M1: SIRS Flashcards

0
Q

Alteration of neuroendocrine, metabolic & immune system. Disequilibrium of internal environmental balance homeostasis.

A

Injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

Inflammatory responses

A

Cell signalling, Cell migration & Mediator release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

No significant sequela

A

Minor injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Overwhelming inflammatory response leads to multiple organfailure then death.

A

Major injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Phase of SIRS: restore tissue function& eradicate MO.

A

Pro inflammatory response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Phase of SIRS: prevent excessive inflammatory activities to restore homeostasis.

A

Anti inflammatory response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Examples of Injury

A

Surgery, Infection & Trauma “SIT”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Presence of bacteria

A

Infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Has two or more of the given criteria. Identifiable source if microbial insult.

A

SIRS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Criteria for SIRS: Temp of

A

38°c

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Criteria for SIRS: Heart rate

A

90bpm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Criteria for SIRS: Respiratory rate

A

20cpm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Criteria for SIRS: PaCO2 of

A

32mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Criteria for SIRS: presence of

A

Bands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Identifiable source of infection + SIRS

A

Sepsis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Sepsis + Organ Dysfunction

A

Severe sepsis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Sepsis + hypotension(CV collapse) requiring vasopressor support

A

Septic shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Purely SIRS give antibiotic

A

Acute Pancreatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Blood component that responds to injury the first 24 hours

A

Neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Type of signaling in which inflammatory mediators in circulation can induce fever & anorexia

A

Humoral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Example of humoral signaling factor

A

TNF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Type of signaling in which parasympathetic vagal stimulation attenuates inflammatory response via ________ release.

A

Neural. Acetylcholine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Neural signaling Parasympathetic vagal stimulation: Heart rate

A

Decreases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Neural signaling Parasympathetic vagal stimulation: gut motility

A

Increase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Neural signaling Parasympathetic vagal stimulation: vessels
Vasodilation
25
Reduces macrophage activation. Reduce release of pro inflammatory receptors
Parasympathetic vagal stimulation(Anti inflammatory)
26
Afferent signals: areas of CNS devoid of blood brain barrier admit passage of inflammatory mediators (TNF) causing anorexia, fever & depression
Circulation pathway
27
Afferent signals: to the vagus nerve like cytokines, baroreceptors(aorta), chemoreceptors, thermoreceptors from the site of injury.
Neural pathway
28
Reduces tissue macrophage and release of inflammatory mediators but not IL10
Acetylcholine in Parasympathetic response
29
Sense by high pressure baroreceptors and low pressure stretch receptors
Effective Circulatory Volume
30
An antidiuretic to preserve fluid volume
Vasopressin
31
Sensed by carotid & aortic bodies. Decrease sympathetic activity. Increase respiratory rate.
Chemoreceptor reflexes
32
Sensed by the pre optic area of the hypothalamus
Temperature
33
Efferent Outputs
Hormonal, Autonomic & Local tissue response
34
Hormone for circadian signals that lost in injury due to pain & anxiety.
ACTH
35
Elevated in types of injury, longest in burn pxs in 4 weeks.
Cortisol
36
Due to adrenal suppression from exogenous administration of glucocorticoid.
Acute Adrenal Insufficiency
37
An effective immuno suppressive agents
Cortisol
38
During severe trauma or injury, there would be an inhibition of this hormone leading to hyperglycemia. Can be also due to resistance.
Insulin
39
Fluid given to patients with hyperglycemia
Plain LR
40
Most potent mediator of the inflammatory response. Eradicates invading MO & promotes wound healing.
Cytokines
41
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
42
Oxygen scavengers that protects the cell from Reactive Oxygen Metabolites
Glutathione & Catalase
43
Are oxidation derivatives of membrane phospholipid arachidonic acids. Secreted by nucleated cells.
Eicosanoids
44
Increases fluid leakage from blood vessels
PGE2
45
Potent vasodilators. Cause by hypoxia & ischemia.
Bradykinin
46
Earliest & most potent mediators. Monocyte/Macrophages and T cells. For muscle catabolism & cachexia during stress. Coagulation activation.
TNF
47
Induces febrile response to injury by stimulating PG.
IL 1
48
Guards the endothelium of blood vessels
Neutrophil
49
Most potent vasoconstrictor present at the endothelial linings
Endothelins
50
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
51
Most commonly observed in patient's with burns
Hyperglycemia
52
Had an anti inflammatory effects. Improves homeostasis effect in inhibiting apoptotic activities.
Insulin
53
Biochemical marker to check the severity of injury
C-Reactive Protein
54
Exerts several homeostatic influences. Including enhancing gut motility, reducing heart rate & regulating inflammation.
Vagus nerve
55
Parasympathetic nervous system activity transmit vagus nerve efferent signals primarily through this neurotransmitter
Acetylcholine
56
For rapid response to inflammatory stimuli and for the potential regulation of early proinflammatory mediator release
TNF
57
Are polypeptide hormones
Cytokines
58
Cytokines, glucagon and insulin are
Polypeptide
59
Epinephrine, serotonin and histamine are
AA
60
Glucocorticoid, prostaglandin & leukotrienes are
Fatty acids
61
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
62
Is an eicosanoid
Thromboxane
63
Is one of the two precursors of the eicosanoids
Arachidonic Acid
64
Examples of cytokines
TNF & IL-10
65
Eicosanoids are derived primarily by oxidation of the membrane phospholipid
Arachidonic acid/Eicosatetraenoic acid
66
The synthesis of of arachidonic acid from phospholipids require the enzymatic activation of
Phospholipase A2
67
Products of the COX pathway include all the
Prostaglandin & Thromboxane
68
The lipoxygenase pathway generates
Leukotrienes & HETE
69
Two pathways in which Eicosanoids are primarily produced
Arachidonic Acid(O3 FA) & Eicosapentanoic Acid(O6 FA)
70
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
71
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
72
TNF is primarily synthesized by
Macrophage, Monocyte & T cells
73
Stimulates muscle breakdown, increase catabolism, insulin resistance, redistribution of AA, mediates coagulation activation, cell migration and macrophage phagocytosis.
TNF
74
Is a member of the selectin family of adhesion molecules
L-selectin
75
Phospholipid which mediates leukocyte function but does not contribute to adhesion
Platelet Activating Factor
76
Is a polypeptide growth factor which is upregulated in some malignant tumors
TGF-B
77
Is a cytokine which is upregulated in inflammatory conditions but does not play a role in adhesion of leukocytes to endothelium
TNF
78
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
79
Normal vascular smooth muscle relaxation is maintained by a constant output of NO and subsequent activation of soluble
Guanylyl cyclase
80
Easily traverses cell membranes and has a short half life of a few seconds and is oxidized into nitrate & nitrite.
NO
81
Member of eicosanoid family and is primarily produced by endothelial cells. Effective vasodilator and also inhibits platelet aggregation.
Prostacyclin
82
Associated with increased cardiac output, splanchnic blood flow and oxygen delivery & consumption with no significant decrease in mean arterial pressure.
Prostacyclin infusion
83
To maintain basal metabolic needs, a normal healthy adult requires approximately ___________ per day drawn from carbohydrate, lipid & protein sources.
20-25kcal/kg/day
84
Primary source of calories during acute starvation (<5 days)
Fat
85
Primary fuel source in prolonged starvation
Ketone bodies
86
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
87
Primary fuel source after acute injury. Are not merely nonprotein, noncarbohydrate fuel sources that minimize protein catabolism in the injured patient.
Lipids
88
Are the predominant energy source during critical illness and after injury.
Triglycerides
89
Fat metabolism occurs mainly in response to catecholamine stimulus of the
Hormone sensitive triglyceride lipase
90
Most abundant AA in the body. A substrate for nucleotide synthesis, major fuel source of enterocytes & immunocytes.
Glutamine
91
Site of synthesis for Glutamine
Skeletal muscles & Lungs
92
Precursor of this is glutamine. Major intracellular oxidant.
Glutathione
93
No identifiable source of infection but presents two of the given criteria
SIRS
94
Is a glucocorticoid steroid hormone released by the adrenal cortex in response to ACTH. Increased during times of stress.
Cortisol
95
How long can cortisol persists in a patient with burn
1 month
96
Used to mitigate cortisol effects on wound healing
Vitamin A
97
Wound healing also is impaired, because cortisol reduces these
TGF B & IGF 1
98
Laboratory finding seen in patients with adrenal insufficiency
Hypernatremia
99
Overfeeding (RQ >1.0) in a critically ill patient can result in
Inc risk of infection
100
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
101
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
102
Vitamin that is not present in commercially prepared IV vitamin preparation and therefore must be supplemented in a patient receiving TPN.
Vitamin K
103
New onset of glucose intolerance in a TPN dependent patient can be due to
Chromium deficiency
104
Associated with copper deficiency
Microcytic anemia
105
The most frequent presentation of trace mineral deficiencies developing both diffusely and at tetriginous areas in zinc deficient patients
Eczematoid rash
106
Is extremely rare and poorly described but may be associated with delayed or poor wound healing
Manganese deficiency
107
Positive nitrogen balance
Anabolism
108
A potential physiologic effect of anabolism
Glycosuria
109
Glycosuria can result from
Hypokalemia
110
Is essential to achieve positive nitrogen balance and replace depleted intracellular stores
Potassium
111
Should not be significantly affected by anabolism
Serum calcium levels