Diet Ht &Sal.cerna 2012

7/26/2019 Diet Ht &Sal.cerna 2012

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Departemen Ilmu Gizi FK USU

MEDAN


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Refers to nonspesific,persistent upper

abdominal discomfort or pain. Causes of discomfort:

Ephageal reflux

Gastritis

Peptic ulcer Gallbladder disease

Other identificable pathologic conditions.

Always misdiagosed with iiritble bowelsyndrome.

Diet,stress and other lifestyle factor maycontribute to the symptoms.


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Goal: Decrease exposure of esophagus to gastric

contents.

Avoid: large meals,dietary fat, alchohol

Goal: Decrease acidity of gastric secretions. Avoid coffee

Fermented alkoholic beverages.

Goal:oPrevent pain and irritation

o Any food that the patient feels exacerbates his/hersymptoms.


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Result when infectious (Heliobacter pylori),chemical

or neural abnormalities disrupt mucosal integrity ofthe stomach.

Other causes of gastritis chronic: used of aspirin or

other NSAID,steroids,alcohol,erosive

substances,tobacco or any combination

acquiring acute or chronic gastritis.

Symptoms of gastritis:

Nausea,vomiting,malaise,anorexia,hemorrhage and

epigastric pain.Prolonged gastritis atrophy and loss of sotmach

parietal cells achlorhydria & intrinsic factor

Pernicious anaemia


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Peptic ulcer:

Typically : evidence of chronic inflammation and

repair processes surrounding the lesion.

Normally involve two major regions: gastric and

duodenal.

Characteristic peptic ulcers Abdominal

discomfort/abdominal pain

Other symptoms are: anorexia,weight loss, nausea

and vomiting and heartburn

In some patients :asymptomatic.


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Complication : hemorrhage and perforation.

Ulcer can perforate into

Peritoneal cavity

Penetrate into an adjacent organ (usually pancreas)

Erode an artery and cause massive hemorrhage

Melena( black,tarry stools) are common in peptic ulcer

disease especially in older adults.

Melena may suggest either acute or chronic upper GIbleeding.


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Atropic gastritis : lack of intrinsic factor and acid

malabsorbtion of vit.B12. Acid


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Omega 3 and omega 6 fatty acids are involved in Inflamatory

Immune of the GI

Cryptoprotective physiologic conditions mucosa

But they have not yet been found to be effectivefor treatment.

High quality diet without nutrient deficiencies mayoffer protection and promote healing.

Advised: Avoid foods that exacerbate their symptoms

Consume a nutritionally complete diet withadequate dietary fiber from fruits and vegetables


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Characterized by chronically recurring

abdominal discomfort or pain and altered

bowel habits.

Other symptoms:

bloating,feelings of incomplete evacuation

Presence of mucus in the stool

Increased GI distress associated with psychosocial

distress.


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Diagnosis is based on international consensuscriteria (Rome criteria): Symptoms of abdominal discomfort must be present for at

least 3 days per month for the past 3 months, include atleast 2 of 3 features:

1. Discomfort relieved by defication

2. Onset associated with a change in frequency of stool

3. Onset associated with a change in form of the stool

o Diagnosis futher categorizes the syndrome into one of 3subtypes:

1. Diarrhea predominant

2. Constipation predominant

3. Mixed (1 + 2)


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The goal :

To ensure adequate nutrient intake Tailor the diet for the spesific GI pattern of IBS

Explain the potential roles of foods in the management ofsymptoms.

Large meals and certain foods may be poorly

tolerated (excess quantities of dietary fat,caffeine,lactose,fructose,sorbitol and alcohol)

found in persons with diarrhea predominant IBS ormixed IBS.

Supplementation of insoluble fibre (wheat bran)worsen symptoms.

Consumption of adequate fluid is recommended.


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Peny.kronik dimana sel liver diganti ojar.fibrosis dan infiltrasi lemak.

Causa: alkohol

hepatitis (post nekrotik)

kelainan biliaris

peny.autoimun

penggunaan obat hepatotoksik

Nutrition intake problem: Adequate nutrition intake is difficult to achieve

because of anorexia,nausea, and other GITsymptoms (+).


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Energy.

In general Energy requirement for ESLD (End StageLiver Disease) 25 35 cal/ kg BW ( if ascites

,infection and malabsorption are present)

Oral nutrition supplement or tube feeding

Increase optimal intake Reducing complication and prolonged survival.

Carbohydrate.

Liver failure reduces glucose production &peripheral glucose use.

CH 60-70% total energy (complexs)


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Lipid.

The body prefers lipids as an energy sThebody preferlipids as an energy substrate.

Range 25-40% of calories as fat is generallyrecommended.

Protein.

Cirrhosispatient increase protein use. 0.8 g/kg/day is the mean requirement to

achieve nitrogen balance in stable cirrhosis.

To promote nitrogen accumulation

(positivebalance) : 1.2-1.3 g/kg daily. Alcoholic hepatitis or decompensated disease

: 1.5 g /kg BW/day.


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Vitamin & Mineral.

Vitamin & mineral supplementation is needed for

ESLD because of the intimate role of the liver in: Nutrient transport

Storage

Metabolosm

Side eefct of drug. Iron stores depleted in GIT bleeding need Fe

supplementation,but do not give to the patient withhemochromatosis or hemosiderosis.

Ca,Mn and Zn may be malabsorbed with steatorrhea

therefore the patient should take mineral

supplement.

For


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The formation of gallstones (calculi) is cholelithia

sis. In most cases :Asymptomatic

Choledocholithiasis (+) when stones slip into thebile ducts obstruction,pain and cramps (+).

Obstruction of the distal common bile ductPancreatitis (+) if the pancreatic duct is blocked.

Most gallstone are unpigmented cholesterol stonescomposed primaliry :Cholesterol,bilirubin,Ca salts.

Causes of gallstone: bacteria

high dietary fat intake over a prolonged period.

Rapid weight loss.


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Risk factors for cholesterol stone

formation

Female gender

Pregnancy

Older age Family history

Obesity

DM

IFD (Inflamatory

Bowel Disease)

Drugs(lipid loweringmedications,oral con-

traseptive,estrogen


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Medical nutrition therapy.

No spesific dietary treatment is available to prevent

cholelithiasis in susceptible persons. Replace simple sugar and refined starches with

high fibre carbohydrate.

Individual who consuming refined CH have 60%

greater risk for developing gallstones >< whoconsumed the most fibre (in particular insolublefibre) plant based diets reduced the risk ofCholelithiasis

After surgical removal of the gallbladderoral feeding can be advance to a regular diet astolerated


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Is the inflammation of the gallbladder(acute or

chronic) Caused by: gallstones obstructing the bile

ducts.

Acute cholecystitis without stones occur in Critically ill patients When the GB (gallbladder) and its bile are stagnant

The walls of the GB become inflamed &distended infection (+).

Symptoms : upper quadrant abdominal pain +nausea, vomiting & flatulence


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Chronic Cholecystitisis :

Long standing inflammation of the GB.

Caused by repeated,mild attack of Acute Chole

cystitis.

Eating food high in fat may aggragavate the

symptoms

More often in women than in men.

Increase after the age of 40

Risk factor :

The presence of gallstones

History of acute cholecystitis.


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cute cholecystitis

In acut attack oral feedings are discontinued. Parenteral Nutrition is indicates if

The patient is malnourished

Not taking anything orally for a prolonged period.

When feeding are resumed: give a low fat diet (30-40 g of fat/day)

Chronic cholecystitis.

Require a long term,low fat diet that contains 25%-

30% of total calories as fat.Stricter limitation is undesirable because fat in the

intestine is important for stimulate and drainage of

the biliary tract.


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Diet Ht &Sal.cerna 2012