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61 Cards in this Set

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What is PROTEIN-ENERGY MALNUTRITION?
PROTEIN-ENERGY MALNUTRITION:
Inadequate intake of protein and calories.
What are the 2 types of malnutrition?
2 types of malnutrition:

1. You can lose Somatic proteins, primarily SKELETAL MUSCLE - affected in MARASMUS- (mid arm circumference)

2. You can lose Visceral proteins in organs, esp. LIVER - affected in KWASHIORKOR- (albumin). With KWASHIORKOR, since you're losing all of your protein, and your oncotic pressure falls very low, you don't have very much albumin, and so you lose a lot of fluid. You also have a lot of edema.

Why? I think because the blood vessels lose protein. Since water wants to travel to the place with the most protein, it tends to go to the tissue instead of the blood vessels, thereby causing edema.

Mechanism to Edema: I believe the mechanism is as follows.

1. The person is malnourished, and therefore doesn't get enough protein.
2. When your body doesn't have enough protein, it doesn't have enough amino acids to make serum albumin.
3. Low levels of albumin (protein) causes low oncotic pressure.
4. The low oncotic pressure allows fluid to leak out from the interstitial spaces and into the tissue (edema) and peritoneal cavity (ascites).
Signs of PROTEIN-ENERGY MALNUTRITION (PEM)
SIGNS OF PEM

1. Loss of fat stores (subcutaneous fat)
2. Loss of muscle mass
3. Loss of serum proteins (albumin, transferin)
4. Loss of total body weight

Total body weight:
< 80% is malnourished
<60% is MARASMUS
What is MARASMUS?
MARASMUS:

- < 60% body weight
- Diet lacks protein & carbohydrate
- Loss of muscle mass (somatic protein)- amino acids are used for energy
- Serum proteins (visceral compartment) NORMAL - so you don't get a lot of edema
- Loss of subcutaneous fat (broomstick)
- EMACIATION- loss of muscle and fat
- Head appears too large; “stick figure”
- Multiple vitamin deficiencies
- Immune deficiency- esp. T cell immunity
- Infection
How do you describe this child?
This child has marasmus.
Marasmus is seen in elderly people, and in people with cancer.
What is KWASHIORKOR?
KWASHIORKOR:

- Protein deprivation > caloric deprivation
- 2nd Child is weaned too soon and put on a high carbohydrate diet because there's not enough milk, the primary source of protein.
- MORE dangerous than Marasmus: these kids don't look as sick as kids with marasmus, but they are more sick
- Severe loss of visceral protein
- Hypoalbuminemia causes generalized EDEMA which can mask the loss of visceral protein
- Subcutaneous fat and muscle are SPARED
What is similar between marasmus and kwashiorkor?
1. Both are often seen in children under the age of 1 year, because these children often don't live to be older.
2. Multivitamin deficiencies because of a lack in enzymes that are required to absorb these vitamins. Therefore, when they do eat, they can't absorb nutrients from the food.
3. Immune defects and infections
4. Anemia- usually hypochromic/microcytic
5. Cerebral atrophy
SIGNS OF KWASHIORKOR
SIGNS OF KWASHIORKOR:

1. Flaky Paint Skin- hypo- and hyper-pigment and desquamation
2. Hair loss or color change
3. FATTY LIVER- due to loss of apolipoproteins; also small intestine atrophy /disaccharidease deficiency and diarrhea (Apolipoproteins are proteins that bind to fat, and then transport that fat to the intestines where it can be broken down.)
4. Kids become apathetic with LOSS OF APPETITE
5. Multivitamin deficiencies because of a lack of the enzymes that are required to absorb these vitamins** Therefore, when they do eat, they can't absorb nutrients from the food.
6. Immune defects and infections**
7. Anemia- usually hypochromic/microcytic**
8. Cerebral atrophy**
9. Pitting edema and ascites due to hypoalbuminemia


** both in MARASMUS AND KWASHIORKOR
What does this child have?
KWASHIORKOR:

You can see:
1. He does not have stick-like features
2. muscle and fat are well preserved
3. Prominent abdomen because of the fatty liver
4. Edema (around the eyes)
5. Even when presented with food, this child will not eat well, and what he does eat, will not be absorbed well.
SECONDARY Protein - Energy Malnutrition
SECONDARY Protein - Energy Malnutrition

Robbins Table 10-20

1. MARASMUS-LIKE- chronic illnesses like cancer; loss of muscle and subcutaneous fat; normal serum proteins

2. KWASHIORKOR-LIKE- acute illness like burns; normal fat and muscle; hypoalbuminemia and edema; VERY POOR PROGNOSIS

With marasmus, if you can get the malignancy under control, the patient tends to recover, but with kwashiorkor, the patients does not tend to recover, even if the malignancy is under control.
COMPARISON OF SEVERE MARASMUS-LIKE AND KWASHIORKOR-LIKE SECONDARY PROTEIN-ENERGY MALNUTRION
Marasmus-like vs Kwashiorkor-like

Marasmus-like Protein energy malnutrition
Clinical: Chronic illness (e.g.,chronic lung disease, cancer)
Time Course: Months
Clinical Features: History of weight loss, Muscle wasting, Absent subcutaneous fat
Laboratory Findings: Normal or mildly reduced serum proteins
Prognosis: Variable; depends on underlying disease

Kwashiorkor-like protein energy malnutrition
Clinical: Acute, catabolic illness (e.g., severe trauma, burns, sepsis)
Time Course: Weeks
Clinical Features: Normal fat and muscle, Edema
Laboratory Findings: Serum albumin <2.8 gm/dl
Prognosis: Poor
CACHEXIA
CACHEXIA:

- CANCER and AIDS
- Loss of muscle and fat
- Good appetite
- Higher metabolic rate
- Cytokines- TNF, interleukins, interferons - Cancer patients have a constant low level of TNF circulating
- Proteolysis-inducing factor (PIF) -
The circulation of these factors leads to protein degradation and a loss of fatty tissue in spite of an adequate diet.
CACHEXIA
ANOREXIA NERVOSA
ANOREXIA NERVOSA:

- Self-induced starvation
- Like PEM plus:
1. Amenorrhea
2. Hypothyroidism
3. Scaly, yellow skin and lanugo ( skin on a new born baby)
4. Osteoporosis-like
5. Anemia, lymphpenia, hypoalbuminemia
6. HYPOKALEMIA AND CARDIAC ventricular ARYTHMIA - this is the main cause of death. (This is also seen in bulimics)
BULIMIA NERVOSA
BULIMIA NERVOSA:

- < ½ have amenorrhea (Unlike, anorexia nervosa, most bulimics still get their periods)
- Weight and gonadotrophins near normal
- Hypokalemia and CARDIAC venticular ARYTHMIA
- Very bad teeth
- Aspiration of gastric contents - aspiration pneumonia
- Mallory-Weiss Syndrome - laceration of the esophagus or stomach
- Boerhaave’s Syndrome - rupture of esophagus or stomach
Mallory-Weiss Syndrome
Mallory-Weiss Syndrome - laceration of the esophagus or stomach
Boerhaave’s Syndrome
Boerhaave’s Syndrome - rupture of esophagus or stomach
Vitamin Deficiencies and Trace Element Deficiencies
Vitamin Deficiencies and Trace Element Deficiencies


VITAMINS: Table 9-9, Robbins p. 438

TRACE ELEMENTS: Table 9-10, Robbins p. 439
VITAMINS
VITAMINS:

Vitamins are divided into:
1. Fat Soluble Vitamins- A, D, E, K

2. Water soluble Vitamins- B’s, C, Folate

Fat soluble vitamins are more readily stored and last longer in the body, BUT they are poorly absorbed in fat malabsorption disorders. Water soluble vitamins can be used up faster, and it's harder to get vitamin intoxication because they can be excreted in the urine. But the fat soluble vitamins, especially vitamins A and D, can give you a toxic reaction if you take in too much.

A. ENDOGENOUS- D, K and Niacin
(THINK: DKNY, no DKN-dogenous.
B. DIET- all the others

Vitamin Deficiency can be PRIMARY (diet) or Secondary (malabsorption).

The boards will ask questions about vitamin deficiencies.
VITAMIN A
VITAMIN A (RETINOL)

- Robbins Figure 9-25- Vitamin A “cycle”
- Vitamin A- liver, fish, eggs, milk, butter
- “pro-vitamins”- (beta-carotene)- carrots, spinach are converted to Vitamin A in the body
- Fats/carotenes/retinoids require bile, pancreatic enzymes and antioxidants for digestion and absorption
- Vitamin A stored in ITO CELLS in the liver; 6-month supply

Not much of this was discussed in class, but it was mentioned that you should have enough Vitamin A if you eat a reasonably balanced diet.
What do you need to eat to get enough Vitamin A, and what is the importance of this vitamin?
Vitamin A is found in meats and veggies. Vit A is metabolized in the body into different products, and it is important in a couple of areas.
1. eyes - for the proper maintenance of vision.
2. mucous membranes or epithelial cells.

THINK: Ist three Vowels AEI
A - Vitamin A
E - Epithelium (mucosa)
I - eye (vision)
VITAMIN A FUNCTIONS
VITAMIN A FUNCTIONS:

Night vision
Growth and differentiation of mucus-secreting epithelium
Immunity (children)

THINK: 1st three vowels AEI
A - Vitamin A
E - epithelium
I - eye and immunity
VITAMIN A DEFICIENCY
VITAMIN A DEFICIENCY

- Night blindness
- Xerophthalmia (dry eye)- keratinized squamous epithelium replaces mucus-secreting epithelium
- Bitot spots (keratin debris) and keratomalacia (destruction of the cornea)
- Squamous metaplasia in LUNG ( increased viral and bacterial infections) in kids that can be life threatening and BLADDER (stones) in adults
- Increased mortality in measles and diarrhea, especially in kids.
What are the effects of Vitamin A deficiency?
1. Bitot Spots
2. Corneal ulcers
3. Keratomalacia
4. Most importantly, squamous metaplasia of the respiratory epithelium which makes children more susceptible to infection.
5. In adults, keratin deposits in the renal pelvis can cause bladder stones.
Keratomalacia caused by Vitamin A deficiency. (Destruction of the cornea)
VITAMIN A TOXICITY
VITAMIN A TOXICITY

- Increased intracranial pressure
- Papilledema, headache, vomiting
- Bone pain and hypercalcemia (chronically)
VITAMIN D
VITAMIN D:

1. Vit D is important in maintaing proper CALCIUM AND PHOSPHORUS levels
2. Diet or endogenous synthesis in the skin (sunlight); about 80% of required Vitamin D can be produced endogenously, so part of it need to come from the diet.
3. Fish, plants (ERGOSTEROL), grains
Robbins Figure 9-27 for Vitamin D metabolism
Vitamin D absorption and processing
Vitamin D is absorbed as a precursor and has to be hydroxylated in order to become metabolically activated. The first hydroxylation is in the liver, and the second is in the kidney. So, if you have either liver to kidney disease, you can get vitamin D deficiency as a secondary problem. The active form of Vit D is activate in absorption of dietary Vit D
Vitamin D Deficiency
Vitamin D deficiency - the active form is not present. This may be the result of a kidney or liver problem. Without enough Vit D, there isn't enough calcium and phosphorus absorbed from the intestines so levels fall. This triggers more parathormone and metabolism of calcium and phosphorus from bone. Also, the kidneys are stimulated to preserve Calcium at the expense of Phosphorus.
What happens when the kidney produces Vitamin D?
Kidney production of Vitamin D:

1. If you have a lot of Vitamin D, it will feedback, and inhibit alpha-1-hydroxylase (Too much Vit D can cause hypercalcemia and many problems, so the body had a feedback mechanism to keep it under control.)
2. If you have inadequate absorption of calcium from the intestine, this hypocalcemia stimulates PTH which activates alpha-1-hydroxylase to make more Vit D
3. Hypophosphatemia activates alpha-1-hydroxylase directly
VITAMIN D FUNCTIONS
VITAMIN D FUNCTIONS:

Ca and P absorption in the intestine
Mobilization of bone Ca (with PTH)
Stimulates PTH-dependent re-absorption of Ca in the distal renal tubule
VITAMIN D DEFICIENCY
VITAMIN D DEFICIENCY:

Cause HYPOCALCEMIA and loss of bone: RICKETS (in kids) or OSTEOMALACIA (in adults)
Robbins Figure 9-29 lists causes of Rickets and Osteomalacia:

1. < diet or sunlight
2. pancreatic insufficiency or obstruction, so you can's absorb it
3. drugs, liver disease, renal disease
4. phosphate depletion

Robbins Figure 9-28
In rickets and osteomalacia there is an excess of UNMINERALIZED matrix. You have a lot of osteoid that doesn't get mineralized, and if it doesn't get mineralized, it's not a strong bone. In children (rickets) endochondral bone growth is also disturbed. (Compared to Vit C, there's a lot of mineralization available, but not a lot of osteoid, so you get weak bones)
Left: Vitamin D Deficient
Right: Normal

In the Vit D deficient bone, there's not enough dark, not enough mineralization
RICKETS
RICKETS:

- Osteoid with inadequate mineralization
- Disorganized fibroblasts and capillaries
- Microfractures
- Deformed bones

Square head, “rachitic” rosary, pigeon breast, and bowed legs (Robbins Figure 9-28)
Rickets: This child has short and bowed legs.
Rickets: This child has short and bowed legs.
OSTEOMALACIA
OSTEOMALACIA: In older children and adults

- Abnormal bone remodeling
- Inadequate mineralization of new bone
- Fractures and microfractures
- Vertebrae and femoral neck

Note: osteoporosis is caused by inadequate osteoid protein and defective Vitamin D receptors with demineralization.
Osteoporosis vs Vit D deficiency vs Vit C deficiency
Osteoporosis: Not enough osteoid or mineralization

Vitamin D deficiency: Lot of osteoid, not enough mineralization.

Vitamin C deficiency: You have enough mineralization, but not enough osteoid.
OSTEOMALACIA: Decreased mineralization in bone
Compare normal bone, osteoporosis and osteomalacia
Normal Bone: Fully mineralized

Osteoporosis: The bone is fully mineralized, but there's less bone mass overall. So you lose osteoid and mineralization, but what is left is fully mineralized.

Osteomalacia: Under mineralized bone.
VITAMIN D TOXICITY
VITAMIN D TOXICITY:

- Metastatic calcification
- Hypercalcemia (deposition of Calcium in the lungs and the kidney primarily), hyperphosphatemia
- Low PTH
Vitamin D Antimicrobial Effect
Vitamin D Antimicrobial Effect (Fig. 9-30): Vitamin D is important in defending against certain infections, especially TB

- Toll-like Reptors- when activated by the micro-organisms, they increase Vit D receptors.
- Increase in Vitamin D receptor - this makes macrophages more efficient in handling TB by making Cathelicidin, an antimicrobial peptide.
- Synthesis of Cathelicidin
- Inhibition of M. tuberculosis
Vit D and TB
Vitamin D Antimicrobial Effect (Fig. 9-30): Vitamin D is important in defending against certain infections, especially TB

- Toll-like Reptors- when activated by the micro-organisms, they increase Vit D receptors.
- Increase in Vitamin D receptor - this makes macrophages more efficient in handling TB by making Cathelicidin
- Synthesis of Cathelicidin
- Inhibition of M. tuberculosis
VITAMIN E
VITAMIN E: The anti-sterility vitamin in mice, so people thought the same would be true in humans

- Alpha-Tocopherol
- “antioxidant”
- Deficiency- nervous system- degeneration of posterior column axons
- Loss of position and vibration sense; ataxia, muscle weakness
“looks like” B-12 deficiency
- Hemolytic anemia of premature infants
VITAMIN E AND HEART DISEASE
VITAMIN E AND HEART DISEASE:

NO protection from coronary heart disease
NO decrease in coronary events

AND no benefit in dementia prevention
VITAMIN K
VITAMIN K:

- Vit K is required for Clotting factors II (prothrombin), VII, IX and X are carboxylated in the liver and Vitamin K is a cofactor
- Also, carboxylation of protein C and S (anticoagulants)
- Vitamin K is “recycled” in the liver and gut bacteria make the vitamin, but some dietary source is required
VITAMIN K DEFICIENCY
VITAMIN K DEFICIENCY:

Bleeding because of an inadequate amount of clotting factors, especially intracranial in infants; also bleeding umbilical stump

Adults can also get bleeding problems and can have easy bruisibility, but it's not life threatening as it is in newborns.
THIAMINE
THIAMINE:

- One of the B Vitamins
- Not in polished rice, white flour or refined sugar
- TPP (a thiamine derivative) is a cofactor in oxidative decarboxylation and deficiency of thiamine results in DECREASED ATP
- Cardiovascular and nervous system problems
- ¼ of all alcoholics are thiamine deficient
THIAMINE DEFICIENCY
THIAMINE DEFICIENCY:


1. Dry beriberi (polyneuropathy)- myelin degeneration
2. Wet beriberi (cardiovascular)- vasodilitation produces heart failure and edema (high output failure)
3. Wernicke-Korsakoff Syndrome- Wernicke- ataxia/confusion;
Korsakoff- amnesia, confabulation (Confabulation is the formation of false memories, perceptions, or beliefs about the self or the environment as a result of neurological or psychological dysfunction. When it is a matter of memory, confabulation is the confusion of imagination with memory, or the confused application of true memories)
THIAMINE DEFICIENCY: Picture
THIAMINE DEFICIENCY:


1. Dry beriberi (polyneuropathy)- myelin degeneration
2. Wet beriberi (cardiovascular)- vasodilitation produces heart failure and edema (high output failure)
3. Wernicke-Korsakoff Syndrome- Wernicke-
ataxia/confusion;
Korsakoff- amnesia, confabulation
NIACIN
NIACIN:

1. Involved in NAD and NADP are coenzymes for dehydrogenases
2. Grains, legumes and seed oils
3. Deficiency- PELLAGRA (3 D’s)
dermatitis (rash) (Robbins Figure 10-28), diarrhea (epithelial atrophy) and dementia (posterior column changes as in B-12 deficiency)
Niacin Deficiency
NIACIN:

1. Involved in NAD and NADP are coenzymes for dehydrogenases
2. Grains, legumes and seed oils
3. Deficiency- PELLAGRA (3 D’s)
dermatitis (rash) (Robbins Figure 10-28), diarrhea (epithelial atrophy) and dementia (posterior column changes as in B-12 deficiency)
NIACIN AND HEART DISEASE
NIACIN AND HEART DISEASE:

- High doses (1-6 grams per day):
1. Lowers LDL
2. Lowers triglycerides
3. Increases HDL

Nothing else does this. Statins may lowed LDL and triglycerides, but it also lower HDL.

When using Niacin, you must start with low doses and under doctor supervision, because it can cause liver necrosis. So start at low doses and check liver enzymes and then increase from there.
VITAMIN C (ASCORBIC ACID)
VITAMIN C (ASCORBIC ACID)

- Found in (Citrus) fruits and vegetables
- Bone disease in growing children
- Abnormal development of mucous membranes results in hemorrhage and poor wound healing in children and adults
- Vitamin C is a cofactor in formation and maturation of procollagen
- Hydroxylation is impaired and crosslinks are not formed
- Antioxidant ???
VITAMIN C DEFICIENCY
VITAMIN C DEFICIENCY:

- SCURVY (Robbins Figure 9-31)
- Capillary and venule walls are weak with hemorrages (purpura and ecchymoses)
- Trauma- hematoma and hemarthrosis (joints)
- Child- too much cartilage and not enough osteoid protein); bowed legs and deformed chest
- Bacterial infection associated with gingival hemorrhage
Scurvy
SCURVY

1. Gum disease because of abnormal development of the mucous membranes around the teeth - Bacterial infection associated with gingival hemorrhage
2. Weird curly hairs on the skin
3. Capillary and venule walls are weak with hemorrages (purpura and ecchymoses)
4. Trauma- hematoma and hemarthrosis (joints) - Weak joints
5. Child- too much cartilage and not enough osteoid protein); bowed legs and deformed chest
6. Poor wound healing
Vitamin C Deficiency:

- You have a lot of mineral, but not enough osteoid.
FOLATE
FOLATE:

- Marginal body stores
- 20% of Americans have low Folate, even though almost everything that's relatively healthy have folate in it.
- Neural tube defects in the fetus
- Macrocytic anemia - this looks like B12 deficiency anemia, but you don't get the neurologic complications.
Zinc Deficiency
Zinc Deficiency:

- Aka Acrodermatitis
- Anorexia
- Growth retardation
- Impaired wound healing
- Hypogonadism
Zinc Deficiency
Zinc Deficiency:

- Aka Acrodermatitis
- Anorexia
- Growth retardation
- Impaired wound healing
- Hypogonadism