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Pathoma > Ch 2 - Inflammation, Inflammatory Disorders, and Wound Healing > Flashcards

Ch 2 - Inflammation, Inflammatory Disorders, and Wound Healing Flashcards

1
Q

ACUTE INFLAMMATION is characterized by

A

Presence of EDEMA and NEUTROPHILS

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2
Q

Conditions in which ACUTE INFLAMMATION arises

A

Response to INFECTION to eliminate pathogen and TISSUE NECROSIS to clear necrotic debris

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3
Q

Acute inflammation in MYOCARDIAL INFARCTION

A

24hrs post-MI there is acute inflammation with NEUTROPHILS to clear necrotic debris –> causes increased WBCs post-MI (mainly neutrophils)

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4
Q

Key HALLMARK 24hrs post-MI

A

Acute inflammation with NEUTROPHILS

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5
Q

Acute Inflammation: innate vs adaptive immunity

A

INNATE - immediate response with limited specificity

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6
Q

How do MACROPHAGES recognize GRAM NEGATIVE BACTERIA?

A

CD14 (a TLR) on MACROPHAGES recognizes LPS (a pathogen assoc molecular pattern - PAMP) on Gram neg bacteriaCD14 (a TLR) on MACROPHAGES recognizes LPS (a pathogen assoc molecular pattern - PAMP) on Gram neg bacteriaCD14 (a TLR) on MACROPHAGES recognizes LPS (a pathogen assoc molecular pattern - PAMP) on Gram neg bacteriaCD14 (a TLR) on MACROPHAGES recognizes LPS (a pathogen assoc molecular pattern - PAMP) on Gram neg bacteriaCD14 (a TLR) on MACROPHAGES recognizes LPS (a pathogen assoc molecular pattern - PAMP) on Gram neg bacteriaCD14 (a TLR) on MACROPHAGES recognizes LPS (a pathogen assoc molecular pattern - PAMP) on Gram neg bacteriaCD14 (a TLR) on MACROPHAGES recognizes LPS (a pathogen assoc molecular pattern - PAMP) on Gram neg bacteriaCD14 (a TLR) on MACROPHAGES recognizes LPS (a pathogen assoc molecular pattern - PAMP) on Gram neg bacteriaCD14 (a TLR) on MACROPHAGES recognizes LPS (a pathogen assoc molecular pattern - PAMP) on Gram neg bacteriaCD14 (a TLR) on MACROPHAGES recognizes LPS (a pathogen assoc molecular pattern - PAMP) on Gram neg bacteria

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7
Q

Result of TLR activation

A

Upregulation of NF-kB which activates immune response genes –> production of multiple immune mediators

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8
Q

Cells involved in INNATE IMMUNITY

A

Mast cells, macrophages, neutrophils, eosinophils, basophils, epithelium on body surfaces, mucous secreted by cells, complement system

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9
Q

Cells involved in ADAPTIVE IMMUNITY

A

lymphocytes, T cells and Ab - very specific target

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10
Q

Arachidonic acid –> PGs

A

AA released from phospholipid membrane by phospholipase A2 and acted upon by COX –> PGs

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11
Q

Arachidonic acid –> Leukotrienes (LT)

A

AA released from phospholipid membrane by phospholipase A2 and acted upon by 5-lipoxygenase –> LTs

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12
Q

PGs that mediate VASODILATION and INCREASED VASCULAR PERMEABILITY

A

PGI2, PGD2, PGE2

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13
Q

Function of PGE2

A

Mediates PAIN, fEver as well as VASODILATION and INCREASED PERMEABILITY

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14
Q

In inflammation, VASODILATION occurs at the level of:

A

ARTERIOLE

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15
Q

In inflammation, increased VASCULAR PERMEABILITY occurs at:

A

POST-CAPILLARY VENULE

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16
Q

Which LEUKOTRIENE ATTRACTS NEUTROPHILS?

A

LTB4

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17
Q

Chemical Mediators that ATTRACT NEUTROPHILS?

A

LTB4, C5a, IL-8, Bacterial products

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18
Q

Leukotrienes that MEDIATE VASOCONSTRICTION, BRONCHOSPASM, and INCREASED VASCULAR PERMEABILITY

A

LTC4, LTD4, LTE4 - cause smooth muscle to contract

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19
Q

SLOW reacting substances of ANAPHYLAXIS

A

LTC4, LTD4, LTE4 - vasoconstriction, bronchospasm, increased vascular permeability

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20
Q

What ACTIVATES MAST CELLS?

A

Tissue trauma, C3a & C5a, cross-linking of surface IgE by Ag

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21
Q

IMMEDIATE RESPONSE of MAST cells?

A

Release of preformed HISTAMINE - mediates VASODILATION (of ARTERIOLES) and INCREASED VASCULAR PERMEABILITY (at post-cap venules)

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22
Q

DELAYED RESPONSE of MAST cells?

A

Production of AA metabolites - particularly LEUKOTRIENES - maintain acute inflamm

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23
Q

Activation of Complement Pathway

A

Classical, Alternative Pathway, Mannose-binding lectin pathway - all pathways result in production of C3 CONVERTASE

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24
Q

Activation of CLASSICAL Complement Pathway

A

GM makes CLASSIC cars - C1 binds IgG or IgM that is bound to Ag

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25
Q

COMPLEMENT proteins that TRIGGER MAST CELL DEGRANULATION

A

C3a and C5a - anaphylatoxins - result in histamine mediated vasodilation and increased vascular permeability

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26
Q

COMPLEMENT protein that is CHEMOTACTIC for NEUTROPHILS

A

C5a

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27
Q

COMPLEMENT protein that acts as OPSONIN for phagocytes

A

C3b (also IgG)

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28
Q

COMPLEMENT proteins that make up MAC?

A

C5b, C6-9

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29
Q

Function of Membrane Attack Complex

A

lyses microbes by creating a hole in the cell membrane

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30
Q

What activates HAGEMAN FACTOR (Factor XII)?

A

inactive proinflamm protein produced in liver that is activated upon exposure to subendothelial or tissue collagen

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31
Q

HAGEMAN FACTOR (Factor XII) activates which processes?

A

COAGULATION and FIBRINOLYTIC systems –> DIC; complement; Kinin system - produces BRADYKININ (mediates VASODILATION, INCREASED VASCULAR PERMEABILITY, and PAIN)

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32
Q

Which chemical proteins mediate PAIN?

A

PGE2 and BRADYKININ

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33
Q

Pathophys of GRAM NEGATIVE SEPSIS –> DIC

A

GRAM NEG organisms have ability to ACTIVATE HAGEMAN FACTOR which activates COAGULATION and FIBRINOLYTIC systems

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34
Q

Primary mediator of REDNESS (rubor) and WARMTH (calor) in inflammation

A

HISTAMINE; also PGs and bradykinin - vasodilation (relaxation of arteriolar smooth muscle)

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35
Q

Primary mediator of SWELLING (tumor) in inflammation

A

HISTAMINE; also tissue damage - cause endothelial cell contaction –> leakage of fluid from postcap venule

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36
Q

Primary mediators of PAIN (dolor) in inflammation

A

BRADYKININ and PGE2 - sensitive nerve endings

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37
Q

Primary mediator of FEVER in inflammation

A

PGE2 raises temp set point - MACROPHAGES release IL-1 and TNF which increase COX activity in perivascular cells of the HYPOTHALAMUS

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38
Q

Steps of NEUTROPHIL arrival and function

A

Margination –> Rolling –> Adhesion –> Transmigration and Chemotaxis –> Phagocytosis –> Destruction of phagocytosed material –> Resolution

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39
Q

How do LEUKOCYTES ROLL on Endothelial cells?

A

P-selectin and E-selectin bind SIALYL LEWIS X on leukocytes

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40
Q

P-SELECTIN

A

Released from WEIBEL-PALADE bodies - mediated by HISTAMINEReleased from WEIBEL-PALADE bodies - mediated by HISTAMINEReleased from WEIBEL-PALADE bodies - mediated by HISTAMINEReleased from WEIBEL-PALADE bodies - mediated by HISTAMINEReleased from WEIBEL-PALADE bodies - mediated by HISTAMINEReleased from WEIBEL-PALADE bodies - mediated by HISTAMINEReleased from WEIBEL-PALADE bodies - mediated by HISTAMINEReleased from WEIBEL-PALADE bodies - mediated by HISTAMINE

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41
Q

Weibel-Palade bodies release:

A

von Willebrand factor and P-selectin von Willebrand factor and P-selectin von Willebrand factor and P-selectin von Willebrand factor and P-selectin von Willebrand factor and P-selectin von Willebrand factor and P-selectin von Willebrand factor and P-selectin von Willebrand factor and P-selectin

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42
Q

How does LEUKOCYTE ADHERE to endothelial cell?

A

INTEGRINS on leukocytes bind to ICAM and VCAM on endothelium

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43
Q

What upregulates ICAM and VCAM?

A

TNF and IL-1

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44
Q

What upregulates INTEGRINS on leukocytes?

A

C5a and LTB4 (both chemotactic for neutrophils as well)

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45
Q

LEUKOCYTE ADHESION DEFICIENCY (LAD)

A

AR defect of INTEGRINS (CD 18 subunit)

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46
Q

Clinical Features of Leukocyte Adhesion Deficiency

A

DELAYED SEPARATION OF UMBILICAL CORD (acute inflamm cannot cross endothelium to clear tissue), INCREASED CIRCULATING NEUTROPHILS (1/2 of body’s neutrophils typically hang out in blood vessels in lungs but with less adhesion –> more circulating), and RECURRENT BACTERIAL INFECTIONS THAT LACK PUS (pus is dead neutrophils in fluid and they can’t cross so no pus)

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47
Q

Where do LEUKOCYTES TRANSMIGRATE across ENDOTHELIUM?

A

POST-CAPILLARY VENULE

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48
Q

CHEDIAK-HIGASHI SYNDROME

A

AR Protein Trafficking Defect –> IMPAIRED PHAGOLYSOSOME FORMATION; railroad (microtubules) that lead from phagosome to lysosome is out

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49
Q

Clinical Features of CHEDIAK-HIGASHI Syndrome

A

Railroad (microtubules) are out –> IMPAIRED PHAGOLYSOSOME formation; INCREASED PYOGENIC INFECTIONS (can’t destroy consumed organisms), NEUTROPENIA, GIANT GRANULES in LEUKOCYTES (accumulation), Defective PRIMARY HEMOSTASIS (abn dense granules in platelets), ALBINISM (can’t transport melanin), PERIPHERAL NEUROPATHY (can’t pass nutients over long distances to end of nerves)

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50
Q

Most Effective Destruction of Phagocytosed material

A

O2 dependent killing is most effective - HOCl* generated by oxidative burst in phagolysosomes

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51
Q

O2 INDEPENDENT Destruction of Phagocytosed material

A

Lysozyme in macrophages and major basic protein in eosinophils

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52
Q

What enzyme converts O2 –> O2*-

A

NADPH oxidase

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53
Q

What enzyme conversts O2*- –> H2O2

A

SUPEROXIDE DISMUTASE (SOD)

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54
Q

What enzyme converts H2O2 –> HOCl*

A

MYELOPEROXIDASE (MPO)

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55
Q

CHRONIC GRANULOMATOUS DISEASE (CGD)

A

Poor O2-dependent killing due to NADPH OXIDASE DEFECT - can’t make HOCl*–> recurrent infection and granuloma formation with CATALASE + organisms in particular STAPH AUREUS and PSEUDOMONAS CEPACIA; also Serratia marcescens, Nocardia and Aspergillus

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56
Q

Pts with CHRONIC GRANULOMATOUS DISEASE are SUSCEPTIBLE to which ORGANISMS?

A

CATALASE + STAPH AUREUS & PSEUDOMONAS CEPACIA; also Serratia marcescens, Nocardia and Aspergillus

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57
Q

Role of CATALASE in bacterial organisms

A

Destorys H2O2 and thus prevents HOCl* formation and prevents O2 dependent killing

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58
Q

NITROBLUE TETRAZOLIUM test

A

Used to screen for CHRONIC GRANULOMATOUS DISEASE (NADPH oxidase deficiency); if leukocytes contain NADPH oxidase they will turn blue but they will remain clear if they do not contain NADPH oxidase

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59
Q

MYELOPEROXIDASE Deficiency

A

Cannot convert convert H2O2 –> HOCl*; Increased risk for CANDIDA infections; most pts Asx, Nitroblue Tetrazolium test is normal

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60
Q

Pts with MYELOPEROXIDASE Deficiency are susceptible to

A

CANDIDA infections

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61
Q

At end of acute inflammation, when and where do neutrophils undergo apoptosis?

A

Undergo apoptosis and disappear in the infected tissue within 24 hours of resolution

62
Q

In acute inflammation, when do NEUTROPHILS reach peak levels?

A

~24 hours

63
Q

In acute inflammation, when do MACROPHAGES reach peak levels?

A

2-3 days after inflammation begins

64
Q

MACROPHAGES role in ACUTE INFLAMMATION

A

Ingest organisms via phagocytosis (augmented by opsonins) and destroy the phagocytosed material using enzymes (lysozyme) in secondary granules (O2 independent killing); they also MANAGE THE NEXT STEP of inflammation - proceed to Resolution/healing, further acute inflamm, abscess formation or chronic inflamm

65
Q

ANTI-INFLAMMATORY CYTOKINES produced by MACROPHAGES to induce resolution and healing

A

IL-10 and TGF-β

66
Q

CYTOKINE produced by MACROPHAGES to CONTINUE ACUTE INFLAMMATION

A

IL-8 recruits ADDITIONAL NEUTROPHILS; marked by PERSISTENT PUS formation

67
Q

Role of MACROPHAGES in ABSCESS formation

A

Mediate FIBROSIS via FIBROGENIC GROWTH FACTORS and cytokines

68
Q

Role of MACROPHAGES in CHRONIC INFLAMMATION

A

Present Ag to active CD4+ helper T cells which promote cyokines –> chronic inflamm

69
Q

CD4+ HELPER T CELL ACTIVATION

A

EXTRACELLULAR Ag is phagocytosed & presented on MHC Class II by APCs (dendritic cells or macrophages); 2nd signal B7 on APC binds to CD28 on CD4+ helper T cellEXTRACELLULAR Ag is phagocytosed & presented on MHC Class II by APCs (dendritic cells or macrophages); 2nd signal B7 on APC binds to CD28 on CD4+ helper T cellEXTRACELLULAR Ag is phagocytosed & presented on MHC Class II by APCs (dendritic cells or macrophages); 2nd signal B7 on APC binds to CD28 on CD4+ helper T cellEXTRACELLULAR Ag is phagocytosed & presented on MHC Class II by APCs (dendritic cells or macrophages); 2nd signal B7 on APC binds to CD28 on CD4+ helper T cellEXTRACELLULAR Ag is phagocytosed & presented on MHC Class II by APCs (dendritic cells or macrophages); 2nd signal B7 on APC binds to CD28 on CD4+ helper T cellEXTRACELLULAR Ag is phagocytosed & presented on MHC Class II by APCs (dendritic cells or macrophages); 2nd signal B7 on APC binds to CD28 on CD4+ helper T cell

70
Q

TH1 cells secrete:

A

IL-2 and IFN-γ

71
Q

TH2 cells secrete:

A

IL-4, IL-5, and IL-10

72
Q

Function of IL-2

A

T cell growth factor and CD8+ T cell activator

73
Q

Function of IFN-γ

A

Activates macrophages; in granuloma formation it converts macrophages to EPITHELIOID HISTIOCYTES & GIANT CELLS

74
Q

Function of IL-4

A

Facilitates B-cell class switching to IgG and IgE

75
Q

Function of IL-5

A

Eosinophil chemotaxis and activation, maturation of B cells to plasma cells, and class switching to IgA

76
Q

Function of IL-10

A

Inhibits TH1 phenotype; also produced by macrophages if they decide its time for resolution prior to chronic inflamm

77
Q

CD8+ CYTOTOXIC T CELL ACTIVATION

A

INTRACELLULAR Ag is processed and presented on MHC Class I (expressed by all nucleated cells and platelets); 2nd signal IL-2 from CD4+ TH1 cellsINTRACELLULAR Ag is processed and presented on MHC Class I (expressed by all nucleated cells and platelets); 2nd signal IL-2 from CD4+ TH1 cellsINTRACELLULAR Ag is processed and presented on MHC Class I (expressed by all nucleated cells and platelets); 2nd signal IL-2 from CD4+ TH1 cellsINTRACELLULAR Ag is processed and presented on MHC Class I (expressed by all nucleated cells and platelets); 2nd signal IL-2 from CD4+ TH1 cellsINTRACELLULAR Ag is processed and presented on MHC Class I (expressed by all nucleated cells and platelets); 2nd signal IL-2 from CD4+ TH1 cellsINTRACELLULAR Ag is processed and presented on MHC Class I (expressed by all nucleated cells and platelets); 2nd signal IL-2 from CD4+ TH1 cells

78
Q

Immunoglobulins expressed by NAÏVE B CELLS

A

IgM and IgD

79
Q

B CELL ACTIVATION –> IgM or IgD Plasma Cell

A

Ag binds to surface IgM or IgD on NAÏVE B cell –> maturation to IgM or IgD secreting plasma cell

80
Q

B CELL ACTIVATION –> IgA, IgG and IgE Secreting Plasma Cells

A

B cell Ag presentation to CD4+ Helper T cells via MHC Class II; 2nd signal comes from CD40 RECEPTOR ON B CELL binding to CD40L on HELPER T CELL – Helper T cell secretes IL-4 (IgG and IgE class switching) and IL-5 (IgA class switching)B cell Ag presentation to CD4+ Helper T cells via MHC Class II; 2nd signal comes from CD40 RECEPTOR ON B CELL binding to CD40L on HELPER T CELL – Helper T cell secretes IL-4 (IgG and IgE class switching) and IL-5 (IgA class switching)B cell Ag presentation to CD4+ Helper T cells via MHC Class II; 2nd signal comes from CD40 RECEPTOR ON B CELL binding to CD40L on HELPER T CELL – Helper T cell secretes IL-4 (IgG and IgE class switching) and IL-5 (IgA class switching)B cell Ag presentation to CD4+ Helper T cells via MHC Class II; 2nd signal comes from CD40 RECEPTOR ON B CELL binding to CD40L on HELPER T CELL – Helper T cell secretes IL-4 (IgG and IgE class switching) and IL-5 (IgA class switching)B cell Ag presentation to CD4+ Helper T cells via MHC Class II; 2nd signal comes from CD40 RECEPTOR ON B CELL binding to CD40L on HELPER T CELL – Helper T cell secretes IL-4 (IgG and IgE class switching) and IL-5 (IgA class switching)B cell Ag presentation to CD4+ Helper T cells via MHC Class II; 2nd signal comes from CD40 RECEPTOR ON B CELL binding to CD40L on HELPER T CELL – Helper T cell secretes IL-4 (IgG and IgE class switching) and IL-5 (IgA class switching)

81
Q

DEFINING CHARACTERISTIC of GRANULOMATOUS INFLAMMATION

A

EPITHELIOID HISTIOCYTES surrounded by GIANT CELLS and a rim of LYMPHOCYTES

82
Q

Difference between NONCASEATING and CASEATING Granulomas

A

Noncaseating LACK central necrosis

83
Q

Reaction to foreign material - noncaseating vs caseating granuloma

A

NONCASEATING granuloma

84
Q

Histo hallmark of SARCOIDOSIS

A

Multiple NONCASEATING granulomas in several tissues, in particular the LUNG

85
Q

Histo hallmark of BERYLLIUM EXPOSURE

A

NONCASEATING granuloma in the LUNG

86
Q

Histo hallmark of CROHN DISEASE

A

NONCASEATING granuloma

87
Q

Histo hallmark of ULCERATIVE COLLITIS

A

CRYPT ABSCESSES

88
Q

Organisms that display CASEATING GRANULOMAS

A

TB and Fungal infections

89
Q

Stains for CASEATING GRANULOMAS

A

AFB stain to look for TB and a GMS (Silver) stain to look for FUNGAL INFECTIONS

90
Q

Histo hallmark of CAT SCRATCH DISEASE

A

STELLATE SHAPED NONCASEATING granuloma

91
Q

Process of GRANULOMA FORMATION (both caseating and noncaseating)

A

MACROPHAGES process and present Ag via MHC Class II to CD4+ HELPER T CELLS –> MACROPHAGES SECRETE IL-12 inducing CD4+ helper T cells to differentiate to TH1 subtype –> TH1 cells secrete IFN-γ which converts macrophages to epithelioid histiocytes and giant cellsMACROPHAGES process and present Ag via MHC Class II to CD4+ HELPER T CELLS –> MACROPHAGES SECRETE IL-12 inducing CD4+ helper T cells to differentiate to TH1 subtype –> TH1 cells secrete IFN-γ which converts macrophages to epithelioid histiocytes and giant cellsMACROPHAGES process and present Ag via MHC Class II to CD4+ HELPER T CELLS –> MACROPHAGES SECRETE IL-12 inducing CD4+ helper T cells to differentiate to TH1 subtype –> TH1 cells secrete IFN-γ which converts macrophages to epithelioid histiocytes and giant cellsMACROPHAGES process and present Ag via MHC Class II to CD4+ HELPER T CELLS –> MACROPHAGES SECRETE IL-12 inducing CD4+ helper T cells to differentiate to TH1 subtype –> TH1 cells secrete IFN-γ which converts macrophages to epithelioid histiocytes and giant cellsMACROPHAGES process and present Ag via MHC Class II to CD4+ HELPER T CELLS –> MACROPHAGES SECRETE IL-12 inducing CD4+ helper T cells to differentiate to TH1 subtype –> TH1 cells secrete IFN-γ which converts macrophages to epithelioid histiocytes and giant cells

92
Q

Function of IL-12 in Granuloma Formation

A

Induce CD4+ helper T cells to become TH1 subtype

93
Q

DIGEORGE SYNDROME

A

Devo failure of 3rd and 4th PHARYNGEAL POUCHES due to 22q11 microdeletion –> T-cell deficiency (lack of thymus), HYPOCALCEMIA (lack of parathyroids), abnormalities of the heart, great vessels and face

94
Q

Severe Combined Immunodeficiency Disorder (SCID)

A

Defective cell-mediated and humoral immunity (defective T and B cell immunity)

95
Q

Pts with SCID are Susceptible to:

A

No T cells –> Fungal and viral No B cells –> bacteria and protozoa

96
Q

Tx for SCID

A

Isolation (bubble boy) and stem cell transplant (hematopoietic stem cells)

97
Q

X-Linked AGAMMAGLOBULINEMIA

A

LACK OF IMMUNOGLOBULIN due to disordered B cell maturation; MUTATED BRUTON TYROSINE KINASE (BTK)

98
Q

INFECTIONS found in X-Linked AGAMMAGLOBULINEMIA patients

A

BACTERIA (no IgG to opsonize), ENTEROVIRUS and GIARDIA (no IgA to protect mucosa); also avoid live vaccines

99
Q

COMMON VARIABLE IMMUNODEFICIENCY (CVID)

A

Low Ig due to B cell or helper T cell defect

100
Q

Pts with Common Variable Immunodeficiency are susceptible to:

A

Susceptible to BACTERIA, ENTEROVIRUSES and GIARDIA LAMBILIA; also increased risk for AUTOIMMUNE DISEASES and LYMPHOMA

101
Q

MC Ig Deficiency

A

IgA –> mucosal infection (esp viral)

102
Q

IMMUNOGLOBULIN DEFICIENCY assoc with CELIAC DISEASE

A

IgA

103
Q

HYPER-IgM SYNDROME

A

MUTATED CD40L (on helper T cells) or MUTATED CD40 RECEPTOR on B cells –> no second signal is delivered –> CYTOKINES necessary for class switching NOT PRODUCED –> LOW IgA, IgG, IgE –> RECURRENT pyogenic infections (poor opsonization - low IgG), esp at mucosal surfaces (low IgA)

104
Q

WISKOTT-ALDRICH SYNDROME

A

Triad - Thrombocytopenia, Eczema, and recurrent infections

105
Q

Pts with C5-9 DEFICIENCY are susceptible to

A

NEISSERIA infection (N gonorrhoeae and N meningitidis)

106
Q

Clinical Features of C1 INHIBITOR DEFICIENCY

A

PERIORBITAL EDEMA and muscoal surfaces (over activation of complement –> increased vasodilation and increased vascular permeability –> edema)

107
Q

Type of Hypersensitivity Reaction in SLE

A

Type II (cytotoxic) and Type III - Ab aginst host damage multiple tissues

108
Q

Clinical Features of SLE

A

Malar butterfly rash, arthritis, pleuritis and pericarditis, CNS psychosis, RENAL DAMAGE, Endocarditis, myocarditis, or pericarditis, ANEMIA, THROMBOCYTOPENIA, or LEUKEMIA

109
Q

MC RENAL injury in SLE

A

Diffuse Proliferative GlomerulonephrITIS

110
Q

Classic ENDOCARDITIS injury in SLE

A

LIBMAN-SACKS endocarditis - small sterile deposits on BOTH sides of the mitral valve

111
Q

HEMATOLOGIC findings in SLE

A

PANCYTOPENIA - due to auto-Ab against cell surface proteins

112
Q

MC cause of death in SLE

A

Renal failure and infection

113
Q

Abs used for screening and Dx in SLE

A

Screen with ANA - sensitive but not specific; Dx made with anti-dsDNA Abs - highly specificScreen with ANA - sensitive but not specific; Dx made with anti-dsDNA Abs - highly specificScreen with ANA - sensitive but not specific; Dx made with anti-dsDNA Abs - highly specific

114
Q

DRUG-INDUCED SLE - Abs and common causes

A

AntihiSTONED Ab; Causes are HIP - Hydralazine, Isoniazid, Procainamide

115
Q

SJOGREN SYNDROME Pathophys and Hypersensitivity Rxn

A

Autoimmune destruction of LACRIMAL and SALIVARY glands; lymphocyte-mediated damage - Type IV

116
Q

Clinical Features of SJOGREN SYNDROME

A

“Can’t chew a cracker with this damn dirt in my eyes” - DRY EYES (keratoconjunctivitis), DRY MOUTH (xerostomia) and recurrent DENTAL CARRIES in older woman (50-60yo)

117
Q

Abs found in SJOGREN SYNDROME

A

ANA (screening) and ANTI-RIBONUCLEOPROTEIN (anti-SS-A/Ro and anti-SS-B/La)

118
Q

Higher risk COMPLICATION of SJOGREN SYNDROME and its presentation:

A

B-cell (marginal zone) lymphoma presenting as UNILATERAL enlargement of PAROTID GLAND late in disease course

119
Q

Abs in SCLERODERMA

A

ANA and ANTI-DNA TOPOISOMERASE I (Scl-70)

120
Q

CREST SYNDROME and its Abs

A

Calcinosis, Raynaud phenomenon, Esophageal dysmotility, Sclerodactyly, and Telangiectasias of the skin; ANTI-CENTROMERE (CRESTomere)

121
Q

Abs in MIXED CONNECTIVE TISSUE DISEASE

A

Abs against U1 RIBONUCLEOPROTEIN

122
Q

LABILE tissues

A

tissues that possess STEM CELLS that continuously cylce to regenerate tissue

123
Q

Examples of LABILE tissues and LOCATION OF STEM CELLS

A

Small and large bowel - SCs in MUCOSAL CRYPTS; Skin - SCs in BASAL LAYER; Bone marrow - hematopoietic SCs

124
Q

MARKER of HEMATOPOIETIC STEM CELLS

A

CD34

125
Q

STEM CELL of the LUNG

A

Type II Pneumocytes

126
Q

STABLE tissues

A

Comprised of cells that are QUIESCENT (G0) but can reenter the cell cycle to REGENERATE TISSUE WHEN NECESSARY

127
Q

Examples of STABLE TISSUES

A

Regeneration of LIVER by compensatory hyperplasia after partial resection; PROXIMAL RENAL TUBULE shows regeneration during acute tubular necrosis

128
Q

PERMANENT tissues

A

LACK significant regenerative potential so they undergo repair (fibrous scar)

129
Q

Examples of PERMANENT TISSUES

A

Myocardium, skeletal muscle and neurons

130
Q

Initial phase of Repair in wound healing

A

Granulation Tissue

131
Q

Granulation Tissue in Wound Healing consists of:

A

FIBROBLASTS (TYPE III COLLAGEN), capillaries, and myofibroblasts (CONTRACT wound)

132
Q

COLLAGEN CHANGE in SCAR formation

A

Type III is REPLACED BY TYPE I COLLAGEN

133
Q

COLLAGENASE in Scar formation

A

REMOVES TYPE III COLLAGEN and REQUIRES Zn as a cofactor

134
Q

COLLAGENASE requires which COFACTOR

A

ZINC

135
Q

TYPE I Collagen CHARACTERISTICS and LOCATION

A

High tensile strength - present in skin bONE, tendons and most organs

136
Q

Type II Collagen LOCATION

A

carTWOlage

137
Q

TYPE III Collagen CHARACTERISTICS and LOCATION

A

Pliable - found in BVs, granulation tissue and embryonic tissue

138
Q

TYPE IV Collagen LOCATION

A

Basement Membrane

139
Q

Role of TGF-α in Tissue Regeneration and Repair

A

EPITHELIAL and FIBROBLAST Growth Factor

140
Q

Role of TGF-β in Tissue Regneration and Repair

A

FIBROBLAST GROWTH FACTOR and INHIBITS INFLAMMATION

141
Q

Role of PLATELET-DERIVED GROWTH FACTOR in Tissue Regeneration and Repair

A

GF for endothelium, smooth muslce and fibroblasts

142
Q

Role of FIBROBLAST GROWTH FACTOR in Tissue Regeneration and Repair

A

ANGIOGENESIS and MEDIATES SKELETAL DEVELOPMENT

143
Q

Role of VASCULAR ENDOTHELIAL GROWTH FACTOR (VEGF) in Tissue Regeneration and Repair

A

ANGIOGENESIS

144
Q

GROWTH FACTORS important in ANGIOGENESIS in Tissue Regeneration and Repair

A

VEGF and FGF

145
Q

Role of MYOFIBROBLASTS in Secondary intention wound healing

A

Edges are not approximated and granulation tissue fills the defect - MYOFIBROBLASTS THEN CONTRACT THE WOUND forming a scar

146
Q

Conditions leading to DELAYED WOUND HEALING

A

INFECTION (MC is S. aureus), VITAMIN C DEFICIENCY, COPPER DEFICIENCY, OR ZINC DEFICIENCY

147
Q

VITAMIN C DEFICIENCY in Wound healing

A

Vit C is impt cofactor in HYDROXYLATION OF PROLINE AND LYSINE PROCOLLAGEN RESIDUES which is necessary for eventual cross-linking

148
Q

COPPER DEFICIENCY in Wound healing

A

COPPER is a cofactor for LYSYL OXIDASE which CROSS-LINKS LYSINE and HYDROXYLYSINE TO FORM STABLE COLLAGEN

149
Q

Type of Collagen in HYPERTROPHIC SCAR

A

TYPE I

150
Q

KELOID - Pathophys, genetics and location

A

Excess production of scar tissue (TYPE III COLLAGEN) that is out of proportion to the wound; AFRICAN AMERICANS more common; affects EARLOBES, FACE and UPPER EXTREMITIES

Pathoma (3 decks)

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