Pharmacology Nervous System Myasthenia Gravis

Lack neural impulse and muscle responses at the myoneural junction Inadequate secretion of acetylcholine or loss of acetylcholine increased enzyme acetylcholinesterase which destroy acetylcholine at the myoneural junction. Treatment has different which strategies: acute, remissions and exacer ation, chronic progressi!e phase. Clinical Manifestation

"atigue, muscle weakness of the respiratory system, facial muscle #tosis $%rooping &yelids': (ranial ner!e in!ol!ement $%ifficulty of )wallowing' *espiratory arrest due to respiratory muscle paralysis. Parkinsonism Im alance of neurotransmitters+dopamine and acetylcholine Lacks sufficient dopamine. Increased acetylcholine at the asal ganglia of the extra pyramidal motor tract. %,#-.I/&: inhi itor neurotransmitter -(&T0L(1,LI/&: excitatory neurotransmitter DRUGS: 2 CA !G"R#!S -nti+cholinergics 2 3lock the cholinergic receptors %opaminergics 2 )timulate the dopamine receptors AN #C$"%#N!RG#CS %ecrease rigidity %ecrease tremors ut decrease effect on radykinesia

 Inhi it release of acetylcholine

)4&: /ausea, %ry mouth, /er!ousness, %izziness, 3lurred !ision, (onstipation, 5rinary retention (4I: 6laucoma, 6I , struction, 5lcerati!e (olitis, 3#/ $3enign #rostatic 1yperplasia' /ursing *esponsi ilities: 7. .onitor 84), urine output, owel sounds 9. Increase fi er4fluids intake :. (andies, gums, ice chips+oral care due to decreased sali!ation ;. *outine eye examination. D"PAM#N!RG#CS: Le!odopa

most effecti!e drug for decreasing s4sx of #arkinson<s disease precursors of dopamine gi!en in increased dosage = %,#- %&(-*3,>0L-)& has short half life $ gi!en :+; times a day ' initially low doses then gradually increased weekly maximum effect after 9+; months )4&: /48, dyskinesia, orthostatic hypotension, cardiac dysfunction and psychosis $ paranoia, increased li ido ' Car&i'o(a: alternati!e to le!odopa inhi its enzyme %,#-%&(-*3,>0L-)& periphery more le!odopa reaches the rain (om ined with le!odopa in a ratio of 7:7? $(ar idopa:Le!odopa' -d!antages: .ore dopamine reaches the asal ganglia )ingle dose4day is administered instead of multiple doses )maller doses of le!odopa are required to achie!e the desired effect %isad!antages: )4&: /48 dystonic mo!ement $in!oluntary a normal mo!ement' , psychotic eha!ior

 #eripheral )4&: not pre!alent howe!er, cardiac dysrrthmia, palpitations and orthostatic hypotension may occur. Do(amine Agonist: )timulate the %opamine receptors &x. )ymmetrel = anti+!iral drug and acts on the %opamine receptors. + used for drug+inducing parkinsonism #arlodel = act directly on the dopamine receptors in the (/), (ardio!ascular )ystem and 6IT + .ore effecti!e the )ymmetrel and anticholinergics ut not as effecti!e -s le!odopa in decreasing #arkinsonian symptoms + )u stitute for le!odopa MA")#nhi&itors: .onoamine oxidase+3 $.-,+3' = enzyme that causes the cata olism of %opamine &x. )elegiline 1(L $&ldepryl' = inhi its .-,+3 Thus prolong effect of le!odopa ,rdered for newly diagnosed #arkinson<s disease

%rug+%rug Interactions: 7. 8itamin 3@+increase %opadecar oxylase action which meta olize Le!odopa in the #eripheral /er!ous )ystem to %omamine: "oods rich in 8itamin 3@ should e a!oided like eans, cereals, anana. 9. -nti+#sychotic drugs should e a!oided: lock dopamine receptors. $1ypertensi!e (risis' /ursing *esponsi ilities , tain aseline 84) especially 3#, &(6, %rugs hx, .ed. 1x (hanging position hypotension+orthostatic -!oid foods rich in 8itamin 3@ -!oid foods rich in Tyramine when patent is recei!ing .-, inhi itors Taper when discontinuing the %rug :. .-, inhi itors should not e gi!en with Le!odopa and anti depressant:

 Inform that the client<s urine may

discolored and will darken

with air exposureA perspiration may e dark = 1armless Instruct client recei!ing (ar idopa+Le!odopa to decrease intake of (1,/ rich food ecause increase (1,/ interfere with drug transport loss Myasthenia Gravis Lack of acetylcholine reaching the cholinergic receptors + -cetylcholinesterase destroys -cetylcholine (haracterized muscle Acetylcholinesterase #nhi&itors 7. /eostigmine $#rostigmin' )hort acting T B : :?mins , + 7 hour: gi!en 9+; hours and must e gi!en on time to pre!ent muscle weakness 9. #yridostigmine 3romide $.estinon' 1as a intermediate action: 6i!en :+@ hours :. -m enonium (L $.ytelase' Long -cting 5sually prescri ed if the client doesn<t respond to #rostigmin or .estinon ; . Tensilon $&ndrophonium (L' "or diagnostic .6 #tosis shoukd e a sent within 7+Cmins )hort acting drug y muscle weakness and fatigue of the skeletal

,!erdose: + (holinergic reaction + )4)> = nausea, a dominal cramps, excessi!e sali!ation, sweating -ntidote: + -tropine ),; for cholinergic crisis )4&: /48, diarrhea, a dominal cramps, Increased sali!ation, tearing miosis $(onstricted #upils' possi le 1#/

/ursing *esponsi ilities: 84) -ssess for s4sxs of myasthenia crisis: muscle weakness with difficulty of reathing an swallowing .onitor drug<s effect -dminister I8 .estinon undiluted at rate of ?.Cmg4min. %o not add to I8 fluids , ser!e for the )4)>) of (holinergic crisis #repare antidote at edside I% racelet &xact time of administration

Multi(le Sclerosis: (haracterized y multiple lesions of the myelin sheath There are remissions and exacer ations of multiple symptoms muscle weakness, spasticity or diplopia 1ard to diagnose treatment There is an increase Ig6, ()"4-l umin ratio is increased .*I re!eals multiple lesions 6oal of treatment: %ecrease inflammatory process of ner!e fi ers and to impro!e conduction of demyelinating axons. Acute Attack: .edication is gi!en: 7. #rednisone = 6lucocorticoids 9. -drenocorticotropic 1ormone I.4I8 -queous -(T1, D? E5F in C?? ml %CG for 7+C days Tapering doses of -(T1 gel I. for 9C+:? d, starting with ;? units 3I% :. @+-lpha .enthylpradnisolone )odium )uccinate .# 7g4d for C+Hdays Tapering doses oral glucocorticoids ecause there is no specific diagnostic

 )4)>: "atigue, motor weakness, optic neuritis

Remission)!*acer&ation +Recurrence of MS, .edication 6i!en: 7. 3etaseron: ?.9C mg $D. EI5F' e!ery other day decrease spasticity and impro!es muscle mo!ement 9. Imuran $Immunosupressant %rug' %ecrease replaces and decrease steroid use

Chronic Progressive: .edication gi!en: 7. (ytoxan @??mg4m9 in 9C? ml or %CG e!ery other day times C does 9. -(T1 )4)>: #rogressi!e .) symptoms, wheelchair ound Skeletal Muscle Rela*ants

+ *elie!es muscle spasm and pain associated with traumatic injuries and chronic de ilitating disorders: .), strokes, cere ral palsy and spinal cord injuries S(asticity Increased muscle tone hyper excita le neurons. Increased stimulation from the cere ral neurons or lack of inhi ition in the )pinal (ord at the )keletal .uscle 2 y(es: 7. (entrally acting muscle relaxants. + + + + + + + %epress neurons acti!ity in the )pinal (ord or 3rain 5se to treat acute spasms from muscle trauma ex. ),.-, .-, late, #araflex, "lexeril, )kelaxin, *o axin, /orflex, Lioresal %ecrease pain and increase range of motion 1a!e sedati!e effect: should not %ecrease muscle spasm act directly on the skeletal muscles e gi!en with (/) depressant like 3ar iturate, /arcotics and -lcohol, 8alium $%iazepam', &quanil 9. #eripherally acting muscle relaxants

+ + + +

&x. %antrolene /- $%antrium' -ct on the muscles directly .ore effecti!e for spasticity or muscle contractions of neurologic origin $.), (8-': Increased doses of %antrium+1epatotoxic $"or Li!er &nzyme .onitoring' Pharmakokinetics:

(arisprodol $),.-'4 %antrium $%antrolene' Gell a sor ed in the 6I decreased :CI .oderate t749 life %antrolene: Increased (1,/+ ound J?I .eta olized in the li!er and exerted thru the urine

Pharmaco'ynamics: %atrolene: -ct directly on skeletal muscle and decrease release of (alcium there y muscle spasticity occurs (arisoprodol: %ecrease muscle spasm

)4&: (-.*+ drowsiness, dizziness, light+headedness, headache, /48, diarrhea and a dominal distress. )4&: #-.*+ hepatotoxic, drowsiness, photosensiti!e, anorexia and /48 %o not gi!e to patients with history of reast cancer ecause it can cause mammary malignancy. Anti)#nflammatory Drugs

Inflammation+ *esponse to tissue injury and infection (ardinal )igns: + 3lood accumulates in the area of tissue injury due to release of the ody<s chemical mediators $kinins, prostaglandins and histamine' histamine dilates arterioles 9. &%&.- $)welling' 9nd phase + #lasma leaks into the interstitial tissue at the injury site. Kinins dilate the arterioles. Increase capillary permea ility :. 1eat+ due to increase lood accumulation and pyrogens that interfere with temperature regulating center $1ypothalamus'

7. &rythema $*edness' 7st phase

;. #ain+ due to tissue swelling release of chemical mediators C. Loss of "unction+ due to accumulation of fluid at the tissue injury site and to pain which decrease mo ility at affected area

Salicylates: &x. -spirin, (holine, )alicylate, )alicylic -cid .echanism of -ction: 7. -nalgesia+ *elief of pain locking the prostaglandin synthesis redness sensiti!ity of peripheral pain receptors to mechanical or chemical acti!ation 9. -nti+pyresis reduce outflow of !asoconstrictor impulse from hypothalamus, thus promote !asodilation, sweating, heat loss, decrease production of prostaglandin & !s. endogen pyrogens :. -nti inflammatory decrease !ascular leakage of fluids and neutrophils, secretory cells, inhi it synthesis of prostaglandin and endogenous su stances ;. -nti+coagulant inhi it platelet aggregation + + -)- $-spirin'+ ,ldest &ffecti!e in pre!ention of recurrent TIThrom olytic condition like .I /ursing (onsiderations 1istory of hypertensi!e to -)-, gastric upset , leeding or li!er disease .onitor serum salicylate if patient is taking high doses of aspirin: /ormal 7C to :? mg4dl $L:? mg4dl+mild: LC? mg4dl se!ere toxicity' , ser!e for sign and symptoms of leeding like dark colored+ stools, leeding gums, patechiae, ecchymosis, purpura )hould not e gi!en to patient suffering from !irus or flu like chicken pox, *eye<s syndrome $8omiting, Lethargy and delirium, coma and death' Take with meals Para)Amino(henol Derivative + -cetaminophen $Tylenol' 5sed widely as analgesis ad anti+pyretic

-d!antage: %ecreased 6I upset, 6I 3leeding, decrease incidence of hypersensiti!ity

Para)Chloro&en-oic Aci' + + Indomethacin $Indocin' #rostaglandin inhi itor 5sed for rheumatoid, gouty and osteoarthritis )ulindac $(linoril' Tolmetin $Tolectin'

Pyra-olone Derivatives .enamates "*icams #iroxincam $"eldene' 5sed for rheumatoid and osteoarthritis .eclofenamate .efenamic -cid To relie!e moderate pain of rief duration ,xyphen utazone #henyl utazone $3utazolidin' 5sed for rheumatoid arthritis, acute gout -d!erse *xn: 3lood dyscrasias+agranulocytosis and a plastic anemia

Central Luzon Doctors Hospital Educational Institution

San Pablo, Tarlac City

Pharmacology Nervous System

)u mitted 3y: .ichael 3. /emir 6erald Louie .ene (ynthia .iranda %aphnie Lorraine /ie!es -!egail #agdanganan .onica *ica #ineda Kaycee Muinsay Neannielyn *amos 1all .ark *amos .em ers: 6rp.9: 3)/ III+& )u mitted to: .a<am: &lynor .aquidang *./

O#harmacologyP