how to approach patient with diarrhoea

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HOW TO APPROACH PATIENT WITH DIARRHOEA SITI NUR ELLYANI BINTI MOHD BOHARI 012010050482 NURHAFIZAH BT MOHD KAMIL 012010050486 NURAZLIN SOFIA BINTI MOHAMMAD MURAD 012010050504 NURLIYANA FATIN BT DARIMIN 012010050485

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8/7/2019 HOW TO APPROACH PATIENT WITH DIARRHOEA

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HOW TO

APPROACH PATIENT 

WITH DIARRHOEASITI NUR ELLYANI BINTI MOHD

BOHARI

012010050482

NURHAFIZAH BT

MOHD KAMIL

012010050486

NURAZLIN SOFIA BINTI

MOHAMMAD MURAD

012010050504

NURLIYANA FATIN

BT DARIMIN

012010050485

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DIARRHEA

� A Greek word = to flow through

� It is a Symptom or a Sign

� NOT a Disease

� It is the most common cause of 

clinical presentations ingastrointestinal practice.

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DIARRHEA

� AS A SYMPTOM

 ± Frequency of bowel action

 ± Looseness of stools ± Increase in stool volume

� AS A SIGN

 ± Stools weight more than 250 gm/24 hours

A CombinationA Combination

of theseof these

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Normal Physiology

� 8-10 liters of fluid enter the duodenum daily

 ± 2 liters from the diet

 ± About 8 liters from secretion;

� Salivary 0.5 L� Gastric 1.0 L

� Pancreatic 1.0 L

� Hepatic 1.0 L

� Small bowel 3.0 L

� The small intestine absorbs all but 1.5 liters of thisfluid

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Normal PhysiologyNormal Physiology

The maximum absorbing capacity of the smallThe maximum absorbing capacity of the small

intestine is unknown.intestine is unknown.

The absorbing capacity of the adult colon is 4The absorbing capacity of the adult colon is 4--

5 liters/day5 liters/day

From the 1.5 liters coming from small bowelFrom the 1.5 liters coming from small bowel

the colon absorbs all but 100 mlthe colon absorbs all but 100 ml

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Diarrhea

Diarrhea is mainly a disorder of the small or large

bowel

� If the small intestine is deranged

 ± The daily volume of intestinal contents presented to the

colon exceeds its absorbing capacity if > 5 liters

� If the colon is deranged

 ± It cannot absorb its daily capacity of 1.5 liters

Diarrhea is anDiarrhea is an imbalanceimbalance between absorption &between absorption &secretionsecretion

Pancreatic and Pancreatic and biliary biliary disorders can also causedisorders can also cause

diarrhea.diarrhea. It can also reflect rimar disorders outside the G.I.It can also reflect rimar disorders outside the G.I.

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TYPES� Diarrhea generally is divided into two types, acute

and chronic.

A

cute diarrhea lasts from a few days up to a week. Chronic diarrhea lasts more than three weeks.

� It is important to distinguish between acute and

chronic diarrhea because they usually havedifferent causes, require different diagnostictests, and require different treatment.

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CAUSES� Infective causes:

 ± Bacterial:

� Eg: salmonella sp, shigella, E.Coli

 ± Viral:

� Rotavirus ± Fungal:

� Histoplasmosis

 ±

Parasitic :� Amoebic dysentry

� Schistosomiasis

� Giardia intestinalis

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� Non-infective causes: ± Inflammatory bowel disease

 ±

Pseudo membrano coloitis ± Malabsorption

 ± Drugs (laxative, metformin, anti cancer drug)

 ± Irritable bowel syndrome

 ± Carcinoma of the colon

� Endocrine ± Zollinger-ellison syndrome

 ± VIPoma

 ± Thyrotoxicosis

� Factitious diarrhoea: ± Purgative abuse

 ± Dilutional diarrhoea

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PATHOPHYSIOLOGY

� Mechanisms:

 ±Osmotic diarrhea

 ±Secretory diarrhea

 ± Inflammatory and infectious diarrhea

 ± Diarrhea associated with deranged motility

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1.Osmotic diarrhea

� arise as a consequence of water

retention by unabsorbed substances in

the intestinal lumen� from one of two situations:

Ingestion of a poorly absorbed substrate

Malabsorption

Stop: fasting or stops consuming

the poorly absorbed solute.

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2.Secretory diarrhea

� Secretory diarrhea means that there is anincrease in the active secretion, or there is aninhibition of absorption.

� caused by hypersecretion of fluids andelectrolytes by the villus crypts

� e.g. in response to stimulation by E.Coli orhydroxylated fatty acids

� will not resolve during a 2-3 day fast.

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3. Inflammatory and Infectious Diarrhea

damage to the intestinal mucosal cell

(mucosal inflammation or infiltration)

or

increased intestinal hydrostatic pressure

(lymphatic obstruction or portal hypertension

increase hydrostatic pressure )

loss of fluid and blood.

� In addition, there is defective absorption of fluids and electrolytes.

� Common cause are infective condition and inflammatoryconditions.

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4. Diarrhea Associated with Deranged

Motility

intestinal contents must beadequately exposed to the

mucosal epithelium

retained long enough toallow absorption.

nutrients and water to beefficiently absorbed

Disorders in motility

accelerate transit time

decrease absorption

diarrhea

(even if the absorptiveprocess per sec wasproceeding properly)

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History Taking

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Personal Data

� Name

� Age

� Gender

� Home Address� Marital Status

� Occupation

� Registration Number

� Date and Time of Admission

� Date and Time of Clerking

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History of Presenting Illness

� Volume, frequency and character of stools?� Presence of blood or mucous in stools?

� Onset and duration?

 ± Onset in relation to pain (which came first?) if diarrhea

first then pain, it could be gastroenteritis� Does anything relieve or exacerbating the condition?

 ± E.g: Drinking or eating?

� Has the patient tried any medication for the diarrhea? Has itworked?

� Associated features?

 ± Nausea, vomiting, fever, abdominal pain, constipation,loss of weight , loss of appetite

� Is diarrhea the biggest problem, or are there other more

pressing concerns?

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Past Medical History

� Underlying diseases?

� Inflammatory bowel disease (IBD)

�Irritable bowel syndrome (IBS)

� Malabsorption syndrome

� Cancer

� HIVEndocrine diseases (diabetes, thyrotoxicosis,

Zollinger-Ellison syndrome)

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Past Surgical History

� Post-vagotomy

 ± History of gastric surgery destruction of the

pylorus or section of the vagus nerve may result in

diarrhea, often associated with dumping

� Transplants

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Drug/Allergy History

� Any recent consumption of drugs:

 ± Antibiotics

 ± Laxative abuse

 ± Ingestion of magnesium-containing antacids

 ± Cytotoxic drugs

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Family History

� Is there anyone in the family or living together

or nearby has similar condition?

� Family history of diseases ± E.g: IBD, cancer, diabetes, hypertension

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Travel History

� Any recent travel for holidays or outstations?

� Recent outdoor activities such as jungle

trekking? If so, what was the food and watersituation?

� Recent dietary history of recent consumptions

of meat (cooked/uncooked), eggs, seafood,

dairy foods and unusual food?

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Social History

� Smoking status?

� Alcohol consumptions?

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PHYSICAL EXAMINATION

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GENERAL EXAMINATION

� General appearance & mental status ± Anxiety, confusion, loss of consciousness

� Vital signs : ± Blood Pressure (hypotension)

 ±

Pulse (tachycardia, weak pulse) ± Respiratory rate (tachypnoeic)

� Hands ± Cold skin

 ± Clammy skin

 ± Pallor ± Loss skin elasticity

 ± Erythematous palms

 ± Plummers nail

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� Face and mouth

 ± Pale

 ± Hydration

 ± Exophtalmos

 ± Lid lag

 ± Oral ulcer

� Neck

 ± Lymphadenopathy

 ± Enlarged thyroid

 ± Reduced Jugular Venous Pressure

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SYSTEMIC EXAMINATION

Endocrine

� Thyroid mass

Cardiorespiratory

� Wheezing and right-sided heart murmurs(carcinoid syndrome)

Musculoskeletal

� Arthritis (IBD, Whipple's disease)

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SKIN LESIONS

� Dermatitis herpetiformis (celiac disease)

� Erythema nodosum and pyoderma gangrenosum(IBD)

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� H yperpigmentation (Addison's disease)

� Flushing (carcinoid syndrome)

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ABDOMINAL EXAMINATION

� Surgical scars

� Abdominal tenderness

� Masses

� Hepatosplenomegaly

� Borborygmus on auscultation ± malabsorption

 ± bacterial overgrowth

 ± obstruction, or rapidintestinal transit.

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PERINEAL AND RECTAL EXAMINATION

� Signs of incontinence ± skin changes from chronic irritation,

 ± gaping anus,

 ± weak sphincter tone.

� Crohn's disease ± perianal skin tags

 ± Ulcers

 ± fissures

 ± abscesses

 ± Fistulas

 ± stenoses.

� Fecal impaction or masses might be noted.

� Anal Sphincter Laxity

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INVESTIGATIONS

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INVESTIGATION

1. Full Blood Count WBC

2. Thyroid function test TSH & T3, T4

3. Serum electrolytes potassium, sodium

4. Serum albumin

5. Stool evaluation leukocytes, fat, ova &parasites , laxative abuse

6. Endoscopy any lesion or mass in bowel

7. Mucosal biopsies rule out any malignancy

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TREATMENT 

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NON-SPECIFIC THERAPIES

� Dietary modifications

 ±Smaller, more frequent meals

 ±

Decrease carbohydrates ±Decrease fat intake

 ±Avoidance of milk

 ±Avoid sorbitol and mannitol

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Bismuth subsalicylate (i.e., Pepto-

Bismol )

� Opioids and opioid agonists ±Loperamide: first line therapy

 ±diphenoxylate-atropine (Lomotil )

 ±Codeine and other narcotics  forrefractory cases

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SPECIFIC THERAPIES

� Clonidine-

 ± Diabetic diarrhea

 ± moderate and severe diarrhea-predominant

irritable bowel syndrome (IBS

)

� Somatostatin

� AIDS,

� post chemotherapy,

� GVHD,

� and hormone secreting tumors.

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� Bile acid binders (ie, cholestyramine)

� Pancreatic enzyme supplementation

� Antimicrobials ²empiricfluoroquinolones therapy

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 Thank

 you