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302: Scientific basis of medicine > Metabolic response to starvation, injury, sepsis > Flashcards

Metabolic response to starvation, injury, sepsis Flashcards

1
Q

Anorexia nervosa

A

Severe restriction of nutritional intake causing severe nutritional deficiency

Features

  • Hypoglycaemia
  • Ketoacidosis
  • High urea- due to increased protein breakdown
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2
Q

Metabolic consequence of starvation

A

Hypoglycaemia causes increase in gluconeogenesis and ketogenesis

Increased glucagon

  • Glycogenolysis
  • Lipolysis
  • Proteinolysis

Low insulin= less glucose uptake
- Ketone bodies use

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3
Q

Anorexia nervosa Rx

A

Psychotherapy

Antidepressants

Diet 1800 Cal.

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4
Q

Ketoacidosis

A

Occurs in response to unutilised glucose or hypoglycaemia

  • Type 1 diabetes
  • Alcoholics
  • Starvation/ Low carb diet

Low insulin and high glucagon= hepatic ketosis
- Activates lipase= lipolysis, increase in FA, glycerols

FA oxidised into Acetyl-CoA

  • Krebs cycle
  • Ketone generation
  • More FFA
  • Cholesterol
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5
Q

Ketone bodies metabolism

A

Synthesised in the liver

Prolonged gluconeogenesis= depleted oxaloacetate
- Inhibits Acetyl-CoA entry into Krebs cycle

Acetyl-CoA converted to ketone bodies

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6
Q

Ketone bodies

A

Acetone

Acetoacetate

Beta-hydroxyburyrate (major ketone)

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7
Q

Ketosis levels

A

1 mmol/L after 12 hour fast
- mild ketosis

Fasting for 20 days
- 8-10 mmol/L

S-bicarbonate falls by 7-8mmol/L

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8
Q

Metabolic mechanisms to stabilise ketone production

A

Insulin release

- Inhibitory effect on adipose tissue= less lipolysis= less ketones

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9
Q

Sepsis 6

A

Give 3

  • O2
  • Fluids
  • IV antibiotics

Take 3

  • Blood culture
  • Lactate
  • Urine output
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10
Q

Metabolic responses to trauma/ critically ill

  • CV
  • Metabolic
A

Increased BP, HT

Peripheral insulin resistance

Increased protein/ lipid catabolism

Increased resting energy expenditure

Increased body temperature

Muscle wasting, protein loss

Increase Acute-phase proteins

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11
Q

Glucose levels in critical illness

A

High
- Stress mediators oppose anabolic effects of insulin

High catecholamines, cortisol

  • Increase glycogenolysis
  • Peripheral insulin resistance due to impairing insulin signalling and GLUT-4 translation in muscle and adipose

Processes enhanced:

  • Lipolysis
  • Skeletal muscle proteolysis
  • Gluconeogenic substrates
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12
Q

Protein and lipid metabolism in illness

A

Increase in pro-inflammatory cytokines= protein breakdown

  • TNF
  • Reduced lipid mobilisation

Protein is major source of glucose

Decreased muscle= insulin resistance due to skeletal muscle responsible for the majority of insulin-dependent glucose uptake.

Consequences

  • Increases infection
  • Delays wound healing
  • Muscle weakness
  • Inhibits cough reflex
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13
Q

Endocrine complications of starvation (gonad)

A

Suppresses HP- Ovaraian axis

  • Hypogonadotropic, hypogonadism
  • Low GnRH, LH, FSH, oestradiol
  • Low leptin

Consequences

  • Amenorrhea
  • Infertility
  • Bone loss
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14
Q

Endocrine complications of starvation (adrenal)

A

Increased HPA axis activity
= High cortisol
- Breakdown of protein into glucose

Consequences

  • Osteopenia (loss of collagen)
  • Muscle weakness
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15
Q

Endocrine complications of starvation (thyroid)

A

Chronic Undernutrition = decreased metabolic rate

  • Low-normal TSH
  • Low-normal FT4
  • Low FT3

Decreased T3 to T4 conversion

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16
Q

Metabolic activity in simple starvation

  • Basal metabolic rate
  • Glucose levels and glucose utilisation
  • Gluconeogenesis
  • Protein and lipid catabolism
  • Ketone utilisation
  • Ketosis and ketosuria
A
  • Decreased BMR
  • Low Glucose levels
  • Limited glucose use
  • Gluconeogenesis increases initially then decreases five to Seven days after
  • Low Protein catabolism
  • High Fat catabolism
  • Increased Ketone utilization
  • Ketosis and ketosuria present
17
Q

Metabolic activity in starvation + stress/ injury

A
  • Decreased/ normal BMR initially
  • Increased Glucose levels
  • Increased glucose use
  • Gluconeogenesis increases
  • High Protein catabolism
  • Low or no Fat catabolism
  • Decreased Ketone utilization
  • Ketosis and ketosuria absent
18
Q

Anorexia treatment

A

Psychotherapy
Antidepressant
Diet of at least 1800 calories.

19
Q

Presentation of anorexia nervosa

A
  • Increased urea due you to protein breakdown or AKI
  • Increased ketones due to FFA breakdown from lipolysis
  • Low glucose= Low insulin, high glucagon

302: Scientific basis of medicine (28 decks)

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