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CASE PRESENTATION
On
DH tqpe a & complications
qpertens|on m|tn |td oard|oegatq m|tn
putonarq oongest|on and neuon|a
VISION:
As u leudlng Chrlstlun lnstltutlon of leurnlng ln Aslu, Sllllmun Unlverslty ls commltted to totul humun development for the well-belng of soclety und
envlronment.
MISSION:
In thls regurd, the Unlverslty:
Infuses lnto the ucudemlc leurnlng the Chrlstlun fulth unchored on the gospel of Jesus Chrlst; provlde un envlronment where Chrlstlun fellowshlp und
relutlonshlp cun be nurtured und promoted.
Provldes opportunltles for growth und excellence ln every dlmenslon of the unlverslty llfe ln order to strengthen churucter, competence, und fulth.
Instllls ln ull members of the unlverslty communlty un enllghtened soclul consclousness, und u deep sense of |ustlce und compusslon.
Promotes unlty umong peoples und contrlbute to nutlonul development
1op|c Descr|pt|on
1hls Loplc focuses on neumonla wlLh uMll and mlld cardlomegaly lL Lackles Lhe anaLomy and physlology paLhophyslology and dlsease condlLlons relaLed
Lo Lhe case as well as Lhe demographlc daLa genogram of Lhe paLlenL growLh and developmenL of a mlddle adulL nurslng responslblllLles pharmacologlcal
lnLervenLlons funcLlonal healLh paLLern and 3 nurslng care plans 1he knowledge on pneumonla uMll and mlld cardlomegaly wlLh pulmonary congesLlon
4
provldes slgnlflcanL daLa and knowledge regardlng Lhe dlfferenL dlseases lL wlll also help lmprove Lhe skllls and aLLlLudes of nurses ln Laklng care of paLlenLs
expelnclng such condlLlons
|acement -urslng Care ManagemenL 10a Medlclne 8oLaLlon
Centra| Cb[ect|ves
AL Lhe end of our dlscusslon Lhe level lv sLudenLs of -CM 104 secLlon P1 shall acqulre knowledge develop skllls and manlfesL poslLlve aLLlLudes
necessary ln glvlng hollsLlc quallLy and safe care Lo paLlenLs experlenclng uM Lype ll and lLs compllcaLlons neumonla PyperLenslonanglna pecLorls
pulmonary congesLlon and Mlld cardlomegaly
Spec|f|c Cb[ect|ves
AL Lhe end of Lhe case presenLaLlon Lhe sLudenL nurses shall
1 Pave a clear vlew abouL Lhe glven lnformaLlon relaLed Lo Lhe paLlenL's case saLlsfacLorlly
2 ulscuss Lhe anaLomy and physlology of Lhe sysLems relaLed Lo Lhe case of Lhe paLlenL correcLly
3 ulscuss Lhe demographlc daLa genogram and Lhe paLlenL's funcLlonal healLh paLLern comprehenslvely
4 ldenLlfy properly Lhe nurslng responslblllLles on Laklng care wlLh paLlenLs havlng such condlLlons
3 ldenLlfy Lhe common medlcaLlons for cllenLs experlenclng such condlLlons and Lhe acLlons and slgnlflcanL conslderaLlons of each
6 CrlLlcally analyze Lhe -Cs for Lhe cllenL aL 73 level of compeLency
7 verballze lncreased level of knowledge Lo aL leasL 73 wlLh regards Lo pneumonla uMll mlld cardlomegaly
8 verbally express appreclaLlon of Lhe concepLs covered ln Lhe case presenLaLlon
Mrs Corazon Crdoez
Cllnlcal lnsLrucLor Medlclne 8oLaLlon
Sllllman unlverslLy College of -urslng
uumagueLe ClLy
5
uear Madam
l 8azlel LsLornlno a Level lv sLudenL of Sllllman unlverslLy College of -urslng care for a 38year old paLlenL Mrs vlllanos Amada 8 She was admlLLed lasL !uly
13 2008 aL 410 M wlLh chlef complalnLs of d dl lf ff fl lc cu ul lL Ly y l ln n b br re ea aL Lh hl ln ng g n no oL Le ed d p pr ro od du uc cL Ll lv ve e c co ou ug gh h w wl lL Lh h w wl lL Lh hl ls sh h s sp pu uL Lu um m e ed de em ma a o of f b bo oL Lh h l le eg gs s a an nd d f fe ee eL L v vo om ml lL Ll ln ng g o of f
l ln ng ge es sL Le ed d f fo oo od d f fo ou ur r L Ll lm me es s p pe er r d da ay y w wh hl lc ch h w we er re e a al ll l n no oL Le ed d 1 1 w we ee ek k p pr rl lo or r L Lo o a ad dm ml ls ss sl lo on n
ln relaLlon Lo Lhls l would llke Lo apply for a case sLudy regardlng my paLlenL who has uM Lype 2 hyperLenslon wlLh mlld cardlomegaly wlLh pulmonary congesLlon
and pneumonla on boLh lung bases ln connecLlon wlLh our relaLed learnlng experlence aL -egros CrlenLal rovlnclal PosplLal uumagueLe ClLy l wlll be prlvlleged
Lo conducL Lhls case sLudy for lL would enhance my knowledge lmprove our skllls and culLlvaLe poslLlve aLLlLudes Loward Lhe care of a paLlenL who experlences
such condlLlons WlLh Lhese l would llke Lo presenL and lmparL knowledge and skllls Lo my fellow learners Lhrough a case presenLaLlon
?our approval would be deeply appreclaLed and noLed as slgn of your concern for Lhe hollsLlc developmenL of Lhe exclLlng and never endlng quesL for knowledge
and wlsdom 1hank you
8especLfully yours
kA2ILL 8 LS1CkNINC
CKNOWLEDGEMENT
6
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7
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8
%#DuO%
labeLeselllLus ls commonly descrlbed as Lhe culprlL/ Lhe klller dlsease/ Lhe rooL of all evlls" 1hls ls
due Lo Lhe rooLlng compllcaLlons afLer ulabeLes MelllLus was lefL unLreaLed or lnefflclenLly unLreaLed ln Lhe case of
Lhe sub[ecL ln Lhls case sLudy Lhe same culprlL wlLh oLher predlsposlng and preclplLaLlng facLors made her suscepLlble
Lo dlfferenL dlsease condlLlons such as hyperLenslon mlld cardlomegaly pulmonary congesLlon and pneumonla
_toetes meIIttos ts o ezoate sgstem dtseose eozoeteztzed g ettez o defteteaeg ta tasoIta oz o deezeosed
otIttg of te odg to ose tasoIta tt ts somettmes zefezzed to os tg sogozs" g ot eIteats oad eoIt eoze pzoetdezs. ge
aottoa ossoetottag sogoz tt dtoetes ts oppzopztote eeoose te possoge of Iozge omooats of sogozIodea oztae ts
eozoeteztstte of poozIg eoatzoIIed dtoetes. goeeez, tg IeeeI of Iood gIoeose oze oaIg oae eompoaeat of te potoIogte
pzoeess oad eItateoI moatfestottoas ossoetoted tt _g. _m eoa e ossoetoted tt seztoos eompIteottoas , ot peopIe tt
dtoetes eoa to/e pzeeeattee meosozes to zedoee te oeeozzeaee of soe It/eItood.
goatasoIta depeadeat _g oz _g tgpe ts te most eommoa tgpe of dtoetes oad oeeooats foz oppzostmoteIg 80 of
oII eoses. geze oze eoztoos eoosottee foetozs ot foz tts speetfte eose stodg, te potteat's geaette pzedtspostttoa to te dtseose
os pzeetpttoted g ez tg tato/e of gIoeose. %ea se os dtogaosed to oee _m tgpe z ot te oge of 8, teze os
taeffeettee tezopeotte moaogemeat ta tezms of medteoI moaogemeat oad os eII os aoapozmoeoIogteoI tatezeeattoas soe
os aotztttoaoI tato/e modtfteottoa oad esezetse. gts taeffeettee eoetoz zesoIted to te oggzoeottoa of te eoadtttoa Ieodtag
to dtffezeat seztoos pzoIems soe os gpezteastoa ezeta te potteat oIso ts geaetteoIIg pzedtsposed. geze oze odded tasoIts
9
to taozg oad ompezed te aozmoI foaettoatag of te /tdaeg, moag eoatztottag foetozs Ieod to te mtId eozdtomoegoIg oad
poImoaozg eoagesttoa, oad oIso te potteat tmmoae zespoase os eompzomtsed oad Ieods ez to e soseepttIe to paeomoato.
ge tafIommottoa oa ez Ioags oad te deezeosed mgoeozdtoI soppIg te zoaeed oot fzom te oztgtaoI staaez eoosed ez
to oee oagtao peetozts.
_toetes meIIttos zepzeseats o etezogeaeoos gzoop of ezoate dtsozdez eozoeteztzed g gpezgIgeemto. gost
eommoaIg offeets omea ogtag eteeaJ to . gts ts doe to totoI oz pozttoI tasoIta defteteaeg oz taseastttettg of eto eeIIs
to seezete tasoIta. 9t ts eozoeteztzed g dtsozdezs ta te metooItsm of eozogdzote, fot, pzoteta, os eII os eoages ta te
stzoetoze of Iood eesseIs. Qoosottee foetozs taeIode geaettes oad aotztttoaoI tg tato/e of gIoeose. ggpezteastoa, oeeozdtag
to te ozId eoIt ozgoatzottoa , ts te pezststeat eIeeottoa of te sgstoIte _g ooee 10 mm gg oad te dtostoIte ooee ?0
mm gg. @ts/ foetozs taeIode fomtIg tstozg oad gpezeoIestezemto. gaeomoato ts te tafIommottoa of te oIeeoIoz spoees
of te Ioag zesoIttag ta eoasoItdottoa of Ioag ttssoe os oIeeoIt ftII te esodotes. gese oze eoosed g eoztoos ozgoatsms.
agtao peetozts ts te tzoasteat pozosgsmoI eest pota pzodoeed g tasoffteteat Iood fIo to te mgoeozdtom zesoIttag ta
mgoeozdtoI tseemto. ge zts/ foetozs oze ggg oad _g.
10
EOGRAPHIC ATA
N Nu um me e: : Vlllunos, Amudu S Se ex x: : F Fe em mu ul le e C Cl lv vl ll l S St tu ut tu us s: : M Mu ur rr rl le ed d H Hu us sb bu un nd d: : V Vl ll ll lu un no os s, , B Be er rn nu ur rd d
A Ag ge e: : 5 58 8 y yr rs s. . o ol ld d B Bl lr rt th hd du uy y: : J Ju ul ly y 1 16 6, , 1 19 94 49 9 R Re el ll lg gl lo on n: : Romun Cuthollc N Nu ut tl lo on nu ul ll lt ty y: : F Fl ll ll lp pl ln no o
A Ad dd dr re es ss s: : L Lu ug gd do on ng gu un n, , D Dl lp po ol lo og g C Cl lt ty y O Oc cc cu up pu ut tl lo on n: : B Bu us sl ln ne es sw wo om mu un n B Bl lr rt th hp pl lu uc ce e: : D Dl lp po ol lo og g, , C Cl lt ty y
E Ed du uc cu ut tl lo on nu ul l A At tt tu ul ln nm me en nt t: : 2 2
n nd d
Y Yr r. . C Co ol ll le eg ge e
R Ro oo om m: : C CC CU U # #5 5 D Du ut te e u un nd d T Tl lm me e o of f A Ad dm ml ls ss sl lo on n: : J Ju ul ly y1 15 5, , 2 20 00 08 8 @ @ 4 4: :1 10 0 P PM M
A At tt te en nd dl ln ng g P Ph hy ys sl lc cl lu un n: : D Dr r. . S So ol lu ut tu un n/ / D Dr r. . C Cu ud dl lz z C Cu us se e # #: :0 01 10 04 42 26 6
C Ch hl le ef f C Co om mp pl lu ul ln nt t: :
D Dl lf ff fl lc cu ul lt ty y l ln n b br re eu ut th hl ln ng g n no ot te ed d, , p pr ro od du uc ct tl lv ve e c co ou ug gh h w wl lt th h w wl lt th hl ls sh h s sp pu ut tu um m; ; e ed de em mu u o of f b bo ot th h l le eg gs s u un nd d f fe ee et t; ; v vo om ml lt tl ln ng g o of f l ln ng ge es st te ed d f fo oo od d f fo ou ur r t tl lm me es s
p pe er r d du uy y ( (u ul ll l n no ot te ed d 1 1 w we ee ek k P PT TA A) )
V Ve er rb bu ul ll lz ze ed d, ," " n nu ug gl ll ls so od d | |u ud d k ko o u ug g g gl ln nh hu uw wu u d du uy y u un ny yu u k ku un nu un ng g g gl lu ub bo o k ko o n nu uu uy y p pl le em mu u, , g gu uh hu ub bu ug g m mu un n p pu ud d u uk ko on ng g t tl ll ll l; ; u un ng g d dl ll ll l n nu uk ko o m mu uk ku uy yu u
k ku uy y g gu us su uk ku u p pu u | |u ud d k ko o, , l lg gu uw wu us s r ru u n nu uk ko o u uk ko on ng g k kl ln nu uo on n b bu u" "
V Vl lt tu ul l S Sl lg gn ns s u up po on n u ud dm ml ls ss sl lo on n: : T T= =3 37 7. .2 2 d de eg gr re ee e C Ce el ls sl lu us s; ; P PR R= = 1 10 06 6 b bp pm m; ; R RR R= = 1 18 8c cp pm m; ; B BP P= =1 13 30 0/ /9 90 0
G Ge en ne er ru ul l I Im mp pr re es ss sl lo on n: :
R Re ec ce el lv ve ed d s sl lt tt tl ln ng g o on n b be ed d, , c co on ns sc cl lo ou us s, , u un nd d v ve er rb bu ul ll ly y r re es sp po on ns sl lv ve e; ;
f fu uc cl lu ul l g gr rl lm mu uc cl ln ng g l ls s n no ot te ed d u un nd d u us se e o of f u uc cc ce es ss so or ry y m mu us sc cl le e l ls s n no ot te ed d u up po on n b br re eu ut th hl ln ng g; ;
r re es st tl le es ss s u un nd d s sw we eu ut tl ln ng g n no ot te ed d o on n f fo or re eh he eu ud d u un nd d f fu uc ce e; ;
11
k ke ee ep ps s o on n m mo ov vl ln ng g t to o f fl ln nd d u u c co om mf fo or rt tu ub bl le e p po os sl lt tl lo on n- -f fr ro om m s sl lt tt tl ln ng g, , l ll le es s o on n b be ed d o on n u u s su up pl ln ne e p po os sl lt tl lo on n w wl lt th h h he eu ud d e el le ev vu ut te ed d u ut t u up pp pr ro ox xl lm mu ut te el ly y 3 30 0 d de eg gr re ee es s
u un nd d k ke ee ep ps s o on n s sh hl lf ft tl ln ng g f fr ro om m l le ef ft t l lu ut te er ru ul l t to o r rl lg gh ht t l lu ut te er ru ul l p po os sl lt tl lo on n. .
H Hl ls st to or ry y o of f P Pr re es se en nt t I Il ll ln ne es ss s: :
S Sh he e w wu us s d dl lu ug gn no os se ed d o of f D DM M t ty yp pe e I II I o on n 1 19 99 97 7 w wh he en n s sh he e w wu us s 4 48 8 y yr rs s. . o ol ld d; ;
S Sh he e w wu us s u ul ls so o u ud dm ml lt te ed d t to o t th he e s su um me e l ln ns st tl lt tu ut tl lo on n 4 4 w we ee ek ks s p pr rl lo or r t to o t th he e p pr re es se en nt t u ud dm ml ls ss sl lo on n d du ue e t to o d dl lf ff fl lc cu ul lt ty y l ln n b br re eu ut th hl ln ng g u un nd d p pr ro od du uc ct tl lv ve e c co ou ug gh h w wl lt th h
w wh hl lt tl ls sh h s sp pu ut tu um m; ; 1 1 w we ee ek k p pr rl lo or r t to o t th he e p pr re es se en nt t u ud dm ml ls ss sl lo on n, , s sh he e h hu ud d t th he e s su um me e c co om mp pl lu ul ln nt ts s u us s h he er r p pr re ev vl lo ou us s u ud dm ml ls ss sl lo on n b bu ut t n no ow w, , b bo ot th h h he er r l le eg gs s u un nd d f fe ee et t
w we er re e e ed de em mu ut to ou us s u un nd d s sh he e v vo om ml lt ts s o ou ut t t th he e f fo oo od d s sh he e l ln ng ge es st te ed d u ur ro ou un nd d f fo ou ur r t tl lm me es s l ln n u u d du uy y. .
G E N O G R M
Amillo Raiz
63yrs old
Vehivular
accident
Gardenia
Raiz
56 yrs. old
Vehicular
accident
Candelario
Reno, 55yrs.
old
hypertension
Pipito Reno
78yr. old
A&W
Amisita
Castillo
78 yrs old
Hypertension
Dalia Raiz
65 yrs. old
DM
Gardorello
Castillo
72 yrs. old
DM
Amando
Castillo
60 yrs. old
DM
Gardo Castillo
53 yrs. old
Hypertension
Gaston Castillo
86 yrs. old
A&W
12
LEGEND:
Female X-
Deceased
Male -
Client
KOW1h and LVLLOMLN1 o[ a midd!g
adu!
Norma| at|ent hys|o|og|c changes
hys|ca| Deve|opment
uecrease ln bone denslLy and mass causes a decrease ln helghL
She sLands 3 feeL 2 lnches and verballzed nagkakuba
Amada C. Villanos
58 yrs. old
Businesswoman
DM type
2;HPN;pneumonia,mil
d cardiomegaly w/
pulmonary congestion
Bernard
Villanos
60 yrs. old
A&W
Nelda
Aguilla
40 yo
Teacher
HPN
Joscilin
Agoncillo
36 yrs. old
Nurse
A&W
Marlon
Villanos
38 yr. old
Teacher;
HPN
Amando Castillo
60 yrs. old
DM; currently
living in Dgte.
city
Bernardo Jr.
Villanos
39 yrs. old
businessman
A&W
Randy
Villanos
33 yrs. old
jobless
A&W
Rudy Villanos
20 yrs. old
Prohibited
Drug User
13
as Lhe lndlvldual geLs older Muscle Lone decreases causlng
Lhe person Lo appear flabbler vlsual aculLy ofLen dlmlnlshes
necesslLaLlng eye glasses 1here ls an ad[usLmenL Lo
menopause
1he mosL vlslble changes aL Lhls perlod are graylng of halr
wrlnkllng of Lhe skln And Lhlckenlng of Lhe walsL uecrease ln
hearlng and vlsual aculLy are ofLen noLed durlng Lhls perlod
Cogn|t|ve changes
Changes ln cognlLlve funcLlon of mlddle adulLs are rare excepL
wlLh lllness or Lrauma 1he mlddle adulL can learn new skllls
and lnformaLlon Some mlddle adulLs enLer educaLlonal or
vocaLlonal programs Lo prepare Lhemselves for enLerlng [ob
markeL and changlng [obs
sychosoc|a| Deve|opment
Learns and ad[usLs Lo role as grandparenLs MalnLalns conLacL
wlLh exLended famlly 8eaches and malnLalns a saLlsfacLory
performance ln career uevelops adulL lelsure Llme acLlvlLles
8eadles self boLh flnanclally and psychologlcally for reLlremenL
llrsL awareness LhaL Lhey are becomlng old"
naman ko kay gulang na dlll na pareha sauna akong
Llnlndugan ba laln man [ud nang baLa pa kay lamlg
Llnundugan" clalmed she wears eye glasses buL noL ln
Lhe hosplLal she uses lL only when she ls readlng buL she
was noL able Lo brlng lL has mlxLure of black and whlLe
halr wrlnkllng of Lhe skln ls noLed on Lhe face and
exLremlLles poor hearlng aculLy due Lo old age
verballzed kaLong haplL na ko mag menopause me[o
naglahl [ud ko kanang sapuLon ba usahay"
ALLends Lo semlnars ln Lhelr barangay regardlng
buslnesses buL Lend Lo sLay home when her healLh
sLarLed Lo become lll verballzed kaLong wala pa ko
sugod nagsaklL [ud kay muaLLend ra man mo kung unsay
mga semlnar labaw na kabahln buslness ba blsan kaLo
naa nako uM2 pero kanang grabe na [ud pundo nlng
balay sa Lv nalang"
Crandchlldren usually vlslL her durlng speclal occaslons
LogeLher wlLh her chlldren when Lhey are sLlll ln
ulpologverballzed layo naman pud sllaa kanang sauna
ra kay dall ra pagadLo nlla mablslLa dayon ko sa mga
baLa mao unLay kallngawan unsaon La man kay layo na
llsod pud magbyahe uy"
Cood performance ln her grocery sLore buslness and
clalmed Lo be Lhe one managlng lL ull Llme compared Lo
her husband SLlll preparlng for her Lhelr llves as an old
couple and verballzed kanang amo kay kung padalan ra
14
Mora| Deve|opment
Accordlng Lo kohlberg Lhe adulL can move beyond Lhe
convenLlonal level Lo Lhe posLconvenLlonal level kohlberg
belleves LhaL exLenslve experlence of personal moral cholce
and responslblllLy ls requlred before people can reach Lhe posL
convenLlonal level 1he person llves auLonomously and deflnes
moral values and prlnclples LhaL are dlsLlncL from personal
ldenLlflcaLlon wlLh group values She llves accordlng Lo
prlnclple LhaL are unlversally agreed on and LhaL Lhe person
conslders approprlaLe for llfe
Sp|r|tua| deve|opment
As an adulL grows flrmer Lhe falLh Lo Cod
pud ml sa akong anak sa gawas pero kung dlll pud kay
kanlng sa negosyo ra lpon ug glnagmay para sa
klnabuhlng Llgulang" She shared LhaL she's geLLlng older
and weaker due Lo her compllcaLed dlsease/condLlon
She doesn'L flnd lL dlfflfflculL Lo follow rules seL by Lhe
communlLy as long as Lhe rules are falr enough Lo
everybody ln maklng declslon she 1
sL
conslders Lhe
welfare of her famlly and consulLs her husband all Lhe
Llme Slnce her chlldren were lefL aL ulpolog clLy she
always cllngs Lo her husband and older broLher when lL
comes Lo declslon maklng and verballzed usahay day
kay slla na lamang akong pasagdan mas maayo kay kusog
pa man slla unya kanang magluya k okay guboL na man
gud hunahuna slla na lamang kabalo naman pud slla
basLa Lama ra"
My cllenL ls a 8oman CaLhollc She clalms LhaL as she
grows older she develops Lhls sLronger falLh Lo Cod
AlLhough she ls sufferlng of Lhls dlsease condlLlon she ls
very Lhankful Lhe she's sLlll allve She Lhanks Plm each
day and asks Plm Lo be able Lo see her chlldren and
grandchlldren compleLely llke a reunlon lf only posslble
because lL wlll make her very happy and forgeL LhaL she ls
lll verballzed nangandoy Lawon ko blsag lmposlble
gamay kay lagyo man slla kanang unLa makareunlon pud
mo blsag slmple ra kay gulang na gud pud Lawon ml nya
15
masaklLon pa gyud ko maayo nang maklLan nako akong
mga apomallpay [ud Lawon konagampo gyud ko nlya"
16
PHYSICAL ASSESSENT
35
Respiratory system
8esplraLory SysLem ln anaLomy and physlology organs LhaL dellver oxygen Lo Lhe clrculaLory sysLem for LransporL Lo all body cells Cxygen ls essenLlal for cells
whlch use Lhls vlLal subsLance Lo llberaLe Lhe energy needed for cellular acLlvlLles ln addlLlon Lo supplylng oxygen Lhe resplraLory sysLem alds ln removlng of
carbon dloxlde prevenLlng Lhe leLhal bulldup of Lhls wasLe producL ln body Llssues uayln and dayouL wlLhouL Lhe prompL of consclous LhoughL Lhe resplraLory
sysLem carrles ouL lLs llfesusLalnlng acLlvlLles lf Lhe resplraLory sysLem's Lasks are lnLerrupLed for more Lhan a few
mlnuLes serlous lrreverslble damage Lo Llssues occurs followed by Lhe fallure of all body sysLems and ulLlmaLely
deaLh
Whlle Lhe lnLake of oxygen and removal of carbon dloxlde are Lhe prlmary funcLlons of Lhe resplraLory sysLem lL
plays oLher lmporLanL roles ln Lhe body 1he resplraLory sysLem helps regulaLe Lhe balance of acld and base ln
Llssues a process cruclal for Lhe normal funcLlonlng of cells lL proLecLs Lhe body agalnsL dlseasecauslng
organlsms and Loxlc subsLances lnhaled wlLh alr 1he resplraLory sysLem also houses Lhe cells LhaL deLecL smell
and asslsLs ln Lhe producLlon of sounds for speech
1he resplraLory and clrculaLory sysLems work LogeLher Lo dellver oxygen Lo cells and remove carbon dloxlde ln a
Lwophase process called resplraLlon 1he flrsL phase of resplraLlon beglns wlLh breaLhlng ln or lnhalaLlon
lnhalaLlon brlngs alr from ouLslde Lhe body lnLo Lhe lungs Cxygen ln Lhe alr moves from Lhe lungs Lhrough blood
vessels Lo Lhe hearL whlch pumps Lhe oxygenrlch blood Lo all parLs of Lhe body Cxygen Lhen moves from Lhe
bloodsLream lnLo cells whlch compleLes Lhe flrsL phase of resplraLlon ln Lhe cells oxygen ls used ln a separaLe
energyproduclng process called cellular resplraLlon whlch produces carbon dloxlde as a byproducL 1he second
phase of resplraLlon beglns wlLh Lhe movemenL of carbon dloxlde from Lhe cells Lo Lhe bloodsLream 1he
bloodsLream carrles carbon dloxlde Lo Lhe hearL whlch pumps Lhe carbon dloxldeladen blood Lo Lhe lungs ln Lhe
lungs breaLhlng ouL or exhalaLlon removes carbon dloxlde from Lhe body Lhus compleLlng Lhe resplraLlon cycle
36
jare palred organs ln Lhe chesL LhaL
carry onresplraLlon ln Lhe adulL human each lung ls 23 Lo 30 cm (10 Lo
12 ln) long and roughly conlcal 1he Lwo lungs are separaLed by a
sLrucLure called Lhe medlasLlnum whlch conLalns Lhe hearL Lrachea
esophagus and blood vessels 1hey are covered by a proLecLlve
membrane called Lhe pulmonary pleura whlch ls separaLed from Lhe
parleLal pleuraa slmllar membrane on Lhe chesL wallby a lubrlcaLlng
fluld lnhaled alr passes Lhrough Lhe Lrachea whlch dlvldes lnLo Lwo
Lubes called bronchl each bronchus leads Lo one lung WlLhln Lhe lungs
Lhe bronchl subdlvlde lnLo bronchloles whlch glve rlse Lo alveolar ducLs
Lhese end ln sacs called alveoll
1he rlghL lung has Lhree lobes Lhe lefL lung wlLh a clefL Lo
accommodaLe Lhe hearL has only Lwo 1he Lwo branches of Lhe Lrachea called bronchl subdlvlde wlLhln Lhe lobes lnLo smaller and smaller alr vessels 1hey
LermlnaLe ln alveoll Llny alr sacs surrounded by caplllarles When Lhe alveoll lnflaLe wlLh lnhaled alr oxygen dlffuses lnLo Lhe blood ln Lhe caplllarles Lo be pumped
by Lhe hearL Lo Lhe Llssues of Lhe body and carbon dloxlde dlffuses ouL of Lhe blood lnLo Lhe lungs where lL ls exhaled
RESPIRATION
uurlng resplraLlon Lhe dlaphragm conLracLs and moves downward Lhe pecLoralls mlnor
and lnLercosLal muscles pull Lhe rlb cage ouLwards 1he chesL cavlLy expands and alr rushes lnLo
Lhe lungs Lhrough Lhe Lrachea Lo flll Lhe resulLlng vacuum When Lhe dlaphragm relaxes Lo lLs
normal upwardly curvlng poslLlon Lhe lungs conLracL and alr ls forced ouL
ln Lhls llfesupporLlng process oxygen from lncomlng alr enLers Lhe blood and carbon
dloxlde a wasLe gas from Lhe meLabollsm of food ls exhaled 1he exchange of gases Lakes place
37
when alr reaches Lhe alveoll 1hese small sacs are only one cell Lhlck and Lhey are surrounded by blood caplllarles LhaL are also only one cell Lhlck Alr dlffuses
Lhrough Lhese cells lnLo Lhe caplllary blood whlch carrles Lhe oxygenrlch alr Lo Lhe hearL Lo be dlsLrlbuLed LhroughouL Lhe body ln Lhe alveoll aL Lhe same Llme
gaseous carbon dloxlde dlffuses from Lhe blood lnLo Lhe lung and ls explred
Alr enLers Lhe lungs when Lhe dlaphragm a sLrong muscle under Lhe lungs forclbly lowers and enlarges Lhe chesL cavlLy ln whlch Lhe lungs are suspended
1hls causes Lhe lungs Lo expand and Lhe alr Lo flll Lhe enlarged lungs When Lhe dlaphragm relaxes Lhe lungs conLracL and Lhe alr ls forced ouL ln Llmes of greaLer
oxygen need Lhe rlb cage can also expand furLher enlarglng Lhe chesL cavlLy for greaLer alr lnLake A healLhy adulL can draw ln abouL 33 Lo 49 llLres (200 Lo 300
cu ln) of alr aL a slngle breaLh buL aL resL only abouL 3 per cenL of Lhls volume ls used 1he lungs also excreLe waLer as gas sLore glycogen a complex
carbohydraLe and fllLer ouL lncomlng organlsms and dangerous parLlcles vla halrs called cllla
CARIOVASCULAR SYSTE
ClrculaLory SysLem or cardlovascular sysLem ln humans Lhe comblned funcLlon of Lhe hearL blood and
blood vessels Lo LransporL oxygen and nuLrlenLs Lo organs and Llssues LhroughouL Lhe body and carry away
wasLe producLs Among lLs vlLal funcLlons Lhe clrculaLory sysLem lncreases Lhe flow of blood Lo meeL
lncreased energy demands durlng exerclse and regulaLes body LemperaLure ln addlLlon when forelgn
subsLances or organlsms lnvade Lhe body Lhe clrculaLory sysLem swlfLly conveys dlseaseflghLlng elemenLs of
Lhe lmmune sysLem such as whlLe blood cells and anLlbodles Lo reglons under aLLack Also ln Lhe case of
ln[ury or bleedlng Lhe clrculaLory sysLem sends cloLLlng cells and proLelns Lo Lhe affecLed slLe whlch qulckly
sLop bleedlng and promoLe heallng.
COPONENTS OF THE CIRCULAORY SYSTE
1he hearL blood and blood vessels are Lhe Lhree sLrucLural elemenLs LhaL make up Lhe clrculaLory sysLem
1he hearL ls Lhe englne of Lhe clrculaLory sysLem lL ls dlvlded lnLo four chambers Lhe rlghL aLrlum Lhe rlghL
venLrlcle Lhe lefL aLrlum and Lhe lefL venLrlcle 1he walls of Lhese chambers are made of a speclal muscle
called myocardlum whlch conLracLs conLlnuously and rhyLhmlcally Lo pump blood 1he pumplng acLlon of
Lhe hearL occurs ln Lwo sLages for each hearL beaL dlasLole when Lhe hearL ls aL resL and sysLole when Lhe
hearL conLracLs Lo pump deoxygenaLed blood Loward Lhe lungs and oxygenaLed blood Lo Lhe body uurlng
38
each hearLbeaL Lyplcally abouL 60 Lo 90 ml (abouL 2 Lo 3 oz) of blood are pumped ouL of Lhe hearL lf Lhe hearL sLops pumplng deaLh usually occurs wlLhln four Lo
flve mlnuLes
8lood conslsLs of Lhree Lypes of cells oxygenbearlng red blood cells dlseaseflghLlng whlLe blood cells and bloodcloLLlng plaLeleLs all of whlch are carrled
Lhrough blood vessels ln a llquld called plasma lasma ls yellowlsh and
conslsLs of waLer salLs proLelns vlLamlns mlnerals hormones dlssolved
gases and faLs
1hree Lypes of blood vessels form a complex neLwork of Lubes LhroughouL
Lhe body ArLerles carry blood away from Lhe hearL and velns carry lL
Loward Lhe hearL Caplllarles are Lhe Llny llnks beLween Lhe arLerles and
Lhe velns where oxygen and nuLrlenLs dlffuse Lo body Llssues 1he lnner
layer of blood vessels ls llned wlLh endoLhellal cells LhaL creaLe a smooLh
passage for Lhe LranslL of blood 1hls lnner layer ls surrounded by
connecLlve Llssue and smooLh muscle LhaL enable Lhe blood vessel Lo
expand or conLracL 8lood vessels expand durlng exerclse Lo meeL Lhe
lncreased demand for blood and Lo cool Lhe body 8lood vessels conLracL
afLer an ln[ury Lo reduce bleedlng and also Lo conserve body heaL
ArLerles have Lhlcker walls Lhan velns Lo wlLhsLand Lhe pressure of blood
belng pumped from Lhe hearL 8lood ln Lhe velns ls aL a lower pressure so
velns have oneway valves Lo prevenL blood from flowlng backwards away
from Lhe hearL Caplllarles Lhe smallesL of blood vessels are only vlslble by mlcroscopeLen caplllarles lylng slde by slde are barely as Lhlck as a human halr lf all
Lhe arLerles velns and caplllarles ln Lhe human body were placed end Lo end Lhe LoLal lengLh would equal more Lhan 100000 km (more Lhan 60000 ml)Lhey
could sLreLch around Lhe earLh nearly Lwo and a half Llmes
1he arLerles velns and caplllarles are dlvlded lnLo Lwo sysLems of clrculaLlon sysLemlc and pulmonary 1he sysLemlc clrculaLlon carrles oxygenaLed blood from
Lhe hearL Lo all Lhe Llssues ln Lhe body excepL Lhe lungs and reLurns deoxygenaLed blood carrylng wasLe producLs such as carbon dloxlde back Lo Lhe hearL 1he
pulmonary clrculaLlon carrles Lhls spenL blood from Lhe hearL Lo Lhe lungs ln Lhe lungs Lhe blood releases lLs carbon dloxlde and absorbs oxygen 1he oxygenaLed
blood Lhen reLurns Lo Lhe hearL before Lransferrlng Lo Lhe sysLemlc clrculaLlon
39
A. SYSTEMIC CIRCULATION
1he hearL e[ecLs oxygenrlch blood under hlgh pressure ouL of Lhe hearL's maln pumplng
chamber Lhe lefL venLrlcle Lhrough Lhe largesL arLery Lhe aorLa Smaller arLerles branch off
from Lhe aorLa leadlng Lo varlous parLs of Lhe body 1hese smaller arLerles ln Lurn branch ouL
lnLo even smaller arLerles called arLerloles 8ranches of arLerloles become progresslvely
smaller ln dlameLer evenLually formlng Lhe caplllarles Cnce blood reaches Lhe caplllary level
blood pressure ls greaLly reduced
Caplllarles have exLremely Lhln walls LhaL permlL dlssolved oxygen and nuLrlenLs from Lhe
blood Lo dlffuse across Lo a fluld known as lnLersLlLlal fluld LhaL fllls Lhe gaps beLween Lhe
cells of Llssues or organs 1he dlssolved oxygen and nuLrlenLs Lhen enLer Lhe cells from Lhe
lnLersLlLlal fluld by dlffuslon across Lhe cell membranes Meanwhlle carbon dloxlde and oLher
wasLes leave Lhe cell dlffuse Lhrough Lhe lnLersLlLlal fluld cross Lhe caplllary walls and enLer
Lhe blood ln Lhls way Lhe blood dellvers nuLrlenLs and removes wasLes wlLhouL leavlng Lhe
caplllary Lube
AfLer dellverlng oxygen Lo Llssues and absorblng wasLes Lhe deoxygenaLed blood ln Lhe
caplllarles Lhen sLarLs Lhe reLurn Lrlp Lo Lhe hearL 1he caplllarles merge Lo form Llny velns
called venules 1hese velns ln Lurn [oln LogeLher Lo form progresslvely larger velns ulLlmaLely
Lhe velns converge lnLo Lwo large velns Lhe lnferlor vena cava brlnglng blood from Lhe lower
half of Lhe body and Lhe superlor vena cava brlnglng blood from Lhe upper half 8oLh of Lhese
Lwo large velns [oln aL Lhe rlghL aLrlum of Lhe hearL
8ecause Lhe pressure ls dlsslpaLed ln Lhe arLerloles and caplllarles blood ln velns flows back Lo Lhe hearL aL very low pressure ofLen runnlng uphlll when a person
ls sLandlng llow agalnsL gravlLy ls made posslble by Lhe oneway valves locaLed several cenLlmeLers aparL ln Lhe velns When surroundlng muscles conLracL for
example ln Lhe calf or arm Lhe muscles squeeze blood back Loward Lhe hearL lf Lhe oneway valves work properly blood Lravels only Loward Lhe hearL and
cannoL lapse backward velns wlLh defecLlve valves whlch allow Lhe blood Lo flow backward become enlarged or dllaLed Lo form varlcose velns
40
. PULMONARY SITUATION
ln pulmonary clrculaLlon deoxygenaLed blood reLurnlng from Lhe organs and Llssues of
Lhe body Lravels from Lhe rlghL aLrlum of Lhe hearL Lo Lhe rlghL venLrlcle lrom Lhere lL ls
pushed Lhrough Lhe pulmonary arLery Lo Lhe lung ln Lhe lung Lhe pulmonary arLery
dlvldes formlng Lhe pulmonary caplllary reglon of Lhe lung AL Lhls slLe mlcroscoplc
vessels pass ad[acenL Lo Lhe alveoll or alr sacs of Lhe lung and gases are exchanged across
a Lhln membrane oxygen crosses Lhe membrane lnLo Lhe blood whlle carbon dloxlde
leaves Lhe blood Lhrough Lhls same membrane -ewly oxygenaLed blood Lhen flows lnLo
Lhe pulmonary velns where lL ls collecLed by Lhe lefL aLrlum of Lhe hearL a chamber LhaL
serves as collecLlng pool for Lhe lefL venLrlcle 1he conLracLlon of Lhe lefL venLrlcle sends
blood lnLo Lhe aorLa compleLlng Lhe clrculaLory loop Cn average a slngle blood cell Lakes
roughly 30 seconds Lo compleLe a full clrculL Lhrough boLh Lhe pulmonary and sysLemlc
clrculaLlon
1he pressure generaLed by Lhe pumplng acLlon of Lhe hearL propels Lhe blood Lo Lhe
arLerles ln order Lo malnLaln an adequaLe flow of blood Lo all parLs of Lhe body a cerLaln
level of blood pressure ls needed 8lood pressure for lnsLance enables a person Lo rlse
qulckly from a horlzonLal poslLlon wlLhouL blood poollng ln Lhe legs whlch would cause falnLlng from deprlvaLlon of blood Lo Lhe braln -ormal blood pressure ls
regulaLed by a number of facLors such as Lhe conLracLlon of Lhe hearL Lhe elasLlclLy of arLerlal walls blood volume and reslsLance of blood vessels Lo Lhe passage
of blood
. LOOD PRESSURE
8lood pressure ls measured uslng an lnflaLable devlce wlLh a gauge called a LhaL ls wrapped around Lhe upper arm 8lood pressure ls measured durlng
sysLole Lhe acLlve pumplng phase of Lhe hearL and dlasLole Lhe resLlng phase beLween hearLbeaLs SysLollc and dlasLollc pressures are measured ln unlLs
of mllllmeLers of mercury (abbrevlaLed mm Pg) and dlsplayed as a raLlo 8lood pressure varles beLween lndlvlduals and even durlng Lhe normal course of a
day ln response Lo emoLlon exerLlon sleep and oLher physlcal and menLal changes -ormal blood pressure ls less Lhan 120/80 mm Pg ln whlch 120
descrlbes sysLollc pressure and 80 descrlbes dlasLollc pressure Plgher blood pressures LhaL are susLalned over a long perlod of Llme may lndlcaLe
hyperLenslon a damaglng clrculaLory condlLlon Lower blood pressures could slgnal shock from hearL fallure dehydraLlon lnLernal bleedlng or blood loss
41
4. -\-*v
idneys palred organ whose funcLlons lnclude removlng wasLe producLs from Lhe blood and regulaLlng Lhe amounL of fluld ln Lhe body 1he baslc
unlLs of Lhe kldneys are mlcroscoplcally Lhln sLrucLures called nephrons whlch fllLer Lhe blood and cause wasLes Lo be removed ln Lhe form of urlne 1ogeLher
wlLh Lhe bladder Lwo ureLers and Lhe slngle ureLhra Lhe kldneys make up Lhe body's urlnary sysLem Puman belngs as well as members of all oLher
verLebraLe specles Lyplcally have Lwo kldneys
Llke kldney beans Lhe body's kldneys are dark red ln color and have a shape ln whlch one slde ls convex or rounded and Lhe oLher ls concave or lndenLed 1he
kldneys of adulL humans are abouL 10 Lo 13 cm (4 Lo 3 ln) long and abouL 3 Lo 73 cm (2 Lo 3 ln) wldeabouL Lhe slze of a compuLer mouse
1he kldneys lle agalnsL Lhe rear wall of Lhe abdomen on elLher slde of Lhe splne 1hey are slLuaLed below Lhe mlddle of Lhe back beneaLh Lhe llver on Lhe rlghL
and Lhe spleen on Lhe lefL Lach kldney ls encased ln a LransparenL flbrous membrane called a renal capsule whlch helps proLecL lL agalnsL Lrauma and lnfecLlon
1he concave parL of Lhe kldney aLLaches Lo Lwo of Lhe body's cruclal blood vessels
Lhe renal arLery and Lhe renal velnand Lhe ureLer a Lubellke sLrucLure LhaL carrles
urlne Lo Lhe bladder
UNCTIONS
A prlmary funcLlon of kldneys ls Lhe removal of polsonous wasLes from Lhe blood
Chlef among Lhese wasLes are Lhe nlLrogenconLalnlng compounds urea and urlc acld
whlch resulL from Lhe breakdown of proLelns and nuclelc aclds LlfeLhreaLenlng
lllnesses occur when Loo many of Lhese wasLe producLs accumulaLe ln Lhe
bloodsLream lorLunaLely a healLhy kldney can easlly rld Lhe body of Lhese
subsLances
42
ln addlLlon Lo cleanlng Lhe blood Lhe kldneys perform several oLher essenLlal funcLlons Cne such acLlvlLy ls
regulaLlon of Lhe amounL of waLer conLalned ln Lhe blood 1hls process ls lnfluenced by anLldlureLlc
hormone (AuP) also called vasopressln whlch ls produced ln Lhe hypoLhalamus (a parL of Lhe braln LhaL
regulaLes many lnLernal funcLlons) and sLored ln Lhe nearby plLulLary gland 8ecepLors ln Lhe braln monlLor
Lhe blood's waLer concenLraLlon When Lhe amounL of salL and oLher subsLances ln Lhe blood becomes Loo
hlgh Lhe plLulLary gland releases AuP lnLo Lhe bloodsLream When lL enLers Lhe kldney AuP makes Lhe
walls of Lhe renal Lubules and collecLlng ducLs more permeable Lo waLer so LhaL more waLer ls reabsorbed
lnLo Lhe bloodsLream
1he hormone aldosLerone produced by Lhe adrenal glands lnLeracLs wlLh Lhe kldneys Lo regulaLe Lhe
blood's sodlum and poLasslum conLenL Plgh amounLs of aldosLerone cause Lhe nephrons Lo reabsorb more
sodlum lons more waLer and fewer poLasslum lons low levels of aldosLerone have Lhe reverse effecL 1he
kldney's responses Lo aldosLerone help keep Lhe blood's salL levels wlLhln Lhe narrow range LhaL ls besL for
cruclal physlologlcal acLlvlLles
AldosLerone also helps regulaLe blood pressure When blood pressure sLarLs Lo fall Lhe kldney releases an enzyme (a speclallzed proLeln) called renln whlch
converLs a blood proLeln lnLo Lhe hormone angloLensln 1hls hormone causes blood vessels Lo consLrlcL resulLlng ln a rlse ln blood pressure AngloLensln Lhen
lnduces Lhe adrenal glands Lo release aldosLerone whlch promoLes sodlum and waLer Lo be reabsorbed furLher lncreaslng blood volume and blood pressure
1he kldney also ad[usLs Lhe bodys acldbase balance Lo prevenL such blood dlsorders as acldosls and alkalosls boLh of whlch lmpalr Lhe funcLlonlng of Lhe cenLral
nervous sysLem lf Lhe blood ls Loo acldlc meanlng LhaL Lhere ls an excess of hydrogen lons Lhe kldney moves Lhese lons Lo Lhe urlne Lhrough Lhe process of
Lubular secreLlon An addlLlonal funcLlon of Lhe kldney ls Lhe processlng of vlLamln u Lhe kldney converLs Lhls vlLamln Lo an acLlve form LhaL sLlmulaLes bone
developmenL
Several hormones are produced ln Lhe kldney Cne of Lhese eryLhropoleLln lnfluences Lhe producLlon of red blood cells ln Lhe bone marrow When Lhe kldney
deLecLs LhaL Lhe number of red blood cells ln Lhe body ls decllnlng lL secreLes eryLhropoleLln 1hls hormone Lravels ln Lhe bloodsLream Lo Lhe bone marrow
sLlmulaLlng Lhe producLlon and release of more red cells
43
Pathophysiology
lor cenLurles lL has been noLed LhaL dlabeLes "runs ln famllles" because abouL 40 of people who develop Lhe dlsease have a poslLlve famlly hlsLory ln
relaLlon Lo Lhe paLlenL's case boLh parenLs and grandfaLher has dlabeLes melllLus buL she cannoL remember whaL Lype of uM 1hls genet|c hered|ty predlsposed
her Lo have uM as well 1he preclplLaLlng facLors are age d|et and stress 1he paLlenL was dlagnosed wlLh uM Lype when she was 48 yrs old lncreaslng age ls
relaLed Lo decllne ln glucose Lolerance and an lncrease ln lnsulln reslsLance along wlLh an lncrease prevalence of dlabeLes 1he frequency rlses sharply afLer 40
yrs old probably reflecLlng a general change ln glucose Lolerance 1he separaLlon beLween beLween dlabeLes and nondlabeLes may presensL a problem lf
Lolerance ls noL ad[usLed for age 1hls lncreaslng frequency has been explalned as a decrease ln body funcLlon such as Lhe pancreas LhaL occurs ln all body cells ln
senescence D|et Lhe effecLs of dleL hlgh ln glucose can as well cause rlse ln blood glucose Stress any form of sLress wlLh Lhe neuroendocrlne response lncreases
gluconeogenesls 1hls ls due Lo Lhe release of AC1P(adenocorLlcoLroplc hormone) whlch sLlmulaLes Lhe adrenal gland Lo release glucocorLlcolds and
mlneralocorLlcolds ClucocorLlcolds wlll release corLlsol whlch ls responslble for gluconeogenesls resulLlng Lo lncrease blood glucose AldosLeroone whlch ls Lhe
mosL abundanL MlneralocorLlcold causes sodlum and waLer reLenLlon lncreaslng blood volume Lhus lncreaslng blood pressure
1he geneLlcs of Lype 2 dlabeLes are complex and noL compleLely undersLood buL presumably Lhls dlsease ls relaLed Lo mulLlple genes Lvldence supporLs
lnherlLed componenLs for boLh pancreaLlc beLa cell fallure and lnsulln reslsLance Conslderable debaLe exlsLs regardlng Lhe prlmary defecL ln Lype 2 dlabeLes
melllLus MosL paLlenLs have boLh lnsulln reslsLance and some degree of lnsulln deflclency lallure ln Lhe funcLlon of beLa cells of Lhe pancreaLlc cells or Lhe lsleLs
of langerhans causes lmpalred lnsulln secreLlon slnce Lhey are responslble for lnsulln secreLlon causlng lncrease on blood glucose level 1hls elevaLlon conLlnues
because Lhe llver cannoL sLore glucose as glycogen wlLhouL sufflclenL lnsulln levels slnce lnsulln ls needed ln glycogenesls ln an aLLempL Lo resLore balance and
reLurn blood glucose levels Lo normal kldney excreLes Lhe excess glucose ln Lhe urlne (g|ucosur|a) ***** lnsulln also exhlblLs vasodllaLory properLles lnsulln
reslsLance have been suggesLed as belng responslble for Lhe lncreased arLerlal pressure causlng secondary hypertens|on hyperLenslon wlLh an ldenLlflable
underlylng cause whlch ls now wldely recognlzed as parL of syndrome x a condlLlon characLerlzed by P- wlLh uM Lype 2
lnsulln reslsLance of cells on Lhe oLher hand occurs when Lhe lnsulln recepLors are less senslLlve -ow slnce Lhe lnsulln acL as Lhe key for glucose Lo enLer cells and
be used as energy Lhe reslsLance made lL more dlfflculL for glucose enLrance causlng lL Lo remaln ln Lhe blood and lncrease Lhe blood glucose level lncreased
blood glucose level ls Lermed as hyperg|ycem|a whlch ls Lhe ma[or characLerlsLlc of DM type 2 *******1he dlfflculLy of glucose enLrance makes glucose
unavallable for energy producLlon lnsLead faL sLores are used for energy producLlon WlLh Lhese llpoproLelns are lncreased Lo provlde dellvery and plckup
44
servlces so LhaL llplds wlll be avallable when cells need Lhem 1hls resulL lncreased llpld levels 1he blood chem shows LhaL Lhe LoLal cholesLerol level ls elevaLed Lo
240 mg]dL as we|| as nDL of 26 mg]dL and LDL of 14 mg]dL 1hls lncrease ln cholesLerol level preclplLaLe Lhe cllenL ln havlng nN
When Lhe blood glucose reaches 160 Lo 200 mg/dL Lhe glucose wlll be forced Lo moved ouL Lhe glomerular membrane causlng Lhe glomerular caplllarles Lo be
damaged and become so permeable LhaL plasma proLelns enLer Lhe glomerular fllLraLe causlng proLelns Lo be found ln Lhe urlne prote|nur|a As a resulL Lhe
fllLraLe exerLs a collold osmoLlc pressure LhaL draws ouL waLer ouL of blood ln Lhls slLuaLlon Lhe -l or neL fllLraLlon pressureLoLal pressure LhaL promoLes
fllLraLlon lncreases whlch means more fluld ls fllLered AL Lhe same Llme Lhe 8CC/ blood collold osmoLlc pressure whlch ls due Lo Lhe presence of proLelns ln
blood plasma whlch also opposes fllLraLlon decreases because plasma proLelns are belng losL ln Lhe urlne 8ecause more fllLers ouL of blood caplllarles lnLo Llssues
LhroughouL Lhe body Lhan reLurns vla reabsorpLlon blood volume decreases and lnLersLlLlal fluld lncreases 1hus loss of plasma proLeln ln Lhe urlne cause edema
an abnormally hlgh volume of lnLersLlLlal fluld 1he paLlenL manlfesL edema on boLh legs and feeL 1 week 1A 1here ls also oLher reason for edema occurrence
whlch wlll be dlscussed on Lhe laLer parL ***When blood glucose ls above 160200 mg/dL Lhe renal symporLers cannoL work fasL enough Lo reabsorb all Lhe
glucose LhaL enLers Lhe glomerular fllLraLe As a resulL some glucose remalns ln Lhe urlne g|ucosur|a 8ased on Lhe urlnalysls resulL of Lhe paLlenL glucose ln Lhe
urlne marked as poslLlve and Lhe color ls llghL yellow due Lo Lhe presence of glucose WlLh Lhe loss of large quanLlLles of glucose and semlsLarvaLlon of cells Lhere
ls compensaLory lncrease ln hunger po|yphag|a And Lhere wlll be lncreased osmolallLy due Lo glucose excreLed ln Lhe urlne acLlng as osmoLlc dlureLlc and causes
excreLlon of excesslve amounLs of waLer leadlng Lo excesslve urlnaLlon po|yur|a resulLlng Lo fluld volume deflclL LxLreme dehydraLlon mlghL lead Lo coma and
evenLually Lo deaLh Lxcesslve urlnaLlon faclllLaLes loss of poLasslum sodlum and chlorlde LlecLrolyLe lmbalance happen whlch as Lhe manlfesLaLlon of weakness
fat|gue ma|a|se Loss of waLer cause an lncrease ln serum osmolallLy whlch sLlmulaLes Lhe LhlrsL cenLer ln Lhe hypoLhalamus and Lhe body response as
po|yd|ps|a
Cne of Lhe mosL common heredofamlllal dlsease ls nN 1he paLlenL ls geneLlcally predlsposed Lo Lhls condlLlon slnce her grandfaLher and uncle are hyperLenslve
reclplLaLlng facLors are Lhe presence of hlgh blood cholesLerol levels whlch causes addlLlonal blood vessel lengLh ln adlpose Llssues maklng lLs lengLh longer Lhus
Lhe vascular reslsLance ls lncreased 1hls ls due Lo Lhe facL LhaL reslsLance Lo blood flow Lhrough a vessel ls dlrecLly proporLlonal Lo Lhe lengLh of Lhe vessel 1he
longer Lhe blood vessel Lhe greaLer Lhe reslsLance 1hls conLrlbuLes Lo rlse ln 8 called nN ln P- Lhe Lunlca medla of Lhe arLerloles are Lhlcken Lhus Lhe
arLerloles ln Lhe kldneys are damaged havlng narrowed lumen 1hls narrowlng of lumen decreases blood supply Lo Lhe kldneys When blood supply Lo Lhe kldneys
decreases [uxLaglomerular cells secreLe rennln Lo Lhe bloodsLream ln sequence ACL acL on Lhelr subsLraLe Lo produce acLlve hormone AngloLensln ll whlch
ralses blood pressure ln Lwo ways llrsL lL ls a poLenL vasoconsLrlcLor lL ralses blood pressure and lncreaslng vascular reslsLance lL wlll also cause perlpheral
arLery consLrlcLlon whlch sLlmulaLes eplnephrlne release Lplnephrlne causes decrease sysLemlc 8 sLlmulaLlng AuP release Second AngloLensln ll sLlmulaLes Lhe
secreLlons of aldosLerone whlch lncreases reabsorpLlon of sodlum and waLer by Lhe kldneys 1he waLer reabsorpLlon lncreases LoLal blood volume whlch
lncreases blood pressure as well 1he reabsorpLlon of sodlum and waLer causes edema
lncrease blood pressure may damage Lhe small blood vessels ln Lhe kldneys causlng lmpalrmenL ln Lhe glomerular funcLlon of fllLerlng blood 1hls resulLs Lo
nlLrogenous wasLe ln Lhe blood as evldenced by Lhe urlnalysls resulL Ur|c ac|d of 108 mg creat|n|ne of 06 mg]dL and urem|a of 227 mg]dL SympLoms of
uremla lnclude drowslness |rr|tab|||ty nausea vom|t|ng breath|ess lf vomlLlng ls exLreme lL mlghL lead Lo convulslon Lhen coma and can lead Lo sudden deaLh
45
lf Lhese lmpalrmenL ln Lhe reabsorpLlon of Lhe kldneys and lmpalred glomerular funcLlon wlll be lefL unLreaLed 8L-AL lAlLu8L ls more llkely Lo occur 1he maln
precursors of eryLhropoleLln or LC are cells ln Lhe kldneys LhaL lle beLween Lhe kldney Lubules (perlLubular lnsLersLlLlal cells) WlLh renal fallure LC release
slows and 88C producLlon ls lnadequaLe 1he hemoglobln oxygen carrylng proLeln ln 88C wlll also be decreased as well as Lhe hemaLocrlL as manlfesLed ln Lhe
C8C of Lhe paLlenL showlng ngb of 2 6 gm and nct of 6gm
1oLal blood volume and lncrease ln 8 forces Lhe hearL Lo work harder Lo pump adequaLe blood LhroughouL Lhe body or for longer dlsLance of longer blood
vessels 1hls glves exLra work Lo cardlac muscles maklng lL enlarged card|omega|y
lncreased vascular reslsLance and eplnephrlne release causes lncrease force of lefL venLrlcular conLracLlon so lL wlll requlre more oxygen supply buL slnce Lhe
coronary arLery consLrlcLlon causes decreased C2 supply Lhe lefL venLrlcle wlll hypoxlc 1hls wlll lead Lo decreased force of lefL venLrlcular conLracLlon whlch
lncreases Lhe lefL venLrlcular end dlasLollc pressure Lhus Lhere ls also lncreased lefL venLrlcular preload Cf course as Lhe normal clrculaLlon suggesL Lhe preload
of lefL aLrlum wlll also be lncreased Lhus fluld wlll be accumulaLed ln Lhe lungs causlng edema and pu|monary congest|on an excesslve accumulaLlon of fluld ln
Lhe lungs 1he reabsorpLlon of sodlum and waLer wlll also cause lncrease lefL venLrlcular preload Lhus conLrlbuLlng Lo edema formaLlon
***Cn Lhe oLher hand Ang|na ector|s sympLom of reduced oxygen supply Lo Lhe hearL muscle usually caused by narrowlng or obsLrucLlon of Lhe coronary
arLery aln may radlaLe from Lhe fronL of Lhe chesL ofLen lnLo Lhe arm
lmpalrmenL ln lnsulln secreLlon causes Lhe lowered sLlmulaLlon of proLeln synLhesls Lhus decreaslng defenslns (proLelns found ln neuLrophlls LhaL exhlblL a broad
range of anLlbloLlc acLlvlLy agalnsL bacLerla and fungl and lL poke holes ln mlcrobe membranes whlch kllls Lhe lnvader due Lo loss of cellular conLenLs) -ow Lhere
wlll be lneffecLlve anLlbloLlc acLlvlLy maklng Lhe neuLrophll handlcapped *** Slnce Lhe paLlenL ls already an elderly aglng 38 ?rs old and was dlagnosed wlLh um
Lype 2 aL Lhe age of 48 Lhe Lhymus gland already aLrophy whlch decreases lymphocyLe and anLlbody producLlon 1he lnflammaLory process ls Lherefore lmpalred
1hls evenL made Lhe cllenL predlsposed Lo pneumon|a 1here are 3 ma[or classlflcaLlons of pneumonla CommunlLy acqulred hosplLal acqulred and asplraLlon
acqulred 1here name suggesL were Lhe causaLlve agenLs came from So afLer Lhe asplraLlon of Lhe organlsm Lhere wlll be normal mucus producLlon and clllary
acLlon buL slnce Lhe mucoclllary escalaLor ls less effecLlve Lhere wlll be adherence of Lhe organlsm Lo Lhe alveolar macrophages ln whlch Lhe cell wall componenLs
are exposed lnflammaLory response Lakes place Lhen red heapLlzaLlon and consolldaLlon of lung parenchyma maklng lL swell Lhus maklng Lhe lung appear reddlsh
and granular llke 1hls ls pneumon|a lnflammaLlon of lung parenchyma also causes chesL paln and Lhen Lhere wlll be leukocyLe nfllLraLlon buL slnce Lhere ls
lmpalred lmmune response as dlscussed earller Lhe lnfecLlon occurs and wlll noL be resolved 1here wlll be lncreased secreLlon of of flulds and shredded cells
pourlng lnLo Lhe passages of alr sacs of lungs 1he presence of exudaLes wlLhln alr spaces cause coughlng and shorLenlng of breaLh******uurlng Lhe
lnflammaLory process Lhe arLerloles ln Lhe area wlll be vasoconsLrlcLs 1he consLrlcLlon sLlmulaLe Lhe release of chemlcal medlaLors LhaL wlll boLh cause
consLrlcLlon(maklng spaces beLween cells Lhus fluld escapes Lo Llssues edema) and vasodllaLlon (faclllLaLlng hyperemla and movemenL of fluld from caplllarles Lo
Llssuesedema) 1hls causes pu|monary congest|on as well
46
47
OvERVIEW OF THE ISEASE
CONITIONS
UHDL1L 1YL L
ln 1ype 2 dlabeLes formerly known as nonlnsullndependenL dlabeLes melllLus (-luuM) and adulLonseL dlabeLes Lhe body's dellcaLe balance beLween
lnsulln producLlon and Lhe ablllLy of cells Lo use lnsulln goes awry SympLoms characLerlsLlc of 1ype 2 dlabeLes lnclude Lhose found ln 1ype 1 dlabeLes as well
as repeaLed lnfecLlons or skln sores LhaL heal slowly or noL aL all generallzed Llredness and Llngllng or numbness ln Lhe hands or feeL
1he onseL of 1ype 2 dlabeLes usually occurs afLer Lhe age of 43 alLhough Lhe lncldence of Lhe dlsease ln younger people ls growlng rapldly 8ecause sympLoms
develop slowly lndlvlduals wlLh Lhe dlsease may noL lmmedlaLely recognlze LhaL Lhey are slck A number of genes are lnvolved ln 1ype 2 dlabeLes ln addlLlon
Lhere ls a sLrong relaLlonshlp beLween obeslLy and 1ype 2 dlabeLes AbouL 80 percenL of dlabeLlcs wlLh Lhls form of Lhe dlsease are slgnlflcanLly overwelghL
COMPLICATIONS
#LNH HU#L
48
lf lefL unLreaLed dlabeLes melllLus may cause llfeLhreaLenlng compllcaLlons 1ype 1 dlabeLes can resulL ln dlabeLlc coma (a sLaLe of unconsclousness caused by
exLremely hlgh levels of glucose ln Lhe blood) or deaLh ln boLh 1ype 1 and 1ype 2 dlabeLes compllcaLlons may lnclude bllndness kldney fallure and hearL
dlsease ulabeLes can cause Llny blood vessels Lo become blocked when Lhls occurs ln blood vessels of Lhe eye lL can resulL ln reLlnopaLhy (Lhe breakdown of
Lhe llnlng aL Lhe back of Lhe eye) causlng bllndness ulabeLes melllLus ls Lhe leadlng cause of new cases of bllndness ln people aged 20 Lo 74 ln Lhe kldneys
dlabeLes can lead Lo nephropaLhy (Lhe lnablllLy of Lhe kldney Lo properly fllLer Loxlns from Lhe blood) AbouL 40 percenL of new cases of endsLage renal
dlsease (kldney fallure) are caused by dlabeLes melllLus 8lockages of large blood vessels ln dlabeLlcs can lead Lo many cardlovascular problems lncludlng hlgh
blood pressure hearL aLLack and sLroke AlLhough Lhese condlLlons also occur ln nondlabeLlc lndlvlduals people wlLh dlabeLes are Lwo Lo four Llmes more
llkely Lo develop cardlovascular dlsorders
ulabeLes melllLus may also cause loss of feellng parLlcularly ln Lhe lower legs 1hls numbness may prevenL a person from feellng Lhe paln or lrrlLaLlon of a
break ln Lhe skln or of fooL lnfecLlon unLll afLer compllcaLlons have developed posslbly necesslLaLlng ampuLaLlon of Lhe fooL or leg 8urnlng paln senslLlvlLy Lo
Louch and coldness of Lhe fooL condlLlons collecLlvely known as neuropaLhy can also occur CLher compllcaLlons lnclude hlgherrlsk pregnancles ln dlabeLlc
women and a greaLer occurrence of denLal dlsease
YL#1LNUN
PyperLenslon or Plgh 8lood ressure medlcal condlLlon ln whlch consLrlcLed arLerlal blood vessels lncrease Lhe reslsLance Lo blood flow causlng an lncrease ln
blood pressure agalnsL vessel walls 1he hearL musL work harder Lo pump blood Lhrough Lhe narrowed arLerles lf Lhe condlLlon perslsLs damage Lo Lhe hearL
and blood vessels ls llkely lncreaslng Lhe rlsk for sLroke hearL aLLack and kldney or hearL fallure CfLen called Lhe sllenL klller" hyperLenslon usually causes
no sympLoms unLll lL reaches a llfeLhreaLenlng sLage
1wo facLors deLermlne blood pressure Lhe amounL of blood Lhe hearL pumps and Lhe dlameLer of Lhe arLerles recelvlng blood from Lhe hearL When Lhe
arLerles narrow Lhey lncrease Lhe reslsLance Lo blood flow 1he hearL works harder Lo pump more blood Lo make sure Lhe same amounL of blood clrculaLes Lo
all Lhe body Llssues 1he more blood Lhe hearL pumps and Lhe smaller Lhe arLerles Lhe hlgher Lhe blood pressure
1he kldneys play a ma[or role ln Lhe regulaLlon of blood pressure kldneys secreLe Lhe hormone renln whlch causes arLerles Lo conLracL Lhereby ralslng blood
pressure 1he kldneys also conLrol Lhe fluld volume of blood elLher by reLalnlng salL or excreLlng salL lnLo urlne When kldneys reLaln salL ln Lhe bloodsLream
Lhe salL aLLracLs waLer lncreaslng Lhe fluld volume of blood As a hlgher volume of blood passes Lhrough arLerles lL lncreases blood pressure
49
SclenLlsLs do noL fully undersLand Lhe causes of hyperLenslon ln up Lo 93 percenL of cases no clear cause can be ldenLlfled 1hls Lype of hlgh blood pressure ls
known as essenLlal hyperLenslon and sclenLlsLs suspecL LhaL geneLlc facLors may play a role ln lLs developmenL ln abouL 3 percenL of cases hlgh blood
pressure develops as a resulL of anoLher medlcal dlsorder such as kldney or llver dlsease or as a slde effecL of cerLaln medlcaLlons 1hls Lype of hlgh blood
pressure ls known as secondary hyperLenslon CLher facLors LhaL may conLrlbuLe Lo elevaLed blood pressure ln some people lnclude a dleL hlgh ln salL physlcal
lnacLlvlLy obeslLy and heavy alcohol consumpLlon
Complications
lf hyperLenslon ls noL deLecLed and LreaLed llfeLhreaLenlng compllcaLlons develop over a course of years lncreased pressure on Lhe lnner walls of blood
vessels makes Lhe vessels less flexlble over Llme and more vulnerable Lo Lhe bulldup of faLLy deposlLs ln a process known as aLherosclerosls (see
ArLerlosclerosls) Weakened porLlons of Lhe blood vessel wall may balloon formlng an aneurysm lf an aneurysm rupLures lnLernal hemorrhaglng (bleedlng)
resulLs 8oLh aLherosclerosls and a rupLured aneurysm ln Lhe braln can lead Lo a sLroke
U LH#UULUHY
PyperLenslon forces Lhe hearL Lo work harder Lo pump adequaLe blood LhroughouL Lhe body 1hls exLra work causes Lhe muscles of Lhe hearL Lo enlarge and
evenLually Lhe enlarged hearL becomes lnefflclenL ln pumplng blood An enlarged hearL may lead Lo hearL fallure ln whlch Lhe hearL can noL pump enough
blood Lo meeL Lhe body's needs
lncreased blood pressure may damage Lhe small blood vessels wlLhln Lhe kldney 1he kldney Lhen becomes unable Lo fllLer blood efflclenLly and wasLe
producLs may bulld up ln Lhe blood ln a condlLlon known as uremla WlLhouL medlcal LreaLmenL kldney fallure wlll resulL
UUNH#Y LUNUL1UN
lL happens when Lhere ls excesslve accumulaLlon of fluld ln Lhe lungs Lhe condlLlon of havlng an excesslve amounL of blood or fluld accumulaLe ln an organ or
body parL as a resulL of dlsease or lnfecLlon
50
NLUUNH
neumonla lnflammaLlon of one or boLh lungs ln people wlLh pneumonla alr sacs ln Lhe lungs flll wlLh fluld prevenLlng oxygen from reachlng blood cells and
nourlshlng Lhe oLher cells of Lhe body SomeLlmes Lhe lnflammaLlon occurs ln scaLLered paLches ln Lhe Llssue around Lhe ends of Lhe bronchloles Lhe smallesL
alr Lubes ln Lhe lungs 1hls ls known as bronchopneumonla ln oLher cases Lhe lnflammaLlon ls wldespread and lnvolves an enLlre lobe of Lhe lung 1hls
condlLlon ls called lobar pneumonla
Lxpand
neumonla lnflammaLlon of one or boLh lungs ln people wlLh pneumonla alr sacs ln Lhe lungs flll wlLh fluld prevenLlng oxygen from reachlng blood cells and
nourlshlng Lhe oLher cells of Lhe body SomeLlmes Lhe lnflammaLlon occurs ln scaLLered paLches ln Lhe Llssue around Lhe ends of Lhe bronchloles Lhe smallesL
alr Lubes ln Lhe lungs 1hls ls known as bronchopneumonla ln oLher cases Lhe lnflammaLlon ls wldespread and lnvolves an enLlre lobe of Lhe lung 1hls
condlLlon ls called lobar pneumonla ln Lhe unlLed SLaLes abouL 3 mllllon cases of pneumonla are reporLed each year and abouL 63300 people dle from Lhe
dlsease
CAuSLLS Cl -LuMC-lA
neumonla has more Lhan 30 dlfferenL causes MosL cases of pneumonla resulL from lnfecLlon wlLh mlcroorganlsms prlmarlly vlruses bacLerla mycoplasmas
(small freellvlng parLlcles wlLh characLerlsLlcs of boLh bacLerla and vlruses) and fungl neumonla may also resulL from cerLaln klnds of allerglc reacLlons
lnhalaLlon of flulds or some gases and Lhe lnhalaLlon of lngesLed foods
vl8AL -LuMC-lA
AbouL 30 percenL of pneumonla cases are caused by vlruses parLlcularly Lhose vlruses LhaL cause upper resplraLory lnfecLlons such as Lhe vlruses LhaL cause
lnfluenza adenovlruses and rhlnovlruses MosL cases of vlral pneumonla are mlld and resolve sponLaneously wlLhouL speclflc LreaLmenL
Cne excepLlon ls severe acuLe resplraLory syndrome (SA8S) a Lype of vlral pneumonla SA8S Lyplcally beglns wlLh a fever of 380C (1004l) or more chllls
headache and malalse 1wo Lo seven days laLer some people develop a dry cough and dlfflculLy breaLhlng lor Lhese people SA8S can cause deaLh
8AC1L8lAL -LuMC-lA
51
lnfecLlon wlLh Lhe SLrepLococcus pneumonlae bacLerlum also called pneumococcus ls Lhe mosL common cause of bacLerlal pneumonla neumococcus
usually causes lobar pneumonla aLLacklng an enLlre lobe or porLlon of a lobe of Lhe lung ln double pneumonla pneumococcus aLLacks boLh lungs
neumococcal lobar pneumonla ofLen occurs ln wlnLer afLer an acuLe vlral upper resplraLory lnfecLlon usual sympLoms lnclude a shaklng chlll followed by a
fever of abouL 40C (104l) paln ln Lhe chesL whlle breaLhlng a cough and bloodsLreaked spuLum
CLher bacLerla LhaL cause pneumonla lnclude klebslella pneumonlae Paemophllus lnfluenzae Leglonella pneumophllla (Lhe bacLerlum LhaL causes
Leglonnalres' dlsease) and varlous sLaphylococcl and sLrepLococcl bacLerla lnfecLlons wlLh Lhese organlsms prlmarlly cause bronchopneumonla CnseL of
sympLoms ls generally slower Lhan wlLh lobar pneumonla and Lhe fever ls lower
C1PL8 1?LS Cl -LuMC-lA
Cne common Lype of pneumonla formerly called prlmary aLyplcal pneumonla ls caused by Mycoplasma pneumonlae a mycoplasma Lpldemlcs of
mycoplasma pneumonla occur ln schools and ln Lhe mlllLary 1he mosL promlnenL sympLom of mycoplasma pneumonla ls a vlolenL dry cough Some paLlenLs
experlence nausea or vomlLlng
neumocysLls carlnll pneumonla (C) ls caused by a normally harmless fungus LhaL may become deadly ln people wlLh lmpalred lmmune sysLems C ls Lhe
mosL common cause of deaLh ln people wlLh acqulred lmmunodeflclency syndrome (AluS)
ulAC-CSlS A-u 18LA1ML-1
A physlclan can dlagnose pneumonla by Lapplng Lhe chesL and llsLenlng wlLh a sLeLhoscope Lo Lhe sound produced 1applng Lhe chesL of a healLhy person
produces a resonanL sound because of Lhe alr conLalned ln Lhe lungs ln a person wlLh pneumonla Lhe alr spaces of Lhe lungs become fllled wlLh fluld and
Lapplng produces a dull flaL sound 1he dlagnosls of pneumonla ls conflrmed by Laklng an xray plcLure of Lhe chesL
1o deLermlne Lhe cause of pneumonla a physlclan Lakes a sample of Lhe paLlenLs spuLum Analysls of Lhe spuLum ln Lhe laboraLory may ldenLlfy Lhe parLlcular
klnd of mlcroorganlsm causlng Lhe lnfecLlon ldenLlflcaLlon of Lhe cause of pneumonla ls lmporLanL ln deLermlnlng LreaLmenL
AnLlbloLlcs can cure bacLerlal pneumonla and speed recovery from mycoplasma pneumonla and C AnLlbloLlcs rarely have an effecL on pneumonla caused
by vlruses Powever paLlenLs wlLh vlral pneumonla ofLen recelve anLlbloLlcs Lo prevenL bacLerlal pneumonla from developlng durlng Lhe course of Lhelr lllness
ln addlLlon Lo drug LreaLmenL a paLlenL wlLh pneumonla should sLay ln bed eaL healLhy meals and drlnk large amounLs of llqulds MedlcaLlon may be glven Lo
relleve chesL paln and vlolenL coughlng and oxygen may be admlnlsLered lf Lhe paLlenL has dlfflculLy breaLhlng A vacclne ls avallable LhaL confers lmmunlLy
52
agalnsL pneumococcus 1he vacclne ls glven Lo people mosL aL rlsk for developlng pneumonlaLhose over Lhe age of 63 and Lhose wlLh chronlc hearL lung or
llver dlsease
Medications
1. Imdur 60mg 1 tab OD
ISOSORBIDE MONONITRATE (eye-soe-sor-bide mo-noe-nye-trate )
Imdur, Ismo, Isotrate ER, Monoket
CLASSIFICATION(S).
Ther. Class. antianginals
Pharm. Class. nitrates
Pregnancy Category C
INDICA1ICNS
Acute treatment oI anginal attacks (SL only)
Prophylactic management oI angina pectoris (dinitrate and mononitrate)
53
Treatment oI chronic CHF (dinitrate).
AC1ICN
Produce vasodilation (venous greater than arterial)
Decrease leIt ventricular end-diastolic pressure and leIt ventricular end-diastolic volume (preload). Net eIIect is reduced myocardial oxygen consumption
Increase coronary blood Ilow by dilating coronary arteries and improving collateral Ilow to ischemic regions.
Therapeutic Effects:
4 RelieI oI anginal attacks and increase in cardiac output.
nAkMACCkINL1ICS
Absorption: Well absorbed aIter PO and SL administration.
Distribution: Unknown.
Metabolism and Excretion: Mostly metabolized by the liver.
Half-life: Isosorbide dinitrate50 min; isosorbide mononitrate5 hr.
CCN1kAINDICA1ICNS AND kLCAU1ICNS
Contraindicated in:
Hypersensitivity
Severe anemia.
Concurrent use oI sildenaIil.
Use Cautiously in:
Head trauma or cerebral hemorrhage
Geriatric patients (start with lower doses)
Pregnancy (may compromise maternal/Ietal circulation)
Children or lactation (saIety not established).
ADVLkSL kLAC1ICNS AND SIDL LIILC1S*
CAPITALS indicate liIe threatening; underlines indicate most Irequent.
CNS: dizziness, headache, apprehension, weakness.
54
CV: hypotension, tachycardia, paradoxic bradycardia, syncope.
GI: abdominal pain, nausea, vomiting.
Misc: cross-tolerance, Ilushing, tolerance.
IN1LkAC1ICNS
Drug-Drug:
Concurrent use oI sildenafil may result in signiIicant and potentially Iatal hypotension (concurrent use is contraindicated)
Additive hypotension with antihypertensives, acute ingestion oI alcohol, beta blockers, calcium channel blockers, and phenothiazines
Aspirin may increase blood levels and eIIects
EIIects may be antagonized by dihydroergotamine.
kCU1L AND DCSAGL
Isosorbide Mononitrate
PO (Adults): Ismo, Monoket20 mg twice daily (may start with 5 mg twice daily), 7 hr apart.Imdur3060 mg once daily; may increase to 120 mg once daily (up to 240 mg/day).
AVAILA8ILI1
4 Isosorbide Mononitrate
Extended-release tablets (Imdur, Isotrate ER): 30 mg
Rx
, 60 mg
Rx
, 120 mg
Rx
Cost: Imdur30 mg $130.03/100, 60 mg $136.86/100, 120 mg $191.60/100, Isotrate ER 60 mg $117.41/100;generic 30 mg $111.55/100, 60 mg $116.11$117.40/100.
TIME/ACTION PROFILE (cardiovascular eIIects)
ONSET PEA DURATION
ISMN-PO 3060 min unknown 7 hr
55
NUkSING IMLICA1ICNS
ASSESSMENT
Assess location, duration, intensity, and precipitating Iactors oI anginal pain.
Monitor blood pressure and pulse routinely during period oI dosage adjustment.
ab 1est Considerations: May cause Ialsely decreased serum cholesterol determinations.
4 Excessive doses may increase methemoglobin concentrations.
4 May cause increased urine vanillylmandelic acid (VMA) concentrations.
POTENTIAL NURSING DIAGNOSES
Tissue perIusion, altered (Indications).
Activity intolerance (Indications).
nowledge deIicit, related to medication regimen (Patient/Family Teaching).
IMPLEMENTATION
Isosorbide Mononitrate
PO: Medication should be taken on an empty stomach with a Iull glass oI water.
PATIENT/AMILY TEACHING
Instruct patient to take medication exactly as directed, even iI Ieeling better. II a dose is missed, take as soon as remembered; doses oI isosorbide dinitrate should be taken at least 2 hr apart
(6 hr with extended-release preparations); daily doses oI isosorbide mononitrate should be taken 7 hr apart. Do not double doses. Do not discontinue abruptly.
Caution patient to make position changes slowly to minimize orthostatic hypotension.
May cause dizziness. Caution patient to avoid driving or other activities requiring alertness until response to medication is known.
Advise patient to avoid concurrent use oI alcohol with this medication. Patients should also consult health care proIessional beIore taking OTC medications while taking isosorbide.
InIorm patient that headache is a common side eIIect that should decrease with continuing therapy. Aspirin or acetaminophen may be ordered to treat headache. NotiIy health care
proIessional iI headache is persistent or severe. Do not alter dose to avoid headache.
Advise patient to notiIy health care proIessional iI dry mouth or blurred vision occurs or iI undigested extended-release isosorbide dinitrate tablets are Iound in stool.
EVALUATION
Effectiveness of therapy can be demonstrated by:
56
Decrease in Irequency and severity oI anginal attacks
4 Increase in activity tolerance.
. ASPIRIN COR 30 mg 1 tab OD
Classification: aspirin
Indication: chronic stable and unstable angina,MI. adjunct treatment oI CV disease in transcient ischemic attack or minor ischemic stroke
Dosage:1 tab daily
AC1ICN
Inhibits the synthesis oI prostaglandins that may serve as mediators oI pain and Iever, primarily in the CNS
Has no signiIicant anti-inIlammatory properties or GI toxicity.
Therapeutic Effects:
4 Analgesia
4 Antipyresis.
nAkMACCkINL1ICS
Absorption: Well absorbed Iollowing oral administration. Rectal absorption is variable.
Distribution: Widely distributed. Crosses the placenta; enters breast milk in low concentrations.
Metabolism and Excretion: 8595 metabolized by the liver. Metabolites may be toxic in overdose situation. Metabolites excreted by the kidneys.
Half-life: 14 hr.
CCN1kAINDICA1ICNS AND kLCAU1ICNS
Contraindicated in:
Previous hypersensitivity
Products containing alcohol, aspartame, saccharin, sugar, or tartrazine (FDC yellow dye #5) should be avoided in patients who have hypersensitivity or intolerance to these compounds.
Use Cautiously in:
Hepatic disease/renal disease (lower chronic doses recommended)
Chronic alcohol use/abuse
Malnutrition.
57
ADVLkSL kLAC1ICNS AND SIDL LIILC1S*
CAPITALS indicate liIe threatening; underlines indicate most Irequent.
GI: HEPATIC FAILURE, HEPATOTOXICITY(overdose).
GU: renal Iailure (high doses/chronic use).
Derm: rash, urticaria.
IN1LkAC1ICNS
Drug-Drug:
Chronic high-dose acetaminophen (~2 g/day) may increase the risk oI bleeding with arfarin (PT should be monitored regularly and INR should not exceed 4)
Hepatotoxicity is additive with other hepatotoxic substances, including alcohol
Concurrent use oI sulfinpyrazone, isoniazid, rifampin, rifabutin, phenytoin, barbiturates, and carbamazepine may increase the risk oI acetaminophen-induced liver damage (limit selI-
medication); these agents will also decrease therapeutic eIIects oI acetaminophen
Combined use with salicylates or NSAIDs increases the risk oI adverse renal eIIects.
Propranolol decreases metabolism and may increase eIIects.
May decrease eIIects oI lamotrigine, zidovudine, and loop diuretics.
NUkSING IMLICA1ICNS
ASSESSMENT
General Info: Assess overall health status and alcohol usage beIore administering acetaminophen. Malnourished patients or chronic alcohol abusers are at higher risk oI developing
hepatotoxicity with chronic use oI usual doses oI this drug.
4 Assess amount, Irequency, and type oI drugs taken in patients selI-medicating, especially with OTC drugs. Prolonged use oI acetaminophen alone or combined with salicylates or
NSAIDs increases the risk oI adverse renal eIIects. For short-term use, combined doses oI acetaminophen and salicylates should not exceed the recommended dose oI either drug
given alone.
Pain: Assess type, location, and intensity prior to and 3060 min Iollowing administration.
ever: Assess Iever; note presence oI associated signs (diaphoresis, tachycardia, and malaise).
ab 1est Considerations: Hepatic, hematologic, and renal Iunction should be evaluated periodically throughout prolonged, high-dose therapy.
4 May alter results oI blood glucose monitoring. May cause Ialsely decreased values when measured with glucose oxidase/peroxidase method, but probably not with
hexokinase/glucose-6-phosphate dehydrogenase (G6PD) method. May also cause Ialsely increased values with certain instruments; see manuIacturer's instruction manual.
4 Increased serum bilirubin, LDH, AST, ALT, and prothrombin time may indicate hepatotoxicity.
1oxicity and Overdose: II overdose occurs, acetylcysteine (Mucomyst) is the antidote.
POTENTIAL NURSING DIAGNOSES
58
Pain (Indications).
Body temperature, risk Ior altered (Indications).
nowledge deIicit, related to medication regimen (Patient/Family Teaching).
IMPLEMENTATION
General Info: When combined with opioids do not exceed the maximum recommended daily dose oI acetaminophen.
PO: Administer with a Iull glass oI water.
4 May be taken with Iood or on an empty stomach.
PATIENT/AMILY TEACHING
Advise patient to take medication exactly as directed and not to take more than the recommended amount. Chronic excessive use oI ~4 g/day (2 g in patients with chronic alcoholism) may
lead to hepatotoxicity, renal, or cardiac damage. Adults should not take acetaminophen longer than 10 days and children not longer than 5 days unless directed by health care proIessional.
Short-term doses oI acetaminophen with salicylates or NSAIDs should not exceed the recommended daily dose oI either drug alone.
Advise patient to avoid alcohol (3 or more glasses per day increase the risk oI liver damage) iI taking more than an occasional 12 doses and to avoid taking concurrently with salicylates or
NSAIDs Ior more than a Iew days, unless directed by health care proIessional.
Advise parents or caregivers to check concentrations oI liquid preparations. Errors have resulted in serious liver damage.
InIorm patients with diabetes that acetaminophen may alter results oI blood glucose monitoring. Advise patient to notiIy health care proIessional iI changes are noted.
Advise patient to consult health care proIessional iI discomIort or Iever is not relieved by routine doses oI this drug or iI Iever is greater than 39.5C (103F) or lasts longer than 3 days.
EVALUATION
Effectiveness of therapy can be demonstrated by:
RelieI oI mild pain
Reduction oI Iever.
3. Metoclopramide 1 AMP IVTT evry 8 hours
METOCLOPRAMIDE
(met-oh-kloe-pra-mide)
Apo-Metoclop, Clopra, Emex, Maxeran, Octamide, Octamide-PFS, Reclomide, Reglan
C$$IFIC1IOA($):
1her. Class: antiemetics
59
Pregnancy Category
INDICA1ICNS
Treatment oI postsurgical and diabetic gastric stasis
Management oI esophageal reIlux .
Unlabelled Uses:
4 Treatment oI hiccups
4 Adjunct management oI migraine headaches.
AC1ICN
Blocks dopamine receptors in chemoreceptor trigger zone oI the CNS
Stimulates motility oI the upper GI tract and accelerates gastric emptying.
Therapeutic Effects:
4 Decreased nausea and vomiting
4 Decreased symptoms oI gastric stasis
4 Easier passage oI nasogastric tube into small bowel.
nAkMACCkINL1ICS
Absorption: Well absorbed Irom the GI tract, Irom rectal mucosa, and Irom IM sites.
Distribution: Widely distributed into body tissues and Iluids. Crosses blood-brain barrier and placenta. Enters breast milk in concentrations greater than plasma.
Metabolism and Excretion: Partially metabolized by the liver; 25 eliminated unchanged in the urine.
Half-life: 2.55 hr.
CCN1kAINDICA1ICNS AND kLCAU1ICNS
Contraindicated in:
Hypersensitivity
Possible GI obstruction or hemorrhage
60
History oI seizure disorders
Pheochromocytoma
Parkinson's disease.
Use Cautiously in:
History oI depression
Diabetes (may alter response to insulin)
Pregnancy and lactation (saIety not established)
Children and geriatric patients (increased incidence oI extrapyramidal reactions).
ADVLkSL kLAC1ICNS AND SIDL LIILC1S*
CAPITALS indicate liIe threatening; underlines indicate most Irequent.
CNS: drowsiness, extrapyramidal reactions, restlessness, anxiety, depression, irritability, tardive dyskinesia.
CV: arrhythmias (supraventricular tachycardia, bradycardia), hypertension, hypotension.
GI: constipation, diarrhea, dry mouth, nausea.
Endo: gynecomastia.
IN1LkAC1ICNS
Drug-Drug:
Additive CNS depression with other CNS depressants, including alcohol, antidepressants, antihistamines, opioid analgesics, and sedative/hypnotics
May increase absorption and risk oI toxicity Irom cyclosporine
May aIIect the GI absorption oI other orally administered drugs as a result oI eIIect on GI motility
May exaggerate hypotension during general anesthesia
Increased risk oI extrapyramidal reactions with agents such as haloperidol or phenothiazines
Opioids and anticholinergics may antagonize the GI eIIects oI metoclopramide
Use cautiously with MAO inhibitors (causes release oI catecholamines)
May increase neuromuscular blockade Irom succinylcholine
May decrease the eIIectiveness oI levodopa.
TIME/ACTION PROFILE (eIIects on peristalsis)
ONSET PEA DURATION
61
IV 13 min immediate 12 hr
NUkSING IMLICA1ICNS
ASSESSMENT
Assess patient Ior nausea, vomiting, abdominal distention, and bowel sounds beIore and aIter administration.
Assess patient Ior extrapyramidal side eIIects (5arkinsoniandiIIiculty speaking or swallowing, loss oI balance control, pill rolling, mask-like Iace, shuIIling gait, rigidity, tremors; and
dystonicmuscle spasms, twisting motions, twitching, inability to move eyes, weakness oI arms or legs) periodically throughout course oI therapy. May occur weeks to months aIter
initiation oI therapy and are reversible on discontinuation. Dystonic reactions may occur within minutes oI IV inIusion and stop within 24 hr oI discontinuation oI metoclopramide. May be
treated with 50 mg oI IM diphenhydramine or diphenhydramine 1 mg/kg IV may be administered prophylactically 15 min beIore metoclopramide IV inIusion.
Monitor Ior tardive dyskinesia (uncontrolled rhythmic movement oI mouth, Iace, and extremities; lip smacking or puckering; puIIing oI cheeks; uncontrolled chewing; rapid or worm-like
movements oI tongue). Usually occurs aIter a year or more oI continued therapy. Report immediately; may be irreversible.
Assess patient Ior signs oI depression periodically throughout therapy.
ab 1est Considerations: May alter hepatic Iunction test results.
4 May cause increased serum prolactin and aldosterone concentrations.
POTENTIAL NURSING DIAGNOSES
Nutrition, altered: less than body requirements (Indications).
Injury, risk Ior (Side EIIects).
nowledge deIicit, related to medication regimen (Patient/Family Teaching).
PATIENT/AMILY TEACHING
Instruct patient to take metoclopramide exactly as directed. II a dose is missed, take as soon as remembered iI not almost time Ior next dose.
May cause drowsiness. Caution patient to avoid driving or other activities requiring alertness until response to medication is known.
Advise patient to avoid concurrent use oI alcohol and other CNS depressants while taking this medication.
Advise patient to notiIy health care proIessional immediately iI involuntary movement oI eyes, Iace, or limbs occurs.
EVALUATION
Effectiveness of therapy can be demonstrated by:
Prevention or relieI oI nausea and vomiting
62
Decreased symptoms oI gastric stasis
Facilitation oI small bowel intubation
Decreased symptoms oI esophageal reIlux.
. Lantus 15 ~u SQ before supper
INSULINS
(in-su-lin)
insulin glargine
Lantus
C$$IFIC1IOA($):
1her. Class: antidiabetics, hormones
!harm. Class: 5ancreatic hormone
Pregnancy Category C (glargine), (all others)
INDICA1ICNS
Treatment oI insulin-dependent diabetes mellitus (IDDM, type 1)
Management oI noninsulin-dependent diabetes mellitus (NIDDM, type 2) unresponsive to treatment with diet and/or oral hypoglycemic agents
Concentrated insulin U-500: Only Ior use in patients with insulin requirements ~200 units/day.
AC1ICN
Lower blood glucose by increasing transport into cells and promoting the conversion oI glucose to glycogen
Promote the conversion oI amino acids to proteins in muscle and stimulate triglyceride Iormation
Inhibit the release oI Iree Iatty acids
Sources include pork, beeI/pork combinations, semisynthetic, biosynthetic, and recombinant DNA.
Therapeutic Effects:
4 Control oI blood sugar in diabetic patients.
63
nAkMACCkINL1ICS
Absorption: Rapidly absorbed Irom SC administration sites. Absorption rate is determined by type oI insulin, injection site, volume oI injectate, and other Iactors.
Distribution: Widely distributed.
Metabolism and Excretion: Metabolized by liver, spleen, kidney, and muscle.
Half-life: 56 min (prolonged in patients with diabetes; biologic halI-liIe is 11.5 hr).
CCN1kAINDICA1ICNS AND kLCAU1ICNS
Contraindicated in:
Allergy or hypersensitivity to a particular type oI insulin, preservatives, or other additives.
Use Cautiously in:
Stress, pregnancy, and inIection (temporarily increase insulin requirements).
ADVLkSL kLAC1ICNS AND SIDL LIILC1S*
CAPITALS indicate liIe threatening; underlines indicate most Irequent.
Derm: urticaria.
Endo: HYPOGLYCEMIA, rebound hyperglycemia (Somogyi eIIect).
Local: lipodystrophy, itching, lipohypertrophy, redness, swelling.
Misc: allergic reactions includingANAPHYLAXIS.
IN1LkAC1ICNS
Drug-Drug:
eta blockers may block some oI the signs and symptoms oI hypoglycemia and delay recovery Irom hypoglycemia
Thiazide diuretics, corticosteroids, diltiazem, dobutamine, thyroid preparations, estrogens, nicotine, protease inhibitor antiretrovirals, and rifampin may increase insulin
requirements
Anabolic steroids (testosterone), alcohol, clofibrate, guanethidine, MAO inhibitors, most NSAIDs, oral hypoglycemic agents, sulfinpyrazone, tetracyclines, phenylbutazone, and
arfarin may decrease insulin requirements.
Drug-Natural:
64
Glucosamine may worsen blood glucose control
enugreek, chromium, and coenzyme Q-10 may produce additive hypoglycemic eIIects.
kCU1L AND DCSAGL
Dose depends on blood sugar, response, and many other Iactors.
etoacidosis-Regular Insulin Only
IV (Adults): 0.1 unit/kg/hr as a continuous inIusion.
Maintenance Therapy
SC (Adults and Children): 0.51 unit/kg/day. Adolescents during ra5id growth0.81.2 units/kg/day.
AVAILA8ILI1
Insulin injection (regular insulin): 100 units/ml
OTC
Cost: $29.65/10 ml vial
Insulin glargine: 100 units/ml in 5 ml vials
Rx
, 10 ml vials
Rx
, 3 ml cartridges
Rx
TIME/ACTION PROFILE (hypoglycemic eIIect)
ONSET PEA DURATION
Insulin
glargine SC
1.1 hr 5 hr 24 hr
f
f
Small amounts oI insulin glargine slowly released resulting in a relatively constant eIIect over time.
NUkSING IMLICA1ICNS
ASSESSMENT
65
Assess patient Ior signs and symptoms oI hypoglycemia (anxiety; chills; cold sweats; conIusion; cool, pale skin; diIIiculty in concentration; drowsiness; excessive hunger; headache;
irritability; nausea; nervousness; rapid pulse; shakiness; unusual tiredness or weakness) and hyperglycemia (drowsiness; Ilushed, dry skin; Iruit-like breath odor; Irequent urination; loss oI
appetite; tiredness; unusual thirst) periodically throughout therapy.
Monitor body weight periodically. Changes in weight may necessitate changes in insulin dose.
ab 1est Considerations: May cause decreased serum inorganic phosphate, magnesium, and potassium levels.
4 Monitor blood glucose and ketones every 6 hr throughout therapy, more Irequently in ketoacidosis and times oI stress. Glycosylated hemoglobin may also be monitored to
determine eIIectiveness oI therapy.
1oxicity and Overdose: Overdose is maniIested by symptoms oI hypoglycemia. Mild hypoglycemia may be treated by ingestion oI oral glucose. Severe hypoglycemia is a liIe-threatening
emergency; treatment consists oI IV glucose, glucagon, or epinephrine.
POTENTIAL NURSING DIAGNOSES
nowledge deIicit, related to medication regimen (Patient/Family Teaching).
Noncompliance (Patient/Family Teaching).
PATIENT/AMILY TEACHING
Instruct patient on proper technique Ior administration. Include type oI insulin, equipment (syringe, cartridge pens, alcohol swabs), storage, and place to discard syringes. Discuss the
importance oI not changing brands oI insulin or syringes, selection and rotation oI injection sites, and compliance with therapeutic regimen.
Demonstrate technique Ior mixing insulins by drawing up regular insulin or insulin lispro Iirst and rolling intermediate-acting insulin vial between palms to mix, rather than shaking (may
cause inaccurate dose).
Explain to patient that this medication controls hyperglycemia but does not cure diabetes. Therapy is long term.
Instruct patient in proper testing oI serum glucose and ketones. These tests should be closely monitored during periods oI stress or illness and health care proIessional notiIied oI signiIicant
changes.
Emphasize the importance oI compliance with nutritional guidelines and regular exercise as directed by health care proIessional.
Advise patient to consult health care proIessional prior to using alcohol or other medications concurrently with insulin.
Advise patient to notiIy health care proIessional oI medication regimen prior to treatment or surgery.
Advise patient to notiIy health care proIessional iI nausea, vomiting, or Iever develops, iI unable to eat regular diet, or iI blood sugar levels are not controlled.
Instruct patient on signs and symptoms oI hypoglycemia and hyperglycemia and what to do iI they occur.
Advise patient to notiIy health care proIessional iI pregnancy is planned or suspected.
Patients with diabetes mellitus should carry a source oI sugar (candy, sugar packets) and identiIication describing their disease and treatment regimen at all times.
Emphasize the importance oI regular Iollow-up, especially during Iirst Iew weeks oI therapy.
EVALUATION
Effectiveness of therapy can be demonstrated by:
Control oI blood glucose levels without the appearance oI hypoglycemic or hyperglycemic episodes.
66
5. Diovan 80 mg 1 tab OD
ANGIOTENSIN II RECEPTOR ANTAGONISTS
valsartan
(val-sar-tan)
Diovan
C$$IFIC1IOA($):
1her. Class: antihy5ertensives
!harm. Class: angiotensin II rece5tor antagonists
Pregnancy Category C (first trimester), D (second and third trimesters)
INDICA1ICNS
Alone or with other agents in the management oI hypertension.
AC1ICN
Blocks the vasoconstrictor and aldosterone-producing eIIects oI angiotensin II at various receptor sites, including vascular smooth muscle and the adrenal glands.
Therapeutic Effects:
4 Lowering oI blood pressure.
nAkMACCkINL1ICS
Absorption: CandesartanCandesartan cilexetil is converted to candesartan in the GI tract during the absorption process where 15 is absorbed; e5rosartan13 absorbed; irbesartan6080
absorbed; losartanwell absorbed but undergoes extensive Iirst-pass hepatic metabolism, resulting in 33 bioavailability; telmisartan4258 absorbed Iollowing oral administration
(bioavailability increased in patients with hepatic impairment); valsartan25 absorbed Iollowing oral administration.
Distribution: Unknown; candesartanminimal penetration oI the blood-brain barrier.
Protein inding: e5rosartan98
Metabolism and Excretion: CandesartanExcreted mostly unchanged in urine and Ieces (via bile); minor metabolism by the liver; e5rosartan90eliminated unchanged in Ieces via biliary
elimination, 7 excreted in urine; irbesartansome hepatic metabolism, some biliary excretion, some elimination as unchanged drug in urine; losartanundergoes extensive Iirst-pass hepatic
67
metabolism; 14 is converted to an active metabolite. 4 oI losartan is excreted unchanged by the kidneys; although 6 oI the active metabolite is excreted unchanged by the kidneys, some biliary
elimination also occurs; telmisartanexcreted mostly unchanged in Ieces via biliary excretion, 11 metabolized by the liver; valsartan20 metabolized by the liver; mostly excreted in Ieces via
bile.
Half-life: Candesartan9 hr; eprosartan59 hr;irbesartan1115 hr; losartan2 hr (69 hr Ior metabolite); telmisartan24 hr; valsartan6 hr.
CCN1kAINDICA1ICNS AND kLCAU1ICNS
Contraindicated in:
Hypersensitivity
Pregnancy or lactation.
Use Cautiously in:
CHF (may result in azotemia,oliguria, acute renal Iailure and/or death)
Volume- or salt-depleted patients or patients receiving high doses oI diuretics (correct deIicits beIore initiating therapy or initiate at lower doses)
Black patients (may not be as eIIective as monotherapy; additional agents may be required)
Impaired renal Iunction due to primary renal disease or CHF (may worsen renal Iunction)
Obstructive biliary disorders or hepatic impairment (lower initial doses oI losartan, temisartan, or valsartan recommended)
Patients with childbearing potential
Children 18 yr (saIety not established).
ADVLkSL kLAC1ICNS AND SIDL LIILC1S*
CAPITALS indicate liIe threatening; underlines indicate most Irequent.
CNS: dizziness, Iatigue, headache.
CV: hypotension.
GI: diarrhea, drug-induced hepatitis.
GU: RENAL FAILURE.
and E: hyperkalemia.
IN1LkAC1ICNS
Drug-Drug:
NSAIDs may decrease antihypertensive eIIects
Additive antihypertensive eIIects with other antihypertensives and diuretics. Risk oI hypotension is increased by concurrent diuretic therapy (use lower initial doses)
68
Telmisartan increases serum digoxin levels.
Concurrent use oI potassium-sparing diuretics or potassium supplements may increase the risk oI hyperkalemia
kCU1L AND DCSAGL
Valsartan
PO (Adults): 80 mg/day as a single dose initially in patients who are not receiving diuretics or other antihypertensives; may be increased to 160320 mg/day.
AVAILA8ILI1
4 Valsartan
Capsules: 80 mg
Rx
, 160 mg
Rx
.
Cost: 80 mg $125.10/100, 160 mg $133.73/100.
1ablets: 80 mg
Rx
, 160 mg
Rx
, 320 mg
Rx
.
In combination with: hydrochlorothiazide (Diovan HCT
Rx
).
TIME/ACTION PROFILE (antihypertensive eIIect
f
)
ONSET PEA DURATION
Valsartan within 2 hr 46 hr 24 hr
f
maximum response may take 23 weeks oI treatment
NUkSING IMLICA1ICNS
ASSESSMENT
Assess blood pressure (lying down, sitting, standing) and pulse periodically throughout therapy.
Monitor Irequency oI prescription reIills to determine adherence.
Assess patient Ior signs oI angioedema (dyspnea, Iacial swelling). May rarely cause angioedema; more common in patients who have had angioedema with ACE inhibitors.
ab 1est Considerations: May rarely cause elevations in BUN and serum creatinine.
4 May cause elevated serum bilirubin.
4 May occasionally cause hyperkalemia.
69
4 Losartan may cause transient elevations oI ALT and AST, hemoglobin, and hematocrit and decreased uric acid concentrations.
POTENTIAL NURSING DIAGNOSES
Injury, risk Ior (Adverse Reactions).
nowledge deIicit, related to medication regimen (Patient/Family Teaching).
Noncompliance (Patient/Family Teaching).
IMPLEMENTATION
General Info: Volume depletion should be corrected, iI possible, prior to initiation oI therapy.
PO: May be administered without regard to meals.
PATIENT/AMILY TEACHING
Emphasize the importance oI continuing to take as directed, even iI Ieeling well. Take missed doses as soon as remembered iI not almost time Ior next dose; do not double doses.
Medication controls but does not cure hypertension. Instruct patient to take medication at the same time each day. Gradual reduction oI dose prior to discontinuation is suggested.
Encourage patient to comply with additional interventions Ior hypertension (weight reduction, low-sodium diet, discontinuation oI smoking, moderation oI alcohol consumption, regular
exercise, stress management).
Instruct patient and Iamily on proper technique Ior monitoring blood pressure. Advise them to check blood pressure at least weekly and to report signiIicant changes.
Caution patient to avoid sudden changes in position to decrease orthostatic hypotension. Use oI alcohol, standing Ior long periods, exercising, and hot weather may increase orthostatic
hypotension.
Advise women oI childbearing age to use contraception and notiIy health care proIessional iI pregnancy is suspected or planned.
May cause dizziness. Caution patient to avoid driving or other activities requiring alertness until response to medication is known.
Advise patient to consult health care proIessional beIore taking any OTC cough, cold, or allergy remedies or other medications.
Instruct patient to notiIy health care proIessional oI medication regimen prior to treatment or surgery.
Emphasize the importance oI Iollow-up exams to evaluate eIIectiveness oI medication.
EVALUATION
Effectiveness of therapy can be demonstrated by:
Decrease in blood pressure without appearance oI excessive side eIIects.
. Capoten 5mg SL every hours for P 10/90 mm Hg
70
ANGIOTENSIN-CONVERTING ENZYME (ACE) INHIITORS
captopril
(kap-toe-pril)
Capoten
C$$IFIC1IOA($):
1her. Class: antihy5ertensives
!harm. Class: ACE inhibitors
Pregnancy Category C (first trimester), D (second and third trimesters)
INDICA1ICNS
Alone or with other agents in the management oI hypertension
Captopril,: Management oI CHF
Captopril,:Reduction oI risk oI death or development oI CHF Iollowing MI
Slowed progression oI leIt ventricular dysIunction into overt heart Iailure (selected agents)
Captopril: Decreased progression oI diabetic nephropathy.
AC1ICN
ACE inhibitors block the conversion oI angiotensin I to the vasoconstrictor angiotensin II. ACE also inactivates the vasodilator bradykinin and other vasodilatory prostaglandins. ACE
inhibitors also increase plasma renin levels and reduce aldosterone levels. Net result is systemic vasodilation.
Therapeutic Effects:
4 Lowering oI blood pressure in hypertensive patients
4 Decreased aIterload in patients with CHF
4 Decreased development oI overt heart Iailure
4 Increased survival aIter MI (selected agents only)
4 Decreased progression oI diabetic nephropathy (captopril only).
71
nAkMACCkINL1ICS
Absorption: ena:e5rilAt least 37 absorbed Iollowing oral administration. Ca5to5rilAt least 75 Iollowing oral administration (decreased to 3055 by Iood). Enala5ril60 absorbed
Iollowing oral administration.
Distribution: All ACE inhibitors cross the placenta. ena:e5ril, bena:e5rilat, ca5to5ril, enala5ril, enala5rilat, and fosino5rilat Enter breast milk in small amounts
Metabolism and Excretion: . Ca5to5ril 50 metabolized by the liver to inactive compounds, 50 excreted unchanged by the kidneys.
Half-life: Ca5to5ril 2 hr (increased in renal impairment)
CCN1kAINDICA1ICNS AND kLCAU1ICNS
Contraindicated in:
Hypersensitivity
Cross-sensitivity among ACE inhibitors may occur
Pregnancy
Angioedema (hereditary or idiopathic).
Use Cautiously in:
Renal impairment, hepatic impairment, hypovolemia, hyponatremia, elderly patients, concurrent diuretic therapy (initial dosage reduction recommended Ior most agents)
Black patients with hypertension (monotherapy less eIIective, may require additional therapy)
Aortic stenosis/hypertrophic cardiomyopathy
Cerebrovascular or cardiac insuIIiciency
Surgery/anesthesia (hypotension may be exaggerated)
Lactation or children (saIety not established Ior most agents).
Exercise Extreme Caution in:
Family history oI angioedema.
ADVLkSL kLAC1ICNS AND SIDL LIILC1S*
CAPITALS indicate liIe threatening; underlines indicate most Irequent.
CNS: dizziness, Iatigue, headache, insomnia, weakness.
Resp: cough, eosinophilic pneumonitis.
CV: hypotension, angina pectoris, tachycardia.
GI: taste disturbances, anorexia, diarrhea, nausea.
72
GU: proteinuria, impotence, renal Iailure.
Derm: rashes.
and E: hyperkalemia.
Hemat: AGRANULOCYTOSIS, NEUTROPENIA (CAPTOPRIL ONLY).
Misc: ANGIOEDEMA, Iever.
IN1LkAC1ICNS
Drug-Drug:
Excessive hypotension may occur with concurrent use oI diuretics
Additive hypotension with other antihypertensives, nitrates, phenothiazines, acute ingestion oI alcohol, and during surgery or general anesthesia
Hyperkalemia may result Irom concurrent use oI potassium supplements, potassium-sparing diuretics, indomethacin, salt substitutes, or cyclosporine
Antihypertensive response may be blunted by nonsteroidal anti-inflammatory agents
Absorption may be decreased by antacids
Increases levels and may increase the risk oI lithium or digoxin toxicity
Probenecid decreases elimination and increases levels oI captopril
Risk oI hypersensitivity reactions increased by concurrent allopurinol
Capsaicin may increase the incidence oI cough
Rifampin may decrease the eIIectiveness oI enalapril
Tetracycline absorption is decreased by quinapril (because oI magnesium in tablets).
Drug-ood:
ood decreases conversion oI perindopril to perindoprilat.
kCU1L AND DCSAGL
Captopril
PO (Adults): y5ertension12.525 mg 23 times daily, may be increased at 12 wk intervals up to 150 mg 3 times daily (usual dose 50 mg 3 times daily; begin with 6.2512.5 mg 23
times daily in patients receiving diuretics). CF12.5 mg 23 times daily, may be increased up to 50100 mg 3 times daily (range 12.5450 mg/day). Post MI6.25-mg test dose,
Iollowed by 12.5 mg 3 times daily, may be increased up to 50 mg 3 times daily. Diabetic ne5hro5athy25 mg 3 times daily.
Renal Impairment
PO (Adults): Initiate therapy at 6.2512.5 mg 23 times daily
73
AVAILA8ILI1
4 Captopril
1ablets: 12.5 mg
Rx
, 25 mg
Rx
, 50 mg
Rx
, 100 mg
Rx
Cost: Ca5oten12.5 mg $88.03/100 m 25 mg $95.15/100, 50 mg $163.18/100, 100 mg 217.30/100; generic12.5 mg $58.06$64.05/100, 25 mg $62.77$68.69/100, 50 mg
$107.55$119.09/100, 100 mg $143.32$156.30/100
In combination with: hydrochlorothiazide (Capozide
Rx
).
TIME/ACTION PROFILE (eIIect on blood pressuresingle dose
f
)
ONSET PEA DURATION
Captopril 1560 min 6090 min 612 hr
f
Full eIIects may not be noted Ior several weeks.
NUkSING IMLICA1ICNS
ASSESSMENT
Hypertension: Monitor blood pressure and pulse Irequently during initial dosage adjustment and periodically throughout therapy. NotiIy health care proIessional oI signiIicant changes.
4 Monitor Irequency oI prescription reIills to determine adherence.
CH: Monitor weight and assess patient routinely Ior resolution oI Iluid overload (peripheral edema, rales/crackles, dyspnea, weight gain, jugular venous distention).
ab 1est Considerations: Monitor BUN, creatinine, and electrolyte levels periodically. Serum potassium may be increased and BUN and creatinine transiently increased, whereas sodium
levels may be decreased. II elevated BUN or serum creatinine concentrations occur, dosage reduction or withdrawal may be required.
4 Monitor CBC periodically during therapy. May rarely cause slight decrease in hemoglobin and hematocrit.
4 May cause elevated AST, ALT, alkaline phosphatase, serum bilirubin, uric acid, and glucose.
4 Assess urine protein prior to and periodically during therapy Ior up to 1 yr in patients with renal impairment or those receiving ~150 mg/day oI captopril. II excessive or increasing
proteinuria occurs, re-evaluate ACE inhibitor therapy.
4 May cause positive ANA titer.
4 Ca5to5ril. May cause Ialse-positive test results Ior urine acetone.
4 WBC with diIIerential should be monitored prior to initiation oI therapy, monthly Ior the Iirst 36 mo, and periodically thereaIter Ior up to 1 yr in patients at risk Ior neutropenia
(patients with renal impairment, collagen-vascular disease, or those receiving high doses) or at Iirst sign oI inIection. Discontinue therapy iI neutrophil count is 1000/mm
3
.
POTENTIAL NURSING DIAGNOSES
74
Cardiac output, decreased (Indications, Side EIIects).
nowledge deIicit, related to medication regimen (Patient/Family Teaching).
Noncompliance (Patient/Family Teaching).
IMPLEMENTATION
PO: Precipitous drop in blood pressure during Iirst 13 hr Iollowing Iirst dose may require volume expansion with normal saline but is not normally considered an indication Ior stopping
therapy. Discontinuing diuretic therapy or increasing salt intake 1 week prior to initiation may decrease risk oI hypotension. Monitor closely Ior at least 1 hr aIter blood pressure has
stabilized. Resume diuretics iI blood pressure is not controlled.
Captopril
Administer 1 hr beIore or 2 hr aIter meals. May be crushed iI patient has diIIiculty swallowing. Tablets may have a sulIurous odor.
4 An oral solution may be prepared by crushing a 25-mg tablet and dissolving it in 25100 ml oI water. Shake Ior at least 5 min and administer within 30 min.
PATIENT/AMILY TEACHING
General Info: Instruct patient to take medication exactly as directed at the same time each day, even iI Ieeling well. Missed doses should be taken as soon as possible but not iI almost time
Ior next dose. Do not double doses. Warn patient not to discontinue ACE inhibitor therapy unless directed by health care proIessional.
4 Caution patient to avoid salt substitutes or Ioods containing high levels oI potassium or sodium unless directed by health care proIessional .
4 Caution patient to change positions slowly to minimize hypotension, particularly aIter initial dose. Patients should also be advised that exercising in hot weather may increase
hypotensive eIIects.
4 Advise patient to consult health care proIessional beIore taking any OTC medications, especially cold remedies.
4 May cause dizziness. Caution patient to avoid driving and other activities requiring alertness until response to medication is known.
4 Advise patient to inIorm health care proIessional oI medication regimen prior to treatment or surgery.
4 Advise patient that medication may cause impairment oI taste that generally resolves within 812 wk, even with continued therapy.
4 Instruct patient to notiIy health care proIessional iI rash; mouth sores; sore throat; Iever; swelling oI hands or Ieet; irregular heart beat; chest pain; dry cough; hoarseness; swelling
oI Iace, eyes, lips, or tongue; diIIiculty swallowing or breathing occur; or iI taste impairment or skin rash persists. Persistent dry cough may occur and may not subside until
medication is discontinued. Consult health care proIessional iI cough becomes bothersome. Also notiIy health care proIessional iI nausea, vomiting, or diarrhea occurs and
continues.
4 Emphasize the importance oI Iollow-up examinations to monitor progress.
Hypertension: Encourage patient to comply with additional interventions Ior hypertension (weight reduction, discontinuation oI smoking, moderation oI alcohol consumption, regular
exercise, and stress management). Medication controls but does not cure hypertension.
4 Instruct patient and Iamily on correct technique Ior monitoring blood pressure. Advise them to check blood pressure at least weekly and to report signiIicant changes to health care
proIessional.
EVALUATION
75
Effectiveness of therapy can be demonstrated by:
Decrease in blood pressure without appearance oI side eIIects
Decrease in signs and symptoms oI CHF
Reduction oI risk oI death or development oI CHF Iollowing MI
Decrease in progression oI diabetic nephropathy (captopril).
. Ranitidine 1 AMP IVTT every 8 hours
nIS1AMINL n
2
AN1AGCNIS1S
kan|t|d|ne
(ran|Lldeen)
Apo8anlLldlne ZanLac ZanLacC ZanLac 73
Dosage: 30 mg q8 hours koute lv11
cL455lllc41lON{5)
1her c/oss ootlolcet oqeots
regnancy Category 8
INDICA1ICNS
ShorLLerm LreaLmenL of acLlve duodenal ulcers and benlgn gasLrlc ulcers
rophylaxls of duodenal ulcers (aL lower doses)
ManagemenL of CL8u
1reaLmenL and prevenLlon of hearLburn acld lndlgesLlon and sour sLomach (C1C use)
ran|t|d|ne IV revenLlon and LreaLmenL of sLresslnduced upper Cl bleedlng ln crlLlcally lll paLlenLs
76
Un|abe||ed Uses
4 ManagemenL of Cl sympLoms assoclaLed wlLh Lhe use of -SAlus
4 revenLlon of sLress ulceraLlon or asplraLlon pneumonlLls
4 revenLlon of acld lnacLlvaLlon of supplemenLal pancreaLlc enzymes ln paLlenLs wlLh pancreaLlc lnsufflclency
4 ManagemenL of urLlcarla
AC1ICN
lnhlblLs Lhe acLlon of hlsLamlne aL Lhe P
2
recepLor slLe locaLed prlmarlly ln gasLrlc parleLal cells resulLlng ln lnhlblLlon of gasLrlc acld secreLlon
1herapeut|c Lffects
4 Peallng and prevenLlon of ulcers
4 uecreased sympLoms of gasLroesophageal reflux
4 uecreased secreLlon of gasLrlc acld
nAkMACCkINL1ICS
Absorpt|onooltlJloe30 absorbed afLer C and lM admlnlsLraLlon
Metabo||sm and Lxcret|on ooltlJloemeLabollzed by Lhe llver mosLly on flrsL pass 30 excreLed unchanged by Lhe kldneys afLer C admlnlsLraLlon 7080
afLer parenLeral admlnlsLraLlon
na|f||fe tooltlJloe173 hr (all are lncreased ln renal lmpalrmenL)
CCN1kAINDICA1ICNS AND kLCAU1ICNS
Contra|nd|cated |n
PypersenslLlvlLy
CrosssenslLlvlLy may occur
Some oral llqulds conLaln alcohol and should be avolded ln paLlenLs wlLh known lnLolerance
Use Caut|ous|y |n
77
8enal lmpalrmenL (more suscepLlble Lo adverse C-S reacLlons lncreased dosage lnLerval recommended for tooltlJloe lf CCr 30 ml/mln
CerlaLrlc paLlenLs (more suscepLlble Lo adverse C-S reacLlons dosage reducLlon recommended)
regnancy or lacLaLlon
ADVLkSL kLAC1ICNS AND SIDL LIILC1S*
*CAl1ALS lndlcaLe llfe LhreaLenlng underllnes lndlcaLe mosL frequenL
CNS confuslon dlzzlness drowslness halluclnaLlons headache
CV A88P?1PMlAS
GI nausea
GU decreased sperm counL lmpoLence
Lndo gynecomasLla
nemat AC8A-uLCC?1CSlS ALAS1lC A-LMlA anemla neuLropenla LhrombocyLopenla
Loca| paln aL lM slLe
M|sc hypersenslvlLy reacLlons
IN1LkAC1ICNS
DrugDrug
ranlLldlne have a much smaller and less slgnlflcanL effecL on Lhe meLabollsm of oLher drugs
Lhe agenLs decrease Lhe absorpLlon of ketoconazo|e
Antac|ds and sucra|fate decrease absorpLlon of Lhe agenLs
C|ar|thromyc|n lncreases ranlLldlne levels
kCU1L AND DCSAGL
kan|t|d|ne
IV IM (Adu|ts) 30 mg q 68 hr (noL Lo exceed 400 mg/day) otlooos lv lofoslo623 mg/hr Costtlc bypetsectetty coJltlos1 mg/kg/hr may be
lncreased by 03 mg/kg/hr (noL Lo exceed 23 mg/kg/hr)
78
kena| Impa|rment
C (Adu|ts) t50 ml/mlo130 mg q 24 hr may be lncreased Lo 130 mg q 12 hr or more frequenLly lf necessary furLher reducLlons may be necessary lf
Lhere ls coexlsLenL hepaLlc lmpalrmenL
1lML/AC1lC- 8CllLL
CNSL1 LAk DUkA1ICN
8anlLldlne lv unknown 13 mln 812 hr
NUkSING IMLICA1ICNS
ASSLSSMLN1
Assess paLlenL for eplgasLrlc or abdomlnal paln and frank or occulL blood ln Lhe sLool emesls or gasLrlc asplraLe
Assess gerlaLrlc and deblllLaLed paLlenLs rouLlnely for confuslon 8eporL prompLly
Lob 1est considerotions C8C wlLh dlfferenLlal should be monlLored perlodlcally LhroughouL Lherapy
4 AnLagonlze effecLs of penLagasLrln and hlsLamlne durlng gasLrlc acld secreLlon LesLlng Avold admlnlsLraLlon for 24 hr before Lhe LesL
4 May cause falsenegaLlve resulLs ln skln LesLs uslng allergenlc exLracLs PlsLamlne P
2
anLagonlsLs should be dlsconLlnued 24 hr before Lhe LesL
4 May cause an lncrease ln serum Lransamlnases and serum creaLlnlne
4 ooltlJloe may cause falseposlLlve resulLs for urlne proLeln LesL wlLh sulfosallcyllc acld
C1LN1IAL NUkSING DIAGNCSLS
aln (lndlcaLlons)
knowledge deflclL relaLed Lo medlcaLlon reglmen (aLlenL/lamlly 1eachlng)
IMLLMLN1A1ICN
79
Genera| Info lf anLaclds or sucralfaLe are used concurrenLly for rellef of paln avold admlnlsLraLlon of anLaclds wlLhln 30 mln1 hr of Lhe hlsLamlne P
2
anLagonlsL and Lake sucralfaLe 2 hr afLer hlsLamlne P
2
anLagonlsL may decrease Lhe absorpLlon of hlsLamlne P
2
anLagonlsLs
C AdmlnlsLer wlLh meals or lmmedlaLely afLerward and aL bedLlme Lo prolong effecL
4 uoses admlnlsLered once dally should be admlnlsLered aL bedLlme Lo prolong effecL
4 Shake oral suspenslon before admlnlsLraLlon ulscard unused suspenslon afLer 30 days
kan|t|d|ne
D|rect IV ulluLe each 30 mg ln 20 ml of 09 -aCl or u3W for ln[ecLlon
ote AdmlnlsLer over aL leasL 3 mln 8apld admlnlsLraLlon may cause hypoLenslon and arrhyLhmlas
Interm|ttent Infus|on ulluLe each 30 mg ln 100 ml of 09 -aCl or u3W ulluLed soluLlon ls sLable for 48 hr aL room LemperaLure uo noL use soluLlon LhaL
ls dlscolored or LhaL conLalns preclplLaLe
ote AdmlnlsLer over 1320 mln
Cont|nuous Infus|on Add ranlLldlne Lo u3W for a concenLraLlon of 130 mg/230 ml (no greaLer Lhan 23 mg/ml for ZolllngerLlllson paLlenLs)
ote AdmlnlsLer aL a raLe of 623 mg/hr ln paLlenLs wlLh ZolllngerLlllson syndrome sLarL lnfuslon aL 1 mg/kg/hr lf gasLrlc acld ouLpuL ls 10 mLq/hr or
paLlenL becomes sympLomaLlc afLer 4 hr ad[usL dose by 03 mg/kg/hr lncremenLs and remeasure gasLrlc ouLpuL
4 poLasslum chlorlde
4 Llcarclllln
4 Lobramycln
4 vancomycln
Add|t|ve Incompat|b|||ty
4 amphoLerlcln 8
4 cllndamycln
A1ILN1]IAMIL 1LACnING
Genera| Info lnsLrucL paLlenL Lo Lake medlcaLlon as dlrecLed for Lhe full course of Lherapy even lf feellng beLLer lf a dose ls mlssed lL should be Laken as
soon as remembered buL noL lf almosL Llme for nexL dose uo noL double doses
4 Advlse paLlenLs Laklng C1C preparaLlons noL Lo Lake Lhe maxlmum dose conLlnuously for more Lhan 2 wk wlLhouL consulLlng healLh care
professlonal -oLlfy healLh care professlonal lf dlfflculLy swallowlng occurs or abdomlnal paln perslsLs
4 lnform paLlenL LhaL smoklng lnLerferes wlLh Lhe acLlon of hlsLamlne anLagonlsLs Lncourage paLlenL Lo qulL smoklng or aL leasL noL Lo smoke afLer
lasL dose of Lhe day
80
4 May cause drowslness or dlzzlness CauLlon paLlenL Lo avold drlvlng or oLher acLlvlLles requlrlng alerLness unLll response Lo Lhe drug ls known
4 Advlse paLlenL Lo avold alcohol producLs conLalnlng asplrln or -SAlus and foods LhaL may cause an lncrease ln Cl lrrlLaLlon
4 lnform paLlenL LhaL lncreased fluld and flber lnLake and exerclse may mlnlmlze consLlpaLlon
4 Advlse paLlenL Lo reporL onseL of black Larry sLools fever sore LhroaL dlarrhea dlzzlness rash confuslon or halluclnaLlons Lo healLh care
professlonal prompLly
LVALUA1ICN
Lffect|veness of therapy can be demonstrated by
uecrease ln abdomlnal paln
revenLlon and LreaLmenL of gasLrlc lrrlLaLlon and bleedlng Peallng of duodenal ulcers can be seen by xrays or endoscopy 1herapy ls conLlnued for aL
leasL 6 wk ln LreaLmenL of ulcers buL noL usually longer Lhan 8 wk
uecreased sympLoms of esophageal reflux
1reaLmenL of hearLburn acld lndlgesLlon and sour sLomach (C1C use)
8 Ceftr|axone 1 Amp IV11 every 8 hours
CEPHALOSPORINS-THIRD GENERATION
ceftriaxone
(seI-try-ax-one)
Rocephin
C$$IFIC1IOA($):
1her. Class: anti-infectives
!harm. Class: third-generation ce5halos5orins
Pregnancy Category
81
INDICA1ICNS
Treatment oI:
4 Skin and skin structure inIections
4 Bone and joint inIections
4 Urinary and gynecologic inIections including gonorrhea or respiratory tract inIections
4 Intra-abdominal inIections
4 Septicemia
4 Otitis media (ceIdinir)
Ceftriaxone: Single-dose treatment oI acute bacterial otitis media
AC1ICN
Bind to the bacterial cell wall membrane, causing cell death.
Therapeutic Effects:
4 Bactericidal action against susceptible bacteria.
Spectrum:
4 Similar to that oI second-generation cephalosporins, but activity against staphylococci is less, whereas activity against gram-negative pathogens is greater, even Ior organisms
resistant to Iirst- and second-generation agents
4 Notable is increased action against
4 Enterobacter
4 aemo5hilus influen:ae
4 Escherichia coli
4 lebsiella 5neumoniae
4 Neisseria
4 Proteus
4 Providencia
4 Serratia
4 Moraxella catarrhalis
4 orrelia burgdorferi
4 Some agents have enhanced activity against:
4 Pseudomonas aeruginosa (ceItazidime, ceIoperazone)
4 All except ceIixime, ceItibuten, and ceIpodoxime have some activity against anaerobes, including acteroides fragilis.
nAkMACCkINL1ICS
Absorption: Well absorbed aIter IM administration. Cefixime, ceftibuten,and cef5odoxime are well absorbed aIter oral administration (ceIixime suspension produces higher blood levels than
tablets); cefdinir 1625 absorbed aIter oral administration. CeItidoren is a prodrug and is broken down prior to absorption (14 absorbed).
82
Distribution: Widely distributed. Cross the placenta; enter breast milk in low concentrations. CSF penetration better than with Iirst- and second-generation agents.
Protein inding: Cefo5era:one and ceftriaxone K90.
Metabolism and Excretion: Cefdinir, cefe5ime, cefta:idime, cef5odoxime, ceftidoren, and cefti:oxime~85 excreted in urine. Cefixime50 excreted unchanged in urine, K10 excreted in
bile. Cefo5era:oneexcreted in the bile. Ceftibuten, ceftriaxone, and cefotaximepartly metabolized and partly excreted in the urine.
Half-life: Cefdinir102 min; cefditoren100 min; cefe5ime120 min; cefixime180240 min; cefo5era:one102156 min; cefotaxime60 min; cef5odoxime120180 min; cefta:idime
114120 min; ceftibuten120144 min; cefti:oxime84114 min; ceftriaxone348522 min (all except cefo5era:one and ceftriaxone are increased in renal impairment).
CCN1kAINDICA1ICNS AND kLCAU1ICNS
Contraindicated in:
Hypersensitivity to cephalosporins
Serious hypersensitivity to penicillins
Hypersensitivity to L-arginine (Ceptaz Iormulation only).
Carnitine deIiciency or inborn errors oI metabolism (ceIditoren only).
Use Cautiously in:
Combined severe hepatic and renal impairment (dosage reduction/increased dosing interval recommended Ior ceftriaxone)
History oI GI disease, especially colitis
Geriatric patients (dosage adjustment due to age-related decrease in renal Iunction may be necessary)
Pregnancy and lactation (have been used saIely).
ADVLkSL kLAC1ICNS AND SIDL LIILC1S*
CAPITALS indicate liIe threatening; underlines indicate most Irequent.
CNS: SEIZURES(high doses).
GI: PSEUDOMEMBRANOUS COLITIS, diarrhea, nausea, vomiting, cramps, pseudolithiasis (ceItriaxone).
Derm: rashes, urticaria.
Hemat: bleeding (increased with ceIoperazone), blood dyscrasias, hemolytic anemia.
Local: painat IM site, phlebitisat IV site.
Misc: allergic reactions includingANAPHYLAXIS andSERUM SICNESS, superinIection.
IN1LkAC1ICNS
Drug-Drug:
83
Ingestion oI alcohol within 4872 hr oI ceIoperazone may result in a disulIiram-like reaction
CeIoperazone may potentiate the eIIects oI anticoagulants and increase the risk oI bleeding with antiplatelet agents, thrombolytics, plicamycin, or valproic acid
Concurrent use oI large doses oI cephalosporins and NSAIDs may increase the risk oI bleeding
Concurrent use oI loop diuretics ornephrotoxic agents including aminoglycosidesmay increase the risk oI nephrotoxicity
Antacids decrease absorption oI ceIdinir and ceIpodoxime (take 2 hr beIore or aIter antacid)
Iron supplements decrease absorption oI ceIdinir (administer 2 hr beIore or 2 hr aIter)
Antacids and H
1|llr,l(]r]l((gl]-l(]g(]-l(g]]|]]|(gl(r]||,|(]l(
]|l|]|jr|-]|]|jr(|l|1|lrjr]l|||jr(]jrjr(rl(((((]-j]l(]/jrl(l(
|(gl]l(((]l(g(g||]|jlj|(rl(gl(jl-]]||l(]1|r|]rl(]|j]|j|,l|,,
j|]-l(g]]|-]|l|((g,(j](((l-]gj,]|j]l(]|gl--l|],l(jr]|l(,g((
j]||(g-];(l]l(-l(]g-g;(gjr]l|l]||l]l|j]()(gl]|]|l,jrjrl(]r(]l(l||j
j|((gl|,|(l(]|j|r(g-]|gl
ibIiography
!ra Souee. Hs. Vrllaios, Aada
143
Seeoida. NO! Chat, H. Eeiad Aada~huslaid
Eooks.
O Elaek, 1. H., awks, 1. . |200J). Hedreal~sureal iusri |7
th
ed.). Sriajoe. Flsevre Sauides.
O Eulloek, E.l. |I00). !athojhsrolo. Adajtatrois Alteatrois ri Fuietroi. +
th
ed. 1.E. lrjjrieott Cojai. !hrladeljhra.
O Feshwate, F. Haslri~!otheo, S. |200J). Elaekwells Nusri Dretroia |2
id
ed). Ll. Elaekwell !ullrshri ltd.
O lell, W. 1. |Fd.). |2007). Nuses du urde 2007. !hrladeljhra. lrjjrieott Wrllras Wrlkris.
O lo:re, E. et al.|200+).Fuidaetals ol Nusri.Coieejts, !oeess, aid !aetree |7
th
edrtroi).New 1ese.!easoi Fdueatroi lie.
O Harel, F. N. |2002). Fsseitrals ol huai aiato aid jhsrolo |
th
ed.). Calrloira. Eeijari,Curis Sereiee !ullrshri.
O Hoiahai, F. Saids, 1., et al. |2007). !hrjjs Hedreal~Sureal Nusri ealth llliess !esjeetrves |8
th
ed.) Hosl lie.
O Seele, R., Stejheis, I. Iate, !. |200). Aiato !hsrolo |
th
ed.) Newok. HeCaw~rll.
O Selt:e, S.C.,Eae, E.C.|200+).Euiie aid Suddaths Iextlook ol Hedreal Sureal Nusri|I0th edrtroi).
O Iotoa, C., Calowskr, S. |200). !rierjles ol huai aiato aid jhsrolo |I0
th
ed.). LSA. 1ohi Wrle aid Sois, lie.
1ouials.
Rolets, S.S.|1ai 200).Draletes Foeeast|Vol J Nu I). Draletes No Reasoi Io esrtate Alout Vaseula Sue. Vrrira.Aereai Draletes
Assoeratroi.j8~8
Iaieile, R.1.|Ajrl 200J).Draletes Foeeast |Vol JJ Nu +).Sue lo Olesrt.Vrrira.Aereai Draletes Assoeratroi.j8I