Session 21 Nutritional Pathology

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Lecture Notes

Session 21: Nutritional Pathology

Alex Simon (MD)

Learning tasks

At the end of this session, students are expected to be able to:

Explain Protein Energy Malnutrition.

Explain eating disorders.

Identify vitamins deficiencies.

Explain obesity and its clinical consequences.

Introduction

A healthy diet provides

Sufficient energy, in the form of carbohydrates, fats, and proteins, for the body’s daily metabolic needs.

Essential (as well as nonessential) amino acids and fatty acids, used as building blocks for synthesis of structural and functional proteins and lipids.

Vitamins and minerals, which function as coenzymes or hormones in vital metabolic pathways or, as in the case of calcium and phosphate, as important structural components.

Malnutrition

Primary malnutrition.

One or all of these components are missing from the diet.

Secondary (conditional) malnutrition.

The dietary intake of nutrients is adequate.

Malnutrition results from nutrient

Malabsorption.

Impaired utilization or storage.

Excess losses.

Increased requirements.

Malnutrition cont…

The causes of secondary malnutrition can be grouped into three general but overlapping categories:

GI diseases.

Chronic wasting diseases.

Acute critical illness.

Causes of dietary insufficiencies

Poverty.

Ignorance.

Chronic alcoholism.

Acute chronic illnesses.

Self-imposed dietary restriction.

Other causes

GI diseases.

Acquired and inherited malabsorption syndromes

Specific drug therapies.

Total parenteral nutrition.

Protein-Energy Malnutrition

PEM manifests as a range of clinical syndromes, all resulting from a dietary intake of protein and calories that is inadequate to meet the body’s needs.

The two ends of the spectrum of syndromes are known as marasmus and kwashiorkor.

In considering these conditions, an important point is that from a functional standpoint, there are two protein compartments in the body.

Somatic compartment.

Visceral compartment.

Protein compartments in the body

Somatic compartment.

Represented by proteins in skeletal muscles.

Affected more severely in marasmus.

Visceral compartment.

Represented by protein stores in the visceral organs, primarily the liver.

Depleted more severely in kwashiorkor.

These two compartments are regulated differently.

Marasmus

The term marasmus originated from the word marasmos meaning wasting.

A child is considered to have marasmus when weight level falls to 60% of normal for sex, height, and age.

A marasmic child suffers growth retardation and loss of muscle mass as a result of catabolism and depletion of the somatic protein compartment.

This seems to be an adaptive response that provides the body with amino acids as a source of energy.

Marasmus cont…

Of interest, the visceral protein compartment, which presumably is more precious and critical for survival, is depleted only marginally, so serum albumin levels are either normal or only slightly reduced.

In addition to muscle proteins, subcutaneous fat is also mobilized and used as fuel.

Marasmus cont…

High levels of cortisol that contribute to lipolysis.

With such losses of muscle and subcutaneous fat, the extremities are emaciated

By comparison, the head appears too large for the body.

Anemia and manifestations of multivitamin deficiencies are present.

There is evidence of immune deficiency, particularly of T cell– mediated immunity.

Hence, concurrent infections are usually present that impose an additional stress on an already weakened body.

Kwashiorkor

Kwashiorkor occurs when protein deprivation is relatively greater than the reduction in total calories.

This is the most common form of PEM seen in children who have been weaned too early and subsequently fed, almost exclusively, with carbohydrate diet.

Kwashiorkor cont…

Marked protein deprivation is associated with severe loss of the visceral protein compartment.

The resultant hypoalbuminemia gives rise to generalized or dependent edema.

The weight of children with severe kwashiorkor typically is 60% to 80% of normal.

However, the true loss of weight is masked by the increased fluid retention (edema).

There is relative sparing of subcutaneous fat and muscle mass.

The modest loss of these compartments may also be masked by edema.

Clinical features of Kwashiorkor

Generalized edema

Skin lesions with alternating zones of hyperpigmentation, desquamation, and hypopigmentation, giving a “flaky paint” appearance.

Hair changes include loss of color or alternating bands of pale and darker color, straightening, fine texture, and loss of firm attachment to the scalp.

Other features include

An enlarged, fatty liver (resulting from reduced synthesis of the carrier protein component of lipoproteins) and

The development of apathy, listlessness, and loss of appetite.

Kwashiorkor cont…

Vitamin deficiencies are likely to be present, as are defects in immunity and secondary infections.

In kwashiorkor, the inflammation caused by infection produces a catabolic state that aggravates the malnutrition.

Of note, marasmus and kwashiorkor represent two ends of a spectrum but considerable overlap exists.

The two main primary PEM syndromes are marasmus and kwashiorkor.

Secondary PEM

Secondary PEM is common in chronically ill or hospitalized patients.

A particularly severe form of secondary PEM, called cachexia, often develops in patients with advanced cancer.

The wasting is all too apparent and often presages death.

Although loss of appetite may partly explain it, cachexia may appear before appetite decreases.

Secondary PEM(Cancer cachexia mechanism)

The underlying mechanisms are complex.

Involve “cachectins” such as proteolysis-inducing factor, which are secreted by tumor cells, and cytokines, particularly TNF, which are released as part of the host response to advanced tumors.

Both types of factors directly stimulate the degradation of skeletal muscle proteins, and cytokines such as TNF also stimulate fat mobilization from lipid stores.

Hallmark anatomic changes in PEM

Growth failure.

Peripheral edema in kwashiorkor.

Loss of body fat and atrophy of muscle, more marked in marasmus.

Morphology in Kwashiorkor

The liver in kwashiorkor is enlarged and fatty.

In kwashiorkor the small bowel shows a decrease in the mitotic index in the crypts of the glands, mucosal atrophy and loss of villi and microvilli.

The bone marrow may be hypoplastic, mainly as a result of decreased numbers of red cell precursors (as in marasmus).

Anemia is usually present, most often hypochromic, microcytic anemia.

Brain shows cerebral atrophy, a reduced number of neurons, and impaired myelination of white matter.

Morphology in Kwashiorkor cont…

Other changes

Thymic and lymphoid atrophy (more marked in kwashiorkor than in marasmus),

Anatomic alterations induced by intercurrent infections, particularly with endemic helminthes and other parasites.

Deficiencies of other required nutrients such as iodine and vitamins.

Protein Energy Malnutrition (PEM)

Marasmus

Kwashiorkor

Eating disorders:Anorexia Nervosa and Bulimia

These are self-imposed dietary restriction disorders.

Anorexia nervosa is a state of self-induced starvation resulting in marked weight loss.

Bulimia is a condition in which the patient binges on food and then induces vomiting.

Bulimia is more common than anorexia nervosa and carries a better prognosis.

Anorexia nervosa

It is a state of self-induced starvation resulting in marked weight loss.

Anorexia nervosa also occurs primarily in previously healthy young women who have acquired an obsession with attaining or maintaining thinness.

The clinical findings in anorexia nervosa generally are similar to those in severe PEM.

Anorexia nervosa cont…

In addition, effects on the endocrine system are prominent

Amenorrhea, resulting from decreased secretion of gonadotropin-releasing hormone.

Decreased thyroid hormone release, include cold intolerance, bradycardia, constipation, and changes in the skin and hair.

Dehydration and electrolyte abnormalities are frequent findings.

The skin becomes dry and scaly and may be yellow-tinged as a result of excess carotene in the blood.

Anorexia nervosa cont…

Body hair may be increased but usually is fine and pale (lanugo).

Bone density is decreased, most likely because of low estrogen levels, which mimics the postmenopausal acceleration of osteoporosis.

As expected with severe PEM, anemia, lymphopenia, and hypoalbuminemia may be present.

A major complication of anorexia nervosa is an increased susceptibility to cardiac arrhythmia and sudden death, both due to hypokalemia.

Bulimia

It is a condition in which the patient binges on food and then induces vomiting.

In bulimia, binge eating is the norm.

Huge amounts of food, principally carbohydrates, are ingested, only to be followed by induced vomiting.

Although menstrual irregularities are common, amenorrhea occurs in less than 50% of bulimic patients.

Medical complications are related to continual induced vomiting and chronic use of laxatives and diuretics.

Bulimia cont…

These complications include

Electrolyte imbalances (hypokalemia), which predispose the patient to cardiac arrhythmias.

Pulmonary aspiration of gastric contents.

Esophageal and stomach rupture.

There are no specific signs and symptoms for this syndrome.

The diagnosis must rely on a comprehensive psychological assessment of the patient.

Vitamin deficiencies

There are fat soluble vitamins (A,D,E,K) and water soluble vitamins.

The distinction between fat- and water-soluble vitamins is important.

Although fat soluble vitamins are more readily stored in the body, they may be poorly absorbed in fat malabsorption disorders, caused by disturbances of digestive functions.

Vitamin deficiencies cont…

Certain vitamins can be synthesized endogenously— vitamin D from precursor steroids, vitamin K and biotin by the intestinal microflora, and niacin from tryptophan, an essential amino acid.

Notwithstanding this endogenous synthesis, a dietary supply of all vitamins is essential for health.

Deficiency of a single vitamin is uncommon, and single or multiple-vitamin deficiencies may be submerged in concurrent PEM.

Fat soluble vitamin deficiencies

VITAMIN

DEFICIENCY

Vitamin A

Night blindness, Xerophthalmia.

Squamous metaplasia.

Vulnerability to infection.

Vitamin D

Rickets in children.

Osteomalacia in adults.

Vitamin E

Spinocerebellar degeneration.

Vitamin K

Bleeding diathesis.

Water soluble vitamin deficiencies

VITAMIN

DEFICIENCY

Vitamin B1

(Thiamine)

Dry, wet and Infantile beriberi

Wernicke-Korsakoff syndrome

Vitamin B2

(Riboflavin)

Cheilosis, stomatitis, glossitis, dermatitis, corneal vascularization

Vitamin B3

(Niacin)

Pellagra—“three Ds”

Dementia, Dermatitis, Diarrhea

Vitamin B5

(Pantothenic acid)

No syndrome recognized

Vitamin B6

(Pyridoxine)

Cheilosis, glossitis, dermatitis, peripheral neuropathy

Water soluble vitamin deficiencies cont…

VITAMIN

DEFICIENCY

Vitamin B7

(Biotin)

No clearly defined clinical syndrome

Vitamin B12

Megaloblastic anemia.

Degeneration of posterolateral spinal cord tracts.

Vitamin C

Scurvy

Folate

Megaloblastic anemia, neural tube defects

OBESITY

A state of increased body weight, due to adipose tissue accumulation, that is of sufficient magnitude to produce adverse health effects.

Measure commonly used

Body Mass Index (BMI) = (weight in kilograms)/(height in meters)2, or kg/m2

Skinfold measurements

Various body circumferences, particularly the waist-to hip circumference ratio

BMI ranges

The BMI is closely correlated with body fat.

It is generally agreed that a BMI higher than 30 kg/m2 imparts a health risk.

BMI RANGE

REMARK

18.5 to 24.9 kg/m2

Normal

25 and 30 kg/m2

Overweight

≥30 kg/m2

Obesity

Obesity cont…

The untoward effects of obesity are related not only to the total body weight but also to the distribution of the stored fat.

Central (visceral) obesity, in which fat accumulates in the trunk and in the abdominal cavity (in the mesentery and around viscera), is associated with a much higher risk for several diseases than is excess accumulation of fat in a diffuse distribution in subcutaneous tissue.

Obesity cont…

The etiology of obesity is complex and incompletely understood.

Involved are genetic, environmental, and psychological factors.

Obesity is a disorder of energy balance.

The two sides of the energy equation (intake and expenditure) are finely regulated by neural and hormonal mechanisms, so that body weight is maintained within a narrow range for many years.

Clinical consequences of Obesity

Atherosclerosis.

Type 2 Diabetes mellitus.

Hypertension.

Cholelithiasis.

Osteoarthritis.

Cancers.

(Esophagus, Thyroid, Colon, Kidney, Gallbladder, Endometrium).

Hypoventilation syndrome.

(Pickwickian syndrome).

Nonalcoholic fatty liver disease (Nonalcoholic steatohepatitis).

Hyperlipoproteinaemia.

Hyperinsulinemia.

Key points

Kwashiorkor is characterized by hypoalbuminemia, generalized edema, fatty liver, skin changes, and defects in immunity.

Marasmus is characterized by emaciation resulting from loss of muscle mass and fat.

Secondary PEM occurs in the chronically ill and in patients with advanced cancer.

Anorexia nervosa is self-induced starvation.

Bulimia is a condition in which food binges alternate with induced vomiting.

Obesity is when BMI is greater than 30 kg/m2.

Review questions

What are the causes of secondary malnutrition?

List five (5) differences between marasmus and kwashiorkor.

Differentiate between anorexia nervosa from bulimia.

List disorders seen in deficiencies of fat soluble vitamins.

Explain clinical consequences of obesity.

References

Goljan E.;(2007): Rapid Review Pathology (2th Ed.) Elsevier Saunders, USA. Pg. 122-133.

Kumar V. ; Abbas A. K. ; Aster J. C.;(2013): Robbins and Contran Pathologic Basis of Disease (9th Ed.) Elsevier Saunders, USA. Pg. 293-306.

Mohan H.;(2010): Text book of Pathology (6th Ed.) Jaypee Brothers Medical Publishers, India. Pg. 243-255.

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Session 21 Nutritional Pathology

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Lecture Notes