Feb8 M2-Starvation Weight Loss Frailty Flashcards
name of disease caused by chronic starvation
protein-energy malnutrition (PEM) (also starvation disease or hunger disease)
weight loss in prolonged starvation is due to what
loss of body cell mass mostly
% fat loss and % BCM lost in prolonged starvation
70% fat lost
25% BCM lost (but muscle is denser than fat) so accounts for more weight
how BCM loss and weight loss are related in prolonged starvation
proportions are similar. if lose 23% body weight, lose 23% BCM (most body weight loss is BCM)
what increases in prolonged starvation and consequence
ECF volume increased. leads to frank edema (hunger edema). may hide extent of lean tissue loss
what happens eventually in prolonged starvation
body adapts (metabolic adaptation) and reaches new equilibrium where energy balance and N balance = 0
how is an energy balance of 0 reached in prolonged starvation
- lower BMR (changes in TH metab and SS activity)
- less BCM
- less NEAT (do less work, less EE)
how is a N balance of 0 reached in prolonged starvation
- loss of BCM (need less protein
- more efficient protein turnover
- increased retention of dietary aa
main costs of starvation adaptation
- loss of insulating fat
- loss of muscle mass and physical power
- easier hypothermia (generating less heat)
- loss of central (organs: heart, intestines, etc.) muscle mass
in a person with a negative N balance, why do we attribute the protein loss and BCM loss to a loss of muscle mass
because to sustain central protein mass, aa from degradation of muscle are used
systemic inflammation link with adapted starvation
are opposed. systemic inflammation increases TEE and aa catabolism. may induce death in starvation adapted person
marasmus def
PEM (protein energy metabolism) in a child
marasmus charact
high ECF, low albumin, good fat store, liver fat
kwashiorkor def
more dangerous form of PEM.
kwashiorkor cause
inflammatory response to infection in infants and children in existing PEM combined with vitamin and mineral deficiencies
frailty def
deterioration of body function with age
most important modifiable contributor to frailty and name for this
muscle atrophy (sarcopenia = muscle atrophy with age)
frailty charact + is it only in old people?
less muscle mass, less immune system regulation, impaired balance and agility, impaired mental cognition (mildly)
younger people can be frail too
to what extent sarcopenia can be stopped and how
life-long lifestyle, physical activity, nutrition (can minimize but not halt sarcopenia)
sarcopenic obesity def
condition of obese patients with muscle atrophy
a patient CAN be frail and obese
how to evaluate frailty and common charact
- physical fct, gait speed and cognition
- charact: slow walking, exhaustion on normal tasks, less voluntary activity
3 causes of diminished muscle mass in frail people
- sarcopenia
- disuse muscle atrophy
- PEM
prevention and treatment of frailty
focus on exercise (formal and NEAT): increases food consumption and muscle mass bc increases TEE
fasting def and metabolic charact of long term fasting
diet devoid of protein, carbs or fat.
long term fasting leads to ketosis
how energy is provided to the brain in fasting and consequent wastes
- glucose from glycerol and aa from muscle
- FAs oxidized but some not completely and yield acetoacetic acid, acetone and beta-hydroxybutyric acid (3 ketone bodies)
why ketone bodies increase in prolonged fasting
liver takes FAs, converts them to ketone bodies and puts ketone bodies back in blood
how serum glucose changes in prolonged fasting
mild decrease even though liver releases much less glucose bc glucose uptake and metab by tissue is decreased
ketoacidosis def
ketosis severe enough to lower serum bicarb
ketoacidemia possible in prolonged fasting?
no but possible in diabetes bc ketoacidosis in diabetes is much more important
syndrome nondiabetic ketoacidemia occurs when + glucose levels
protracted (prolonged) vomiting, volume depletion in binge drinkin + no food consumption
NORMAL glucose levels
NDKA vs diabetic ketoacidemia
NDKA often less severe bc glucose levels are normal
prolonged fasting labs
low glucose, low insulin, moderate ketosis
ketoacidosis of severe diabetes associated with what (and why it differs from NDKA)
- hyperglycemia
- volume depletion
- hypermetabolic state
- severe ketosis
