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GI / Hepatology > 30 - Clinical Manifestation of Malnutrition > Flashcards

30 - Clinical Manifestation of Malnutrition Flashcards

1
Q

Malnutrition

A

Condition resulting from a diet in which certain nutrients are lacking, in excess or in the wrong proportions

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2
Q

Hunger, and its associated malnutrition

A

Greatest single threat to the world’s public health

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3
Q

Protein-Energy Malnutrition (PEM)

A

Body’s needs for:

Protein
Energy fuels
or
Both

cannot be satisfied by diet

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4
Q

Protein-Energy Malnutrition (PEM) Syndromes

A

Kwashiorkor (edematous) - Predominant Protein Deficiency

Marasmus - Predominant Energy Deficiency

Marasmic Kwashiorkor (edematous) - Chronic Energy Deficiency PLUS acute or chronic Protein Defiiciency

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5
Q

Edematous PEM

A

Kwashiorkor

Marasmic Kwashiorkor

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6
Q

Secondary PEM - Causes

A

Diseases causing poor intake - Anorexia of disease

Inadequate nutrient absorption or utilization with increased losses - IBD, Celiac, CF

Increased nutritional requirements - CF, Lung, Heart, Kidney

Increasd nutrient losses - CF, Celiac

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7
Q

Where do most malnourished patitents live?

A

Developing countries
30% in Africa and Far East
15% in Latin America and Near East
33% o chidlren

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8
Q

PEM - Social & Economic Factors

A 
Poverty - Low food availability, overcrowding, unsanitary conditions
Ignorance
Decline in practice and duration of breast feeding
Inadequate weaning practices
Abuse
Deprivation
Abandonment
Dependence
Taboo
Fads
Migration
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9
Q

PEM - Biologic Factors

A

Maternal Malnutrition

Infectious Diseases:
Measles
Diarrhea
Respiratory

Diets

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10
Q

PEM - Environmental Factors

A

Overcrowding
Unsanitary living conditions

Agricultural patterns:
Droughts
Floods
Wars
Forced migration
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11
Q

PEM - Age

A

Increased frequency in infants and young children

Older kids experience milder forms

Pregnant and lactating women have increased nutritional requirements that can lead to PEM

Elderly and unable to care for themselves also experience PEM

Adolescents, adult men, non-pregnant, non-lactating women have a low prevalence of PEM

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12
Q

Marasmus - Age

A

Most common form of PEM in children

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13
Q

Kwashiorkor - Age

A

More frequent in children >18 mo

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14
Q

PEM - Pathophysiology

A

Develops gradually over weeks to months

Series of metabolic and behavioral adjustments:
Decreased nutrient demands and nutritional equilibrium compatible with lower level of nutrient availability

The slower PEM develops, the better adaptation to current nutritional status - Maintain a less fragile metabolic equilibrium.

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15
Q

PEM - Adaptive mechanisms

A 
Energy mobilization and expenditure
Protein breakdown and synthesis
Endocrine changes
Hematologic changes
Cardiovascular and renal function changes
Immune changes
Monokines
Electrolytes
GI function
CNS & PNS
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16
Q

PEM - Energy mobilization and expenditure

A

Decreased energy intake
Decreased energy expenditure (body fat mobilized)
Decreased adiposity with weight loss as subQ fat is reduced
Protein catabolism with muscle wasting

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17
Q

PEM - Energy mobilization and expenditure - Marasmic Patients

A

Visceral protein usually preserved
Increased basal O2 consuption
Increased basal metabolic rate

More severe:
Decreased basal metabolic rate
Blood glucose usually normalized by glycerol from fats & gluconeogenesis of AA

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18
Q

PEM - Energy mobilization and expenditure - Kwashiorkor Patients

A

Early visceral depletion of amino acids
Decreased basal O2 consumption
Decreased basal energy expenditure/unit body mass

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19
Q

PEM - Protein Breakdown & Synthesis

A

Poor availability of dietary proteins
Decreased protein synthesis

Initial adaptations:
Sparing body protein and essential protein dependent functions

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20
Q

PEM - Protein Breakdown & Synthesis - Long term deficits

A

Loss of skeletal muscle
Increased loss of visceral protein
Death

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21
Q

PEM - Amino Acid Recycling

A

90 - 95% of dietary AAs are recycled (normal metabolism is 75%)
Proportional decrease in AA catabolism (normally 25%)
Decrease in urea synthesis
Decrease in urinary nitrogen excretion.

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22
Q

PEM - Albumin

A

Decreased rate of synthesis and breakdown

Shift of albumin from extravascular to intravascular to maintain oncotic pressure

Severe depletion:
Adaptive mechanisms fail
Decreased serum protein
Decreased intravascular oncotic pressure
Outflow of water into extravascular space
Edema of Kwashiorkor
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23
Q

PEM - Cardiovascular & Renal Function

A

Decreased Cardiac Output
Decreased Heart Rate
Decreased Blood Pressure

Central circulation takes precedence over peripheral circulation

Altered cardiovascular reflexes
Postural hypotension
Decreased venous return

Severe:
Peripheral circulatory failure
Hemodynamic compensation
Tachycardia
Decreased renal plasma flow & GFR (secondary to decreased cardiac output)

Normal water clearance with normal concentration and acidification of urine

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24
Q

PEM - Immune System

A

Depletion of T-Lymphocytes from Thymus
Atrophy of Thymus gland

Decrease in complement production
Increased susceptibility to Gram (-) sepsis

Decreased functional activity of the complement system
Increased susceptibility to Gram (-) sepsis

Decreased opsonic activity of serum
Increased susceptibility to Gram (-) sepsis

Decreased phagocytosis
Decreased chemotaxis
Decreased intracellular killing

Possible defects in secretory IgA
Increased predisposition to infections and severe complications from otherwise less-important infectious diseases.

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25
Q

PEM - Monokines

A

Peptide/glycoprotein mediators of the body’s response to injury.

Decreased IL-1 - Poor febrile response and decreased leukocyte counts in infection

Increased TNF - Anorexia, muscle wasting, lipid abnormalities

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26
Q

PEM - Electrolytes

A

Decrease of total body potassium

Altered cellular exchange Na+ and K+ loss
Potassium loss
Increased intracellular Na+
Intracellular overhydration

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27
Q

PEM - GI Function

A

Impaired absorption of:
Lipids
Disaccharides
Glucose

Decreased gastric, pancreatic & bile production

Normal - low enzyme and conjugated bile
Further impairment of absorption
Diarrhea

Irregular intestinal motility
Diarrhea

Bacterial overgrowth
Diarrhea

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28
Q

PEM - CNS & PNS

A

Severe PEM at early age:

Decreased brain growth
Decreased nerve myelination
Decreased neurotransmitter production
Decreased velocity of nerve conduction

29
Q

PEM - Hormones

A

Gonadotropins - Decreased

Hypothalamic - Pituitary Axis & Medulla Oblongata are preserved, so patients can still respond to stress. Epi and corticosteroids can still go up in response to stress.

30
Q

PEM - Classifications (Severity)

A

Normal (90 - 110% weight for height)
Mild (80 - 89% weight for height)
Moderate (70 - 79% weight for height)
Severe (

31
Q

PEM - Classifications (Course-based)

A

Acute
Chronic
Acute w/chronic background

32
Q

PEM - Classifications (Main defect)

A

Protein
Energy
Both

33
Q

Anthropometric Measurements

A

Weight/Height - Index of CURRENT nutritional status
Height/Age - Index of PAST nutritional history
Wasting - Deficit weight/height
Stunting - Deficit height/age

34
Q

4 Anthropometric Categories

A

Normal
Wasted (acute PEM)
Wasted and stunted (acute and chronic PEM)
Stunted (Past PEM)

35
Q

Intensity of wasting

A

Calculate as percent of reference median wt/ht

% Weight/Heigh = Observed Weight/Reference weight/height

% Height/Age = Observed height/Reference height/age

BMI = Weight/Height^2

Recommended for adolescents and adults

36
Q

PEM - BMI

A

> = 18.5 - Normal

  1. 0 - 18.4 - Mild
  2. 0 - 16.9 - Moderate
37
Q

Mild/Moderate PEM - Clinical Features

A

Weight Loss
Decreased SubQ fat
Decreased adiposity (

38
Q

Extreme Marasmus - Physical Findings

A 
Severely wasted
Shorter
Look wasted/ill
Irritable
Apathetic
Look of anxiety
Sunken cheeks (monkey)
Hair dry and brittle
Hair pulls out without pain
Hypothermia
Slow pulses
Eye infections (Vitamin A deficiency)
Respiratory infections
Diarrhea
39
Q

Extreme Kwashiorkor - Physical Findings

A

Edema (face, perineum, legs, feet, arms, hands)
Growth not as stunted as marasmic patients
Apathetic
Irritable
Look ill
Hair turns lifeless & dull
Color of hair turns to yellowish white, dull brown or red
Irritation and skin lesions in areas of edema.
Depigmented skin
Hyperkeratotic skin
Scales of dermis coming off in large patches
Big bellies
Hepatomegaly
Fatty liver
Vitamin deficiencies

40
Q

Extreme Marasmus - Labs

A

Everything is normal or slightly reduced
EXCEPT glucose
Glucose is much lower than in Kwashiorkor patients

Total body water high
Extracellular water high
Total body protein low

41
Q

Extreme Kwashiorkor - Labs

A

Everything is reduced or markedly reduced

Total body water high
Extracellular water higher
Total body protein low
Liver fatty infiltration severe

42
Q

Flag Sign

A

During malnutrition, hair becomes depigmented

Hair is pigmented, then not pigmented, then pigmented. Not pigmented signifies malnutrition period.

43
Q

Mild/Moderate PEM - Prognosis

A

Good
Patients normalize signs of malnutrition quickly
Maintain normal wt/height
May take longer for height to reach normal, or they may never reach normal height.

Decreased work capacity
Behavioral problems
Decreased capacity for social interaction and creativity.

These don’t persist if you “give them good stimulation when you treat them”

44
Q

Severe PEM - Prognosis

A

40% die without proper treatment

10% die with proper treatment

45
Q

Severe PEM - Markers for poor prognosis

A 
Younger child
Poor wt/height
Infection (measles)
Hemorrhagic tendencies
Mental status changes
Electrolyte disturbances
Low serum protein
Severe anemia
46
Q

Mild/Moderate PEM - Treatment

A

Treat in ambulatory setting
GOAL - 2 times protein, 1.5 times energy requirements

Food supplements:
Appetizing
Easy to prepare
Feed others in household
No commercial value

Avoid decrease in breast feeding
Vitamin and mineral supplements

47
Q

Severe PEM - Treatment

A

Home vs. Hospital Care
Probably hospital

Resolve life threatening conditions
Restore nutritional status without disrupting homeostasis
Ensure nutritional rehabilitation.

48
Q

Severe PEM - Fluid/Electrolyte Disturbances

A

Hypoosmolarity
Moderate hyponatremia
Metabolic acidosis
Increased tolerance to hypocalcemia
Decreased body potassium without hypokalemia
Decreased body magnesium without hypomagnesemia

49
Q

Severe PEM - Infection

A

Clinical manifestations may be mild
Antigen antibody reactions may be impaired
False negative skin tests
Altered drug metabolism & detoxification mechanisms

50
Q

Severe PEM - Hemodynamic alterations

A

Cardiac failure secondary to anemia, fluids or improper treatment
Pulmonary edema

51
Q

Severe PEM - Other conditions to resolve

A 
Severe anemia
Hypothermia
Hypoglycemia
(impaired thermoregulatory mechanisms)
Severe vitamin A deficiency
52
Q

Severe PEM - Treatment - Homeostatic restoration of nutritional status

A

Replace nutrient tissue deficits
Begin to slowly avoid metabolic disruptions
LIquid formula best (PO/NG) in small frequent feeds
Marasmus - Larger amounts of dietary energy needed
Increased mortality with TPN
K+, Na+, Ca, Mg, Zn, Folic acid, Vitamin A supplementation
Add iron after 1 week of diet therapy
Protein source of high biologic value, and easily digested
Cow, goat, ewe, buffalo, camel milk
Eggs, meat, fish, soy/vegetable mixtures are good too…

53
Q

If you feed these patients too quickly, you get

A

Refeeding syndrome!!!!

54
Q

Refeeding Syndrome

A

Fluid, electrolyte & metabolic abnormalities:

Chronic malnutrition - Body stores of nitrogen, phosphorous, magnesium & potassium are depleted, but serum levels are near normal

Refeeding - Proteins synthesized and insulin released. Increased cellular uptake of these cations, so HUGE drops in serum concentration!!!!

Common pathway ascribed to hypophosphatemia, but may include fluxes in K+, Mg+, Na+

55
Q

Patients at risk for refeeding syndrome

A 
Anorexia nervosa
Classic Kwashiorkor
Classic Marasmus
Chronic malnutrition (underfeeding)
Chronic alcoholism
Morbid obesity with massive weight loss
Unfed patient 7 - 10 days with evidence of stress and depletion
Prolonged fasting
Prolonged IV hydration
Cancer cachexia
56
Q

How to avoid refeeding syndrome

A

Test for electrolyte abnormalities before initiating nutrition support. Follow these values!
Judiciously restore circulatory volume
Increase caloric delivery slowly
Administer vitamins routinely

Monitor:
Phosphorous
Potassium
Magnesium
Glucose
Urinary electrolytes
57
Q

Ensuring Nutritional Rehabilitation

A 
Introduction of traditional foods
High calories
High protein
Emotional and physical stimulation
Seek underlying cause of persistent or recurrent diarrhea or other health problems
58
Q

Criteria for recovery from PEM

A

Weight gain
Adequate wt/ht
Normal CHI 0.9

59
Q

PEM - Prevention and Control

A 
Food production and distribution
Preventative medicine
Education
Social development
Economic improvement
60
Q

Vitamin A Deficiency

A 
Dry skin
Decreased resistance to infection
Night blindness
Decreased hair growth
1/3 of all children on earth under 5
500,000 deaths yearly
61
Q

Rickets

A 
Vitamin D deficiency
OR
Calcium deficiency
OR
Phosphate deficiency
Softening/weakening of bones
Bone pain or tenderness
Dental deformities
Impaired growth
Bone fractures
Skeletal deformities
62
Q

Beriberi

A 
Vitamin B1 (Thiamine) deficiency
Common in alcoholics
CHF
Fluid in lungs
Tachycardia
Swelling of legs
Memory loss
Delusions
Coordination problems
Death
63
Q

Wet Beriberi

A

Dyspnea
Tachycardia
Swelling

64
Q

Dry Beriberi

A 
Difficulty walking
Loss of sensation
Nystagmus
Tingling
Vomiting
65
Q

Wernicke-Korsakoff Syndrome

A

Brain disorder secondary to thiamine deficiency

66
Q

Pellegra

A

Vitamin B3 (Niacin) deficiency

Diarrhea
Dermatitis
Dementia
Death

67
Q

Scurvy

A 
Vitamin C deficiency
Lethargy
Skin spots
Bleeding gums
Loss of teeth
Fever
Death

Treat with horse meat and citrus fruits

68
Q

Ariboflavinosis

A

Vitamin B2 (Riboflavin) deficiency

Malnourished and alcoholics

Bright pink tongues
Cracked lips
Throat swelling
Bloodshot eyes
Low RBC count
69
Q

Vitamin K Deficiency

A

Half of all newborns worldwide affected

Alcoholics, bulimics, dieters, CF

Bleeding

GI / Hepatology (28 decks)

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