Acute Inflammation And Cardinal Manifestations Of Disease Flashcards
1
Q
What is the first line of defense?
A
Skin and mucous membranes, tears, saliva, gut flora, and stomach acid
2
Q
What is the second line of defense?
A
Inflammatory response that is not specific to injury and acute inflammation
3
Q
What is the third line of defense?
A
The immune system
4
Q
What is etiology
A
Cause
5
Q
What are some etiologies of acute inflammation
A
Microorganisms, hypoxia/ischemia, nutritional deficiencies, trauma/surgery, radiation, caustic chemicals, and extreme heat/cold
6
Q
What are the 2 major components of acute inflammation?
A
Vascular response and cellular response
7
Q
What happens in vascular response?
A
Increased blood flow to injury site and increased blood vessel permeability at the injury site
8
Q
What is the function of the cellular response?
A
Removal of offending agent and damaged tissue
9
Q
Why is the vascular response important in inflammation?
A
It enables cells in the body responsible for clotting, tissue repair, and immunity to travel to the site of injury
10
Q
What are the specific physiological phenomenon that occur in the vascular response
A
-transient vasoconstriction
vasodilation to increase blood flow to the area and enhance transport of blood and cells
-the endothelial cells lining vessels contract to increase the permeability
-increased permeability allows plasma and cells to travel into the injured tissue
-exudation of fluid dilutes the offending agent
-flow in vessels decreases to slow the spread of offending agent
-clotting elements move to the injury site
11
Q
What are the 3 types of capillaries?
A
Continuous capillaries- most common type
Fenestrated capillaries- little holes, present in endocrine organs, intestinal walls, and choroid plexus
Sinusoids- big gaps to let bigger cells out, present in bone marrow, liver, and spleen
12
Q
What are the three major patterns of vascular responses?
A
Immediate transient, immediate sustained, and delayed hemodynamic
13
Q
When does an immediate transient vascular response occur?
A
Following a minor injury, resolves quickly
14
Q
When does a immediate sustained pattern of vascular response occur?
A
Following a major injury, lasts longer
15
Q
When does a delayed hemodynamic pattern of vascular response occur?
A
4-24 hours after an injury
16
Q
What occurs during the cellular response?
A
Phagocytic white blood cells move into the injury site (granulocytes and monocytes)
17
Q
What are the four steps of cellular response?
A
Margination/adhesion, migration (diapedesis), chemotaxis, and phagocytosis
18
Q
What specifically happens in margination/adhesion?
A
Chemical mediators (cytokines) are released, adhesion molecules (selectins) are expressed, leukocytes slow migration and begin marginating (pavementing), and adhere to the cell wall
19
Q
What happens during migration?
A
Leukocytes extend pseudopods and pass through the capillary wall via an ameboid movement
20
Q
What happens during chemotaxis?
A
Leukocytes travel through the tissue to the site of injury. Cytokines draw cells towards site and complement proteins bind to the bad cells to tag
21
Q
What happens during phagocytosis?
A
Leukocytes recognize and attach through opsonization. Then they engulf and intracellularly kill the harmful agent
22
Q
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What type of cell is this?
A
Neutrophil
23
Q
Which WBC is the “first responder”
A
Neutrophils
24
Q
When do neutrophils arrive and how long can they survive in the tissue?
A
90 minutes and they can survive for 10 hrs
25
What is the name of the condition of elevated WBC count?
Leukocytosis
26
What are immature forms of neutrophils called?
Bands or left shift
27
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What type of cell is this?
A band
28
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Which cell is this?
Lymphocyte
29
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What cell type is this?
PMN neutrophil
30
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What cell type is this?
Monocyte (kidney shaped nucleus)
31
What are eosinophils active in?
Allergic reactions and parasitic infections. They are responsive to IgE
32
What are the 3 types of granulocytes
Eosinophils, basophils, and mast cells
33
What is the function of basophils?
They are active in inflammation and allergic reactions. They release histamine and they bond with IgE
34
What is the function and location of mast cells?
Found in connective tissue, similar to basophils. They are on mucosal surfaces-lung, GI tract, and dermis.
They are always ready in a “sentinel position” and are active in allergic reaction (IgE) and parasitic infections
35
What is the largest WBC?
Monocyte
36
What role do monocytes play?
They have a long lifespan and arrive 24 hours after injury to become the predominant cell type 48 hours after injury. They engulf larger and greater quantities of foreign material than neutrophils and play a role in adaptive response
37
What is the difference between a monocyte and a macrophage
A monocyte is in the blood and a macrophage is in tissue. Otherwise they are closely related
38
What is the common name of an erythrocyte and what role do they play??
Red blood cell, transport of oxygen to tissues
39
What is the common name of a thrombocyte and what role do they play?
Platelet, helps to mediate the vascular response, hemostasis and thrombosis. Release inflammatory mediators
40
What is the role of endothelial cells?
Synthesize and release inflammatory mediators and play role in vascular response
41
Which cell is the “street cop”
Neutrophil, rapid response
42
Which cell is the “fumigator” and why?
Eosinophil, kills parasites
43
Which cell is the “fireman” and why?
Basophil, inflammation
44
Which cell is the “riot police” and why?
Macrophage, longer lasting
45
Which cell is the “signal man” and why?
Dendritic cell, relays info
46
Which cell is the “special forces” and why?
Lymphocytes (B and T cells), specific targeted response
47
What is the role of inflammatory mediators?
Modify and enhance inflammatory response
48
What are the 6 types of inflammatory mediators?
Plasma proteins, histamine, interleukin and other cytokines, platelet activating factor, prostaglandins, leukotrienes
49
What are the three types of plasma proteins?
Complement system, kinins, and clotting system
50
What is the most important kinin?
Bradykinin
51
What are the functions of kinins?
Vasodilation and vascular permeability, smooth muscle contraction, pain response.
52
What breaks down kinins?
Kininase and angiotensin-converting enzyme
53
What is the function of the clotting system?
Expression of endothelial adhesion molecules, production of prostaglandins, PAF, and chemokines
54
What is the key protease in the clotting process?
Thrombin
55
What proteins and enzymes are involved in the clotting system?
Fibrinopeptides, thrombin is a key protease enzyme
56
Where are complement proteins found?
They are inactive in plasma
57
What do complement proteins do when they are activated?
They become proteolytic enzymes that degrade other complement proteins in a cascade
58
What are the functions of complement proteins
Vasodilation and increased vascular permeability, smooth muscle contraction
leukocyte recruitment and augmentation of phagocytosis, mast cell degradation
59
What are the 2 key complement proteins?
C3a and C5a
60
What cells release histamine?
Mast cells, basophils, platelets
61
What is the role of histamine in vascular response?
Vasodilation and increased vascular permeability
62
What receptor does histamine use to impact vascular response?
H1
63
What are the types of cytokines?
Chemokines, interferons, interleukins, lymphokines, and tumor necrosis factor
64
What is the function of IL-1 and TNFa
mediate early inflammatory response responsible for fever and pain
adhesion, chemotaxis, general acute-phase response
65
What is arachidonic acid?
A fatty acid precursor derived from cell membrane phospholipids
66
What is created from arachidonic acid in the cyclooxygenase pathway?
Prostaglandins and thromboxane
67
What is created from arachidonic acid through the lipoxygenase pathway?
Leukotrienes
68
What do corticosteroid medications block?
The synthesis of arachidonic acid from phospholipids
69
What end product can’t be created if arachidonic acid is not created?
Leukotrienes, prostaglandins, and thromboxane
70
What blocks the cyclooxygenase pathway?
NSAIDS/aspirin
71
What can’t be created if the cyclooxygenase pathway is blocked?
Prostaglandins and thromboxane
72
What is the function of prostaglandins?
Vascular permeability and vasodilation, pain response
73
What is the function of prostaglandin E1 and prostaglandin E2?
Induce inflammation and poténciate effects of other inflammatory mediators, especially histamine
74
What is the function of thromboxane A2?
Promotes platelet aggregation and vasoconstriction
75
What is the function of leukotrienes?
Vascular permeability, adhesion of endothelial cells, chemotaxis, further histamine release
76
What is function of slow-reacting substance of anaphylaxis?
It is a group of leukotrienes that causes slow and sustained constriction of the bronchioles. It is important in asthma and anaphylaxis
77
What are leukotriene receptor antagonists used for
The treatment of asthma
78
What are 5-lipoxygenase inhibitors used for?
Block enzyme in lipoxygenase pathway to convert arachidonic acid to leukotrienes
79
Where does platelet activating factor come from
Cell membrane phospholipids
80
What is the function of platelet activating factor?
-Induces platelet aggregation and stimulates platelets to release vasoactive mediators
- stimulates synthesis of thromboxanes
-increase vascular permeability
-neutrophil activation, and chemoattractant for eosinophils
81
What is the function of nitric oxide
Smooth muscle relaxant, antagonism of platelet functions, reduction of leukocyte recruitment, assists in microbicidal action by phagocytes
82
What is erythema and why is it present?
Redness. Increased blood flow
83
What is heat (calor) and what causes this response?
Heat. Increased blood flow
84
What causes swelling (edema, tumor)
Increased permeability of vessels causes leakiness into tissues of fluid
85
What causes pain?
Chemical mediators released cause pain, but it can also be caused due to swelling pushing into neighboring tissues
86
What causes loss of function?
Swelling or injury itself
87
What are the 5 cardinal signs of inflammation?
Redness, swelling, heat, pain, loss of function
88
What is an exudate?
Fluid excreted from site of injury due to vascular response
89
What is a water, low in protein, derived from plasma entering inflammatory site exudate
Serous
90
Thin, red or pink, water, plasma with a few RBCs mixed in exudate
Sanguinous
91
Large amount of fibrinogen, thick, sticky mesh work exudate
Fibrinous
92
Pus from degrading WBCs, protein, and tissue debris exudate
Purulent/suppurative
93
Severe tissue injury causing damage to blood vessels or significant RBC leakage from capillaries (hematoma) exudate
Hemorrhagic
94
Exudate that is formed on mucous membranes with necrotic cells in fibropurulent base
Membranous/Pseudomembranous
95
What is an abscess?
Localized area of inflammation containing Purulent exudate
96
What is an ulceration?
Necrotic, eroded area of epithelium with subepithelial inflammation
97
What are the signs/symptoms of the acute-phase response of systemic inflammation?
Changed plasma proteins concentration, fever, increased leukocytes, lethargy, and skeletal muscle catabolism, increased erythrocyte sedimentation rate
98
What causes fever?
IL-1, IL-6, and TNFa reset the thermoregulatory set point in the hypothalamus
99
What mediates the increase in leukocytes?
IL-1 and other cytokines
100
What mediates lethargy?
IL-1, TNFa action on CNS
101
What are the acute-phase proteins involved in systemic inflammation?
CRP, fibrinogen
102
If someone has elevated CRP what is that indicative of?
Inflammation, HTN, DM, smoking, aging, obesity, depression, sleep disturbance`
103
What is the function of CRP?
Binds to surface of invading microorganisms to assist their destruction, aids with regulating immune response, clears necrotic cell
104
What is an elevated CRP associated with?
Increased risk of cardiovascular disease
105
When would you see an increase in erythrocyte sedimentation rate?
Acute phase of systemic inflammation, non-inflammatory conditions (obesity) and anemic patients (falsely elevated)
106
What can cause leukocytosis?
Medication, bone marrow disease, inflammation or infection
107
What infections cause neutrophilia?
Bacterial infection
108
What infections cause eosinophilia?
Parasitic infection, allergic reaction
109
What condition causes neutropenia and/or lymphocytosis?
Viral infection
110
What are the signs/symptoms of lymphadenitis?
Swollen, tender, mobile, rubbery, possibly erythematous or fluctuant lymph node
111
What is the cause of lymphadenitis?
An inflammatory reaction in lymph nodes draining injured area. It is caused by filtering lymph fluid with infectious/necrotic material
112
What is the treatment of lymphadenitis?
Treatment of underlying inflammatory process, antimicrobial therapy, analgesics, anti-inflammatory es, cool compresses, abscessed nodes may require drainage
113
What is the cause of lymphangitis?
Inflammation or infection of lymph channels draining an injured area
114
What are the signs and symptoms of lymphagenitis?
Red, tender streaks extending proximal y
115
What is the treatment of lymphadenitis?
Treatment of underlying inflammatory process, antimicrobial therapy, analgesics, anti-inflammatories, cool compresses
116
What is shock?
Life threatening condition caused by lack of adequate circulation and oxygenation of the body
117
Why is shock an emergency?
There is a high risk of multiple organ damage and failure
118
What are the main signs/symptoms of shock?
Hypotension, oliguria, pale/cool/clammy skin, altered mental status, metabolic acidosis, also possible: shallow breathing and/or rapid breathing, elevated heart rate, dehydration, chest pain/irregular heartbeat
119
What are the 5 types of shock?
Cardiogenic, hypovolemic, Distributive, anaphylactic, neurogenic, septic
120
What type of shock is due to the inability of heart to pump required amount of blood?
Cardiogenic shock
121
What are some of the causes of Cardiogenic shock?
Cardiac arrhythmias, damaged heart muscle or valves, pressure around heart, or rupture of heart muscle
122
What type of shock is due to decreased intravascular volume leading to decreased perfusion of vital organs?
Hypovolemic shock
123
What type of shock is related to severe vasodilation causing loss of peripheral vascular resistance?
Distributive shock
124
What types of shock fall under distributive shock?
Anaphylactic, neurogenic, and septic
125
What is the type of shock where severe, rapid allergic or hypersensitive reaction has potential to be fatal?
Anaphylactic
126
What is the type of shock with damage to the autonomic pathways in the CNS that causes loss of sympathetic stimulation to blood vessels which causes vasodilation and sudden hypotension?
Neurogenic
127
What type of shock is caused by systemic vasodilation after an infection and desregulaciones of inflammatory response?
Septic shock
128
What is SIRS? What is it mediated by?
Systemic inflammatory response system, mediated by IL-1 and TNFa.
129
What happens in septic shock?
A exaggerated inflammatory response leads to vasodilation, tissue ischemia, direct cell injury, and altered apoptosis
130
What are the effects of septic shock on the circulatory and lungs?
Hypotension and hypo perfusion, pulmonary edema
131
What are the effects of septic shock on the GI tract, liver, and kidney?
Increased intestinal permeability allows bacteria and endotoxins to enter systemic circulation, impaired elimination of bacteria and endotoxins from gut due to cellular injury, and impaired filtration of toxins and waste products from blood due to hypoperfusion and renal damage in kidney
132
What is the impact of septic shock on the nervous system?
Encephalopathy due to changes in cell signaling by inflammatory mediators and dysfunction of the blood-brain barrier
133
Which immune mediators are responsible for pain?
Kinins, cytokines, and prostaglandins
134
Which immune mediators are responsible for expression of endothelial adhesion molecules?
Clotting system, cytokines, leukotrienes
135
Which immune mediators are responsible for fever?
Cytokines
