Inflammation Flashcards

1
Q

what are thin bands of collagenous connective tissue which may restrict motion or cause retraction to an abnormal position of internal organs

A

adhesion

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2
Q

shrinking of the nucleus

A

nuclear pyknosis

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3
Q

when the nucleus and chromatin are “broken into pieces”

A

karyorrhexis

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4
Q

when the nucleus disappears (being autodigested by cellular enzymes)

A

karyolysis

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5
Q

what type of cellular injury is reversible

A

cellular and organelle swelling

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6
Q

what is the most common and least common outcomes of inflammation

A

complete resolution is the most common
scar formation and partial or complete loss of function is less common (ulcer, fistula, peritonitis, abscesses)

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7
Q

the following list is an example of primary or secondary intetion wound healing:
- clear surgical wounds
- close wound margins
- injured tissues composed of labile cells (epithelium)
- accomplished through the process of granulation

A

primary intention

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8
Q

the following list is an example of primary or secondary intetion wound healing:
- crashed extensive wounds
- tissues, composed of permanent cells
- risk factors for poor healing
- produces scar/adhesion
- leads to deformity

A

secondary intention
*the mesh produced by fibroblasts cannot be filled with the same type of cells that were there before, so the area has to heal with a scar

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9
Q

What kind of cells recreuit stem cells in the area to perform restoration?
What kind of cells can restore completely on their own?
What kind of cells do not have stem cells to regenerate themselves so restoration takes place via fibroplasia/scaring

A

stable cells
labile cells
permanent cells

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10
Q

when do we see an increase in PMNs or neutrophilia

A

during acute bacterial infections or acute necrosis

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11
Q

what is the term for when RBC’s stack together in long chains causing them to sediment more readily? Why does this happen? What is ESR?

A

this concept is known as rouleaux formation and the rate in which it happens is called ESR (erythrocyte sedimentation rate).
The mechanism for the sedimentation rate, increases non-specifically with inflammation and increased acute phase serum proteins.

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12
Q

when do we often see an increase in eosinophils and basophils?

A

during allergic reactions and with parasitic infestations

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13
Q

monocytes can migrate out of the bloodstream and become tissue macrophages under the influence of ______

A

cytokines

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14
Q

if we see neutrophils in the blood, it is _____; if we see monocytes and lymphocytes in the blood, it is _____

A

acute; chronic

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15
Q

what are the two major types of chronic inflammation

A
  • interstitial/diffuse: asthma, COPD, colitis
  • granulomatous: TB, Crohn’s disease
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16
Q

what are non-specific markers of inflammation

A

CRP (C-Reactive Protein)
Fibrin - increased ESR

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17
Q

what do we call a bunch of proteins the LV gives to the blood plasma to fight intruders

A

complement

18
Q

explain the platelet aggregation factor (PAF)

A

platelets are activated –> they release histamine and serotonin –> causes vasodilation and bronchoconstriction

19
Q

Arachidonic Acid gives rise to what chemical mediators of inflammation

A
  • prostaglandins
  • prostacyclins
  • thromboxane A2
  • Leukotrienes
  • Cytokines
20
Q

which chemical mediator for inflammation is responsible for vasodilation and pain

A

prostaglandins

21
Q

which chemical mediator for inflammation is responsible for vasodilation and platelet inhibition

A

prostacyclins

22
Q

which chemical mediator for inflammation is responsible for vasodilation and increase in platelet activity

A

thromboxane A2

23
Q

which chemical mediator for inflammation is responsible for promoting chemotaxis

A

leukotrienes

24
Q

which chemical mediator activates immune responses by other blood cells –> fever, thrombisis, attraction of PMN, & liver activation

A

cytokines

25
Q

what is the difference between monocytes and macrophages

A

monocytes are found in blood and macrophages are found in tissues

26
Q

mast cells

A

were at one time monocytes but evolved to develop granules inside of them; mast cells along with basophils are major cells for allergies

27
Q

which two chemical mediators of inflammation are released from inflammatory cells: basophils, mast cells, and platelets

A

histamine and serotonin

28
Q

what are the fucntions of histamine and serotinin when inflammation is present in the body

A

they cause vasodilation and increased vascular permeability (fluid escapes into the interstital space - how edema is formed)
also cause bronchoconstriction (ex: asthma attack)

29
Q

what is another name for a young or immature neutrophil

A

band cell (immediate precursor for mature neutrophil)

30
Q

what is another name for a mature neutrophil

A

segmented neutrophil

31
Q

bandemia

A

abundance of immature neutrophils in the blood (usually at the beginning of a acute bacterial infection)

32
Q

list the 6 vascular events of acute inflammation

A
  1. brief constriction of arterioles
  2. following dilation of arterioles
  3. increased blood flow to the area
  4. hyperemia (redness)
  5. increased hydrostatic pressure (edema)
  6. venous stasis of blood (heat)
33
Q

rubor

A

redness

34
Q

calor

A

heat

35
Q

dolor

A

pain

36
Q

functio laesa

A

loss or diminution of function

37
Q

which type of inflammation is most commonly a result of an infection or tissue necrosis/infarction; clinical presentation starts abruptly

A

acute infmmation

38
Q

which type of inflammation is either due to non-healing acute process, foreign materials within the body, or auto-immune reactions; clinical presentation is insidious

A

chronic

39
Q

T/F - inflammation is regarded as a vascular and cellular response to injury

A

T

40
Q

the purpose of inflammation

A

removal/elimination of an injurous agent; cleaning of debris and repair