( BETA EDITION)

With
Prof. Dr Mohammed Abo El-Asrar

Edited By
El-Azhar Medical students 2012


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51

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Diarrhea

electrolyte disturbance

colic , bleeding, .......etc.

liver

Mechanism of hepatomegaly and veno-occlusive dis.

hepatitis & portal hyper tension 

diarrhea
The second commonest presentation after respiratory disease

In winter  80% of patient respiratory tract diseases
In summer  80 % of patient diarrhea
-:
- Definition


....................................................................................
- degree of diarrhea.
- Mechanism of diarrhea.
- Etiology of diarrhea.
- Gastroenteritis { precipitating factors, C/P, complications, investigations and TTT}.
Definition
:
- passing loose stool
" "
container
+
- frequent 
frequency
1.

if breast feeding  according to usual habits 

intake
called exaggerated gastro-colic reflex
*
*

2.

if artificial feeding  if > 3 times /day.

Diarrhea & dysentery
Dysentery  diarrhea with mucous and blood + tenesmus ( painful defecation )
+

Degrees
Degrees of Diarrhea

- Water loss / 1 motion Diarrhea  100 ml water /1 motion

... 6 10 :

mild or moderate or severe
600 ml water /day 6 X 100

60 ml / kg / day = 600/ 10

so, mild diarrhea

1.

Mild diarrhea..... loss 50-70 ml /kg /day

2.

Moderate diarrhea.... loss 70-90 ml /kg / day

3.

Severe diarrhea..... loss > 90 ml /kg /day

Mechanism of diarrhea

vein .... branch of artery .... .... columnar cells intestinal villi


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The main function.... absorption of water & well digested food.

1.

Digestive function....

2.

Excretion of abnormal toxins as K+ (after kidney), urea ...

3.

.....lactase

- also in colon..... Excrete excess bicarbonate.

Its function .... Mucous secreting cells .... GIT
) ( 1- lubrication of food
mucous gut Mucous ..... .... jejunum ...  neutral media acidic alkaline  duodenum PH
Ileum colon ... stool bulky2- mucous also , protect mucosa from digestive juice & PH of the lumen
Mechanism of diarrhea
EnteroEntero- toxinogenic pathway:

1.

Organism toxins organism Entero toxin to cells ......invasion of the wall

 ......... increase CAMP ..... absorption ) secretion Organism (
..... digestive food absorption
) ( ) Mucous watery ( blood
???? DD from osmotic diarrhea
Here organism (infection) so, fever.

Also, fermentation of food.... bad odour ...

Osmotic diarrhea

2.

mechanism
1- unrib food:
.... No organism unrib food ) (
- ...
lumen stool

2- excess CHO:
absorption CHO ... food poisoning ...
 GIT Lumen
3- excess fat:
excess fat bile ... ... absorption Lumen Increase motility of the gut
No complete absorption of food.
DD from osmotic diarrhea

3.


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.... Here with severe abdominal colic ...
as in:
- thyrotoxicosis .... where increased motility.
- pheochromocytoma...... increase motility.
4.

EnteroEntero-invasive pathway:
Organism Lumen toxins villi absorption surface No digestion ....No absorption
ulcers stool Mucous protective mechanism ulcers ..
colon (dysentery) tenesmus amoeba, bilharziasis and Shigella  sigmoid colon or rectum
 dysentery sigmoid and rectum
)combined mechanism ( Excretory diarrhea

5.

liver cell failure urea Urea KEtiology

1- infective diarrhea
-

gastro enteritis

:
1- 1ry
Organism GIT bacteria : shigella, salmonella, cholera, cambylobacter
) (
virus :   Rota virus parasite giradia  ....

amoeba Not now
fungal Moniliasis .. .. .. ) ( monilia Gastroenteritis


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2- 2ry -:
GIT

* Lumen respiratory throat

.... tonsillitis ) ( Organism

Due to post nasal discharge ... sinusitis
....bronchitis
... pneumonia
* blood
Organisms GIT Urinary tract pyelonephritis GE
Or any other septic focus

infective Gastroenteritis non infective

Here there is fever & bad general conditions

1ry 2ry

1ry
) NB mechanism of diarrhea in GE is entero- toxinogenic ( entero invasive


2 - Non infective diarrhea

1- Dietetic errors
.... May over feeding .. absorption
... stool diarrhea

Gastro enteritis
......

.... GE Stool
feeding or under feeding as starvation diarrhea
artificial feeding diarrhea


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CHO ) ( fat Low protein marasmus absorption osmoticdiarrhea

2- Malabsorption
3- drug induced
common
) ( .. .. .. ...
..
diarrhea Induced diarrhea
- Also, ampicillin, oral penicillin..... not complete absorption
4- endocrinal ...... as thyrotoxicosis & pheochromocytoma
5- 2ry to systemic disease

Definition
Def : Infective diarrhea with or without fever and vomiting.

Precipitating factors:
more in summer time ....

1.

Non breast feeding > breast feeding.

2.

in bad nutritional & general condition as marasmus and Kwash.

3.

Immune deficient

4.

bad hygiene

5.

) (Clinical presentations:
Non complicated (simple GE).

1.

Fever, anorexia and malaise..... Etc.

 convulsions
Diarrhea
) ( diarrhea ... ... )... 8 (





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to determine the degree
fermentation motility stool bile
tenesemus ... .. Mucous ..
2.

Complicated:
complications ...
Complications of GE

1.

Dehydration.... water loss

2.

Electrolyte disturbance....

3.

Decrease of Bicarb.... .... stool ...... acidosis

Alkalosis ..... vomiting only
acid base
base disturbance ... diarrhea & vomiting diarrhea

Only diarrhea

4.

Decrease of water.... decrease renal blood flow.... decrease GFR.... decrease urine output
Pre renal acute renal failure & acute tubular necrosis ... -

5.

Decrease of water..... increase blood viscosity ... increase thrombosis

DIC Infection -

6.

Destruction of ( brush border of the intestine )

lactase destruction Intestine brush border ... lactase ( lactose free milk ) B  ... intolerance

7.

Malnutrition..... if repeated attacks >> IDA, marasmus , rickets.......Etc.

8.

Decrease in immunity ...... undercurrent infection.

9.

If viral GE.... antibodies.... auto immune disorders >> as reactive arthritis , Guillian Barre syndrome...

etc.
10.

If bacterial GE ....toxins... May cause septicemia, bacteremia, endocarditis ......etc.

11. Hemolytic uremic syndrome ( )

: hemolytic uremic syndrome
hemolytic bicytopenia pan cytopenia hemolytic uremic syndrome
.... gastroenteritis Intestine certain strains E.coli uremic
blood toxins entero toxins toxins gastroenteritis
Hemolysis of the RBCs
thrombocytopenia platelets toxins .... intra vascular hemolysis
thrombocytopenia
nephritis

immune complexes immune complexes

hemolytic uremic syndrome

anemia thrombocytopenia


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E.coli gastroenteritis hemolytic uremic syndrome
gastroenteritis Intestine E.coli
toxins entero toxins toxins certain strains gastroenteritis
hemolytic anemia RBCs blood
thrombocytopenia platelets
nephritis immune complexes ...
pan cytopenia nephritis
GIT

DIC viscosity thrombosis

thrombosis
rapid blood flow
normal blood viscosity
viscosity
DIC WBCs wall roughness Infection

Causes of convulsions in GE
1.

Febrile convulsion.

2.

Electrolyte disturbance.
Hypomagnesmia hypocalcemia ... tetany . bicarbonate acidosis - May also, due to hypernatermia cause convulsion

3.

May intracranial hemorrhage.

DIC

4.

May cerebral infarction ... thrombosis only.

5.

Meningitis or encephalitis. .... Due to septicemia or bacteremia.

Investigations

1.

Stool analysis.

2.

CBC... ..... due to hematocrit

dehydration -

3.

Urine analysis  UTI

& renal function   Renal failure

4.

Blood gases.... acid base disturbance.

5.

Serum electrolytes.
Treatment


....................................................................................
prophylactic:

1.

- proper breast feeding
- proper hygiene
 Rota virus  - proper vaccination
- proper nutritional state
GE weaning
Treatment of the cause.

2.

You must treat the underlying cause.

etiology symptomatic treatment onlyIf bacterial ...... give antibiotic.

)a

Fungal ....antifungal.....etc.

)b

Diet :

3.

Breast feeding....

)a

Artificial feeding.

)b

)- mild or moderate GE ( mild or moderate diarrhea

- But if Severe GE ... give lactose free milk
lactose intolerance
... ) - (
Symptomatic treatment:

4.

Fever.... antipyretic.

)a

Colic ... anti spasmodic.

)b

Vomiting..... Antiemetic.

)c

Anti diarrheal ( whatever the mechanism ) is contra indicated.
.. Motility .. paralytic illeus .. toxins ) ( .. <<<
.. stool <<< .. stool .. bulky ...brush border of intestine  inflamed & friable
Treatment of the complications.
51 52

5.


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Body fluids.

Dehydration

Electrolyte disturbance......

treatment.

acid base imbalance.

70 % body weight

) 60 %
(






30 % of body weight .... extra cellular.

40 % ..... intra cellular.

Extra cellular fluids:

5 % of body weight .... plasma.
25 % of body weight .... interstitial fluids.

Dehydration
...negative water balance
body fluids .. ... .. negative water balance
either .. intake loss
Intake Loss diarrhea vomiting Poly uria (Not hyperventilation) sweating .. Clinical manifestations of dehydration:

dehydration
) ( dehydration
70 % .. ... acute loss of body weight
!!!!
<<< loss of weight Degree of dehydration


....................................................................................
less than or equal to 10 kg

1.

mild ....

5 % body weight
moderate ....

10 % body weight
severe .....

15 % body weight
more than 10 kg.

2.

mild .....

3 % body weight
moderate .....

6 % body weight
severe .....

9 % body weight

..

100 .... 5 % 1000 ... .... 3 % ..

.. compartments .. body fluids
If extra cellular fluids ...

1.

.. plasma .. blood volume .. venous return stroke volume

cardic out put
stroke volume x heart rate
COP

... heart rate as compensatory mechanism

:
Weak pulse..... Due to decrease stroke volume.

Rapid pulse..... Increase heart rate.

heart compensation
Decrease heart rate.  Decrease COP Decrease RBF Decrease GFR oliguria


 redistribution of circulation V.C.
 as extremities and skin
) pale skin, cold skin (of the extremities only
sign
impaired capillary filling
bony prominence
.. capillaries


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capillaries << <<
................
severe hypotension & hypovolemic shock <<
2.

Decrease of interstitial fluids:

- Decrease CSF.... if still not closed anterior fontanelle

depressed anterior fontanell
- Eyes.... decrease of lacrimation ... dry eye.
decrease of retro orbital fat.... sunken eyes
Decreases of aqueous.... decrease of intra occular pressure.... soft globe.
- skin: decrease of its water .... dry skin as no sweat .... inelastic skin

3.

Decrease of intra cellular fluids:

a)

Dry mucous membrane as dry mouth.

b)

Dry tongue.
..
Peripheral receptors of thirst sensation tongue

c)

brain cells
if mild .... drowsy
if sever ... marked irritation and may lead to convulsions.
( ) dehydration in general C/P
Which degree????

1.

According to weight loss.

2 degree ... ...

2.

Clinically

a)

If no signs or symptoms of dehydration except thirst sensation

mild.....

b)

If all present but not shocked .... moderate.

c)

if shocked ..... severe.

Types of dehydration
Na , glucose and urea 3 ... blood osmolarity (dehydration Na )
275 -295 ml osmole / liter normal osmolarity 130 -150 mEq / liter Normal serum Na -

1- isotonic :


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.plasma << loss of Na and water ( .. )
this is called iso-tonic = iso-osmoler = iso natremic
intra cellular fluids extra cellular 2- Hypotonic:
So, decrease in Na more than loss of water
Na < 130  so, osmolarity < 275
Called hupotonic = hyponatremic = hypoosmolar dehydration
N.B.
.. intracellular Na .. .. extracellular fluids .. hypotonic Na .. Intra cellular Intra cellular << Extra cellular << extra cellular
..
<< relatively Na 
Intracellular fluids extracellular <<
extracellular
1- external loss ..... due to causes of dehydration.
2- internal loss .... due to intracellular fluids.

. Intra cellular C/P .. extra cellular C/P over hydration of intracellular brain edema ( coma ) .. ( )
complications fluids
3- Hypertonic dehydration :

- Na > 150 mEq/L So,
So osmolarity > 295  called hypertonic= hypernatermic = hyperosmolar
 Intra cellular relatively extracellular
So,
So, both extracellular and intra cellular are decreased but more intra cellular loss
So, may C/P of extracellular and marked manifestations of intracellular
convulsions shrunken brain cells
markedly dry mucous membranes
Marked thirst sensation
(15 )
Investigations
1.

Increase of hematocrite ... due to hemo concentration

2.

Serum Na and osmalarity according to the type

3.

Other electrolyte and acid base

4.

Renal function.
Treatment


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Rehydration therapy
1- oral
A- Indications:

)in mild and moderate cases not in severe cases .... (Shocked so, give IV.
)
B- components:

"ORS" Oral rehydration solution
Na Cl + NHCO3 + KCL + glucose
Na Cl ...... 3.5 gram - Na HCO3.... 2.5 gram - KCL.... 1.5 gram - glucose.... 20 gram
) ( 27.5 gram 1/5 C- preparations:
preparation :
200 ) ( ) (

-1
-2 GE congestion wall of the stomach decongestion

) ( 7 UP
Mental retarded ) D.D. (
alkaline  media Iron Ca absorption
N.B
D - Method of administration:
) ( cup and spoon ) (

naso-gastric tube give IV

E - Dose :
1- deficit

mild ... 60-80 ml/kg.

)a

moderate . 80-100 ml/kg.

)b

severe . 100-120 ml/kg.

)c


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4-6
2- Maintenance :
100 ml 50 ml 2- IV
Oral severe
A initial therapy ... if shocked >>> give 20 ml /kg
bicarbonate lactate Liver ringer lactate correction of acidosis

B maintenance


1st 10 kg. .. 10 ml / kg.

2nd 10 kg. . 50 ml / kg.

more than 20 kg. . 20 ml/ kg.

C - Deficit
...... dehydration degree
10 10 -1
If mild . 50 ml /kg.
If moderate
moderate
derate. 100 ml / kg.
If severe
severe.. 150 ml /kg.
10 -2
If mild..... 30 ml / kg.
If moderate.... 60 ml /kg.
If severe.... 90 ml /kg.

dehydration ...Iv type of solution


If isotonic dehydration .... isotonic solution.

if hypertonic dehydration .... hypotonic solution.

if hypotonic dehydration .... hypertonic solution.

......
......
Duration: if IV

1- if isotonic or hypotonic dehydration ...

24 correction


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-1 deficit 8 maintenance 16
-2 .. deficit  maintenance 8 16

2- if hypertonic dehydration
brain cells shrunken shrunken
.... edematous ... correction 3 ) 3 maintenance
(
maintenance


+ maintenance .... deficit

+ maintenance .... deficit

+ maintenance .... deficit

1- Hyopkalemia
3.5-4.5 mEq/L
normal serum K
serum k ... 3 hypokalemia
Excess loss of K

1.

May be . GIT . as vomiting , diarrhea or fistula

)a

gut secretion
loss of K inside the cells

)b

1- entry to inside the cells

glucose DKA
K
2- In alkalosis

... Na pump H K H ..... K Hypo kalemia ... H  ) ( alkalosis
So, alkalosis is associated with hypokalemia

Hypo kalemia tetany tetany
alkalosis


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hypo calcemia Hypokalemia hyper insulinemia
consumption of Ca+2 insulin
Hyperinsulinemia Insulin .. hypo magenesemia + Hypo calcemia + Hypokalemia
tetany and hypokalemia
alkalosis
hyper insulinemia
3- stimulation of B2 receptors in bronchus cause entry of K inside cells

C - loss of K+ in urine

distal convoluted tubules aldosterone Urine K
Angiotensin 1 angiotensin 2  aldosterone Ang. converting Enzyme
juxta glomerular apparatus renin angiotensinogen Ang. 1 : urine aldosterone -1


increase from supra renal as in conn's syndrome.

also, increase of cortisone .... has aldosterone like action as in cushing.

loss of water and K lasix loop diuretics -2
renal  as fanconi etc  re absorption of K renal tubules -3

Clinical manifestations of hypokalemia

cardic arrest bradyarrythmiac HR K -1
cause paralytic illeus ( distention ) & constipation.... abdominal motility -2
only if associated with alkalosis or hyper insulinemia.... Muscle tetany -3
Investigations
Serum
Serum K+ & investigation of the underlying causes
causes
Treatment

53 52

hyper kalemia.

hyper natremia and hypo natremia.

acidosis and alkalosis.

congenital hypertrophy pyloric stenosis.


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congenital mega colon.

mechanism of hepatomegaly.

5.5 mEq
mEq/
K /l

Causes:
1- increase intake :
K

A IV fluids
 IV fluids K IV fluid administration
B Old blood :
..
48 platelets K .... WBCs K ... RBCs 120C - drugs: as KCL containing drugs.
) K syrup ( lasix
transient
 2- Renin, angiotensin system.
kidney receptors aldosterone K Na
) (
cycle aldosterone K
) 1- captopril . (ACE inibitor
- block angiotensin converting enzyme >> no conversion of Angiotensin one to angiontensin two, >> no
aldosterone >> No K in urine
2- addison disease :
supra renal aldoesterone addison disease
3- spirolactone :
receptors )as spirolactone  ( K retaining diuretics
4- chronic renal failure :
Kidney aldosterone chronic renal failure
3-


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1- DM
Insulin DM K hyper kalemia low dose
hyperkalemia DKA 2- Acidosis
( ) H
K Na H2 as in acidosis
3- tumor lysis syndrome
as in tumor lysis syndrome K K K assessment chemotherapy tumor Oncology side effect K
Clinical manifestations :
1- On heart
heart
eart.. tachyarrhythmia.
2- On GIT
GIT. increase motility
colic and diarrhea
3- Generalized muscle weakness

threshold ionizable Ca acidosis
Investigations :
serum K > 5.5 mEq/L
Treatment :
treatment Nephrology
1- treatment of the underlying etiology.
2- Decrease of intake of K :
( K citrate )
3- increase k entry to the cells .
hypoglycemia ... insulin + glucose K
4- increase its entry to smooth ms of bronchi :
inhalation ventolin .. B2 agonist .. smooth muscle of the bronchi
5- Ca. gluconate :
.....
1- Ca inhibition of SA node act as cardio protective.
2- formation of K gluconate
excreted with bile 

K-gluconate K gluconate

6- dialysis :


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K 7 dialysis

130 -150 mEq/ L .

Normal serum sodium.....
sodium
Hyper natremia if Na > 155 mEq/ L.

Causes

mainly extracellular

3
2/3 ..
hyper natremia

1- increase of Na

1- Salty food etc.
2- IV fluids but hypertonic solution.
3- excess saline enema :
abdominal ultra sound plain X-ray abdomen ) enema (
 excess saline enema)4- slat water drinking (accedintly
hypernatremia
5- excess NaCHO3
Na  So, if excess NaCHO3 ... NaHCO3 Hyper natremia
6- increase aldosterone + cushing or steroid therapy
K
2- decrease of water

1- excessive sweating

2- Diarrhea or vomiting
pathology
3- Polyuria; as in D.M.


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Clinical manifestations :
1- Manifestations of the underlying etiology
2- if eat salt food :

a)

Dryness in mouth

b)

Increase of thirst sensation.

c)

May convulsion if brain dehydration.

Treatment :
hypotonic solution

causes
1.

Decrease in intake.
decrease intake ....
.. hypo tonic solution

2.

Excess loss.
K retention
ACE inhibitors
addison




spironolactone
chronic renal failure
3.




Excess water.

1- Psychogenic polydepsia

...
2- Excess tape water enema.
saline ... 
3- State of inapropriate secretion of ADH SIADH
... ADH
4- Diarrhea and vomiting if water loss < Na loss


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Manifestations of hyponatremia
generalized ms weakness  drowsy  due to brain odema  excessive salivation  Treatment
Treatment of the cause + hypertonic
hypertonic solution

Types:
1- ALKALOSIS
bicarb/CO2  dissolved CO2 and bicarb ratio PH either increased bicarbonate or decreased CO2 .... alkalosis PH Respiratory CO2 Metabolic HCO3 Causes of metabolic alkalosis
metabolic alkalosis
1.

Over correction of acidosis ( iatorgenic )

2.

Vomiting
bicarbonate H .. carbonic acid stomach praietal cell H2CO3  H + HCO3
bicarbonate ... HCL H
HCO3 HCL -

alkalosis bicarbonate HCL parietal cells HCL vomiting Causes of respiratory alkalosis
Respiratory alkalosis
(CO2 )
1- hypervetilation :
hyperventilation Lung
alkalosis ( Hyper ventilation ) female tetany
tetany
2- Whooping cough
CO2 CO2 prolonged expiration

( Prolonged expiration .... 5-6 )


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Clinical manifestations
tetany ionizable Ca alkalosis
2- Acidosis
acidosis PH
:
Metabolic acidosis (decrease HCO3 ) or respiratory acidosis (increase CO2)
Causes of metabolic acidosis
1- decrease HCO3  HCO 3
A from GIT :
( alkalosis vomiting ) HCO3 stool ... Diarrhea
B from Urinary system
reabsorption kidney
1- chronic renal failure 
2- Tubular defect:
-as in Fanconi syndrome , lowe syndrome , light wood syndrome (renal tubular acidosis ) and liginac
syndrome.
(acidosis tubular defect )
2- or excess consumption of HCO3 :

increase orgsnic acid release .. acids neutralization

1- any tissue hypoxia  anerobis glycolysis  increase lactic acid  lactic acidosis
2- DKA  icrease ketoacids
Causes of Resp. Acidosis
- increase CO2  as in any problem in resp. system.
C/P of acidosis
Kaussmle respiration
Investigations of acid base disturbance
BLOOD GASES
( PH,HCO3 & PCO2 ) bl. Gases 3 1- if decreased PH  means acidosis
HCO3 & PCO2 levels
- if decreased HCO3 & decreased PCO2 = Metabolic 


....................................................................................
 PH  - if increasd HCO3 & increased PCO2 = Respiratory
)  metabolic acidosis resp acidosis PH (

..
normal PH = 2 HCO3/CO2 = PH
normal HCO3 = 8  normal co2 = 4 PH = 2
1- In metabolic acidosis :
HCO3  6 1.5 = 6/4 = PH
 compensation  hypertachypnea  CO2 3
3.5
PH  metabolic HCO3 CO2 compensation
2- In Respiratory acidosis :
: CO2 retention 6  1 1/3  8/6  PH -  compensation  HCO3 synthesis HCO3 10

1 2/3  10/6  PH

PH HCO3 & CO2  due to normal compensation Respiratory CO2 HCO3 compensation
..
2- if increase PH  alkalosis
PH  - if increased both HCO3 & PCO2  metabolic
 - if both decreased  respiratory

muscle of the pylorus Lumen ) ( - more in males than in females

Age of onset.... one week after birth
at birth ) (
never present at the 1st week

C/P
1- projectile vomiting not preceded by nausea
Milk cardic sphincter Pyloric wall of the stomach


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cardic sphincter stomach Pressure lumen of the pylorus projectile vomiting not preceded by nausea
2- constipation & failure to thrive :
failure to thrive constipation
3- also, dehydration , malnutrition & oliguria
Investigations
1- clinically :
clinically
abdomen palpation contraction pylorus suckling suckling -1
( ) Pylorus
Olive green mass in right upper quadrant of the abdomen especially on suckling
2- X ray with barium meal :
string sign X-ray Barium meal
Treatment
muscle

colon stool
spinal cord signals stretch receptors called ganglion cells colon wall stool contraction fecal mass segment direct stimulation neurons
rectum
suppression of segment ( suppressors ) Inter neurons stimulation relaxation mass
ganglion cells


Rectum only..... 30 %

Recto sigmoid ....44

....44 %

All the colon.....8

colon.....8 %
segment stretch stool
Clinical Pictures

1- Prolonged constipation 
2- abdominal distention   even vomiting of feces


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Intestinal obstruction
3- palpable colon :
colon
4- if pass stool  huge amount of waztery stool of very bad odour
stool fermentation floora stool
Huge amount of watery stool
5- empty rectum :
No stool reach to it .... rectum
glycerin test prolonged constipation defecation stimulation of stretch receptors
mega colon defecation
Investigations


Barium enema.... Markedly distended colon.

Daignostic ... Biopsy of rectum ... abscence of ganglion cells

Treatment
Surgical >> Colostomy then resection anastomsis
desire ...... N.B.
54 53

basic
5 % Neonates Liver adult 2 % - Normally in newborn.... liver is palpable 3.5 cm under costal margin
12 costal margin 2 cm
hepatomegally ptosed liver ptosis & hepatomegally
5th space maximum 4th space upper border of the liver lower percussion Upper border heavy percussion
Liver span Palpation border
Normal liver span:


4-4.5 cm ...... at birth.

7 cm ............. 3 years.

9 cm ............. 12 years.
1- ptosis only

upper border ( right lobe) 5 cm costal margin 2 cm liver ptosis only Normal Liver span Hepatomegally


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2- hepatomegally only
Liver span upper border 2 cm Lower border 3- both
span 2 cm Lower upper border ptosis and hepatomegally
size comment liver palpation
costal margin cm right lobe
xiphisternum cm Left lobe
smooth or nodular surface
firm consistency
rounded or sharp border
tender
respiration
infra diaphragmatic organ  Liver
Causes of hepatomegally
hepatomegally
Liver
1- vascular space
2- biliary tract.
vascular causes dilatation of vascular spaces
1- vascular causes
... congestive liver
vascular space dilatation
obstruction heart portal
Heart hepatic Portal
:
1- Small intra hepatic venules obstruction veno-occlusive disease.
2- Obstruction of 2 common hepatic veins. Budd chiari syndrome.
3- Obstruction of IVC high (not low) IVC obstruction.
4- Constricting precarditis....
thin wall heart IVC fibrosis
5-Tricuspid stenosis or regurge ...... +++ RT atrium pressure.... Systemic congestion.
6- Right ventricular failure.
2- Dilation of biliary system
biliary obstruction

Intra hepatic and extra hepatic bile duct
1- congenital
congenital extra hepatic biliary atresia


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biliary cirrhosis intra hepatic dilation
2- may occlus
occlused by thick bile
severe hemolysis
3- may congenital dilation
choledochal cyst cyst bile duct
duct stones bile salts bile stagnation
4- pressure
biliary obstruction lymph nodes ... Cancer of pancreas Hepatomegally .... obstructive jaundice biliary system vascular causes
Liver cells
3- Liver cells

1- Increase the size of the cells.

inborn error of metabolism storage disease
2- Increase the number of the cells.
malignancy
1- From liver ... 1ry ...
as hepato balstoma. Or cirrhosis  hepato cellular carcinoma.
as leukemia, lymphoma.....etc.

2- 2ry.... Infiltration
3- Both 1&2.

Hepatitis Liver Infalmmation
size and number
edematous cells
due to infiltration with inflammatory cells number
hepatomegally Liver Inflammation
So , all causes of Hepatits lead to Hepatomegally as :
1- May be viral :


Hepato-tropic.

Non hepato-tropic.... EBV, rubella ...etc.

2- May be bacterial :


Pyogenic liver abscess.

from septicemia

Aslo syphilis

3- Parasitic or protozoal :


Toxoplasma, amoeba, fasciola, Bilharziasis.

4- May be auto immune hepatitis.


....................................................................................

1- Glycogen storage diseases:

Lactose di sacarrides lactase glucose and galactose absorption Liver galactose glucose
glucose glycogen glycogen glucose Liver glycogen glucose
) ( ... -: -1 heart stores glycogen
-2 Muscles
-3 renal tubules ... ATP

12 ) ( type 0 Liver glycogen glucose

  type 0
liver , Heart , muscles & renal tubules
C/P
1- Liver
1-History of frequent attacks of hypoglycemia
Liver In between meals
 hypoglycemia attack

2- heptomegally :
20 glycogen
hepatomegally increased glycogen stores
3- liver cirrhosis :
stores Liver cells
 may portal   liver cirrhosis destruct cells & replaced by fibrous tissue
hypertension, hepato cellular failure and carcinoma.
4- short stature :
somatomediens  short stature growing child
) (inborn error of metabolism


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2- Herat
..... heart
1- So, no hypoglycemia
2- cardiomyopathy and heart failure
ATP glucose glycogen Heart muscle
So, degeneration >>>> cardiomyopathy and heart failure 

3- Muscles
myopathy manifestation degeneration of muscle fibers Muscles affected
In ability to walk , generalized muscle weakness and hypotonia and hyporeflexia
4- renal tubules
Fanconi syndrome no reabsorptive function ... renal tubules
Fanconi Rickets

1- Failure to thrive.
2- Frequent hypoglycemic attack.
3- Hepatomegally.
4- May cirrhosis & jaundice.
5- May cardiomyopathy.
6- May myopathy.
7- May rachetic manifestations.
Investigations
glycogen
glycogen storage disease

1- glucose level
hypoglycemia attack of hypoglycemia
2- biopsy  diagnostic
glycogen cells
3- enzymatic assay
Enzymatic assay
Treatment :
1- Give small frequent meals.
2- Severe hypoglycemia
Life saving glucagon
3- The best.... liver transplantation
2- Galactosemia


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galactose- 1- phosphate galactokinase galactose
 galactose -1- Ph uridyl transferase UDP- glucose
UDP galactose + glucose -1-Ph
Epemerase enzyme UDP glucose UDP galactose

A  B
C
A  C
B
Types & C/P
galactosemia
1- Type i defect in galactokinase
cataract glactyrol Polydepsia polyuria Urine galactose
2- type ii
Defect in galactose -1- Ph uridyl transferase >>> increase in galactose -1- Ph
which is
1- hepato toxic >>>> acute hepatitis manifestations + frequent attacks of hypo glycemia
chronic
2- Also, nephro toxic.... Fanconi syndrome
3- Also, neuro toxic. MR & microcephaly
as type i  galactose

galacto kinase

3- type iii
-defect in epimerase  Increase of UDP galactose
as type ii  galactose -1-PH
Investigations
galactose and galactose 1 Ph
( ) enzymatic assay diagnostic
Treatment
Lactose & galactose free diet
Fat errors .. CHO errors

........ Gaucher disease & Neimann pick disease

Gaucher  
C/P
: abnormal sites lipid 1- liver & spleen  hepatosplenomegally


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- In Gaucher spleen > liver
- In Neimann Pick Liver > spleen
2- in Bone marrow cavity :
Pancytopenia , Pallor, purpura & repeated infection
3- In bone cortex
bony bowing and fracture
4- In CNS
neurological manifestations
5- In kidney
may Fanconi syndrome
Investigations
fat ....Biopsy
enzymatic assay
Treatment
1- Supportive and symptomatic treatment.
2- May need Bone marrow transplant, kidney transplant etc.
3- Enzymatic replacement therapy.
4 800
( )

para hydroxy phenyl pyruvic acid transaminase tyrosine

aceto acetic acid para hydroxy phenyl pyruvic acid oxidase
Para hydroxy phenyl pyruvic acid oxidase
C/P
1- increase Para hydroxy phenyl pyruvic acid which is :
A- Hepato toxic effect
hepatitis like manifestation idiopathic hepatitis
B- Frequent attacks of hypoglycemia.
C- Chronic hepatitis.
D- Nephrotoxic.... Fanconi syndrome.
2- Also, increase tyrosine.... tyrosinemia

inflammation in cornea ....corneal ulcer -1
thick palm and soles Hyperkeratosis -2
Investigations
Investigations
Enzymatic assay + Biopsy


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Treatment
inborn errors
supporting treatment + liver transplantation
Minerals
N.B.
muscle weakness Hyper kalemia

which increase ionizable Ca .... associated with acidosis ....

cupper
( - - )
cupper ceruloplasmin Liver cupper
Urine
C/P
ceruloplasmin Liver cells cupper ceruloplasmin mitochondria & lysosomes of the liver cell
destruction of the cell which is energy producer of the cell
5
.......... with un explained hepatomegaly
cupper liver cell
1- in RBCs
1st presentation hemolytic anemia RBCs 2- in Kidney
Fanconi syndrome Kidney Fanconi  tubules 1000 40 Urine cupper 3- in CNS
athetosis, chorea, parkinsonism basal ganglia neuronal cells 4- in Eye
Slit lamp Kayser flisher ring cornea 5- in Liver
Liver cirrhosis Investigations
- Increase serum cupper + decrease ceruloplasmin + Increased urinary cupper.
- Liver biopsy.
Treatment


....................................................................................
- Decrease cupper intake.
- Cupper chelating agent  penicillamine.

hematology

Infection WBCs organism Infection destructive proteolytic enzymes Organism proteolytic enzymes ... WBCs
enzymes
suppression of proteolytic enzymes Liver alpha 1 antitrypsin suppression Liver
Proteolytic inflammation effect biliary system
C/P
severe inflammation in biliary proleolytic enzyme alpha 1 antitrypsin system
biliary cirrhosis ..... cholestasis & biliary obstruction Treatment
Liver transplantation or gene therapy

hepatomegally
1- Abnormal features or not.
dull apathetic features ... mucopolysaccharidosis thalassaemic features ... chronic hemolytic anemia 2- Measures
Liver  if short stature .... measures  as in metabolic disease or congenital infections or any cause of early cirrhosis
3- Eye

1- Jaundice or not.
2- Kayser flesher ring.
3- Herpitiform corneal ulcer.... Herpes or tyrosenemia.


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4- Cataract.... galactosemia or cong. infection.
5- Cystein crystals.... lignac syndrome.
4- extremities
extremities
1- Edema.
2- Clubbing. in 1ry biliary cirrhosis.
3- Hyper keratosis in palm and soles.
4- Abnormal movement. if extra pyramidal.
5- Rachetic manifestations ( Fanconi )
5- Skin
1- Color ... pallor
2- Hemosidrosis.... dark.
3- Jaundice.
4- Purpura ... if BM failure or hypersplenism.
5- Palmer erythema.
6- Severe itching.... Due to biliary obstruction.
55 54

Splenic & superior mesentric veins  ..2 veins portal vein Liver.. portal v. Behind the head of the pancreas ..  small branch to left lobe & large branch to right lobe
: Portal tract tributaries 1- branch of hepatic artery
2- tributary of portal vein
3- branch of intrahepatic bile duct
Liver cell hepatic lobule Which is:
- Columnar cells (hepatocytes).... column of cells
small intra hepatic venules ... collect in central vein

 Called hepatic sinusoids  space -

2 common hepatic veins to IVC just below the diaphragm  -

Etiology
Etiology of portal hypertension


....................................................................................
7 mm Hg .. 5-7 mmHg portal pressure portal hyper tension
: obstruction 1- Pre sinusoidal
1- Infra hepatic.....
- mainly due to thrombus formation as in :
1- infection:
.. thrombus

activation of platelets rough wall

- As in umblical infection 
- Also as in peritonitis 
2- Increased viscosity of the blood.
- Decrease water.... As dehydration.
- Increased cells.... as polycythemia.
3- Congenital narrowing of portal vein .
2- intra hepatic :
congenital hepatic fibrosis Portal tract .. Inflammation healed by fibrosis portal tract schistosoma  Not cirrhosis
2- Sinusoidal  Cirrhosis
sinusoidal regeneration and formation cirrotic nodules degeneration of liver cell 3- Post sinusoidal :
- Budd chirari syndrome.
- Hight IVC obstruction.
- Constrictive pericarditis.
- Right failure & tricuspid regurge.
Clinical Picture
Symptoms
portal vein related congestion portal flow
1- Congestion in wall of stomach .
dyspepsia vomiting
2- Intestinal congestion.
- If mild  motility  distention and constipation
- If severe congestion  congestion.... ... congestion of villi..... Decrease absorption and secretion ...... may
lead to excretory diarrhea.
3- portal & systemic anastomosis:
To bypass the obstruction  portal & systemic flow Union


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hematemesis and melena rupture varices 
bleeding per rectum rupture Piles 
4- congested spleen.... pain in the left hypochondrium
Signs
1- Splenomegaly.
2- May mild ascites. ( Mild )
3- Massive ascites if associated with liver cell failure.
4- liver :
- If pre hepatic ...... normal.
- If hepatic..... As cirrhosis..... Shrunked.
- If post hepatic.... Enlarged with rounded border.
Investigations
1- Abdominal sonar 
 Liver & spleen condition.
 Pressure in portal vein.
2- varices or not  Do endoscopy.
Barium meal 3- Search for underlying etiology .
Treatment
No curative treatment of portal hypertension .Only supportive & symptomatic
portosystemic shunt
Acute massive hematemesis ttt 
canula -1
fresh blood as soon as possible -2
fresh blood ..
coagulation factor platelets correct anemia RBCs
.. fresh blood
fresh frozen plasma (FFP) packed RBCs
: 2-3 Vitamin K administration  -3
 fresh frozen plasma with or without packed RBCs
No advanced liver cirrhosis .. liver
varices compression Sungestaken tube -4


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. ......
Age of onset .... 1st 5 years of life

Etiology
small intra hepatic venules thrombosis

toxins
1- Aphlatoxin
2- Pyrolizidine toxin

Liver Not destroyed by heating
small intra hepatic venules thrombosis
Clinical manifestations
Acute stage
Symptoms:
1- severe pain in the right hypochondrium .
2- abdominal distention 
Signs:
Congested tender enlarged liver + ascites + jaundice.
2-3 weeks  Then partial recanalization where relieve of the pain , normal liver (not
- Acute stage last....
last
tender) but still mild enlargment & decrease in ascites
also, May liver cirrhosis .....etc.
Treatment
liver transplantation symptomatic treatment cortisone liver congested omentopexy  perotoneal sac ascites
venothrombolytic
ytic drug
veno-occlusive thrombol

thrombolytic liver hemorrhage

veno-occlusive recent thrombus
clot  Pain congested  Liver
congestion ligation of hepatic artery

hepatic artery flow Precipitating factor of hepatic coma

massive infraction in liver


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Etiology and diagnosis

1-overfeeding
50 ) 6(  13 - 12) (oliguria + constipation
 Polyuria 12 3-4
colic
over feeding
2- May gastrogastro-esophageal refelux .

cardic sphincter contraction stomach

constipation + oliguria + may under weight Mild regurge  Only wheezy chest esophagus Stomach
3- Stomach  gastritis
N.B.

....  symptom +

) - - (
antipyretics severe gastritis ) antacids (peptic ulcer antipyretics
4- Intestine
intestinal obstruction

1- Abdominal distention.
2- Increased motility.... Abdominal colic.
abdominal colic paralytic illeus
3- Absolute constipation.
4- Persistent vomiting.


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5- Gastroenteritis..... Diarrhea and vomiting.
6- Appendicitis ...
rigidity in the right iliac fossa tender
7- Accessories of the gut.
1- As acute pancreatitis.
severe pain Pain pancreas viscera
So, severe pain + Prone position + vomiting
2- Acute hepatitis
3- Cholecystitis
- Right hypochondrium pain plus or minus jaundice.
8- Non GIT causes :
1- Increased intra cranial pressure.
..
+ projectile vomiting not proceeded by nausea
2- Infectious.... toxins.... nausea and vomiting.
As pneumonia, sore throat
3- Food poisoning .
group manifestation
4- Inborn errors of metabolism.
5- Drug induced.
6- Hysterical.
" "
7- Bulimia
Induction of vomiting

constipation


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1- Esophagus: Stricture or foreign body .
2- Stomach
by stricture of forign body  pylorus
3- Intestinal obstruction
1- Dudenal atresia.
2- Mal-rotation....

3- Volvulus.....
rotation tube
4- Inguinal hernia.
5- Intussusceptions.
6- Meconium ileus.
7- Crohn's disease.... mass obstruct pathway.
8- Anal stenosis .

hematemesis & melena 2nd part of the duodenum bleeding per rectum Causes
1- Esophagus
Ulcers HCL reflux
2- Gastritis and peptic ulcer.
3- dysentery
4- Polyp.....
Ulcer
5- Intussusceptions.
6- Inflammatory bowel disease." IBD "
7- Pile or fissure.
8- Bleeding disorder 

1- Feeding disorder .
1- Over feeding.
2- under feeding .( )
3- If no eructation.... Aerphagia.
4- Milk allergy
5- Irritable mothers....


....................................................................................
catecholamines sphincter contraction wall relaxation 2- Stomach :
- Gastritis or peptic ulcer.
3- Liver :
- Hepatitis, liver abscess, congested liver, biliary stones.
4- Pancreatitis ....... pain.
5- All causes of intestinal obstruction.
6- Appendicitis.
7- Infestation with parasites as amoeba and Giardia.
8- Spleen  as stretch of its capsule
9- Acute peritonitis.
10- Renal stone or pyleonephritis.
11- Refered pain :
- Chronic cough ...... muscle strain.
- From spine..... Radicular pain.
- Basal pneumonia.
12- Systemic causes :
As uremia. - Rheumatic fever.
13- Hysterical pain........
55