This document is meant to accompany the
Bailey 28th T&D course by Surgtest. This is mainly
intended to help students revise concepts from the
Bailey 28th edition taught in the live course. At times,
faculty might have referred to other textbooks in
order to efficiently cover concepts. But for a more
comprehensive resource for NEET SS preparation
please check out the MCQ bank and video lecture
series available on the Surgtest app.
The Surgtest ‘General Surgery + Sub-specialty’ MCQ
Bank has more than 2800 unique MCQs.
Get it on Play Store Get it on App Store
Get it on Play Store Get it on Play Store
Metabolic Response to Injury
Bailey and Love 28th edition updates
Dr Praveen G Sekaran
M.S.,DNB (General Surgery), MRCS (Edin)
Homeostasis
• Role of surgical critical care
• Role in sepsis and MODS.
• Elective surgical practice now seeks to actively reduce the need for a homeostatic response
by minimising the primary insult via minimal access surgery and by ‘stress-free’ perioperative
care or enhanced recovery after surgery (ERAS).
Homeostasis
Which is the first stage of tissue injury?
a. Ebb phase
b. Flow phase
c. Catabolic
d. Anabolic
Homeostasis
Which is the first stage of tissue injury?
a. Ebb phase
b. Flow phase
c. Catabolic
d. Anabolic
Metabolic injury is now divided into initial period of catabolism (which may include period of
shock) followed by anabolic phase of repair and tissue healing.
Modern surgical care
• Role of surgical critical care is stressed - to work with resuscitation and organ support
alongside metabolic effects of injury to restore homeostasis.
• Systemic effects of injury impact heavily on survival and complications through loss of muscle
mass, sepsis and MODS.
• Catabolic effects + inflammatory processes + immunosuppression
Mediators of the metabolic response
• Tissue damage and inflammation
• Neuroendocrine response
• Agonists and antagonists
Tissue damage and inflammation
Tissue damage causes the release of all the following except,
a. Alarmins
b. Damage associated molecular patterns (DAMPs)
c. Heat shock proteins
d. High mobility group protein B1 (HMGB1)
e. None of the above
Tissue damage and inflammation
Tissue damage causes the release of all the following except,
a. Alarmins
b. Damage associated molecular patterns (DAMPs)
c. Heat shock proteins
d. High mobility group protein B1 (HMGB1)
e. None of the above
Tissue damage and inflammation
DAMPs
Pattern recognition preceptors
(Toll-like receptors, NOD-like) on innate immune system
Inflammasome formation
Caspases
IL-1, 6, TNF, interferons, chemokines
SIRS
Neuroendocrine response to injury
Neuroendocrine response to injury includes all except,
a. Pro-inflammatory cytokines
b. Prostanoids (via cycloxygenase-2)
c. Endothelin-1
d. Complement and kinin pathway
e. None of the above
Neuroendocrine response to injury
Neuroendocrine response to injury includes all except,
a. Pro-inflammatory cytokines
b. Prostanoids (via cycloxygenase-2)
c. Endothelin-1
d. Complement and kinin pathway
e. None of the above
CARS
CARS can be prolonged as part of a chronic critical illness which is also known as,
a. Persistent inflammation
b. Hypermetabolism
c. Immunosuppression
d. Catabolism
CARS
CARS can be prolonged as part of a chronic critical illness which is also known as,
a. Persistent inflammation
b. Hypermetabolism
c. Immunosuppression
d. Catabolism
CARS
If the anti-infammatory response dominates or is accentuated and prolonged in critical
illness, it is characterised as a compensatory anti-infammatory response syndrome (CARS),
resulting in immunosuppression and an increased susceptibility to opportunistic (nosocomial)
infection.
Further sepsis, with its associated catabolism, results. CARS can be prolonged by ongoing critical
illness as part of an ongoing vicious cycle of chronic critical illness (also known as Persistent
Infammation, Immunosuppression and Catabolism) syndrome.
Managing the response
• Hypermetabolism
• Alterations in skeletal muscle protein metabolism
• Alterations in hepatic protein metabolism
• Insulin resistance
Which of the following is true regarding metabolism following trauma?
A. Energy expenditure increases above 15-25%
B. Hyper metabolism completely abolished by nutritional supplementation
C. Cori cycle utilises hepatic glycogen
D. Cytokines involved in proteolysis are IL4,5,9,13, TGF beta
Which of the following is true regarding metabolism following trauma?
A. Energy expenditure increases above 15-25%
B. Hyper metabolism completely abolished by nutritional supplementation
C. Cori cycle utilises hepatic glycogen
D. Cytokines involved in proteolysis are IL4,5,9,13, TGF beta
Energy expenditure increases above 15-25%
During hypermetabolism protein catabolism increases by 15-25%. Hyperalimentation leads to an increase in free
radical formation. Therefore hypermetabolism can never be fully abolished and in many cases and may be
detrimental. In contrast, in starvation metabolic response is abolished by nutritional supplementation.
Cori cycle utilizes muscle glycogen, ATP consumption pathway.
Proinflammatory cytokines IL 1, IL 6 and IL 8 are involved in proteolysis. IL 4, IL 5, IL 9, IL 13 and TGF beta are anti-
inflammatory cytokines.
Which of the following is not an anti-inflammatory cytokine?
A. IL 4
B. IL 5
C. IL 8
D. IL 9
Which of the following is not an anti-inflammatory cytokine?
A. IL 4
B. IL 5
C. IL 8
D. IL 9
C. IL 8
IL 4, IL 5, IL 9, IL 13, IL 10 and TGF beta are anti-inflammatory cytokines.
IL 1, IL 6 and IL 8 are pro-inflammatory cytokines.
Which muscle is spared in protein catabolism after trauma?
A. Skeletal muscle
B. Cardiac muscle
C. Smooth muscle
D. Respiratory muscle
Which muscle is spared in protein catabolism after trauma?
A. Skeletal muscle
B. Cardiac muscle
C. Smooth muscle
D. Respiratory muscle
Cardiac muscle
The major site of protein loss is peripheral skeletal muscle, although nitrogen losses also occur in the
respiratory muscles (predisposing the patient to hypoventilation and chest infections) and in the gut
(reducing gut motility). Cardiac muscle appears to be mostly spared.
Jacob Devaraj, 29 year old body-builder who also drives a truck suffered a major road traffic
accident at NH 5 highway after his bus overturned. He was kept in the ICU after undergoing
damage control surgery. There was a significant drop in his albumin levels. The fall in albumin
levels can be attributed to,
A. Decreased production of albumin by liver
B. Increased albumin binding to protein molecules released by catabolism
C. Increased trans-capillary escape rate
D. Diversion of albumin to more vital sites like gut and heart
Jacob Devaraj, 29 year old body-builder who also drives a truck suffered a major road traffic
accident at NH 5 highway after his bus overturned. He was kept in the ICU after undergoing
damage control surgery. There was a significant drop in his albumin levels. The fall in albumin
levels can be attributed to,
A. Decreased production of albumin by liver
B. Increased albumin binding to protein molecules released by catabolism
C. Increased trans-capillary escape rate
D. Diversion of albumin to more vital sites like gut and heart
The increase in trans-capillary escape rate (TER) of albumin is said to be responsible for falling
albumin levels after trauma rather than decreased production by liver. This happens because of
increased micro-vascular permeability. Albumin trans-capillary escape rate may be increased
three-fold following major injury/sepsis.
The acute phase protein response brings about an alteration in the hepatic protein
metabolism. Which of the following is not a positive acute phase reactant?
A. Transferrin
B. Alpha 2 macroglobulin
C. CRP
D. Fibrinogen
The acute phase protein response brings about an alteration in the hepatic protein
metabolism. Which of the following is not a positive acute phase reactant?
A. Transferrin
B. Alpha 2 macroglobulin
C. CRP
D. Fibrinogen
Protein catabolism is a major part of metabolic response to injury. Which statement regarding
protein catabolism is not true?
A. Muscle protein synthesis and breakdown at the rate of 1-2%
B. In extreme catabolism urinary nitrogen loss 14-20g/day
C. Muscle protein degrades into amino acids
D. 1 gm of Nitrogen is equal to 6.25 gm of wet weight tissue
Protein catabolism is a major part of metabolic response to injury. Which statement regarding
protein catabolism is not true?
A. Muscle protein synthesis and breakdown at the rate of 1-2%
B. In extreme catabolism urinary nitrogen loss 14-20g/day
C. Muscle protein degrades into amino acids
D. 1 gm of Nitrogen is equal to 6.25 gm of wet weight tissue
Within lean tissue, each 1 g of nitrogen is contained within 6.25 g of protein, which is contained
in approximately 36 g of wet weight tissue. Thus, the loss of 1 g of nitrogen in urine is
equivalent to the breakdown of 36 g of wet weight lean tissue.
1g Nitrogen = 6.25g protein = 36g wet weight tissue
Muscle protein is continually synthesised and broken down with a turnover rate in humans of
1–2% per day.
Under extreme conditions of catabolism (e.g. major sepsis), urinary nitrogen losses can reach
14–20 g/day; this is equivalent to the loss of 500 g of skeletal muscle per day. Muscle protein
degrades into amino acids.
Avoidable factors
• Volume loss
• Hypothermia
• Tissue oedema
• Tissue undwrperfusion
• Starvation
• Immobility
Volume receptors are present in:
a. Carotid body
b. Aortic arch
c. Atrium
d. Kidney
Volume receptors are present in:
a. Carotid body
b. Aortic arch
c. Atrium
d. Kidney
c. Atrium
Pressure receptors are present in aortic arch and carotid body
Volume receptors are present in the Left atrium.
THANK YOU
