B1U3- Imp Stuff3

Front 1

enteral tube feedings
vs. parenteral feeding

Back 1

enteral:
**passes thru intestine**
-only use if can't do oral feeding!!
-relatively inexpensive

parenteral:
**nut go straight into bpd
-second chioice- only if you can't do oral feeding
-short term use only!!
expensive

Front 2

estimate E and protein req
to recover from PEM

Back 2

1-2gm protein/kg body wt
(instead of 0.8gm/kg body wt normally used)
...more but not a ton more...

Front 3

fasting progression
-what is being metabolized?
-change in numbers
-urinary NH3 levels during progg
-change in albumin??
-change in BMR
***what is used for glucose toward the end??***

Back 3

24 hr- glycogen & muscle aa
-body stops degrading protein
(less glucose 180--> now 80g)
(less aa 75g -->20g now)
(urine NH3 inc then dec)
-ketone production (mostly 3-hydroxybuterate)
(body inc ammonia for pH reg)
***no change in albumin**
**metabolic mod protect lean body mass & fat in CHRONIC PEM***
***dec BMR**
~~~ketone bodies used for obligatory glucose req~~~
*((well-fed people don't use ketones for glucose)))

Front 4

Nitrogen/protein balance
in PEM

Back 4

-large neg nitrogen balance
nit balance = nit uptake - nit loss

**measure of degree of protein catabolism**

Front 5

Acute Catabolic Insult-Induced PEM
-change in BMR
-inc gluconeogen?
glucose sparing
-physical appearance
-nitrogen balance
-albumin levels

Back 5

CATABOLIC PHASE (10d)
-inc BMR
-inc gluconeogenesis
-inc glucose util by injured region
-dec gluceose util by un-nec regions
-physical apprearance normal
-lrg neg balance
-albumin INC in ~4d

Front 6

CHRONIC PHASE
-term

Back 6

chronic = 'marasmus'
body adapts, starts using ketone bodies to supply glucose to the brain
NS and erythrocytes require GLUCOSE for E

**nerve cells typicall use only 20% ketone bodies; but this is greatly inc during marasmus**

Front 7

significance of muscle's lack of
G6phosphatase &glycogen

Back 7

muscle cannot break down G16
**stored glycogen can only be used by the muscle cell itself***

Front 8

how can muscle supply E for the body in times of starvation??

Back 8

-muscle cannot help out w/ its glycogen stores
-can supply aa breakdown:
intermediates --> liver (ala-glu cycle)
-used for glucnoneogenesis in liver

Front 9

why is insulin bad for CVD & CHD??

Back 9

IR prev inhibition of LPL --> lipotoxicity
**inc FAA and TAG --> VLDL ---> LDL --> plaque

Front 10

3 GLUT transporters:
where are they located???

Back 10

GLUT 4= muscle
GLUT 2 = beta cell (2nd in alpha)
GLUT 1= RBC (constit on)

Front 11

Atherogenic Triad

Back 11

high TG
high (small) LDLs
low HDL

Front 12

microvascular complication from hyperglycermia

Back 12

(impaired cap circulation))
**micro means narrow focused**
-retinopathy
-nephropathy
-neuropathy