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Benjamin's Pathology > Pathology (Acute Inflammation) > Flashcards

Pathology (Acute Inflammation) Flashcards

To learn Acute Inflammation Lecture 1

1
Q

How does the body protect itself from injury?

A

Neural Reflexes Flight or fight reflexes Skin barrier Enzymes in tears/saliva Acid in stomach Bacteria in gut Mucous and cilia in airways Macrophages in alveoli

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2
Q

Inflammation

A

Protective response of living vascularised tissues to injury To eradicate cause and consequence of injury Closely linked with repair and healing Variable cell regeneration and or scarring to repair any tissue damage Various patterns Important features: Blood components: Cells: selected white blood cells Proteins Blood vessels and endothelium Numerous chemical mediators Cellular and extra cellular components of connective tissue

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3
Q

Acute inflammation

A

Earliest response Lasts days, sometimes longer Features: neutrophils, oedematous exudate, vasodilation Non specific

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4
Q

Chronic inflammation

A

Later response Lasts weeks/months/years Features: macrophages, lymphocytes, plasma cells, associated fibrosis/scarring Specific or non-specific

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5
Q

Causes of Acute inflammation

A

Certain infections Trauma Burns Infarction

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6
Q

Aims of Acute inflammation

A

Deliver nutrients, defence cells Destroy any infective agents Remove debris

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7
Q

3 Features of Acute inflammation

A

Vascular response Exudate Variable tissue necrosis

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8
Q

Steps of Vascular and Cellular responses of Acute inflammation

A

Dilation of BV –> increase blood flow –> blood flow slows Vessels become permeable –>passage of water, salts and small proteins from plasma into the damaged area (Exudate) Circulating neutrophils are attracted to damaged area and ahere to swollen endothelial cells (Margination) and migrate through BM (emigration) into damaged area Later, macrophages and lymphocytes migrate to damaged area.

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9
Q

Definition: Exudate

A

Protein rich fluid and cells that have escaped from blood vessels due to an increase in vascular permeability e.g. in inflammation

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10
Q

Definition: Transudate

A

Extravascular fluid that results from increased hydrostatic pressure or diminished colloid oncotic pressure in the blood vessel. (not inflammation)

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11
Q

Composition of Acute inflammatory exudate

A

Fluid (nutrients, mediators, immunoglobulins) Fibrin (Prevents micro-organism movement, produces scaffold for movement of neutrophils and macrophages) Many neutrophils Few Macrophages Few lymphocytes

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12
Q

Why are only a few macrophages and lymphocytes found in acute inflammation?

A

Because they are primarily involved in chronic inflammation.

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13
Q

Functions of Acute inflammatory exudate

A

Carries proteins, fluid and cells from local blood vessels into the damaged area to mediate local defences The components of the exudate are able to destroy the infective causative agent Break down and remove damaged tissue

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14
Q

Types and production of Chemical mediators of inflammation

A

Produced locally by cells at the site of inflammation, or they may be circulating in the plasma as inactive precursors which can be activated at the site of inflammation. Cell derived Plasma Derived

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15
Q

Cell-derived mediators

A

Circulating neutrophils, monocytes, platelets and tissue mast cells, macrophages and endothelial cells at the site of injured tissue are all cellular sources of inflammatory mediators. Arachidonic acid metabolite Vasoactive amines Derived from abnormal production of normal vascular function regulators Cytokines

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16
Q

Plasma-derived mediators

A

Short lived –> intrinsic mechanisms to turn off response and allow resolution Circulating proteins of 3 interrelated systems - complement, kinin and coagulation

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17
Q

Neutrophils

A

Produced by maturation of precursor cells in bone marrow Most numerous white cells in blood Short life span Motile and move easily from vessels to tissues Chemical mediators attract them Bacteria = ^^^ neutrophil Phagocytotic and destroys bacteria Release free radicals Enzymes released on death that destroys extracellular matrix.

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17
Q

How do neutrophils get into tissues?

A

Aggregate and move along endothelium (margination) Into tissues via diapedes Attracted to damaged area (chemotaxis)

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18
Q

What is Neutrophilia?

A

Increased concentration of neutrophils in the blood. Increased amount released and increased production in bone marrow

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19
Q

Macrophages

A

Derived from blood monocytes Longer lived then neutrophils Pagocytic Assist in repair Important in chronic inflammation and immunity.

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20
Q

The four signs of Acute inflammation

A

Redness Heat Pain Swelling

21
Q

Redness caused by?

A

Vessel dilatation and increased blood flow

22
Q

Heat caused by?

A

Vessel dilatation and increased blood flow

23
Q

Pain caused by?

A

Pressure effects on nerve endings and chemical factors

24
Q

Swelling caused by?

A

Due to accumulation of exudate

25
Q

Three types of Acute inflammation

A

Purulent Fibrinous Serous

26
Q

Purulent Acute inflammation

A

Pus Neutrophils Necrotic cells Oedema Abscesses

27
Q

Fibrinous Acute inflammation

A

More severe injuries = greater vascular permeability and vessels are permeable to fibrin

28
Q

Serous Acute inflammation

A

Outpouring of thin fluid e.g. blisters

29
Q

Purulent (Suppurative) inflammation - Complications

A

Abscess Caused by pyogenic bacteria Localised area of tissue necrosis with live and dead neutrophils May become walled off by fibrosis/scar tissue to become chronic

30
Q

Acute inflammation - body responses

A

Fever Malaise Decreased appetite Increased acute phase proteins Increased pulse rate Leukocytosis (High neutrophils in acute, high monocytes in viral)

31
Q

Fever 3 stages

A

Release of exogenous pyrogens from bacteria, viruses or injured cells stimulate production of endogenous pyrogens and interferons Endogenous pyrogens stimulate prostaglandin synthesis within the vascular and perivascular cells of the hypothalamus These prostaglandins stimulate production of neutrotransmitters to reset body temperature at a high level (shivering)

32
Q

Lymphatics roles in inflammation

A

Lymph flow is increased to help drain oedema fluid from the extravascular space Lymph also drains WBCs and cell debris In severe inflammatory reactions the lymphatics will tranport the bacteria and the lymphatics may become inflamed as well as the draining lymph nodes.

33
Q

Outcomes of Acute inflammation

A

Resolution Variable regeneration and organization (repair) Chronic inflammation Depends on tissue type, extent of damage and type and duration of injury.

34
Q

What is resolution?

A

Return of the structure of damaged tissue to normal In situations where tissue damage is minimal and any dead cells can be replaced by cells of the same type Phagocytes clear fluid, leukocytes and dead tissue and fluid and proteins are removed by lymphatic drainage.

35
Q

What is repair/healing?

A

Variable cell replication and organization Organization: Formation of a scar Scar is formed by an intermediary tissue: Granulation tissue

36
Q

What is Granulation tissue composed of?

A

Macrophages Small vessel proliferation Lymphocytes Fibroblasts

37
Q

Cell-derived mediators (Histamine) Source and Actions

A

Mass cells, basophils, platelets Vasodilation, increased vascular permeability, endothelial activation

38
Q

Cell-derived mediators (Serotonin) Source and Actions

A

Platelets Vasodilation, increased vascular permeability

39
Q

Cell-derived mediators (Prostaglandins) Source and Actions

A

Mast cells, leukocytes Vasodilation, pain, fever

40
Q

Cell-derived mediators (Leukotrienes) Source and Actions

A

Mast cells, leukocytes Increased vascular permeability, chemotaxis, leukocyte adhesion and activation

41
Q

Cell-derived mediators (Platelet activating factor) Source and Actions

A

Leukocytes, mast cells Vasodilation, increased vascular permeability, leukocyte adhesion, chemotaxis, degranulation, oxidative burst

42
Q

Cell-derived mediators (ROS) Source and Actions

A

Leukocytes Killing of microbes, tissue damage

43
Q

Cell-derived mediators (Nitric Oxide) Source and Actions

A

Endothelium, macrophages Vascular smooth muscle relaxation, killing of microbes

44
Q

Cell-derived mediators (Cytokines IL - 1, TNF) Source and Actions

A

Macrophages, endothelial cells, mast cells Local endothelial activation, fever, pain, anorexia, hypotension, shock

45
Q

Demolition

A
46
Q

Repair

A
47
Q

Heart Acute Inflammation

A
48
Q

Lung Acute Inflammation

A
49
Q

Margination of neutrophils: Label following:

A

A: RBC

B: Endothelium

C: Neutrophil

50
Q
A

Benjamin's Pathology (10 decks)

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