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/