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Pathology 1 RUSVM > Block 4 > Flashcards

Block 4 Flashcards

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)
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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
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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

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4
Q

Arachidonic Acid Metabolites act on many cell types and mediate all

step

Vasoconstriction and platelet
aggregation (procoagulant)

A

TXA2(thromboxane)

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5
Q

Arachidonic Acid Metabolites act on many cell types and mediate all

step

Vasoconstriction and
bronchoconstriction

A

Leukotrienes C-E

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6
Q

Arachidonic Acid Metabolites act on many cell types and mediate all

step

Chemotaxis

A

L2B4

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7
Q

Arachidonic Acid Metabolites act on many cell types and mediate all

step

Inhibitors of inflammation

A

Lipoxins

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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

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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

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10
Q

? is a complex systemic early-defence system
activated by trauma, infection, stress, neoplasia, and inflammation

A

Acute Phase Response

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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)

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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

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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
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14
Q

Clotting System

The clotting system
and ? are
intimately connected

A

inflammation

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15
Q

Clotting System

The clotting system is
divided into two
converging pathways–>
what?

A

→ activation of
THROMBIN and the
formation of FIBRIN

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16
Q

Clotting Cascade

Plasma Derived

intrinsic or extrinsic?

A

(Intrinsic)

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17
Q

Clotting Cascade

Tissue Derived
intrinsic or extrinsic?

A

(extrinsic)

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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)

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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)

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20
Q

Summary: Acute Inflammation

Causes

A

are many and include anything that causes cell injury

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21
Q

Summary: Acute Inflammation

Purpose

A

destroy harmful agents & limit their spread, prepare damaged tissue
for repair

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22
Q

Summary: Acute Inflammation

Cardinal signs of inflammation

A

Redness, Swelling, Heat, Pain, Loss of function
(vasodilation, ↑permeability, oedema, bradykinin release)

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23
Q

Summary: Acute Inflammation

Chemical mediators from plasma

A
  • Complement - lyses microbes, increases permeability, chemotaxis
  • Coagulation - fibrin, production, controls bleeding
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24
Q

Summary: Acute Inflammation

Chemical mediators derived from cells

A
  • Preformed : histamine, serotonin, lysosomal enzymes
  • Synthesized : PGs/LK, ROS, cytokines (including chemokines)
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25
Q

Summary: Acute Inflammation

Vascular changes

A

Vasodilation, Increased permeability, Fluid exudation

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26
Q

Resolution of infection if….

Macrophages…

A

can lymphatic vessels remove the exudate.

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27
Q

Resolution of infection if…

The inciting agent or substance is…

A

eliminated.

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28
Q

Resolution of infection if….

The connective tissue of the affected tissue can…

A

still support
epithelial cells.

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29
Q

Resolution of infection if….

Damaged epithelium can…

A

regenerate on an intact basement
membrane.

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30
Q

a loalized collection of puss in a cavity formed by disintegration of tissue is called…

A

ABSCESS FORMATION

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31
Q

ABSCESS FORMATION

caused by what?
is it acute or chronic?

A

Failure of acute inflammatory response
- Not necessarily classified as acute or chronic

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32
Q

ABSCESS FORMATION

what is it made up of?

A

Liquified tissue and neutrophils (pus) surrounded by
fibrous capsule

Suppurative exudate and liquefactive necrosis
- lots of cellular debris!

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33
Q

ABSCESS FORMATION

what must be done?
will antibiotics work?

A

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

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34
Q

what is this?

A

ABSCESS

Large number of neutrophils, and lesser numbers of
macrophages, lymphocytes and bacteria

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35
Q

WHAT IS CHRONIC INFLAMMATION?

A

Prolonged inflammatory response

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36
Q

WHAT IS CHRONIC INFLAMMATION?

How does chronic inflammation arise?

A

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

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37
Q

Systemic mycoses
what is it, what might it cause?

A

Chronic Inflammation
Examples of causes
* Systemic mycoses
* Cryptococcus neoformans
* Histoplasmosis, Blastomycosis

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38
Q

Intracellular bacteria
what is it, what might it cause?

A

Chronic Inflammation
Examples of causes
Intracellular bacteria
* Mycobacteria spp
* Rhodococcus sp

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39
Q
  • Toxoplasma, Leishmania
    what is it, what might it cause?
A

Chronic Inflammation
Examples of causes

  • Protozoa
  • Toxoplasma, Leishmannnia
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40
Q
  • Toxocara, Habronema larvae
    what is it, what might it cause?
A

Chronic Inflammation
Examples of causes
* Parasites
* Toxocara, Habronema larvae

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41
Q
  • grass seeds, splinters, suture material.
    Injections
    what is it, what might it cause?
A

Chronic Inflammation
Examples of causes

  • Foreign bodies
  • grass seeds, splinters, suture material.
    Injections
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42
Q
  • allergic dermatitis eg. FAD (Flea allergy dermatitis)
    what is it, what might it cause?
A

Chronic Inflammation
Examples of causes
* Autoimmune diseases
* allergic dermatitis eg. FAD (Flea allergy dermatitis)

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43
Q

Macrophages in Inflammation
describe

A
  • Activated macrophages within tissues are relatively large cells
    – abundant clear cytoplasm, slightly eccentricreniform nuclei
    –“epithelioid”
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44
Q

Macrophages in Inflammation

With time they can what?

A

With time they can further differentiate

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45
Q

Macrophages in Inflammation

With time they can further differentiate:
–Multinucleate Giant Cells
what are they?

A
  • collection of fused macrophages
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46
Q

Macrophages in Inflammation

With time they can further differentiate:
–Multinucleate Giant Cells
name 2 types

A
  • Langhans (peripheral nuclei)
    or Foreign body type (central nuclei)
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47
Q

Macrophages in Inflammation

With time they can further differentiate:
–Multinucleate Giant Cells
when are they frequently seen?

A
  • seen frequently in granulomatous inflammation
    especially when it is difficult to eliminate the
    cause of the inflammation eg Mycobacterium spp,
    fungi, foreign body
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48
Q

WHO IS THE POSTER CHILD FOR CHRONIC
INFLAMMATION?

A

Macrophages

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49
Q

WHO IS THE POSTER CHILD FOR CHRONIC INFLAMMATION?

Macrophages:
name3 types?

A
  1. Tissue-specific macrophages
  2. M1 Macrophages
  3. M2 Macrophages
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50
Q

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?

A

Tissue-specific macrophages

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51
Q

WHO IS THE POSTER CHILD FOR CHRONIC INFLAMMATION?

Macrophages:
phagocytic cells that respond to
inflammatory stimuli
is an example of what?

A

M1 Macrophages
*When you think macrophage, the #1 thing is phagocytosis clean up

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52
Q

WHO IS THE POSTER CHILD FOR CHRONIC INFLAMMATION?

Macrophages:

tissue repair
is an example of what?

A

M2 Macrophages

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53
Q

WHO IS THE POSTER CHILD FOR CHRONIC INFLAMMATION?

what are syncytial cells formed by fusion of 2 or more activated macrophages?

A

MNGC

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54
Q

WHO IS THE POSTER CHILD FOR CHRONIC INFLAMMATION?

Can form Multinucleated Giant Cells (MNGCs) through
what?
examples?

A

Can form Multinucleated Giant Cells (MNGCs) through
fusion
- characteristic of chronic granulomatous inflammation
ex. Mycobacteria, mycotic infections or FBs

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55
Q

Some types of Chronic inflammation

name 4

A

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

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56
Q

GRANULOMATOUS INFLAMMATION

Cell Types?

A

Macrophages and MNGCs

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57
Q

GRANULOMATOUS INFLAMMATION

2 Forms?

A

Diffuse form
Nodular/Tuberculoid form

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58
Q

GRANULOMATOUS INFLAMMATION

accumulation of macrophages within the tissue
- Johne’s Disease ĺ Mycobacterium avium subsp. paratuberculosis
- Th2 response

is an example of?

A

Cell Types: Macrophages and MNGCs
2 Forms:
Diffuse form:

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59
Q

GRANULOMATOUS INFLAMMATION

tissue forms into granulomas
- granulomas are nodular masses of inflammatory tissue
- Tuberculosis ĺ Mycobacterium bovis

is an example of?

A

Cell Types: Macrophages and MNGCs
2 Forms:
Nodular/Tuberculoid form:

60
Q

GRANULOMATOUS INFLAMMATION

Stains?
what are the 2 and when do you use them?

A

Ziehl-Neelsen (ZN) an acid-fast stain used for Mycobacteria
Silver Stain or Periodic Acid Schiff (PAS) used to identify fungi

61
Q

what is this?
Acute or Chronic:
Type of Inflammation:
Cell types?
etiology?

A

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
Q

HISTOLOGY - GRANULOMAS

what is this?

A

Fish-Nodular Granulomatous
Inflamation-Mycobacterium ssp.

63
Q

HISTOLOGY - GRANULOMAS

what is this?

A

Acid Fast (Ziehl Neelson/ZN) stain for Mycobacteria

64
Q

WHAT IS YOUR MDX AND ETIOLOGY?

A

MDx:Multifocal, coalescing, granulomatous pneumonia
Etiology: Mycobacterium bovis

65
Q

EOSINOPHILIC INFLAMMATION

Cell Type ?
what might you see?

A

Cell Type: Eosinophils and macrophages
- may see lymphocytes
- secondary to migrating parasites, allergic
conditions or fungi

66
Q

PYOGRANULOMATOUS INFLAMMATION

Cell Types ?
what might you see?
ex?

A

Cell Types: Neutrophils and Macrophages
- Probably will see lots of pus!

Ex. Histoplasma capsulatum

67
Q

LYMPHOCYTIC INFLAMMATION

Cell Types?
what might you see?
ex?

A

Cell Types: Lymphocytes and plasma cells
- May see some macrophages as well

Ex. Leptospirosis
- Chronic tubulointerstitial nephritis

68
Q

Summary

Causes of chronic inflammation:

A

Failure to eliminate stimulus, repeated acute
inflammation, unique virulence factors of microbes

69
Q

Summary

  • Morphologic features:
A

Mononuclear cells (macrophages, lymphocytes), attempts at
repair: Angiogenesis (new vessels), Fibrosis (fibroblasts, fibrocytes, collagen)

70
Q

Summary

Role of macrophages:

A

tissue injury, phagocytosis, stimulate adaptive immunity,
initiate repair & fibrosis

71
Q

Summary

Granulomatous inflammation:

A

Predominant cell is macrophage, often Multinucleate
Giant Cells, often also lymphocytes, eosinophils, fibroblasts, fibrous tissue, necrosis
* Diffuse vs Nodular (granuloma)

72
Q

Summary

Other forms of chronic inflammation include

A

eosinophilic, pyogranulomatous,
lymphocytic

73
Q

WOUND REPAIR

Neutrophils and macrophages
Lasts 1-4 days
Removal of dead tissue(s) and exudate

is what?

A

Inflammation:

74
Q

WOUND REPAIR

Macrophages
Lasts up to 3 weeks
Angiogenesis: formation of new blood vessels
Filling with granulation tissue, a delicate vascular
tissue
Is what?

A

Proliferation:

75
Q

WOUND REPAIR

**Macrophages
Lasts up to 3 weeks
Angiogenesis: formation of new blood vessels
Filling with granulation tissue, a delicate vascular
tissue
Is what?

A

Proliferation:

76
Q

WOUND REPAIR

formation of new blood vessels
Filling with granulation tissue, a delicate vascular
tissue

A

Angiogenesis

77
Q

WOUND REPAIR

**fibrosis - scar formation
Lasts up to 2 years
Collagen disposition and remodeling

A

Maturation:

78
Q

WOUND REPAIR

necrotic cells/tissues are replaced by tissue similar to original

A

regeneration

79
Q

WOUND REPAIR

injured tissue is replaced by fibrous tissue

A

repair

80
Q

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?

A

GRANULATION TISSUE

81
Q

nodular structure formed primarily of macrophages, and is a type of chronic inflammatory response

A

Granuloma

82
Q

orderly proliferation of fibroblasts and capillaries formed during the repair process in damaged tissue

A

Granulation tissue

83
Q

Granulation tissue is another word for granuloma?
t/f

A

f
NOT THE SAME AS GRANULOMA

84
Q

Scar formation (chronic)

Formation of fibrous connective tissue

Composed of collagen which is made by
fibroblasts
what is it?

A

FIBROSIS

85
Q

FIBROSIS same as FIBRIN?

A
  • NOT FIBRIN!!!! (acute inflammation
    leakage of fibrinogen from the blood
    vessels) *
86
Q

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?

A

FIRST INTENTION HEALING

87
Q

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?

A

SECOND INTENTION HEALING

88
Q

Excessive formation of granulation tissue and
fibrosis

Seen in horses

“Hypertrophic scar”

what is this?

A

PROUD FLESH

89
Q

Excessive formation of granulation tissue and
fibrosis

Seen in horses

“Hypertrophic scar”

what is this?

A

PROUD FLESH

90
Q

WHAT CAN AFFECT TISSUE REPAIR?

what 4 systemic causes?

A

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
Q

WHAT CAN AFFECT TISSUE REPAIR?

what 3 local factors?

A

Local Factors:
- Infection
-FBs
-Wound characteristics: size, location and type

92
Q
  • 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?

A

Labile cells or continuously dividing cells

93
Q

Labile cells or continuously dividing cells

stratified squamous surfaces of the skin, oral
cavity, vagina and cervix
describes what?

A
  • Surface epithelia
94
Q

Labile cells or continuously dividing cells

what effect to Lining mucosa?

A

Lining mucosa of all the excretory ducts of the glands of the body
(e.g., salivary glands, pancreas, biliary tract)

95
Q

Labile cells or continuously dividing cells

in addition to surface epithelia and lining mucosa, what other 3 locations?

A
  • 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
Q

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?

A

Stable or quiescent cells

97
Q

what is this?

A

Stable or quiescent cells

Mouse kidney: tubular epithelial cells,
endothelial cells, smooth muscle cells.

98
Q
  • 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?

A

Nondividing or permanent cells

99
Q

Pathological Aspects of Wound Repair

what happens to the granulation tissue?
wound dehiscence?
ulceration?

A

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
Q

Summary

Granulation tissue:

A

New tissue, repair of wounds, pink, soft,
bleeds easily, mainly fibroblasts & fibrocytes (fibroplasia) & young blood vessels
(angiogenesis)

101
Q

Summary

Tissue healing & scar formation

A

angiogenesis, fibroblast proliferation & fibrosis

102
Q

Summary

Healing by first intention:

A

simple, opposed edges, uninfected surgical wounds

103
Q

Summary

Healing by second intention:

A

complicated, separated edges, large defect, granulation tissue
forms, replaced by fibrous tissue

104
Q

Summary

Factors influence wound healing Systemic:

A

Nutrition, Metabolic status, Circulatory status,
Hormones;

105
Q

Factors influence wound healing Local:

A

Infection, Mechanical factors, Foreign bodies, Size, location, type of wound

106
Q

Summary

Pathological consequences of chronic inflammation & inadequate healing:

A

Inadequate granulation tissue (dehiscence, ulceration) Excessive granulation
tissue (keloid scar).

107
Q

CIRCULATORY SYSTEM

What makes up the circulatory system?

A

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
Q

WHAT IS THE VASCULAR ENDOTHELIUM?

A

It acts as a barrier between intravascular and extravascular spaces

109
Q

WHAT IS THE VASCULAR ENDOTHELIUM?

What is its role?
name 3

A

Hemostasis:
Modulates perfusion through mediators:
Inflammatory Response:

110
Q

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?

A

Hemostasis:

111
Q

WHAT IS THE VASCULAR ENDOTHELIUM?

Endothelin –> vasoconstriction
Nitric oxide (NO) –> vasodilation

2 types of what?

A

Modulates perfusion through mediators:

112
Q

WHAT IS THE VASCULAR ENDOTHELIUM?

Production of pro-inflammatory cytokines
Directs traffic of inflammatory cells
Tissue repair

describes what?

A

Inflammatory Response:

113
Q

WHAT IS THE VASCULAR ENDOTHELIUM?

what is primary homostasis

A
114
Q

WHAT IS THE VASCULAR ENDOTHELIUM?

what is secondary homostasis

A
115
Q

INTERSTITIUM AND ECM

The medium through which all metabolic products
must pass between the microcirculation and cells
- composed of the Extracellular Matrix (ECM)

A

Interstitium:

116
Q

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)

A

Characteristics of the ECM:

117
Q

INTERSTITIUM AND ECM

Structural molecules: collagen, reticulin, elastic fibers
Ground substances: glycoproteins, glycosaminoglycans,
proteoglycans

A

Composition of the ECM:

118
Q

NUMBERS TO KNOW!!!

Total Body Water:

A

60% of body weight

119
Q

NUMBERS TO KNOW!!!

Intracellular Fluid:

A

40%
- the majority

120
Q

NUMBERS TO KNOW!!!

Extracellular Fluid:

A

20%
- Interstitial Fluid: 15%
- Plasma: 5%

121
Q

FLUID PRESSURES

drives fluid out of
vessels (into ECF)
- Blood pressure

A

Hydrostatic Pressure:

122
Q

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)

A

Oncotic Pressure:

123
Q

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)

A

Oncotic Pressure:

124
Q

EDEMA

what is edema?

A

What is edema? - Accumulation of excess extracellular
fluid in the interstitial space or in body
cavities. - Can be localized or generalized

125
Q

EDEMA

4 PATHOMECHANISMS:

A
  1. Increased blood hydrostatic pressure
  2. Decreased oncotic pressure
  3. Lymphatic obstruction or damage
  4. Increased vascular permeability
126
Q

EDEMA - INCREASED HYDROSTATIC PRESSURE

what is it?

A

Increased BP (hydrostatic pressure) due to impaired
venous blood flow, forcing fluid out of the vasculature

127
Q

EDEMA - INCREASED HYDROSTATIC PRESSURE

what does generalized mean?
what is an example?

A

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
Q

EDEMA - INCREASED HYDROSTATIC PRESSURE

what does localized mean?
what is an example?

A

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
Q

EDEMA - INCREASED HYDROSTATIC PRESSURE

what is lymphatic obstruction/damage?

A

typically causes localized edema
damage/obstruction of lymphatics (e.g. surgery)

130
Q

EDEMA - DECREASED ONCOTIC PRESSURE

what does it cause?

A

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
Q

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?

A

Hypoproteinemia:

132
Q

EDEMA - LYMPHATIC OBSTRUCTION

what is it?
when does it occur?
why does it occur?

A

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
Q

EDEMA - INCREASED VASCULAR PERMEABILITY

what is it?

A

**Localized **edema
Endothelium damage by viruses and toxins

134
Q

EDEMA - INCREASED VASCULAR PERMEABILITY

Why would there be increased vascular permeability
with inflammation?

A

Release of inflammatory mediators changes the
permeability of the vasculature!

135
Q

EDEMA - INCREASED VASCULAR PERMEABILITY

How would this change the composition of the
edema?

A

With the increase in permeability, both** fluid AND small proteins are able to escape the vasculature**

136
Q

CLASSIFICATION OF EDEMA

what are the 2 types?

A

Non-inflammatory - Transudate
Inflammatory - Exudate

137
Q

CLASSIFICATION OF EDEMA

  • increased vascular permeability (think
    inflammation!)
  • high protein content, high specific
    gravity, high nucleated cell count

what is it?

A

Inflammatory - Exudate

138
Q

CLASSIFICATION OF EDEMA

  • increased hydrostatic, decreased osmotic,
    lymphatic obstruction
  • CHF/liver failure
  • protein poor, low specific gravity, low
    cellularity

what is it?

A

Non-inflammatory - Transudate
*think transparent-nothing in it

139
Q

Wet, gelatinous and heavy

Swollen organs

When cut, fluid will seep

May also appear yellow

what is it?

A

GROSS APPEARANCE OF EDEMA

140
Q

HISTOLOGICAL APPEARANCE OF EDEMA

describe

A

-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
Q

EDEMA ACCORDING TO LOCATION

A

Ascites (Hydroperitoneum)
abdomen

142
Q

EDEMA ACCORDING TO LOCATION

A

Submandibular Edema “Bottle Jaw”
jaw

143
Q

EDEMA ACCORDING TO LOCATION

A

Hydrothorax
thorax

144
Q

EDEMA ACCORDING TO LOCATION

A

Pericardial Effusion “Mulberry Heart Disease”
paracardim/heart (spelling?)

145
Q

EDEMA ACCORDING TO LOCATION

A

Anasarca
fetus

Pathology 1 RUSVM (7 decks)

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