Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Block 7 Week 4 > Acute Phase response and fever-Hunter > Flashcards

Acute Phase response and fever-Hunter Flashcards

1
Q

The host response to invading microbes begins with recognition of (Blank) by (blank) on macrophages and other innate immune cells.

A

PAMPs (pathogen associated molecular patterns)

PRRs (pattern recogntion receptors)

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

Microbes also cause tissue damage which elicits (blank) patterns

A

damage-associated molecular patterns

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

Once you have PAMPs and DAMPs what happens next?

A

a variety of secreted inflammatory mediators are produced that orchestrate the initial response to infection or tissue damage.

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

Mediators like (blank) change the properties of vascular endothelium, prompting an increase in vascular permeability, vasodilation, upregulation of adhesion molecules and clotting.

A

TNF-alpha

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

Most responses to pathogens remain (blank)

A

local

some responses are systemic

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

Some systemic inflammatory responses to pathogens can be positive and protective such as (blank). Other systemic responses can be negative and harmful such as (blank)

A

acute phase response and fever

sepsis and septic shock

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

Where do you find this PAMP:

f-met-leu-phe receptor

A

Bacteria

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

Where do you find this PAMP:

mannose receptor

A

bacteria, fungi, viruses

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

Where do you find this PAMP

scavenger receptors

A

acetylated lipoproteins on bacteria

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

Where do you find this PAMP

dectin-1 glucan receptor

A

fungi

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

Where do you find this PAMP

LPS binding protein and CD14

A

bacteria

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

Pathogens cause (blank) to release various mediators of inflammation.

A

macrophages

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

Activation of the kinin system produces (blank)

A

bradykinin (pain)

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

Cytokines produced by macrophages cause (blank) of local small blood vessels

A

dilation

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

Leukocytes move to periphery of blood vessel as a result of increased expression of (blank)

A

adhesion molecules

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

Once leukocytes move to periphery of blood vessel and adhere what do they do next?

A

leukocytes extravasate at site of infection and blood clotting occurs in the microvessels

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

Summarize what happens if you get trauma resulting in a bleed

A

blood vessel dilation and increased vascular permeability

  • upregulation and expression of adhesion molecules
  • local coagulation in microvessels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

(blank) cytokines released by macrophages in response to microbial produts have both local and systemic effects

A

Proinflammatory

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

On sensing microbial products, macrophages secrete a variety of pro-inflammatory cytokines. What are they?

A 
IL-6
TNF alpha
IL-1B
CXCL8
IL-12
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What does TNF alpha do locally?

A

activates vascular endothelium and increases vascular permeability which leads to increased entry of complement and cells to tissues and increased fluid drainage to lymph nodes

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

What does IL-Ib do locally?

A
  • activates vascular endothelium
  • activates lymphocytes
  • local tissue destruction
  • increases access of effector cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What does CXCL8 do locally?

A

chemotactic factor that recruits neutrophils and basophils to site of infection

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

What does IL-12 do locally?

A

activates NK cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the systemic effects of IL-6?

A

fever

induces acute-phase protein production by hepatocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the systemic effects of TNF-alpha?

A

fever, mobilization of metaboites, shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the systemic effects of IL-1b?

A

fever, production of IL-6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What mediates the acute phase response and fever?

A

cytokines! (IL-6, TNF-alpha, IL1b)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

(blank) (blank) and (blank) are the principle cytokines that mediate the systemic effects of inflammation

A

IL-1, IL-6, TNF-alpha

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

(blank) is predominantly involved in the acute phase response in the liver

A

IL-6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

(blank) and (blank) are involved in the induction of fever

A

IL-1, TNF-alpha

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What does IL-1, IL-6, and TNF-alpha do to the liver?

A

acute phase proteins (c-reactive protein, mannose-binding lectin)
-> activation of complement opsonization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What does IL1, IL6, TNF alpha do to the bone marrow and endothelium?

A

neutrophil mobilization-> phagocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What does IL1, IL6 and TNF alpha do to the hypothalamus?

A

increases body temp and results in decreased viral and bacterial replication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What does IL1, IL6 and TNF alpha do to the fat, muscle?

A

protein and energy mobilization to generate increased body temp-> resulting in decreased viral and bacterial replication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

(blank) is predominantly involved in the acute phase response in the liver

A

IL-6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

(blank) and (blank) are involved in the induction of fever

A

IL-1, TNF alpha

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the acute phase response?

A

a systemic reaction to disturbances in homeostasis caused by infection, tissue injury, trauma or surgery, neoplastic growth, or immunological disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

The APR (acute phase response) is orchestrate by the proinflammatory cytoknes (blank, blank, blank) and other mediators produced by macrophages and other cells

A

IL-1, IL-6, TNF alpha

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

APR involves changes in plasma levles of acute phase proteins, many produces in the (blank) in response to IL-6

A

liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

In the acute phase response, what proteins are increased?

Which are decreased?

A

Positive acute phase proteins -> increased

negative acute phase proteins-> decreased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

The “positive” APP are regarded as have general functions in….?

A
  • opsonization and trapping of microorganisms
  • activating complement
  • coagulation and fibrinolysis
  • scavenging free hemoglobin and iron
  • neutralizing enzymes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Negative APP decrease in (blank)

A

inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are some negative APPs?

A

albumin, transferrin, transthyretin, retinol-binding protein, antithrombin, transcortin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What does C-reactive protein do?

A

opsonin on microbes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What does mannan-binding lectin do?

A

mannan-binding lectin pathway of complement activation

46
Q

What does fibrinogen, prothrombin, factor 8, von willebrand factor do?

A

coagulation factors, trapping invading microbes in blood clots

47
Q

What does ferritin do?

A

binding iron, inhibiting microbe iron uptake

48
Q

What does alpha-1-antitrypsin do?

A

serpin, downregulates inflammation

49
Q

What family does C-reactive protein (CRP) belong to?

A

pentraxin family

50
Q

What does CRP bind to in the cell membranes of microorganisms (including lipopolysacchardies of gram-neg bacteria)

A

phosphocholine

51
Q

How does CRP promote opsonization?

A

by binding C1q, triggering the classical pathway of complement activation and generating C3b

52
Q

CRP is normal present at (blank) levels in the plasma but can (blank) 50,000 fold during the inflammation-induced acute phase response

A

low

increase

53
Q

Measurement of CRP is used clinically as a good diagnostic marker of (blank)

A

systemic inflammation

54
Q

Inflammation associated coagulation begins when cytokines, TLR agonists or other stimuli induce (Blank) expression on the surfaces of monocytes and vascular endothelial cells

A

Tissue factor

55
Q

How do you get the procoagulant effects of the acute phase response?

A
  • increased plasminogen activator inhibitor (PAI-1)

- hepatic synthe of protein C and AT-III decreases

56
Q

What does plasinogen activator inhibitor do?

A

inhibits plasmin formation thus inhibits fibrinolysis :)

57
Q

What is the end result of the procoagulant effects of the acute phase?

A

increased thrombin activity and decreased fibrinolysis, which promotes fibrin formation and thrombosis

58
Q

In the acute phase response, (blank) molecules are also produced

A

anti-inflammatory

59
Q

The acute phase response increases the blood concentrations of numerous molecules that have (blnk) actions

A

anti-inflammatory actions

60
Q

Blood levels of (blank) can inhibit the binding of IL-1 to its receptors

A

IL-1 receptor antagonist

61
Q

High levels of soluble (blank) neutralize TNF-alpha that enters the circulation

A

TNF-alpha receptors

62
Q

(blank) hormones downregulate the immune response

A

Neuroendocrine hormones (cortisol, ACTH, epi, alpha MSH)

63
Q

What are protease inhibitors or antioxidants?

A

acute phase proteins that neutralize potentially harmful molecules released from neutrophils and other inflammatory cells

64
Q

What are the ways that the acute phase respone can cause anti-inflammatory effects?

A
  • IL-1 antagonists
  • high levels of soluble TNF alpha receptors
  • neuroendocrine hormones
  • protease inhibitors or antioxidants
65
Q

The acute phase response engages the (Blank) reflex

A

inflammatory

66
Q

The nervous system interacts with the immune system through the (blank)

A

inflammatory reflex

67
Q

Inflammatory mediators produced by infection or injury activate sensory neurons traveling to the brainstem in the (Blank)

A

vagus nerve

68
Q

When you get an injury and sensory neurons of the vagus send a signal the brain about this, what happens?

A

action potentials are generated from brainstem to the spleen and other organs

69
Q

The action potentials produced by the brainstem will synapse with (blank) to activate these cells to release the neurotransmitter (blank)

A

T lymphocytes

acetylocholine

70
Q

(blank) binds to receptors on macrophages and stimulates an intracellular signaling pathway that blocks secretion of (blank)

A

Acetycholine

inflammatory mediators like TNF-alpha

71
Q

Body temp is a vital sign that is controlled by the (blank)

A

hypothalamus

72
Q

Neurons in both the preoptic anterior hypothalamus and posterior hypothalamus received 2 kinds of signals, what are they?

A
  • one from peripheral nerves that transmit info from warm/cold receptors in the skin
  • one from the temp of blood bathing the region
73
Q

The 2 signals sent to the hypothalamus are integrated by the (blank) of the hypothalamus to maintain normal temp (hypothalamic set point)

A

thermoregulatory center

74
Q

What is the mean oral temp and when do you have the lowest temp? highest?

A

36.8 C (98.2 F)
6 AM
4-6 PM

75
Q

Fever is defined as a temp in the morning greater than (Blank) or a temp in the afternoon greater than (blank)

A
  1. 2 (98,9)

37. 7 (99.9)

76
Q

Fever is an elevation of normal body temp caused by resetting of the (blank)

A

hypothalamic set point

77
Q

Once the hypothalamic set point is raised neurons in the (blank) are activated and (blank) commences

A

vasomotor center

vasoconstriction

78
Q

A febrile individual first notices vasoconstriction in the (blank) and (Blank).

A

hands and feet

79
Q

Why do you feel cold when you have a fever? When do you get shivering

A

you get vasoconstriction in hands and feet and blood is shunted from periphery to internal organs.
At this time

80
Q

For most fevers caused by infections, body temp only increases (blank) degrees celcius.

A

1-2

81
Q

The term (blank) is used to describe any substance that causes fever

A

pyrogen

82
Q

(blank) are derived from outside the patient; most are microbial products, microbial toxins, or whole microorganisms

A

Exogenous pyrogens

83
Q

The classic example of an exogenous pyrogen is the (blank) produced by all gram-negative bacteria.

A

LPS (endotoxin)

84
Q

Pyrogenic products of gram- positive organisms include the enterotoxin of (Blank) and the group A and B streptococcal toxin also called (blank)

A

Staph aureus

superantigens

85
Q

Some cytokines also cause fever; formerly referred to as endogenous pyrogens, they are now called (blank)

A

pyrogenic cytokines

86
Q

What are the pyrogenic cytokines?

A

IL1, IL6, TNF apha, ciliary neutropic factor (CNTF), nd interferons-a/b

87
Q

A wide spectrum of bacterial, fungal, viral and parasitic products induce the synthesis and release of (blank)

A

pyrogenic cytokines

88
Q

(blank) can be a manifestation of disease in the absence of microbial infection (e.g inflammatory processes, trauma, tissue necrosis, and antigen-antibody complexes); these processes also trigger the hypothalamus to raise the set point to febrile levels

A

fever

89
Q

What is a FUO?

A

fever of unknown origin

90
Q

(blank) and (blank) can reset the hypothalamic thermal set point

A

Pyrogenic cytokines and microbial products

91
Q

Pyrogenic cytokines mediate the coordinate induction of (blank) and microsomal (blank) in the endothelium of blood vessels in the preoptic hypothalamic area to form the arachdonic acid metabolite PGE2

A

COX-2

PGE synthase-1 (mPGES-1)

92
Q

What does PGE2 do?

A

triggers EP-3 receptors on glial cells and this stimulation results in the rapid release of cyclic AMP

93
Q

What does cyclic AMP do?

A

changes the hypothalamic set point via activation of neurons in thermoregulatory center

94
Q

What type of distinct receptors are located on the hypothalamic endothelium?

A

PAMPs and DAMPs

95
Q

Binding of PAMPs and DAMPs also results in (blank) production and upregulation of the (Blank)

A

PGE2

hypothalamic set point

96
Q

So give me a quick breakdown how you get a fever

A

Endotoxin, inflammation. pyrogenic stimuli-> monocytes, macrophages, kupffer cells release cytokines-> preoptic area of hypothalamus->prostaglandins released-> raise temp set point-> fever

97
Q

A team of investigators has designed a new drug that lowers fever by blocking the formation of this key arachidonic acid metabolite responsible for resetting of the hypothalamic set point.

A

PGE2

98
Q

Reducing the level of (blank) in the thermoregulatory center lowers the elevated hypothalamic set point

A

PGE2

99
Q

The synthesis of PGE2 depends on the consitutively expressed enzyme (blank), and the antipyretic drugs inhibit brain (blank)

A

cyclooxygenase

cyclooxygenase

100
Q

What are good antipyretics?

A

acetaminophen, aspirin NSAIDS, COX-2 inhibitors

101
Q

Chronic high-dose therapy with antipyretics such as aspirin or any NSAID (does/does not) reduce normal core body temp.

A

Does not, so does not affect normal thermoregulation

102
Q

Glucocorticoids are (Blank) and work by reducing PGE2 synthesis by inhibiting the activity of (blank) which is needed to release arachidonic acid from the cell membrane.

A

antipyretics

phospholipase A2

103
Q

Glucocorticois block the transcription of the (blank) for the pyrogenic cytokines

A

mRNA

104
Q

A 5-year boy with no history of immunization presents with an exanthematous skin rash. You notice the presence of Koplik spots in the buccal mucosa and make the diagnosis of measles. He has a fever of 38.5° C and is very uncomfortable, so you recommend acetaminophen to lower his fever. Which of the following enzymes is inhibited by acetaminophen, aspirin, and other non-steroidal anti-inflammatory drugs?

A

Cyclooxygenase (COX)

105
Q

What is a fever awesome?

A

kills pathogens! Also can help with anthrax, pneumococcal pneumonia, leprosy, and various fungal, rickettsial and viral diseases.

106
Q

Before the advent of antibiotics, fevers were artificialy induced for the treatment (blank) and proved to be beneficial

A

neurosyphilis

107
Q

(blank) production is increased when body temp is elevated

A

antibdy

108
Q

When does a fever become a bad thing? What do you call this?

A

with a rectal temp greater than 41.5 C (greater than 106.7 F)
-hyperpyrexia

109
Q

When does hyperpyrexia usually occur?

A

with CNS hemorrhages (can also occur w. sever infections)

110
Q

When the temp is over (blank), heat stroke develops and death is common

A

43 degrees C

Block 7 Week 4 (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions