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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
Q

Describe role of LV in inflammation response.

A

LV is a major supplier of active phase proteins which makes the blood compartment more viscous, keeping acute inflammation localized

26
Q

What are expected outcomes of acute inflammation?

A

elimination of injurious agent via phagocytosis

27
Q

List cells that mainly participate in chronic inflammation

A

macrophages, lymphocytes, plasma cells,

28
Q

The two types of chronic inflammation are _______

A

diffuse (nonspecific)

granulomatous

29
Q

Describe diffuse chronic inflammation

A

accumulation of macrophages at site of injury lead to fibroblast proliferation, with subsequent scar formation that replaces normal tissue

30
Q

Describe granulomatous inflammation

A

macrophages aggregate around foreign body forming granulomas

31
Q

A granuloma is ________

A

a lesion in which there is a massing of macrophages surrounded by lymphocytes

32
Q

Capacity for healing depends on _______

A

tissue type, cell type, immunocompetence, age, retention of debris, underlying chronic conditions, lifestyle, risk factors, environment, quality of health care

33
Q

The two types of wound healing are __________

A

primary and secondary intention

34
Q

Describe primary intention wound healing

A

wound margins are close together, injured tissues composed of labile cells, typically found in clean surgical wounds, minimal scarring

35
Q

Describe secondary intention wound healing

A

extensive wounds where tissues are composed of permanent cells, granulation leads to scarring, possible adhesion

36
Q

What tissues usually heal by primary intention?

A

Tissues composed of labile cells

37
Q

What tissues usually heal by secondary intention?

A

Tissues composed of permanent cells

38
Q

Labile cells are those that __________

A

continue to divide and replicate throughout life, e.g.epithelial cells of skin, oral cavity, vagina, cervix

39
Q

Stable cells are those that ________

A

normally stop dividing when growth ceases unless appropriately stimulated, e.g. LV, KD, smooth muscle, vascular endothelial cells

40
Q

Permanent cells are those that _______

A

cannot undergo mitotic division, e.g. nerve cells, skeletal muscle, cardiac muscle

41
Q

Adhesions often occur _________

A

as a natural part of the body’s healing process after surgery

42
Q

CRP stands for _____. Its function is to _________

A

C-Reactive Protein

assists in increasing viscosity of blood

43
Q

ESR stands for _______. How will ESR change during inflammation? Why?

A

Erythrocyte Sedimentation Rate

ESR will increase since CRP along with complement proteins and fibrin increase blood viscosity

44
Q

List vascular components of inflammation

A

increase in vascular permeability
vasodilatation
endothelial injury

45
Q

List cellular components of inflammation

A

neutrophils extravasate (let force of fluids out) from circulation to injured tissue to participate in inflammation through phagocytosis, degranulation, and inflammatory mediator release

46
Q

Describe acute inflammation

A

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
Q

Describe chronic inflammation

A

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
Q

Compare dystrophic calcification
vs
metastatic calcification

A

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
Q

List the chemical mediators of inflammation ___. They are derivatives of ____?

A
  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
Q

What inhibits chemical meditators of inflammation?

A

anti-inflammatory drugs

fat free food (chemical garbage)

51
Q

List non-specific markers of inflammation from LV

A

CRP - C reactive protein

Fibrin - increases ESR

52
Q

Chronic inflammation is organized by which cells?

A

macrophages (in tissue), lymphocytes (b-in blood t-in thymus), plasma cells

53
Q

List 2 types of chronic inflammation

A
  1. interstitial/diffuse ie. asthma, COPD

2. granulomatous (granuloma/cellular rosette) ie. TB, Crohn’s

54
Q

What is the outcome of inflammation?

A
  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
Q

When is cellular injury reversible?

A

cellular and organelle swelling is reversible

ie. increase cranial pressure due to edema of brain

56
Q

Describe irreversible cellular injury

A
  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
Q

Describe granulation

A

healing of inflammation often involves ingrowth of capillaries and fibroblasts
ie MI

Pathophysiology I (11 decks)

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