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Patho > Ch4: Injury, inflammation and repair > Flashcards

Ch4: Injury, inflammation and repair Flashcards

1
Q

parenchymal cells

A

cells that carry out the main function of an organ; most abundant; and often unique to that organ

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2
Q

nucleus

A

vital to cells- genetic code in DNA is ultimate regulator of cell’s function surrounded by nuclear membrane, contains loosely arranged CHROMATIN- high content of DNA during cell division, chromatin aggregates into discrete strands (chromosomes) which replicate and separate to form 2 daughter cells

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3
Q

cytoplasm

A

enclosed by highly specialized cell membrane

CYTOPLASMIC ORGANELLES:

  1. mitochondria
  2. endoplasmic reticulum
  3. Golgi apparatus
  4. smooth ER
  5. lysosomes

CYTOSOL: soluble component

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4
Q

Mitochondria

A

complex, membranous structures that generate energy for use by the cell

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5
Q

endoplasmic reticulum

A

tortuous set of membranes

rough: lined by small basophilic granules= RIBOSOMES
smooth: also transport materials through the cell and is the site of production of many biochemical substances other than proteins

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6
Q

Golgi apparatus

A

proteins under ribosome control are carried through the RER to the GA where they are modified, sorted and stored for secretion

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7
Q

Lysosomes

A

membrane bound packets of digestive enzymes

may surround and digest foreign substances that have been engulfed (phagocytosed) by the cell

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8
Q

epithelial cells

A

work with each other as coherent units to carry out specialized functions:

  1. protection
  2. secretion
  3. metabolism

injury interfere with their functions- have to revert to purposes of reproduction to replace dead cells

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9
Q

CT cells

A

more loosely arranged, involved in general support function:

  1. provide physical support
  2. facilitates movement of fluids and nutrients

tissues that give support:

  1. bone
  2. cartilage
  3. ligaments
  4. tendons
  5. fascia
  6. other fibrous tissues
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10
Q

leukocytes

A

WBC; mobile CT type cells specialized to attack foreign substances

neutrophils & monocytes

lymphocytes

basophils and eosinophils

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11
Q

neutrophils and monocytes

A

can engulf and digest foreign materials such as bacteria

monocytes -> macrophages when they leave the bloodstream

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12
Q

lymphocytes

A

direct the attack against persistent foreign materials by remembering their chemical structure

they release substances that kill cells in the area of the foreign material and other substances that attract macrophages to the area. the macrophages then phagocytose the material and dead cells to prevent further spread.

B-cells also transform into plasma cells to produce ANTIBODIES- attach to unique chemical structure of foreign substance (antigen) to aid in neutralizing/destroying it

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13
Q

basophils and eosinophils

A

much less abundant

involved in allergic reactions

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14
Q

collagen

A

most abundant component of CT

amount of collagen= strength and fibrous nature of CT

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15
Q

events following injury

A

intensities depend on magnitude, duration and location of the injury

  1. necrosis: death of cells/tissues as result of endo/exogenous injury.
  2. Inflammation: vascular & cellular response to necrosis or sublethal cell injury. body’s mechanism of limiting spread of injury and removing necrotic debris
  3. Repair: body’s attempt to replace dead cells. doesn’t happen until necrosis ceases

degeneration=changes w/out necrosis

sublethal= can recover

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16
Q

Apoptosis

A

“programmed cell death”

when not all cells generated are needed, rids the body of excess lymphocytes following injury

differs in appearance from necrosis

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17
Q

nuclear changes

A

pyknosis= condensation of the nucleus

karyorrhexis= fragmentation of the nucleus

karyolysis= lysis or fading of the nucleus

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18
Q

anoxia

A

lack of oxygen

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19
Q

hypoxia

A

=reduced oxygen

most common cause of acute injury and necrosis

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20
Q

ischemia

A

localized hypoxia resulting from poor BF

when severe leads to necrosis of the cells in the area

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21
Q

infarct

A

area of ischemic necrosis

most commonly caused by obstruction of arteries

artherosclerotic placques that obstruct coronary arteries and lead to myocardinal infarcts are responsible for high percent of deaths

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22
Q

immunologic mechanisms

A

important part of inflammatory reaction and also contribute to the damage produced by inflammation

less damaging than no resolve though!

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23
Q

autoimmune reaction

A

body reacting to own tissues >producing damaging diseases

RA, lupus

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24
Q

coagulation necrosis

A

caused by anoxia; coagulation process evolves slowly over days.

can recognize coagulation necrosis of an infarct by its pale, yellow color and solid but soft texture

size, location and shape depend on area supplied by blocked artery

25
Q

liquefaction necrosis

A

caused by certain types of bacteria

pyogenic bacteria-attracts neutrophils into area & enzymes released by neutrophils liquefy the dead tissue

thick creamy mixture of dead tissue and neutrophils=pus/purulent exudate

26
Q

caseous necrosis

A

caused by mycobacterium tuberculosis or by certain fungi

necrosis of diseased tissue

produces solid, amorphous cheesy mass

27
Q

enzymatic fat necrosis

A

occurs following injury to pancreas and surrounding adipose tissue as a result of leakage of that organs digestive enzymes

chalky, yellow-white nodules

location limited to pancreas and surroundings

28
Q

gangrenous necrosis

A

coagulation necrosis with superimposed decompisition by saprophytic bacteria

similar to postmortem decomposition except that only a part of the body is dead

caused by bacteria clostriditum- produces gas and a necrotizing toxin

29
Q

chronic injury

A

may produce decrease in tissue size or number (atrophy) or accumulation of material within cells or between. or large cells with decreased function

chronic cell/tissue degeneration classified according to cause of atrophy or type of material

  1. senile atrophy
  2. disuse atrophy
  3. denervation atrophy
  4. pressure atrophy
  5. endocrine atrophy

Accumulations: fatty, adiposity, glycogen, hyaline, minerals& pigments

30
Q

senile atrophy

A

caused by aging

tissues become smaller and decrease in functional capacity

31
Q

disuse atrophy

A

when cells are unable to carry out their normal function

reversible

32
Q

denervation atrophy

A

permanent loss of nervous stimulation

33
Q

pressure atrophy

A

from steady pressure on tissue (tumor, bedsores)

34
Q

endocrine atrophy

A

decreased hormonal stimulation= atrophy in that organ

35
Q

accumulations

A
  1. fatty change/fatty metamorphosis: lipid w/in cells
  2. adiposity: fat in fat cells
  3. glycogen storage: increased carbs
  4. hyaline:
  5. minerals and pigments
36
Q

hyaline

A

dense, homogeneous, eosinophilic deposit- produced by excess protein accumulating w/in cells and becomes compact

Amyloid= hyaline deposit that has crystalline chemical structure, polarizes light & stains with the due congo red

deposits develop very slowly, affect organ function late in the course of disease and are not reversible

37
Q

accumulation of minerals and pigments

A

calcification, hemosiderosis and brown atrophy

  • metastatic calcification
  • dystrophic calcificationhemosiderosis
  • hemochromatosis
  • brown atrophy
38
Q

metastatic calcification

A

excessive bloow calcium (maybe from metabolic disorders)

leads to calcium accumulation in normal tissues

39
Q

dystrophic calcification

A

dying cells take on calcification when this calcium remains as a deposit in the area of necrosis

causes no problem but bc calcium is radiopaque, it allows radiologist to sport areas of disease

40
Q

hemosiderosis

A

iron accumulation in tissues

excess iron in the form of ferritin combines with protein-forms hemosiderin- a brown pigment that accumulates in cells

41
Q

hemochromatosis

A

implies a more serious condition associated with tissue damage

usually caused by a genetic defect in regulation of iron uptake

damaging effects are most felt in the liver and pancreatic islets with resultant cirrhosis of the liver and diabetes

42
Q

brown atrophy

A

brown color of the heart and liver that develops with aging as a result of accumulation of lipdusion pigment in myocardinal fibers and hepatocytes

43
Q

inflammation

A

process by which fluid, chemicals and cells are brought to injured area to limit the extent of injury, remove necrotic debris and prepare for healing process

44
Q

acute inflammation

A

tightly coordinated vascular and cellular responses to injury

increased BF and vascular permeability to leak into interstitial spaces

45
Q

cardinal signs of inflammation

A
  1. redness: HYPEREMIA (increased BF)
  2. swellng: EDEMA (leakage of fluid into tissue)
  3. heat: (increased BF)
  4. pain: from pressure of swelling
  5. loss of function: from pain
46
Q

phagocytes

A

neutrophils and macrophages

margination -> adhesion -> emigration

47
Q

margination

A

phagocytes (neutrophils &macrophages) move from normal location in the bloodstream to periphery as the venula dilates and flow of blood slows. phagocytes then adhesion to endothelial cells

48
Q

emigration

A

leukocytes crawl between endothelial cells into tissue.

*neutrophils move faster but die quicker and are more important in bacterial infections

49
Q

chemotaxis

A

movement of WBCs in response to chemical gradient

50
Q

opsonins

A

phagocytosis- promoting antigens

51
Q

pyogenic

A

organisms that fight neutrophils

neutrophils reaction to these bacteria result in death and tissue breakfown to produce pus

52
Q

macrophages

A

arrive late but are much hardier

carry the major load in cleaning up debris including dead neutrophils

53
Q

chemical mediators

A

HISTAMINE: diffuses from inured site to cause vasodilation and increased ermeability of adjacent small venules

released from mast cells

54
Q

3 chemical systems

A
  1. Kinin system
  2. coagulation system
  3. compliment system
55
Q

kinin system

A

hageman factor:

kinins leak through venule made permeable to histamine

activate to become bradykinin- cause increased vascular permeability and its a major factor in sustaining flow of fluid and chemicals to inflammatory site by self perpetuating reaction

also acts on nerve endings to cause pain

deactivated faster than formed, and vascular response gradually subsides

56
Q

coagulation system

A

activated when fibrinogen leaks through permeable vessels along with other blood coagulation factors

polymerization of fibrinogen to fibrin (barrier to spread of injurous agent)

similar to kinin- inited by Hageman factor-clotting system

57
Q

compliment system

A

splitting of compliment proteins

antigens compliment antibodies

58
Q

transudate

A

collection of fluid in tissue or body space that accumulates bc of increased hydrostatic or decreased osmotic pressure

low protein content

59
Q

exudates

A

result of increased osmotic pressure in tissue bc of high protein content and are caused by inflammation or obstruction of lymphatic flow

Patho (11 decks)

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