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Patho I > Powerpoint-Chap2 > Flashcards

Powerpoint-Chap2 Flashcards

1
Q

What are the acute inflammatory cell

A

granulocytes

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2
Q

What are the 3 main involvements of acute inflammation

A

vascular dilation and increased flow
microvasculature alterations to allow egress of cells and proteins
emigration, accumulation and activation of leukocytes

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3
Q

What are the 4 cardinal signs of inflammation

A

dolor-pain
calor-heat
rubor-redness
tumor-swelling

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4
Q

What is the 5th cardinal sign of acute inflammation

A

functio laesa-loss of function

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5
Q

What is the Lewis Triple response

A

red line(vasodilation)
red flare- after 15-30 seconds (vasodilation)
wheal in 1-3 minutes (vascular leakage)

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6
Q

what cells release histamine

A

mast cells

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7
Q

how can we completely stop inflammation

A

cutting the nerves involved

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8
Q

What can cause acute inflammation

A

infections, necrotic tissues, hypoxia, foreign bodies, immune reactions

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9
Q

what factor during hypoxia causes inflammation

A

hypoxic induced factor 1 alpha

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10
Q

what is released in necrotic tissue to cause inflammation

A

uric acid, ATP, HMGB-1 DNA

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11
Q

what are the main triggers of inflammation in an infection(foreign)

A

toll like R and cytoplasmic R

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12
Q

In a blood smear describe what neutrophils look like

A

have 3+ nuclei usually. young neutrophils have the banded nucleus

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13
Q

In a blood smear what do the eosinophils look like

A

hace 2 nuclei usually

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14
Q

In a blood smear what do the basophils look like

A

stain darker and very punctuated

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15
Q

What do the lymphocytes look like in blood smear? how do you tell them from monocytes

A

have oval purple nucleus

monocytes stain lighter, and have more cytoplasm(nucleus usually kidney shaped

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16
Q

What are majority of cells in a virus caused inflammation

A

lymphocytes

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17
Q

what are majority of cells in a pseudomonas caused reaction

A

neutrophil dominance

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18
Q

what is the normal pattern of cell population in acute inflammation

A

granulocytes early followed by monocytes

neutrophils followed by macrophages

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19
Q

What chemical mediators cause vascular permeability

A

histamine, bradykinin and leukotrienes

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20
Q

what is exudation and what causes it

A

fluid, proteins, RBC and WBC in intravascular space as a resuls of increased osmotic pressure extravascular, and increased hydrostatic pressure intravascular

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21
Q

What is vascular stasis

A

slowing of blood with vasodilation and fluid exudation to allow chemical mediators and inflammatory cells to collect and respond to stimulus

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22
Q

what 2 componenets contribute to vascular stasis

A

less blood (fluid loss) and vasodilation

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23
Q

what is the term margination

A

leukocytes accumulating on vascular endothelium

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24
Q

What are the two manifestations from vasodilation

A

erythema and warmth

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25
Q

what is histamines mechanism that leads to vascular permeability

A

causes endothelial cells to contract and so then there are gaps between cells

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26
Q

What are the other chemicals that increase vascular permeability

A

NO and VEGF

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27
Q

WBC have what barrier to escape through when endothelial cells contract and make pathways

A

basement membrane

have collagenase to chew through

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28
Q

what is transudate

A

ultrafiltrate of plasma leaking from vessls due to increase hydrostatic P or decrease P

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29
Q

what is exudate

A

mixture of cells and plasma leaking out of vessels in response to chemical mediators

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30
Q

What is purulent exudate

A

granulocyte rich, cellular debris, +/- microbes (pus)

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31
Q

Why is the nucleus on one side of the cell in a plasma cell

A

because rER is so large, squishes nucleus over to one side

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32
Q

what causes fibrinous pericarditis

A

exudate

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33
Q

What are the types of body cavity effusion

A 
serous- yellow/clear
serosanguinous- mixed
sanguinous- blood
purulent
chylous
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34
Q

white and milky effusion is called what

A

chylous

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35
Q

which is more alkaline, transudate or exudate

A

transudate

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36
Q

if pressure increases in body, like increased Cardiac output, what leaks out

A

fluid- transudate

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37
Q

inflammation and increased P, what will leak out of cells

A

exudate- proteins, enzymes, maybe bacteria. Acidic. maybe odorous

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38
Q

what is dermatographism a reaction to

A

histamine. when we scratch ourselves and redness and wheal forms. this is when it lasts for more than 30 minutes

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39
Q

what is the immediate transient response

A

the leakage of histamines because vasodilation and endothelial cells contract. 15-30 minutes
No neutrophils!

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40
Q

What is the immediate sustained response

A

thermal chemical burns or lytic bacterial infection
leakage starts and lasts several hours to days
endothelial cell necrosis occurs
venules, capillaries and arterioles may be affected

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41
Q

What is delayed prolonged leakage

A

leakage 2-12 hours after injury
inflammation lasts hours to days
bacterial toxins, mild to moderate thermal burns
capillaries and venules affected- mechanism unclear

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42
Q

How does leakage drain

A

lymphatics

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43
Q

what is lymphangitis

A

inflammation of lymph vessels

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44
Q

what is lymphadenitis

A

inflammation of vessels and lymph nodes

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45
Q

what is adenitis

A

inflammation of lymph node

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46
Q

what are the steps in leukocyte emigration

A

stasis- margination- rolling- adhesion- migration

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47
Q

how do leukocytes migrate across the endothelium

A

chemotaxis towards concentration gradient

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48
Q

how do leukocytes migrate across basement membrane

A

chemotaxis, cytoskeleton, collagenases

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49
Q

how do leukocytes migrate into tissues

A

chemotaxis, integrins and CD44

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50
Q

what occurs first in leukocyte migration, crossing endothelium or basement membrane

A

crossing endothelium

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51
Q

TNF and IL1 increase expression of what on endothelium

A

P selectin, E selectin and integrin ligand (CAM1)

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52
Q

what cell has a weibel palade bodies

A

endothelial cells

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53
Q

Where is L selectin located

A

on the leukocyte

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54
Q

recurrent bacterial infections(not pustular), periodontitis and impaired wound healing are key to what pathology

A

rare, deficiencies in leukocyte adhesion molecules

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55
Q

What is CD99

A

normally repulses cells but changes to homophillic state and allows leukocytes to migrate through endothelial cells

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56
Q

When neutrophils bind and the GPCR is activated what occurs

A

increase Ca, kinases causing polymerization of actin (filopodia) can move towards signals

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57
Q

what are chemoattractants

A

cytokines, complement C5a, leukotriene B4

bacterial products

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58
Q

which complement component is chemotactic

A

C5a

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59
Q

what are the humoral endogenous chemotactic factors

A

fibrin split products (PMNs)

complement C5a and C567

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60
Q

What cells can be phagocytes

A

macrophages

neutrophils

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61
Q

what do phagocyte WBC recognize on targets

A

mannose R
scavenger R- LDL
opsonins

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62
Q

what does a classically activate macrophage do

A

kill bacteria

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63
Q

what do alternatively activated macrophages do

A

wound repair and anti-inflammatory

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64
Q

What are the antiinflammatory substances secreted from macrophages

A

IL10 and TGF beta

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65
Q

Chronic arthritis is due to what cells and molecules

A

lymphocytes macrophages and antibodies

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66
Q

chronic atherosclerosis is from what cells

A

macrophages and lymphocytes

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67
Q

what cells are responsible for chronic transplant rejection

A

lymphocytes and cytokines

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68
Q

what cells are responsible for pulmonary fibrosis

A

macrophages and fibroblasts

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69
Q

what cell is responsible for lug abscess

A

neutrophils

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70
Q

what chemicals are responsible for septic shock

A

cytokines

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71
Q

what cells and molecules are responsible for acute transplant rejection

A

lymphocytes, Ab and complement

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72
Q

what cells are responsible for acute respiratory distress sydnrome

A

neutrophils

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73
Q

What is chediak higashi syndrome

A

lysosome fusion disorder. phagolysosomes

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74
Q

what are problems with leukocytes with microbial activities. (deficiency)

A

decreased phagocyte oxidase leading to dec in ROS and results in chronic granulomatous disease and decreased MPO leading to recurrent candida infections

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75
Q

What type of diseases have impaired WBC production

A

bone marrow suppression, tumors, radiation and chemotherapy

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76
Q

what are our innate mechanisms to end acute response

A

mediators and neutrophils have short half lives

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77
Q

what are the active mechanisms in our bodies to end acute response

A

switch AA products
liberation of anti-inflammatory cytokines TGFb
prduction of anti-inflammatory lipid mediators (resolvins and protections)
neural changes (dec TNF by macrophages)

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78
Q

Describe how cell derived chemical mediators of inflammation are made

A

preformed or newly synthesized by simple splice to activate

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79
Q

what are the plasma derived mediators of inflammation

A

coagulation
complement and kinin
activation of normally present proteins by cascades

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80
Q

what cells make histamine

A

mast cells, basophils and platelets

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81
Q

what cell release serotonin

A

platelets and neuroendocrine cells

82
Q

What cell releases NO

A

macrophages and the endothelium

83
Q

What factor in coagulation cascade is key to set everything off

A

factor XII

84
Q

what does serotonin do for inflammation

A

vasodilation, increased vascular permeability

85
Q

What cells release TNF and IL 1

A

macrophages, endothelial cells and mast cells

86
Q

where are complement and kinins produced

A

in the liver

87
Q

what causes release of histamine

A 
physical injury (triple response)
neuropeptides (subP)
Ab binding
anaphylatoxins (C3a and C5a)
leukocyte histamine releasing proteins
cytokines (IL1 and IL8)
88
Q

serotonin has similar activity to what other mediator

A

histamine

89
Q

What R does histamine worked through

A

H1 R on endothelial cells

90
Q

what are the primary roles of histamine

A

constrict large arteries
vasodilation
increase venular permeability via endothelial contraction

91
Q

What inactivates histamine

A

histaminase

92
Q

What sets off serotonin release

A

collagen, thrombin, ADP and Antigen Ab complexes

93
Q

What are eicasanoids

A

AA metabolites

94
Q

steroids inhibit what

A

phospholipases which make AA

95
Q

Cox1 and 2 inhibitors block what

A

cyclooxygenase

96
Q

Prostaglandin is converted into what

A

prostacyclin and thromboxane A2

97
Q

what is the role of prostacyclin

A

vasodilation, inhibits platelet aggregation

98
Q

what is the role of thromboxane A2

A

vasoconstriction, promotes platelet aggregation

99
Q

What are derivatives produced via cycloocygenases

A

thromboxane A2
prostacycline
PGD2
PGE2 and PGF2

100
Q

what is the effect of PGE2

A

pain and vasodilates

101
Q

What does PGD2 cause

A

attracts neutrophils, vasodilates

pain and fever via cAMP action on temp set point

102
Q

What do leukotrienes cause

A

bronchoconstriction, increase vascular permeability
cause vasoconstriction
attract leukocytes

103
Q

what do lipoxins do

A

inhibit leukocyte recruitment and inflammation

104
Q

Which leukotriene is responsible to attract leukocytes

A

B4

105
Q

What do aspiring and other NSAIDs inhibit

A

Cox1 and 2

106
Q

cox 1 makes what

A

thromboxane

107
Q

cox 2 makes what

A

prostacyclines

108
Q

cox 2 inhibitors impair what

A

endothelial cell production or prostacyclin (which is a vasodilator and inhibitor of platelet aggregation)

109
Q

what is the problem with cox 2 inhibitors

A

increase risk of clot because cox1 unnopposed

110
Q

lipoxogenase inhibitors are used for what

A

asthma

111
Q

What cells make platelet activating factor

A

platelet, endothelial cells and leukocytes

112
Q

what activates release of platelet activating factor

A

platelet aggregation, vasoconstriction, bronchoconstriction
enhanced leukocyte adhesion
at low concentrations causes vasodilation

113
Q

What are the primary reactive species

A

O2-, H2O2, and OHelctron

114
Q

when reactive species combine with NO what is product

A

ONOO electron

115
Q

what causes ROS

A

endothelial cell damage
damage to parenchymal cells and erythrocytes
inactivate proteases

116
Q

smoking kills what protein

A

alpha1 antitrypsin

117
Q

What is the role of NO

A

relaxes smooth m
inhibits leukocyte rolling, adhesion and degranulation
inhibits platelet aggregation and adhesion
inhibits mast cell activated inflammation

118
Q

What are the 3 types of nitrous oxide synthetase

A

constituitive: endothelial eNOS and Neuronal nNOS

inducible (iNOS) from monocytes and macrophages activated by TNF and INF gamma

119
Q

what are cytokines

A

general category of messenger molecules

120
Q

what are chemokines

A

special cytokines that direct leukocyte migration

121
Q

How do chemokines work

A

bind to GPCRs

122
Q

What activates TNF and IL 1

A

macrophages

123
Q

What controls IL 1 production

A

inflammasome

124
Q

what is the action of TNF and IL 1 generally

A

endothelial activation to activate adhesion molecules in the acute phase, fever and also activates fibroblasts and nuetrophils

125
Q

Increased active IL 1 with mutation result in what

A

inherited autoinflammatory syndromes

126
Q

Which cytokine is responsible for cachexia when sick( don’t want to eat)

A

TNF

127
Q

what is happens to iron when we are sick

A

more hepcidin available which binds up all the iron. so looks like iron deficient(anemia) but not really

128
Q

What are the azurophil granules

A

primary neutrophils that show up first

129
Q

what are the specific granules(neutrophil)

A

secondary, show up second

130
Q

What type of enzymes are in specific granules

A

more enzymes for digestion, like collagenase, lysozyme

131
Q

What reaction is substance P known for

A

wheal formation

132
Q

where are majority of neurons with substance P located

A

GI tract and lungs

133
Q

what does sub P cause

A

pain, endocrine cells secretion, mast cell activation, vascular permeability

134
Q

What is hageman factor XII involved in

A

activates clotting cascade, kinin cascade, fibrinolytic cascade, complement cascade

135
Q

What do fibrin split products produce

A

chemostasis, inflammation

136
Q

Which cascade results in production of bradykinin? what is bradykinins role

A

the kinin cascade from kallikrein make bradykinin

bradykinin activates C5 to C5a which causes more inflammation

137
Q

plasmin has what affect on complement

A

splits C3 into C3a and b

138
Q

Which Complement parts make MAC

A

C5b-Cp

139
Q

What are the anaphylatoxins of complement cascade

A

C3a, C4a and C5a

140
Q

what else does C5a do

A

leukocyte activation
chemotaxis
lipoxygenase increased activity

141
Q

which complement parts are opsonins

A

C3b and iC3b

142
Q

What do protease activated receptors cause

A 
mobilization P selectin
chemokine production
Cox2 induction
increased PGs PAF and NO
endothelial adhesion
endothelial conformation change
143
Q

what are the actions of bradykinin

A

increased vascular permeability
smooth m contraction
pain

144
Q

what is the role of kallikrein

A

positive feedback to XII, creates bradykinin

145
Q

What is the role of plasmin in the fibrinolytic system of inflmmation

A

breaks down fibrin into split products
increase vasc permeability
chemotactic for leukocytes

146
Q

what is the role of an anaphylatoxin

A

release histamine

147
Q

What mediators play a role in vasodilation

A

PGs NO and histamine

148
Q

what mediators increase vasc permeability

A

histamine, serotonin, C3a C5a bradykinin Leukotrienes

PAG and sub P

149
Q

what mediators are included in chemotaxis

A

TNF IL 1 chemokines, C3a C5a leukotriene B4

150
Q

What mediators induce fever

A

IL 1 TNF and PGs, PGE2!

151
Q

what mediators induce pain

A

PGs and bradykinin!!!

152
Q

what mediators induce tissue damage

A

lysosomal enzymes of leukocytes
ROS
NO

153
Q

what is resolution

A

complete repair after inflammation

154
Q

What is fibrosis from inflammation

A

collagen deposition and loss of function

155
Q

if inflammation never goes away what is the problem

A

chronic inflammation

156
Q

What is exudative acute inflammation

A

stuff coming out

157
Q

what is serous inflammation

A

serous fluid coming out

158
Q

what is fibrinoid vs fibrinous

A

fibrinous we can see it

fibrinoid is under microscope

159
Q

urticarial inflammation means what

A

itchy

160
Q

what is catarrhal inflammation

A

runny nose

161
Q

What is cellulitis

A

inflammation of skin

162
Q

what is necrotizing inflammation

A

necrotic inflammatory process

163
Q

what type of inflammation is granulomatous

A

chronic

164
Q

what is interstitial inflammation

A

in between layers

acute or chronic

165
Q

what is cytopathic inflammation

A

cell has been modified- like in viruses

166
Q

what is purulent vs serous

A

serous clear yellow

purulent- pus

167
Q

pericarditis and endocarditis are examples of what inflammation

A

fibrinous

168
Q

what does fibrinous inflammation look like under scope

A

very pink- lots of protein, lots of fibrin

169
Q

what is pseudomembranous inflammation

A

form of exudative inflammation involving mucous and serous membranes
fibrin in exudate causes membrane like covering that is adherent to inflamed tissue

170
Q

what types of infections cause pseudomembranous inflammation

A

c difficile colitis

corynebacterium diptheriae pharyngitis

171
Q

what are mononuclear cell infiltrates in chronic inflammation

A

macrophages, lymphocytes, plasma cells, other cells

172
Q

what does chronic inflammation arise from

A

continued infections
prolonged exposure to toxic/foreign agents
autoimmune diseases
malignancies

173
Q

In acute viral infections what happens to neutrophil count

A

neutrophils go down. lymphocytes up

174
Q

what are the characteristics of chronic inflammation

A

chronic inflammatory cells

destruction of parenchyma and replacement by CT

175
Q

Describe life of monocytes

A

live in blood 1 day unless activated into macrophages which can live longer

176
Q

What is the hallmark of chronic inflammation

A

tissue damage

177
Q

What are the macrophages of body

A 
alveolar macrophages in lungs
microglia in CNS
kupffer in liver
osteoclasts in bone
dendritic cells of many tissues
langerhans are the dendritic cells of the skin
178
Q

what are the 2 roles of macrophages

A

increase inflammation or begin repair

179
Q

Why are benign cells found surrounding malignant cell

A

all the cehmoattractancts that the malignant cell is releasing

180
Q

what is the perinuclear huff

A

the edge of the plasma cell that is dark around cytoplasm

181
Q

what are produced in eosinophils

A

IL 3, IL 5

granulocyte/monocyte colony stim factor GM-CSF

182
Q

what are the chemoattractans for eosinphils

A

LTB4, CCL5(RANTES) and eotaxin 1 and 2

183
Q

what are in the granules in eosinophils

A 
basic protein(toxic to parasites)
cytotoxic agents like cationic proteins, neurotoxin and peroxidase
184
Q

Which parasites that get attacked by eosinophils

A

helminths

185
Q

what is the most common cause eosinophilia

A

allergies

186
Q

How do you know if a cell is a basophil

A

cannot see the nucleus because it is so dark

187
Q

what are the main components that are staining dark in basophils

A

histamine and heparin

188
Q

big cell lots of cytoplasm

A

macrophages

189
Q

what is the most common granulomatous disease

A

TB

190
Q

If the nuclei of a giant cell are around the edge what are they called

A

langhans type giant cell

191
Q

Describe histo sarcoidosis

A

granulomas
no central necrosis like we see in TB
mainly macrophages

192
Q

describe difference of cat scratch fever compared to other granulomas

A

has neutrophils in the areas as well

193
Q

What cytokines are responsible for fever in inflammation

A

IL1 IL 6 TNF and IFN gamma

194
Q

What cytokines are generated in large amounts that causes sepsis

A

TNF IL1

195
Q

what is neutropneia or agranulocytosis

A

too few circulating neutrophils

196
Q

What can cause neutrophil adherence molecule problems

A

hereditary, DM, glucocorticoid admin, ehtanol

197
Q

what chronic disease can cause failure of neutrophils to move properly

A

DM

198
Q

what can cause failure of neutrophils to phagocytose

A

DM, complement of Ig deficiencies

199
Q

Insufficient Oxygen radicals can lead to what type diseases

A

chronic granulomatous diseases

200
Q

Major burns can cause what deficiency

A

chemotaxis

201
Q

what can lead to deficiencies in phagocytosis and microbial activity

A

leukemia, anemia, sepsis, DM, neonates and malnutrition

Patho I (6 decks)

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