An African mother brings her 18-month-old child to the clinic because - she says - he was poisoned.

Taking the history we note that her child was breast-fed till 1 year of age. Then another pregnancy started

and the mother abruptly weaned the child, who has since been fed almost exclusively on sweet potatoes

and sorghum porridge. The child has been presenting liuid stools for the last ! weeks. According to his

mother he refuses to eat.

"hysical examination reveals a sad, apathetic child. #is face is swollen, there are generali$ed oedema,

low weight, decreased arm-circumference and muscle-wasting. #is hair is pale, straight and easily pulled

off. #is skin is depigmented, the liver and spleen are palpable.

Which of the following statements are correct?

A) This child presents the clinical picture of protein-energy malnutrition of the

marasmus type.

B) The aetiology of this child's protein-energy malnutrition is multifactorial.

C) The laboratory inestigation of this child should include a thic! smear" a

microscopic e#amination of the stools and a stool culture.

$) Therapy will aim at introducing foods rich in proteins to this child's diet.

%) A good part of any successful outcome will rely on dietary education of the

mother.

%&-year-old peasant farmer complains of loss of weight, anorexia, sore tongue, indigestion and diarrhoea.

'ymmetrical bilateral erythematous pruritic lesions are present on the backs of the hands and the

forearms.

(hich of the following statements are correct)

A* This condition is often associated with a mai$e diet.

+* A psychosis may occur in advanced stages of this disease.

* 'ignificant hypoalbuminaemia is usually present

* asals necklace is a feature of this condition.

/* The 0ecommended ietary Allowance of the deficient nutrient is about 1 mg2day for an adult

male

• Are cardiovascular diseases a growing problem)

• 3.! #ow can diet and physical activity affect cardiovascular diseases)

• 3.% (hat nutrients are known to affect cardiovascular diseases)

• 3.4 (hat food items are known to affect cardiovascular diseases)

• 3.& #ow could cardiovascular diseases be prevented)

 

Table 1. &ummary of strength of eidence on lifestyle factors and ris! of deeloping cardioascular

diseases

%idence $ecreased ris! o relationship (ncreased ris!  

Conincing 0egular physical activity

5inoleic acid

6ish and fish oils 7/#A and #A*

egetables and fruits 7including berries*

"otassium

5ow to moderate alcohol intake7for coronary

heart disease*

itamin /

supplements

9yristic and palmitic

acids

Trans fatty acids

#igh sodium intake

:verweight

#igh alcohol intake 7for

stroke*

robable a-5inolenic acid

:leic acid

 ;'"

(holegrain cereals

 ;uts 7unsalted*

"lant sterols2stanols

6olate

'tearic acid ietary cholesterol

<nfiltered boiled coffee

ossible 6lavonoids

'oy products

6ats rich in lauric acid

=mpaired fetal nutrition

+eta-carotene supplements

(nufficient alcium

9agnesium

itamin

arbohydrates

=ron

Dietary Suggestions to Reduce CVD Risk • %at more fruits and egetables.

• %at more whole grains.

• *se low-fat snac!s.

• +educe fat inta!e to ,?/ percent of the diet.

• +educe cholesterol inta!e to less than // mg. per day.

• +educe consumption of egg yol!s to three to fie per wee!.

• 0inimi1e use of whole mil! and its products2 use low-fat or nonfat mil! products.

• Aoid red meats2 eliminate all cured meats and lunchmeats.

• 3imit the use of nuts and seeds" not more than a handful daily.

• Aoid e#cess inta!e of aocados" olies" crab" and shrimp.

• %at more coldwater fish" such as sardines and salmon.

• *se fresh" monounsaturated" mechanically pressed oils" such as olie or fla#seed oils" to

proide the essential fatty acids.

+ole of the 3ier in ormal utrition

 

The liver is the primary metabolic organ within the body that coordinates a complex array of biochemical

and physiological processes linked to nutrition. =t influences nutritional status through its role in macro-

and micronutrient metabolism, including carbohydrate, protein, lipid, and vitamins 71%,14,!!,!%,!4*.

'trategically located between the portal and systemic circulation, the liver is exposed to most ingested

nutrients and drugs, enabling its key role in metabolism and detoxification within the body 7!%,!4*. As

 part of its metabolic role, the liver enables the maintenance of homeostasis of glucose, protein2amino

acids, and lipids, and also the synthesis of clotting factors, albumin, and plasma proteins 714,!%,!4*. The

excretion of lipid-soluble waste material into bile and the removal of bacteria and other factors delivered

 by the portal or systemic circulation are additional activities of the liver 7!%,!4*. As well, the

detoxification of chemicals entering the body, for example in foods, fluids, and drugs, is another primary

role of the liver 7!%,!4*.

5iver failure does not become obvious until most of the hepatocytes have been destroyed, at which point

it becomes difficult for the body to maintain nutritional homeostasis, utili$e nutrients appropriately,

synthesi$e plasma proteins, and detoxify noxious substances 7!%,!4*.

The liver plays an important role in intermediary metabolism within the body 7!%,!4*. The synthesis and

degradation of protein occurs in this organ, as the en$ymes that metaboli$e amino acids and synthesi$e

urea are located within the liver 7!%,!4*. "lasma proteins, which include albumin, transferrin, coagulation

factors, and ceruloplasmin, account for about half of the protein synthesi$ed within in the liver 7!%*.

#ormones such as insulin, glucagon, and glucocorticoids, as well as nutritional status, all influence

 protein synthesis by the liver 714,!!,!%,!4*. =n addition, carbohydrate metabolism is regulated through the

synthesis, storage, and breakdown of glycogen within the liver 7!%,!4*. >lycogen synthesis occurs when

the intake of glucose, or glucose precursors, exceeds energy reuirements, and glycogen is readily

metaboli$ed when dietary intake is deficient in energy. ?ey en$ymes and hormones such as epinephrine,

insulin, and glucagon are also an important part of carbohydrate metabolism regulated through this organ

7!%*. Triglyceride synthesis and fatty acid degradation also occur primarily in the liver. (hen

carbohydrate intake exceeds energy reuirements, glycogen storage within the liver is probably exceeded

and triglyceride synthesis is then stimulated 7!!,!%,!4*.

Chronic 3ier $isease and utritional 4actors

A decrease in the number of functioning hepatocytes results in a decrease in the nutrients, immune cells,

and hormones that are being delivered to the remaining functional hepatocytes 7!!,!%,!4*. Thus, ongoing

impairment of hepatic function will increase ones risk of nutritional deficiencies, particularly when

cirrhosis develops.

<nfortunately there is no clear, consistent approach to the nutritional management of chronic liver

disease. To date there is no @gold standard for evaluating nutritional efficacy in this population, probably

as a result of an incomplete understanding of the pathophysiological processes responsible for protein

energy malnutrition 7"/9*, and also due to a lack of agreement about appropriate outcome measures

$ietary (nta!e

=nadeuate dietary intake is likely one of the primary causes of nutritional deficiencies in patients with

chronic liver disease 74,&*. 'uboptimal nutrient intake is prevalent in !3-83B of patients with alcoholic

and nonalcoholic liver disease, and might arise secondary to a number of factors, such as nausea,

anorexia, and early satiety, particularly in the presence of ascites. The therapeutic restriction of dietary

sodium and protein 71%*, changes in taste acuity 7&1*, or the etiology and severity of liver failure 7&!* may

all impact on the daily intake of dietary nutrients. The pattern of food intake might also be an important

consideration when trying to maximi$e the dietary intake of subCects with cirrhosis 7&%,&*. A recent

 published study indicates that the spontaneous dietary intake of cirrhotic patients was lower than that of

controls, and than recommended intake levels 7&4*.

0aldigestion and 0alabsorption

A reduction in bile salt secretion and in the bile salt pool si$e has been reported in patients with cirrhosis.

The smaller bile salt pool probably interferes with micelle formation and fat assimilation, ultimately

increasing the risk of deficiencies of fat, and fat soluble vitamins .

0etabolic Alterations in Chronic 3ier $isease

A decrease in glucose oxidation along with an increase in the oxidation of lipid has been observed in

cirrhotic patients, which is independent of nutritional status . =mpaired glucose tolerance with

accompanying insulin resistance and hyperinsulinemia occurs commonly in cirrhotic patients with about

 

!B developing diabetes mellitus . A recently published study suggests that chronic hyperinsulinemia

causes insulin resistance in cirrhosis, possibly due to diminished hepatic insulin degradation, which would

 be the primary metabolic defect in cirrhosis.

=n the fasting state, plasma free fatty acids, as well as glycerol and ketone bodies, are increased 714*.

"lasma clearance and lipid oxidation rates are, however, normal in cirrhotic patients 7&*, and therefore,

their net capacity to store exogenous lipid does not seem to be impaired 714*. ecreased polyunsaturated

fatty acids 7"<6A* have been found in cirrhotic patients, correlating to nutritional status 7D* and the

severity of liver disease 7D1*. :f interest, a recent study determined that the "<6A content of erythrocyte

membranes in cirrhotic patients is decreased compared to healthy controls, with a more pronounced effect

noted in patients with alcoholic cirrhosis compared to those whose disease is viral in origin 7D!*.

"olyunsaturated fatty acids are potent precursors of free radicals, which will increase oxidative stress

7D%*, in a population of patients who have already been identified as being oxidatively stressed 7%4,%&*.

6urther studies need to be undertaken to determine whether increased fat intake should be encouraged in

this population, using "<6A, which are an important source of essential fatty acids 7/6A*.

"atients with insulin resistance have not been found to have impaired protein and amino acid metabolism

7D4*. "rotein turnover has been reported to be normal in fasted cirrhotic patients 714,!%,!4*E however,

after refeeding, protein flux has been found to increase 7!%,!4*, with an increase in protein degradation in

some patients 714*. 'table cirrhotic patients appear to be capable of efficient nitrogen retention, able to

maintain lean body mass 7D4*, and able to consume protein intakes similar to those of people without

cirrhosis 7!%,!4*. "rotein catabolism influences amino acid balance, and can indirectly cause an

overloading of nitrogenous waste within the liver. #yperammonia, which is an end-product of amino acid

catabolism, can ultimately contribute to hepatic encephalopathy if the liver is not able to detoxify the

nitrogenous waste71%,14,!%,!4*. The synthesis of albumin correlates with uantitative liver function tests

and the clinical status of cirrhosis 71%,14,D&*.

rotein %nergy 0alnutrition 5%0)

"rotein energy malnutrition is uncommon in the precirrhotic stages of liver diseaseE however, it is a

common finding in advanced liver disease 748*. The prevalence and severity of "/9 are related to the

clinical stage of chronic liver disease 71%,14*. Anthropometric evaluation indicates that about !B of

 patients with compensated liver cirrhosis have "/9, while about DB of patients with severe liver failure

have "/9 714,DD*. #owever, more sensitive body composition measures suggest that the prevalence is

likely higher 714,D3,D8*. 'evere non-alcoholic liver disease has been found to be characteri$ed by

significant reductions in body fat and body cell mass 7D8*, with a significant reduction in some nutritional

compartments, with the tissue loss possibly reflecting mechanisms of tissue wasting 7D8*.

"/9 impairs liver function but rarely causes morphological alterations 71%,14*. Fuantitative liver

function tests can be used as global indicators of functional impairment but are not capable of

distinguishing between malnutrition-induced and disease-induced liver failure 71%,14*. #owever,

malnutrition does have a negative effect on clinical outcome of this population considering survival and

complications 714*.

Assessment of utritional &tatus

The assessment of nutritional status reuires information on energy balance, body composition, and tissue

function 71%,14*. 6actors to consider in the assessment of nutritional status are outlined.

linical /valuation 7!!,D*

1. 0edical 6istory

GAssessment of changes in weight, including factors that affect the evaluation of weight such as fluid

retention states

Ghanges in appetite, including anorexia, changes in taste acuity, nausea, and vomiting

/valuation of gastrointestinal function, considering diarrhea, and steatorrhea

!. hysical %#am

G /valuation for physical signs of protein energy malnutrition 7"/9*

%. $iet 6istory

G /valuation of energy intake, as well as protein, sodium, and fluid

G Alcohol use

G 6ood intake pattern, intolerances

G itamin2mineral supplements

 

Body Composition $ates

+ody weight

G +ody weight measurements are not always valid in liver failure due to fluid shifts that occur because of

edema, ascites, and also diuretic therapy.

G 9alnutrition is associated with a shift of fluid from the intravascular to the extravascular space, with a

concurrent decrease in lean body mass 7loss of lean body mass may occur with no change in body

weight*.

'omatic protein compartment

G The anthropometric measures, which include mid-arm circumference 79A*, mid-arm muscle

circumference 79A9*, and skin fold thickness 7T'6* can be used for patients with liver failure.

G These measures should be ideally used for serial measures to assess changes over timeE comparisons

with standard measures are not helpful.

G reatinine height index 7#=* is affected by several factorsH hepatocyte damage can decrease the

formation of creatinine and alter measures of #=E also, "/9 and aging can decrease body cell mass and

result in a decrease in #=.

isceral protein compartment 71%,!!*

G isceral proteins provide a measure of hepatic transport proteinsE they correlate more accurately with

the degree of liver damage than with the degree of "/9.

G 'erum albumin will remain normal until less than !&B of hepatocytes are functioning. =t functions to

maintain colloid oncotic pressure within the bodyE in liver disease, serum albumin levels may be used as

markers of liver function as well as nutritional status.

G Transferrin is generally thought to be a more accurate measure of nutritional status due to its shorter

half-lifeE however, serum concentrations are affected by many of the same factors as albumin.

GThyroxine-binding pre-albuminH non-nutritional factors, such as bleeding and infection that cause an

immediate need for protein synthesis, will acutely decrease levelsE thyroid function will also affect levels.

+%C700%$AT(7& 47+ *T+(T(7A3 (T%+8%T(7

The goals of nutritional intervention are to provide adeuate energy and protein to facilitate hepatocyte

regeneration, which will improve liver metabolism and overall nutritional status 71%,14,!!* 7see Table 1*.

6urther goals are to avoid the excess production of ammonia from endogenous or exogenous protein

catabolism, and to provide adeuate vitamins and minerals. As well, the avoidance of complications

related to the role of the liver in intermediary metabolism associated with carbohydrate, lipids and

 proteins, the avoidance of fluid and electrolyte imbalance, and death related to nutritional factors, are of

 primary concern

"atients who are not consuming adeuate energy should be offered the opportunity of nutritional

evaluation and monitoring by a ualified dietitian.

A modified meal pattern with freuent small meals four to seven times per day, including an evening

snack, has been found to improve nitrogen and substrate utili$ation in stable cirrhotic patients :ral

 protein2energy supplements may be helpful in conCunction with the usual diet regimen. The use of branch

chain amino acids might be useful in selected cirrhotic patients who have an intolerance to the usual

dietary proteins, to enable them to attain positive nitrogen balance 73D*. 5ong-term supplementation with

 branch chain amino acids has been associated with improved liver function and nitrogen accretion in

 protein-intolerant patients 733,38*. 'ome interesting research involving the branch chain amino acid

leucine was undertaken in cirrhotic patients. 0esults suggest that in this population, degraded leucine is

 being oxidi$ed completely, and is therefore not available to provide a carbon skeleton for use by other

metabolic pathways within the body, such as lipid synthesis 73*.

=f nutritional intake is inadeuate by the oral route, the enteral route should be considered. "arenteral nu-

trition is an option that is generally reserved for those who are otherwise unable to meet their

reuirements. 6ormulae for cirrhotic patients should be high energy 71.& kcal2 ml* with

a lower sodium content 74 mmol2day*, so that they can be readily used by patients who have problems

with fluid retention

Nutritional Status Assessment Form 5+%9*(+%$ 47+0)

 

$etermine :our utritional 6ealth form below

The warning signs of poor nutritional health are often overlooked. <se this checklist to

find out if you or someone you know is at risk.

0ead the statement below. ircle the number in the IyesI column for those that apply to you or someone you know. 6or each IyesI answerE score

the number in the box. Total your nutritional score

  :%&

= have an illness or condition that made me change the kind and2or amount of

food = eat.!

= eat fewer than ! meals per day. %

= eat few fruits or vegetables, or milk products !

= have % or more drinks of beer, liuor, or wine almost every day. !

= have tooth or mouth problems that make it hard for me to eat. !

= dont always have enough money to buy the food = need. 4

= eat alone most of the time. 1

= take ! or more different prescribed or over-the-counter drugs a day. 1

(ithout wanting to, = have lost or gained 1 pounds in the last D months. !

= am not always physically able to shop, cook, and2or feed myself. !

T7TA3  

Total :our utritional &core

/ - , ;ood< 0echeck your nutritional score in D months

- :ou are at moderate nutritional ris!.  'ee what can be done to improve

your eating habits and lifestyle. Jour office on aging, senior nutrition

 program, senior citi$ens center, or health department can help. 0echeck

your nutritional score in % months.

= or more :ou are at high nutritional ris! . +ring this checklist the next time your

see your doctor, dietitian, or other ualified health or social service

 professional. Talk with them about any problems you may have. Ask for

help to improve your nutritional health.

 ;:T/H 0emember that warning signs suggest risk, but do not represent diagnosis of any condition.

$iagnosis of *ndernutrition(eight and weight loss - primary diagnostic indicator for undernutrition

"arameters for undernutrition

• (eight loss - & lbs. lossE &B loss in % daysE 1B loss in 18 days

• Fuantification of food intake K3&B of meals for three consecutive days

• Albumin level K %.& g2dl

• holesterol K 1D mg2dl

• +ody 9ass =ndex weight in kg -K!!

  height in meters! 

<nderweight K !!, :verweight L !8