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Pathology Mindmaps 2023 Youne
Pathology Mindmaps 2023 Youne
D
Defination Alteration In Structure,
Function Resulting From
Inabilty Of Cell To Adapt
With Ingurius Agent
Ischemia
Anemia
arbon Monoxid
C
Posning
Bacteria
Infection Viruses
Toxins
Hypersensitivity
Drugs
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
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
⇓Production Of Protein
Mediatory
Atrophy ⇓Production Organelles
occur after denervation
Example Ischemic Atropy
Gross
Organ Small
Examination
Mic Cell Small
Nuclei Small
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
Cardiac M.
Not Occur In
Skeletal M
Neurons M.
Gross
Organ Enlarged
Examination
Mic
Cell ⇑Number
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
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
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
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
I nability To Return To
Previous Normal State
Long Duration
Maximal Intensity
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
Caogulative
Caseous
Necrosis Fat
Next
Liquefactive
Fibrinoid
Type
Gangrenous
Apoptosis Next
YOUNES_AL_7AMADY
I rreversible Death Of
Definition
Group Of Cells
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
Brain Infraction
EXAMPLE
Pyogenic Abscess
YOUNES_ALHAMADY Pus
Definition
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
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
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
Plasma Mediators
Next
Chemical Mediator
Cellular Mediator
Next
V.C
V.D
Vascular Event
⇑VP
Leukodiapedesis
INFLAMMATION Phagocytosis
Loaclaized
Suppurative
Diffuse
Serous
Pseudomembranous
Fibrinous
Non-suppurative
Serofibrinous
Next
Hemorrhageic
Type
Necrotizing
Allergic
Primary
Causes
Scondary
Chronic Inflammation
Specific
Causes & Morphological
Non-specific
If Mild
Resolution
Septicemia
Blood
Pyemia
Bad
Chronicity
Non Suppurative ⇒
Suppurative
YOUNES_AL-7AMADY
Main Mediators Sources Action
erotonin
S Mast Cell - VD
Histamin Platelets -⇑VP
- 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
Thromboxaine A2
V.C Cause
Leukotrienes C4, D4, E4
Histamin
Serotonin
Cause
Prostaglandins
V.D
Bradykinin
Transudate
Due to ⇡ IVHP
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
ecreased Intravascular
D
Osmotic Pressure
Loss Of Fluid
Cause I ncrease Concentration of
RBCs
Stasis
Increase Vasosity
Leukodiapedesis
Next
Chemotaxis
Cellular Event Next
Phagocytosis YOUNES_AL-7AMADY
Next
Activation of WBCs
Cause
L-selectin
On Leukocytes
S-selectin
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
LTB4
Cause Chemotactic Factors
C5a
Firm Adhesion
CELLULAR Mediated By Interaction Of
EVENT 1
I ntegrin With Endothelial
Adhesion Molecules
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
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
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
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
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
I ncrease Permeability
Mechanism (Widening Of Gaps)
Hematogenous Part
Protein
Type
Histogenous Part
WBCs
Dilute
Neutrophile Macrophage
Giant Cells
Pus Cells
Fate Endothelial Cells
Apoptosis
Foam Cells
YOUNES_AL-7AMADY
Definition
Necrotic Tissue
Neutrophils
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
ctivation Of Blood
A
Plasma Systems
Present
Mostly Non-specific
Characters Suppurative
Necrosis
Present Only In : ecrotizing Type Of
N
Non-suppurative
Inflammation
ain
M Neutrophils
Inflammatory Cells Macrophage
Pus Cells
Microscopic Eosinophils
Fibrin Deposition
Thin Wall
Examination Congested Blood Vessels
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
Lymphadenitis Lymphangitis
Sings
Septic Shock In Severe Acute Infection
Loss Of Function
Suppurative Next
Type
Non-suppurative Next
Resolution
Removal Cause
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
ecrotizing
N
Suppurative Inflammation
Acute
Inflammation Cause
Streptococcus Aureus
ecrets Streptokinase
S
Diffuse Lead To Dissolve Matrix
Of Tissue And Fibrin
Cellulitis
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
Small Abscess
oil
B
"Furuncle" Hair Follicles
Sebaceous Glands
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
Granulation Tissue
Healing By
Fibrosis
Sinus
Tract With One Opening
Tract Formation
Fistula
Tract With Tow Opening
ocal Defect On
L
Endothelial Surface
Necrosis
Stages
Inflammatory Ulcer
Different Diagnotic Bw: Slight Elevation Of Edge
-Inflammatory Ulcer
Malignant Ulcer
-Malignant Ulcer Slight Elevation Of Edge
Direct
With Enlargement Of Abscess
Non-evacuated Lymphangitis
In Lymphatic Vessels
Lymphatic
Spread Lymphadenitis
In Lymph Nodes
Weak
Bacteraemia Bacteria Only On 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
Mild
Exudate
Mucin Exudate
Severe
Uremic Toxins
Cause
Severe Injury By Bacteria
Lung Parenchyma
Labor Pneumonia
Site
Pericardium
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
RBCs
Severe
Rich In Erythrocytes
Exudate ue To Severe Vascular
D
Damage
Hemorrhagic
Highly Virulent Organisms
Cause
Bacterial Exotoxins, Endotoxins
ue To Hypersensitivity
D
Reactions
Cause Allergens
Allergic Mechanism
Hypersensitivity Type 1
Severe
Cause
Highly Virulent Organisms
Necrotizing Focal Ulceration
Gangrenous Type
YOUNES_AL-7AMADY
Onest Gradually
Duration prolonged
ollowing Acute
F
Inflammation
ecurrent Attacks Of
R
Acute Inflammation
Pathogenesis
hronic Inflammation
C
From Begining
ctivation Of Blood
A
Absent
Plasma Systems
Necrosis Present
ain
M
Inflammatory issue
T issue
T
Cells estructive
D Fibrosis
Lymphocytes
Epitheloid Cells
Gaint Cells
Tissue Fibrosis
issue Necrosis
T
"Destructive Change"
Thick Wall Blood Vessels
Granulation Tissue
hronic Non-
C
inflammation
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
Stypilis
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
rolonged Exposure To
P
Non-degradable Foreign Silicosis
Cause Material
Asbestosis
According Cause
Auto-immune Reactions
Unknown Etiology
Sarcoidosis
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
ononuclear Cells
M
Infiltrate
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
Alchohol Fibrosis
Fibroplasia 17
C.T deposition
Gliosis 5
Healing By Regeneration
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
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
I ngestion Of Contaminated
HAV, T.B
Water , Milk, Food
I nhalation Of
Influenza
Exogenosis Contaminated Air
trept Viridans In
S
hange Normal Bacteria
C
hange Position Of
C Mouth
In Body To Pathogenic
Bacteria
Bacteria E Coli In Intestine
Bacteria
Plasma
Hepatitis B Virus
Blood
Herpes Virus
Spread Cells
HIV
Pleural Cavity
Tissue Fluids
Peritoneal Cavity
Respiratory System
Natural
Urinary System
Direct Inflammation
Cause Disease
By acteria Ag From
B
Hypersensetivity
Nontoxin Organism
Bacteremia
Toxemia
Blood Spread
Bacteria Infection Septicemia
Pyaemia
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
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
cute
A
Membranoprolifera
Postinfectious apid Progressive
R IgA Nephrophathy
tive
Glomerulonephri Glomerilonephritis (Berger Disease)
Glomerulonephritis
tis
hickening Of
T
Hypercellilar Glomerular Basement
rescent
C
Micro Neutrophils Different Change Membrane Only
Formation "Lobulated
Monocytes
Architecture"
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
YOUNES_AL-7AMADY embranoproliferative
M
Glomerulonephritis Is
Type Of:
Nephritic Nephrotic
Vasculitis
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
Notes
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