1
Q
Cell Derived : Newly synthesized Arachidonic Acid Metabolites
Damage to cell membranes–> ?
that acts on cell membranes–> releasing what?
A
- Damage to cell membranes → activation of Phospholipase A2
that acts on cell membranes → releasing Arachidonic Acid (AA)
2
Q
Cell Derived : Newly synthesized Arachidonic Acid Metabolites
Two major classes of enzymes then act on AA to produce
metabolites?
A
- Cyclooxygenase (Cox 1 and 2)
- Prostaglandins and prostacyclins
- COX1 constitutive in gut and kidney
- Lipoxygenase
- Leukotrienes (LTs) and lipoxins
3
Q
Arachidonic Acid Metabolites act on many cell types and mediate all
step
Vasodilation (protective in gut
and kidney), fever and pain,
platelet aggregation inhibition
A
Prostaglandins/Prostacyclins
4
Q
Arachidonic Acid Metabolites act on many cell types and mediate all
step
Vasoconstriction and platelet
aggregation (procoagulant)
A
TXA2(thromboxane)
5
Q
Arachidonic Acid Metabolites act on many cell types and mediate all
step
Vasoconstriction and
bronchoconstriction
A
Leukotrienes C-E
6
Q
Arachidonic Acid Metabolites act on many cell types and mediate all
step
Chemotaxis
A
L2B4
7
Q
Arachidonic Acid Metabolites act on many cell types and mediate all
step
Inhibitors of inflammation
A
Lipoxins
8
Q
Arachidonic Acid Metabolites act on many cell types and mediate all
step
Corticosteroids (prednisone, dexamethasone) and many Non-Steroidal Anti-inflammatory Drugs
(NSAIDs like meloxicam, phenylbutazone, ibuprofen) act on this pathway
true/false?
A
true
9
Q
Arachidonic Acid Metabolites act on many cell types and mediate all
step
-main actions are on endothelium, leukocytes, fibroblasts and induction of acute phase response.
-primarily responsible for the “acute phase response”
A
Inflammatory Cytokines: IL1,TNFa
10
Q
? is a complex systemic early-defence system
activated by trauma, infection, stress, neoplasia, and inflammation
A
Acute Phase Response
11
Q
Acute Phase Response
When tissue is injured, what secrete cytokines into the bloodstream (e.g.
interleukins like IL-1, IL-6 and TNFα)
A
local inflammatory cells (neutrophils, granulocytes
and macrophages)
12
Q
Acute Phase Response
what in response, produces a large number of acute-phase reactants
(e.g. C-reactive protein, complement factors, mannose-binding protein &
ferritin)
A
The liver
13
Q
Acute Phase Response
What are the 7 steps that take place?
A
- Fever
- ↑ sleep
- Pain
- Neutrophilia
- ↓ Appetite (TNF promotes lipid and protein mobilization by
suppressing appetite) - Prolonged production of TNF → cachexia (weight loss and
anorexia – cancer and infection) - Corticotropin and corticosteroids released
- If severe → hypotension, decreased vascular resistance, increased
heart rate and decreased blood pH → shock
14
Q
Clotting System
The clotting system
and ? are
intimately connected
A
inflammation
15
Q
Clotting System
The clotting system is
divided into two
converging pathways–>
what?
A
→ activation of
THROMBIN and the
formation of FIBRIN
16
Q
Clotting Cascade
Plasma Derived
intrinsic or extrinsic?
A
(Intrinsic)
17
Q
Clotting Cascade
Tissue Derived
intrinsic or extrinsic?
A
(extrinsic)
18
Q
Clotting Cascade
-Hageman Factor(F12) activated 2° to exposure of
collagen & basement membrane when
endothelium is damaged
is an example of what?
A
Plasma Derived (Intrinsic)
19
Q
Clotting Cascade
- Tissue factor released when sub-endothelial damage
Coagulation Cascade
Fibrinogen Fibrin
- fibrin strands (pink) seen histologically
- framework for repair
is an example of what?
A
Tissue Derived (extrinsic)
20
Q
Summary: Acute Inflammation
Causes
A
are many and include anything that causes cell injury
21
Q
Summary: Acute Inflammation
Purpose
A
destroy harmful agents & limit their spread, prepare damaged tissue
for repair
22
Q
Summary: Acute Inflammation
Cardinal signs of inflammation
A
Redness, Swelling, Heat, Pain, Loss of function
(vasodilation, ↑permeability, oedema, bradykinin release)
23
Q
Summary: Acute Inflammation
Chemical mediators from plasma
A
- Complement - lyses microbes, increases permeability, chemotaxis
- Coagulation - fibrin, production, controls bleeding
24
Q
Summary: Acute Inflammation
Chemical mediators derived from cells
A
- Preformed : histamine, serotonin, lysosomal enzymes
- Synthesized : PGs/LK, ROS, cytokines (including chemokines)
25
# Summary: Acute Inflammation
Vascular changes
Vasodilation, Increased permeability, Fluid exudation
26
# Resolution of infection if....
Macrophages...
can lymphatic vessels remove the exudate.
27
# Resolution of infection if...
The inciting agent or substance is...
eliminated.
28
# Resolution of infection if....
The connective tissue of the affected tissue can...
still support
epithelial cells.
29
# Resolution of infection if....
Damaged epithelium can...
regenerate on an intact basement
membrane.
30
a loalized collection of puss in a cavity formed by disintegration of tissue is called...
ABSCESS FORMATION
31
# ABSCESS FORMATION
caused by what?
is it acute or chronic?
Failure of acute inflammatory response
- Not necessarily classified as acute or chronic
32
# ABSCESS FORMATION
what is it made up of?
Liquified tissue and **neutrophils (pus) surrounded by
fibrous capsule**
Suppurative exudate and liquefactive necrosis
- lots of cellular debris!
33
# ABSCESS FORMATION
what must be done?
will antibiotics work?
**Must be drained**! Antibiotics will not be able to penetrate
the fibrous capsule
https://www.youtube.com/watch?v=jnQi5J9atZk - literally the
best video you will ever watch
34
what is this?
ABSCESS
Large number of neutrophils, and lesser numbers of
macrophages, lymphocytes and bacteria
35
WHAT IS CHRONIC INFLAMMATION?
Prolonged inflammatory response
36
# WHAT IS CHRONIC INFLAMMATION?
How does chronic inflammation arise?
Failure of acute inflammatory response to
eliminate injurious stimulus
- ineffective response to phagocytosis or
enzymatic digestion
Continuous periods of acute inflammation
Intense response to virulence factors or special
biochemical characteristics of pathogens like
mycobacteria
37
Systemic mycoses
what is it, what might it cause?
Chronic Inflammation
Examples of causes
* Systemic mycoses
* Cryptococcus neoformans
* Histoplasmosis, Blastomycosis
38
Intracellular bacteria
what is it, what might it cause?
Chronic Inflammation
Examples of causes
Intracellular bacteria
* Mycobacteria spp
* Rhodococcus sp
39
* Toxoplasma, Leishmania
what is it, what might it cause?
Chronic Inflammation
Examples of causes
* Protozoa
* Toxoplasma, Leishmannnia
40
* Toxocara, Habronema larvae
what is it, what might it cause?
Chronic Inflammation
Examples of causes
* Parasites
* Toxocara, Habronema larvae
41
* grass seeds, splinters, suture material.
Injections
what is it, what might it cause?
Chronic Inflammation
Examples of causes
* Foreign bodies
* grass seeds, splinters, suture material.
Injections
42
* allergic dermatitis eg. FAD (Flea allergy dermatitis)
what is it, what might it cause?
Chronic Inflammation
Examples of causes
* Autoimmune diseases
* allergic dermatitis eg. FAD (Flea allergy dermatitis)
43
Macrophages in Inflammation
describe
* Activated macrophages within tissues are relatively large cells
– abundant clear cytoplasm, slightly eccentricreniform nuclei
–“epithelioid”
44
# Macrophages in Inflammation
With time they can what?
With time they can further differentiate
45
# Macrophages in Inflammation
With time they can further differentiate:
–Multinucleate Giant Cells
what are they?
* collection of fused macrophages
46
# Macrophages in Inflammation
With time they can further differentiate:
–Multinucleate Giant Cells
name 2 types
* Langhans (peripheral nuclei)
or Foreign body type (central nuclei)
47
# Macrophages in Inflammation
With time they can further differentiate:
–Multinucleate Giant Cells
when are they frequently seen?
* seen frequently in granulomatous inflammation
especially when it is difficult to eliminate the
cause of the inflammation eg Mycobacterium spp,
fungi, foreign body
48
WHO IS THE POSTER CHILD FOR CHRONIC
INFLAMMATION?
Macrophages
49
# WHO IS THE POSTER CHILD FOR CHRONIC INFLAMMATION?
Macrophages:
name3 types?
1. Tissue-specific macrophages
2. M1 Macrophages
3. M2 Macrophages
50
# WHO IS THE POSTER CHILD FOR CHRONIC INFLAMMATION?
Macrophages:
Alveolar (lung) macrophages,
splenic macrophages (spleen), osteoclasts(bone), Kupffer cells(liver), microglial (brain)cells
is an example of what?
Tissue-specific macrophages
51
# WHO IS THE POSTER CHILD FOR CHRONIC INFLAMMATION?
Macrophages:
phagocytic cells that respond to
inflammatory stimuli
is an example of what?
M1 Macrophages
*When you think macrophage, the #1 thing is phagocytosis clean up
52
# WHO IS THE POSTER CHILD FOR CHRONIC INFLAMMATION?
Macrophages:
tissue repair
is an example of what?
M2 Macrophages
53
# WHO IS THE POSTER CHILD FOR CHRONIC INFLAMMATION?
what are syncytial cells formed by fusion of 2 or more activated macrophages?
MNGC
54
# WHO IS THE POSTER CHILD FOR CHRONIC INFLAMMATION?
Can form Multinucleated Giant Cells (MNGCs) through
what?
examples?
Can form Multinucleated Giant Cells (MNGCs) through
fusion
- characteristic of chronic granulomatous inflammation
ex. Mycobacteria, mycotic infections or FBs
55
# Some types of Chronic inflammation
name 4
1) Granulomatous Inflammation – diffuse and nodular
2) Eosinophilic granuloma
3) Pyogranulomatous
4) Lymphocytic
nb. can have a mixture of these cell types, but type
that predominates, and histology dictate category
56
# GRANULOMATOUS INFLAMMATION
Cell Types?
Macrophages and MNGCs
57
# GRANULOMATOUS INFLAMMATION
2 Forms?
Diffuse form
Nodular/Tuberculoid form
58
# GRANULOMATOUS INFLAMMATION
accumulation of macrophages within the tissue
- Johne's Disease ĺ Mycobacterium avium subsp. paratuberculosis
- Th2 response
is an example of?
Cell Types: Macrophages and MNGCs
2 Forms:
**Diffuse form:**
59
# GRANULOMATOUS INFLAMMATION
tissue forms into granulomas
- granulomas are nodular masses of inflammatory tissue
- Tuberculosis ĺ Mycobacterium bovis
is an example of?
Cell Types: Macrophages and MNGCs
2 Forms:
**Nodular/Tuberculoid form:**
60
# GRANULOMATOUS INFLAMMATION
Stains?
what are the 2 and when do you use them?
**Ziehl-Neelsen (ZN)** an acid-fast stain used for **Mycobacteria**
Silver Stain or Periodic Acid Schiff (PAS) used to identify **fungi**
61
what is this?
Acute or Chronic:
Type of Inflammation:
Cell types?
etiology?
JOHNE'S DISEASE
mdx: chronic granlamatous exteritis
Ileum of a cow - dense infiltrate of inflammatory cells in lamina propria
Chronic
Diffuse Granulomatous
Macrophages and MNGCs
Mycobacterium avium subsp.
paratuberculosis
62
# HISTOLOGY - GRANULOMAS
what is this?
Fish-Nodular Granulomatous
Inflamation-Mycobacterium ssp.
63
# HISTOLOGY - GRANULOMAS
what is this?
Acid Fast (Ziehl Neelson/ZN) stain for Mycobacteria
64
# WHAT IS YOUR MDX AND ETIOLOGY?
MDx:Multifocal, coalescing, granulomatous pneumonia
Etiology: Mycobacterium bovis
65
# EOSINOPHILIC INFLAMMATION
Cell Type ?
what might you see?
Cell Type: **Eosinophils and macrophages**
- may see lymphocytes
- secondary to migrating parasites, allergic
conditions or fungi
66
# PYOGRANULOMATOUS INFLAMMATION
Cell Types ?
what might you see?
ex?
Cell Types: Neutrophils and Macrophages
- Probably will see lots of pus!
Ex. Histoplasma capsulatum
67
# LYMPHOCYTIC INFLAMMATION
Cell Types?
what might you see?
ex?
Cell Types: **Lymphocytes and plasma cells**
- May see some macrophages as well
Ex. **Leptospirosis**
- Chronic tubulointerstitial nephritis
68
# Summary
Causes of chronic inflammation:
Failure to eliminate stimulus, repeated acute
inflammation, unique virulence factors of microbes
69
# Summary
* Morphologic features:
Mononuclear cells (macrophages, lymphocytes), attempts at
repair: Angiogenesis (new vessels), Fibrosis (fibroblasts, fibrocytes, collagen)
70
# Summary
Role of macrophages:
tissue injury, phagocytosis, stimulate adaptive immunity,
initiate repair & fibrosis
71
# Summary
Granulomatous inflammation:
Predominant cell is macrophage, often Multinucleate
Giant Cells, often also lymphocytes, eosinophils, fibroblasts, fibrous tissue, necrosis
* Diffuse vs Nodular (granuloma)
72
# Summary
Other forms of chronic inflammation include
eosinophilic, pyogranulomatous,
lymphocytic
73
# WOUND REPAIR
Neutrophils and macrophages
Lasts **1-4 days**
Removal of dead tissue(s) and exudate
is what?
Inflammation:
74
# WOUND REPAIR
Macrophages
Lasts up to 3 weeks
Angiogenesis: formation of new blood vessels
Filling with granulation tissue, a delicate vascular
tissue
Is what?
Proliferation:
75
# WOUND REPAIR
****Macrophages
Lasts up to **3 weeks**
Angiogenesis: formation of new blood vessels
Filling with granulation tissue, a delicate vascular
tissue
Is what?
Proliferation:
76
# WOUND REPAIR
formation of new blood vessels
Filling with granulation tissue, a delicate vascular
tissue
Angiogenesis
77
# WOUND REPAIR
****fibrosis - scar formation
Lasts **up to 2 years**
Collagen disposition and remodeling
Maturation:
78
# WOUND REPAIR
necrotic cells/tissues are replaced by tissue similar to original
regeneration
79
# WOUND REPAIR
injured tissue is replaced by fibrous tissue
repair
80
Fills tissue defect during repair
Provides support and allows for remodeling
Proliferation of **fibroblasts** (helps lay down callogen) and endothelial cells
Very vascularized **red/pink** in color
Soft and fragile bleed relatively easily
what is it?
GRANULATION TISSUE
81
nodular structure formed primarily of macrophages, and is a type of chronic inflammatory response
Granuloma
82
orderly proliferation of fibroblasts and capillaries formed during the repair process in damaged tissue
Granulation tissue
83
Granulation tissue is another word for granuloma?
t/f
f
*NOT THE SAME AS GRANULOMA*
84
Scar formation **(chronic)**
Formation of fibrous connective tissue
Composed of **collagen which is made by
fibroblasts**
what is it?
FIBROSIS
85
FIBROSIS same as FIBRIN?
* NOT FIBRIN!!!! (acute inflammation
leakage of fibrinogen from the blood
vessels) *
86
Simple and uncomplicated healing that is **rapid**
Leaves **very little scarring**
Clean edges
Skin for the most part has **normal tensile
strength after healing**
Ex. Ovariohysterectomy
what is this called?
FIRST INTENTION HEALING
87
Complicated healing
Messy edges - wide open wounds
Contraction and healing of wound with
**fibrous connective tissue**
Large **defects - reduced tensile
strength
**
May see granulation tissue
what is this called?
SECOND INTENTION HEALING
88
Excessive formation of **granulation tissue and
fibrosis**
Seen in horses
"Hypertrophic scar"
what is this?
PROUD FLESH
89
Excessive formation of **granulation tissue and
fibrosis**
Seen in horses
"Hypertrophic scar"
what is this?
PROUD FLESH
90
# WHAT CAN AFFECT TISSUE REPAIR?
what 4 systemic causes?
Systemic:
** Nutrition** **Vitamin C Deficiency** (scurvy--bleeding and inflammation of joints) in Guinea Pigs
**Metabolic Status** Diabetes Mellitus
** Circulatory Status** Congestive Heart Failure (CHF)
** Hormonal** **Glucocorticoids are anti-inflammatory**
91
# WHAT CAN AFFECT TISSUE REPAIR?
what 3 local factors?
Local Factors:
- Infection
-FBs
-Wound characteristics: size, location and type
92
* They follow the cell cycle from one mitosis to the next.
* They continue to proliferate throughout life, continuously replacing
cells that have being destroyed.
* Tissues
regenerate after injury, provided that
**enough stem cells remain.**
what are they?
Labile cells or continuously dividing cells
93
# Labile cells or continuously dividing cells
stratified squamous surfaces of the skin, oral
cavity, vagina and cervix
describes what?
* Surface epithelia
94
# Labile cells or continuously dividing cells
what effect to Lining mucosa?
Lining mucosa of all the excretory ducts of the glands of the body
(e.g., salivary glands, pancreas, biliary tract)
95
# Labile cells or continuously dividing cells
in addition to surface epithelia and lining mucosa, what other 3 locations?
* The columnar epithelium of the gastrointestinal tract, uterus, and
fallopian tubes
* The transitional epithelium of the urinary tract
* Cells of the splenic, lymphoid, and hematopoietic tissue.
96
These cells usually demonstrate
a low normal level of
replication. However, stable
cells can undergo rapid division
in response to a variety of
stimuli.
* Stable cells are capable of
reconstituting the tissue of
origin.
* Examples:
* Epithelial cells of the liver,
kidney, lung, pancreas.
* Smooth muscle cells
* Fibroblasts
* Vascular endothelial cells
what are they?
Stable or quiescent cells
97
what is this?
Stable or quiescent cells
Mouse kidney: tubular epithelial cells,
endothelial cells, smooth muscle cells.
98
* These cells have left the
cell cycle and cannot
undergo mitotic division
in postnatal life.
* Examples of permanent
cells:
* Neurons
* Cardiac muscle cells
what are they?
Nondividing or permanent cells
99
# Pathological Aspects of Wound Repair
what happens to the granulation tissue?
wound dehiscence?
ulceration?
1.Inadequate formation of granulation
tissue
* wound dehiscence (breakdown)
* infection
* excessive activity
* after abdominal surgery if ↑
abdominal pressure
* ulceration
* inadequate vascularisation
during healing
How will this incision heal?
100
# Summary
Granulation tissue:
New tissue, repair of wounds, pink, soft,
bleeds easily, mainly **fibroblasts & fibrocytes** (fibroplasia) & **young blood vessels**
(angiogenesis)
101
# Summary
Tissue healing & scar formation
angiogenesis, fibroblast proliferation & fibrosis
102
# Summary
Healing by first intention:
simple, opposed edges, uninfected surgical wounds
103
# Summary
Healing by second intention:
complicated, separated edges, large defect, granulation tissue
forms, replaced by fibrous tissue
104
# Summary
Factors influence wound healing Systemic:
Nutrition, Metabolic status, Circulatory status,
Hormones;
105
Factors influence wound healing Local:
Infection, Mechanical factors, Foreign bodies, Size, location, type of wound
106
# Summary
Pathological consequences of chronic inflammation & inadequate healing:
Inadequate granulation tissue (dehiscence, ulceration) Excessive granulation
tissue (keloid scar).
107
# CIRCULATORY SYSTEM
What makes up the circulatory system?
What makes up the circulatory system?
Heart Ǖ central pump
Arteries Ǖ high velocity blood flow, strong walls
Veins Ǖ slow blood flow, elastic, extra blood reserve
Microcirculation Ǖ capillaries: fluid and waste exchange
Lymphatics Ǖ drain fluid from extravascular spaces
108
# WHAT IS THE VASCULAR ENDOTHELIUM?
It acts as a barrier between intravascular and extravascular spaces
109
# WHAT IS THE VASCULAR ENDOTHELIUM?
What is its role?
name 3
Hemostasis:
Modulates perfusion through mediators:
Inflammatory Response:
110
# WHAT IS THE VASCULAR ENDOTHELIUM?
Stopping blood via vasoconstriction and
coagulation
Normal state ĺ anti-thrombotic & pro-fibrinolytic
Injured state ĺ pro-thrombotic and anti-fibrinolytic
what is this?
Hemostasis:
111
# WHAT IS THE VASCULAR ENDOTHELIUM?
Endothelin --> vasoconstriction
Nitric oxide (NO) --> vasodilation
2 types of what?
Modulates perfusion through mediators:
112
# WHAT IS THE VASCULAR ENDOTHELIUM?
Production of pro-inflammatory cytokines
Directs traffic of inflammatory cells
Tissue repair
describes what?
Inflammatory Response:
113
# WHAT IS THE VASCULAR ENDOTHELIUM?
what is primary homostasis
114
# WHAT IS THE VASCULAR ENDOTHELIUM?
what is secondary homostasis
115
# INTERSTITIUM AND ECM
The medium through which all metabolic products
must pass between the microcirculation and cells
- composed of the Extracellular Matrix (ECM)
Interstitium:
116
# INTERSTITIUM AND ECM
This is Physio 1 Review!!!
Lipid soluble substances (lipophilic) can move across the
membrane
Water moves through pores
Cell volume maintained through pumps (ATPases)
Characteristics of the ECM:
117
# INTERSTITIUM AND ECM
Structural molecules: collagen, reticulin, elastic fibers
Ground substances: glycoproteins, glycosaminoglycans,
proteoglycans
Composition of the ECM:
118
# NUMBERS TO KNOW!!!
Total Body Water:
60% of body weight
119
# NUMBERS TO KNOW!!!
Intracellular Fluid:
40%
- the majority
120
# NUMBERS TO KNOW!!!
Extracellular Fluid:
20%
- Interstitial Fluid: 15%
- Plasma: 5%
121
# FLUID PRESSURES
drives fluid out of
vessels (into ECF)
- Blood pressure
Hydrostatic Pressure:
122
# FLUID PRESSURES
drives fluid into vessels
- Plasma proteins
- any change in net hydrostatic and oncotic
pressure will be altering the fluid distribution
within the ECF (ex. Increased hydrostatic
pressure)
Oncotic Pressure:
123
# FLUID PRESSURES
drives fluid into vessels
- Plasma proteins
- any change in net hydrostatic and oncotic
pressure will be altering the fluid distribution
within the ECF (ex. Increased hydrostatic
pressure)
Oncotic Pressure:
124
# EDEMA
what is edema?
What is edema? - Accumulation of excess extracellular
fluid in the interstitial space or in body
cavities. - Can be **localized or generalized**
125
# EDEMA
4 PATHOMECHANISMS:
1. Increased blood hydrostatic pressure
2. Decreased oncotic pressure
3. Lymphatic obstruction or damage
4. Increased vascular permeability
126
# EDEMA - INCREASED HYDROSTATIC PRESSURE
what is it?
Increased BP (hydrostatic pressure) due to impaired
venous blood flow, forcing fluid out of the vasculature
127
# EDEMA - INCREASED HYDROSTATIC PRESSURE
what does generalized mean?
what is an example?
Generalized: throughout the entire body
Ex. Right-sided Congestive Heart Failure (CHF)
*venus blook can't be pumped to lings so it builds up
increased hydro ??? (I cant read the notes? slide 44)
128
# EDEMA - INCREASED HYDROSTATIC PRESSURE
what does localized mean?
what is an example?
Venous occlusion
- ex. a bandage wrapped too tightly around a limb
*when venous blood can't flow--> increased hydrostatic pressure
Or how about when you fall off your horse and the idiots put the cast on too tight and you are in so much pain your parents have to call 911?
129
# EDEMA - INCREASED HYDROSTATIC PRESSURE
what is lymphatic obstruction/damage?
typically causes localized edema
damage/obstruction of lymphatics (e.g. surgery)
130
# EDEMA - DECREASED ONCOTIC PRESSURE
what does it cause?
Causes **generalized edema *- you lose proteins
everywhere, not just one area!
Remember: Plasma proteins play a role in
maintaining this pressure, so if those proteins are
altered, edema can result!
131
# EDEMA - DECREASED ONCOTIC PRESSURE
Proteins not absorbed from diet or starvation
Decrease in protein production by the liver (hepatic
diseases)
Glomerular diseases
what is it?
Hypoproteinemia:
132
# EDEMA - LYMPHATIC OBSTRUCTION
what is it?
when does it occur?
why does it occur?
**Localized edema**
Common complications from **surgery and neoplasms**
**The lymphatic system normally drains excess fluid, so if
the lymphatics are obstructed then fluid is able to
accumulate!**
133
# EDEMA - INCREASED VASCULAR PERMEABILITY
what is it?
**Localized **edema
Endothelium damage by viruses and toxins
134
# EDEMA - INCREASED VASCULAR PERMEABILITY
Why would there be increased vascular permeability
with inflammation?
Release of inflammatory mediators changes the
permeability of the vasculature!
135
# EDEMA - INCREASED VASCULAR PERMEABILITY
How would this change the composition of the
edema?
With the increase in permeability, both** fluid AND small proteins are able to escape the vasculature**
136
# CLASSIFICATION OF EDEMA
what are the 2 types?
Non-inflammatory - Transudate
Inflammatory - Exudate
137
# CLASSIFICATION OF EDEMA
- increased vascular permeability **(think
inflammation!)**
- **high protein content, high specific
gravity, high nucleated cell count**
what is it?
Inflammatory - Exudate
138
# CLASSIFICATION OF EDEMA
- increased hydrostatic, decreased osmotic,
lymphatic obstruction
- CHF/liver failure
- protein poor, low specific gravity, low
cellularity
what is it?
Non-inflammatory - Transudate
*think transparent-nothing in it
139
Wet, gelatinous and heavy
Swollen organs
When cut, fluid will seep
May also appear yellow
what is it?
**GROSS APPEARANCE** OF EDEMA
140
# HISTOLOGICAL APPEARANCE OF EDEMA
describe
-Clear or pale **eosinophilic staining** depending
on whether is non-inflammatory or inflammatory
edema
- Spaces are distended
- Blood vessels may be filled with RBCs
Lymphatics are **dilated**
Why?
-they are trying hard to soak in as much extra fluid as possible.
141
# EDEMA ACCORDING TO LOCATION
Ascites (Hydroperitoneum)
abdomen
142
# EDEMA ACCORDING TO LOCATION
Submandibular Edema "Bottle Jaw"
jaw
143
# EDEMA ACCORDING TO LOCATION
Hydrothorax
thorax
144
# EDEMA ACCORDING TO LOCATION
Pericardial Effusion "Mulberry Heart Disease"
paracardim/heart (spelling?)
145
# EDEMA ACCORDING TO LOCATION
Anasarca
fetus
Pathology 1 RUSVM
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