chapter 2 inflammation Flashcards
1
Q
what are the two causes of desease
A
congenital and acquired
2
Q
congenital
A
inherited, Intrauterine Lesions- malformation
3
Q
acquired
A
Inflammation – Neoplasia (cancer) – Immunologic (rhematoid arthritis) – Vascular (heart 0failure, heart attack – Endocrine (afrenal galnd) – Degeneration (alzheimers disease) – Iatrogenic (caused by the health care provider- example didn't wash hands properly)
4
Q
what causes inflammation
A
Infection – Chemical Agents – Physical Agents (Radiation, Heat, Cold) – Trauma – Chronic Irritation
5
Q
what is he difference btw acute and chronic inflamation
A
Inflammation of sudden onset and short
duration is characterized as acute, in contrast to
chronic inflammation, which lasts a long time
6
Q
what is inflammation
A
Response of living tissue to irritation or injury
Inflammation occurs only in multicellular
organisms capable of mounting a
neurovascular and cellular response to injury
• In contrast to cell injury, which occurs at the
level of single cells, inflammation is a
coordinate reaction of the animal and human
body, and it involves nerves, vessels, blood
cells, and soluble mediators of inflammation
7
Q
what is inflammations role
A
protective role, Some times the process may become
uncontrollable, producing more harm than
good. For example, pulmonary tuberculosis
elicits a protective tissue reaction. This
inflammatory response may erode pulmonary
vessels and cause massive bleeding
8
Q
what are some side effects of inflammation
A
noxious. For example, fever, which initially
has a beneficial effect, may be so high that it
may cause death
9
Q
can a gangrenous foot become inflammed
A
no because Inflammation occurs only in living
tissues
• Necrotic or dead tissue cannot
mount an inflammatory response.
10
Q
what are the signs of inflammation
A
exam q: calor (heat) • rubor (redness) • tumor (swelling) • dolor (pain) • functio laesa or disturbed function, as the classical symptom
11
Q
what is the bodies first response to blood flow
A
Hemodynamic (vascular) changes - change in blood flow represent the body’s first response
injury.
– The redness and swelling of the skin following a slap
on the face or spanking are typical examples of such a vascular response
12
Q
what does an increase in blood flow do to regulate hemodynamic chages
A
The mechanic stimulus (ex. hand) stimulates nerves that
transmit signals to smooth muscle cells on precapillary arterioles. The smooth muscle cells
act as sphincters, regulating the inflow of blood into the capillaries
13
Q
what is the first response of arterioles to an injurious stimulus, what is the second
A
vasoconstriction,
which lasts only a few seconds
• This is followed by vasodilatation (ie.,
relaxation of the precapillary sphincter), which results in flooding of
the capillary network with arterial
blood, manifested by redness and mild
swelling of the tissue engorged by blood
14
Q
what is hyperemia
A
• Increased blood flow to capillaries (Vasodilatation) → Hyperemia – Red – Swelling → Pain – Heat – → Congestion The blood flow in dilated capillaries and venules is slow, which leads to congestion (the Latin root of which means “heaping together”)
15
Q
what do rbc do in inflammation
A
Sludge & form rouleaux (stacks like
coins) - delay circulation further
16
Q
what do wbc do in inflammation
A
are marginalized & attached to
endothelium (pavementing)
17
Q
where are surface adhesion molecules found
A
e normally present on leukocytes and endothelial cells
18
Q
what is the role of interleukins
A
soluble mediators of inflammation- which activates surface components of cells
19
Q
what initiates clotting
A
Platelets adhere to endothelium-
20
Q
The permeability of the vessel wall of
capillaries and postcapillary venules changes in response to inflammation as:
A
Increased pressure inside the congested blood vessels
• Slowing of the circulation, which reduces the
supply of oxygen and nutrients to endothelial
cells
• Adhesion of leukocytes and platelets to
endothelial cells
• The release of soluble mediators of
inflammation from inflammatory cells,
platelets, endothelial cells, and plasma
21
Q
what two classes of substances do the mediators of inflammation belong to
A
plasma-derived
and
cell-derived
22
Q
how do plasma-derived mediators circulate
A
in an inactive form and must be
transformed into an active form by an activator. There are numerous specific
and non-specific activators
23
Q
how do cell-derived mediators mediate
A
Cell-derived mediators may be preformed and stored in granules of platelets and leukocytes, or they may be
synthesized de novo on demand.
24
Q
what is an example of a preformed mediator
A
histamine( from Platelets & Mast Cells)
25
what is an example of a slower mediator
bradykinin Protein formed in plasma from
| Hageman activation)
26
what is histamine
: Early in inflammation, the vessels become leaky because of the action of biogenic amines, like histamine, and inflammatory
polypeptides, like bradykinin
27
what is bradykinin
A plasma protein formed through the action of the enzyme kallikrein on a precursor kininogen. It has effects similar to those of
histamine, but at a slower pace (in Greek, bradys means slow, and kinein means acting)
28
what does the activation of haegeman factor lead to
to increased
| vascular permeability, clotting and thrombolysis
29
what are complemental cascades
another important source of mediators of inflammatoin 9 different proteins
30
how can the complement cascades be activated
through two pathways:
– Classical
– Alternate
31
what is the classcal pathway
typically activated by antigenantibody
complexes formed in immune reactions. It can
also be initiated by some proteolytic enzymes,
32
what is the alternate pathway
activated by bacterial endotoxins,
| fungi, snake venom, and some other substances.
33
what is the MAC
membrane attack complexe • Both pathways converge toward a common
terminal pathway, which finally leads to the
formation of the membrane attack complex
(MAC)
• The MAC is enzymatically active and is able to
destroy cells by literally boring holes in
membranes
34
WHAT ARE Arachidonic Acid Derivatives
```
An important group of mediators of
inflammation:
• Derived from the phospholipids of cell
membranes through the action of
phospholipase. splits into 2 metabolic pathways
```
35
what are the 2 ways that arachidonic acid derivitaives that are already formed be further metabolized
The lipoxygenase pathway
| – The cyclooxygenase pathway
36
whatis the lipoxygenase pathway
The lipoxygenase pathway leads to the
formation of leukotrienes, which are active in
chemotaxis , increase vascular permeability,
also known as the slow-reacting substances of
anaphylaxis (SRS-A), and they cause
bronchospasm in asthma and anaphylactic
shock by contracting the smooth muscles in
the bronchi
37
what is the cyclooxygenase pathway
leads to
formation of the prostaglandins, prostacyclin
and thromboxane, which cause vasodilatation.
Thromboxane promotes platelet aggregation
and thrombosis, whereas prostacyclin
counteracts this effect
38
what are the two major cellular events in inflammation
Emigration of Leukocytes
| and Phagocytosis
39
what is transudation
leakage of fluid from the
| vessels into the interstitial spaces
40
what is edema and how does it form
-transudation accounts
| for the formation of edema, rich in protein, but contains few cells
41
how is exudate formed
Emigration, or diapedesis, of cells across the vascular wall
leads to the formation of exudate which contains much
more protein than transudate and inflammatory cells.
42
what is Emigration, or diapedesis
is the movement of leukocytes out of the circulatory system and towards the site of tissue damage or infection
43
during emigration or diapedesis of an acute inflammation what type of cells are they
```
polymorphonuclear leukocytes, also called
polymorphonuclear neutrophils (PMNs)
```
44
• Increased permeability → leakage of
| fluid (transudation) → edema fluid
remember
45
• Emigration of cells out of vessel →
exudate (Mainly PMNs)
(PMN = Polymorphonuclear Leukocyte)
remember
46
what becomes apparent in the exudate within the
| first 48 hours
• As the inflammation evolves, PMNs are joined by
| other cells, such as monocytes and eosinophils
47
as the inflammation becomes chronic, what replaces the PMNS
macrophages, lymphocytes, and
| plasma cells
48
The emigration of leukocytes from blood
vessels is an active process that occurs in
several phases. These phases include:
Adhesion of PMNs to the endothelial cells
• Insertion of cytoplasmic pseudopods between the junctions of endothelial cells
• Passage through the basement membrane
• Ameboid movement away from the vessel toward the cause of inflammation (e.g.,
bacteria)
49
chemotaxis
• Active movement of PMNs along a
| concentration gradient
50
how do PMNs move towards the chemoattractant
The chemoattractant is derived from bacteria
or tissues destroyed by inflammation, or
from activated complement. Chemotactic
substances stimulate PMNs to move along a
chemical concentration gradient until they
reach its source or the site that has the
highest concentration
51
how do PMNs act like scavengers
• PMNs that reach the bacteria or other sources
of chemotactic substances lose their mobility
and begin acting as scavengers
52
how are bacterium killed by phagocytosis
• Engulfment of the bacterium is a process by
which the cytoplasm of the PMN surrounds
the foreign particle and encloses it into an
invagination of the cell membrane. Inside
the nascent vacuole, the bacterium is killed
by bactericidal substances released from
the cytoplasm of the PMN. The bacterium is
internalized into a phagocytic vacuole,
which fuses with lysosomes
Inflammati
53
what s are the primary mediators of acute inflammation caused by bacteria
PMNs
54
along with PMNs, what else is also present from the earlies stages of inflammation
platelets
55
what are the latcomers to inflmmation
eosinophils,
| macrophages, and lymphocytes
56
what are the most numerous white blood
cells in the circulating blood, accounting
60 to 70 percent of all white blood cells
PMNs
57
why are PMNs called p (polymorphous)
have a segmented nucleus
and a well developed cytoplasm filled with
granules
• They are called PMNs because their
nucleus may have one to five segments - it
is “polymorphous” (
58
what are some important feature of PMNs
```
• Highly mobile
• Bacteriocidal – Granules contain
bacteriocidal elements
• Phagocytosis
• Cytokines – release various chemicals
including interleukin-I (→ Fever)
endogenous pyrogen—hypothalamic centre--fever
```
59
which is bigger macrophages or PMNs
macros
60
when do macrophages appear
3-4 days
61
what are macrophages
• Mononuclear cells derived from
| blood monocytes
62
what is the fct of macrophages
Phagocytosis
| – Release cytokines
63
what do lymphocytes do
```
Primarily
involved
with
antibody
production
```
64
do platelets have nucleouses
no
65
lymphocytes and plasma cells are components of _____ inflammation
chronic
66
what are the four perameters that inflammation can be classified under
• Duration (acute-chronic)
Etiology (how it happened)
• Location
•Morphology, or pathologic characteristics
67
what causes inflammation
infectious pathogens or by
| chemical, physical, and immune factors
68
how are infections classified as
bacterial, viral, protozoal and fungal
69
chemical causes can be classified as
organic or inorganic, industrial or medicinal, exogenous or endogenous
70
physical causes of inflammation
foreign bodies, heat, irradiation, and trauma
71
what is systemic inflammation
involving multiple
organs is common in immunologically
mediated diseases, such as systemic lupus
erythematosus. Sepsis, characterized by a
spread of bacteria through the blood, is also a
systemic disorder.
72
itis
inflammation
73
serous inflammation
```
Mild
• Exudation of Serum
• Early stages of most
inflammations
• Typical of Viral Infections
– ie. Skin vesicles (herpes virus)
```
74
Fibrinous Inflammation
```
• Exudate rich in Fibrin
• Indicates more severe inflammation
• Seen in many bacterial infections
• Resolves more slowly (requires
macrophages to lyze fibrin)
• May be organized
(space filled with blood vessels)
• May form fibrous (scar) tissue
```
75
purulent inflammation
Usually caused by bacterial infection
(Staph, strep)
• Viscous yellow fluid filled with tissue
debris and dying PMNs (pus)
76
abscess
• Closed pocket of Purulent
inflammatory exudate (Pus)
• If not drained, may become chronic
• Usually requires surgical drainage
77
what happens in chronic abscesses
```
the wall of the cavity is
composed of a capsule, which consists of
fibrotic granulation tissue. Abscesses do
not heal spontaneously and must be
evacuated surgically
• Large abscesses tend to rupture,
forming a sinus or fistula
```
78
what is a sinus
a cavity, usually occupied
previously by an abscess that drains
through a tract to the surface of the body
79
fistula
a (in Latin, meaning tube) is a
similar channel formed between two preexisting
cavities or hollow organs and the
surface of the body
80
in appendicitis, what are two important clinical findings
```
fever and leukocytosis-• Fever – response caused by
endogenous pyrogens
– Interleukin I
– Tumor Necrosis Factor (TNF)
• Leukocytosis (↑ WBC)
```
81
fever
n elevation in body temperature that
exceeds 37°C-is a typical response to acute
inflammation caused by endogenous pyrogens.
These substances-primarily IL-l and tumor
necrosis factor (TNF)-act on the
thermoregulatory centers in the hypothalamus,
which serve as a thermostat. If the threshold
of the thermostat (like the heating sensor in a
house) is raised, the temperature of the body
rises
82
what are fever mediated by
prostaglandins-released by pyrogens in the
hypothalamic center. Prostaglandin
synthesis can be inhibited by antipyretic
drugs, such as aspirin. However, in most
cases, the fever will abate on its own as
soon as the inflammation is eradicated
83
what are constitutional symptoms of inflammation
```
non-specific and are called
constitutional. These include:
– Fatigue
– Weakness
– Depression
– Lack of appetite
– Generalized pain
– Exhaustion
The pathogenesis of
```
84
can acute inflammation heal
may heal without any
consequences, or it may progress to chronic
inflammation
85
can mild inflammation heal
usually resolves
spontaneously after the inciting stimuli have
disappeared and mediators of inflammation
are no longer being created. However, if the
inflammation was accompanied by
considerable destruction of tissue, complete
healing may be postponed or never
accomplished
86
cells can be classified into three
groups according to their ability to
proliferate:
– Continuously dividing or mitotic cells (labile cells)
– Quiescent(dormancy), facultative (occurring optionally in response to circumstances rather than by nature.) mitotic cells (stable cells)
– Nondividing, postmitotic cells (permanent cells)
87
labile cells
cells divide throughout entire
lifespan (eg. stem cells, basal layer of skin,
mucosa of internal organs)
88
stable cells
(stable cells) – cells do not divide regularly,
can be stimulated to divide (eg. Parenchymal
organ – liver or kidney)
89
permanent cells
– Do not have the capacity to
proliferate under any circumstances (eg.
neurons/ myocardial cells)
90
what cells are most important for wound healing
```
leukocytes, macrophages, stay at site -
produce cytokines, growth factors,
mediators - act on connective tissue
cells: epithelial cells, myofibroblasts,
angioblasts, fibroblasts and collagen
```
91
myofibroblasts
hybrid properties (smooth muscle
cell/fibroblast)
– Able to contract like muscle cells.
– Secrete matrix substances
92
angioblasts
Precursors of blood vessels/proliferate
– Provide a route for the scavenger cells,
influx of blood (oxygen, nutrients)
93
fibroblasts
Produce most of the extracellular matrix
| fibronectin and collagen – form a scar
94
what is the path for healing by first intention
```
Incision site contains clotted
blood forming a scab
• PMN’s invade, followed by
macrophages → fibroblasts
• Vascularized connective tissue
becomes granulation tissue Granulation tissue is cleared out
and replaced by fibrous tissue (scar
tissue) changing from pink to white
• Skin cells proliferate and cover
wound, replacing the scab
```
95
what are the most important determinants of wound
| healing
```
Site of the wound
• Mechanical factors
• Size
• Presence or absence of infection
• Circulatory status
• Nutritional factors
• Age
```
96
```
• Infection: Sterile Wounds Heal faster
• Circulation:
– Well Oxygenated Wounds Heal
faster
– Ischemic (Hypoxic) Wounds Heal Slowly
(eg Diabetes)
```
remember
97
what may cause deficient scar formation
```
– Diabetics, Steroids
– ↓ Tensile strength → dehiscence
(separation of tissue margin may
occur)
•
```
98
keloids
Scars that grow beyond the boundaries
of the healing injury and are also
discolored are known as keloid- super gross growth
99
transmural inflammation
lots of neutrafils
100
what causes inflammation
infection, chemicals, heat, cold (red) ,trauma,irritation
101
what is the pathogenesis of inflammation
changes in circulation of blood
changes in vessel wall permeability
white blood cell response
the release of soluble mediators
102
what is pavementing
WBC’s are marginalized & attached to endothelium (pavementing) –also changes;
103
what becomes a rouleaux
RBC’s Sludge & form rouleaux (stacks like coins) - impede circulation further
104
endotheliuim cells are the surronding tube thing- the adhesion molecules are on that
remember
105
what is opsonin
coats the bacteria- so that they are more succeptible to be engulfed
106
what does asprin black
the formation of protaglandins
107
what are PMNs
polymorphonuclear neutrophils
108
what is chemotaxid
Active movement of PMNs along a concentration gradient is called chemotaxis (in Greek, taxis means order)
109
what is acute
last a few days
110
what is systemic inflammation
inflammation involving multiple organs is common in immunologically mediated diseases, such as systemic lupus erythematosus. Sepsis, characterized by a spread of bacteria through the blood, is also a systemic disorder.
111
what is a fever caused by
response caused by endogenous pyrogens
Interleukin I
Tumor Necrosis Factor (TNF)
112
what is secondary wound healing
Wound healing may be complicated by local or systemic influences. Overall, the most important determinants of wound healing are:
```
Site of the wound (ex hand)
Mechanical factors
Size
Presence or absence of infection
Circulatory status
Nutritional factors
Age
- take s a long time
```
113
site
skin is easy, brain poorly
114
mechanical factors
tension movement , small is better, foreign bodies
115
infectoin
sterile is faster
116
circulations
more is better
117
dehicense
very red scar
