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
2
Q
the second line of defense in our body is_______
A
inflammatory response
3
Q
third line of defense in the body is
A
immune response
4
Q
what is considered inflammation
A
anything that causes damage or alteration to normal tissue is
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)
6
Q
What is the cellular response to acute inflammation?
A
removal of offending agents and damaged tissue
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
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.
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
10
Q
Increased permeability allows fluid into the inflamed tissue which therefore
A
dilutes the offending agent in the tissue
11
Q
What is the most common types of capillaries
A
continuous capillary
12
Q
what capillaries are found in the endocrine organs, intestinal walls, and choroid plexus
A
fenestrated capillaries
13
Q
Where are fenestrated capillaries found
A
in endocrine organs, intestinal walls, choroid plexus
14
Q
Where are sinusoid (discontinuous capillaries) found
A
bone marrow, liver, spleen
15
Q
give an example of immediate transient response and explain what it is
A
slapping, follwing minor injuries
16
Q
give an example of immediate sustained and explain what it is
A
broke ankle, following major injuries
17
Q
delayed hemodynamic example and explain what it is
A
sunburn/frostbite, 4-24 hours after injury before results occur
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
19
Q
What is the cellular response of white blood cells in inflammation
A
to move phagocytic WBCs into the area of the injury
20
Q
What are the two main types of phagocytic WBCs
A
granulocytes and monocytes
21
Q
What are cytokines
A
the cells that signal to the body that something is wrong (known as chemical mediators)
22
Q
What are selectins
A
acts as the velcro to stop the white blood cels to the point of inflammation (adhesion molecules)
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
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
25
How do leukocytes kill invading cells
through engulfment and phagocytosis.
26
once injury begins to heal the amount of _________ in that injury is decreased
cytokines
27
Once WBC get to the site of the injury what do they do
participate in phagocytosis and absorb and destroy pathogens or damaged cells
28
Neutrophil
-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.
29
What is the process of increasing circulation and creation of WBCs
leukocytosis
30
eosinophils
cells are especially elevated in allergic reactions and parasitic infections
31
basophils
cells are most reactive with general inflammation, allergic reactions and release histamine. found in blood
32
mast cells
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.
33
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 _____________________.
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.
34
macrophage v monocyte
monocyte is in blood and once it gets to the tissue its called a macrophage
35
What are the 5 cardinal signs of inflammation
heat, erythema, loss of function, pain, swelling.
36
erythrocytes job
transport of oxygen to tissues
37
thrombocytes job
AKA platelets
Help mediate vascular response
hemostasis and thrombosis
Release inflammatory mediators
38
endothelial cells job
key role in vascular response
synthesize and release inflammatory mediators
39
street cop (rapid response) =
fumigator (kills parasites) =
fireman (inflammation) =
riot police (longer lasting) =
signal man (relays info) =
special forces soldiers (specific target response) =
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)
40
The plasma protein system includes three main inflammatory mediators, what are they.
kinins (specifically bradykinin), clotting system (specifically thrombin), and complement (specifically C3a and C5a).
41
what is the role of kinins in the plasma protein system.
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.
42
What is the most important kinin in inflammatory response
bradykinin
43
What is the most important enzyme in the clotting system and why
thrombin allows expression of selectins (adhesion molecules) and produces prostaglandins, PAF, and chemokines
44
Explain complements in the plasma protein system (where are they found, what do they do, which are most important in inflammatory response)
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
What is histamine released by.
what is its job
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
Explain cytokines ( what are the main cytokines involved in inflammation, what types of cytokines are there)
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
Arachidonic Acid is a ________________ that is derived from __________ and is released when ____________ (_______)
the two pathways that arachidonic acid is released from are ______________ and ________________
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
What is the product of arachidonic acid broken down by lipoxygenase and what is the function of that product
Leukotrienes
Similar to histamine
vasc permeability, adhesion, chemotaxis, and further histamine realease
SRS-A
49
What is the product of arachidonic acid broken down by cylooxygenase and what is the function of that product
prostaglandins and thromboxane
prostaglandins induce vasodilation and bronchoconstriction and inhibits inflammatory cell function
thromboxane increases vasoconstriction bronchoconstriction and promotes platelet function.
50
What is the function of corticosteroids
to stop cell membrane phospholipids from being converted to arachidonic acid
51
what is the function of aspirin and NSAIDs
to prevent the cyclooxygenase pathway from being converted to prostaglandins and thromboxane.
52
What is the job of prostaglandins and what are the main prostaglandins
- 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
What is the job of thromboxane A2
to promote platelet aggregation and vasoconstriction.
54
What inhibits the enzyme used in the cyclooxygenase pathway for prostaglandin synthesis
NSAIDS and Aspirin
55
Is thromboxane a prostaglandin
apparently yes
56
What is the difference between histamine and leukotrienes
histamine is produced rapidly and is quicker to get to the inflammation site whereas leukotrienes are slower and show up later.
57
Explain a scenario in which Leukotrienes could cause a problem in the ER
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
What are leukotrienes also known as
slow-reacting substance of anaphylaxis. (SRS-A)
59
What is the main job of leukotrienes
increase adhesion of endothelial cells
chemotaxis, permeability, and SRS-A
increase histamine release
60
What is the difference between leukotriene receptor antagonists and 5-lipoxygenase inhibitors
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
Platelet Activaitng factor job
increases platelet aggregation, stimulates production of thromboxane (aka stimulates clotting mechanisms) and increases vascular permeability, neutrophil activation and eosinophil attraction.
62
what is the main job of NO nitric oxied
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
What are the five cardinal signs
erythema (redness, rubor)
heat (calor)
swelling (edema, tumor)
pain (dolor)
Loss of function.
64
Endothelial cells job
key role in vascular response
synthesize and release inflammatory mediators.
65
serous
exudate that is watery, lower in protein derived from plasma entering inflammatory site
66
sanguinous
thin, red or pink, watery, plasma with a few RBCs
67
fibrinous
large amount of fibrogen
thick, sticky meshwork
usually with large wounds
68
purulent/suppurative
pus (degraded WBCs, protein, tissue debris)
69
hemorrhagic
severe tissue injury causing damage to blood vessels or significant leakage of RBCs from capillaries (hematoma)
70
membranous/pseudomembranous
form on mucous membrane; necrotic cells in fibro purulent base
71
Inflammation is always considered an ____________
exudate
72
abscess
localized area of inflammation containing putulent exudates
often walled off from healthy tissue by fibroblasts
73
ulceration
necrotic, eroded area of epithelium with subepithelial inflammation (can be due to taumatic injury or vascular compromise)
74
Local V systemic manifestations
local says in one place, systemic travels to other parts of the body
75
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 ____________________
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
What causes fever also known as __________
"pyrexia"
IL-1, IL-6, TNF-a
77
increased number of leukocytes during acute phase response is mediated largely by _________
IL-1 as well as other cytokines
78
lethargy in acute phase response is mediated by actions of ______ and ______ on ____
IL-1 and TNF-a on the CNS
79
What are the main plasma proteins that are increased during the acute-phase response
C-reactive protein and fibrinogens
80
What is the job of CRP (c reactive protien in inflammation
To bind to the surface of invading microorganisms and aid in their destruction.
81
What could an elevated CRP be indicative of
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
What is he main job of fibrinigen
to increase the erythrocyte sedimentation rate.
83
What is the erythrocyte sedimenation rate
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
Why is anemic patieints have higher ESR
because they have less red blood cells so it takes less time for them to all settle at the bottom of the tube.
85
normal WBC range
10-12k
86
leukocytosis
the increased production of WBCs
87
neutrophilia is indicative of _________
bacterial infections
88
eosinophilia is indicative of
parasitic infection or allergic reaction
89
neutropenia and/or lymphocytosis is indicative of
viral infection
90
What is a left shift
an increased number of immature neutrophils in the blood at a site of infection
91
What is a left shift indicative of
an infection
92
Lymphadenitis (what is it and how does it present)
inflammatory reaction in lymph nodes that are draining infectious and/or necrotic fluids created by an injured or infected area.
swollen lymph node
93
lymphangitis
inflammation or infection of lymph channels fraining an injured area.
present by red, tender streaks that extend proximally along the lymph vessel
94
how are lymphangitis and lymphadenitis different
lymphangitis involves the lymph vessels and nodes whereas lymphadenitis involves just the nodes.
95
What is shock
life-threatening condition caused by lack of adequate circulation and oxygenation of the body
96
What are the major features of shock
-extremely _______________
-decreased ________________
-________________ skin
-____________________ (early is ________________ later on is ____________________)
-kidneys________________ and cause ______________
-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
what causes hyperventilation during shock
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
Why is there high heart rate during shock
heart rate increases to compensate for low blood pressure
99
This typeof shock is due to the inability of the heart to pump the required amount of blood.
cardiogenic shock
100
this type of shock is caused by decerased intravascular volume which leads to decreased perfusion of vital organs
hypovolemic shock
101
this type of shock is related to severe vasodilation causing loss of peripheral vascular resistance
distributive shock (this is not technically its own category but is an overarching ASK KB AND KC
102
what includes anaphylactic shock, neurogenic shock and septic shock.
distributive shock
103
severe, rapid allergic or hypersensitivity reaction with potential to be fatal is
anaphylactic shock.
104
damage to the autonomic pathways within the CNS is
neurogenic shock
105
systemic vasodilation secondary to infection and dysregulation of inflammatoy response is
septic shock
106
sudden loss of sympathetic stimulation to blood vessles > massive vasodilation > sudden extreme hypotension
neurogenic shock
107
What is septic shock caused by
Systemic inflammatory response syndrome (SIRS) which is a systemic uncontrolled inflammatory response mediated by IL-1 and TNF-a
108
What does SIRS lead to
excessive vasodilation, and direct cell death due to cells turning on themselves.
109
How does septic shock affect the organ systems:
circulatory - severe _________________
lungs - pulmonary _________-
gi tract - ______________
liver
kidney
nervous system
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.
