Lec 4/5: Disaster Planning and Metabolic Stress Flashcards
Disaster Planning Basics
-> Disasters =
-> Plans at different levels:
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-> Plans cover meeting basic needs
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Who else?
Specifically - 2 from above
= natural disasters, war or unrest, power outages, pandemics….
- National, provincial, municipal, institutional
- Prevent, protect against, respond and recover
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- Clothing, shelter, FOOD, information, services
- Chain of command
2 - Emergency Food Service Coordinator - Institutions (ie. hospitals) also have a coordinator
? - any food service establishment / food retailers&distributers / health care professionals / volunteer food organizations
Emergency Food Service Coordinator:
- assembles a committee to make a disaster plan / creates a plan / revisits the plan on a reg basis / tests plan / executes plan when needed
What is included in a plan?
1-12 - slide 8 , name 3
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- communication plans
- where food service will happen / supply chain / staff requirements & training / distribution plans
METABOLIC STRESS =
Catabolic =
What results in M.S:
** read slides specifically example throughout **
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The MAJOR result =
= group of conditions that result in:
= hypermetabolic, catabolic response to acute injury or disease
= breakdown of complex molecules (CHO, PRO, FAT) for energy {aka - energy requirements skyrocket}
: Trauma, surgery, burns and sepsis all do
- Trauma (blunt, penetrating)
- Surgery (controlled trauma)
- Burn (thermal trauma)
- Sepsis (generalized infection - bacteria in the blood)
= REE INCREASED majorly
Hormone Review
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-> Insulin
-> Counter-regulatory hormones (countering the effects of insulin)
- Glucagon
- Catecholamines, eg. epinephrine
- Glucocorticoids / corticosteriods eg. cortisol
-> ADH
-> ACTH - Adrenocorticotropic hormone
Physiological Responses - Ebb Phase =
- I like to think of it as the body being in
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-> Metabolic response
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Describe Figure - slide 20:
= Immediately post-trauma; lasts 2-48h
- in shock
- Wound response - coagulation, inflammation
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- Shock, hypovolemia, decreased O2 availability
- Low cardiac and urinary output
- Low core temperatures
- Low insulin
- Elevated blood glucose, catecholamines, free fatty acids, ACTH release leads to glucocorticoid secretion
- ADH increases to preserve fluid balance
(Result: Reduced (or no) urination)
Figure:
- in the ebb phase plasma osmolality increases (AKA solutes in blood increase + fluid into tissues) and atrial pressure decreases: this increases ADH hormone = water resorption = urine volume reduced (antidiuresis)
Flow Phase =
- Lasts from
-> Classic Signs and Symptoms of M.S
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Back to figure - but flow phase:
-> Increased…
- from hours to days
(patient may slip back and forth between ebb and flow)
-> - Increased cardiac output
- Increased temperature d/t cytokine release (IL-1, IL-2, IL-6, TNF-α)
- Increase O2 consumption and REE
- Increased insulin but also insulin resistance result: high blood glucose levels
- Increased counter-regulatory hormones
- ADH decreases (increased urine output)
- Wound response - angiogenesis / collagen synthesis / growth of epithelium
: Atrial Pressure increases, Plasma Osmolality decreases (fluid back into vascular system): ADH is cancelled = decreased water resorption = urine volume increased (Diuresis)
-> Increased energy metabolism
(Major Burns are by far the most increase in metabolism)
Glucose metabolism during flow phase
-> Hyperglycemia
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-> Insulin resistance
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-> Muscle and wound switch to anaerobic glycolysis
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- Hepatic (liver) gluconeogenesis
- Increased uptake of gluconeogenic amino acids by liver
- Glycogenolysis
- Reduced glucose oxidation (max 4-5 mg/kg/min)
- Decreased glucose uptake - insulin resistance
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- Maintains glucose availability for non-insulin dependent organs
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- Wound is hypoxic (low in oxygen)
- Lactate is a biproduct of glycolysis
- Cori Cycle converts lactate to glucose
(esp in burns patients)
Protein metabolism during the flow phase
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1 2 3
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Positive acute phase proteins
What are they?
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Why?
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Examples:
-> Negative nitrogen balance
- Protein (muscle) breakdown for energy
- Production of positive acute phase proteins
[Hormones encourage breakdown proteins]
- Amino acid efflux
1 Substrate for protein synthesis
2 Converted to glucose
3 Source of glutamine for gut fuel - Greater N loss with greater severity of trauma
? - Proteins whose concentrations increase in the blood during metabolic stress
Why? - Release is stimulated by inflammatory cytokines
- Generally have a role to play in the immune response and healing
Ex’s: C reactive protein (inflamm, O2 + blood to wound) , fibronectin (wound healing), ceruloplasmin (iron metabolism)
- ## LOTS: -->
N excretion (g/day) Graph:
Why all the fuss about Negative N balance?
Loss of___
- Concentrations in the blood decrease during metabolic stress
- LOTS - Albumin, Pre-Albumin, many others [not a good nutr protein assessment - just tells us they are in metabolic stress]
-> This becomes very important when interpreting blood test results
: Major Burn by far has the most
___ of 1g N = 30g loss of lean body mass
Complications associated with loss of lean body mass
[% loss of lean body mass VS associated complications]
10%
20%
30%
40%
10% - impaired immunity, increased risk of infection
20% - decreased wound healing, weakness, infection
30% - too weak to sit, pressure sores, pneumonia, no wound healing
40% death, usually from pneumonia
(Flow Phase CON’D)
Lipid Metabolism:
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What is RQ?
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- Increased lipolysis
- Free fatty acids used as energy source
- RQ = Co2 produced / O2 consumed
- Days to weeks to months
- Metabolic response
- Wound response:
- remodeling of wound, collagenases lyse (breakdown) collagen
- New collagen synthesized
- Replacing dead/injured tissue
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- Good apposition of margins (the wound edges line up)
- Minimal necrotic tissue and infection
- Good perfusion of blood
- Endocrine status - challenges for those with DM, those on corticosteriods
(both have poor circulation, increased risk of infection) - Wound dehiscence = failure of wound to knit
(need to re-cut and debride (remove dead tissue) to encourage inflammatory response)
Medical Management of Metabolic Stress
-> Trauma
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Human Skin Diagram - slide 48 LOOK AT **
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- Stop bleeding, support vascular system, IV fluids
- Mechanical ventilation
- Drugs for paralysis (pt unable to move muscles), sedation (calming agitation)
- Insulin
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- Caused by heat, chemicals, radiation or electricity
- Burned skin loses its function
- Burns described by thickness of the burn area
- Injury described in terms of surface area of body burned
- Ebb phase 2-5 days
- Flow phase sustained until wound closure
(infections, surgical procedures etc. reinitiates flow phase)
(protein loss through wound exudate (fluid that oozes from a wound - high in protein, keeps the wound clean))
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- Support vascular and respiratory systems
- Fluid replacement
- Begin feeding ASAP
- Cover open areas
- Avoid sepsis
- Debride eschar - remove necrotic tissue
- Grafts and Jobst garments
Sepsis - Background:
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-> Initial signs:
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- trauma VS sepsis
-> Generalize (blood-borne) infection
- Mortality 20-40%
- Severe sepsis includes organ dysfunction and/or tissue hypo-perfusion (low blood flow to tissues)
-> Can be caused by bacterial translocation
-> May also be caused by TPN
-> increased WBC, HR, fever, hypothermia
-> Gut Dysfunction
-> Comparing metabolic responses
VS
- if well nourished, similar responses seen
- Poorly nourished sepsis patients may have low or normal metabolic rate
- With sepsis, response will not weaken until infection is under control
- Sepsis has greater insulin resistance
- Sepsis more likely to have hypertriglyceridemia
