How stool is formed?

1. Stool propelled via colon to rectum (reaches rectum 7-8 hours after ingestion) 2. When stool enters rectum: Stool distends rectum Rectum contracts reflexively Stool forced into anal canal Stool crosses 90 degree angle 3. When stool enters anal canal: Internal anal sphincter (involuntary control) automatically relaxes on stool entrance! "xternal anal sphincter (voluntary control) voluntary relaxation results in defecation . !efecation: "xternal anal sphincter opens Intra#a$dominal pressure increases with and stool moved out What are the results of chronically ignoring urge to defecate? Sensor" receptor refle# arc less responsive Stool collects in distal colon Stool desiccates and $orsens %onstipation

%hat is the stool analysis test?

& stool anal"sis is a series of tests done on a stool (feces) sample to help diagnose certain conditions affecting the digestive tract.

%hy It Is &one

'elp identif" diseases of the digestive tract( liver( and pancreas. 'elp find the cause of s"mptoms affecting the digestive tract( including prolonged diarrhea( )lood" diarrhea( an increased amount of gas( nausea( vomiting( loss of appetite( )loating( a)dominal pain and cramping( and fever. *oo+ for intestinal parasites. *oo+ for the cause of an infection( such as )acteria( a fungus( or a virus. %hec+ for poor a)sorption of nutrients )" the digestive tract (mala)sorption s"ndrome).

=>0?930 :85;< 489630 )73 4561 '1230 +,-./0 )* '(

1. 2. 3. . -. ,atient $ith a)dominal pain or a)dominal discomfort ,atient $ith diarrhea ,atient $ith anemia ,atient $ho is too thin or do not gro$ $ell ,atient $ith stool color that is changed to a)normal color

Stool sampling D1?E53 @,ABC(

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pass stool may be painful.

.1 .2 .3 . .-

FoteG: There is no pain while collecting a stool sample, but if you are constipated, straining to

:EHE53 @,ABC(
H>I/2> PQ EFc3o .Fgo CDA PQ C4? .1 rFgZ=i2 pFq\ R3G@ b<n@ PQ C4? .2 (.G3` 5OD uM62> 9:6; @ .FiF6t2> T><7s> U<gS ? J=K) fIF/o .F1QH fCQ .1FX2> JiG Ig; ? .3 FoteG: Exposing the stool sample to air or room temperature will affect the test result. U3:;</2> @ U3FiF6t2> T<z{ EyIc @ 9Fi2> 5><7 rgZQ 31x H>I/2> j?) 9:cs> wx Io3/2> v3/k2> .1FG (I/o> .t|12> T><7s> 9=[S 3z\s 5367s> C1G .y3D H>I/234 5</2> NO=D> ^CG f3G>IQ etD uF_|=2> ~ 9FiM=2> j<; ? J=K .;Iz|2> fT@C2> R31~A R3012> C1G ^C234 H>I/2> NO=D> ^CG f3G>IQ .Xs> CX4 PFQ<; 5OD ./k234 .XA ]InA d2> u_|2> PQ .1FX2> cIS FoteG: sample rejected from patient recently had an X-ray test using barium contrast
material, such as a barium enema

. ..} .7 .8

. HI/Q3/2> I|S .ZF=\ 3n H>I/2> j3o > cIS U336M2> Jc 5367s> .1FG . FoteG: Samples from babies and young children may be collected from diapers (if the stool is
not contaminated with urine or from a small-diameter glass tube inserted into the baby!s rectum.

:9Q 9FiM=2> R>InA 9/B .1FXg2> E;@be2> X4 CDA PG 31=Q?> YZ; "ntacids, antidiarrheal medications, antiparasite medications, antibiotics, enemas, and laxati#es

.1

.23M2> Y0K 3z1G 5>02>@ 3z4 9gXg2> T3tD PQ C4? H>I/2> JiG I~S .;@bA ]A dD> .23K Jc .11 H>I/2> E1FG rFgZS C1G U31Fig2> ^>C_=`> PG CX=4> .12 .R3G<2> wiG .1FX2> YK3y U3\3F4 r@ YZ; .13 9iM=2 3 X1Q PF=G302> PG C;S ? fI=c Jc 9gXg2> J2 .1FX2> R3tG 9:6; 9gXg2> T3D .1FX2> UdDA > .1 U3FiF6t2> X4 b34H @A ;Io ./iG Jc \3o > 9gXg2> T3D PQ H>I/2> U31FG 9/[S ? .1FoteG: Sometimes a stool sample is collected using a rectal swab that contains a
preser#ati#e (if patient is unable to gi#e stool . The swab is inserted into the rectum, rotated gently, and then withdrawn. $t is placed in a clean, dry container and sent to the lab right away.

IJK;5(

E\A @IXg2> Pgc .1FX2> FoIS .[;I7@ uM6234 ^<[; d2> w3kD?> fI/D <x H>I/2> uMc Jc 9Q3G xA 3gio j<` .23K Jc 9F6t2> j3o @A .6F67 .43yW> \3o 3gio@ uF_|=2> 9z` 3gio fC;C .43yW> \3o 3gio . I/oA fI/D J2 3=M;@ YXyA uF_|=2> j3o IJK;5( fCK>@ .1FG JiG b3g=Gs> jA FK .F23==Q ^3;A .~O~ Jc 9Bs> JiG H>I4 U31FG .~O~ uMc YZ; E\A L3M4s> =/~A >@ 9gXg2> etD JcOS =; J=K .6i=_Q 9Q3XQ .~O~ 9:6;@ U3FiF6t2> .;T Jc .yI62> fb3;2 m2@ J6; ? h[c .u_ PQ IoA U31FX2> ]I; jA 9:6; 9gXg2> 6\ Jc =F` uM62> j3o

>0?930 IM8N '1L-<

3zS<Q 9/B .t|12> T><7s> .;I2 .yI62> fb3;2 m2@ 53M2> Jc .1FX2> uMc 9:6; .;<Q .nTb C1G .nO234 j_; ~ ?@A (YF`I=234) aIF:MS =Fc H>I/2> P;_S fT@I j3o > PF23QT<62> @ .nO2> Jc </`A PQ IoA H>I/2> .1FG 6M2 PF23QT<c 5<iMQ 53gX=`> Pg; ..iy<M=g2> T><7s> JiG c3M; .3XQ .t|12> @ .iy<M=g2> T><7s> JiG c3M; U31FX2> 6K Jc 5<M2> ^>C_=`> ) .t|12> T><7s> 9=B J2 ]b; .1FXi2 36n LCM; ? J=K R><zi2 3IXQ .1FX2> <o VIS Y1ZS coprooic)wnT3_2> <Z2> U3FiF6t4 .1FX2> L<i=S ? J=K @ (larva)U3BIF2> @ (trophooite .(protooa -1 -2 -3 --

>0?930 RM8N ?8Q;< O?P

RM8H30 ?8Q;< WMN I(,* ST,UVG
_;Y3,^ b,8c30 I3 dMe\1 d\B :85;\3,^ :EH^ bKc8] a230 _-`30 R6]0K^ ?8Q;\30 )\1 Z[ :QY1 !?8Q;\30 g,Mh[ f?*,A30 0 f?*,A30 _;Y3,^ Rr,-30 @,V,8930 :q 'N RM8H30 ?QB '( o0p] '( W^n m3j lLH< 0jk !o,;30 dt _;Y< )3 0jk m3j WH^ RyCe30 dt ,7M1L-< )h vwx u?][ dt RM8H30 ?8Q;< )\1 '( gL~30 m3j _;t :QY1 },-( x[ W1Wr x[ Ce( bW3,q {H89P ?8| g{. f[ >0?930 RM8H^ Z,q 0jk !RM8H30 ?8Q;< dt gW930 :9w K]x?8E30 v;< nx[ RM8H30 !X !i !s !z

reparation methods
&irect smear oncentration techniue Sedimentation method Saline sedimentation ech!

 ormal "ther oncentration ech! loatation method ato techniue

&irect smear
Ic1?630 v;< ,7U;t0 )h S5E30 oK5;( '( I6cV ( ,7yL(0 x IY8AV I;1?. d5N >0?930 '( ?8r RH6w !X z0 I]WH30 )h X0 I]WH30 ,(W-\( K]x?8E30 gL~30 0W* _;Y^ gW930 4~1 },-( x0 W1Wr x0 b I^ gLy IM8H3,^ Z,q 00 !i g,H(n0 x0 Ic8wW30 g,H(n,^ @,858YP Kyx o,E\Bn I50 '( IM8N x >0?930 S6] '( RM8N _;t 4~1 !s IA8530 _;t0 m325t `M30 lK630 :\c1 K830 '3 I5rK;\E30 l0KPn0 R1?3 RM8H30 9U3 K830 b0W-\]0 'E1 !z nx0 K830 ZxW^ @0L8EE30 @,858Y653 I5rK;\E30 ,8qn0 _;Y3 ,],][ bW-\<x RH1?]x R57] Rc1?630 K8H30 Ir?Yt I585w IM8H30 dt @,858Y630 0WN0 vV,q K3 ,(0 W1W. :8Y63,^ I^,rn0 ZK1 Z0 ,\;< x Ic8w ?8| Ic1?P 0Wy IY8H Ic1?630 W7^ ,7\1l

oncentration techniue
Sedimentation method Saline sedimentation ech! Ic1?630 !K30 d30 S5E30 oK5;( ,Q1 )h 8AV Kq {t K<x >0?930 '( RH6w 2p< !X !0W8y oK5;E30 {t >0?930 45c1 !i !K30 g,6| x0 ,. IH6w b0W-\],^ I^K9V0 dt >0?930 {YU1 !s !Rc8w s0 i0 WE3 I^K9Vn0 ?\< !z K]x?8E3,^ 4]0?30 _;Y1 ! d30 fp1 Z0 'E1 fKc30 ?1xW\30 '3 48]?\30 '( 1?\30 x IM8H30 ?1xW\3 K8t?\M30 b0W-\]0 'E1 IJK;5( !@,w?830 x @,Q1K930 l0Wy ?8< @0L8EE30 G:e( I^K9Vn0 u,w dt 4]?\< d3,\3,^ x S5E30 oK5;( '( ,V>x :chn0 @,858Y653 R9],M( Ic1?630 W*

"scaris
Shistosoma mansoni

%asciola Strongyloides stercoralis

K8H30 g,Y30 YM^ @,858Y630 8E~3 S5U< n ormal ether concentration ech! Ic1?630 !K30 d30 S5E30 oK5;( ,Q1 )h 8AV Kq {t K<x >0?930 '( RH6w 2p< !X !0W8y oK5;E30 {t >0?930 45c1 !i !K30 g,6| x0 ,. IH6w b0W-\],^ I^K9V0 dt >0?930 {YU1 !s !WB0x Rc8w WE3 K8t?\M30 {t I^K9Vn0 lxW< !z a?[ Rc8w WE3 I^K9Vn0 lxW< x ?( '( ?eq[ S5E30 oK5;( ,Q1 ?H\( o0> ,( aK5H30 :T,30 Z,q 0jk ! !,cT0l aK5H30 :T,30 S9U1 d\B !R^K9V/0 {t 4]0?30 ?\1x T0?30 :T,30 41 ! !T,w WE3 ?\1x W8y LE1x R^K9V/,^ 4]0?30 {3k '83,(lKY30 oK5;( ,Q1 ! !Rc8w WE3 K8t?\M30 {t l0W< )h Rc8w WE3 W`^ ?<x R^K9V/0 5<x ?8h/0 ,Q1 ! @,c9P ^l[ I^K9Vn,^ ZK\1 Zn0 ?8e1[ G{3x/0 Rc9630 @CQt GR8V,e30 Rc9630 '83 ,(lKt oK5;( GRe3,e30 Rc9630 @,858Y630 {5N aK\;( 4]0?30 GRH^0?30 Rc9630 !0W8y 4]0?30 02* LE1x ct 4]0?30 ?\1x R^K9V/0 '( RhCe30 R1K5H30 @,c9630 '( _5-\30 )\1 !K]?8E30 v;< 4]0?30 '( I6cV _;Y< !K]?8E30 v;< _;Y< x K830 ( 4]0?30 '( I6cV LE< !9 !X0 !XX K8H30 I9Hr x I51KP Ic1?P

loatation method Ic1?630 !K30 d30 S5E30 oK5;( ,Q1 )h 8AV Kq {t K<x >0?930 '( RH6w 2p< !X !0W8y oK5;E30 {t >0?930 45c1 !i !K30 g,6| x0 ,. IH6w b0W-\],^ I^K9V0 dt >0?930 {YU1 !s !T,w X0 WE3 I^K9V00 ?<0 !z !S5E30 oK5;E^ ,85H30 ,7\*Kt d\B I^K9Vn0 :Eq0 ! !I^K9Vn0 R*Kt OKt R;1?. K< ! !Rc8w s0 i0 WE3 I^K9Vn0 ?\< !

!_;Y< x K]x?8E30 v;< K<x 45c<x 0?\B,^ R;1?`30 t?< ! @0L8EE30 G:e( I^K9Vn0 dt :T,30 S6] d5N KY6< d3,\3,^ x S5E30 oK5;( '( ,V>x n0 @,858Y653 R9],M( Ic1?630 W* Entrobius "n&ylestoma Tricuris K8H30 g,Y30 YM^ @,858Y630 8E~3 S5U< n

ato techniue
Ic1?630 IY8AV I8y,y> I;1?. ?QB !X K<,q ^?( I;1?`30 d5N !i >0?930 IM8H^ K<,q ^?( 0?t gC(0 !s '1?y v8qC( I9U^ IM8H30 9r0 !z _;Y< )h '8\N,] WE3 Ryl s {5N 'Q;<x 0W8y ?Y<x 9`E30 Z,tK583,^ RM8H30 {6< ! @0L8EE30 !R^,r 0 W. ?1Wc\3 @,Q1K930 WH3 m32qx _;Y53 bW-\< !lK7. {30KB WE3 R|K9UE30 ST0?`3,^ ,Y\Bn0 'E1 K8H30 !K<,q {3k Rt, ,^ f?0 Rc1?6^ _;Y30 4~1 023 W1K5~V?\]n0 @,w?1 x[ ,98(,\Vn0 'N `53 S5U< n

Laboratory stool report

Stool Examination
Test
Physical examination Color Odour Reaction Consistency Mucus Appearance Pus Blood Gross Parasite (naked eye) Microscopic examination Pus cells RBCs pithelial cells State of digestion !tarch granules "at glo#ules %egeta#le cells Muscle fi#ers i0#i # $sent 0 # H 0 # s H $sent
rown ffensive aria$le ormed $sent $sent $sent $sent rown ffensive aria$le ormed $sent $sent $sent $sent

Result

Normal

$$ $$$

Parasites Proto&oa ' %egetati(e ' Cysts )el*inthes ' +ar(ae ' O(a

$sent $sent $sent H! nana

$sent $sent $sent $sent

ross examination
olor
FormalG
ro$n color is the normal color of stool Why stool color is #ro,n? he characteristic )ro$n color of feces is due to stercobilin and urobinin( )oth of $hich are produced )" )acterial degradation of )iliru)in.

$normalG
Black color' indicate iron medication (for treatment of anemia) or upper )leeding (due to peptic ulcer( stomach carcinoma or esophageal varices). Bright red color' indicate lo$er )leeding (due to piles and anal fissure). Clay color(gray-,hite)' indicate o)structive aundice !il(er color' indicate com)ination of aundice and )lood (cancer of ampulla of ater). Red #ro,n color' indicate drugs as etrac"clines( and ifam)icin anti)iotics Green color' indicate medications as !iathiaine( ercurous chloride also vitamins cause green color of stool and in some cases of intestinal putrefaction.
mpulla of ater FoteG red stool color may be seen if there are undigested beets or tomatoes . he ampulla of ater( also +no$n as the hepatopancreatic a*pulla( is formed )" the union ofFoteG the pancreatic duct is and the and common duct. if stool color blac& there)ile is no history of iron medication %'(T is recommended. unction arious smooth muscle sphincters regulate the flo$ of )ile and pancreatic uice through the ampulla: the sphincter of the pancreatic duct( the sphincter of the )ile duct( and the hepatopancreatic sphincter (Sphincter of ddi)( $hich controls the introduction of )ile and pancreatic secretions into the duodenum( as $ell as preventing the entr" of duodenal contents into the &mpulla.

dour
FormalG
ormall" offensive Why stool odour is offensi(e? ecal odor results from gases produced )" )acterial meta)olism( including s+atole( mercaptans( and h"drogen sulfide.

$normalG
Odorless' usuall" seen if there is no fecal matter as in )acterial infection. %ery offensi(e' usuall" seen in cases of constipation and $ith certain t"pes of food that produce e#cessive gases.

pH ( reaction )
FormalG
ormall" varia)le Why stool p) is (aria#le ecause stool p' mainl" depends on the t"pe of diet.

$normalG
High alaline stool hysiological 'igh protein diet High acidic stool hysiological 'igh car)oh"drate diet athological ,oor a)sorption of sugars as in lactose intolerance athological ,oor fat a)sorption

onsistency
FormalG
ormall" $ell formed

$normalG
"bnormal consistency may be graded as follow) %ery hard' seen in cases of constipation !e*i for*ed' seen in the cases of parasitic infection !oft' seen in the cases of parasitic infection +oose' seen in the cases of diarrhea Watery' mostl" seen in cases of )acterial infection

ucus
FormalG
ormall" undetecta)le amount produce )" and found in the stool.

$normalG
&)normal mucus in the sample appears as $hite patches and usuall" present $ith appearance pus and indicate )acterial infection. &ccording to the amount of mucus it can )e graded using signs (( ( ) FoteG mucus with fresh blood in stool usually indicate amoebic dysentery

ppearance pus
FormalG
ormall" not found (pus can )e found normall" in the stool )ut "ou cannot see it )" na+ed e"e).

$normalG
suall" detected $ith mucus and appear as $hite patches in the stool( it indicate ulcerative colitis or )acterial infection as bacillary dysentery. &lso it can )e graded using signs (( ( ). ,resence of detecta)le pus )" na+ed e"e means that the microscopic pus must )e over 1. 9Z0S j> 9/B S CB E1FX2> IF:MS j> @> Ix3q2> uM6234 >@ IFl N3_g2> @> C;Ck2> j3o >b> : E{<MiQ >b> FK Ix3q2> uM62> Jc N3_g2> @> C;Ck2> E43=2 J4<`@IFg2> uM62> JiG Cg=G3c Ix3q2> uM62> @> Ix3q2> uM62> Jc N3_g2> @ C;Ck2> Y=o> 8 PQ JiG> <`IFg2> MS C;Cy UCn@

ross $lood
FormalG

ormall" no )lood seen in the stool ("ou cannot see it )" na+ed e"e).

$normalG
"bnormal fresh blood seen in cases of lower *$T bleeding caused by) ilharias (schistosoma mansoni infection) anal fissure piles J4<`@IFg2> uM62> Jc %s 5> bCG E43=o PQ C4Oc ]Ix3q2> uM6234 .1FX2> Jc ^b UCn@ >> : E{<MiQ .(over 1) 1 PQ Io>

Faed eye parasite

FormalG no parasites or larva appear in the stool $normalG
n some cases the $hole $orm or parts of its )od" appear in the stool and can )e seen )" na+ed e"e. hree $orms can )e seen )" na+ed e"e in the stool: "scaris lumbericoides Entrobius #ermicularis Taenia sp.

icroscopic examination
_;Y53 R;1?`30 ?8Q;<
vI0g2>@ fR3W> FK PQ@ U3`CX2> .c3q\@ .QO` FK PQ 9gXi2 23y <`@IFg2> j> Coe=2> YZ; . >I|2> R3tl m2do@ .F4<`@IFg2> >I|2> .c3q\ PQ Coe=2> IF/o j><1G fR>IB PQ m1gS .M;I|2> adx ((not too thin not too thic& .Fn<g\ .M;I IF:MS .3zB<c X@ >b> .iZQ Jc CX4 ~ 3zio .M;I|2> 0Q =; J=K 1 .FF|2> .`CX234 <`@IFg2> MS .1FX2> uMc AC/; jA P0M=0; .(.Fi_2> U>CFK@ ZK Ik2 >Iq\ m2@) .FF|2> .`CX234 uM62> =; m2b .1 .2 .3 .

R(,* @,ABC(
igag bCMQ IF` hD r/S> @ EM;I|2> JiG .1FXQ .t[\ PQ uM62> >C4> VIS j@b EiQ3o EM;I|2> uMc =; J=K overlapping .iD>C=Q .[;It4 .M;I|2> uM6S j> 5@3K .U3l>Ic J=K .6i=_Q Po3QA PQ E1FG T3=D> E_ti2> E[;I7 ^C_=0S 1o >b> @ .1FG 92 9B?> JiG PF=M;I uMc> .>CFn .1FX2> .ZF=\ wiG M2> Pg; j>C;b b<n@ ^CG PQ ^3=2> Coe=i2 PF=M;I PQ Io> uMc> .M;I|2> Jc ^b @> C;Cy b<n@ C1G .1 .2 .3 .

OQ E1FXQ ova PG M/S j> 9Q .1FX2> Jc M/S \> @ PFXQ RJ VIF6S Jc r:S? .uM6; ]d2> u_|2> 3k;? J=K )inocular ) <`@IFQ ) uM62> Jc PF1FX2> ^>C_=`> 9:6; .} fCK>@ PFG ^C_=`> >> >Ck234 PF4 ;I6=i2 aI/_2> VC1G j<; j> C4? m2C2 ^<:zg2> IF2> ^3Xti2 >Cn fIFo 53> JiG ]<=M; H>I/2> .7 .U3:;</2> @ EFXF/t2> 53?> 3=2> PQ T<k234 PFX=`> @> 3zkM6; VIF2 .1FX2> VIS> 3zcIXS ? 3Q .:;<4 b<n@ 53g=K> Jc m|2> C1G .8 .1FG ;Ig2> PQ Yi7> @ 3zFc V<|g2> .:;</2> .43=o ^CG 9:c?> Pgc m2 Ic<=; 2 >>@ IS<F/g2> @> .]ID> fIQ uM6i2 v3/k2> Jc ]ID> Jc b<n<g2> 9F6t2> rB<S @ miFiMS EMy PQ Coe=2> PQ m1gS ;Ig2> JiG EFIg2> >IG?> X4 . .E1FX2> Jx uF_|=2> 93`@ CK> j> 94 ;Ig2> .i|Q uF_|=2 H>I/234 U3FiF67 b<n@ 37I F2 .1 @> U3:;<4 b<n@ ^CG PQ Coe=2> CX4 @ J\e=g2> @ .1FXi2 >Cn CFZ2> uM62> C1G m2d2 U3FiF67 b<n@ b3X/=`> .U3FiF67 j@C4 9FiM=2> Y=o> 3z4 larva

verlapping

-igag

K]x?8E30 v;< RM8H30 _;t

ells
RBCs
ppearanceG
R3|4 @C/S @ (C;Ck2> EFiD PQ Iy> ) ZM2> aIFy EFi_o <`@IFg2> MS R>IgM2> ^C2> U>Io IzqS >Cx JtX; ]C2> PF4<in<gFz234 3zO=Q> EZF1S >Cx Izq; 3g\> @ @bQ F2 3z3|l E[F[M2> Jc P2) @bQ .(3/t\?> E{<MiQ E;I2> Co; 3gQ ]Ix3q2> uM62> R31~> 3:;> Izq; @ p;\ .ZF=\ Y232> Jc LCM; H>I/2> Jc ^b b<n@ <`@IFg2> MS

MS IzqS j3FK?> X4 Jc @ 3z2 j<2 ? 94 IgK> F2 <`@IFg2> MS R>IgM2> ^C2> U>Io j<2 4Og2> PQ 3F2> Jx 94 >C4> ^b F2 Jx @ 9;<7 hD @> E_t2 9 JiG R>IgK Y>< <`@IFg2> .73gt2> @ Ft/2> .y3D 9o?> PQ @>

FormalG
ormall" fe$ amounts of %s (-3) are seen under high po$er field of microscope.

ountingG
%s are counted under ', of microscope and the range of count is $ritten for e#ample 1-12 or 3- and so on.

InterpretationG
&)normal %s under microscope is seen in: ilharias (schistosoma mansoni infection) anal fissure piles ntame)a histol"tica infection

PUS
ppearanceG
. a><\ 3z4 @ ZM2> aIF/o EFi_o <`@IFg2> MS C;Ck2> @> R3:F/2> ^C2> U>Io IzqS E{<MiQ U3XgZS Jc Cn<; 3g>b C;Ck2> Cn<S ? E\> K? 31x @ E;IF=/2> U343y?> U?3K Jc m2b @ C;Cy 3zio .1FX2> j<S j3FK?> X4 Jc .:z2> E23K JiG M2> Pg; Oc E;H>I4 ab3Q EFiG @ N3_Q j<S 3Q 3/23l 3z\? .M;I|2> JiG fbIZg2> PFX234 R3:F4 IzqS J=2> Po3Q?> PG 3g>b M4> . C;Ck2> PQ rgZS

FormalG
ormall" fe$ amounts of pus (--) are seen under high po$er field of microscope.

ountingG
,us is counted under ', of microscope and the range of count is $ritten as in the case of %s. FoteG if pus count is o#er +,, stool culture is recommended.

InterpretationG
&)normal pus under microscope is seen in: acterial infection as Shigellosis ( Salmonellosis nflammation of the intestines( such as lcerative colitis FoteG usually pus is absent or few in cases of -iral diarrheas (.ota#irus infection ) and
/arasitic infestations.

Epithelial cells
ppearanceG
3zgZK P2 Egq=1Q IFl @ EF7@I_Q @> E;I>b j<S j> Pgg2> PQ Jzc 3z2 FgQ 9 Cn<; ? EFOt2> 3;O_2> .<`IFg2> MS 3xFFgS 9z02> PQ 9XZ; 3ziD>C4 a><12> @ IF/2>

FormalG
ormall" it is fe$ or a)sent.

InterpretationG
pithelial cells increased $ith gastrointestinal tract irritation FoteG absence of epithelial cells in meconium of newborn may aid in diagnosis of intestinal
obstruction in the newborn. econium is the earliest stools of an infant. nli+e later feces( meconium is composed of materials ingested during the time the infant spends in the uterus: intestinal epithelial cells( ( mucus( amniotic fluid( )ile( and $ater. econium is almost sterile( unli+e later feces( is viscous and stic+" li+e tar( and has no odor .

&igestive state
Starch
ppearanceG
JiG j<S 94 .[F[M2> Jc IF/o 9|4 Cn<S ? P2 @ .F`3FB 53> E2@ @ HT?> @ g[2> 9Q .gX7> 5@31S PQ Izq; .H>I/i2 Fgg2> J1/2> j<i2> dDeS @ J><|G 9 .Fx

FormalG
ormall" found in the stool and graded as () $hen seen under ',.

InterpretationG

ncreased starch in stool ( or ) indicate a case of indigestion.

Fat
ppearanceG
E/|S .6i=_Q ^3ZK> E2 @ J\><FK TCkQ @> JS3/\ TCkQ PQ \3o R><` ^3Xt2> Jc j<xC2> 5@31S PQ Izq; . J23[SI/2> I6y?> j<i2> dDeS UO=`I2> FoteG 0eutral fat globules can be stained with Sudan stain and counted.

FormalG
ormall" found in the stool and graded as () $hen seen under ',.

InterpretationG
$ncreased fat in stool may indicate) ,ancreatic insufficienc" as in pancreatitis due to reduced pancreatic uice secretion. !isorders affect the a)sorption of fats as sprue (celiac disease) and infection $ith *iardia.

Vegetable cells
ppearanceG
._2> 9Q 3F2?34 .F12> .gX7?> 5@31S PQ Izq; Cn<S .;I:_2> 3;O_2> UCn@ >b> .Q3G @ U3:;</2> PF4@ 3z1F4 ;I6=i2 fI/D 3=MS m2C2 U3:;</2> E/|S 3z\> K? ..1FX2> Jc U3:;<4 ]> Cn><S PQ IF4 Io> fIF/o .Fg4

FormalG
ormall" found in the stool and graded as () $hen seen under ',.

InterpretationG
ncreased vegeta)le cells in stool have no clinical significance and considered as residual food.

Muscle fibers
ppearanceG
Pg;@ H>I/2> Jc ID> RJ ]> rQ hi=_S ? @ (aIFkM2> 9 9Q)>@@ FgQ 3zi @ ^<Mi2> 5@31S PQ IzqS ..2<z04 3xI;C[S E{<MiQ

Y=S m2C2 @ JXF/7 ^3X7 9oe; ? E\? muscle fibers JiG ]<=M;? Iz> } 5@> Jc rI2> 5367?> H>I4 .]b3X2> u_|2> 9Q H>I/2> j<;@ .FXF/7 fT<k4 96t2> 9oeFc Iz> } CX4 3Q> absent

FormalG
ormall" found in the stool and graded as () $hen seen under ',.

InterpretationG
ncreased muscle fi)ers in stool have no clinical significance and considered as residual food. FoteG the presence of large amount of undigested meat fibers in the stool may be caused by
pancreatitis. FoteG Some studies ha#e shown an excellent correlation between excessi#e fecal muscle fibers and hypo- or achlorhydria.

ther findings Formal constituents of stoolG

acteria: normall" non pathogenic )acteria are found in the stool and usuall"
)acilli such as Escherichia coli and 1actobacillus sp. FoteG pathogenic bacteria may be found in stool (such as Salmonella, Shigella, and
Staphylococcus aureus and this will leads to pus formation, stool culture can differentiate between pathogenic and non pathogenic bacteria.

east: normall" stool contain harmless "east cells such as blastocystis hominis rystals: normall" stool contain triple phosphate( calcium o#alate and
cholesterol cr"stal due to food ingestion.

i$ers: normall" stool contains man" fi)ers that ma" arise from clothes or
undigested plant food.

ir $u$$les: normall" found and has no clinical significance. il droplets: normall" found( the" are ver" )right and completel" rounded.
FoteG some times oil droplets are muddled with cysts but cysts are not so bright and not so
rounded and if you stain the smear with iodine nucleus of cyst will be seen.

-ndigested food: normall" found( it has man" shapes.

$normal constituents of stoolG

Hematoidin crystals: sometimes found after tract hemorrhage. harcot#eyden crystals : sometimes found in parasitic infestation
(especiall" ame)iasis) and in cases of ulcerative colitis.

arasites
&efinitionsG
edical parasitologyG
he stud" of the parasites of man and their medical conseuences

arasitismG
s an ecological relationship )et$een t$o different organisms( one designated the parasite( the other the host.

HostG
organism har)oring a parasite.

&efinitive or primary hostG

&nimal har)oring the adult or se#uall" mature stage of the parasite.

Intermediate or secondary hostG

&nimal in $hich development occurs )ut in $hich adulthood is not reached.

ife cycleG

or survival and reproduction reasons man" parasites evolve through a num)er of morphologic stages and several environments or different hosts. he seuence of morphologic and environmental stages is referred to as the life c"cle.

Infective stageG
t is a stage in the life c"cle of the parasite that can infect human.

Reservoir hostG
&n animal that har)ors a species of parasite that can )e transmitted to and infect man.

ectorG
an arthropod or other living carrier that transports a pathogenic organism from an infected to a non-infected host.

arrierG
a host that har)ors a parasite )ut e#hi)its no clinical signs or s"mptoms.

oonosisG
a disease involving a parasite for $hich the normal host is an animal( and $herein man can also )e infected.

What are the types of parasites that attack hu*an?

"ctoparasites live outside on the human )od" as common )ed)ugs "ndoparasites live inside the human )od"( e.g. amoe)as( $orms( or flu+es.

What is the difference #et,een parasitic infection and parasitic infestations?

,arasitic infection means that parasite live in host as the case of intestinal parasites $hile parasitic infestations means that parasite live on host as the case of )ed)ugs.

What is the *ode of parasitic infection?

ral-facial ite of vector

&utoinfection %ongenital Se#ual contact ,enetration nhalation

What are the general effects of the parasite on the host?

ating nourishment echanical destruction )struction &llergic reaction Secondar" )acterial infection &nemia &)dominal pain and diarrhea

What is the tests that can #e done to diagnose parasitic infection?

Stool anal"sis urine anal"sis( )lood film( %S e#amination( and serological tests

Classify parasites according to ha#itat?

ntestinal parasites as *iardia lamblia issue parasites as trichenlla spiralis lood parasites as plasmodium malaria rinar" tract parasites as trichomonas #aginalis

What are the co**on types of intestinal parasites that infect hu*an? rotooa
ntame)a histol"tica iardia lam)lia

Helminthes
rematoda Schistosoma mansoni asciola gigantica estoidea aenia solium

aenia saginata '"menolepis nana Fematoda ascaris lum)ericoides strong"loides stercoralis

entro)ius vermicularis

an+"lestoma duodenale

trichuris trichiura

What is the for*s of proto&oa that ca appears in stool? colu)riformis

trichostrang"lus

rophooiteG meta)olicall" active invasive stage. yst: vegetative inactive form resistant to unfavora)le environmental conditions.

What is the for*s of hel*inthes that ca appears in stool?

vaG that is results from se#ual reproduction of helminthes. arvaG the stage that is come from the ova.

ommon uestions
)o, can . pre(ent parasitic infection?
rg=Zg2> ]@CX2 5@s> TCkg2> <x j30\?> ) JIg2> OG <x U3FiF6t234 .43yW> PQ .;3B<i2 9/02> 5@A j> -1 r`>@ T3[G j> J=K Cn<;? E\s FMk2> OXi2 > Cn zQ 9Q3G .43y2 FMk2> uF_|=2> jA Iod\ 31x@ ( RJ r73[2>@ Fi02> uF_|=23c aCK JiG 9F67 92 3D OG Cn<; 94 .FiF6t2> U343yW> rFgn OX2 ]Cg2> . .Q@3[g2> Jc > Cn ^3x CZ\ m2d2 .F/2> L<iS PG =1;@ .MFMy IFl U3`T3gQ ;I7 PG JSe; E\s > Cn 9z` U3FiF6t234 .43yW> j> -2 : YZ; E\A . 3QHO4<0=2>@ .Ft;I|2> j>C;C2> 9Q U343y PQ j30\?> .;3B<2 ( V3g`s>@ ^<Mi2> ) ^3Xt2> Jz7 T3`?> 9Q j>C;C2> PQ IF234 .43yW> PQ j30\?> .;3B<2 ( E7O02> ) 3zioA 9/B > CFn U>@I:_2> 90l . 3/FQs> 9Q >@H<S@I/2>@ . 3/FQs> 3FoA 9gM; ]d2> 34d2> PQ ><`s>@ 5H31g2> Jc ^3Xt2> 6K >@H<S@I/2> @A j>C;C2> @A 3F`T3zi/234 .43yW> PQ j30\?> J[; 3gQ 5</2>@ H>I/234 a3Fg2> Tb3kQ L<iS ^CG

PQ 9[=1S CB J=2> .FiF6t2> >IQs> PQ .;3B<i2 3 FMy .6F2s> U3\><FM2> .;3GT .[;I7 .cIXg2 312> .FG<S . j30\?> J2 j><FM2> .Fk_|2> .c3q12> m2do@ ^3gM2> PQ @I_2> CX4@ 9os> 9/B ]C;s> 90l 9Q .gFi02> .FMk2> U3`T3gg2> m2do .FiF6t2> >IQs34 .43yW> PQ fCFoA .;3B@

Once . ha(e had parasitic infection can . #e re infected?

es there is no long immunit" after parasitic infection.

Can stool analysis detect all parasites?

o it can detect onl" intestinal parasites.

Can a #a#y #eco*e infected ,ith parasites ?

es speciall" protooa from contaminated hands and food.

Can an e*#ryo (fetus) #eco*e infected ,ith parasite?

es for e#ample to#oplasmosis can )e transmitted from mother to here fetus.

Can parasite cause the e/cess in gases that . ha(e?

o( parasites do not cause an" e#cessive gas production.

What is the cause of e/cess in gases in the intestine?

u[\ 3zgxA PQ 9Q><G fCG J2 b<X; wg:z2> H3zZ2> wc U3D36=\ L@CK@ Pt/2> U>H3l j<S 3/`A xA PQ j wc 9o3|Q L@CK@ T>Ig=`34 ^3gM2> J2 @I_2> ^CG @ i[2> @ IS<=2> @ ^3Xt2> :z2 .QHO2> U3g;\W> X4 wc @ fCXg2> wc fC>H .<gK @ j<2<[2> wc U3[[|S @ .;<Xg2> vI[2> @ R3XQs> wc U3;Itc j<S@ w/kX2> j<2<[2> I3kX2> @ ?<2> I@ .GI04 9os> m2do@ w[i=0Q u_|2> @ 9os> 3:;A@ 9os> R31~A R><z2> ri4 @ bI/2> @ fIx2> @ 6i2> @ ^<2> @ 9k/2> @ 9Z62> @ <6ig2> @ j3/ns> @ j3/2s> @ YFiM2> @ 53[SI/2> IFkG @ .;H32> ? .gX7s> ><\A PF4 rgZ2> @ fI4 9os> @ j<4I2> JiG <=Mg2> 9os> U3F2<[/2> ><\A 9o@ 5<62>@ ugM2> . .[F:2> 4Og2> /2 ( Pt/2> .[t1Q wc uDs34 @ jH<2> fb3;H U3;<|12> @ U3;I02> 3 XQ :zS

What is the treat*ent of e/cess in gases or ho, . can a(oid this?

. ^3Xt2> wc `C2> @ ^<Mi2>@ U3F2<[/2> 5@31S PQ 9Fi[=2> . U<;2> @ w23[g2>@ 2><g2> @ UOi_g2> 5@31S PQ 9Fi[=2> .IFnIZ2> @ 9Z62> 5@31S PQ 9Fi[=2> . PFDC=2> PG OBW> .U3;<iM2> @ w23[g2> 9Q fCXg2> .<gK C;S w=2> UOos> PG b3X=4W> . ^<12> 9/B 9os> Y1ZS @ .g_=2> PG b3X=4W> . 0Z2> .cCS fT@I@ bI/234 .43y?> Y1ZS . r3n 02 \A @ ^3Xt2> 9oA ^CG .1 .2 .3 . ..} .7 .8

.> CFn <ztQ IF2> 9os> PG b3X=4W> . .:g2> R31~A R><z2> ri4 Y1ZS .1 ..cI[2> @ j<0\3F2> @ j<g2> I .11 .U>H32> u=gS :gi2 >IB> ^>C_=`> .12 2hew tablets as luftal or acti#ated charcoal as ultra carbon tablets

Are there are any parasite (accines?

here are successful vaccination programs against viral and )acterial diseases( )ut unfortunatel"( progress to$ards parasite vaccines has )een slo$. his limited progression is due in part to the multi-factorial immune response to parasite infection( parasite immune avoidance strategies and the comple# nature of parasite antigens. 'o$ever( in recent "ears molecular )iolog" research has identified and produced ne$ protective recom)inant antigens for vaccine trials. !& )ased vaccination has also )een successful in trials.

)o, parasites can #e treated?

ost protooa can )e treated )" metronidaole (flag"l or fasig"m). ost helminthes can )e treated )" vermiole. 9=[S ?@ j>C;C2> 9=[S 3z\? m2@ Iz CX4 ~ PFG</`> CX4 TIS ~ ^3;> 3 .GIZ2> dDS j>C;C2> .23K Jc : E{<MiQ .j>C;C2> nID> U3BIF2> j<S J=K fCQ CX4 JtXS m2d2 @ U3BIF2>

Why ,e need to count parasitic egg?

t is used to determine the intensit" of infection.

)o, ,e can count parasitic egg?

he simplest and most effective method for determining the num)er of eggs per gram of stool is the McMaster counting techni0ue

rocedure
1) Weigh 2) 3) ) -) }) 7) g of faeces and place into container. &dd -} ml of saline. i# the contents thoroughl" $ith a stirring device. ilter the faecal suspension. a+e a sample $ith pasture pipette. ill the )oth slides of the counting cham)er $ith the samples &llo$ the counting cham)er to stand for - minutes.

8) #amine the sample of the filtrate under a microscope. ) %ount all eggs $ithin the engraved area of )oth cham)ers. 1) he num)er of eggs per gram of faeces can )e cal calculated as follo$: &dd the egg count of the t$o cham)ers together ultipl" the total )" -. his gives the e.p.g. of faeces.

What are the i*itations of stool e/a*ination in the diagnosis of gastro-intestinal parasites?
1. he demonstration of parasite eggs or larvae in the stool provides positive evidence that an animal is infected )ut does not indicate the degree of an infection. 2. he failure to demonstrate eggs or larvae does not necessaril" mean that no parasites are present the" ma" )e present in an immature stage or the test used ma" not )e sufficientl" sensitive. 3. arious factors can limit the accurac" and significance of a stool egg count. here is a fairl" regular fluctuation in faecal egg output. ggs are not evenl" distri)uted throughout the faeces. he uantit" of faeces passed $ill affect the num)er of eggs per unit $eight. he egg output is influenced )" the season of the "ear (large infections ma" )e acuired during rain" seasons). ggs ma" not )e detected due to lo$ num)ers of them or to a lo$ test sensitivit".

ommon diseases of I
Hemorrhoid
'emorrhoids or piles are varicosities or s$elling and inflammation of veins in the rectum and anus.

auses
ncreased straining during )o$el movements( )" constipation or diarrhea( ma"

lead to hemorrhoids t is a common condition due to constipation caused )" $ater retention in $omen e#periencing menstruation. '"pertension( particularl" portal h"pertension( can also cause hemorrhoids )ecause of the connections )et$een the portal vein and the vena cava $hich occur in the rectal $all -- +no$n as portocaval anastomoses.
)esit" can )e a factor )" increasing rectal vein pressure.

Sitting for prolonged periods of time can cause hemorrhoids.

,regnanc" causes h"pertension and increases strain during )o$el

movements( so hemorrhoids are often associated $ith pregnanc". #cessive consumption of alcohol or caffeine can cause hemorrhoids. FoteG caffeine ingestion increases blood pressure transiently, but is not thought to cause
chronic hypertension. "lcohol can also cause alcoholic li#er disease leading to portal hypertension.

Symptoms
'emorrhoids usuall" are not dangerous or life threatening. n most cases( hemorrhoidal s"mptoms $ill go a$a" $ithin a fe$ da"s.

 &lthough man" people have hemorrhoids( not all e#perience s"mptoms. he most common s"mptom of internal hemorrhoids is )right red )lood covering the stool. an internal hemorrhoid ma" protrude through the anus outside the )od"( )ecoming irritated and painful. his is +no$n as a protruding hemorrhoid. S"mptoms of e#ternal hemorrhoids ma" include painful s$elling or a hard lump around the anus that results $hen a )lood clot forms. his condition is +no$n as a throm)osed e#ternal hemorrhoid. microc"tic h"pochromic anemia occurs due to chronic )leeding.

reatments
or man" people( hemorrhoids are mild and temporar" conditions that heal spontaneousl". here is no medicine that $ill cure hemorrhoids( )ut local treatments such as topical analgesic( can provide temporar" relief. n the case of e#ternal hemorrhoids $ith a visi)le lump of small sie( the condition can )e improved $ith $arm )ath causing the vessels around rectal region to )e rela#ed. ating fruit helps avoid conditions that lead to hemorrhoids. ating fi)er-rich )ul+ing agents to help create a softer stool that is easier to pass( to lessen the irritation of e#isting hemorrhoids. !urgical treat*ents Some people reuire the follo$ing medical treatments for chronic or severe hemorrhoids: u))er )and ligation lastic )ands are applied onto an internal hemorrhoid to cut off its )lood suppl". Within several da"s( the $ithered hemorrhoid is sloughed off during normal )o$el movement. 'emorrhoidol"sisalvanic lectrotherap" !esiccation of the hemorrhoid )" electrical current. Sclerotherap" (in ection therap") 'ardening agent is in ected into hemorrhoids. his causes the vein $alls to collapse and the hemorrhoids to shrivel up. 'emorrhoidectom" & true surgical procedure to e#cise and remove hemorrhoids. an"

patients complain that pain during recover" is severe. or this reason is often no$ recommended onl" for severe hemorrhoids.

nal fissure
&nal fissure is a crac+ or tear in the anus s+in. &s a fissure( these tin" tears ma" sho$ as )right red rectal )leeding and cause severe periodic pain after defecation.

auses
ost anal fissures are caused )" stretching of the anal mucosa )e"ond its capa)ilit". &nal fissures are common in $omen after child)irth follo$ing e#cessive anal intercourse after difficult )o$el movements and in infants follo$ing constipation.

revention
reating constipation )" eating food rich in dietar" fi)er( avoiding caffeine

($hich can increase constipation) ( drin+ing a lot of $ater and ta+ing stool softener.
reating diarrhea.

&voiding straining or prolonged sitting on the toilet. eeping the anus dr" and h"gienic.

reatment
reatment included $arm )aths( topical anesthetics( stool )ul+ing agents( mechanical anal stretching( and( sometimes( surger". sphincteroto*y ,ainful deep chronic fissures( on the other hand( $ill not heal )ecause of poor )lood suppl" caused )" sphincter spasm. Surgical intervention ma" )e reuired for persisting deep anal fissures.

$structive aundice
aundice( also +no$n as icterus is "ello$ish discoloration of the s+in( sclerae ($hites of the e"es) and mucous mem)ranes caused )" h"per)iliru)inemia.

Post-hepatic 1aundice ,ost-hepatic aundice( also called o)structive aundice( is caused )" an interruption to the drainage of )ile in the )iliar" s"stem. he most common causes are gallstones in the common )ile duct( and pancreatic cancer in the head of the pancreas. &lso( a group of parasites +no$n as liver flu+es live in the common )ile duct( causing o)structive aundice. ther causes include strictures of the common )ile duct( )iliar" atresia(

at mala$sorption
ala)sorption is a state arising from a)normalit" in digestion or a)sorption of food nutrients across the gastrointestinal () tract. at mala)sorption is characteried )" a)normal fecal e#cretion of fat (steatorrhea) and varia)le mala)sorption of fats and fat solu)le vitamins.

auses
o$el mucosal damage acterial and viral infections ,arasites infections e. g. *iardia lamblia nsufficient concentrations of digestive en"mes !rug induced

&iarrhea
!iarrhea( also spelled diarrhoea( is freuent loose or liuid )o$el movements.

auses
!iarrhea is most commonl" caused )" viral infections( parasites or )acterial

to#ins. !iarrhea can also )e a s"mptom of more serious diseases( such as d"senter"( cholera( or )otulism( and can also )e indicative of a chronic s"ndrome such as %rohns disease. !iarrhea can also )e caused )" dair" inta+e in those $ho are lactose intolerant.

ypes of diarrhea
Secretory diarrhea Secretor" diarrhea means that there is an increase in the active secretion( or there is an inhi)ition of a)sorption. he most common cause of this t"pe of diarrhea is a cholera to#in that stimulates the secretion of anions( especiall" chloride ions. smotic diarrhea smotic diarrhea occurs $hen too much $ater is dra$n into the )o$els. his can )e the result of maldigestion (e.g.( pancreatic disease or %oeliac disease)( in $hich the nutrients are left in the lumen to pull in $ater. n health" individuals( too much vitamin % or undigested lactose can produce osmotic diarrhea and distention of the )o$el. otility#related diarrhea otilit"-related diarrhea is caused )" the rapid movement of food through the intestines (h"permotilit"). f the food moves too uic+l" through the tract( there is not enough time for sufficient nutrients and $ater to )e a)sor)ed. his can )e due to a dia)etic neuropath"( as a complication of menstruation or '"perth"roidism $hich can produce h"permotilit". Inflammatory diarrhea nflammator" diarrhea occurs $hen there is damage to the mucosal lining or )rush )order( $hich leads to a passive loss of protein-rich fluids( and a decreased a)ilit" to a)sor) these lost fluids. t can )e caused )" )acterial infections( viral infections( parasitic infections( or autoimmune pro)lems such as inflammator" )o$el diseases.

reatment
n man" cases of diarrhea( replacing lost fluid and salts is the onl" treatment needed. edicines that are availa)le $ithout a doctors prescription include aopectate and strepto+eine. ID; m2 j? fI3/Q ( >Cn C;C j3o >> ?> )53z`?> pB<S .;@b> 53z`?> ;IQ dDe; j> et_2> PQ : E{<MiQ En@ID ^CG @ R3XQ?> Jc Y/0g2> 9Q3X2> H3Z=K34 Ig2> PQ R36|2> Ic PQ

constipation
%onstipation( is a condition of the digestive s"stem in $hich a person e#periences hard feces that are difficult to e#pel. his usuall" happens )ecause the colon a)sor)s too much $ater from the food.

symptoms
n common constipation( the stool is hard( difficult( and painful to pass. suall"( there is an infreuent urge to void. the a)domen ma" )ecome distended ( tender and cramp"( occasionall" $ith enhanced )o$el sounds

complication
Straining to pass stool ma" cause hemorrhoids and anal fissures( $hich are painful in themselves. &lso constipation can lead to headache and testicular varices.

auses
he main causes of constipation include: 'ardening of the feces mproper mastication (che$ing) of food nsufficient inta+e of dietar" fi)er inadeuate fluid inta+e edication( e.g. diuretics and those containing iron( calcium( aluminum slo$ed transit( $here peristaltic action is diminished or a)sent( so that feces are not moved along '"poth"roidism '"po+alemia edications( such as( opioids (e.g. codeine morphine) ( certain tric"clic antidepressants and cough drugs. *ead poisoning %onstriction( $here part of the intestine or rectum is narro$ed or )loc+ed( not allo$ing feces to pass Smo+ing cessation (nicotine has a la#ative effect) irregular )o$el ha)it

reatment
reventionG !rin+ing orange uice. !iet rich in fi)ers as vegeta)les and fruit and $hole meal )read ncrease the inta+e of fluids (prefera)l" $ater) Wal+ing to facilitate )o$l movement o coffee or tea. edicationsG *a#atives as apila#in( la#in and cisapride. FoteG Enemas can be used to pro#ide a form of mechanical stimulation. 3owe#er, enemas
are generally useful only for stool in the rectum, not in the intestinal tract.

spastic colon
n gastroenterolog"( irrita)le )o$el s"ndrome (S) is a functional )o$el disorder characteried )" a)dominal pain( discomfort or )loating relieved )" defecation and alteration of )o$el ha)its. !iarrhea or constipation ma" predominate( or the" ma" alternate (classified as S-!( S-% or S-&( respectivel").

Symptoms
he primar" s"mptoms of S are a)dominal pain or discomfort in association $ith freuent diarrhea( constipation( or a change in )o$el ha)its. here ma" also )e urgenc" for )o$el movements( a feeling of incomplete evacuation (tenesmus)( )loating or a)dominal distention.

auses
nitiall"( S $as considered a ps"chosomatic illness )ut ne$ evidences sho$ that organic factors contri)ute for the disease such as immune reaction and infections.

reatment
Initial treatments

edications ma" consist of stool softeners and la#atives in constipationpredominant S( and antidiarrheals in diarrhea-predominant S. ntispasmodics he use of antispasmodic drugs (e.g. colospasmine and li)ra#) ma" help patients( especiall" those $ith cramps or diarrhea. &rugs affecting serotonin !rugs affecting serotonin (--') in the intestines can help reduce s"mptoms. 88 Serotonin stimulates the gut motilit" and so agonists can help constipation predominate irrita)le )o$el $hile antagonists can help diarrhea predominant irrita)le )o$el:

rohns disease
%rohns disease (also +no$n as regional enteritis) is a chronic( episodic( inflammator" )o$el disease (!) and is generall" classified as an autoimmune disease. t can affect an" part of the gastrointestinal tract from mouth to anus

Symptoms
an" people $ith %rohns disease have s"mptoms for "ears prior to the diagnosis. he usual onset is )et$een 1- and 3 "ears of age )ut can occur at an" age. astrointestinal symptoms
&)dominal pain ma" )e the initial s"mptom of %rohns disease. he pain is

commonl" cramp-li+e and ma" )e relieved )" defecation. t is often accompanied )" diarrhea( $hich ma" or ma" not )e. ,erianal discomfort ma" also )e prominent in %rohns disease. tchiness or pain around the anus ma" )e suggestive of inflammation. he mouth ma" )e affected )" non-healing sores (aphthous ulcers). Systemic symptoms

%rohns disease( li+e man" other chronic( inflammator" diseases( can cause a variet" of s"stemic s"mptoms. &mong children( gro$th failure is common. &mong older individuals( %rohns disease ma" manifest as $eight loss. his is usuall" related to decreased food inta+e( since individuals $ith intestinal s"mptoms from %rohns disease often feel )etter $hen the" do not eat and might lose their appetite. "xtra intestinal symptoms n addition to s"stemic and gastrointestinal involvement( %rohns disease can affect man" other organ s"stems. nflammation of the interior portion of the e"e( +no$n as uveitis( can cause e"e pain( especiall" $hen e#posed to light. nflammation ma" also involve the $hite part of the e"e (sclera)( a condition called episcleritis. oth episcleritis and uveitis can lead to loss of vision if untreated. %rohns disease is associated $ith inflammation of one or more oints (arthritis).

omplications
%rohns disease can lead to several mechanical complications $ithin the intestines( including o)struction( and a)scesses. )struction t"picall" occurs from strictures or adhesions $hich narro$ the lumen( )loc+ing the passage of the intestinal contents. %rohns disease also increases the ris+ of cancer in the area of inflammation.

ause
he e#act cause of %rohns disease is un+no$n. 'o$ever( environmental and genetic factors have )een invo+ed in the pathogenesis of the disease. utations in the %&!1- gene (also +no$n as the !2 gene) are associated $ith %rohns disease.

lood tests for rohns disease

& complete )lood count ma" reveal anemia( $hich ma" )e caused either )" )lood loss or vitamin 12 deficienc".

 r"throc"te sedimentation rate( or S( and %-reactive protein measurements can also )e useful to gauge the degree of inflammation. esting for anti-neutrophil c"toplasmic anti)odies (&%&) has )een evaluated to identif" inflammator" diseases of the intestine and to differentiate %rohns disease from ulcerative colitis.

reatment
%urrentl" there is no cure for %rohns disease reatment for %rohns disease is onl" $hen s"mptoms are active and involve first treating the acute pro)lem( then maintaining remission. &cute treatment uses medications to treat an" infection (normall" anti)iotics) and to reduce inflammation (normall" aminosalic"late anti-inflammator" drugs and corticosteroids). When s"mptoms are in remission( treatment enters maintenance $ith a goal of avoiding the recurrence of s"mptoms.

-lcerative colitis
lcerative colitis is a form of inflammator" )o$el disease (!)( a disease of the intestine( specificall" the large intestine or colon( that includes characteristic ulcers( or open sores( in the colon.

auses
While the cause of ulcerative colitis is still un+no$n( several( possi)l" interrelated( causes have )een suggested: enetic factors & genetic component to the etiolog" of ulcerative colitis can )e h"pothesied )ased on the aggregation of ulcerative colitis in families. "nvironmental factors an" h"potheses have )een raised for environmental contri)utions to the pathogenesis of ulcerative colitis. nclude the follo$ing:

 the colon is e#posed to man" dietar" su)stances $hich ma" encourage

inflammation. & diet lo$ in fermenta)le dietar" fi)er ma" affect ulcerative colitis incidence. utoimmune disease Some sources list ulcerative colitis as an autoimmune disease.

linical presentation
I symptoms he clinical presentation of ulcerative colitis depends on the e#tent of the disease process. ,atients usuall" present $ith diarrhea mi#ed $ith )lood and mucus( of gradual onset. he disease is usuall" accompanied $ith different degrees of a)dominal pain( from mild discomfort to severel" painful cramps.

"xtra intestinal features &s ulcerative colitis is a s"stemic disease( patients ma" present $ith s"mptoms and complications outside the colon. hese include the follo$ing: aphthous ulcers of the mouth ritis or uveitis( $hich is inflammation of the iris &n+"losing spond"litis( arthritis of the spine r"thema nodosum( $hich is inflammation of su)cutaneous tissue involving the lo$er e#tremities &utoimmune hemol"tic anemia

complications
-lcerative colitis and colorectal cancer here is a significantl" increased ris+ of colorectal cancer in patients $ith ulcerative colitis after 1 "ears. rimary sclerosing cholangitis

lcerative colitis has a significant association $ith primar" sclerosing cholangitis (,S%)( a progressive inflammator" disorder of small and large )ile ducts.

reatment
Standard treatment for ulcerative colitis depends on extent of in#ol#ement and disease se#erity. he goal is to induce remission initiall" $ith medications( follo$ed )" the administration of maintenance medications to prevent a relapse of the disease. &rugs used
&minosalic"lates as sulfasalaine %orticosteroids as prednisone

mmunosuppressive drugs as aathioprine Surgery nli+e %rohns disease( ulcerative colitis can generall" )e cured )" surgical removal of the large intestine. Surger" is indicated for patients $ith severe colitis or patients $ith s"mptoms that are disa)ling and do not respond to drugs.

&yspepsia
!"spepsia (ndigestion) is a medical condition characteried )" indigestion $ith chronic or recurrent pain in the upper a)domen( upper a)dominal fullness and feeling full earlier than e#pected $ith eating. t can )e accompanied )" )loating( )elching( nausea or heart)urn.

symptoms
he characteristic s"mptoms of d"spepsia are upper a)dominal pain( )loating( fullness and tenderness on palpation. FoteG /ain worsened by exertion and associated with nausea and sweating may also indicate
angina.

causes

over eating spic" food too fast eating

 alcohol drug eat stress

reatment
!rugs that facilitate digestion as &mrae or digestin. ,roton pump inhi)itors (,,s)( $hich are effective for the treatment of heart)urn.

sprue (celiac disease)

%oeliac disease ( also spelled celiac disease( and it has several other names( including: non-tropical sprue( endemic sprue( gluten enteropath" or glutensensitive enteropath"( and gluten intolerance( it is an autoimmune disorder of the small intestine that occurs in geneticall" predisposed people of all ages.

Symptoms
nclude chronic diarrhea( failure to thrive (in children)( and fatigue.

ause
%oeliac disease is caused )" a reaction to gliadin( a gluten protein found in $heat. pon e#posure to gliadin( the en"me tissue transglutaminase modifies the protein( and the immune s"stem cross-reacts $ith the )o$el tissue( causing an inflammator" reaction. hat leads to flattening of the lining of the small intestine (called villous atroph"). his interferes $ith the a)sorption of nutrients )ecause the intestinal villi are responsi)le for a)sorption.

reatment
he onl" effective treatment is a lifelong gluten-free diet.

chlorhydria
&chlorh"dria and h"pochlorh"dria refer to states $here the production of gastric acid in the stomach is a)sent or lo$( respectivel".

Symptoms
he decreased acid level itself causes fe$ s"mptoms( )ut lo$ acid levels in the stomach are lin+ed $ith )acterial overgro$th (as the stomach does not +ill

micro)es normall" present in food)( $hich can manifest as diarrhoea or decreased a)sorption of nutrients or vitamins.

auses
&utoimmune disorders $here there is anti)od" production against parietal cells

$hich normall" produce gastric acid. he use of antacids or drugs that decrease gastric acid production & s"mptom of 3elicobacter pylori infection $hich neutralies and decreases secretion of gastric acid to aid its survival in the stomach.