Rog Nidan Basic Pathology –Part 2

Rog Nidan- Basic Pathology –Part 2
• Presented By –
Prof.Dr.R.R.Deshpande
(M.D in Ayurvdic
Medicine & M.D. in
Ayurvedic Physiology)
• www.ayurvedicfriend.c
om
• Mobile – 922 68 10 630
• professordeshpande@g
mail.com
12/21/2016 1Prof.Dr.R.R.Deshpande

Rog Nidan –Basic Pathology
• This PPT is based on the –
• Syllabus of CCIM ( 2014) for 3rd BAMS of
Rognidan
• Points are from Paper 1 Part A ,Point III –
Basic Pathology

Basic Pathology
• 1. Introduction to pathology and its sub-
divisions
• 2. Introduction to Cell Injury and Cellular
adaptations
• 3. Definition and brief description of
inflammation – Healing/repair

Contents of this PPT
• Definition and brief description of –
• Inflammation
• Healing & repair
12/21/2016 Prof.Dr.R.R.Deshpande 4

Inflammation – Definition
• This is a nonspecific local response to injury
• This defense mechanism helps to eliminate or
to control the spread of injurious agents.


Inflammation
Pneumonitis Cervicitis

Injurious agents
• i) Physical Agents --  Heat (sun stroke) cold
(frost bite) radiation.
• ii) Chemical Agents --  Poison
• iii) Infective Agents --  Bacteria, viruses
• iv) Immunological Agents --  Antigen,
antibody complex.

Signs of Inflammation

• i) Rubor – redness.
• ii) Tumor – Swelling
• iii) Calor – Heat
• iv) Dolor – Pain
• v) Functio laesa – loss of function.

Types of Inflammation
• i) Acute
• ii) Chronic

Acute Inflammation
• Short Duration – Usually atomatic repair
• Changes divided into
• 1) Vascular changes
• 2) Cellular changes
• Vascular Events --
• a) Hemodynamic changes
• b) Altered Vascular permeability

Acute Inflammation
• a) Haemodynamic changes --
• i) Transient Vasoconstriction of arterioles --
The blood flow may be re established  in 5 sec.
to 5 min.
• ii) Persistent progressive vasodialatation – It
is observed in the first half an hour of injury –
Transudation of fluid in ECF (Extra Cellular
fluid)

Acute Inflammation
• a) Haemodynamic changes –
• iii) Slowing or Stasis
• iv) Leukocytic migration --  Leukocytes stick to
vascular endothelium & then move & migrate
through the gaps  between endothelial cells
into ECF. This is called Emigration

b) Altered Vascular Permeability
• Due to vasodilatation – Fluid comes out from
Blood plasma, so accumulation of oedema
fluid, around the injured tissue.
• This fluid is transudate. Generally little fluid is
taken up by lymphatics and no oedema occurs.
• If the trauma is severe – more fluid come out
and lymphatics can not take it back naturally
& oedema occurs

2) Cellular Events
• a) Exudation of leucocytes –
• The polymorphonuclear neutrophils (PMNs)
comprise the 1st line of defense, followed by
monocytes and macrophages.

b) Margination and pavementing
• Due to stasis and increased permeability, the
layer of plasma close to vessel wall goes out
into ECF and so the central stream of cells
come in close contact with the cell wall
• This phenomenon is known as Margination
or Pavementing.


Margination and pavementing

Emigration
• Neutrophils move along the wall of capillary to
find suitable place to escape from vessel
• Then they put the out of the capillary wall and
then stick to the outer surface of capillary
• With the help of pseudopodia, Neutrophill
migrates into EC. This is Emigration.

Emigration of Neutrophil

Dipediasis
• After neutrophills, escape of RBCs through
the gaps between endothelial cells is called
Dipediasis
• This dipediasis give haemorrhagic appearance
to inflammatory exudates.

Diapedesis

Chemotaxis
• Emigration due to some chemical stimuli in
called chemotaxis
• Many chemicals liberated at the site of injury
brings about Chemotaxis

Chemotaxis

Phagocytosis – Definition
• Process of engulfment of solid material by
Phagocytes. ( e.g Specific cells like Kuffer’s
cells in liver)
• Divided in 3 stages --- see Next Slides

Phagocytosis

1 ) Stage of Attachment
• Microorganisms and Neutrophills both are
negative, so naturally they repeal each other
• Hence bacteria get coated with some specific
substances (Opsonins),from serum
• e.g. i) IgE opsonin ii) C3b opsonin.

2 ) Stage of Engulfment
• Opsonised particle is now ready for
engulfment
• There is formation of pseudopoda by
phagocyte around the particle, enveloping it
in a vacuole
• The plasma membrane from cellular surface
break and thus the particle enters inside cell.


3 ) Stage of killing and degradation
• There are some antibacterial substances
inside the cell, which kill the engulfed
bacteria
• Killed bacteria then degraded by lysosomes
of the Phagocytic cells
• This mechanism fails in some cases like
Tubercle bacilli

Chemical Mediators of Acute Inflammation
• These are classified into –
• 1) Mediators released by cells of injured
tissue
• 2) Mediators from plasma

I) Mediators released by cells of injured tissue

• i) Vasoactive amines -- a) Histamine:
• Secreted by Eosinophil. It’s main function is
vasodilation, it increases the vascular permeability.
It also act as a neurotransmitter, which helps in the
conduction of itching sensation.
• In the majority of the allergic reactions it is one of
the transmitter
• so antihistaminic drugs like AVIL is used in the
treatment.

• b) 5 – hydroxy tryptamine (5-HT) –
• It is same as histamine but is less potent.
• It is present in gastro intestinal tract and in
spleen.

• c) Prostaglandin -- The name is given because
this substance initially found in human
seminal fluid, but now it could be isolated
from various body tissues.
• Names -- PGD2, PGE2, PGF2
• Functions -- Vasodilatation & increase
permeability

I)Mediators released by cells of injured tissue
• iv) Thromboxane A2
• This is vasoconstrictor substance and its
main function is platelet aggregation ( Fast
healing of Cell injury )
• v) Leukotrienes (LTs) :
• They are derived from leukocytes . Act as
chemotatic agent. Also helps in smooth
muscle contraction.

• vi) Lysosomal Enzymes
• Neutrophills and monocytes release these
enzymes which help in degradation of
bacterial wall and extra cellular component.

• vii) PAF (Platelet Activating Factor)
• Released from basophill and mast cells .It’s main
function is to aggregating the platelets.
• viii)Cytokines
• Released by lymphocytes and monocytes &
important mediators liberated by these cells are
Tumor Necrosis Factor (TNF) & Interleukin 1

II) Chemical Mediators from Plasma
• The following four systems are inter linked and
are derived from plasma in inflammatory
reactions
• i) Kinin system
• ii) Clotting system
• iii)Fibrinolytic system
• iv)Complement system
•

II)Chemical Mediators from Plasma
• Hagemen Factor (Factor No. XII) Plays a key
role in an interaction of these 4 systems
• i) Kinin System –
• It generates bradykinin. It brings about slow
contraction of smooth muscles.

II) Chemical Mediators from Plasma
• ii) Clotting System –
• Activated factor XII initiates the chain reaction
of clotting.

II)Chemical Mediators from Plasma
• iii) Complement System --
• Activation of complement system takes place
by stimulation of antigen of by bacterial toxins
• Function: It release histamine from mast cells
& acts as a chemotatic agent for leukocytes.
• e.g. C3a, C1a, C5a are working substances

The inflammatory Cells
• i) Neutrophills (Polymorphs): These are
predominant in acute infections.
• Enzymes – Proteases & lysosomes
• Function : i) Phagocytosis (hence Neutrophillia is
common in bacterial infection)
• ii) Engulfment of antigen, antibody
complex
• Normal Count -- 60 – 70 %

• ii) Eosinophil:
• Eosinophils have the enzyme --
Myeloperoxidase.
• Eosinophillia is seen in Tropical Eosinophillia,
allergy, worms, skin diseases, and malignant
lymphoma.
• Eosinopenia or disappearance can occur in
high level of steroid.

• iii) Basophil --
• Basophils secrete heparin & histamines. They
are similar to the mast cells
• Function: Useful in hypersensitivity reaction
• Histamine is released by IgE sensitized
basophills.

• iv) Lymphocyte -- These are present in lymph nodes
& spleen.
• Antibodies are formed by B- lymphocytes.
• T-lymphocytes are useful in cell mediated immune
response.
• Function : These cells are more dominant in the late
stage of acute inflammation. They also play a
important role in chronic inflammation.


• v) Plasma Cells --
• These cells are derived from B-lymphocytes.
These are rich in RNA and gamma globulins &
they are active in antibody synthesis.
• They are increased in immunological reactions
e.g. Autoimmune response like Rheumatoid
arthritis (RA), Hypersensitivity reactions,
Allergies & in Multiple Myeloma.

• vi) Monocytes --
• They constitutes 4 – 5 % of the total WBCs
• In addition to this they are present in the
tissue in the form of macrophages (Kuffers
cells in Liver)


Inflammatory Response
• A) Factors related with Organism: Following
factors of an organism are important in an
inflammation.
• i) Type of injury and infection- In the
streptococcal infection the skin gives the
response by producing the boil or furuncle.

• ii) Virulence of an organism –
• It is the capacity of an organism to harm the
host cells.


• iii)Dose of an organism -- To produce the
host cells damage the certain number of
organisms are required and generally this is
tested by culture grown on specific media and
the sensitivity test is carried out
• Urine, Blood, Sputum & Stool samples are
generally send for the culture sensitivity test.

• iv) Route of Entry --
• Vibrio cholerae causes cholera only when
ingested and not when injected.

Factors Related to the host
• i) General health of the patient
• ii) Immune status
• iii) Leucopenia – It is observed in Steroid use
especially in RA, Asthma, skin allergy &
Nephrotic syndrome.
• iv) Site and type of the tissue --The spread of
infection is rapid through the mucus
membrane.
•

Inflammation Exudate
• The nature of the secretion of the
inflammation may be ---
• i) Serous
• ii) Purulent
• iii) Hemorrhagic, fibrinous T.B., cold abscess
etc.

Morphology of Infection
• The lesions of an infections show the
responses like -----
• i) Membrane formation
• ii) Ulcer
• iii) Suppuration
• iv) Cellulitis
• v) Bacterial Infection (Bacteraemia,
septicaemia, pyemia)

• i) Membrane formation: Inflammatory
response to specific toxins of bacteria e.g.
Diphtheria produces the membrane which is
the hallmark of the disease
• ii) Ulcer: In Ulcerative colitis there is an ulcer
in the colon.

Membrane Formation & Ulcer
Diphtheria Ulcerative colitis

• iii) Suppuration: Pus formation. e.g.
Staphylococcal abscess

• iv) Cellulitis: Diffused inflammation of soft
tissue due to the enzyme hyaluronidase,
which is released by some bacteria

Suppuration & Cellulitis
Staphylococcal Abscess Cellulitis

• v) Bacterial Infection –
• i) Bacteramia --- Presence of small number
of bacteria in blood.
• Blood culture is done to detect Salmonella
Typhi.

v) Bacterial Infection
• ii) Septicemia -- Presence of rapidly
multiplying highly pathogenic bacteria in
blood.e.g. bacilli of Plague.
• They develop fast systemic effects like
toxaemia.
• iii) Pyaemia -- Dissemination of small septic
thrombi in blood. They can form pyaemic
abscess e.g. liver abscess.

Systemic Effects of Acute Inflammation
• i) Fever
• ii) Leukocytosis
• iii) Lymphangitis
• iv) Lymphadenitis

Fate of Acute Inflammation
• Acute inflammatory response may subside or
convert into the chronic response
• Following are the stages of the inflammatory
response
• Continued with Next slide --

• i) Resolution
• ii) Healing by Scarring
• iii) Suppuration
• iv) Chronic inflammation


• i) Resolution --
• Complete return to normal tissue.
• ii) Healing --
• When destruction is more, that deficit can not
be filled up by parenchymal tissue (normal
tissue) . So fibrosis takes place. (e.g. burn,
surgery)

• iii) Suppuration ---
• When pyogenic bacteria are the cause of
acute inflammation, they results in severe
necrosis ,which then leads to suppuration.

• iv) Chronic Inflammation –
• If the stimuli persist then the inflammation
turns into the chronic form
• The chronic inflammation takes place in
tubercular reaction

Chronic Inflammation – Definition
• This is a prolonged process --
• In which tissue destruction and inflammation
occur at the same time

Chronic Inflammation - Causes
• i) Chronic inflammation occurs after acute
inflammation
• Tissue destruction is an extensive and the
small number of bacteria survives at the site
of acute inflammation and then chronic
inflammation take place. e.g. 'Osteomylitis'

Chronic Inflammation-Osteomyelitis

Chronic Inflammation - Causes
• ii) Recurrent attack of acute inflammation:
e.g. Recurrent UTI may turn into chronic
pyelonephritis
• iii) Chronic inflammation from the beginning
-
• e.g. Mycobacterium tubercle.

Chronic Inflammation - Pyelonephritis

Features of Chronic Inflammation
• 1) Mononuclear Cell Infiltration --
• Lesions are infiltrated with phagocytes
(monocytes) and lymphoid cells. Macrophages
are the most common cells
• 2) Tissue destruction or necrosis takes place

Features of Chronic Inflammation
• 3) Proliferative changes --- Proliferation of
small blood vessels and fibroblast (fibrous
tissue) is very common
• So formation of granulation tissue & healing
by fibrosis occurs

Types of chronic Inflammation
• 1) Chronic Non-specific Inflammation:-- Non
specific inflammatory cell infiltration .Ex is
Osteomylitis
• 2) Chronic granulomatous inflammation e.g.
T.B.

Food – useful to reduce Inflammation

Gramuloma
• Definition -- It is a circumscribed lesion, 1- mm
in diameter composed by modified
macrophages (epithelioid cells) and this
granuloma is rimmed by lymphoid cells in
periphery.
• Chronic Inflammation also has giant cells. (A
fusion of adjacent epithelioid cells) They also
follows same track of necrosis and fibrosis.

Healing
• Definition --
• It is defined as the body's response to injury to
restore normal structure and function.
• There are mainly 3 phages
• i) Regeneration
• ii) Repair
• iii) Contraction of wound

Healing
• 1) Regeneration –
• The original tissue healing and restoration
when occurs with the parenchymal cells then
the process is called as Regeneration.

Regeneration
• Regeneration mainly involves 3 types of cells
• i) Liable Cell –
• Under normal physiological condition, these
cells continue multiply through out the life. e.g.
Epidermal cells (skin cells)

1) Regeneration
• ii) Stable Cell -- They loose their ability of
proliferation after adolescence e.g.
Parenchymal cells of liver. (But can multiply in
response to appropriate stimuli in adult life)
• iii) Permanent Cells -- Loose their ability to
proliferate around at the time of birth e.g.
Neurons and cardiac muscle cells.

2) Repair
• When the tissue is replaced by the connective
tissues which causes the fibrosis and scar
formation then the process of healing is called
as “Repair”
• This process has 2 stages
• Continued in Next slide --

Repair
• 1) Granulation tissue formation –
• i) Phase of inflammation: After trauma, blood clot
is formed at the site of injury.
• The inflmmatory cells migrate to the site of injury
and liberate chemical mediators of inflammation.
• Some chemicals are released through plasma also.
• Monocytes , macrophages and Neutrophils are
predominant at this phase.

Repair
• ii) Phase of clearance --
• Proteolytic enzymes are liberated from
Neutrophils, autolytic enzymes are released
from dead tissue and phagocytic activity is
carried out by macrophages
• In this process the necrotic tissue, debris and
RBCs are cleared


iii) Phase of Growth of Granulation Tissue
• It consists of ---- a) Angiogenesis -- Formation
of new blood vessels, by the proliferation of
endothelial cells from the margins of wound of
neighboring blood vessels
• Initially they are solid buds but within few
hours develop a lumen and start carrying
blood. Soon they are differentiated into
arterioles and venuoles

Angiogenesis

• b) Fibrous tissue Formation: The new fibroblast
originates from fibrocytes.
• Collagen fibers begin to appear on 6th day.
• As healing progresses, the number of proliferating
fibroblasts and new vessels decreases.
• Gradually more and more collagen is formed and
new blood vessels decreased.
• At last inactive looking scars is formed.
(Cicatrisation)

• c) Contraction of Wound –
• Wound starts contracting after 3 days and is
completed on 14th day
• Wound is reduced approximately 80 % of
original size

Theories about contraction
• How does the wound contraction take place?
• It is a question for the scientists and the
theories have established for the explanation
of this question.
• some of the explanations are as follow-

Theories about contraction
• 1) Dehydration or drying of wounds
• 2) Contraction of collagen fibers
• 3) Appearance of myofibroblast in active
granulation tissue

Wound Healing
• This is a classical example of regeneration and
repair

Stages of wound healing

1) Primary Union or 1st Intension
• Features ----
• This is a healing of external type of wounds
e.g. a) An uninfected wound.
b) Surgically incised wound.
c) Without much loss of tissue.
d) Edges of wound -----approximated
by surgical sutures.

10 unions take place as follows
• i) Initial haemorrhage -- Bleeding  clot
 Seal
• ii) Acute inflammatory response -- It is seen
within 24 hours. Initially the polymorphs
appear and then they are replaced by
macrophages on 3rd day.

• iii) Epithelial changes ---Basal cells of
epidermis start to proliferate towards the
incised tissue or site
• Approximated wound is covered by a layer of
epithelium within 48 hours.
• By 5th day new multilayered epidermis is
formed.

• iv) Organisation --
• By the 3rd day fibroblast appears in the wound
area & by 5th day new collagen fibers start
forming and continue till the wound heal.
Within 1 month – 10 wound healing is
completed.
• v) Suture Track -- Each suture track is a
separate wound and follows like original
wound.

2) 20 - Secondary Intension
• This is applicable for the following types of
wound.
• i) Open wound with large tissue deficit
and infected.
• ii) Extensive loss of tissue.
• iii) Wound is not approximated (i.e. not
sutured)
•

2) 20 Secondary Intension
• In above situations basic events of wound
healing are similar to primary type of healing
• However the process is slow and
• The scar is generally ugly in appearance

Wound Healing

Complications of wound healing

• 1. Infection
• 2. Implantation cyst.
• 3. Pigmentation
• 4. Deficient scar formation
• 5. Incisional hernia
• 6. Hypertrophied scar.
• 7. Excessive contraction.
• 8. Neoplasia.

Complications of wound Healing

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Rog Nidan Basic Pathology –Part 2

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