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Pathology > Inflammation and Repair > Flashcards

Inflammation and Repair Flashcards

1
Q

inflammation

A

the response of vascularized tissue to injury

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2
Q

acute inflammation (2 important things)

A

steryotyped, after the INITIAL vasoconstriction:

Vessels dilate (histamine, etc.)
vessels leak protein (histamine etc)
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3
Q

RUBOR

A

red - from vessel dilation

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4
Q

CALOR

A

hot - from vessel dilation

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5
Q

TUMOR

A

swelling - grom leaky vessels

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6
Q

Vessels leak protein in acute inflammation
hurt a little
hurt worse
hurt really bad

A

-
albumin comes out
IgG comes out
fibrinogen/fibrin for mesh comes out

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7
Q

Neutrophils in acute inflammation

A

pass through the venues and damage anything they think may be bacteria and whatever tissue is nearby

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8
Q

DOLOR

A

pain

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9
Q

Chronic inflammation

A

orchestrated by T cells mostly
B cells become plasma cells and make antibodies
Macrophages gobble things up, if they get mad–> form walls=granulomas
eosinophils kill worms

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10
Q

Granulation tissue

A

fibrin meshwork if not destroyed by plasmin will be ORGANIZED into granulation tissue
by endothelial cells and fibroblasts

macrophages eat the firing, endothelial cells make new vessels, and fibroblasts make collagen fibers

at the end, fibroblast grow contractile fibers like little muscles and this is how SCAR CONTRACTS

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11
Q

myofibroblasts

A

cause scars to contract

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12
Q

Band cell

A

immature neutrophil. child soldier, baby neutrophyl

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13
Q

lymphocyte

A

dense chromatin

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14
Q

monocyte

A

dent in nucleus. name changes to macrophage as soon as it leaves the bloodstream

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15
Q

neutrophil

A

segmented nucleus. made daily just to protect and help you

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16
Q

eosinophil

A

pink

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17
Q

basophil

A

blue

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18
Q

the _____ are the commandos of acute inflammation

A

neutrophils
72 hour life span, clear, packed up on glycogen. Rambo on sugar. can burn up fuel source because they may move to a place where they don’t have access to other nutrients.

segmented nucleus so they can squeeze into places other cells can’t and they can do it fast

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19
Q

diapedisis

A

transmigration of neutrophils through a blood vessel in a combat zone. takes place primarily in venues - because they have a low flow rate and aren’t as fragile as capillaries

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20
Q

Neutrophils are heavily armed troops with a variety of weapons in various

A

granules

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21
Q

azurophil granules

A

myeloperoxidase, elastase, cathepsins

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22
Q

specific granules

A

alkaline phophatase, lactoferrin, and collagenase

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23
Q

both granules have

A

lysozyme

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24
Q

Myeloperoxidase

A

a heme based protein that produces hypochlorite like in household bleach
H2O2–> OCl-

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25
Q

myeloperoxidase deficiency/absence

A

people without it can still kill germs fine, they have other potent weapons

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26
Q

ongoing inflammation makes neutrophils

A

stick better to the endothelium (selections and integrins)

get through endothelium

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27
Q

Deficiencies in selectins, integrins and ligands

A

WBC adhesion defects - can be bad

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28
Q

Gonococcal infection of the finger

A

the redness from extra blood flow through dilated arteries (HYPEREMIA). One joint inflamed, gonorrhea until proven otherwise

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29
Q

All human tissue is gram

A

negative

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30
Q

pus

A

liquid composed of neutrophils and the body tissues their enzymes have liquefied during combat

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31
Q

adjective for pus

A

purulent

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32
Q

verb for make pus

A

supperate

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33
Q

pus surrounded by mor normal tissue

A

abscess

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34
Q

puss filing a body cavity (pleural space, gall bladder)

A

empyema

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35
Q

gonorrhea can cause

A

purulent urethritis

fatal infections of joints

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36
Q

neutrophils lose their ____ after death

A

segmentation

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37
Q

in health and illness, neutrophils tend to stick to

A

vessel endothelium= marginate

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38
Q

aside from neutrophils, you may see ___ in pus

A

fibrin strands

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39
Q

pus builds up pressure because

A

osmotic pull of the small molecules produced by hydrolysis of big proteins

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40
Q

pus is yellow because

A

necrosis is yellow - lipid goes out of the aqueous phase

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41
Q

greenish tinge on exposure to air (of pus)

A

due to neutrophil myeloperoxidase

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42
Q

pseudomonas infections

A

fluorescent green pus that smells like grapes

pigment= pyocyanin

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43
Q

clostridial infections

A

thin (hydrolyzed) gray (lipolyzed) dishwater pus

[clostridia cause your body to decompose, tear up proteins, everything]

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44
Q

left shift

A

lots of band cells, lots of child neutrophils. something bad is probably going on

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45
Q

Leukemoid reaction (what you find in blood)

A

severe infection where so many neutrophils including young ones may be present in the blood that you’ll suspect leukemia

> 50,000 WBC in the absence of true leukemia. in leukemia the wbcs probably aren’t powered up. no toxic granulation

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46
Q

toxic granulation

A

powered up neutrophil. more active. something bad probably going on.

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47
Q

leukemoid reaction will have

A

high leukocyte alkaline phosphatase (low in leukemia)
usually toxic granulation
will lack the chromosome markers for leukemia

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48
Q

if in doubt of leukemia reaction vs leukemia

A

treat for infection. leukemia can wait for days. if the la testing leaves the diagnosis uncertain, do a history and physical exam

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49
Q

Systemic inflammatory response

A

current term for multiple organ failure developing as a result of a bad infection.

extreme elevations of IL-1 and TNF-a.

Once its underway, treating the cause may not save the patient

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50
Q

first line of defense agains the bacteria we meet as we go through life

A

neutrophils

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51
Q

staphylococci

A

try to sequester themselves from their principal enemies (the neutrophils)

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52
Q

streptococci

A

try to outrun neutrophils

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53
Q

necrosis always attracts some

A

inflammatory cells early on

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54
Q

Neutrophils in the lung - damaging effects

A

good that they are there to help, but can –> no air in the lungs–> death

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55
Q

Chediak Higashi features

A

problems with organelles (lysosomes, melanocytes) and thus impaired neutrophil killing of microbes

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56
Q

Chronic Granulomatous disease

A

any of several defects in neutrophil killing of common staph

the body walls off staph using granulomas instead. trivial skin lesions turn into long standing TB-like lesions; if staph get access to lungs death can result if unrecognized

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57
Q

Exudate

A

potein rich fluid released from vessels in inflammation.

in acute inflammation, blood vessels dilate and leak protein, and neutrophils come to the scene

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58
Q

friction blister

A

epidermis detached from the dermis. mild inflammatory cellular reaction

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59
Q

ROS

A

reactive oxygen species, free radicals

need these to kill germs. this may be one reason that antioxidants do so poorly as health promoters in real studies

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60
Q

Neutrophils self destruct after _____. if needed, they can turn into ______

A

72 hours

traps that bind nearby bacteria (neutrophil extracellular traps, NETS)

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61
Q

Sunburn

A

cells that recognize themselves to be radiation-damaged undergo apoptosis

apoptosis of endothelial cells causes vasodilation and delayed-prolonged leakage (causes capillaries to relax)

peeling= desquamation

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62
Q

special reasons for vessel dilation

A

ie sunburn, where the ‘molecular and cellular mediators of inflammation’ aren’t even involved

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63
Q

Triple Response of Lewis

A
  1. local redness (capillaries dilate)
  2. flare surrounding the scratch (capillaries dilate)
  3. swelling/edema (a wheal) surrounds the scratch

only the flare depends on an intact nerve supply. This led to the discovery of histamine, the first known inflammatory mediator

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64
Q

Histamine (released from, and functions in inflammation - 3)

A

major mediator, released from mast cells. functions in inflammation:
dilate blood vessels
make them leaky to proteins, especially albumin
may contribute to pain and itching

bronchoconstriction and a host of other effects

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65
Q

Seratonin

A

in small amounts is released from platelets and constricts vessels (help us stop the bleeding, thanks)
not a targetable factor in what we usually call inflammation
its role in emotional health completely overshadows this

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66
Q

Bradykinin

A

inflammatory peptide that famously DILATES vessels, at least partly by producing prostacyclin.
mediates som pain of inflammation

also a bronchoconstrictor and inflames the airwaymucosa.

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67
Q

Bradykinin production

A

produced in the blood by the kinin-kallikrein system.

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68
Q

Brady kinin and ace inhibitors

A

ace inhibitors famously interfere with the breakdown of bradykinin, which explains the cough side effect (bronchoconstriction and inflamed airway mucosa are effects of bradykinin)

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69
Q

prostaglandins and trhomboxanes are made from _____ by means of _____.

A

arachidonic acid
cyclooxygenase
COX can be inhibited by a variety of medications

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70
Q

Prostaglandin E2

A

variety of effects in acute inflammation

FEEEver, making vessels permeable, and making vessels dilate

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71
Q

PGD2

A

making vessels permeable

making vessels dilate

72
Q

porstacyclin

A

PGI2,

inhibits platelet aggregation and dilates blood vessel (keep blood vessels open for troops)

73
Q

Thromboxane A2

A

promotes platelet aggregation and constricts blood vessels (lets not have a hemorrhage right now troops)

74
Q

When COX is inhibited, AA gets sunned into the _____ path instead. Favoring production of ______

A

lipo-oxygenase pathway
other mediators, especially by neutrophils and macrophages

leukotriene B4, Leukotrienes C4 D4 and E4

75
Q

leukotriene B4

A

famous promotor of neutrophil attachment and chemotaxis

76
Q

Leukotrienes C4, D4, and E4

A

constrict vessels, make them permeable, and constrict airway smooth muscle. there are medications for asthmatics that block their action

77
Q

5-HETE produced by _________ via the _____ pathway is a __________

A

neutrophils and lymphocytes
lypooxygenase pathway
chemotactic agent

78
Q

Lipoxins

A

made via lipooxygenase pathway
produced by neutrophils and macrophages when inflammation is about to end

“brakes”

79
Q

C3a

A

fragment of complement that is a powerful chemotactic agent

80
Q

C3b

A

fragment of complement that binds to microbes via antibodies and allows more complement activation nearby as well as promoting opsonization and thus phagocytosis

81
Q

C5a

A

powerful promotor of inflammation (KING OF THE CASCADE)
promotes chemotaxis
makes more adhesion molecules on endothelium
makes vessels dilate
makes vessels leak

82
Q

MAC

A

produced at end of complement cascade, punches holes in membranes

83
Q

IL-1

A

family of cytokines produced mostly by MACROPHAGES, but also other cells
mostly powerful pro inflammatory cytokine

Fever (endogenous pyrogen)
increased neutrophil production
increase in adhesion molecules
increased movement of and killing by phagocytes
recruitment of lymphocytes to sites of inflammation
causes fatigue and increased sensitivity to pain
dilates blood vessels
increases insulin resistance, changes protein production by liver (acute phase reaction

84
Q

Anakinra

A

blocks IL-1Ra, works agains rheumatoid arthritis

85
Q

IFN-g

A

made by T cells mostly, is another strong pro inflammatory cytokine

recruiting neutrophils and macrophages to sites of inflammation
activating macrophages and making them more deadly
making cells produce more IL1, IL12, and IL23

used for chronic granulomatous disease and osteopetrosis

86
Q

used for chronic granulomatous dz and osteopetrosis

A

IFN-g

87
Q

IL-2

A

cytokine that has little to do with inflammation, but seems to regulate whether T cells respond to antigens or tolerate them
as a recombinant medication, its in use against malignant melanoma and renal cell carcinoma

88
Q

A form of IL-2 complexed with diphtheria toxin is used

A

against cancer cells that express the IL2 receptor, most famously some cutaneous T cell lymphomas

89
Q

IL-4 and IL-13

A

antiinflammatory. produced by macrophages, direct other macrophages to produce anti-inflammatory mediators
TGF-b and IL-10
Alternatively activated macrophages

90
Q

M2 macrophages produce

A

TGF b and IL10 as well as

osteopontin - granuloma glue - lets not fight, but wall it off instead

91
Q

IL-5

A

from Th2 and mast cells
attacts and activates eosinophils.

may use an antibody against Il5 to treat type I allergen illness, esp in severe asthma

92
Q

IL-6

A

some effects similar to IL-1 (fever, neutrophil production)
some anti-inflammatory
the one major cytokine produced by skeletal muscle and is increased by exercise. from sk m= anti-inflammatory

credited for much of the acute phase reaction, with changes in the levels of proteins made by the liver for the blood stream

93
Q

IL-12

A

from stimulated dendritic macrophages and stimulated B cells
turns undifferentiated Tcells into Th1 cells and causes Tcells to produce IFN-g and TNF-a

powerful pro inflammatory effects and is among usual suspects in various autoimmune diseases

94
Q

IL-23

A

up and com ing molecule with effects that may have previously been attributed to IL-12

95
Q

IL-17

A

produced by Th17 promote recruitment of neutrophils, macrophages, and mor Th17 cells to sites of inflammation

famously bad actor that is everywhere

main suspects in rheumatoid arthritis, inflammatory bowel disease, and psoriasis

96
Q

TNF

A 
produced by macrophages and by many other cells.
proinflammatory
causes fever ('endogenous pyrogen')
causes neutrophil production
activates neutrophils and macrophages
helps mediate the acute phase reaction
promotes thrombosis
promotes insulin resistance
induces apoptosis
97
Q

TNF is worth knowing bc

A

its used as an immunostimulant itself.
medicines that block its receptor are among the most important meds for asthma, rheumatoid arthritis, anklyosing spondylitis, inflammatory bowel did, psoriasis and others

TB and fungal infections are the chief risks of these meds

98
Q

PDGF

A

produced by platelets and other mesenchymal cells
powerfully promotes growth of NEW VESSELS as in granulation tissue/young scar

use to treat ulcers, and by surgeons and periodontists

99
Q

TGF-b

A

produced by many cells including macrophages
LAYING DOWN SCAR, sometimes great, sometimes not

seems to be key to effective collagen production in scar, and is blamed for fibrosis in chronic inflammation

slows inflammation, promotes fibrosis and restoration of damaged epithelial cell populations, and can turn other T lymphocytes into t suppressor cells

100
Q

Platelet activating factor

A

small molecule with several known or suspected actions in inflammation

101
Q

chemokines

A

peptides that get neutrophils moving faster when needed

102
Q

C-reactive protein and SAA protein

A

produced by liver in response to the acute phase reaction

CRP has become a pop blood test that supposedly is one more coronary risk factor. some clear value in rheumatology
SAA is protein that is often B pleated to amyloid in the presence of chronic inflammation (leprosy famously)

103
Q

Results from mutations in relatively obscure molecules that act as brakes, or gain of function mutations in cytosine receptors

A

several auto inflammatory diseases. the most familiar is FAMILIAL MEDITERRANEAN FEVER, which can mimic almost anything

104
Q

Neutrophil monocyte topics

A 
adhesion
margination
opsonization
chemotaxis
chemokines
phagocytosis
degranulation
microbe killing
whats in what sort of neutrophil lysosomal granule
105
Q

common clinical problems interfere with neutrophil function in a variety of ways

A

ie diabetes, glucocoritcoid rxs

106
Q

Acute phase reaction

A

quantities of various proteins in the plasma change when significant inflammation has been going on for a while

RBC sink faster in the plasma= increased erythrocyte sedimentation rate

107
Q

anemia of inflammation

A

changes in one’s chemistry also result in less uptake of iron by developing red cells. that will appear if this goes on for very long (part of acute phase reaction)

108
Q

neutrophils

A

classic bacterial infection, candida, bad injury

109
Q

lymphocytes

A

autoimmunity, viruses, pertussis

110
Q

monocytes

A

mycobacteria, other fungi, typhoid

111
Q

eosinophils

A

worms, asthma, hodgkins’s, dermatitis, herpetiformis, dermatomyositis, IgE allergy less often

112
Q

plasma cells/activated B cells

A

especially abundant with spirochetes (syphilis, Lyme dz)

113
Q

no inflammatory cells

A

prions, gas gangrene (very aggressive clostridia), the immunocompromised

114
Q

Eosinophil granules are specialized for

A

chemical warfare against worms, their intended target

extremely alkaline granules (major basic protein) - pour base all over worms

115
Q

Lymphocytes with nuclear dent is often a

A

T killer cell

116
Q

plasma cells

A

nucleus is always pushed to one side of the ell. clock face/soccer ball nucleus

117
Q

the harness of a chancre, the lesion of primary syphilis is due to the great abundance of

A

mostly plasma cells

118
Q

A circulating monocyte/mononuclear phagocyte

A

dent in the nucleus. changes its name to macrophage when it leaves the bloodstream

119
Q

ink used to make tattoos

A

more or less fixed macrophages contain the ink

macrophages loaded with pigment

120
Q

____ come first, ____ move in later on

A

neutrophils (24hrs)

monocytes/macrophages

121
Q

macrophages, can _____

A

stick tight together

122
Q

How our body rids itself of splinters

A

epithelium does not tolerate a free edge, so it grows along the splinter
macrophages adhere to the splinter and to one another, forming a granuloma

123
Q

Macrophages stuck tight together form a

A

granuloma

they are called epitheliod, by sticking together they mimic epithelium

124
Q

Histoplasmosis

A

KC

histoplasmosis granuloma with caseous center

125
Q

foreign body giant cells are

A

fused clusters of macrophages with nuclei distributed throughout

126
Q

Langhans cell

A

is fused macrophages with nuclei in a horseshoe around the edge

127
Q

Most foreign bodies end up surrounded by

A

granulomas

128
Q

TB

A

caseating granuloma

129
Q

giant cell with asteroid body

A

altered cytoskeleton, but no one know whether it means anything

130
Q

The sealant on your own abrasion

A

fibrin

131
Q

fibrous means

A

collagen

132
Q

fibrous means

A

fibrin

133
Q

Ulcer

A

the epithelium and a significant amount of connective tissue underneath have been lost to necrosis

ulcer is a portion of epithelium plus at least some underlying CT that has been lost to necrosis

the crater of an ulcer is always inflamed and fibrin sealed

134
Q

Erosion

A

loss of epithelium WITHOUT significant damage to the underlying CT. in a stomach erosion, only the epithelium and a bit of the lamina propria are gone

135
Q

pseudomembrane

A

very broad, very shallow ulcer. seen famously in diphtheria and C. difficult colitis

136
Q

Scab

A

fresh clot - just a scratch

factor XIII crosslinks fibrin. vessels and fibroblasts invade the fibrin meshwork

ready to fall off - immature scar tissue below

will fill it in with fibrin. the soft clot becomes harder after a few hours. factor XIII cross linking the fibers. red gell stuff under a scab - granulation tissue - fibrin that’s been grown into by the fibrobasts

137
Q

Granulation tissue

A

fibrin that’s been grown into by epithelial tissue, vascuature. gribroblasts

138
Q

scar

A

is collagen

139
Q

Law of epithelium

A

epithelium does not tolerate a free edge. if an epithelial cell is missing a neighbor on one side, it divides to replace it.
everybody wants a neighbor

140
Q

healing skeletal muscle fiber

A

purply RNA rich cytoplasm and big, active nuclei with a whole lot of euchromatin

141
Q

new collagen laid down at site of healing injury

A

scar

142
Q

if you damage the CT below lamina propria,

A

you’ll get at least a tiny scar afterwards

143
Q

Langers lines

A

if you cut along the lines of a scar it will show less
elastic fibers of skin run in a certain way. if you cut the direction the elastic pulls, you wil get a smaller scar. if you cut so that the elastic fibers pull it open, you will get a bigger scar

144
Q

Labile cell populations

A

bone marrow, gut epithelium, epidermis

are always renewing themselve

145
Q

stable cell populations

A

will renew themselves if some members die

liver, other glands, fibroblasts

146
Q

permanent cell populations

A

have very limited ability to replace lost members

brain, heart

147
Q

Wounds healing

A
  1. fibrin
  2. becomes granulation tissue
  3. becomes scar
  4. scar contracts
148
Q

bread and butter pericarditis

A

fibrin on outer surface of the heart. looks like butter and ketchup

149
Q

exuberant granulation tissue after injury

A

an exaggeration of normal healing, with granulation tissue rising above the surface, that may require surgical debridement

no on really understands why this sometimes hapens

150
Q

New vessels sprout and grow

A

into fibrin, and wherever else they seem to be needed for healing.

most famous angiogenic factor is VEGF A. but even without, some vessels would surely sprout where needed

151
Q

VEGF a

A

for vascular sprouting. cancer needs to trick blood vessels into going into tumor, does this through vegf-a

152
Q

granulation tissue redness and softness

A

prominent vessels impart the redness

edema the softness

153
Q

developing granulation tissue has

A

nice new vessels, fibroblasts

maturing vessels. plasma cells too

154
Q

Collagen in trichrome stain

A

dense collagen is deep blue - lots of it in mature scar

155
Q

wounds heal by ____ and ___ intention

A

primary
secondary
(old surgeons terms)

156
Q

primary intention

A

edges are carefully approximated and everything goes perfectly –> tiny scar, everyone happy

well approximated, non infect, well nourished, no diabetes, not on glucocorticoids, clean, well vascularized area

157
Q

secondary intention

A

messy cut, diabetic, etc –> healing by second intention, takes longer, not all that clen cut, bigger scar

158
Q

adhesions

A

scar after surgery able to obstruct the bowel

gut is held tight by fibrous tissue, peritonitis, fibrous bands between loops of bowel that can cause obstruction down the road

159
Q

myofibroblasts

A

fibroblasts with some contractile cytoskeleton. SCAR CONTRACTS at the end of the healing process

160
Q

scar contraction can be detrimental if

A

it kinks the bowel (adhesion) or hinders joint movement

161
Q

Keloid scar

A

a scar that’s overly large, tends to expand over time, and has thick, glassy collagen fibers. serrations on edge of scar (crab claw). tend to keep expanding

162
Q

hypertrophic scar

A

related to keloid. but lacks serrated edges. don’t tend to keep expanding

163
Q

result of longstanding ongoing epithelial damage

A

scar, according to big robbins.
increased damage of CT rather than epithelial tissue is what erf says causes ongoing scarring.

we see this in alcoholic liver cirrhosis and smokers lungs. cells maintain structure, but it’s moot - if you’re mangling an organ, you’re mangling an organ

164
Q

how does bone heal

A

fibroblasts to cartilage to new bone, like in kids

165
Q

Inflammation 9 R’s

A 
Recognize the injury
Recruit white cells
Remove the threat
Regulate the immune response
Resolve the inflammation
Repair the damage

in Real life, most deaths Result from our final inflammatory Reaction

166
Q

-tomy

A

cut something

167
Q

-ectomy

A

cut something out

168
Q

-ostomy

A

made a mouth to outside/between two organs

169
Q

-plasty

A

reshaped

170
Q

-pexy

A

moved something to the right place

171
Q

-rraphy

A

sewed something up

172
Q

-desis

A

made two things stick together

173
Q

Aching pain

A

periosteum/tooth/dura/circuit in brain

174
Q

burning pain

A

mucosal injury/nerve injury

175
Q

crampy pain

A

hollow organ

176
Q

stabbing pain

A

serosal membrane

177
Q

ischemia, most everything else

A

something other than aching, burning, cramping, stabbing

Pathology (15 decks)

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