30 - Clinical Manifestation of Malnutrition Flashcards

(69 cards)

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
PEM - Monokines
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
26
PEM - Electrolytes
Decrease of total body potassium Altered cellular exchange Na+ and K+ loss Potassium loss Increased intracellular Na+ Intracellular overhydration
27
PEM - GI Function
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
28
PEM - CNS & PNS
Severe PEM at early age: Decreased brain growth Decreased nerve myelination Decreased neurotransmitter production Decreased velocity of nerve conduction
29
PEM - Hormones
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.
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PEM - Classifications (Severity)
Normal (90 - 110% weight for height) Mild (80 - 89% weight for height) Moderate (70 - 79% weight for height) Severe (
31
PEM - Classifications (Course-based)
Acute Chronic Acute w/chronic background
32
PEM - Classifications (Main defect)
Protein Energy Both
33
Anthropometric Measurements
Weight/Height - Index of CURRENT nutritional status Height/Age - Index of PAST nutritional history Wasting - Deficit weight/height Stunting - Deficit height/age
34
4 Anthropometric Categories
Normal Wasted (acute PEM) Wasted and stunted (acute and chronic PEM) Stunted (Past PEM)
35
Intensity of wasting
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
PEM - BMI
>= 18.5 - Normal 17. 0 - 18.4 - Mild 16. 0 - 16.9 - Moderate
37
Mild/Moderate PEM - Clinical Features
Weight Loss Decreased SubQ fat Decreased adiposity (
38
Extreme Marasmus - Physical Findings
``` 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
Extreme Kwashiorkor - Physical Findings
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
Extreme Marasmus - Labs
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
Extreme Kwashiorkor - Labs
Everything is reduced or markedly reduced Total body water high Extracellular water higher Total body protein low Liver fatty infiltration severe
42
Flag Sign
During malnutrition, hair becomes depigmented Hair is pigmented, then not pigmented, then pigmented. Not pigmented signifies malnutrition period.
43
Mild/Moderate PEM - Prognosis
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
Severe PEM - Prognosis
40% die without proper treatment | 10% die with proper treatment
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Severe PEM - Markers for poor prognosis
``` Younger child Poor wt/height Infection (measles) Hemorrhagic tendencies Mental status changes Electrolyte disturbances Low serum protein Severe anemia ```
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Mild/Moderate PEM - Treatment
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
Severe PEM - Treatment
Home vs. Hospital Care Probably hospital Resolve life threatening conditions Restore nutritional status without disrupting homeostasis Ensure nutritional rehabilitation.
48
Severe PEM - Fluid/Electrolyte Disturbances
Hypoosmolarity Moderate hyponatremia Metabolic acidosis Increased tolerance to hypocalcemia Decreased body potassium without hypokalemia Decreased body magnesium without hypomagnesemia
49
Severe PEM - Infection
Clinical manifestations may be mild Antigen antibody reactions may be impaired False negative skin tests Altered drug metabolism & detoxification mechanisms
50
Severe PEM - Hemodynamic alterations
Cardiac failure secondary to anemia, fluids or improper treatment Pulmonary edema
51
Severe PEM - Other conditions to resolve
``` Severe anemia Hypothermia Hypoglycemia (impaired thermoregulatory mechanisms) Severe vitamin A deficiency ```
52
Severe PEM - Treatment - Homeostatic restoration of nutritional status
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...
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If you feed these patients too quickly, you get
Refeeding syndrome!!!!
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Refeeding Syndrome
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
Patients at risk for refeeding syndrome
``` 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 ```
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How to avoid refeeding syndrome
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 ```
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Ensuring Nutritional Rehabilitation
``` Introduction of traditional foods High calories High protein Emotional and physical stimulation Seek underlying cause of persistent or recurrent diarrhea or other health problems ```
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Criteria for recovery from PEM
Weight gain Adequate wt/ht Normal CHI 0.9
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PEM - Prevention and Control
``` Food production and distribution Preventative medicine Education Social development Economic improvement ```
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Vitamin A Deficiency
``` Dry skin Decreased resistance to infection Night blindness Decreased hair growth 1/3 of all children on earth under 5 500,000 deaths yearly ```
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Rickets
``` 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 ```
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Beriberi
``` Vitamin B1 (Thiamine) deficiency Common in alcoholics ``` ``` CHF Fluid in lungs Tachycardia Swelling of legs Memory loss Delusions Coordination problems Death ```
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Wet Beriberi
Dyspnea Tachycardia Swelling
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Dry Beriberi
``` Difficulty walking Loss of sensation Nystagmus Tingling Vomiting ```
65
Wernicke-Korsakoff Syndrome
Brain disorder secondary to thiamine deficiency
66
Pellegra
Vitamin B3 (Niacin) deficiency Diarrhea Dermatitis Dementia Death
67
Scurvy
``` Vitamin C deficiency Lethargy Skin spots Bleeding gums Loss of teeth Fever Death ``` Treat with horse meat and citrus fruits
68
Ariboflavinosis
Vitamin B2 (Riboflavin) deficiency Malnourished and alcoholics ``` Bright pink tongues Cracked lips Throat swelling Bloodshot eyes Low RBC count ```
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Vitamin K Deficiency
Half of all newborns worldwide affected Alcoholics, bulimics, dieters, CF Bleeding