Rog Nidan –Basic Pathology Part 2 - PPT
By Prof. Dr. R. R. Deshpande
• 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
• Contents of PPT are – Inflammation & Healing Topics are explained in detail .Details are as follows – Definition of Inflammation, Injurious agents, Signs of Inflammation, Types of Inflammation, Vascular & Cellular changes in Acute Inflammation, What is Emigration, Diapedesis , Chemotaxis, Phagocytosis , Chemical mediators of Acute Inflammation, Which are Inflammatory cells, Inflammatory response, Morphology of Infection, Systemic effects of Acute Inflammation, Fate of Acute Inflammation, Causes of Chronic Inflammation, Features of chronic inflammation, Three phages of Healing, What is Primary Union & Secondary Union, Complications of wound healing .
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13. 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)
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14. 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
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16. 2) Cellular Events
• a) Exudation of leucocytes –
• The polymorphonuclear neutrophils (PMNs)
comprise the 1st line of defense, followed by
monocytes and macrophages.
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31. 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.
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34. 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.
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36. I) Mediators released by cells of injured tissue
• 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
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40. 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
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42. The inflammatory Cells
• 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.
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43. The inflammatory Cells
• 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.
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44. The inflammatory Cells
• 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.
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45. The inflammatory Cells
• 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.
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46. The inflammatory Cells
• 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)
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63. Fate of Acute 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)
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64. Fate of Acute Inflammation
• iii) Suppuration ---
• When pyogenic bacteria are the cause of
acute inflammation, they results in severe
necrosis ,which then leads to suppuration.
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65. Fate of Acute Inflammation
• iv) Chronic Inflammation –
• If the stimuli persist then the inflammation
turns into the chronic form
• The chronic inflammation takes place in
tubercular reaction
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77. Healing
• 1) Regeneration –
• The original tissue healing and restoration
when occurs with the parenchymal cells then
the process is called as Regeneration.
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81. 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.
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82. 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
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94. 10 unions take place as follows
• 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.
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