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Group 5, Section B1
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OUTLINE
I. Diarrhea
II. Presentation of Case 1
III. Mechanism of Diarrhea
IV. Management
VI. Cholera
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I. Diarrhea
A. Definition
Defined as passage of abnormally liquidor unformed stools at an increased
frequency
> 200-300 gm/day
> 3 stools/day
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I. Diarrhea
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I. Diarrhea
Classification:
Duration of the illness
Mechanism
SeverityAcute - < 2 weeks
Persistent- 2 to 4 weeks
Chronic- > 4 weeks Stool Characteristic
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I.Diarrhea
Acute Diarrhea
common cause of death in developing countries.
< 2 weeks
Causes
90 % - INFECTIOUS AGENTS
10 % - Medications , Toxic ingestions,Ischemia
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I.Diarrhea
Chronic Diarrhea
> 4 weeks
Caused by:
Infection
Allergy
IBD (inflammatory bowel disease)
or Crohnsdisease.
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I. Diarrhea
Types of Diarrhea
Secretory diarrhea
Infections increase the secretion of water and
electrolytes which override the re-absorptive ability ofthe large intestine.
Cause:
Bacterial
Viral
Protozoan Drugs (Laxatives)
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I.Diarrhea
Osmotic diarrhea
- Maldigestion and Malabsorption
- Water and electrolyte retention in Large Intestine
Causes:
Lactose Intolerance
Malabsorption
Pancreatic disease
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The most common pathogens causing diarrhea are :
Rotavirus
(15-25%)
Enterotoxigenic
Escherichia coli
10-20%
Shigella
5-15%Campylobacter jejuni
10-15%
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I.Diarrhea
Transmission
Most of the diarrheal agents are transmitted by
the fecal-oral route
Airborne (viruses)
Nosocommial transmission is possible
Shigella(the bacteria causing dysentery) is mainly
transmitted person-to-person
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I. Diarrhea
Signs and Symptoms
Loose and watery stool
Increase in frequency of bowel movements Presence of mucus, pus, blood or excessive
amounts of fat
Dehydration
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I.Diarrhea
Person at Risk: Cholera: 2 years and above, uncommon in very
young infants
Shigellosis: more common in young children agedbelow 5 years
Rotavirus diarrhea: more common in young
infants and children aged 1-2 years
E. colidiarrhea: can occur at any age
Amebiasis: more common among adults
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I.Diarrhea
Management:
A. Prevention
Hand washing Proper preparation and storage of food
Clean water source
Clean environment Proper waste management
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Management
B. Non-pharmacological
Diet
Avoid high fiber diet, caffeine, alcohol
Continuing solids Improve mothers diet
Continue breast feeding as usualduring and after rehydration therapy.
Rehydration50-200ml/kg/day of ORAL REHYDRATION
SOLUTION (ORS)
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Case I Discussion
A mother brought her 10-months old, 8-kgdaughter to a health center because of diarrheaof one day duration which occurred 4 times.There was no accompanying vomiting. She has
been breastfed since birth. At 5 months old.Lugaw with fish and vegetables were started. Atthe onset of diarrhea, the mother stoppedbreastfeeding and giving of solid foods and
instead shifted to giving am with sugar. Thechild is alert, with good skin turgor and adequateurine output.
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Metabolic Changes Observed in
Diarrhea
QUESTION 1: Describe the sequence of the
various metabolic changes observed in
diarrhea and correlates these to the clinical
manifestations observed in the patient.
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Normal Intestinal Physiology
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Secretory
diarrhea
Osmotic
diarrheaMotility-related
diarrheaExudative
diarrhea
oMaldigestion
oOsmotic laxativesoLactose intolerance
oFructose malabsorptionon
water is drawninto the bowels
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Osmotic
Digestive enzyme deficiencies
Ingestion of un-absorbable solute
i i l f i d ili
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Gastrointestinal function and motility
INCREASED GI FUNCTION AND MOTILITY
- movement of food, water absorption
- Parasympathetic NS increases GI motility
- Bacteria causes the Crypts of Liberkuhn to
secrete large amounts of choride andbicarbonate.
Osmotic movement of water
propels the movement of stool out of the system.
LOOSE WATERY STOOL
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Alteration in fluid volume
DEFICIENT FLUID VOLUME
secretion of water by the Crypts of
Liberkuhn in the small intestine causes the
fecal matter to travel faster to anus.
DEHYDRATION
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Acid- base balance
Metabolic acidosis- precursor to diarrhea
Hypokalemia- prolonged diarrhea
< 3.0 meq/L- muscle weakness, muscle cramps
and cardiac arrhythmias.
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Composition
Semisolid or loose stool
Mucous
Blood
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Evaluation of nutritional status and state
of hydration of the patient.
QUESTION 2: Evaluate the nutritional status
and state of hydration of the patient (use
growth chart and assessment of hydration
table). Compute for the ideal weight for ageof the patient.
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DATA:
Sex: Female
Age: 10 months old
Weight: 8 kg Does the young infant have diarrhea? YES
For how long? One day
Frequency : Four times
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Mild Moderate Severe
-Irritable -Irritable
-Weak pulse
-Some reduction in urine
volume
-Moribund, apathetic
-Peripheral circulatory
failure (cold extremities,
warm body, excessiveblanching, weak pulse)
-Marked reduction in urine
volume
Thirsty Thirsty Thirsty
-Fontanelle depressed
-Eyeballs sunken
-Facies dry and pinched
-Buccal mucosa dry
-Lips parched
-Loss of skin turgor (exceptin in hypernatremic
variety)
-Fontanelle markedly
depressed
-Eyeballs markedly sunken
-Facies markedly dry and
pinched
-Buccal mucosa dry-Lips parched
-Loss of skin turgor (except
hypernatremic in which it
may not be variety
prominent)
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ASSES AND CLASSIFY SICK CHILD
AGED 2 MONTHS UP TO 5 YEARS ASK: Does the child have diarrhea?
If YES, ask:
For how long?
Is there blood in the stool?
Look and feel:
Look at the childs general condition.
Is the child:
Abnormally sleepy or difficult to awaken?
Restless and irritable?
Look for sunken eyes.
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Classify Diarrhea
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If diarrhea for 14 days or more
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If blood in stool
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Based on Integrated Management of childhoodIllness the infant is considered NO DEHYDRATION
status. Based on the assessment that the child isalert, with good skin turgor and adequate urineoutput.
Computation:
Formula: [ AGE (month) + 9] / 2 ( weight forkilograms)
WHO Weight standards
= 10 months + 9/ 2 = 9.5 kg The infant has poor nutritional status based on
her low weight for age.
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Cycle of Malnutrition and Diarrhea
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NET SECRETION
X
+++++
Impaired absorption of Na
Cl , HCO3
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Exudative
Inflammation
Decreased colonic
reabsorption
Increased motility Decreased transit time
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CONTINUATION
Evaluation of nutritional status and
state of hydration of the patient.
QUESTION 3: Determine the adequacy of the
patients diet before and during diarrhearelate this to the cycle of malnutrition and
diarrhea.
f h
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Before diarrhea: inadequate.
10 months- eat variety of foods (rice and meatproducts) sustain her nutritional requirement to boost her immune system thus preventing
malnutrition.
During diarrhea: inadequate
Discontinue breast feeding am or rice water was given- alternative for starch
requirement, supplementary source of fluid andelectrolytes
WHO: Am has the nutritional advantage of providingmore calories during rehydration than does ORS
d f b f d d l
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Advantages of breastfeeding and oral
rehydration solution.
QUESTION 4: What advice should be given to
the patients mother regarding breastfeeding,
use of home fluids/oral rehydration solutions
and other nutritional support for the patient.
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ADVANTAGES
A. Breastfeeding/Colostrums
-Continued during diarrhea.
-As often as the infant desires
-Less prone to diarrhea.
-Low buffering capacity, stools of breast-
fed babies are acidic.
-Low E. coli count, high Lactobacillus
bitidus-Viable phagocytes, IgA and IgM which
protect against most enteropathogens
-Better growth performance.
Has right amount of fat, sugar, water, and
protein that is needed for a baby's growth
and development
-Greater Immune Health: IgA antibodies
against infections on the childs intestinal
flora.
Side Note: The quality of a mother's
breast milk may be compromised by
alcoholic beverages, caffeinated drinks,marijuana, methamphetamine, heroin,
and methadone.
vantage
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g
B. Oral Rehydration Solutions
(ORS)
-prepared at home by mixing
eight level teaspoonfuls of cane
sugar (40 grams of sucrose), one
level teaspoonful of table salt
(five grams of NaCl) with or
without a lemon squeezed in
one litre of potable water. Since
2 g of sugar releases I g of
glucose, 40 g of sucrose is used.
Alternatively a 3 finger pinch
(upto the first crease) of table
salt and closed fistful of cane
sugar are mixed in half a litre of
water.
-Replenishes lost essential fluids
that maintain body
homeostasis.
-patient treated with ORS do not
require an intravenous access, a
potentially painful and difficult
procedure in young children.
Although effective in
rehydration, it do not decreases
stool volume because of the
relatively high osmolality of
glucose they contain.
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Advantage
C. Nutritional Support
Zinc Greatly reduces the
severity and duration of
diarrheaPotassium Influences osmotic balance
between cells and
interstitial fluid (Na-K-
ATPase Pump)
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QUESTION 5: What biochemical significance if
any, can be given to the use of am with
sugar in diarrheic patients?
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Sodium glucose transport mechanism
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Sodium- glucose transport mechanism
High concentration of sodium, water and
glucose in the gut lumen
High concentration will enter the epithelial
cell using SGLT1 carrier protein
Glucose and sodium entered the cell water
will follow through
Where sodium goes,
water follows
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Outline
I. Definition
II. Presentation of the Case
III. Biochemical Aspect of Cholera
IV. Mode of Transmission
V. Signs and SymptomsVI. Diagnosis and Treatment
WHAT i
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WHAT is
CHOLERA?
Acute Intestinalinfection
Caused by anenterotoxin releasedby bacterium, Vibrio
cholera
Profuse waterydiarrhea
ib i h l
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Vibrio cholerae
no known animal
hosts
attach themselveseasily to the shells of
crabs, shrimps and
other shellfish
Fecal contamination
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Vibrio Cholerae
2 out of 150 serotypes
of cholera toxin:
O1 and O139
C 2
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Case 2: A 21-year-old female medical student at FEU-NRMF
suddenly began to pass profuse watery stoolscontinuously. This was associated with 6 episodes
of vomitingof previous ingested food, her general
condition declined abruptly, and she was rushed to
the FEU-NRMF emergency room. On admission, she
was cyanotic, skin turgor was poor, with blood
pressure of 70/50 mmHg palpatory, her pulse was
weak and rapid. The ER physician on dutydiagnosed her as acute gastroenteritis probably
viral T/C cholera,he took some blood and stool
sample and was treated immediately.
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BIOCHEMICAL BASIS OF
CHOLERA
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Biochemical Basis
2 subunits of Enterotoxin:
1. one A subunit
2. five B subunits
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Biochemical Basis
2 subunits of Enterotoxin:
1. one A subunit
a. one A1 peptide
b. one A2 peptide
2. five B subunits
A1
A2
Five B subunits
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Ganglioside
GM1
Enterotoxin
Extracellular Space
Enterotoxin
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Epithelial cell of the
Small Intestine
BLOOD VESSEL
Interstitial
Spce
Ganglioside
1
Extracellular Space
Enterotoxin
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G Protein
Epithelial cell of the
Small Intestine
BLOOD VESSEL
Interstitial
Spce
Ganglioside
1
2
Extracellular Space
Enterotoxin
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Inactive
Adenylate
Cyclase
G Protein
Epithelial cell of the
Small Intestine
BLOOD VESSEL
Interstitial
Spce
Ganglioside
1
2
3
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How G Protein normally
works?
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G Protein
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Biochemical Basis
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Biochemical Basis
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video
Extracellular Space
Enterotoxin
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Inactive
Adenylate
Cyclase
G Protein
Epithelial cell of the
Small Intestine
BLOOD VESSEL
Interstitial
Spce
Ganglioside
1
2
3
Adenylate cyclase NAD Adenylyl cyclase
ADP-Ribosylation
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ADP Ribosylation
ADENYLATE CYCLASE
NAD
Nicotinamide ADP ribose
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ADP-Ribosylation
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ADP Ribosylation
ADENYLATE CYCLASE
NAD
Nicotinamide ADP ribose + G protein
A1
ADP-Ribosylation
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ADP Ribosylation
ADENYLATE CYCLASE
NAD
Nicotinamide ADP ribose + G protein
+ nicotinamide
G protein
ADPRibose
A1
ADP-Ribosylation
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ADP Ribosylation
ADENYLATE CYCLASE
NAD
Nicotinamide ADP ribose + G protein
+ nicotinamide
G protein
ADPRibose
= ACTIVATE ADENYLYL CYCLASE
Extracellular Space
Enterotoxin
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Inactive
Adenylate
Cyclase
G Protein
Epithelial cell of the
Small Intestine
BLOOD VESSEL
Interstitial
Spce
Ganglioside
1
2
3
Adenylate cyclase NAD Adenylyl cyclase
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Extracellular Space
Enterotoxin
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ATP
CAMP
Adenylyl
CyclaseG Protein
Epithelial cell of the
Small Intestine
BLOOD VESSEL
Interstitial
Spce
Ganglioside
1
2
3
4
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ATP
Active Adenylyl
Cyclase
cAMP(cyclic AdenosineMonophosphate)
Extracellular Space
Enterotoxin
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ATP
CAMP
Adenylyl
CyclaseG Protein
Epithelial cell of the
Small Intestine
BLOOD VESSEL
Interstitial
Spce
Ganglioside
1
2
3
4
Extracellular Space
Enterotoxin
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ATP
CAMP
Protein
Kinase
Adenylate
CyclaseG Protein
Epithelial cell of the
Small Intestine
BLOOD VESSEL
Interstitial
Spce
Ganglioside
1
2
3
45
Extracellular Space
Enterotoxin
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ATP
CAMP
Protein
Kinase
CFTR
Cl
Adenylate
CyclaseG Protein
Epithelial cell of the
Small Intestine
BLOOD VESSEL
Interstitial
Spce
Ganglioside
1
2
3
45
6
Na
Extracellular Space
Enterotoxin
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ATP
CAMP
Protein
Kinase
CFTR
Cl
Adenylate
CyclaseG Protein
Epithelial cell of the
Small Intestine
BLOOD VESSEL
Interstitial
Spce
Ganglioside
1
2
3
45
6
7
Na H2O
Extracellular Space
Enterotoxin
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ATP
CAMP
Protein
Kinase
CFTR
Cl
Adenylate
CyclaseG Protein
Epithelial cell of theSmall Intestine
BLOOD VESSEL
Interstitial
Spce
Ganglioside
1
2
3
45
6
7
8
Na, H2O
V Ch l
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V. Cholera
Uses NAD to transform the G protein
Inactivates the GTPase function of G protein
Adenylyl cyclase is activated for longer period
100 fold increase in cAMP
Activation of ion channels
Ions flow out and water follows
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