Biochem Final Protein Malnutrition

Front 1

primary malnutrition

Back 1

primary- problem with supply

secondary- problem with abs, or increased need,

Front 2

what happens with PEM

Back 2

your missing protein so you cant build new molecules (anabolism is bad)

Front 3

waht disease affects...
somatic protein
visceral protein

Back 3

somatic- marasmus

visc-kwash

Front 4

how do you look when...
marsa
kwash

Back 4

Marsa: you looked starved, no mm protein

Kwash: you look like a fatty belly, visceral protein

Front 5

what does RMR look like
mars
kwash

Back 5

mars: decreased

kwash: increased, barely getting by and then you get sick

Front 6

name the disease

"wasting away"

"the disease the first child gets when the second child id born"

Back 6

marsu

kwash

Front 7

what is the development of,,,
mara
kwash

Back 7

marsa: gradula

kwash: acute, fast

Front 8

what PEM disease is brough on slowly? what adaptations does this allow?

Back 8

marau

*allows body to adapt, use sk mm, decrease RMR, less O2 required so anemia

Front 9

what proteins are attacked in marsa, what are spared

Back 9

attack: myosin

spared: albumin from liver (does NOT go below 2.8)

Front 10

what is a comorbid condition of marsa

Back 10

physiological anemia, less o2 required due to lower RMR

Front 11

what disease needs refeeding? what is refeeding?

Back 11

marsa, slow onset so slow reintroduction of food. body not prepared to digest

*repletion heart failure: overwork of atrophied heart
*Hypophosphatemia:

Front 12

what are 2 problems that happen if food is introduced too fast for a marsa pt

Back 12

1. Repletion heart Failure- the heart is atrophied and introcution of food will increase RMR and plasma volume, this over works the heart

2. Hypophosphatemia: youve not needed Pi for lipid metabolism, when glocose is given many Pi are needed and none are left for ATP

Front 13

what 3 conditions will give you a fatty liver

Back 13

1. kwash **
2. obesity **
3. alcoholic

**due to IR

Front 14

wht disease is characterized by marginal nutrition, an infection, and increase in RMR and then the disease

Back 14

kwarsh

Front 15

TNFa and IL6 are secreted during infection, what does this do to insulin? what diesase

Back 15

creates IR ---> fatty liver
kwarsh

Front 16

waht does the IR in kwash do to protein/ metabolism

Back 16

IR so you degrade protein to make glucose (gluconeogenesis), BUT... your kwarsh so you dont have any extra protein to give up. So you get...
1. edema, decreased albumin
2. decreased immune fx
3. skin leisions and varying pigmentation
4. hair changes

Front 17

what disease has edema, how does it happen

Back 17

kwash

**you have decreased albumin synthesis, recall albumin is the driving force for fluid reabs at the capillary

Front 18

besides IR what else leads to fatty liver in kwarsh

Back 18

insifficient AA

**lots of FA being made and no protein is available to make APO B for VLDL formation

**IR increases lipolysis, IR creates hyperglycemia and the extra glucose is used to make FA

Front 19

so the symptoms of kwarsh are:
edema
poor immune fx: wound healing
skin/hair changes

**what is the underlying cause of all of thses

Back 19

lack of protein!

Front 20

why is there IR in kwarsh

Back 20

bc there is an infection, infections prefer IR so that glucose is available for brain and vital immune organs

Front 21

how is kwarsh dx

Back 21

albumin less than 2.8
no weight loss
at least one of the following:
1. lympophenia
2. impaired wound healing
3. edema
4. hair is pluckable

Front 22

Kwarsh and mars
etiology
adaptation to starvation
time course

Back 22

Mars: primary malnutrion (inadequate intake), normal response to starvation, month/years

Kwarsh: metabolic response to infection and marginal nutrition, abnormal response to starvation, weeks

Front 23

kwarsh and mars

Clinical features
Labs
course
mortality

Back 23

Mars: look starved, weight loss, loose subcu fat, keep visceral protein. Anemic, normal albumin, good response to short term stress, low mortality, needs refeeding

Kwarsh: look nourished, keep subcu fat, normal weight, edema, hair pluckable. LOW albumin, poor wound healing, ulcers, skin breakdown, high mortality

Front 24

what disease increases blood glucose

Back 24

kwarsh

**blood glucose is low in mara

Front 25

what happens to urea excretion in kwarch and mars

Back 25

Kwarsh: increase
Marsa: decrease

Front 26

what happens to gluconeogensis in marsa/kwarsh

Back 26

marsa: decrease
Kwarsh: increase

Front 27

what disease is due to a secondary cause of malnutrition

Back 27

cachexia

Front 28

what causes hte mm wasting/weight loss in cachexia

Back 28

1. no appetite
2. increases RMR

Front 29

cytokines play a role in what 2 diseases

Back 29

1. Cachexia: secondary malnutrition due to disease, cyto assoc with disease --> IR

2. Kwarsh: cyto due to infection and create IR

Front 30

besides the biggies, mara, kwarsh, cachexia are there other malnutritions?

Back 30

1. poverty: homeless, old
2. alcolohics: folate, pyridoxal pi, Vit a, riboflavin, vit e, niacin, thiamin
3. ilness
4. hospitalized: dextrose has no protein
5. sef inposed: bulemia, anorexia

Front 31

what are alcoholics deficient in

Back 31

folate
pyridoxal pi
vit a
vit e
riboflavin
niacin
thiamin

Front 32

who gets artificial feeding

Back 32

1. malnutriation
2. risk of malnutrition
3. cachexia that will die of starvation and not the disease

Front 33

enteral nutrition
paraenteral nutrition

Back 33

enteral: enters upper GI
paraenteral: directly into blood

Front 34

what is preferred enteral or paraenteral ntn

Back 34

enteral: get it in GI, use it or loose it

Paraenteral enters blood directly and requires no work by GI

Front 35

why do we want to use enteral ntn other than just keeping intestine moveing (bacteria)

Back 35

reduce infection from colonic bacteria

Front 36

entry for enteral nutrition

Back 36

NG: simple, less than 10 days
PEG: abdomen port,

Front 37

when is a PEG good to use to deliver enteral ntn?

what are advantages for PEG

Back 37

1. neurological condiction
2. oral cancer


1. larger diameter, can use blendered food,
2. decreased apriration
3. looks nicer

**always used for long term (>10days) ntn

Front 38

so usually enteral ntn is preferred over paraenteral, what are 2 disadvantages of enteral

Back 38

1. aspiration risk
2. Diarrhea

Front 39

are paraenteral solns hyper or hypo tonic

Back 39

hypertonic

Front 40

TPN

Back 40

total paraenteral nutrition

**complete nutrition delivered via central vein that was placed surgically

Front 41

central veins receive what NTS
peripheral veins receive what NTS

Back 41

central: TPN, hyperosmotic

peripheral: PPN, NOT hyperosmotic

Front 42

what is added to TPP, why

Back 42

insulin, to decrease IR and hyperglycemia.

**less mortality with insulin administered too

**IR is a stress response to illness

Front 43

what happens to insulin sensitivity in ill pts

Back 43

IR

IR is a stress response, supply brain and vital organs with glucose

Front 44

name 4 advantages of enteral over paraenteral ntn

Back 44

1. physiological: liver helps maination homeostasis of aa pool and decrease hyperglycemia
2. immunological: preserve GI tract and reduce GI infection
3. safe: less aspiration, no complications assoc with IV access- catheter sepsis, pneumothorax, catheter embolism, arterial laceration
4. Cost: EN is cheap just blend up what you eat!

Front 45

what method of feeding is associated with the lever maintaining aa pool and glucose regulation

Back 45

Enteral

Front 46

what method of feeding is associated with preservation of GI tract

Back 46

Enteral

Front 47

what method of feeding is cheap

Back 47

enteral

Front 48

what method of feeding is safe?

Back 48

enteral

NO aspiration
NO complications with catherter
* sepsis, embolism
*arterial laceration
*pneumothorax