[SURG] 1.01 Systemic Response to Injury and Metabolic Support

A systemic inflammatory response activated by traumatic injury to produce a systemic inflammatory response in an attempt to limit damage.

The stress response follows extensive tissue damage or systemic insult and is mediated by a complex signaling system and systemic washout of locally produced substances.

Acute proinflammatory response resulting in the activation of the innate immune system.

To produce a systemic inflammatory response in an attempt to limit damage.

Activating the innate immune response to stimulate the proinflammatory phase.

To modulate the pro-inflammatory phase to return to homeostasis.

It appears to be directly proportional.

5-10%.

To prevent or reverse the catabolic effects of the injury and to give adequate nutritional support.

It can result in multiple organ failure and/or early death.

Preserves gut integrity, decreases likelihood of bacterial translocation, preserves immunologic function of gut, increases compliance with intake, cost-effective vs parenteral, prevents intestinal villi atrophy.

Thermal injuries and severe infections.

Shorter periods of time (<2 weeks).

To meet the energy requirements for essential metabolic and tissue repair, and to meet the substrate requirement for protein synthesis.

Presence of 2 or more of the following: fever, tachycardia, tachypnea, abnormal WBC count.

Mechanical complications (e.g. tube migration and obstruction), labor-intensive assessment (e.g. site care), risk of aspiration, applicable for nasogastric.

It gives more, leading to muscle wasting.

Patients with severe malnutrition.

Carbohydrates (49-53%), Fat (29-30%).

Identifiable source of infection + SIRS.

A cellular response to stress that aims to reestablish appropriate protein folding through signaling proteins in the endoplasmic reticulum (ER).

Immunonutrients, standard polymeric formula, fiber-containing, immune enhancing, calorie dense formulas, high protein/bariatric, elemental, renal failure formula, hepatic failure formula.

A form of cellular response where the cell death is dependent on the activity of caspase enzyme.

Hypoglycemia is the primary stimulus.

Peripheral veins.

It is protective of the enteral epithelial barrier function and helps to maintain the diversity of the microbiome.

Sepsis + Organ dysfunction.

Cytokines, eicosanoids, plasma contact system, serotonin, histamine.

Sepsis + Cardiovascular collapse (requiring vasopressor support).

Electrolytes, amino acids, intravenous vitamin preparation.

Systemic Inflammatory Response Syndrome (SIRS).

They increase heart rate, myocardial activity, blood pressure, cellular metabolism, and promote glycogenolysis, gluconeogenesis, lipolysis, and ketogenesis.

ERAS (Early Resumption of feeding After Surgery) recommends early feeding as early as Day 2-3 with general liquids, and on day 3-4, food is given.

Apoptosis is programmed cell death, an energy-dependent, organized mechanism for clearing senescent or dysfunctional cells without promoting an inflammatory response.

Muscle protein, body fat, and hepatic glycogen, with fat being the most abundant source of energy.

Cardiovascular collapse.

Non-functioning GI tract, NPO for more than 5 days, GI fistula, acute pancreatitis, short bowel syndrome, malnutrition with more than 15% weight loss.

Large veins.

22 to 25 kcal/kg per day.

Ischemia, inflammation, and trauma.

They are reduced.

Autophagy is the process of disposing of damaged organelles and debris aggregates, induced during hypoxia and stress to provide energy.

Increased cortisol, catecholamines, glucagon, and growth hormone.

The steps include the engulfment of cytoplasm/organelle by a phagophore, fusion of the phagophore edges to form the autophagosome, and fusion of the autophagosome with a lysosome to form an autolysosome for degradation.

Essential for both innate and adaptive immune responses, mediate cellular responses, eradicate invading microorganisms, and promote wound healing.

Anuria (no urine output) and no response to fluid resuscitation resulting in cardiovascular collapse.

Contamination of central venous catheter, contamination of solution, complications of catheter placement.

Approximately 9 kcal of energy.

ROS are highly reactive molecules formed as by-products of oxygen metabolism in mitochondria, peroxisomal fatty acid metabolism, cytochrome P450 reactions, and respiratory burst of phagocytic cells.

Impaired ingestion, inability to consume adequate nutrition orally, patient is unable to eat, impaired digestion, absorption and metabolism, severe wasting.

The extrinsic pathway, activated through the binding of death receptors, and the intrinsic pathway, which proceeds through protein mediators that influence mitochondrial membrane permeability.

They are rapidly depleted.

The UPR is triggered by cellular stress that decreases calcium concentration in the endoplasmic reticulum (ER), leading to the accumulation of unfolded or misfolded proteins. It is a process to reestablish appropriate folding and decrease protein synthesis.

Gluconeogenesis and for the synthesis of acute phase proteins.

Same as short term fasting plus ketone bodies, with ketone bodies being the principal fuel source.

A reprioritization of substrate use ensues to preserve vital organ function and support repair of injured tissue.

Sepsis or surgical or traumatic injury in seriously ill patients for whom use of the GI tract for feedings is not possible.

Necroptosis.

Cortisol is essential for survival during significant physiologic stress and results in a net anti-inflammatory effect when it binds to glucocorticoid receptors.

Adipose stores within the body (triglycerides).

Autophagy process is controlled by numerous autophagy-specific genes and by the specific kinase, mammalian target of rapamycin (mTOR).

It is activated almost immediately after a traumatic injury and acts as the required 'first line of defense' for the host against pathogens by binding and clearing them from the circulation.

Identifiable bug.

Hyperglycemia, electrolyte abnormalities, CO2 retention and respiratory insufficiency, hepatic steatosis or marked glycogen deposition, cholestasis and formation of gallstones.

4 kcal of energy.

Too much ROS can lead to cellular injury through the oxidation of cell membrane substrates, cellular proteins, and DNA, and can result in the death of host cells.

To minimize muscle wasting.

Necroptosis is the premature, uncontrolled death of cells in living tissue, typically caused by accidental exposure to external factors which result in extreme cellular stress.

Premature uncontrolled death of cells in living tissue typically caused by accidental exposure to external factors which result in extreme cellular stress.

A form of cellular response where the cell death is dependent on the activity of your caspase enzyme.