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Pathophysiology I > Class 2 - Inflammation > Flashcards

Class 2 - Inflammation Flashcards

1
Q

Inflammation is regarded as a ______ and ______ response to injury

A

vascular

cellular

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2
Q

The purpose of inflammation is _______

A
  • removal of an injurious agent

- cleaning of debris and repair

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3
Q

List types of inflammation and their etiologies

A

Acute - infection or tissue necrosis/infarction

Chronic - non-healing acute process, foreign material in body, auto-immune reaction

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4
Q

The classic signs of inflammation are __________

A 
redness (rubor)
swelling (tumor)
heat (calor)
pain (dolor)
loss of function (functio laesa)
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5
Q

List vascular events of acute inflammation

A

1) brief constriction of arterioles
2) following dilatation of arterioles
3) increased blood flow to the area
4) hyperemia
5) increased hydrostatic pressure - edema
6) venous stasis of blood - heat

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6
Q

In terms of vascular event of acute inflammation, why is there pain?

A

increased hydrostatic pressure in area leads to accumulation of fluids in interstitial space, putting pressure on sensory receptors

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7
Q

The major cells of acute response to inflammation are _____ aka ________

A

PMNs - polymorphonuclear leukocytes

neutrophils

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8
Q

The process of leukocyte accumulation is called ______

A

margination

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9
Q

List sequence of cellular stage of acute inflammation

A

1) Margination and adhesion to endothelium
2) Transmigration across endothelium (Diapedesis)
3) Chemotaxis
4) Activation and phagocytosis

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10
Q

Leukocyte adhesion and transmigration across endothelium is facilitated by _________ on the leukocyte and endothelial surfaces.

A

complementary adhesion molecules (e.g. selectins, integrins)

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11
Q

Chemotaxis is ___________

A

locomotion oriented along a chemical gradient

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12
Q

Band cells are _______. They are released from _____ when __________

A

immature neutrophils with horseshoe (band) shaped nuclei

bone marrow

there is excessive demand for phagocytes (acute inflammation)

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13
Q

Phagocytes are attracted to inflamed tissues through a process called _______.

A

chemotaxis

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14
Q

High Neutrophil count can be attributed to _____

A

Bacterial infection, burns, stress, inflammation

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15
Q

High Lymphocyte count can be attributed to ______.

A

Viral infection, leukemia

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16
Q

High Monocyte count can be attributed to _________.

A

Viral or fungal infection, chronic diseases

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17
Q

High Eosinophil count can be attributed to _____

A

allergic reaction, parasites, autoimmune disorder

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18
Q

High Basophil count can be attributed to_______

A

allergic reaction, cancers, hyperthyroidism

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19
Q

Histamine and serotonin are released from (which type of cells)______ during acute inflammation

A

basophils, mast cells, platelets

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20
Q

Describe function of histamine and serotonin in acute inflammation.

A

Cause vasodilation and increased vascular permeability (fluid escape into interstitial space). Also cause bronchoconstriction

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21
Q

Prostaglandins and cytokines are derived from _________

A 
arachidonic acid
(both are chemical mediators of inflammation)
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22
Q

Prostaglandins function to _________

A

induce vasodilation and bronchoconstriction
pain
(chemical mediators of inflammation)

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23
Q

Cytokines function to _______

A

“kines” to move
activate immune response by other blood cells, attraction of neutrophils, thrombosis, activate liver
LV makes blood more viscous so it’s easier to prevent by localizing
(chemical mediators of inflammation)

24
Q

PAF stands for ______. Describe its function.

A

Platelet aggregating factor -
it activates neutrophils, acts a eosinophil attractant, and stimualates histamine and serotonin release leading to vasodilation and bronchoconstriction

25
Describe role of LV in inflammation response.
LV is a major supplier of active phase proteins which makes the blood compartment more viscous, keeping acute inflammation localized
26
What are expected outcomes of acute inflammation?
elimination of injurious agent via phagocytosis
27
List cells that mainly participate in chronic inflammation
macrophages, lymphocytes, plasma cells,
28
The two types of chronic inflammation are _______
diffuse (nonspecific) | granulomatous
29
Describe diffuse chronic inflammation
accumulation of macrophages at site of injury lead to fibroblast proliferation, with subsequent scar formation that replaces normal tissue
30
Describe granulomatous inflammation
macrophages aggregate around foreign body forming granulomas
31
A granuloma is ________
a lesion in which there is a massing of macrophages surrounded by lymphocytes
32
Capacity for healing depends on _______
tissue type, cell type, immunocompetence, age, retention of debris, underlying chronic conditions, lifestyle, risk factors, environment, quality of health care
33
The two types of wound healing are __________
primary and secondary intention
34
Describe primary intention wound healing
wound margins are close together, injured tissues composed of labile cells, typically found in clean surgical wounds, minimal scarring
35
Describe secondary intention wound healing
extensive wounds where tissues are composed of permanent cells, granulation leads to scarring, possible adhesion
36
What tissues usually heal by primary intention?
Tissues composed of labile cells
37
What tissues usually heal by secondary intention?
Tissues composed of permanent cells
38
Labile cells are those that __________
continue to divide and replicate throughout life, e.g.epithelial cells of skin, oral cavity, vagina, cervix
39
Stable cells are those that ________
normally stop dividing when growth ceases unless appropriately stimulated, e.g. LV, KD, smooth muscle, vascular endothelial cells
40
Permanent cells are those that _______
cannot undergo mitotic division, e.g. nerve cells, skeletal muscle, cardiac muscle
41
Adhesions often occur _________
as a natural part of the body’s healing process after surgery
42
CRP stands for _____. Its function is to _________
C-Reactive Protein | assists in increasing viscosity of blood
43
ESR stands for _______. How will ESR change during inflammation? Why?
Erythrocyte Sedimentation Rate | ESR will increase since CRP along with complement proteins and fibrin increase blood viscosity
44
List vascular components of inflammation
increase in vascular permeability vasodilatation endothelial injury
45
List cellular components of inflammation
neutrophils extravasate (let force of fluids out) from circulation to injured tissue to participate in inflammation through phagocytosis, degranulation, and inflammatory mediator release
46
Describe acute inflammation
neutrophil, eosinophil, and antibody mediated acute inflammation is rapid onset (sec to min), lasts min to days. outcomes incl. complete resolution, abscess formation, and progression to chronic
47
Describe chronic inflammation
mononuclear cell and fibroblast mediated; characterized by persistent destruction and repair. associated with blood v. proliferation, fibrosis. granuloma: nodular collections of epithelioid macrophages and giant cells. outcomes include scarring and amyloidosis.
48
Compare dystrophic calcification vs metastatic calcification
both types of calcification consist of calcium phosphate crystals. differ is that dystrophic calcification (post mi) occurs in damaged tissue, and metastatic calcification occurs in normal tissue in the setting of hypercalcemia dystrophic = damaged
49
List the chemical mediators of inflammation ___. They are derivatives of ____?
1. prostaglandins - vasodilatation, pain 2. prostacyclins - vasodilatation, platelets inhibition 3. thromboxane A2 - vasoconstriction, increase platelet activity 4. leukotrienes - promotes chemotaxis (encourage WBC) 5. cytokines - activate immune response by other blood cells ... 6. PAF "platelet aggregation factor" activates platelets to release histamine, serotonin they are derivatives of ARACHIDONIC ACID
50
What inhibits chemical meditators of inflammation?
anti-inflammatory drugs | fat free food (chemical garbage)
51
List non-specific markers of inflammation from LV
CRP - C reactive protein | Fibrin - increases ESR
52
Chronic inflammation is organized by which cells?
macrophages (in tissue), lymphocytes (b-in blood t-in thymus), plasma cells
53
List 2 types of chronic inflammation
1. interstitial/diffuse ie. asthma, COPD | 2. granulomatous (granuloma/cellular rosette) ie. TB, Crohn's
54
What is the outcome of inflammation?
1. complete resolution: most common 2. scar formation & partial or complete loss of fx (less common) 3. ulcer 4. fistula 5. peritonitis 6. abscess 7. becoming more general/ extensive rather than local
55
When is cellular injury reversible?
cellular and organelle swelling is reversible | ie. increase cranial pressure due to edema of brain
56
Describe irreversible cellular injury
1. disintegration of cellular & organelle membranes (ribo, mtio, nucl) 2. nuclear pyknosis: shrinking necleus 3. karyorrhexis: nucleus and chromatin are broken to pieces 4. karyolysis: nucleus disappears (autodigested by cellular enzymes)
57
Describe granulation
healing of inflammation often involves ingrowth of capillaries and fibroblasts ie MI

Pathophysiology I (11 decks)

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