Homesleeping healthBsc Nursing NotesNecrosis, Inflammation, Thrombosis, Embolism- BSc Pathophysiology Nursing Notes

Necrosis, Inflammation, Thrombosis, Embolism- BSc Pathophysiology Nursing Notes

BSc Pathophysiology Nursing Notes of unit I on necrosis, Inflammation, Thrombosis


  • Morphologic changes that follow cell death in a living tissue or organ
  • Defined as a localized area of death of tissue followed by degradation of tissue  by hydrolytic enzymes liberated by dead cells
  • Necrotic cells cannot maintain membrane integrity and their contents often leak out.
  • The enzymes responsible for the digestion of the cells are from lysosomes of dying cells or lysosomes of leukocytes as part of the inflammatory reaction
  • Cell digestion by lytic enzymes
  • Denaturation of protein in the cell

Morphologic alternation during the necrosis

Morphologic alternation

  • Cytoplasmic changes- causing increased eosinophilia
  • Nuclear changes- pyknosis/karyolysis/karyorrhexis
  • Fragmentation and dissolution
  • Discontinuity-Breakdown of the plasma membrane and organellar membranes
  • Myelin figures- dead cells replaced by large phospholipid masses
  • Leakage- Leakage and enzymatic digestion of cellular contents

Cause of necrosis

  • Hypoxia
  • Chemical and physical agents
  • Microbial agents
  • Immunological injury

Types of Necrosis

  • Coagulative Necrosis
  • Liquefactive Necrosis
  • Caseous Necrosis
  • Fat Necrosis
  • Fibrinoid Necrosis

Coagulative necrosis

  • The most common type and Mostly from sudden cessation of blood flow
  • Due to denaturation of protein
  • Characteristic of infarcts in solid organs
  • This form of necrosis is where component cells are dead but the basic tissue architecture is preserved
  • Commonly occurs in the heart, kidneys, spleen
  • Example- Sudden occlusion of blood flow in coronary arteries (myocardial infarction) which leads to necrosis
  • Bacterial and chemical agents can also cause but less often

Liquefactive or colliquative Necrosis

  • Occurs due to degradation of tissue by the action of hydrolytic enzymes
  • Whatever the pathogenesis, completely digests the dead cells resulting in the transformation of tissue into a liquid viscous mass

Causes of Liquefactive necrosis

  • ischemic injury and bacterial or fungal infections
  • Example- infracted brain, abscess cavity in gums

Caseous Necrosis

  • The term “caseous” means cheese-like
  • Derived from the friable yellow-white appearance of the area of necrosis
  • The tissue is cheesy white in appearance
  • Example- Tuberculous infections

Fat Necrosis

  • Refers to focal areas of fat destruction
  • Presence of shadowy outlines of necrotic cells
  • Seen in the pancreas, breast
  • Example- acute pancreatitis necrosis, traumatic fat necrosis

Fibrinoid necrosis

  • Characterized by deposition of fibrin-like material in necrosed areas
  • Example- autoimmune diseases, vasculitis


  • Derived from Latin “Inflammare”
  • This means burn and swelling
  • Defined as the local response of living tissues to an injury
  • It is a body defense mechanism which eliminates or limits the spread of injurious agents in the body

Why Inflammation?

The purpose is to

  • To dilute, localize, and destroy the injurious agent
  • To limit tissue injury
  • To restore the tissue to normal

Causes of Inflammation

  • Physical agents
  •  such as heat, cold, radiation, trauma
  • Chemical agents
  • such as acids, alkalis, poisons
  • Infective agents
  • such as virus, bacteria, toxins
  • Immunological agents
  • such as antigen-antibody reactions

Types of Inflammation

  • Acute Inflammation
  • Chronic Inflammation

Acute inflammation

  • It is of short duration represents the early body reaction and is usually followed by repair
  • Occurs  vascular and cellular events, Migration, and Pavements

vascular events- chemotaxis

cellular events

  • During cellular events, it occurs by leukocytosis and phagocytosis.
  • Neutrophils are the act of first line of body defense, followed by monocytes and macrophages.
  • When blood flow slows down leukocytes are pushed to periphery (margination and pavementing)
  • Pro-inflammatory cytokines released by macrophages and mast cells causes endothelial cells and leukocytes to express adhesion molecules (selectins and sialyl lewis x proteins). These slows leukocytes and tumble along endothelium (rolling) and adhere with endothelial cells
  • Transmigration of adherent leukocytes through endothelial gaps to extravascular space (Diapedesis)
  • Once the extravascular space, leukocytes migrate towards the site of infection (chemotaxis)
  • It is induced by chemokines produced by mast cells, complement proteins such as leukotriene B4, platelet factor 4, etc
  • Neutrophils remain site of infection for 6- 24hrs followed by monocytes (24-48 hrs)
  • Then leukocytes recognize dead cells or microbes and kill them (phagocytosis)

Signs of inflammation

  • Dolor
  • Calor
  • Rubor
  • Tumor
  • Functio laesa

Signs of inflammation

5 cardinal signs

  • Rubor- Redness caused by vasodilatation
  • Tumor- Swelling due to extra-vascular accumulation of fluid
  • Calor- Heat caused by increased blood flow
  • Dolor- Pain due to high pressure by accumulation of fluid/chemical mediators
  • Functio laesa- Loss of function (swelling and pain)

Consequences of Acute inflammation

  • Resolution- return to normal following acute inflammation
  • Healing by scarring- when tissue is destroyed, healing occurs by fibrosis
  • Suppuration- collection of pus
  • Chronic inflammation- when acute inflammation persist, it may progress to chronic inflammation

Chronic inflammation

  • It is an inflammation of prolonged duration (weeks/months/years) in which active inflammation, tissue injury and healing proceed simultaneously

Causes of Chronic Inflammation

  • Following acute inflammation e.g. oesteomyelitis, pneumonia
  • Recurrent attacks of acute inflammation e.g, recurrent UTI leads to pyelonephritis

Clinical features of Chronic inflammation

  • Mononuclear cell infiltration- macrophages, lymphocytes
  • Tissues destruction- induced by inflammatory cells
  • Proliferative change- repair (angiogenesis and fibrosis)

Types of Chronic Inflammation

  • Chronic nonspecific inflammation
  • Chronic granulomatous inflammation
  • Chronic nonspecific inflammation
  • Characterized by nonspecific inflammatory cell infiltration
  • For example, chronic osteomyelitis

Types of Chronic Inflammation

Chronic granulomatous inflammation

  • Characterized by the formation of granuloma
  • For example, TB, leprosy


  • Process of formation of the thrombus within blood vessels
  • Platelet deposition on the vascular surface is the initial stage of thrombosis
  • Thrombus- solid mass consisting of platelets (thrombocytes) and fibrin in which red and white cells are trapped

Pathogenesis of Thrombosis

Virchow’s triad

Endothelial Injury

  • Causes- ulcerated plaque, vegetation, mural thrombus, smoking, infectious agents, trauma, etc
  • This disrupts the pathway of coagulation

Alternation in normal blood flow-stasis-turbulence

  • Stasis- slowing of the circulation and a major factor for the development of thrombi
  • Turbulence- unstable movement that contributes to arterial and cardiac thrombosis by causing endothelial injury
  • Normal blood flow is laminar

Stasis and turbulence cause

  • Disrupts laminar blood flow and brings platelets in contact with endothelium
  • Prevent dilution by activated clotting factors
  • Retard the inflow of clotting factor inhibitors and permits thrombosis
  • Promote endothelial cell activation resulting in thrombosis

Hypercoagulability of blood

  • Any alteration in the coagulation pathway that predisposes to thrombosis
  • Less contribution
  • Divided into primary and secondary

Hypercoagulability of blood cont.

  • Primary or genetic-inherited causes such as mutation in factor V, Antithrombin III deficiency
  • Secondary or acquired- pathogenesis such as MI, cancer, prolonged bed rest, use of heparin


  • Thrombi are attached to the underlying blood vessels or heart wall at the point of origin
  • Thrombi vary in shape and size of origin, cause, and pathogenesis

Types of Thrombi

  • Based on color and components- platelet thrombus, coagulation thrombus
  • Based on site and mode of formation- occlusive thrombus
  • Based on infection- septic

Effects of thrombi

  • They causes obstruction of arteries and veins
  •  Formation of emboli
  • Example- coronary thrombosis causes MI


  • When the thrombus travels from its site of origin resulting in partial or complete occlusion of a vessel causing smaller passage
  • 90 % emboli arise from thrombi and called thromboemboli


  • It is a detachable intravascular solid, liquid or gaseous mass that is carried by the blood to a site distant from its point of origin

Types of Emboli

  • Thromboemboli (solid)
  • Malignant cell emboli (solid)
  • Ruptured atherosclerotic plaques (solid)
  • Amniotic fluid (liquid)
  • Droplets of fat (liquid)
  •  Parasites (solid)
  • Foreign bodies such as silk, bullets (solid)
  • Air embolism (gas)


  • Lodging of thrombus and emboli in pulmonary circulation  or systematic circulation
  • Site of Origin of thromboembolism

Types of Thromboembolism

  • Pulmonary
  • Systemic
  • Air
  • Amniotic fluid

Pulmonary Thromboembolism

Thrombus and Emboli lodge in Pulmonary Circulation

Systemic Thromboembolism

  • Due to emboli that travel through the arterial circulation

Site of origin

  • Heart- 80 % arises
  • Aorta-20%
  • Unknown origin (10-15%)

Air embolism

  • Air forms as Emboli
  • About 100 ml of air required to obstruct vascular flow
  • Air may enter venous during
  • during delivery or abortion, air is forced into ruptured uterine vein
  • During artificial pneumothorax, hemodialysis,
  •  accidental opening of large veins

Fat embolism

  • Fat globules in the circulation
  • Causes
  • fracture of the shaft of long bone,
  • trauma of fat tissue,
  • burn of adipose tissue

Pathogenesis of Fat Embolism

  • Mechanical obstruction- micro aggregates of fat causes occlusion of pulmonary or cerebral microvasculature
  • Chemical injury- free fatty acids released from globules cause toxic injury to vascular endothelium
  • Thrombocytopenia due to coating of fat globules with platelets
  • Amniotic fluid embolism
  • Occurs during complication of labour and immediate postpartum period
  • occurs due to infusion of amniotic fluid into maternal circulation via a tear in placental membrane and rupture of uterine veins
  • Characterized by sudden sever dysponea, cyanosis, hypertensive shock followed by seizure and coma


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