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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
liquefaction necrosis
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
caseous necrosis
caused by mycobacterium tuberculosis or by certain fungi necrosis of diseased tissue produces solid, amorphous cheesy mass
27
enzymatic fat necrosis
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
gangrenous necrosis
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
chronic injury
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
senile atrophy
caused by aging tissues become smaller and decrease in functional capacity
31
disuse atrophy
when cells are unable to carry out their normal function reversible
32
denervation atrophy
permanent loss of nervous stimulation
33
pressure atrophy
from steady pressure on tissue (tumor, bedsores)
34
endocrine atrophy
decreased hormonal stimulation= atrophy in that organ
35
accumulations
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
hyaline
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
accumulation of minerals and pigments
calcification, hemosiderosis and brown atrophy * metastatic calcification * dystrophic calcificationhemosiderosis * hemochromatosis * brown atrophy
38
metastatic calcification
excessive bloow calcium (maybe from metabolic disorders) leads to calcium accumulation in normal tissues
39
dystrophic calcification
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
hemosiderosis
iron accumulation in tissues excess iron in the form of ferritin combines with protein-forms hemosiderin- a brown pigment that accumulates in cells
41
hemochromatosis
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
brown atrophy
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
inflammation
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
acute inflammation
tightly coordinated vascular and cellular responses to injury increased BF and vascular permeability to leak into interstitial spaces
45
cardinal signs of inflammation
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
phagocytes
neutrophils and macrophages margination -\> adhesion -\> emigration
47
margination
phagocytes (neutrophils ¯ophages) 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
emigration
leukocytes crawl between endothelial cells into tissue. \*neutrophils move faster but die quicker and are more important in bacterial infections
49
chemotaxis
movement of WBCs in response to chemical gradient
50
opsonins
phagocytosis- promoting antigens
51
pyogenic
organisms that fight neutrophils neutrophils reaction to these bacteria result in death and tissue breakfown to produce pus
52
macrophages
arrive late but are much hardier carry the major load in cleaning up debris including dead neutrophils
53
chemical mediators
HISTAMINE: diffuses from inured site to cause vasodilation and increased ermeability of adjacent small venules released from mast cells
54
3 chemical systems
1. Kinin system 2. coagulation system 3. compliment system
55
kinin system
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
coagulation system
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
compliment system
splitting of compliment proteins antigens compliment antibodies
58
transudate
collection of fluid in tissue or body space that accumulates bc of increased hydrostatic or decreased osmotic pressure low protein content
59
exudates
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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