( 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
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- frequent
1.

2.

frequency
if breast feeding according to usual habits
intake
called exaggerated gastro-colic reflex *
*
if artificial feeding if > 3 times /day.
Diarrhea & dysentery
Dysentery diarrhea with mucous and blood + tenesmus ( painful defecation )
+

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

, ... 6 10 :
,
mild or moderate or severe
ml water /day 600 X 100 6
600/ 10 = 60 ml / kg / day
so, mild diarrhea
1.
2.
3.

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

Moderate diarrhea.... loss 70-90 ml /kg / day
Severe diarrhea..... loss > 90 ml /kg /day
Mechanism of diarrhea

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

vein

1.
The main function.... absorption of water & well digested food.
2.
Digestive function.... .....lactase
3.
Excretion of abnormal toxins as K+ (after kidney), urea ...
- also in colon..... Excrete excess bicarbonate.
GIT .... Mucous secreting cells .... Its function
1- lubrication of food ( )
mucous ... .... jejunum ..... Mucous gut PH duodenum alkaline acidic media neutral

stool bulky ... colon Ileum 2- mucous also , protect mucosa from digestive juice & PH of the lumen
Mechanism of diarrhea
1.
Entero- toxinogenic pathway:
invasion of the wall ...... Entero toxin organism toxins Organism
Organism ) secretion absorption ......... to cells ..... increase CAMP
(
absorption ..... digestive food
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) ( ) Mucous blood ) watery
???? 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
3.
Increase motility of the gut
No complete absorption of food.
DD from osmotic diarrhea
.... Here with severe abdominal colic ...
as in:
- thyrotoxicosis .... where increased motility.
- pheochromocytoma...... increase motility.
4.
Entero-invasive pathway:
Organism Lumen toxins villi absorption surface No digestion .... No absorption
ulcers stool Mucous protective mechanism ulcers ..
colon (tenesmus (dysentery sigmoid colon or rectum amoeba, bilharziasis and Shigella
dysentery sigmoid and rectum
)5.combined mechanism ( Excretory diarrhea
liver cell failure urea Urea KEtiology

1- infective diarrhea
gastro enteritis
:
1- 1ry
Organism GIT - bacteria :


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shigella, salmonella, cholera, cambylobacter
) (
virus : Rota virus parasite giradia ....

amoeba Not now
fungal Moniliasis .. .. .. ) (
monilia Gastroenteritis
2- 2ry : GIT

* Lumen respiratory throat

.... tonsillitis ) ( Organism

sinusitis ... Due to post nasal discharge
....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
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feeding or under feeding as starvation diarrhea
artificial feeding diarrhea
CHO ) ( fat Low protein marasmus absorptionosmotic diarrhea

2- Malabsorption
3- drug induced
common
) ( .. .. .. ...
..
diarrhea Induced diarrhea
Also, ampicillin, oral penicillin..... not complete absorption4- endocrinal ...... as thyrotoxicosis &pheochromocytoma
5- 2ry to systemic disease

Definition
Def : Infective diarrhea with or without fever and vomiting.
Precipitating factors:
1.more in summer time ....
2.Non breast feeding > breast feeding.
3.in bad nutritional & general condition as marasmus and Kwash.
4.Immune deficient
5.bad hygiene
) (Clinical presentations:
1.Non complicated (simple GE).
Fever, anorexia and malaise..... Etc.
convulsions
Diarrhea
) (diarrhea ... ... )... 8 (
to determine the degree
bile stool motility fer
mentation
.. Mucous .. ... tenesemus
2.Complicated:
... complications
Complications of GE
1.
Dehydration.... water loss
2.
Electrolyte disturbance....
3.
.... stool ...... acidosis Decrease of Bicarb....
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vomiting only ..... Alkalosis
acid base ... diarrhea & vomiting diarrhea
disturbance

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 ( B ( lactose free milk ... 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
bicytopenia pan cytopenia hemolytic uremic syndrome
gastroenteritis Intestine certain strains E.coli hemolytic 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

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


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1.
2.

3.
4.
5.

Causes of convulsions in GE
Febrile convulsion.
Electrolyte disturbance.
Hypomagnesmia hypocalcemia ... tetany . bicarbonate acidosis - May also, due to hypernatermia cause convulsion
May intracranial hemorrhage.
DIC
May cerebral infarction ... thrombosis only.
Meningitis or encephalitis. .... Due to septicemia or bacteremia.

Investigations
Stool analysis.
CBC........ due to hematocrit
dehydration 3.
Urine analysis UTI
& renal function Renal failure
4.
Blood gases.... acid base disturbance.
5.
Serum electrolytes.
Treatment
1.
2.

1.

prophylactic:

proper
proper
proper
proper

2.
a)
b)
3.
a)
b)

breast feeding
hygiene
vaccination Rota virus
nutritional state

weaning GE
Treatment of the cause.
You must treat the underlying cause.
symptomatic treatment only etiology If bacterial ...... give antibiotic.
Fungal ....antifungal.....etc.
Diet :
Breast feeding....
Artificial feeding.

- mild or moderate GE ( mild or moderate diarrhea)

- But if Severe GE ... give lactose free milk
lactose intolerance
( - ) ...
4.
Symptomatic treatment:
a)
Fever.... antipyretic.
b)
Colic ... anti spasmodic.
c)
Vomiting..... Antiemetic.

.Anti diarrheal ( whatever the mechanism ) is contra indicated


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.. Motility .. paralytic illeus .. toxins ) ( .. >>>

.. stool >>> .. stool .. bulky ... brush border of intestine inflamed & friable
Treatment of the complications.

5.

51 52

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 (sweating (Not hyperventilation
..
Clinical manifestations of dehydration:

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

:
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1.

2.

1.

less than or equal to 10 kg

mild ....
body weight % 5
moderate ....
body weight % 10
severe .....
body weight % 15
more than 10 kg.
mild .....
body weight % 3
moderate .....
body weight % 6
severe .....
body weight % 9

..

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

.. body fluids .. compartments
If extra cellular fluids ...
stroke volume .. venous return .. blood volume .. plasma
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.

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


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

2.

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3.
a)
b)

c)

Decrease of intra cellular fluids:

Dry mucous membrane as dry mouth.
Dry tongue.
..
Peripheral receptors of thirst sensation tongue
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 )
ml osmole / liter 295- 275 normal osmolarity mEq / liter 150- 130 Normal serum Na 1- isotonic :
. 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
Na .. .. extracellular fluids .. hypotonic >> Intra cellular Extra cellular >> extra cellular .. intracellular
.. Na .. Intra 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 ( brain edema ( coma .. ( )

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intracellular fluids complications
3- Hypertonic dehydration :

- Na > 150 mEq/L So, osmolarity > 295 called hypertonic= hypernatermic = hyperosmolar
extracellular relatively Intra cellular
So, both extracellular and intra cellular are decreased but more intra cellular loss
So, may C/P of extracellular and marked manifestations of intracellular
shrunken brain cells convulsions
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
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
) ( gram 27.5 1/5 C- preparations:
preparation :
200 ) ( ) (

-1
-2 GE congestion wall of the stomach
decongestion

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

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naso-gastric tube give IV
E - Dose :
1- deficit
)a
mild ... 60-80 ml/kg.
)b
moderate . 80-100 ml/kg.
)c
severe . 100-120 ml/kg.

6-4
2- Maintenance :
ml 100 ml 502- IV
severe Oral
A initial therapy ... if shocked >>> give 20 ml /kg
ringer lactate Liver lactate bicarbonate 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
degree ...... dehydration
-1 10 10
mild . 50 ml /kg.
moderate. 100 ml / kg.
severe.. 150 ml /kg.
-2 10
mild..... 30 ml / kg.
moderate.... 60 ml /kg.
severe.... 90 ml /kg.

If
If
If

If
If
If

type of solution ...Iv dehydration

If isotonic dehydration .... isotonic solution.
if hypertonic dehydration .... hypotonic solution.
if hypotonic dehydration .... hypertonic solution.
......
......

Duration: if IV

1- if isotonic or hypotonic dehydration ...
correction 24

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

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

+ maintenance .... deficit

+ maintenance .... deficit

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

May be . GIT . as vomiting , diarrhea or fistula
gut secretion
loss of K inside the cells

)a
)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
hyper insulinemia Hypokalemia hypo calcemia
insulin consumption of Ca+2
.. Hypokalemia + Hypo calcemia + hypo magenesemia Insulin
Hyperinsulinemia
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

K Urine aldosterone distal convoluted tubules
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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
re absorption of K as fanconi etc renal tubules -3
renal
Clinical manifestations of hypokalemia
cardic arrest bradyarrythmiac HR K -1
( abdominal motility ....& constipation cause paralytic illeus ( distention -2
Muscle tetany ....only if associated with alkalosis or hyper insulinemia -3

Investigations
Serum K+ & investigation of the underlying causes
Treatment

53 52

hyper kalemia.
hyper natremia and hypo natremia.
acidosis and alkalosis.
congenital hypertrophy pyloric stenosis.
congenital mega colon.
mechanism of hepatomegaly.

mEq/l 5.5 K

Causes:
1- increase intake :
K

A IV fluids
IV fluid administration K IV fluids
B Old blood :
..
.... K platelets 48 ... K WBCs 120 RBCs C - drugs: as KCL containing drugs.
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lasix ) ( K syrup
transient
2- Renin, angiotensin system.
Na K aldosterone receptors kidney
( )
K aldosterone cycle
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 :
addison disease aldoesterone supra renal
3- spirolactone :
(as spirolactone ( K retaining diuretics receptors
4- chronic renal failure :
chronic renal failure aldosterone Kidney
3-
1- DM
Insulin DM K hyper kalemia low dose
hyperkalemia DKA 2- Acidosis
( ) H
K Na H2 as in acidosis
3- tumor lysis syndrome
K as in tumor lysis syndrome K K assessment chemotherapy tumor Oncology side effect K
Clinical manifestations :
1- On heart.. tachyarrhythmia.
2- On 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.

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2- formation of K gluconate
gluconate K , K-gluconate excreted with bile
6- dialysis :
K 7 dialysis

Normal serum sodium..... 130 -150 mEq/ L .

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 NaHCO3 ...So, if excess NaCHO3 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.
Clinical manifestations :
1- Manifestations of the underlying etiology
2- if eat salt food :
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a)
b)
c)

Dryness in mouth
Increase of thirst sensation.
May convulsion if brain dehydration.
Treatment :
hypotonic solution

causes
1.
2.

3.

Decrease in intake.
decrease intake ....
.. hypo tonic solution
Excess loss.
K retention
ACE inhibitors

addison

spironolactone

chronic renal failure

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

Types:
1- ALKALOSIS
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1.

dissolved CO2 and bicarb bicarb/CO2 ratio PH alkalosis .... either increased bicarbonate or decreased CO2 PH Respiratory CO2 Metabolic HCO3 Causes of metabolic alkalosis
metabolic alkalosis
Over correction of acidosis ( iatorgenic )

2.

Vomiting

bicarbonate H .. carbonic acid stomach praietal cell H2CO3 H + HCO3

bicarbonate ... HCL H
HCO3 HCL bicarbonate HCL parietal cells HCL vomiting alkalosis
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 .... 6-5 (
Clinical manifestations
tetany ionizable Ca alkalosis
Acidosis -2
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
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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
3 bl. Gases ( ( PH,HCO3 & PCO21- 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 PH = HCO3/CO2
normal HCO3 = 8 normal co2 = 4 PH = 2
: In metabolic acidosis -1
HCO3 6 PH = 6/4 = 1.5
compensation hypertachypnea CO2 3
3.5
PH metabolic HCO3 CO2 compensation
: In Respiratory acidosis -2
: CO2 retention 6 PH 8/6 1 1/3 compensation HCO3 synthesis HCO3 10 PH 10/6 12/3
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 stomach Pressure lumen of the pylorus projectile vomiting not preceded by nausea sphincter
2- constipation & failure to thrive :
constipation
failure to thrive
3- also, dehydration , malnutrition & oliguria
Investigations
1- clinically :
clinically
palpation contraction pylorus suckling suckling -1
( ) Pylorus abdomen
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
signals stretch receptors called ganglion cells colon wall contraction fecal mass segment direct stimulation neurons spinal cord
rectum stool
suppression of ( suppressors ) Inter neurons stimulation relaxation mass segment
ganglion cells

Rectum only..... 30 %

Recto sigmoid ....44 %

All the colon.....8 %

segment stretch stool
Clinical Pictures
1- Prolonged constipation
2- abdominal distention even vomiting of feces
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

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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 cm 2
hepatomegally ptosed liver ptosis & hepatomegally
5th space maximum 4th space upper border of the liver percussion Upper border heavy percussion
Liver span Palpation lower border
Normal liver span:

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

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

9 cm ............. 12 years.
1- ptosis only
upper border ( cm (right lobe 5 costal margin cm 2 liver Normal Liver span Hepatomegally
ptosis only
2- hepatomegally only
Liver span upper border cm 2 Lower border 3- both
span cm 2 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
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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.
Dilation of biliary system -2
biliary obstruction

Intra hepatic and extra hepatic bile duct
1- congenital extra hepatic biliary atresia
biliary cirrhosis intra hepatic dilation
2- may 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 obstructive jaundice .... Hepatomegally biliary system vascular causes
Liver cells
Liver cells -3

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.
2- 2ry.... Infiltration as leukemia, lymphoma.....etc.
3- Both 1&2.

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

Hepato-tropic.
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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
Liver -1
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
2- Herat
..... heart
1- So, no hypoglycemia

24


....................................................................................
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 renal tubules ... no reabsorptive function
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 storage disease

1- glucose level
attack of hypoglycemia
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

galactose- 1- phosphate galactokinase galactose

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

AB
C
A C
B
Types & C/P
galactosemia
1- Type i defect in galactokinase
glactyrol Polydepsia polyuria Urine galactose
cataract
25


....................................................................................
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
galactose -1-PH as type ii
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
- 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
26

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

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

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 tubules 1000 40 Urine cupper Fanconi
3- in CNS
athetosis, chorea, parkinsonism basal ganglia neuronal cells 4- in Eye
Slit lamp Kayser flisher ring cornea 5- in Liver
Liver cirrhosis 27


....................................................................................
-

Investigations
Increase serum cupper + decrease ceruloplasmin + Increased urinary cupper.
Liver biopsy.
Treatment
Decrease cupper intake.
Cupper chelating agent penicillamine.

hematology

Infection WBCs organism Infection proteolytic enzymes Organism proteolytic enzymes ... WBCs
destructive enzymes
suppression of proteolytic enzymes Liver alpha 1 antitrypsin suppression Liver
Proteolytic inflammation effect biliary system
C/P
severe inflammation in proleolytic enzyme alpha 1 antitrypsin biliary 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 measures .... if short stature as in metabolic disease or congenital infections or any cause of early cirrhosis
3- Eye

1234541234-

Jaundice or not.
Kayser flesher ring.
Herpitiform corneal ulcer.... Herpes or tyrosenemia.
Cataract.... galactosemia or cong. infection.
Cystein crystals.... lignac syndrome.
extremities
extremities
Edema.
Clubbing. in 1ry biliary cirrhosis.
Hyper keratosis in palm and soles.
Abnormal movement. if extra pyramidal.
28


....................................................................................
55123456-

Rachetic manifestations ( Fanconi )

Skin
Color ... pallor
Hemosidrosis.... dark.
Jaundice.
Purpura ... if BM failure or hypersplenism.
Palmer erythema.
Severe itching.... Due to biliary obstruction.
55 54

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

Etiology of portal hypertension

mm Hg 7 .. mmHg 7-5 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 29


....................................................................................
Not cirrhosis
2- Sinusoidal Cirrhosis
regeneration and formation cirrotic nodules degeneration of liver cell sinusoidal
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:
portal & systemic flow To bypass the obstruction Union 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
Abdominal sonar
Liver & spleen condition.
Pressure in portal vein.
varices or not Do endoscopy.
Barium meal 3- Search for underlying etiology .
1

2-

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
30


....................................................................................
.. fresh blood
( fresh frozen plasma (FFP packed RBCs
: 3-2 Vitamin K administration -3
fresh frozen plasma with or without packed RBCs
No advanced liver cirrhosis .. liver
varices compression Sungestaken tube -4

. ......
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.
- Acute stage last.... 2-3 weeks Then partial recanalization where relieve of the pain , normal liver
(not tender) but still mild enlargment & decrease in ascites
also, May liver cirrhosis .....etc.
Treatment
- liver transplantation
symptomatic treatment cortisone liver congested perotoneal sac omentopexy ascites
veno-occlusive thrombolytic drug

thrombolytic liver hemorrhage

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

hepatic artery flow Precipitating factor of hepatic coma

massive infraction in liver

31

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

Etiology and diagnosis

1-overfeeding
50 ) 6( 12 13 ) (oliguria + constipation Polyuria 12 4-3
colic
over feeding
2- May gastro-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.
5- Gastroenteritis..... Diarrhea and vomiting.
6- Appendicitis ...
tender rigidity in the right iliac fossa
7- Accessories of the gut.
1- As acute pancreatitis.
severe pain viscera pancreas Pain
So, severe pain + Prone position + vomiting
2- Acute hepatitis
32


....................................................................................
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
1- Esophagus: Stricture or foreign body .
2- Stomach
pylorus by stricture of forign body
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
33


....................................................................................
2- Gastritis and peptic ulcer.
3- dysentery
4- Polyp.....
Ulcer
5678-

Intussusceptions.
Inflammatory bowel disease." IBD "
Pile or fissure.
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

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