
Administer narcotic antagonist
Comfort, safety measures
Thorough health teaching abt. drug ( brand name , dosage, time of taking, cautions etc. )

MIGRAINE HEADACHES- sev. Throbbing headaches on one side of the head. 2° to arterial dilation
COMMON- occurs s aura, sev. Unilat. Pulsating pain usu. accompanied by N&V light & sound sensitivity (aggravated by physical activity)
CLASSIC- preceded by aura, sensation (sensory & motor disturbances .5 hrs prior to headache
CLUSTER HEADACHES- starts during sleep (Sharp, steady eye pain 15-90mins) c sweating, flushing, tearing & nasal congestion
TENSION HEADACHE-during stress (dull band of pain around entire head 30mins-1wk.) anorexia, fatigue, mild intoleranec to light / sound.

ERGOT DERIVATIVES-cause cranial vasocontrictions, ↓ pulsations of cranial arteries
DIHYDROERGOTAMINE (Migranal)-po, iv,nasal spray
ERGOTAMINE- previous drug of choice, SL
Actions: blocks alpha adrenergic & serotonin sites in the brain causing constriction of vessels & ° ↓ arterial pulsation
Ix: prevent & abort vascular & migraine headaches
Pharmacokinetics: rapidly absorbed c in 30 mins.
CIx ^Cautions : allergy, pregant & lactating px, ^ pruritus, GI reactions.
Adverse effects: numbness, tingling fingers & toes, Ms pain, thready pulse, chest pain

Nsg implementation:
Know px drug Hx/allergy,
Hx taking for CV dse.
r/o pregnancy & lactation
Continous monitoring for any adverse reaction post drug administration.
Health teaching abt drug being administered.

TRIPTANS- new class. Causes cranial vasoconstriction & migraine relief (-) CV, GI effects vs ergot derivatives
SUMATRIPTAN (Imitrex)- very effective in cluster headache
NARATRIPTAN ( Amerge) – causes birth defects
RIZATRIPTAN (Maxalt) – for migraine (c / s )aura
Actons: binds to selective serotonin sites causing vasoconstriction
Ix: Tx but not prevention of migraines
Pharmacokinetics: liver metabolizes, excreted by kidney, crosses placenta

CIx ^ Cautions: allergy, pregnant / lactating px. ^ elderly px , CAD px
Adverse effects: dizziness, vertigo, weakness, myalgia, chest pain, tingling, numbness
Nsg. Implementation:
know drug allergy / Hx
Use 10 R’s of drug administration
Px comfort & safety
Monitor CV functioning & other VS
Observe for any adverse effects
Health teaching

ANESTHETICS: drugs that cause complete/partial loss of sensation
GENERAL- CNS depressants produces loss of pain & consciousness. blocks body reflex
Goals: (analgesia, unconsciousness, amnesia)
Risk Factors:
CNS= neurological d/o dse (SE, CVA, MG)
CV= cv dse/abnormality (CAD, hypotension)
RESPI= abnormal V/Q perfussion ratio (COPD, Asthma, etc)
Renal & Hepatic: altered met & excretion of drug (ARF, ESRD, Hepa A-E, cirrhosis, etc.)
LOCAL- cause loss of pain sensation & feeling in a designated area or body part

Balance Anesthesia- use of combination of drug(s) each c a specific effect (analgesia,Ms relaxation, unconsciousness, amnesia)
Pre op meds- anticholinergics, atropine SO4
Sedative-hypnotics - dormicum
Antiemetics - plasil
Antihistamines - benadryl
Narcotics - nubain (nalbuphine)
Stages of Anesthesia
Stage 1: Analgesia stage(loss of pain sensation) px is still consciouss & able to communicate
Stage 2: Excitement stage(excited & may be combative behavior) usu. c SNS response ( ↑ PR, BP, RR)

Stage 3 Surgical Anesthesia (relaxed skeletal Ms, Normal RR, loss of eye reflexes, dilated pupil) surgery can be safely performed
Stage 4 Medullary Paralysis CNS depression, respiratoty & vasomotor stimuli loss. (death can occur)
INDUCTION- from beginning of anesthesia – stage 3. *stage 2 = danger pd.
MAINTENANCE –from stage 3- until surgery is complete (usu. Gas anesthetics given)
RECOVERY- from dc anesthesia-cosnciousness regained (movement, ability to communicate) *px must be continously monitored*

TYPES OF GEN. ANESTHESIA
BARBITURATES
THIOPENTAL (Pentothal)-most common, rapid onset, short recovery pd (- analgesic prop.)
METHOHEXITAL (Brevital)- rapid onset, must not be in contact c silicon, (- analgesic prop.) causes resp. depression, apnea.
NON BARBITURATES
MIDAZOLAM (Dormicum)peaks 30-60mins, N&V are often
KETAMINE (Ketalar)- causes hallucinations,dreams, psychotic episodes
DROPERIDOL (Inapsine)- CIx in renal & liver dse.

ANESTHETIC GASES- enters the bronchi & alveoli  capillary system  heart  systemic circulation  tissues/fats (nerves)  brain= CNS depression
NITROUS OXIDE ( BLUE CYLINDER )- potent analgesic, least toxic usu in dental practice
Cyclopropane ( orange cylinder ) – not good analgesic,causes headache, N & V,
Ethylene ( red cylinder )- less toxic, unpleasant taste in mouth

VOLATILE LIQUIDS- unstable gas @ rm T° & release gases
HALOTHANE (Fluothane)- rapid onset & recovery,( ↓HR, BP, ) liver toxic
DESFLURANE (Suprane)- causes cough & laryngospasm
ENFLURANE (Enthrane)- causes renal toxicity, arrythmia
METHOXYFLURANE (Penthrane)- slow onset, used in labor & delivery
SEVOFLURANE ( Uthane)- newest form,

LOCAL ANESTHETICS-loss of sensation in local area of the body ( T°, touch, proprioception, skeletal Ms tone)
TYPES OF ADMINISTRATION:
TOPICAL-cream, spray, lotion (skin, nose, throat, mouth, urethra, rectal)
INFILTRATION-injecting directly in area (wound dehis) that needs resuturing
FIELD BLOCK-injected all around the area that ill be affected by the operation (tooth extraction)

NERVE BLOCK-injected some point along the nerve that’s responsible for the sensation of area involve
peripheral nerve block- blocks sensory & motor aspectsof a particular nerve for a relief of pain.
central nerve block-injected into the roots of the nerves
epidural block-injected in the space where the nerves emerge from the SC
caudal block-injection in sacral canal below the epidural area

INTRAVENOUS & REGIONAL ANESTHESIA- carefully draining all blood from the extremities, securing it c torniquet (prevent anesthesia from entering the general circulation) & injecting it in the vein.
GEN. KINDS:
ESTERS : BENZOCAINE, PROCAINE, TETRACAINE
AMIDES: LIDOCAINE, BUPIVACAINE, DIBUCAINE, ROPIVACAINE
OTHERS: DYCLONE, PRAMOXINE

Action: temporary interruption in production & conduction of nerve impulse.
Affects permeability of nerves membranes to Na ions thereby preventing the nerve from depolarization
Ix: infiltration, nerve blocks, spinal anesthesia, local pain relief
Pharmacokinetics: ester types are easily broken down by plasma esterases. amides types are broken down much longer (toxicity prone)
CIx: ^Cautions: allergy, heart block, shock, ^liver & kidney dse. hypotension

Adverse effects: skin injury, headache, restlessness, anxiety, tremors, blurred vision, N & V, arrythmia, cardiac depression
Nsg Intervention:
assess CV & Respiratory function
Maintain patent airway
check for gag & swallowing reflex
Spinal anesth px must remain flat on bed x 12hrs
Proper hydration

NMJ- area of communication bet. the nerve & Ms.
Neuromuscular Junction Blocking Agents- blocks the area of communication bet. Nerve & Ms.
Non Depolarizing NMJ agent: ( CURARE) TUBOCURARINE-adjunct to Gen. anesthesia
Action: occupies the muscular cholinergic receptor site preventing Ach from reacting c the receptor
Ix: induce skeletal relaxation, ECT, Ventilated px.
Pharmacokinetics: metabolized by liver & excreted unchange by the liver
Adverse effects: respiratory depression, apnea, bronchospasm, cardiac arrythmia.

Depolarizing NMJ blocker: attaches to the Ach receptor site on the Ms cell, depolarizing it.hydrophillic & does not cross BBB
Succinylcholine - adjunct to gen. anesthesia
Action: combines c ACh receptors causing flaccid paralysis. Prolongs depolarization (Ms contracts first & then leading to paralysis)
Ix: facilitate ET intubation, induce skeletal Ms relaxation, ECT,
Pharmacokinetics: metabolize in the plasma & liver by the use of cholinesterase
CIx ^ Caution: allergy, MG, renal & hepatic Dse. pregnant^ CV dse. Malignant hyperthermia,

Adverse effects: respiratory depression, Ms paralysis, bronchospasm, hypotension, arrythmias,, GI, dysfxn, paralysis, decubitus ulcer
Nsg. Implementation:
Must be given by specialist
Not be mixed c alkaline soln.
Monitor px’s overall status & recovery
Maintain cholinesterase inhibitor
Maintain cmfort & safety
Close monitoring of VS & neuro VS

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Nursing Pharmacology Prelim

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