Nutrition and Intensive Care- Week 2 Flashcards Preview

Nutrition > Nutrition and Intensive Care- Week 2 > Flashcards

Flashcards in Nutrition and Intensive Care- Week 2 Deck (36)
Loading flashcards...

What are the stages of critical illness?

1. Primary Insult (burns, acute pancreatitis, trauma, etc)
2. Hypermetabolic inflammatory catabolic state (hyper-metabolism anorexia, catabolism, neuroendocrine/cytokine mediated)
3. Sepsis ------ leads to either recovery or death


There are two responses to critical illness: simple fasting and severe stress. What is the pathway for simple fasting in response to critical illness?

Simple Fasting ------ glycogen and protein mobilized to provide glucose ------ ketogenesis and ketosis increases and glucose needs fall ----- metabolic rate slows ----- energy needs fall ----- protein and energy conservation


What is the pathway for severe stress in response to critical illness?

Severe Stress ----- glycogen and protein mobilized for glucose and acute phase reactants ------ less or no ketogenesis and ketosis: gluconeogenesis from protein remains high ---- metabolic rate rises -----energy needs increase ----accelerated protein and energy depletion


In the hyper-metabolic, inflammatory catabolic state the physiological responses increases, in the systemic, skeletal muscle, liver and adipose tissue. What are the specific increase in changes systemically?

1. metabolic rate
2. Body temp
3. Water retention
4. Cardiac output
5. Blood volume
6. Tissue perfusion
7. Free radical production
8. Nitric oxide production


What are the specific increase in changes in the skeletal muscle?

1. Net proteolysis
2. Amino acid oxidation


What are the specific increase in changes in the liver?

1. Amin acid oxidation/N. excretion
2. Acute phase protein synthesis
3. Gluconeogenesis
4. Cori cycle


What are the specific increase in changes in the adipose tissue?

1. Lipolysis/TG turnover


What are the specific decreases in changes that happens in the hyper-metabolic inflammatory state

1. Plasma Albumin
2. Plasma IGF-1


What is the order of the hypermetabolic inflammatory catabolic state?

Insult ------- SIRS/hyper-inflammation (Systemic inflammatory response syndrome) ------ sepsis ------ severe sepsis and multi organ failure ----- septic shock


In addition to the SIRS pathway for sepsis what is another pathway in the hypermetabolic inflammatory state that will lead to sepsis?

CARS, immuno-suppression
--compensatory anti-inflammatory response syndrome
--pathway to sepsis stays the same as in the SIRS pathway
--associated with increased mortality risk


In the SIRS septic shock pathway there are symptoms within the pathway. Identify the symptoms for SIRS, Sepsis, multi organ failure, and septic shock

SIRS: 2 or more of ---- temperature greater than or equal to 38C or less than or equal to 36C ; Heart rate greater than or equal to 90bpm ; respiratory rate greater than or equal to 20/min ; and Leukocytes greater than or equal to 12000mL or less than or equal to 4000ml
Sepsis: SIRS with assumed or certain infection
Multi Organ Failure: sepsis with greater than or equal to 1 organ failure
Septic Shock: metabolic acidosis and refractory hypertension


Finally in the SIRS septic shock pathway what is the mortality risk associated with each step?

1. SIRS: 10%
2. Sepsis: 20%
3. Multi Organ Failure: 20-40%
4. Septic Shock: 40-80%


There is a neuro endocrine-cytokine response to stress. What is the response of the hyporthalamus, pituitary and adrenal cortex in this response system?

Hypothalamus: stimulation of SNS acting on the cardio/pulm system, GIT, adrenal medulla, pancreas, and kidney
Pituitary/Adrenal Cortex: Increased Catabolic hormones: adrenalin glucagon, cortisol, GH
--these responses lead to reduced anabolic hormones and insulin resistance: reduced IGF-1 and T3


Within the neuro endocrine-cytokine response to stress there are local reactions (mediator release, recruitment of cells and wound healing), what immuno cytokines do these local reactions produce?

Pro-Inflammatory Mediators: TNFalpha, IL-1b, IL-6, IL-8, PGE2, NO and ROS
--these lead to SIRS (Systemic inflammatory response syndrome)


What is the neuroendocrine response that leads to SIRS (systemic inflammatory response syndrome)?

Increased catabolic hormone
Reduced Anabolic hormones


Critical illness is an unstable state with failed _______, increased ____ ______, and tissue ______

Failed Homeostasis
Increased energy expenditure
Tissue Catabolism


What are potential outcomes of critical illness?

Sepsis and death


Hyper-inflammation SIRS or immuno suppression CARs, can occur mediated by what?

Neuro endocrine-cytokine response to stress


The intestinal barrier normal function is critical for what?

Survival in critical illness


What microorganisms play a critical role in preventing pathogenic bacteria binding to the intestinal barrier and causing illness?

1. Aerobic Micro-organisms
2. Anaerobic Micro-organisms


The gut is the largest immunological system in the body. What are the local and systemic immunological responses in the body?

1. Gut-associated lymphoid tissues
2. Intra-epithelial lymphocytes
3. Submucosal Aggregates
4. Peyer's Pathches
5. Mesenteric lymph nodes
6. Secretory IgA
1. Circulatory lymphocytes
2. Hepatic Kupffer cells


What are mechanical aspects of the gut which allow for the intestinal barrier to stay functional?

1. Healthy enterocyte
2. Tight junction
3. Cell turnover
4. Normal Motility


What are the chemical aspects of the gut which allow for the intestinal barrier to stay functional?

1. Gastric acidity
2. Salivary lysozyme
3. Lactoferrin
4. Mucus Secretion
5. Bile Salts


If these barriers to the intestine fails then the barrier is compromised and can mediate systemic inflammatory responses. What are some of these responses?

1. Release of cytokines: IL-1, IL-6, TNF, PAF, etc
2. Multiple organ dysfunction and failure
3. Activation of complement system: C3A,C3B,C3C,C3D
4. Decreased splanchnic blood flow
5. Catabolic hormones catecholamines
6. Acute phase proteins
7. Release of arachidonic acid metabolites pGE2, thromboxane, and leukotrienes


Again if a patient has a compromised gut barrier this can lead to mediation of the systemic inflammatory response. In disease states, how does this compromise in the barrier lead to sepsis?

Bacteria and endotoxins can translocate through the epithelial mucosa
----mesenteric lymph node
----liver and spleen


What are the two options for nutritional support in a critical ill patient?

1. TPN (total parenteral intravenous nutrition)
2. EN (enteral feeding)


type of feeding used for patients in intensive care and how much it reduces mortality

parenteral or enteral



Bowel rest (delayed EN) increases risk of system infection by 66%. Therefore which is the better option for feeding EN or TPN?

EN is better than TPN


Why doesn't TPN protect against infection?

1. Failure to enable proper maintenance of the gut immune system
2. Failure to provide adequate nutrition to the enterocyte


The outcome of critical illness can be influenced by nutritional support in terms of what?

1. duration and consequences of the hypermetabolic phase
2. The occurrence of sepsis
3. The recovery from sepsis


Nutrients must provide what in a critically ill patient?

1. Systemic metabolic support
2. Gastrointestinal support
3. Immune system support


Intestinal barrier function is crucial to survival and failure can result in what?



Nutritional support of immune barrier function by _____ _____ may be inadequate and some ____ _____ is needed

parenteral nutrition may be inadequate and some enteral nutrition is needed


Outcome will depend on nutritional support at key stages of critical illness with targeted _____ _______.

Nutritional support


translocation through the epithelial mucosa in in a compromised gut is due to

-􏰁increased intestinal permeability,(lack of oral feeding)
-􏰁decreased host immune defense (eg CARS)
-􏰁increased bacteria due to bacterial overgrowth.


why should some enteral nutrition be maintained whenever possible

because though TPN can provide for most of energy, you need sufficient enteral energy --> stimulate CCK/ gut trophic factors and maintain immune function