WEEK 8 Inflammation Flashcards

1
Q

What is the best definition for inflammation

A

an immunologic defense against tissue, injury, or allergy.

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2
Q

the body’s reaction to injury, irritation, or infection characterized by redness, swelling, warmth, and/or pain; caused by accumulation of immune cells and substances around the injury or infection, this is known as what ?

A

inflammation

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3
Q

True or false. Inflammation is protective process initiated to or remove the pathologic agent or stimulus triggering the inflammation, and to promote healing

A

true

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4
Q

Inflammation is not always with infection , but it can also occur in the absence of infection

A

false, it’s always present with infection

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5
Q

what are the concepts connected with inflammation

A

infection
tissue integrity
thermoregulation
gas exchange
clotting
fatigue
stress
immunity

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6
Q

Scope of inflammation
inflammation can be

A

acute
chronic
repair/restorative

local or systemic

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7
Q

scope of inflammation triggers: Inflammation

A

mechanical trauma
thermal, electrical or chemical injury
radiation damage
biological assault ( infections )

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8
Q

We know that inflammation can be chronic o acute but what does repair/restorative mean ?

A

this means they are going to be both chronic and acute

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9
Q

generally if organ is involved it will be what type of inflammation?

A

it will be systemic

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10
Q

Which is acute and chronic ?

rolling an ankle
bowl disease

A

first is acute and second is chronic

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11
Q

would this be an example of acute systemic ?

pneumonia and appendicitis

A

yes both are true

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12
Q

Normal inflammatory response : the goal

A

the goal is to restore normal function of cells
and fibrous repair when cells can’t be restored

white blood cells and chemicals that serve to protect the body from invaders or cellular/tissue damage are involved

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13
Q

Protective mechanisms, certain cells cannot regenerated ( our cardiac muscle, brain cells )

A

this is true–> they cannot replace

scar tissue all over and over again when having a heart attack

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14
Q

types of white blood cells Granulocytes and Agranulocytes ( what are the categories under it )

A
  1. neutrophil ( helps in phagocytosis )
  2. eosinophil ( fights against parasitic infection)
  3. basophil ( produces inflammatory and allergic reactions)

Agranulocytes
4. lymphocyte ( produces specific immune responses)
5. Monocyte `( fights off bacteria viruses and fungi)

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15
Q

what are the 3 type of lymphocytes

A
  1. B lymphocytes
  2. T lymphocytes
  3. natural killer cell
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16
Q

immature neutrophils are called what ? and what can they not perform?

A

they are called bands and they canot perfrom endocytosis

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17
Q

how many days does bands turn into segmented ?

A

12 days

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18
Q

( agranulocytes) this is essentially in immune response, they keep calling for help ( operators) this is activated when there is inflammatory response.

A

true

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19
Q

mature neutrophils are called what?

A

segmented neutrophils

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20
Q

When injury has occurred this will occur and call for help, what is this being referred to?

A

chemotaxis ( realising pro inflammatory response)

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21
Q

a complex process involving more than a dozen different chemicals ( proinfalmamtory hormone)

A

chemotaxis

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22
Q

Chemotaxis is stimulated by :

A

bacterial or viral exotoxins

degenerative- by products of inflammation

products of complement system activation

reactive products of plasma clotting

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23
Q

True or false. White blood cells head to an inflammation when chemotaxis occurs

A

true

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24
Q

what are the 3 hormones linked to proinflammatory hormones ?

A

prostaglandins
histamines
cytokines

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25
The characteristics of Prostaglandin histamines an cytokines combined together
increase blood flow to the area of injury increase vascular permeability activate components of an immune response attract leukocytes to area of injury promote angiogenesis ( blood vessel creation making more blood vessels ) stimulate connective tissue growth ( talking about that repair) cause fever
26
basophil release ____ that is why we take antihistamine
histamines
27
give me an example of acute inflamattion
rolling the ankle
28
what is the stage one acute inflammation?
vascular response
29
what do you have to think of when thinking about stage one : vascular repsonse?
think of blood focus response
30
name what undergoes stage one vascular response
injured tissues and local granulocytes and tissue masts secrete pro inflammatory hormones - small veins constrict and arterioled dilate - blood flow increases delievering nurtrients, ( oxygen and glucose) to injured tissues
31
What is a tissue masts ?
this is a type of connective tissue glucose site ( they are involve in throwing off pulmonary hormone to help the response)
31
what are the clinical manifestations of stage one vascular response?
- hyperemia/redness, warmth
32
True or false. Stage one vascular response causes capillary to leak/permeability?
this is true
33
true or false in stage one vascular response it Causes our capillaries to leak our plasma fluid out ( our plasma is now leaking in the vascular intersial space)
true
34
True or false. Define if this is true in terms of the characteristics amongst stage one vascular repsonse. Tons of blood flow going constricting that blood return, the blood flow is going to increase ( this is going to heal)-> we use oxygen for atp, glucose for energy replace for those that needs it.
true
35
Does macrophages not secrete pro-inflammatory hormones ? in stage one vascular repsonse
false, it does secrete it
36
Mature WBC's are quicker and promote neutrophil invasion. 12 days of maturing will be 12 hours instead, because it's quick.
true
37
When inflammation is occurring, how can we simplify that explanation ?
increased blood flow--> leakage of plsma proteins= edema --> neutrophil emigration
38
What is occurring in stage two cellular response?
granulocytes and tissue mast cells become activated ) neutrophils occurs) 12 hrs after injury -phagocytosis
39
what promotes continuous inflammatory response in stage two cellular response?
eosinophils,basophils, and mast cells
40
True or false. Stage two : cellular response does not exudate forms ?
false, it does
41
What are the clinical manifestations of stage two : cellular response
dead WBCs, necrotic tissue, leaked cell fluid
42
This is telling neutrophils to mature and head out ( they are going to cause phagocytosis) , where does this occur?
stage two: cellular response
43
Macrophages increase and stimulate monocyte production in stage two cellular response, is that true or false?
that is true
44
What type of cascade occurs in stage 2 cellular response? and what does it increase ?
arachidonic acid cascade, it increases inflammation
45
Fill in the blanks : Stage two : cellular response Fatty acids in memebranes of injured cells turn into arachidonic acid which is then converted by ______ enzyme into subtances histamine ______, prostaglandins, ____ , _____ that promote inflammation
COX , leukotrines, serotonin, kinins ( protein in the blood that cause inflammation and affect bp).
46
TRUE OR FALSE. ibuprofen stops COX from getting worse?
this is true
47
This occurs stimulaneously with stage one vascular response and stage two cellular response ( scar tissue is no longer functional, there is a 'bandaid')
this is stage three : tissue repair and replacement
48
Characteristics of stage 3 : tissue repair and replacement
1. all white blood cells invovled start the replacement of lost/damaged tissues by stimulating healthy cells to divide 2. White blood cells trigger blood vessel growth and scar tissue formation for those cells that cannot divide - function of these cells are lost
49
true or false: healing can only occur if inflammation occurs
true!!!
50
this starts as an acute inflammation
chronic inflammation
51
this is diffuclt to detect, may feel run down, tired, achy, and no symptoms ( asymptomatic)
this is a chronic inflammation
52
true or flase. Chronic inflmmation is a pronlonged inflmmation and the star here is neutrophils!
false, although it is a prolonged inflmmation, macrophages are the star!
53
what is a type of phagocyte?
macrophage
54
What does macrophages release in chronic inflmmation?
release tissue thromboplastin--facilitates hemostasis, promotes fibroblasts - removes necrotic tissue and pathogens ( debridement ) continous release
55
Select all that is true in terms of chronic inflammation Thickening and scarring of connective tissue may also be subclinical - no overt symptoms - more systemic manifestations - investigate through blood tests: CPR and ESR -may need a WBC scan to identify areas of inflammation
all is true
56
what does hemostais and fibroblasts do in chronic inflmmation?
hemostasis= stop bleeding fibroblasts = making more scar tissue
57
when investigating an inflmmation for acute and chronic which blood tests are we giving for the apteint for acute and chronic ?
acute CPR c - reactive protein chronic ESR euthrocyte sedementation rate
58
Outcomes of acute inflammation Select all that is true vascular changes neutrophil recruitment mediators Injury that can occur Infraction bacterial infections toxins trauma
they are all true
59
what is the resolution for acute inflammation?
clearance of injurious stimuli clearance of mediators and aucte inflmmatory cells replacement of injured cells normal function
60
Define if these charcateristics are true in terms of chronic inflammation angiogenesis mononuclear cell infiltraete fibrosis ( scar) injury : - viral infections chronic infections persistent injury autoimmune diseases
they are all true
61
name the clinical manifestations for local response vs systemic repeponse ( how do we determine if it's localize or systemic)
1. extensiveness 2.location 3.dependent on pateint's immune response 4. dependent on acute vs chronic
62
True or false. Location matters when determining sytsemic or local as we would need a good neutrophils system to help rejevunate healing.
true
63
Proinflmamtory hormone explains the clinical maifestations of local response ?
yes it does
64
If it's not open , you can see exudate. True or false?
false, if its not open you cannot see exudate, since exudate means you can see leakge ( pus ) etc.
65
You have to visualize this on the outside
this is a local response
66
Local response : what are the charcateristics
swelling pain heat redness exudate/impaireed function serous/fibrinous/purulent/hemorrhagic
67
This is typically seen witch chronic inflammation pateints
systemic response
68
what are the characteristics of systemic response?
neutrophilia ( abnormally high nuetrophils in the body) fever malaise loss of apetite muscle catabolism
69
why do you have a fever when having a chronic inflammation pateint in systemic repsonse?
because this is your pro inflammatory response
70
What occurs when you loss petite in systemic response ?
we are gonna ahve muscle loss
71
Whata are the assessment ( nursing process) in terms of inflammation
history physical assessment diagnostics
72
go more in depth of physical assesment when assesing a patient with inflammation
look for trauma check for colour temeprature pain swelling look for any drainage ( what you see, smell)?
73
WHat undergoes diagnosis when assessing a patient with inflmmation?
radiographic blood
74
Why are these important when assessing? Vital signs Blood work
vital signs can detect that fever tieing to that inflammation blood work if they have neutrophil change
75
Trueor false. Anemia causes you to have loss of apetite and not having a good diet, which causes to be more prone to chronic inflammation?
true
76
who's more prone to getting inflammation in terms of population?
older adults and babies ( have no antiboodies yet) and they are a bit more fragile
77
Name the the different inflammation blood work values we look at
WBC total segmented bands monocytes lymphocytes eosinophils basophils hemoglobin
78
How can we stop inflammation from stoping to the first place ( select all that is true) a. eat well b. take care of yourself c.hand hygiene d. safety
these are all true
79
what are the clinical management for inflammation
primary prevention ( eat well, hand hygiene, safety, etc) Secondary prevention- screening ( there is no screening ) collaborative approaches
80
What undergoes collaborative interventions in clinical management ( inflammation)
goals : mediate inflammatory process and promote healing and repair treat underlying cause
81
Define all that when treating the underlying cause of inflammation Infection-eliminate cause hypersensitivity response - only manage inflammation Sprain/Strain: Rice and NSAIDS Chronic-monitor to prevent further tissue damage, treat cause, support ongoing tissue function, medications ( type 1 diabetes, provide insulin)
2nd one is wrong, yes u have to manage the inflammation, however you also have to manage the pathologic issue ( e.g DM, RA, MS)
82
What does rice stands for ?
Rest on ice compression on elevation
83
Characteristics of RICE
first 24-48 hours after injury Rest to prevent further reinjury and trigger inflmmation ce for 10 minutes at a time every 2-3. hours
84
True or false. Using the Rice methods, we use comprehension to reduce swelling
true
85
Why do we elevate above level when using the RICE method?
we elevate above level of heart to minimize swelling
86
What are the Pharmacology therapy we use to reduce inflammation, manage fever, and pain relief when dealing
Reduce inflammation - steroidal agents - glucocorticoids- prednisone Non-steroidal anti- inflammatory drugs (NSAIDS) - ibuprofen Manage fever - antipyretics 1) acetaminophen 2) aspirin 3) NSAIDs Pain Relief -analgesics 1) acetaminophen 2)aspirin 3) NSAIDS 4) OPIOIDS ( if pain is severe)
87
This is given but side effects is bleeding, this is at the bottom of managing fever ( as a lot of side effects)
aspirin
88
What stops the COX enxyme?
Ibuprofen
89
What is the difference in the MOA of presidone vs. NSAIDS
steroids is either life or death ibuprofen has side effects ( renal, and liver)
90
Define if these characteristics are true or false within the Prednisone You want to use this long term to avoid the inflammation coming back When administering the medication, we follow up frequently to make sure the effects are controlled as possible
the first one is wrong, we use this for a short term but in a high dose
91
What are we monitoring when taking Prednisone
fluid retention blood pressure ( making sure weights , sodium ) and if they have fluid or no fluid in the body
92
DRUG CARD : Corticosteroids : Prednisone
MOA: Decrease inflammation through suppressing immune responses ( inhibit macrophage accumulation, reduce capillary permeability ) Administration Do not stop abruptly, must be tapered slowly Give with or after meals to prevent GI upset Indiciations : Severe allergic conditions endocrine disorders respiratory disorders Contraindication: active untreated infections Drug to drug: use with caution with NSAIDS/ASA (GI side effects increased )
93
what are the side effects of Prednisone
CVS: fluid retention- HTN Endo: adrenal insufficient Gi: peptic ulder Psych: mood disturbances, depression, psychosis, insomnia Labs: hyperglycaemia long term : cushings
94
What type of prednisone do we use if it's systemic and localize?
pill for systemic and lotion for localized
95
true or false. Prednisone can be taken oral and iv as well
true, iv causes more side effects tho
96
Define if this these statements are true in the therapeutic effects of prednisone less likely to see results however for active inflammation it can reduced inflammation ( if lungs-reduced brochical inflammation revealing improved work of breath, reduced wheezing and reduces mucus production for treatment for endocrine disroder : reduced active disease ( addisons's )
both are true
97
Sudden withdrawal and adrenal crisis : corcotocoids is not important in our body?
false, it is
98
What is controlled by the release of ACTH (Adrenocorticotropic hormone)from pituitary glad through negative feedback ?
adrenal galnds
99
Sudden withdrawal and adrenal crisis define the characteristics
negative feedback : exogenous control suppresses pituitary release of ACTH and suppresses production of natural cortisol by adrenal glands Adrenal crisis - hypotension seizure shock flu symptoms - therapy is kept short term ( less than 10 days) if long term, may give eod: requires dose to be tapered as it is discontinued so adrenals resume production
100
Where does adrenal crisis results from ?
results from sudden withdrawal such as hypotenesion, flu symptoms, seizures, shock
101
is inflammation the agent causing the injury as seen with infection?
no it is a protective factor
102
what kind of inflammation is this? Inflammation that continues for weeks to years after the initial injury
chronic
103
what are the four categories of chemotaxis?
(1) bacterial or viral exotoxins, (2) degenerative by-products of inflammation, (3) products of complement system activation, and (4) reactive products of plasma cloing in the inflamed area.
104
what is the source and inflammatory response for bradykinin?
Source: plasma protein and kinins inflammatory response: Increase vascular permeability and vasodilation responsible for pain production
105
what is the inflammatory response prostaglandins do?
mediate late stages of acute inflammatory response increase vasodilation increase vascular permeability active in anaphylactic hypersensitivity reactions
106
where is the source and inflammatory response to histamine?
mast cells mediates early acute inflammatory response
107
what term is this describing? this is essentially when an alarm goes off when the White blood cells are notified, singing "clean up clean up everything do your share"
chemotaxis
108
what does Arachidonic acid cascade do? what stage does it fall under?
this is responsible for anti and pro inflammatory process, falls under stage 2: cellular response
109
what stage of inflammation does this fall under? ■ Fatty acids in membranes of injured cells turn into arachidonic acid which is then converted (by COX enzyme) into substances (histamine, leukotrienes, prostaglandins, serotonin, kinins) that promote more inflammation
stage 2: cellular response
110
what does the scope of inflammation range from?
from no inflammation to active inflammation localized or systemic
111
true or false: Inflammation is a process involving white blood cells (WBCs) and a number of different chemicals that serve to protect the body against invading pathogens or cellular/tissue trauma.
true
112
what are prostaglandins, cytokines and histamines known for?
they are the three major hormone groups (pro inflammatory)
113
true or false: the proinflammatory hormones increase blood flow to the injured area, increase vascular membrane permeability, activate various components of an immune response, removes leukocytes to the area of injury, promote angiogenesis, stimulate growth of connective tissue, and cause fever.
false it attracts leukocytes
114
when does this occur in acute inflammation Release of nitric oxide and prostacyclin, endothelin, thromboxane A2, angiotensin II, growth factor, and chemokines from activated endothelial cells
the last step
115
true or false: Neutrophils are of significant importance in an acute inflammatory response.
true
116
true or false: The chemotaxic factors bind to the surface of the neutrophils and cause them to release additional factors, resulting in pathogen breakdown from lysosomal cytoplasmic enzymes. The neutrophils are also directly involved in phagocytosis after they bind to antibodies already connected to the antigen.
true
117
true or false: macrophages are critical in a chronic inflammatory response.
true
118
true or false: The liver will respond by releasing a number of proteins, called acute phase proteins, that include complement system proteins, cloing factors, and protease inhibitors.
true