Cellular Injury

1
Cellular Injury Ageing

• Disease
• Dis Ease Disease.
• Discomfort due to Structural or functional
  abnormality
• Disease is caused by an agent.
• Causes (etiology) can be
• External / Environmental. E.g.. Heat, Bacteria.
• Internal E.g. stress, genes, ageing.

2
Cellular Injury Adaptation

• Normal cell is in a steady state Homeostasis
• Change in Homeostasis due to stimuli - Injury
• Injury - Reversible / Irreversible
• Adaptation / cell death

3
Response to Injury

• Adaptations (reversible)
• Hydropic degeneration
• Hypertrophy
• Hyperplasia
• Atrophy
• Accumulations - hyaline, fat, etc.
• Necrosis (irreversible) cell death.

4
Terminology

• Necrosis Morphologic changes seen in dead cells
  within living tissue.
• Autolysis Dissolution of dead cells by the cells
  own digestive enzymes. (not seen)
• Apoptosis Programmed cell death. Physiological,
  for cell regulation.

5
Types of Necrosis

• Coagulative Eg. Infarction
• Liquifactive - Brain, abscess
• Caseous - Bacterial / Tuberculosis
• Gangrene - With infection

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Sequels of Necrosis

• Cell Death
• Necrosis
• Autolysis
• Phagocytosis
• Organization fibrous repair.

7
Ageing

• Progressive time related loss of structural and
  functional capacity of cells leading to death
• Senescence, Senility, Senile changes.
• Ageing of a person is intimately related to
  cellular ageing.

8
Factors affecting Ageing

• Genetic Clock genes, (fibroblasts)
• Diet malnutrition, obesity etc.
• Social conditions -
• Diseases Atherosclerosis, diabetes etc.
• Werners syndrome.

9
Cellular mechanisms of ageing

• Cross linking proteins DNA.
• Accumulation of toxic by-products.
• Ageing genes.
• Loss of repair mechanism.
• Free radicle injury
• Telomerase shortening.

10
Telomerase in ageing
Germ Cells Somatic Cells
11
Ageing changes

• Gradual atrophy of tissues and organs.
• Dementia
• Loss of skin elasticity
• Greying and Loss of hair
• BV damage atherosclerosis/bruising.
• Loss of Lens elasticity ? opacity ? vision
• Lipofuscin pigment deposition Brown atrophy in
  vital organs.

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Pathology of elderly
13
Factors affecting ageing

• Stress
• Infections
• Diseases
• Malnutrition
• Accidents

• Diminished stress response.
• Diminished immune response.
• Good health.

14
Conclusions

• Cellular Injury - Various causes
• Reversible Injury ? Adaptations
• Hypertrophy, Hyperplasia, Atrophy
• Accumulations - Hydropic, hyaline, fat..
• Irreversible Injury - Necrosis
• Coagulative, Liquifactive, Caseous
• Ageing - Causes, Changes, Factors

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Inflammation

• Inflame to set fire.
• Inflammation is dynamic response of vascularised
  tissue to injury.
• Is a protective response.
• Serves to bring defense healing mechanisms to
  the site of injury.

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Lewis Triple Response

• Flush capillary dilatation.
• Flare arteriolar dilatation.
• Weal exudation, edema.

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Red, Warm Swollen
(Flare, Flush Weal Lewis)
Triple response
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Cardinal Signs of Inflammation

• Rubor Redness Hyperaemia.
• Calor Warm Hyperaemia.
• Dolor Pain Nerve, Chemical med.
• Tumor Swelling Exudation
• Loss of Function

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Inflammation - Mechanism

1. Vaso dilatation
2. Exudation - Edema
3. Emigration of cells
4. Chemotaxis

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Mechanism of Inflammation
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Chemical Mediators

• Chemical substances synthesised or released which
  mediate the changes in inflammation.
• Histamine by mast cells - vasodilatation.
• Prostaglandins Cause pain fever.
• Bradykinin - Causes pain.

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Morphologic types

• Acute
• Exudative Inflammation excess fluid. TB lung.
• Suppuration/Purulent Bacterial - neutrophils
• Fibrinous pneumonia fibrin
• Serous excess clear fluid Heart, lung
• Haemorrhagic b.v.damage - anthrax.
• Chronic inflammation with healing.
• Grannulomatous clusters of epitheloid cells
  eg. TB, Fungus, Foreign body.

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Inflammation Outcome
Fungus Virus Cancers T.B. etc.
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Acute Vs Chronic

• Flush, Flare Weal
• Acute inflammatory cells - Neutrophils
• Vascular damage
• More exudation
• Little or no fibrosis

• Little signs - Fibrosis,
• Chronic inflammatory cells Lymphocytes
• Neo-vascularisation
• No/less exudation
• Prominent fibrosis

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Stages of Healing

• Hemorrhage
• Inflammation
• Granulation tissue (soft callus)
• Scar Fibrosis (hard callus)
• Remodeling Wound strength

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Repair

• Regeneration of injured tissue by parenchymal
  cells of the same type
• Replacement by connective tissue
• In other words
• Regeneration
• Scar

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Proliferative Potential

• Labile cells - continuously dividing
• Epidermis, mucosal epithelium, GI tract
  epithelium etc
• Stable cells - low level of replication
• Hepatocytes, renal tubular epithelium, pancreatic
  acini
• Permanent cells - never divide
• Nerve cells, cardiac myocytes, skeletal mm

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Polypeptide growth factors

• Most Important Mediators affecting Cell Growth
• Present in serum or produced locally
• Exert pleiotropic effects proliferation, cell
  migration, differentiation, tissue remodeling
• Regulate growth of cells by controlling
  expression of genes that regulate cell
  proliferation

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Repair by connective tissue

• Occurs when repair by parenchymal regeneration
  alone cannot be accomplished
• Involves production of Granulation Tissue
• replacement of parenchymal cells with
  proliferating fibroblasts and vascular
  endothelial cells

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Components of the processof fibrosis

• Angiogenesis - New vessels budding from old
• Fibrosis, consisting of emigration and
  proliferation of fibroblasts and deposition of
  ECM
• Scar remodeling, tightly regulated by proteases
  and protease inhibitors

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Wound healing

• Induction of acute inflammatory response by an
  initial injury
• Parenchymal cell regeneration
• Migration and proliferation of parenchymal and
  connective tissue cells

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Wound healing (contd)

• Synthesis of ECM proteins
• Remodeling of parenchymal elements to restore
  tissue function
• Remodeling of connective tissue to achieve wound
  strength

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Healing byFirst IntentionFocal Disruption of
Basement Membrane and loss of only a few
epithelial cellse.g. Surgical Incision
35
Healing by Second IntentionLarger injury,
abscess, infarctionProcess is similar
butResults in much larger Scar and then
CONTRACTION
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Wound Strength

• After sutures are removed at one week, wound
  strength is only 10 of unwounded skin (Walker
  Law)
• By 3-4 months, wound strength is about 80 of
  unwounded skin (Walkers Law)

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Factors affecting Healing

• Systemic
• Age
• Nutrition
• Vitamin def.
• Immune status
• Other diseases

• Local
• Infection
• Size or extent.
• apposition
• Blood supply
• Mobility
• Foreign body

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Summary

• Healing Proliferation Differentiation.
• Labile, Stabe Permanent cells
• Stages of Healing 1-2-3-4.
• Healing by First or Second intention.
• Skin wound healing - bone healing.
• Factors affecting healing Local / Systemic

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Circulatory disorders

• BV - Narrowing, rupture, aneurism.
• Thrombosis
• Embolism
• Venous congestion
• Edema
• Shock

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Thrombosis

• Intravascular coagulation
• Vessel damage - atheroma, toxins
• Blood changes - stasis, coagulation factors
• Types White, Red Mixed.
• Sites
• Arterial Brain, Heart, limbs, eys.
• Venous Leg
• Capillary DIC in septicemia

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Embolism

• Abnormal solid mass carried in blood.
• Source destination
• Types.
• Thromboembolism - atherosclerosis
• Fat - Fractures
• Tumor - cancers
• Gas Caisson disease
• Liquid Amniotic fluid in new born.
• Rapid onset of infarction vs. Thrombosis

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Sequels of Block

• Collateral circulation
• Ischemia,
• Infarction, Gangrene
• Haemorrhage

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Common Sites of B.V block
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Edema Shock.!
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Normal Microcirculation
Capillary Arterial
Venous Hydrostatic Pressure 36 16 Oncotic
Pressure - 26 - 26 Net filtration Pressure
10 mmHg - 9 mm Hg (leak-out) (Reabsorb)
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Edema

• Increased interstitial fluid volume
• Two major types
• Local - inflammation
• Generalised - anasarca - Systemic causes.

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Edema mechanism

• Leaky vessels inflammation.
• Increased capillary hydrostatic pressure
• Venous obstructions
• Cardiac failure
• Decreased Osmotic pressure
• Hypoproteinemia liver disease, anemia.
• Lymphatic obstruction
• Elephantiasis

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Shock

• Depressed vital functions due to decreased
  circulating blood volume
• Types
• Hypovolaemic - true/vasovagal
• Cardiogenic Heart failure, MI.
• Obstructive Pulm embolism.
• Anaphylactic vasodilation due to allergy.
• Septic capillary damage by infection.

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Shock Featurs

• Hypotension
• Tachycardia
• Cold clammy skin
• Rapid shallow respiration.
• Drowsiness, confusion, irritability
• Multi organ failure.

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Shock Mechanisms

• Compensatory mechanisms
• Adrenaline ? cold, clammy skin
• Complications Ischemic damage.

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Shock Management

• Position, clothing vital organs.!
• Airway
• Stimulants ammonia inhalation.
• Fluids, electrolytes, Blood pressure
• Treat the cause.

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Disorders of Growth

• Understand Growth disorders.
• Difference between Neoplastic Non neoplastic
  growths.
• Classification of growth disorders.
• Characters of tumors Biology of tumors
• Diagnosis management of tumors. (Basic)

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New Cancer Statistics USA 1996
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Introduction

• Inflammatory, Degenerative Neoplastic
• Tumor Swelling / new growth / mass
• Two types of growth disorders
• Non-Neoplastic
• Secondary / adaptation due to other cause.
• Neoplastic.
• Primary growth abnormality.

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Non-Neoplastic Proliferation

• Controlled Reversible
• Hypertrophy Size
• Hyperplasia Number
• Metaplasia Change
• Dysplasia Disordered

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Neoplastic Proliferation

• Uncontrolled Irreversible
• Benign
• Localized, non-invasive.
• Malignant (Cancer)
• Spreading, Invasive.

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Pathogenesis Smoke - Lung Dis.
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Normal Adaptation Benign
Malignant
Mechanism of Growth Disorders
Polyclonal Monoclonal
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Nomenclature

• Cell of origin Suffix
• (Oma, Carcinoma Sarcoma)
• Fibroma - Fibrosarcoma
• Osteoma - Osteosarcoma
• Adenoma - Adencarcinoma
• Papilloma - Squamous cell carcinoma
• Chondroma Chondrosarcoma

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Diagnosis

• History of Clinical examination
• Radiographic analysis X-Ray, US, CT, MRI
• Laboratory analysis Tumor markers
• Cytology Pap smear, FNAB
• Biopsy - Histopathology, markers.
• Autopsy Research, learning teaching

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Biology of Tumor

• Grading Differentiation
• Staging Progression

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TNM Staging of tumor
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TNM Staging of tumor

• T1N1M0 Means primary tumor is within the organ
  but cancer cells have spread to local lymphnodes,
  there is no metastasis.
• T3N0Mo - Means tumor has spread beyond primary
  organ but has not spread to lymphnodes or other
  sites.

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Immune Disorders

• Humoral Immunity
• B lymphocytes - Antibody
• Cell mediated Immunity
• T lymphocytes Macrophages
• Non-Specific immunity
• Neutrophils, Macrophages

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Introduction

• Immunity is not inherited.
• Antigen / Antibody
• Active / Passive immunity.
• Vaccine, Toxoid, Live/Killed
• Primary response slow, weak.
• Learning period, memory cells.
• Secondary response rapid, strong

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Immune Disorders

• Immunodeficiency disorders
• AIDS, antibody deficiency
• Hypersensitivity Disorders (allergy)
• Type-I (IgE), II-IgG, III-Immunecomplex, IV-Cell
  mediated.
• Autoimmune disorders
• SLE, Rhematoid, Rheumatic fever.

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Rheumatic fever

• Autoimmune disorder.
• Group A, streptococcal pharyngitis.
• Antibody cross react with connective tissue in -
  susceptible individuals
• 2-3 weeks Autoimmune reaction.
• Inflammation - T lymphocytes, macrophages.
• Heart, skin, brain joints.

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Morphology

• Acute Rheumatic Fever
• Acute Inflammatory Phase
• Heart Pancarditis
• Skin Erythema Marginatum
• CNS Sydenham Chorea
• Migratory polyarthritis
• Chronic Rheumatic Fever
• Deforming fibrotic valvular disease.

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What is Asthma?

• Hypersensitivity Allergy , Type I
• of airways of lungs - Bronchi
• Allergens in the air, mast cell - IgE ab.
• Inflammation of airways Bronchitis.
• Genetic, Environmental, Race, Age.
• High in industrial cities 4-19, Fiji lt 1
• Increasing incidence !

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Pathogenesis - Atopic Asthma
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Asthma Mechanism

• Allergy
• Inflammation Of Bronchi
• Obstruction
• Mucous Plugs

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INFLAMMATION
Airflow Limitation
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Asthma - Bronchial morphology

• inflammation
• Eosinophils
• Gland hyperplasia
• Mucous plug in lumen
• Hypertrophy of muscle layer

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Autoimmune Disorders

• Immune response against self antigen resulting in
  Tissue damage.
• Single organ or systemic multi organ.
• Common in females.
• Normally immune system is tolerant to self
  antigens (learns during fetal development).
• Autoimmune disorders result from Defective
  tolerance, cross reacting antibodies or antigenic
  mimicry.

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Immunodeficiency AIDS

• Serious, persistent, unusual, recurrent
  Opportunistic infections.
• Secondary causes more common.
• Antibody deficiency Bacterial inf.
• Cell Mediated imm def. viral / fungal
• AIDS infection by HIV virus destruction of T
  helper cells deficiency of humoral CM
  immunity.

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Introduction

• Specific Immune System
• Humoral
• Cell medicated
• Non-Specific Immune System
• Phagocytes
• Complements
• Single or multiple component deficiency.
• Susceptibility - Opportunistic infections.

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Classification

• Primary Deficiencies (Inherited)
• B cell defects Ig def. Bacterial infections.
• T cell defects T cells. Viral fungal
  infect.
• Combined defects T B
• Secondary Deficiencies (Acquired) T
• Malnutrition Protein
• Immunosuppressive therapy, drugs.
• Infections viral, chronic bacterial, malaria.
• Chronic diseases Diabetes, Malignancy.

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History

• 1979 Increased Kaposi sarcoma and Pneumocystis
  carinii infections in homosexuals noted in
  Africa.
• 1981 First case in California.
• gt 30 million in world 1999 increasing
• 0.01 incidence in Australasia
• 67 in Sub-Saharan Africa!

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Pathogenesis
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HIV
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Retrovirus Replication
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Immune Response to HIV
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Genetic Disorders Congenital Disorders

• Non Genetic
• Developmental defects Malformations
• Genetic Disorders
• Chromosomal
• Gene - Mendelian
• Multifactorial

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Mutations

• Genome whole set Polyploidy 4n, 8n etc.
• Chromosomal change in chromosome.
• Number Trisomy, monosomy
• Structure Deletion, Translocation etc.
• Gene Submicroscopic.
• Point mutation single base sequence
• Deletions -
• Insertions

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Cell Cycle
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Mitosis
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Meiosis

• Reduction Division (4n-2n)
• Prophase-1(Synapsis, g.rec)
• Metaphase-1
• Anaphase-1
• Telophase-1
• Equatorial Division (2n-n)
• Prophase-2
• Metaphase-2
• Anaphase-2
• Telophase-2

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Cytogenetic Abnormalities

• Abnormal number of chromosomes
• Non-disjunction - Downs Syndrome
• Anaphase lag - Turners xxx
• Abnormal Structure (normal no)
• Deletion of short arm 5q- Cri-du-chat syndrome
• Inversion -
• Translocation - Ph Chromosome - t(922) CML,

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Non-disjunction
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Downs Sy.Trisomy-21
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Downs Syndrome

• Mental retardation
• Neck folds
• Epicanthic folds
• Flat facial profile
• Simian crease
• Hypotonia
• Umbilical hernia
• Leukemia

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Anatomy of Heart
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Circulation
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Coronary Arteries
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Major Disorders of CVS

• Atherosclerosis
• Hypertension
• Myocardial Infarction (MI)
• Stroke
• IHD - Ischemic Heart Disease
• VHD - Valvular Heart Disease
• RHD Rheumatic Heart Disease
• CHD - Congenital Heart Disease

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Atherosclerosis

• Chronic inflammatory disorder of intima of large
  blood vessels characterised by formation of
  fibrofatty plaques called atheroma.
• Hardening of arteries - Arteriosclerosis

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Introduction

• Large elastic arteries Starts in Intima
• Fat deposits, Hardening and destruction.
• Major cause of IHD, MI Stroke.
• Incidence is decreasing since 1995
• Better understanding Change in life style.

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Risk Factors

• Non modifiable
• Age middle to late.
• Sex Males, complications
• Genetic - Hyperchol.
• Family history.

• Potentially Modifiable
• Hyperlipidemia HDL/LDL ratio.
• Hypertension.
• Smoking.
• Diabetes
• Life style, diet, excercise

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Pathogenesis

• Unknown etiology Hyperlipidemia, life style,
  hypertension, smoking, genetic etc.
• Starts with Initial intimal injury,
  inflammation, necrosis, Lipid accumulation,
  Fibrosis - Atheroma.
• Leads to Obstruction or destruction of vessel
• Organ damage due to ischemia.
• Complications - Thrombosis, embolism, aneurism,
  dissection rupture.

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Common Sites

• Aorta, Carotid Iliac. (large vessels)
• Major Vessels - Heart, Brain Kidney.
• Coronary
• Renal
• Abdominal
• Limbs

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Morphology

• Fatty Dots
• Fatty Streaks
• Atheromatous Soft Plaque
• Fibrofatty Hard Plaque
• Complications
• Ulceration, Rupture,Hemorrhage, Thrombosis
• Atheroemboli or cholesterol emboli.

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Complications

• Heart attack Myocardial infarction.
• Stroke Cerebral infarction
• Gangrene tissue infarction.
• Kidney failure Kidney infarction.
• Aneurysms
• Rupture
• Thromboembolism.

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Hyperlipidemia

• Hypercholesterolemia Risk
• Hypertriglyceridemia - less significant
• LDL Increased risk
• HDL lowers the risk Reverse transport
• Mobilises the cholesterol from tissues to liver.

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Good Fats

• Mono unsaturated fats
• Poly unsaturated fats
• Omega-3 fatty acids (Fish)

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Lipoprotiens - LDL HDL

• Good and Bad Fats?
• Lower LDL, Increase HDL
• Mono unsaturated fats
• Poly unsaturated fats
• Omega-3 fatty acids (Fish)
• LDL indicate Positive lipid balance, HDL
  negative.
• No Cholesterol in any vegetable oil?

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Ischaemic Heart Disease

• Common Health problem.
• High Mortality Morbidity.
• Etiology common Atherosclerosis
• Two major types Angina MI.
• Risk factors
• Hypertension
• Hypercholesterolemia
• Diabetes
• Smoking, Life style, Diet, Genetic.

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Patterns of CHD

• Angina Pectoris
• Acute Myocardial Infarction
• Sudden cardiac death

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Pathogenesis

• Obstruction to blood flow.
• Atheroma, Thrombosis Embolism
• Diminished coronary perfusion.
• Ischemia Angina
• Infarction Necrosis
• Inflammation
• Granulation tissue
• Fibrous scarring.

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Myocardial Infarction-MI

• Death of heart tissue due to lack of blood
  supply
• Atherosclerosis is the common cause.
• Coagulative necrosis intact cell shape.
• Severe chest pain, breathlessness sweating
• Complications cardiogenic shock, Death or
  Cardiac failure.

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Gross - Morphology - Micro
Myocardial Infarction-MI

• None
• Edema, inflammation
• Necrosis, granulation
• Granulation tissue
• Dense Fibrosis

• 1-18h none
• 24h Pale, edema
• 3-4D Hemorrhage
• 1-3W Thin, yellow
• 3-6W Tough white

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Complications

• Cardiogenic shock, death
• Arrhythmias and conduction defects,
• Congestive heart failure (pul edema)
• Mural thrombosis, - embolization
• Myocardial wall rupture, tamponade
• Ventricular aneurysm

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Laboratory Diagnosis

• LDH - 1-5 (1 - 2 flip)
• CK- Isoenzymes (Fractions)
• MM - Muscles
• MB - Cardiac muscle.
• BB - Brain
• Troponins

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Management

• Aimed to prevent complications.
• Rest sedation
• Supportive mesures
• Thrombolytic agents - Streptokinase

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HEMATOLOGYRBC DisordersC.B.C

• Haemoglobin - 152.5, 14 2.5 - g/dl
• PCV - 0.47 0.07, 0.42 0.05 - l/l ()
• Haematocrit, effective RBC volume - better
• RBC count - 5.5 1, 4.8 1 x1012/l
• MCHC - Hb/PCV - 30-36 - g/dl
• Hb synthesis within RBC
• MCH - Hb/RBC - 29.5 2.5 pg/l
• Average Hb in RBC
• MCV - PCV/RBC 85 8 - fl

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RBC disorders (Anemias)

• Anemia is decreased red cell mass affecting
  tissue oxygenation
• Low Hb lt13.5 (males), lt11.5 (females)

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RBC disorders

• Decreased Production
• Aplastic, Hypoplastic anemias - drugs
• Deficiency anemias Iron, B12, Folate etc.
• Increased loss/destruction
• Blood loss anemias - parasites, bleeding
• Hemolytic anemias Immune, mechanical, drugs
  toxins.
• Congenital disorders Sickle cell, thalassemia

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Iron Deficiency Anemia

• Most abundant metal, common deficiency..!
• Limited absorption and no excretory mech.
• Recycling of iron dead cells to new cells
• 1mg/day ? 3-6G body ? 1mg/day

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Microcytic Anemia (IDA)
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Iron Metabolism

• 10 of the 10 to 20 mg of dietary iron is
  absorbed each day to balance the 1 to 2 mg daily
  loss.
• Iron is absorbed in Jejunum.
• Stored as Ferritin Hemosiderin.
• Laboratory tests
• Serum iron(1mg/l)
• Serum iron binding capacity (3mg)
• Serum ferritin (gt20ug)

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Causes of Iron deficiency Anemia

1. Chronic Blood loss parasites, ulcers, hernia,
   drugs (NSAID), Carcinoma, colitis, diverticulosis
   etc. Rarely hematuria.
2. Increased need Pregnancy, children
3. Malabsorption gastrectomy, coeliac disease.
4. Poor diet Contributory but rarely the sole
   cause.

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Clinical Features

• Anemia
• Pallor, Weakness, Lethargy
• Breathlessness on exertion
• Palpitations may lead to heart failure - edema
• IDA
• Angular cheilosis, atrophic glossitis,
• dysphagia, koilonychia, gastric atrophy.

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Megaloblastic anemia

• Vitamin B12/Folic acid deficiency
• Low DNA less division more cell size
• Megaloblasts, Abnormal destruction
  pan-cytopenia
• Multi System disease All organs with increased
  cell division.
• Macrocytic anemia, pancytopenia.
• Pernicious anaemia
• autoimmune, Gastric atrophy, VitB12 def.

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Macrocytic Anemia (Meg.)
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Blood Loss anemias

• All have Polychromasia (Marrow response)
• Acute blood loss
• Hemolytic anemias ( Jaundice)
• Immune Auto immune Allo immune
• Mechanical - Valve, DIC
• Hereditary Sickle, Thalassemia
• Infection Clostridia, malaria.

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Hemolytic anemias

• Laboratory evaluation
• Blood smear Morphology very important
• CBC, Bilirubin levels
• Direct and indirect Coombs test (antibody)
• Hemoglobin electrophoresis abnormal Hb.
• Tests for parasites.
• Kidney Liver function tests important

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SHOCK
Introduction
Definition SHOCK is an acute
circulatory failure, characterized by
dysfunction of the microcirculation , inadequate
blood flow to vital organs and inability of
the body cell mass to metabolize the nutrients
normally.
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Different kind of Reason
Inadequate Blood Flow
Metabolic Disturbances
Circulatory Failure

Special Clinical Syndrome
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SHOCK
Etiology and Classification of Shock

• 1. Classification of Shock by Causes
• (1) Hypovolemic shock Hemorrhagic shock
• 
  Traumatic shock
• (2) Cardiogenic shock
• (3) Neurogenic shock
• (4) Anaphylactic shock
• (5) Infectious shock

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2. Classification of Shock according to
hemodynamic changes ?Hypodynamic Shock
Cardiac Output ?,
Vascular Resistace?,
Cold Skin ? Hyperdynamic
Shock Cardiac Output ?,
Vascular Resistace ?,
Worm Skin
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SHOCK
Pathophysiologic process of Shock by severity
? Stage ? Early reversible shock (compensated
shock) ? Stage ? Late reversible shock
(decompensated shock) ? Stage ? Refractory
shock
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SHOCK
Systemic pathophysiologic responces of Shock

• Initial changes of shock
• ? Reduction of blood volume volume and rate
• ? Decrease in myocardial contractility
  infarction
• ? Increased vascular-bed volume

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Systemic pathophysiologic responces of Shock
Redistribution of blood flow

Low blood flow
Skin,fat,skeletal
muscls,kidney,intestines
Heart,brain normal or
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Systemic pathophysiologic responces of Shock
2. Changes of Microcirculation ? Neurogenic
mechanisms carotid, aortic ?sympathetic NS,
BP ?(50mmHg)
? CNS ? Cellular mechanisms Polymorphonuclear
leukocytes, ? Humoral mechanisms ?
Noradrenaline and adrenaline
? Renin and angiotensin
?
Vasopressin (posterior pituitary)
? Histamine and
serotonin
? Kinin
? Neuropeptides

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SHOCK
Systemic pathophysiologic responces of Shock
1. Stage of Vasoconstriction (Ischemic Anoxia)

• Changing in the microcirculation catecholamine
  

• Maintenance of blood pressure, shift of fluid,
  redistribution of
• of blood supply, conservation of sodium and
  water

• Clinical aspects pale, cool limbs, clammy skin,
  
• fast and weak impulse, decreased urine
  output, BP n

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SHOCK
Systemic pathophysiologic responces of Shock
2. Stage of Vasodilation (Stagnant Anoxia)

• Changing in the microcirculation acidosis,
  histamine ,
• endotoxin

• Blood in the liver, intestine, lung ? venous
  return ?
• shift of fluid, blood concentrated BP? no
  urine

• Clinical aspects BP ?, poor heart beat,
  unconscious,
• less to no urine, cynosis

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SHOCK
Systemic pathophysiologic responces of Shock

• 3. Stage of Vasofailure
• DIC
• MOF septa

139
SHOCK
Responses of specific organ systems of shock
1. Disturbance of cell metabolism a.
Hypoxia, anaerobic metabolism ? b.
Disturbance of Na-Ka pump, cell swelling
c. Local acidosis ?
2. Effects on kidneys (shock kidney), oliguria
, hyperkalemia,
acidosis a. Functional renal failure
b. Parenchymal renal failure
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SHOCK
Responses of specific organ systems of shock
5. Effects on Gastrointestinal tract and Liver
peptic ulcer, acidosis and sepsis

6. Effects on brain restless, lassitude and
coma
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Clinical manifestation of shock
Skin system Pale of the
skin,
Cool and wet limbs
Kidney Oliguria
Heart
Weak and Fast Impulse
BP Lung
Rapid and Deep rest
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Monitoring of shock
1.Phsychologic States
General monitoring Heart rate Breathing
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Monitoring of shock
2.Colour and temprature of skin
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Monitoring of shock
3.BP
Systolic Pressure was lower than 12kPa(90mmHg)
4. Urina
Oliguria
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Monitoring of shock
Special monitoring 1.CVP
5-10cmH2O
CVPlt5cmH2O Inadequecy of blood volume
CVPgt12cmH2O Cardiac dysfunction
2.Lung arterial pressure 3.Cardiac
output 4.Blood gas PO2
75-100mmHg
Pco2 40mmHg
PH 7.357.45 5.Coagulation
test
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SHOCK
Treatment of the shock
Fundamental principle

• 1.Emergency care
• 2.Restore of the blood volume
• 3.Correction of the acidosis
• 4.Application of vasoactive drugs

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Treatment of the shock
Pulmonary dysfunction
1.Recognition of ventilatory insufficiency 2.Esta
blishment of airway 3.Oxygenation and ventilation
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Treatment of the shock
Establishment of Airway
150
Treatment of the shock
Other Emergency Care
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Treatment of the shock
Position of Body 30?
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Treatment of the shock
Keep the body worm
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Treatment of the shock
Control the bleeding
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Treatment of the shock
Common Reason 1. Big vascular rupture 2.
Organ rupture 3. Intestinal bleeding 4. Bone
fracture