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8/13/2019 FIRM 4_Diarrhea Presentation 2013_2014 - Copy
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DIARRHOEALDISEASES
A SEMINAR PRESENTATION BYFIRM 4 RENAL UNIT) MEDICALSTUDENTSDATE: December 2013
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OUTLINE
INTRODUCTION AND DEFINITION
BRIEF HISTORY
EPIDERMIOLOGY
TYPES/CLASSIFICATION OF DIARRHEA BASED ON:
DURATION
PATHOGENETIC MECHANISMS
PATHOGENESIS
AETIOLOGY
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Outline contd
PATIENT EVALUATIONS
INVESTIGATION OF DIARRHEA
DISCUSSION OF SPECIFIC DIARRHEAL DISEASES
MANAGEMENT
CONCLUSION
REFERENCES
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Familiar with purging?
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Diarrhoea is defined as an abnormal increase
in daily stool fluidity, frequency and volume.
W.H.O defines diarrhea as having 3 or more
loose or liquid stools per day, or as having
more stools than is normal for that person. It is a reversal of the normal net absorptive
status of water and electrolytes absorption to
secretions
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Introduction continued.
Acute diarrhoea are usually caused by
infections
Chronic diarrhoea are due to inadequately
treated amoebic or bacillary dysentery,
schistosomiasis, pancreatic diseases,
abdominal tuberculosis, etc
HIV infection is important cause of both acute
and chronic diarrhoea
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In developing countries diarrhoeal disease isthe leading cause of death among childrenunder 5 years of age
The CDC (centre for disease control) estimatedthat 42-47% reduction in diarrhoea can occurwhen hand-washing with soap and water isintroduced into a community
Diarrhea is mainly spread by person-to-personcontact faeco-oral route and, many times,contaminated hands.
Introduction continued.
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Studies conducted by the W.H.O in the year 2004showed that child mortality due to diarrhea
in Africa was approximately 350-400 thousand deaths &
in Nigeria, about 175,000 deaths.
Global estimates of the number of deaths due todiarrhea in the Sub-Saharan Africa have shown asteady decline, from 4.6 million (in the 1980s) to
3.3 million (in the 1990s) to 2.5 million (year 2000).
Diarrhoeal diseases remain among the five major
killers of children under five years of age.
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Epidemiology of diarrhea contd
In Nigeria, according to UNICEF, diarrhoea: has a prevalence rate of 18.8%, account for
16% of child death &
Has an estimate of about 150,000deaths/year (esp. of children < 5 years)mainly caused by poor sanitation andhygiene practices
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CLASSIFICATION BASED ON DURATION
Acute diarrhoea
Chronic diarrhoea
CLASSIFICATION BASED ON PATHOGENETIC
MECHANISMS Osmotic diarrhoea
Secretory diarrhoea
Inflammatory diarrhoea( mucosal destruction)
Abnormal motility
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ACUTE DIARRHOEA
Diarrhoea of suddenonset
often short-lived (i.e does not last more than fourteendays)
may not require investigation or treatment
Clinical features associated with the acute diarrhoeainclude
fever,
abdominal pain and
Vomiting. Common causes include
Viral infection ( e.g norovirus),
bacterial infection( e.g staphylococus aureus) and
parasitic infections( giardia lamblia)
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CHRONIC DIARRHOEA
This usually lasts for more than fourteen days
always needs investigation
Colonoscopy is usually necessary if stool cultures are
negative and small bowel disease is not suspected
Common causes include
Colitis usually caused by campylobacter, shigella, E coli,
Yersiniaand salmonella
Parasitic infection ( e.g Entamoeba histolytica)
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PATHOGENESIS OF DIARRHOEA
OSMOTIC DIARRHOEA
Due to excessive osmotic force exerted by the luminal
solutes. E.g. purgatives such as MgS or Mg- containingantacids
It leads to more than 500ml of stool per day
It abates upon fasting
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SECRETORY DIARRHOEA
In this disorder, there is both: Active intestinal secretions of fluid and electrolytes and
decreased absorption
Common cause of secretory diarrhoea
Enterotoxins (Cholera toxins, E. colitoxins)
Hormones
Bile salts and
Fatty acids
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Pathogenesis of diarrhea contd
INFLAMMATORY DIARRHEA Damage to the intestinal mucosa cell
Loss of fluid and blood
There is also defective absorption of fluid andelectrolytes
Common causes: infective conditions (e.g. dysentry
due to shigella) and inflammatory conditions (e.g.
ulcerative colitis and Crohnsdisease)
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Pathogenesis of diarrhea contd
ABNORMAL MOTILITY:Diabetic, post-vagotomy and
hyperthyroid diarrhoea are all due
to abnormal motility of the upper
gut
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INFECTIVE CAUSES
Bacteria
Campylobacter jejuni
Salmonella spp Escherichia coli
Staphylococcal enterocolitis
Clostridium botulism
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Viral Rotavirus
Parasitic
Giardia intestinalis
Entamoeba histolytica
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RISK FACTORS
Poor environmental hygiene
Poor personal hygiene
Poor food hygiene
Contaminated water source
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BIODATA: name, age, sex, religion address
(locality may predispose to diarrhoea),
occupation
PRESENTING COMPLAINTS
Is the diarrhoea the major problem or is there any
other pressing concern?
Blood or mucus in stool
Onset in relation to duration
P i l i i d
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Patient evaluation continued
HISTORY OF PRESENTING COMPLAINT Onset of stool and duration
Volume, frequency and character of stool Normal stool frequency => 3 time a day to 3 times per week
character => golden brown, easy to pass, sausage
Does anything exacerbate or relieve the diarrhea?
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Associated Features: nausea, vomiting, fever,
abdominal, Tenesmus
Recent travel to another part of the country
Recent dietary history? E.g. half boiled meat, eggs,
usual foods e.t.c. HIV, transplant, malignancy, abdominal surgery?
Anyone else around you have diarrhoea?
Smoker? Appetite? Weight loss?
Medication? to know if laxatives have been
abused
P ti t l ti ti d
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PHYSICAL EXAMINATION
INSPECTION: abdominal distension
PALPATION: palpable mass or abdominal
tenderness
PERCUSSION: any area of dullness
BOWEL SOUNDS
ITCHING BLISTERING RASH => Coeliac disease DRE (digital rectal examination)
COLONOSCOPY
Patient evaluation continued
P ti t l ti ti d
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INVESTIGATIONS
STOOL TESTS Microscopy, culture and investigation
Faecal leucocyte level => leucocyte infiltration
Faecal fat analysis to evaluate malabsorption
Stool laxative screening
BLOOD TESTS
Full blood count
ESR (erythrocyte sedimentation rate) LFT (liver function test)
Electrolyte levels
Blood culture to test for clostridium difficile
Patient evaluation continued
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ACUTE GASTROENTRITIS
Causative organism: Rotavirus
Transmission:
faecal-oral,
close contact,
Contaminated food and water and
Respiratory droplet
Host: cow and monkeys. Animal strains areantigenically distinct from human strains.
Persons:All ages and sexes.
Ac te gastroenteritis contin ed
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Acute gastroenteritis continued.
Pathogenesis:
1. Ingestion of virus
2. Proteolytic cleavage of the outer capsid in GIT
activates the virus for infection and produces an
intermediate infectious sub-viral particle (ISVP)3. ISVP enters absorptive columnar epithelium of
alimentary tractlining apical half of intestinal villi.
4. Thus, absorptive apical are destroyed anddiarrhoea sets in.
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CHOLERA
An acute intestinal infection Causative organism: Vibrio cholerae
Transmission: ingestion of food or
water contaminated with the
bacterium.
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Pathogenesis:
The bacterium has a short incubation period
(varies from a few hours to 6 days) It produces an enterotoxin (esp. holera toxin;
others are zona occludens toxin, ZOT and
accessory cholera toxin, ACT) that causes a
copious, painless, watery diarrhoea (secretive
diarrhoea) that can quickly lead to severe
dehydration and death if treatment is not
promptly given. Vomiting also occurs in mostpatients.
Achlorhydria or hypochlorhydria facilitates
passage of the bacterium into the intestine
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Cholera continued
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CLINICAL FEATURES:
Most persons infected do not become ill.
When illness does occur, about 80-90% of
episodes are of mild or moderate severityand are difficult to distinguish clinically
from other types of acute diarrhoea.
the typical ricewater stool, flecked withmucus, may be seen.
Cholera continued
Clinical features of cholera
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Clinical features of cholera.
Massive fluid loss hypovolaemicshock (cold clammy skin, tachycardia,
hypotension and peripheral cyanosis)
and dehydration (sunken eyes,hollow cheeks and a diminished urine
output)
muscle cramp which could be severe
Convulsionowing to hypoglycaemia
Ch l ti d
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Cholera continued.
INVESTIGATIONS:Fresh stool examination
(microscopy and culture)
Rapid dipstick test [detects
lipopolysaccharide antigens ofVibrio cholerae serotypes O1 andO139 from rectal swabs]
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AIM OF TREATMENT
To replace the lost fluids andelectrolytes
Oral rehydration therapy is most
preferred
In severe cases Intravenous
Rehydrationcan be used
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ORAL REHYDRATION THERAPY
The standard oral rehydration salt by theW.H.O. and UNICEF has an osmolality of
310mmol/kg and contains 90 mmols/L of
sodium
This high sodium content can theoritically
induce hypernatraemia but there is few
evidence supporting this
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REFEEDING
The W.H.O. and CDC have advised that childrenand adults suffering from diarrhoea continue toeat and drink normally
In children breastfeeding should be continuedalong with the administration of ORTthroughout the course of diarrhoea
Early refeeding reduces intestinal permeability,
enhances enterocyte regeneration andpromotes recovery of disaccharides in thebrush border membranes
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THERAPY WITH ANTI-DIARRHEAL
COMPOUNDS
COMPOUNDS THAT ALTER INTESTINAL
MOTILITY
Loperamide
COMPOUNDS THAT ALTER SECRETIONS
Opiates and opiate-antispasmotic combinations
e.g. Bismuth subsalycylate, Racecadotril
(acetorphan)
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IMMUNIZATION
There can be
Active immunization:
against Rotavirus is as effective as a natural infection in
preventing subsequent rotavirus diarrhoea
Passive immunization: Oral ingestion of immunoglobulins extracted from
immunized bovine colostrum is effective in managing
children with Acute Rotavirus diarrhoea
Zincreduces the severity and duration ofdiarrhoea
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ANTIBIOTICS
There should be limited use of antibiotics dueto their self-limiting nature and risk of
worsening antibiotic resistance
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CONCLUSION Diarrhoea depletes body water quickly and
anybody experiencing frequent watery stoolshould seek medical help immediately.
The dehydrating resulting from diarrhoea can be
treated using oral rehydration solution around,and even drinking plain water
But as we all know that prevention trumps cure
anyday, regular washing of hands with soap andwater after visits to the rest-room and before and
after any meals will save us a lot of trouble. In
this case it saves us a lot of body water.
REFERENCES
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REFERENCES American Family Physicians website. www.aafp.org
A.O. Falase, 2009. An introduction to Clinical diagnosis inthe Tropics.
Curtis V. and Cairneross S., 2003. Effect of washing handswith soap on diarrhoea risk in the community: A systematicreview. The Lancet Infectious Disease. 275-281
Cynthia B-P, Claudio F. L., Walter M. and Demissie H.Diarrheal Diseases. Disease and Mortality in Sub-SaharanAfrica. 2ndedition
Kumar P. & Clark M., 2012. Kumar and Clarks ClinicalMedicine, 8thedition.
Oxford Handbook of clinical medicine, Longmore, M.,Wilkinson, I.B., Davidson, E.H., et al, 8thedition
http://www.medicinenet.com/http://www.medicinenet.com/http://www.medicinenet.com/http://www.medicinenet.com/http://www.medicinenet.com/