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acute inflammation and cardinal manifestations of disease Flashcards

1
Q

first line of defense in our body is ______ give examples

A

skin and the mucous membranes
tears, saliva, gut flora, stomach acid

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2
Q

the second line of defense in our body is_______

A

inflammatory response

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3
Q

third line of defense in the body is

A

immune response

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4
Q

what is considered inflammation

A

anything that causes damage or alteration to normal tissue is

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5
Q

What is the vascular response to inflammation

A

increased blood flow to the injury site and increased blood vessel permeability at the injury site (allows WBC RBC and nutrients out of the vessels and to the tissues that actuallly ned them)

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6
Q

What is the cellular response to acute inflammation?

A

removal of offending agents and damaged tissue

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7
Q

Vascular response enables cells in the body responsible for _________, _________, and _________ to travel to the site of injury. This begins ______________.

A

Vascular response enables cells in the body responsible for clotting, tissue repair, and immunity to travel to the site of injury. This begins almost immediately after injury

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8
Q

What are the two major anatomic changes to vessels that occur during a vascular response and what are they

A

increased dilation (which increases blood flow to area and enhances transport of blood and cells )and increased permeability which increases separation of intercellular junctions and increases permeability.

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9
Q

Why does the body initiate vasoconstriction prior to vasiodilation when inflammation occurs? This is termed ___________

A

to limit blood loss, this only lasts a few seconds or minutes, this is ermed transient vasocontriction

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10
Q

Increased permeability allows fluid into the inflamed tissue which therefore

A

dilutes the offending agent in the tissue

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11
Q

What is the most common types of capillaries

A

continuous capillary

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12
Q

what capillaries are found in the endocrine organs, intestinal walls, and choroid plexus

A

fenestrated capillaries

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13
Q

Where are fenestrated capillaries found

A

in endocrine organs, intestinal walls, choroid plexus

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14
Q

Where are sinusoid (discontinuous capillaries) found

A

bone marrow, liver, spleen

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15
Q

give an example of immediate transient response and explain what it is

A

slapping, follwing minor injuries

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16
Q

give an example of immediate sustained and explain what it is

A

broke ankle, following major injuries

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17
Q

delayed hemodynamic example and explain what it is

A

sunburn/frostbite, 4-24 hours after injury before results occur

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18
Q

what type of vascular response is the flu considered

A

an immediate sustained response because as soon as the cells recognize the flu in your body it will start kicking in inflammtion

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19
Q

What is the cellular response of white blood cells in inflammation

A

to move phagocytic WBCs into the area of the injury

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20
Q

What are the two main types of phagocytic WBCs

A

granulocytes and monocytes

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21
Q

What are cytokines

A

the cells that signal to the body that something is wrong (known as chemical mediators)

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22
Q

What are selectins

A

acts as the velcro to stop the white blood cels to the point of inflammation (adhesion molecules)

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23
Q

What happens once leukocytes (WBC) are stopped by the selectins

A

they migrate through the capillary wall. this is called diapedisis. this is occuring such as an ameboid during phagocytosis

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24
Q

once a leukocyte is on the other side of a capillary wall, what do they do

A

look for the most amount of cytokines so that the site of infection can be located

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25
Q

How do leukocytes kill invading cells

A

through engulfment and phagocytosis.

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26
Q

once injury begins to heal the amount of _________ in that injury is decreased

A

cytokines

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27
Q

Once WBC get to the site of the injury what do they do

A

participate in phagocytosis and absorb and destroy pathogens or damaged cells

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28
Q

Neutrophil

A

-first on scene
-arrive in 90 min, survive 10 hrs in tissue
-if inflammation persists and neutrophils are depleted immature neutrophils may be released called bands or left shift.

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29
Q

What is the process of increasing circulation and creation of WBCs

A

leukocytosis

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30
Q

eosinophils

A

cells are especially elevated in allergic reactions and parasitic infections

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31
Q

basophils

A

cells are most reactive with general inflammation, allergic reactions and release histamine. found in blood

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32
Q

mast cells

A

are parked in connective tissues and line mucosal tissues (lung , GI tract, dermis.). they are first line of defense for releasing histamin for anything hurting tissues

allergic and parasitic infections.
very similar to basophils except in connective tissue.

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33
Q

Give the 5 facts about monocyte:
1. largest ________
2. significantly longer lifespan than _________
3. arrive _____ hours after injury
4. predominant cell type _____ hours after injury
5. engulf larger and greater quantities of foreign material than ____________
6. play a role in _____________________.

A

Give the 5 facts about monocyte:
1. largest WBCs
2. significantly longer lifespan than PMNs
3. arrive 24 hours after injury
4. predominant cell type 48 hours after injury
5. engulf larger and greater quantities of foreign material than neutrophils
6. play a role in adaptive immune response.

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34
Q

macrophage v monocyte

A

monocyte is in blood and once it gets to the tissue its called a macrophage

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35
Q

What are the 5 cardinal signs of inflammation

A

heat, erythema, loss of function, pain, swelling.

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36
Q

erythrocytes job

A

transport of oxygen to tissues

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37
Q

thrombocytes job

A

AKA platelets
Help mediate vascular response
hemostasis and thrombosis
Release inflammatory mediators

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38
Q

endothelial cells job

A

key role in vascular response
synthesize and release inflammatory mediators

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39
Q

street cop (rapid response) =
fumigator (kills parasites) =
fireman (inflammation) =
riot police (longer lasting) =
signal man (relays info) =
special forces soldiers (specific target response) =

A

street cop (rapid response) = neutrophil
fumigator (kills parasites) = eosinophil
fireman (inflammation) = basophil
riot police (longer lasting) = macrophage
signal man (relays info) = dendritic cell
special forces soldiers (specific target response) = lymphocytes (B and T cells)

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40
Q

The plasma protein system includes three main inflammatory mediators, what are they.

A

kinins (specifically bradykinin), clotting system (specifically thrombin), and complement (specifically C3a and C5a).

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41
Q

what is the role of kinins in the plasma protein system.

A

They increase vasodilation and vascular permeability as well as smooth muscle contraction in some areas ( think of airway and gut contracton). It is also involved with pain response.

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42
Q

What is the most important kinin in inflammatory response

A

bradykinin

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43
Q

What is the most important enzyme in the clotting system and why

A

thrombin allows expression of selectins (adhesion molecules) and produces prostaglandins, PAF, and chemokines

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44
Q

Explain complements in the plasma protein system (where are they found, what do they do, which are most important in inflammatory response)

A

they are always present in plasma but are inactivated until one of them becomes activated and creates a chain reaction to all of the complements.

They increase vasodilation and vascular permeability, increase smooth muscle contraction, increase WBC activation, adhesion and chemotaxis, degranulates mast cells.

Key complements are C3a and C5a

45
Q

What is histamine released by.

what is its job

A

Released by Mast cells, basophils and platelets

one of the first mediator molecules to be released. major role in vascular inflammatory response via the H1 receptors (dont need to know details). increases vasodilation and vascular permeability

46
Q

Explain cytokines ( what are the main cytokines involved in inflammation, what types of cytokines are there)

A

includes chemokines, interferon (INFs), interleukins (ILs), lymphokines, and tumor necrosis factor (TNF)

The major ones are IL-1 and TNF-a which are major mediators of early inflammatory response. ( fever, adhesion of WBC, chemotaxis, pain response)

47
Q

Arachidonic Acid is a ________________ that is derived from __________ and is released when ____________ (_______)

the two pathways that arachidonic acid is released from are ______________ and ________________

A

Arachidonic Acid is a fatty acid precursor that is derived from phospholipids in the cell membrane and is released when there is damage to the cells (rupture, viral/bacterial infection)

The two pathways that it is released from is the cyclooxyrgenase pathway and the lipoxygenase pathway

48
Q

What is the product of arachidonic acid broken down by lipoxygenase and what is the function of that product

A

Leukotrienes

Similar to histamine
vasc permeability, adhesion, chemotaxis, and further histamine realease
SRS-A

49
Q

What is the product of arachidonic acid broken down by cylooxygenase and what is the function of that product

A

prostaglandins and thromboxane

prostaglandins induce vasodilation and bronchoconstriction and inhibits inflammatory cell function

thromboxane increases vasoconstriction bronchoconstriction and promotes platelet function.

50
Q

What is the function of corticosteroids

A

to stop cell membrane phospholipids from being converted to arachidonic acid

51
Q

what is the function of aspirin and NSAIDs

A

to prevent the cyclooxygenase pathway from being converted to prostaglandins and thromboxane.

52
Q

What is the job of prostaglandins and what are the main prostaglandins

A
  • increase vascular permeability and vasodilation
  • play a large role in pain response
    Prostaglandin E1 (PGE1 and Prostaglandin E2 (PGE2) increase potency of other inflammatory mediators especially histamine.
53
Q

What is the job of thromboxane A2

A

to promote platelet aggregation and vasoconstriction.

54
Q

What inhibits the enzyme used in the cyclooxygenase pathway for prostaglandin synthesis

A

NSAIDS and Aspirin

55
Q

Is thromboxane a prostaglandin

A

apparently yes

56
Q

What is the difference between histamine and leukotrienes

A

histamine is produced rapidly and is quicker to get to the inflammation site whereas leukotrienes are slower and show up later.

57
Q

Explain a scenario in which Leukotrienes could cause a problem in the ER

A

if a person comes in with severe asthma attackor allergy anaphyaxis, giving them an antihistamine drug will stop the reaction but sometimes this is only short term and the reaction will return worse a few hours later. This is because the leukotrienes later kick in and bring the reaction back even though the histamines are inhibited. Therefore if you need to give someone an antihistamine they probably need a leukotriene receptor agonist as well.

58
Q

What are leukotrienes also known as

A

slow-reacting substance of anaphylaxis. (SRS-A)

59
Q

What is the main job of leukotrienes

A

increase adhesion of endothelial cells
chemotaxis, permeability, and SRS-A
increase histamine release

60
Q

What is the difference between leukotriene receptor antagonists and 5-lipoxygenase inhibitors

A

leukotriene receptor antagonist doesn’t stop leukotrienes from being made, it just block them from interacting with the receptors. whereas 5-lipooxygenase inhibitors stop leukotrienes from being made at all.

61
Q

Platelet Activaitng factor job

A

increases platelet aggregation, stimulates production of thromboxane (aka stimulates clotting mechanisms) and increases vascular permeability, neutrophil activation and eosinophil attraction.

62
Q

what is the main job of NO nitric oxied

A

to work to counteract inflammatory mediators as things start to get better and less inflamed.

-promotes smooth muscle relaxation
- reduces leukocyte recruitment
-antagonizes platelet functions

63
Q

What are the five cardinal signs

A

erythema (redness, rubor)
heat (calor)
swelling (edema, tumor)
pain (dolor)
Loss of function.

64
Q

Endothelial cells job

A

key role in vascular response
synthesize and release inflammatory mediators.

65
Q

serous

A

exudate that is watery, lower in protein derived from plasma entering inflammatory site

66
Q

sanguinous

A

thin, red or pink, watery, plasma with a few RBCs

67
Q

fibrinous

A

large amount of fibrogen
thick, sticky meshwork
usually with large wounds

68
Q

purulent/suppurative

A

pus (degraded WBCs, protein, tissue debris)

69
Q

hemorrhagic

A

severe tissue injury causing damage to blood vessels or significant leakage of RBCs from capillaries (hematoma)

70
Q

membranous/pseudomembranous

A

form on mucous membrane; necrotic cells in fibro purulent base

71
Q

Inflammation is always considered an ____________

A

exudate

72
Q

abscess

A

localized area of inflammation containing putulent exudates
often walled off from healthy tissue by fibroblasts

73
Q

ulceration

A

necrotic, eroded area of epithelium with subepithelial inflammation (can be due to taumatic injury or vascular compromise)

74
Q

Local V systemic manifestations

A

local says in one place, systemic travels to other parts of the body

75
Q

What is the first phase of systemic manifestations and what occurs during this phase:

the “__________________”
-_________
-changed concentrations of ______________
-increased number of ____________
-_________
-Skeletal muscle ________ for _________
-increased ____________________

A

the acute-phase response
-fever
-changed concentrations of plasma proteins
-increased number of leukocytes
-lethargy
-skeletal muscle catabolism for amino acid production
-increased erythrocyte sedimentation rate (ESR)

76
Q

What causes fever also known as __________

A

“pyrexia”
IL-1, IL-6, TNF-a

77
Q

increased number of leukocytes during acute phase response is mediated largely by _________

A

IL-1 as well as other cytokines

78
Q

lethargy in acute phase response is mediated by actions of ______ and ______ on ____

A

IL-1 and TNF-a on the CNS

79
Q

What are the main plasma proteins that are increased during the acute-phase response

A

C-reactive protein and fibrinogens

80
Q

What is the job of CRP (c reactive protien in inflammation

A

To bind to the surface of invading microorganisms and aid in their destruction.

81
Q

What could an elevated CRP be indicative of

A

inflammation, however this is not always the case because it can increase due to many things such as stress, obesity, elderly, and lack of sleep.

82
Q

What is he main job of fibrinigen

A

to increase the erythrocyte sedimentation rate.

83
Q

What is the erythrocyte sedimenation rate

A

causes proteins to clump together faster than normal.
can be indicative of inflammation but sed rate changes slower than CRP

this test is how fast a patients RBCs settle at the bottom of the tube

84
Q

Why is anemic patieints have higher ESR

A

because they have less red blood cells so it takes less time for them to all settle at the bottom of the tube.

85
Q

normal WBC range

A

10-12k

86
Q

leukocytosis

A

the increased production of WBCs

87
Q

neutrophilia is indicative of _________

A

bacterial infections

88
Q

eosinophilia is indicative of

A

parasitic infection or allergic reaction

89
Q

neutropenia and/or lymphocytosis is indicative of

A

viral infection

90
Q

What is a left shift

A

an increased number of immature neutrophils in the blood at a site of infection

91
Q

What is a left shift indicative of

A

an infection

92
Q

Lymphadenitis (what is it and how does it present)

A

inflammatory reaction in lymph nodes that are draining infectious and/or necrotic fluids created by an injured or infected area.

swollen lymph node

93
Q

lymphangitis

A

inflammation or infection of lymph channels fraining an injured area.

present by red, tender streaks that extend proximally along the lymph vessel

94
Q

how are lymphangitis and lymphadenitis different

A

lymphangitis involves the lymph vessels and nodes whereas lymphadenitis involves just the nodes.

95
Q

What is shock

A

life-threatening condition caused by lack of adequate circulation and oxygenation of the body

96
Q

What are the major features of shock

-extremely _______________
-decreased ________________
-________________ skin
-____________________ (early is ________________ later on is ____________________)
-kidneys________________ and cause ______________

A

-extremely low blood pressure
-decreased urine output (oliguria
-pale, cool, clammy skin
-altered mental status (ealry is agitation/irritation later on is confusion, delerium and coma)
-kidneys excrete acid in urine and cause metabolic acidosis.

97
Q

what causes hyperventilation during shock

A

since kidneys are producing acid into urine and your body is not excreting urine you are increasing acid in body therefore metabolic acidosis. Your body then incerases ventilation to attempt to decrease the pH and blow off CO2

98
Q

Why is there high heart rate during shock

A

heart rate increases to compensate for low blood pressure

99
Q

This typeof shock is due to the inability of the heart to pump the required amount of blood.

A

cardiogenic shock

100
Q

this type of shock is caused by decerased intravascular volume which leads to decreased perfusion of vital organs

A

hypovolemic shock

101
Q

this type of shock is related to severe vasodilation causing loss of peripheral vascular resistance

A

distributive shock (this is not technically its own category but is an overarching ASK KB AND KC

102
Q

what includes anaphylactic shock, neurogenic shock and septic shock.

A

distributive shock

103
Q

severe, rapid allergic or hypersensitivity reaction with potential to be fatal is

A

anaphylactic shock.

104
Q

damage to the autonomic pathways within the CNS is

A

neurogenic shock

105
Q

systemic vasodilation secondary to infection and dysregulation of inflammatoy response is

A

septic shock

106
Q

sudden loss of sympathetic stimulation to blood vessles > massive vasodilation > sudden extreme hypotension

A

neurogenic shock

107
Q

What is septic shock caused by

A

Systemic inflammatory response syndrome (SIRS) which is a systemic uncontrolled inflammatory response mediated by IL-1 and TNF-a

108
Q

What does SIRS lead to

A

excessive vasodilation, and direct cell death due to cells turning on themselves.

109
Q

How does septic shock affect the organ systems:
circulatory - severe _________________
lungs - pulmonary _________-
gi tract - ______________
liver
kidney
nervous system

A

circulatory - severe hypotension and hypo perfusion
lungs - pulmonary edema and hypoxemia
GI tract - increased intestinal permeability allowing bacteria and bacterial endotoxins in gut to enter systemic circulation
liver - impaired elimination of bacteria and endotoxins
kidney - impaired filtration of toxins and waste products
nervous system - encephalopathy due to changes in cell signaling caused by inflammatory mediators.

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