Roga nidan Basic Pathology -part 1

Rog Nidan- Basic Pathology –Part 1
• 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
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12/19/2016 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

Basic Pathology
• 4. Definition and brief description of edema –
shock – hemorrhage, Thrombosis , embolism,
Ischemia and Infarction
• 5. Types of Immunity – different types of
immune responses in the body – Basic
knowledge of auto immune diseases, Acquired
immune deficiency disease and
hypersensitivity

Contents of this PPT
• 1) Cell Injury & Cell death ,Necrosis
• 2) Oedema
• 3) Haemorrhage
• 4) Shock
• 5) Thrombosis
• 6) Embolism

Cell Injury and Cell Death
• Cell is a restless, pulsating microcosm,
constantly modifying its structure and function
in response to changing demands and stress

• Cell tries its level best to maintain the internal
environment within the normal limits i.e
homeostasis

Cell Injury and Cell Death
• . But when cell exposes to the excess stress it
fails to maintain the homeostasis
• In this situation cell adapts itself by changing
its shape or its numbers.

Cell Injury due to free Radicals

Hypertrophy, Atrophy and Hyperplasia
• Examples of cellular adapatations –
• If the stress is beyond the limits of cellular
adaptation then the cell injury take place
• Up to some extend the cell injury is reversible
but when the patho physiological stress is in
excess and persistent then the irreversible cell
injury occurs.


Atrophy & Hypertrophy

Hypertrophy & Hyperplasia

Causes of cell Injury
• 1) Hypoxia ---- low level of oxygen supply
• 2) Chemical agents ---- Drugs and other
chemicals
• 3) Physical agents --- Trauma, heat, cold etc.
• 4)Micro organisms --- Bacteria, Viruses, Fungi
etc.

Cell Injury

Causes of cell Injury
• 5) Immunological reactions --- Anaphylactic and
allergic reactions
• 6) Genetic defects --- Gross congenital anomalies like
Down’s syndrome and subtle effects like HbS in
Sickle cell anemia
• 7) Nutritional imbalances -- Various vitamin
deficiency related disorders or Ion deficiency anemia
• 8) Ageing – cataract, prostate enlargement etc.


Cell Death
• The principal adaptive responses are atrophy,
hypertrophy, hyperplasia, and metaplasia
• If the adaptive capability is exceeded, cell
injury develops.

Cell Death
• Within certain limits, injury is reversible, and
cells return to a stable baseline; however, with
severe or persistent stress, irreversible injury
results, and the affected cells die
• There are two principal patterns of cell death
are recognized and those are ---
• Necrosis and Apoptosis

Necrosis & Apoptosis

1) Necrosis
• It means the cell death
• It occurs after a loss of blood supply or after
an exposure to toxins
• Characterized by cellular swelling, protein
denaturation, and organelle breakdown.

1) Necrosis- Causes
• Hypoxia (O2 )
• Chemical and physical agents
• Microbial agents
• Immunological injury (Autoimmune diseases)

Types of Necrosis
• 1) Coagulative Necrosis
• 2) Liquefaction Necrosis
• 3) Caseous Necrosis
• 4) Fat Necrosis
• 5) Fibrinoid Necrosis


1) Coagulative necrosis
• Sudden stoppage of the blood supply may
lead to coagulative necrosis
• It is seen commonly in heart ,kidneys, brain
and spleen.

1) Coagulative necrosis
• In this type of the injury the acidosis develops
which denatures the structural proteins as
well as the enzyme proteins
• The important feature of this type is
conversion of normal cell into thrombus.
(Thromb stones)

Coagulative necrosis –Left Ventricle

2) Liquefactive necrosis
• It is characteristic of focal bacterial or
sometimes fungal infections
• It is characterized by the accumulation of
white cells
• In a surgical practice the most of the
abscesses are of this type

Liquefactive necrosis in Brain

3) Caseous necrosis
• It is a special form of necrosis observed in
a Tuberculous infection.
• The term "caseous" is derived from the
cheesy, white gross appearance of the
central necrotic area

Caseous Necrosis
Tuberculosis Lungs

3) Caseous necrosis
• Microscopically, the necrotic focus is
composed of structureless, amorphous
granular debris enclosed within a distinctive
ring of granulomatous inflammation

4) Fat Necrosis
• This occurs in the abdominal emergency
like acute pancreatitis
•
• It results from pathologic release of
activated pancreatic enzymes into
adjacent parenchyma or the peritoneal
cavity.

4) Fat Necrosis
• Activated pancreatic enzymes escape from
acinar cells and ducts, liquefying fat cell
membranes and hydrolyzing the triglyceride
esters contained within them
• The released fatty acids combine with
calcium to produce grossly visible chalky
areas

Fat Necrosis -Pancreas

5) Fibrinoid Necrosis
• It is characterized by the deposition of
the fibrin like material and commonly
observed in -----
• Rheumatoid arthritis and in Auto
Immune Diseases like SLE.

Fibrinoid Necrosis

Apoptosis
• It occurs as a result of ----
• Set and internally controlled "suicide"
program, ---
• After which the dead cells are removed
with minimal disruption of the
surrounding tissue.

Apoptosis
• This occurs in physiologic states when
unwanted cells are to be eliminated
• e.g., embryogenesis, menstrual
discharge
• As well as in a variety of pathologic states
e.g., Irreparable mutational damage

Autoloysis
• It is the mechanism in which the cell death
occurs due to its own hydrolytic enzymes
liberated from lysosomes It is commonly
observed in a post mortem change
• This is rapid in tissues ,which are rich in
hydrolytic enzymes e.g. Pancreas & gastric
mucosa.

Gangrene
• It is a type of necrosis of tissue with super
added putrification.
• Types :
• 1) Dry Gangrene: It is commonly observed in
the toes and feet of old patients.
• It appears black due to the liberation of
hemoglobin and reaction with H2S producing
iron sulphate.

Gangrene

2) Wet Gangrene
• It Occur in the moist tissues (mouth,
bowel, lungs, cervix etc.).
• It is very common in Diabeteic patients
especially in the toe


2) Wet Gangrene
• The affected part becomes soft,edematous
and blackish in colour
• The foul smell is the characteristic feature
• The Toxic products formed by bacteria are
absorbed through blood and septicemia can
develop in these patients

Dry & Wet Gangrene

3) Gas Gangrene
• It is caused by gas forming Gram positive
anaerobic bacteria -- Clostridium perfringen
• The open, contaminated wound may develop
this condition
• The affected par is swollen, painful and typical
crepitus is heard, due to gas bubbles.

Gas Gangrene

Oedema

• Excess accumulation of the fluid in an
interstitial space is called as ‘Oedema’.
• Oedema can be localized or may be
generalized
• Generalized form is called as ‘Anasarca’.

Oedema
• There are four types of pressures which
contribute in the exchange of the fluid.
• The hydrostatic pressure of plasma and
interstitial oncotic pressure are responsible
for the net outward flow of the fluid.

Oedema
• Whereas the interstitial hydrostatic pressure
and plasma oncotic pressure lead the inward
directional flow of the fluid.
• In the formation of the oedema the outward
directional pressures are increased.

Unilateral Localised Oedema
• 1) Cellulitis
• 2) Deep vein thrombosis (DVT)
• 3) Filariasis
• 4) Gout.

1) Cellulitis
• It is an inflammation of the tissue

• Affected part shows the signs of inflammation
like swelling, redness, raised local
temperature and pain
• The affected part show the tenderness.

Cellulitis

2) Deep Vein Thrombosis (DVT)
• The swelling in the calf muscles ----
• With signs of inflammation is the typical
feature of DVT.
• Calf tenderness is a typical feature
• Fear of Embolism – So Massage should not be
done –otherwise fear of Pulmonary Embolism
& death

Deep Vein Thrombosis
Calf Pain Defective valve

Deep Vein Thrombosis

3) Filariasis
• It is also known as Elephantitis
• The oedema is initially pitting but later on
turns into non pitting due to fibrosis

• It is characterized by intermittent fever
especially in the night.


Filariasis

4) Gout
• It is also an inflammatory condition secondary
to raised level of serum uric acid
• The inflammatory response is very common
behind the great toe
• The part becomes red and tender

Gout

B) Generalized Oedema
• Generalized form of oedema is common in ----
• Heart diseases like CCF
• Nephrotic syndrome
• Liver disorders
• Hypothyroidism
• Anaemia

Paedal oedema & Ascites in CCF

Generalised Oedema -- Causes
• 1) Anaemia with Hypoprotenemia
• 2) Drug induced oedema
• 3) Venous insufficiency
• 4) Angioneurotic oedema
• 5) Myxoedema
• 6) Premenstrual oedema

Oedema
Nephrotic Syndrome Myxoedema

1) Anaemia with Hypoproteinaemia
• In these conditions the oedema is
common in an areolar tissue i.e
periorbital & pedal edema
• The patient is pallor, the extremities are
cold and complains recurrent stomatitis

2) Drug induced oedema
• Sudden onset with swelling of face and feet.
• H/o steroids – Cushing’s syndrome (Moon
shaped face) -- Side effects of the drugs like
NSAIDs e.g. Diclofenac (Voveran), Ibuprofen
(Brufen)
• Side Effect -- If the women is taking the oral
contraceptive pills (Mala – D)

Steroid –Cushing’s syndrome

3) Venous Insufficiency
• It is very common in middle aged women
• Typically appears on the ankle region

4) Angioneurotic or Allergic Oedema
• It is the type of hypersensitivity reaction to
the allergen.
• It releases the mast cells secretions
(Histamine) into the tissues.
• Due to the Histamine the itching takes place.
• The other symptoms of allergic reactions are
oedema, rashes, dyspnoea and hoarsenes of
the voice.

Angioedema

5) Myxoedema or Hypothyroidism
• The low level of thyroid hormones in the
plasma reduces the BMR
• Secondary to this the water retention takes
place in the body
• Patient complaints of heaviness in the body,
lethargy, lack of confidence, bradycardia and
puffiness

6) Premenstrual Oedema
• Due to the retension of water and sodium the
oedema develops in premenstrual syndrome
• Many times Diuretics are given as a
symptomatic releif


Haemorrhage
• Definition: It is defined as escape of
blood from blood vessels due to trauma
or disease

• The clinical significance of hemorrhage
depends on the volume, rate of blood
loss and the site.

Haemorrhage
• 1) Haematoma --  Escape of blood in tissues with
swelling
• 2) Ecchymosis ---  Large extravasation of blood
into skin and mucous membrane
• 3) Purpura ---  Small areas of haemorrhages,
below 1 cm in skin or mucus membrane.
• ii) Diapedesis --  Microscopic escape of RBC in
loose tissue.


Haemorrhage
Petechiae & Purpura Patechiae & Purpura

Haematoma

Diapedesis

Skin lesions

Shock
• Definition –
• It is a clinical state of circulatory collapse and
• Inadequate perfusion of the cell and tissues
• Specially less blood supply to Brain


Shock

Types of Shock
• 1) Hypovolumic Shock
• 2) Septicaemic Shock
• 3) Cardiogenic shock
• 4) Neurogenic shock
• 5) Anaphylactic shock

Shock: Types
• 1) Hypovolemic Shock:
• Common in the conditions like ----
• Road accidents
• Severe haemorrhage
• Severe dehydration
• In severe burns

Shock: Types
• 2) Septicemic Shock:
• It is the severe condition secondary to
infections
• The bacteria produces the exotoxins and
endotoxins which are responsible for this type
of shock


Shock: Types
• 3) Cardiogenic Shock ---
• Heart is the pump of the body & if fails to
pump the blood as per the demand of the
tissues then the cardiogenic shock occurs
• It is observed in CCF and in cardiac
arrhythmias.


Shock: Types
• 4) Neurogenic Shock -----
• Secondary to ----
• The severe painful conditions
• Emotional upsetting situation
• In spinal injuries especially in road traffic
accidents

Shock: Types
• 5) Anaphylactic Shock ----
• It is the Hypersensitivity type-1 reaction in
which, the body gives over response to the
antigens
• The mast cells degranulation, IgE antibodies
response, histamine and other inflammatory
mediators are responsible for the
pathophylogical events
•

Shock -- Signs and Symptoms
• 1) Pulse --- Feeble with tachycardia
• 2) Low systolic B.P. < 60 mm of Hg
• 3) Severe perspiration (sweating increases),
limbs are cold
• 4) Subnormal temperature (i.e. temperature
decreases)

Thrombosis
• Definition -----
• It is defined as the formation of solid mass in
a circulation from the constituents of the
blood
• In the formation of the Thrombus the
endothelial cells, platelets and the clotting
factors play a central role

Harmful Effects of Thrombosis
• 1) Ischaemia --- Less Blood supply
• 2) Thrombo - embolism

Coronary Thrombosis

Fate of Thrombosis
• 1) Anti thrombotic mechanisms are also
functioning in the body to arrest the on going
Thrombus formation
• t-PA i.e tissue plasminogen activator is
antithrombotic factor present in the body
• Plasminogen dissolves the fibrin and hence the
clot too

Fate of Thrombosis
• 2) Organisation – Phagocytic cells start eating
fibrin and cell debris. New fibroblasts develop
• 3) Propagation --- Thrombus enlarged in size.

Predisposing factors of Thrombosis
• 1) Advanced Age.
• 2) Prolonged bed rest (Due to decrease
movements ,circulation hampers )
• 3) Immobilization
• 4) Use of O.C. pills
• 5) Cigarette smoking – Nicotine causes
vasoconstriction
• 6) Tissue damage due to burn & fracture.


Clinical Conditions which can Cause Thrombosis
• 1) Valvular defects in the Heart
• 2) Atherosclerosis
• 3) Varicose Veins – DVT
• 4) Disseminated cancers
• 5) Nephrotic Syndrome
• 6) Late pregnancy and
• 7) After delivery

Embolism
• Definition: Any mass carried in circulation
and which cause partial or complete
obstruction in the circulation.
• 1) Brain -- Stroke (CVA – Cerebro Vascular
Accident) leads to hemiplegia.
• 2) Heart --- Heart attacks
• 3) Kidney --- Renal failure – Oliguria (Initially
polyuria then oliguria)
•

Embolism

Effects of embolism
• 1) Sudden death ( Many times due to
Pulmonary Embolism )
• 2) Infarction- AMI (Acute Mycardial Infarction)
• 3) Gangrene


Ischaemia
• Less blood supply to the part of a tissue. This
may be total or partial
• Effects:
• 1) Tissue hypoxia.
• 2) Inadequate supply of nutrients.
• 3) Inadequate drainage of metabolites.

Infarction
• The necrosis of the tissue is called as Infarction
• Infarction – Total stoppage of blood supply
• It is secondary to circulatory insufficiency
• Infarction takes place due to
• 1) Thrombosis
• 2) Embolism
• 3) Ischaemia


Prof.Dr.R.R.Deshpande
• Sharing of Knowledge
• FOR
• Propagating Ayurved

Roga nidan Basic Pathology -part 1

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