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Pathoma > Chapter 2: Inflammation, Disorder and Wound Healing > Flashcards

Chapter 2: Inflammation, Disorder and Wound Healing Flashcards

1
Q

What is the overall effect of inflammation ?

A

To allow inflam. cells, plasma protein and fluids to exit blood vessels and go into the interstitial space.

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2
Q

What are the two kinds of inflammation

A

Acute and Chronic

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3
Q

What two things are always present in acute inflammation ?

A

Edema and Neutrophils (neutrophils are really the hallmark of acute inflammation)

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4
Q

What two occurrences lead to the presence of acute inflammation ?

A

Acute infection (figh pathogen) and tissue necrosis (Clear dead tissue)

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5
Q

Toll Like Receptors are found on cells of the innate immune system and are implicit in Acute Inflammation. What is the co-receptor for these and what do they respond to ?

A

CD14

Respond to PAMPS (Pathogen Associated Molecular Patterns)
CD14 specifically responds to LPS (Gram -)

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6
Q

The activation of CD14 and TLR will lead to the activation of which intracellular immune mediator ?

A

NF-kB (translocates to the nucleus and cause activation of multiple immune mediator genes etc.

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7
Q

Which cells are part of the innate immune system ?

A

Mast, Macrophages, Neutrophils, Eosinophils

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8
Q

What releases Arachadonic Acid (AA) from the membrane ?

A

Phospholipase A2

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9
Q

What are the two enzyme systems that act on AA ?

A

Cyclooxygenase –> PG’s

Lipoxygenase 5 –> LT’s

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10
Q

Which PG’s are responsible for VASODILATION and VASCULAR PERMEABILITY ?

A

PG D2 ,E2 and I2

PG will make you DIE (mnemonic) due to hypotension and edema.

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11
Q

Where in the vasculature does vasodilation occur ?

A

Arteriole

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12
Q

Where in the vasculature does vascular permeability occur ?

A

Post capillary venule

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13
Q

Which prostaglandin is related to production of Pain and Fever (also vasodilation and permeability) ?

A

PGE2

Feever = E2

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14
Q

Which LT is responsible for neutrophils attraction and activation ?

A

LTB4

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15
Q

What other molecules besides LTB4 is responsible for neutrophil attraction ?

A

C5a, IL8 and Bacterial Products.

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16
Q

What do LTC4, D4 and E4 mediate ?

A

Vasoconstriction, Bronchospasm and Increased Permeability ( post capillary venule).

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17
Q

How do LTC4, D4 and E4 increase vascular permeability despite causing vasoconstriction ?

A

They cause the vascular pericyte cells to contract. This pulls the epithelial cells apart creating a gap in which vascular fluids can leak out of.

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18
Q

What three things activate Mast Cells ?

A

Direct Damage to Tissue
C3a and C5a
Crosslinking of antigen with IgE on cell surface

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19
Q

What is the immediate effect occurs due to Mast Cell activation by the three processes listed ?

A

Release of prestored histamine vesicles

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20
Q

What does Histamine release lead to in the vasculature ?

A

Vasodilation
Vascular permeability

(Much like PGD,E,I2)

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21
Q

What is the common effector created by the Classical, Alternative and MBL pathways in complement activation ?

A

C3 Convertase

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22
Q

Explain the components of the Classical Pathway of Complement activation ?

A

IgG or IgM bind to pathogen.
C1 binds to IgG or IgM on pathogen
Leads to Activation of C3 Convertase

(GM makes Classical Cars, lets go see one (C1))

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23
Q

Explain the components of the Alternative Pathway of Complement activation ?

A

Microbial products directly activate complement

Leads to C3 Convertase production

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24
Q

Explain the components of the MBL Pathway of Complement activation ?

A

MBL binds to Mannose moieties on pathogen leading to activation of complement and formation of C3 convertase

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25
Q

Products of C3 Convertase activity

A

C3 –> C3a and C3b

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26
Q

C3b leads to the production of ..

A

C5 convertase

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27
Q

Products of C5 Convertase

A

C5a and C5b

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28
Q

What does C5b complex with to lead to the formation of the MAC ?

A

C6-9

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29
Q

What is the overall effect of MAC ?

A

Lyse cells

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30
Q

C5a and C3a are also known as …. and lead to …..

A

Anyphylaxotoxins

Mast Cell degranulation and release of Histamine (anaphylaxis is due to huge amount histamine release )

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31
Q

Besides leading to the activation of the C5 Convertase, C3b also allows for …

A

Opsonization

It is an opsonin that Ab’s bind to. Helps phagocytes internalize pathogens and necrotic cells>

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32
Q

Besides being and anayphylaxotoxin, C5a is also a chemoattractant for …..

A

Neutrophils

Other Neutrophils attractants : LTB4, IL8 and Bacterial Products.

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33
Q

Where is Hageman Factor (Factor XII) produced and what activates its circulating form ?

A

Liver

Exposed sub endothelial COLLAGEN.

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34
Q

Hageman Factor leads to the activation of which three systems ?

A

Coagulation and Fibrinolytic (Major Roll Player in DIC***)

Complement

Kinnin System

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35
Q

Hageman Factor Activation of Kinnin leads to the cleavage of HMWK to ….

A

Bradykinin

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36
Q

What processes does Bradykinin mediate ?

A

Vasodilation
Vascular Permeability
PAIN (other mediator of pain ? PGE2 !)

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37
Q

What are the 4 Major Signs of Acute Inflammation ?

A

Redness and Warmth
Swelling
Pain
Fever

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38
Q

Which processes lead to Redness and Warmth ? Which molecules mediate this ?

A

Vasodilation
PGD,E,I2
Histamine
Bradykinin

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39
Q

What leads to swelling ? What molecules mediate this ?

A

Increased vascular permeability (post capillary venule)

HISTAMINE**, PGD,E,I2. LTC,D,E4 , Bradykinin and Tissue Damage.

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40
Q

Which molecules mediate pain ?

A

PGE2 and Bradykinin (sensitize sensory nerve endings)

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41
Q

What mediators do Macrophages release that activates COX in the perivascular cells of the hypothalamus ?

A

IL-1 and TNF

Macrophages are activated by pyrogens

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42
Q

What is produced by COX in the perivascular cells of the hypothalamus that leads to increased temperature set point and thus fever ?

A

PGE2

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43
Q

What are the 4 processes that lead to movement of Neutrophils out of the blood vessels ?

A

Margination
Rolling
Adhesion
Transmigration/Chemotaxis

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44
Q

What leads to margination of WBC’s ?

A

Vasodilation (arteriole) and slowing of the blood so that WBC’s can move out of the central blood flow towards the periphery.

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45
Q

Rolling requires the interaction between Sialyl Lewis X and selections. Which cells are these found on respectively ?

A

Sialyl Lewis X (WBC)

E and P Selectins (Endothelium)

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46
Q

What molecules lead to the up regulation of P selectins on the vascular endothelium ?

A

Histamine

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47
Q

What molecules lead to the up regulation of E selections on the endothelium ?

A

TNF and IL-1

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48
Q

Adhesion of WBC’s to the endothelium is due to the interaction between Integrins and ICAM/VCAM. What cells are these found on respectively ?

A

Integrins: WBC’s

ICAM/VCAM: Vascular endothelium

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49
Q

What molecules lead to the up regulation of Integrins on WBC’s ?

A

C5a and LTB4 (These are also chemoattractant for neutrophils)

What other molecules are chemo-attractants for neutrophils ? IL8 and Bacterial Products.

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50
Q

What molecules up-regulate CAM/VCAM on endothelium ?

A

TNF and IL-1 (the same molecules that regulate Selectins on vascular endothelium)

(TNF and IL-1 are also released by macrophages and lead to COX activity in the Hypothalamus –> PGE2 activation and fever.)

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51
Q

Leukocyte Adhesion Deficiency is caused by an autosomal recessive defect in …..

A

Integrins (CD18 subunit)

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52
Q

What is the earliest manifestation of Leukocyte Adhesion Deficiency ?

A

Delayed Separation of Umbilical Cord. (Necrotic tissue that is usually phagocytically removed by the presence of neutrophils –> separation)

Two other signs of LAD: Increased circulating neutrophils and frequent infections that do not produce pus (non-pyogenic).

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53
Q

Where do WBC’s migrate across the endothelium ?

A

POST CAPILLARY VENULE (this is the site of increased permeability KNOW IT !!!)

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54
Q

Again, what are the molecules that lead to chemotaxis and migration by WBC’s (neutrophils in this case) ?

A

C5a, LTB4, IL-8 and Bacterial products

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55
Q

What two opsonins enhance the phagocytosis of pathogens and necrotic tissue ?

A

IgG and C3b (C3b is an opsonin and also leads to activation of the C5 Convertase)

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56
Q

Formation of which intracellular organelles are needed for proper functioning of phagocytes ?

A

Phagolysosome (Phagosome + Lysosome)

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57
Q

This syndrome is characterized by neutropenia, increased risk for pyogenic infection, giant granules in leukocytes, albinism, defective hemostasis and peripheral neuropathy ?

A

Chediak-Higashi Syndrome

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58
Q

What is the main cause of Chediak Higashi syndrome ?

A

Autosomal recessive defect in protein trafficking that leads to inhibited phagolysosome formation.

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59
Q

What is the most effective form in intracellular killing by phagocytes ?

A

O2 dependent

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60
Q

What is the ultimate final molecule that is responsible for oxygen dependent killing ?

A

Bleach (HOCL)

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61
Q

What is the first step in production of HOCL ?

A

O2 –> superoxide (via NADPH Oxidase)

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62
Q

What is the second rxn in creating HOCL ?

A

Superoxide –> H2O2 (via Superoxide Dismutase)

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63
Q

What is the last rxn in creating HOCL ?

A

H2O2 –> HOCL (via Myeloperoxidase, MPO)

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64
Q

Chronic Granulomatous Disease (CGD) is due to a defect in which enzyme ?

A

NADPH Oxidase

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65
Q

CGD is marked by recurrent infection and granuloma formation involving which kind of organisms ?

A

Catalase Positive (Catalase is capable of breaking down H202)

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66
Q

Which organisms (5) are often seen in granulomas of CGD ?

A 
S.aureus
P. cepacia
S.marcescens
Nocardia
Aspergillus
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67
Q

How does catalase allow organisms to survive in CGD ?

A

Normally, organisms produce a small amount of H202. People with CGD can use this (since their endogenous H202 production is inhibited) to make HOCL.
Organisms with Catalase break down H2O2 making this form of killing impossible.

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68
Q

What is the test that screens for CGD ? What is a positive result for CGD ?

A

Nitroblue Tetrazolium

Normal patients have NADPH Oxidase and can metabolize NBT to a blue color. Those w/o NADPH oxidase will not metabolize this and will not produce a blue color : Positive Screen = Colorless.

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69
Q

MPO deficiency leads to ineffective production of HOCL. What organisms will patients with this defect be at high risk for ?

A

Candida

(Patients with MPO still have effective NADPH so they will have an oxidative burst that can kill Catalase + organisms (will have Negative NBT test = blue color produced)

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70
Q

In what granules will you see oxygen independent killing ?

A

Secondary Granules of leukocytes etc.

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71
Q

Review: what are the three phases of Acute Inflammation ?

A

Fluid
Neutrophil
Macrophage

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72
Q

How do macrophages enter the peripheral tissue ?

A

Same as neutrophils: Margination, Rolling, Adhesion and extravasion.

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73
Q

What type of granules help Macrophages destroy ingested material ?

A

Secondary (02 independent mechanisms).

Note: Opsonins help macrophages phagocytize material ( c3b and IgG)

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74
Q

What are the anti-inflammatory molecules secreted by Macrophages that mediate resolution and healing ?

A

IL-10

TGF-B

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75
Q

What are the pro-inflammatory molecules secreted by Macrophages that mediate the continued recruitment of neutrophils and therefore Acute Inflammation ?

A

IL-8

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76
Q

Structure formed by Macrophages due to acute inflammation and fibrosis

A

Abscess (cytokines and growth factors mediate this)

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77
Q

What cells do macrophages present antigen to in order to mediate CHRONIC INFLAMMATION ?

A

CD4+ Helper cells.

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78
Q

What cells are characteristic of Chronic Inflammation ?

A

Lymphocytes and Plasma Cells in Tissue

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79
Q

What are some stimuli for chronic inflammation ?

A 
Viral Infection
Mycobacteria
Fungus
Parasites
AI Disease
Foreign Material 
Certain Cancers
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80
Q

What constitutes the T-cell Receptor Complex ?

A

TCR

CD3

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81
Q

Antigen presented to the TCR comes attached to which molecules ?

A

MHC-I

MHC-II

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82
Q

MHC-I complexes with which class of T-Cells ?

A

CD8 T-Cells

83
Q

MHC-II complexes with which class of T-Cells ?

A

CD4 T-Cells

84
Q

CD4+ recognize what kind of antigen that is presented on MHC-II molecules ?

A

Extracellular !

85
Q

CD4+ activation involving TCR + MHC-II also requires a secondary signal between B7 and CD28 to cause activation. Which cells have B7 on them ? Which Cells have CD28 on them ?

A

APC has B7 and MHCII

CD4+ Cells has TCR and CD28

28/7 = 4 ~

86
Q

TH1 cells are required for the proper function of which 3 cells ?

A

Macrophages
B-cells
CD8 Killer Cells

87
Q

What do TH1 cells secrete to activate Macrophages ?

A

IFN-g (causes them to turn into histiocytes, more about this later)

88
Q

What do TH1 cells secrete to affect B-cells ?

A

INF-g (causes class switching from IgM–>IgG)

89
Q

What do TH1 cells secrete to activate CD8 Killer Cells ?

A

IL-2 !!

90
Q

TH2 cells are important in the activation/differentiation of which cells ?

A

B-Cells

91
Q

What do TH2 cells secrete to cause class switching of B-cells to IgE ?

A

IL-4

92
Q

What do TH2 cells secrete to cause class switching of B-cells to IgA ?

A

IL-5

93
Q

What are the two ways in which B-cells are activated ?

A
  1. Antigen Binds IgM or IgD leading to either IgM or IgD secreting plasma cells
  2. TH2 interactions
94
Q

Initially which CD40 on the B-cell must bind CD40L on the TH2 cell. After this occurs, what does the TH2 cell secrete to activate the B-cell ?

A

IL-4 (IgM –> IgE)

IL-5 (IgM –> IgA, maturation to plasma cell)

95
Q

CD8 Cytotoxic T-Cells complex with MHC-I which presents which kind of antigen ?

A

INTRACELLULAR ! (intracellular pathogens)

96
Q

In order to be activated, CD8 T-Cells must bind antigen on MHC-I and receive which stimulatory signal from TH1 cells ?

A

IL-2 (already a card, just wanted to test my recall).

97
Q

What are the two ways in which CD8 Cells kill infected cells ?

A

Perforin/Granzyme –> perforin creates a hole in the membrane for granzyme to enter. Granzyme activates apoptosis

CD8 FasL binds Fas on target cell activating apoptosis.

98
Q

Granulomatous Inflammation is divided into two sub-types. What are they ?

A

Caseating

Non-caseating.

99
Q

What is the CHARACTERISTIC cell of granulomatous inflammation ?

A

EPITHELIOD HISTIOCYTE. (Tranformed macrophage)

100
Q

What is the characteristic of Non-caseating granulomas ?

A

Lack Central Necrosis

101
Q

What are some conditions that lead to Non-caseating granulomas ?

A 
Foreign Body
Sarcoid
Beryllium
Crohn disease (Crypt Abscess, no necrosis)
Cat Scratch (stellate shaped granuloma)
102
Q

What is the characteristic of caseating granulomas ?

A

central necrosis

103
Q

What are some conditions that lead to caseating granulomas ?

A

Tuberculosis

Fungal infection

104
Q

the initial step in granuloma production involves Macrophages presenting antigen on MHCII to TH cells. What doe the secretion of IL-12 from the macrophage lead to ?

A

Differentiation of TH to TH1 cell !

105
Q

After differentiation to TH1, what will this cell secrete to transform macrophage into an epitheliod histiocyte (and giant cells) ?

A

INF-g.

106
Q

DiGeorge Syndrome is caused by a developmental failure of which embryonic structure to form ?

A

3/4th pharyngeal pouch

107
Q

What deletion is responsible for DiGeorge ?

A

22q11

108
Q

What anatomical structures are effected by developmental failure of the 3/4th pharyngeal pouch to form ?

A

Thymus
Parathyroid
Upper portion of Heart/Great Vessels
Closure of palate

109
Q

Characteristics of DiGeorge syndrome include T-Cell deficiency and hypocalcemia. Why ?

A

Lack of Thymus and Parathyroid (respectively)

110
Q

SCID is caused by defective cell mediated and humoral immunity and is usually due to which three etiologies ?

A

Cytokine Receptor Defect
Adenosine Deaminase Deficiency ***
MHC-II deficiency

111
Q

Why will Cytokine Receptor Defect lead to SCID ?

A

Cytokines (like IL-4,5,12 and INF-g) are all needed for proper formation of T and B Cells

112
Q

Why will Adenosine Deaminase Deficiency lead to SCID ?

A

ADA is responsible for the deamination of adenosine and deoxyadenosine. Build up of these two is cytotoxic to lymphocytes (T/B cells)

MOST HIGH YIELD

113
Q

Why will MHC-II deficiency lead to SCID ?

A

MHC-II is needed to activate both B and T-cells. Without this there will be no maturation!

114
Q

What is the TOC for SCID ?

A

Stem Cell Transplant

115
Q

X-Linked Agammaglobulinemia is related to a complete lack of …

A

immunoglobulin (due to disordered T-cell maturation)

116
Q

What receptor is defective in X-Linked Agammaglobulinemia ?

A

Bruton Tyrosine Kinase (x-linked)

BTK is signal for immature B-cell to become a plasma cell.

117
Q

What kind of infections are seen in X-Linked Agammaglobulinemia ?

A

**Bacterial, Enteroviral and Giardia ***

Enteroviral and Giardia due to lack of IgA

118
Q

What must be avoided in X-Linked Agammaglobulinemia ?

A

Live Vaccines

119
Q

Like in X-Linked Agammaglobulinemia, Common Variable Immunodeficiency will result in infection from…

A

bacteria, Enteroviruses and Giardia ! Due to defect in B and T Cells.

120
Q

What else are patients with Common Variable Immunodeficiency at high risk for ?

A

Autoimmune disease and lymphoma !

121
Q

What is the most common immunoglobulin deficiency ?

A

IgA deficiency ! –> Low mucosal IgA

122
Q

What kind of infections are people with IgA deficiency at most risk for ?

A

Mucosal, especially viral

123
Q

What is the cause of Hyper IgM Syndrome ?

A

Either a defect in CD40L (on TH2) or CD40R(On B-cell)

124
Q

Why will you see IgM secretion but low or absent levels of IgA,E and G ?

A

The first mechanism of B-Cell activation is intact (i.e antigen binds IgM or IgD on B-cell surface –> IgM or D secreting Plasma Cells). Lots of IgM will be made but no class switching occurs since TH2 cells cannot be activated to release IL-4/5).

But the second mechanism the involves TH2 cell mediated activation of B-cell and class switching is impaired due to CD40 defect that inhibits activation.

125
Q

What is defective in Wiskott-Aldrich Syndrome ?

A

WASP gene (X-linked)

126
Q

What are the three common manifestations seen in Wiskott-Aldrich Syndrome ?

A

Thrombocytopenia (Petechiae), Eczema, recurrent infection

127
Q

what is the leading cause of death in Wiskott-Aldrich Syndrome ?

A

Bleeding

128
Q

What kind of infection are patients with deficiency in complement molecules C5-9 at higher risk for ?

A

Neisseria!

MAC is main way we deal with Neisseria

129
Q

C1 inhibitor deficiency is mostly characterized by what manifestation ?

A

Angiodema especially at the mucosal surfaces especially PERIORBITAL EDEMA

130
Q

Autoimmune disorders are characterized by immune mediated damage of tissues and involve..

A

A loss of self tolerance

131
Q

AI is more common in men or women ?

A

Women of child bearing age.

132
Q

What kind of hypersensitivity is Systemic Lupus Erythematosus ?

A

Type II (Cytotoxic) and Type III ( Immune Complex)

133
Q

Typical signs associated with SLE include

A 
Fever/Weight loss
Malar Rash (Butterfly)
Arthritis
Renal Disease 
Cardiac damage
Anemia
134
Q

What is the most common cause of Renal Damage ?

A

Diffuse Proliferative Glomerulonephritis

135
Q

What kind of syndrome is Diffuse Proliferative Glomerulonephritis: Nephritic or Nephrotic ?

A

Nephritic

136
Q

Cardiac inflammation is seen in all tissues of the heart (Endocarditis, Myocarditis, Pericarditis). One of the characteristics is Libman-Sachs Endocarditis Describe this..

A

small sterile deposits on either side of the mitral valve

137
Q

What causes anemia, thrombocytopenia and leukopenia ?

A

Ab’s to RBC’s, platelets and leukocytes respectively.

138
Q

Is ANA specific for for SLE ?

A

NO , sensitive but not specific.

139
Q

What Ab is highly specific for SLE ?

A

dsDNA antibodies

140
Q

What are the main causes of death in SLE ?

A

RENAL (Diffuse Glomerular GN)
Infection
Endocarditis

141
Q

What is the Ab present in Drug Induced SLE ?

A

Anti-Histone Ab

142
Q

What drugs lead to Drug Induced SLE ?

A

Hydralazine, Isoniazid and Procainamide

143
Q

What is the treatment for Drug Induced SLE ?

A

REMOVAL OF THE DRUG !

144
Q

Antiphospholipid Antibody syndrome is seen in 30% of patients with SLE. What are the two most common anti-bodies ?

A

Anti-Cardiolipin

Lupus Anticoagulant

145
Q

Abberent positive Syphilis tests are seen in the presence of what Ab’s in SLE ?

A

Anti-Cardiolipin

146
Q

Lupus Anticoagulant leads to an aberration of which test ?

A

PTT (Increases it)

147
Q

Although Lupus Anticoagulant causes an increased PTT, what is it associated with ?

A

THROMBOSIS

Hepatic –> Budd-Chiari
DVT
Placental –> loss of baby

148
Q

What is the TOC for Lupus Anticoagulant Ab ?

A

Lifelong anticoagulation.

149
Q

What is destroyed in Sjogrens Syndrome ?

A

Lacrimal and salivary Glands

150
Q

What kind of hypersensitivity is seen in Sjogrens Syndrome ?

A

Type IV

151
Q

What are the three chacrteristic signs of Sjogrens ?

A

Dry Eyes
Dry mouth (can’t chew cracker)
Recurrent Dental Carries ( Dry mouth

152
Q

Along with ANA, what is the Ab associated with Sjogren Syndrome ?

A

Anti-ribonucleoprotein antibodies

153
Q

Sjogrens Syndrome is associated with rheumatoid arthritis and what other disease ?

A

B-cell (Marginal) Lymphoma

Presents as unilateral parotid gland enlargement, which is unusual since most are bilateral

154
Q

What cells are activated in Scleroderma ?

A

Fibroblasts –> deposition of collagen (Fibrosis)

155
Q

Scleroderma can be split into two large categories: Localized and Systemic. What organ is involved in Localized Scleroderma ?

A

Skin Only

156
Q

What Anti-body is present in Localized Scleroderma ?

A

DNA Topoisomerase II

157
Q

Systemic Scleroderma is can be split into two sub-categories. What are they ?

A

Limited and Diffuse

158
Q

Does Limited Systemic Scleroderma is associated with which syndrome ?

A

CREST !

Early Skin involvement with late stage visceral

159
Q

What does CREST stand for ?

A 
Calcinosis
Reynaud
Esophageal dysmotility
Sclerodactly
Telangiectasias
160
Q

What auto-Ab is CREST associated with ?

A

Anti-Centromere Ab

161
Q

Diffuse Systemic Scleroderma involves both skin and visceral organs. What are the organist that are most affected ?

A

GI Tract
Lungs
Kidneys

162
Q

What Anti-body is associated with Diffuse Systemic Scleroderma ?

A

Anti-Topoisomerase I (Scl 70)

163
Q

Characteristics of which three diseases are seen in Mixed Connective Tissue Disease ?

A

SLE
Systemic Sclerosis
Polymyositis.

164
Q

What AB is associated with Mixed Connective Tissue Disease ?

A

Anti -U1 Ribonucleoprotein.

165
Q

What are the two processes that work in combination during wound healing ?

A

Regeneration and Repair

166
Q

When does wound healing begin ?

A

At the onset of inflammation

167
Q

What is regeneration ?

A

Replacement of damaged tissue with native tissue !

Does not occur in all cell types

168
Q

What are the three kinds of tissues based on regenerative capacity ?

A

Labile
Stabile
Permanent

169
Q

Labile

A

possess stem cells that continually regenerate the tissue

170
Q

What are the major tissues that are labile ?

A

Small/Large Bowel
Skin
Bone Marrow

171
Q

Where are the stem cells of the bowel found ?

A

Crypts

172
Q

Where are the stem cells of the skin found ?

A

Basal layer

173
Q

Where are the stem cells of the blood found ?

A

Bone marrow Hematopoeitic Cells

174
Q

What are the stem cells of the lung ?

A

Type II Pneumocytes

175
Q

Stable

A

Typically quiescent in Go phase but are stimulated on injury to re-enter the cell cycle

176
Q

What are some examples of Stable Cells ?

A

Liver

Kidney Tubule

177
Q

Permanent Tissue

A

Lacks significant regenerative potential

178
Q

What tissues are Permanent ?

A

Myocardium, Skeletal Muscle, Neurons

179
Q

What is Repair ?

A

Regeneration of damage tissue with fibrous scar

180
Q

When doe repair occur ?

A

When stem cells are lost or if cell lacks regen capability

181
Q

What is first step or repair ?

A

FORMAITON OF GRANULATION TISSUE

182
Q

What three structures/cells are found in granulation tissue ?

A

Fibroblasts: Deposit Tyoe III Collagen

Capillaries: Bring blood to tissue (lots of neovascularization in granulation tissue)

Myofibroblasts: Lead t contraction of wound

183
Q

What is the eventual result of Repair ?

A

Scar Formation

184
Q

What occurs to type III collagen in the course of repair ? What enzyme does this ?

A

It is replaced by Type I

Collagenase Enzyme

185
Q

Where do you find Type I Collagen ?

A

Bone
SKin
Tendon

186
Q

Where do you find Type II Collagen ?

A

Cartilage

187
Q

Where do you find Type III Collagen ?

A

Granulation Tissue
Blood vessels
Embryonic

188
Q

Where do you find Type IV Collagen ?

A

Basement membrane

189
Q

What kind of signaling regulates regeneration and repair ?

A

paracrine (via growth Factors)

190
Q

TGF-a

A

Epithelial and Fibroblast GF

191
Q

TGF-b

A

fibroblast growth factor
INHIBITS INFLAMMATION (along with IL-10)
Secreted by macrophages

192
Q

Platelet Derived Growth Factor

A

From Platelets

Growth Factor for Endothelium, Smooth Muscle and Fibroblasts

193
Q

Fibroblast Growth Factor

A

Sort Of A Misnomer: IMPORTANT FOR ANGIOGENESIS

194
Q

VEGF

A

Important for Angiogenesis

195
Q

Primary Intention

A

Wound edges are brought together ( like suturing)

Minimal scar formation

196
Q

Secondary intention

A

Edges of wound not approximated. Repair and Regenertion –> Granulation tissue which fills the defect
Myofibroblasts contract the wound –> Scar

197
Q

What is the most common cause of delayed wound healing ?

A

INFECTION

S.aureus is the most common offender

198
Q

Vitamin C deficiency leads to delayed wound healing because it is an important factor for what process ?

A

Hydroxylation of Proline and Lysine Procollagen Residues needed for collagen cross linking.

199
Q

Copper deficiency leads to delayed wound healing because it is an important factor for what process ?

A

Cofactor for Lysly oxidase which cross links lysine and hydroxylysine to form stable collagen.

200
Q

Zinc deficiency leads to delayed wound healing because it is an important factor for what process ?

A

Cofactor for Collagenase which is necessary for replacing Type III with Type I Collagen in granulation tissue

201
Q

What is the most commonly seen site of Dehiscence (wound rupture) ?

A

Abdominal (after surgery)

202
Q

This scar deformity is due to an Excess of Type I collagen being put down

A

Hypertrophic Scar

203
Q

This scar deformity is due to an Excess of Type III collagen being put down

A

Keloid

204
Q

Which scar deformity is seen most often in african americans and often involves the earlobes, face and upper extremities ?

A

Keloid

Pathoma (15 decks)

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