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PRINCIPLES OF DISEASE > Acute inflammation 2 > Flashcards

Acute inflammation 2 Flashcards

1
Q

Name some anatomical locations and their subsequent name if they were to become inflamed.

A

Meninges - meningitis
Appendix - appendicitis
Lungs - pneumonia
Pleural cavity - pleurisy

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2
Q

Describe neutrophils as “mobile phagocytes”

A

Neutrophils recognise foreign antigen and then move towards it - Chemotaxis.
They adhere to the organism.
The granules that they release possess oxidants and enzymes.
They phagocytose and destroy foreign antigens and then…
Die as a result.

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3
Q

Describe the consequences of neutrophil action.

A

Neutrophils die when their granule contents are released.
They “fall apart” and produce a soup of fluids, PUS.
Might extend into other tissues, progressing the inflammation.

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4
Q

Describe the role of fibrinogen in acute inflammation.

A

Fibrinogen is a coagulation factor (part of the coagulation cascade) - it forms fibrin and clots exudate.
= Localises the inflammatory process.

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5
Q

Describe the role of immunoglobulins in acute inflammation.

A

Immunoglobulins in plasma specific for antigen - humoral immune response.

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6
Q

Describe the collective effects of Mediators of acute inflammation.

A

Vasodilation
Increased permeability
Neutrophil adhesion
Chemotaxis
Itch and pain

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7
Q

Describe the cell surface mediators of acute inflammation.

A

Adhesion molecules appear on endothelial cells
E.g. ICAM<-1 helps neutrophils stick, by P-selectin that interacts with neutrophil surface.

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8
Q

List the mediators of acute inflammation that are released from cells.

A

Histamine
Prostaglandins
Cytokines and Chemokines
Nitric Oxide
Oxygen free radicals
5-hydroxytryptamine

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9
Q

Describe the role of histamine as a mediator of acute inflammation.

A

Histamine is preformed in mast cells beside vessels, platelets, basophils.
Released as a result of local injury; IgE mediated reactions.
Causes vasodilation, increased permeability.
Acts via H1 receptors on endothelial cells.

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10
Q

Describe the role 5-hydroxytryptamine as a mediator of acute inflammation.

A

Preformed in platelets.
Released when platelets degranulate in coagulation
Vasodilation
= Prevention of blood loss.

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11
Q

Describe the role of prostaglandins as mediators of acute inflammation.

A

Many promote histamine effects and inhibit inflammatory cells.
Thromboxane A2 promotes platelet aggregation and vasoconstriction.

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12
Q

Describe the role of cytokines and chemokines as mediators of acute inflammation.

A

Small molecules produced by macrophages, lymphocytes, endothelium in response to inflammatory stimuli.
Pro-inflammatory and anti-inflammatory effects.
Stimulate intracellular pathway are signalling.

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13
Q

Describe the role of Nitric oxide as a mediator of acute inflammation.

A

Smooth muscle relaxation, anti-platelet regulate leukocyte recruitment to inflammatory focus.

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14
Q

Describe the role of oxygen free radicals as mediators of acute inflammation.

A

Released by neutrophils on phagocytosis
Amplify other mediator effects.

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15
Q

List the mediators of acute inflammation that are intracellular signalling molecules.

A

Pattern associated molecular patterns.
Danger associated molecular patterns

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16
Q

Describe the role of pattern associated molecular patterns.

A

Microbial antigen
Genetically hardwired to recognise
Innate and adaptive immunity
Stimulate pattern recognition receptors on cell membranes.
Activate inflammatory response.

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17
Q

Describe the role of danger associated molecular patterns.

A

Substances released in response to stimulus.
Stimulate pattern recognition receptors on cell membranes.
Activate inflammatory response.

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18
Q

Name some intracellular inflammatory pathways.

A

NF-kB (nuclear factor kappa - B) pathway.
MAPK (mitogen-activated protein kinase) pathway
JAK-STAT (Janus kinase -signal transducer and activator to transcription) pathway.
***
All lead to inflammatory cytokine production (nucleus).

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19
Q

Describe the blood-coagulation pathways involved in acute inflammation.

A

Clots fibrinogen in exudate and interacts widely with other systems.

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20
Q

Describe the fibrinolysis process involved in acute inflammation.

A

Breaks down fibrin, helps maintain blood supply.
This happens after the inflammatory process/after formation of the thrombus.

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21
Q

Describe the kinin system involved in acute inflammation.

A

Kinins are kinds of plasma proteins and the most important one is Bradykinin.
Bradykinin (in combination with prostaglandins) sensitizes the nerves, alerting the brain - with pain - that something is wrong at the site.

22
Q

Describe the process of the complement cascade involved in acute inflammation.

A

Complement system ties inflammation with immune system.
Active components stimulate increased permeability, chemotaxis, phagocytosis, cell breakdown.
= acute inflammatory response.

23
Q

List the main outcomes of action by mediators.

A

Have positive and negative effects
= dynamic balance.
Favours and inhibits acute inflammation
Relative to need.

24
Q

Name the IMMEDIATE systemic effects of acute inflammation.

A

Pyrexia
Feel unwell
Neutrophilia

25
Q

Explain “pyrexia” as a systemic effect of acute inflammation.

A

Pyrexia = raised temperature.
Endogenous pyrogens from white cells act centrally.
(act in the brain, causes increase in temperature of brain stem, causes “ill feeling”)

26
Q

Explain “feeling unwell” as a systemic effect of acute inflammation.

A

Malaise, anorexia, nausea.
Abdominal pain and vomiting in children.

27
Q

Explain “neutrophilia” as a systemic effect of acute inflammation.

A

Neutrophilia = raised WBC count.
Released from bone marrow.
Detected in peripheral blood - indicates an ongoing response

28
Q

Name some LONGER TERM systemic effects of acute inflammation.

A

Lymphadenopathy
Weight loss

29
Q

Explain “lymphadenopathy” as a systemic effect of acute inflammation.

A

Lymphadenopathy = regional lymph node enlargement.
This is an immune response.

30
Q

Explain weight loss as a systemic effect of acute inflammation.

A

Catabolic anaemia, acute inflammation also uses energy .

31
Q

Define “suppuration”.

A

Suppuration is a potential outcome of acute inflammation.
Means PUS formation.

32
Q

Describe - in outline - the process of suppuration.

A

Pus formation
Pyogenic membrane surrounds pus
Collection of pus (abscess).

33
Q

Explain the formation of pus in suppuration.

A

The pus is composed of dead tissue, organisms, exudate, neutrophils, fibrin, red cells and debris.

34
Q

Explain the pyogenic membrane involved in suppuration.

A

Pyogenic membrane surrounds the pus, this membrane is where capillaries can then start to sprout and allow capillaries to grow in.
The membrane holds neutrophils.
Fibroblast cells ‘wall off the pus’ and hold it in one place.

35
Q

Explain the process of localisation of pus.

A

This is where pus collects under pressure.
Creating a single locule or multiloculated abscess.
The abscess comes to a point and discharges.
It then collapses after discharge allowing for healing and repair.

36
Q

Describe the process of suppuration in a single locule abscess.

A

Ingrowth of granulation tissue occurs, there is discharge of pus.

37
Q

Describe the process of suppuration in a multiloculated abscess.

A

Pus bursts through the pyogenic membrane and forms new cavities.

38
Q

Define an “empyema”.

A

Empyema’s occur in a hollow viscus
-e.g. gall bladder, pleural cavity

39
Q

Define a “pyaemia”.

A

This is where an abscess discharges to the blood stream.

40
Q

Describe organisation as an outcome of acute inflammation.

A

Granulation tissue is central to organisation.
Results in healing and repair.
Leads to fibrosis and formation of a scar.

41
Q

Describe “granulation tissue”.

A

Granulation is essentially a universal patch - repair kit - for all damaged formed.
It is accompanied by:
Angiogenesis
Fibroblasts and collagen
Macrophages

42
Q

Describe dissemination as an outcome of acute inflammation.

A

“SEPSIS”.
Usually has microbial cause
Where infection has spread to blood stream - patient “septic”

43
Q

Define “bacteraemia”.

A

Bacteria in blood

44
Q

Define “septicaemia”.

A

Growth of bacteria in blood.

45
Q

Define “toxaemia”.

A

Toxic products in blood.
= sick

46
Q

Define “SEPSIS”.

A

Life threatening organ dysfunction caused by a dysregulated (no longer local= systematised) host response to infection.

Characterised by increasing organ dysfunction.

47
Q

Describe septic shock.

A

A subset of sepsis.
Profound circulatory, cellular and metabolic abnormalities.
Greater risk of mortality than sepsis alone.

48
Q

Describe the clinical picture of sepsis.

A

Peripheral vasodilation
Tachycardia
Hypotension
Often pyrexia
Sometimes haemorrhagic skin rash

49
Q

Describe the pathogenesis of septic shock.

A

Systemic release of chemical mediators from cells to plasma.
Mediators cause vasodilation causing loss of systemic vascular resistance.
Results in catecholamine release.
- Tachycardia (increased heart rate), follows to maintain cardiac output (CO=SV x HR)
Bacterial endotoxin released.
- interleukin-1 acts on hypothalamus - pyrexia.
Activation of coagulation - disseminated intravascular coagulation and vasodilation (vasoactive chemical) = haemorrhagic skin rash.

50
Q

Describe the outcome of septic shock IF, the compensation (by tachycardia) failed.

A

If the raised heart rate was insufficient to maintain cardiac output,
The SVR (systemic vascular resistance) is low, so blood pressure falls.
This ultimately leads to refused perfusion of tissues = tissue hypoxia and loss of cell, tissue and organ function.
= systemic collapse.

51
Q

Describe the outcome of septic shock.

A

Rapidly fatal.
Tissue hypoxia - cell death.
Haemorrhage
Requires urgent intervention and support
- awareness and early recognition
- ability of young people to compensate
- admit to hospital and intensive care.

PRINCIPLES OF DISEASE (44 decks)

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