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SURGERY > M1: SIRS > Flashcards

M1: SIRS Flashcards

0
Q

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

A

Injury

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1
Q

Inflammatory responses

A

Cell signalling, Cell migration & Mediator release

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2
Q

No significant sequela

A

Minor injury

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3
Q

Overwhelming inflammatory response leads to multiple organfailure then death.

A

Major injury

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4
Q

Phase of SIRS: restore tissue function& eradicate MO.

A

Pro inflammatory response

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5
Q

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

A

Anti inflammatory response

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6
Q

Examples of Injury

A

Surgery, Infection & Trauma “SIT”

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7
Q

Presence of bacteria

A

Infection

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8
Q

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

A

SIRS

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9
Q

Criteria for SIRS: Temp of

A

38°c

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10
Q

Criteria for SIRS: Heart rate

A

90bpm

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11
Q

Criteria for SIRS: Respiratory rate

A

20cpm

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12
Q

Criteria for SIRS: PaCO2 of

A

32mmHg

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13
Q

Criteria for SIRS: presence of

A

Bands

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14
Q

Identifiable source of infection + SIRS

A

Sepsis

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15
Q

Sepsis + Organ Dysfunction

A

Severe sepsis

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16
Q

Sepsis + hypotension(CV collapse) requiring vasopressor support

A

Septic shock

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17
Q

Purely SIRS give antibiotic

A

Acute Pancreatitis

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18
Q

Blood component that responds to injury the first 24 hours

A

Neutrophils

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19
Q

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

A

Humoral

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20
Q

Example of humoral signaling factor

A

TNF

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21
Q

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

A

Neural. Acetylcholine.

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22
Q

Neural signaling Parasympathetic vagal stimulation: Heart rate

A

Decreases

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23
Q

Neural signaling Parasympathetic vagal stimulation: gut motility

A

Increase

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24
Q

Neural signaling Parasympathetic vagal stimulation: vessels

A

Vasodilation

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25
Q

Reduces macrophage activation. Reduce release of pro inflammatory receptors

A

Parasympathetic vagal stimulation(Anti inflammatory)

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26
Q

Afferent signals: areas of CNS devoid of blood brain barrier admit passage of inflammatory mediators (TNF) causing anorexia, fever & depression

A

Circulation pathway

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27
Q

Afferent signals: to the vagus nerve like cytokines, baroreceptors(aorta), chemoreceptors, thermoreceptors from the site of injury.

A

Neural pathway

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28
Q

Reduces tissue macrophage and release of inflammatory mediators but not IL10

A

Acetylcholine in Parasympathetic response

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29
Q

Sense by high pressure baroreceptors and low pressure stretch receptors

A

Effective Circulatory Volume

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30
Q

An antidiuretic to preserve fluid volume

A

Vasopressin

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31
Q

Sensed by carotid & aortic bodies. Decrease sympathetic activity. Increase respiratory rate.

A

Chemoreceptor reflexes

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32
Q

Sensed by the pre optic area of the hypothalamus

A

Temperature

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33
Q

Efferent Outputs

A

Hormonal, Autonomic & Local tissue response

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34
Q

Hormone for circadian signals that lost in injury due to pain & anxiety.

A

ACTH

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35
Q

Elevated in types of injury, longest in burn pxs in 4 weeks.

A

Cortisol

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36
Q

Due to adrenal suppression from exogenous administration of glucocorticoid.

A

Acute Adrenal Insufficiency

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37
Q

An effective immuno suppressive agents

A

Cortisol

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38
Q

During severe trauma or injury, there would be an inhibition of this hormone leading to hyperglycemia. Can be also due to resistance.

A

Insulin

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39
Q

Fluid given to patients with hyperglycemia

A

Plain LR

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40
Q

Most potent mediator of the inflammatory response. Eradicates invading MO & promotes wound healing.

A

Cytokines

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41
Q

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.

A

Oxygen radicals

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42
Q

Oxygen scavengers that protects the cell from Reactive Oxygen Metabolites

A

Glutathione & Catalase

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43
Q

Are oxidation derivatives of membrane phospholipid arachidonic acids. Secreted by nucleated cells.

A

Eicosanoids

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44
Q

Increases fluid leakage from blood vessels

A

PGE2

45
Q

Potent vasodilators. Cause by hypoxia & ischemia.

A

Bradykinin

46
Q

Earliest & most potent mediators. Monocyte/Macrophages and T cells. For muscle catabolism & cachexia during stress. Coagulation activation.

A

TNF

47
Q

Induces febrile response to injury by stimulating PG.

A

IL 1

48
Q

Guards the endothelium of blood vessels

A

Neutrophil

49
Q

Most potent vasoconstrictor present at the endothelial linings

A

Endothelins

50
Q

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.

A

Intensive Insulin Therapy

51
Q

Most commonly observed in patient’s with burns

A

Hyperglycemia

52
Q

Had an anti inflammatory effects. Improves homeostasis effect in inhibiting apoptotic activities.

A

Insulin

53
Q

Biochemical marker to check the severity of injury

A

C-Reactive Protein

54
Q

Exerts several homeostatic influences. Including enhancing gut motility, reducing heart rate & regulating inflammation.

A

Vagus nerve

55
Q

Parasympathetic nervous system activity transmit vagus nerve efferent signals primarily through this neurotransmitter

A

Acetylcholine

56
Q

For rapid response to inflammatory stimuli and for the potential regulation of early proinflammatory mediator release

A

TNF

57
Q

Are polypeptide hormones

A

Cytokines

58
Q

Cytokines, glucagon and insulin are

A

Polypeptide

59
Q

Epinephrine, serotonin and histamine are

A

AA

60
Q

Glucocorticoid, prostaglandin & leukotrienes are

A

Fatty acids

61
Q

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.

A

Heat Shock Proteins

62
Q

Is an eicosanoid

A

Thromboxane

63
Q

Is one of the two precursors of the eicosanoids

A

Arachidonic Acid

64
Q

Examples of cytokines

A

TNF & IL-10

65
Q

Eicosanoids are derived primarily by oxidation of the membrane phospholipid

A

Arachidonic acid/Eicosatetraenoic acid

66
Q

The synthesis of of arachidonic acid from phospholipids require the enzymatic activation of

A

Phospholipase A2

67
Q

Products of the COX pathway include all the

A

Prostaglandin & Thromboxane

68
Q

The lipoxygenase pathway generates

A

Leukotrienes & HETE

69
Q

Two pathways in which Eicosanoids are primarily produced

A

Arachidonic Acid(O3 FA) & Eicosapentanoic Acid(O6 FA)

70
Q

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.

A

Omega-3 Fatty Acids

71
Q

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.

A

TNF

72
Q

TNF is primarily synthesized by

A

Macrophage, Monocyte & T cells

73
Q

Stimulates muscle breakdown, increase catabolism, insulin resistance, redistribution of AA, mediates coagulation activation, cell migration and macrophage phagocytosis.

A

TNF

74
Q

Is a member of the selectin family of adhesion molecules

A

L-selectin

75
Q

Phospholipid which mediates leukocyte function but does not contribute to adhesion

A

Platelet Activating Factor

76
Q

Is a polypeptide growth factor which is upregulated in some malignant tumors

A

TGF-B

77
Q

Is a cytokine which is upregulated in inflammatory conditions but does not play a role in adhesion of leukocytes to endothelium

A

TNF

78
Q

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.

A

Nitric Oxide

79
Q

Normal vascular smooth muscle relaxation is maintained by a constant output of NO and subsequent activation of soluble

A

Guanylyl cyclase

80
Q

Easily traverses cell membranes and has a short half life of a few seconds and is oxidized into nitrate & nitrite.

A

NO

81
Q

Member of eicosanoid family and is primarily produced by endothelial cells. Effective vasodilator and also inhibits platelet aggregation.

A

Prostacyclin

82
Q

Associated with increased cardiac output, splanchnic blood flow and oxygen delivery & consumption with no significant decrease in mean arterial pressure.

A

Prostacyclin infusion

83
Q

To maintain basal metabolic needs, a normal healthy adult requires approximately ___________ per day drawn from carbohydrate, lipid & protein sources.

A

20-25kcal/kg/day

84
Q

Primary source of calories during acute starvation (<5 days)

A

Fat

85
Q

Primary fuel source in prolonged starvation

A

Ketone bodies

86
Q

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.

A

Brain

87
Q

Primary fuel source after acute injury. Are not merely nonprotein, noncarbohydrate fuel sources that minimize protein catabolism in the injured patient.

A

Lipids

88
Q

Are the predominant energy source during critical illness and after injury.

A

Triglycerides

89
Q

Fat metabolism occurs mainly in response to catecholamine stimulus of the

A

Hormone sensitive triglyceride lipase

90
Q

Most abundant AA in the body. A substrate for nucleotide synthesis, major fuel source of enterocytes & immunocytes.

A

Glutamine

91
Q

Site of synthesis for Glutamine

A

Skeletal muscles & Lungs

92
Q

Precursor of this is glutamine. Major intracellular oxidant.

A

Glutathione

93
Q

No identifiable source of infection but presents two of the given criteria

A

SIRS

94
Q

Is a glucocorticoid steroid hormone released by the adrenal cortex in response to ACTH. Increased during times of stress.

A

Cortisol

95
Q

How long can cortisol persists in a patient with burn

A

1 month

96
Q

Used to mitigate cortisol effects on wound healing

A

Vitamin A

97
Q

Wound healing also is impaired, because cortisol reduces these

A

TGF B & IGF 1

98
Q

Laboratory finding seen in patients with adrenal insufficiency

A

Hypernatremia

99
Q

Overfeeding (RQ >1.0) in a critically ill patient can result in

A

Inc risk of infection

100
Q

Initial enteral formula for the majority of surgical patients. Standard or first line formula for stable patients with an intact GIT.

A

Low residue isotonic formula

101
Q

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.

A

Fat

102
Q

Vitamin that is not present in commercially prepared IV vitamin preparation and therefore must be supplemented in a patient receiving TPN.

A

Vitamin K

103
Q

New onset of glucose intolerance in a TPN dependent patient can be due to

A

Chromium deficiency

104
Q

Associated with copper deficiency

A

Microcytic anemia

105
Q

The most frequent presentation of trace mineral deficiencies developing both diffusely and at tetriginous areas in zinc deficient patients

A

Eczematoid rash

106
Q

Is extremely rare and poorly described but may be associated with delayed or poor wound healing

A

Manganese deficiency

107
Q

Positive nitrogen balance

A

Anabolism

108
Q

A potential physiologic effect of anabolism

A

Glycosuria

109
Q

Glycosuria can result from

A

Hypokalemia

110
Q

Is essential to achieve positive nitrogen balance and replace depleted intracellular stores

A

Potassium

111
Q

Should not be significantly affected by anabolism

A

Serum calcium levels

SURGERY (3 decks)

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