Innate Defenses: Inflammation Q&A
1 - When a pathogen enters your body, what
NONSPECIFIC reaction occurs?
Inflammation
2 – Which line of body defense is inflammation?
2nd
3 – Which system response comprises of the
following:
- Initiates response to pathogen or injury
- Walls off dangerous pathogens
- Enhances immune response
- Destroy & remove debris
- Repairs & heals wounds
Inflammatory system
4 – Body defense lines:
1st Skin
2nd Inflammatory  Nonspecific
3rd Immune  Specific
5 – Inflammation responds to body tissues that
undergo what?
Immune reaction
Injury
Ischemic damage
6 – Infectious microbes, trauma or surgery,
caustic chemicals and extremes of heat/cold
may cause what nonspecific response?
Inflammatory response
7 – Two basic patterns of inflammation are?
Acute & Chronic
8 – This is the EARLY response to inflammation
Acute Inflammation
*Note: Review Figures: Sequence of events –inflammation & Sequence of Wound healing
9 – What are 5 Cardinal signs to inflammation?
Pain
Heat
Redness
Swelling
Loss of function
10 – This nonspecific pattern of inflammation
occurs BEFORE the immune response
Acute
11 – Two major components of this pattern
consists of- Vascular & Cellular stages
Acute inflammation
12 – What are 2 major components to Acute
inflammation?
Vascular & Cellular
Acute Inflammation
Vascular level
Cellular level
IMMEDIATE changes- 5 Cardinal signs seen here
LEUKOCYTES classes Granulocytes: “granules in cytoplasm”
 Vasodilation: erythemia (red), heat
Neutrophils
Eosinophils
Basophils
 Vasoconstriction: pain, loss of function,
Mobile
--Biochemical
--Contains
edema (swell)
Get there first
Response patterns
1) Immediate transient 15-30 min
2) Immediate sustained
3) Delayed hemodynamic


mediators:
serotonin &
histamine
--Control vascular
response
histamine
--Control
vascular
response
Monocytes/Macrophages -ECF
Mast cells
13 – A patient with an allergic reaction would
have which leukocyte/biochemical mediator
increased?
Eosinophils  incr histamine
14 – Where are Monocytes found in the Cellular
inflammatory stage?
Extracellular fluid (ECF)
15 – A shift to the left is a hallmark of what?
Neutrophil hallmark (PMN) or bands
16 – These leukocytes are: predominantly
phagocytic cells in the early inflammation
response, short-lived, constantly replaced
(requires leukocytosis).
PMN
17 – the primary role of this short-lived
phagocytic cell- PMN
Remove debris (bacteria phagocytic)
18 – a patient with increased bands indicates
what?
Incr baby neutrophils  Bacterial infection
19 – these blood cells are the largest, longest life
span than Granulocytes, lives in ECF/interstitial
space & migrates to the inflammatory site where
it develops into a macrophage
Monocyte
20 - __________ have the same function as PMNs,
engulfing foreign bodies
Monocytes
21 – Where are (inactivated) monocytes found?
ECF/interstitial space
22 – leukocytes that engulf larger, greater
amounts of foreign material than neutrophils,
that also mature from monocytes are called?
Macrophage
23 – these blood cells secrete mediators that
promote tissue re-growth and healing 
angiogenesis & fibroblasts, also signals
hallmark of chronic inflammation
Macrophage
24 – Which WBCs surrounds & walls off foreign
material that cannot be digested?
a. Which pattern of inflammation?
Macrophage
a. Chronic inflammation hallmark
25 – C/C hallmarks of acute & chronic
inflammation:
Acute inflammation hallmark:
Baby neutrophils
5 cardinal signs
Chronic inflammation hallmark:
Macrophage walls off foreign material
26 – The cells are sensitized or activated
during allergic/hypersensitive responses and
are armed with IgE
a. These cells are found along what types
surfaces? (i.e. lung, GI, dermis)
b. Give an example of when these cells are
activated
27 – On a larger scale, a patient injures
himself/herself  activates this multicomponent beginning with  Margination &
Diapedesis, leading to ?
a. What is Margination (or pavementing)?
b. Describe Diapedesis (or transmigration)
28 – After pavementing & transmigration
(Margination & Diapedesis) 3 steps
Phagocytosis take place:
Mast cells
a. Mucosal surfaces
b. Asthma, causes edema + swelling in the
lungs  mast cell response; meds are
taken to control this response
Phagocytosis
a. Phagocytes line up and stick on the
epithelial
b. Vascular permeability; phagocytes move
to surrounding tissue by emigration
through retracted endothelial junctions
a. Opsoniazation plus attachment
- attract antigen due to *complement*
(attract bacteria)
b. Engulfment
-cytoplasmic extensions surrounds &
extends around particle
c. Intracellular killing
- enzymes & toxins
*attract  engulf  destroy
Vasoactive & Smooth
Muscle Constriction
-Histamine, Serotonin
-Prostaglandin,
Leukotrienes
Chemical Mediators (by Function)
Plasma Protein
Chemotactic factors
Systems (3)
1 –Complement
-Chemical gradient by
2 –Clotting Cascade
which phagocytes
3 –Kinin System
progress to inflamed site
*Attraction
Cytokines
-Protein messengers made by
immune cells
-Regulate movement, proliferation,
differentiation of WBCs
-Exe:
Interleukins
Interferons
Tumor necrosing factor
Stimulating factor
29 – Where are Chemical mediators found?
a. They assist in producing what?
b. How are they classified?
Plasma or inside cells
a. S&S
b. Function
30 – Chemical mediators are classified by how
they function, what are the classifications?
1. Vasoactive + smooth muscle Constriction
(Histamine, serotonin, prostaglandins,
leukotrienes)
2. Plasma Protein Systems
(Complement, Clotting Cascade, Kinin Systems)
3. Chemotactic
4. Cytokines
31 – Directional movement of cells along a
chemical gradient formed by chemoactic factor
is called?
Chemotaxis
32 – A Chemical mediator is the –Complement
System, this is the primary effector system for
innate & adaptive humoral responses.
A - Enhances phagocytosis
Enhances engulfing/clearing complex w/
macrophage
A - How do these group proteins affect
inflammation in the circulation?
Trigger WBC influx through chemostatic factors
B – The Complement Sys. is initiated by…
Activates proper sequence & inhibitor proteins
B – antibody bound epitopes on microbes
through immune complexes
*Major mediator and enhances functions going
on
33 – Regulatory proteins (messengers) are
made by immune cells & produced in all phases
of the immune response, called?
a. How do these messengers modulate
reactions of host to foreign anitigens/
injurious agents?
Local Manifestations
Exudates (protein-rich fluid)
-serous –watery, low in protein
-fibrinous –thick & sticky, lots of fibrinogen
-sanguineous –reddish, thick, watery
-purulent –“milk”, tissue debri (WBCs), protein
-hemorrhagic –red, thick
Abscess (pus)
-contains purulent exudate
-walled off by fibroblasts
-require I&D
Ulceration
-epithelial becomes necrotic & eroded
-origin: traumatic injury or vascular compromise
(decr blood source)
Cytokines (aka Immune Response Messengers)
a. Regulates 1. Movement, 2. Proliferation
and 3. Differentiation of WBCs
- Cascade affects production subsequent
cytokines
Inflammation
Systemic Manifestations (affect total body systems)
Acute
Chronic
Response:
1 –Fever, shift-to-left,
leukocytosis, plasma protein
changes, skeletal muscle
catabolism
2 –Proteins
o Incr Liver production
o Fibrinogen & CRP
3 –Incr ESR (Erythrocyte
Sedimentation Rate)
o General inflame. Marker*
Self-perpetuating & prolonged
healing & destruction all at once
Examples:
Alteration in WBC count
Lead to:
Scar Tissue
Granulomas
o Lymphocytes
surround
macrophages
surrounding small
lesions
o Exe. Typical w/ foreign
bodies –splinter,
sutues, TB
Lymphadenopathy
Sepsis & septic shock
*hours to days
o
o
Infiltration mostly by
macrophages,
lymphocytes
Evoked by low-grade,
persistent irritants
(virus, pathogen) that
can’t spread rapidly/
penetrate deep
*two weeks or longer
*Review Acute Inflammation Figure
34 – This “milky” exudate contains protein,
degraded WBCs and tissue debri, present in
local manifestation of inflammation
a. This localized inflammatory area
contains purulent exudate that is walled
off by fibroblasts, may require incision &
drainage.
Purulent
35 – A localized inflamed area caused from
traumatic injury or when vessels are
compromised, leading to blood loss is called?
Ulceration
a. Abcess or pus
36 – A patient is experience a fever, their lab
results indicate a shift-to-the-left, increased
proteins- fibrinogen and CRP, lymphadenopathy
and apparent alterations in WBC count.
a. Which type of inflammation is occurring
in this pt?
b. What does shift to the left indicate?
c. Incr of these proteins indicates what?
a. Systemic, Acute
b. Bacterial infection
c. Incr liver production
37 – The pt is infiltrated by macrophages (and
lymphocytes), which was evoked by a persistent
virus or pathogen that was unable to rapidly
spread. This pt is likely to develop scar tissue
and granulomas. Which type of inflammation is
manifesting?
Chronic (systemic) inflammation
38 – Response to tissue injury & attempt to
maintain normal body structure & function
indicates this.
Tissue Repair
*the site is usually weakened/never the same
Tissue Repair
Regeneration (“Resolution”)
Injured cell replaced with same cell type
Two structure types
1 –Parenchymal

Contains function cells of body organ
2 –Supporting CT (stromal)

Everything else; tissues supporting organs

Exe. Blood vessels, extracellular matrix (ECM),
nerve fibers

For instance, the liver goes through this
Replacement
Fibrous CT leaves permanent scar

Severe or persistent injury to parenchyma & ECM

Granulation tissue & Scar tissue development 
replaces CT
39 – A pt is undergoing tissue repair from a
persistent injury to a ligament which leaves a
permanent scar
Replacement
40 – A pt’s liver is damaged from alcohol abuse.
The stromal tissues begin repairing this organ.
What is this tissue repair called?
Regeneration
41 – C/C Primary Intention v. Secondary
Intention of wound healing:
Primary Intention
o Restore the original structure & function
o Replacement occurs if restoration is not
possible
Secondary Intention
o Replacement occurs through collagen
scar tissue
Inflammatory 
o
Prepares environment for
healing; engulf debris
o
Neutrophils & Macrophages
*begins at time of injury
Wound Healing: 3 phases
Reconstruction (proliferate)
Maturation (remodel).
o
Building new tissue
o
Scar tissue remodeling
o
FIBROBLASTS –key cell,
synthesize + secrete
collagen for healing &
growth factors needed for
angiogenesis & wound
contraction
o
Collagen & lysis
simultaneous synthesis by
collagenase enzymes
o
Scar incr strength
*3 weeks (upto >6 mo)
*2-3 days (upto 3 weeks)
42 – What are the 3 phases to wound healing?
Inflammatory, Reconstruction, Maturation
a. This phases builds new tissue through
CT –fibroblasts that make/use collagen
a. Restoration
b. A patient is healing from a wound from 5
weeks ago. A scar has formed. What
phase is the pt in?
b. Maturation
c.
Inflammatory
c. This phase begins at the time of injury
43 – Granulation tissue is a highly vascular CT.
What does it contain other than oozing exudate?
Newly formed capillaries
Fibroblasts
Residual inflammatory cells
Answer the following:
1. What are the five cardinal signs of inflammation?
2. The difference between hemodynamic & cellular phases of inflammation?
a. Acute & Chronic
3. Describe the types of inflammatory exudates
4. The role of the complement system
5. Characteristics of acute-phase response
6. Parenchymal vs. Stromal
7. The difference between healing by primary & secondary intention
8. Trace the would-healing process (through inflammation—proliferative—remodel phases)