CH 9 P2

DRUG THAT BEST ILLUSTRATES CLASS'S COMMON PROPERTIES

• BRAIN SPINAL CORD
• NERVES THAT TERMINATE WITHIN

• ALL NERVOUS TISSUE
• OUTSIDE OF CNS

CONTROLS INVOLUNTARY

"AUTOMATIC" FUNCTIONS

• MOTOR FUNCTIONS
• VOLUNTARY

• FIGHT OR FLIGHT
• PART OF AUTOMATIC NS

• FEED OR BREED
• PART OF AUTONOMIC NS

MED THAT RELIEVES SENSATION OF PAIN

ABSENCE OF ALL SENSATION

MED THAT ENHANCES THE EFFECTS OF OTHER DRUGS

• CHEMICALLY SIMILAR TO OPIUM
• POPPY PLANT
• SIM TO ENDORPHINS
• 5 RECEPTORS

SALICYLATES, NSAIDS, PARA AMINOPHENOL

AFFECT PROSTAGLANDINS AND CYCLOOXYGENASE

NARCAN

COMPETIVELY BINDS W/ OPIATE RECEPTORS

BENZOS, ANTIHISTAMINES

TALWIN

BOTH AGONIST AND ANTAGONISTIC EFFECTS

MED THAT INDUCES LOSS OF SENSATION TO TOUCH OR PAIN

COMBINES DECREASED PAIN WITH AMNESIA WHILE PT REMAINS CONSCIOUS

AS A GROUP CAUSE RES DEPRESSION

AND CARIDIOVAS DEPRESSION

INHALATION OR INJECTION

ETHER

*HYPERPOLARIZE NEURAL MEMBRANES; MAKING DEPOLARIZATION MORE DIFFICULT--WHICH DECREASE FIRING RATES

ONSET DEPENDS ON CARD OUTPUT, GAS, PUL MIN VOLUME, PERFUSION

HALOTHANE

RSI

• LIDOCAINE

USED TO DECREASE ANXIETY

2 MAIN BARBITUATES AND BENZOS

HYPERPOLARIZE MEMBRANE OF CNS SYS

STATE OF DECREASED ANXIETY AND INHIBITIONS

INSTIGATION OF SLEEP

CHIEF INHIBITORY NT OF CNS SYS

GABA RECEPTORS THRUOUT ON CHLORIDE ION CHANNELS

GABA OPENS "CHANNELS" CHLORIDE(CL-) MORE PRESENT OUT OF CELL RUSHES IN .....IN MORE NEG THAN OUT...HYPERPOLARIZES...MORE DIFFICULT TO DEPOLARIZE....LARGER STIM REQUIRED TO DEPOLARIZE

BENZO ONLY ENHANCE GABA EFFECTIVENESS LIMITED...

BARBITUATES MIMIC GABA AS WELL...NOT LIM BY AMOUNT OF GABA

FLUMANZENIL (ROMAZICON) =ANTAGONIST= COMP BINDS WITH BENZO RECEPTORS

SEIZURE STATE OF HYPERACTIVITY OF BRAIN OR PART OF BRAIN

MAY OR NOT HAVE CONVULSIONS

BALANCE CONTROL OF SEIZURE VS SIDE EFFECTS

BOTH HEMI OF BRAIN; DESCRIBED BY MOTOR ACTIVITY

• MUSCLE RIGIDITY(TONIC CLONIC)
• SPASMODIC TWITCHING (CLONIC STAGE)
• SLOW RETURN TO CONSCIOUSNESS (POST ICTAL)

• GENERALIZED ...nO CONVULSIONS
• 100'S A DAY

• UNINTERRUPTED TONIC CLONIC SEIZURE ...LASTING MORE THAN 30 MIN
• 2 OR MORE W/O LUCID INTERVAL

ACTION ON NA AND CALCIUM ION CHANNELS (DILANTIN)...INHIBITS INFLUX OF SODIUM INTO CELL DECREASE CELLS ABILITY TO DEPOLARIZE AND PROPOGATE SEIZURE

BENZOS AND BARBS ETC...

AMPHETAMINES, METHAMPHETAMINES, METHYLXANTHINES

2 WAYS WORK

1. INCREASE RELEASE EFFECTIVENESS OF EXCITATORY NTS

2. DECREASE RELEASE OF INHIBITORY NT'S

INCREASE RELEASE OF EXCITATORY NT'S ....NOR EPI & DOPAMINE

INCREASED WAKEFULNESS AND AWARENESS........ TACHY, HTN, DECREASEDAPPETITE

RITALIN...ADHD

CLASS 2 CONTROLLED SUB

MOA SIMILAR TO AMPHETAMINES

CAFFEINE, AMINOPHYLLINE, THEOPHYLINE

FEW CLINICAL USES

BLOCK ADENOSINE RECEPTORS...LARGER DOSE REQ

TREAT MENTAL DYSFUNCTION

• DO NOT UNDERSTAND PATHOPHYS
• BASE RX ON CLINICAL CORELATION (SCIENTIC OBSERVATION OF EFFECTIVENESS)

INVOLVE MONOAMINE NT'S (NOREPI,DOPAMINE,SEROTONIN)= REGULATION OF EMOTION

IMBALANCE OF MONOAMIN=MENTAL DYSF

INCREASED RELEASE OF DOPAMINE

RX AIMED AT BLOCKING DOPA

lACK OF CONTACT W/ REALITY AND DISORGANIZED THINKING...DELUSIONS/HALLUCINATIONS/INCOHERENT SPEECH/CATATONIC

=INADEQUATE AMOUNTS OF MONOAMINES

RX TO INCREASE THE RELEASE OF THESE MEDS....

SIDE EFFECT OF ANTI PSYCHOTIC MEDS

MUSCLE TREMORS, PARKINSON-LIKE

PHENOTHIAZENES &BUTYROPHENONES

• BLOCK DOPAMINE RECEPTORS
• DIFFER IN POTENCY=AMOUNT
• &STRENGTH=CONCENTRATION

• THORAZINE
• SIDE EFFECT:EPS FROM CHOLINERGIC BLOCKADE IN THE BASAL GANGLIA
• ORTHO HYPO
• SEDATION
• SEX DYSFUNCTION

TREAT eps W/ DIPHENHY=ANTICHOLINERGIC

LOSS OF INTEREST, DEPRESSED MOOD, WEIGHT LOSS OR GAIN,

INSUFF MONOAMINES

RX INCREASE REL OF NT'S RELEASED IN BRAIN

• 1 PRODUCE MORE
• 2. INHIBIT UPTAKE

BLOCK REUPTAKE OF NOREPI AND SEROTONIN

LESS COMMONLY USED

MANY seFFECTS

• OD=CARDIOTOXIC EFFECTS= SUICIDE ATTEMPTS COMMON
• TOFRANIL

• MOST COMMON
• SELECTIVE SEROTONINREUPTAKE iNHIBITOR

• NO DOPA/ NO NOREPI
• NO CHOLINERGIC RECEPTORS BLOCKED-LIKE TCAS

MONOAMINE OXIDASE REUPTAKE INHIBITORS

BLOCKS BREAKDOWN OF MONOAMINES

MAJOR SE= HTN CRISIS---rICH FOODS

NO LONGER COMMONLY USED

NARDIL

MAJOR SWINGS

HYPERACTIVITY GRANDEUR

• LITHIUM W BENZOS
• MOA UNKNOWN DECREASES SIGNS OF MANIA

DEPAKOTE SUCCESFUL!

NERVOUS DISORDER CAUSED BY DESTRUCTION OF DOPAMINE RELAEASING NEURONS-IN BASAL GANGLIA

DYSKINESIA=DYSFUNCTIONAL MOVEMENTS+BRADYKINESIA=SLOW MOVEMENTS+aKINESIA......DEMENTIA....INCAPACITATION

NO CURE, TREAT SYMPTOMS...

BASAL GANGLIA=CONTROLS FINE MOTOR CONTROL

• IN BASAL GANGLIA
• DOPAMINE =INHIBITORY NT OPPOSES
• ACETYLCHOLINE =EXCITATORY NT

RX-RESTORE BALANCE B/W THE 2

• DOPAMENERGIC EFF OR
• ANTICHOLINERGIC

N(n)= AUTONOMIC GANGLIA, PRESYNANPTIC NT BOTH PARA & SYMPATH

N(m)=NEUROMUSCULAR JUNCTION PART OF SOMATIC NS

M = ORGANS PARASYMPATHETIC NS

• DIRECT=STIM CHOLINERGIC RECEPTORS (SAME RESPONSE=FEED/BREED)
• MUSCARINIC RECEPTORS
• SIDE EFF...BRADYCARDIA, HYPOT,
• SLUDGEM

• INDIRECT
• AFFECT ACYTLCHOLINESTERASE(INHIBIT)
• FOR-MYASTHENIA GRAVIS, GLAUCOMA, REVERSE rsi

• REVERSIBLE VS
• IRREVERSIBLE= NERVE GAS=SLUDGEM RESPONSE

OPPOSE THE PNS

• MUSCARINIC CHOLINERGIC ANTAGONIST=
• PARASYMPATHOLYTICS=COMPETIVETLY BIND WITH MUSCARINIC RECEPTORS

ATROPINE= INCREASE HR, DECREASE SLUDGEM, "HOT AS HELL, BLIND AS BAT, DRY AS BONE, RED AS BEET, MAD AS A HATTER"

TURN OFF AUTONOMIC NS

TREAT HTN

PARALYSIS W/O AFFECTING CONSCIOUSNESS

POLARIZING VS DEPOLARIZING

NICOTINE

STIM PARA AND SYMPA NS

CHAIN GANGLIA VS COLLATERAL GANGLIA

• STIM SYMPA=FIGHT OR FLIGHT
• (CHAIN GANGLIA)
• 1. SWEAT
• 2. CONSTRICT OF BV OF SKIN
• 3. BLOOD FLOW TO SKEL MUSC
• 4. HR INCREASE
• 5. BRONCHODILATION

• COLLATERAL GANGLIA(ABD CAVITY)
• REDUCE BF TO ABD ORGANS
• DECREASE DIGESTION
• RELEASE GLUCOSE STORES

• DIRECT STIM OF ADRENAL GLAND
• -RELEASE 20%NOREPI AND 80%EPI IN CIRC

• a1=peri vasoconstrict, stim metabolism
• a2=inhibitory- prevent overstim of norepi
• b1 heart=increased intro, chrono, dromo eff
• b2 lungs= bronchodilation, vasodilation

dopamenerGIC= UNSURE

meds that stim sympa NS

adrenergic

• increase preload= increased co
• increase afterload= increased bp

meds that inhibit stim of sympa ns

antiadrenerics

stim = local vasocontrict= systemic absorption decreased

anatag= controlling HTN, LOCAL VASODILATION

STIM= INCREASED HR BP CCF

ANTAG= CONTROL BP, DECREASE HR CCF BP

STIM= TREAT ASTHMA= RELAX BRONCH SM=BRONCHODILATON

ANTAG= NO CLINICAL PURPOSE

AFFECT RATE

AFFECT CONDUCTIVITY

AFFECTS CONTRACTILITY

AGONIST= ENDOGENOUS NT'S= NOREPI, EPI,DOPAM, SOME SYNETHITIC DOBUTUMAINE

ADRENERGIC ANTAGONIST= BETA BLOCKER

INDERAL/LOPRESSOR= BLOCK BETA 1

SIDE EFFECT/LARGE DOSE = BLOCK BETA 2 BRONCHOCONSTRICTION

• CENTRAL ACTING (GENERAL SEDATION)VS DIRECT ACTING (DECREASED RELEASE OF CALCIUM = REQUIRED FOR CONTRACTION
• TREAT MS

• 1. ELECTRICAL STIMULATION
• 2. ADEQUATE ATP
• 3. ADEQUATE AMOUNTS OF ION CALCIUM

SA NODE = HEARTS DOMINATE PACEMAKER

GENERATES ELECTRICAL IMPULSES(ACTION POTENTIALS)

INTRAATRIAL PATHWAYS----TO AV NODE ---DELAY

AV NODE THROUGHOUT VENTRICLES THRU(BUNDLE OF HIS&PERKINJE FIBERS)

ALL HAS AUTOMATICITY(GEN ELEC IMPULSE)

ACHIEVED THRU MOVEMENT OF IONS ACROSS CELL MEMBRANES


AT REST = POLARIZED= +OUTSIDE -INSIDE

NA+ OUT K+ INSIDE

SARCOPLASMIC RETICULUM=CAL++ STORAGE OUTSIDE CELL

DEPOLARIZE= CHARGE ELIMINATED OR REVERSED

FAST POTENTIALS= CARDIAC MUSCLE TISS, VENT COND SYS

SLOW POTENTIALS= AV & SA NODES

0= INFLUX OF NA+ INTO CELL (INSIDE MORE+ THAN OUTSIDE) CAUSED BY IMPULSE GENERATED ELSEWHERE- sa NODE

• 1-3 REPOLARIZATION
• 1-K+ LEAVES THE CELL= RETURN CELL TO NEG CHARGE

2-INFLUX OF CA++ INTO THE CELL- PLATEAU

3-END OF CA++ INFLUX, RAPID EFFLUX OF K+(INTO CELL)

• 4 RESTING MEMBRANE POTENTIAL OR
• PATHOLOGY - SLOW INFLUX OF SODIUM= DEPOLARIZE WITHOUT ELEC IMPULSE
• ***MANY ANTI DYS MOA -IN 4***

SA AV NODES NOT CONTRACTILE TISSUE

DEPOLARIZE DIFFERENTLY - CAUSED BY CALCIUM NOT SODIUM

GRADUAL UP GRADUAL DOWN

TACHY AND BRADY MOST COMMON

MOST OFTEN CAUSED BY IMBALANCE BETWEEN SNS - PNS

• BRADY EXCESS PNS- ANTICHOLINERGICS
• TACHY VARIETY OF CAUSES

PATHOLOGIC COND= ISCHEMIA, MI INFARCT, EXCESS SNS = PHASE 4 RESTING POTENTIAL BECOMES PHASE 4 DEPOLARIZATION....ABNORMAL IMPULSE PROPOGATED THRU HEART

FOCUS FOR ELECTRICAL IMPULSE GENERATED SOME PLACE OTHER THAN WHERE IT SHOULD

PERKINJE FIBER HAS A "ONE WAY VALVE"

CAN CAUSE AN EARLY BEAT OR RAPID REENTERANT RHTYM "CIRCUS RTHYM"

ANTI DYSRYTHMIAS

ANTIHYPERTENSIVES

HEMOSTATIC AGENTS

ANTIHYPERLIPIDEMIC AGENTS

MED USED TO TREAT AND PREVENT ABNORMAL RHYTHMS

• 1SODIUM CHANNEL BLOCKERS
• 11BETA BLOCKERS
• 111POTASSIUM CHANNEL BLOCKERS
• 1111CALCIUM CHANNEL BLOCKERS

AFFECT NA+ INFLUX IN PHASE 0 AND 4 OF FAST POTENTIALS

*SLOWS PROPAGATION OF IMPULSES DOWN CONDUCTION SYSTEM

*1A "PROCANIMIDE" DECREASE REPOLARIZATION RATE;WIDENS QRS COMPLEX, PROLONGS QT INTERVAL

*1B "LIDOCAINE" ****INCREASE RATE OF REPOLARIZATION*** REDUCE AUTOMATICY****

1C DECREASE CONDUCTION VELOCITY THROUGH ATRIA AND VENTRICLES

ADRENERGIC ANTAGONIST

INDICATED FOR TREATMENT OF DYSRTHY RESULTING FROM EXCESSIVE SNS STIM

BETA 1 RECEPTOR = ATTACHED TO CALCIUM CHANNELS= BLOCKS CAL CHANNELS

PROPRANOLOL

MOA IS ON K+ CHANNELS ON FAST POTENTIALS

V- FIB AND REFRACTORY V - TACH

PROLONGS REPOLARIZATION AND REFRACTORY PERIOD WHICH PROLONGS QT INTERVAL

EFFECT ON HEART IS ALMOST IDENTICAL TO BETA BLOCKERS

• DECREASE CONDUCTIVITY THRU AV NODE
• DECREASE SA & AV AUTOMATICITY

CARDIZEM & VERAPAMIL

ADENOSINE = ACTS ON BOTH K AND NA+ CHANNELS = HYPERPOLERAZATION THAT SLOWS CONDUCTON OF SLOW CHANNELS

• DIGOXIN DO NOT UNDERSTAND MOA
• INCREASES STRENGTH OF PSNS EFFECTSETC.....

MAGNESIUM FOR TOSARDES DE POINTES

BP = CO X PVR

CO = SV X HR

ANTI HTN CAN COUNTERACT ALL OF THESE FACTORS

• 1DIURETICS
• 2BETA BLOCKERS
• 3ACE INHIBITORS
• 4CAL CHAN BLOCKERS
• 5DIRECT VASODILATORS

MED USED TO REDUCE CIRCULATING BLOOD VOLUME BY INCREASNG URINE OUTPUT

REDUCES PRELOAD

DIFF CLASS = DIFF PART OF NEPHRON AFFECTED

1LASIX = LOOP DIURETIC= LOOP OF HENLE

REFLEX TACHY

• 2 THIAZIDES= DISTAL CONVOLUTED TUBULE= DEPEND ON GLUMERULAR FILT
• LOOP DIUR DO NOT....

3 K+ SPARING DIURETICS

• BETA ADRENERGIC ANTAGONISTS (METOPROLOL)
• CENTRALLY ACTING ADRENERGIC INHIB
• PERIPHERAL ADRENERGIC INHIBITORS
• ALPHA 1 ANTAGONISTS
• COMBINED ALPHA/BETA

AGENTS INTERUPT THE RENIN ANGIOTENSIN ALDOSTERONE SYSTEM

PREVENT CONVERSION FROM ANGIOTENSIN 1 TO 2

RENIN - ANGIOTENSIN- AANGIO1-ACE - ANGIO2 = ALDOSTERONE, INCREASED SNS STIM ETC

CAPOTEN

ABSENCE OF SIDE EFF OF OTHERS

SIMILAR TO ACE INHIBITORS

BLOCK CAL CHANNELS IN

1MYOCARDIUM

2VASCULATURE

3bOTH

1 DILATE ARTERIOLES

2. DILATE ART AND VEINS

• DIFF BETWEEN DILATE THE 2?
• VEIN=STORAGE SYSTEM

GANGLIONIC BLOCKING AGENTS

CARDIAC GLYCOSIDES

OTHER VASO DILATORS

PG359 DID NOT READ

• HEMOSTASIS = STOPPAGE OF BLEEDING
• SERIES OF EVENTS IN RESPONSE TO A TEAR...

ADP & TXA RELEASED ---AGGREGATION PF PLATLETS--VASOCONSTRICTION--PLATLETS FORM A PLUG--ENDING WITH THROMBIN-FIBRINOGEN--FIBRIN

VITA K NECC

FIBRINOLYSIS PLASMINOGEN PLASMIN

BLOOD CLOTS THAT OBSTRUCT VESSELS OR HEART CAVITIES

CAUSE MI, STROKE, PULMONARY EMBOLISM

DRUGS THAT DECREASE FORMATION OF PLATLET PLUGS

CURBS FORMATION ON NEW; NO EFFECT ON EXISTING

ASA

SE BLEEDING

INTERRUPT THE CLOTTING CASCADE

• HEPARIN
• COUMADIN(ORAL) RAT POISON ANTAGON VITA K

BLEEDING AND DECREASED PLATTLET COUNTS

THROMBOLYTICS

ACT DIRECTLY ON THROMBI

ACTIVATE ENZYMES THAT BREAK UP THROMBI

STREPTASE DERIVED FROM STREPTOCOCCI BACTERIUM

MEDS USED TO TREAT HIGH BLOOD CHOLESTEROL

EVELVATED LDL SCLARLY INDICATED AS A CAUSE OF CAD

HDL GOOD CHOLESTEROL= CARRY CHOLESTEROL TO LIVER TO BE BROKEN DOWN

LDL = BAD = CARRY CHOLESTEROL FROM LIVER TO PERIPHERY

LDL ^ FATTY PLAQUE DEPOSITS^ ATHERSCLEROSIS

THROW A CLOT---THROMBUS

"STATINS"