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‎ amage Cell With

D
‎Defination ‎Alteration In Structure,
‎Function Resulting From
‎Inabilty Of Cell To Adapt
‎With Ingurius Agent

‎Ischemia

‎Anemia

‎Hypoxia ‎ ardiac, Pulmonary


C
‎Diseases

‎ arbon Monoxid
C
‎Posning

‎Bacteria

‎Infection ‎Viruses

‎Toxins

‎Hypersensitivity

‎Cause ‎Autoimmune Reactions


‎Immunologic Reaction
I‎ mmune Copmlex
‎Reactions

‎Drugs

‎Chemical Injury ‎Alcohol

‎Acids

‎Trauma
‎CELL INJURY ‎Physical Injury ‎Burns

‎Radiation

‎Cell Membrane

‎Aerobic Respiration

‎ATP Product
‎ ell Component
C ‎Protein Synthesis
‎Target To Injury
‎Cytoskeleton

‎ enetic apparatus
G
‎DNA/RNA

‎Depletion of ATP

‎Damage To Mitochondria

‎Influx Of Calcium

‎Oxidative Stress
‎Mechanism
‎ efects In Memb.
D
‎Permeability

‎Nuclear Damage

‎Adapation ‎Next

‎Type ‎Reversible ‎Next

‎Irreversible ‎Next
‎YOUNES_ALHAMADY 
‎ eversible Cellular
R
‎Changes In Function,
‎Size, Number In Response
‎DEFINITION ‎To Changing In
‎Environmental Conditions
‎Of Cell.

‎Physiologic ‎ s Response To
A
‎Normal Stimulation
‎CAUSE
‎Pathologic ‎ odified Response To
M
‎Avoid Injury

‎ ecreas In Cell Size And


D
‎Definition
‎Functional Ability

‎⇓Production Of Protein
‎Mediatory
‎Atrophy ‎⇓Production Organelles
occur after denervation
‎Example ‎Ischemic Atropy

‎Gross
‎Organ Small
‎Examination
‎Mic ‎Cell ‎Small

‎Nuclei ‎Small

‎Definition ‎Increas In Cell Size


‎ADAPTATION
‎⇑Protein Synthesis
‎Mediatory
‎⇑ Production Organelles

‎ k. M. In
S
‎Body Builder
‎Hypertrophy
‎Phys ‎ terus In
U
‎Pregnancy
‎Example
‎Patho ‎Ventericular
‎Hypothyroidism

‎Gross
‎Organ Enlarged
‎Examination
‎Mic ‎Cell ‎Large

‎Nuclei ‎Large

I‎ ncrease In Number Of
‎Definition
‎Cell

‎⇑DNA
‎Mediatory
‎⇑Mitosis

‎Phys ‎ PH
B
‎TYPE ‎in old age

‎Hyperplasia ‎Patho ‎ ndomatrial


E
after nerphrectomy hepatectomy
‎Example ‎Hyperplasia

‎Cardiac M.
‎Not Occur In
‎Skeletal M

‎Neurons M.

‎Gross
‎Organ Enlarged
‎Examination
‎Mic
‎Cell ‎⇑Number

‎ onversion Of Cell Type To


C
‎Another
‎Definition
‎-Usually Reversible
‎-Can Progress To Dysplasia

‎Chronic Irrtattion
‎Mediatory
‎Metatrophy ‎Prolong Inflammation

‎ olumnar
C
‎ pithelial
E ‎Metaplasia
‎Metaplasia
‎(Most Common) ‎ quamous
S
‎Metaplasia
‎Example
‎ sseous
O
‎ esenchymal
M ‎Metaplasia
‎Metaplasia ‎ artilagenous
C
‎Metaplasia

‎ ellular Proliferation Of
C
‎Atypical Cell With Change
‎Definition
‎In Size , Shape, Loss Of
‎Dysplasia ‎Cellular Organization

‎ ervical Intra-epithelial
C
‎YOUNES_AL_7AMADY  ‎Example ‎CIN
‎Neoplasia(most Common)
‎Feature

‎ bility Of Cell To Return


A
‎To Previous Normal

‎Early Stage Of Cell Injury

‎Short Duration

‎Minimal Intensity

‎ ltrastructure
U
‎Changes

‎Swelling ‎Mitochondria

‎ER

‎Clumping Of Chromatin

‎ etachment Of
D
‎Ribosoms

‎ ell Memb.
C ‎ oss Of
L
‎Characters ‎Alteration ‎Microvilli
‎Types Of Changes
‎ embrane
M
‎Blebs

‎ iochemical
B
‎Changes

‎Decrease Of Atp

‎Anaerobic Glycolysis

‎Morphological
‎Changes

‎Swelling
‎ EVERSIBLE
R
‎CELL INJURY ‎Fatty Change

I‎ ntracellular
‎Accumulation

‎Examination

‎Gross ‎Soft Enlarged Tissue

‎Micro ‎Clear Vacules Of Water

‎Cell Swelling

‎Cloudy
‎ ‎Next
‎Type
‎Hydropic

‎ atty Change
F ‎YOUNES_AL_7AMADY 
‎(Steatosis)
‎Definition ‎ eversible Cell Injury
R
‎With Accumulation
‎Water In Cytoplasm

‎cause
‎Mild Injury

‎ ll Site In Body
A
‎Site ‎Except In Bones

‎Size ‎Enlarged

‎3 S ‎Shape ‎Round

‎Surface ‎Smooth
‎Gross ‎Color ‎Pale
‎ ut
C
‎Cloudy
‎3 C ‎Section ‎Pulging

‎Soft
‎Consistency
‎Firm
‎Cell Swelling ‎Membrane ‎Intact

‎Cell ‎Normal
‎Micro
‎Nucleus ‎Normal

‎Cytoplasm ‎Esonophile

‎EM ‎Flatting

‎cause
‎severe injury

‎Size ‎Enlarged

‎3 S ‎Shape ‎Round

‎Surface ‎Smooth
‎Gross ‎Color ‎Pale
‎ ut
C
‎3 C ‎Section ‎Pulging
‎Hydropic
‎Soft
‎Consistency
‎Firm
‎ YPE OF
T
‎REVERSIBLE ‎Membrane ‎Intact
‎INJURY ‎Cell ‎Normal
‎Micro
‎Nucleus ‎Normal

‎Cytoplasm ‎Pale

‎EM ‎Flatting

‎Definition ‎ eversible Cell Injury


R
‎With Accumulation
‎Fat In Non Fatty Cells

‎ ame Cause Of
S
‎Cell Injury
‎cause ‎ Obesity, Starvation,
+
‎Alchohol

‎Liver

‎Site ‎Heart

‎Kidney

‎ atty Change
F ‎ ‎Size ‎Enlarge
‎(Steatosis) ‎3 S ‎Shape ‎Round

‎Surface ‎Smooth
‎Gross
‎Color ‎Yellow

‎ ut
C
‎3 C
‎Section ‎Pulging

‎Consistency ‎Soft

‎Membrane ‎Intect

‎Cell ‎Enlarge
‎Micro ‎Nucleus ‎Normal

‎ ignet Ring
S
‎ OUNES_AL_
Y ‎Cytoplasm ‎Appearance

‎7AMADY
‎Result From

‎ rogression Of
P
‎Reversible Injury

‎ evere Injury From


S
‎Begining

I‎ nability To Return To
‎Previous Normal State

‎Long Duration

‎Maximal Intensity

‎Features ‎Late Stage

‎ evere Injury Of
S
I‎ rreversible
‎Lysosomal Memb.
‎Cell Injury
‎ hanges In
C
‎Characters ‎Cytoplasm & Nucleus

‎Severe Swelling
‎ ltrastructure
U ‎Mitochondria
‎Change ‎Rupture Of Lysosome

‎DNA& RNA damage

‎Caogulative

‎Caseous

‎Necrosis ‎Fat ‎
‎Next
‎Liquefactive

‎Fibrinoid
‎Type
‎Gangrenous

‎Apoptosis ‎Next
‎YOUNES_AL_7AMADY 
I‎ rreversible Death Of
‎Definition
‎Group Of Cells

‎ ame Cases Of Cell Injury


S
‎Cause
‎But It Lasted Longer

‎ ame Mechanism Of Cell


S
‎Mechanism
‎Injury But It Lasted Longer

‎Color ‎Mostly Yellow


‎Gross
‎Firm
‎Consistency
‎Soft

‎Membrane ‎Lost

‎Cell ‎Large

‎Cytoplasm ‎Eosinophile
‎Micro
‎Shrinking Of Nucleus
‎Pyknosis
‎Due To Decrease PH

‎Fragments Of Nucleus
‎Nucleus ‎Karyorrhexis
‎NECROSIS ‎Due To DNA Chromatin Damage

‎Dissolve Of Nucleus
‎Karyolysis
‎Due To Activation Of DNA Enzyme

‎Inflammation

‎ ormation Of
F
‎New Cells

‎Fibrosis
‎Fate
‎Phagocytosis

‎Capsulation

‎Calcification

‎Putrefaction

‎Caogulative ‎Next

‎Caseous ‎Next

‎Fat ‎Next
‎Type
‎Liquefactive ‎Next

‎Fibrinoid ‎Next

‎Gangrenous ‎Next
‎YOUNES_AL-7AMADY 
‎Cause
‎Autoimmune Disease
‎Cause
‎Color ‎Sudden Ischemia
‎Pink Eosinophile
‎Gross ‎Color
‎Consistency ‎Pale
‎Gross
‎Glassy
‎Consistency
‎Membrane ‎Firm
‎Lost
‎Membrane
‎Cytoplasm ‎Fibrinoid ‎Lost
‎Acidophilic ‎Micro
‎Caogulative ‎Cytoplasm
‎Micro ‎Acidophilic
‎Pyknosis most important

‎Nucleus
‎Karyorrhexis ‎Pyknosis
‎Nucleus
‎Karyolysis ‎Karyorrhexis

‎EXAMPLE ‎Karyolysis
‎Systemic Lupus Erytho
‎EXAMPLE
‎Myocardial Infraction
‎Tramatic
‎Self- Digestion
‎Cause ‎Cause
‎Enzymatic ‎Hypersensitivity
‎ anceatic
P
‎Saponification ‎Lipase
‎Color
‎Yellowish
‎Gross
‎Fatty Acid ‎Ca ‎Consistency
‎Soft Cheesy
‎Color
‎White ‎Membrane
‎Gross
‎Lost
‎Consistency
‎Hard ‎ YPE OF
T ‎Caseous ‎Cytoplasm
‎NECROSIS ‎Micro ‎Acidophilic
granulomatous inflammation
‎Membrane
‎Lost ‎Pyknosis
‎Fat ‎Nucleus
‎Cytoplasm ‎Karyorrhexis
‎Basophilic
‎Karyolysis
‎Pyknosis ‎Micro
‎Nucleus ‎EXAMPLE
‎Karyorrhexis ‎TB
‎Karyolysis
‎Cause ‎⇑Lipid Content
‎Fat Cells ‎Cells
‎Pus
‎Inflammatory Cells
‎Color
‎Tramatic ‎Yellowish
‎Breast Fat ‎Gross
‎EXAMPLE
‎Consistency
‎Acute Hemorrhagic ‎Enzymatic ‎Liquefied
‎Pancreatitis
‎Membrane
‎Lost

‎Liquefactive ‎Cytoplasm
‎Micro ‎Acidophilic
suppurative inflammation

‎NEXT ‎Wet Gangrenous ‎Pyknosis


‎Nucleus
‎NEXT ‎Dry Gangrenous ‎Gangrenous ‎Karyorrhexis

‎NEXT ‎Gas Gangrenous


necrotizing inflammation ‎Karyolysis

‎Brain Infraction
‎EXAMPLE
‎Pyogenic Abscess
‎YOUNES_ALHAMADY  ‎Pus
‎Definition

‎ ype Of Necrosis With


T
‎Superadded Putrefaction
‎Most Following
‎Coagulative Nerosis
‎Due To Ischemia

‎Artery And Vein

‎Cause By
‎Growing Bacteria

‎Color
‎Dark
‎GANGRENOUS ‎Gross
‎Wet Gangrenous
‎Consistency ‎ oft
S
‎Swollen
‎Rotten

‎Mouth

‎Site ‎Bowels

‎Lungs

‎Artery Only

‎Line Of Demarcation

‎Cause By
‎Arterial Occlusion
‎Types ‎Color
‎Dry Gangrenous
‎Black
‎Gross
‎Consistency ‎ ry
D
‎Shrunken

‎Limb Of Elderly Patients ‎Feet


‎Site ‎With Arteriosclerosis
‎Toes

‎Cause By
‎Formin Clostridia

‎Color
‎Dark Black
‎Gas Gangrenous ‎Gross
‎Consistency
‎Swellen

‎Open Wounds
‎Site
‎Especially In Muscles

‎YOUNES_AL_7AMADY 
-‎ Programmed Cell Death
‎-(Single Cell Death)
‎Definition
‎Or Small Group Of Cells
‎-Energy Dependent

‎Physiologic Processes
‎Cause
‎Pathologic Processes

‎Cell Shrinkage

‎ ormation Of Apoptotic
F
‎Bodies
‎Mechanism
‎ hagocytosis Of
P
‎Apoptotic Bodies

‎ ell Disappear
C
‎Completely

‎Membrane ‎Intact

‎Cell ‎Small
‎Micro
‎Nucleus ‎Fragmented

‎Cytoplasm ‎Acidophilic

‎Cell Injury
‎APOPTOSIS
‎DNA damage

‎Hormones
‎Stimulus
‎Lack Of ‎Cytokines

‎Growth Factors

‎Receptor Ligand Signals

‎ revent Realeas
P
‎Cytochrom C From
‎Mitochondria
‎ cl-2
B
‎(Inhibited) ‎ ind pro-apoptotic
B
‎protease activating
‎Regulated Genes ‎factor
‎(Apaf-l)

‎ -53
P
‎(Stimulate)

‎Digest Nuclear

‎ igest Cytoskeletal
D
‎Execution ‎Caspases
‎Proteins

‎Activate Endonucleases

‎No Inflammation
‎Fate
‎Phagocytosis
‎YOUNES_ALHAMADY 
‎ rotective Response
P
‎Definition ‎Tissue To Eliminate
‎The Case Of Cell Injury

‎Infection Agents ‎Bacteria


‎Virus
‎ ediated
M
‎Immunologic Injury ‎Antigen
‎ ntibody Cell
A
‎Causes ‎Reaction
‎Physical ‎Trauma
‎Heat
‎Chemical ‎Acids
‎Alkalis

‎Plasma Mediators
‎Next
‎Chemical Mediator
‎Cellular Mediator
‎Next

‎V.C

‎V.D
‎Vascular Event
‎⇑VP

‎Major Event ‎Srasis ‎ ‎Next

‎Leukodiapedesis

‎Cellular Event ‎Chemotaxis

‎INFLAMMATION ‎Phagocytosis

‎Loaclaized
‎Suppurative
‎Diffuse

‎Serous

‎Acute Inflammation ‎Catarrhal

‎Pseudomembranous

‎Fibrinous
‎Non-suppurative
‎Serofibrinous
‎ ‎Next

‎Hemorrhageic
‎Type
‎Necrotizing

‎Allergic

‎Primary
‎Causes
‎Scondary
‎Chronic Inflammation
‎Specific
‎Causes & Morphological
‎Non-specific

‎If Mild
‎Resolution

‎Good I‎ f Destraction Of ‎Regenration ‎Same Type Of Tissue


‎Tissue
‎Repair ‎ ny Site
A
‎Fibroplasia
‎ .T
C ‎Except CNS
‎ eposition
d
‎Gliosis ‎CNS
‎Fate ‎Lymph ‎Lymphangitis
‎Spread ‎Toxemia

‎Septicemia
‎Blood
‎Pyemia
‎Bad
‎Chronicity

‎Non Suppurative ‎⇒
‎Suppurative
‎YOUNES_AL-7AMADY 
‎Main Mediators ‎Sources ‎Action

‎ erotonin
S ‎Mast Cell -‎ VD
‎Histamin ‎Platelets ‎-⇑VP

‎Thromboxane ‎Platelets ‎VC

-‎ VD
‎-fever
‎-pain

‎ Prostaglandins ‎WBCs
‎Chrmotaxin

‎LTB4 ‎ eukocyte
L
‎Activation
‎Lukotriens ‎WBCs ‎VC
‎ ellular
C
‎Mediators ‎(LTC, D, E)4 ‎⇑VP

‎ ysosome
L ‎WBCs ‎ issue
T
‎Enzyme ‎Macrophages ‎Destraction

‎Macrophages -‎ VD
‎Nitric Oxide
‎Endothelial Cell ‎-tissue damage

‎Granuloma Formation

‎Interferon ‎T-lymphocyte

‎ cute Phase
A
‎Response Of
‎ hemical
C ‎Cytokines ‎Inflammation
‎Mediator
‎ ndothelial Cell
E
‎Activition
‎ILI–TNF ‎Macrophages
‎ ibroblastic
F
‎Proliferation

‎⇑VP
‎Bradykinin ‎VD
‎Kinin System
‎pain

‎⇑VP
‎C3a

‎ C3a ‎Phagocytosis
‎ lasma
P ‎C3b
‎ C3b
‎Mediators
‎ C5a ‎⇑VP
from complement
system ‎C5a ‎Chrmotaxin

‎⇑VP
‎Fibrinopeptide
‎Clothing System ‎Chrmotaxin

‎ ‎ ‎Kallikrein
‎Factor Xll ‎Prekallikrein ‎Kallikrein ‎Kininogen ‎Bradykinin

‎Thrombin ‎Plasmin
‎Fibrinogen ‎Fibrin ‎Fibrin Spelt Products

‎Kallikrein ‎⇑Vp
‎C5 ‎C5b
‎Chemotaxis

‎Plasmin ‎C3a ‎⇑Vp


‎C3 ‎ OUNES_AL-
Y
‎C3b ‎Phagocytosis 
‎7AMADY
‎Definition ‎ ransient Contraction Of
T
‎Blood Vessele

‎Thromboxaine A2
‎V.C ‎Cause
‎Leukotrienes C4, D4, E4

‎Effect ‎ arrowing Of Blood


N
‎Vessel Lumen

‎Definition ‎ ilation Of Blood Vessel


D
‎Lumen

‎Histamin

‎Serotonin
‎Cause
‎Prostaglandins
‎V.D
‎Bradykinin

‎Redness ‎1st Sing

‎Due To ⇡ Blood Flow

‎Effect ‎Hotness ‎2nd Sing

‎Due To ⇡ Blood Flow

‎Transudate
‎Due to ⇡ IVHP

‎Definition ‎ ndothelial Cell Change


E
‎With Widening Inter-
‎endothelial Spases

‎Histamine
‎ ndothelial Cell
E
‎Contraction By: ‎Bradykinin
‎Vascular Event
‎Leukotriene

‎ ndothelial Cell
E ‎IL-1
‎Retraction By:
‎Cause
‎TNF

‎ irect Tissue
D
‎⇑VP ‎Damage
‎ ndothelial Cell
E ‎Cell Injury
‎Injury
‎ ction Of Enzymes
A
‎Of Leukocyte
‎Leukocyte Activation

‎ oss Of High Protein


L
‎Molecules And Blood Cells

‎ ecreased Intravascular
D
‎Osmotic Pressure

‎Effect I‎ ncreased Extravascular


‎Osmotic Pressure
‎Major Event ‎Loss Of Fluid
‎Of
‎Formation Of Exudate
‎Inflammation
‎Definition
‎Slowing Of Circulation

‎Loss Of Fluid
‎Cause I‎ ncrease Concentration of
‎RBCs
‎Stasis
‎Increase Vasosity

‎Loss Of Axial Blood Flow


‎Effect ‎ idening Central Blood
W
‎Flow

‎Loss Of Plasmatic Zone

‎Leukodiapedesis
‎Next

‎Chemotaxis
‎Cellular Event ‎Next

‎Phagocytosis ‎YOUNES_AL-7AMADY 
‎Next
‎Activation of WBCs

‎Margination ‎ indening Of Central


W
‎Blood Flow

‎Pavementation ‎ ovement Leukocytes


M
‎Toward Endothelial
‎Surface

‎Definition ‎ eukocytes Roll The


L
‎Endothelial Surface

‎Cause

‎TNF & lF-1


‎by activation
‎selectin
‎Rolling
‎P-selectin ‎ n Endothelial
O
‎Cells
‎E-selectin

‎L-selectin
‎On Leukocytes
‎S-selectin

‎Effect ‎ oosing Binding Of


L
‎Leukocytes To
‎Endothelium

‎Definition ‎ eukocytes Adhere To


L
‎Endothelial Cells

‎Cause

(‎ ICAM1,2 )
‎On Endothelial
‎Cells
‎Leukodiapedesis
leukocyte extravasation ‎TNF & lF-1
‎by activation ‎Binds ‎LFA-1
‎On Leukocytes
‎adhesion molecules ‎Mac-1
‎Adhesion
(‎ VCAM1 )
‎On Endothelial
‎Cells

‎Binds
‎VLA-4 ‎On Leukocytes

‎IL-1
‎Cause
‎TNF
‎Weak Adhesion
‎Mediated By Interaction Of

I‎ ntegrin With Endothelial


‎Effect
‎Adhesion Molecules

‎Integrin In This Case Is Inactive

‎LTB4
‎Cause ‎Chemotactic Factors
‎C5a
‎Firm Adhesion
‎CELLULAR ‎Mediated By Interaction Of
‎EVENT 1
I‎ ntegrin With Endothelial
‎Adhesion Molecules

‎Integrin In This Case Is Active

‎Definition ‎ eukocytes Pass Through


L
‎Inter-endothelial Gaps

‎TNF & lF-1


‎Of Both Leukocytes ,Endothelial Cells

‎PECAM-1
‎Transmigration ‎Of Both Leukocytes ,Endothelial Cells
‎Cause
diapedesis
‎Collagenases

‎Pseudopodial Extension
‎Of Leukocytes

‎Effect ‎ ormation Of
F
‎Inflammatory
‎||Cellular Exudate||

‎Chemotaxis ‎Next

‎Phagocytosis ‎Next
‎YOUNES_AL-7AMADY 
‎Leukodiapedesis ‎Leukocyte Extravasation

‎Definition ‎ ttraction Of Leukocytes


A
‎To The Sit Of Injury

‎Cause
‎Chemotactic Agents

‎ ctivation Of
A
‎Chemotaxis
‎Phospholipase C

I‎ ncreased Cytosolic
‎Calcium
‎Effect
‎Activation Of Contractile
‎Proteins

‎Cell Movement
‎CELLULAR
‎EVENT 2 ‎Definition I‎ ngestion Of Bacteria
‎And Foreign Particales
‎Neutrophils

‎Phagocytic Cells ‎Monocytes

‎Macrophages
‎Cause
‎Plasma Factors

‎Opsonins ‎IgG

‎C3b

‎Effect
‎Killing Or Failure

‎ ecognition And
R
‎Attachment
‎Phagocytosis
‎ ngulfement And
E
‎Formation
‎Phagolysosome

‎ xidative Mechanism
O
‎(More Common )

‎ roduction Oxygen
P
‎Free Radical

‎Superoxid

‎H2O2
‎ egeneration Of
D
‎Micro-organism By: ‎HOCL
‎Mechanism ‎ ecretion Of
S
‎Lysolysosomal
‎Granules

‎Neutrophils

‎Macrophages

‎Non-oxidative Mechanism

‎Lysosomal Hydrolases

‎Proteases

‎Result Pus Cells

‎ iving Bacteria Continue To


L
I‎ f Failure To Kill
‎YOUNES_AL-7AMADY  ‎Live Inside Macrophages
‎The Engulfed Bacteria
‎ ransfers By Lymphatic
T
‎To Adjacent Part To
‎Produce New Lesions
‎Definition ‎ xtravascular Non-inflammatory
E
‎Fluid Of Blood Plasma
‎- Non Oedema, Water Only

‎Cause -‎ Due To Osmotic Or Hydrostatic


‎Imbalance Across Vessel Wall
‎Without ⇑ V P

‎Gravity
‎Less Than 1018
‎Transulate
‎Color
‎Pale Yellow

‎Aspect
‎Clear

‎Gross ‎Protein
‎low than 3 gm

‎Fibrin
‎No Fibrin

‎Coagulation
‎Absent

‎Cells
‎Minimal Or Absent

‎Definition ‎ xtravascular Inflammatory


E
‎Fluid Of Blood Plasma
‎-With Oedema

‎ ‎Cause
‎Due To ⇑ V P , With Oedema

‎Gravity
‎More Than 1018

‎Color
‎Straw

‎Aspect
‎Turbid

‎Gross ‎Protein
‎More Than 3 gm

‎Fibrin
‎Rich

‎Coagulation
‎Present

‎Cells
‎Rich In Inflammatory Cells

‎Exudate I‎ ncrease Hydrostatic


‎Pressure (VD)

I‎ ncrease Permeability
‎Mechanism ‎(Widening Of Gaps)

I‎ ncrease Tissue Osmotic


‎Pressure

‎Hematogenous Part
‎Protein
‎Type
‎Histogenous Part
‎WBCs

‎Dilute

‎Antibodies ‎Hematogenous Part


‎Function
‎Localization

‎Phagocytosis ‎Histogenous Part

‎Fate ‎ rainage By Lymphatic To


D
‎Venous Circulation
‎YOUNES_AL-7AMADY 
‎ PHAGOCYTIC CELL

‎Neutrophile ‎Macrophage

‎Name ‎Microphage ‎Monocytotic

‎Respone ‎Early ‎Late

‎Aim ‎Killing ‎Cleaning And Killing

‎present ‎Acute Inflammation Only ‎Acute And Chronic

‎Giant Cells
‎Pus Cells
‎Fate ‎Endothelial Cells

‎Apoptosis
‎Foam Cells

‎YOUNES_AL-7AMADY 
‎Definition

‎Inflammatory Fluid Exude

‎Site Of Injury With

‎Necrotic Tissue

‎Neutrophils

‎Pus Cells

‎Formation ‎ ction Of Proteolytic


A
‎Enzymes Of Pus Cells

‎ iquifactive Of Necrosis
L
‎PUS ‎Tissue

I‎ nflammatory Fluid
‎ (Purulent= Pus)

‎Color
‎Yellow

‎Appearance ‎Clearance
‎Turbid

‎Clotting ‎Non-clotting

‎Bacteria

‎ us Cells(dead
P
‎Neutrophils)
‎Component ‎ iquifactive Of Necrosis
L
‎Tissue

‎Fluids
‎YOUNES_AL-7AMADY 
‎Onest
‎Sudden

‎Duration
‎Short Duration

‎Cardinal Sings
‎Present

‎VC ‎VD
‎Vascular Event
‎Pathogenesis ‎⇑VP ‎Stasis

‎Leukodiapedesis ‎Chemotaxis
‎Cellular Event
‎Phagocytosis

‎Plasma Exudate
‎Present

‎Sever VD and ⇑VP


‎Present

‎ ctivation Of Blood
A
‎Plasma Systems
‎Present

‎Mostly Non-specific

‎Characters ‎Suppurative
‎Necrosis
‎Present Only In : ‎ ecrotizing Type Of
N
‎Non-suppurative
‎Inflammation

‎May Lead To Death ‎Severe Infection


‎Due To
‎Severe Vasodilation "VD"

‎ ain
M ‎Neutrophils
‎Inflammatory Cells ‎Macrophage
‎Pus Cells

‎Microscopic ‎Eosinophils
‎Fibrin Deposition
‎Thin Wall
‎Examination ‎Congested Blood Vessels

‎In Mild Cases ‎Oedematous


‎Grossly ‎congested changed
‎In Chronic Cases ‎ uppurative With
S
‎Necrotic Changes

‎Followed By Repair

‎Abscess

‎Ulcers
‎Main Morphology
‎Bacteremia
‎Through Blood ‎Pyaemia
‎Septicemia
‎ cute
A
‎Inflammation ‎Fever ‎Hight Grade

‎Due To Leucotaxine
‎Leucocytosis ‎Neutrophilia ‎Bacteria Infections
‎General ‎Eosinophilia ‎Parasites Infections

‎Neutropenia ‎Viral Infections

‎Lymphadenitis ‎Lymphangitis
‎Sings
‎Septic Shock ‎In Severe Acute Infection

‎Redness "Rubor" ‎Hotness "Calor"


‎Local
‎Swelling "Tumor" ‎Pain "Dolor"

‎Loss Of Function

‎Suppurative ‎Next
‎Type
‎Non-suppurative ‎Next

‎Common Example ‎Pyogenic Abscess ‎Cellulitis ‎Pneumonia

‎Resolution
‎Removal Cause

‎Suppuration ‎ ccur In Infection With:


O
‎- Pyogenic Organisms
‎-Severe Tissue Necrosis

‎ ealing By:
H
‎Fate ‎- Fibrosis ‎ hen There Is:
W
‎-Scarring ‎ ‎- Afibrinous Exudate
‎-Tissue Non-
‎regeneration

‎ hange To Chronic
C ‎ hen There Is:
W
‎Inflammation ‎-Persistence Cause
‎-Recurrent Of The ‎YOUNES_AL-7AMADY 
‎Inflammation
‎ evere Acute
S
‎Inflammation
‎Definition
‎Characterized By
‎Exudate Called Pus

‎Characters ‎Formation Of Pus

‎Cause ‎Pyogenic Bacteria

‎Site ‎Any Part Of Body

‎ ecrotizing
N
‎Suppurative ‎Inflammation
‎Acute
‎Inflammation ‎Cause

‎Streptococcus Aureus

‎ ecrets Streptokinase
S
‎Diffuse ‎Lead To Dissolve Matrix
‎Of Tissue And Fibrin

‎Cellulitis

‎In Subcutaneous Tissue

‎Phlegmonous
‎Type
‎In Mucous Membrane

‎Examples
‎Acute Appendicitis

‎ ocalized
L
‎"Abscess"

‎Next ‎YOUNES_AL-7AMADY 
‎ cute Localized Suppurative
A
‎Definition ‎Inflammation Formed Of
‎Cavity Containing Pus

‎Staphylococcus Aureus

‎ ecrets Coagulase Enzyme


S
‎Cause ‎Lead To Fibrin Formation
‎Lead To Localization

‎Site ‎Any Organ Of Body

‎Small Abscess
‎ oil
B
‎"Furuncle" ‎Hair Follicles

‎Related To : ‎Sweat Gland

‎Sebaceous Glands

‎Variants ‎ ultiple Communicating


M
‎Abscess In
‎Subcutaneous Tissue
‎Carbuncle ‎Opening To Surface By
‎Multiple Sinuses

‎Central Zone
‎Zon Of Necrosis
‎Mid Zone
‎Zones ‎Cavity Filled With Pus

‎ ocalized
L ‎Peripheral Zone ‎ ibrioplastic Proliferation
F
‎Pyogenic Membrane
‎With Vascular Dialation
‎Abscess

‎Multiple Differently In Size

‎Examples ‎Lung ‎Pale-pink Color

‎Granulation Tissue
‎Healing By
‎Fibrosis

‎Sinus
‎Tract With One Opening
‎Tract Formation
‎Fistula
‎Tract With Tow Opening

‎ ocal Defect On
L
‎Endothelial Surface

‎Cause ‎ ysosomal Enzymes


L
‎Of Neutrophils
‎ lcer Formation
U
‎"Ulcerative ‎Mouth
‎Site
‎Inflammation " ‎GIT
‎Evacuated
‎ cute
A ‎Neutrophils
‎Stage
‎Vascular Dilation ‎In Edges Of Ulcer

‎Necrosis
‎Stages

‎Chronic ‎Mononuclear Cell


‎Stage I‎ n Edges And
‎Fibroblastic Proliferation
‎Base Of Ulcer
‎Fate ‎Fibrosis

‎Inflammatory Ulcer
‎Different Diagnotic Bw: ‎Slight Elevation Of Edge
‎-Inflammatory Ulcer
‎Malignant Ulcer
‎-Malignant Ulcer ‎Slight Elevation Of Edge

‎Change To Chronic Abscess

‎Direct
‎With Enlargement Of Abscess
‎Non-evacuated ‎Lymphangitis
‎In Lymphatic Vessels
‎Lymphatic
‎Spread ‎Lymphadenitis
‎In Lymph Nodes

‎Weak
‎Bacteraemia ‎Bacteria Only On Blood

‎Blood Spread ‎Toxemia ‎Bacteria Toxin Only In Blood


‎Virulent
‎Septicemia ‎Bacteria + Their Toxin In Blood

‎YOUNES_AL-7AMADY  ‎Pyaemia
‎ hrombophilipitis + Septic
T
‎Emboli In Blood
‎ ore In:
M
‎Site ‎-Subcutaneous Tissue
‎-Connective Tissue

‎No Pus

‎ ot Cause By Pyogenic
N
‎Characters
‎Bacteria

‎Mild

‎Exudate
‎Serous Exudate

‎Burns
‎Cause
‎Many Bacteria Infection
‎Serous
‎Mainly In Serous Cavity
‎Site
‎Skin

‎ cute Glottal And


A
‎Examples ‎Vesicular Skin ‎Laryngeal Edema

‎Mild

‎Exudate
‎Mucin Exudate

‎ acterial And Viral


B
‎Infections
‎Cause ‎ llergy With
A
‎Catarrhal
‎Non-suppurative ‎Hypersensitivity Reaction
‎Acute ‎Site ‎Respiratory Tract
‎Inflammation ‎Mucous Membranes Of
‎GIT

‎Examples ‎Catarrhal Appendicitis ‎Catarrhal Rhinitis ‎Catarrhal Bronchitis

‎Severe

-‎ Most Important Acute


‎Inflammation
‎-Type Of Healing

‎Exudate ‎ ibrin With Neutrophils


F
‎Exudate

‎Uremic Toxins
‎Cause
‎Severe Injury By Bacteria

‎Fibrinous ‎Serosal Layer

‎Lung Parenchyma
‎Labor Pneumonia
‎Site
‎Pericardium

‎Serous Membrane ‎Pleura

‎Peritoneum

‎ ypes Of Serous
T ‎Serous Type Character By
‎Predomination Of Fluids
‎Membrane
‎Fibrinous Type Character By
‎Predomination Of Fibrin

‎Type ‎Severe

I‎ f We Remove It Lead To
‎Severe Hemorrhage

‎Cause
‎Toxigenic Bacteria

‎commonly in GIT
‎Site
‎Upper Respiratory Tract
‎ seudo-membranous
P
‎(Membranous) ‎Examples ‎Diphtheric Laryngotracheitis ‎Amoebic Dysentery

‎Grayish Yellow
‎Grossly
‎Dirty

‎ ecrotic Mucosa With


N
‎Fibrin Deposition

‎Microscopic ‎Dead, Living Neutrophils

‎RBCs

‎Severe

‎Rich In Erythrocytes
‎Exudate ‎ ue To Severe Vascular
D
‎Damage
‎Hemorrhagic
‎Highly Virulent Organisms
‎Cause
‎Bacterial Exotoxins, Endotoxins

‎Examples ‎Smallpox ‎Pancreatitis

‎Exudate ‎Rich In Eosinophils

‎ ue To Hypersensitivity
D
‎Reactions

‎Cause ‎Allergens

‎Allergic ‎Mechanism
‎Hypersensitivity Type 1

‎Site ‎RTS ‎GIT ‎Skin ‎Other Sites

‎Examples ‎Bronchial Asthma ‎Allergic Rhinitis ‎Allergic Eczema

‎Severe

‎Cause
‎Highly Virulent Organisms
‎Necrotizing ‎Focal Ulceration

‎Diffuse Necrotizing Type


‎Main Forms
‎"Cellulitis "

‎Gangrenous Type
‎YOUNES_AL-7AMADY 
‎Onest ‎Gradually

‎Duration ‎prolonged

‎Cardinal Sings ‎generally imperceptible

‎ ollowing Acute
F
‎Inflammation

‎ ecurrent Attacks Of
R
‎Acute Inflammation
‎Pathogenesis
‎ hronic Inflammation
C
‎From Begining

‎Plasma Exudate ‎Absent

‎Sever VD and ⇑VP ‎Absent

‎ ctivation Of Blood
A
‎Absent
‎Plasma Systems
‎Necrosis ‎Present

‎Characters ‎Immune Response


‎Associated With
‎Production Of Antibodies
‎Associated With Repair
‎Plasma Cells ‎Diagnosis Cells

‎ ost Important Cell In


M
‎Macrophages ‎Chronic Inflammation
‎Because They Cause:

‎ ain
M
‎Inflammatory ‎ issue
T ‎ issue
T
‎Cells ‎ estructive
D ‎Fibrosis

‎Lymphocytes

‎Epitheloid Cells

‎Gaint Cells

‎Microscopic ‎Forgeign Body


‎Study
‎Langhan's

‎Tissue Fibrosis
‎ issue Necrosis
T
‎"Destructive Change"
‎Thick Wall Blood Vessels

‎Granulation Tissue

‎ hronic Non-
C
‎inflammation

‎Main Morphology ‎TB

‎Leprosy
‎Granulomatous
‎Sacoidosis
‎ HRONIC
C
‎INFLAMMATION ‎Stypilis

‎Fever
‎Mild

‎Lymphocytic
‎Leucocytosis
‎Monocytic
‎General ‎Lymphadenitis

‎Lymphangitis

‎Anaemia
‎Sings
‎Amyloidosis

‎Local
‎No Local Sings

‎Granulation Tissue

‎TB

‎Common Example ‎Chronic Osteomyelitis

‎Stypilis

‎According Cause: ‎Primary ‎Next

‎Secondary ‎Next
‎Type ‎ ccording Cause
A
‎And Morphology: ‎Specific ‎Next

‎Non-specific ‎Next

‎Resolution
‎Regeneration
‎Fate ‎Healing
‎Fibrosis
‎ ystrophic
D
‎Calcification ‎ OUNES_AL-
Y

‎7AMADY
‎ sually Starts From
U
‎Beginning

‎Slowly, Gradually Onset

‎ ithout Preceding Acute


W
‎Inflammation Reaction
‎Primary
‎TB
‎Persistence Infection
‎Leprosy

‎ rolonged Exposure To
P
‎Non-degradable Foreign ‎Silicosis
‎Cause ‎Material
‎Asbestosis
‎According Cause
‎Auto-immune Reactions

‎Unknown Etiology
‎Sarcoidosis

‎Secondary ‎Result Of Conversion Of


‎Due To Persistence Of The
‎Acute Inflammation To
‎Injurious Agents
‎Chronic Inflammation

‎Specific Injurious Agents


‎Cause
‎Mostly Infective Agents

‎ ononuclear Cells
M
‎Infiltrate

‎Tissue Fibrosis
‎ ype Of
T
‎Characters
‎Chronic ‎Tissue Destruction
‎Inflammation ‎ pitheloid Cells
E
‎Specific ‎( Granuloma )

‎TB ‎Granuloma
‎+
‎Caseous Necrosis

‎Syphilis ‎Granuloma
‎+
‎ oagulative Necrosis
C

‎Leprosy ‎Granuloma
‎Histological Features
‎+
‎Involving Dermal Nerve

‎ oreign Body
F
‎Granuloma ‎Foreign Body
‎ ccording Cause
A ‎+
‎And Morphology ‎Multiple Nucleated Cells

‎Sarcoidosis ‎Granuloma Without


‎Necrosis
‎Non-specific Injurious
‎Agents
‎Cause ‎Mostly Non Infective
‎Agents

‎ ononuclear Cells
M
‎Infiltrate

‎Non-specific ‎Tissue Fibrosis


‎Characters
‎Tissue Destruction
No Epitheloid Cells

‎No Epitheloid Cells


‎( Granuloma )

‎Histological Features ‎No Specific Histological


‎Features
‎YOUNES_AL-7AMADY 
‎ eplacement Of
R
‎Damaged Tissue By
‎New Tissue
‎Definition

‎Labile Cells

‎Stable Cells
‎Cells
‎Permanent Cells

f‎ actors secreted by
‎-macrophage
‎Defi.
‎-fibroblast
‎-inflammatory crellho


‎Effect
‎Growth Factors ‎


‎Mechanism

‎EGF

‎Example ‎FGF

‎Defi. ‎TG


‎ actor Control
F ‎ xtracellular
E ‎Effect
‎Of Repair ‎
‎Matrix

‎Mechanism


‎Repair ‎Example

‎Defi. ‎
‎ ell To Cell
C

‎Intraction ‎Characters


‎Example

‎Regenration

‎Type ‎ ny site
A
‎Fibroplasia
‎ .T
C ‎except CNS
‎ eposition
d
‎Gliosis ‎CNS

‎Labile
‎Regeneration

‎ ype Of
T ‎Regeneration
‎Cell Damage ‎Stable
‎Gliosis

‎Regeneration
‎Damage ‎Permanent
‎C.t Deposition

‎ xtent Of
E
‎Local
‎Tissue Damage

‎Blood Supply
‎2 B
‎Foreign Body
‎Factor Effect Of ‎Age
‎Repair ‎repair better in young age

‎Nutration
‎Nutritional Deficiency
‎Systemic ‎Cytotoxic Drugs
‎Drugs
‎Cytotoxic Drugscortisone

‎D.M
‎Disease
‎YOUNES_ALHAMADY  ‎Endocrinal Diseases ‎Cushing Syndrome
‎ eplacement Of
R
‎Definition ‎Damaged Tissue By New
‎Tissue Of The Same Type

‎ roliferation Of The
P
‎Occur By
‎New Cell

‎Site 2

‎Characters 2

‎Regenration ‎Abrasion
‎Epidermis
‎& ‎ omplete
C
‎Epidermis Injury
‎Mucous Membrane ‎Regeneration
‎Skin Wounds

‎Epidermis Injury ‎Regeneration


‎Example
‎Dermis Injury ‎Fibrosis
‎Mild Injury
‎ rocesses
P
‎Of Repair
‎Liver Cells ‎ omplement
C
‎Acute Hepatitis
‎Regeneration
‎ isturbance Of
D
‎Framework

‎Chronic Hepatitis ‎Fibrosis

‎Alchohol ‎Fibrosis

‎Fibroplasia 17

‎C.T deposition
‎Gliosis 5

‎Repair 2 ‎ ontinuously Dividing


C
‎Definition
‎Cells

‎Characters ‎High Proliferative Activity


‎Labile Cells
‎Skin Epidermal Surface
‎Example
‎Hematopoietic Cells

‎Healing By ‎Regeneration

‎ ell With Limited Capacity


C
‎Definition
‎Of Cell Division

‎Stable Cells ‎Characters ‎Low Proliferative Activity

‎Example ‎Parenchymal Cells


‎Cells
‎Limit Damage ‎Regeneration
‎Healing By
‎Very Damage ‎Fibrosis
‎Mesenchymal Cells
‎Definition
‎ on-dividing Cell Still G0
N
‎Phase

‎Characters ‎Non Proliferative Activity

‎Cardiac Muscle
‎Permanent Cells
‎Example ‎Smooth Muscel
‎Nerve

‎Cardiac Muscle
‎YOUNES_ALHAMADY  ‎Fibrosis
‎Smooth Muscel
‎Healing By

‎Gliosis ‎Nerve
‎Steps

‎Haematoma Formation

‎ ocal Inflammatory
L
‎Response
‎Traumatic Inflammation

‎ hagocytosis With
P
‎Secretion Growth Factors

‎ ormation Of Soft Callus


F
‎" Procallus" ‎ allus: Tissue Make
C
‎Collection Bw 2 End Of
‎ ealing Of
H uformation of chondroblasts and osteoblasts from
prei and endostum ‎Bone
‎Bone Fracrure
‎ ormation Provisional
F
‎Callus
‎Non Amellar Bone

‎Formation Hard Callus


‎Lamellar Bone

‎Callus Remodeling
‎By Osteoblasts

‎ - Regeneration Of
8
‎Bone Marrow

‎Complications

‎Fibrous Union

‎Non-union
‎YOUNES_ALHAMADY 
‎Delayed Union
I‎ nvasion Of The Body By
‎Definition ‎Pathogenic Micro-organism

‎Bacteria
‎More Commonly
‎Causes ‎ Virus

‎Fungi ‎Less Commonly

‎Skin Mucous Memberane ‎Ventral Disease

I‎ ngestion Of Contaminated
‎HAV, T.B
‎Water , Milk, Food

I‎ nhalation Of
‎Influenza
‎Exogenosis ‎Contaminated Air

‎Blood Transfusion ‎HBV, HCA

‎Sexual Transmission ‎AIDS, HBV

‎Transplacental ‎Toxoplasmosis, HBV

‎Method ‎Hypersensitivity Reaction ‎HR

‎ trept Viridans In
S
‎ hange Normal Bacteria
C
‎ hange Position Of
C ‎Mouth
‎In Body To Pathogenic
‎Bacteria
‎Bacteria ‎E Coli In Intestine

‎Endogenosis ‎ e-activation Of Old


R
‎Infected

‎ eactive Old Infected


R
‎Lesions
‎Infection
‎Local
‎Lymphangitis
‎Lymphatic
‎Lymphadenitis

‎Bacteria
‎Plasma
‎Hepatitis B Virus
‎Blood
‎Herpes Virus
‎Spread ‎Cells
‎HIV

‎Pleural Cavity
‎Tissue Fluids
‎Peritoneal Cavity

‎Neural ‎Rabies Virus

‎Respiratory System
‎Natural
‎Urinary System

‎Toxin Production ‎Cell Injury

‎Direct ‎Inflammation
‎Cause Disease
‎By ‎ acteria Ag From
B
‎Hypersensetivity
‎Nontoxin Organism

‎Bacteremia

‎Toxemia
‎Blood Spread
‎Bacteria Infection ‎Septicemia

‎Pyaemia

‎Weak ‎Bacteraemia ‎Bacteria Only On Blood

‎Type ‎ acteria Toxin Only In


B
‎Toxemia
‎Blood

‎ acteria + Their Toxin In


B
‎Virulent ‎Septicemia
‎Blood

‎YOUNES_ALHAMADY  ‎ hrombophilipitis +
T
‎Pyaemia
‎Septic Emboli In Blood
‎ Types Of Nephrotic
‎. ‎.. ‎... ‎....

‎ embranous
M ‎Membranoprolifera
‎Minimal Change ‎ ocal Segmental
F
‎ ‎Glomerulonephriti ‎tive
‎Disease ‎Glomerulosclerosis
‎s ‎Glomerulonephritis

‎Incidence ‎Children ‎Adult ‎Adult ‎Any Age


‎ hickening Of
T
‎Lipid Accumulation In ‎ hickening Of
T
‎ ocal Segmental
F ‎Glomerular Basement
‎Proximal ‎Glomerular Capillary
‎ Micro ‎Sclerosis, ‎Membrane Only
‎Intracytoplasmic ‎Walls And
‎Hyalinization ‎"Lobulated
‎Tubular Cells ‎Basement Membrane
‎Architecture"

‎ ve for ICx
- ‎ Ve for ICx
-
‎ E.M ‎+Ve for ICx Deposition ‎+Ve for ICx Deposition
‎Deposition ‎Deposition

‎ Ve for Ig
- ‎ Ve for IgM
+ ‎ Ve for IgG Deposition+
+ ‎ Ve for IgG Deposition+
+
‎ IF
‎Deposition ‎Deposition+C3 ‎C3 ‎C3

‎ ll Characterized By
A
‎ inimal Change
M
‎ Gross ‎Mild Bilateral Kidney
‎Glomerulonephritis
‎ ‎ ‎
‎Enlarged Except :

‎ ocal Segmental
F
‎ ll Cause
A ‎Glomerulosclerosis
‎ Histo ‎Enlargement ‎ ‎ ‎
‎Glomeruli Except: ‎ inimal Change
M
‎Glomerulonephritis

‎Good Prognosis

‎ I‎n Minimal
‎Prognosis ‎Change Disease ‎ ‎ ‎
‎Prognosis To CRF

‎In Other Type


‎YOUNES_AL-7AMADY 
‎ Types Of Nephritic
‎. ‎.. ‎... ‎....

‎ cute
A
‎Membranoprolifera
‎Postinfectious ‎ apid Progressive
R I‎gA Nephrophathy
‎ ‎tive
‎Glomerulonephri ‎Glomerilonephritis ‎(Berger Disease)
‎Glomerulonephritis
‎tis

‎Incidence ‎ Children ‎Any Age ‎Children+adult ‎Any Age

‎ hickening Of
T
‎ Hypercellilar ‎Glomerular Basement
‎ rescent
C
‎ Micro ‎ Neutrophils ‎Different Change ‎Membrane Only
‎Formation ‎"Lobulated
‎ Monocytes
‎Architecture"

‎ +Ve for ICx ‎ Ve for ICx


-
‎ E.M ‎+Ve for ICx deposition ‎+Ve for ICx deposition
‎ deposition ‎deposition

‎ +Ve for IgG+IgM ‎ Ve for IgG Deposition+


+ ‎ Ve for IgA Deposition+
+ ‎ Ve for IgG Deposition+
+
‎ IF
‎ deposition +C3 ‎C3 ‎C3 ‎C3

‎ All Characterized By
‎ Gross ‎ Mild Bilateral Kidney ‎ ‎ ‎
‎ Enlarged

‎ ll Cause
A
‎ Histo ‎ Enlargement ‎ ‎ ‎
‎ Glomeruli
I‎n Acute
‎Good Prognosis ‎Postinfectious
‎Glomerulonephritis

‎ are In Acute
R
‎Postinfectious
‎Prognosis ‎Glomerulonephritis ‎ ‎ ‎

‎Prognosis To ARF
‎ ommon In Rapid
C
‎Progressive
‎Glomerulonephritis

‎Prognosis To CRF ‎In Other Type

‎YOUNES_AL-7AMADY  ‎ embranoproliferative
M
‎Glomerulonephritis Is
‎ Type Of:

‎Nephritic ‎Nephrotic
Vasculitis

* it is inflemation of the blood vessels wall


the immuon mediated vasculitis
poly arteritis nodosa kawasaki desease Buergers disease Wegners disease Takayasu disease temporal arteritis*

size medium and small arteries large & medium large ,medium & small
superfascial temporal artery
ESPICALLY ____ coronary artery arteris of extermtiies arteries of kidney & lung ____
retenal artery
OTHER mucoctenous lymph Thromboangitis Gaint cell
_____ _______ pulse less disease **
NAME node syndrome obliterans arteritis
Age all ages Infant & children yeang male 40 to 50 years yeang & middle female old age above 50 years
1.lyemphadenopathy
2.lyphangitis
acossated heptitis B infaction smoking ____________
adema & arthema of
mucoctenous membrane
effect arteries of leads to thrombosis formation of thrombosis syptomes involve pulse abcence Severe unilatral
many orgens wich couse MI and macroabcess kidney and lung dicrease in prussere headache
NOTES ther is nudules which nerve also involve so there is hypertention , blandness
form fiprous nudules lag pain & gangren if effect the jow claudication
then rupture at end occur disceanding artery

P-ANCA AECA AECA c-ANCA HLA __

Notes

* temporal arteritis is the most common type of vasculitis

* *other name of Takayasu disease : 1. occlusive thromboaortopathy 2.aortic arch syndrome


Primary CNS Tumor
Meningiomas Glioma
(The Most Common Benign Intracranial Tumer)
Astrocytoma (80% Of Adult 1ry Tumor) (Mutation In IDH1,IDH2) Oligodendrogliomas(deletion of chromosom 1p,19q) Ependymomas
Association With Genetal Disorder: NF2,Gorlin Syndrome
Benign Meningioma Atypical Anaplastic Pilocytic Diffuse Anaplastic Glioblastoma Multiform(Mutation In P53&RB) Oligodendroglioma Anaplastic Ependymoma Anaplastic
1ry (de novo) , 2ry (diffuse fibrillary astrocytoma) (The Most Malignant Astrocytoma)
Meningioma Meningioma Oligodendroglioma Ependymoma
Grade I ii iii I ii iii iv ii iii ii iii

Age Female Predominace Common In Children Adult (30-50) Years Adult >40 Years Old Age Adult Adult All age 1-90 years All age 1-90 years
(male=female) (male=female)
External-Internal (Ventricular) -Cerebellum -Brainstem Cerebellum Cerebellum -Cerebellum Cerebellum Cerebellum In Children: Typically In Children: Typically
Site Near 4th Ventricle Near 4th Ventricle
-Spinal Cord-Opetic Nerve -Rare In Brainstem -Spinal Cord *White Matter
In Adult: Spinal Cord In Adult: Spinal Cord
Associated With NF2 Associated With NF2
Gross -Round Well Formed-Capsulated-Whorly Pattern Soft Gray Mass Infiltrating Mass -ill Defined -ill Defined -Red Line Hemorrhage -Well defined grey mass -Well Defined Grey -Well Demarcated Mass -Well Demarcated
-Grayish_White Nodule -Firm In Cosistency Cystic Lesion Without Destruction -Destructive Surrounding Tissue - High Destructive Surrounding Tissue -Gelatination Mass -Grey Soft To Firm Mass
-Ring Enhancement In MRI -Calacification -Calacification -Hemorrhage -Grey Soft To Firm
-Hemorrhage -Necrosis -Hemorrhage

Micro -No Atypia -Hypercellularity -Hypercellularity -Biphasic Pattern -Mild To Moderate -High Cellularity -High Cellularity 3 Cs: -High Cytology Atypia -High Ependymal -High Cellular
-Low Mitotic Rate<4 -Intermediat -High Mitotic -Cystic Like Spase Cellularity -Cellular And Nuclear -Marked Cellular And Nuclear .Clear Halo of Cytoplasm -High Mitotic Activity Proliferation With Proliferation
-Psammomatus Mitotic Rate>4 Rate>20 -Bibolar Cells With -Small Dense Nuclei Pleomorphism Pleomorphism -Necrosis Monotonous Dark -High Cytology
.Calcification
-Syncytic -Macronucleoli -Macronucleoli Nuclei Atypia
Hairlike Process -No Mitotic Activity -High Mitotic Activity -High Mitotic Activity .Checken Wire Appearance -Vascular Proliferation
(Meningiothelial) _Larg Cell _Larg Cell -True Rosette -High True Rosette
-Transitional(Mixed) _Prominent _Prominent -Rosenthal Fibers -No Necrosis -No Necrosis -Serpentine Necrosis of Branching Capillaries -Calacification
(It's Tumor Cells Around Lumen) -High Perivascular
-Fibrioblastic Nucleoli Nucleoli -Eosinophilic Granular -No Vascular -No Vascular Proliferation -High Vascular Proliferation -monotonous round cells - Branching Capillaries -Perivascular Pseudorosettes
-Angiomatuous _Necrosis Bodies Proliferation (Glomerular Vascularization) -fried egg appearance of Pseudorosettes (Pseudo > True)
-Microscytic -Sheet Like Growth - Rhabdoid -Fibrillary -Pseudopalisading cell (It's Tumor Cells Around Blood Vessels) -High Mitosis
-Secretory -Clear Cell - Papillary Background -prominent central nuclei (Pseudo > True) -High Necrosis
-Metaplastic -Chordoid -No Or Few Mitosis (Pseudopalisading)
-Lymphoplasmacyte-Rich -No Necrosis
Prognosis Depends on size location grade Good Good good Poor Better than astrocytoma Poor With Recurrence Poor Poor

Younes-AL7amadi
P-Medicin 37

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