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Disease And Defense > Unit 2 Exam Material > Flashcards

Unit 2 Exam Material Flashcards

1
Q

Regeneration of Injured cells in essence is…

A

cell proliferation, drive by growth factors and dependent on integrity of ECM

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2
Q

Cell types proliferating during tissue repair

A

Remnants of injured tissue; vascular endothelial cells; fibroblasts

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3
Q

Fibroblasts in tissue repair

A

source of fibrous tissues that form scar to fell defects that cannot be corrected via regeneration

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4
Q

Three groups of tissues

A

1) Labile 2) Stable 3) Permanent

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5
Q

Labile Tissues

A

Continuous cell turnover due to stem cells and proliferation of mature cells

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6
Q

Labile Tissue examples

A

Bone marrow, surface epithelium on skin, GI, ducts, urothelium

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7
Q

Stable Tissues

A

Quiescent with minimal replication; capable of proliferation in response to injury of loss of tissue mass; limited regenerative capacity

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8
Q

Stable Tissue Examples

A

parenchyma of solid organs - liver, kidney; Endothelial cells, fibroblasts, smooth muscle cells.

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9
Q

Permanent Tissues

A

terminally differentiated and non-proliferative; insufficient regeneration, dominated by scar formation.

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10
Q

Permanent Tissue examples

A

Nuerons and cardiac muscle

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11
Q

Stem cells are characterized by two properties…

A

Self renewal; asymmetric replication

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12
Q

Two types of stem cells

A

embryonic and adult

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13
Q

Embryonic Stem Cells

A

most undifferentiated; gives rise to ectoderm, endoderm, mesoderm

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14
Q

Adult Stem cells

A

tissue stem cells; less undifferentiated. Found among differentiated cells within organ/tissue; more limited in self-renewal capacity and lineage potential. Important in tissue homeostasis!

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15
Q

What do growth factors do?

A

stimulate survival and proliferation, promote migration, differentiation, other responses

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16
Q

Where are growth factors produced?

A

macrophages; lymphocytes; parenchymal/stromal cells

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17
Q

mechanism of growth factor activation

A

recruited to site of injury by macrophages or lymphocytes or inactive and activated at sight of injury

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18
Q

autocrine

A

signaling occurs directly on same cell that produces factor

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19
Q

paracrine

A

signaling between adjacent cells

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20
Q

Endocrine

A

signaling over great distances

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21
Q

Three main types of growth factor Receptors

A

Tyrosine Kinase; G protein; receptors without intrinsic enzymatic activity

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22
Q

ECM function

A

mechanical support, control cell proliferation; scaffolding for tissue renewal; establish tissue microenvironments

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23
Q

Components of ECM

A

1) fibrous structural proteins 2) water-hydrated gels 3) adhesive glycoproteins

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24
Q

Function of Fibrous structural proteins in ECM

A

collages, elastins - tensile strength and recoil

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25
Q

Water hydrated gel in ECM - function

A

proteoglycans and hyaluronon - resilience and lubrication

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26
Q

Adhesive glycoproteins in ECM - function

A

connect matrix elements to one another and to cells

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27
Q

Interstitial Matrix

A

Between cells in connective tissue that is synthesized by mesenchymal cells.

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28
Q

Components of Interstitial matrix

A

fibrillar and non-fibrillar collagen; fibronectin; elastin; proteoglycans; hyaluronate

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29
Q

Basement Membrane

A

beneath epithelial, endothelial and smooth muscle that is synthesized by overlying epithelium and underlying mesenchyme

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30
Q

Components of basement membrane

A

type IV collagen; laminin; proteoglycan

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31
Q

what happens if ECM is damaged?

A

tissue repair can only be accomplished by scar formation

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32
Q

Repair of labile tissues

A

injured cell are rapidly replaced by residual cells and differentiation of stem cells - basement membrane must be intact

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33
Q

Stable tissue repair

A

Regeneration can occur, but is usually more limited (exception of the liver)

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34
Q

Liver Regeneration/Repair capabilities

A

40-60% of liver can be removed in living donor transplant; can also regnerate after insults (hepatitis) if enough framework is intact

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35
Q

Liver Regneration biochemistry

A

TNF triggers Kuppfer cell to release IL-6, which triggers the priming of hepatocytes. In transition from G0 to G1, EGF, TGFalpha, and HGF trigger cell proliferagion

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36
Q

When do scars form?

A

if tissue injury is severe or chronic that results in damage to parenchymal cells and epithelia, as well as connective tissue; OR when non-dividing cells are injured

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37
Q

What is scar formation?

A

replacement of non-regenerated cells with connective tissue OR by a combo of regeneration and scar formation

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38
Q

Steps in Scar Formation

A

Angiogenesis; migration and proliferation of fibroblasts and deposition of CT; maturation and reorganization of fibrous tissue to produce scar

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39
Q

Granulation Tissue

A

Connective tissue in scar formation

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40
Q

Steps in Angiogenesis in scar formation

A

1) Vasodliation 2) separation of pericytes and breakdown of basement membrane 3) migration of endothelial cells toward area of injury 4) proliferation of endothelial cells just behind migratory cells 5) remodeling into capillary tubes 6) recruitment of periendothelial cells to form mature vessel 7) suppression of proliferation and migration and deposition of basement membrane

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41
Q

What triggers vasodilation in angiogenesis

A

VEGF in induces NO and increased permeability

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42
Q

Periendothelial Cells include

A

Pericytes and smooth muscle

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43
Q

Deposition of connective tissue

A

migration and proliferation of fibroblasts; deposition of ECM proteins

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44
Q

What induces deposition of CT in scar formation

A

cytokines and GFs inlcuding PDGF, FGF, TFG-beta from inflammatory cells (activated M2 macrophages)

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45
Q

TGF-Beta

A

most important cytokine for deposition of CT in scar formation

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46
Q

Remodeling of CT is dependent on…

A

balance between synthesis and degradation of ECM proteins

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47
Q

Degradation of collagen and ECM is accomplished by…

A

Matrix Metalloproteinases

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48
Q

where are MMPs produced?

A

lots of cell types (fibroblasts, macrophages, neutrophils)

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49
Q

What are the types of MMPs

A

interstitial collagenases, gelatinases, stromelysins

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50
Q

what factors influence tissue repair?

A

Nutritional deficiencies, metabolic diseases, vascular impairment; whether the inciting insult has been terminated or persists or whether a new insult is introduced (infection)

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51
Q

Nutritional Factors that influence tissue repair..

A

Protein deficiency, Vit C deficiency both impair collagen synthesis

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52
Q

Metabolic Factors that influence tissue repair..

A

Diabetes and glucocorticoids delay tissue repair

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53
Q

how do glucocorticoids affect tissue repair

A

inhibit TFG-beta production and dimish fibrosis

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54
Q

Vascular factors that influence tissue repair..

A

thrombosis, ateriosclerosis and atherosclerosis, venous drainage impairment all lead to ischemia

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55
Q

Hypertrophic scar

A

scar close to the boundaries of injury; increased collagen syntehsis; parallel collagen arrangement; regresses; infrequently recurs after resection

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56
Q

Keloid

A

lots and lots of disorganzed collagen, way outside of boundary of injury; Does not regress, recur following resection

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57
Q

pathologic scar

A

accumulation of excessive amounts of collagen

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58
Q

contracture

A

injury that occurs across a joint line

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59
Q

Repair sequence

A

1) vascular reaction - dilation and increased permeability 2) acute or chronic inflammatory phase 3) repair phase with collagen deposition, angiogenesis, and regeneration if possible

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60
Q

First intention healing

A

First: epithelial regeneration is principle mechanism

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61
Q

second intention healing

A

second: complex involving regeneration and scarring

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62
Q

Differences in first and second intention healing..

A

2: larger clot or scab rich in fibrin forms at surface of wound; inflammation crease more necrotic debris and exudate; larger defects require greater volume of granulation tissue to fill gaps to lead to greater mass of scar tissue

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63
Q

Wound Contraction

A

involved in secondary healing, attributed to myofibroblasts

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64
Q

composition of granulation tisue

A

fibroblast, new capillaries, loose eCM, inflammatory cells

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65
Q

sutured wound strength

A

70% normal strength

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66
Q

wound strength with suture removal

A

10%

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67
Q

Wound strength three months after suture removal

A

70-80%

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68
Q

Cell adaptations to stress

A

reversible changes in number, size, phenotype, metabolic activity or function in response to physiologic or pathologic changes

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69
Q

types of cell adaptations

A

hypertrophy, hyperplasia, atrophy, metaplasia

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70
Q

Hypertrophy

A

increase in size of cells to result in increase in size of organ due to functional demand or GF or hormone stimulation

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71
Q

Hyperplasia

A

increased number of cells; both physiologic or pathologic

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72
Q

Physiologic hyperplasia

A

hormonal: female breast or compensatory: liver regneration

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73
Q

Pathologic hyperplasia

A

due to excessive hormonal or GF stimulation (endometrial hyperplasia)

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74
Q

Atrophy

A

decrease/shrinkage in size and functional capacity of cell

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75
Q

Physiologic Atrophy

A

due to loss of hormone stimulation, decreased workload, aging

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76
Q

Pathologic atrophy

A

due to denervation or diminished blood supply

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77
Q

Mechanism of atrophy

A

decreased protein synthesis and increased protein degradation

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78
Q

Metaplasia

A

reversible change in which one differentiated cell type is replaced by another differentiated cell type

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79
Q

Metaplasia mechanism

A

cell type sensitive to stress is reaplaced by another cell type better able to withstand stress

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80
Q

Barret Esophagus

A

example of metaplasia - long standing acid reflux changes from squamous epithelium to intestinal type epithelium

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81
Q

Reversible Cell injury

A

recoverable if damaging stimulus is removed; injury has not progressed to severe membrane damage and nuclear dissolution

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82
Q

Irreversible cell injury

A

Cell death - necrosis, apoptosis

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83
Q

Reversible Injury - morphology

A

Cellular swelling, accumulation of fats, plasma membrane alterations, mitochondrial changes, dilation of ER and detachment of ribosomes, nuclear alterations

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84
Q

Cellular swelling

A

failure of energy dependent ion pumps in PM to disrupt ionic and fluid homeostasis

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85
Q

Fatty Changes in reversible cell injury

A

accumulation of lipid vacuoles within cytoplasm; increased entry and synthesis of FFA and decreased FA oxidation

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86
Q

Plasma membrane alterations with reversible injury

A

blebbing, blunting, distortion of microvilli, loosening intracellular attachments

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87
Q

myelin figures

A

seen in reversible injury - phospholipid masses derived from damaged cell membranes

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88
Q

Mito changes with reversible injury

A

swelling and phospholipid rich amorphous densities

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89
Q

Nuclear alterations with reversible injury

A

clumping of chormatin

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90
Q

Cell size in Necrosis and Apoptosis

A

Necrosis: enlarged
Apoptosis: shrinkage

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91
Q

Nucleus in Necrosis and Apoptosis

A

Karyolysis in Necrosis; fragmentation in apoptosis

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92
Q

Plasma membrane in Necrosis and Apoptosis

A

Necrosis: disrupted
Apoptosis: intact but with altered structure

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93
Q

Cellular contents in Necrosis and Apoptosis

A

Necrosis: enzymatic digestion that leaks out of cells
Apoptosis: are intact

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94
Q

Adjacent Inflammation in Necrosis and Apoptosis

A

Necrosis: frequent
Apoptosis: none

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95
Q

Physiologic or pathologic role in Necrosis and Apoptosis

A

necrosis: invariably pathologic (irreversible cell injury)
Apoptosis: physiologic - means of eliminating unwanted cells

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96
Q

Irreversible injury cellular morphology

A

Cytoplasmic Changes: increased eosinophilia and loos of RNA Basophilia Nuclear changes: breakdown of DNA and chromatin

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97
Q

Eosinophilia

A

increased binding of eosin to to denatured cytoplasmic proteins; increased pink stain

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98
Q

Pyknosis

A

nuclear shrinkage and increased basophilia (DNA condenses); condensed blue/purple nuclues

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99
Q

Karyorrhexis

A

pyknotic nulcues fragments

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100
Q

Karyolysis

A

dissolution of nucleus - breakdown of denatured ; basophilia of chromatin fades

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101
Q

Steps in nuclear changes

A

Pyknosis, karyorrhexis, karyolysis

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102
Q

Pattens of tissue necrosis

A

coagulative (gangrenous), liquefacative, caseous, fat, fibrinoid

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103
Q

Coagulative necrosis

A

Tissue architecture preserved for several days, pale ghost-like cells; most often seen due to infarcts

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104
Q

Liquefactive Necrosis

A

accumulation of inflammatory and leukocyte enzymes; due to focal bacteria and fungal infections hypoxia in CNS

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105
Q

Caseous Necrosis

A

necrotic appears as collection of fragmented of lysed cells and amorphous granular debris enclosed within inflammatory border

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106
Q

Fat Necrosis

A

fat destruction due to activated pancreatic lipases. Fats are hydrolyzed into FFAs that precipitate with calcium to make a chalk gray material

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107
Q

What causes fat necrosis

A

activation of pancreatic lipases following acute pancreatitis or trauma.

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108
Q

Fibroid Necrosis

A

antigens and antibodies are deposited on walls of arteries; immune complexes combine with fibrin to form bight pink amorphous appearance

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109
Q

Mechanism of Cell injuries

A

ATP depletion, mito damage, influx of Calcium, accumulation of reactive oxygen, increased permeability of membranes, accumulation of damaged DNA and misfolded proteins

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110
Q

ATP is generated by

A

ATP is made from oxidative phos, ADP in mito or glycolysis.

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111
Q

Low ATP leads to…

A

decreased action of NA pump —> influx of Ca, H20, Ka and efflux of K –> ER swelling; Increased lactic acid and decreased pH to nuclear clumping; detachment of ribosomes and decreased protein synthesis

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112
Q

Which wells are most susceptible to ischemic injury

A

Neurons (3-5 minutes)

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113
Q

Mitochondrial damage in cell injury

A

failure of oxidative phosphorylation –> ATP depletion, formation of ROS, formation of high conductance channels and loss of Membrane potential, release of proteins that activate apoptosis.

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114
Q

Dangers of the influx of calcium…

A

activation of cellular enzymes that lead to membrane damage and nuclear damage, decreased activity of ATPase that leads to increased mitochondrial permeability transition..

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115
Q

Accumulation of ROS is due to..

A

1) Redox reactions during mitochondrial respiration that lead to H2O2 and OH- radicals
2) phagocytic leukocytes (neutrophils and macrophages)

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116
Q

Consequence of Free Radicals…

A

increased production –> oxidative stress. (membrane damage, misfolding of proteins, mutations in DNA)

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117
Q

what converts O2- to H2O2?

A

SOD

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118
Q

Have decomposes H2O2?

A

glutathione peroxidase converts to H2O

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119
Q

what contributes to membrane damage?

A

phospholipid loss due to ROS, phospholipid reacylation and phospholipid degradation; lipid breakdown productions; cytoskeletal damage due to protease activation (intracellular Ca)

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120
Q

apoptotic bodies

A

membrane bound vesicles of cytosol and organelles

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121
Q

activation of apoptosis

A

Mitochondrial (intrinsic) and Death receptor (extrinsic)

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122
Q

Anti-apoptotic intrinsic pathway

A

BCL2, BCL-XL, MCL1

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123
Q

Pro apoptotic intrinsic pathway

A

Bax and Bak

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124
Q

Intrinsic Pathway of Apoptosis

A

BCL2 senses cell injury that acts on effectors to increase mito permeability to release cytochrome C and pro-apoptotic proteins which start a cascade to lead to endonuclease activation and breakdown.

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125
Q

Extrinsic Pathway of apoptosis

A

death receptor interacts with ligand to activate adaptor proteins and initiator and executioner caspase 8

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126
Q

Autophagy

A

process by which cell eats own contents

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127
Q

Intracellular accumulations result from..

A

inadequate removal, accumulation of abnormal endogenous substance, failure to degrade due to enzyme deficiencies, deposition and accumulation of abnormal exogenous substances.

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128
Q

Lipofuscin

A

wear and tear pigment that accumulates with age or atrophy. Marker of past free radical injury

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129
Q

Melanin

A

endogenous brown-black pigment synthesized by melanocytes in epidermis; finder lan lipofuscin

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130
Q

Hemosiderin

A

Hb bound granular pigments that accumulate when local or systemic excess of iron

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131
Q

Cholesterolosis

A

deposits of cholesterol in macrophages of gallbladder

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132
Q

Pathologic Calcification

A

abnormal deposition of calcium salts (with small amounts of iron, mg, and mierals)

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133
Q

Dystrophic calcification

A

occurs in dead/dying tissues; absence of derangements in Ca metabolism

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134
Q

Metastatic calcifications

A

occurs in normal tissue; derangement is calcium metabolism

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135
Q

Psammoma body

A

calcification - sign of increased degeneration and cell turn over.

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136
Q

Acute vs Chronic Inflammation - Onset

A

Acute: Fast - minutes/hours
Chronic: slow - days

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137
Q

Acute vs Chronic Inflammation - Cellular infiltrate

A

Acute: neutrophils
Chronic: monocytes/macrophages, lymphocytes

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138
Q

Acute vs Chronic Inflammation - tissue injury

A

Acute: mild and self limited
chronic: severe and progressive

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139
Q

Acute vs Chronic Inflammation - local and systemic signs

A

acute: prominent
Chronic: less, may be subtle.

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140
Q

Acute vs Chronic Inflammation - with innate vs. adaptive

A

acute: largely innate
chronic: involves both innate and adaptive in coordination

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141
Q

stimuli of acute inflammation

A

Infection; Trauma, Foreign material, immune reaction

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142
Q

what type of infections cause acute inflammation?

A

bacteria, virus, fungus, parasites; toxins from infectious organisms

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143
Q

The process of acute inflammation

A

1) receptor activation 2) vascular changes 3) leukocyte recruitment 4) leukocyte activation

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144
Q

Receptor Activation in acute inflammation

A

PRRs are triggered on PM (extracellular); endosomes (ingested) cytosol (intracellular)

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145
Q

what do TLRs do?

A

stimulate transcription factors to create mediators for inflammation, interferons for viral infections (in response to microbe infection)

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146
Q

what TFs do TLRs activate?

A

p28, JNK, NFkB

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147
Q

Inflammasome

A

mediate cellular response todead and damaged cells (some microbes)

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148
Q

what activates inflammasomes?

A

uric acid from DNA breakdown; ATP, decreased intracellular K from PM injury, DNA free in cytosol

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149
Q

Where are inflammasomes located?

A

cytosplasm

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150
Q

where are TLRs located?

A

PM and endosomes

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151
Q

result of inflammasome activation?

A

Activates caspase-1 which cleaves IL1Beta into active form

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152
Q

IL1-beta

A

recruits luekocytes to come in and clean up dead cells (activated by inflammasomes)

153
Q

Gout

A

urate crystals that stimulate IL1-Beta

154
Q

Vascular Changes in Acte Inflammation

A

increase blood flow and permeability to bring cells and materials for response to injury or threat

155
Q

Rubor

A

Redness - due to increased blood flow that causes congested capillary beds

156
Q

Erythema

A

redness

157
Q

Calor

A

warmth, due to increased blood flow

158
Q

Tumor

A

increase permeability causing exudate of fluid into tissues and swelling

159
Q

what dilates in vascular changes in acute inflam?

A

arterioles - so they flood the capillaries with blood.

160
Q

Histamine - acute inflam

A

acts on smooth muscle cells of arterioles to cause vasodilation

161
Q

Permeability in Acute inflammation

A

1) endothelial cells contract due to mediators 2) endothelial injury 3) transcytosis
This is done in the post-capillary venules

162
Q

endothelial cell contraction mediators in acute inflammation

A

Early: histamine, bradykinin
Later: IL1, TNF

163
Q

Transcytosis

A

material transported through cells in vesicles

164
Q

Exudate vs transudate- common cause

A

Ex: due to vascular permeability
Trans: increased hydrostatic or decreased osmotic pressure

165
Q

Exudate vs transudate- protein content

A

Ex: increased
trans: decreased

166
Q

Exudate vs transudate- cell content

A

Ex: increased inflammation, RBC
Trans: few cells

167
Q

Exudate vs transudate- Specific gravity

A

Ex: high
Trans: low

168
Q

Exudate

A

results form increased vascular permeability due to inflammation. Causes cells and proteins in extracellular environment

169
Q

Transudate

A

due altered intravascular pressure; filters just the fluid. (increased capillary pressure, decreased blood protein)

170
Q

Leukocyte Recruitment

A

1)migration/rolling 2) adhesion 3) transmigration 4) chemotaxis

171
Q

Margination

A

vasodilation slows blood flow in post-capillary venule, causing larger/slower moving luekocytes into periphery.

172
Q

Stasis

A

thicker and slower blood due to leakage into interstitial space; gives things more opportunity to contact.

173
Q

Rolling

A

stimulated endothelial cells express Selectins which have affinity for sugars on leukocyte surface

174
Q

What stimulates P-selectin?

A

Histamine

175
Q

what stimulates E selectin

A

IL-1

176
Q

Adhesion (acute inflammation)

A

chemokines signal specific area of luekocytes to act.

Integrins are activated on leukocyte surface and Cellular adhesion molecules are on endothelial cells

177
Q

Integrins

A

cell surface structures on leukocytes that are activated in adhesion – CD11 and CD18

178
Q

What triggers cell adhesion molecules in adhesion step of acute inflammation?

A

IL-1 and TNF

179
Q

Leukocyte adhesion deficiency

A

AR, defective integrin CD18; delayed sep of umbilical cord, increased circulating neutrophils; recurrent bacterial infection

180
Q

Transmigration

A

Leukocytes squeeze between endothelial cells in post-capilary venules and cells secrete collagenase

181
Q

Diapedesis

A

when leukocytes squeees between endothelial cells

182
Q

Collagenase

A

breaks up basement membrane in transmigration

183
Q

Chemotaxis

A

leukocytes move toward inflammation following chemical gradient.

184
Q

Chemotatic agents

A

endogenous and exogenous - bacterial products, cytokines, C5b, Arachidonic acid metabolites.

185
Q

Activation of leukocytes in acute inflammation

A

Phagocytosis, killing/degrade engulfed material, secrete material to kill; produce inflammatory mediators

186
Q

Phagocytosis in Activation - acute inflammation

A

1) recognition of particle to leukocyte (receptors for microbes, necrotic cells, opsonins) 2) engulfment and formation of vacule 3) killing of vauolated material

187
Q

Destruction of Phagocytosed material - acute inflam

A

Done by HOCl strong radical, NO, and lysosomal enzymes (elastase, lysozymes)

188
Q

NADPH oxidase

A

converts O2 into O2-

189
Q

SOD

A

converts O2- into H2O2

190
Q

What converts H2O2 into HOCl

A

myeloperoxidase

191
Q

Secretion of compounds for degradation - acute inflammation

A

enzymes or antimicrobial proteins; Neutrophil extracellular traps

192
Q

Neutrophil extracellular traps

A

nuclear chromatin is imbedded with antimicrobial material and extruded to trap microbes.

193
Q

Outcomes of Acute Inflammation

A

Resolution; chronic Inflammation; scarring

194
Q

Resolution of acute inflammation

A

injured tissue can regenerate due to minimal tissue injury

195
Q

when does acute inflammation turn into chronic

A

offending agent is not removed; often results in scarring or resolution.

196
Q

Stimuli of Chronic inflammation

A

Persistent infection; immune mediated disease; prolonged exposure to toxins

197
Q

Immune mediated diseases that cause chronic inflammation

A

autoimmune, allergic disease

198
Q

Endogenous substances that cause chronic inflammation

A

atherosclerosis, cancer

199
Q

Steps in Chronic Inflammation?

A

1) mononuclear cell infiltrate 2)tissue destruction 3) repair: neovascularization and fibrosis

200
Q

Mononuclear cell infiltrate in chronic inflammation

A

lymphocytes and monocytes circulate and give rise to macrophages that infiltrate into tissues to ingest microbes and debris, initiate tissue repair and secrete inflammatory mediators.

201
Q

Classical Activation - what activates these

A

M1-

endotoxins, IFNgamma (T-cell cytokine), foreign material

202
Q

Classical Activation -what do these macrophages produce?

A

ROS, NO, lysozymal enzymes, proinflammatory cytokines

203
Q

Classical Activation - function of macrophages

A

killing microbes, chronic inflammation

204
Q

Alternative activation - activation of macrophages

A

IL-4, IL-13 (t cells, eosinophils, mast cells)

205
Q

Alternative activation - what does these macrophages produce?

A

growth factors for new vessels and fibroblast activation

206
Q

Alternative activation - function of macrophages

A

tissue repair and fibrosis

207
Q

Players in chronic inflammation

A

Lymphocytes, eosinophils, mast cells

208
Q

Lymphocytes in Chronic Inflammation

A

CD4+ T cells secrete cytokines to promote inflammation.

209
Q

Th1 CD4+ secretes…

A

IFN-gamma to activate classical macrophage pathway

210
Q

Th2 CD4+ secretes…

A

IL-4, IL-5, IL-13 to activate alternative

211
Q

Th17 CH4+ secretes

A

IL-17 to recruit neutrophils and monocytes

212
Q

Eosinophils in chronic inflammation

A

T cell secrete eoxtaxin.

Most notable in parasite infection and allergic reactions with IgE.

213
Q

Mast cells in chronic inflammation

A

quickly release inflammatory mediates (histamine and AA); coated with IgE to trigger mediated release; known for anaphylactic reactions

214
Q

Granulmatous Inflammation

A

Enlarged marcophages form a nodule that is composed of epitheloid histiocyte that is surrounded by lymphocytes; forms capsule to prevent spread

215
Q

What disease are characteristic of granulomatous inflammation?

A

TB, leprosy, fungi, crohn’s disease, sarcoidosis

216
Q

Systemic effects of inflammation

A

Fever, Acute phase proteins in blood,

217
Q

Fever

A

due to increased COX activity in perivascular cells of hypothalamus to increase PGE2 to raise temp.

218
Q

Endogenous pyrogens

A

IL-1, TNF

219
Q

Acute phase proteins in blood - systemic effects of inflammation

A

AL-6 cuases hepatocytes to increase protein secretion that can be used to monitor inflammation process

220
Q

What are the acute phase blood proteins?

A

C-Reactive proteins, Serum Amyloid A; Fibrinogens

221
Q

Serum Amyloid A

A

adheres to cell walls and act as opsonins

222
Q

Fibrinogen

A

binds to blood cells and causes them to form stacks that sediment – erythrocyte sedimentation rate

223
Q

what triggers leukocyte release from bone marrow

A

TNF and IL-1 - leukocytosis

224
Q

Left shift in leukocytosis

A

increase in number of immature WBCs

225
Q

Colony Stimulating Factors in chronic inflammation

A

In continue inflammation, increase bone marrow production of leukocytes

226
Q

Neutrophilia is due to…

A

bacterial infection

227
Q

Lymphocytosis is due to..

A

viral infections

228
Q

eosinophilia is due to..

A

asthma, parasite infection

229
Q

Leukopenia is due to..

A

decreased luekocytes, specific infections (typhoid)

230
Q

Hydrostatic Pressure

A

increase pressure on arterial end to push fluid outside of capillaries. Increased due to high blood pressure that can lead to fluid build up.

231
Q

Osmotic Pressure

A

is the pull of the fluid back into veins due to high protein content in vasculature. Drop in osmotic: due to liver disease with lack of albumin; block in lymphatics, vessel wall damage

232
Q

what causes extravasation of fluid into tissues?

A

Increased capillary hydrostatic pressure, decreases plasma osmotic pressure, increase vascular permeability; exceeds capacity for lymphatic drainage.

233
Q

Edema

A

fluid buildup in tissue;

234
Q

Effusion

A

Fluid build up in spaces

235
Q

Transudate results from..

A

increased Hydrostatic pressure, reduced oncotic pressure

236
Q

Exudate results from..

A

increased vascular permeability: inflammation and direct damage to endothelial cells

237
Q

Specific Gravity of transudate vs exudate?

A

Tran is low = less than 1; exudate is higher = greater than 1

238
Q

Total protein conc. in transudate vs. exudate

A

Trans: 3.0 g/dL

239
Q

Protein fluid/serum ratio in transudate/exudate

A

0.5 for exudate

240
Q

Glucose Fluid/Serum ratio in transudate and exudate

A

> 0.5 in transudate;

241
Q

why is glucose higher in transudate than exudate?

A

you have bacteria and other things to metabolize glucose in the fluid outside of the vessel

242
Q

WBC count in transudate vs. exudate?

A

Trans: non for few
Exudate: many

243
Q

Hyperemia

A

Arteriolar dilation; physiological reasoning to bring more oxygenated or nutritional blood to area.

244
Q

Hyperemia occurs during

A

exercise and inflammation

245
Q

Congestion

A

Outflow obstruction in venous end; backs up into capilaries and arterioles. deoxygenated blood gets suck and causes ischemia in adjacent tissues.

246
Q

What causes congestion?

A

local obstruction, congestive heart failure

247
Q

appearance of hyperemia vs congestion?

A

hyperemia: red
Congestion: dark/purple color

248
Q

what causes pulmonary edema and plural effusion?

A

Left heart failure (fluid buildup in lungs)

249
Q

what does decreased blood flow out of heart from left ventricular failure lead to?

A

decreased blood flow to kidney.

250
Q

Decreased renal blood flow..

A

compensates by holding onto Na and H20, which increases volume of dilute blood. This causes fluid to leak out and causes peripheral edema.

251
Q

Right heart failure leads to..

A

back up in venous system –> liver congestion, splenic congestion, GI varices.

252
Q

Ascites

A

fluid in the abdomen, when cirrosal surface starts moving fluid into abdominal cavity due to right heart failure.

253
Q

Hemorrhage

A

blood outside of vasculature due to vessel damage, low level/function of platelets; low level/function of coagulation factors

254
Q

how are small breaks in blood vessels repaired?

A

small clots form on the surface to cover damage, but does not block flow and vessels.

255
Q

Petechiae

A

hemorrahge 1-2 mm in size; very small due to ineffective platelet and clotting factors

256
Q

Pupura

A

> 3 mm hemorrhage

257
Q

Ecchymoses

A

1-2 cm hemorrhage; usually resembles a bruise

258
Q

Hematoma

A

large blood collection within tissue

259
Q

Thrombosis (three factors)

A

Endothelial lining, abnormal blood flow; hypercoagulability

260
Q

Thrombosis is most common in what age group?

A

elderly because of accumulation of epithelial damage - hypercholesteremia, diabetes, athersclerosis

261
Q

Factor V leiden

A

mutation that makes them prothrombotic; usually occurs as young adults

262
Q

Formation of a thrombis

A

layering of platelets and fibrin mesh. Usually it stops after a few layers that do not obstruct flow; but if out of control, thrombosis does not stop accordingly.

263
Q

Lines of Zahn

A

lines of platelets and RBC in throbis

264
Q

Post-morten thrombis

A

not layered and thick, because blood is not flowing.

265
Q

Abnormal blood flow in thrombosis causes.

A

Stasis (atrial fibrilation, bed rest) turbulance (atherosclerosis, vessel narrowing)

266
Q

Hypercoagulability in thrombosis - causes

A

inherited (factor V leiden); acquired (disseminated cancer)

267
Q

Thromboembolus

A

Most due to immobility. But also due to estrogen, pregnancy, previous or current cancer, coagulation abnormalities, limb trauma or orthopedic procedures, obesity.

268
Q

Laminar flow

A

large things flowing in center and small particles move towards edge.

269
Q

what does stasis do to laminar flow?

A

decreases it, and platlets and WBC move towards endothelium and stick and bind –> fluid build up, congestion, edema.

270
Q

how does estrogen promote emboli

A

pushes liver to make more coagulants and less anticoagulants.

271
Q

Pulmonary Embolus stymptoms

A

chest pain, poor flow to area of lung, decreased oxygenation, lung infarction

272
Q

Recanalization

A

process of long term thrombus. that sometimes breaks down to left fluid leak through.

273
Q

Embolus in venous system

A

Thromboemboli, fat/bone marrow, amniotic fluid, tumor

274
Q

Embolus in Arteriole system

A

Thromboemboli, arteroemboli

275
Q

why do emboli form in venous over arteriole?

A

flow is too fast in arteriole, mostly forms due to atherosclerosis

276
Q

DIC

A

Disseminated Intravascular Coagulation

Thrombosis and hemorrhage can occur simultaneously

277
Q

DIC - pathology

A

an underlying condition that promotes widespread damage leads to systemic activation of coagulation which leads to widespread fibrin deposition and thrombosis. But as you use all your platelets and coagulants, you start bleeding in new areas.

278
Q

DIC symptoms

A

Respiratory insufficiency, MSC, convulsions, acute renal failure, petechiae/purpura, GI and oral hemorrhage, Shock

279
Q

Causes of DIC

A

hemolytic anemia, thrombocytopenia, low fibrinogen, elevated D-dimer, and other fibrin degradation produces

280
Q

Infarction

A 
tissue death (necrosis) caused by vessel occlusion.
most often coagulative and liqueficative in brain.
281
Q

White Infarction

A

due to arterial insuffidicney, single blood supply, no reperfusion, often in dense tissue like heart, kidney, spleen.

282
Q

Red Infarction

A

block of blood flow temporarily, or in tissue with multiple sources of blood flow. Due to venous insuffidiency, dual bloodflow, yes to repurfusion, loose tissue in lung, liver, intestine.

283
Q

Shock

A

circulating blood volume or BP is not adequae to perfuse body tissues –> muliorgan damage.

284
Q

Cardiogenic shock

A

myocardial pump failure; caues myocardial damage, extrinsic compression, outflow obstruction

285
Q

Hypovolemic shock

A

low blood volume due to severe dehydration, hemorrhage, bruns

286
Q

Pathophysiology of shock

A

low cardiac output, low BP leads to vasoconstriction, increased DR, renal conservation of fluid –> coolness, pallor, tachycardia, low urine output

287
Q

SIRS

A

system inflammatory response syndrome

SubsetL septic Shock: due to microbial infection.

288
Q

SIRS pathophysiology

A

Elevated inflammatory mediators leads to fever, DIC, , acute respiratory distress
Arterial vasodilation, vascular leakage, venous blood pooling

289
Q

arterial vasodilation leads to

A

hypotension, warm, flushed skin

290
Q

Vascular leakage leads to..

A

hypotension, edema

291
Q

Venous blood pooling leads to..

A

reduced cardiac output, increased HR

292
Q

Is septic shock responsive to IV fluids

A

NO!

293
Q

what inflammatory mediators are Vasoactive Amines?

A

Histamine and Serotonin

294
Q

Synthesis of Vasoactive Amines

A

Storage in cells, ready for quick release

295
Q

Effects of Histamine - basic

A

Arterial dilation, endothelial contraction

296
Q

What cell types is histamine release from?

A

Mast cells, basophils, platelets

297
Q

how is histamine released?

A

Mast cells release them based on physical features, immune binding to IgE, complement (C3a and C5a), releasing proteins, neuropeptides, cytokines

298
Q

what complement factors cause histamine release?

A

C3a and C5a

299
Q

What cytokines cause histamine release?

A

IL-1 and IL-8

300
Q

How is histamine inactivated?

A

histaminase

301
Q

Is histamine plasma or cell derived?

A

Cell

302
Q

Serotonin basic effects

A

Vasoconstriction to aid in clotting

303
Q

Source of serotonin

A

platelet granules

304
Q

Is serotonin plasma or cell derived?

A

Cell

305
Q

What inflammatory mediators are Arachidonic Acid Metabolites?

A

Prostaglandin, Thromboxane, leukotriene, lipoxin

306
Q

synthesis of arachidonic Acid metabolites?

A

From cell membrane phospholipids; from cyclooxyrgenase and lioxygenase

307
Q

Cycoloxygenase Pathway produces…

A

produces prostalandins and thromboxanes

308
Q

Lipoxygnase pathway produces…

A

Leukotrienes and lipoxins

309
Q

Basic effects of Arachidonic Acid?

A

inflammation and homeostasis

310
Q

Arachidonic acids are released from

A

leukocytes, mast cells, enothelium, platelets

311
Q

How do arachidonic acid metaboites let inactivated?

A

spontaneous decay and enzymes

312
Q

prostaglandin is produced by what pathway?

A

cyclogyogenase from Arachidonic acid metabolites in many sites throughout the body

313
Q

What are the basic effects of prostaglandin?

A

Pain, Fever, vasodilation, increased vascular permeability, inhibit clotting

314
Q

how are prostaglandins inactivated?

A

NSAIDs, croticosteroids, COx2 selective

315
Q

what does corticosteroids inhibit?

A

phospholipase A2 in prostaglandin syntehsis

316
Q

Thronboxane synthesis pathway

A

cycooxygenase pathway: prostaglandin H2 to thromboxane

317
Q

Thromboxane basic effects

A

vasoconstriction, promotes platelet aggregation

318
Q

how is thromboxane inhibited?

A

COX inhibitors, naproxen, synthase inhibitors

319
Q

Leukotriene sythesis

A

lioxygenase pathway

320
Q

Leukotriene basic effects

A

bronchospasm, chemotactic for neutrophils, increase vascular permeability

321
Q

LTB4

A

Leukotriene that is chemotactic for neutrophils

322
Q

LTC4, LTD4, LTE4

A

leukotrienes to increase vascular permeability

323
Q

Lipoxin sythesis

A

lipoxygenase pathway generated as leukocytes enter tissue

324
Q

Lipoxin basic effects

A

inhibit neutrophils adhesion and chemotaxis; antagonize leukotrienes

325
Q

which arachidonic acid inflammatory mediator is anti-inflammatory?

A

lipoxin

326
Q

Platelet Activating Factor Sythesis

A

Phospholipase A2 leaves lipids from cell membranes

327
Q

Platelet Activating Factor Storage

A

continuously produced at low quantity, regulated by enzymes

328
Q

Platelet activating factor effects

A

platelet activation, aggregation, vasodilation, vascular permeability, bronchoconstriction, stimulation of platelets to produce mediators

329
Q

Tumor Necrosis Factor

A

A cytokine

330
Q

what are major cytokines?

A

TNF, IL-1, Chemokines (CXC, CC)

331
Q

synthesis of cytokines

A

stimulated by microbes, immune complex, T-mediators

332
Q

TNF Effects

A

endothelial activation, leukocyte binding and recruitment, Systemic effects: fever, acute phase protein synthesis

333
Q

IL-1 effects

A

endothelial activation, leukocyte binding and recruitment Systemic effects: fever, acute phase protein synthesis

334
Q

IL-1

A

Cytokine, very similar to TNF

335
Q

TNF and IL-1 is produced from

A

macrophages, mast cells, endothelial cells

336
Q

Are cytokines pro or anti-inflammatory?

A

all are pro inflammatory except IL-10

337
Q

Chemokines

A

CXC and CC

338
Q

Chemokine Effect

A

Chemotaxis, activation of leukocytes

339
Q

Chemokines are produced from…

A

macrophages, mast cell, endothelial cells

340
Q

CXC

A

chemokine, chemotactic for neutrophils

341
Q

CC

A

chemokine, chemotactic for a variety of cells

342
Q

Eotaxin

A

Chemokine, chemotactic for Eosinophils

343
Q

Chronic Cytokines

A

INF-gamma, IL-12

344
Q

INF-gamma

A

Cytokine, classical macrophage activation

345
Q

IL-12

A

cytokine, growth/function of T-cells

346
Q

Reactive oxygen radicals types

A

superoxide radical, hydroxyl radical, hypochlorous radical

347
Q

How are reactive oxygen radicals synthesized?

A

NAPDH oxidase pathway using NADPH oxidase, SAD, myeloperoxidase

348
Q

Effects of Oxygen Radicals

A

Damage microbes and host tissues

349
Q

what cells produced oxygen radicals

A

activated neutrophils

350
Q

what inhibit/deactivated oxygen radicals

A

endogenous antioxidants (superoxide dimutase)

351
Q

Nitric Oxide

A

Reactive oxygen sepecies produced from Nitric oxide synthase and L-arginine

352
Q

NO - effect

A

kill microbes, vasodilation, antagonizes platelet activation, reduces leukocyte recruitment

353
Q

NO is produced by…

A

Type II macrophages and endothelial cells produced by IL-1, INFgamma, and bacterial endotoxins.

354
Q

Lysosomal Enzyme inflammatory Mediators

A

Azuorphil specific gelatinous Secretary granules

355
Q

Azurophil speicic gelatinase secretory granules effect

A

kill microbe and ingest digested material with acid proteases and neutral proteases

356
Q

Acid proteases

A

produced by lysosomal enzymes that are active within phagolysosomes at low pH

357
Q

Neutral proteases

A

produced by lysosomal enzymes that are active outside of cell in neutral pH (collagenase)

358
Q

Substance P category

A

Neuropeptide inflammatory mediator

359
Q

Where is Substance P released from?

A

nerves and inflammatory cells (macrophages, eosinophils, lymphocytes, dendritic cells)

360
Q

Substance P effects

A

initiation inflammation, vascular tone, permeability. Active in lung and GI, binds to neurokinin-1 receptor to generage proinflammatory effect in immune and epithelial cells

361
Q

Complement synthesis

A

inactive molecules in circulation that are activated and produce proeolysis. C3 converts converts C3 to C3a to C3b. C3b activates C5 converts to initiate MAC. Classical, alternative, lectin

362
Q

Complement effects

A

inflammation, immunity, increased vascular permeability and release of histamine, leukocyte activation, opsonin

363
Q

what complement proteins cause leukocyte activation?

A

C5a, C4a, and C3a

364
Q

What complement has opsonin properties?

A

C3b

365
Q

What cells produce complement?

A

Hepatocytes, tissue macrophages, monocytes, epithelial cells

366
Q

What inhibits complement pathway

A

C1-inhibitor and Decay-Accelerating factor and Factor H

367
Q

C1-inhibitor

A

blocks activation of C1

368
Q

Decay-Accelerating factor and Factor H

A

limit C3 and C5 convertase formation

369
Q

Factor XII

A

a coagulation/kinin

370
Q

Hageman factor

A

Factor XII

371
Q

Coagulation/kinin inflammatory mediators

A

Factor XII (hageman) Factor Xa, Thrombin

372
Q

Hageman factor effect

A

activated kinin sytem, clotting factor, leads to bradykinin and increased vascular permeability, dilation and pain.

373
Q

Positive feedback in Hageman factor

A

Kallikrein is chemotactic and activates Factor XII

374
Q

Factor Xa effects

A

increased vascular permeability

375
Q

Thrombin effect

A

activates protease activated receptor on Endothelial cells, cleaves fibrinogen to increase finrinopeptides that increase vascular permeability and are chemotactic, cleaves factor 5 into 5a

376
Q

Thrombin

A

Factor IIa

377
Q

Fibrinolytic Sytem

A

inflammatory mediators that result in vascular permeability, dilation, and C3a formation

378
Q

Anti-Inflammatory Mediators

A

Destruction of circulating pro-inflammatory, lipoxins, complement regulatory, IL-10 to down regulate activated macrophages, TGF-Beta, intracellular compounds that antagonize pro-inflammatory cell states.

379
Q

IL-10

A

secreted by macrophages to down regulate activated macrophages - anti-inflammatory

Disease And Defense (7 decks)

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