CH 9 P2

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CH 9 P2
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CHAPTER 9 P2
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  1. PROTOTYPE
    DRUG THAT BEST ILLUSTRATES CLASS'S COMMON PROPERTIES
  2. CNS
    • BRAIN SPINAL CORD
    • NERVES THAT TERMINATE WITHIN
  3. PNS
    • ALL NERVOUS TISSUE
    • OUTSIDE OF CNS
  4. ANS
    CONTROLS INVOLUNTARY

    "AUTOMATIC" FUNCTIONS
  5. SOMATIC NS
    • MOTOR FUNCTIONS
    • VOLUNTARY
  6. SYMPA NS
    • FIGHT OR FLIGHT
    • PART OF AUTOMATIC NS
  7. PARA NS
    • FEED OR BREED
    • PART OF AUTONOMIC NS
  8. ANALGESICS
    MED THAT RELIEVES SENSATION OF PAIN
  9. ANESTHESIA
    ABSENCE OF ALL SENSATION
  10. ADJUNCT MED
    MED THAT ENHANCES THE EFFECTS OF OTHER DRUGS
  11. OPIOD AGONIST
    • CHEMICALLY SIMILAR TO OPIUM
    • POPPY PLANT
    • SIM TO ENDORPHINS
    • 5 RECEPTORS
  12. NONOPIOD ANALGESICS
    SALICYLATES, NSAIDS, PARA AMINOPHENOL

    AFFECT PROSTAGLANDINS AND CYCLOOXYGENASE
  13. OPIOD ANTAGANOIST
    NARCAN

    COMPETIVELY BINDS W/ OPIATE RECEPTORS
  14. ADJUNCT MEDS
    BENZOS, ANTIHISTAMINES
  15. OPIOD AGONIST ANTAGONISTS
    TALWIN

    BOTH AGONIST AND ANTAGONISTIC EFFECTS
  16. ANESTHETICS
    MED THAT INDUCES LOSS OF SENSATION TO TOUCH OR PAIN
  17. NEUROLEPTANESTHSIA
    COMBINES DECREASED PAIN WITH AMNESIA WHILE PT REMAINS CONSCIOUS
  18. ANESTHICS
    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
  19. ANTIANXIETY - SEDATIVE HYPNOTIC DRUGS
    USED TO DECREASE ANXIETY

    2 MAIN BARBITUATES AND BENZOS

    HYPERPOLARIZE MEMBRANE OF CNS SYS
  20. SEDATION
    STATE OF DECREASED ANXIETY AND INHIBITIONS
  21. HYPNOSIS
    INSTIGATION OF SLEEP
  22. GABA
    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
  23. BENZO AND BARBITUATES
    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
  24. ANTISEIZURE/ANTIEPILEPTIC DRUGS
    SEIZURE STATE OF HYPERACTIVITY OF BRAIN OR PART OF BRAIN

    MAY OR NOT HAVE CONVULSIONS

    BALANCE CONTROL OF SEIZURE VS SIDE EFFECTS
  25. GENERALIZED SEIZURES
    BOTH HEMI OF BRAIN; DESCRIBED BY MOTOR ACTIVITY

    • MUSCLE RIGIDITY(TONIC CLONIC)
    • SPASMODIC TWITCHING (CLONIC STAGE)
    • SLOW RETURN TO CONSCIOUSNESS (POST ICTAL)
  26. ABSCENCE SEIZURES
    • GENERALIZED ...nO CONVULSIONS
    • 100'S A DAY
  27. STATUS EPILEPTICUS
    • UNINTERRUPTED TONIC CLONIC SEIZURE ...LASTING MORE THAN 30 MIN
    • 2 OR MORE W/O LUCID INTERVAL
  28. SEIZURE RX
    ACTION ON NA AND CALCIUM ION CHANNELS (DILANTIN)...INHIBITS INFLUX OF SODIUM INTO CELL DECREASE CELLS ABILITY TO DEPOLARIZE AND PROPOGATE SEIZURE
  29. ANTI SEIZURE MEDS
    BENZOS AND BARBS ETC...
  30. CNS STIMULANTS
    AMPHETAMINES, METHAMPHETAMINES, METHYLXANTHINES

    2 WAYS WORK

    1. INCREASE RELEASE EFFECTIVENESS OF EXCITATORY NTS

    2. DECREASE RELEASE OF INHIBITORY NT'S
  31. AMPHETAMINES
    INCREASE RELEASE OF EXCITATORY NT'S ....NOR EPI & DOPAMINE

    INCREASED WAKEFULNESS AND AWARENESS........ TACHY, HTN, DECREASEDAPPETITE
  32. METHYLPHENIDATE
    RITALIN...ADHD

    CLASS 2 CONTROLLED SUB

    MOA SIMILAR TO AMPHETAMINES
  33. METHYLXANTHINES
    CAFFEINE, AMINOPHYLLINE, THEOPHYLINE

    FEW CLINICAL USES

    BLOCK ADENOSINE RECEPTORS...LARGER DOSE REQ
  34. PSYCHOTHERAPEUTIC MEDS
    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
  35. SCHIZOPHRENIA
    INCREASED RELEASE OF DOPAMINE

    RX AIMED AT BLOCKING DOPA

    lACK OF CONTACT W/ REALITY AND DISORGANIZED THINKING...DELUSIONS/HALLUCINATIONS/INCOHERENT SPEECH/CATATONIC
  36. DEPRESSION
    =INADEQUATE AMOUNTS OF MONOAMINES

    RX TO INCREASE THE RELEASE OF THESE MEDS....
  37. EXTRAPYRAMIDAL SYMPTOMS
    SIDE EFFECT OF ANTI PSYCHOTIC MEDS

    MUSCLE TREMORS, PARKINSON-LIKE
  38. AKA NEUROLEPTIC DRUGS...AFFECTING THE NERVE=ANTIPSYCHOTIC DRUGS
    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
  39. ANTI DEPPRESSANTS
    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
  40. TCA'S
    BLOCK REUPTAKE OF NOREPI AND SEROTONIN

    LESS COMMONLY USED

    MANY seFFECTS

    • OD=CARDIOTOXIC EFFECTS= SUICIDE ATTEMPTS COMMON
    • TOFRANIL
  41. SSRI'S
    • MOST COMMON
    • SELECTIVE SEROTONINREUPTAKE iNHIBITOR

    • NO DOPA/ NO NOREPI
    • NO CHOLINERGIC RECEPTORS BLOCKED-LIKE TCAS
  42. MAOIS
    MONOAMINE OXIDASE REUPTAKE INHIBITORS

    BLOCKS BREAKDOWN OF MONOAMINES

    MAJOR SE= HTN CRISIS---rICH FOODS

    NO LONGER COMMONLY USED

    NARDIL
  43. BIPOLAR (MANIC DEPRESSION)
    MAJOR SWINGS

    HYPERACTIVITY GRANDEUR

    • LITHIUM W BENZOS
    • MOA UNKNOWN DECREASES SIGNS OF MANIA

    DEPAKOTE SUCCESFUL!
  44. PARKINSONS DISEASE
    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
  45. cholinergic receptors= ACH RECEPTORS
    N(n)= AUTONOMIC GANGLIA, PRESYNANPTIC NT BOTH PARA & SYMPATH

    N(m)=NEUROMUSCULAR JUNCTION PART OF SOMATIC NS

    M = ORGANS PARASYMPATHETIC NS
  46. CHOLINERGICS

    DIRECT VS INDIRECT
    • 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
  47. ANTICHOLINERGICS

    CUTTING THE BRAKE LINE
    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"
  48. GANGLIONIC BLOCKING AGENTS
    TURN OFF AUTONOMIC NS

    TREAT HTN
  49. NEUROMUSCULAR BLOCKING AGENTS
    PARALYSIS W/O AFFECTING CONSCIOUSNESS

    POLARIZING VS DEPOLARIZING
  50. GANGLIONIC STIM AGENTS
    NICOTINE

    STIM PARA AND SYMPA NS
  51. DRUGS USED TO AFFECT 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
  52. ADRENERGIC RECEPTORS
    • a1=peri vasoconstrict, stim metabolism
    • a2=inhibitory- prevent overstim of norepi
    • b1 heart=increased intro, chrono, dromo eff
    • b2 lungs= bronchodilation, vasodilation

    dopamenerGIC= UNSURE
  53. sympathomimetics

    "step on gas"
    meds that stim sympa NS

    adrenergic

    • increase preload= increased co
    • increase afterload= increased bp
  54. sympatholytics

    "cut gasline"
    meds that inhibit stim of sympa ns

    antiadrenerics
  55. alpha 1

    stim vs antag
    stim = local vasocontrict= systemic absorption decreased

    anatag= controlling HTN, LOCAL VASODILATION
  56. BETA 1
    AGONSIST VS ANATG
    STIM= INCREASED HR BP CCF

    ANTAG= CONTROL BP, DECREASE HR CCF BP
  57. BETA 2

    STIM VS ANTAG
    STIM= TREAT ASTHMA= RELAX BRONCH SM=BRONCHODILATON

    ANTAG= NO CLINICAL PURPOSE
  58. CHRONTROPIC
    AFFECT RATE
  59. DROMOTROPIC
    AFFECT CONDUCTIVITY
  60. INOTROPIC
    AFFECTS CONTRACTILITY
  61. ADRENERGIC AGONIST

    VS

    ADRENERGIC ANTAGONIST
    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
  62. SKEL MUSC RELAXANTS
    • CENTRAL ACTING (GENERAL SEDATION)VS DIRECT ACTING (DECREASED RELEASE OF CALCIUM = REQUIRED FOR CONTRACTION
    • TREAT MS
  63. DRUGS TREAT CARDIO VASCULAR SYSTEM
  64. CARDIAC A&P

    MYOCARDIAL MUSCLE CONTRACTION DEPENDS ON 3 FACTORS
    • 1. ELECTRICAL STIMULATION
    • 2. ADEQUATE ATP
    • 3. ADEQUATE AMOUNTS OF ION CALCIUM
  65. IMPULSE GENERATION AND CONDUCTION
    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)
  66. MYOCARDIAL TISSUE
    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
  67. DEPOLARIZE
    DEPOLARIZE= CHARGE ELIMINATED OR REVERSED

    FAST POTENTIALS= CARDIAC MUSCLE TISS, VENT COND SYS

    SLOW POTENTIALS= AV & SA NODES
  68. FAST POTENTIAL 5 PHASES
    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***
  69. SLOW POTENITIALS

    DISTICTIONS
    SA AV NODES NOT CONTRACTILE TISSUE

    DEPOLARIZE DIFFERENTLY - CAUSED BY CALCIUM NOT SODIUM

    GRADUAL UP GRADUAL DOWN
  70. DYSRHYTHMIA GENERATION

    ABNORMAL AUTOMATICITY
    ABNORMAL CONDUCTIVITY
    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
  71. ECTOPIC FOCI
    FOCUS FOR ELECTRICAL IMPULSE GENERATED SOME PLACE OTHER THAN WHERE IT SHOULD
  72. ABNORMAL CONDUCTION
    PERKINJE FIBER HAS A "ONE WAY VALVE"

    CAN CAUSE AN EARLY BEAT OR RAPID REENTERANT RHTYM "CIRCUS RTHYM"
  73. CLASSES OF CARDIOVASCULAR DRUGS

    4
    ANTI DYSRYTHMIAS

    ANTIHYPERTENSIVES

    HEMOSTATIC AGENTS

    ANTIHYPERLIPIDEMIC AGENTS
  74. ANTI DYSRYTHMICS
    MED USED TO TREAT AND PREVENT ABNORMAL RHYTHMS

    • 1SODIUM CHANNEL BLOCKERS
    • 11BETA BLOCKERS
    • 111POTASSIUM CHANNEL BLOCKERS
    • 1111CALCIUM CHANNEL BLOCKERS
  75. 1SODIUM CHANNEL BLOCKERS

    1A
    1B
    1C
    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
  76. CLASS 2 BETA BLOCKERS
    ADRENERGIC ANTAGONIST

    INDICATED FOR TREATMENT OF DYSRTHY RESULTING FROM EXCESSIVE SNS STIM

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

    PROPRANOLOL
  77. POTASSIUM CHANNEL BLOCKERS
    MOA IS ON K+ CHANNELS ON FAST POTENTIALS

    V- FIB AND REFRACTORY V - TACH

    PROLONGS REPOLARIZATION AND REFRACTORY PERIOD WHICH PROLONGS QT INTERVAL
  78. CLASS 4 CALCIUM CHANNEL BLOCKERS
    EFFECT ON HEART IS ALMOST IDENTICAL TO BETA BLOCKERS

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


    CARDIZEM & VERAPAMIL
  79. MISC ANTI DYSRTHYMICS
    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
  80. ANTI HYPERTENSIVES

    50 MILLION AFFECTED

    5 CLASES
    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
  81. DIURETICS
    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
  82. ADRENERGIC INHIBITING AGENTS
    • BETA ADRENERGIC ANTAGONISTS (METOPROLOL)
    • CENTRALLY ACTING ADRENERGIC INHIB
    • PERIPHERAL ADRENERGIC INHIBITORS
    • ALPHA 1 ANTAGONISTS
    • COMBINED ALPHA/BETA
  83. ACE INHIBITORS
    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
  84. ANGIOTENSIN 2 RECEPTOR ANTAGONIST'S
    SIMILAR TO ACE INHIBITORS
  85. CALCIUM CHANNEL BLOCKING AGENTS
    BLOCK CAL CHANNELS IN

    1MYOCARDIUM

    2VASCULATURE

    3bOTH
  86. DIRECT VASODILATORS
    1 DILATE ARTERIOLES

    2. DILATE ART AND VEINS

    • DIFF BETWEEN DILATE THE 2?
    • VEIN=STORAGE SYSTEM
  87. OTHER ANTIHYPERTENSIVE MEDS
    GANGLIONIC BLOCKING AGENTS

    CARDIAC GLYCOSIDES

    OTHER VASO DILATORS

    PG359 DID NOT READ
  88. HEMOSTATIC AGENTS
    • 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
  89. THROMBI
    BLOOD CLOTS THAT OBSTRUCT VESSELS OR HEART CAVITIES

    CAUSE MI, STROKE, PULMONARY EMBOLISM
  90. ANTIPLATLETS
    DRUGS THAT DECREASE FORMATION OF PLATLET PLUGS

    CURBS FORMATION ON NEW; NO EFFECT ON EXISTING

    ASA

    SE BLEEDING
  91. ANTICOAGULANTS
    INTERRUPT THE CLOTTING CASCADE

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

    BLEEDING AND DECREASED PLATTLET COUNTS
  92. FIBRINOLYTICS
    THROMBOLYTICS

    ACT DIRECTLY ON THROMBI

    ACTIVATE ENZYMES THAT BREAK UP THROMBI

    STREPTASE DERIVED FROM STREPTOCOCCI BACTERIUM
  93. ANTI HYPERLIPIDEMIC AGENTS
    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"

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