m




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

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

0
m



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
m




à Autolysis is termed self digestion

by lysosomes enzymes .

à Heterolysis is termed digestion

by lysosomes of other cells
m



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
m



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
m




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
11
 m




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)
m




Cellular injury depends on injury:

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

1
 m 
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
   

m 
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
1¬
   
 
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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

1Œ
   

m 

Intracellular accumulation
1 Cellular swelling or hydropic
dystrophy

| Lipid accumulation

 Glycogen accumulation |0
   

m 

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

|Œ

( 
*
'
& 
(
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

|
Ã *

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
Ã 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..

Œ
 "$

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