Metabolic 3: metabolic response to stress vs starvation Flashcards

You may prefer our related Brainscape-certified flashcards:
1
Q

how does simple starvation differ from catabolic weight loss ?

A

simple starvation = metabolic adaptation and lean tissue conserved
catabolic weight loss = lean tissue breakdown which continues despite nutritional intake.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is anorexia nervosa and how does it affect the body?

A
Nutritional deficiency, severe
Severe restriction of nutritional intake
Despite extremely low body weight
Glucose: Low
Starvation ketosis 
Physiological response for alternative 				energy supply
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what changes would you see in urea and ketones in starvation?

A

Serum analysis showed increased urea, ketones
High urea indicates protein (muscle) breakdown & /or AKI

Ketones indicate use of an alternative energy supply from TG - FFA breakdown

In liver FFA for energy & conversion to ketones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what happens to glucose metabolism in starvation?

A

Low glucose causes decline in insulin & increase in glucagon release

Resulting in degradation: glycogen, fat stores, protein

To maintain glucose supply to cells without mitochondria: RBCs Brain requires some glucose
Brain adapts further to ketones for energy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

describe normal glucose metabolism

A

Postprandial increase blood glucose
Stimulates insulin release
Insulin mediates glucose uptake into skeletal muscle, fat tissue
Suppresses hepatic gluconeogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

describe the process of ketoacidosis and what stimulates it.

A

Liver production of ketones
Stimulated by low insulin & high glucagon
Secondary to low glucose: fasting, low carbohydrate diet, diabetes
Lipase activated
Fat stores - triglycerides - long chain fatty acids & glycerol
Fatty acids transported to liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

name the 2 main ketone bodies

A

beta-hydroxybutyric acid

acetoacetic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

describe the process of a fasting ketosis

which is the major ketone?

A

Liver generation of ketones is the physiological response to fasting
Mild ketosis ~1mmol/L after 12h fast
Fasting for 20 days: 8 - 10mmol/L
β-hydroxy butyrate is major ketone
Synthesis matches utilization : in brain, muscle, kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are the 3 stabalisation methods in a fasting ketosis ?

A

Stabilization:3 mechanisms:
Stimulation insulin release, despite low glucose
Increased sensitivity of adipose tissue to insulin inhibitory effect on fatty acid release
Direct inhibition of lipolysis by ketones
No adverse effects with fasting ketosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

why do we need to give nutritional support in critical illness?

A

Catabolism exceeds anabolism
Carbohydrates are preferred energy
Fat mobilization is impaired
Protein administration to decrease breakdown of muscle protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

List the sepsis 6

A
Give 
1) oxygen 
2) fluids 
3) antibiotics 
Take 
1) urine output 
2) blood cultures 
3) lactate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

why is there lactic acidosis in sepsis?

A
Usual cause is Tissue hypoperfusion
Impaired tissue oxygenation, leading to 		increased anaerobic metabolism
Hypovolemia
Cardiac failure
Sepsis
Cardiopulmonary arrest
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

list the hypermetabolic response to injury/trauma/surgical/critically ill

A
Increased blood pressure & heart rate
Peripheral insulin resistance 
Increased protein and lipid catabolism
Increased resting energy expenditure
Increased body temperature
Total body protein loss
Muscle wasting
Acute-phase protein response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what happens to glucose in critically unwell patient?

A

High catecholamines, cortisol
Increased gluconeogenesis Catecholamines:
Enhance glycogen breakdown
Impair glucose disposal via alterations of the insulin-signaling pathway; & GLUT4 translocation in muscle & adipose tissue, resulting in peripheral insulin resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

why is there insulin resistance in critical illness?

A

Skeletal muscle is responsible for 75% of whole-body insulin-stimulated glucose uptake
Decreases in muscle contribute to this persistent insulin resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

loss in lean mass complications?

A
Increase in infection 
Delays wound healing
Muscle weakness 
Prolongs mechanical ventilatory utilization
Inhibits cough reflexes
Delays mobilization 
Contributing to mortality
17
Q

how is the adrenal axis affected?

A

Increased hypothalamic-pituitary-adrenal activity
Stress of chronic starvation
High cortisol (glucocortcoid ):
Breakdown of protein (muscle, collagen) to glucose & urea
Loss of collagen: Osteopenia
Loss of muscle: Weakness

18
Q

list the endocrine complications of critical illness

A
Hypogonadotropic hypogonadism
Low GnRH, LH, FSH, estradiol 
Amenorrhea, infertility
Due to energy deficit, low fat mass, leptin low
Bone loss - severe
19
Q

how is the thyroid affected in critical illness?

A
Sick euthyroid pattern: 
TSH low-normal, FT4 low-normal, FT3 low
Due to chronic undernutrition
Decreased metabolic rate
Decreased conversion FT4 to FT3 (low) 
TSH & FT4 levels: low normal or low
Reduced metabolic rate