roga nidan basic pathology -part 1
TRANSCRIPT
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.com
• Mobile – 922 68 10 630• [email protected]
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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
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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
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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
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Contents of this PPT
• 1) Cell Injury & Cell death ,Necrosis• 2) Oedema
• 3) Haemorrhage• 4) Shock
• 5) Thrombosis • 6) Embolism12/19/2016 5Prof.Dr.R.R.Deshpande
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
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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.
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Cell Injury due to free Radicals
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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.
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Atrophy & Hypertrophy
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Hypertrophy & Hyperplasia
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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.
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Cell Injury
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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.
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Cell Death
• The principal adaptive responses are atrophy, hypertrophy, hyperplasia, and metaplasia
• If the adaptive capability is exceeded, cell injury develops.
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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
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Necrosis & Apoptosis
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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.
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1) Necrosis- Causes
• Hypoxia (O2 )
• Chemical and physical agents
• Microbial agents
• Immunological injury (Autoimmune diseases)
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Types of Necrosis
• 1) Coagulative Necrosis• 2) Liquefaction Necrosis
• 3) Caseous Necrosis
• 4) Fat Necrosis• 5) Fibrinoid Necrosis 12/19/2016 20Prof.Dr.R.R.Deshpande
1) Coagulative necrosis
• Sudden stoppage of the blood supply may lead to coagulative necrosis
• It is seen commonly in heart ,kidneys, brain and spleen.
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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)
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Coagulative necrosis –Left Ventricle
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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
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Liquefactive necrosis in Brain
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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
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Caseous Necrosis
Tuberculosis Lungs
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3) Caseous necrosis
• Microscopically, the necrotic focus is composed of structureless, amorphous granular debris enclosed within a distinctive ring of granulomatous inflammation
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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.
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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
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Fat Necrosis -Pancreas
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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.
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Fibrinoid Necrosis
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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.
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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
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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.
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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.
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Gangrene
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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
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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
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Dry & Wet Gangrene
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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.
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Gas Gangrene
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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’.
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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.
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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.
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Unilateral Localised Oedema
• 1) Cellulitis
• 2) Deep vein thrombosis (DVT)
• 3) Filariasis
• 4) Gout.
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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.
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Cellulitis
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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
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Deep Vein Thrombosis
Calf Pain Defective valve
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Deep Vein Thrombosis
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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.
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Filariasis
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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
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Gout
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B) Generalized Oedema
• Generalized form of oedema is common in ----
• Heart diseases like CCF• Nephrotic syndrome• Liver disorders• Hypothyroidism • Anaemia
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Paedal oedema & Ascites in CCF
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Generalised Oedema -- Causes
• 1) Anaemia with Hypoprotenemia• 2) Drug induced oedema• 3) Venous insufficiency
• 4) Angioneurotic oedema• 5) Myxoedema• 6) Premenstrual oedema
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Oedema
Nephrotic Syndrome Myxoedema
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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
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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)
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Steroid –Cushing’s syndrome
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3) Venous Insufficiency
• It is very common in middle aged women
• Typically appears on the ankle region
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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.
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Angioedema
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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
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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
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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.
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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.
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Haemorrhage
Petechiae & Purpura Patechiae & Purpura
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Haematoma
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Diapedesis
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Skin lesions
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Shock
• Definition –
• It is a clinical state of circulatory collapse and
• Inadequate perfusion of the cell and tissues
• Specially less blood supply to Brain 12/19/2016 75Prof.Dr.R.R.Deshpande
Shock
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Types of Shock
• 1) Hypovolumic Shock• 2) Septicaemic Shock• 3) Cardiogenic shock
• 4) Neurogenic shock • 5) Anaphylactic shock
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Shock: Types
• 1) Hypovolemic Shock: • Common in the conditions like ----
• Road accidents • Severe haemorrhage • Severe dehydration • In severe burns
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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
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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.
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Shock: Types
• 4) Neurogenic Shock ----- • Secondary to ---- • The severe painful conditions
• Emotional upsetting situation
• In spinal injuries especially in road traffic accidents
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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
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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)
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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
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Harmful Effects of Thrombosis
• 1) Ischaemia --- Less Blood supply
• 2) Thrombo - embolism
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Coronary Thrombosis
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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
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Fate of Thrombosis
• 2) Organisation – Phagocytic cells start eating fibrin and cell debris. New fibroblasts develop
• 3) Propagation --- Thrombus enlarged in size.
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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.
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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
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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)
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Embolism
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Effects of embolism
• 1) Sudden death ( Many times due to Pulmonary Embolism )
• 2) Infarction- AMI (Acute Mycardial Infarction)
• 3) Gangrene
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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.
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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 12/19/2016 95Prof.Dr.R.R.Deshpande
Prof.Dr.R.R.Deshpande
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