Chronic Diarrhea: Causes and Consequences
undefined
C
h
r
o
n
i
c
D
i
a
r
r
h
e
a
Presented by:
•
Bandar Dallak
•
Faisal Al-Qahtani
•
Ali Al-Zahrani
•
Saeed Al-Shreef
I
n
t
r
o
d
u
c
t
i
o
n
:
Diarrhea is an increase in fluidity, volume
and frequency of stools relative to the
usual habits of an individual.
≥
3/day loose, watery stool.
I
n
t
r
o
d
u
c
t
i
o
n
:
The great majority of diarrhea episodes
last less than one week;
When diarrhea persists for more than 14
days, it is called persistent, intractable, or
chronic diarrhea.
I
n
t
r
o
d
u
c
t
i
o
n
:
In the developing world, persistent
diarrhea usually follows an acute episode
and typically is associated with serial
enteric infections without time to recover
between episodes.
Children are at risk of malnutrition and
often have other intercurrent illnesses,
such as respiratory infections.
I
n
t
r
o
d
u
c
t
i
o
n
:
In developed countries, children are less
likely to be exposed to serial enteric
infections and malnutrition.
In these populations, chronic diarrhea is
more likely to be caused by underlying
disease, such as celiac disease or other
food allergy.
I
n
t
r
o
d
u
c
t
i
o
n
:
Sequelae:
Dehydration.
Marked weight loss and malnutrition.
FTT.
T
h
e
r
e
a
r
e
f
o
u
r
b
a
s
i
c
p
a
t
h
o
p
h
y
s
i
o
l
o
g
i
c
a
l
c
a
t
e
g
o
r
i
e
s
o
f
d
i
a
r
r
h
e
a
(1)
Osmotic Diarrhea
: when an ingested
solute is not absorbed properly, the higher
concentration gradient within the gut lumen
acts to draw water into intestinal lumen and
greatly increases the water content of the
stool. The classic example of this is the
diarrhea caused by lactose intolerance.
Enteric infections may also cause
malabsorption via damage to intestinal
epithelial cells (ex. Rotavirus or Shigella).
(
2
)
S
e
c
r
e
t
o
r
y
D
i
a
r
r
h
e
a
:
t
h
i
s
d
i
a
r
r
h
e
a
i
s
c
a
u
s
e
d
b
y
t
h
e
i
n
t
e
s
t
i
n
e
a
c
t
i
v
e
l
y
s
e
c
r
e
t
i
n
g
w
a
t
e
r
i
n
t
o
t
h
e
g
u
t
l
u
m
e
n
.
I
n
f
e
c
t
i
o
n
s
s
u
c
h
a
s
C
h
o
l
e
r
a
,
C
l
o
s
t
r
i
d
i
a
P
e
r
f
r
i
n
g
e
n
s
,
C
l
o
s
t
r
i
d
i
a
D
i
f
f
i
c
i
l
e
,
E
.
C
o
l
i
,
S
t
a
p
h
.
A
u
r
e
u
s
,
a
n
d
S
h
i
g
e
l
l
a
a
l
l
c
a
u
s
e
s
e
c
r
e
t
o
r
y
d
i
a
r
r
h
e
a
m
a
i
n
l
y
v
i
a
p
r
e
f
o
r
m
e
d
e
n
t
e
r
o
t
o
x
i
n
s
.
(
3
)
I
n
f
l
a
m
m
a
t
o
r
y
D
i
a
r
r
h
e
a
:
I
n
t
e
s
t
i
n
a
l
i
n
f
l
a
m
m
a
t
i
o
n
c
a
n
l
e
a
d
t
o
b
l
o
o
d
,
m
u
c
u
s
,
a
n
d
p
r
o
t
e
i
n
e
x
u
d
a
t
e
l
o
s
s
e
s
,
a
c
c
o
m
p
a
n
i
e
d
b
y
f
l
u
i
d
a
n
d
e
l
e
c
t
r
o
l
y
t
e
s
.
T
h
e
m
o
s
t
c
o
m
m
o
n
c
a
u
s
e
o
f
t
h
i
s
t
y
p
e
o
f
d
i
a
r
r
h
e
a
i
s
i
n
f
e
c
t
i
o
n
b
u
t
c
a
n
a
l
s
o
b
e
d
u
e
t
o
c
h
r
o
n
i
c
d
i
s
e
a
s
e
s
s
u
c
h
a
s
I
B
D
o
r
C
e
l
i
a
c
D
i
s
e
a
s
e
.
(
4
)
D
i
a
r
r
h
e
a
d
u
e
t
o
M
o
t
i
l
i
t
y
D
i
s
o
r
d
e
r
s
:
a
l
t
h
o
u
g
h
u
n
c
o
m
m
o
n
,
b
o
t
h
a
n
i
n
c
r
e
a
s
e
a
n
d
a
d
e
c
r
e
a
s
e
i
n
g
u
t
m
o
t
i
l
i
t
y
c
a
n
b
e
a
c
a
u
s
e
o
f
d
i
a
r
r
h
e
a
.
N
o
t
e
:
d
i
a
r
r
h
e
a
c
a
n
b
e
c
a
u
s
e
d
b
y
o
n
e
o
r
a
n
y
c
o
m
b
i
n
a
t
i
o
n
o
f
t
h
e
s
e
c
a
t
e
g
o
r
i
e
s
C
a
u
s
e
s
C
A
U
S
E
S
:
Viral, parasitic, bacterial,..
•
Hyperthyroidism.
•
Adrenal insufficiency.
•
Lactase deficiency.
•
Glucose-glactose
malabsorption.
Cow’s Milk/soy
protein intolerance.
Agammaglobulinemia
IgA deficiency.
AIDS.
Familial chloride
diarrhea.
Cystic fibrosis.
Celiac disease.
I
n
f
e
c
t
i
o
n
s
T
y
p
h
o
i
d
:
Caused by
S. typhi and S.
paratyphi
.
Transmitted through contact
with infected animals e.g.,
chicken, or through
contaminated food e.g.,
eggs, dairy products.
T
y
p
h
o
i
d
:
C/P:
Bactremia and high grade fever that usually
precede the enteric phase.
Diarrhea (usually after 1 week)
Abdominal pain.
Nausea.
Loss of appetite.
CNS signs ( severe) : coma, meningism, fits..
If untreated, the disease persists 2-3 weeks with
marked weight loss, hematochezia, melena.
T
y
p
h
o
i
d
:
Treatment:
Ciprofloxacin (best)
Alternative for ciprofloxacin resistance
Ceftriaxone or
azithromycin
Co-trimoxazole (TMP-SMZ)
Dexamethazone
P
a
r
a
s
i
t
i
c
:
Giardia Lamblia.
Entamoeba histolytica.
Cryptosporidium parvum.
A
m
e
b
i
a
s
i
s
:
C/P:
Intestinal:
Acute onset of mild diarrhea. or
Amebic dysentry: perfuse diarrhea with
blood, tenesmus, severe abd. pain
Extra intestinal:
- amebic liver abscess (fever, sweats, RUQ
pain, high WBCs..)
-may invade lung or brain also..
A
m
e
b
i
a
s
i
s
:
Diagnosis:
Stool microscopy
Fecal antigen detection
Serology
US/CT .. Aspiration
Treatment:
metronidazole:
With diloxanide furoate (cyst)
Tinidazole ( severe )
G
i
a
r
d
i
a
l
a
m
b
l
i
a
:
is transmitted through ingestion of cysts
from contaminated food or drinks.
Adheres to microvilli of dudenal or jejunal
epithelium.
G
i
a
r
d
i
a
l
a
m
b
l
i
a
:
C/P :
diarrhea
Bloating , flatulence
Abdominal pain
Explosive diarrhea
Malapsorption
Weight loss
Diagnosis:
Direct fluorescent antibody (DFA) >> gold
standard
Stool microscopy>> may be (--)
Treatment:
Tinidazole
paromomycin
C
e
l
i
a
c
D
i
s
e
a
s
e
C
e
l
i
a
c
D
i
s
e
a
s
e
:
abnormal small intestine mucosa due to intestinal
reaction to gliadin, a component of gluten.
Etiology
Only autoimmune disease in which androgen (alpha-
gliadin) is recognized.
Associated with other autoimmune diseases, especially
thyroid disease.
Gluten, a protein in cereal grains, is toxic factor.
Associated with HLA-DQ2 and with HLA-DQ8
C
e
l
i
a
c
D
i
s
e
a
s
e
:
Clinical Features
classically: diarrhea, weight loss, anemia,
symptoms of vitamin/ mineral deficiency, failure
to thrive; now more commonly bloating, gas,
iron deficiency.
improves with gluten-free diet, deteriorates
when gluten reintroduced.
disease is usually most severe in proximal bowel;
therefore iron, calcium, and folic acid
deficiency common
C
e
l
i
a
c
D
i
s
e
a
s
e
:
Investigations:
small bowel mucosal
biopsy
(usually
duodenum) :
villous atrophy and crypt hyperplasia
increased number of plasma cells and
lymphocytes in lamina propria.
C
e
l
i
a
c
D
i
s
e
a
s
e
:
Investigations:
Evidence of Malabsorption:
Steatorrhea
Low levels of ferritin/iron saturation, Ca, Fe,
albumin, cholesterol, carotene, B12
absorption
C
e
l
i
a
c
D
i
s
e
a
s
e
:
Investigations:
Serology:
anti-transglutaminase antibodies, TTG
Fecal fat >7% over 72 hrs
C
e
l
i
a
c
D
i
s
e
a
s
e
:
Treatment:
Dietary counselling:
Gluten free diet: avoid barley, rye, wheat,
maybe oats (if not contaminated by other
grains).
Starchy foods e.g., rice are safe.
Iron, folate supplementation (with
supplementation of other vitamins as needed)
C
e
l
i
a
c
D
i
s
e
a
s
e
:
Prognosis:
associated with increased risk of
lymphoma, carcinoma including small
bowel and colon.
These can be avoided if adherent to diet.
C
y
s
t
i
c
F
i
b
r
o
s
i
s
C
y
s
t
i
c
F
i
b
r
o
s
i
s
:
Autosomal Recessive.
Gene on long arm of chromosome 7
encoding for CFTR (
Cystic Fibrosis Transmembrane
Regulator
).
CFTR is a Chloride channel regulating
Chloride transport and possibly sodium.
This is responsible for elevated sweat chloride
in 99% of patients.
C
y
s
t
i
c
F
i
b
r
o
s
i
s
:
CF is characterized by widespread
exocrine dysfunction.
C
y
s
t
i
c
F
i
b
r
o
s
i
s
:
GI Manifestation:
More prominent in infants.
Meconium ileus.
Greasy stools and fl atulence.
Pancreatitis.
Biliary cirrhosis.
Jaundice.
C
y
s
t
i
c
F
i
b
r
o
s
i
s
:
GI symptoms are more prominent in infancy,
while pulmonary manifestations predominate
thereafter.
C
y
s
t
i
c
F
i
b
r
o
s
i
s
:
Dx.:
Sweat chloride Test:
> 60 mEq/L.
Genetic analysis:
Are confirmatory.
C
y
s
t
i
c
F
i
b
r
o
s
i
s
:
Others:
DM.
Infertility.
Unexplained hyponatremia.
Fat soluble vitamins (A, D, E, K) deficiency.
..etc.
C
y
s
t
i
c
F
i
b
r
o
s
i
s
:
Management.:
Pulmonary manifestations :are managed with chest
physical therapy, bronchodilators, corticosteroids,
antibiotics, and DNase.
Administer pancreatic enzymes and fat-soluble
vitamins A, D, E, and K for malabsorption.
Nutritional counseling and support with a high-calorie
and high-protein diet are essential for health
maintenance.
I
B
D
I
n
f
l
a
m
m
a
t
o
r
y
B
o
w
e
l
D
i
s
e
a
s
e
s
I
B
D
s
:
Epidemiology:
More common Jewish.
The incidence of IBDs is increasing especially in
industrialized countries.
Environmental factors are needed to drive the
disease in genetically susceptible individuals.
30 folds increased risk in those with first degree
relatives involved.
C
r
o
h
n
’
s
D
i
s
e
a
s
e
:
May involve any part of GIT.
The commonest site is illeocecal junction.
Discontinuous pattern “ SKIP LESIONS ”.
Rectum is often spared.
C
r
o
h
n
’
s
D
i
s
e
a
s
e
:
C/P:
Abdominal pain.
Abdominal tenderness.
Abdominal mass.
Low grade fever.
Weight loss.
Watery diarrhea.
Perianal fissure/fistula.
U
l
c
e
r
a
t
i
v
e
C
o
l
i
t
i
s
:
Mainly affect the colon.
The rectum is always involved.
May extend proximally in a continuous
fashion.
U
l
c
e
r
a
t
i
v
e
C
o
l
i
t
i
s
:
C/P:
Bloody diarrhea.
Lower abdominal cramps.
Tenesmus.
Urgency.
Abdominal pain/tenderness.
Blood on rectum.
Usually, no abdominal mass.
E
x
t
r
a
i
n
t
e
s
t
i
n
a
l
M
a
n
i
f
e
s
t
a
t
i
o
n
s
o
f
I
B
D
s
:
Aphthous stomatitis,
Episcleritis/uveitis,
Arthritis,
Erythema nodosum,
Pyoderma gangrenosum.
I
n
f
l
a
m
m
a
t
o
r
y
B
o
w
e
l
D
i
s
e
a
s
e
s
I
B
D
s
:
Investigations:
Blood test.
Endoscopy.
Colonscopy.(biopsy)
Plane Abdominal XR.
US, CT.
I
n
f
l
a
m
m
a
t
o
r
y
B
o
w
e
l
D
i
s
e
a
s
e
s
I
B
D
s
:
Management:
5-ASA.
Steroids.
Azathioprine.
Infliximab
MTX.
-surgical
G
l
u
c
o
s
e
-
g
a
l
a
c
t
o
s
e
m
a
l
a
b
s
o
r
p
t
i
o
n
Glucose-Galacose
Malabsorption:
a condition in which the cells lining
the intestine cannot take in the
sugars glucose and galactose.
Generally becomes apparent in the first few
weeks of a baby's life.
Glucose-Galacose
Malabsorption:
C/P:
Severe diarrhea.
Life-threatening dehydration,
Increased acidity of the blood and tissues
(acidosis), and
weight loss
This occurs when fed breast milk or regular infant
formulas.
Glucose-Galacose
Malabsorption:
C/P:
However, they are able to digest fructose-based
formulas that do not contain glucose or
galactose.
Some affected children are better able to
tolerate glucose and galactose as they get
older.
Glucose-Galacose
Malabsorption:
C/P:
Small amounts of glucose in the urine (mild
glucosuria).
Affected individuals may also develop
kidney
stones
or more widespread deposits of calcium
within the kidneys.
Familial Chloride
Losing Enteropathy
Familial Chloride Losing
Enteropathy:
An inherited defect of chloride absorption in
ileum and colon.
Defect in chloride-bicarbonate exchange
protein.
Presents since birth with abdominal distension
and watery diarrhea.
A
p
p
r
o
a
c
h
History:
Age:
Duration:
Consistency? Blood? Mucus? Pus?
Offensive?
Frequency?
Volume?
Associated symptoma:
Vomiting? Fever? Abdominal pain? Tenesmus?
Convulsion? Cough? Appetite? Weight loss? Height
intolerance? Tremorr?
Type and quantity of milk? Food?
History:
Allergy to food?
Past history of similar attack? How frequent?
Past Medical and Surgical Histoty?
Family hx of a similar condition?
Living conditions?
Drug history?
Travel history?
P
H
Y
S
I
C
A
L
E
X
A
M
I
N
A
T
I
O
N
G
E
N
E
R
A
L
:
General appearance and mental status
Vital signs
Growth Parameters: FTT???
Hydration assessment.
Orthostasis- volume depletion,autonomic
dysfunction
Pallor?
Exophthalmos
(hyperthyroidism)
Aphthous ulcers
(IBD and celiac disease)
Lymphadenopathy
(malignancy, infection
or Whipple's disease)
Thyroid Examinations:
Clubbing
(liver disease, IBD, laxative abuse,
celiac disease,)
S
K
I
N
L
E
S
I
O
N
S
Dermatitis herpetiformis
(celiac disease)
Erythema nodosum and pyoderma
gangrenosum
(IBD)
Hyperpigmentation
(Addison's disease)
A
B
D
O
M
I
N
A
L
E
X
A
M
I
N
A
T
I
O
N
Surgical scars
Abdominal tenderness
Masses
Hepatosplenomegaly
Auscultation:
Malabsorption
bacterial overgrowth
obstruction, or rapid intestinal
transit.
P
E
R
I
N
E
A
L
A
N
D
R
E
C
T
A
L
E
X
A
M
I
N
A
T
I
O
N
Ulcers
fissures
abscesses
Fistulas
stenoses.
S
Y
S
T
E
M
I
C
E
X
A
M
I
N
A
T
I
O
N
Chest Examinations?
Joints: Arthritis (IBD, Whipple's disease)
I
N
V
E
S
T
I
G
A
T
I
O
N
S
I
N
V
E
S
T
I
G
A
T
I
O
N
S
:
Investigations are directed by clinical findings:
CBC.
Stool culture.
Electrolytes.
RFTs.
endoscopy, clonoscopy,
TFTs,
Antibody test for celiac disease.
Sweat chloride test.
Trial of lactose restriction? Lactose breath
hydrogen.
C
o
n
c
l
u
s
i
o
n
:
C
o
n
c
l
u
s
i
o
n
:
Chronic diarrhea lasts more than 2 weeks.
Has wide range of causes.
Causes can be infectious, familial , inherited,
metabolic,…
May interfere with normal growth of child.
Careful assessment and detection of the
underlying cause is needed to prevent serious
sequele.
Chronic diarrhea is characterized by persistent loose, watery stools lasting more than 14 days. The condition can be caused by various factors such as osmotic, secretory, inflammatory, or motility disorders. In developing countries, it often follows acute infections, while in developed countries, underlying diseases like celiac disease or food allergies may be the culprits. Children are particularly at risk of malnutrition and dehydration due to chronic diarrhea, making early diagnosis and management crucial.
Download Presentation
Please find below an Image/Link to download the presentation.
The content on the website is provided AS IS for your information and personal use only. It may not be sold, licensed, or shared on other websites without obtaining consent from the author. Download presentation by click this link. If you encounter any issues during the download, it is possible that the publisher has removed the file from their server.
E N D
Presentation Transcript
Chronic Diarrhea Presented by: Bandar Dallak Faisal Al-Qahtani Ali Al-Zahrani Saeed Al-Shreef
Introduction: Diarrhea is an increase in fluidity, volume and frequency of stools relative to the usual habits of an individual. 3/day loose, watery stool.
Introduction: The great majority of diarrhea episodes last less than one week; When diarrhea persists for more than 14 days, it is called persistent, intractable, or chronic diarrhea.
Introduction: In the developing world, persistent diarrhea usually follows an acute episode and typically is associated with serial enteric infections without time to recover between episodes. Children are at risk of malnutrition and often have other intercurrent illnesses, such as respiratory infections.
Introduction: In developed countries, children are less likely to be exposed to serial enteric infections and malnutrition. In these populations, chronic diarrhea is more likely to be caused by underlying disease, such as celiac disease or other food allergy.
Introduction: Sequelae: Dehydration. Marked weight loss and malnutrition. FTT.
There are four basic pathophysiological categories of diarrhea (1) Osmotic Diarrhea: when an ingested solute is not absorbed properly, the higher concentration gradient within the gut lumen acts to draw water into intestinal lumen and greatly increases the water content of the stool. The classic example of this is the diarrhea caused by lactose intolerance. Enteric infections may also cause malabsorption via damage to intestinal epithelial cells (ex. Rotavirus or Shigella).
(2) Secretory Diarrhea: this diarrhea is caused by the intestine actively secreting water into the gut lumen. Infections such as Cholera, Clostridia Perfringens, Clostridia Difficile, E. Coli, Staph. Aureus, and Shigella all cause secretory diarrhea mainly via preformed enterotoxins. (3) Inflammatory Diarrhea: Intestinal inflammation can lead to blood, mucus, and protein exudate losses, accompanied by fluid and electrolytes. The most common cause of this type of diarrhea is infection but can also be due to chronic diseases such as IBD or Celiac Disease. (4) Diarrhea due to Motility Disorders: although uncommon, both an increase and a decrease in gut motility can be a cause of diarrhea. Note: diarrhea can be caused by one or any combination of these categories
CAUSES: Viral, parasitic, bacterial,.. Infections Hyperthyroidism. Adrenal insufficiency. IBS IBD Endocrine Chronic nonspecific diarrhea. Small intestine Celiac disease. Chronic Diarrhea Carbohydr ates malabsorpt ion Cystic fibrosis. Pancreas Lactase deficiency. Glucose-glactose malabsorption. Cow s Milk/soy protein intolerance. Metabolic defects Dietary Familial chloride diarrhea. Immune defects Agammaglobulinemia IgA deficiency. AIDS.
Salmonella. Campylobacter Bacterial Antibiotic induced: C. difficile Parasitic Giardasis. Ascaris. Amoeba. Ankylostoma. Post infectious secondary lactase deficiency Infections
Typhoid: Caused by S. typhi and S. paratyphi. Transmitted through contact with infected animals e.g., chicken, or through contaminated food e.g., eggs, dairy products.
Typhoid: C/P: Bactremia and high grade fever that usually precede the enteric phase. Diarrhea (usually after 1 week) Abdominal pain. Nausea. Loss of appetite. CNS signs ( severe) : coma, meningism, fits.. If untreated, the disease persists 2-3 weeks with marked weight loss, hematochezia, melena.
Typhoid: Treatment: Ciprofloxacin (best) Alternative for ciprofloxacin resistance Ceftriaxone or azithromycin Co-trimoxazole (TMP-SMZ) Dexamethazone
Parasitic: Giardia Lamblia. Entamoeba histolytica. Cryptosporidium parvum.
Amebiasis: C/P: Intestinal: Acute onset of mild diarrhea. or Amebic dysentry: perfuse diarrhea with blood, tenesmus, severe abd. pain Extra intestinal: - amebic liver abscess (fever, sweats, RUQ pain, high WBCs..) -may invade lung or brain also..
Amebiasis: Diagnosis: Stool microscopy Fecal antigen detection Serology US/CT .. Aspiration Treatment: metronidazole: With diloxanide furoate (cyst) Tinidazole ( severe )
Giardia lamblia: is transmitted through ingestion of cysts from contaminated food or drinks. Adheres to microvilli of dudenal or jejunal epithelium.
Giardia lamblia: C/P : diarrhea Bloating , flatulence Abdominal pain Explosive diarrhea Malapsorption Weight loss
Diagnosis: Direct fluorescent antibody (DFA) >> gold standard Stool microscopy>> may be (--) Treatment: Tinidazole paromomycin
Celiac Disease: abnormal small intestine mucosa due to intestinal reaction to gliadin, a component of gluten. Etiology Only autoimmune disease in which androgen (alpha- gliadin) is recognized. Associated with other autoimmune diseases, especially thyroid disease. Gluten, a protein in cereal grains, is toxic factor. Associated with HLA-DQ2 and with HLA-DQ8
Celiac Disease: Clinical Features classically: diarrhea, weight loss, anemia, symptoms of vitamin/ mineral deficiency, failure to thrive; now more commonly bloating, gas, iron deficiency. improves with gluten-free diet, deteriorates when gluten reintroduced. disease is usually most severe in proximal bowel; therefore iron, calcium, and folic acid deficiency common
Celiac Disease: Investigations: small bowel mucosal biopsy (usually duodenum) : villous atrophy and crypt hyperplasia increased number of plasma cells and lymphocytes in lamina propria.
Celiac Disease: Investigations: Evidence of Malabsorption: Steatorrhea Low levels of ferritin/iron saturation, Ca, Fe, albumin, cholesterol, carotene, B12 absorption
Celiac Disease: Investigations: Serology: anti-transglutaminase antibodies, TTG Fecal fat >7% over 72 hrs
Celiac Disease: Treatment: Dietary counselling: Gluten free diet: avoid barley, rye, wheat, maybe oats (if not contaminated by other grains). Starchy foods e.g., rice are safe. Iron, folate supplementation (with supplementation of other vitamins as needed)
Celiac Disease: Prognosis: associated with increased risk of lymphoma, carcinoma including small bowel and colon. These can be avoided if adherent to diet.
Cystic Fibrosis: Autosomal Recessive. Gene on long arm of chromosome 7 encoding for CFTR (Cystic Fibrosis Transmembrane Regulator). CFTR is a Chloride channel regulating Chloride transport and possibly sodium. This is responsible for elevated sweat chloride in 99% of patients.
Cystic Fibrosis: CF is characterized by widespread exocrine dysfunction.
Cystic Fibrosis: GI Manifestation: More prominent in infants. Meconium ileus. Greasy stools and fl atulence. Pancreatitis. Biliary cirrhosis. Jaundice.
Cystic Fibrosis: GI symptoms are more prominent in infancy, while pulmonary manifestations predominate thereafter.
Cystic Fibrosis: Dx.: Sweat chloride Test: > 60 mEq/L. Genetic analysis: Are confirmatory.
Cystic Fibrosis: Others: DM. Infertility. Unexplained hyponatremia. Fat soluble vitamins (A, D, E, K) deficiency. ..etc.
Cystic Fibrosis: Management.: Pulmonary manifestations :are managed with chest physical therapy, bronchodilators, corticosteroids, antibiotics, and DNase. Administer pancreatic enzymes and fat-soluble vitamins A, D, E, and K for malabsorption. Nutritional counseling and support with a high-calorie and high-protein diet are essential for health maintenance.
Crohns Disease Ulcerative Colitis IBD
Inflammatory Bowel Diseases IBDs: Epidemiology: More common Jewish. The incidence of IBDs is increasing especially in industrialized countries. Environmental factors are needed to drive the disease in genetically susceptible individuals. 30 folds increased risk in those with first degree relatives involved.
Crohns Disease: May involve any part of GIT. The commonest site is illeocecal junction. Discontinuous pattern SKIP LESIONS . Rectum is often spared.
Crohns Disease: C/P: Abdominal pain. Abdominal tenderness. Abdominal mass. Low grade fever. Weight loss. Watery diarrhea. Perianal fissure/fistula.
Ulcerative Colitis: Mainly affect the colon. The rectum is always involved. May extend proximally in a continuous fashion.
Ulcerative Colitis: C/P: Bloody diarrhea. Lower abdominal cramps. Tenesmus. Urgency. Abdominal pain/tenderness. Blood on rectum. Usually, no abdominal mass.
Extraintestinal Manifestations of IBDs: Aphthous stomatitis, Episcleritis/uveitis, Arthritis, Erythema nodosum, Pyoderma gangrenosum.
Inflammatory Bowel Diseases IBDs: Investigations: Blood test. Endoscopy. Colonscopy.(biopsy) Plane Abdominal XR. US, CT.
Inflammatory Bowel Diseases IBDs: Management: 5-ASA. Steroids. Azathioprine. Infliximab MTX. -surgical
Glucose-galactose malabsorption
Glucose-Galacose Malabsorption: a condition in which the cells lining the intestine cannot take in the sugars glucose and galactose. Generally becomes apparent in the first few weeks of a baby's life.
