Investigations

Coeliac Disease – Investigations
Blood Tests
- serology by blood test; useful in diagnosing and excluding coeliac disease
- 4 types: modern – IgA antibodies against endomysium or tissue transglutaminase
older – IgA antibodies against reticulin or gliadin
- should still be followed by an endoscopy
- based on indirect immunofluorescence or ELISA
- total serum IgA level should be checked as some patients may have IgA deficiency

Endoscopy
- upper endoscopy with biopsy of the distal duodenum or proximal jejunum should be performed
- important to obtain multiple samples from the duodenum because not all areas equally affected (false negative)
- most have a small bowel that appears normal on endoscopy; main findings are scalloping of the small bowel folds, paucity in the folds, mosaic pattern to the mucosa, prominence of the submucosal blood vessels, and a nodular pattern to the mucosa
The classic pathology changes of coeliac disease in the small bowel are categorized by the "Marsh classification":
- Marsh stage 0: normal mucosa
- Marsh stage 1: increased number of intra-epithelial lymphocytes, usually exceeding 20 per 100 enterocytes
- Marsh stage 2: proliferation of the crypts of Lieberkuhn
- Marsh stage 3: partial or complete villous atrophy
- Marsh stage 4: hypoplasia of the small bowel architecture

Other tests
- full blood count
- electrolytes
- calcium
- renal function
- liver enzymes
- vitamin B12
- folic acid level
- coagulation tests (PT & aPTT) for vitamin K deficiency

(Posted by: Vivian)

cause and incidence of IDA, CAM of Coeliac disease

Cause of IDA

Iron deficiency anemia causes include:

• Blood loss. Blood contains iron within red blood cells. If you lose blood, you lose some iron. Women with heavy periods are at risk of iron deficiency anemia because they lose a lot of blood during menstruation. Slow, chronic blood loss from a source within the body — such as a peptic ulcer, a kidney or bladder tumor, a colon polyp, colorectal cancer, or uterine fibroids — can cause iron deficiency anemia. Gastrointestinal bleeding can result from regular use of aspirin or other nonsteroidal anti-inflammatory drugs (NSAIDs). While not common in the United States, hookworm infestation can cause blood loss.Blood lost from within the body may show up in your urine or stools, producing black or bloody stools. Inform your doctor if you notice blood in your urine or stools.
  

• A lack of iron in your diet. Your body regularly gets iron from the foods you eat. If you consume too little iron, over time your body can become iron deficient. Examples of iron-rich foods include meat, eggs, dairy products or iron-fortified foods. For proper growth and development, infants and children need iron from their diet, too.

• An inability to absorb iron. Iron from food is absorbed into your bloodstream in your small intestine. An intestinal disorder, such as Crohn's disease or celiac disease, which affects your intestine's ability to absorb nutrients from digested food, can lead to iron deficiency anemia. If part of your small intestine has been bypassed or removed surgically, that may affect your ability to absorb iron and other nutrients. Some medications can interfere with iron absorption. For example, regular use of prescription-strength stomach acid blockers called proton pump inhibitors may lead to iron deficiency anemia, although this is unusual. Your body needs stomach acid, which these products suppress, to convert dietary iron into a form that can readily be absorbed by the small intestine.

• Pregnancy. Without iron supplementation, iron deficiency anemia occurs in many pregnant women because their iron stores need to serve their own increased blood volume as well as be a source of hemoglobin for the growing fetus. A fetus needs iron to develop red blood cells, blood vessels and muscle.

Incidence

High-risk groups include:

Women of child-bearing age who have blood loss through menstruation
Pregnant or lactating women who have an increased requirement for iron
Infants, children, and adolescents in rapid growth phases
People with a poor dietary intake of iron

Complementary medicine for coeliac disease

Calcium (for deficiency only)

Enzymes

Folic acid (for deficiency only)

Iron (for deficiency only)

Magnesium (for deficiency only)

Multivitamin-mineral

Vitamin A (for deficiency only)

Vitamin D (for deficiency only)

Vitamin K (for deficiency only)

Zinc (for deficiency only)

Lipase

Vitamin B6 (for depression unresponsive to a gluten-free diet)

Contributed by Lawrence Oh

The Psychosocial Challenges of Living with Celiac Disease

The Psychosocial Challenges of Living with Celiac Disease

Komack explains that a diagnosis of CD often puts a strain on relationships because advocating for a gluten-free diet can be very taxing. “I’ve heard some people say they stop accepting social invitations because it is too difficult to talk about their needs. Others tell me friends and family minimize the importance of the diet or do not understand it sufficiently to make accommodations.” Solving such interpersonal problems involves give and take, so Komack advises her clients to have patience and a willingness to educate. “I tell people with celiac disease that the process may begin with an offer to bring their own food to a dinner party to illustrate the importance of the diet. And who knows? Over time, you might find the host segregating food to avoid accidents and cross-contamination for a friend with celiac disease.”

Prognosis & Complications of Celiac Disease

Prognosis

Prognosis for celiac disease is generally good. For most people, following a gluten-free diet plan will stop symptoms, heal existing intestinal damage, and prevent further damage. Improvements begin within days of starting the diet. The small intestine is usually completely healed in 3 to 6 months in children and younger adults and within 2 years for older adults. Healed means a person now has villi that can absorb nutrients from food into the bloodstream.

However, sometimes, depending on a person’s age at diagnosis, some problems will not improve, such as delayed growth and tooth discoloration. For example, young patients who are diagnosed with celiac disease after their growth period will continue to have a short stature.

Some people with celiac disease show no improvement on the gluten-free diet. This condition is called unresponsive celiac disease. The most common reason for poor response is that small amounts of gluten are still present in the diet. Advice from a dietitian who is skilled in educating patients about the gluten-free diet is essential to achieve the best results.

Rarely, the intestinal injury will continue despite a strictly gluten-free diet. People in this situation have severely damaged intestines that cannot heal. Because their intestines are not absorbing enough nutrients, they may need to receive nutrients directly into their bloodstream through a vein, or intravenously. People with this condition may need to be evaluated for complications of the disease. Researchers are now evaluating drug treatments for unresponsive celiac disease.

Complications of celiac disease

Complications of Celiac Disease are secondary conditions, symptoms, or other disorders that are caused by Celiac Disease. In many cases the distinction between symptoms of Celiac Disease and complications of Celiac Disease is unclear or arbitrary.

Damage to the small intestine and the resulting nutrient absorption problems put a person with celiac disease at risk for several diseases and health problems.

Some of the more common ones are listed below:

· Anaemia caused mainly by deficiencies in iron and vitamin B12 absorption.
· Lymphoma and adenocarcinoma are cancers that can develop in the intestine.
· Osteoporosis caused by poor calcium absorption.
· Miscarriage and congenital malformation of the baby, such as neural tube defects, are risks for pregnant women with untreated celiac disease because of nutrient absorption problems.
· Short stature results when childhood celiac disease prevents nutrient absorption during the years when nutrition is critical to a child’s normal growth and development. Children who are diagnosed and treated before their growth stops may have a catch-up period.
· Seizures, or convulsions, result from inadequate absorption of folic acid. Lack of folic acid causes calcium deposits, called calcifications, to form in the brain, which in turn cause seizures.

Contributed by John Lee

Sources:

National Institute of Diabetes and Digestive and Kidney Diseases (US):
http://digestive.niddk.nih.gov/ddiseases/pubs/celiac/#6

WrongDiagnosis.com:
http://www.wrongdiagnosis.com/c/celiac_disease/complic.htm

Pathophysiology of Celiac Disease

Pathophysiology of Coeliac Disease with correlation with its histologic presentation
Ji Keon LOOI
Monash University Sunway Campus

Introduction
•A.k.a. Gluten-sensitive enteropathy
•an autoimmune inflammatory disease of the small intestine
•Precipitated by the ingestion of gluten
•genetically susceptible persons
Oral tolerance
•Ingested protein does not normally provoke an immune response - "oral tolerance"

Oral intolerance / true allergy to an ingested protein (milk or soy protein)
•a typical IgE-mediated response
–urticaria,
–angioedema, and
–bronchoreactivity

Pathophysiology (1)
•involves plasma cells - IgA and IgG
•little or no IgE involvement

Current theory
•Ingested alpha-gliadin and related peptides bind with tissue transglutaminase in enterocytes
•The alpha-gliadin is rich in glutamine; transglutaminase deamidates glutamine residues, forming glutamic acid.
•Deamidation enhances the immunogenicity of alpha-gliadin by creating epitopes that are recognized as foreign by host cell­mediated immunity

Pathophysiology (2)
•IgA and IgG (by plasma cells) direct against a variety of antigens
–transglutaminase, endomysium, gliadin, and reticulin.
•Locally elaborated lymphokines attract inflammatory cells à villous flattening appearance
•Followed by malabsorption of micronutrients and macronutrients
•Small-bowel involvement is most prominent proximally and may be "patchy," especially in patients with "silent" celiac disease (i.e., minimal or no symptoms) and those with dermatitis herpetiformis.

My Task
•To explain the histologic charateristics of Coeliac Disease

Note: These slides were provided by Dr Rakesh Naidu on Monday's PCL.

Histologic Findings of Coeliac Disease
Histology
•In untreated coeliac disease
•inflammed lining of the intestine becomes inflamed
•villous atrophy
–flat appearance
•reduced surface area à nutritional deficiencies

Histological Description of CD
•Disease causality was established when the characteristic features of
–villous flattening,
–crypt hyperplasia, and
–increased intraepithelial lymphocytes

Before - After
A At time of diagnosis. There is severe villous abnormality associated with marked enterocyte damage (black arrows), in keeping with untreated coeliac disease.
B After 6 months of gluten-free diet. There is partial improvement of the previous villous abnormality, but a moderate villous abnormality with associated crypt hyperplasia remains

Remember……
•Exclusion of dietary gluten results in healing of the mucosa, resolution of the malabsorptive state, and reversal of most, if not all, effects of celiac disease.

Thank you!
•http://www.aafp.org/afp/20021215/2259.html
•http://content.answers.com/main/content/wp/en/6/60/CoeliacDisease.png

Management for Coeliac disease

self management...

No medication required. Just avoid food with gluten forever.


Supplementing the Gluten-Free Diet
Celiac disease prevents the body from absorbing nutrients properly. There are no longer as many functioning "holes in the sieve" for nutrients to get through to the blood stream. Even after the villi in the small intestine are described as being "back to normal," there remains the potential of some nutrients being absorbed at lower levels. Because of this, the monitoring physician may recommend a blood test analysis to learn if selected vitamins or nutrients are being absorbed at adequate levels.
Once a determination is made, supplementation of the GF diet may be advised. This recommendation may include selected intake of iron and folate and, in a few cases, one of the B vitamins. Occasionally there is need for replacement of fluids and electrolytes, including calcium, potassium and magnesium. Both men and women with low bone density may require vitamin D replacement. If there are associated conditions, such as lactose intolerance or diabetes, a series of additional treatment elements may apply.
It is important to remember that the immune system of a person with celiac disease is weak. The auto-immune system functions at a lower-than-normal level. Infections may not be handled as well as in other people. Stamina and resilience may not be at the level they once were. Most vitamins, food supplements and over-the-counter medications are based on and measured for persons at full-functioning, full-absorbing levels. A person with CD may need less or perhaps more of a particular vitamin, mineral or medication. Again, working with a monitoring physician will help determine what and how much is the appropriate allowance of a particular medical or supplemental product.
If symptoms persist after adopting a GF diet, further refinement may be necessary.

chris

Tasks for this week

Celiac Disease
1. Definition (also for IBS and UC) - Madhura
Risk Factors + Causes - Madhura
2. Pathophysiology - Ji Keon
3. Epidemiology (also for IBS and UC) - Shanthini
4. Signs and Symptoms - Sri
5. Investigation and Examination - Vivian
6. Management (include diet/lifestyle) - Chris
7. Prognosis and Complication - John
8. Psychosocial - Christine
9. CAM - Lawrence
(also IDA causes and incidence) - Lawrence

IBS = Irritable Bowel Syndrome
UC = Ulcerative Colitis
IDA = Iron Deficiency Anemia

Investigation for GERD

Barium Esophagram

• A barium esophagram or swallow is used as an initial diagnostic test for several esophageal conditions such as Barrett's esophagus, dysphagia (difficulty swallowing) as well as complications such as stricture, obstruction, narrowing, ulcers and tumors.
• During this procedure, the patient swallow barium, a while, chalky substance, which can then be viewed via x-ray. Using this procedure the physician can view many abnormalities associated with the esophagus.
  
• The disadvantage of this procedure is that it can miss smaller ulcers and tumors. This test is also not very effective for diagnosing gastro-esophageal reflux with GERD.

Esophagogastroduodenoscopy

• a diagnostic endoscopic procedure that visualises the upper part of the gastrointestinal tract up to the duodenum.
• (EGD) identifies the presence and severity of esophagitis and the possible presence of Barrett esophagus.
• EGD also excludes the presence of other diseases (eg, peptic ulcer) that can present similarly to GERD.
• Although EGD is frequently performed to help diagnose GERD, it is not the most cost-effective diagnostic study because esophagitis is present in only 50% of patients with GERD.

Esophagus monetary

• Esophageal manometry measures pressure within the esophagus. This test may also be referred to as an esophageal motility or function study.
• During esophageal manometry, a tiny, pressure-sensitive tube is inserted through your nose — or sometimes your mouth — and into your esophagus. There, it measures the effects of muscle contractions as you swallow. The test takes less than one hour.
• Manometry may also be used to measure pressures in your stomach (gastric motility), small intestine (small intestine manometry) and rectum (anorectal function).
  

24-hours Esophageal pH test

• An esophageal pH test measures and records the pH in your esophagus to determine if you have gastroesophageal reflux disease (GERD). The test can also be done to determine the effectiveness of medications or surgical treatment for GERD.
• A thin, small tube with an acid sensing device on the tip is gently passed through your nose, down the esophagus ("food tube"), and positioned about 2 inches above the lower esophageal sphincter. The tube is secured to the side of your face with clear tape. The end of the tube exiting from your nose is attached to a portable recorder that is worn on your belt or over your shoulder.
  
• The recorder has several buttons on it that you will press to mark certain events. A nurse will review the monitoring instructions with you.
  

Contributed by Lawrence Oh

Epidemiology of GORD

Gastro-oesophageal Reflux Disease - considered a common disease in the West.

The study of the epidemiology of GORD is restricted by the lack of consensus over the basic definition of the disease. To review the global epidemiology of GORD is currently problematic as there is no internationally applied definition.

An approximate prevalence of 10–20% was identified for GORD, defined by at least weekly heartburn and/or acid regurgitation in the Western world while in Asia this was lower, at less than 5%.

The disease is more common in the Western world than in Asia. This appears to be related to the high fat diet typically consumed by Westerners.

There is little difference between the prevalence of GORD (as defined by heartburn and/or acid regurgitation at least weekly) in North America (19.8–20%, n = 2) and in Europe (9.8–18%, n = 3). There is some indication that the prevalence may be lower in Southern than Northern Europe. There is a definite trend, however, towards a lower prevalence of GORD in Asia (2.5–4.8%, n = 2).

The incidence in the Western world was approximately 5 per 1000 person year. No data available from Asia. The low rate of incidence relative to prevalence reflects its chronicity.

Studies have shown a positive relationship between obesity and gastro-oesophageal reflux symptoms. This may explain the high prevalence of GORD in the USA compared with the rest of the world.

Contributed by John Lee

Sources:

http://gut.bmj.com/cgi/content/full/54/5/710
Dent J., El-Serag H.B., Wallander M-A. & Johansson S. 2005,
‘Epidemiology of gastro-oesophageal reflux disease: a systematic review’, Gut 2005, 54:710-717.

http://www.emedicine.com/radio/topic300.htm - Gastroesophageal Reflux

The cardia!

The cardia (or esophagogastric junction or gastroesophageal junction) is the anatomical term for the junction orifice of the stomach and the esophagus. At the cardia, the mucosa of the esophagus transitions into gastric mucosa.
The cardia is also the site of the lower esophageal sphincter (also termed cardiac sphincter, gastroesophageal sphincter, and esophageal sphincter


The stomach generates strong acids and enzymes to aid in food digestion. This digestive mixture is called gastric juice. The inner lining of the stomach has several mechanisms to resist the effect of gastric juice on itself, but the mucosa of the esophagus does not. The esophagus is normally protected from these acids by a one-way valve mechanism at its junction with the stomach. This one-way valve is called the lower esophageal sphincter (LES), and prevents gastric juice from flowing back into the esophagus.
During peristalsis, the LES allows the food bolus to pass into the stomach. It prevents chyme, a mixture of bolus, stomach acid, and digestive enzymes, from returning up the esophagus. The LES is aided in the task of keeping the flow of materials in one direction by the diaphragm.

chris

Signs & Symptoms

Heart Burn – Signs and Symptoms

• A burning feeling that starts in the chest, just behind the breastbone (the sternum). It usually occurs just after eating and can last a few minutes to several hours.
• Chest pain, especially after bending over, lying down or eating, more frequent or worse at night
• A burning feeling in the throat
• Sour or bitter taste in the throat/mouth
• Feeling of food “sticking” in the middle of the chest or throat

Gastro esophageal reflux disease

• Heart burn
• Difficulty swallowing
• Belching (burping)
• Chronic coughing
• Hoarseness
• Loss of voice for no apparent reason
• Wheezing or other asthma-like symptoms
• In babies, spitting up or throwing up almost after every meal.

Symptoms of heartburn are often mistaken for signs of a heart attack. Pain from a heart condition is usually made worse by physical activity, but heartburn is not usually caused by physical activity. However, if you think you are having a heart attack, or you're not sure, it's important that you go to the emergency room immediately.

Possible signs of heartburn that could be mistaken for a heart attack include:

• A sharp, burning sensation just below the breastbone or ribs.
• Pain generally does not radiate to the shoulders, neck, or arms, but it can.
• Pain usually comes after meals, when lying on the back, when exercising or when experiencing anxiety.
• Symptoms usually respond quickly to antacids.
• Rarely accompanied by a cold sweat.

Possible signs of angina (severe pain in chest area) or heart attack:

• A feeling of fullness, tightness, or dull pressure or pain generally in the center of the chest.
• The feeling of a belt being tightened around your chest.
• Sudden chest pain or pressure that worsens.
• Dizziness.
• Pain may spread to the shoulders, neck, jaw or arms.
• Pain often responds quickly to nitroglycerin.
• Shortness of breath.
• Often accompanied by a cold sweat.

(Posted by: Vivian)

mx and px of GORD

Management and prognosis of gastro-oesophageal reflux disease (gord)

Mx:
Lifestyle: ENCOURAGE weightloss, raise bed head, small regular meals
AVOID hot drinks, alcohol, and eating <3h before bed. Avoid drugs affecting oesophageal motility (nitrates, anticholinergics, tricyclic anti-depressants) or that damage mucosa (NSAID, K+ salts, alendronate)




Drugs: antacids such as magnesium trisilicate mixture(10ml/8h) or alginates( gaviscon, 10-20ml/8h) to relieve symptoms

If sx persists for >4wks, or weight decreases, dysphagia, excessive vomiting, GI bleeding, refer for GI endoscopy.

Prokinetic drugs: help with gastrc emptying( metoclopramide)


Surgery: not indicated unless sx are bad and there is radiological or PH monitoring evidence of severe reflux.

PX is generally good

Gastro-esophageal reflux disease

Gastro-oesophageal Reflux Disease(GORD/GERD)
prepared by: Ji Keon Looi
for pcl 9 Empty Nest

Introduction
•GOR is a normal physiologic event. However excessive exposure of the esophagus to stomach contents can lead to symptoms of complications (GORD)

Definition
•symptoms or mucosal damage (oesophagitis) resulting from the exposure of the distal oesophagus to refluxed gastric contents
•NB symptoms =/= mucosal damage

Pathophysiology
•Failure of the antireflux barrier
–Lower esophageal sphincter (LoS)
–Crural diaphragm (ext sphincter)
•Postprandial à Gastric distention àTransient relaxations of the LoS à Reflux episodes
•Decreased pressure of LoS (caffeine, nicotine, alcohol, fatty foods, chocolate)
Other factors
•Delayed gastric emptying
•Impaired oesophageal clearance
•Decreased salivary production

A myraid of causes
•Hiatus hernia (discussed later)
•Oesophagitis
–Acute inflammatory process in esophagus
•H. pylori
–Distal (antral) gastritis increases the production of gastric acid

Hiatus Hernia
•Part of the stomach protrudes through the oesophageal hiatus in the diaphragm
Hiatus hernia
•Most cases asymptomatic
•Impairs LoS function, increases likelihood of reflux
•large volumes of gastric contents pass unimpeded into the hiatal sac
•increased abdominal pressure on straining and even deep breathing may be enough to force refluxate into the oesophagus

Take home message
•The structure and function of the gastro-oesophageal junction is of key importance in reflux disease—as the condition becomes more severe, the risk of reflux during transient relaxations of the lower oesophageal sphincter rises and the volume of refluxate increases

•Fox M, Forgacs Ian, GORD, ; BMJ 2006

Dysphagia

• Difficulty in swallowing, commonly associated with disorders of the oesophagus
• dys meaning difficulty or disordered; phagia meaning "to eat"
• Aphagia - Inability to swallow
• Odynophagia - severe pain on swallowing due to a disorder of the esophagus
• Risks of dysphasia:
• aspiration pneumonia
• malnutrition
• dehydration
• weight loss
• airway obstruction
• Disorders leading to dysphagia may affect the oral, pharyngeal, or esophageal phases of swallowing; disorders of swallowing may be categorized according to the swallowing phase affected
• Oral phase
• Oral preparatory phase: chewing/processing of bolus
• Oral propulsive phase: initiation of swallowing: bolus propelled to oropharnyx (involuntary swallowing reflex is triggered here)
• Pathophysiology: Impaired control of the tongue, difficulty chewing solid food and initiating swallows. When drinking a liquid, patients may find it difficult to contain the liquid in the oral cavity before swallowing. As a result, liquid spills prematurely into the unprepared pharynx, often resulting in aspiration.
• Pharyngeal phase
• Involuntary
• Bolus passed down into esophagus
• Upper esophageal sphincter relaxes during the pharyngeal phase of swallowing and closes after passage of the food
• Pathophysiology: In case of weakness or lack of coordination of the pharyngeal muscles, or poor opening of the upper esophageal sphincter, patients may retain excessive amounts of food in the pharynx and experience overflow aspiration after swallowing
• Esophageal phase
• Bolus is propelled downward by a peristaltic movement
• Lower esophageal sphincter relaxes at initiation of the swallow
• Closes after the bolus enters the stomach, thereby preventing gastroesophageal reflux
• Pathophysiology: Mechanical obstruction, motility disorder, or impaired opening of the lower esophageal sphincter can result in retention of food and liquid in the esophagus after swallowing
• Treatment:
• Disorders of oral and pharyngeal swallowing are usually amenable to rehabilitation, including dietary modification and training in swallowing techniques and maneuvers.
• Surgery is rarely indicated for patients with swallowing disorders.
• In patients with severe disorders, bypassing the oral cavity and pharynx in their entirety and providing enteral nutrition may be necessary. Options include percutaneous endoscopic gastrostomy and intermittent oroesophageal catheterization.

Source: http://www.emedicine.com/pmr/topic194.htm

PCL tasks week 9

1) definition and normal physiology (gastroesophageal spinchter)- Chris
2) pathophysiology -Ji Keon
3) Risk factors (diet-what kind of diet?precisely when it occurs?, lifestyle-smoking?alcohol intake?, pregnancy-hormonal changes?fetus?)-Shantz
4) Investigations-to rule out(H.pylori culture? ECG? rule out possible tumor?, to rule in-endoscope-Lawrence
5) Signs and symptoms-Vivian
6) Management and Prognosis- Christine
7) Epi-John
8) difficulty in swallowing-Madhura
9) Complications + Esophageal cancer-Sri

NJOY!!!!!

Socio-Economic-Environmental challenge of rural community

Social Challenge
- poor education
- language barrier
- lack of awareness
- lack of access to health care facilities
- high level of self-harm, drug-misuse and violence
- high rates of incarceration
- poor nutrition

Economic Challenge
- financial problem, lower income
- lack of job opportunity

Environmental Challenge
- health care facilities are not easily accessible
- risk of being exposed to natural disaster such as flood
- poor sanitation
- poor hygiene

Contributed by Lawrence Oh

Healthcare Delivery in Rural Malaysia

Healthcare services in rural Malaysia are mainly provided by the government in the form of a two-tier system. This system consists of the Klinik Kesihatan (Health Clinic) and the Klinik Desa (Community Clinic) which are under the management of the District Health Office.

Klinik Desa:
- Provides healthcare to a population of about 4000 (or a kampong)
- Handled by 1-2 Jururawat Masyarakat (community nurse)
- Focus on maternal & child health, particularly antenatal, postnatal care, contraception, immunisation and development assessment
- Provides home visit

Klinik Kesihatan:
- One KK with 4 KD
- Caters to a population of 20,000
- Managed by Medical Officers, with the help of Medical Assistants
- Accept referrals from Medical Assistants, nurses, midwives & private GPs
- Larger KKs have a Family Medicine Specialist (e.g KK Segamat) + more facilities like laboratory, diagnostic imaging facilities, maternal & child clinics and dental services

Serious cases which cannot be handled by the KKs will be refered to the nearest district hospital, which is under the charge of the hospital department of the Ministry of Health.

Non-government Healthcare Providers in Rural Areas
- Private GPs
- Traditional Medicine Practitioners ( particularly for the treatment of musculoskeletal problems, psychological illness and illness perceived to be supernatural in origin)
- Estate Clinics (provided by Palm Oil Companies to serve the health needs of the estate workers/ managed by a Health Assistant)

Contributed by John Lee

Source: Review Article- Rural Health Care in Malaysia by Kamil Mohamad Ariff & Teng Cheong Lieng