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m 

LECTURE ON PATHOLOGICAL
ANATOMY IS PRESENTED BY
AS.PROF. SERDOBINTSEVA T.S.

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à Structures of living systems are not
constant
à They are destructured and restored
continuously
à All living organisms absorb and
extract proteins, lipids (fats),
carbohydrates, and their
components as well as water, ions,
and pigments.
|
 
à All living systems including cells and
extra cellular matrix absorb fresh
substances and extract products of
their metabolisms.

à Polypeptides, polynucleotides and


polysaccharides play the most
significant role to metabolize.

 
à Every organism (body) consists of
organs

à Every organ consists of tissues

à Tissue consists of cells

à Cell consists of ultrastructures


u
 

à There are tissues: epithelium,


à derivations from mesenchymal tissue (
connective tissue, fatty tissues, bones,
cartilages, muscles, vessels )
à Nervous tissues
à Bone marrow tissues
à Lymphatic tissues
¬
 

à The chain of changes develops


under super normal (hyper
normal) and pathological
processes inside cells and extra
cellular matrix

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à ETIOLOGIC AGENT MAY BE EVERY
ONE EXOGENIC OR INTRAGENIC
à BUT CHAIN OF CELLULAR CHANGES
CONSISTS OF STAGES AS FOLLOW:
1ADAPTATION
| REVERSIBLE CHANGES
 IRREVERSIBLE CHANGES as
NECROSIS(CELLULAR DEATH)
u autolysis and heterolysis G
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à Autolysis is termed self digestion


by lysosomes enzymes .

à Heterolysis is termed digestion


by lysosomes of other cells
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à Reversible changes or cellular
degeneration or parenchymal dystrophy
à According to metabolic disturbance
there are protein, fatty, carbohydrate, and
ion degenerations.
According to localization
there are parenchymal (cellular),
mesenchymal (stromal-
(stromal-vascular),
And mixed reversible changes or
degenerations Œ
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à Causes or etiology:
à Hypoxia
à Ischemia
à Physic agents
à Chemical agents including medicine, drug
à Infective agents
à Immunologic reaction
à Genetic injury
à Nutrition disbalance 10
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Mechanisms of reversible injury


à Decomposition of membranes
à Hyper infiltration of substances
(intracellular accumulation)
à Unnatural syntheses
Disbalance of calcium metabolism
à ATP depletion
à Free radical-
radical-induced injury
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Cellular injury depends on cell:


à 1 type (myocardial cells dies in |0-
|0-0
min. ,but epidermis cells dies in weeks,
after cause (etiologic agents ) acted.
à | genetic makeup
à  adaptability ( hepatic cells are more
adaptive cells, then neurons)
1|
à u status( normal or hypertrophic)
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Cellular injury depends on injury:


1 type (ischemia or infective agent)
| its duration
 its severity

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à Myocardiac cell becomes no contractile in1
in1
to | minutes after ischemia stated.
à It dies in |0
|0--0 minutes after ischemia
started
But ultra structural evaluation of changes
appears in |- hours after ischemia started
and
light microscopical evaluation becomes
possible in 0-1| hours after ischemia
started. 1u
  
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INTRACELLULAR RESPONSE INCLUDS
1 Aggregation of intramembranous particles
| Endoplasmic reticulum swelling
 Dispersion of ribosomes
u Cell swelling
¬ Clumping of nuclear chromatin
0 Mitochondrial swelling
G Small densities within mitochondrii

   
 
 !
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10
m# 
#%" 
à 1classification according to location
à Parenchymal (cellular) degeneration or
dystrophy

à Stromal vascular

à Mixed

1G
m# 
#%" 
| classification according to type
metabolism abnormality
à Disproteinosis
à Lipidosis
à Carbohydrate abnormality

à Mineral abnormality
à Pigment abnormality
1
mm&
 
'
(  )
LIPID METABOLISM ABNORMALITY

à INTRACELLULAR ACCUMULATION

à STROMAL VASCULAR
ACCUMULATION


  
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Intracellular accumulation
1 Cellular swelling or hydropic
dystrophy

| Lipid accumulation

 Glycogen accumulation |0
  
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Classification according to cellular


disproteinosis
1 Cellular swelling or hydropic (vacuole)
dystrophy or degeneration
| Hyaline droplet dystrophy or
degeneration
 Hyper keratinization
|1
m! 


à Ions disbalance between sodium


and potassium with water bubble
formation

à Protein infiltration within cells

à Cellular membranes destruction


||
m! 


à Diseases:
à 1Infective diseases
à | Nephropathy
à  Chronic glomerulonephritis
à u Alcoholic disease
à Alzheimer disease

|
m! 


Organs are as follow:


1 Kidney
| Liver
 Skin (epidermis)
u Brain (neurons)

|u
m! 

The tubular
vacuolization and
tubular dilation here is
a result of the toxic
effect of ethylene
glycol poisoning.

The kidney

( 
  

à Here are Mallory


bodies (the red
globular material)
composed of
cytoskeletal filaments
in liver cells
chronically damaged
from alcoholism

|0

m 
mm&
 
*

m() +

,

PARENCHYMAL LIPIDOSIS
IS CHARACTERIZED BY ABNORMAL
ACCUMULATION OF TRIGLYCERIDES
WITHIN PARENCHYMAL CELLS
ORGANS: THE LIVER,
THE MYOCARDIUM,
THE KIDNEYS.
.
|G
*

m() 

(  
à ETIOLOGY IS TOXINS, PROTEIN
MALNUTRITION, DIABETES
MELLITUS, OBESITY AND ANOXIA.
à PATHOGENESIS IS
DISBALANCE BETWEEN REMOVE,
UTILISATION AND EXCRETION
OF LIPIDS BY HEPATOCYTES.

|
'
( )   *
*

 
à EXCESS ABSORPTION OF fatty acids
and triglycerides
à Reduced Utilization of them on
mitochondrii
à Decrease in apoprotein production



( 
* ' 
&  
(
à FIGURATIYE NAME IS GOOSE
LIVER

à DISEASES ARE
1 ALCOHOL ABUSE
| DIADETES MELLITUS
 OBESITY
u STARVATION
¬ POISONING 0

( 
* ' 
&  
(

Gross sample

Micro sample
stain is Sudan  1
 


à REVERSE TO NORMAL
STRUCTURE

à HEPATITIS

à CIRRHOSIS

|
à *

m() 

( ( 

  
' $


*

m() 

( ( 

à ETIOLOGY
HYPOXIA, INTOXICATION .
à PATHOGENESIS
LACK of OXYGEN LEAD TO decreasing
oxidative phosphorylation
anaerobic glycolysis
decreasing ATP synthesis
mitochondrion destruction
inhibition of fatty acid oxidation

toxins cause severe damage of membranes


and enzyme systems
u
à GROSSLY
' $- 
# #

APPEARANT BANDS OF YELLOWED


MYOCARDIUM ALTERNATING WITH
BANDS OF DARKER, RED-BROWN
UNINVOLVED HEART ³TIGERET
³EFFECT´ ± TIGER HEART´

Severe fatty change is


produced by profound
hypoxia with diffused yellow ¬
±colored myocardium
1Small droplets of lipid
are found within
myocardial cells.
Prolonged moderate
hypoxia results in local
intracellular fat deposits
according to venous
blood collection Micro sample
stain is Sudan 
0
*

m() 
( 
 
 ) 

à Atherosclerotic plaque contains
cholesterol and its esters within
macrophages and smooth muscle cells
(foam cells).
After cell death, cholesterol and its
esters are seen out of cells.

G
!
.
grossly

Stage of atherosclerosis
is termed lipidosis

micro

Foam cells within


atherosclerotic plaque

m ( 

 &

à Carbohydrate Parenchymal abnormality
is divided into disorders of glycogen and
glycoproteids.
Diseases are diabetes mellitus and
hereditary glycogen storage diseases
named Glycogenoses or tezaurismosis
tezaurismosis..


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à Hyperglycosemia lead to
glycogen accumulation
within renal tubular
epithelium
à Best¶s stained by
Carmine
à Crimson ±colored
granules of glycogen

u0
m 

à The end

u1