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A_PLE > SX_SYTEMIC RESPONSE TO INJURY AND METABOLIC SUPPORT > Flashcards

SX_SYTEMIC RESPONSE TO INJURY AND METABOLIC SUPPORT Flashcards

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1
Q

Protein signaling compounds that are essential for both innate and adaptive immunity

A. Cytokines
B. Heat shock proteins
C. ROS
D. Eicosanoids
E. FA metabolites
F. Kallikrein-Kinin system
G. Serotonin
H. Histamine (H4)

A

Cytokines

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2
Q

Mediate cellular responses including cell migration and turnover, DNA replication, and immunocyte proliferation

A. Cytokines
B. Heat shock proteins
C. ROS
D. Eicosanoids
E. FA metabolites
F. Kallikrein-Kinin system
G. Serotonin
H. Histamine (H4)

A

Cytokines

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3
Q

Group of intracellular proteins that are increasingly expressed during time of stress

A. Cytokines
B. Heat shock proteins
C. ROS
D. Eicosanoids
E. FA metabolites
F. Kallikrein-Kinin system
G. Serotonin
H. Histamine (H4)

A

Heat shock protein

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4
Q

Bind both autologous and foreign proteins and thereby function as intracellular chaperones for ligands such as bacterial DNA and endotoxin

A. Cytokines
B. Heat shock proteins
C. ROS
D. Eicosanoids
E. FA metabolites
F. Kallikrein-Kinin system
G. Serotonin
H. Histamine (H4)

A

Heat shock protein

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5
Q

Protect cells from deleterious effects of traumatic stress and when released by damaged cells, alert the immune system of the tissue damage

A. Cytokines
B. Heat shock proteins
C. ROS
D. Eicosanoids
E. FA metabolites
F. Kallikrein-Kinin system
G. Serotonin
H. Histamine (H4)

A

Heat shock protein

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6
Q

Small molecules that are highly reactive due to the presence of unpaired outer orbit electrons

A. Cytokines
B. Heat shock proteins
C. ROS
D. Eicosanoids
E. FA metabolites
F. Kallikrein-Kinin system
G. Serotonin
H. Histamine (H4)

A

ROS

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7
Q

Derived primarily by oxidation of membrane phospholipid, arachidonic acid

A. Cytokines
B. Heat shock proteins
C. ROS
D. Eicosanoids
E. FA metabolites
F. Kallikrein-Kinin system
G. Serotonin
H. Histamine (H4)

A

Eicosanoids

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7
Q

Cause cellular injury to both host cells and invading pathogens through oxidation of unsaturated FA within cell membranes

A. Cytokines
B. Heat shock proteins
C. ROS
D. Eicosanoids
E. FA metabolites
F. Kallikrein-Kinin system
G. Serotonin
H. Histamine (H4)

A

ROS

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8
Q

Composed of subgroups including prostaglandins, prostacyclin, hydroxy eicosatetraenoic acid, thromboxane and leukotriene

Generate a proinflammatory response

A. Cytokines
B. Heat shock proteins
C. ROS
D. Eicosanoids
E. FA metabolites
F. Kallikrein-Kinin system
G. Serotonin
H. Histamine (H4)

A

Eicosanoid

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9
Q

Omega 3-FA have anti-inflammatory effects including inhibition of TNF release from hepatic Kupffer cells, leukocyte adhesion and migration

A. Cytokines
B. Heat shock proteins
C. ROS
D. Eicosanoids
E. FA metabolites
F. Kallikrein-Kinin system
G. Serotonin
H. Histamine (H4)

A

FA metabolites

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10
Q

Group of proteins that contribute to inflammation, BP control, coagulation, and pain responses

A. Cytokines
B. Heat shock proteins
C. ROS
D. Eicosanoids
E. FA metabolites
F. Kallikrein-Kinin system
G. Serotonin
H. Histamine (H4)

A

Kallikrein-Kinin system

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11
Q

Levels of this protease are increased during gram negative bacteremia, hypotension, hemorrhage, endotoxemia, and tissue injury

A

Kallikrein

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12
Q

A hypotensive protease that liberates kinins from blood plasma proteins and is used therapeutically for vasodilation

A

Kallikrein

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13
Q

Mediate
-Vasodilation
-Increased cap permeability
-Tissue edema
-Pain pathway activation
-Inhibition of GNG
-Increased bronchoconstriction

A

Kinins

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14
Q

Any of various polypeptide hormones that are formed locally in tissues and cause dilation of bv (vasodilation) and contraction of smooth muscles

A

Kinin

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15
Q

Released at the site of injury, primarily platelets

A. Cytokines
B. Heat shock proteins
C. ROS
D. Eicosanoids
E. FA metabolites
F. Kallikrein-Kinin system
G. Serotonin
H. Histamine (H4)

A

Serotonin

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16
Q

Stimulates
-Vasoconstriction
-Bronchoconstriction
-Platelet aggregation

A. Cytokines
B. Heat shock proteins
C. ROS
D. Eicosanoids
E. FA metabolites
F. Kallikrein-Kinin system
G. Serotonin
H. Histamine (H4)

A

Serotonin

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17
Q

Receptor blockade of this hormone is associated with decreased production of TNF and IL-1 in edotoxin-treated monocytes

(napapababa ang TNF and IL-1)

A. Cytokines
B. Heat shock proteins
C. ROS
D. Eicosanoids
E. FA metabolites
F. Kallikrein-Kinin system
G. Serotonin
H. Histamine (H4)

A

Serotonin

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18
Q

Associated with eosinophil and mast cell chemotaxis

A. Cytokines
B. Heat shock proteins
C. ROS
D. Eicosanoids
E. FA metabolites
F. Kallikrein-Kinin system
G. Serotonin
H. Histamine (H4)

A

Histamine (H4)

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19
Q

Increased release has been documented in hemorrhagic shock, trauma, thermal injury, endotoxemia, and sepsis

A. Cytokines
B. Heat shock proteins
C. ROS
D. Eicosanoids
E. FA metabolites
F. Kallikrein-Kinin system
G. Serotonin
H. Histamine (H4)

A

Histamine (H4)

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20
Q

Among earliest responders after injury

Induces muscle breakdown and cachexia through increased catabolism

A. TNF-a (Tumor necrosis factor)
B. IL-1 (Interleukin 1)
C. IL-2 (Interleukin 2)
D. IL-6 (Interleukin 6)
E. IL-8 (Interleukin 8)
F. IFN-y (Interferon-y)

A

TNF-a (Tumor necrosis factor)

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21
Q

Induces fever through prostaglandin activity in anterior hypothalamus

Promotes E-endorphin release from pituitary

A. TNF-a (Tumor necrosis factor)
B. IL-1 (Interleukin 1)
C. IL-2 (Interleukin 2)
D. IL-6 (Interleukin 6)
E. IL-8 (Interleukin 8)
F. IFN-y (Interferon-y)

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A

IL-1 (Interleukin 1)

22
Q

Promotes lymphocyte proliferation, immunoglobulin production, gut barrier integrity

Attenuated production after major blood loss lead to immunocompromise

A. TNF-a (Tumor necrosis factor)
B. IL-1 (Interleukin 1)
C. IL-2 (Interleukin 2)
D. IL-6 (Interleukin 6)
E. IL-8 (Interleukin 8)
F. IFN-y (Interferon-y)

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A

IL-2 (Interleukin 2)

23
Q

Elicited by all immunogenic cells as mediator of acute phase response

Prolongs activated neutrophil survival

A. TNF-a (Tumor necrosis factor)
B. IL-1 (Interleukin 1)
C. IL-2 (Interleukin 2)
D. IL-6 (Interleukin 6)
E. IL-8 (Interleukin 8)
F. IFN-y (Interferon-y)

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A

IL-6 (Interleukin 6)

23
Chemoattractant for neutro, baso, esosinophils, lymphocytes A. TNF-a (Tumor necrosis factor) B. IL-1 (Interleukin 1) C. IL-2 (Interleukin 2) D. IL-6 (Interleukin 6) E. IL-8 (Interleukin 8) F. IFN-y (Interferon-y)
IL-8 (Interleukin 8)
24
Activates macrophages via TH1 cells that demostrate enhanced phagocytosis and microbial killing Found in wounds 5-7 days after injury A. TNF-a (Tumor necrosis factor) B. IL-1 (Interleukin 1) C. IL-2 (Interleukin 2) D. IL-6 (Interleukin 6) E. IL-8 (Interleukin 8) F. IFN-y (Interferon-y)
IFN-y (Interferon-y)
24
-NSAID prototype -MOA: Nonselective and irreversible COX inhibitor inhibiting both COX1 and COX 1 isoenzymes A. Aspirin (ASA) B. Ketorolac C. Indomethacin D. Celecoxib
Aspirin (Acetylsalicylic acid, ASA)
25
MOA: Anti-inflammatory effect is mediated by COX-2 inhibition via decreasing platelet production of TXA2, a potent stimulator of platelet aggregation A. Aspirin (ASA) B. Ketorolac C. Indomethacin D. Celecoxib
Aspirin (Acetylsalicylic acid, ASA)
26
Side effect of Aspirin (Acetylsalicylic acid, ASA) due to inhibition of COX-1 and thereby PG synthesis
Gi toxicity
27
Side effect is GI toxicity due to inhibition of COX-1 and thereby PG synthesis A. Aspirin (ASA) B. Ketorolac C. Indomethacin D. Celecoxib
Aspirin (Acetylsalicylic acid, ASA)
28
Uncoupler of oxidative phosphorylation and is associated with Reye syndrome in children A. Aspirin (ASA) B. Ketorolac C. Indomethacin D. Celecoxib
Aspirin (Acetylsalicylic acid, ASA)
29
Nonselective but reversible COX inhibitors A. Aspirin (ASA) B. Ketorolac C. Indomethacin D. Celecoxib
Ketorolac Indomethacin
30
Selective COX-2 inhibitor with a reduced risk of GI toxicity A. Aspirin (ASA) B. Ketorolac C. Indomethacin D. Celecoxib
Celecoxib
31
Hormonal response to injury Glucocorticoid steroid hormone released by the adrenal cortex in response to adrenocorticotropic hormone (ACTH) A. Cortisol B. Macrophage migration-inhibiting factor C. Growth Hormone (GH) D. Catecholamines E. Insulin
Cortisol
32
Hormonal response to injury Released is increased during times of stress and may be chronically elevated in certain disease process (burn-injured patients may exhibit elevated levels for 4 weeks) A. Cortisol B. Macrophage migration-inhibiting factor C. Growth Hormone (GH) D. Catecholamines E. Insulin
Cortisol
33
Hormonal response to injury Reduces transforming growth factor-beta (TGF-B) and insulin-like growth factor (IGF-1) so wound repair is impaired A. Cortisol B. Macrophage migration-inhibiting factor C. Growth Hormone (GH) D. Catecholamines E. Insulin
Cortisol
34
Hormonal response to injury Neurohormone that is stored and secreted by the anterior pituitary and by the intracellular pools within macrophages A. Cortisol B. Macrophage migration-inhibiting factor C. Growth Hormone (GH) D. Catecholamines E. Insulin
Macrophage migration-inhibiting factor
35
Hormonal response to injury A counter regulatory mediator that potentially reverses the anti-inflammatory effects of cortisol A. Cortisol B. Macrophage migration-inhibiting factor C. Growth Hormone (GH) D. Catecholamines E. Insulin
Macrophage migration-inhibiting factor
36
Hormonal response to injury Neurohormone expressed primarily by the pituitary gland that has both metabolic and immunomodulatory effects A. Cortisol B. Macrophage migration-inhibiting factor C. Growth Hormone (GH) D. Catecholamines E. Insulin
Growth hormone
37
Hormonal response to injury Exerts its downstream effects through direct interaction with GH receptors and secondarily through the enhanced hepatic synthesis A. Cortisol B. Macrophage migration-inhibiting factor C. Growth Hormone (GH) D. Catecholamines E. Insulin
Growth hormone
38
Hormonal response to injury Promote protein synthesis and insulin resistance and enhances mobilization of fat stores A. Cortisol B. Macrophage migration-inhibiting factor C. Growth Hormone (GH) D. Catecholamines E. Insulin
Growth hormone (GH) and Insulin growth factor (IGF-1)
39
Hormonal response to injury Include epinephrine, norepinephrine, and dopamine which have metabolic, immunomodulatory and vasoactive effects A. Cortisol B. Macrophage migration-inhibiting factor C. Growth Hormone (GH) D. Catecholamines E. Insulin
Catecholamines
40
Hormonal response to injury After sever injury, plasma levels of this hormones are increased 3-4x with elevations lasting 24-48h before returning to baseline levels A. Cortisol B. Macrophage migration-inhibiting factor C. Growth Hormone (GH) D. Catecholamines E. Insulin
Catecholamines
41
Hormonal response to injury Mediates an overall host anabolic state A. Cortisol B. Macrophage migration-inhibiting factor C. Growth Hormone (GH) D. Catecholamines E. Insulin
Insulin
42
Hormonal response to injury Are hallmarks of critical illness due to catabolic effects of circulating mediators including catecholamines, cortisol, glucagon and GH
Insulin resistance and hyperglycemia
43
Hormonal response to injury During critical illness has immunosuppresive effects and thus is associated with an increased risk for infection
Hyperglycemia
44
Hormonal response to injury This therapy to manage hyperglycemia decreased mortality and reduced in infections complications in select patient populations
Insulin therapy
45
CNS regulation of inflammation Nerve highly influential in mediating afferent sensory input to the CNS
Vagus nerve
46
CNS regulation of inflammation Parasympathetic nervous system transmits its efferent signals via this neurotransmitter
Acetylcholine
47
CNS regulation of inflammation Exerts homeostatic influences such as -enhancing gut mobility -reducing heart rate -regulating inflammation
Vagus nerve
48
CNS regulation of inflammation Allows for rapid response to inflammatory stimuli and also for the potential regulation of early proinflammatory mediator release specifically tumor necrosis factor (TNF)
Vagus nerve
49
CNS regulation of inflammation Inhibit cytokine activity and reduce injury from disease process
Vagus nerve
50
Burn patients may exhibit elevated levels of this hormone for 4 weeks
Cortisol
51
Plasma levels of this hormone are increased 3-4x lasting for 24 to 48 hours before returning to baseline after severe injury
Catecholamines

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