M1: SIRS Flashcards
Alteration of neuroendocrine, metabolic & immune system. Disequilibrium of internal environmental balance homeostasis.
Injury
Inflammatory responses
Cell signalling, Cell migration & Mediator release
No significant sequela
Minor injury
Overwhelming inflammatory response leads to multiple organfailure then death.
Major injury
Phase of SIRS: restore tissue function& eradicate MO.
Pro inflammatory response
Phase of SIRS: prevent excessive inflammatory activities to restore homeostasis.
Anti inflammatory response
Examples of Injury
Surgery, Infection & Trauma “SIT”
Presence of bacteria
Infection
Has two or more of the given criteria. Identifiable source if microbial insult.
SIRS
Criteria for SIRS: Temp of
38°c
Criteria for SIRS: Heart rate
90bpm
Criteria for SIRS: Respiratory rate
20cpm
Criteria for SIRS: PaCO2 of
32mmHg
Criteria for SIRS: presence of
Bands
Identifiable source of infection + SIRS
Sepsis
Sepsis + Organ Dysfunction
Severe sepsis
Sepsis + hypotension(CV collapse) requiring vasopressor support
Septic shock
Purely SIRS give antibiotic
Acute Pancreatitis
Blood component that responds to injury the first 24 hours
Neutrophils
Type of signaling in which inflammatory mediators in circulation can induce fever & anorexia
Humoral
Example of humoral signaling factor
TNF
Type of signaling in which parasympathetic vagal stimulation attenuates inflammatory response via ________ release.
Neural. Acetylcholine.
Neural signaling Parasympathetic vagal stimulation: Heart rate
Decreases
Neural signaling Parasympathetic vagal stimulation: gut motility
Increase
Neural signaling Parasympathetic vagal stimulation: vessels
Vasodilation
Reduces macrophage activation. Reduce release of pro inflammatory receptors
Parasympathetic vagal stimulation(Anti inflammatory)
Afferent signals: areas of CNS devoid of blood brain barrier admit passage of inflammatory mediators (TNF) causing anorexia, fever & depression
Circulation pathway
Afferent signals: to the vagus nerve like cytokines, baroreceptors(aorta), chemoreceptors, thermoreceptors from the site of injury.
Neural pathway
Reduces tissue macrophage and release of inflammatory mediators but not IL10
Acetylcholine in Parasympathetic response
Sense by high pressure baroreceptors and low pressure stretch receptors
Effective Circulatory Volume
An antidiuretic to preserve fluid volume
Vasopressin
Sensed by carotid & aortic bodies. Decrease sympathetic activity. Increase respiratory rate.
Chemoreceptor reflexes
Sensed by the pre optic area of the hypothalamus
Temperature
Efferent Outputs
Hormonal, Autonomic & Local tissue response
Hormone for circadian signals that lost in injury due to pain & anxiety.
ACTH
Elevated in types of injury, longest in burn pxs in 4 weeks.
Cortisol
Due to adrenal suppression from exogenous administration of glucocorticoid.
Acute Adrenal Insufficiency
An effective immuno suppressive agents
Cortisol
During severe trauma or injury, there would be an inhibition of this hormone leading to hyperglycemia. Can be also due to resistance.
Insulin
Fluid given to patients with hyperglycemia
Plain LR
Most potent mediator of the inflammatory response. Eradicates invading MO & promotes wound healing.
Cytokines
Produced by reduction of oxygen to superoxide anion and metabolize to form H202 & hydroxyl radicals. Causes injury by oxidation of unsaturated FA within cell membranes.
Oxygen radicals
Oxygen scavengers that protects the cell from Reactive Oxygen Metabolites
Glutathione & Catalase
Are oxidation derivatives of membrane phospholipid arachidonic acids. Secreted by nucleated cells.
Eicosanoids
Increases fluid leakage from blood vessels
PGE2
Potent vasodilators. Cause by hypoxia & ischemia.
Bradykinin
Earliest & most potent mediators. Monocyte/Macrophages and T cells. For muscle catabolism & cachexia during stress. Coagulation activation.
TNF
Induces febrile response to injury by stimulating PG.
IL 1
Guards the endothelium of blood vessels
Neutrophil
Most potent vasoconstrictor present at the endothelial linings
Endothelins
In severely burned pediatric patient, this is beneficial to use to improve post-burn morbidity. Decreased incidence of infection & sepsis. Improves hepatic adrenal functions. Partially restore the depleted and compromised immune system.
Intensive Insulin Therapy
Most commonly observed in patient’s with burns
Hyperglycemia
Had an anti inflammatory effects. Improves homeostasis effect in inhibiting apoptotic activities.
Insulin
Biochemical marker to check the severity of injury
C-Reactive Protein
Exerts several homeostatic influences. Including enhancing gut motility, reducing heart rate & regulating inflammation.
Vagus nerve
Parasympathetic nervous system activity transmit vagus nerve efferent signals primarily through this neurotransmitter
Acetylcholine
For rapid response to inflammatory stimuli and for the potential regulation of early proinflammatory mediator release
TNF
Are polypeptide hormones
Cytokines
Cytokines, glucagon and insulin are
Polypeptide
Epinephrine, serotonin and histamine are
AA
Glucocorticoid, prostaglandin & leukotrienes are
Fatty acids
Intracellular proteins that are increasingly expressed during the times of stress such as burn injury, inflammation & infection. Includes protein misfolding and protein targeting. Bind both autologous and foreign proteins and thereby function as intracellular chaperones for ligands such as bacterial DNA & endotoxin.
Heat Shock Proteins
Is an eicosanoid
Thromboxane
Is one of the two precursors of the eicosanoids
Arachidonic Acid
Examples of cytokines
TNF & IL-10
Eicosanoids are derived primarily by oxidation of the membrane phospholipid
Arachidonic acid/Eicosatetraenoic acid
The synthesis of of arachidonic acid from phospholipids require the enzymatic activation of
Phospholipase A2
Products of the COX pathway include all the
Prostaglandin & Thromboxane
The lipoxygenase pathway generates
Leukotrienes & HETE
Two pathways in which Eicosanoids are primarily produced
Arachidonic Acid(O3 FA) & Eicosapentanoic Acid(O6 FA)
Have specific anti inflammatory effects, including inhibition of NF-B activity, TNF release from the hepatic Kupffer cells, as well as adhesion and migration. Inhibits inflammation, ameliorate weight loss, increase small bowel perfusion and increase gut protection.
Omega-3 Fatty Acids
Is a cytokine that is rapidly mobilized in response to stressors such as injury and infection, and is a potent mediator of the subsequent inflammatory response.
TNF
TNF is primarily synthesized by
Macrophage, Monocyte & T cells
Stimulates muscle breakdown, increase catabolism, insulin resistance, redistribution of AA, mediates coagulation activation, cell migration and macrophage phagocytosis.
TNF
Is a member of the selectin family of adhesion molecules
L-selectin
Phospholipid which mediates leukocyte function but does not contribute to adhesion
Platelet Activating Factor
Is a polypeptide growth factor which is upregulated in some malignant tumors
TGF-B
Is a cytokine which is upregulated in inflammatory conditions but does not play a role in adhesion of leukocytes to endothelium
TNF
AKA endothelium derived relaxing factor due to its effects on vasuclar smooth muscle and has important functions in both physiologic & pathologic control of vascular tone.
Nitric Oxide
Normal vascular smooth muscle relaxation is maintained by a constant output of NO and subsequent activation of soluble
Guanylyl cyclase
Easily traverses cell membranes and has a short half life of a few seconds and is oxidized into nitrate & nitrite.
NO
Member of eicosanoid family and is primarily produced by endothelial cells. Effective vasodilator and also inhibits platelet aggregation.
Prostacyclin
Associated with increased cardiac output, splanchnic blood flow and oxygen delivery & consumption with no significant decrease in mean arterial pressure.
Prostacyclin infusion
To maintain basal metabolic needs, a normal healthy adult requires approximately ___________ per day drawn from carbohydrate, lipid & protein sources.
20-25kcal/kg/day
Primary source of calories during acute starvation (<5 days)
Fat
Primary fuel source in prolonged starvation
Ketone bodies
In extended fasting, ketone bodies become an important fuel source for this organ after 2 days and gradually become the principal fuel source by 24 days.
Brain
Primary fuel source after acute injury. Are not merely nonprotein, noncarbohydrate fuel sources that minimize protein catabolism in the injured patient.
Lipids
Are the predominant energy source during critical illness and after injury.
Triglycerides
Fat metabolism occurs mainly in response to catecholamine stimulus of the
Hormone sensitive triglyceride lipase
Most abundant AA in the body. A substrate for nucleotide synthesis, major fuel source of enterocytes & immunocytes.
Glutamine
Site of synthesis for Glutamine
Skeletal muscles & Lungs
Precursor of this is glutamine. Major intracellular oxidant.
Glutathione
No identifiable source of infection but presents two of the given criteria
SIRS
Is a glucocorticoid steroid hormone released by the adrenal cortex in response to ACTH. Increased during times of stress.
Cortisol
How long can cortisol persists in a patient with burn
1 month
Used to mitigate cortisol effects on wound healing
Vitamin A
Wound healing also is impaired, because cortisol reduces these
TGF B & IGF 1
Laboratory finding seen in patients with adrenal insufficiency
Hypernatremia
Overfeeding (RQ >1.0) in a critically ill patient can result in
Inc risk of infection
Initial enteral formula for the majority of surgical patients. Standard or first line formula for stable patients with an intact GIT.
Low residue isotonic formula
Is usually increased to 50% of the total calories, with a corresponding reduction in carbohydrate content. Increased in pulmonary failure to reduce carbon dioxide production and alleviate ventilation burden for failing lungs.
Fat
Vitamin that is not present in commercially prepared IV vitamin preparation and therefore must be supplemented in a patient receiving TPN.
Vitamin K
New onset of glucose intolerance in a TPN dependent patient can be due to
Chromium deficiency
Associated with copper deficiency
Microcytic anemia
The most frequent presentation of trace mineral deficiencies developing both diffusely and at tetriginous areas in zinc deficient patients
Eczematoid rash
Is extremely rare and poorly described but may be associated with delayed or poor wound healing
Manganese deficiency
Positive nitrogen balance
Anabolism
A potential physiologic effect of anabolism
Glycosuria
Glycosuria can result from
Hypokalemia
Is essential to achieve positive nitrogen balance and replace depleted intracellular stores
Potassium
Should not be significantly affected by anabolism
Serum calcium levels