SlideShare uma empresa Scribd logo
1 de 53
CHAPTER 2
   Inflammation
        (5 OBJECTIVES)
1) (Concept) Understand the chain,
 progression, or sequence of
 vascular and cellular events in
 the histologic evolution of acute
 inflammation
2) (Rote?) Learn the roles of various
“chemical mediators” of acute
inflammation
3) Know the three possible outcomes of
acute inflammation
4) Visualize the morphologic patterns of
acute inflammation
5) Understand the causes, morphologic
patterns, principle cells, minor cells, of
chronic and granulomatous
inflammation
SEQUENCE OF EVENTS
• NORMAL HISTOLOGY 
• VASODILATATION 
• INCREASED VASCULAR PERMEABILITY 
• LEAKAGE OF EXUDATE 
• MARGINATION, ROLLING, ADHESION 
• TRANSMIGRATION (DIAPEDESIS) 
• CHEMOTAXIS 
• PMN ACTIVATION 
• PHAGOCYTOSIS: Recognition, Attachment,
  Engulfment, Killing (degradation or digestion) 
• TERMINATION 
• 100% RESOLUTION, SCAR, or CHRONIC
  INFLAMMATION are the three possible outcomes
ACUTE INFLAMMATION
• “PROTECTIVE”
  RESPONSE
•NON-specific
ACUTE INFLAMMATION
• VASCULAR EVENTS
• CELLULAR EVENTS (PMN or
 PolyMorphonuclear Neutrophil,
 Leukocyte?, “POLY”, Neutrophil,
 Granulocyte, Neutrophilic
 Granulocyte
• “MEDIATORS”
ACUTE
INFLAMMATION
     Neutrophil
     Polymorphonuclear
     Leukocyte, PMN, PML
     “Leukocyte”
     Granulocyte, Neutrophilic
     granulocyte
     “Poly-”
     Polymorph
HISTORICAL
 HIGHLIGHTS
   (Egypt, 3000 BC)

Rubor
Calor
Tumor
Dolor
5th (functio laesa)
STIMULI
    for acute inflammation
• INFECTIOUS
• PHYSICAL
• CHEMICAL
• Tissue Necrosis
• Foreign Bodies (FBs)
• Immune “responses”, or “complexes”
Vascular Changes
• Changes in Vascular Flow
  and Caliber

• Increased Vascular
  Permeability
INCREASED PERMEABILITY
• DILATATION
• Endothelial “gaps”
• Direct Injury
• Leukocyte Injury
• Transocytosis (endo/exo)
• New Vessels
LEAKAGE OF
PROTEINACEOUS FLUID
(   EXUDATE, NOT
     TRANSUDATE)
EXTRAVASATION of
         PMNs
• MARGINATION
  (PMN’s go toward
  wall)
• ROLLING (tumbling
  and HEAPING)
• ADHESION
• TRANSMIGRATION
  (DIAPEDESIS)
ADHESION MOLECULES
    (glycoproteins) affecting
ADHESION and TRANSMIGRATION
• SECRETINS (from
  endothelial cells)
• INTEGRINS (from many
  cells)
CHEMOTAXIS
PMNs going to the site of “injury”
AFTER transmigration
LEUKOCYTE
       “ACTIVATION”
• “triggered” by the offending stimuli for PMNs to:
   – 1) Produce eicosanoids (arachidonic acid
     derivatives)
     • Prostaglandin (and thromboxanes)
     • Leukotrienes
     • Lipoxins
  – 2) Undergo DEGRANULATION
  – 3) Secrete CYTOKINES
PHAGOCYTOSIS
• RECOGNITION

• ENGULFMENT

• KILLING
  (DEGRADATION/
  DIGESTION)
CHEMICAL MEDIATORS
• From plasma or cells
• Have “triggering” stimuli
• Usually have specific
  targets
• Can cause a “cascade”
• Are short lived
CLASSIC MEDIATORS
                 • PLATELET
• HISTAMINE        ACTIVATING
• SEROTONIN        FACTOR (PAF)
• COMPLEMENT     • CYTOKINES
• KININS         • /CHEMOKINES
• CLOTTING       • LYSOSOME
  FACTORS          CONSTITUENTS
• EICOSANOIDS    • FREE RADICALS
• NITRIC OXIDE   • NEUROPEPTIDES
HISTAMINE
• Mast Cells,
  basophils
• POWERFUL
  Vasodilator
• Vasoactive
  “amine”
• IgE on mast
  cell
SEROTONIN
• (5HT,   5-Hydroxy-
  Tryptamine)
• Platelets and
  EnteroChromaffin Cells
• Also vasodilatation, but
  more indirect
• Evokes N.O. synthetase
  (a ligase) from argenine
COMPLEMENT SYSTEM
• >20
  components,
  in circulating
  plasma
• Multiple sites
  of action, but
  LYSIS is the
  underlying
  theme
KININ SYSTEM
• BRADYKININ is KEY component, 9 aa’s
• ALSO from circulating plasma
• ACTIONS
  – Increased permeability
  – Smooth muscle contraction, NON vascular
  – PAIN
CLOTTING
      FACTORS
• Also from circulating plasma
• Coagulation, i.e., production of
  fibrin
• Fibrinolysis
EICOSANOIDS
(ARACHIDONIC ACID DERIVATIVES)
 • Part of cell membranes
 • 1) Prostaglandins (incl.
   Thromboxanes)
 • 2) Leukotrienes
 • 3) Lipoxins (new)
  MULTIPLE ACTIONS AT MANY LEVELS
Prostaglandins
(thromboxanes included)

• Pain
• Fever
• Clotting
Leukotrienes
• Chemotaxis
• Vasoconstriction
• Increased Permeability
Lipoxins
• INHIBIT chemotaxis
• Vasodilatation
• Counteract actions of
  leukotrienes
Platelet-Activating Factor
           (PAF)
• Phospholipid
• From MANY cells,
  like eicosanoids
• ACTIVATE
  PLATELETS,
  powerfully
CYTOKINES/CHEMOKINES
• CYTOKINES are PROTEINS produced by
  MANY cells, but usually LYMPHOCYTES
  and MACROPHAGES, numerous roles in
  acute and chronic inflammation

  –TNFα, IL-1, by
   macrophages
• CHEMOKINES are small proteins which are
  attractants for PMNs (>40)
NITRIC OXIDE
• Potent vasodilator
• Produced from the action
  of nitric oxide synthetase
  from arginine
LYSOSOMAL CONSTITUENTS
• PRIMARY            • SECONDARY
• Also called        • Also called SPECIFIC
  AZUROPHILIC, or
  NON-specific       •   Lactoferrin
                     •   Lysozyme
• Myeloperoxidase    •   Alkaline Phosphatase
• Lysozyme (Bact.)   •   Collagenase
• Acid Hydrolases
FREE RADICALS
• O2 – (SUPEROXIDE)
• H2O2 (PEROXIDE)
• OH- (HYDROXYL RADICAL)

• VERY VERY DESTRUCTIVE
NEUROPEPTIDES
• Produced in CNS (neurons)
• SUBSTANCE P
• NEUROKININ A
OUTCOMES OF
  ACUTE INFLAMMATION
• 1) 100% complete
  RESOLUTION

• 2) SCAR

• 3)CHRONIC inflammation
Morphologic PATTERNS
   of Acute INFLAMMATION
          (EXUDATE)
• Serous (watery)
• Fibrinous (hemorrhagic,
 rich in FIBRIN)
• Suppurative (PUS)
• Ulcerative
BLISTER, “Watery”, i.e., SEROUS
FIBRINOUS
PUS
    =
PURULENT


 ABSCESS
    =
 POCKET
    OF
   PUS
    =
NEUTROPHILS
PURULENT, FIBRINOPURULENT
ULCERATIVE
SEQUENCE OF EVENTS
• NORMAL HISTOLOGY 
• VASODILATATION 
• INCREASED VASCULAR PERMEABILITY 
• LEAKAGE OF EXUDATE 
• MARGINATION, ROLLING, ADHESION 
• TRANSMIGRATION (DIAPEDESIS) 
• CHEMOTAXIS 
• PMN ACTIVATION 
• PHAGOCYTOSIS: Recognition, Attachment,
  Engulfment, Killing (degradation or digestion) 
• TERMINATION 
• 100% RESOLUTION, SCAR, or CHRONIC
  inflammation
CHRONIC INFLAMMATION
     (MONOS)



             “MONO”CYTE

LYMPHOCYTE   MACROPHAGE
CAUSES of
CHRONIC INFLAMMATION
 • 1) PERSISTENCE of
   Infection
 • 2) PROLONGED
   EXPOSURE to insult
 • 3) AUTO-IMMUNITY
Cellular Players
• LYMPHOCYTES
• MACROPHAGES
  (aka, HISTIOCYTES)
• PLASMA CELLS
• EOSINOPHILS
• MAST CELLS
MORPHOLOGY
• INFILTRATION
• TISSUE DESTRUCTION
• HEALING
GRANULOMAS
GRANULOMATOUS INFLAMMATION
                     4 COMPONENTS


                     FIBROBLASTS


                       LYMPHS



                     HISTIOS

                     “GIANT” CELLS
GRANULOMAS
GRANULOMATOUS INFLAMMATION


  CASEATING (TB)
 NON-CASEATING
LYMPHATIC
     DRAINAGE
• SITE REGIONAL LYMPH NODES
SYSTEMIC MANIFESTATIONS
       (NON-SPECIFIC)
• FEVER, CHILLS
• C-Reactive Protein (CRP)
• “Acute Phase” Reactants, i.e., α1-α2
• Erythrocyte Sedimentation Rate (ESR)
  increases
• Leukocytosis
• Pulse, Blood Pressure
• Cytokine Effects, e.g., TNF(α), IL-1
NORMAL SPE


Serum
Protein
Electrophoresis




In ACUTE
Inflammation
Alpha-1 & alpha-2
are increased, i.e.,
“acute phase”
reactants.

Mais conteúdo relacionado

Mais procurados (20)

Acute inflammation
Acute inflammationAcute inflammation
Acute inflammation
 
Inflammation....
Inflammation....Inflammation....
Inflammation....
 
Serous Inflammation
Serous InflammationSerous Inflammation
Serous Inflammation
 
Inflammation, role and types.
Inflammation, role and types.Inflammation, role and types.
Inflammation, role and types.
 
Inflammation acute and chronic
Inflammation acute and chronicInflammation acute and chronic
Inflammation acute and chronic
 
Inflammation
InflammationInflammation
Inflammation
 
Inflammation and Healing
Inflammation and HealingInflammation and Healing
Inflammation and Healing
 
Inflammation- General Pathology seminar PG 1st year
Inflammation- General Pathology seminar PG 1st yearInflammation- General Pathology seminar PG 1st year
Inflammation- General Pathology seminar PG 1st year
 
Chronic inflammation
Chronic inflammationChronic inflammation
Chronic inflammation
 
chronic inflammation
chronic inflammationchronic inflammation
chronic inflammation
 
Inflammation
InflammationInflammation
Inflammation
 
Inflammation
InflammationInflammation
Inflammation
 
Chronic inflammation
Chronic inflammationChronic inflammation
Chronic inflammation
 
Chronic inflammation
Chronic inflammationChronic inflammation
Chronic inflammation
 
Acute inflammation handouts 30 9-2016
Acute inflammation handouts 30 9-2016Acute inflammation handouts 30 9-2016
Acute inflammation handouts 30 9-2016
 
Chronic inflammation
Chronic inflammationChronic inflammation
Chronic inflammation
 
Inflammation
InflammationInflammation
Inflammation
 
Inflammation
Inflammation Inflammation
Inflammation
 
Acute And Chronic Inflammation
Acute And Chronic InflammationAcute And Chronic Inflammation
Acute And Chronic Inflammation
 
inflammation
 inflammation inflammation
inflammation
 

Semelhante a Chronic inflamation

Ch2-Inflam (1).ppt
Ch2-Inflam (1).pptCh2-Inflam (1).ppt
Ch2-Inflam (1).pptLearta Asani
 
Minarcik robbins 2013_ch2-inflam
Minarcik robbins 2013_ch2-inflamMinarcik robbins 2013_ch2-inflam
Minarcik robbins 2013_ch2-inflamElsa von Licy
 
Pathology cptr2 ( acute & chronic inflammation)
Pathology    cptr2 ( acute & chronic inflammation)Pathology    cptr2 ( acute & chronic inflammation)
Pathology cptr2 ( acute & chronic inflammation)MBBS IMS MSU
 
Inflammation & Repair ( Endodontics point of view)
Inflammation & Repair ( Endodontics point of view)Inflammation & Repair ( Endodontics point of view)
Inflammation & Repair ( Endodontics point of view)MettinaAngela
 
Inflammation dr. ihsan alsaimary
Inflammation dr. ihsan alsaimaryInflammation dr. ihsan alsaimary
Inflammation dr. ihsan alsaimarydr.Ihsan alsaimary
 
Inflammation & healing & dental Implications
Inflammation & healing & dental ImplicationsInflammation & healing & dental Implications
Inflammation & healing & dental ImplicationsRupali623
 
basic chemical mediator
basic chemical mediatorbasic chemical mediator
basic chemical mediatorKd Sudarsan
 
ACUTE INFLAMMATION.pptx
ACUTE    INFLAMMATION.pptxACUTE    INFLAMMATION.pptx
ACUTE INFLAMMATION.pptxdraaankurgupta
 
Acute and chronic inflammation
Acute and chronic inflammation Acute and chronic inflammation
Acute and chronic inflammation AsgharullahKhan
 
Apoptosis - programmed cell death that occurs in multicellular organisms
Apoptosis - programmed cell death that occurs in multicellular organismsApoptosis - programmed cell death that occurs in multicellular organisms
Apoptosis - programmed cell death that occurs in multicellular organismsMeethuRappai1
 

Semelhante a Chronic inflamation (20)

Ch2-Inflam.ppt
Ch2-Inflam.pptCh2-Inflam.ppt
Ch2-Inflam.ppt
 
Ch2-Inflam (1).ppt
Ch2-Inflam (1).pptCh2-Inflam (1).ppt
Ch2-Inflam (1).ppt
 
Minarcik robbins 2013_ch2-inflam
Minarcik robbins 2013_ch2-inflamMinarcik robbins 2013_ch2-inflam
Minarcik robbins 2013_ch2-inflam
 
2 inflam
2 inflam2 inflam
2 inflam
 
2 inflam
2 inflam2 inflam
2 inflam
 
Inflammation General Pathology
Inflammation General PathologyInflammation General Pathology
Inflammation General Pathology
 
Pathology cptr2 ( acute & chronic inflammation)
Pathology    cptr2 ( acute & chronic inflammation)Pathology    cptr2 ( acute & chronic inflammation)
Pathology cptr2 ( acute & chronic inflammation)
 
Inflammation1.pptx
Inflammation1.pptxInflammation1.pptx
Inflammation1.pptx
 
Inflammation
InflammationInflammation
Inflammation
 
Inflammation & Repair ( Endodontics point of view)
Inflammation & Repair ( Endodontics point of view)Inflammation & Repair ( Endodontics point of view)
Inflammation & Repair ( Endodontics point of view)
 
Inflammation dr. ihsan alsaimary
Inflammation dr. ihsan alsaimaryInflammation dr. ihsan alsaimary
Inflammation dr. ihsan alsaimary
 
Inflammation & healing & dental Implications
Inflammation & healing & dental ImplicationsInflammation & healing & dental Implications
Inflammation & healing & dental Implications
 
Acute Inflammation
Acute InflammationAcute Inflammation
Acute Inflammation
 
basic chemical mediator
basic chemical mediatorbasic chemical mediator
basic chemical mediator
 
ACUTE INFLAMMATION.pptx
ACUTE    INFLAMMATION.pptxACUTE    INFLAMMATION.pptx
ACUTE INFLAMMATION.pptx
 
Priya blood
Priya bloodPriya blood
Priya blood
 
6.immune
6.immune6.immune
6.immune
 
Acute and chronic inflammation
Acute and chronic inflammation Acute and chronic inflammation
Acute and chronic inflammation
 
Acute inflammation 1& 2
Acute inflammation 1& 2Acute inflammation 1& 2
Acute inflammation 1& 2
 
Apoptosis - programmed cell death that occurs in multicellular organisms
Apoptosis - programmed cell death that occurs in multicellular organismsApoptosis - programmed cell death that occurs in multicellular organisms
Apoptosis - programmed cell death that occurs in multicellular organisms
 

Mais de Forensic Pathology (20)

Stat3 central tendency & dispersion
Stat3 central tendency & dispersionStat3 central tendency & dispersion
Stat3 central tendency & dispersion
 
Exercise 1 12 no solution
Exercise 1 12 no solutionExercise 1 12 no solution
Exercise 1 12 no solution
 
Writing a research protocol 2011
Writing a research protocol 2011Writing a research protocol 2011
Writing a research protocol 2011
 
Some statistical defenition
Some statistical defenitionSome statistical defenition
Some statistical defenition
 
Prac excises 3[1].5
Prac excises 3[1].5Prac excises 3[1].5
Prac excises 3[1].5
 
Exercise 1 12 no solution
Exercise 1 12 no solutionExercise 1 12 no solution
Exercise 1 12 no solution
 
Analysis of variance
Analysis of varianceAnalysis of variance
Analysis of variance
 
Stat6 chi square test
Stat6 chi square testStat6 chi square test
Stat6 chi square test
 
Stat5 the t test
Stat5 the t testStat5 the t test
Stat5 the t test
 
Stat3 central tendency & dispersion
Stat3 central tendency & dispersionStat3 central tendency & dispersion
Stat3 central tendency & dispersion
 
Stat 4 the normal distribution & steps of testing hypothesis
Stat 4 the normal distribution & steps of testing hypothesisStat 4 the normal distribution & steps of testing hypothesis
Stat 4 the normal distribution & steps of testing hypothesis
 
Stat 2 data presentation2
Stat 2 data presentation2Stat 2 data presentation2
Stat 2 data presentation2
 
Correlation 3rd
Correlation 3rdCorrelation 3rd
Correlation 3rd
 
Stat 1 variables & sampling
Stat 1 variables & samplingStat 1 variables & sampling
Stat 1 variables & sampling
 
Pancreas 2
Pancreas 2Pancreas 2
Pancreas 2
 
Pancreas 1
Pancreas 1Pancreas 1
Pancreas 1
 
Liver 3
Liver 3Liver 3
Liver 3
 
Liver 2
Liver 2Liver 2
Liver 2
 
Liver 1
Liver 1Liver 1
Liver 1
 
The biliary tract
The biliary tractThe biliary tract
The biliary tract
 

Último

Jual Obat Aborsi Di Dubai UAE Wa 0838-4800-7379 Obat Penggugur Kandungan Cytotec
Jual Obat Aborsi Di Dubai UAE Wa 0838-4800-7379 Obat Penggugur Kandungan CytotecJual Obat Aborsi Di Dubai UAE Wa 0838-4800-7379 Obat Penggugur Kandungan Cytotec
Jual Obat Aborsi Di Dubai UAE Wa 0838-4800-7379 Obat Penggugur Kandungan Cytotecjualobat34
 
Gorgeous Call Girls Dehradun {8854095900} ❤️VVIP ROCKY Call Girls in Dehradun...
Gorgeous Call Girls Dehradun {8854095900} ❤️VVIP ROCKY Call Girls in Dehradun...Gorgeous Call Girls Dehradun {8854095900} ❤️VVIP ROCKY Call Girls in Dehradun...
Gorgeous Call Girls Dehradun {8854095900} ❤️VVIP ROCKY Call Girls in Dehradun...Sheetaleventcompany
 
Nagpur Call Girl Service 📞9xx000xx09📞Just Call Divya📲 Call Girl In Nagpur No💰...
Nagpur Call Girl Service 📞9xx000xx09📞Just Call Divya📲 Call Girl In Nagpur No💰...Nagpur Call Girl Service 📞9xx000xx09📞Just Call Divya📲 Call Girl In Nagpur No💰...
Nagpur Call Girl Service 📞9xx000xx09📞Just Call Divya📲 Call Girl In Nagpur No💰...Sheetaleventcompany
 
💚Call Girls In Amritsar 💯Anvi 📲🔝8725944379🔝Amritsar Call Girl No💰Advance Cash...
💚Call Girls In Amritsar 💯Anvi 📲🔝8725944379🔝Amritsar Call Girl No💰Advance Cash...💚Call Girls In Amritsar 💯Anvi 📲🔝8725944379🔝Amritsar Call Girl No💰Advance Cash...
💚Call Girls In Amritsar 💯Anvi 📲🔝8725944379🔝Amritsar Call Girl No💰Advance Cash...Sheetaleventcompany
 
Call Girls Mussoorie Just Call 8854095900 Top Class Call Girl Service Available
Call Girls Mussoorie Just Call 8854095900 Top Class Call Girl Service AvailableCall Girls Mussoorie Just Call 8854095900 Top Class Call Girl Service Available
Call Girls Mussoorie Just Call 8854095900 Top Class Call Girl Service AvailableJanvi Singh
 
👉Chandigarh Call Girl Service📲Niamh 8868886958 📲Book 24hours Now📲👉Sexy Call G...
👉Chandigarh Call Girl Service📲Niamh 8868886958 📲Book 24hours Now📲👉Sexy Call G...👉Chandigarh Call Girl Service📲Niamh 8868886958 📲Book 24hours Now📲👉Sexy Call G...
👉Chandigarh Call Girl Service📲Niamh 8868886958 📲Book 24hours Now📲👉Sexy Call G...Sheetaleventcompany
 
💚Chandigarh Call Girls Service 💯Piya 📲🔝8868886958🔝Call Girls In Chandigarh No...
💚Chandigarh Call Girls Service 💯Piya 📲🔝8868886958🔝Call Girls In Chandigarh No...💚Chandigarh Call Girls Service 💯Piya 📲🔝8868886958🔝Call Girls In Chandigarh No...
💚Chandigarh Call Girls Service 💯Piya 📲🔝8868886958🔝Call Girls In Chandigarh No...Sheetaleventcompany
 
VIP Hyderabad Call Girls KPHB 7877925207 ₹5000 To 25K With AC Room 💚😋
VIP Hyderabad Call Girls KPHB 7877925207 ₹5000 To 25K With AC Room 💚😋VIP Hyderabad Call Girls KPHB 7877925207 ₹5000 To 25K With AC Room 💚😋
VIP Hyderabad Call Girls KPHB 7877925207 ₹5000 To 25K With AC Room 💚😋mahima pandey
 
7 steps How to prevent Thalassemia : Dr Sharda Jain & Vandana Gupta
7 steps How to prevent Thalassemia : Dr Sharda Jain & Vandana Gupta7 steps How to prevent Thalassemia : Dr Sharda Jain & Vandana Gupta
7 steps How to prevent Thalassemia : Dr Sharda Jain & Vandana GuptaLifecare Centre
 
Cara Menggugurkan Kandungan Dengan Cepat Selesai Dalam 24 Jam Secara Alami Bu...
Cara Menggugurkan Kandungan Dengan Cepat Selesai Dalam 24 Jam Secara Alami Bu...Cara Menggugurkan Kandungan Dengan Cepat Selesai Dalam 24 Jam Secara Alami Bu...
Cara Menggugurkan Kandungan Dengan Cepat Selesai Dalam 24 Jam Secara Alami Bu...Cara Menggugurkan Kandungan 087776558899
 
❤️Amritsar Escorts Service☎️9815674956☎️ Call Girl service in Amritsar☎️ Amri...
❤️Amritsar Escorts Service☎️9815674956☎️ Call Girl service in Amritsar☎️ Amri...❤️Amritsar Escorts Service☎️9815674956☎️ Call Girl service in Amritsar☎️ Amri...
❤️Amritsar Escorts Service☎️9815674956☎️ Call Girl service in Amritsar☎️ Amri...Sheetaleventcompany
 
Most Beautiful Call Girl in Chennai 7427069034 Contact on WhatsApp
Most Beautiful Call Girl in Chennai 7427069034 Contact on WhatsAppMost Beautiful Call Girl in Chennai 7427069034 Contact on WhatsApp
Most Beautiful Call Girl in Chennai 7427069034 Contact on WhatsAppjimmihoslasi
 
Control of Local Blood Flow: acute and chronic
Control of Local Blood Flow: acute and chronicControl of Local Blood Flow: acute and chronic
Control of Local Blood Flow: acute and chronicMedicoseAcademics
 
Intramuscular & Intravenous Injection.pptx
Intramuscular & Intravenous Injection.pptxIntramuscular & Intravenous Injection.pptx
Intramuscular & Intravenous Injection.pptxsaranpratha12
 
💰Call Girl In Bangalore☎️63788-78445💰 Call Girl service in Bangalore☎️Bangalo...
💰Call Girl In Bangalore☎️63788-78445💰 Call Girl service in Bangalore☎️Bangalo...💰Call Girl In Bangalore☎️63788-78445💰 Call Girl service in Bangalore☎️Bangalo...
💰Call Girl In Bangalore☎️63788-78445💰 Call Girl service in Bangalore☎️Bangalo...gragneelam30
 
Call Girl In Indore 📞9235973566📞 Just📲 Call Inaaya Indore Call Girls Service ...
Call Girl In Indore 📞9235973566📞 Just📲 Call Inaaya Indore Call Girls Service ...Call Girl In Indore 📞9235973566📞 Just📲 Call Inaaya Indore Call Girls Service ...
Call Girl In Indore 📞9235973566📞 Just📲 Call Inaaya Indore Call Girls Service ...Sheetaleventcompany
 
❤️Chandigarh Escorts Service☎️9814379184☎️ Call Girl service in Chandigarh☎️ ...
❤️Chandigarh Escorts Service☎️9814379184☎️ Call Girl service in Chandigarh☎️ ...❤️Chandigarh Escorts Service☎️9814379184☎️ Call Girl service in Chandigarh☎️ ...
❤️Chandigarh Escorts Service☎️9814379184☎️ Call Girl service in Chandigarh☎️ ...Sheetaleventcompany
 
Dehradun Call Girls Service {8854095900} ❤️VVIP ROCKY Call Girl in Dehradun U...
Dehradun Call Girls Service {8854095900} ❤️VVIP ROCKY Call Girl in Dehradun U...Dehradun Call Girls Service {8854095900} ❤️VVIP ROCKY Call Girl in Dehradun U...
Dehradun Call Girls Service {8854095900} ❤️VVIP ROCKY Call Girl in Dehradun U...Sheetaleventcompany
 
Dehradun Call Girl Service ❤️🍑 8854095900 👄🫦Independent Escort Service Dehradun
Dehradun Call Girl Service ❤️🍑 8854095900 👄🫦Independent Escort Service DehradunDehradun Call Girl Service ❤️🍑 8854095900 👄🫦Independent Escort Service Dehradun
Dehradun Call Girl Service ❤️🍑 8854095900 👄🫦Independent Escort Service DehradunSheetaleventcompany
 
tongue disease lecture Dr Assadawy legacy
tongue disease lecture Dr Assadawy legacytongue disease lecture Dr Assadawy legacy
tongue disease lecture Dr Assadawy legacyDrMohamed Assadawy
 

Último (20)

Jual Obat Aborsi Di Dubai UAE Wa 0838-4800-7379 Obat Penggugur Kandungan Cytotec
Jual Obat Aborsi Di Dubai UAE Wa 0838-4800-7379 Obat Penggugur Kandungan CytotecJual Obat Aborsi Di Dubai UAE Wa 0838-4800-7379 Obat Penggugur Kandungan Cytotec
Jual Obat Aborsi Di Dubai UAE Wa 0838-4800-7379 Obat Penggugur Kandungan Cytotec
 
Gorgeous Call Girls Dehradun {8854095900} ❤️VVIP ROCKY Call Girls in Dehradun...
Gorgeous Call Girls Dehradun {8854095900} ❤️VVIP ROCKY Call Girls in Dehradun...Gorgeous Call Girls Dehradun {8854095900} ❤️VVIP ROCKY Call Girls in Dehradun...
Gorgeous Call Girls Dehradun {8854095900} ❤️VVIP ROCKY Call Girls in Dehradun...
 
Nagpur Call Girl Service 📞9xx000xx09📞Just Call Divya📲 Call Girl In Nagpur No💰...
Nagpur Call Girl Service 📞9xx000xx09📞Just Call Divya📲 Call Girl In Nagpur No💰...Nagpur Call Girl Service 📞9xx000xx09📞Just Call Divya📲 Call Girl In Nagpur No💰...
Nagpur Call Girl Service 📞9xx000xx09📞Just Call Divya📲 Call Girl In Nagpur No💰...
 
💚Call Girls In Amritsar 💯Anvi 📲🔝8725944379🔝Amritsar Call Girl No💰Advance Cash...
💚Call Girls In Amritsar 💯Anvi 📲🔝8725944379🔝Amritsar Call Girl No💰Advance Cash...💚Call Girls In Amritsar 💯Anvi 📲🔝8725944379🔝Amritsar Call Girl No💰Advance Cash...
💚Call Girls In Amritsar 💯Anvi 📲🔝8725944379🔝Amritsar Call Girl No💰Advance Cash...
 
Call Girls Mussoorie Just Call 8854095900 Top Class Call Girl Service Available
Call Girls Mussoorie Just Call 8854095900 Top Class Call Girl Service AvailableCall Girls Mussoorie Just Call 8854095900 Top Class Call Girl Service Available
Call Girls Mussoorie Just Call 8854095900 Top Class Call Girl Service Available
 
👉Chandigarh Call Girl Service📲Niamh 8868886958 📲Book 24hours Now📲👉Sexy Call G...
👉Chandigarh Call Girl Service📲Niamh 8868886958 📲Book 24hours Now📲👉Sexy Call G...👉Chandigarh Call Girl Service📲Niamh 8868886958 📲Book 24hours Now📲👉Sexy Call G...
👉Chandigarh Call Girl Service📲Niamh 8868886958 📲Book 24hours Now📲👉Sexy Call G...
 
💚Chandigarh Call Girls Service 💯Piya 📲🔝8868886958🔝Call Girls In Chandigarh No...
💚Chandigarh Call Girls Service 💯Piya 📲🔝8868886958🔝Call Girls In Chandigarh No...💚Chandigarh Call Girls Service 💯Piya 📲🔝8868886958🔝Call Girls In Chandigarh No...
💚Chandigarh Call Girls Service 💯Piya 📲🔝8868886958🔝Call Girls In Chandigarh No...
 
VIP Hyderabad Call Girls KPHB 7877925207 ₹5000 To 25K With AC Room 💚😋
VIP Hyderabad Call Girls KPHB 7877925207 ₹5000 To 25K With AC Room 💚😋VIP Hyderabad Call Girls KPHB 7877925207 ₹5000 To 25K With AC Room 💚😋
VIP Hyderabad Call Girls KPHB 7877925207 ₹5000 To 25K With AC Room 💚😋
 
7 steps How to prevent Thalassemia : Dr Sharda Jain & Vandana Gupta
7 steps How to prevent Thalassemia : Dr Sharda Jain & Vandana Gupta7 steps How to prevent Thalassemia : Dr Sharda Jain & Vandana Gupta
7 steps How to prevent Thalassemia : Dr Sharda Jain & Vandana Gupta
 
Cara Menggugurkan Kandungan Dengan Cepat Selesai Dalam 24 Jam Secara Alami Bu...
Cara Menggugurkan Kandungan Dengan Cepat Selesai Dalam 24 Jam Secara Alami Bu...Cara Menggugurkan Kandungan Dengan Cepat Selesai Dalam 24 Jam Secara Alami Bu...
Cara Menggugurkan Kandungan Dengan Cepat Selesai Dalam 24 Jam Secara Alami Bu...
 
❤️Amritsar Escorts Service☎️9815674956☎️ Call Girl service in Amritsar☎️ Amri...
❤️Amritsar Escorts Service☎️9815674956☎️ Call Girl service in Amritsar☎️ Amri...❤️Amritsar Escorts Service☎️9815674956☎️ Call Girl service in Amritsar☎️ Amri...
❤️Amritsar Escorts Service☎️9815674956☎️ Call Girl service in Amritsar☎️ Amri...
 
Most Beautiful Call Girl in Chennai 7427069034 Contact on WhatsApp
Most Beautiful Call Girl in Chennai 7427069034 Contact on WhatsAppMost Beautiful Call Girl in Chennai 7427069034 Contact on WhatsApp
Most Beautiful Call Girl in Chennai 7427069034 Contact on WhatsApp
 
Control of Local Blood Flow: acute and chronic
Control of Local Blood Flow: acute and chronicControl of Local Blood Flow: acute and chronic
Control of Local Blood Flow: acute and chronic
 
Intramuscular & Intravenous Injection.pptx
Intramuscular & Intravenous Injection.pptxIntramuscular & Intravenous Injection.pptx
Intramuscular & Intravenous Injection.pptx
 
💰Call Girl In Bangalore☎️63788-78445💰 Call Girl service in Bangalore☎️Bangalo...
💰Call Girl In Bangalore☎️63788-78445💰 Call Girl service in Bangalore☎️Bangalo...💰Call Girl In Bangalore☎️63788-78445💰 Call Girl service in Bangalore☎️Bangalo...
💰Call Girl In Bangalore☎️63788-78445💰 Call Girl service in Bangalore☎️Bangalo...
 
Call Girl In Indore 📞9235973566📞 Just📲 Call Inaaya Indore Call Girls Service ...
Call Girl In Indore 📞9235973566📞 Just📲 Call Inaaya Indore Call Girls Service ...Call Girl In Indore 📞9235973566📞 Just📲 Call Inaaya Indore Call Girls Service ...
Call Girl In Indore 📞9235973566📞 Just📲 Call Inaaya Indore Call Girls Service ...
 
❤️Chandigarh Escorts Service☎️9814379184☎️ Call Girl service in Chandigarh☎️ ...
❤️Chandigarh Escorts Service☎️9814379184☎️ Call Girl service in Chandigarh☎️ ...❤️Chandigarh Escorts Service☎️9814379184☎️ Call Girl service in Chandigarh☎️ ...
❤️Chandigarh Escorts Service☎️9814379184☎️ Call Girl service in Chandigarh☎️ ...
 
Dehradun Call Girls Service {8854095900} ❤️VVIP ROCKY Call Girl in Dehradun U...
Dehradun Call Girls Service {8854095900} ❤️VVIP ROCKY Call Girl in Dehradun U...Dehradun Call Girls Service {8854095900} ❤️VVIP ROCKY Call Girl in Dehradun U...
Dehradun Call Girls Service {8854095900} ❤️VVIP ROCKY Call Girl in Dehradun U...
 
Dehradun Call Girl Service ❤️🍑 8854095900 👄🫦Independent Escort Service Dehradun
Dehradun Call Girl Service ❤️🍑 8854095900 👄🫦Independent Escort Service DehradunDehradun Call Girl Service ❤️🍑 8854095900 👄🫦Independent Escort Service Dehradun
Dehradun Call Girl Service ❤️🍑 8854095900 👄🫦Independent Escort Service Dehradun
 
tongue disease lecture Dr Assadawy legacy
tongue disease lecture Dr Assadawy legacytongue disease lecture Dr Assadawy legacy
tongue disease lecture Dr Assadawy legacy
 

Chronic inflamation

  • 1.
  • 2. CHAPTER 2 Inflammation (5 OBJECTIVES) 1) (Concept) Understand the chain, progression, or sequence of vascular and cellular events in the histologic evolution of acute inflammation
  • 3. 2) (Rote?) Learn the roles of various “chemical mediators” of acute inflammation 3) Know the three possible outcomes of acute inflammation 4) Visualize the morphologic patterns of acute inflammation 5) Understand the causes, morphologic patterns, principle cells, minor cells, of chronic and granulomatous inflammation
  • 4. SEQUENCE OF EVENTS • NORMAL HISTOLOGY  • VASODILATATION  • INCREASED VASCULAR PERMEABILITY  • LEAKAGE OF EXUDATE  • MARGINATION, ROLLING, ADHESION  • TRANSMIGRATION (DIAPEDESIS)  • CHEMOTAXIS  • PMN ACTIVATION  • PHAGOCYTOSIS: Recognition, Attachment, Engulfment, Killing (degradation or digestion)  • TERMINATION  • 100% RESOLUTION, SCAR, or CHRONIC INFLAMMATION are the three possible outcomes
  • 5. ACUTE INFLAMMATION • “PROTECTIVE” RESPONSE •NON-specific
  • 6. ACUTE INFLAMMATION • VASCULAR EVENTS • CELLULAR EVENTS (PMN or PolyMorphonuclear Neutrophil, Leukocyte?, “POLY”, Neutrophil, Granulocyte, Neutrophilic Granulocyte • “MEDIATORS”
  • 7. ACUTE INFLAMMATION Neutrophil Polymorphonuclear Leukocyte, PMN, PML “Leukocyte” Granulocyte, Neutrophilic granulocyte “Poly-” Polymorph
  • 8. HISTORICAL HIGHLIGHTS (Egypt, 3000 BC) Rubor Calor Tumor Dolor 5th (functio laesa)
  • 9. STIMULI for acute inflammation • INFECTIOUS • PHYSICAL • CHEMICAL • Tissue Necrosis • Foreign Bodies (FBs) • Immune “responses”, or “complexes”
  • 10. Vascular Changes • Changes in Vascular Flow and Caliber • Increased Vascular Permeability
  • 11. INCREASED PERMEABILITY • DILATATION • Endothelial “gaps” • Direct Injury • Leukocyte Injury • Transocytosis (endo/exo) • New Vessels
  • 12. LEAKAGE OF PROTEINACEOUS FLUID ( EXUDATE, NOT TRANSUDATE)
  • 13. EXTRAVASATION of PMNs • MARGINATION (PMN’s go toward wall) • ROLLING (tumbling and HEAPING) • ADHESION • TRANSMIGRATION (DIAPEDESIS)
  • 14. ADHESION MOLECULES (glycoproteins) affecting ADHESION and TRANSMIGRATION • SECRETINS (from endothelial cells) • INTEGRINS (from many cells)
  • 15. CHEMOTAXIS PMNs going to the site of “injury” AFTER transmigration
  • 16. LEUKOCYTE “ACTIVATION” • “triggered” by the offending stimuli for PMNs to: – 1) Produce eicosanoids (arachidonic acid derivatives) • Prostaglandin (and thromboxanes) • Leukotrienes • Lipoxins – 2) Undergo DEGRANULATION – 3) Secrete CYTOKINES
  • 17. PHAGOCYTOSIS • RECOGNITION • ENGULFMENT • KILLING (DEGRADATION/ DIGESTION)
  • 18. CHEMICAL MEDIATORS • From plasma or cells • Have “triggering” stimuli • Usually have specific targets • Can cause a “cascade” • Are short lived
  • 19. CLASSIC MEDIATORS • PLATELET • HISTAMINE ACTIVATING • SEROTONIN FACTOR (PAF) • COMPLEMENT • CYTOKINES • KININS • /CHEMOKINES • CLOTTING • LYSOSOME FACTORS CONSTITUENTS • EICOSANOIDS • FREE RADICALS • NITRIC OXIDE • NEUROPEPTIDES
  • 20. HISTAMINE • Mast Cells, basophils • POWERFUL Vasodilator • Vasoactive “amine” • IgE on mast cell
  • 21. SEROTONIN • (5HT, 5-Hydroxy- Tryptamine) • Platelets and EnteroChromaffin Cells • Also vasodilatation, but more indirect • Evokes N.O. synthetase (a ligase) from argenine
  • 22. COMPLEMENT SYSTEM • >20 components, in circulating plasma • Multiple sites of action, but LYSIS is the underlying theme
  • 23. KININ SYSTEM • BRADYKININ is KEY component, 9 aa’s • ALSO from circulating plasma • ACTIONS – Increased permeability – Smooth muscle contraction, NON vascular – PAIN
  • 24. CLOTTING FACTORS • Also from circulating plasma • Coagulation, i.e., production of fibrin • Fibrinolysis
  • 25.
  • 26. EICOSANOIDS (ARACHIDONIC ACID DERIVATIVES) • Part of cell membranes • 1) Prostaglandins (incl. Thromboxanes) • 2) Leukotrienes • 3) Lipoxins (new) MULTIPLE ACTIONS AT MANY LEVELS
  • 27.
  • 30. Lipoxins • INHIBIT chemotaxis • Vasodilatation • Counteract actions of leukotrienes
  • 31. Platelet-Activating Factor (PAF) • Phospholipid • From MANY cells, like eicosanoids • ACTIVATE PLATELETS, powerfully
  • 32. CYTOKINES/CHEMOKINES • CYTOKINES are PROTEINS produced by MANY cells, but usually LYMPHOCYTES and MACROPHAGES, numerous roles in acute and chronic inflammation –TNFα, IL-1, by macrophages • CHEMOKINES are small proteins which are attractants for PMNs (>40)
  • 33. NITRIC OXIDE • Potent vasodilator • Produced from the action of nitric oxide synthetase from arginine
  • 34. LYSOSOMAL CONSTITUENTS • PRIMARY • SECONDARY • Also called • Also called SPECIFIC AZUROPHILIC, or NON-specific • Lactoferrin • Lysozyme • Myeloperoxidase • Alkaline Phosphatase • Lysozyme (Bact.) • Collagenase • Acid Hydrolases
  • 35. FREE RADICALS • O2 – (SUPEROXIDE) • H2O2 (PEROXIDE) • OH- (HYDROXYL RADICAL) • VERY VERY DESTRUCTIVE
  • 36. NEUROPEPTIDES • Produced in CNS (neurons) • SUBSTANCE P • NEUROKININ A
  • 37. OUTCOMES OF ACUTE INFLAMMATION • 1) 100% complete RESOLUTION • 2) SCAR • 3)CHRONIC inflammation
  • 38. Morphologic PATTERNS of Acute INFLAMMATION (EXUDATE) • Serous (watery) • Fibrinous (hemorrhagic, rich in FIBRIN) • Suppurative (PUS) • Ulcerative
  • 41. PUS = PURULENT ABSCESS = POCKET OF PUS = NEUTROPHILS
  • 44. SEQUENCE OF EVENTS • NORMAL HISTOLOGY  • VASODILATATION  • INCREASED VASCULAR PERMEABILITY  • LEAKAGE OF EXUDATE  • MARGINATION, ROLLING, ADHESION  • TRANSMIGRATION (DIAPEDESIS)  • CHEMOTAXIS  • PMN ACTIVATION  • PHAGOCYTOSIS: Recognition, Attachment, Engulfment, Killing (degradation or digestion)  • TERMINATION  • 100% RESOLUTION, SCAR, or CHRONIC inflammation
  • 45. CHRONIC INFLAMMATION (MONOS) “MONO”CYTE LYMPHOCYTE MACROPHAGE
  • 46. CAUSES of CHRONIC INFLAMMATION • 1) PERSISTENCE of Infection • 2) PROLONGED EXPOSURE to insult • 3) AUTO-IMMUNITY
  • 47. Cellular Players • LYMPHOCYTES • MACROPHAGES (aka, HISTIOCYTES) • PLASMA CELLS • EOSINOPHILS • MAST CELLS
  • 48. MORPHOLOGY • INFILTRATION • TISSUE DESTRUCTION • HEALING
  • 49. GRANULOMAS GRANULOMATOUS INFLAMMATION 4 COMPONENTS FIBROBLASTS LYMPHS HISTIOS “GIANT” CELLS
  • 50. GRANULOMAS GRANULOMATOUS INFLAMMATION CASEATING (TB) NON-CASEATING
  • 51. LYMPHATIC DRAINAGE • SITE REGIONAL LYMPH NODES
  • 52. SYSTEMIC MANIFESTATIONS (NON-SPECIFIC) • FEVER, CHILLS • C-Reactive Protein (CRP) • “Acute Phase” Reactants, i.e., α1-α2 • Erythrocyte Sedimentation Rate (ESR) increases • Leukocytosis • Pulse, Blood Pressure • Cytokine Effects, e.g., TNF(α), IL-1
  • 53. NORMAL SPE Serum Protein Electrophoresis In ACUTE Inflammation Alpha-1 & alpha-2 are increased, i.e., “acute phase” reactants.

Notas do Editor

  1. Think of it as a Cecil B. DeMille epic movie!
  2. Who was Cecil B. DeMille?
  3. The sequence of changes occurring in acute inflammation are NOT specific for the stimuli which cause them
  4. These are the three “phases”, in order, of acute inflammation. Please NOTE they, in no way, are the independent of each other, and as you might suspect by now, quite the contrary, CRUCIALLY all wrapped up with each other!
  5. Many names, same cell
  6. The four “cardinal”, i.e., “classic” signs of inflammation, translated, literally, 1) redness, 2) heat, 3) swelling, 4) pain. Just like a fith Marx bother, Gummo, was often added, so was the term “functio laesa” or “loss of function”
  7. The usual suspects, again. “Stimuli”, like “etiologic agents” is a very elusive term if you like to think in terms of ultimate causes.
  8. Vascular changes occur BEFORE any infiltration of inflammatory cells arrive.
  9. These are all events which either cause, or result, from the phenomenon of “increased permeability”
  10. Transudate vs. Exudate. Transudates can be thought of as being fairly pure water. Transudates are water PLUS most serum proteins, fibrin, and many blood cells often. So which one do you think requires bigger holes in the endothelium, transudates or exudates?
  11. The four things neutrophils do, in order, in acute inflammation. This is beautifully demonstrated in live cell imaging!
  12. Secretins and integrins are classes of substances to help neutrophils stick to vessel walls and migrate through the wall. Yes they are CAMs.
  13. CHEMOkines induce CHEMO-taxis, that why their called CHEMO -kines.
  14. These three events are the results of leukocytes (i.e., neutrophils) being “activated”
  15. The three phases of phagocytosis, in correct order. 1) Recognition  2) Engulfment  3) Digestion (cell probably already dead)
  16. These are the common features of ALL “chemical mediators” in acute inflammation. This is the shovelling part!
  17. How many of the 4 cardinal signs of inflammation can histamine cause, by virtue of its being a powerful vasodilator? 3-4?
  18. Serotonin is widely and primarily thought as being a neurotransmitter involved in the full spectrum of emotional responses, but its role in acute inflammation is just as powerful.
  19. Complement fixation is the end stage of a cascade of multiple chemical events, similar to coagulation, which ultimately result in lysis of cell membranes, hopefully, membranes of bad cells.
  20. Bradykinin is a potent endothelium -dependent vasodilator , causes contraction of non-vascular smooth muscle , increases vascular permeability and also is involved in the mechanism of pain .
  21. Coagulation is also a cascade, like complement fixation.
  22. Three classic eicosanoids, new classes are also being discovered. ALL are derivatives from arachidonic acid. Eicosanoids can also be directly attributed to causing the 4 cardinal signs of inflammation. http://en.wikipedia.org/wiki/Eicosanoid The problem with Eicosanoids is that you NEVER get the BIG picture: Here’s the BIG PICTURE NOW!
  23. Arachidonic acid
  24. When you think of the three main things that ASPIRIN does, you can remember the three main properties of the prostaglandins.
  25. Click back to the previous slide on LEOKITRIENES and realize that LIPOXINS generally do the OPPOSITE of what LEUKOTRIENES do.
  26. It is produced in response to specific stimuli by a variety of cell types, including neutrophils , basophils , platelets , and endothelial cells . From wiki: Platelet-activating factor , also known as a  PAF ,  PAF-acether  or  AGEPC  (acetyl-glyceryl-ether-phosphorylcholine) is a potent phospholipid  activator and mediator of many leukocyte functions, including platelet aggregation and degranulation, inflammation, and anaphylaxis. It is also involved in changes to vascular permeability, the oxidative burst, chemotaxis of leukocytes, as well as augmentation of arachidonic acid metabolism in phagocytes.
  27. There are gazillions of cytokines/chemokines. The two most classical and famous ones are TNF-alpha and Interleukin-1. TNF-alpha, also called tumor necrosis factor, or cachectin, is a substance that is destructive of human tissues, and is a key player in “cachexia”. Interleukin-1 was the first of many interleukins discovered and generally propagates the inflammatory response at many levels and also has a significant effect on T-cells.
  28. Which drug INCREASES the effect of nitric oxide? Hint: you get spam ads for it 10 times a day in your spam, even if you are a female.
  29. MPO produces hypochlorous acid and tyrosyl radical are cytotoxic, so they are used by the neutrophil to kill bacteria and other pathogens. It is what makes pus look greenish yellow. Lactoferrin  (LF), also known as  lactotransferrin  (LTF), is a globular multifunctional protein with antimicrobial activity (bacteriocide, fungicide) Lysozymes , also known as muramidase or  N-acetylmuramide glycanhydrolase , are a family of enzymes (EC 3.2.1.17) which damage bacterial cell walls by causing hydrolysis.
  30. Substance P is an 11 amino acid polypeptide tied into many things including mood disorders, anxiety, stress, reinforcement, respiration rate, neurotoxicity, nausea, emesis, and pain. The Neurokinins are also peptide neurotransmitters involved in many things.
  31. Three classic outcomes of acute inflammation
  32. FOUR patterns of acute inflammation: (OneLook.com has 133 adjectives to the word “inflammation”)
  33. FIBRIN is the endpoint of coagulation and had a characteristic appearance both grossly and microscopically. Do you remember hearing the term fibrin-OID necrosis too?
  34. It is EXTREMELY important to be able to recognize neutrophils (Polys) in H&E sections. The key tip is, OFTEN, they might NOT look multilobulated at first, but upon close examination, they are!
  35. ULCERS (i.e., pathologic LOSS of mucosal or epithelial coverings, are both the CAUSE as well as a RESULT of acute inflammation. WHY? Identify the FOUT layers of the colon here, mucosa, submucosa, muscularis, and finally adventitia/serosa.
  36. If there was only ONE slide you needed to memorize for this chapter, THIS would be it!
  37. Please understand the DIFFERENCE between a MONO-cyte, and a generic MONO-nucleated cell.
  38. What does chronic inflammation look like? ANS: Infiltrates of lymphs and monos “peppering” normal histology. Most auto-immune inflammations are long standing, or “chronic” clinically as well.
  39. Please note that the “cellular” players of chronic inflammation are NOT the baseball players who play in US Cellular Field in Chicago, i.e., the White Sox.
  40. Know, ALWAYS, the FOUR cells of granulomatous inflammation, and the FOUR common types of granulomatous infections: 1) TB, 2) Sarcoid, 3) Fungi, 4) Foreign Bodies. Why do granulomas form, rather than just acute or chronic inflammation? Very simple, you need to bring your friends if your enemy is too big?
  41. The drainage patters of acute or chronic inflammation follow the same general drainage patterns of tumor cells.
  42. CRP is a member of the class of acute phase reactants as its levels rise dramatically during inflammatory processes occurring in the body. It is thought to assist in complement binding to foreign and damaged cells and affect the humoral response to disease. It is also believed to play an important role in innate immunity, as an early defense system against infections.
  43. Which TWO of these 5 “hills” are significantly higher in nonspecific systemic acute inflammation? Answer: alpha-1 and alpha-2