Lecture 2 Flashcards
(88 cards)
1
Q
First line of defense
A
skin and mucous membranes
2
Q
second line of defense
A
inflammation
3
Q
third line of defense
A
immune response
4
Q
cellular response steps (4)
A
marginization/adhesion
migration
chemotaxis
phagocytosis
5
Q
marginalization/adhesion
A
- cytokines released leads sto increase in selectins
- leukocytes slow down *stick to vessel walls
6
Q
migration
A
leukocytes extend pseudopods PASS thru cell wall via ameboid movement
7
Q
chemotaxis
A
leukocytes travel thru tissues to injury
8
Q
phagocytosis
A
- recognition *adherence
- engulfment
- intercellular killing
9
Q
3 vascular response patterns
A
- immediate transient
- immediate sustained
- delayed hemodynamic
10
Q
immediate transient
A
follows minor injury (ex. being snapped)
11
Q
immediate sustained
A
follows major injury (surgical incision)
12
Q
delayed hemodynamic
A
4 to 24 hours after injury (ex sunburn, vaccine)
13
Q
types of white blood cells
A
neutrophils, eosinophils, basophils, mast cells, monocytes
14
Q
neutrophils
A
1st responder! arrives approximately 90 minutes and stay / live for approximately 10 hours.
Bands or left shift=immature neutrophil
Primary phagocyte
neutrophilia due to bacterial infection.
15
Q
Eosinophils
A
Red under microscope
parasitic
16
Q
basophils
A
inflammation x allergic rxns
release histamine & bonds with IGE
17
Q
mast cells
A
last basophils but In connective tissues & mucosal surfaces
allergic rxn and parasitic
“sentinel position” -immediately releases anti-histamine
18
Q
monocytes
A
Swat team
acts like macrophage
slowest to respond (approximately 24 hours) but last 48 hours
19
Q
What do inflammatory mediators do?
A
modify and enhance inflammatory response
20
Q
types of inflammatory mediators
A
plasma protein systems, histamines, cytokines, cyclooxygenase pathway, nitric oxide
21
Q
Plasma Protein systems
A
Kinins, clotting system, complements
22
Q
What do kinins do?
A
inflammatory mediators that do vasodilstion + increased permeability
feel pain via smooth muscle contraction
bradykinin
kinins broken down by 1. ace inhibitors
2. Kininase
23
Q
What breaks down kinins?
A
- ACE inhibitors
- Kininase
24
Q
Clotting system
A
expresses adhesion molecules and produces prostaglandins and chemokines
key clotting enzyme: thombin
25
Complements-what do they do?
vasodilation + inc. permeability
adhesion and chemotaxis
leukocute activation
augmentation of phagocytes
26
what do histamines help with?
helps with vasodilation and permeability via H1 receptor
27
What cells release histamines?
released by mast cells, platelets, and basophils
28
what do cytokines consist of?
1. niterferons (IFNs)
2. intereukins (ILs)
3. chemokines
4. lympohkines
5. tumor necrosis factor (TNF)
29
what are the 5 actions-->
1. fever
2. adhesion of leukosytes
3. pain
4. chemotaxis
5. acute phase response
30
2 major cytokines (major mediators of early inflammatory response
IL-1 and TNF-alpha
31
what is arachidonic acid
it is a fatty acid precursor derived from phospholipids in cell membrane
32
3 types of granulocytes
eosinophils, basophils, and mast cells
33
pathway that converts arachidonic acid to prostaglandins and thromboxane
cyclooxygenase pathway
34
pathway that converts arachidonic acid to leukotrienes
lipoxygenase pathway
35
What is a leukotriene antagonist
5-lipoxygenase inhibitor
IE: singulair--used to treat asthma
36
fxn of leukotreienes
induces smooth muscle contraction
constricts pulmonary airway (with smooth muscle contraction)
increases microvascular permeability
adhesion of endothelial cells
chemotaxis
further histamine release
37
fxn of prostaglandins
vascular permeability and vasodilation
induces inflammation
involved in pain response
potentiate effects of other inflammatory mediators (especially histamine)
38
fxn of thromboxane A2
promotes platelet aggregation and vasoconstriction
NSAIDs and Aspirin--inhibit enzyme in cyclooxygenase pathway for prostaglandin synthesis
39
Nitric oxide
slows/stops inflammation:
smooth muscle relaxation
antagonism of platelet functions (adhesion, aggregation, degranulation)
40
5 cardinal signs of inflammation
erythema, heat, swelling, pain, loss of function
41
erythema
redness due to vasodilation, increase in RBC, and increase in blood flow
42
heat
vasodilation, increased blood flow
43
Swelling
also known as edema or tumor
increase vascular permeability
increase fluid in extracellular space
44
Pain
compression in tissues due to swelling, direct elicitation of pain due to inflammatory mediators
45
loss of fxn
direct damage or due to pain or swelling
46
Types of local manifestations of inflammation (3)
exudates, abscess, ulceration
47
What is a exudate?
fluid excreted from site of injury
48
what is an absess?
localized collection of purulent (PUS) walled off by fibroblasts
49
what is an ulceration?
necrotic or eroded epithelium due to Trauma or Vascular compromise
50
Types of exudates?
serous, sanguinous, fibrinous, purulent, hemorrhagic, membranous/pseudomembranous
51
describe serous exudate
yellow and watery, derived from plasma. Lower in protein
52
describe sanguinous exudate
thin, red or pink, watery; plasma with a few RBCs mixed in
53
describe fibrinous exuate
large amounts of fibringen-thick sticky meshwork (adhesions) usually inside the body
54
describe Purulent/Suppurative exudate
pus (degraded WBC, proteins, tissue debris)
55
describe a hemorrhagic exudate
severe tissue injury causing damage to blood vessels or significant leakage of RBCs from capillaries (hematoma)
56
describe a membranous/pseudomembranous
form on mucous membranes; necrotic cells in fibropurulent base
57
3 types of capillaries
continuous, fenestrated, sinusoid
58
Systemic manifestations of inflammation
fever, increase in leukocytes, lethargy, skeletal muscle catabolism, increase in erythrocyte sedimentation rate (ESR)
59
What is leukocytosis?
increase in overall number of WBCs in the serum
60
if someone has a bacterial infection, they would see an increase in what kind of leukocyte? and what would that be called?
increase in neutrophil
would be called neutrophilia
61
if someone has a parasitic infection, they would see an increase in what kind of leukocyte? and what would that be called?
eosinophilic cells would increase to site
would be called eosinophilia
62
if someone has an allergic reaction, they would see an increase in what kind of leukocyte? and what would that be called?
eosinophilic cells would increase to site
would be called eosinophilia
63
if someone has a viral infection, they would see an increase in what kind of leukocyte? and what would that be called?
neutrophils or lymphocytes would increase
would be called neutropenia and/or lymphocytosis
64
what are an increase in left shift cells suggestive of?
an infection
65
what is lymphadenitis?
inflammatory reaction in lymph nodes draining an injured area
66
what causes lymphadenitis?
caused by filtering lymph fluid with infectious and/or necrotic material draining from local injured or infected area
67
What is the treatment for lymphadenitis?
antimicrobial therapy, analgesics, anti-inflammatories, cool compress
+abscessed nodes may require drainage
68
what is lymphangitis?
inflammation or infection of lymph channels draining an injured area
69
most common cause of lymphangitis?
streptococcus pyogeneses
70
characteristics of lymphangitis?
red, tender streaks extending proximally
71
how is lymphangitis treated?
antimicrobial therapy, analgesics, anti-inflammatories, cool compress
72
what causes shock?
lack of O2 and circulation
73
what are the fatality rates if you have a patient in septic shock?
35-60% mortality rate
74
what are the fatality rates if a patient presents themselves with cardiogenic shock?
60-90% mortality
75
Major symptoms of shock
extremely low blood pressure (hypotension)
decreased urine output (oliguria)
pale, cool, clammy skin
altered mental status:
early-agitation, irritabily, and or anxiety
late-confusion, delirium, coma
metabolic acidosis
76
What causes cardiogenic shock?
inability of heart to pump the required amount of blood
causes include: cardiac arrhythmia, damaged heart muscle or valves, rupture of heart muscle
77
hypovolemic shock causes?
decreased intravascular volume leading to decreased perfusion of vital organs.
can be caused by hemorrhage or fluid loss
78
types of distributive shock?
anaphylactic shock, neutrogenic shock, septic shock
79
what causes anaphylactic shock?
severe, rapid allergic or hypersensitivity reaction with potential to be fatal
80
what causes neurogenic shock?
damage to the autonomic pathways within the CNS?
sudden loss of sympathetic stimulation to blood vessels-->massive vasodilation-->sudden hypotension
81
what causes septic shock?
systemic vasodilation secondary to infection and dysregulation of inflammatory response
Most common cause- G+ bacteria, followed by G- endotoxin-producing bacteria
82
Systemic inflammatory response syndrome (SIRS)
systemic uncontrolled inflammatory response
happens when exaggerated, unregulated, self sustaining inflammatory response to an infection
largely mediated by IL-1 and TNF-alpha
83
how does septic shock affect the circulatory system?
severe hypotension and hypoperfusion
84
how does septic shock affect the lungs?
pulmonary edema and hypoxemia
85
how does septic shock affect the GI tract?
increased intestinal permeability allowing bacterial in gut to enter systemic circulation
86
how does septic shock affect the Liver?
impaired elimination of bacteria and endotoxins from gut due to hypoperfusion and direct renal damage
87
how does septic shock affect the kidneys?
impaired filtration of toxins and waste products from blood due to thypoperfusion and direct renal damage
88
how does septic shock affect the nervous system?
encephalopathy due to changes in cell signaling caused by inflammatory mediators; dysfunction of blood-brain barrier?
