Nutritional pathology Flashcards
A child is considered malnourished when
weight is <80% of normal
2 protein compartments in body
Somatic
Visceral
What makes up the somatic protein compartment
Skeletal muscle
What makes up the visceral protein compartment
Liver stores
4 examples of Protein Energy Malnutrition
Kwashiorkor
Marasmus
Cachexia
Anorexia nervosa
Kwashiorkor predominantly affects
Visceral protein - protein deficiency
Marasmus predominantly affects
SOMATIC protein
Protein AND energy - caloric deficiency
Marasmus~ starvation characterized by
Severe reduction in carloric intake weight <60% of normal growth retardation, loss of muscle PRESERVE visceral compartment mobilize subcutaneous fat - decreased leptin REDUCED BMR - opposite of cachexia
Marasmus may show clinical signs such as
- emaciation of extremeties
- Anemia
- Vitamin def
- Immune deficiency - T cell mediated - infections
- poor wound healing
Kwashiorkor characterized by
Greater protein deprivation than reduction in calories
Which PEM is more severe
Kwashiorkor IS MORE SERVERE than marasmus
Kwashiorkor may PRESENT as
60-80% normal weight
HYPOalbuminemia and EDEMA
FLAKY Paint skin lesions hyperpigmentation and hypo
Loos of color on hair
Clinical presentation of Kwashiorkor
1- Liver steatosis 2- Apathy, listlessnes,anorexia 3- vitamin deficiencies 4 - immune deficiency and infection 5- poor wound healing
Cachexia characterized by
- loss of fat and muscle
- INCREASED resting energy and BMR
- result of TNF, IL-2, IL-6 and proteolysis inducing factor - PIF - tumor secretions
What does proteolysis inducing factor lead to
Breakdown of skeletal muscle
Clinical findings of anorexia nervosa are most similar to
Marasmus
- effects on endocrine system
- dehydration and electrolyte imbalance
- lethal cardiac arrythmias
Medical complications of bulimia
- electrolyte imbalance- HYPOKALEMIA
- Pulmonary aspiration
- Esophageal and gastric cardia tears
What % of adults overweight? and obese?
30% … and additional 30% (bmi>30)
Obesity is a disorder of…
ENERGY balance
Central processing of food intake/expenditure is through 2 anorexigenic factors
POMC
CART
Central processing of food intake/expenditure is through 2 ORExigenic neurons - make you hungry
Neuropeptide Y
AgRP
Leptin is secreted by (means thin)
Adipocytes
- binds to POMC and CART neurons
Net effect of leptin is TO
REDUCE food intake
INCREASE energy expenditure
Loss of function mutations in leptin lead to
Early onset severe obesity
Adiponectin is produced by
Adipocytes
- directs FA to muscle for oxidation
- Decrease INFLUX of FA to liver
- Decrease glucose production in liver
What is the ONLY known hormone to increase FOOD intake - Orexigenic effect
GHRELIN
- binds to NPY, and AgRP pathway
- short term initiator of feeding
- levels rise before meals
Obesity leads to increased expression of
IGF-1 - mitogenic and anti-apoptotic
HIF 1 and
VEGF
and leads to conversion of androgens to estrogen
Insulin increases
Androgen synthesis in adrenals and ovaries
Which vitamins can be synthesized endogenously?
D
K
Biotin
Niacin
Which minerals are needed in large amounts - still micronutrients
- Sodium
- potassium
- Calcium
- phosphorus
Which trace minerals are needed
Cobalt, Copper
Flourine, Iodine
Iron, Mg
Selenium, Zn
Case: Flat occipital bones, Frontal bossing, deformation of chest, Rachitic rosary
Vitamin D deficiency
Deficiency of vitamin K will cause
Bleeding
Source of Vitamin D
Fish liver, plants, grains
>80% ENDOGENOUS SOURCE
Vitamin D on skin synthesized from
7-dehydrocholesterol - need UV light
What happens to Vitamin D in liver
add 25-OH
What happens to Vitamin D in kidney
1,25 - added 1, from 1a hydroxylase
What activates alpha-1-hydroxylase
- PTH
2. Hypophosphatemia
What down regulates alpha-1-hydroxylase
High levels of 1,25 OH Vit D
What is the function of Vitamin D
intestinal absorption of Ca and P
stimulate Ca reasborption from bone and from distal renal tubules via PTH
and for normal mineralization of bone
Result of a Vitamin D deficiency
HYPOcalcemia - increased PTH production
Clinical manifestation of Vit D deficiency
- rickets - inadequatemineralization
- inadequate calcification and overgrowth of epiphyseal cartilage
- rachitic costochondral junction
- in adults leads to osteomalacia
Case: Alcohol abuse, bilateral foot drop, sensory loss, retrograde amnesia
Vitamin B1 - Thiamin deficiency
Source of Vitamin B1 - Thiamin
- in diet, not in polished rice, white flour, white sugar
Function of Vitamin B1 -
Synthesis ATP- energy production
Cofactor for transketolase
Maintain neural membrane
3 causes of thiamine deficiency
1- dietary insufficiency
2- Chronic alcoholism
3- excess vomiting diarrhea
- can get subclinical def - if you refeed/give glucose
3 main areas affected by thamine deficiency
- Peripheral nerves - dry beriberi
- Heart - wet beriberi
3- CNA - wernicke-kosrsakoff sybdrome
What does dry beriberi result in
1 - symmertric polyneuropathy
2- first appears in legs
- toe drop, foot drop, sensory loss with hyporeflexia
What does wet beriberi result in
1- CVD - peripheral vasodilation
2- rapid AV shunting of blood
3- High output cardiac failure
4- peripheral edema - enlarged heart
What is Wernicke-Korsakoff syndrome
1- encephalopathy - confusion, opthalmoplegia
2- Korsakoff- retrograde amnesia, confabulation
CNS lesions due to thiamine deficiency are found in
Mamillary bodies
Periventricular regions of thalams
Floor of 4th ventricle
Anterior cerebellum
Case: Partial gastrectomy, megaloblastic anemia -
vitamin b12 deficiency
Sources of Vitamin B12
animal proteins, meat, eggs
Excess vitamin B12 stored in
Liver
What is the function of B12
binds to Intrinsic factor (produced by parietal cells)
- forms a complex - dissociates in ileum - binds transcobalamin, delivered to bone liver, marrow, etc.
Vitamin B12 deficiency can be due to
- decreased intake
- Intrinsic factor deficiency - gastrectomy - or pernicious anemia -
- other malabsorption syndrome
How does Vitamin B12 present
1- Megaloblastic anemia - (needed for DNA synthesis - and leads to defective erythrocyte maturation)
2- Neurological complications
Case: DM, Hepatomegaly, slate-grey skin
Iron excess
Normal iron absorption is
limited - iron efficiently re-utilized in the body
Increase absorption of iron with
Ascorbic acid
Iron excess can result frmo
Primary Hereditary Hemochromatosis
Secondary - ineffective erythropoiesis, increased intake, chronic liver diseaes
Hereditary Hemochromatosis is a common
Autosomal recessive trait
more common in men
HIGH absorption - accummulation of iron in tissues
Clinical manifestations of hemochromatosis
1 - hepatomegaly, fibrosis
2 -DM - pancreas
3- altered skin pigmentation
- cardiac problems - testicular atrophy
how do you treat hemochromatosis?
Regular phlembotomy - and supportive treatment
What risk has vitamin A shown in lung cancers
Increased risk
Risk of vitamin A supplementation in head and neck cancers
Success in preventing squamous cell carcinomas
Lycopene has been shown to have some
Antioxidant properties
- tomatoes -
