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omar sawas

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Transcript of Pathology

* Cellular Injury :
- cell adaptations
- cell injury ( morphology , reversible Vs irreversible )
- Mechanism of cell injury
- Apoptosis Vs Necrosis
- Intracellular Accumulations
- Calcification
First Exam
Second Exam
Syllabus + What is the Subject ?!
First Exam
Second Exam
Final Exam
How to Study ?
- 3 Credit Hours
- 2 lectures / week
- Lab : No Quizzes
Molecular and morphologic changes: structural alterations in cells or tissues.
Molecular and immunologic aspects of the disease/tissue/organ.

Aspects of disease

Etiology/ cause:
Genetic: mutations
Acquired: infectious, nutritional, chemical..

Aspects of disease

- Pathology: the study (logos) of suffering or disease (pathos).
- The study of the structural, biochemical, and functional changes in cells, tissues, and organs that underlie disease.
- A bridge between the basic sciences and clinical medicine.
- Uses molecular, microbiologic, immunologic, and morphologic techniques trying to reach a diagnosis and explanation.


Biopsies: excisional and incisional.
Smears: exfoliative and fine needle aspiration.

Diagnosis in Histopathology

Subspecialties: neuropathology, dermatopathology,
oral pathology……

Anatomic pathology

Anatomical/ surgical pathology or histopathology: Gross examination and microscopic examination to reach a diagnosis.
Clinical pathology: hematology, microbiology, immunology and biochemistry.

Classification of Pathology


In clinical life

Functional derangements and clinical manifestations: the end results of changes in cells and tissues.
(functional abnormalities leading to the clinical manifestations of disease and the way it progresses).

Pathogenesis: sequence of events in the response of cells or tissues to the etiologic agent,
from the initial stimulus to the ultimate expression of the disease. (mechanism).

Aspects of disease

- General pathology: reactions of cells and tissues to abnormal stimuli. Cell injury,
inflammation and repair, hemodynamic disorders, genetic disorders, immune system diseases, infectious disease and environmental diseases.
Systemic pathology: alterations in specialized organs and tissues in diseased status.

- General Vs systemic
- Book , slides , sheets ?!
5 topics
- Cell injury
- Inflammation
- Tissue Repair
- Neoplasia
- Hemodynamic
- 4
# ( cause / mechnism / morphology / function )
* how we deal with patients ?
( deal with biopsies from ORGANS or TISSUES )
( deal with cells , eg : thyroid mass or breast mass )
whole mass
for examine the thyroid & breast mass

like the pap smear

# ( Histopathology : tissue , organ , biopsies )
# ( cytopathology : cells , smears )
# ( hypertrophy, hyperplasia, atrophy, metaplasia )
- Mechanism
- Example
( lec 2 )

Past year : all these are adaptive ways except:

a- hypertrophy
c- reversible cell injury
d- hyperplasia
# pathological to have hyperplasia of the endometrium
# physiological to have hyperplasia of the myometrium
# ciliated columner >> stratified squamous
stratified >> columner
# irreversible = cell death
# hypoxia (deficiency ) Vs ischemia ( decrease )
how can i know that there is injury ?
# function before morphology
# cytoplasm
# Plasma membrane
# mitochondria
# ER
# nucleus
Necrosis Vs apoptosis
# ischemia
# hypoxia
# infarction
# coagulative
# Liquefactive
# Gangrenous
Try to understand .. not memorize
# Coagulative # Caseous
# Liquefactive # Fat
# Gangrenous # Fibrinoid
( no drug for tt )
( status )
low ATP leads to 3 things
protein + heme !
Release of cytochrome C --> activation of caspases --> activation of nucleic acid -- > fragmentation of the cell.
* caspases = enzyme degrade proteins
ferrous : Fe +2
ferric : Fe +3
# Catalase : H2O2 --> H2O
# Superoxide disumtase : O-2 -- > H2O2 + O2
# Glutathione peroxidase : OH or H2O2 --> H2O
2OH- + 2 GSH --> 2H2O + GSSG
* GSSG : oxidized form
* GSH : reduced form , important for cell safety
if its present , the reaction will take place
# lipids
# proteins
good DNA = good protein
#1 ATP depleation
#2 Mito. Damage
#3 Influx C
#4 ROS
#5 Membrane
#6 DNA & Proteins
#7 chemical
# phagocytosis by macrophages but NO inflammation
A - Normal
B- Apoptosis
C- Necrosis ( pulse batch Exam )
# 2 pathways for apoptosis :
intrinsic & extrinsic
sensors of damage
Fatty change
lysosomal storage disease
antitrypsin defecincy
silica and carbon
cholesterol-laden macrophages: macrophages filled with cholesterols (foamy macrophages)
urinary bladder
Proteinuria hypoalbuminemia
( found in plasma cells undergoing excess production of immunoglobulin. )
found in the brain and it is the primary marker of Alzheimer disease
black lung disease


marker for fee radical injury ,
not dangerous
( screen against UV )
( golden brownish yellow pigment ) / Prussian-blue stain
accumulation in
* ( parathyroid increase [ca] in blood )

- Susceptibility to infections
- Defective innate immunity

- Delayed repair
- Delayed clearance of debris and necrotic tissue
- Lack of stimuli for repair

Consequences of Defective Inflammation

Chronic Inflammation

- Allergic reactions : ( relationship between T & macrophages )
- Autoimmune disorders
- Atherosclerosis : ( accumulation cause CI)
- Ischemic heart disease

Consequences of Excessive Inflammation

- Ulceration
Ulcer: Local defect or loss of continuity in surface epithelia

- Chronic abscess cavity

- Induration & fibrosis

- Thickening of the wall of a hollow organ

- Caseous necrosis

Morphologic Appearance of Chronic Inflammation

Examples of Granulomatous Inflammation

Histopathology of Granuloma

A distinctive form of chronic inflammation characterized by collections
of epithelioid macrophages→ GRANULOMA

Granuloma, in addition to epithelioid macrophages, may have one or more of the following:

- a surrounding rim lymphocytes & plasma cells
- a surrounding rim of fibroblasts & fibrosis
- giant cells
- central necrosis due to hypoxia & FR injury
e.g. caseous necrosis in Tuberculosis (TB)

Granulomatous Inflammation

- Plasma cells

- Eosinophils
Parasitic infections and allergic conditions
Recruited by Eotaxin (chemokine) and other mediators
Release Major Basic Protein

- Mast cells
Allergic reactions
release histamine & AA metabolites

- Neutrophils with necrotic cells , persistent microbes, or mediators → Acute on Chronic Inflammation

Other cells in chronic inflammation

Macrophage-lymphocyte interaction

- Proteases
- Complement and clotting factors
- Oxygen species and NO
- AA metabolites
- IL-1 & TNF
- Growth factors (PDGF, FGF, TGFb)

Products Activated macrophages

* Macrophages:

- Derived from circulating monocytes >> tissue >> Macrophage

- Scattered in tissues & act as filters

* Examples :
- Kupffer cells (liver),
- Sinus histiocytes (spleen & LN)
- Alveolar macrophages (lung),
- Microglia (CNS)

Macrophages & the Mononuclear Phagocytic System

- Progression from acute inflammation
Tonsillitis, osteomyelitis ( inf of bone marrow ) , etc.

- Repeated exposure to toxic agent
Silicosis, asbestosis, hyperlipidemia, etc.

- Persistent viral infections

- Persistent microbial infections difficult to clear
Mycobacteria, Treponema, Fungi, etc.

- Immune mediated (Autoimmune ) disorders
Rheumatoid arthritis, Systemic Lupus,

Under what circumstances does chronic Inflammation develop ?

** Chronic inflammatory cell infiltrate :
- Macrophages
- Lymphocytes
- Plasma cells

** Tissue destruction

** Repair by :
- Neovascularization
- Fibrosis

Chronic Inflammation Components :

Inflammation of prolonged duration, in which there is :
Continuing inflammation
Tissue injury
With or without repair

Characterized by :
- Persistent injurious agent
- Inability of the host to overcome the injurious agent



3- Leukocytosis :
Due to action of cytokines & Colony Stimulating
Factors (CSFs) on BM , WBC count rises to
15,000- 20,000cells/ ml. or more.
Bacterial infections : Neutrophilia
Viral infections : Lymphocytosis
Parasitic infections & allergy : Eosinophilia

4- Increased heart rate, BP, anorexia… etc

5- Severe infections , Septic shock, DIC…
Induced by: TNF

Caseating Granuloma

Histopathology of Granuloma


Activated mainly by IFN-‎g secreted from T lymphocytes,
bacteria, Chemokines, C5a, PDGF, TGF α, fibrinopeptides, fibronectin, collagen
breakdown fragments
Other cytokines from lymphocytes, eosinophils…etc

Increased cell size : Epitheloid cell
Increased lysosomal enzymes, NO, ROS….
More active metabolism, with greater ability to kill ingested organisms

Result in death of macrophage or accumulation of many macrophages at site of injury ,



Chronic inflammation

Duration: days to years

Predominance of lymphocytes and macrophages

Vascular proliferation and fibrosis

Acute inflammation

Duration: minutes to days

Predominance of neutrophils

Fluid & plasma protein exudation

Inflammation Comparison:


Systemic Effects of Inflammation
(Acute phase reactions)

Mainly produced by cytokines : TNF, IL-1 & IL-6 from leukocytes:

1- Fever :
Endogenous pyrogens: synthesis of prostaglandins
Exogenous from bacteria : IL-1 & TNF

2- Elevated plasma level of acute phase proteins
C- reactive protein **
Fibrinogen** correlates with level of ESR
Serum amyloid A

3-Catabolism ( in general , we need more ATP )
4-Increased slow wave sleep ( need more sleep )
5-Hypotension and other hemodynamic changes

AFB Stain in Caseating Granuloma


1. Ingest & destroy microbes, FB

2. Initiate repair

3. Secrete mediators of inflammation e.g IL-1

4. Antigen presenting cells

Role of macrophages in defense &
inflammation :


Tissue Injury >> Monocyte migration >> site of injury >> MACROPHAGE activation by various cytokines : Two pathways

* Classical macrophage activation important in
- host defense against ingested microbes
chronic inflammatory reactions

* Alternative macrophage activation : important in

tissue repair
through angiogenesis & fibroblast
activation >> Collagen synthesis

Mechanisms :

Chronic and Acute Pneumonia

Chronic Inflammation
Acute Inflammation !
Tissue Repair
* Inflammation :
- Acute
- Chronic

* Tissue Repair

* Neoplasia
# move what in the blood vessel
( fluid , plasma proteins , inf. cells ) to the battle area in order to get rid of the bad things .
( AIM = why it happens ? )
( double edge weapon .. ex : if there is a
problem in the immune system of the pt
, inf will not stop )
# Note : by response not time , cause macrophages ( managers ) can induce Acute for weaks !
# work in 2 levels
( rubor ) = by blood flow | vasod | His , PGs , bradykinin
( calor ) same as redness | vasod
( tumor ) = fluid accumulation | His , tissue damage
( dolor ) | PGE2 , Bradykynin
* Fever ( IL-1 , TNF , PGE2 )
(( At the ARTERIOL ))
What the event that occur firstly in inflammation :
a - Arteriolar vasoconstriction
b- Arteriolar Vasodilation
c – Capillary vasodilation
d - Venous vasodilation
e – non of the above
Answer :

(( by increase permeability at post capillary venules ))
Increase Permeability
* contraction of EC
• At the region of inflammation we will have a very
(takes few seconds) period of
then the Arteriolar dilatation. Subsequently there is an increase in vascular permeability.
* First : fluid with little pro. ( Transudate )
* after : Pro. rich fluid ( Exudate )
( 7 )
leakiness induced by leuckocytes
Burn Bluster
accumulation of fluid
( 8 steps )
( chemotaxis )
# 1 Margination
# 2 Rolling ( selectins )
# 3 Adhesion ( integrins )
# 4 Trasnmigration
# 5 chemotaxis ( migrate )
# 6 Phagocytosis
# 7 Killing
# 8 Resolution ( tissue repair )
( Diapedisis )
and lecuko
# ON leukocytes
# chemokinesis factors :
C5a , IL-8 , LTB4 , Bac products
In resting phase, selectins are stored inside weibel-palade bodies inside the endothelial cells, but once stimulation occur, specific chemical mediators (histamine and thrombin) induce the selectins, getting them out of weibel-palade bodies and
exposing them as p-selectins on the surface of the endothelial cell.
( recognition Receptors : TLR , Inflammasoe )
( Final exam qus )
( Neutralizing factors )
( found all the time )
* There is 2 Pathways
IL-10 & TGFB : healing
** Cytokines are the general category of messenger molecules, while chemokines are a special type of cytokine that direct the migration of white blood cells to infected or damaged tissues



9 ( help by 8 )

( help by 5 )

2 ( help 8 , 5 , 13 )

1 ( fibrin , need 13 )



10 , 9 , 7 , 2 >> vit K
* Fibronegic system : degrade fibrin
* C3 convertase , C3a & C3b
* C5 convertase , C5b
* MAC ( C5b + C6-9 )
# Macrophages act as managers :
- Healing : IL - 10 , TGFB
- cont . acute : IL-8
- abscess : fibrosiss , close area
- chronic
** whats the difference ?!
# Persistent / Autoimmune
# Chronic inf is divided into :
- Granulomatous inf. >>> Granuloma = Epitheloid histocyte
- non grnulomatous inf.
# macrophage is APCs
# presentation to dr ?
commonest consequence in the acute inflammation is complete resolution →
everything will go back to normal.
stable cells
in G0 or G1 and after injury they will enter the S phase and the
G2 … etc.
- Embryonic stem cells : Pluripotent cells that can give rise to all tissues of the body
- Adult stem cells
- Induced pluripotent stem cells (IPS cells)
# from the name indicate the func
* How do these factors work?
( EGF & HGF )
( Chemokine )
3 pathways
* Acute :
- def. , signs , mechanism , factors .. etc
- Apoptosis results from the activation of enzymes called caspases.

- The activation of caspases depends on a finely tuned balance between production of pro- and anti-apoptotic proteins.

-Two distinct pathways converge on caspase
1 ) the mitochondrial pathway
2 ) and the death receptor pathway.

- Regulated mechanism of cell death
that serves to eliminate unwanted and irrevesibly damaged cells, with the least possible host reaction.

- Characterized by enzymatic degradation of proteins and DNA, initiated by caspases; and by recognition and removal of dead cells by phagocytes.

Mitochondrial (intrinsic) pathway is triggered by loss of survival signals, DNA damage and accumulation of misfolded
proteins (ER stress); associated with leakage of
pro-apoptotic proteins from mitochondrial membrane into the cytoplasm, where they trigger caspase activation.

Inhibited by anti-apoptotic members of the Bcl family, which are induced by survival signals including growth factors.

Death receptor (extrinsic) pathway is responsible for elimination of self-reactive lymphocytes and damage by cytotoxic T lymphocytes; is initiated by engagement of
death receptors (members of the TNF receptor family) by ligands on adjacent cells.

Cells normally function under hemostasis, if this condition is altered there will be changes on the

a) biochemical
b) structural
c) functional

levels of the cell that will affect the tissues and therefore the organ.
*So the disease affects the body at its different levels according to the severity of the disease.
Anatomical Vs Clinical
(dissect dead bodies)
Double pathogenicity :
There might be many potential causes for the symptoms; so
when diagnosing, don’t look for only one cause
(may respond by having some accumulative material inside it)
( in pt with hypertension )
(both hypertrophy & hyperplasia will end up in increasing the size of the organ)
Some women at the age of 50(and they are not pregnant) have hyperplasia of the glands of
endometrium. She has excess in hormone production, or ovarian mass, or ovarian abnormality, so this is totally pathological NOT physiological.

(( first and second labs here : http://ar.utmb.edu/webpath/cinjhtml/cinjidx.htm ))
** Required slides are ( 1-54 Except : 13 , 38 , 42 , 43 , 48 , 49 , 50 )
The new mesenchymal does not have to be better than the old
one, but it is more resistant for the condition that made the old one
metaplasia to dysplasia and malignancy
The esophagus is composed of squamous epithelium, and
the stomach has columnar epithelium, which stands the acidity of the
stomach contents more than the squamous,
stem cells
(( we can't have morphological changes in the cell without having molecular/biochemical changes and changes in the function of the cell )).
whatever it is Na+ or K+ that will enter the cell
(prominent nucleoli)
(irreversible cell injury )
any stress or stimulus that will over exceed the power of the
capability of the cell
what happened is a severe denaturation of proteins … so even the enzymes will be denaturated and eventually they will lose their function .
* so here we will have cell death and the enzymes will not digest the remnants of the cell membrane so we won't lose the architecture of the cell
Apoptosis: cell death-----------> irreversible .
Atrophy :decrease in size -----> reversible .
external death signal or stimulus from the body to kill the cell
(9 & 8)
(3 & 6)
<Q1> One of the following about apoptosis is FALSE:
<C> Is an active process
<C+> Associated with heavy inflammatory cell infiltrate
<C> Could be physiological
<C> Occur in single cells
<C> May occur in viral infections
<Q2>Release of cytochrome C into the cytosol is necessary for :
<C> Necrosis
<C> Autolysis
<C+> Apoptosis
<C> Lipid peroxidation
<C> Metaplasia
<Q3>Which of the following provides an example of concomitant
hyperplasia & hypertrophy?
<C> Left ventricular hypertrophy in hypertension
<C> Enlargement of skeletal muscle in athletics
<C+> Uterine growth during pregnancy
<C> Endometrial hyperplasia in response to certain ovarian tumors
<C> Regenerating myocardial fibers after infarction
Page 14 of 15

Q8)All of the following are cell adaptations to stresses except:
a- hypertrophy
b- metaplasia
c- atrophy
d- hyperplasiae-
e- reversible injury
Answer : e

Q9) autophagy is accompanied with :
a- metaplasia
b- hyperplasia
c- abundance of nutrients
d- atrophy
answer: d

Q10)which of the following is acentral factor in necrosis :
a- chromatin clumping
b- extensive membrane damage
c- appearance of densities
d- ribosomes detachment
answer: b
<Q3>Phagocytosis is facilitated by all of the following EXCEPT:
<C> IgG
<C> C3
<C> Collectins
<C+> TNF
<C> Opsonins.

<Q4>Apoptotic bodies are most likely due to :
<C> Activation of lipases
<C+> Activation of caspases
<C> Lipid peroxidation
<C> Activation of superoxide dismutase
<C> Activation of catalase

Q5) Which of the following is anti-apoptic factor:
answer: c

Q6)The initiator caspases :
a- 3&6 caspases
b-8&9 caspases
answer: b

Q7)the main difference between
apoptosis and necrosis is:
answer: the presence of inflammatory
Inflammation is a
for the
cell injury,
Once we have cell injury the body
will react with inflammation trying to get rid of the cause that has lead to cell injury
from the beginning
( asthma )
(play a role in inflammatory process especially in
the process of
after injury have taken place)
(CT cells )
( take what in BV out )
normally we are supposed to
see the alveoli as white empty
spaces under the microscope
= lower resp tract inf
it is a place of " free MO " in normal situation ( micro )
but here the alveoli is full of inflammatory cells (
Neutrophils , lymphocytes, plasma cells), also fibrin and exudates inside the alveoli , and u can see the blood vessels dilated and congested. so all of these are changes of acute inflammation , we have vascular changes and then the cells will accumulate outside the blood vessel
who's first ?!
* what is the 5th event in acute inflammation :
a - Rolling
b – adhesion
c- margination
d - migration
e – chemotaxis
Answer :
increment in the hydrostatic pressure inside the blood vessel and
this increment will drive the fluid outside the vessel
in retraction there will be changes n the Ultra
structure of the same E.cell (change in
(Think about ways to separate Ec )
(channels allow fluid to leak out of the vessel)
inflammation in the
Specific gravity is a machine based measurement , (ratio of the density of a substance to the
density of a reference substance )
* Normal physics : in any flow , heavy things
should be in the center .
* In case of inflammation: fluid leaks out --> RBC's & leukocytes become in contact with the E.cells and this migration of the blood cells from centeral to
periphery called MARGINATION
important for achieving adherence
slow down the cells
( part of it will be inside )
In normal condition integrenes are
inactive (closed) & they open when
integrins affinity increased by
chemical mediators ; so that it will
be capable to bind to the
endothelial cell to achieve firm
adherence .
* R = receptor
* L = Ligand
(GlyCAM-1 (glycosylation-dependent cell adhesion molecule-1) is one of the sialomucin-like ligands for L-selectin)-wiki
CD's !
CD62 : selectins
CD11 : P150 , an integrin
CD54 : ICAM , adhesion
CD106 : VCAM , adhesion
CD31 : PECAM-1
CD 18 : integrins
(selectins - carbohydrate)
(integrins - Ig superfamily)
loose adhesion =
(firm adherens)
selectins will dind to sialylated Lewis X , and the sugar will bind to mucin lie cam
(no reaction btw
and EC )
# chemokine play a role not only in chemotaxis, it also play a role in a process of :
1) increasing avidity of integrin on leukocytes
2) expression the receptors on surface of endothelial cells
** Note : edema first , Neutrophil , Macrophage

( plasma carbohydrate-binding lectine) that bind to
microbial cell wall sugar groups
( ferrin means iron , bac need iron , lactoferrin bind iron , no iron for bact :( .. bac die )
(host defense proteins)
Which of the following is least effective in killing microbes :
a -h2o2
b -NO
c -O2
d- IBT4
Answer :
(they are good)
We have 2 types of lysosomes :
1) Acid protease : need low PH, to be active.
2) Neutral protease ,like : Elastases, collagenases, and cathepsin
(( activate them ))
phagocytosis is normal,but the problem is that the phagocytes can not get rid of the pathogen
(formed by liver)
(come form inside the cell)
injury --> activate PhosphoLipase-A2

I : go with inhibition
D&E : increase VP
A : go with activation
In chediac- Higashi disease which of the following is true :
A- Phagocytoses is impared
B-Phagocytic vacuoles are not formed
C- Lysosomes are deficient
D-Fusion of phagocytic vacuoles with lysosomes is
Answer :
they are not present in normal situations
** Histamine activate what ?!
go back to slide 30 :)
cell-derived BUT they are only formed upon stimulation
** PGI2 and TXA2 come from the same pathway of
cyclooxigenase but have opposing functions
** 3 ways
** 5-HPETE has 3 ways
( from 12-lipoxigenase )
** Note : asthma patients have PAF, LTC4 ,LTD4,LTE4
(( remmber : also lipoxin inhibit infm ))
** Note : IL-1 can promote other leukocytes to secrete more IL-1 ,IL-6.
regulation of chemotaxis and
activation of leukocytes
Plasma-derived mediators:
i > E
1 ) Coagulation system: The main goal is to form a blood clot
( intrinsic , extrinsic )

2 ) Fibrinolytic system : lysis the clot ( plasmin )

3 ) Kinin system : bradykinin --> increase VP , arteriolar dilation , PAIN
** Clinical note
( not required from you , just to understand the topic )
- Some bacteria ( like staph aureus ) contain enzymes that can degrade
fibrin , and other enzymes that can form fibrin !
Degrade fibrin --> to escape from the clot that is formed by IS
Form fibrin --> to hide itself
(fibrinogen produces them on its way while forming fibrin)
(( what else activate complement )) ?
** Pain - PGE2 also
activated factor XII (XIIa) initiates FOUR systems : 1- the kinin system
2- the clotting system
3-the fibrinolytic system
4-the complement system
can also act on plasminogen to give plasmin
activated by
* C3a , C5a : anaphylaxoins
* C3b : opsonin
* C5b : MAC
C3 ( the most important component and the meeting
point of the 3 pathways)
functions of the complement system are :
- recrutement of leukocytes , phagocytosis, and killing the Microorganism
* DAF (decay accelerating factor)
(healing !)
(ulcer Vs erosin)
Serous Inflammation
(mononuclear phagocytic system)
** Remember : in full pic , inf is just a part of immune response
chronic pneumonia
acute inflammatory
most of the viral infections will induce chronic
status of inflammation rather than acute inflammatory status because the viral
genome is going to be integrated into the DNA material of the cells.
(things for inf + Repair )
** Story start from something bad enter the body
Role of Activated Macrophages in Chronic Inflammation
** bidirectional
Complete Resolution of Inflammation
healing is a combination of regeneration and fibrotic process
(Cytokine) .. t go with t
(integrin)-(fibronectin) | ( laminin )
(part of repair by CT)
** Granulation tissue :
blood vessels
few inflammatory cells
collagen bundles
Full transcript