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.
External anal sphincter (voluntary control), voluntary relaxation
results in defecation

4. Defecation:
External anal sphincter opens
Intra-abdominal pressure increases with and stool moved out

What are the results of chronically ignoring urge to defecate?

Sensory receptor reflex arc less responsive
Stool collects in distal colon
Stool desiccates and worsens Constipation

What is the stool analysis test?

A stool analysis is a series of tests done on a stool (feces) sample to help

diagnose certain conditions affecting the digestive tract.

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Why It Is Done

Help identify diseases of the digestive tract, liver, and pancreas.

Help find the cause of symptoms affecting the digestive tract, including
prolonged diarrhea, bloody diarrhea, an increased amount of gas,
nausea, vomiting, loss of appetite, bloating, abdominal pain and
cramping, and fever.
Look for intestinal parasites.
Look for the cause of an infection, such as bacteria, a fungus, or a virus.
Check for poor absorption of nutrients by the digestive tract
(malabsorption syndrome).

‫ل ا راز؟‬ ‫صاذن طب ماط ب‬ ‫ن ھم ا‬

1. Patient with abdominal pain or abdominal discomfort
2. Patient with diarrhea
3. Patient with anemia
4. Patient who is too thin or do not grow well
5. Patient with stool color that is changed to abnormal color

Stool sampling

‫رض‬ ‫ظت‬
‫دث ا ط‬ ‫اا راز‬ ‫ل ا ول أو ل أ د‬ ‫ط ل‬ .1
‫دم أداه (ل‬ ‫* ب (ل ا 'دوى أو ا‬ ‫" ك ' ا راز‬%‫( ل ا‬gloves) ‫د "ن ار داء زات‬ .2
‫ او ء‬- '‫ا‬
(toilet bowl)‫ا راز "ن دة ا " م‬ ‫ ذ‬/ .3
‫ ون‬2 ‫" ء أو ا‬ ' ‫ط ا‬1 .4
' ‫ ل د ك * دا 'د أ د ا‬3‫ا‬ .5

Note:: There is no pain while collecting a stool sample, but if you are constipated, straining to
pass stool may be painful.

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 ‫ل‬ ‫ظت‬

‫ "ن ا راز‬- 4 "4 ‫د "ن أ د‬ .1

5 "* 1 ‫د "ن و*ود و ء ظ ف‬ .2
( ‫ل‬ ‫لا ص‬ ‫ و‬1 ‫طوار ا ط‬8‫"وت ا‬ ) ‫ رة‬4 "‫ ا ' "دة ز‬1 ‫"ر‬ .3

Note:: Exposing the stool sample to air or room temperature will affect the test result.

(‫ ر‬4‫ت ا‬ ‫ ت و ا و‬1 ‫ ظ=ور ا ط‬2‫ر‬- ‫ ل و‬1 ‫ طوال ا‬5"*" ‫ ل ) ن ا راز ھ‬-8‫ر ھ; ا‬4 ‫ ح ا‬2 ‫ا‬ .4
‫طوار ا >ط‬8‫ = ( ل ا‬8 ‫ط ل‬8‫ د ا‬2 ‫"را ة دم ا ط ا ول راز‬ .5
/‫ ل ?م ا > ص ط‬1 ‫ون ا‬4 ‫"را ة دم ا ط ا راز دم د ا ء أ? ء ا دورة ا >=ر‬ .6
'>8‫ل و" ن 'د ا‬ B 2 '>‫ض ا ' "ن ا > ص ا ذي أ*رى أ‬-‫ر‬ .7
.8
Note:: sample rejected from patient recently had an X-ray test using barium contrast material,
such as a barium enema
. ‫* >رب ا " رز‬ ‫ ن ا راز * ف‬4 ‫ض إذا‬-‫ت ر‬ ‫ ا‬- ‫ط ل‬8‫ا‬ .9

Note:: 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.

:‫ ل "?ل‬1 ‫ل أ*راء ا‬ '" ‫دو ا‬8‫*ب ا " ع ن أ د 'ض ا‬ .10

Antacids, antidiarrheal medications, antiparasite medications, antibiotics, enemas,

and laxatives

‫با‬ = ‫ا راز د "ن إ ط ر ا "'"ل = وا ؤال‬ 1 ‫ا ذ أى أدو ؤ?ر‬ - .11

‫ا راز‬ 5 "* ‫ ت د‬1" ‫ ا 'د ن ا دام ا‬.12
. ‫; ا و ء‬1 ' ‫ ب ا‬2 ‫ ت‬5 ‫ *ب و‬.13
‫ل‬1 ً'"‫ن‬ ‫ رة ز د ن ا‬- - ‫ل إ ط ء ا ' إ ا "'"ل‬ ‫رج ا "'"ل‬ ' ‫ إذا أ ذت ا‬.14
‫ ت‬1 ‫'ض ا ط‬
‫ر م أو ز دي‬4 1 - ‫ ت‬4 ‫ت ا راز "ن رج ا "'"ل إذا‬ ‫(ل‬ .15

Note:: Sometimes a stool sample is collected using a rectal swab that contains a preservative
(if patient is unable to give stool). The swab is inserted into the rectum, rotated gently, and then
withdrawn. It is placed in a clean, dry container and sent to the lab right away.

‫وظ‬

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 ‫‪"- ،‬ن ا "'روف أ ‪"14‬‬ ‫ص وطر ( ر‪ 4‬ز ا '‬ ‫أھم "ل ‪ - -‬ص ا راز ھو رة ا ‪ ;J 2‬ا ذي (وم‬
‫‪4‬ون ‪ 4 "14‬ن‬ ‫ط أو ‪ 4‬ن ا ط ل ‪-‬‬ ‫‪ 4‬ت ا‪> 2%‬د دة ‪= "14‬ل ا > ص و‪ 4 "14‬ت ا‪2%‬‬
‫رة أ‪ 4‬ر ‪.‬‬ ‫ا > ص أ‪'2‬ب و ج إ‬

‫وظ‬
‫وا دة‬ ‫ث أن ا‪ " 8‬د ‪1‬‬ ‫ت راز ‪ 1‬ا‪ 8‬ل ‪ ? ? -‬أ م "‬ ‫أ? ت ا‪ 8‬ث أ *ب ‪ -‬ص ? ?‬
‫م ‪ -‬ط‪ /‬ا "'"ل وإذا‬ ‫‪(-‬ط ‪ 4‬وذ ك ز دة ا ر‪ - 2‬رؤ ا ط ‪ 1‬ت و ل ? ? "' "ل " ‪1‬‬
‫ل أن رى ا ' ت أ‪?4‬ر "ن > ص‪.‬‬ ‫‪ 4‬ن ا ص م ‪ -‬س ا "'"ل‬

‫ز ن " ! ا راز‬
‫ل ‪ -‬ص ا ' ‪ -‬ا ل وذ ك ز دة ا ر‪ 2‬رؤ ا‪8‬طوار ا >ط ل "و =‬ ‫‪-1‬‬
‫ره ) ر ب( أو ?م زن ? * د در* ‪J" 4‬و‬ ‫إذا ‪ 4‬ن رورة ز ن ا راز ‪ -‬م‬ ‫‪-2‬‬
‫ا راز أ‪?4‬ر "ن أ وع ‪ -‬ا ? * و ا ور" ن ‪-‬ظ‬ ‫"‪4‬ن ا '" ل " ‪1‬ول ‪-‬ور" ن ‪ %40‬ظ‬ ‫‪-3‬‬
‫‪ 1‬ا‪8‬طوار ا " و‪. 12‬‬
‫ظ ا ' ت ‪-‬ظ ‪ 1‬ا‪8‬طوار ا " و‪ 12‬و ا >ط "' ‪.‬‬ ‫ا دام ا ‪ 4‬ول ‪-‬‬ ‫‪-4‬‬
‫ل ا‪8‬طوار ا >ط‬ ‫دث * ف ‪ '1‬ؤدى إ‬ ‫‪=1‬واء‬ ‫* ب رك ‪4‬وب ا ' "'ر‬ ‫‪-5‬‬
‫‪1‬وث ا ' ط ‪ 1‬ت ا *و ا ر*;) ‪coprozoic‬‬ ‫)‪ (trophozoite‬و ا ر ت)‪ (larva‬و‬
‫‪.(protozoa‬‬

‫‪ $‬ر " !‪ #‬ا راز‬ ‫طرق‬

‫‪ $‬ر ا !‪:#‬‬ ‫"!د‬ ‫!* )( ھ‬
‫‪ /‬ص‬ ‫ا‪ +‬م‬ ‫‪0!1 0‬‬ ‫ل‬ ‫ل‬ ‫ص ا ذي ‪+ ,‬وم‬
‫‪$/‬ل أن م ا ‪ $‬ر وا‪,‬ط‪ #‬ا‬ ‫‪.1‬‬
‫ا ظ ھرى أ‪ !1‬ء ا ‪ $‬ر‪.‬‬
‫إذا زر ذ ك ‪ 7‬د ن ‪,‬ؤال ن ‪$‬ر ا !‪" #‬ن ‪5‬ل ا ! ت ا *‪ / #‬ص ا ظ ھرى‪0‬‬ ‫‪.2‬‬
‫م ‪ $‬ر ا !‪ 0< #‬أ‪,‬رع و‪:‬ت ‪1‬م ز ! <‪ 0‬ا ‪ #= 1‬د ذ ك إذا م ‪ /‬ص <‪ 0‬ا ل‪.‬‬ ‫‪.3‬‬
‫إذا ‪ 5‬ن !‪ #‬ا راز أى >ء ? ر ط > ‪ 5‬دم ‪ 1‬أو *د د أو ط ‪$/‬ل < ص ذ ك ا =زء ن‬ ‫‪.4‬‬
‫ا !‪ #‬أو‪ 7‬ت ا ‪5‬رو‪5,‬وب ‪ :‬ل ا دء <‪ $ 0‬ر ا !‪.#‬‬

‫‪Preparation methods‬‬
‫‪Direct smear‬‬
‫‪Concentration technique‬‬
‫‪Sedimentation method‬‬
‫‪Saline sedimentation Tech.‬‬
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 ‫‪Formal Ether Concentration Tech.‬‬
‫‪Floatation method‬‬
‫‪Kato technique‬‬

‫‪Direct smear‬‬

‫ا طر ‪+‬‬
‫ت‬ ‫ول ا ( ‪1‬م ا< *‬ ‫ن‬ ‫@ !‪+‬ط‬ ‫ز=‬ ‫‪: @$ .1‬ط ‪ B* #‬رة ن ا راز " ‪ 0‬ر !ظ ‪ /‬و ا‬
‫ا ‪5‬رو‪5,‬وب ‪ ,‬د ا د‪1 10 ,‬م ا د‪40 ,‬‬
‫دء ‪ /‬ص ھدا ا =زء‬ ‫! =زء دم او *د د او ط =ب ا‬ ‫‪ .2‬ادا ‪ 5‬ن‬
‫ء‬ ‫ء ا د‪ + :‬او ا‪7‬‬ ‫‪ 7‬ل و=ود ط‪ /‬ت ‪7‬‬ ‫‪= .3‬ب < ص " !‪ #‬ن ‪,‬ط( ا راز و " ! ن دا‬
‫ا‪ B‬ظ‬
‫‪5‬ن ا ود ‪ +‬ل ا طور ا ! ط < ذ ك ا< ص‬ ‫و*‬ ‫‪5 .4‬ن ا‪ ,‬دام ا ود * ‪ C‬ا !‪ #‬رؤ ‪ #‬ا‪7‬طوار ا‬
‫دون ا ود او‪7‬‬

‫ا زات‬
‫ت‬ ‫ط‪/‬‬ ‫و*‬ ‫ا طر ‪ # , #+‬و‪,‬ر ‪ #‬و ‪ ,‬دم أ‪ / , ,‬ص ا‪ 57‬س ا‬

‫ا وب‬
‫<‪/‬ر*‬ ‫و ‪! 5‬ت ا"داد ا ط‪ /‬ت <‪ 0‬ا ! ‪:‬‬ ‫ط‪ /‬ل د ده ا‬ ‫ج ان ‪5‬ون ا‪*7‬‬ ‫طر ‪ ? +‬ر د‪ + :‬و‬
‫ده ا طر ‪= / $ +‬دا‬ ‫رؤ‬

‫‪Concentration technique‬‬

‫‪Sedimentation method‬‬

‫‪Saline sedimentation Tech.‬‬

‫ا طر ‪+‬‬
‫‪ .1‬ؤ ذ ‪:‬ط ‪ #‬ن ا راز و و‪5 >< @$‬وب !ظ ف ‪1‬م ‪ $‬ف ول ا ( ا ‪ 0‬ا ‪5‬وب‪.‬‬
‫‪ + .2‬ب ا راز <> ا ول = دا‪.‬‬
‫ش او ?ط ء ا ‪5‬وب‪.‬‬ ‫‪ >/* .3‬ا راز <‪ 0‬ا! و ‪ ,‬دام ‪:‬ط‬
‫دة ‪ 30 – 20‬د‪.#+ :‬‬ ‫‪ .4‬رك ا‪ !7‬و‬
‫‪5‬رو‪5,‬وب‬ ‫‪ / .5‬ص ا را‪,‬ب‬
‫‪5‬ن ا‪ ,‬دام ا ‪ !,‬ر< وج دو ر ا ! و ا ‪,‬ر @ ن ا ر‪ ,‬ب ‪5‬ن ا دو ر ا ‪+‬وى ‪5‬ن ان ؤدى ا ‪0‬‬ ‫وظ‬
‫‪ ,5‬ر =دار ا و ‪ $‬ت و ا ر‪ :‬ت‪.‬‬

‫ا زات‬
‫‪1‬ل‪:‬‬ ‫‪ 0‬ر‪,‬ب <‪ : 0‬ع ا‪ !7‬و‬ ‫ول ا ( و‬ ‫ت ا‪+17‬ل وز! ن‬ ‫! ‪ # ,‬ط‪/‬‬ ‫ھده ا طر ‪+‬‬
‫‪Ascaris‬‬
‫‪Shistosoma mansoni‬‬
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 ‫‪Fasciola‬‬
‫‪Strongyloides stercoralis‬‬
‫ا وب‬
‫‪ @ = ( * 7‬ا ط‪ /‬ت !‪/‬س ا ‪ /5‬ءه‬

‫‪Formal ether concentration Tech.‬‬

‫ا طر ‪+‬‬
‫ول ا ( ا ‪ 0‬ا ‪5‬وب‪.‬‬ ‫ؤ ذ ‪:‬ط ‪ #‬ن ا راز و و‪5 >< @$‬وب !ظ ف ‪1‬م ‪ $‬ف‬ ‫‪.1‬‬
‫‪ +‬ب ا راز <> ا ول = دا‪.‬‬ ‫‪.2‬‬
‫ش او ?ط ء ا ‪5‬وب‪.‬‬ ‫*‪ >/‬ا راز <‪ 0‬ا! و ‪ ,‬دام ‪:‬ط‬ ‫‪.3‬‬
‫دور ا‪ !7‬و <> ا ‪ !,‬ر< وج دة د‪ #+ :‬وا دة‪.‬‬ ‫‪.4‬‬
‫دة د‪ #+ :‬أ ري‬ ‫إذا ‪ 5‬ن ا ‪) ,‬ل ا وي زال ‪5‬ر ‪ $‬ف ول ا ( أ‪15‬ر ن رة و دور ا‪ !7‬و‬ ‫‪.5‬‬
‫‪ ( * 0‬ا ‪) ,‬ل ا وي را)‪. +‬‬
‫‪5, .6‬ب ا ‪) ,‬ل ا را)ق و رك ا را‪,‬ب <> ا ! و ‪.#‬‬
‫‪ $ .7‬ف ول ا ‪/‬ور ن إ > ا را‪,‬ب ! و ‪ #‬و زج = د و رك دة ‪ 5‬د‪) :‬ق‪.‬‬
‫‪ $ .8‬ف ا ‪ 1‬ر و ‪ B‬ق ا ! و ‪ #‬و رج دة دة د‪1 #+ :‬م دار <> ا ‪ !,‬ر< وج دة د‪.#+ :‬‬

‫ا‪7‬ن ‪5‬ون ‪ !7‬و أر @ ط ‪ +‬ت‬

‫ا ط ‪ #+‬ا و > ‪:‬أ ‪ 1‬ر‬
‫ا ط ‪ #+‬ا ‪ $<: # ! 1‬ت‬
‫ا ط ‪ #+‬ا ‪ : #1 1‬ول <ور ن‬
‫ت‬ ‫ا ط ‪ #+‬ا را ‪: #‬ا را‪,‬ب وي " > ا ط‪/‬‬

‫ص ن ا ط ‪ +‬ت ا و ‪ #‬ا ‪ #1 1‬ن ا ! و ‪ #‬و رك ا را‪,‬ب <‪+‬ط و زج ھذا ا را‪,‬ب = دا‪.‬‬ ‫ما‬ ‫‪.9‬‬
‫‪ /‬ص !‪+‬ط ن ا را‪,‬ب ت ا ‪5‬ر‪5,‬وب‪.‬‬ ‫‪.10‬‬
‫زج !‪+‬ط ن ا را‪,‬ب @ ا ود و ‪ /‬ص ت ا ‪5‬ر‪5,‬وب‪.‬‬ ‫‪.11‬‬
‫ا وب‬
‫و*‬ ‫طر ‪ +‬طو‬

‫‪Floatation method‬‬
‫ا طر ‪+‬‬
‫ول ا ( ا ‪ 0‬ا ‪5‬وب‪.‬‬ ‫ؤ ذ ‪:‬ط ‪ #‬ن ا راز و و‪5 >< @$‬وب !ظ ف ‪1‬م ‪ $‬ف‬ ‫‪.1‬‬
‫‪ +‬ب ا راز <> ا ول = دا‪.‬‬ ‫‪.2‬‬
‫ش او ?ط ء ا ‪5‬وب‪.‬‬ ‫*‪ >/‬ا راز <‪ 0‬ا! و ‪ ,‬دام ‪:‬ط‬ ‫‪.3‬‬
‫ده ‪ 10‬د‪) :‬ق‪.‬‬ ‫ا رك اا! و‬ ‫‪.4‬‬
‫ول ا (‪.‬‬ ‫‪< 0‬وھ ا‬ ‫ا‪ 5‬ل ا‪ !7‬و‬ ‫‪.5‬‬
‫و‪ @$‬ر ‪< #‬وق <وھ‪ #‬ا‪ !7‬و ‪.‬‬ ‫‪.6‬‬
‫دة ‪ 30 – 20‬د‪.#+ :‬‬ ‫رك ا‪ !7‬و‬ ‫‪.7‬‬

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 ‫ت ا ‪5‬رو‪5,‬وب و ‪ /‬ص‪.‬‬ ‫راس و ‪ +‬ب و و‪@$‬‬ ‫‪ .8‬ر<@ ا ر ‪#‬‬

‫ا زات‬
‫‪1‬ل‪:‬‬ ‫‪ 0‬ط‪/‬و " ‪, 0‬ط( ا ‪) ,‬ل <‪ 0‬ا‪ !7‬و‬ ‫ت ا‪ 7‬ف وز! ن ول ا ( و‬ ‫! ‪ # ,‬ط‪/‬‬ ‫ھده ا طر ‪+‬‬
‫‪Entrobius‬‬
‫‪Ankylestoma‬‬
‫‪Tricuris‬‬
‫ا وب‬
‫‪ @ = ( * 7‬ا ط‪ /‬ت !‪/‬س ا ‪ /5‬ءه‬
‫‪Kato technique‬‬

‫ا طر ‪+‬‬
‫ز= = !ظ ‪/‬‬ ‫‪$‬ر ر‬ ‫‪.1‬‬
‫ر@‪ 5‬و‬ ‫ر‬ ‫‪ 0 " @$‬ا‬ ‫‪.2‬‬
‫ر @ ‪ 5‬و ! ا راز‬ ‫ا ء <راغ‬ ‫‪.3‬‬
‫‪ 5‬ت =ر ن‬ ‫*‪B‬‬ ‫ا* ‪ C‬ا !‬ ‫‪.4‬‬
‫@ و ‪/‬رد = دا و ‪$‬ن " > ‪ 37‬در=‪ #‬دة ‪ " ,‬ن ‪1‬م ‪ /‬ص‬ ‫‪ ,‬و< ن ا‬ ‫‪B‬ط> ا !‪#‬‬ ‫‪.5‬‬

‫ا زات‬
‫‪ ,‬دم ‪ /‬ص و‪5‬ذ ك د ا و ‪ $‬ت ‪+‬د ر دة ا‪. # *J‬‬
‫را)( ا * و?‪ #‬دة وا > ‪ 6‬ور ‪.‬‬ ‫‪5‬ن ا‪ / 7‬ظ‬

‫ا وب‬
‫أو ر‪ :‬ت ا‪ ,7‬ر!= و دس ‪ ،‬ذا =ب ا ‪ /‬ص طر ‪ #+‬ا رى ‪ #< $J‬إ > ‪ 5‬و ‪.‬‬ ‫‪ 5 ( * 7‬ف "ن ا‪!7‬‬

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 Laboratory stool report

Stool Examination
Test Result Normal

Physical examination

Color Brown Brown

Odour Offensive Offensive
Reaction Variable Variable
Consistency Formed Formed
Mucus Absent Absent
Appearance Pus Absent Absent
Blood Gross Absent Absent
Parasite (naked eye) Absent Absent

Microscopic examination

Pus cells 20-25 0 - 5 / HPF

RBCs 5-6 0 - 3 / HPF
Epithelial cells Absent Absent

State of digestion
Starch granules + +
Fat globules ++ +
Vegetable cells +++ +

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 Muscle fibers + +

Parasites
Protozoa : Vegetative Absent Absent
: Cysts Absent Absent
Helminthes : Larvae Absent Absent
: Ova H. nana Absent

Gross examination
Color

Normal:
Brown color is the normal color of stool
Why stool color is brown? The characteristic brown color of feces is due to
stercobilin and urobinin, both of which are produced by bacterial degradation of
bilirubin.

Abnormal:
Black color: indicate iron medication (for treatment of anemia) or upper GIT
bleeding (due to peptic ulcer, stomach carcinoma or esophageal varices).
Bright red color: indicate lower GIT bleeding (due to piles and anal fissure).
Clay color(gray-white): indicate obstructive jaundice
Silver color: indicate combination of jaundice and blood (cancer of ampulla of
Vater).
Red brown color: indicate drugs as Tetracyclines, and Rifambicin antibiotics
Green color: indicate medications as Diathiazine, Mercurous chloride also
vitamins cause green color of stool and in some cases of intestinal putrefaction.

Note: red stool color may be seen if there are undigested beets or tomatoes.

Note: if stool color is black and there is no history of iron medication FOBT is recommended.

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 Ampulla of Vater

The ampulla of Vater, also known as the hepatopancreatic ampulla, is formed by the
union of the pancreatic duct and the common bile duct.

Function
Various smooth muscle sphincters regulate the flow of bile and pancreatic juice through
the ampulla: the sphincter of the pancreatic duct, the sphincter of the bile duct, and the
hepatopancreatic sphincter (Sphincter of Oddi), which controls the introduction of bile and
pancreatic secretions into the duodenum, as well as preventing the entry of duodenal
contents into the Ampulla.

Odour
Normal:
Normally offensive
Why stool odour is offensive? Fecal odor results from gases produced by
bacterial metabolism, including skatole, mercaptans, and hydrogen sulfide.

Abnormal:
Odorless: usually seen if there is no fecal matter as in bacterial infection.
Very offensive: usually seen in cases of constipation and with certain types of
food that produce excessive gases.

pH ( reaction )
Normal:
Normally variable
Why stool pH is variable? Because stool pH mainly depends on the type of diet.

Abnormal:
High alkaline stool

Physiological Pathological
High protein diet Poor fat absorption

High acidic stool

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 Pathological
Physiological
Poor absorption of sugars
High carbohydrate diet
as in lactose intolerance

Consistency
Normal:
Normally well formed

Abnormal:
Abnormal consistency may be graded as follow:
Very hard: seen in cases of constipation
Semi formed: seen in the cases of parasitic infection
Soft: seen in the cases of parasitic infection
Loose: seen in the cases of diarrhea
Watery: mostly seen in cases of bacterial infection
Mucus
Normal:
Normally undetectable amount produce by GIT and found in the stool.

Abnormal:
Abnormal mucus in the sample appears as white patches and usually present
with appearance pus and indicate bacterial infection.
According to the amount of mucus it can be graded using signs (+, ++, +++)

Note: mucus with fresh blood in stool usually indicate amoebic dysentery

Appearance pus
Normal:
Normally not found (pus can be found normally in the stool but you cannot see
it by naked eye).

Abnormal:
Usually detected with mucus and appear as white patches in the stool, it
indicate ulcerative colitis or bacterial infection as bacillary dysentery.
Also it can be graded using signs (+, ++, +++).
Presence of detectable pus by naked eye means that the microscopic pus
must be over 100.

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‫ر ا ' د م ل ان *ل ا ص‬ ‫ص ا ظ ھري او ان‬ N ‫ ر وا‬3 ‫د د او ا " ط‬2 ‫ ن ا‬4 ‫ ادا‬: ‫ وظ‬1"
‫د د‬2 ‫ ا ص ا ظ ھري ث ادا و*دت‬- ‫د د او ا " ط‬2 ‫ا‬ 4 ‫و‬4 ‫رو‬4 " ‫ ا ص ا‬1 ‫ "د‬- ‫ا ظ ھري‬
++ ‫ او‬+ ‫ ا ص ا ظ ھري‬- ‫د د و ا " ط‬2 ‫ ب ا‬4‫ ا‬80 ‫ "ن‬1 ‫وب ا‬4 ‫ر‬4 " ‫ت ا‬

Gross blood
Normal:
Normally no blood seen in the stool (you cannot see it by naked eye).

Abnormal:
Abnormal fresh blood seen in cases of lower GIT bleeding caused by:
Bilharzias (schistosoma mansoni infection)
anal fissure
piles

‫و‬4 ‫رو‬4 " ‫ ا ص ا‬- RBCs ‫دد ال‬ 4 ‫ د "ن‬- ‫ص ا ظ ھرى‬ ' ‫ ا‬- ‫ اذا و*دت دم‬: ‫ وظ‬1"
.(over 100) 100 ‫?ر "ن‬4‫ا‬

Naked eye parasite

Normal: no parasites or larva appear in the stool

Abnormal:
In some cases the whole worm or parts of its body appear in the stool and can be
seen by naked eye.
Three worms can be seen by naked eye in the stool:
Ascaris lumbericoides
Entrobius vermicularis
Taenia sp.

Microscopic examination
‫ ص‬/ # ‫را ر‬$
‫ءة وا " رح‬ %‫ث ا‬ ‫ ا 'د ت و"ن‬- ‫'"ل "ن ث " و ظ‬1 N 2 ‫وب‬4 ‫رو‬4 " ‫د ان ا‬4/ ‫*ب ا‬ .1
.NJ‫ط ء ا >را‬3 ‫ذ ك‬4‫و و‬4 ‫رو‬4 " ‫ ا‬NJ‫ ا >را‬- ‫د "ن ظ‬4/ ‫ا‬ .2
- ‫ ر‬4 ‫وان‬ ‫ ك "ن راءة‬4" ‫( ھذه ا >ر‬not too thin not too thick) *‫"وذ‬ ‫ر >ر‬ .3
. = ‫و‬- ‫ ادا و 'ت‬1*"
‫= ?م 'د‬14 ‫ ا >ر‬N " ‫م‬ 10 J > ‫وب 'د ا‬4 ‫رو‬4 " ‫ت ا‬ ' ‫ ص ا‬- ‫ن أن دأ‬ .4
.( 1 ‫ر *م و دات ا‬B2 ‫ )وذ ك ظرا‬40 J > ‫د ك م ا ص 'د ا‬

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 ‫ظتھ ‪#‬‬
‫‪ 1‬ا >ر و ا ‪ 5‬ط ر " دد ‪zigzag‬‬ ‫‪ .1‬ا دا ا ص "ن (ط "'‬
‫م ‪ -‬ص ا >ر ‪ 1" 4‬دون رك‬ ‫طر ( " دا ‪overlapping 1‬‬ ‫‪ .2‬ول ان ص ا >ر‬
‫‪-‬را‪ 3‬ت‪.‬‬
‫"ن أ" ‪4‬ن " ‪1‬‬ ‫دم طر ( ا ‪1‬ط ا ر‬ ‫و ادا ‪ 4‬ت‬ ‫‪ .3‬ا‪ -‬ص >ر ن ‪ 1‬ا ل ‪4‬ل‬
‫"‪4‬ن ا ‪4‬م ‪ * ;1‬ا ' * دا‪.‬‬
‫‪ .4‬د و*ود ‪2‬د د او دم ‪ -‬ا >ر ا‪ -‬ص ا‪?4‬ر "ن >ر ن ‪4/ 1‬د ا م "ن دم و*ود د دان‬
‫‪ 4 - 5‬رك > ء "' ن و ا ت ث ‪ -‬ا ' "?ل ان ث ن ‪?" '" ova‬‬ ‫‪.5‬‬
‫‪ 2‬ب ا > ص ا ذى ص‬ ‫ل ا دام ا ' ن ‪ -‬ا ص ) " ‪4‬رو ‪4‬وب ‪( binocular‬‬ ‫‪.6‬‬
‫‪2‬داع اذا ا دم ن وا دة‬
‫‪ .7‬ا راز وى ‪ 1‬ا>‪ 4‬ل ‪ ?4‬رة *دا ‪1‬ط' م ا ‪ B‬ر ا "= وم د ك د ان ‪4‬ون دك ا ره ‪ 1‬ر ق ن‬
‫ا >‪ 4‬ل ا ط ' و ا و ت‪.‬‬
‫'ر‪ =-‬ا رك ا ' ‪ B‬رك ‪ =2‬او ا ' ن ‪2‬ور "ن ا ‪ 4‬ب‬ ‫"‬ ‫‪ .8‬د ا >ك ‪ -‬ا " ل و*ود و‬
‫ا ">‪4‬وك ‪ = -‬و اط‪1‬ب "ن ا "ر ض‬ ‫او ا ‪ "4‬و ر واذا م و‪-‬ر ذ ك ‪"-‬ن ا ‪ -‬ل دم ‪ 4‬ا و‬
‫ا رى ‪ -‬ا ‪ 2‬ح ‪ 1‬ص "رة ا رى‪.‬‬
‫‪1 1‬ك و و ‪ 5‬ا ط ل ا "و*ود ‪-‬‬ ‫‪ 1‬ا "ر ض "‪ 4‬ك "ن ا ‪4/‬د "ن ‪2‬‬ ‫‪' .9‬ض ا راض ا "ر‬
‫ا' ‪.‬‬
‫س >رط و*ود ط ‪ 1‬ت راز > ص ">‪ 14‬ا "ر ض ل ان ا د و ‪J‬ل ا > ص ھ‬ ‫‪.10‬‬
‫ا ' د و*ود ط ‪ 1‬ت ذ ك د ا ص ا * د *دا ‪ '1‬و ا " ‪ /‬و 'د ا ‪4/‬د "ن دم و*ود و ت‬
‫او‪ = larva‬ا‪ 4‬ب ا ‪ 1‬ل دون ط ‪ 1‬ت‪.‬‬

‫‪Overlapping‬‬ ‫‪Zigzag‬‬

‫ت ا ‪5‬رو‪5,‬وب‬ ‫< ص ا !‪#‬‬

‫‪Cells‬‬

‫‪RBCs‬‬

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Appearance:
‫> ء "زدوج‬B ‫د د( و دو‬2 ‫ ا‬1 ‫ر "ن‬B2‫ ره ا *م ) ا‬B2 1 4 ‫وب‬4 ‫رو‬4 " ‫رات ا دم ا "راء ت ا‬4 ‫ظ=ر‬
.(‫و ن ا دى 'ط ھدا ا ط ع‬1*‫= = "و‬J "‫دا * ا‬4‫= س "زدوج و ا " ظ=ر ھ‬J >3 ( ( ‫ ا‬- ‫ن‬4 )

‫ وظ‬1"
Q ‫د ا رؤ‬Q4‫ ؤ‬Q"" ‫ ھرى‬Q‫ص ا ظ‬Q ‫ ء ا‬Q ?‫ ا‬Q ‫ر ا‬Q=‫ف و ظ‬Q ‫ ز‬Q* ‫ ب‬B ‫ ا‬- ‫دث‬
‫ ا راز‬- ‫و*ود دم‬
‫وب‬4 ‫رو‬4 " ‫ت ا‬
‫ت‬Q ‫ر‬Q=‫ ن ظ‬Q ‫ض ا‬Q' Q- ‫ و‬Q= ‫ون‬Q ‫ل‬Q ‫ر‬Q" ‫ س ا‬Q ‫وب‬4Q ‫رو‬4 " ‫ت ا‬Q ‫راء‬Q" ‫دم ا‬Q ‫رات ا‬4 ‫ون‬
‫ل ط او ط طو ل و ھ س دم ا دا ل ھ ا ف "ن ا " س او‬4> 1 ‫ب "راء‬J‫وب >وا‬4 ‫رو‬4 " ‫ا‬
.‫ و ا ط" طم‬R ‫ ا ط‬2 ‫ل‬4 ‫"ن ا‬
Normal:
Normally few amounts of RBCs (0-3) are seen under high power field of
microscope.

Counting:
RBCs are counted under HPF of microscope and the range of count is written for
example 10-12 or 30-40 and so on.

Interpretation:
Abnormal RBCs under microscope is seen in:
Bilharzias (schistosoma mansoni infection)
anal fissure
piles
Entameba histolytica infection

PUS

Appearance:
. ‫ ره ا *م و = واه‬4 1 4 ‫وب‬4 ‫رو‬4 " ‫ت ا‬ ‫د د‬2 ‫ء او ا‬ ‫رات ا دم ا‬4 ‫ظ=ر‬

‫ وظ‬1"
‫ *"' ت‬- ‫" و*د‬J‫د د دا‬2 ‫ا‬
‫و*د " ده‬ ‫ظا‬ ‫ ر وھ‬4 ‫ تا‬2 ‫تا‬ - ‫د د و د ك‬2 =14 ' ‫ون ا‬4 ‫ن‬ ‫ 'ض ا‬-
.‫ا = م‬ 1 ‫م‬4 ‫ن ا‬4" - ‫راز‬
Q 1 ‫ ط و‬Q " ‫ون‬Q4 Q" Q 3 = ‫ ا >ر‬1 ‫ء ' ن ا "*ردة‬ ‫ظ=ر‬ ‫ن ا‬4 " ‫" ن ا‬J‫ا ث دا‬
. ‫د د‬2 ‫ "ن ا‬5"*
Normal:
Normally few amounts of pus (0-5) are seen under high power field of microscope.
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Counting:
Pus is counted under HPF of microscope and the range of count is written as in
the case of RBCs.

Note: if pus count is over 100 stool culture is recommended.

Interpretation:
Abnormal pus under microscope is seen in:
Bacterial infection as Shigellosis , Salmonellosis
Inflammation of the intestines, such as Ulcerative colitis

Note: usually pus is absent or few in cases of Viral diarrheas (Rotavirus infection) and
Parasitic infestations.

Epithelial cells

Appearance:
Q="* ‫ن‬Q4 Q"‫ر " ظ‬Q 3 ‫ و‬Q ‫ او " روط‬Q ‫ر‬J‫ون دا‬Q4 ‫ن ان‬Q4"" ‫ن ا‬Q" Q=- = ‫ل "" ز‬4> ‫و*د‬ J ‫اط‬ ‫ا‬
.‫وب‬4 ‫ر‬4 " ‫= *'ل "ن ا =ل " زھ ت ا‬1 ‫ ر و ا واه دا‬4 ‫ا‬
Normal:
Normally it is few or absent.

Interpretation:
Epithelial cells increased with gastrointestinal tract irritation

Note: absence of epithelial cells in meconium of newborn may aid in diagnosis of intestinal
obstruction in the newborn.

Meconium is the earliest stools of an infant. Unlike later feces, meconium is composed of
materials ingested during the time the infant spends in the uterus: intestinal epithelial
cells, , mucus, amniotic fluid, bile, and water. Meconium is almost sterile, unlike later
feces, is viscous and sticky like tar, and has no odor.

Digestive state

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 Starch

Appearance:
Q1 ‫ون‬Q4 ‫ ا ( ( ل‬- ‫ ر‬4 ‫ل‬4> ‫و*د‬ ‫ن‬4 ‫و‬ ‫ ل‬4>‫ و ا رز و و ا‬N"( ‫ظ=ر "ن ول اط'" "?ل ا‬
.‫ راز‬1 ‫ا "" ز‬ ‫ون ا‬1 ‫ ذ ا‬/ ‫ و‬J‫ل >وا‬4> J ‫ھ‬
Normal:
Normally found in the stool and graded as (+) when seen under HPF.

Interpretation:
Increased starch in stool (++ or +++) indicate a case of indigestion.

Fat

Appearance:

Q> Q 1 " ‫ م‬Q* ‫ ا‬Q ‫و‬ ‫وا‬QQ ‫در‬QQ2" ‫او‬ Q ‫در‬QQ2" ‫ن‬QQ" ‫ت‬QQ 4 ‫واء‬QQ ‫ م‬Q '‫ ا ط‬Q - ‫دھون‬QQ ‫ ول ا‬Q ‫ن‬QQ" ‫ر‬QQ=‫ظ‬
. ( ‫ ر ا ر‬2 ‫ون ا‬1 ‫ ذ ا‬/ ‫ر ت‬4 ‫ا‬
Note: Neutral fat globules can be stained with Sudan stain and counted.

Normal:
Normally found in the stool and graded as (+) when seen under HPF.

Interpretation:
Increased fat in stool may indicate:
Pancreatic insufficiency as in pancreatitis due to reduced pancreatic juice
secretion.
Disorders affect the absorption of fats as sprue (celiac disease) and infection with
Giardia.

Vegetable cells

Appearance:
.‫ف "?ل ا س‬ B ‫ظ=ر "ن ول ا ط'" ا‬
‫د‬Q*‫و‬ ‫ر‬ ‫ا‬ ‫" ادا و*دت ا‬ ‫تو‬ ‫ ر ق = و ن ا و‬1 ‫ج رة‬ ‫ظ ا= > ا و ت دك‬
. ' ‫ ا‬- ‫? ر "ن وا*د اى و ت‬4 ‫?ر‬4‫ رة ا‬4 "4
Normal:
Normally found in the stool and graded as (+) when seen under HPF.

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Interpretation:
Increased vegetable cells in stool have no clinical significance and considered as
residual food.

Muscle fibers

Appearance:

‫ن‬Q4" ‫راز و‬Q ‫ ا‬Q- ‫ر‬Q ‫ اى > ء ا‬5" ‫ط‬1 ‫ ره( و‬2 ‫ل ا‬4> ‫)"?ل‬N ‫= "" ز ووا‬14> ‫ وم و‬1 ‫ظ=ر "ن ول ا‬
. ‫(د رھ =و‬
‫ وظ‬1"
‫ب‬Q 4 ‫د ك‬Q ‫ و‬Q' ‫ م ط‬Q'‫ل ط‬Q4/ Q muscle fibers Q1 ‫وى‬Q ‫=ر‬Q>‫ ا‬6 ‫ اول‬Q- 5Q ‫راز ا ط ل ا ر‬
.‫ون ا راز "?ل ا > ص ا ' دى‬4 ‫ورة ط ' و‬2 ‫ل ا ط ل‬4/ - ‫ ا>=ر‬6 ‫ ا" 'د‬absent

Normal:
Normally found in the stool and graded as (+) when seen under HPF.

Interpretation:
Increased muscle fibers in stool have no clinical significance and considered as
residual food.

Note: the presence of large amount of undigested meat fibers in the stool may be caused by
pancreatitis.
Note: Some studies have shown an excellent correlation between excessive fecal muscle
fibers and hypo- or achlorhydria.

Other findings

Normal constituents of stool:

Bacteria: normally non pathogenic bacteria are found in the stool and usually
bacilli such as Escherichia coli and Lactobacillus sp.

Note: 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.
Yeast: normally stool contain harmless yeast cells such as blastocystis hominis

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Crystals: normally stool contain triple phosphate, calcium oxalate and
cholesterol crystal due to food ingestion.

Fibers: normally stool contains many fibers that may arise from clothes or
undigested plant food.

Air bubbles: normally found and has no clinical significance.

Oil droplets: normally found, they are very bright and completely rounded.

Note: 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.

Undigested food: normally found, it has many shapes.

Abnormal constituents of stool:

Hematoidin crystals: sometimes found after GI tract hemorrhage.

Charcot-Leyden crystals : sometimes found in parasitic infestation

(especially amebiasis) and in cases of ulcerative colitis.

Parasites
Definitions:
Medical parasitology:
The study of the parasites of man and their medical consequences

Parasitism:
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Is an ecological relationship between two different organisms, one designated the
parasite, the other the host.

Host:
organism harboring a parasite.

Definitive or primary host:

Animal harboring the adult or sexually mature stage of the parasite.

Intermediate or secondary host:

Animal in which development occurs but in which adulthood is not reached.

Life cycle:
For survival and reproduction reasons many parasites evolve through a number of
morphologic stages and several environments or different hosts. The sequence of
morphologic and environmental stages is referred to as the life cycle.

Infective stage:

It is a stage in the life cycle of the parasite that can infect human.

Reservoir host:
An animal that harbors a species of parasite that can be transmitted to and infect
man.

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

Carrier:
a host that harbors a parasite but exhibits no clinical signs or symptoms.

Zoonosis:
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a disease involving a parasite for which the normal host is an animal, and wherein
man can also be infected.

What are the types of parasites that attack human?

Ectoparasites live outside on the human body as common bedbugs
Endoparasites live inside the human body, e.g. amoebas, worms, or flukes.

What is the difference between parasitic infection and parasitic

infestations?
Parasitic infection means that parasite live in host as the case of intestinal
parasites while parasitic infestations means that parasite live on host as the case
of bedbugs.

What is the mode of parasitic infection?

Oral-facial
Bite of vector
Autoinfection
Congenital
Sexual contact
Penetration
Inhalation

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

Eating nourishment
Mechanical destruction
Obstruction
Allergic reaction
Secondary bacterial infection
Anemia
Abdominal pain and diarrhea
What is the tests that can be done to diagnose parasitic infection?
Stool analysis urine analysis, blood film, CSF examination, and serological tests

Classify parasites according to habitat?

Intestinal parasites as Giardia lamblia
Tissue parasites as trichenlla spiralis
Blood parasites as plasmodium malaria
Urinary tract parasites as trichomonas vaginalis

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What are the common types of intestinal parasites that infect
human?
Protozoa
Entameba histolytica Giardia lamblia

Helminthes
Trematoda
Schistosoma mansoni

Fasciola gigantica

Cestoidea

Taenia solium

Taenia saginata

Hymenolepis nana

Nematoda

ascaris lumbericoides strongyloides stercoralis

entrobius vermicularis ankylestoma duodenale

trichuris trichiura trichostrangylus

What is the forms of protozoa that ca appears in stool?
Trophozoite: metabolically active invasive stage.
Cyst: "vegetative" inactive form resistant to unfavorable environmental conditions.

What is the forms of helminthes that ca appears in stool?

Ova: that is results from sexual reproduction of helminthes.
Larva: the stage that is come from the ova.

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Common questions
How can I prevent parasitic infection?
، ( 5" *" ‫ول 'دوى ا‬8‫در ا‬2" ‫ن ھو ا‬ ‫)ا‬ ‫ ت ھو ج ا "ر‬1 ‫ط‬ 2%‫و "ن ا‬1 ‫ ان أول ا ل‬-1
‫ ا "دى‬5 ‫ن ( ر وا‬S‫ا‬ ‫و*د‬ ً
8 N 2 ‫' ج ا‬1 ‫"ل "=م *دا‬ 2T N 2 ‫ر أن ا > ص ا‬4‫وھ ذ‬
‫ > ء ھ م‬5‫ م وا ( ط‬1 ‫ > ص ا‬- ، ‫ ده‬1 ‫ل ط ل‬4 ‫ ل و*د ج ص‬، 1 ‫ ت ا ط‬2%‫ ا‬5 "* ‫' ج‬
. "‫ ا "( و‬- ً‫*دا‬

‫ ذ ك *د‬، J ‫وث ا‬1 ‫ ن‬U ‫و‬ 2 ‫ ر‬3 ‫ن طر ق "" ر ت‬ / 8 ً‫ ت =ل *دا‬1 ‫ط‬ 2%‫ ان ا‬-2
: ‫أ *ب‬

. "‫ و ز‬4 ‫ ت "?ل ا د دان ا >ر ط وا‬2‫ن "ن إ‬ ‫ا‬ ‫ " ك ( و‬8‫ وم وا‬1 ‫ط= ا ط' م ) ا‬
‫ رس‬4 ‫? ر "ن ا د دان "?ل ا‬4 2%‫ن "ن ا‬ ‫ط ( و ا‬ ‫= ) ا‬14‫روات * داً ل أ‬ ‫ لا‬3
. "8‫وا رو وزوا "?ل ا‬
. "8‫ س ا‬4‫ واق "ن ا ذ ب ا ذى "ل أ‬8‫ ا " زل وا‬- ‫ظ ا ط' م‬
‫= ر أو ا د دان أو ا رو وزوا‬1 2%‫ن "ن ا‬ ‫ در ا " ه راز وا ول "" ( ا‬2" ‫وث‬1 ‫دم‬
‫د (ل "ن‬ ً
‫ ا‬1 ‫"راض ا ط‬8‫و "ن ا‬1 2 8‫ا وا ت ا‬ ‫ طر ( ر‬-‫و ا س "'ر‬
.‫ن‬ ‫ا وان إ ا‬
2 > ‫ ا‬- ‫ذ ك ا ظ‬4‫ل و 'د ا روج "ن ا " م و‬48‫ دى ل ا‬8‫ ل ا‬3 ‫ " "?ل‬1 ‫ ا‬2 ‫ذ ك ا "" ر ت ا‬4
1 ‫"راض ا ط‬8 2%‫ دة "ن ا‬4‫و أ‬

Once I have had parasitic infection can I be re infected?

Yes there is no long immunity after parasitic infection.

Can stool analysis detect all parasites?

No it can detect only intestinal parasites.

Can a baby become infected with parasites ?

Yes specially protozoa from contaminated hands and food.

Can an embryo (fetus) become infected with parasite?

Yes for example toxoplasmosis can be transmitted from mother to here fetus.

Can parasite cause the excess in gases that I have?

No, parasites do not cause any excessive gas production.

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What is the cause of excess in gases in the intestine?
‫ص‬Q( Q="‫ن أھ‬Q" ‫ل‬Q"‫دة وا‬Q ‫; ا *= ز ا = "; 'ود إ‬- ‫ت‬ ‫ زات ا طن و دوث إ‬3 ‫ون‬4 ‫إن "ن أھم أ ب‬
;Q- ‫ل‬4 >" ‫"رار و دوث‬ ‫ق و دم ا روج إ ا " م‬1( ‫ ز " ت ا ز" = م ا ط' م و ا و ر و ا‬%‫; 'ض ا‬-
‫دة و‬Q'" ‫; ا‬Q- ‫دة‬QJ‫ زا‬Q ‫ون و "و‬Q ‫; ا (و‬Q- ‫(( ت‬Q> ‫"' ء و ا (رح ا "'و و‬8‫; ا‬- ‫طر ت‬- ‫ون‬4 ‫ ; و‬2' ‫ا (و ون ا‬
‫ر‬J Q2' ‫و و ا‬Q4 ‫رب ا‬Q>‫ و‬، ‫ر‬Q ‫ل‬Q48‫ذ ك ا‬Q4‫(; و‬1 Q " ‫ ص‬Q> ‫ل و ا‬Q48‫ ا‬Q ‫ل وأ‬Q48‫ ء ا‬Q ?‫ ا =واء أ‬51 ‫ا رد و‬
‫رة و‬Q‫ت و ا زھ‬Q 1 ‫وم و ا‬Q? ‫ل و ا‬Q2 ‫ل و ا‬Q* ‫وف و ا‬Q 1" ‫ ن و ا‬Q *8‫ ن و ا‬8‫ ب و ا‬1 ‫ ر ا ر ( ل و ا‬2 ‫ ز و‬B ‫ا‬
Q"'‫ط‬8‫واع ا‬Q ‫ ن أ‬5"* ‫?رة و ا‬4 ‫ل‬48‫ر ون و ا‬4 ‫ ا‬1 ‫ل ا " وي‬48‫ ا‬، ‫ل أ واع ا (و ت‬4‫ و‬، ‫ا "ص وا ول‬
. ( ‫ س ا " س ا‬, ‫; " ط( ا طن‬- ‫ ص‬8 ‫ ز دة ا وزن و‬، ‫ر ت و ا >و ت‬4 ‫ ا‬، ً '" ‫= م‬

What is the treatment of excess in gases or how I can avoid this?

.‫; ا ط' م‬- ‫ وم و ا د م‬1 ‫ ل "ن ول ا (و ت وا‬1( ‫ ا‬.1

.‫ وا "( ; و ا ز وت‬N ‫ ت و ا "وا‬1 " ‫ ل "ن ول ا‬1( ‫ ا‬.2
.‫ ل "ن ول ا *ل و ا *ر* ر‬1( ‫ ا‬.3
.‫ ع ن ا د ن‬%‫ ا‬.4
.‫و ت‬1 ‫ ت ا ; ز د "و ا "'دة "?ل ا "( ; و ا‬48‫ ' د ن ا‬%‫ ا‬.5
.‫ل ل ا وم‬48‫ ' د ن ا " و * ب ا‬%‫ ا‬.6
.‫ ا * م‬J-‫رد و رورة د‬ 2 ‫ * ب ا‬.7
.5J * ‫ل ا ط' م و أ ت ت‬4‫ دم أ‬.8
ً.‫ ر "ط=و * دا‬B ‫ل ا‬48‫ ' د ن ا‬%‫ ا‬.9
.V " ‫ ا =واء أ? ء ا‬51 ‫* ب‬ .10
. -‫"ون و ا ون و ا (ر‬4 ‫>رب ا‬ .11
.‫ زات‬B ‫ " ص ا‬V "1 ‫ا دام ا راص‬ .12
Chew tablets as luftal or activated charcoal as ultra carbon tablets

Are there are any parasite vaccines?

There are successful vaccination programs against viral and bacterial diseases,
but unfortunately, progress towards parasite vaccines has been slow. This limited
progression is due in part to the multi-factorial immune response to parasite
infection, parasite immune avoidance strategies and the complex nature of
parasite antigens. However, in recent years molecular biology research has
identified and produced new protective recombinant antigens for vaccine trials.
DNA based vaccination has also been successful in trials.

How parasites can be treated?

Most protozoa can be treated by metronidazole (flagyl or fasigym).
Most helminthes can be treated by vermizole.

‫(ل‬ ‫= ( ل ا د دان و‬
‫رر 'د ا و ن ?م 'د >=ر وذ ك‬4 ‫ ا م ?م‬3 ‫ا د دان ؤ ذ ا *ر‬ - : ‫ وظ‬1"
.‫ون ا ر ت ا ر*ت ا د دان‬4 ‫ا ر ت و ذ ك 'ط 'د "دة‬
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Why we need to count parasitic egg?
It is used to determine the intensity of infection.

How we can count parasitic egg?

The simplest and most effective method for determining the number of eggs per
gram of stool is the McMaster counting technique

Procedure
1) Weigh 4 g of faeces and place into container.
2) Add 56 ml of saline.
3) Mix the contents thoroughly with a stirring device.
4) Filter the faecal suspension.
5) Take a sample with pasture pipette.
6) Fill the both slides of the counting chamber with the samples
7) Allow the counting chamber to stand for 5 minutes.
8) Examine the sample of the filtrate under a microscope.
9) Count all eggs within the engraved area of both chambers.
10) The number of eggs per gram of faeces can be cal calculated as
follow:

♦ Add the egg count of the two chambers together

♦ Multiply the total by 50. This gives the e.p.g. of faeces.

What are the imitations of stool examination in the diagnosis of

gastro-intestinal parasites?

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 1. The demonstration of parasite eggs or larvae in the stool provides positive
evidence that an animal is infected but does not indicate the degree of an
infection.
2. The failure to demonstrate eggs or larvae does not necessarily mean that no
parasites are present; they may be present in an immature stage or the test
used may not be sufficiently sensitive.
3. Various factors can limit the accuracy and significance of a stool egg count.

There is a fairly regular fluctuation in faecal egg output.

Eggs are not evenly distributed throughout the faeces.
The quantity of faeces passed will affect the number of eggs per unit
weight.
The egg output is influenced by the season of the year (large
infections may be acquired during rainy seasons).
Eggs may not be detected due to low numbers of them or to a low test
sensitivity.

Common diseases of GIT

Hemorrhoid
Hemorrhoids or piles are varicosities or swelling and inflammation of veins in the
rectum and anus.
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Increased straining during bowel movements, by constipation or diarrhea, may
lead to hemorrhoids

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 It is a common condition due to constipation caused by water retention in
women experiencing menstruation.
Hypertension, particularly portal hypertension, can also cause hemorrhoids
because of the connections between the portal vein and the vena cava which
occur in the rectal wall -- known as portocaval anastomoses.
Obesity can be a factor by increasing rectal vein pressure.
Sitting for prolonged periods of time can cause hemorrhoids.
Pregnancy causes hypertension and increases strain during bowel movements,
so hemorrhoids are often associated with pregnancy.
Excessive consumption of alcohol or caffeine can cause hemorrhoids.

Note: caffeine ingestion increases blood pressure transiently, but is not thought to cause
chronic hypertension. Alcohol can also cause alcoholic liver disease leading to portal
hypertension.

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Hemorrhoids usually are not dangerous or life threatening. In most cases,
hemorrhoidal symptoms will go away within a few days.
Although many people have hemorrhoids, not all experience symptoms.
The most common symptom of internal hemorrhoids is bright red blood
covering the stool.
an internal hemorrhoid may protrude through the anus outside the body,
becoming irritated and painful. This is known as a protruding hemorrhoid.
Symptoms of external hemorrhoids may include painful swelling or a hard lump
around the anus that results when a blood clot forms. This condition is known
as a thrombosed external hemorrhoid.
microcytic hypochromic anemia occurs due to chronic bleeding.
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For many people, hemorrhoids are mild and temporary conditions that heal
spontaneously.
There is no medicine that will cure hemorrhoids, but local treatments such as
topical analgesic, can provide temporary relief.
In the case of external hemorrhoids with a visible lump of small size, the
condition can be improved with warm bath causing the vessels around rectal
region to be relaxed.
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 Eating fruit helps avoid conditions that lead to hemorrhoids.
Eating fiber-rich bulking agents to help create a softer stool that is easier to
pass,
to lessen the irritation of existing hemorrhoids.
Surgical treatments
Some people require the following medical treatments for chronic or severe
hemorrhoids:
• Rubber band ligation
Elastic bands are applied onto an internal hemorrhoid to cut off its
blood supply. Within several days, the withered hemorrhoid is
sloughed off during normal bowel movement.
• Hemorrhoidolysis/Galvanic Electrotherapy
Desiccation of the hemorrhoid by electrical current.
• Sclerotherapy (injection therapy)
Hardening agent is injected into hemorrhoids. This causes the vein
walls to collapse and the hemorrhoids to shrivel up.
• Hemorrhoidectomy
A true surgical procedure to excise and remove hemorrhoids. Many
patients complain that pain during recovery is severe. For this reason
is often now recommended only for severe hemorrhoids.

Anal fissure
Anal fissure is a crack or tear in the anus skin. As a fissure, these tiny tears may
show as bright red rectal bleeding and cause severe periodic pain after
defecation.
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Most anal fissures are caused by stretching of the anal mucosa beyond its
capability.
Anal fissures are common in women after childbirth; following excessive anal
intercourse; after difficult bowel movements; and in infants following constipation.

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Prreevveen
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Treating constipation by eating food rich in dietary fiber, avoiding caffeine
(which can increase constipation) , drinking a lot of water and taking stool
softener.
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 Treating diarrhea.
Avoiding straining or prolonged sitting on the toilet.
Keeping the anus dry and hygienic.

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Treatment included warm baths, topical anesthetics, stool bulking agents,
mechanical anal stretching, and, sometimes, surgery.

sphincterotomy
Painful deep chronic fissures, on the other hand, will not heal because of poor
blood supply caused by sphincter spasm.
Surgical intervention may be required for persisting deep anal fissures.

Obstructive jaundice
Jaundice, also known as icterus is yellowish discoloration of the skin, sclerae
(whites of the eyes) and mucous membranes caused by hyperbilirubinemia.

Post-hepatic jaundice

Post-hepatic jaundice, also called obstructive jaundice, is caused by an

interruption to the drainage of bile in the biliary system.

The most common causes are gallstones in the common bile duct, and pancreatic
cancer in the head of the pancreas.

Also, a group of parasites known as "liver flukes" live in the common bile duct,
causing obstructive jaundice.

Other causes include strictures of the common bile duct, biliary atresia,

Fat malabsorption
Malabsorption is a state arising from abnormality in digestion or absorption of food
nutrients across the gastrointestinal (GI) tract.

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Fat malabsorption is characterized by abnormal fecal excretion of fat (steatorrhea)
and variable malabsorption of fats and fat soluble vitamins.

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Bowel mucosal damage
Bacterial and viral infections
Parasites infections e. g. Giardia lamblia
Insufficient concentrations of digestive enzymes
Drug induced

Diarrhea
Diarrhea, also spelled diarrhoea, is frequent loose or liquid bowel movements.

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Diarrhea is most commonly caused by viral infections, parasites or bacterial
toxins.
Diarrhea can also be a symptom of more serious diseases, such as dysentery,
cholera, or botulism, and can also be indicative of a chronic syndrome such as
Crohn's disease.
Diarrhea can also be caused by dairy intake in those who are lactose intolerant.

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Secretory diarrhea

Secretory diarrhea means that there is an increase in the active secretion, or

there is an inhibition of absorption. The most common cause of this type of
diarrhea is a cholera toxin that stimulates the secretion of anions, especially
chloride ions.

Osmotic diarrhea

Osmotic diarrhea occurs when too much water is drawn into the bowels. This
can be the result of maldigestion (e.g., pancreatic disease or Coeliac disease),
in which the nutrients are left in the lumen to pull in water.

In healthy individuals, too much vitamin C or undigested lactose can produce

osmotic diarrhea and distention of the bowel.

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 Motility-related diarrhea

Motility-related diarrhea is caused by the rapid movement of food through the

intestines (hypermotility). If the food moves too quickly through the GI tract,
there is not enough time for sufficient nutrients and water to be absorbed. This
can be due to a diabetic neuropathy, as a complication of menstruation or
Hyperthyroidism which can produce hypermotility.

Inflammatory diarrhea

Inflammatory diarrhea occurs when there is damage to the mucosal lining or

brush border, which leads to a passive loss of protein-rich fluids, and a
decreased ability to absorb these lost fluids. It can be caused by bacterial
infections, viral infections, parasitic infections, or autoimmune problems such
as inflammatory bowel diseases.

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In many cases of diarrhea, replacing lost fluid and salts is the only treatment
needed.

Medicines that are available without a doctor's prescription include Kaopectate

and streptokeine.

‫ ن >د د *دا ( " >رة ن ذ ك ؤ ر‬4 ‫ ذ "ر ض ا = ل ادو و ف ا = ل) ا اذا‬/ ‫ ان‬/‫ "ن ا ط‬: ‫ وظ‬1"
*‫ ا "' ء و دم رو‬- ‫* ز ا ' "ل ا " ب‬ ‫رص ا > ء "ن ا "رض‬- ‫"ن‬

constipation
Constipation, is a condition of the digestive system in which a person experiences
hard feces that are difficult to expel. This usually happens because the colon
absorbs too much water from the food.

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In common constipation, the stool is hard, difficult, and painful to pass.
Usually, there is an infrequent urge to void.
the abdomen may become distended , tender and crampy, occasionally with
enhanced bowel sounds

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Straining to pass stool may cause hemorrhoids and anal fissures, which are
painful in themselves.
Also constipation can lead to headache and testicular varices.

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The main causes of constipation include:

Hardening of the feces

Improper mastication (chewing) of food
Insufficient intake of dietary fiber
inadequate fluid intake
Medication, e.g. diuretics and those containing iron, calcium, aluminum
slowed transit, where peristaltic action is diminished or absent, so that feces
are not moved along
Hypothyroidism
Hypokalemia
Medications, such as, opioids (e.g. codeine & morphine) , certain tricyclic
antidepressants and cough drugs.
Lead poisoning
Constriction, where part of the intestine or rectum is narrowed or blocked, not
allowing feces to pass
Smoking cessation (nicotine has a laxative effect)
irregular bowel habit

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Prevention:
Drinking orange juice.
Diet rich in fibers as vegetables and fruit and whole meal bread
Increase the intake of fluids (preferably water)
Walking to facilitate bowl movement
No coffee or tea.

Medications:
Laxatives as apilaxin, laxin and cisapride.

Note: Enemas can be used to provide a form of mechanical stimulation. However, enemas are
generally useful only for stool in the rectum, not in the intestinal tract.

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spastic colon
In gastroenterology, irritable bowel syndrome (IBS) is a functional bowel disorder
characterized by abdominal pain, discomfort or bloating relieved by defecation and
alteration of bowel habits. Diarrhea or constipation may predominate, or they may
alternate (classified as IBS-D, IBS-C or IBS-A, respectively).

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ommss
The primary symptoms of IBS are abdominal pain or discomfort in association with
frequent diarrhea, constipation, or a change in bowel habits.

There may also be urgency for bowel movements, a feeling of incomplete

evacuation (tenesmus), bloating or abdominal distention.

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Initially, IBS was considered a psychosomatic illness but new evidences show that
organic factors contribute for the disease such as immune reaction and infections.

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Initial treatments

Medications may consist of stool softeners and laxatives in constipation-

predominant IBS, and antidiarrheals in diarrhea-predominant IBS.

Antispasmodics

The use of antispasmodic drugs (e.g. colospasmine and librax) may help patients,
especially those with cramps or diarrhea.

Drugs affecting serotonin

Drugs affecting serotonin (5-HT) in the intestines can help reduce symptoms.[88]
Serotonin stimulates the gut motility and so agonists can help constipation
predominate irritable bowel while antagonists can help diarrhea predominant
irritable bowel:

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Crohn's disease
Crohn's disease (also known as regional enteritis) is a chronic, episodic,
inflammatory bowel disease (IBD) and is generally classified as an autoimmune
disease. It can affect any part of the gastrointestinal tract from mouth to anus;

S
Syym
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Many people with Crohn's disease have symptoms for years prior to the diagnosis.
The usual onset is between 15 and 30 years of age but can occur at any age.

Gastrointestinal symptoms

Abdominal pain may be the initial symptom of Crohn's disease. The pain is
commonly cramp-like and may be relieved by defecation. It is often
accompanied by diarrhea, which may or may not be.
Perianal discomfort may also be prominent in Crohn's disease. Itchiness or
pain around the anus may be suggestive of inflammation.
The mouth may be affected by non-healing sores (aphthous ulcers).

Systemic symptoms

Crohn's disease, like many other chronic, inflammatory diseases, can cause a
variety of systemic symptoms.

Among children, growth failure is common.

Among older individuals, Crohn's disease may manifest as weight loss. This is
usually related to decreased food intake, since individuals with intestinal
symptoms from Crohn's disease often feel better when they do not eat and
might lose their appetite.

Extra intestinal symptoms

In addition to systemic and gastrointestinal involvement, Crohn's disease can

affect many other organ systems.

Inflammation of the interior portion of the eye, known as uveitis, can cause eye
pain, especially when exposed to light.

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 Inflammation may also involve the white part of the eye (sclera), a condition
called episcleritis. Both episcleritis and uveitis can lead to loss of vision if
untreated.
Crohn's disease is associated with inflammation of one or more joints (arthritis).

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Coom
mpplliiccaattiio
onnss
Crohn's disease can lead to several mechanical complications within the
intestines, including obstruction, and abscesses. Obstruction typically occurs from
strictures or adhesions which narrow the lumen, blocking the passage of the
intestinal contents.

Crohn's disease also increases the risk of cancer in the area of inflammation.
C
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The exact cause of Crohn's disease is unknown. However, environmental and
genetic factors have been invoked in the pathogenesis of the disease.

Mutations in the CARD15 gene (also known as the NOD2 gene) are associated
with Crohn's disease.

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A complete blood count may reveal anemia, which may be caused either by
blood loss or vitamin B12 deficiency. T
Erythrocyte sedimentation rate, or ESR, and C-reactive protein measurements
can also be useful to gauge the degree of inflammation.
Testing for anti-neutrophil cytoplasmic antibodies (ANCA) has been evaluated
to identify inflammatory diseases of the intestine and to differentiate Crohn's
disease from ulcerative colitis.

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Currently there is no cure for Crohn's disease

Treatment for Crohn's disease is only when symptoms are active and involve first
treating the acute problem, then maintaining remission.

Acute treatment uses medications to treat any infection (normally antibiotics) and
to reduce inflammation (normally aminosalicylate anti-inflammatory drugs and
corticosteroids).
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When symptoms are in remission, treatment enters maintenance with a goal of
avoiding the recurrence of symptoms.

Ulcerative colitis
Ulcerative colitis is a form of inflammatory bowel disease (IBD), a disease of the
intestine, specifically the large intestine or colon, that includes characteristic
ulcers, or open sores, in the colon.

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While the cause of ulcerative colitis is still unknown, several, possibly interrelated,
causes have been suggested:

Genetic factors

A genetic component to the etiology of ulcerative colitis can be hypothesized

based on the aggregation of ulcerative colitis in families.

Environmental factors

Many hypotheses have been raised for environmental contributions to the

pathogenesis of ulcerative colitis. Include the following:

the colon is exposed to many dietary substances which may encourage

inflammation.
A diet low in fermentable dietary fiber may affect ulcerative colitis incidence.

Autoimmune disease

Some sources list ulcerative colitis as an autoimmune disease.

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Clliin
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GI symptoms

The clinical presentation of ulcerative colitis depends on the extent of the disease
process.

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Patients usually present with diarrhea mixed with blood and mucus, of gradual
onset.

The disease is usually accompanied with different degrees of abdominal pain,

from mild discomfort to severely painful cramps.

Extra intestinal features

As ulcerative colitis is a systemic disease, patients may present with symptoms

and complications outside the colon. These include the following:

aphthous ulcers of the mouth

Iritis or uveitis, which is inflammation of the iris
Ankylosing spondylitis, arthritis of the spine
Erythema nodosum, which is inflammation of subcutaneous tissue involving the
lower extremities
Autoimmune hemolytic anemia

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Ulcerative colitis and colorectal cancer

There is a significantly increased risk of colorectal cancer in patients with

ulcerative colitis after 10 years.

Primary sclerosing cholangitis

Ulcerative colitis has a significant association with primary sclerosing cholangitis

(PSC), a progressive inflammatory disorder of small and large bile ducts.

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Standard treatment for ulcerative colitis depends on extent of involvement and
disease severity. The goal is to induce remission initially with medications,
followed by the administration of maintenance medications to prevent a relapse of
the disease.

Drugs used

Aminosalicylates as sulfasalazine

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 Corticosteroids as prednisone
Immunosuppressive drugs as azathioprine

Surgery

Unlike Crohn's disease, ulcerative colitis can generally be cured by surgical

removal of the large intestine.

Surgery is indicated for patients with severe colitis or patients with symptoms that
are disabling and do not respond to drugs.

Dyspepsia
Dyspepsia (Indigestion) is a medical condition characterized by indigestion with
chronic or recurrent pain in the upper abdomen, upper abdominal fullness and
feeling full earlier than expected with eating. It can be accompanied by bloating,
belching, nausea or heartburn.

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The characteristic symptoms of dyspepsia are upper abdominal pain, bloating,
fullness and tenderness on palpation.

Note: Pain worsened by exertion and associated with nausea and sweating may also indicate
angina.

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over eating
spicy food
too fast eating
alcohol drug eat
stress
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Drugs that facilitate digestion as Amraze or digestin.
Proton pump inhibitors (PPIs), which are effective for the treatment of
heartburn.

sprue (celiac disease)

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Coeliac disease , also spelled celiac disease, and it has several other names,
including: non-tropical sprue, endemic sprue, gluten enteropathy or gluten-
sensitive enteropathy, and gluten intolerance, it is an autoimmune disorder of the
small intestine that occurs in genetically predisposed people of all ages.

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Include chronic diarrhea, failure to thrive (in children), and fatigue.

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Coeliac disease is caused by a reaction to gliadin, a gluten protein found in wheat.
Upon exposure to gliadin, the enzyme tissue transglutaminase modifies the
protein, and the immune system cross-reacts with the bowel tissue, causing an
inflammatory reaction. That leads to flattening of the lining of the small intestine
(called villous atrophy). This interferes with the absorption of nutrients because the
intestinal villi are responsible for absorption.

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The only effective treatment is a lifelong gluten-free diet.

Achlorhydria
Achlorhydria and hypochlorhydria refer to states where the production of gastric
acid in the stomach is absent or low, respectively.

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The decreased acid level itself causes few symptoms, but low acid levels in the
stomach are linked with bacterial overgrowth (as the stomach does not kill
microbes normally present in food), which can manifest as diarrhoea or decreased
absorption of nutrients or vitamins.

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Autoimmune disorders where there is antibody production against parietal cells
which normally produce gastric acid.
The use of antacids or drugs that decrease gastric acid production
A symptom of Helicobacter pylori infection which neutralizes and decreases
secretion of gastric acid to aid its survival in the stomach.
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