Diarrhea case - cholera combined.pptx

8/14/2019 Diarrhea case - cholera combined.pptx

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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


Small Intestine

BLOOD VESSEL

Interstitial

Spce

Ganglioside

1

2

Extracellular Space

Enterotoxin


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Inactive

Adenylate

Cyclase

G Protein


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


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

G protein

ADPRibose

A1

ADP-Ribosylation


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ADP Ribosylation

ADENYLATE CYCLASE

NAD


+ nicotinamide

G protein

ADPRibose

= ACTIVATE ADENYLYL CYCLASE

Extracellular Space

Enterotoxin


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Inactive

Adenylate

Cyclase

G Protein


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


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


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


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


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


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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Diarrhea case - cholera combined.pptx